SAMJ Vol 106, No 6 (2016) by HMPG

JUNE 2016

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EDITORIAL Response to the Central Drug Authority’s position statement on cannabis CME Adolescent health (part 1) IN PRACTICE Antibiotic stewardship and respiratory infections Heavy alcohol use in patients on HAART Central Drug Authority: Position statement on cannabis CASE REPORT Right ventricular outflow tract aneurysms and endomyocardial fibrosis RESEARCH Where have all the gun deaths gone? Screening for retinopathy of prematurity Changing Kaposi’s sarcoma presentation with HAART

AN IDEAL

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Adding Apidra® to Lantus® helps patients to regain their glycaemic control1- 4

1. Apidra® EU Summary of Product Characteristics – December 2013 2. Lankisch MR, et al. Diabetes Obes Metab 2008;10:1178–85. 3. Bergenstal RM, et al. Diabetes 2008; 31:1305–10. 4. Schreiber SA, et al. Diabetes Stoffw Herz 2011;20:69-77 S C H E D U L I N G S TAT U S : S 3 P RO P R I E TA RY N A M E A N D D O S AG E F O R M: A P I D R A ® (s olu t ion for injec t ion). COMP OSITION: 1 ml cont ains 3,5 mg insulin glulisine, corresponding to 10 0 U human insulin, 3.15 mg of the preser vative met acresol and 0.01 mg of st abilising agent polysorbate 2 0. REGISTR ATION NUMBER: A 3 8 / 21.1/0 5 0 6. N A ME A ND BUSINE S S A DDRE S S OF THE HOLDER OF THE CERTIFICATE OF REGISTR ATION: sanofi-aventis south africa ( pt y) ltd, 2 B ond S treet, Midrand, 16 8 5. Tel: 011 25 6 370 0. Reg. No. 19 9 6 /10 3 81/07. ZA.GLU.11-05-15

JUNE 2016

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GUEST EDITORIAL

Health financing lessons from Thailand for South Africa on the path towards universal health coverage M Blecher, A Pillay, W Patcharanarumol, W Panichkriangkrai, V Tangcharoensathien, Y Teerawattananon, S Pannarunothai, J Davén

EDITOR’S CHOICE

CORRESPONDENCE

Essential skills for rural surgery R F Ingle

Medical malpractice crisis deepens: New approach C Archer

Quality of life in patients with seborrhoeic dermatitis in KwaZulu-Natal, South Africa N Moodley, K Hoosen, N C Dlova

IZINDABA

12 16 16

Quality of care responsible for soaring maternal deaths – report Occupational injuries – radiologists lose patience, sue government Newer drugs keep multiple sclerosis patients out of wheelchairs – expert

EDITORIALS

Gun control saves lives R Matzopoulos

Comment on the Central Drug Authority’s position statement on cannabis K Scott

ACTING EDITOR Bridget Farham, BSc (Hons), PhD, MB ChB EDITORS EMERITUS Daniel J Ncayiyana, MD (Groningen), FACOG, MD (Hon), FCM (Hon) JP de V van Niekerk, MD, FRCR ASSOCIATE EDITORS Q Abdool Karim, A Dhai, N Khumalo, R C Pattinson, A Rothberg, A A Stulting, J Surka, B Taylor, M Blockman HMPG CEO AND PUBLISHER Hannah Kikaya | Email: hannahk@hmpg.co.za MANAGING EDITORS Ingrid Nye Claudia Naidu TECHNICAL EDITORS Emma Buchanan Paula van der Bijl NEWS EDITOR Chris Bateman | Email: chrisb@hmpg.co.za PRODUCTION MANAGER Emma Jane Couzens

CME 22

GUEST EDITORIAL Mental health of and substance use by adolescents Q Abdool Karim

ARTICLES Update on adolescent mental health S Paruk, E Karim

Addressing adolescent alcohol use in South Africa N K Morojele, L Ramsoomar

DTP AND DESIGN Carl Sampson HEAD OF SALES AND MARKETING Diane Smith | Tel. 012 481 2069 Email: dianes@hmpg.co.za JOURNAL ADVERTISING Charles William Duke Benru de Jager Reneé van der Ryst Ladine van Heerden Azad Yusuf ONLINE SUPPORT Gertrude Fani FINANCE Tshepiso Mokoena

IN PRACTICE 30

CLINICAL PRACTICE The role of appropriate diagnostic testing in acute respiratory tract infections: An antibiotic stewardship strategy to minimise diagnostic uncertainty in primary care A J Brink, J van Wyk, V M Moodley, C Corcoran, P Ekermans, L Nutt, T Boyles, O Perovic, C Feldman, G A Richards, M Mendelson

CLINICAL ALERT Emergence of vancomycin-resistant Enterococcus at a tertiary paediatric hospital in South Africa H Lochan, C Moodley, D Rip, C Bamford, M Hendricks, A Davidson, B Eley

Heavy alcohol use in patients on highly active antiretroviral therapy: What responses are needed? C D Parry, C Kekwaletswe, P A Shuper, S Nkosi, B J Myers, N K Morojele

POSITION STATEMENT Position statement on cannabis D J Stein, for the Executive Committee of the Central Drug Authority

HEALTHCARE DELIVERY Complex adaptive HIV/AIDS risk reduction: Plausible implications from findings in Limpopo Province, South Africa C J Burman, M A Aphane

June 2016, Print edition

HMPG BOARD OF DIRECTORS Prof. M Lukhele (Chair), Dr M R Abbas, Dr M J Grootboom, Mrs H Kikaya, Prof. E L Mazwai, Dr M Mbokota, Dr G Wolvaardt ISSN 0256-9574 SAMA website: www.samedical.org Journal website: www.samj.org.za

For further product information contact PHARMA DYNAMICS P O Box 30958 Tokai Cape Town 7966 Tel 021 707 7000 Fax 021 701 5898 Email info@pharmadynamics.co.za CUSTOMER CARE LINE 0860 PHARMA (742 762) www.pharmadynamics.co.za SERRAPRESS 20 mg. Each tablet contains paroxetine hydrochloride equivalent to 20 mg paroxetine. Reg. No.: RSA S5 A38/1.2/0069 NAM NS3 08/1.2/0101. SSC94/02/2015.

CASE REPORT 52 A case of biventricular endomyocardial fibrosis complicated by right ventricular outflow tract aneurysms R Gonçalves, R Meel

RESEARCH Where have all the gun deaths gone?* R Matzopoulos, P Groenewald, N Abrahams, D Bradshaw

Screening for retinopathy of prematurity in a provincial hospital in Port Elizabeth, South Africa* M R Jacoby, L du Toit

Retinopathy of prematurity screening criteria and workload implications at Tygerberg Children’s Hospital, South Africa: A cross-sectional study* E Visser Kift, N Freeman, C Cook, L Myer

HAART in hand: The change in Kaposi’s sarcoma presentation in KwaZulu-Natal, South Africa* L Naidoo, J S Jacobson, A I Neugut, N C Dlova, A Mosam

Clinical findings and genetic screening for copy number variation mutations in a cohort of South African patients with Parkinson’s disease* A C Mahne, J A Carr, S Bardien, C-M Schutte

Identity tags: A vehicle for cross-infection?* S G Cox, A Burahee, A Lucier, C Fernando, S M Machoki

*Full article available online only.

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ONLINE CONTENTS LISTED IN Index Medicus (Medline) Excerpta Medica (EMBASE) Biological Abstracts (BIOSIS) Science Citation Index (SciSearch) Current Contents/Clinical Medicine SAMJ SUBSCRIPTION RATES Local subscriptions ZAR 1 368.00 p.a. Foreign subscriptions ZAR 3 108.00 p.a. Single copies ZAR114.00 local, ZAR 259.00 foreign Members of the South African Medical Association receive the SAMJ only on request, as part of their membership benefit. Subscriptions: Tel. 012 481 2071 Email: members@samedical.org The SAMJ is published monthly by the Health and Medical Publishing Group (Pty) Ltd, Co. registration 2004/0220 32/07, a subsidiary of SAMA. HEAD OFFICE Health and Medical Publishing Group (Pty) Ltd Block F, Castle Walk Corporate Park, Nossob Street, Erasmuskloof Ext. 3, Pretoria, 0181 Tel. 012 481 2069 Email: dianes@hmpg.co.za EDITORIAL OFFICE Suites 9 & 10, Lonsdale Building, Gardener Way, Pinelands, 7405 Tel. 021 532 1281 | Cell. 072 635 9825 Email: publishing@hmpg.co.za Please submit all letters and articles for publication online at www.samj.org.za © Copyright: Health and Medical Publishing Group (Pty) Ltd, a subsidiary of the South African Medical Association Use of editorial material is subject to the Creative Commons Attribution – Non-commercial Works Licence. http://creativecommons.org/licenses/by-nc/3.0 Printed by TANDYM PRINT

JUNE 2016

Additional content available in the full online issue, SAMJ Vol. 106 No. 6 Background photo: Doctors working in rural clinics at retirement age | Mykola Komarovskyy

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Hexagon photos: Type 1 retinopathy of prematurity in a child, stage 2/zone 2/plus | Shuan Dai; Ascending aortic aneurysm | kalus’ Teenage girls teasing boy | Digital vision

June 2016, Print edition

CASE REPORT Right ventricular outflow tract aneurysms and endomyocardial fibrosis RESEARCH Where have all the gun deaths gone? Screening for retinopathy of prematurity Changing Kaposi’s sarcoma presentation with HAART

GUEST EDITORIAL

Health financing lessons from Thailand for South Africa on the path towards universal health coverage Five years after the release of its Green Paper on National Health Insurance (NHI),[1] 4 years after the institution of NHI pilot sites and following the recent release of the White Paper on NHI,[2] South Africa (SA) needs to move beyond the phase 1 plans , policy making and health system strengthening activities to phase 2 – putting into place the legal and institutional frameworks and systems for implementation of its universal health coverage (UHC) system. In doing so, SA can draw on considerable practical lessons from other countries’ reforms in managing UHC with favourable equity outcomes over the past decade.[2,3] We outline some potentially significant lessons from the Thai health financing system for SA. Thailand has received widespread international recognition as one of several middle-income countries that have made enormous progress in building a UHC system and in achieving ‘good health at low cost’.[4] Although its per capita GDP is below that of SA, Thailand has not only massively improved health outcomes (e.g. infant mortality 9.8/1 000[4]) but made great improvements in social security objectives (>99% population coverage, high level of financial risk and impoverishment protection). It has low out-of-pocket payments and health-related catastrophic expenditure has fallen from 2.7% to 0.49%,[5] but there is some room for improvement for urban poor populations. SA can learn a range of practical lessons from Thailand’s experience. Firstly, SA wants to establish an NHI fund. Thailand has a strong national fund called the Universal Coverage (UC) Fund, established in 2002, which covers 75% of its population, the rest being covered by social health insurance and the Civil Servant Medical Benefit Scheme (CSMBS). Thailand has a well-developed purchaser-provider split, with the independent UC Fund established by legislation, with a multi-stakeholder governing body including private and civil society representatives. Its internal structure, operating systems, procedures and information technology are firmly established, accessible and affordable in the middle-income country context. In the early stages, both countries’ funds will cover the majority of the population not covered by other insurance arrangements: medical schemes in the case of SA (16% of the population), and social security (15%) and the CSMBS (9%) in the case of Thailand. Both funds will initially focus mainly on public sector provision, but will progressively explore mixed public and private provision options (for example, Thailand has used private healthcare providers to clear a large cataract backlog). Despite fairly sophisticated population registration, reimbursement and audit systems, the administration cost of the Thai UC Fund is a remarkably efficient 1.2% of its total annual budget. The National Health Security Office (NHSO), which manages the UC Fund, concentrates on pooling and strategic purchasing; it has no revenue collection function, as the scheme is financed through an annual budget. The successes of the UC Fund are such that the CSMBS and social security have adopted a number of its systems (e.g. diagnosis-related groups (DRGs)). In addition, the NHSO manages the disease prevention and health promotion budget for all Thai citizens, thus assisting the other schemes and providing a strong focus on prevention and promotion beyond the conventional scope of insurance. Secondly, SA is keen to embark on reimbursement reform and put in place a system of capitation for primary care and DRGs for hospital inpatients in order to contain hospital spending, adjust for case-mix

severity, fund primary care more equitably and improve technical efficiency.[6] While the development of such systems is still in early planning phase in SA, they have been practically implemented and refined in Thailand over several years. Thailand’s civic registration system (covering 98.4% of total births and deaths[7]) operates mainly through the national ID card and is an impressive sign of citizenship; all citizens are visible, along with their health provider unit in the electronic system of the UC Fund, at every hospital and primary care centre. The Thai capitation system uses an interesting contracting unit called the CUP (Contracting Unit for Primary Care), which is the district hospital along with its referring primary care centres. The UC Fund contracts with 800 CUPs, each with a manageable number of 50 000 catchment population,[5] which is operationally feasible, while within each CUP the district hospital and its primary care centres work together, sharing the outpatient capitation budget from the UC Fund and collaborating as a horizontally integrated provision unit. The Thai DRG system, now in its version 5.1, is well developed and has drawn on the Australian grouper systems in its development. Both hospitals and health centres in Thailand have their own bank accounts and can retain surplus revenue for operation and additional incentives for staff. This decentralised holding of funds has provided greater flexibility to health facilities to solve local problems. These use simpler accounting systems and are audited by the auditorgeneral. In addition to the main capitation and DRG reimbursement mechanisms, certain expensive and prioritised activities also receive additional payments to encourage their provision. Thirdly, Thailand has a very deep primary care system with over 10 000 public health centres[8] (approximately 1/6 000 population v. 1/13 000 in SA). In addition to nursing and public health officers, each health centre has up to 30 community health volunteers who also work closely with health centres and local government on prevention and promotion. Substantial investments were made in infrastructure for rural health centres, often using attractive but standardised design options, lowering infrastructure costs. In a farsighted funding arrangement, every CUP (and therefore district hospital and health centres) receives a dedicated funding stream for prevention and promotion activities from the UC Fund. In addition, each CUP has a co-funding arrangement with the local government for prevention, promotion, rehabilitation and public health, where the local government contributes between 10% and 50% depending on fiscal capacity.[9] Thailand also has a national Health Promotion Foundation, established by law as an independent public organisation and funded through a mandatory 2% additional surcharge on excise tax on alcohol and tobacco, which implements a wide variety of nonclinical health promotion activities using a wide range of media and stakeholders. Fourthly, Thailand has achieved impressive health outcomes, financial risk protection, and universal coverage with advanced reimbursement systems at remarkably low cost. With the progression towards UHC, public health expenditure has grown from only 3.4% of the GDP in 2005 to 5.6% in 2014, and total health expenditure from 4.6% to 6.5%.[10] Many factors contribute to its low costs, particularly on the supply side. Total inpatient payments using DRGs are capped, primary care spending is limited by the capitation mechanisms, and there is substantial use of central procurement of certain high-cost medicines by the NHSO and use of generic

June 2016, Print edition

GUEST EDITORIAL

medicines by contractor providers. The primary care system is highly accessible; patients who bypass their registered CUP are liable to pay full user fees. CUP fund holding is applied, by which higher-level hospitals can bill lower-level hospitals for OPD services (money follows the patient). The use of one main large UC Fund simplifies administration. Relatively low wage costs along with a strong work ethic and the use of mainly public providers contribute to the low costs. There is a sophisticated process of and institutional capacity for health technology assessment using economic evaluation techniques before new expensive interventions and medicines are included into the benefit package of the UC Fund. The Thai Ministry of Public Health and the UC Fund are supported by a number of independent or semi-independent institutions that provide independent technical support. These include, among others, the International Health Policy Program and its capacity development arm for UHC, the Health Intervention and Technology Assessment Program (HITAP), which undertakes economic evaluation of new interventions, the Centre for Health Equity Monitoring and the Thai CaseMix Centre, which develop and refine the DRG system, the Thai Health Foundation and the Healthcare Accreditation Institute. SA could benefit from a health technology assessment institution like the HITAP to assess new interventions and technologies and refine the NHI benefit package over time. However, Thailand and SA also differ in important ways that may make their health financing systems differ. One of the most important of these is that provinces in SA have greater legally derived powers than in Thailand. The relative role and co-ordination between the centre and the provinces still needs to be finally resolved in the SA reforms and in the legislation that defines SA’s new UHC system. While SA has a large private medical scheme system, Thailand has significant CSMBS and social security funds outside the UC Fund. For both countries the progressive alignment and ultimate integration of funding pools into a single fund, as the universal arrangements are progressively built and strengthened, will remain a key agenda. Both countries face a challenge to find the right mix of public and private provision. Although the Thai UC system uses mainly public provision (public sector infrastructure, services and benefits were strengthened over several decades, and the number of health science graduates was increased), public primary care in urban cities remains weak while the private sector concentrates on tertiary specialised care. Thailand has a strong market economy that has achieved large GDP improvements over two decades, rising from a low-income to an upper middle-income country. It has a relative small private sector (25% and 21% of hospitals and beds, respectively, and spending considerably less than in SA), and both countries will

be challenged to find a more diverse provision mix as wealthier urban populations grow. The Thai UC Fund has built strong administrative capacity, reimbursement tools and audit mechanisms that will allow for contracting with a wider range of provider options. Mark Blecher National Treasury, South Africa mark.blecher@treasury.gov.za Anban Pillay National Department of Health, South Africa Walaiporn Patcharanarumol, Warisa Panichkriangkrai, Viroj Tangcharoensathien International Health Policy Program, Ministry of Public Health, Thailand Yot Teerawattananon Health Intervention and Technology Assessment Program, Ministry of Public Health, Thailand Supasit Pannarunothai Centre for Health Equity Monitoring Foundation, Thailand Jonatan Davén National Treasury, South Africa 1. National Department of Health. Policy on National Health Insurance. Government Gazette 2011;554:34523. 2. National Department of Health. National Health Insurance for South Africa: Towards universal health coverage. Government Gazette 2015;1230:39506. 3. Prakongsai P, Limwattananon S, Tangcharoensathien V. The equity impact of the universal coverage policy: Lessons from Thailand. In: Chernichovsky D, Hanson K, eds. Innovations in Health System Finance in Developing and Transitional Economies. London: Emerald Group Publishing, 2009:57-81. 4. Tangcharoensathien V, Pitayarangsarit S, Patcharanarumol W, et al. Promoting universal financial protection: How the Thai universal coverage scheme was designed to ensure equity. Health Res Policy Syst 2013;11(25):1-9. DOI:10.1186/1478-4505-11-25 5. Patcharanarumol W, Tangcharoensathien V, Limwattanaon S, et al. Why and how Thailand achieved good health care at low cost. In: Bababalinova D, McKie M, Mills A, eds. ‘Good health at low cost’ 25 years on: What makes a successful health system. London: London School of Tropical Medicine and Hygiene, 2011:193-233. 6. Busse R, Geissler A, Quentin W, Wiley M. Diagnosis-Related Groups in Europe Moving towards Transparency, Efficiency and Quality in Hospitals. Maidenhead, UK: Open University Press, 2011. 7. National Statistical Office. Survey of Population Changes 2005-2006. Nonthaburi, Thailand: Ministry of Information and Communication Technology, 2006. 8. Jongudomsuk P, Srithamrongsawat S, Patcharanarumol W, et al. The Kingdom of Thailand Health System Review. 2015;5(5):1-265. http://www.wpro.who.int/asia_pacific_observatory/hits/series/ thailand_health_systems_review.pdf (accessed 6 May 2016). 9. Srithamrongsawat S, Aekplakorn W, Jongudomsuk P, et al. Funding health promotion and prevention – the Thai experience. World Health Report (2010) Background Paper, 45. www.who.int/healthsystems/ topics/financing/healthreport/ThailandNo45FINAL.pdf (accessed 6 May 2016). 10. World Health Organization. Global Health Expenditure Database. apps.who.int/nha/database (accessed 21 April 2016).

S Afr Med J 2016;106(6):533-534. DOI:10.7196/SAMJ.2016.v106i6.10953

June 2016, Print edition

20 6 SAGES CONGRESS INCORPORATING SAGINS & SASPEN

CSIR INTERNATIONAL CONVENTION CENTRE • PRETORIA

INTERNATIONAL VISITORS

Sunday 7 August Continued

Dr Peter Irving – United Kingdom Prof Joseph Sung – Hong Kong CONGRESS HIGHLIGHTS Friday 5 August Academic free papers Saturday 6 August Best of AGA Sunday 7 August Session highlights IBD

Barrett’s Oesophagus Colorectal Twilight Symposium IBD, iron deficiency & GI bleeding Monday 8 August Gastro Foundation Hepatocellular Carcinoma a Festschrift Symposium in honour of Prof Michael Kew Invited Speakers: Prof Adrian Di Bisceglie – United States Prof Geoff Dusheiko – United Kingdom Dr Jay Hoofnagle – United States Prof Massimo Pinzani – United Kingdom Dr Lewis Roberts – United States

Friday 5 August 2016: Academic Day Saturday 6 – Monday 8 August 2016: Congress

www.sages2016.co.za CONGRESS MANAGEMENT: EASTERN SUN EVENTS Tel: +27 41 374 5654 • Email: sages@easternsun.co.za

EDITOR’S CHOICE

CME: Adolescent health

Almost 40% of the population of sub-Saharan Africa are between the ages of 12 and 24 years. Adolescence is a time of important bio logical, physiological, neurological, behavioural and social transitions towards adulthood, characterised by higher impulsivity, increased sensation-seeking behaviour, increased risk-taking behaviours relating to substance use and/or sexual experimentation, a heightened sense of self-awareness/invincibility, and social relationships involving partners and peers being more important than those with parents and older siblings. Not surprisingly, the psychological stressors of going through adolescence, coupled with major hormonal, physiological and identity development and peer pressures to fit into dominant peer norms, result in enormous stress levels that sometimes lead to a variety of mental health disorders from, among other things, inadequate coping and/or support structures. In this issue of CME – continuing the theme of adolescent health from last year – the two articles highlight the challenges of mental health and substance use, individually and in combination.

Antibiotic stewardship and acute respiratory tract infections

Antibiotic resistance (ABR) is a critical threat to public health globally that, if unchecked, could result in 10 million deaths per year at a cumulative cost of USD100 trillion by 2050. Overuse and misuse of antibiotics have resulted in the emergence of multidrug-resistant (MDR), extensively drug resistant (XDR) and pan-drug resistant (PDR) bacteria, which are increasingly common in South Africa (SA). Antibiotic stewardship (AS) has emerged as a concept that embodies the appropriate use of antibiotics with the goal of optimising patient outcomes while reducing the emergence of resistant bacteria. The consequences of ABR in terms of patient outcomes and economic impact are not a distant threat; they are here right now. In SA, MDR, XDR and PDR organisms at increasing levels have been spawned by rampant over-use and incorrect use of antibiotics. As such, antibiotics should be seen as a precious resource and the prescribing doctor, particularly the GP, as the guardian of this resource. AS requires collaborative effort from all stakeholders, including patients. This will involve drastic behavioural changes on the part of both doctors and patients, with more emphasis on non-antibiotic treatments, particularly in the community. Acute respiratory tract infections are common presentations in primary care, and focusing on these alone would be a major step in the direction of reducing over- and misuse of antibiotics.[1]

Emergence of vancomycin-resistant Enterococcus at a tertiary paediatric hospital in SA

Emphasising the points made by Brink et al.,[1] during February 2013 the haematology/oncology unit at Red Cross War Memorial Children’s Hospital in Cape Town isolated vancomycin-resistant organisms causing bloodstream infections from blood culture specimens in two patients, 2 days apart.[2] Alarmingly, 7 and 9 months later, vancomycin-resistant Enterococcus (VRE) was isolated from blood culture specimens in two more patients. This is the first documented report of VRE infection in children in SA. Treatment for this resistant organism is limited to linezolid and daptomycin, the latter difficult to access in the public health system. In these cases, patient-to-patient transfer was implicated, emphasising the need for infection control practices. However, the emergence of the resistant organism is a strong case for antibiotic stewardship.

Delayed and poor diagnosis of Down syndrome in KwaZulu-Natal (online only)

Down syndrome (DS) is the most common chromosomal disorder among newborns, with a birth prevalence of approximately 2 in 1 000 live births in SA, but little is known of the epidemiological profile of this syndrome in KwaZulu-Natal (KZN) – a province with a large population. The many abnormalities associated with DS make early diagnosis important in the care of children with the disorder. Early detection of treatable disorders associated with DS, such as hypothyroidism, may prevent further irreversible mental and physical disabilities. The high cost of medical care for patients affected with DS also highlights the need for a largely preventive healthcare programme for these patients. Most of the improvements in quality of life for patients with DS are related to early intervention programmes and improving support for parents. The findings of this study[3] show that both doctors and nurses have problems in making an accurate clinical diagnosis of DS in KZN, resulting in missed opportunities for early intervention. Sadly, even though we know that DS is largely unrecognised in SA, little has changed, with potentially poor outcomes for patients and their families. It even seems that the ability to diagnose DS may be declining. The implications for children with less easily diagnosed and less common congenital disorders are grave.

Where have all the gun deaths gone?

It would appear that stricter gun control, coinciding with the implementation of the Firearms Control Act of 2000, is one of the reasons for the 60% decrease in firearm assaults from a peak in 2000. Matzopoulos et al.[4] conducted a review of all gunshot injuries recorded in Statistics South Africa death notifications from 1997 to 2013. They identified 105 694 gunshot-related injury deaths over the 17-year period, an average of 6 217 per annum. The total annual number of gunshot injuries increased from 1997 to 2000, at which point firearm-related deaths peaked at 9 540 recorded cases. Thereafter there was a steadily decreasing trend (interrupted only in 2006 and 2008) until 2011, when 3 793 deaths were attributed to gunshot-related injuries as the underlying cause – a decrease of >60% from the peak in 2000. In a linked editorial, Matzopoulos[5] points out that in 2000 SA had one of the world’s highest homicide rates, estimated at 67 per 100 000 population, but this had almost halved by 2009 to 38 per 100 000, the decrease coinciding with the introduction of stricter gun control legislation. 2000 was the year in which the Firearms Control Act (FCA) was adopted by Parliament. Thereafter, the annual number of firearm deaths began to decrease, and at a faster rate following the adoption of the regulations related to the FCA in 2004. The study provides further support for the hypothesis that stricter gun control accounted for the decrease in firearm homicide in SA. The findings are not surprising, and echo an expanding body of international evidence. BF 1. Brink AJ, van Wyk J, Moodley VM, et al. The role of appropriate diagnostic testing in acute respiratory tract infections: An antibiotic stewardship strategy to minimise diagnostic uncertainty in primary care. S Afr Med J 2016;106(6):554-561. DOI:10.7196/SAMJ.2016.v106i6.10857 2. Lochan H, Moodley C, Rip D, et al. Emergence of vancomycin-resistant Enterococcus at a tertiary paediatric hospital in South Africa. S Afr Med J 2016;106(6):562-566. DOI:10.7196/SAMJ.2016. v106i6.10858 3. Willoughby M, Aldous C, Patrick M, Kavonic S, Christianson A. Delay and poor diagnosis of Down syndrome in KwaZulu-Natal, South Africa: A retrospective review of postnatal cytogenetic testing. S Afr Med J 2016;106(6):626-629. DOI:10.7196/SAMJ.2016.v106i6.10105 4. Matzopoulos R, Groenewald P, Abrahams N, Bradshaw D. Where have all the gun deaths gone? S Afr Med J 2016;106(6):589-591. DOI:10.7196/SAMJ.2016.v106i6.10379 5. Matzopoulos R. Gun control saves lives. S Afr Med J 2016;106(6):544. DOI:10.7196/SAMJ.2016. v106i6.11034

June 2016, Print edition

CORRESPONDENCE

Essential skills for rural surgery

To the Editor: In Chris Bateman’s Izindaba article entitled ‘Consciously cutting to the bone of SA’s surgical/anaesthetic delivery’,[1] Dr Joe Pahla is quoted as saying ‘It was “critical” to put together a package of basic surgical skills that could be used in district and regional hospitals.’ Of the challenges faced in rural medicine, it is surgery in particular that can engender feelings of lack of confidence, incompetence and anxiety. A common approach to strengthening preparation is to identify lists of surgical procedures that need to be performed most frequently. But that is not the same, and not as constructive, as a list of skills. It is what presents that was not on such ‘lists of procedures’ that can be the bigger challenge. A first and basic essential is the ingraining of the skills of using scalpel, forceps, retractors and suckers, knot-tying, making and closing incisions and control of bleeding, which may be called the ‘knife, fork and spoon’ skills of surgery. These are vital to avoiding uncertainty in the theatre and for being free to proceed knowingly, step by step, with another skill that I call ‘procedural imprinting’. Reading up on a procedure is itself an intensive exercise and a practice to be acquired. It involves bringing to the mind’s eye the reality of a text and its diagrams, and a mentally rehearsed and summarised sequence of practical steps to be followed. Hamilton Bailey, Watson Jones and Harold Gillies used to be leading books on operative surgery. To take notes or even a textbook into theatre should not be embarrassing. Today there will be a variety of computer-based resources that can be used. I see the deliberate and reflective process I have outlined as an essential skill to be taught and practised. I have summarised here what I published in 2003, based on 18 years of practising surgery at a former mission hospital in Transkei.[2] Ronald F Ingle

Hillcrest, KwaZulu-Natal, South Africa (retired) inglerf@iafrica.com 1. Bateman C. Consciously cutting to the bone of SA’s surgical/anaesthetic delivery. S Afr Med J 2016;106(2):132-134. DOI:10.7196/SAMJ.2016.v106i2.10526 2. Ingle R. Preparing for rural surgery: Procedures or skills? S Afr Fam Pract 2003;45(9):7-8.

S Afr Med J 2016;106(6):535. DOI:10.7196/SAMJ.2016v106i6.10720

Medical malpractice crisis deepens: New approach

To the Editor: The medical indemnity insurance crisis has entered a new phase with one hospital group informing its doctors that they will be barred from use of its facilities after February 2016 if they do not have an indemnity policy with at least ZAR30 million cover. This attitude is likely to be adopted by the other hospital groups, who are all under pressure to ensure that they are adequately insured for any negligent act that may involve them or their staff jointly with the doctor against whom a claim is being raised. According to one source, the minimum excess that a hospital has to pay per insurable event is ZAR10 million. This requirement will, by some margin, trump the hospital income earned through admissions by an individual practitioner. This means that no individual practitioner can expect leniency from the hospital based solely on their incomegenerating capacity. Add to this new requirement the premium of ZAR650 000 the Medical Protection Society (MPS) has commenced charging its obstetric customers for its occurrence-based cover this year (an increase of ZAR200 000 since 2015), and it becomes easy to appreciate the enormity of the crisis. Further adding to the obstetricians’ woes, and impacting the pocket of their patients, is the continued lack of an appropriate response from

the medical scheme industry at large. Many in the industry continue to peg their professional fee maternity benefit at about ZAR3 500, seemingly oblivious of the impact that the rising cost of funding malpractice insurance is having on obstetricians. This is forcing doctors to charge a hefty co-payment for their services in order to meet this burgeoning obligation. A malpractice summit held under the auspices of the Department of Health last year, and the MPS meeting calling for legal reform, have provided some hope for the future, but regulatory change is unlikely to have an impact for several years. Clark et al.,[1,2] in describing their experience in the Hospital Corporation of America (HCA) hospital network, have suggested that another approach is needed. The HCA approach was based on an analysis of 89 closed malpractice claims that indicated that >80% of claims against their doctors were the result of substandard care. This led the HCA to restructure their entire approach to labour ward management. Through the application of unambiguous guidelines and protocols in the management of high-risk situations, utilising a team approach involving both doctors and midwives, they were able to reduce the number of claims fourfold and the value fivefold over a period of 10 years. The HCA found that the adoption of their guidelines and protocols was insufficient to bring about the required behaviour change. What was also needed was a way to enforce the adoption of these guidelines. This was made possible in the HCA case through the introduction of a whistle-blower function, whereby even the most lowly member of the obstetric team was encouraged to report any episode of dangerous practice. Mandatory peer review was facilitated by most doctors being employed in HCA hospitals. Independent practitioners who refused to co-operate had their admission privileges withdrawn. A new approach based on the HCA experience, to be known as the Medical Indemnity Insurance Fund (MIIF), is to be launched in South Africa soon. MIIF will establish a new self-funding insurance scheme by doctors in co-operation with the insurance industry in which agreed guidelines and protocols are adopted and a team approach to obstetrics is established in collaboration with the private hospital networks. Mandatory peer review with leverage provided by fund membership, mediation before litigation, and a policy to defend defendable claims will form a part of the package. The critical success factors will be the establishment and implementation of unambiguous, appropriate guidelines and protocols aimed at reducing episodes of substandard care that compromise patient safety; funding through doctor support; full transparency in relation to costs; spending and financial performance; and the support of experienced insurance market practitioners, insurers and reinsurers. Chris Archer

CEO, South African Private Practitioners Forum (SAPPF), Johannesburg, South Africa ceo@sappf.co.za 1. Clark SL, Belfort MA, Dildy GA, Meyers JA. Reducing obstetric litigation through alterations in practice patterns. Obstet Gynecol 2008;112(6):1279-1283. DOI:10.1097/AOG.0b013e31818da2c7 2. Clark SL, Belfort MA, Byrum SL, Meyers JA, Perlin JB. Improved outcomes, fewer cesarean deliveries, and reduced litigation: Results of a new paradigm in patient safety. Am J Obstet Gynecol 2008;199(2):105.e1-e7. DOI:10.1016/j.ajog.2008.02.031

S Afr Med J 2016;106(6):536. DOI:10.7196/SAMJ.2016.v106i6.10407

Quality of life in patients with seborrhoeic dermatitis in KwaZuluNatal, South Africa

To the Editor: Skin diseases may have a severe effect on the quality of life (QOL) of affected individuals,[1,2] but their impact has rarely been investigated in the developing world. In South Africa,

June 2016, Print edition

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there have been no studies conducted on patients with seborrhoeic dermatitis (SD). A cross-sectional study was undertaken in the ILembe District, KwaZulu-Natal Province, assessing the QOL of patients presenting with SD, correlating clinical severity and demographic parameters. Forty-five consenting participants, with a clinical diagnosis of SD, were invited to participate. QOL was assessed using the Dermatology Life Quality Index (DLQI).[3] The severity of the condition was assessed by a dermatologist and graded at individual sites for erythema, thickness, scaling and pruritus on a three-point scale. Body surface area involvement was calculated using the rule of nines and the sites of involvement were recorded. A detailed demographic profile was completed for each patient (Table 1). The median severity score was 24 and the median DLQI score was 17, which equates to a very large effect on the QOL.[3] The QOL varied depending on sex, educational level, ethnic origin, home language, marital status, residence, HIV status and site of involvement. Female patients were more negatively influenced by the disease, confirming the findings in three other studies.[4-6] Patients with no formal schooling were more adversely affected. The way the questions were interpreted and the perception of disability may explain the differences in DLQI between the groups. Visible body areas and groin involvement had a greater impact on a patient’s QOL. As appearance plays an important role in our society, patients felt more embarrassed and self-conscious. In addition groin involvement may affect intimacy with a partner. SD has a higher prevalence in patients with HIV and has been found in up to 40% of seropositive patients,[7] notably, HIV-

Table 1. Demographic profile of study sample and DLQI scores (N=45) n (%) Mean age (years)

DLQI

Sex

Male

19 (42.2)

Female

26 (57.8)

17.5

Ethnic origin

the introduction of ARVs has reduced the number of opportunistic dermatological conditions seen, there has been no change in the prevalence of primary HIV-related inflammatory diseases.[7] This is illustrated by a lack of significant associations between HIV-positive patients on ARVs v. those who were not on ARVS and QOL (on ARVs n=29, median 18; not on ARVs n=8, median 17). This study highlights that QOL tools are valuable in understanding the impact of skin disorders and will help in providing holistic, comprehensive management, offering a patient’s own perspective of their debilitating skin condition.

Black

40 (88.9)

Asian

3 (6.7)

White

2 (4.4)

4.5

Single

31 (68.9)

Married

4 (8.9)

Divorced

1 (2.2)

Widowed

2 (4.4)

9.5

Dermatology Medical Officer, Stanger Regional Hospital, KwaZulu-Natal, South Africa nerissazn@yahoo.com

Living together

7 (15.6)

Koraisha Hoosen, Ncoza Cordelia Dlova

isiZulu

39 (86.7)

English

6 (13.3)

Urban

34 (75.6)

Rural

9 (20.0)

Marital status

Home language

Residence

Level of education

Primary

9 (20.0)

Secondary

27 (60.0)

Tertiary

4 (8.9)

19.5

No schooling

5 (11.1)

positive patients (n=37, 82.2%), with a CD4 count <350 cells/mm3 (n=19, 51.4%), and patients who had been on antiretrovirals (ARVs) for >1 year (n=13, 46.6%) had higher DLQI and severity scores. Although

June 2016, Print edition

Nerissa Moodley

Department of Dermatology, King Edward VIII Hospital, Durban, KwaZulu-Natal, South Africa

1. Harlow D, Poyner T, Finlay AY, Dykes PJ. Impaired quality of life of adults with skin disease in primary care. Br J Dermatol 2000;143(5):979-982. DOI:10.1046/j.1365-2133.2000.03830 2. Jobanputra R, Bachmann M. The effect of skin diseases on quality of life in patients from different social and ethnic groups in Cape town, South Africa. Int J Dermatol 2000;39(11):826-831. DOI:10 .1046/j.1365-4362.2000.00073 3. Finlay AY, Khan GK. Dermatology Life Quality Index (DLQI) – a simple practical measure for routine clinical use. Clin Exp Dermatol 1994;19(3):210-216. DOI:10.1111/j.1365-2230.1994.tb01167 4. Szepietowski JC, Reich A, Wesołowska-Szepietowska E, et al. Quality of life in patients suffering from seborrheic dermatitis: Influence of age, gender and education level. Mycoses 2009;52(4):357-363. DOI:10.1111/j.1439-0507.2008.01624 5. Araya M, Kulthanan K, Jiamton S. Clinical characteristics and quality of life of seborrheic dermatitis patients in a tropical country. Indian J Dermatol 2015;60(5):519. DOI:10.4103/0019-5154.164410 6. Peyri J, Lleonart M. Clinical and therapeutic profile and quality of life of patients with seborrhoeic dermatitis. Actas Dermosifiliogr 2007;98(7):476-482. DOI:10.1016/S1578-2190(07)70491-2 7. Cedeno-Laurent F, Gómez-Flores M, Mendez N, et al. New insights into HIV-1 primary skin disorders. J Int AIDS Soc 2011;14:5. DOI:10.1186/1758-2652-14-5

S Afr Med J 2016;106(5):428. DOI:10.7196/SAMJ.2016v106i5.10551

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Quality of care responsible for soaring maternal deaths – report The National Department of Health (NDoH) is moving across provinces to centralise obstetric skills to a handful of district hospitals, urgently briefing district healthcare chiefs and ensuring they have sufficient blood supplies in a bid to further lower the 63% rise in caesarean section deaths due to bleeding between 2008 and 2014. This was said by Dr Yogan Pillay, NDoH Deputy Director-General of Strategic Health Programmes, who added that provinces were being told to buy and/or dedicate ambulances for quicker interfacility transport of pregnant women and sick infants. He was speaking days after the figures, described as ‘scandalous and a disgrace’, were published in the SAMJ last month. The report, from the National Committee on Confidential Enquiries into Maternal Deaths (NCCEMD), came soon after the National Committee on Perinatal Mortality (NaPeMMCo) and Committee on Mortality and Morbidity in Children under Five (Child CoMMiC) reports, also completed last year and highlighting high numbers of avoidable deaths. It blames a low skill set among junior and inexperienced doctors, especially in rural under-resourced areas where they perform emergency or unnecessary caesarean sections, too often without supervision or proper obste tric/anaesthetic care. Findings include delays in calling for help with ongoing bleeding, inappropriate discharges from post-theatre recovery, and poor monitoring in postnatal wards.

Pillay said that while maternal and newborn/under-5 mortality had been reduced overall (mainly due to prevention of motherto-child HIV transmission and improved antiretroviral drug and adherence interventions), ‘we’ve clearly been less successful with other causes of maternal mortality’ The first author of the article, NCCEMD deputy chairperson Dr Sue Fawcus, said the figures were alarming because causes had been highlighted previously. ‘It’s got worse and cannot be explained by the increase in C-sections – there’s something else going on with quality of care.’ (Public sector

positive airway pressure (CPAP) machines, 35 of which had already been delivered to as many district hospitals, with another 30 ‘on the way’. Echoing the report, he said far too many newborns were still dying of asphyxia, so an audit to find out which hospitals did not have CPAP machines was immediately ordered. ‘We’ve been far more interventionist over the past 3 years than previously, when we merely provided the information and hoped provinces would do the right thing,’ he admitted.

The bleeding was often missed because it was into the abdomen, and the blood pressure and pulse rate remained normal for a long period.

Dr Yogan Pillay, NDoH Deputy Director-General of Strategic Health Programmes.

C-sections rose by 30% from 2008 (181 405) to 2012 (236 149), raising suspicions that many were medically unnecessary.) Pillay said that while maternal and newborn/ under-5 mortality had been reduced overall (mainly owing to preven tion of motherto-child HIV trans mission and improved antiretroviral drug and adherence interventions), ‘we’ve clearly been less successful with other causes of maternal mortality’. Safe C-section care had been centralised in the Free State, with dramatically improved results over 12 months. The template of key recommendations was being implemented in KwaZulu-Natal and North West and would soon move to the other six provinces. ‘We’re insisting interventions get to every health district,’ Pillay said.

‘Far more interventionsist’

The NDoH team, led by national health minister Dr Aaron Motsoaledi, had begun their interventions in the struggling Sekhukhune district in Limpopo and was, at the time of writing, arranging dates with the health chiefs in North West and the Eastern Cape. Pillay said the recommendations of all three reports were being implemented, one of which was the purchase of continuous

June 2016, Print edition

Fawcus said that C-section deliveries should only be done for good medical reasons. ‘It’s a major operation and should not be performed lightly,’ she added. Dr Stefan Gebhardt, head of general specialist services at Tygerberg Hospital, said that junior doctors were not always skilled enough to do complicated C-sections, but there were often no more senior or experienced doctors available to help out. Bleeding only started after the abdomen was closed and the patient was in the recovery room, while pregnant women did not show signs of blood loss until it was very late. The bleeding was often missed because it was into the abdomen, and the blood pressure and pulse rate remained normal for a long period. Peter de Jong, a consulting gynaecologist at Groote Schuur Hospital and the University of Cape Town, described the figures as ‘a scandal; it’s a disgrace. You need to have people explain what those preventable factors are in the rural areas and what is being done about it. There has to be accountability.’ The three national committee chair persons, Prof. Jack Moodley of the NCCEMD, Dr Natasha Rhoda of the NaPeMMCo and Dr Neil McKerrow of Child CoMMiC, outlined the key drivers of the three mortality groups to all NDoH departmental heads at a workshop early this year. Obstetric haemorrhage and safer C-sections emerged as top priorities. Earlier this year Izindaba reported on a total absence of supervisory support

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Specialists in human biosimilar insulins The economic burden of diabetes is increasing worldwide, with the greatest demands and increases in developing countries.1 Globally 415 million people have diabetes, with more than 14 million people in the African Region; The International Diabetes Federation predicts that by 2040 these figures will more than double.2 Three-and-a-half million South Africans (about 6 % of the population) suffer from diabetes and there are many more who are undiagnosed. It is estimated that another five million South Africans have pre-diabetes, a condition where insulin resistance causes blood glucose levels to be higher than normal, but not high enough yet to be type 2 diabetes.3 The need for more cost-effective insulin therapy is critical in reducing the financial burden on patients and health care systems.1 Biosimilars are distinctly different from generic drugs, as they are protein compounds that rely on modification for efficacy and are therefore bioequivalent rather than bioidentical. Biosimilars must follow precise manufacturing, processing and purification procedures, and are regulated to pass stringent laboratory and clinical trials before approval.1 BIOSULIN insulins were approved for use in South Africa more than 10 years ago and are marketed by BIOSWISS, a wholly owned subsidiary of Ascendis Pharma. Biosimilar insulins have the potential to dramatically lower healthcare costs by delivering insulin with similar anti-glycaemic effect and adverse reaction profile to standard, more expensive insulin preparations.1

HbA1c at baseline and after 6 months of therapy with BIOSULIN 30/70 Baseline 6 months

p=0.41

HbA1c (%)

p=0.14

8.4

p=0.19

8.0

7.9

7.7

7.6

Overall

7.4

Type 1

Type 2

Adapted from Segal D et al 1

In the BEST study (SAMJ July 2013) BIOSULIN 30/70 insulin was tested to confirm equivalence to other human premixed insulin preparations on the South African market.1 Seventy-seven subjects with type 1 (n = 18) and type 2 diabetes mellitus (n = 59) were switched from their existing human premix insulin to BIOSULIN 30/70. The change in HbA1c from baseline to 6 months was considered the primary endpoint of the study.1 BIOSULIN 30/70 achieved at least equivalent glycaemic control with no reported new or severe adverse events. In addition there was no significant difference in body weight in the study subjects during the 6-month period on BIOSULIN 30/70.1 Despite the more complex production process and regulatory requirements for biosimilars, they offer a price reduction of between 21 % and 47 % of the parent insulin and analogue insulin.4

Increased use of biosimilar insulins has the potential for significant cost savings with no loss in patients’ glycaemic outcomes.1 Biosimilar insulins, such as BIOSULIN, will play an ever increasing role in the management of diabetes.1

BIOSWISS offers a comprehensive range of human insulins in cartridge form, from the short acting BIOSULIN R, to the intermediate acting BIOSULIN N and BIOSULIN L, as well as the biphasic insulin BIOSULIN 30/70. They have 2 Biosulin insulin delivery devices, namely the YPSOMED BIOSULIN PEN, and GENSUPEN. In addition they provide blood glucose monitoring devices and strips, GLUCOPLUS® and newly launched GLUCOPLUS PRO®, as well as INSUPEN® NEEDLES and LORIS® SAFETY LANCETS.

For more information regarding BIOSWISS and their products, please contact Laurett Correia on laurett@bioswiss-med.co.za. References: 1. Segal D, Tupy D, Distiller L. The Biosulin equivalence in standard therapy (BEST) study − a multicentre, open-label, non-randomised, interventional, observational study in subjects using Biosulin 30/70 for the treatment of insulin-dependent type 1 and type 2 diabetes mellitus. SAMJ 2013;103(7):458-460:1-4. 2. South Africa | International Diabetes Federation. Available from https://www.idf.org/membership/afr/south-africa Accessed 15 February 2016. 3. Prevalence of diabetes in South Africa | Health24. Available from http://www.health24.com/Medical/Diabetes/About-diabetes/Diabetes-tsunami-hits-South-Africa- Accessed 15 February 2016. 4. Database of Medicine Prices February 2016. Available from http://www.mpr.gov.za/ Accessed February 2016 S3 Biosulin R (solution for injection). Each Biosulin R solution for injection contains 100 I.U/ml biosynthetic human insulin. Reg. No: 37/21.1/0670 S3 Biosulin N (solution for injection). Each Biosulin N solution for injection contains 100 I.U/ml biosynthetic human insulin. Reg. No: 37/21.1/0671 S3 Biosulin L (solution for injection). Each Biosulin L solution for injection contains 100 I.U/ml biosynthetic human insulin. Reg. No: 37/21.1/0672 S3 Biosulin 30/70 (solution for injection). Each Biosulin 30/70 solution for injection contains 100 I.U/ml biosynthetic human insulin. Reg. No: 37/21.1/0673 Applicant: Dezzo Trading 392 (Pty) Ltd. Co. Reg No: 2002/001923/07 Cnr Birch Road and Bluegum Avenue, Anchorville, Lenasia, 1827. P. O. Box 725 Lawley 1824. Tel: 011 857 2090 Fax: 086 664 6223. Customer Careline: 086 111 4721 www.bioswiss-med.co.za ZA.BIOS.01 05/2016

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in Limpopo, where the NCCEMD found that 10% of all C-section patients died due to anaesthesia in 2014. Unsupervised community service doctors with no anaesthetic training were performing on

average between two and three C-sections per week in the province’s 70 mainly rural district hospitals, conducting spinal blocks with no airway skills, no intubation equipment and insufficient drugs.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(6):540-541. DOI:10.7196/SAMJ.2016.v106i6.11041

Occupational injuries – radiologists lose patience, sue government In spite of a new electronic claims system and ZAR52 billion in its coffers, the Compensation Fund keeps doctors waiting for payments for up to a year – prompting 19 radiologists to sue it for ZAR121.5 million in unpaid claims this March, in what could prove a landmark case. The Radiological Society of South Africa (RADSA) and 19 individual radio logy practices are suing the labour minister over the fund’s failure to process and pay out this amount in claims for services they have provided to injured workers. The litigant group represents less than a quarter of existing private radiology practices, with most using third-party agencies to collect money for them – at a cost of 20% of debt recovered. RADSA’s Executive Director‚ Richard Tuft‚ says that it’s iniquitous for doctors to have to forfeit a fifth of their income just to increase their chances of getting paid. Last June the biggest company handling claims on behalf of doctors‚ CompSol‚ chose to temporarily suspend its services, so difficult had its job become. The South African Medical Association (SAMA) revealed that many doctors were refusing to attend to ‘injured-on-duty’ cases because

Dr Richard Tuft, Executive Director of RADSA.

they had no confidence that they would be paid by the fund.

A history of unpaid claims

Compensation Commissioner Vuyo Mafata conceded that the fund has a history of unpaid claims‚ but said it had improved its turnaround time – now averaging 60

days – by automating processes with an electronic claims system called Umehluko. The fund had ZAR52 billion in reserves and paid claims totalling ZAR6 billion this year. ‘We don’t want to not pay anyone,’ he said. Tuft said the average debtors’ days for claims from the Compensation Fund was 350 days‚ compared with an average 12 - 20 days for claims from medical schemes. Repeated engagement with the fund’s administrators came to nothing. Mafata said the fund tried to engage with RADSA after becoming aware of litigation last November‚ but to no avail. The Department of Labour would oppose the matter‚ but would have preferred to resolve the matter out of court. Claims could be outstanding because there was documentation missing or because employers had failed to register the claim‚ as required by law‚ he asserted. The fund had set up a team to try to help SAMA’s doctors resolve their outstanding claims‚ he added. Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(6):542. DOI:10.7196/SAMJ.2016.v106i6.11040

Newer drugs keep multiple sclerosis patients out of wheelchairs – expert There are fewer multiple sclerosis (MS) patients in wheelchairs than ever before in South Africa (SA), mainly owing to the advent of interferon drugs over the past decade and better second-line drugs over the past 3 years, says Prof. Girish Modi, Head of Neurology at the University of the Witwatersrand. He was responding to claims last month

by the Biokinetics Association of South Africa (BASA) that physical activity helps manage symptoms and prevent compli c ations and can perhaps even slow progression of MS. Last month (May) marked International Multiple Sclerosis Awareness Month, and Izindaba was testing assertions by BASA that movement and exercise were therapeutic

June 2016, Print edition

(contrary to decades-old ‘wisdom’ that exercise worsens MS). Modi, who is also Head of Neurology at Charlotte Maxeke Hospital in Johannesburg, said a sense of wellbeing had been shown to have ‘some relevance’ in autoimmune diseases, ‘so a healthy lifestyle is a good thing, but there’s no scientific evidence that exercise will reduce attacks or control the disease’. Areta

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activity to try to reduce the symptoms of fatigue.

Medical aids had ‘come to the party with interferon’, and most MS sufferers in the private sector were now on it. Any patient who had had two or more MS attacks within the past 12 months should be on interferon, which cost R7 000 - 9 000 per month.

Prof. Girish Modi, Head of Neurology at the University of the Witwatersrand.

Potgieter, an executive member of BASA and a practising biokineticist, had claimed that one of the most ‘profound’ recent changes in MS treatment and management related to exercise, with fatigue affecting 75 - 90% of all MS patients, many of whom avoided physical

However, Modi said the most profound change was in pharmaceuticals, with inter feron or the similar Copaxone becoming far more widely available in the private sector over the past decade. Second-line drugs such as Tysabri and Gilenya now helped modify the immune response and avoid relapse, though they carried some very significant risk. Evidence following the use of interferon ‘clearly shows fewer people now in wheelchairs’, he said. Medical aids had ‘come to the party with interferon’, and most MS sufferers in the

June 2016, Print edition

Multiple sclerosis is a chronic, typically progressive disease that causes demyelination (disruption of the myelin that insulates and protects nerve cells) of spinal nerve and brain cells. The significant risk in the second-line drugs that Modi refers to is a condition known as progressive multifocal leucoencephalopathy (PML), caused by activation of what’s called the JC virus in the brain – which can be fatal.

private sector were now on it. Any patient who had had two or more MS attacks within the past 12 months should be on interferon, which cost R7 000 - 9 000 per month. Only ‘a handful’ of patients were on it in the public sector because of cost considerations. There are an estimated 5 000 known MS sufferers in SA. Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(6):543. DOI:10.7196/SAMJ.2016.v106i6.11039

EDITORIAL

Gun control saves lives In the January edition of SAMJ, Prinsloo et al.[1] reported that data from the police and a recent study of injury mortality based on postmortem investigations showed a significant decrease in homicide in South Africa (SA). In 2000, SA had one of the world’s highest homicide rates, estimated at 67 per 100 000 population,[2] but this had almost halved by 2009 to 38 per 100 000.[3] Several studies have shown that the decrease has been most evident in firearm-related homicides[3-5] and that it coincided with the introduction of stricter gun control legislation. One study estimated that more than 4 500 lives were saved across five SA cities from 2001 to 2005.[5] Pro-gun interest groups seeking to promote gun ownership and diffusion have attacked these findings, suggesting that stricter gun control was only enacted in 2004 following the publication of regulations pertaining to the Firearms Control Act (FCA) of 2000. They also argue that the 5-year study period ignored a pre-existing downward trend in firearm homicide, and that postmortem figures conflicted with official statistics, such as those presented by Statistics South Africa (SSA). SA is fortunate to have good coverage of death notification nationally, alongside injury mortality surveillance in certain provinces. In this issue of SAMJ, we draw on SSA’s death notifications from 1997 to 2013 to ask the question Where have all the gun deaths gone?[6] We found that in death notification data, the trend in gunshot-related injury deaths – irrespective of intent – was consistent with the findings of other studies. The annual number of firearm deaths was increasing during the 1990s and peaked in 2000, the year in which the FCA was adopted by parliament. Thereafter, the annual number of firearm deaths began to decrease, increasingly following the adoption of the regulations related to the FCA in 2004. The study provides further support for the hypothesis that stricter gun control accounted for the decrease in firearm homicide in SA. The findings are not surprising and echo an expanding body of international evidence. In a recent systematic review, SantaellaTenorio et al.[7] identified 130 studies in 10 countries and found that reductions in firearm deaths were associated with the simultaneous implementation of laws encompassing multiple firearm restrictions in certain countries. The authors cited, alongside examples from the USA, Canada, Australia, New Zealand and Brazil, SA’s FCA, which banned certain types of firearm, required training tests for licences, additional licences for each gun owned, increased age requirements for ownership and compulsory background checks. While mortality data reflect the ‘good news’ of gun control policy saving lives, they are equally adept at showing the deleterious effects of laxity in its enforcement. A concerning finding from our study was that the decrease in homicide had not been sustained for the duration of the study period. We observed an increasing number of gunshot-related deaths in 2012 and 2013. This is also reflected in the increase in murder reported in recent police crime statistics. The timing of the observed increase in gunshot deaths also corresponds noticeably with the police finalising the fast-tracking of more than a million firearm-related applications between November 2010 and

July 2011, alongside allegations of corruption in the licensing and selling of firearms. In its series of evidence briefings, the World Health Organization includes reducing access to firearms among its ‘best buys’ for violence prevention.[8] Although reduced access does not address the root causes of violence, it does, more often than not, reduce the severity and lethality of interpersonal conflict. In a high-violence setting such as SA, there are limited opportunities to effect a significant reduction in violence and homicide at the population level, and to do so relatively quickly. Most evidence-based strategies to reduce violence, such as investing in the early development stages of childhood and increasing positive adult involvement in child monitoring and supervision, establishing positive sociocultural norms, reducing socioeconomic inequalities and improving criminal justice and social welfare systems, all require long-term commitment and investment. As such, they can be difficult to sustain over relatively short political cycles.[9] Reducing firearm mortality by means of stricter gun control is one of the most important short- to medium-term measures to address the burden of violence in SA, while longer-term interventions and policy options take effect. When we have evidence that policies and interventions are working, we need to ensure that they are applied rigorously and consistently. We should be wary of attempts to deny the evidence by groups and individuals promoting their own narrow ideological and commercial interests ahead of the public good. R Matzopoulos South African Medical Research Council Burden of Disease Research Unit, Cape Town, South Africa, and School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, South Africa richard.matzopoulos@mrc.ac.za 1. Prinsloo M, Matzopoulos R, Laubscher R, Myers J, Bradshaw D. Validating homicide rates in the Western Cape Province, South Africa: Findings from the 2009 Injury Mortality Survey. S Afr Med J 2016;106(2):193-195. DOI:10.7196/SAMJ.2016.v106i2.10211 2. Bradshaw D, Nannan N, Laubscher R, et al. South African National Burden of Disease Study 2000: Estimates of Provincial Mortality. Cape Town: Medical Research Council, 2004. http://www.mrc.ac.za/ bod/estimates.htm (accessed 9 May 2016). 3. Matzopoulos R, Prinsloo M, Pillay-Van Wyk V. Injury-related mortality in South Africa: A retrospective descriptive study of postmortem investigations. Bull World Health Organ 2015;93(5):303-313. DOI:10.2471/BLT.14.145771 4. Abrahams N, Mathews S, Martin LJ, Lombard C, Jewkes R. Intimate partner femicide in South Africa in 1999 and 2009. PLoS Med 2013;10(4):e1001412. DOI:10.1371/journal.pmed.1001412 5. Matzopoulos RG, Thompson ML, Myers JE. Firearm and nonfirearm homicide in five South African cities: A retrospective population-based study. Am J Public Health 2014;104(3):455-460. DOI:10.2105/ AJPH.2013.310650 6. Matzopoulos RG. Where have all the gun deaths gone? S Afr Med J 2016;106(6):589-591. DOI:10.7196/ SAMJ.2016.v106i6.10379 7. Santaella-Tenorio J, Cerdá M, Villaveces A, Galea S. What do we know about the association between firearm legislation and firearm-related injuries? Epidemiol Rev 2016;mxv012. DOI:10.1093/epirev/ mxv012 8. World Health Organization. Violence prevention. The evidence. Geneva: WHO, 2010. http://www. who.int/violence_injury_prevention/violence/4th_milestones_meeting/publications/en/ (accessed 9 May 2016). 9. Matzopoulos R, Bowman B, Mathews S, Myers JE. Applying upstream interventions for interpersonal violence prevention: An uphill struggle in low- to middle-income contexts. Health Policy 2010;97(1):62-70. DOI:10.1016/j.healthpol.2010.03.003

S Afr Med J 2016;106(6):544. DOI:10.7196/SAMJ.2016.v106i6.11034

June 2016, Print edition

EDITORIAL

Comment on the Central Drug Authority’s position statement on cannabis The Central Drug Authority (CDA)’s ‘Position statement on cannabis’[1] is a welcome, if somewhat belated, article that gives an indication of the South African (SA) government’s response to the shifting sands of local and international public opinion and global drug policies. Most of the policies outlined in this document can be found in the CDA’s National Drug Master Plan (NDMP).[2] This article appears to be an attempt to clarify some of those policies, emphasise others and introduce one or two new strategies. Although the title of the paper points to a focus on cannabis, the CDA correctly ties in cannabis issues with those of alcohol, tobacco and other illicit psychoactive substances.

Decriminalisation of cannabis

The most important new policy to appear in the position statement[1] is a recommendation for the decriminalisation of cannabis. This represents a major shift in government thinking, as the proposed decriminalisation of cannabis or any other drug does not appear in the NDMP (2013 - 2017),[2] and it is something that the CDA has previously opposed.

Medical marijuana

Unfortunately, the CDA continues to use stale arguments such as the dangers of cannabis to oppose its use as a medicinal herb. As we know, all medicines, including potentially lethal over-the-counter drugs such as aspirin and paracetamol, have many undesirable effects. Cannabis is no exception, but it is far less harmful than the above two drugs. It is also far less toxic than alcohol, which is associated with many kinds of cancer, cardiovascular disease, and other diseases.[3,4] Alcohol is directly responsible for the deaths of over three million people annually,[5] while deaths attributed to cannabis are insignificant in comparison.[6] The CDA continues to justify the illegal status of cannabis and other drugs by using confirmation bias in its selective presentation of evidence to oppose the legalisation of medical marijuana.[7] If it used the same standards regarding alcohol and tobacco, those two drugs would also be banned. Ironically, if the CDA’s recommendation for the decriminalisation of cannabis does bear fruit, individuals will be able to legally self-medicate with this herb even if the failure to legalise medical marijuana does not allow doctors to prescribe it. An unintentional, illogical policy clash? As the CDA recommends cannabis decriminalisation rather than legalisation (cf. legal regulation), it is important to consider the substantial differences between the two policies.

Decriminalisation

Two pertinent definitions of decriminalisation are: • The removal of criminal sanctions for personal use and possession of limited quantities of a drug. • De facto decriminalisation is the intentional ignoring of drug laws without changing them. A good example is employed in The Netherlands, where the possession and sale of cannabis are allowed despite the relevant laws remaining on the statute books. Decriminalisation would certainly be preferable to the present SA situation, where the law criminalises people for drug use and possession. However, it is completely ineffective as a means of controlling the production, supply and purity of illegal drugs. As it

also fails to address the fundamental reasons for the massive growth in the international criminal drug trade, decriminalisation is neither an effective nor distinct control model – it is simply a mild form of prohibition.[8] Decriminalisation rarely provides for users to legally obtain their drugs, but implicitly directs them to continue sourcing drugs of unknown purity and potency. It also requires them to engage with criminals who sell their wares to anyone – including minors. Although it does contribute to harm-reduction strategies relating to the drugs themselves, decriminalisation has a negligible effect on the criminal drug trade – at least as important a cause of drug-related medical and social ills as substance use itself.[9,10] The prohibition-based drug laws implemented by 185 countries (including SA) that signed the 1961 United Nations Single Convention on Narcotic Drugs[11] are primarily responsible for the disastrous failure by the international community to contain drug use and the concomitant multibillion dollar global trade in illicit drugs.[8,10] Although this and its associated treaties allow countries to use their discretion as to how they structure their laws in relation to drug use, they specifically forbid the production and trade in those drugs deemed illicit by the United Nations (UN). Those countries, such as Portugal, that would prefer to go the legal regulation route are therefore having to make do with decriminalisation instead.

Legal regulation – a proven, holistic and humanistic approach to the control of psychoactive drugs

While legalisation is the process of making something illegal legal, legal regulation is the creation of a legal framework governing the production, supply and use of any drugs. The term ‘legal regulation’ does not imply an unregulated free market model of drug control. Rather it involves the implementation of strict controls in a policy area where there are currently very few. Supporters of the status quo – i.e. prohibition – oppose the less punitive model of legal regulation as a radical drug policy strategy. However, historical evidence demonstrates that it is prohibition that is a (failed) radical policy. The legal regulation of drug production, supply and use is far more in line with currently accepted ways of managing health and social risks in almost all other spheres of life such dangerous sports, road traffic accidents and sexually transmitted infections. Any drug will be safer if its production and availability is regulated rather than left in the hands of criminals. This rationale applies to the riskier drugs too; drugs need to be regulated because they are dangerous, not because they are safe. The laws governing alcohol and tobacco products can be found in variations of the legal regulation model that are operational in most countries. The abandonment of legal regulation (in favour of prohibition) of alcohol products in the USA in 1920, and its reintroduction 13 years later, is the most graphic demonstration that legal regulation of even a highly toxic psychoactive drug like alcohol is far better than its prohibition.[8,10] Prohibition gifted a massive source of revenue to the criminal world. Contaminated alcohol products killed and maimed people, organised crime structures such as the Mafia became very powerful, and corruption among politicians, law enforcement structures and the judiciary rose dramatically.[10]

June 2016, Print edition

EDITORIAL

The UN conventions prohibiting psychoactive drugs such as heroin, cocaine, cannabis, methamphetamines, psychedelics and others have caused even more widespread damage and misery than did Prohibition in America. These outdated treaties were built on a foundation of wilful ignorance, fear, racism and the distortion of scientific evidence[10] – influences that continue to prevail over contemporary scientific evidence, rationality and a humanistic approach to drug use. Unfortunately, most of the signatories of the UN treaties, including SA, continue to enforce their outdated, harmful and crime-friendly regulations. It is to be hoped that its position statement[1] is a signal that the CDA is moving away from being a laggardly government body that has been reluctant to take a lead in advocating the most basic harmreduction policies. It would be heartening to see SA take the bull by the horns and become a global leader in drug law reform. Before it does that, it needs to accept a few fundamental realities: • The ‘war on drugs’ has failed. The widespread use of drugs and the criminal edifice that controls the drug trade is not a result of legalising drugs, it is a result of criminalising them.[8-10,12,13] • As humans have and always will seek out psychoactive substances, a drug-free society is unattainable.[14] • The majority – over 80% – of people who use licit drugs or illicit drugs do not develop substance use disorders.[15-17] Moreover, these casual users of drugs form the largest body of customers who drive both the legal and illegal drug trades. • Most of the <20% of people who do develop substance use disorders have significant psychosocial issues.[15,16] They are the unfortunate ones whom the drug laws force onto the margins of society and into lives of crime.[10,13] The CDA needs to take a wider look at the drug problem when drawing up its policies. Using confirmation bias to justify a drug such as cannabis’s illegal status – without taking the harms of prohibition into account – is unworthy of a body that continually emphasises its commitment to evidence-based policies. In spite of ample evidence supporting its use in the control of all psychoactive drugs, the SA drug laws only allow for the legal regulation of the two most harmful drugs, alcohol and tobacco. Moreover, the CDA recommends the legal status quo of prohibition for all others except cannabis, for which it now proposes decriminalisation in preference to legalisation. These confused positions are based neither on logic nor the considerable body of evidence supporting legal regulation. The SA drug laws exacerbate rather than counter drug-related harms in several ways: • Enable organised crime and gangsterism to flourish and (unintentionally) facilitate easy access by minors to illicit drugs.[13]

• Instead of helping drug users, they marginalise them and drive them into lives of crime.[10,13] • Enforce the spraying of harmful herbicides on indigent, subsistence farmers’ cannabis and food crops.[18] • Trample on the human rights of adults who should be free to choose psychoactive drugs of their choice. It is to be hoped that the next CDA position statement or NDMP will reflect a more scientific, evidence-based approach to the broader drug problem, as recommended by organisations such as the Global Commission on Drug Policy and the International Centre for Science in Drug Policy.[19,20] Keith Scott Simon’s Town, Cape Town, South Africa Corresponding author: K Scott (zcottz@gmail.com) 1. Stein DJ, for the Executive Committee of the Central Drug Authority. Position statement on cannabis. S Afr Med J 2016;106(6):569-570. DOI:10.7196/SAMJ.2016.v106i6.10863 2. Central Drug Authority of South Africa. The National Drug Master Plan 2013 - 2017. Pretoria: Department of Social Development, 4 July 2013. 3. Nutt DJ, King LA, Phillips LD, Independent Scientific Committee on Drugs. Drug harms in the UK: A multicriteria decision analysis. Lancet 2010;376(9752):1558-1565. DOI:10.1016/S01406736(10)61462-6 4. Lachenmeiera D, Rehm J. Comparative risk assessment of alcohol, tobacco, cannabis and other illicit drugs using the margin of exposure approach. Sci Rep 2015;5:8126. DOI:10.1038/srep08126 5. World Health Organization. Global Status Report on Alcohol and Health. Geneva: WHO, 2014. 6. Calabria B, Degenhardt L, Hall W, Lynskey M. Does cannabis use increase the risk of death? Systematic review of epidemiological evidence on adverse effects of cannabis use. Drug Alcohol Rev 2010;29(3):318-330. DOI:10.1111/j.1465-3362.2009.00149.x 7. Ksir C, Hart C. Cannabis and psychosis: A critical overview of the relationship. Curr Psychiatry Rep 2016;18(2):12. DOI:10.1007/s11920-015-0657-y 8. Taylor S, Buchanan J, Ayres T. Prohibition, privilege and the drug apartheid: The failure of drug policy reform to address the underlying fallacies of drug prohibition. Criminol Crim Justice 2016 (accessed 6 May 2016, online only). DOI:10.1177/1748895816633274 9. Nadelmann E. Drug prohibition in the United States: Costs, consequences, and alternatives. Science 1989;245(4921):939-947. DOI:10.1126/science.2772647 10. Hari J. Chasing the Scream: The First and Last Days of the War on Drugs. London: Bloomsbury, 2015. 11. United Nations. Single Convention on Narcotic Drugs. New York: UN, 1961. 12. Drucker E. Drug prohibition and public health: 25 years of evidence. Public Health Rep 1999;114(1):1429. 13. Goga K. The Drug Trade and Governance in Cape Town. Pretoria: Institute for Security Studies, 2014:263. 14. Crocq M. Historical and cultural aspects of man’s relationship with addictive drugs. Dialogues Clin Neurosci 2007;9(4):355-361. 15. Robins L, Helzer J, Davis D. Narcotic use in Southeast Asia and afterward: An interview study of 898 Vietnam returnees. Arch Gen Psychiatry 1975;32(8):955-961. DOI:10.1001/ archpsyc.1975.01760260019001 16. Clarke H, Soneji N, Ko D, Yun L, Wijeysundera D. Rates and risk factors for prolonged opioid use after major surgery: Population based cohort study. BMJ 2014;348:g1251. DOI:10.1136/bmj.g1251 17. Mann J. British drugs survey 2014: Drug use is rising in the UK – but we’re not addicted. The Guardian 5 October 2014. 18. Fezisa M. War on dagga puts rural people at toxic risk. Mail and Guardian 19 March 2015. 19. Global Commission on Drug Policy. Taking Control: Pathways to Drug Policies that Work. Geneva: GCDP, 2014. 20. International Centre for Science in Drug Policy. Using Evidence to Talk about Cannabis. Toronto: ICSDP, 2015. http://www.icsdp.org/publications (accessed 6 May 2016).

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GUEST EDITORIAL

Mental health of and substance use by adolescents Almost 40% of the population of sub-Saharan Africa are between the ages of 12 and 24 years. Adolescence is a time of important biological, physiological, neurological, behavioural and social transitions towards adulthood. This period of transition is characterised by higher impulsivity, increased sensation-seeking behaviour, higher risk-taking behaviours relating to substance use and/or sexual experimentation, an increased sense of self-awareness/invincibility, and a higher importance of social relationships involving partners and peers rather than parents and older siblings. Not surprisingly, the psychological stressors of going through adolescence, coupled with major hormonal, physiological and identity development and peer pressure (to fit in with dominant peer norms), result in enormous stress levels that sometimes lead to a variety of mental health disorders, e.g. inadequate coping and/or support structures. In much of sub-Saharan Africa, this transition is taking place in the context of increased economic stress, high youth unemployment, high levels of crime, increasing access to information through modern technology, and high levels of rape and gender-based violence, where adolescent girls and young women bear a disproportionate burden. The risk of adolescents experiencing mental health and/or substance use disorders has increased. It is estimated that about 20.0% of children and adolescents experience a mental health disorder, while 5.6% of adults and adolescents have alcohol and substance use disorders. Mental health illnesses and substance use disorders often converge, and many adolescents with mental health illnesses also experience poorer academic performance, higher rates of suicide, violence, substance abuse, pregnancy and psychopathology with ageing. In addition to an increased risk of mental health problems, high rates of alcohol dependence and the early initiation of, or participation in, binge drinking may increase the risk of negative sexual health outcomes by increasing the chances of unwanted pregnancy, risky sexual practices, and gender-based violence. In the context of subSaharan Africa, where HIV rates remain high, particularly among young women, mental health and substances use disorders could play a mediating role in further enhancing the risk of HIV infection in this already vulnerable group. In sub-Saharan Africa, there are critical inadequacies with regard to access to and adequacy of the provision of mental health and/or substance use services, which are more evident in adolescents. In addition to the limitations of the adolescent-friendliness of primary healthcare services, there is often insufficient capacity and preparedness of providers to screen, identify and treat mental health or substance use cases. While treatment for substance use is often through specialised non-governmental and private organisations, there remains

a gap with mental health issues, exacerbated by social stigma and shame. Adolescents with mental health problems are less likely to disclose substance use to health practitioners. Specialised and targeted screening of adolescents for these disorders, especially when comorbid, is essential to improve adolescent mental health and substance use outcomes. The vulnerability of adolescents to mental health issues, and the increased prevalence of binge drinking and hazardous drinking habits of young people, not only increase the risk of social problems but may also heighten their risk of HIV infection, highlighting the importance of addressing these issues within the rubric of a holistic wellness service targeted at these young people. In this issue of SAMJ, two articles highlight the challenges of mental health and substance use â&#x20AC;&#x201C; individually and in combination. The article by Paruk and Karim[1] highlights the importance of psychiatric disorders among adolescents, and notes that despite affecting 20.0% of children and adolescents, this group of young people remains poorly detected and treated suboptimally. The authors describe how the majority of psychiatric disorders experienced by adolescents, including mood, anxiety and substance-related disorders, are often linked to a combination of genetic, behavioural and psychosocial factors. The authors provide ways of screening and treating adolescents, which can easily be built into health services. The article by Morojele and Ramsoomar[2] focuses on substance use disorders, in particular alcohol abuse. The magnitude of alcohol abuse among young South Africans is highlighted, as are the risk factors associated with the disorder and its comorbid relationship with mental health problems. An essential component of ensuring the wellbeing of adolescents is being better prepared with adequately trained staff and facilities to meet the needs of adolescents, including mental health and subÂstance use. Quarraisha Abdool Karim Guest editor Centre for the AIDS Programme of Research in South Africa, Durban, South Africa quarraisha.abdoolkarim@caprisa.org 1. Paruk S, Karim E. Update on adolescent mental health. S Afr Med J 2016;106(6):548-550. DOI:10.7196/ SAMJ.2016.v106i6.10943 2. Morojele NK, Ramsoomar L. Addressing adolescent alcohol use in South Africa. S Afr Med J 2016;106(6):551-553. DOI:10.7196/SAMJ.2016.v106i6.10944

S Afr Med J 2016;106(6):547. DOI:10.7196/SAMJ.2016.v106i6.11026

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Update on adolescent mental health S Paruk, MB ChB, FCPsych (SA), Child Psych (SA), MMed; E Karim, MB ChB, FCPsych (SA), Child Psych (SA) Discipline of Psychiatry, School of Clinical Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban; and King Dinizulu Hospital, Durban, South Africa Corresponding author: S Paruk (paruks4@ukzn.ac.za)

Adolescence is a period of significant physical, social and emotional change and therefore a vulnerable period for the development of mental illness. Many psychiatric disorders have their onset during adolescence. Approximately 20% of children have a mental health disorder, but the majority of disorders are not detected and treated. Risk factors for mental illness include: genetic vulnerability, neurobiological factors and psychosocial stressors. Common mental disorders during this period are mood, anxiety and substance related, with adolescents often presenting with comorbidity. Healthcare practitioners should screen for adolescent mental illness and assoÂciated suicide risk. Brief screening tools such as the Strengths and Difficulties Questionnaire are useful in detecting mood and anxiety disorders in primary care settings. While there is increasing evidence for the efficacy of psychotropic medications in adolescents, more research is still required. Management of adolescent mental health problems generally requires a combination of psychotropic medication and psychosocial interventions. Early intervention and support in an integrated medical and psychiatric healthcare system is required. S Afr Med J 2016;106(6):548-550. DOI:10.7196/SAMJ.2016.v106i6.10943

Scope of mental health problems in adolescence

It is estimated that about 20% of children and adolescents have a mental health disorder and approximately half of all mental illness and substance-related problems start at the age of 14 years.[1] The risk of mental health problems is further exacerbated in vulnerable environments with poor social support and socioeconomic inequalities, such as developing countries.[2] In a study of mental health among 15 - 19-year-old youth in five cities globally, female adolescents from Johannesburg reported the highest levels of depression and post-traumatic stress symptoms (44.6% and 67.0%, respectively).[2] Suicide remains the second leading cause of death among young people worldwide.[3] Common psychiatric disorders in adolescents, including anxiety-, mood-, trauma- and stressorrelated disorders, are all associated with increased suicide risk.[3]

Importance of assessing and treating mental health problems in adolescence

The majority of adolescents with mental illness remain undiagnosed and untreated, and services are often fragmented.[4] Mental illness in adolescents is associated with significant disease burden, such as poor academic achievement, suicide, violence, substance use, pregnancy and potentially increased risk of psychopathology later in adulthood.[4] The aetiology of mental illness in adolescents is multifactorial and includes biological factors, such as genetic vulnerability, in utero exposure to toxins, substance abuse and head trauma. Psychosocial factors include abuse, neglect, bereavement, family conflict, bullying and stressful life events.[4] Protective factors include familial ties and social support.[2] While the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) diagnostic criteria are generally the same for adolescents and adults, the psychiatric assessment of the adolescent can be more challenging.[5] Adolescence is a period of significant emotional and behavioural change, which makes distinguishing normal development from psychiatric illness difficult. Most adolescents are not able to independently access health services, and are often accompanied by a caregiver. This may raise challenges, as adolescents may be reluctant to engage with the practitioner, may

fear disclosure of personal information to the caregiver, or may fear stigmatisation by others. Practitioners should guard against any perception of collusion with the caregiver. Adolescents may often present with vague, nonspecific symptoms, as they may be unable to express their emotional distress. Finally, there is often comorbidity between the psychiatric disorders, substance use and medical disorders, which may further contribute to the challenge.[4] The substantial evidence of a high prevalence and burden of mental illness in adolescence suggests a need for greater awareness of psychiatric disorders. Primary healthcare practitioners should consider mental illness and suicide risk when assessing adolescents. A variety of screening tools are available to assist with assessment, including: the Paediatric Symptom Checklist, the Strengths and Difficulties Questionnaire (SDQ), and the Reporting Questionnaire for Children.[6-8] The SDQ has been used in the South African setting and is available in several languages. Although the evidence base for management of psychiatric disorders in adolescents is improving, there is still a dire need for further pharmacological and psychosocial intervention studies.[4] General treatment principles include establishing a therapeutic alliance, involvement of family and school, and use of a multimodal treatment plan that includes psycho-education and pharmacological and psychosocial interventions. There is increasing recognition of the efficacy of psychotropic medication in this age group. Medication use is determined by the type and severity of the psychiatric disorder, past psychiatric history, family history, medical history and patient and family preference.[9] When prescribing medication, one has to consider the appropriate dosage and slow titration, and avoid polypharmacy.

Identifying common mental health problems

The objective of this article is to highlight the high prevalence of psychiatric disorders in adolescents and to provide a casebased clinical overview of common mental health disorders and interventions available for adolescents.

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Case report

A 15-year-old girl presented after a panic attack. The patient and her parents reported that she suffered from irritable mood, withdrawal, tearful bouts, excessive worry, poor concentration at school (poor marks in last school report), loss of weight and disturbed sleep for 4 months. There were no psychotic symptoms and she did not use substances. On further enquiry the patient revealed that she was almost raped while out with friends. Collateral information from the teacher revealed that the patient had always been anxious, especially during public speaking and interacting with others, and that there was deterioration in her academic work more recently. The assessment of this patient includes a comprehensive history from the patient and her family, collateral information from the school, a physical examination, a mental state examination and any relevant investigations to exclude a medical disorder. The diagnostic considerations of the abovementioned adolescent should include the disorders listed below.

Mood disorders Depression

The prevalence of depression ranges from 4% to 8% in adolescents.[10] The DSM-5 diagnostic criteria for depression in adolescents and adults are the same.[5] Adolescents are more likely to present with irritable mood, apathy, sadness, low self-esteem, social withdrawal, insomnia and impaired concentration. They often describe themÂselves as useless or life as boring. The diagnosis of depression may be missed in older adolescents, as they may present with oppositional or antisocial behaviour, use of substances and problems at school. Fifty percent of adolescents with depression have two or more comorbid disorders, including disruptive behaviour disorders and anxiety disorders.[9] A suicide risk assessment must be part of every evaluation. Hospitalisation may be indicated if the patient is actively suicidal or has recent suicidal behaviour. The treatment of depression is multimodal, with a combination of psychotherapy and increasing evidence for the use of antidepressants in this age group. Psychotherapeutic interventions include psycho-education of the patient and family, supportive therapy and cognitive behavioural therapy.[9] Treatment with antidepressants is indicated for moderate to severe depression, recurrent depression and poor response to psychotherapy. Selective serotonin reuptake inhibitors (SSRIs) are considered as the first-line intervention for adolescents with depression. In this regard, the most evidence has currently been accumulated for the SSRI, fluoxetine.[11] Tricyclic antidepressants are not effective for paediatric depression. The risk of suicide with SSRI antidepressant initiation in children and adolescents is controversial.[11] The potential risk of treatment-emergent agitation and suicidal ideation associated with SSRI medication can be managed with close monitoring of the patient for self-harm and informed consent from the caregiver for the use of psychotropic medication. Treatment with antidepressants should be continued for 6 - 12 months after recovery and should be tapered off over 6 - 12 weeks at the end of treatment.[9]

Trauma- and stressor-related disorders Post-traumatic stress disorder

There is a high prevalence of trauma in our society and approximately a quarter of all individuals who experience significant trauma may develop post-traumatic stress disorder (PTSD).[12] Adolescents with PTSD develop symptoms in response to a traumatic event involving actual or threatened death, serious injury or sexual violence. The patient may have experienced the event personally or it may have occurred to another, with the patient witnessing or being informed of it. Patients with this disorder,

experience intrusive symptoms such as recurrent recollections, dreams, flashbacks and persistent severe psychological and physioÂ logical reactions to reminders of the event. They attempt to avoid thinking about the occurrence and external reminders of the trauma. Disturbances in mood and cognition occur, such as fear, guilt, detachment and memory impairment. Furthermore, there may be alterations in arousal and reactivity levels, such as hypervigilance and increased startle response.[5]

Acute stress disorder

Acute stress disorder (ASD) presents very similarly to PTSD. While the traumatic event criteria and symptoms are identical, it differs with regard to duration. ASD symptoms last for 3 days - 1 month, while PTSD symptoms are present for >1 month.[5] It is estimated that half of PTSD patients will first present with ASD. After exposure to a traumatic event, many adolescents experience a degree of distressing symptoms, but will not progress to developing a trauma-related disorder. For those manifesting only mild symptoms for <4 weeks, it may be appropriate to adopt a watchful waiting position.[12] The evidence base supports the use of trauma-focused psychoÂ therapy, in particular cognitive behavioural therapy.[12] Medication may be warranted for severe and persisting symptoms, as well as for symptoms that fail to respond to psychotherapy. There is a marked paucity of pharmacological treatment studies in adolescents. Based on the available data, an SSRI is an appropriate choice, noting the abovementioned cautions. Psychotherapy and medication are often combined.[13]

Adjustment disorder

Adolescents may also react to stressors of lesser severity than those associated with the conditions noted above. An adjustment disorder refers to the development of emotional or behavioural symptoms in response to and within 3 months of a stressor that does not meet the criteria for a traumatic event. The reaction is disproportionate to the severity of the stressor and is associated with functional impairment.[5] The disorder may present with varied symptoms, such as anxiety, depression and behavioural disturbances. Adjustment disorder in adolescents is associated with an increased risk of suicidal behaviour and, at a later stage, psychiatric disorders.[14] Crisis intervention and brief psychotherapy may be useful options. Pharmacotherapy is generally not indicated, except for short-term relief of insomnia and anxiety symptoms.[14]

Anxiety disorders

Social anxiety disorder (social phobia)

Patients with this disorder experience marked fear or anxiety in response to social situations in which they are under the scrutiny of others. They fear that their behaviour will be embarrassing, humiliating or lead to rejection, or be perceived as offensive to others. The severity of symptoms is in excess of the actual risks posed by the situation. Patients avoid such situations or endure them with intense fear or anxiety.[5] While many people experience some degree of anxiety in social situations, it is generally only those with the disorder that experience resultant functional impairment.

Generalised anxiety disorder

The prevalence of generalised anxiety disorder (GAD) among children and adolescents has been estimated to be as high as 10%.[15] GAD is characterised by excessive anxiety and worry over a variety of day-to-day issues. The excessive anxiety occurs almost daily and persists for at least 6 months. The symptoms may include

June 2016, Print edition

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restlessness, muscle tension, fatiguability, irritability, disturbed concentration and sleep,[5] and panic attacks. Panic attacks refer to brief periods of intense anxiety. During an attack a multitude of somatic symptoms may occur, such as tachy cardia, shortness of breath, nausea and paraesthesia. Psychological symptoms such as fear of dying or losing control, derealisation, and depersonalisation may also occur.[5] Panic attacks frequently occur in association with other psychiatric disorders. For example, a learner with social anxiety disorder may experience a panic attack if required to deliver a speech in front of an audience, or someone with PTSD may have an attack if reminded of their trauma. These panic attacks can be anticipated because they are triggered by identifiable situations.

Panic disorder

Panic disorder comprises recurrent panic attacks that are unexpected, as they do not occur in response to an identifiable situation. Furthermore, the attacks induce a prolonged period (at least 1 month) of persistent worry or maladaptive behavioural change.[5] As somatic symptoms predominate, it is important to first exclude the possibility that the symptoms are the result of another medical condition or are substance related. Patients often display symptoms of more than one anxiety dis order.[5] The anxiety disorders share commonalities in aetiology and symptomatology; therefore, similar treatment approaches are used. The established treatments for anxiety disorders are psychotherapy (with a good evidence base for cognitive behavioural therapy), medications (most evidence favouring the SSRIs), and combinations of these approaches.[13] There is only a small role for the use of benzodiazepines owing to side-effects and the risk of addiction. While adolescents may also suffer from other anxiety disorders, such as separation anxiety disorder, specific phobias and agoraphobia, these are not common in this age group and therefore beyond the scope of this article.

Conclusion

Psychiatric disorders in adolescents are common and often pose many clinical challenges with regard to assessment and treatment. Mental illness in adolescents is associated with significant short- and long-term morbidity. There is therefore an urgent need to increase awareness, and improve screening, detection and treatment of mental illness in this vulnerable group. An integrated healthcare system that provides medical and mental healthcare at primary and secondary level is critical to address the mental healthcare gap in adolescent services. References 1. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age of onset distributions of DSMIV in the National Comorbidity Survey Replication. Arch Gen Psychiatry 2005;62(6):593-602. DOI:10.1001/archpsyc.62.6.593 2. Cheng Y, XianChen L, Chaohua L, et al. The association between social support and mental health among the vulnerable adolescents in five cities: Findings from the study of the well-being of adolescents in vulnerable environments. J Adolesc Health 2014;55:S31-S38. DOI:10.1016/ jadohealth.2014.08.020 3. Hawton K, Saunders KEA, O’Conner RC. Self-harm and suicide in adolescents. Lancet 2012;23:2773-2782. 4. Patel V, Flisher AJ, Hetrick S, McGorry P. Mental health of young people: A global public health challenge. Lancet 2007;369:1302-1313. 5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association, 2013. 6. Jellinek MS, Murphy JM. Brief psychosocial screening in outpatient pediatric practice. J Pedriatr 1986;109:371-378. 7. Goodman R. The Strengths and Difficulties Questionnaire: A research note. J Child Psychol Psychiatry 1997;38:581-586. 8. Tedesse B, Kabede D, Tegegne T, Alem A. Childhood behavioural disorders in Ambo district, Western Ethiopia. II. Validation of the RQC. Acta Psychiatr Scand Suppl 1999;397:98-101. 9. Birmaher B, Ryan ND, Williamson DE, et al. Childhood and adolescent depression: A review of the past 10 years. Part I. J Am Acad Child Adolesc Psychiatry 2003;35:1427-1439. 10. Costello J, Erkanli E, Angold A. Is there an epidemic of child or adolescent depression? J Child Psychol Psychiatry 2006;47:1263-1271. 11. Birmaher B, Brent D; AACAP working group on quality issues. Practice parameters for the assessment and treatment of children and adolescents with depressive disorders. J Am Acad Child Adolesc Psychiatry 2007;46:1503-1526. 12. National Institute for Health and Clinical Excellence. Post-Traumatic Stress Disorder (PTSD): The Management of PTSD in Adults and Children in Primary and Secondary Care. Clinical Guideline 26. London: NICE, 2006. 13. Rynn M, Puliafico A, Heleniak C, et al. Advances in pharmacotherapy for pediatric anxiety disorders. Depress Anxiety 2011;28:76-87. DOI:10.1002/da.20769 14. Casey P, Bailey S. Adjustment disorders: The state of the art. World Psychiatry 2011;10:11-18. 15. Keeton CP, Kolos AC, Walkup JT. Pediatric generalized anxiety disorder: Epidemiology, diagnosis, and management. Paediatr Drugs 2009;11(3):171-83. DOI:10.2165/00148581-200911030-00003

Further reading World Health Organization. Child and Adolescent Mental Health Resources: Global Concerns and Implications for the Future. Geneva: WHO, 2005. http:www.who.int/mental_health/publications (accessed 26 April 2016).

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Addressing adolescent alcohol use in South Africa N K Morojele,1,2 PhD; L Ramsoomar,2 PhD Alcohol, Tobacco and Other Drug Research Unit, South African Medical Research Council, Pretoria; and School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 2 School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 1

Corresponding author: N K Morojele (neo.morojele@mrc.ac.za)

Excessive alcohol consumption constitutes a significant public health problem for South Africans. Alcohol use by South African (SA) adolescents is characterised mainly by binge/heavy episodic drinking. Levels of binge drinking have been high, but relatively stable, among males since 2002, while there has been a significant increase in binge drinking by females since then. Binge drinking is a major risk factor for a range of alcohol-related harms in SA, including traffic-related accidents and deaths, interpersonal violence, fetal alcohol spectrum disorder (FASD), crime, sexual risk behaviour, HIV, tuberculosis and the resultant burden of all of these on the economy. Clinicians may play a key role in addressing adolescent alcohol use and alcohol-related harm. Such a role may involve screening, brief interventions and referrals to treatment. There are several assessment, screening and diagnostic tools to detect alcohol use and misuse, specifically among adolescents. Furthermore, various pharmacological and psychological approaches are available to treat adolescent alcohol problems. Special issues to consider when dealing with alcohol use problems among adolescents in SA include recognising the risk factors, and acknowledging and addressing the harms associated with alcohol use (including sexual risk behaviour and FASD) and the possible existence of comorbid mental health problems. S Afr Med J 2016;106(6):551-553. DOI:10.7196/SAMJ.2016.v106i6.10944

Definitions

• Adolescents are defined as young people aged 10 - 19 years.[1] • Alcohol use disorder (AUD) constitutes a combination of alcohol use and alco hol dependence in a single disorder, according to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5).[2] AUD is diagnosed when someone presents with the harmful use of alcohol, social and interpersonal problems related to alcohol use, and neglect of major roles owing to use. Furthermore, a diagnosis is made when someone presents with at least two of 11 criteria in the past 12 months.[2] The greater the number of criteria met, the greater the severity of the disorder.[2] The recent transition from the DSM-IV to DSM-5 has removed the previous distinction between alcohol abuse and alcohol dependence, as problems with alcohol are assumed to exist on a continuum. AUDs can be mild (2 - 3 symptoms), moderate (4 - 5 symp toms), or severe (≥6 symptoms). • Binge/heavy episodic drinking refers to the consumption, on one occasion, of ≥5 drinks for males and ≥4 for females.

Introduction and epidemiology

Excessive alcohol consumption constitutes a significant public health problem for South Africans. The current drinking situation in South Africa (SA) is characterised by absti nence from alcohol use juxtaposed with

and Health indicated a prevalence of 5.6% of AUDs among SA adults and adolescents (10.0% among males and 1.5% among females),[1] and a prevalence of 2.4% for alcohol dependence (4.2% for males and 0.7% for females).[1]

heavy episodic drinking. From a global perspective, almost half of the SA population (42.0% of people >15 years of age) abstain from alcohol during their lifetime, 17.3% are former drinkers, and 59.4% have abstained from drinking during the past 12 months. Females abstain more than males in all categories of abstinence.[1] The patterns of drinking that are common among South Africans are of major concern for public health. Apart from achieving global status as one of the most risky drinking countries,[3] a recent national review indicated the high levels of binge/heavy episodic drinking.[4] The study specifically found that the prevalence of hazardous or harmful drinking among current drinkers was 31.5% (39.4% among males and 16.6% among females).[4] There are very clear variations among South Africans with regard to drinking, most notably by gender, race and province. The most recent World Health Organiza tion (WHO) Global Status Report on Alcohol

Drinking among SA adolescents

Adolescence represents a critical developmental period during which young people often experiment with and initiate alcohol use. It is also a period when several physiological changes occur in the brain, physical changes occur in the body (e.g. onset of puberty) and young people experience other sociopsychological transitions. Lifetime alcohol use among adolescents in SA can be characterised as stable but high during 2002 - 2011, with age of initiation <13 years having been stable at 12% over the same period (Table 1).[4] Drinking among SA adolescents is characterised by binge/heavy episodic drink ing.[1,5] According to the national Youth Risk Behaviour Survey (YRBS), binge drinking

Table 1. SA adolescents’ alcohol consumption by gender: findings from the YRBS[5-7] 2002

2008

2011

Alcohol consumption

Male

Female

Male

Female

Male

Female

Ever used alcohol, %

56.1

43.5

54.4

45.1

53.8

44.9

Current alcohol use (past 30 days), %

38.5

26.4

40.5

29.5

36.6

28.2

Binge drinking during past month, %

29.3

17.9

33.5

23.7

30.3

20.1

Age of initiation <13 years, %

15.8

9.0

15.3

8.6

16.3

8.7

YRBS = Youth Risk Behaviour Survey.

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increased between 2002 and 2008 and stabilised in 2011 among males. For females there was a significant increase between 2002 and 2008, which was not sustained in 2011.

Consequences of adoles cent drinking in SA

Binge drinking has important implications for long-term progression to problem drinking and acute alcohol-related harms, highlighted in both the global and the national literature.[1,4,7] Binge drinking is a major risk factor for a range of alcohol-related harms in SA, including traffic-related accidents and deaths, interpersonal violence, fetal alcohol syndrome, crime, sexual risk, tuberculosis, pneumonia and the resultant burden of all these harms on the economy.[8] The most recent findings of the South African Community Epidemiological Network on Drug Use (SACENDU) revealed that, with the exception of one site, between 11% and 19% of patients being treated were <20 years of age.[9] In light of SA’s status as one of the countries with the most risky drinking patterns, it is essential to address binge and problem drinking early in life to prevent both its direct effects on individual health and wellbeing and the associated harms. The WHO Global Status Report on Alcohol and Health highlights the important role of health professionals in ‘monitoring alcohol consumption in their patients and providing brief interventions, counselling and pharmacotherapy, as appropriate, in all cases of identified hazardous drinking or alcohol use disorder’.[1] Given the ubiquity of alcohol consumption in SA, it is important that clinicians regard alcohol and other drug use problems as central to patient care.

Assessment, screening and diagnosis

Since adolescents are often not readily inclined to seek treatment for problems related to their alcohol use, routine screening is recommended.[10] Screening, brief interventions and referral to treatment is advised, particularly to allow for early intervention, and to prevent alcohol-related harms and the progression to more serious AUDs. There are several assessment, screening and diagnostic tools to detect alcohol use and misuse. However, not all of these are recommended for adolescent populations. Among the tools applicable to adolescent populations in primary care are: the Alcohol Use Disorders Identification Test (AUDIT), its shorter adaption (AUDIT-C) (Box 1), the CRAFFT (Car, Relax, Alone, Forget, Family or Friends, and Trouble) instrument

(Box 2), and the Problem Oriented Screening Instrument for Teenagers (POSIT).[11] The AUDIT has been validated for identify ing adolescents at risk for alcohol misuse. However, a practical challenge of administering the AUDIT, particularly in busy clinical settings, is its length (10 items). Therefore, a shorter version of the AUDIT (AUDIT-C) is the preferred instrument, comprising only the first three items, which assess different aspects of alcohol consumption (Box 1). The AUDIT-C is scored on a scale of 0 12, with 0 indicating the absence of alcohol problems. Gender-specific scoring has been applied, with a score of ≥4 for men and ≥3 for women considered to be optimal for identify ing hazardous drinking or active AUDs. A recent review of the CRAFFT concluded that it had adequate psychometric properties Box 1. Items of the AUDIT-C How often do you have a drink containing alcohol? Never Monthly or less 2 - 4 times a month 2 - 3 times a week ≥4 times a week How many standard drinks containing alcohol do you have on a typical day when drinking? 1 or 2 3 or 4 5 or 6 7-9 ≥10 How often do you have ≥6 drinks on one occasion? Never Less than monthly Monthly Weekly Daily or almost daily AUDIT-C = shorter version of the AUDIT.

Box 2. Items of the CRAFFT • Have you ever ridden in a Car driven by someone else (or yourself) who was ‘high’ or had been using alcohol and drugs? • Do you drink to Relax? • Do you ever drink while you are Alone? • Do you ever Forget things you did while using alcohol or drugs? • Do any of your closest Family or Friends ever tell you that you should cut down on your drinking? • Have you ever gotten into Trouble while you were using alcohol or drugs?

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for the detection of AUDs among adoles cents[12] and is widely used to detect alcohol misuse in this age group. CRAFFT is an acronym that consists of six operative words as indicated in Box 2. A score of ≥2 on the CRAFFT is indicative of the presence of an alcohol- or drug-related problem. The POSIT consists of 139 items relating to 10 different problem areas, including alcohol and other drug use, mental health problems and other psychosocial problems. It is most suitable for more comprehensive screening in settings where time constraints are not a major concern.

Treatment and management Brief interventions

Brief interventions are generally of short duration and can be effective for use as part of universal and/or selective and/or indicated prevention approaches.[13] These interventions can be delivered by different categories of healthcare providers, including physicians, nurses, social workers and psychologists. According to a recent metaanalysis, brief interventions are effective (with modest effects) for reducing alcohol consumption and alcohol-related harm among adolescents.[13] Such improvements were sustained for as long as 1 year, although the studies in the review did not have long follow-up periods for adolescents. The review included interventions of up to 5 hours’ contact time, and a maximum of 4 weeks between the first and last intervention session (with booster sessions in some cases). Overall, brief interventions were found to be effective regardless of inter vention modality (e.g. cognitive behavioural therapy (CBT) only, or motivational enhancement therapy (MET) only, or MET/CBT, or feedback/ information); delivery site (primary care/ health centre, or school/university, or emergency room or self-administered); or format (alone, individual, or group). However, interventions that included decisional balance and/or goal-setting exercises were particularly effective, and brief interventions had stronger effects on alcohol-related problems among younger adolescents than older ones Finally, the review indicated that adolescents who were identified as high risk may benefit more than those not so identified (i.e. non-drinkers or low-risk drinkers).

Specialised treatment

Where referral is needed, adolescent patients may receive a range of treatments, comprising psychosocial treatments alone or in combination with pharmacotherapy. The most com-

CME

mon types of psychosocial treatments for adolescents have been identified as: (i) family-based therapy; (ii) individual and group therapy – these mainly include CBT, brief interventions and motivational approaches, and contingency management reinforcement approaches; (iii) 12-step programmes; and (iv) therapeutic communities.[14] Different types of pharmacological therapies may be used for treating and managing AUDs. According to Clark,[15] these are most effective in conjunction with psychotherapy and are used for addressing withdrawal, reducing craving, minimising alcohol’s reinforcing proper ties, and/or addressing other mental health conditions. Alcohol withdrawal, which is extremely rare among adolescents, is generally treated using benzodiazepines, as in adults. These drugs are assumed to be appropriate for adolescents, but such use is not supported by empirical evidence.[15] Benzodiazepines are best used under medical supervision and with caution in pregnant women, given their teratogenic effects. Disulfiram (Antabuse) is used to increase physical aversion to alcohol, as it gives rise to negative symptoms (flushing, nausea, vomiting) when used with alcohol.[15] It is rarely used for adolescents, and requires close supervision and high levels of adherence to abstinence, particularly given the effects (arrhythmias, hypotension[15]) when alcohol is consumed in large quantities.[15] The most common medications for reducing craving are acamprosate and naltrexone.[15] Evidence for the effectiveness of these drugs in adolescents is limited.[15] Finally, certain pharmacotherapies are recommended for treating common comorbid conditions, such as attention-deficit hyperactivity disorder, major depressive disorder, conduct disorder and posttraumatic stress disorder. Treatment of these disorders may improve the outcomes of AUD treatment, and may include antidepressant and stimulant medications.[15] However, the limited evidence to support the use of these medications for adolescents and their abuse potential should be taken into account when they are being considered.[15] In spite of the availability of a range of treatment approaches for addressing alcohol use and other disorders among adolescents, many of the existing services have several shortcomings, and access to treatment is often difficult in SA.[8] SA has very few adolescent-focused or adolescent-exclusive treatment centres, and many existing services do not employ evidence-based approaches. Based on the limitations identified,[8] it is recommended that several factors, such as whether or not the service is adolescent focused, whether or not the programme is evidence based, and the extent of family involvement, should be considered when referring adolescents for treatment.

Special considerations Screening

Factors that may influence decisions about whom to screen may depend on whether the interventions involve a universal, selected or indicated approach. Moreover, in a high-risk community, where the prevalence of AUDs is relatively high, routine screening may be particularly important. One may also consider the presence of other individual risk factors, including a family history of alcohol problems and other mental health problems, e.g. risk factors, when deciding whom to screen and target for further assessment and treatment.

Treatment goal(s)

Total abstinence is generally accepted as the most appropriate treat ment goal for adolescents with an AUD. The findings of a number of studies showing cardioprotective effects of alcohol may tempt the clinician to suggest moderate drinking as an ideal treatment goal. However, these studies have not typically involved adolescents, and

the effects have been observed to diminish in cases of heavy episodic drinking.[1] Consequently, for all adolescents, the message that a little drinking may be good for them is best avoided, while the conclusions with regard to adults are more open to debate.

Comorbidity

Adolescents who engage in heavy drinking or are identified as having an AUD are typically at increased risk of other mental health, social or behavioural problems. For example, alcohol increases the risk of engagement in sexual risk behaviour, leading to sexually transmitted infections (STIs), including HIV. It is important to highlight these risks when engaging with adolescents, and to refer them for further assessment to screen for possible STIs, including HIV, where indicated.

Adolescent girls

Adolescent girls who drink alcohol are also at increased risk of unprotected sex, unplanned pregnancy and sexual assault. Alcohol consumption during pregnancy increases the risk of development of fetal alcohol spectrum disorders (FASDs) in the unborn child. Clinicians are advised to inform sexually active adolescents about the risk of FASDs, and to recommend total abstinence from alcohol among those who are not using contraceptives, given the current uncertainty about the exact threshold (if any) at which drinking becomes harmful.

Summary

Excessive alcohol consumption constitutes a significant public health problem among adolescents in SA. General practitioners are well placed to screen, treat and/or refer them for alcohol-related treatment. Several screening tools are available to guide practitioners on how best to manage their patients, while psychosocial and pharmacological approaches are also available (the latter under medical supervision) for the few instances in which they may be required. Notwithstanding time and other constraints in their busy practices, routine screening to detect alcohol use among adolescents and early intervention by physicians are highly recommended. References 1. World Health Organization. Global Status Report on Alcohol and Health. Geneva: WHO, 2014:20. http://apps.who.int/iris/handle/10665/112736 (accessed 22 June 2014). 2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association, 2013. 3. Peltzer K, Davids A, Njuho P. Alcohol use and problem drinking in South Africa: Findings from a national population-based survey. Afr J Psychiatry (Johannesburg) 2011;14(1):30-37. 4. Ramsoomar L, Morojele NK. Trends in alcohol prevalence, age of initiation and association with alcoholrelated harm among South African youth: Implications for policy. S Afr Med J 2012;10:609-612. 5. Reddy SP, James S, Sewpaul R, et al. Umthente Uhlaba Usamila – the 3rd South African National Youth Risk Behaviour Survey 2011. Cape Town: South African Medical Research Council, 2013. 6. Reddy SP, James S, Sewpaul R, et al. Umthente Uhlaba Usamila – the 2nd South African Youth Risk Behaviour Survey 2008. Cape Town: South African Medical Research Council, 2010. 7. Reddy SP, James S, Sewpaul R, et al. Umthente Uhlaba Usamila – the 1st South African Youth Risk Behaviour Survey 2002. Cape Town: South African Medical Research Council, 2003. 8. Morojele N, Rich E, Flisher A, Myers B. Youth and substances. In: Ellis G, Stein D, Meintjies E, Thomas K, eds. Substance Use and Abuse in South Africa: Insights from Brain and Behavioural Sciences. Cape Town: University of Cape Town, 2012:231-256. 9. Dada S, Harker Burnhams N, Erasmus J, et al. South African Community Network on Drug Use (SACENDU): Monitoring Alcohol, Tobacco and Other Drug Abuse Trends in South Africa (July December 2014). Cape Town: South African Medical Research Council, 2015. http://www.mrc.ac.za/ adarg/sacendu/SacenduUpdateJune2015.pdf (accessed 11 September 2015). 10. Mitchell SG, Gryczynski J, O’Grady KE, et al. SBIRT for adolescent drug and alcohol use: Current status and future directions. J Subst Abuse Treat 2013;44(5):463-472. DOI:10.1016/j.jsat.2012.11.005 11. Rumpf HJ, Wohlert T, Freyer-Adam J, Grothues J, Bischof G. Screening questionnaires for problem drinking in adolescents: Performance of AUDIT, AUDIT-C, CRAFFT and POSIT. Eur Addict Res 2013;19(3):121-127. DOI:10.1159/000342331 12. Mitchell SG, Kelly SM, Gryczynski J, et al. The CRAFFT cut-points and DSM-5 criteria for alcohol and other drugs: A re-evaluation and re-examination. Subst Abus 2014;35(4):376-380. DOI:10.1080 /08897077.2014.936992 13. Tanner-Smith EE, Lipsey MW. Brief alcohol interventions for adolescents and young adults: A systematic review and meta-analysis. J Subst Abuse Treat 2015;51:1-18. DOI:10.1016/j.jsat.2014.09.001 14. Winters KC, Botzet AM, Fahnhorst T. Advances in adolescent substance abuse treatment. Curr Psychiatry Rep 2011;13(5):416-421. DOI:10.1007/s11920-011-0214-2 15. Clark DB. Pharmacotherapy for adolescent alcohol use disorder. CNS Drugs 2012;26(7):559-569. DOI:10.2165/11634330-000000000-00000

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IN PRACTICE

CLINICAL PRACTICE

The role of appropriate diagnostic testing in acute respiratory tract infections: An antibiotic stewardship strategy to minimise diagnostic uncertainty in primary care A J Brink,1 MB ChB, MMed (Micro); J van Wyk,2 MB ChB, MMed (Clin Path); V M Moodley,2 MB ChB, DTM&H, FCPath (Micro) SA, MMed (Micro); C Corcoran,3 MB ChB, FCPath (Virol), DTM&H, MMed (Virol); P Ekermans,4 MB ChB, DTMH, MMed (Clin Path); L Nutt,5 MB ChB, MMed (Clin Path); T Boyles,6 MA, BM BCh, MRCP, MD, DTM&H, Cert ID SA; O Perovic,7,8 FC Path (SA) (Micro), MMed (Micro), DTM&H, MD; C Feldman,9 MB BCh, DSc, PhD, FRCP, FCP (SA); G A Richards,10 MB BCh, PhD, FCP (SA), FRCP; M Mendelson,6 BSc, PhD, MBBS, FRCP, DTM&H mpath National Laboratory Services, Milpark Hospital, Johannesburg, South Africa A Ampath National Laboratory Services, Cape Town, South Africa 3 Department of Molecular Biology, Ampath National Reference Laboratory, Centurion, South Africa 4 D epartment of Clinical Microbiology, Ampath National Reference Laboratory, Centurion, South Africa 5 Ampath National Laboratory Services, Port Elizabeth, South Africa 6 D ivision of Infectious Diseases and HIV Medicine, Department of Medicine, Groote Schuur Hospital and Faculty of Health Sciences, University of Cape Town, South Africa 7 Centre for Opportunistic, Tropical and Hospital Infections, National Institute for Communicable Diseases, Johannesburg, South Africa 8 D epartment of Clinical Microbiology and Infectious Diseases, School of Pathology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 9 D ivision of Pulmonology, Charlotte Maxeke Johannesburg Academic Hospital and Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 10 Department of Critical Care, Charlotte Maxeke Johannesburg Academic Hospital and Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 1 2

Corresponding author: A M Brink (brinka@ampath.co.za)

Antibiotic resistance has increased worldwide to the extent that it is now regarded as a global public health crisis. Interventions to reduce excessive antibiotic prescribing to patients can reduce resistance and improve microbiological and clinical outcomes. Therefore, although improving outpatient antibiotic use is crucial, few data are provided on the key interventional components and the effectiveness of antibiotic stewardship in the primary care setting, in South Africa. The reasons driving the excessive prescription of antibiotics in the community are multifactorial but, perhaps most importantly, the overlapping clinical features of viral and bacterial infections dramatically reduce the ability of GPs to distinguish which patients would benefit from an antibiotic or not. As a consequence, the need for tools to reduce diagnostic uncertainty is critical. In this regard, besides clinical algorithms, a consensus of collaborators in European and UK consortia recently provided guidance for the use of C-reactive protein point-of-care testing in outpatients presenting with acute respiratory tract infections (ARTIs) and/or acute cough, if it is not clear after proper clinical assessment whether antibiotics should be prescribed or not. A targeted application of stewardship principles, including diagnostic stewardship as described in this review, to the ambulatory setting has the potential to affect the most common indications for systemic antibiotic use, in that the majority (80%) of antibiotic use occurs in the community, with ARTIs the most common indication. S Afr Med J 2016;106(6):554-561. DOI:10.7196/SAMJ.2016.v106i6.10857

origin and are self-limiting, so non-antibiotic treatment options should be preferred, they still account for most of the antibiotics prescribed in primary healthcare. It is estimated that almost 60% of patients with an ARTI receive an unnecessary antibiotic, which is unlikely to be of benefit.[5,6,8-10] The reasons for the excessive prescription of antibiotics in the community are complex and include the lack of a precise diagnosis of the cause of the presenting respiratory illness, perceived patient and parental preference for the receipt of an antibiotic, and a lack of appreciation of the negative impact of unnecessary prescriptions, particularly with regard to the development of resistance in the community. Fear of litigation, both consciously and unconsciously, may also be a factor. Perhaps equally important are constraints on the time available to perform a full clinical assessment and

June 2016, Print edition

IN PRACTICE

the considerable diagnostic uncertainty that arises as a consequence of overlapping clinical features between bacterial and viral infections and even non-infectious respiratory illnesses.[10,11] This problem is exacerbated in community practice by the lack of availability of sensitive, specific and cost-effective tests to distinguish viral from bacterial infections. Even the presence of bacteria at the site of a suspected infection does not necessarily identify whether it is bacterial or not, as without evidence of inflammation it probably represents colonisation or contamination.[12,13] This implies that a good clinical history and examination alone may not be sufficient, and the judicious use of biomarkers, such as point-of-care testing (POCT) for C-reactive protein (CRP), may aid in diagnosis and thus reduce antibiotic consumption.[11] The purpose of this review is to provide a simple framework for clinical decisionmaking regarding antibiotic use and, where applicable, the appropriate use of laboratory tests for common ARTI syndromes in pri mary practice. This ‘diagnostic stewardship’ should be a key component of AS, providing assistance to clinicians in everyday practice to differentiate bacterial from viral infect ions or non-infectious conditions and, in so doing, boosting confidence in decisionmaking. Conceptually, this review should be understood as one strategy within a multi modal primary care AS programme with the ultimate aim of reducing redundant antibiotic use (Fig. 1).[14]

Patients presenting with acute cough

Acute cough, defined as lasting <3 weeks (and without more worrying features such as haemoptysis, weight loss or other symptoms of tuberculosis, chest pain or a history of aspiration) is estimated to represent the most common cause for consultation with a general practitioner (GP) and one of the commonest reasons for prescription of antibiotics in community practice; in one study, 52.7% of adult patients presenting with acute cough received an antibiotic.[15] This is despite Whaley et al.[16] having recently demonstrated that the most common infective causes of acute cough were viral: the common cold, nonspecific upper respiratory tract infections (URTIs) and acute bronchitis, for which antibiotic therapy is not indicated. Non-infectious conditions causing cough include postnasal drip from allergic rhinitis, gastro-oesophageal reflux, smoking, angiotensin-converting enzyme inhibitors and undiagnosed asthma. The symptoms of an acute cough can take up to 3 weeks to settle, and it is this prolonged duration that often

precipitates the initial antibiotic prescription (and possibly even a second one), out of desperation either on the part of the patient or the doctor.[17]

The common cold

It should be understood that the clear nasal secretions character istic of the common cold frequently become purulent without signi fying superimposed bacterial infection (Fig. 2). This is a common misperception and hence, even with coughing, which is a normal accompaniment of a postnasal drip, antibiotics are not required.[8] Patients should be advised that the average duration of the illness (before and after seeing the doctor) is in the region of 10 - 11 days. [17] Obtaining nasal swabs for culture is strongly discouraged even if the cough is persistent, and is particularly wasteful in resource-challenged low- and middle-income countries. Only symptomatic treatment should be provided, which may include analgesics such as paracetamol (for relief of fever, headache or sinus discomfort). Aspirin should be avoided

in children <18 years of age because of the risk of Reye’s syndrome. In those ≥12 years of age, oral or topical decongestants may relieve rhinorrhoea and nasal congestion; however, these should not be used for >5 days as longer durations may lead to rebound congestion known as rhinitis medicamentosa. Early use of a nasal steroid may reduce the duration of the postnasal drip-induced cough.

Acute bronchitis

Clinically, it can be difficult to differentiate acute bronchitis from other conditions that may present with cough.[18] The major differential diagnosis is community-acquired pneumonia (CAP), which does require antibiotics (Fig. 3). However, the presentation is very similar to that of the common cold.[19] The latter is usually associated with nasal congestion and rhinorrhoea and typically lasts only 7 - 10 days, but it is important to recognise that bronchitis also seldom occurs in isolation as it frequently results from a ‘sinobronchitis’ occurring as a consequence of a virally induced postnasal drip. The

Healthy person Susceptible to infections

Vaccination

Transmission of virus

Physical barriers (e.g. hand washing)

Complementary and alternative medicine (e.g. probiotics)

Exercise

Person with symptoms of a respiratory infection Need for reassurance

Expectations of antibiotics

Public campaigns

GP education

Behavioural intentions

Complementary and alternative medicine (e.g. zinc)

Patient consulting a GP

GP prescribing Perceived Patient habits patient demand expectations

Shared decisionmaking

Diagnostic tests and biomarkers

Steroids

Diagnostic uncertainty

Safety netting

Delayed antibiotic prescribing

Symptom relief

Shared decisionmaking Time pressure

Policy

Patient prescribed antibiotics

Over-thecounter medicine (e.g. non-steroidal anti-inflammatory drugs)

Therapeutic vacuum

Complementary and alternative medicine (e.g. Echinacea)

Mismatch between guidelines and packet size Policy

Person with redundant antibiotics

Fig. 1. Overview of strategies to minimise antibiotic use in primary care at each stage of the path from healthy person to antibiotic prescription (reproduced with permission from Hansen et al.[14]). Nasal stuffiness and throat irritation • Low-grade fever • Malaise • Myalgia

+/–

• Sneezing • Watery nasal discharge

+/–

Coughing

Mucopurulent secretions* 1 - 3 days

Persists up to 10 days in 31% of cases Persists up to 10 days in 35% of cases *Obtaining nasal swabs for culture is strongly discouraged.

Fig. 2. Natural history of the common cold.[8]

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presence of discoloured sputum should also not be used as an indicator of bacterial as opposed to viral infection, as both of these, and also non-infectious conditions such as asthma, frequently present with purulent or purulent-looking sputum.[18] In most cases, history and physical exami nation are sufficient to identify more serious conditions requiring chest radiography (CXR). Only in select circumstances may additional diagnostic testing be required. If it is suspected that an outbreak of bronchitis may be due to Mycoplasma pneumoniae or Chlamydophila pneumoniae, especially when presenting in young adults, a specimen for molecular confirmation may be warranted. A swab for Bordetella pertussis polymerase chain reaction (PCR) is warranted in unvaccinated patients with a paroxysmal or ‘whooping’ cough.[18]

Data are limited regarding the management of acute bronchitis in children. Most would regard it as an extension of a nonspecific viral URTI and no laboratory testing would be advised. Microscopy, culture and sensitivity (MC&S) on sputum specimens is strongly discouraged, as antibiotics may inappropriately be prescribed for growth of colonisers or normal flora. Perhaps the most important feature of a more severe condition requiring a CXR is tachypnoea. Antibiotics do not alter the natural course of acute bronchitis and should not be prescribed unless comorbid risk factors [18] are present (Fig. 3). Despite most cases being viral in origin, doctors in the USA continue to prescribe antibiotics to adults with this diagnosis despite clear-cut guideline recommendations to the contrary.[16] In fact, despite significant interventions, including

Patients presenting with acute cough and/or other LRTI symptoms

Clinical examination The following features favour CAP over acute bronchitis: • Fever ≥38°C • Tachypnoea ≥24/min • Tachycardia ≥100/min • Evidence of consolidation on examination: · Crackles · Bronchial breathing · Increased tactile fremitus or vocal resonance Where there is diagnostic uncertainty, follow the CRP algorithm Diagnostic uncertainty

POCT CRP (mg/L)

>100

CAP

20 - 100

<20

Acute bronchitis

Severity assessment Inpatient antibiotic treatment

Outpatient antibiotic treatment Routine sputum and CXR not indicated

• No further laboratory investigations indicated • Symptomatic treatment * • No antibiotic prescribed unless exception criteria met

• No antibiotic prescribed unless: · Risk factors present for a complicated course† · Patient deteriorates clinically • Alternatively, provide delayed antibiotic script if follow-up possible

*For patients with acute cough >80 years with one or more, or >65 years with two or more, of the following features, the noantibiotic prescribing strategy and the delayed-antibiotic prescribing strategy should not be considered:[17] • Hospitalisation in the past year • Current use of oral steroids or other immunosuppressive drugs • HIV/AIDS • Type 1 or type 2 diabetes mellitus • History of congestive heart failure. †

Risk factors:[45] • Patients <3 months or >75 years • Comorbid conditions: · Heart failure · Diabetes mellitus · COPD · Asthma · Immunocompromised.

Fig. 3. The use of POCT CRP measurement to distinguish CAP from acute bronchitis in the primary care setting.

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guidelines, quality measures and more than 15 years of educational effort by the Centers for Disease Control and Prevention (CDC), the antibiotic prescribing rates for acute bronchitis, which should be zero, have remained at 71% and even increased between 2006 and 2010.[20] Management should include advice to the patient as to the benign nature and course of the condition, with the potential for symptom resolution to take up to 3 weeks, together with a nasal steroid and with instructions for the patient to return should symptoms fail to resolve or if pyrexia, pleuritic chest pain or haemoptysis develop. A macrolide antibiotic should be prescribed for confirmed B. pertussis infections and, although it has limited symptomatic effect, it does reduce the risk of transmission.

Acute pharyngo tonsillitis

Respiratory viruses are the most common causes of acute pharyngitis/tonsillitis, while group A β-haemolytic streptococci (GABHS) (Streptococcus pyogenes) is the most impor tant bacterial pathogen; these account for 15% and 40% of adult and paediatric cases, respectively.[21,22] It is important to note that asymptomatic carriage of GABHS occurs in up to 20% of children and in up to 5% of adolescents and young adults.[23] Certain clinical features may assist in distinguishing viruses from GABHS (Fig. 4), and several clinical prediction rules to diagnose GABHS have been published.[24] However, reliance on these rules alone may still lead to antibiotic overprescription.[25] Currently, rapid antigen testing (RADT) methods have not been validated in SA and are therefore not routinely available. In a recent meta-analysis, the accuracy of RADT in children with pharyngitis selected as likely to have GABHS by means of clinical prediction rules, ranged from 24% (95% confidence interval (CI) 21 - 27) to 86% (95% CI 84 - 89).[25] According to the authors, none of 16 RADTs tested had good correlation with the diagnosis of GABHS by culture, particularly as the disease spectrum, the size of the bacterial inoculum and the skill of the operator all affect test performance.[25,26] Molecular methods, including PCR, offer the highest accuracy for GABHS detection (approaching 95 - 100%), but widespread use is limited by limited resources.[25] CRP POCT does not distinguish between those who do or do not require antibiotic therapy.[27] In addition, CRP values of 10 60 mg/L measured in the laboratory may not be able to distinguish between viral and bacterial pathogens in patients with symptoms of <7 days’ duration.[28] Although measurement

IN PRACTICE

of the absolute neutrophil count may increase diagnostic accuracy for GABHS when rapid antigen testing is not available, routine use is also not recommended;[29] nor are antistreptococcal antibody titres, as they reflect past and not current infections. [30] Taking all these factors into account, the diagnostic and antibiotic treatment criteria are summarised in Fig. 4. Correctly performed throat cultures are still considered the gold standard for the diagnosis of acute GABHS pharyngotonsillitis, with a high sensitivity of 90 - 95%.[30] To achieve this, it is recommended that the tonsils and posterior pharyngeal wall be vigorously swabbed.[21] It is important to note that a delay in antibiotic prescription pending availability of culture results does not reduce efficacy in the prevention of acute rheumatic fever and, as such, a delayed antibiotic prescription strategy is advised for all patients where a throat swab has been sent for MC&S. However, throat swabs for confirmation of GABHS may not be feasible in many SA settings owing to increased direct and indirect financial costs and the need for additional healthcare visits. In such cases, empirical antibiotic therapy is advised for all patients aged 3 - 21 years who fit the clinical prediction rules. Generally speaking, the mainstay of the management of acute pharyngitis is symptomatic and includes adequate analgesia and antipyretics.

Diagnose all-cause pharyngotonsillitis when the following are present: • Sore throat • Fever • Dysphagia • Halitosis Viral features • Coryza • Cough • Conjunctivitis • Hoarseness • Anterior stomatitis • Discrete ulcerative lesions • Diarrhoea

Bacterial features • Tender anterior cervical lymphadenopathy • Pharyngeal erythema • Pharyngeal oedema or exudate

GABHS more likely

GABHS unlikely

Perform throat swab

• Symptomatic treatment only • No antibiotic prescribed

No throat swab

• Symptomatic treatment • Provide delayed antibiotic script If GABHS grown, contact patient to have antibiotic dispensed • Symptomatic treatment • Provide antibiotic script only if 3 - 21 years old

Fig. 4. Diagnostic and treatment criteria for acute pharyngotonsillitis. Diagnose acute otitis media when rapid onset of signs and symptoms of inflammation in the middle ear is present:

Acute otitis media

Correct clinical diagnosis of acute otitis media (AOM) is the key to reducing overall antibiotic prescribing for this very common condition. Approximately 75% of children have had at least one episode by 3 years of age.[8] Time and clinical acumen is required to visualise the eardrum. Symp tom presentation varies with age and, because typical symptoms overlap with other conditions, a clinical history alone is insufficient to predict whether AOM is present or not. To confirm the diagnosis, inflammation of the eardrum and a middle ear effusion, i.e. fullness, bulging, cloudiness and redness of the tympanic membrane (TM), must be identified (Fig. 5). Although redness of the TM is an early sign of otitis media, it is not diagnostic on its own as there are numerous other causes, including crying, otitis externa, myringitis and barotrauma.[8] As a consequence, AOM is frequently mis- or overdiagnosed. Although clear visualisation of the TM is difficult at times, and because AOM is typically self-limiting, a high degree of diagnostic certainty is essential to minimise antibiotic overuse. Previous studies have shown that

Symptoms include: • Otalgia • Irritability • Otorrhoea* • Fever

Signs include: • Bulging +/– • Erythema +/– • Oedema +/– • Immobility of the TM on visualisation

Enhance judicious antibiotic use by categorising: • Severity • Laterality • Age

Patients with:

Patients who:

• More severe symptoms · Severe otalgia · Otalgia for >48 hours · Temperature ≥39°C • Bilateral involvement • Age ≤2 years

• Have non-severe disease • Have unilateral ear involvment • Age ≥2 years

• Symptomatic treatment • Provide immediate antibiotic script as such patients are more likely to benefit

• Symptomatic treatment • Provide delayed antibiotic script · If follow-up possible, observation · Watchful waiting for 48 hours

*Obtaining swabs and/or aspirations of otorrhoea (clear or purulent secretions) from a fresh tympanic perforation that is neither chronic nor recurring, in patients without prior exposure to antibiotics, is not routinely advised.

Fig. 5. Diagnostic and treatment criteria for acute otitis media.

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IN PRACTICE

with correct diagnosis unnecessary anti biotic use can be reduced by up to 66%. [31] Pneumotoscopy and tympanometry are very useful in determining the presence of a middle ear effusion. Routine tympano centesis on children with uncomplicated otitis is not feasible because of ethical and resource-related considerations. Swabs and/ or aspirations of otorrhoea (clear or purulent secretions) that are neither recurring nor chronic, from a fresh tympanic perforation in patients without prior exposure to anti biotics, are also not routinely advised. However, with cases of AOM that closely follow swimming in children with perfor ations or grommets, an MC&S is very useful in excluding Pseudomonas aeruginosa that might be critical. Of note, CRP is unhelpful in determining whether antibacterial therapy can be withheld. As AOM is often viral in aetiology (50% of cases) and with most bacterial cases (commonly S. pneumoniae, Haemophilus influenzae) resolving spontaneously, treatment of pain is the most critical aspect of the management of AOM. Antibiotics may be deferred for 48 hours in children ≥2 years of age while symptomatic therapy is administered (particularly where good follow-up is possible) if there is unilateral involvement and if the disease is not severe[8,32] (Fig. 5). Antibiotic prophylaxis in recurrent cases is of no value.

Acute bacterial rhinosinusitis

Acute bacterial rhinosinusitis (ABRS) is usually preceded by a viral URTI (Fig. 6). Allergy, trauma, dental infection or other factors that cause inflammation of the nose and paranasal sinuses may also predispose individuals to ABRS.[8] A raised CRP has been suggested as a potential discriminator between coryza and sinusitis, but absolute values have not been validated.[11] Attempts to establish an aetiological diag nosis of sinusitis are typically reserved for patients who have not responded to convent ional medical treatment within 48 - 72 hours, immunocompromised patients and those with complications. Sinus puncture and aspiration are the reference standard for a bacteriological diagnosis of ABRS. As most studies have shown poor correlation between nose and throat cultures and maxil lary sinus aspirates, nasal or nasopharyngeal swabs are not recommended; neither is the use of X-rays, which is strongly discouraged. A recent meta-analysis of treatment out comes for ABRS has shown marginal benefit of antibiotics over placebo.[33] Overall, the number needed to treat for one adult to benefit is 13 (95% CI 9 - 22). Neither topical

nor oral decongestants and/or antihistamines are recommended as adjunctive treatment, whereas both intranasal irrigation with either physiological or hypertonic saline and intranasal corticosteroids are recommended, the latter primarily in patients with allergic rhinitis.

Influenza

Influenza epidemics occur every year in SA during winter, typically from April to September, and should be considered in the differential diagnosis during this period. The clinical presentation varies from asymptomatic to severe and life-threatening infections. Typical and atypical presentations

are depicted in Fig. 7.[34] The clinical diagnosis of influenza is often difficult and unreliable and, where indicated, laboratory testing should be performed.[35] Situations where this is necessary include where there is a cluster of cases in institutions such as nursing homes, or in severe illness, where neuraminidase inhibitors (such as oseltamivir) are indicated. The latter appears to provide only marginal benefit in the non-hospitalised (in contrast to the hospitalised) patient in the community and is not recommended outside of highly immunocompromised patients or those with severe chronic respiratory, cardiac or neurological conditions.[36] The laboratory test of choice is a respiratory tract PCR on

Diagnose all-cause rhinosinusitis when the following are present: One of either: • Anterior or postnasal discharge* • Nasal obstruction With or without: • Facial pain/pressure • Change in sense of smell

Diagnose acute viral rhinosinusitis (often associated with the common cold): • Symptoms <10 days • Non-severe symptoms • No ‘second sickening’ occurred

Diagnose acute viral rhinosinusitis: • Symptoms >10 days and <3 months • Severe long-lasting purulence or fever • Worsening of above symptoms (’second sickening’) occurs in <10 days

• Symptomatic treatment only • No antibiotics prescribed

• Symptomatic treatment • Provide antibiotic script

*Obtaining nose or throat swabs for culture is strongly discouraged.

Fig. 6. Diagnostic and treatment criteria for acute bacterial rhinosinusitis. Diagnosis of influenza Acute onset characterised by: • • • •

High fever Headache Myalgia Dry cough

Atypical presentation in children may include: • Nausea • Vomiting • Diarrhoea

In the elderly, influenza may present as: • Confusion • Drowsiness

Laboratory testing is only indicated for those for whom specific antiviral therapy (e.g. oseltamivir) is recommended, namely: • Those with severe or complicated infection • Institutionalised patients • Those at high risk of developing severe or complicated infections The laboratory test of choice is influenza PCR: • On a nasopharyngeal swab • Alternatively, on a throat or nasal swab

Fig. 7. Diagnostic and treatment criteria for influenza.

June 2016, Print edition

High-risk patients include: • Pregnant women • Age ≥65 years • Age ≤2 years • Chronic respiratory disease • Significant cardiovascular disease • Chronic renal or hepatic disease • Obesity • Diabetes melltus • Immunosuppression, including HIV infection • Asthma

IN PRACTICE

a nasopharyngeal swab. Rapid tests are not recommended, as their sensitivity is often low and negative results do not exclude the diagnosis.[37]

Acute exacerbations of chronic obstructive pulmonary disease

With regard to chronic obstructive pulmonary disease (COPD), there are two situations in which antibiotics may be used. The first is for the treatment of acute exacerbations of COPD (AECOPD), which is the focus of this section. The second is long-term antibiotic use for COPD patients who continue to have recurrent exacerbations despite optimal COPD treatment; description of this is beyond the scope of this article. For AECOPD, antibiotics are not always required and there is still uncertainty as to which patients would benefit most from antibiotic use. Up to 60% of AECOPD is said to be due to airway infection, but not all of these are bacterial, and viral infections play a significant role.[38] In general terms, however, antibiotic use appears to be of more value in patients with more severe COPD and in those with more severe exacerbations of COPD. Severity of AECOPD is usually classified using the Anthonisen criteria.[39] Type 1 exacerbations, which are considered to be severe, have all three cardinal symptoms: increasing dyspnoea, increasing sputum volume and sputum purulence, while type 2 exacerbations (moderate exacerbations) have two of those three symptoms and type 3 exacerbations have one of the symptoms together with one other symptom such as URTI, fever, wheeze, cough, or increased respiratory or heart rate.[39] The recommendations for routine antibiotic use in non-hospitalised patients and CRP testing are summarised in Fig. 8.[40-42]

Routine CXR is not always available in primary care. If readily available, an X-ray is recommended if the signs and symptoms of CAP, as described above, are present or the POCT CRP is >100 mg/L, and if the diagnosis is uncertain. The former is useful to exclude conditions other than pneumonia such as empyema, lung abscess and bronchiectasis. Owing to low sensitivity, routine microbio logical tests such as Gram staining, sputum or blood cultures are also not indicated for the management of outpatients with low-severity CAP. [43,46,47] In children, urinary pneumococcal antigen testing is not recommended for the diagnosis of pneumococcal pneumonia owing to a high rate of false-positive results.[46]

Outpatient v. inpatient management: Severity assessment

In adults, once a clinical diagnosis of CAP has been made the primary care doctor should establish the optimal site for therapy (out patient or inpatient) using clinical judgement together with a severity-of-illness score such as the CURB-65 or CRB-65. [17,48] According to Bradley et al,[46] severity assess ment for children aged ≥3 - 6 months should also be performed on the grounds of the presence or absence of major and minor risk factors, but this is complex and may require referral.[49]

The role of biomarkers in differentiating types of ARTI

There is increasing evidence of a role for biomarkers, such as CRP and procalcitonin

(PCT), in the management of patients presenting with ARTI.[45] In fact, a recent Cochrane review concluded that POCT for biomarkers (e.g. CRP) to guide antibiotic treatment of ARTIs in primary care can reduce antibiotic use and be used as an adjunct to a doctor’s clinical examination; this reduction in antibiotic use did not affect patient-reported outcomes, including recovery from and duration of illness.[45,50] PCT is produced primarily by the C cells of the thyroid gland. Markedly raised levels are seen with bacterial infections and only minimal increases are reported with viral infections, which, through the stimulation of interferongamma, inhibit PCT release. Conditions such as asthma or allergic rhinitis also do not result in PCT release. However, PCT lacks accuracy in less severely ill patients with ARTI seen in primary care[51] and does not perform any better than a POCT CRP measurement in this setting.[45] Because the negative predictive value for exclusion of bacterial infection is enhanced only by serial measurements and by concomitant negative cultures, and because rapid PCT testing on uncentrifuged venous blood is not readily available, this test is currently unlikely to influence management of RTI in primary care.[51,52] In contrast, where there is diagnostic uncertainty, measurement of CRP levels can assist the physician in the management of patients presenting with features of ARTI. Recommendations for the use of CRP are based on reports from two large research groups: the IMPAC3T programme and the

COPD patients presenting with the following cardinal symptoms: • Increased dyspnoea • Increased sputum volume • Increased sputum purulence

All 3 symptoms (type 1 exacerbation*)

2/3 symptoms with one being increased sputum purulence (type 2 exacerbation*)

2/3 symptoms without increased sputum purulence (type 2 exacerbation*)

Community-acquired pneumonia

Most definitions of CAP include symptoms of an LRTI (produc tive cough, pleuritic pain and dyspnoea) and focal chest signs (dullness to percussion, bronchial breathing and crackles), as well as systemic features such as tachypnoea, tachycardia and a temperature of ≥38°C. [43] These features are, however, nonspecific and can be present in other infections, such as acute bronchitis, acute sinusitis and non-infectious conditions, although tachypnoea and tachycardia are uncommon. Symptoms and signs are also often less pronounced in elderly patients.[44] If there is doubt as to the diagnosis,[45] POCT of CRP may be helpful and is discussed below and depicted in Fig. 3.

1/3 symptoms together with one other symptom such as: • An URTI in previous 5 days • Increased wheezing • Increased coughing • Fever without obvious source • 20% increase in respiratory or heart rate above baseline (type 3 exacerbation*)

Symptomatic treatment Provide antibiotic script

CRP POCT (mg/L)

<40

>40

Symptomatic treatment only No antibiotic recommended

Symptomatic treatment Provide antibiotic script

*Anthonisen classification.

Fig. 8. Recommendations for antibiotic use in non-hospitalised patients with AECOPD.[40-42]

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IN PRACTICE

GRACE consortium study. These studies, incorporated into the 2014 NICE guidelines,[53] are very useful in providing evidence to support the clinician who is uncertain as to whether to include antibiotics in the management of LRTI or not.[45] Based on POCT CRP level measurement, the following is recommended (Fig. 3): • CRP <20 mg/L: CAP is unlikely, and antibiotic therapy is not routinely indicated • CRP 20 - 100 mg/L: A watchful waiting approach is recommended, where antibiotic prescription is provided only if the clinical condition deteriorates and if comorbid risk factors are present. These would include age <3 months or >75 years; in children, cardiovascular and pulmonary conditions (except asthma); and in adults, heart failure, severe COPD, diabetes mellitus (especially with use of insulin), neurological conditions, severe renal insufficiency or immune compromise • CRP >100 mg/L: CAP is more likely, and antibiotic therapy would be appropriate.[53-55] These cut-offs should be used as a guide, and CRP values should not be utilised in isolation without a clinical examination. Of note, it is also possible that viral infections, including uncomplicated influenza, may present with CRP values >100 mg/L.[56,57] It is also useful to use CRP to identify patients presenting with AECOPD who are most likely to benefit from antibiotics. In one study of AECOPD comparing amoxicillin/clavulanate with placebo, the best CRP cut-off for predicting clinical failure in the placebo arm was 40 mg/L, with an area under the curve of 0.732 (95% CI 0.614 0.851)[42] (Fig. 8). The practical implications and considerations for POCT CRP in the SA setting that warrant closer attention include: • Validation/verification of the POCT CRP assay used (to confirm the performance specifications as specified by the manufacturer) • The cost of acquiring the desktop analyser • Running costs, including calibration, internal and external quality control, and maintenance • Training (initially and continuously) on daily operation • Instrument storage specifications, including temperature and humidity control, etc. Detailed discussion of these aspects falls outside the scope of this article. It cannot be overemphasised that the results produced by a desktop analyser need to adhere to quality standards.

Conclusion

The consequences of ABR in terms of patient outcomes and economic impact are not a distant threat, but are being played out ‘here and now’. In SA, increasing levels of MDR, XDR and PDR organisms have been spawned by rampant over-use and incorrect use of anti biotics.[1,58] As such, antibiotics should be seen as a precious resource and the prescribing physician, particularly the GP, the guardian of this resource. AS requires a collaborative effort on the part of policymakers, healthcare providers, healthcare insurance companies and patients. Besides the urgent need for AS governance in primary care, including optimal process and outcome measures, a drastic behavioural change is required by both doctors and patients, with more emphasis on non-antibiotic treatment options, particularly in the outpatient setting. To achieve this, primary care physicians need to assess their patients’ clinical presentation carefully, attempt to follow simple frameworks for clinical decision-making regarding antibiotic use and, where applicable, make appropriate use of POCT

testing of biomarkers and cultures in order to minimise diagnostic uncertainty.[59] Understanding their patients’ expectations, along with improved communication of ABR principles, education and empowerment, are key to reducing antibiotic use in the outpatient setting. Without techniques to change behaviour, such as goal setting for GPs to reduce antibiotic prescriptions, provision of feedback to enable self-monitoring and action planning based on guidelines such as these to reduce diagnostic uncertainty, antibiotic prescribing rates will remain stagnant.[60] Furthermore, according to the so-called ‘Pareto Principle’ or ‘Law of the Vital Few’ (derived from economic theory and implying that 80% of outcomes result from only 20% of potential causes), by focusing on a few vital interventions, one can have a significant impact on outcome with less effort.[61] From a community stewardship point of view, it implies that even if the focus is placed on the appropriate diagnosis of ARTIs alone, this would represent a major target, with effect sizes of sufficient magnitude to have the potential to reduce the incidence of ABR bacteria in the community.[11] Disclaimer. This clinical practice article is not intended as a sole source of guidance in the management of patients with the conditions described. Rather, it is intended to assist clinicians in decision-making. It is not intended to replace clinical judgement or establish a protocol for the care of all patients with the conditions described. These recommendations may not provide the only appropriate approach to the management of patients with such conditions. 1. Review on antimicrobial resistance. Tackling a global health crisis: Initial steps. February 2015. http:// amr-review.org/sites/default/files/Report-52.15.pdf (accessed 22 June 2015). 2. Brink AJ, Feldman C, Richards GA, Moolman J, Senekal, M. Emergence of extensive drug resistance (XDR) among Gram-negative bacilli in South Africa looms nearer. S Afr Med J 2008;98(8):586-592. 3. Dellit TH, Owens RC, McGowan JE Jr, et al. Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship. Clin Infect Dis 2007;44(2):159-177. DOI:10.1086/510393 4. Butler CC, Dunstan F, Heginbothom M, et al. Containing antibiotic resistance: Decreased antibioticresistant coliform urinary tract infections with reduction in antibiotic prescribing by general practices. Br J Gen Pract 2007;57(543):785-792. 5. Lee GC, Reveles KR, Attridge RT, et al. Outpatient antibiotic prescribing in the United States: 2000 to 2010. BMC Med 2014;12(1):96. DOI:10.1186/1741-7015-12-96 6. Shapiro DJ, Hicks LA, Pavia AT, Hersh AL. Antibiotic prescribing for adults in ambulatory care in the USA, 2007-09. J Antimicrob Chemother 2014;69(1):234-240. DOI:10.1093/jac/dkt301 7. Gerber JS, Prasad PA, Fiks AG, et al. Effect of an outpatient antimicrobial stewardship intervention on broad-spectrum antibiotic prescribing by primary care pediatricians. A randomized trial. JAMA 2013;309(22):2345-2352. DOI:10.1001/jama.2013.6287 8. Brink AJ, Cotton M, Feldman C, et al. Updated recommendations for the management of upper respiratory tract infections in South Africa: 2015. S Afr Med J 2015;105(5):345-352. DOI:10.7196/ samj.8716 9. Van der Velden A, Duerden MG, Bell J, et al. Prescriber and patient responsibilities in treatment of acute respiratory tract infections – essential for conservation of antibiotics. Antibiotics 2013;2(2):316327. DOI:10.3390/antibiotics2020316 10. Altiner A, Knauf A, Moebes J, Sielk M, Wilm S. Acute cough: A qualitative analysis of how GPs manage the consultation when patients explicitly or implicitly expect antibiotic prescriptions. Fam Pract 2004;21(5):500-506. DOI:10.1093/fampra/cmh505 11. Brink AJ. Antimicrobial stewardship (AMS) in the community. Clin Pulm Med 2016;23(1):1-10. DOI:10.1097/CPM.0000000000000107 12. Boyles T, Wasserman, S. Diagnosis of bacterial infection. S Afr Med J 2015;105(5):419. DOI:10.7196/ SAMJ.9647 13. Wasserman S, Boyles T, Mendelson M, on behalf of the South African Antibiotic Stewardship Programme (SAASP). A pocket guide to antibiotic prescribing for adults in South Africa, 2015. http:// www.fidssa.co.za/images/SAASP_Antibiotic_Guidelines_2015.pdf (accessed 15 July 2015). 14. Hansen MP, Hoffmann TC, McCullough AR, van Driel ML, del Mar CB. Antibiotic resistance: What are the opportunities for primary care in alleviating the crisis? Frontiers Public Health 2015;3:1-7. DOI:10.3389/fpubh.2015.00035 15. Butler CC, Hood K, Verheij T, et al. Variation in antibiotic prescribing and its impact on recovery in patients with acute cough in primary care: Prospective study in 13 countries. BMJ 2009;338:b2242. DOI:10.1136/bmj.b2242 16. Whaley LE, Businger AC, Dempsey PP, Linder JA. Visit complexity, diagnostic uncertainty, and antibiotic prescribing for acute cough in primary care: A retrospective study. BMC Fam Prac 2013;14(1):120. DOI:10.1186/1471-2296-14-120 17. National Institute for Health and Clinical Excellence guidelines. Respiratory tract infections – antibiotic prescribing. Prescribing of antibiotics for self-limiting respiratory tract infections in adults and children in primary care. NICE clinical guideline 69, 2008. www.nice.org.uk/CG069 (accessed 28 October 2015). 18. Albert RH. Diagnosis and treatment of acute bronchitis. Am Fam Physician 2010;82(11):1345-1350. 19. Irwin RS. Guidelines for treating adults with acute cough. Am Fam Physician 2007;75(4):476-482. 20. Barnett ML, Linder JA. Antibiotic prescribing for adults with acute bronchitis in the United States, 1996-2010. JAMA 2014;311(19):2020-2022. DOI:10.1001/jama.2013.286141

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IN PRACTICE

21. Claassen J. The sore throat. Antibiotics are overprescribed for sore throats in general practice. CME 2012;30(9):306-313. 22. Sanchez GV, Hicks LA. Acute sinusitis and pharyngitis as inappropriate indications for antibiotic use. Antimicrob Agents Chemother 2014;58(6):3572. DOI:10.1128/AAC.02696-14 23. Linder JE. Sore throat: Avoid overcomplicating the uncomplicated (Editorial). Ann Intern Med 2015;162(4):311-312. DOI:10.7326/M14-2899 24. Ebell MH. Point-of-care Guides. Diagnosis of streptococcal pharyngitis. Am Fam Physician 2014;89(12):976-977. 25. Hernandez DR, Wolk DM. Does your ‘backup’ method have your back? Controversies surrounding backup of rapid antigen detection methods for group A streptococcus. Clin Micro News 2015;37(14):111-118 DOI:10.1016/j.clinmicnews.2015.07.001 26. Science M, Bitnun A, McIsaac W. Identifying and treating group A streptococcal pharyngitis in children (Commentary). CMAJ 2015;187(1):13-14. DOI:10.1503/cmaj.141532 27. Calviño O, Llor C, Gómez F, Sarvisé C, Hernández S. Association between C-reactive protein rapid test and group A streptococcus infection in acute pharyngitis. J Am Board Fam Med 2014;27(3):424-426. DOI:10.3122/jabfm.2014.03.130315 28. Melbye H, Hvidsten D, Holm A, Nordbø SA, Brox J. The course of C-reactive protein response in untreated upper respiratory tract infection. Br J Gen Pract 2004;54(506):653-658. 29. Christensen AM, Thomsen MK, Oversen T, et al. Are procalcitonin or other infection markers useful in the detection of group A streptococcal acute tonsillitis? Scand J Infect Dis 2014;46(5):376-383. DOI:10.3109/00365548.2014.885656 30. Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis 2012;55(10):e86-e102. DOI:10.1093/cid/cis629 31. Lieberthal AS, Carroll AE, Chonmaitree T, et al. The diagnosis and management of acute otitis media. Paediatrics 2013;131(3):e964-e999. DOI:10.1542/peds.2012-3488 32. Hersh AL, Jackson MA, Hicks LA, et al. Principles of judicious antibiotic prescribing for upper respiratory tract infections in pediatrics. Pediatrics 2013;132(2):1146-1154. DOI:10.1542/peds.2013-3260 33. Chow AW, Benninger MS, Brook I, et al. IDSA clinical practice guideline for acute bacterial rhinosinusitis in children and adults. Clin Infect Dis 2012;54(8):1041-1045. DOI:10.1093/cid/cir1043 34. Call SA, Vollenweider MA, Hornung CA, Simel DL, McKinney WP. Does this patient have influenza? JAMA 2005;293(8):987-997. DOI:10.1001/jama.293.8.987 35. Van Vugt SF, Broekhuizen BDL, Zuithoff NPA, Validity of a clinical model to predict influenza in patients presenting with symptoms of lower respiratory tract infection in primary care. Fam Pract 2015;32(4):408-414. DOI:10.1093/fampra/cmv039 36. Jefferson T, Jones M, Doshi P, Spencer EA, Onakpoya I, Heneghan CJ. Oseltamivir for influenza in adults and children: Systematic review of clinical study reports and summary of regulatory comments. BMJ 2014;348:g2545. DOI:10.1136/bmj.g2545 37. Healthcare Workers Handbook on Influenza - 2015. May 2015. http://nicd.ac.za (accessed 24 February 2016). 38. Wedzicha JA, Donaldson GC. Exacerbations of chronic obstructive pulmonary disease. Respir Care 2003;48(12):1204-1215. 39. Anthonisen NR, Manfreda J, Warren CPW, Hershfield ES, Harding GK, Nelson NA. Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease. Ann Intern Med 1987;106(2):196-204. DOI:10.7326/0003-4819-106-2-196 40. Woodhead M, Blasi F, Ewig S, et al. Guidelines for the management of adult lower respiratory tract infections. Clin Microbiol Infect 2011;17(Suppl 6):1-24. DOI:10.1111/j.1469-0691.2011.03602.x 41. Vollenwieder DJ, Jarrett H, Steurer-Stey CA, Garcia-Aymerich J, Puhan MA. Antibiotics for exacerbations of chronic obstructive pulmonary disease (Review). Cochrane Database Syst Rev 2012;12:CD010257. DOI:10.1002/14651858.CD010257 42. Llor C, Moragas A, Hernández S, Bayona C, Miravitlles M. Efficacy of antibiotic therapy for acute exacerbations of mild to moderate chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2012;186(8):716-723. DOI:10.1164/rccm.201206-0996OC

43. Lim WS, Baudouin SV, George RC, et al. Pneumonia Guidelines Committee of the BTS Standards of Care Committee, The British Thoracic Society: Guidelines for the management of community-acquired pneumonia in adults: Update 2009. Thorax 2009;64(Suppl 3):iii1-iii55. DOI:10.1136/thx.2009.121434 44. Bartlett JG, Mundy LM. Community-acquired pneumonia. N Engl J Med 1995;333(24):1618-1624. DOI:10.1056/NEJM199512143332408 45. Cooke J, Butler C, Hopstaken R, et al. Narrative review of primary care point-of-care testing (POCT) and antibacterial use in respiratory tract infection (RTI). BMJ Open Respir Res 2015;2(1):e000086. DOI:10.1136/bmjresp-2015-000086 46. Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired pneumonia in infants and children older than 3 months of age: Clinical Practice Guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis 2011;53(7):e25-e76. DOI:10.1093/cid/cir531 47. Plouffe JF, McNally C, File TM Jr. Value of non-invasive studies in community-acquired pneumonia. Infect Dis Clin North Am 1998;12(3):689-699. DOI:10.1016/S0891-5520(05)70205-1 48. Feldman C, Brink AJ, Richards GA, et al. Guideline: Management of community-acquired pneumonia in adults. S Afr Med J 2007;97(12):1295-1306. 49. Zar HJ, Jeena J, Argent A, et al. Diagnosis and management of community-acquired pneumonia in childhood – South African Thoracic Society guidelines. S Afr Med J 2005;95(12):977-990. 50. Aabenhus R, Jensen JU, Jørgensen KJ, Hróbjartsson A, Bjerrum L. Biomarkers as point-of-care tests to guide prescription of antibiotics in patients with acute respiratory infections in primary care (Review). Cochrane Database Syst Rev 2014;11:CD010130. DOI:10.1002/14651858.CD010130.pub2 51. Holm A, Pedersen SS, Nexoe J, Obel N, Nielsen LP, Koldkjaer O, Pedersen C. Procalcitonin versus C-reactive protein for predicting pneumonia in adults with lower respiratory tract infection in primary care. Br J Gen Pract 2007;57(540):555-560. 52. Dunne WM Jr. Laboratory diagnosis of sepsis? No SIRS, not just yet. J Clin Microbiol 2015;53(8):24042409. DOI:10.1128/JCM.03681-14 53. National Institute for Health and Clinical Excellence. Pneumonia: Diagnosis and management of communityand hospital-acquired pneumonia in adults. Guideline Development Group, NICE, 2014. https://www.nice. org.uk/guidance/cg191/resources/pneumonia-in-adults-diagnosis-and-management-35109868127173 (accessed 15 November 2015). 54. Van der Meer MV, Neven AK, van den Broek PJ, Assendelft WJ. Diagnostic value of C reactive protein in infections of the lower respiratory tract: Systematic review. BMJ 2005;331(7507):26. DOI:10.1136/ bmj.38483.478183.EB 55. Falk G, Fahey T. C-reactive protein and community-acquired pneumonia in ambulatory care: Systematic review of diagnostic accuracy studies. Fam Pract 2009;26(1):10-21. DOI:10.1093/fampra/cmn095 56. Sadovsky R. Value of C-reactive protein measurements in children. Am Fam Physician 1998;57:1384-1386. 57. Chew KS. What’s new in emergencies trauma and shock? C-reactive protein as a potential clinical biomarker for influenza infection: More questions than answers. J Emerg Trauma Shock 2012;5(2):115117. DOI:10.4103/0974-2700.9647758. 58. Mendelson M, Matsoso MB. A global call for action to combat antimicrobial resistance: Can we get it right this time? S Afr Med J 2014;104(7):478479. DOI:10.7196/SAMJ.8534 59. Meili M, Muller B, Kulkarni P, Schutz P. Management of patients with respiratory infections in primary care: Procalcitonin, C-reactive protein or both? Expert Rev Respir Med 2015;9(5):587-601. DOI:10.1 586/17476348.2015.1081063 60. Davey P, Peden C, Charani E, Marwick C, Michie S. Time for action – improving the design and reporting of behaviour change interventions for antimicrobial stewardship in hospitals: Early findings from a systematic review. Int J Antimicrob Agents 2015;45(3):203-212. DOI:10.1016/j. ijantimicag.2014.11.014 61. Hamilton KW, Fishman NO. Antimicrobial stewardship interventions: Thinking inside and outside the box. Infect Dis Clin North Am 2014;28(2):301-313. DOI:10.1016/j.idc.2014.01.003

Accepted 11 April 2016.

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CLINICAL ALERT

Emergence of vancomycin-resistant Enterococcus at a tertiary paediatric hospital in South Africa H Lochan,1,2* MB ChB, DCH, FCPaed (SA), Cert ID (SA) Paed; C Moodley,3,4* PhD (Mol Cell Biol); D Rip,3,4 PhD (Biotechnol); C Bamford,3,4 MB ChB, DCH (SA), MPhil (Mat Child Health), FCPath (Microbiol), MMed (Med Microbiol); M Hendricks,2,5 MB ChB, DIP PEC (SA), DCH (SA), FCPaed (SA), CMO Paed (SA); A Davidson,2,5 MB ChB, DCH (SA), FCPaed (SA), CMO Paed (SA), MPhil; B Eley,1,2 MB ChB, FCPaed (SA), BSc Hons aediatric Infectious Diseases Unit, Red Cross War Memorial Children’s Hospital, Cape Town, South Africa P Department of Paediatrics and Child Health, School of Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa 3 Division of Medical Microbiology, Department of Pathology, Faculty of Health Sciences, University of Cape Town, South Africa 4 National Health Laboratory Service, Groote Schuur Hospital, Cape Town, South Africa 5 Haematology/Oncology Service, Red Cross War Memorial Children’s Hospital, Cape Town, South Africa * These authors contributed equally to the work (joint first authors). 1 2

Corresponding author: B Eley (brian.eley@uct.ac.za)

Background. During 2013, the haematology/oncology unit at a tertiary level paediatric hospital in South Africa experienced the emergence of infection with vancomycin-resistant Enterococcus (VRE). Objective. To describe the clinical and molecular aspects of the cases identified. Methods. VRE isolates identified from blood culture specimens processed at the National Health Laboratory Service were screened for the presence of the vancomycin resistance genes vanA, B and C1, 2 and 3. Further characterisation of these isolates was carried out using pulsedfield gel electrophoresis (PFGE) and multilocus sequence typing (MLST). Clinical records of infected patients were reviewed to identify possible risk factors, while surveillance with rectal swabs was performed to identify VRE-colonised patients. Results. Four patients with haematological malignancies were identified with VRE bloodstream infections. Patients were immuno compromised at the time of the bloodstream infection (BSI), with receipt of vancomycin prior to VRE-BSI, and infections were treated with linezolid. Colonisation with VRE was found in 8 of 55 patients screened. Infected and colonised patients were isolated in the unit during their admission and strict contact precaution infection control practices were instituted. The vanA gene was identified in all of the isolates but one. PFGE and MLST results showed a degree of genetic relatedness between certain isolates obtained from rectal swab and blood culture samples, suggesting possible patient-to-patient transmission or persistence of the isolates in the unit. Conclusion. Strict infection control practices are necessary to prevent infection and transmission of resistant organisms among vulnerable patients. S Afr Med J 2016;106(6):562-566. DOI:10.7196/SAMJ.2016.v106i6.10858

Multidrug-resistant organisms are an increasing threat to healthcare worldwide. Treatment options for these so-called ‘superbugs’ are limited, with very few new antimicrobials currently in development. One such organism is vancomycin-resistant Enterococcus (VRE). This organism has been detected worldwide in hospitalised adult and paediatric patients since the first description in 1986.[1] Infection and/or colonisation with VRE has been described in patients who are potentially immunosuppressed, especially those with malignancies, solid organ transplant recipients, those with chronic renal disease requiring haemodialysis, neonates and those requiring long-term ventilation.[2,3] Resistance to vancomycin occurs in E. faecium and E. faecalis species primarily owing to the vanA and vanB resistance genes. The first clinical reports of VRE in South African (SA) adults appeared in 1997 and there is currently a paucity of SA paediatric studies describing the incidence of VRE or outbreaks of this organism.[4] We report on the first identification of VRE infections in the paediatric oncology ward at a tertiary-level paediatric hospital in Cape Town, SA, over two time periods in 2013.

Methods

Identification

The first two VRE organisms causing bloodstream infections (VREBSI) were isolated from blood culture specimens of two patients, 2 days apart, in February 2013. Seven and 9 months later, in September and November 2013, respectively, VRE was once again isolated from blood culture specimens in an additional two patients. Following the two time periods, patient hospital records were accessed to identify possible risk factors associated with acquiring VRE-BSI in this setting. Patient records were anonymised and de-identified prior to analysis. Routine screening is not carried out for drug-resistant organisms on admission to the hospital.

Setting

The haematology/oncology unit at Red Cross War Memorial Children’s Hospital (RCWMCH) in Cape Town, SA, is a 17-bed unit with a high-care unit and isolation cubicles. There is a daily outpatient service and a day ward in the area adjoining the main ward. It serves as a referral centre for children with haematological and solid organ malignancies from other local or distant hospitals in the country. Children are admitted from home or long-term

June 2016, Print edition

Alive and received an HSCT 11 13.7 8 Yes 14 No Maintenance chemotherapy 4

HSCT = haemopoeitic stem cell transplant. * Neutropenia: absolute neutrophil count ≤0.5 × 109 cells/L.

63 Positive

Acute myeloid leukaemia

Died of septic shock

Died of septic shock 14

3 9.8

29.6 13

3 Yes

Yes 77

9 Yes

No Cyclosporin

Induction chemotherapy 23

Not done

Burkitt’s lymphoma

Positive

Aplastic anaemia

10 4.2 6 Yes 11

Outcome Mucositis

Yes Maintenance chemotherapy 67 Positive

Patient

Acute promyelocytic leukaemia

Linezolid duration (days) Vancomycin trough levels (µg/mL) Vancomycin use before specimen (days) Duration of neutropenia* before BSI (days) Immunosuppressive therapy Duration of hospitalisation before BSI (days)

Isolates of interest were analysed using pulsed-field gel electrophor esis (PFGE), as described by the Centers for Disease Infection control Control and Prevention, with the following Infected patients were isolated in single changes: cultures were grown on BHI cubicles until discharged. Contact precau medium, at 37°C, aerobically overnight, tions during patient interaction were insti and cell densities were standardised to an tuted for patients, family and staff members. OD610nm≈1.0, using a spectrophotometer Colonised patients were cohorted until discharged. Medical records were marked (BioDrop, UK).[9] Cells were embedded in to ensure isolation, and re-screening by a 1.0% SeaKem Gold agarose gel (Lonza, rectal swab occurred during subsequent Switzerland) and were digested for 2 hours admissions. Staff and parents were re- at 25°C using SmaI (Thermo Scientific, educated regarding correct handwashing USA) restriction endonuclease and ApaI technique, use of alcohol hand sanitiser and as a secondary enzyme (2 hours at 37°C). contact precautions. Digested plugs were electrophoresed through a 1.0% SeaKem Gold agarose gel (Lonza, Switzerland) in 0.5% TBE buffer Microbiological methods (14 °C), using the Gene Navigator (Amer All microbiological and molecular analyses sham Biosciences, UK) at 200 V, with a were conducted by the National Health ramped switching time of 3.5 - 23.5 Laboratory Service at Groote Schuur Hospital seconds over 18 hours. The resultant gel and the Division of Medical Microbiology, was visualised using ethidium bromide University of Cape Town (UCT), SA. staining, and the gel image analysed and Surveillance specimens were plated directly dendrogram generated using Gel Compare onto selective media (colistin nalidixic blood II (BioNumerics v.6.6, Applied-Maths, agar impregnated with a 30 µg vancomycin USA), with an optimisation of 1.0 and a disc) and incubated for up to 48 hours. band tolerance of 1.5. The dendrogram Identification and susceptibility testing of was constructed using the pairwise average colonies growing within the inhibition zone from the SmaI and ApaI results, with the close to the vancomycin disc were performed UPGMA (unweighted pair group method using the Vitek 2 GP and AST-P603 cards with arithmetical mean) method and branch respectively, with interpretation according to quality was calculated using the cophenetic contemporary Clinical Laboratory Standards correlation. E. faecalis ATCC 51299 was Institute criteria.[6] Vancomycin minimum used as a control and for normalisation. inhibitory concentrations (MICs) were determined using the Etest method.[6] MICs ≥32 μg/mL were considered resistant. Multilocus sequence typing Isolates were characterised genotypically Cellular DNA was extracted from selected with the Hain Genotype Enterococcus line isolates and PCR was carried out as probe assay according to the manufacturer’s described above using the conditions instructions, or in-house polymerase chain described by Homan et al.[10] Amplicons reaction (PCR) assay as described below. were sequenced bidirectionally (Inqaba

Central venous catheter

Pulsed-field gel electrophoresis

Underlying diagnosis

Following identification of the first two VRE infections, collaboration between the paediatric oncologists, microbiologists, paediatric infectious diseases physicians, infection control nursing staff and ward nursing staff was instituted to limit further spread by improving infection prevention and control measures. Active surveillance for rectal colonisation with VRE of patients in the ward and discharged patients who had prior contact with the index cases was carried out by means of culture and sensitivity testing using rectal swabs or stool samples. If rectal swabs were negative for VRE at initial screening, a repeat was taken at 1 - 2-weekly intervals until three consecutive negative swabs were documented.[5]

All vancomycin-resistant isolates were screened for the presence of the vanco mycin resistance genes vanA, B and C1, 2, 3 with DNA purified using the ZR Fungal/Bacterial DNA MiniPrep kit (Zymo Research, USA) according to the manufacturer’s instructions.[7] PCR reactions (25 µL) were carried out using GoTaq Flexi (Promega, USA) with an annealing temperature of 60°C, for 35 cycles, in a GeneAmp 9700 thermocycler. PCR amplicons were visualised by agarose gel electrophoresis and ethidium bromide staining. Amplicons were confirmed with DNA sequence analysis (Inqaba Biotech, SA) and BLASTN (http://blast.ncbi.nlm. nih.gov/Blast) comparisons.[8]

Rectal screening swab

Surveillance

In-house PCR assay for genotyping enterococci

Table 1. Summary of patients with VRE-BSI

care facilities. The unit has approximately 2 000 admissions, with an additional 5 500 outpatient visits, per year

Alive and discharged from the unit

IN PRACTICE

Biotech, SA) and the consensus sequences uploaded and typed at using an E. faecium multilocus sequence typing (MLST) database.[11]

Ethical considerations

Ethics approval to perform this study was obtained from the Human Research Ethics Committee, UCT (HREC Ref. No. 022/2015).

Results

Description of the infection

The ward had 100% occupancy during the months of VRE isolation. All four BSI patients were long-term residents in the unit at the time of the infections and were therefore classified as hospital-acquired infections. Patients 2 and 4 were transferred from a referral hospital outside Cape Town, where VRE had previously been isolated. Neither of these patients was screened prior to their transfer to RCWMCH. The clinical features and underlying risk factors at the time of BSI were similar in all four identified patients (Table 1). Three of the infected patients cultured vancomycin-sensitive E. faecium (VSE) isolates from blood in the week preceding the VRE-BSI. All four were treated with vancomycin in the week prior to the the VRE-BSI, and three had suboptimal vancomycin trough drug levels (≤15 µg/ mL). Patient 2 had renal impairment which resulted in the increased trough levels of vancomycin. Central venous catheters were removed from all infected patients after detection of the VRE-BSI. Infected patients were treated with intravenous linezolid. Patients 2 and 3 had protracted periods of illness prior to the BSI and demised from a new Gram-negative BSI and typhilitis following the VRE-BSI, respectively.

Surveillance

Two of 29 (6.9%) patients who were residing in the ward or recently discharged were screened (as identified above) by rectal swab for VRE during February and March 2013 and a further 6 of 26 (23.1%) patients screened between September and October 2013 were positive for VRE. Patient 4 screened positive on rectal swab and

20 25

40 45

55 60 65

subsequently progressed to develop a VRE-BSI a week later. Although the overall number of patients colonised with VRE was 14.5% (8/55), surveillance swabbing was not routinely performed between March and September, and the true prevalence was therefore not established. There were, however, no cases of clinical disease due to VRE documented between March and September 2013. Environmental screening for VRE was not conducted in the unit.

Microbiology

All but one isolate obtained (surveillance and infection) was identified as E. faecium, using the Vitek 2 system. The additional isolate obtained on rectal swab was identified as E. faecalis based on vancomycin sensitivity testing. Vancomycin MICs on Etest were ≥256 µg/mL for the four BSI isolates, confirming high-level resis tance of E. faecium to vancomycin.[8]

Molecular testing

PCR analysis detected the vanA gene in all of the VRE isolates obtained from infected patients and all but one of the VRE screening isolates. This isolate tested positive for the vanB gene. PFGE analysis of these isolates showed that there was genetic diversity among the isolates, which was not indicative of an outbreak. There was, however, a high level of genetic relatedness (>85% confidence interval) between some of the strains tested (Fig. 1). The E. faecalis isolate obtained during the February - March surveillance screening did not undergo any further molecular typing, even though the vanA gene was detected on PCR. Patients 1 and 2, who were considered to be the index cases of a suspected outbreak, had isolates which shared 92.5% homology, indicating a strong possibility of patient-to-patient transmission of the same clone. This result was unusual since the patient 2 isolate in question (No. 13) was obtained from a rectal swab and the isolate obtained from the blood culture of Patient 2 (No. 3) did not show strong homology with each other.

80 85

95 100 07 Patient 1 Blood ST817

92.5 44.8 97

13 Patient 2 Swab ST817 97.2

91.4 100 33.3 97

97.9 28.0 96

54.2 97 64.1 93

23.9 93 12.4

87.8

33 Patient 5 Swab 34 Patient 6 Swab ST117 14 Patient 7 Tissue ST262 05 Patient 1 Blood ST817 30 Patient 3 Blood ST18 37 Patient 8 Swab 36 Patient 9 Swab ST203 35 Patient 10 Swab 39 Patient 4 Swab ST80

61.1

62 Patient 4 Blood ST80 03 Patient 2 Blood ST817 15 Patient 11 Swab 57 ATCC 51299

57.8

85% confidence interval Fig. 1. Dendrogram of isolates obtained during investigation. Shaded bars indicate branch error flags and unshaded values indicate the levels of relatedness. Patients 1 - 4 represent the patients with VRE-BSIs. Patients 5, 6 and 8 - 11 indicate the patients colonised with VRE (patient 11 in February and March, and patients 5, 6, 8, 9 and 10 in September and October; patient 7 was not a haematology/oncology patient). The specimen types and MLST sequence types are indicated in the last two columns, respectively.

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The second isolate from patient 1 (No. 5), obtained from a blood culture, shared 97.2% homology with the blood culture isolate from patient 3 (No. 30). Isolate No. 30 was faintly positive for the vanA gene on PCR and susceptible to vancomycin. Previous isolates from this patient produced strong positive PCR results and high levels of vancomycin resistance. None of the resistant isolates from patient 3 showed significant homology to the sensitive isolate or to any of the other strains tested (data not shown). The two isolates obtained from blood in patient 1 (Nos 5 and 7), however, shared very little genetic homology. These data indicated the possibility of a rapid rate of strain variation, even within the same patient, in this setting. The two isolates from patient 4 (Nos 39 and 62) shared only 61.1% homology with each other and very low homology with any of the other strains tested. There were five screening strains, in two clusters, that shared high genetic homology with each other. Cluster 1 (91.4% homology) comprised patients 5, 6 and 7 and cluster 2 (87.8% homology) comprised patients 8 and 9. Patient 7 (No. 14) in cluster 1 was PCRpositive for the vanB gene, but still shared high homology with the other two isolates, which were both vanA-positive. This patient had no prior contact with the haematology/oncology unit. The isolate was obtained from autopsy of the lung tissue and was probably a contaminant and not a comorbidity. Cluster 2 comprised two isolates that were obtained from different patients on the same day. These results indicated the possibility of spread within the hospital. MLST analysis revealed that the four isolates from patients 1 and 2 (Nos 3, 5, 7 and 13) all shared the same sequence type (ST817). Even though these isolates do not share significant homology in the dendrogram, it strengthens the assumption that these two patients probably had patient-to-patient transmission of the same clone that may have changed over time. The two isolates from patient 4 (Nos 39 and 62) that shared 61.1% homology also shared the same sequence type (ST80). They are single-locus variants of ST817, with a single polymorphism in the adk gene (189G>A).

Infection control

A multidisciplinary approach was instituted to prevent further spread of the organism within the oncology unit. Infection control staff assisted with ensuring that infected patients were isolated and all ward staff members were educated about contact precautions. Colonised patients were cohorted in the multi-bed cubicles for the duration of their hospital stay. Discharged patients were identified to determine who required screening on their next visit. The ward was closed off to all new admissions until all colonised or infected patients were discharged. Once all colonised or infected patients were discharged, the ward was comprehensively cleaned. Following the first two cases of VRE-BSI, antibiotic stewardship ward rounds were instituted in the oncology unit, to improve antibiotic management including optimisation of vancomycin dosing. All patients who required transfer from other hospitals to the oncology unit at RCWMCH, where VRE had previously been documented, were screened for VRE by rectal swab prior to transfer.

Discussion

This is the first documented report of VRE infection in children in SA. A prevalence study in SA found 10.9% (20/184) of screening rectal swabs in at-risk patients to be positive for enterococal isolates.â&#x20AC;&#x160;[12] This study also showed clonal spread of the vanA and vanB genotypes in different hospitals, as well as persistence of the vanA carrying strain over time. The vanA genotype has been commonly isolated in previous outbreak settings.[2,3] Even though the PFGE results indicated overall genetic diversity between the isolates analysed, there was a degree of genetic relatedness

between specific blood and rectal swab samples on both PFGE and MLST analysis. These results may suggest possible patient-to-patient transfer of VRE or persistence of the organism in the haematology/ oncology unit between the two time periods described. Patient 4 was infected by a molecularly distinct, unrelated isolate, possibly before transfer to RCWMCH at a referral hospital where VRE had previously been isolated. The identified sequence type (ST80) along with ST203 (No. 36) and ST18 (No. 30) have previously been assigned to clonal complexes (CC) CC117, CC78, and CC17, respectively, which are known to form part of the CC17 meroclone. The CC17 meroclone has been described as highly diverse with documented worldwide spread.[13] These data again highlight the high levels of strain variation observed in this setting. The purpose of screening is to identify carriers during outbreaks, and in non-outbreak settings to prevent transmission, especially to vulnerable patient groups.[14] Active screening outside outbreak settings can be a costly exercise and especially difficult in resourceconstrained health systems. Screening in children has revealed low rates of colonisation. Active screening of paediatric patients found that 3.4% (41/1 211) were colonised with VRE, of whom 39/41 (95.1%) had an underlying chronic disease.[15] Risk factors for acquiring a BSI or colonisation with this highly resistant organism have been investigated. There are few paediatric studies regarding the risk factors for acquiring VRE. Acquisition of VRE has been associated with previous treatment with broad-spectrum antimicrobials, especially third-generation cepholosporins, and the carbapenems, as well as immunosuppression with antineoplastic chemotherapy, haemotology/oncology and renal patients, increased length of stay in hospital, and a younger age in children.[13] Progression from VRE colonisation to VRE-BSI in patients was associated with admission from a long-term care facility, infection of an additional body site other than blood and receipt of vancomycin.[16] In contrast, Pentima et al.[17] found that VRE-BSI was independent of patient vancomycin exposure. Risk factors in our patient cohort are similar to those described. All the patients with VRE-BSI had an underlying haematological condition requiring immunosuppressive therapy for treatment and received vancomycin for treating presumed Gram-positive infections. Central venous catheters were present in all four infected patients and, although not found to be a risk factor in the studies mentioned, could represent a possible clinical source for BSI. The colonised patients, although not clinically ill at the time, also had similar risk factors: all were exposed to vancomycin at some period during their illness and had underlying immunosuppression in the period preceding the screening. As mentioned, only one of the colonised patients progressed to developing bacteraemia with VRE. Treatment for this resistant organism is limited to the use of linezolid and daptomycin. In SA, daptomycin is difficult to access in the public health system. Linezolid, an oxazolidinone antibacterial agent, has proven to be effective in the treatment of the glycopeptideresistant Enterococcus, as well as methicillin-resistant Staphylococcus aureus and penicillin-resistant Streptococcus pneumoniae in children, and was used to treat the infected patients in this study.[18]

Study limitations

The limitations of this study include lack of a case-control group to conclusively identify risk factors associated with VRE acquisition in our patients, and an insufficient sample size to ascertain whether an outbreak had occurred and to determine the definitive phylogenetic relationships of the VRE strains present in this setting. Owing to financial constraints, no active surveillance was possible after October 2013, so whether or not further transmission occurred and

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the duration of colonisation with VRE were not established. However, no further VRE cases were reported in the oncology unit or the hospital after November 2013.

Conclusion

In conclusion, effective infection control practices are important to limit or prevent transmission of multidrug-resistant pathogens among vulnerable hospitalised populations. Furthermore, the emergence of glycopeptide-resistant enterococci has emphasised the importance of antibiotic stewardship in the haematology/oncology unit and the institution overall. Conflicts/disclosures. Parts of this work have been previously presented as a poster at the 16th International Congress on Infectious Diseases (ICID) in 2014 and published in the conference preceedings in the International Journal of Infectious Dieases (2014), as well as a poster presentation at the 9th World Congress of the World Society for Pediatric Infectious Diseases (WSPID) in 2015. Authorsâ&#x20AC;&#x2122; contributions. HL and CM participated in the drafting of the manuscript. BE conceived the study and helped in the drafting of the manuscript. CM and DR carried out the molecular typing of all the isolates. All authors read and approved the final manuscript. 1. Leclercq R, Derlot E, Duval J, Courvalin P. Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N Engl J Med 1988;319(3):157-161. 2. Iosifdis E, Karakoula K, Protonotariou E, et al. Polyclonal outbreak of vancomycin-resistant Enterococcus faecium in a paediatric oncology department. J Pediatr Hematol Oncol 2012;34(7):511516. DOI:10.1016/j.ajic.2013.02.005

3. Singh J, Esparza S, Patterson M, Vogel K, Patel B, Gornick W. Vancomycin-resistant Enteroococcus in paediatric oncology patients: Balancing infection prevention and family-centered care. J Pediatr Hematol Oncol 2013;35(3):227-231. DOI:10.1097/MPH.0b013e318257a6ca 4. Budavari SM, Saunders GL, Liebowitz LD, Khoosal M, Crewe-Brown, HH. Emergence of vancomycinresistant enterococci in South Africa. S Afr Med J 1997;87(11):1557. 5. Siegel JD, Rhinehart E, Jackson M, Chiarello L. Management of Multidrug-Resistant Organisms in Healthcare Settings. Atlanta, Ga, USA: Centers for Disease Control and Prevention, 2006. 6. Clinical and Laboratory Standards Institute. Performance Standards for Antimicrobial Susceptibility Testing. Wayne, Penn., USA: CLSI, 2013. 7. Bell JM, Paton JC, Turnidge J. Emergence of vancomycin-resistant enterococci in Australia: Phenotypic and genotypic characteristics of isolates. J Clin Microbiol 1998;36(8):2187-2190. 8. Altschul SF, Gish W, Miller W, Lipman DJ. Basic local alignment search tool. J Mol Biol 1990;215(3):403410. 9. Centers for Disease Control. Unified Pulsed-Field Gel Electrophoresis (PGFE). Protocol for Gram Positive Bacteria. Atlanta, Ga, USA: CDC, 2012. http://www.cdc.gov/hai/pdfs/labSettings/Unified_ PGFE_Protocol.pdf (accessed 9 December 2014). 10. Homan WL, Tribe D, Poznanski S, et al. Multilocus sequence typing scheme for Enterococcus faecium. J Clin Microbiol 2002;40(6):1963-1971. DOI:10.1128/jcm.40.6.1963-1971.2002 11. Enterococcus faecium MLST Databases. http://pubmlst.org/efaecium (accessed 25 September 2015). 12. Von Gottberg A, van Nierop W, Duse A, et al. Epidemiology of glycopeptide-resistant enterococci colonizing high risk patients in hospitals in Johannesburg, Republic of South Africa. J Clin Microbiol 2000;38(2):905-909. 13. Ergani-Ozcan A, Naas T, Baysan BO, et al. Nosocomial outbreak of vancomycin-resistant Enterococcus faecium in a paediatric unit at a Turkish university hospital. J Antimicrob Chemother 2008;61(5):10331039. DOI:10.1093/jac/dkn066 14. Humphreys H. Controlling the spread of vancomycin-resistant enterococci: Is active screening worthwhile? J Hosp Infect 2014;88(4):191-198. DOI:10.1016/j.jhin.2014.09.002 15. Weddle G, Jackson MA, Selvarangan R. Utility of a focused vancomycin-resistant enterococci screening protocol to identify colonization in hospitalized children. Am J Infect Control 2012;40(9):891-892. DOI:10.1016/j.ajic.2011.12.005 16. Olivier CN, Blake RK, Steed LL, Salgado C. Risk of vancomycin-resistant Enterococcus (VRE) bloodstream infection among patients colonized with VRE. Infect Control Hosp Epidemiol 2008;29(5):404-409. DOI:10.1086/587647 17. Pentima MCD, Chan S, Briody C, Power M, Hossain J. Driving forces of vancomycin-resistant E. faecium and E. faecalis blood-stream infections in children. Antimicrob Resist Infect Control 2014;3(1):29-33. DOI:10.1186/2047-2994-3-29 18. Dotis J, Iosifidis E, Ioannidou M, Roilides E. Linezolid use in paediatrics: A critical review. Int J Infect Dis 2010;14(8):e638-e648. DOI:10.1016/j.ijid.2009.10.002

Accepted 11 April 2016.

CLINICAL ALERT

Heavy alcohol use in patients on highly active antiretroviral therapy: What responses are needed? C D Parry,1,2 PhD; C Kekwaletswe,3 PhD; P A Shuper,4 PhD; S Nkosi,3 MA; B J Myers,1,5 PhD; N K Morojele,3,5,6 PhD Alcohol, Tobacco and Other Drug Research Unit, South African Medical Research Council, Cape Town, South Africa epartment of Psychiatry, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa D 3 Alcohol, Tobacco and Other Drug Research Unit, South African Medical Research Council, Pretoria, South Africa 4 Centre for Addiction and Mental Health, Toronto, Canada; Dalla Lana School of Public Health, University of Toronto; Center for Health, Intervention, and Prevention, University of Connecticut, Mansfield, USA 5 Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, South Africa 6 School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa; School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 1 2

Corresponding author: C D Parry (cparry@mrc.ac.za)

Background. Alcohol has a negative effect on antiretroviral therapy (ART) adherence and HIV treatment outcomes. Method. As part of formative work for a project to test the efficacy of an alcohol-focused intervention to reduce alcohol consumption and improve HIV treatment outcomes, we investigated the extent of problem drinking among patients at ART clinics in Tshwane, South Africa (SA), using the Alcohol Use Disorders Identification Test (AUDIT). Results. The finding that a third of drinkers reported hazardous drinking, roughly 10% reported harmful drinking, and a further 10% were possibly alcohol dependent replicates the findings of similar research in the Western Cape and Gauteng provinces of SA. It also points to the need for more routine screening of ART patients for problematic alcohol use. Conclusion. The 10-item AUDIT may be too time consuming for health workers in busy ART clinics to administer and score, necessitating even briefer screening instruments for assessing hazardous and harmful drinking. S Afr Med J 2016;106(6):567-568. DOI:10.7196/SAMJ.2016.v106i6.10639

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The number of people on antiretroviral therapy (ART) in South Africa (SA) is the highest globally, accounting for over 20% of all persons on ART worldwide.[1] This places an enormous burden on the health budget and on the human and other resources necessary to deliver ART to a greater proportion of HIV patients. However, increasing access to ART has made HIV a manageable, chronic condition. It is well established that hazardous or harmful alcohol use is causally linked to HIV disease progression. This occurs as a result of the effect of alcohol on ART adherence and on the immune system, and its interaction with ART and medications used to treat opportunistic infections.[2] Yet little is known about the drinking behaviour of patients on ART in SA or how best to intervene. In 2014, the South African Medical Research Council funded a randomised controlled trial (RCT) to determine the efficacy of an alcohol-focused intervention for improving adherence to ART and HIV treatment outcomes.[3] As part of the formative work undertaken for this RCT, we investigated the extent of problem drinking among patients on ART seen at ART clinics in district hospitals in the Tshwane Metropolitan Municipality, Gauteng Province, SA.

Methods

Participants comprised patients who were screened to take part in the pilot study of the RCT[3] as they waited for their clinic appointment. Patients were eligible to participate if they were at least 18 years old, lived in Tshwane or the general area served by the selected clinics, were HIV-positive, had been receiving ART for at least 3 months, were not currently on treatment for tuberculosis (TB), and were not currently enrolled in another study. The Alcohol Use Disorders Identification Test (AUDIT) was then completed with consenting patients.[4] The screener collected information on demographic characteristics, duration of ART, receipt of TB treatment, and alcohol use during the past 12 months. The 10-item AUDIT[4] was administered to participants who reported any alcohol consumption in the past year. Responses were summed to yield a total score, with a possible range of 0 - 40. Higher total scores indicate a greater risk for problem drinking. The AUDIT cut-off scores of 8 - 15 for hazardous drinking, 16 - 19 for harmful drinking and ≥20 for possible alcohol dependence were used.[4]

Results

The sample comprised 196 participants who reported alcohol use in the past 12 months – one-third of those who reached this point in the screening process. Of these, 190 completed all items on the AUDIT. Roughly half were female (49.5%). Among those who reported alcohol use in the past 12 months, a high proportion (46%) were in the low-risk category. A third (33%) of the participants were in the hazardous risk category, 11% were in the harmful risk category and 10% were in the possible dependence category. Overall, 69% of male drinkers and 39% of female drinkers scored in the highest three risk categories (i.e. total AUDIT score ≥8). The mean total AUDIT

score was significantly higher for men (11.4) than for women (7.9) (t=–3.724; p<0.0001). One in five female drinkers (21%) reported heavy episodic drinking at least once a month, compared with a third (32%) of male drinkers (heavy episodic drinking being defined as four or more drinks for women and six or more drinks for men).

Discussion

Although the sample size was relatively small and excluded individuals who refused screening or reported no drinking in the past year, the findings broadly align with those of Kader et al.,[5] who found that 91% of male and 89% of female drinkers (most of whom were receiving ART) attending eight HIV clinics in Cape Town reported hazardous or harmful alcohol consumption when screened with the AUDIT. A similar study conducted in Tshwane in two HIV clinics among patients on ART found slightly lower corresponding figures of 75% for male and 55% for female drinkers, but like the findings of Kader et al.,[5] these are somewhat higher than ours reported above. The high proportions of men and women who drink heavily is of grave concern given the associated risk for reduced ART adherence,[6] forward transmission of HIV, and other health problems.[7] Given the high levels of problematic drinking that were evident among patients on ART in Tshwane, we agree with recommendations made previously[2,5] that there should be more screening of patients attending HIV clinics for problematic alcohol use as a prelude to implementing brief interventions to reduce the negative impact of drinking on HIV treatment outcome, or where necessary referring HIV patients to more intensive treatment. However, the 2 - 4 minutes typically taken to administer and score the AUDIT[4] is likely to serve as a barrier to its routine use in primary care settings, and as a result further research is also needed to assess the possibility of using briefer screening instruments in primary care settings. Acknowledgements. We acknowledge funding from the South African Medical Research Council (Flagship Research) for the study referred to and for our time in preparing this article. 1. UNAIDS. How AIDS Changed Everything – MDG6: 15 Years, 15 Lessons of Home from the AIDS Response. Geneva: UNAIDS, 2015. 2. Schneider M, Neuman M, Chersich, M, Parry, C. Alcohol and antiretroviral therapy – a lethal cocktail. J AIDS Clin Res 2012;S1:005. DOI:10.4172/2155-6113.S1-005 3. Parry CDH, Morojele NK, Myers BJ, et al. Efficacy of an alcohol-focused intervention for improving adherence to antiretroviral therapy (ART) and HIV treatment outcomes – a randomised controlled trial protocol. BMC Infect Dis 2014;14:500. DOI:10.1186/1471-2334-14-500 4. Babor TF, Higgins-Biddle JC, Saunders JB, Monteiro MG. The Alcohol Use Disorders Identification Test: Guidelines for Use in Primary Care. Geneva: World Health Organization, Department of Mental Health and Substance Abuse Dependence, 2001. http://whqlibdoc.who.int/hq/2001/WHO_MSD_ MSB_01.6a.pdf (accessed 6 May 2016). 5. Kader R, Seedat S, Govender R, Parry CD. Hazardous and harmful use of alcohol and/or other drugs and health status among South African patients attending HIV clinics. AIDS Behav 2014;18(3):525534. DOI:10.1007/s10461-013-0587-9 6. Hendershot CS, Stoner SA, Pantalone DW, Simoni JM. Alcohol use and antiretroviral adherence: Review and meta-analysis. J Acquir Immune Defic Syndr 2009;52:180-202. DOI:10.1097/ QAI.0b013e3181b18b6e 7. Rehm J, Baliunas D, Borges GLG, et al. The relation between different dimensions of alcohol consumption and burden of disease – an overview. Addiction 2010;105(5):817-843. DOI:10.1111/ j.1360-0443.2010.02899.x

Accepted 4 April 2016.

June 2016, Print edition

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POSITION STATEMENT

Position statement on cannabis D J Stein, FRCPC, PhD, for the Executive Committee of the Central Drug Authority Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, South Africa Corresponding author: D J Stein (dan.stein@uct.ac.za)

There is an ongoing national debate around cannabis policy. This brief position statement by the Executive Committee of the Central Drug Authority outlines some of the factors that have contributed to this debate, delineates reduction strategies, summarises the harms and benefits of marijuana, and provides recommendations. These recommendations emphasise an integrated and evidence-based approach, the need for resources to implement harm reduction strategies against continued and chronic use of alcohol and cannabis, and the potential value of a focus on decriminalisation rather than the legalisation of cannabis. S Afr Med J 2016;106(6):569-570. DOI:10.7196/SAMJ.2016.v106i6.10863

Why now?

A national debate on cannabis has gathered momentum for several reasons. First, the introduction of a bill that focuses on the use of cannabis for medical purposes has raised issues about the access to and the efficacy of the psychoactive ingredients of the cannabis plant for the management of medical conditions. Second, there have been changes in the legal status of cannabis in several countries around the world, including Uruguay and the USA. Third, in South Africa (SA), the abuse of alcohol, tobacco, cannabis and other psychoactive substances or drugs continues to be a major problem, causing immense suffering to individuals, families and communities and costing the national economy severely.[1-3]

Brief history

Cannabis is subject to several international and national conventions and laws. The International Drug Convention of 1961 agrees that states should not commercialise cannabis, but allows states to decide for themselves the extent to which laws and policies should focus on the different strategies of supply, demand and harm reduction. The Prevention of and Treatment for Substance Abuse Act 70 of 2008 speaks to The National Drug Master Plan, which emphasises all three of these strategies for combating the abuse of alcohol, tobacco, cannabis and other psychoactive substances.

Reduction strategies

Supply reduction refers to policing efforts to curb the manufacture and distribution of alcohol, tobacco, cannabis and other psychoactive substances. Demand reduction refers to preventive efforts to decrease demand for such substances. Harm reduction refers to policies and interventions aimed at reducing the harmful consequences of alcohol, tobacco, cannabis and other psychoactive substance use. A focus on harm reduction does not intend to send a message to the community that risky behaviours and the use of psychoactive substances or drugs are acceptable. Rather, such policies are formulated based on the scientific evidence regarding what works to improve public health and reduce social harms when tobacco, alcohol, cannabis and other psychoactive substances are already being used.[4-6]

Harms of marijuana

Scientific research has established that cannabis is associated with a range of potential harms to individuals and to society. Data on smoking cannabis indicate that this practice is linked to cardio

vascular and respiratory disorders, as well as to cognitive impairment and mental disorders.[7] Exposure to cannabis in adolescence, a time of significant neurodevelopment, is associated with a higher risk for psychotic disorders in later life. The risk is dose related.[8] Highly potent cannabis represents a significant public health problem. Acute cannabis use, for example, is associated with increased risk of motor vehicle collisions, including fatal crashes.[9] Cannabis use should therefore be prevented, and its continued use treated, using evidencebased approaches.

Benefits of marijuana

Medications such as dronabinol and nabilone consist of psychoactive ingredients of the cannabis plant, and are available in a number of countries for the treatment of medical conditions, such as nausea after chemotherapy, pain and spasticity. There is ongoing interest in the use of psychoactive ingredients of the cannabis plant in various other medical contexts, including for weight gain in HIV-positive patients. However, there are relatively few rigorous data in this area, and little is known about safe dose limits.[10] In the SA setting, there is a need for greater health research in general, including work on cannabis. This needs to be balanced against national health research priorities, which have highlighted the importance of additional research on several aspects of mental health that are relevant to SA’s burden of disease, including mortality and morbidity.[11]

Recommendations

• The National Drug Master Plan emphasises the importance of an integrated approach to supply reduction, demand reduction, and harm reduction strategies for combating alcohol, tobacco, cannabis and other psychoactive substance use and abuse in SA. For any particular substance, the balance between these three strategies, and the precise nature of the approach taken, should be evidence based. • An assessment of currently available data in other countries indicates that alcohol is the substance that causes the most individual and societal harm,[12] and it is therefore key to put particular efforts into implementing the most evidence-based policies and interventions for combating such harm. This would encompass addressing a range of upstream drivers of alcohol use, as well as prevention and intervention efforts.[13] • Efforts at harm reduction have been particularly poorly resourced in SA, and given the enormous profits made by the liquor industry

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•

there is a need and obligation for this industry to be substantively more involved in evidence-based harm-reduction efforts. In terms of cannabis, local school survey data suggest high rates of experimentation during early adolescence;[14] hence, evidencebased interventions that include a strong focus on harm reduction are also needed in this population, which comprises a large proportion of South Africans. There are few data to indicate that supply reduction via criminalisation is effective in reducing cannabis abuse. At the same time there are insufficient data to indicate that the legalisation of cannabis will not be harmful. The immediate focus should therefore be decriminalisation rather than legalisation. With regard to medical marijuana, products based on ingredients of the cannabis plant should undergo standard evaluation by the Medicines Control Council to assess their benefits and risks for the treatment of particular medical conditions. Evidence-based approaches that reduce harm from continued and chronic use of alcohol and cannabis (particularly among vulnerable groups such as adolescents and people with mental disorders) deserve greater attention and additional resources. Mental, neurological, and substance use disorders contribute significantly to SA’s burden of disease. Proportionally and quantitatively, more research attention and resources need to focus on this area.

Acknowledgement. We thank Prof. Bronwyn Myers of the SA Medical Research Council for her inputs.

The Executive Committee of the Central Drug Authority: Carol du Toit, Dan Stein, David Bayever, Eva Manyedi, Johlene Ntwana, Lethiwe Ndlovu, Mogotsi Kalaemodimo, Moses Gama, Pelmos Mashabela, Peter Ucko. 1. Van Niekerk JP. Medical marijuana and beyond. S Afr Med J 2014;104(6):387. DOI:10.7196/SAMJ.8335 2. Parry CD, Myers BJ. Legalising medical use of cannabis in South Africa: Is the empirical evidence sufficient to support policy shifts in this direction? S Afr Med J 2014;104(6):399-400. DOI:10.7196/ SAMJ.8135 3. Matzopoulos RG, Truen S, Bowman B, Corrigall J. The cost of harmful alcohol use in South Africa. S Afr Med J 2014;104(2):127-132. DOI:10.7196/SAMJ.7644 4. Anderson P, Chisholm D, Fuhr DC. Effectiveness and cost-effectiveness of policies and programmes to reduce the harm caused by alcohol. Lancet 2009;373(9682):2234-2246. DOI:10.1016/S01406736(09)60744-3 5. Jones L, Hughes K, Atkinson AM, Bellis MA. Reducing harm in drinking environments: A systematic review of effective approaches. Health Place 2011;17(2):508-518. DOI:10.1016/j. healthplace.2010.12.006 6. Babor TF. Linking science to policy: The role of international collaboration and problem-focused integrative reviews. Addiction 2015;110(2):40-46. DOI:10.1111/add.12911 7. Karila L, Roux P, Rolland B, et al. Acute and long-term effects of cannabis use: A review. Curr Pharm Des 2014;20(25):4112-4118. DOI:10.2174/13816128113199990620 8. Radhakrishnan R, Wilkinson ST, D’Souza DC. Gone to pot - a review of the association between cannabis and psychosis. Front Psychiatry 2014;22(5):54. DOI:10.3389/fpsyt.2014.00054 9. Asbridge M, Hayden JA, Cartwright JL. Acute cannabis consumption and motor vehicle collision risk: Systematic review of observational studies and meta-analysis. BMJ 2012;344:e536. DOI:10.1136/bmj.e536 10. Whiting PF, Wolff RF, Deshpande S, et al. Cannabinoids for medical use: A systematic review and meta-analysis. JAMA 2015;313(24):2456-2473. DOI:10.1001/jama.2015.6358 11. Stein DJ. Psychiatry and mental health research in South Africa: National priorities in a low and middle income context. Afr J Psychiatry 2012;15(6):427-431. DOI:10.4314/ajpsy.v15i6.54 12. Nutt DJ, King LA, Phillips LD. Independent Scientific Committee on Drugs. Drug harms in the UK: A multicriteria decision analysis. Lancet 2010;376(9752):1558-1565. DOI:10.1016/S01406736(10)61462-6 13. Ferreira-Borges C, Dias S, Babor T, Esser MB, Parry CD. Alcohol and public health in Africa: Can we prevent alcohol-related harm from increasing? Addiction 2015;110(9):1373-1379. DOI:10.1111/add.12916 14. Parry CD, Myers B, Morojele NK, et al. Trends in adolescent alcohol and other drug use: Findings from three sentinel sites in South Africa (1997 - 2001). J Adolesc 2004;27(4):429-440. DOI:10.1016/j. adolescence.2003.11.013

Accepted 11 April 2016.

June 2016, Print edition

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Transforming public health ! education and practice’

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Complex adaptive HIV/AIDS risk reduction: Plausible implications from findings in Limpopo Province, South Africa C J Burman, PhD; M A Aphane, M Development The Rural Development and Innovation Hub, University of Limpopo, Polokwane, South Africa Corresponding author: C J Burman (burmanc@edupark.ac.za)

This article emphasises that when working with complex adaptive systems it is possible to stimulate new social practices and/or cognitive perspectives that contribute to risk reduction, associated with reducing aggregate community viral loads. The process of achieving this is highly participatory and is methodologically possible because evidence of ‘attractors’ that influence the social practices can be identified using qualitative research techniques. Using findings from Limpopo Province, South Africa, we argue that working with ‘wellness attractors’ and increasing their presence within the HIV/AIDS landscape could influence aggregate community viral loads. While the analysis that is presented is unconventional, it is plausible that this perspective may hold potential to develop a biosocial response – which the Joint United Nations Programme on HIV and AIDS (UNAIDS) has called for – that reinforces the biomedical opportunities that are now available to achieve the ambition of ending AIDS by 2030. S Afr Med J 2016;106(6):571-574. DOI:10.7196/SAMJ.2016.v106i6.10255

We introduce an innovative intervention in Limpopo Province, South Africa (SA) that was designed to respond to complex aspects of the HIV/AIDS landscape. The embryonic findings suggest that this style of intervention may be a step towards developing a contribution to the biosocial response to the epidemic that the Joint United Nations Programme on HIV and AIDS (UNAIDS) has called for in the context of ending AIDS by 2030. The reflection is structured in the following way: we explain how we incorporated complex adaptive systems into the intervention design, follow ed by a brief overview of the findings. In the discussion we highlight the possibility that something similar may have happened in Zimbabwe, from 1997 to 2007, and then discuss the plausible ramifications of this type of intervention in the context of 2030.

end of AIDS by 2030.[1] It was also influenced by the UNAIDS statement that ‘we need to develop a biosocial response’ to reinforce the biomedical opportunities that are now available to achieve the 2030 ambition. From this platform, the objective of the partnership developed into reducing the aggregate community viral load by developing biosocial tools and techniques to reinforce the biomedical opportunities available to end AIDS and reduce HIV transmission opportunities.[2]

Managing complex adaptive systems

Managing a complex adaptive system requires knowledge about the basics of complexity the

ory and the laws associated with the functioning of complex adaptive systems. The literature on the former is colossal and the literature on the latter is equally daunting.[3] However, managing complex adaptive systems has been synthesised into more compact bundles. Managing a com plex adaptive system places emphasis on working with the dynamics of the system within which the challenge is situated because the dynamics are co-constitutive parts of the challenge.

An iceberg metaphor and the dynamics of complex adaptive systems

Futures scientist, Inayatullah[4] developed an iceberg metaphor to describe the workings of

Producing unpredictable emergent outcomes

The focus of the partnership

The partnership is between an HIV/AIDSfocused community-based organisation called the Waterberg Welfare Society (WWS) and the University of Limpopo. The primary focus of the partnership was to respond to frustrations identified by WWS about the effectiveness of the tools and techniques that were at their disposal to promote wellness within the communities they work with. The partnership became influenced by Vision 90-90-90 and the claim by UNAIDS that ‘business as usual’ is unlikely to achieve the

Feedback between the characteristics and the properties

Characteristics: visible descriptor

Properties: submerged, non-linear dynamic relationships and feedback that enable self-organisation and self-regulation

Fig. 1. The iceberg metaphor: the functioning of a complex adaptive system (based on Inayatullah’s[4] iceberg metaphor).

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complex systems. He argued that the visible aspect of the metaphor is one descriptive layer of the phenomenon that is generally represented in the name attributed to the challenge, such as ‘stigma’ or ‘disclosure’. He then argued that the submerged aspect of the metaphor represents discrete layers that influence, sustain and co-constitute the visible descriptor.[4] In complex adaptive systems, the visible part of the iceberg represents the characteristics of the issue and the submerged aspects of the metaphor demonstrate some distinctive properties which co-constitute the visible descriptor. Feedback between – and within – all of the layers provides a dispositional, self-regulating identity to the system. The properties include: a variable number of interacting agents, with an agent being anything that influences the system; feedback mechanisms that connect and influence different agents within the system; and linear – or cause-effect – and non-linear interactions (Fig. 1). The dispositional, self-regulating identity of complex adaptive systems reflects two issues: first, although there are multiple inter actions between agents, these interactions are constrained – or restricted – within permeable boundaries; second, the agents tend to interact more with specific aspects of the complex adaptive system than with other parts. The sites within the system with which agents most commonly interact are called ‘attractor sites’. In social systems, the interactions with specific attractor sites ‘are reflected in patterns of behaviour which are never exactly repeated but are always similar to each other’,[5] such as the ebb and flow of rumour and myth associated with HIV/AIDS.[6]

Incorporating attractors into the intervention framework

From the perspective of an intervention design, attractors become critical for both methodological reasons and implementation. Methodologically, most of the functionings of a complex adaptive system are so discrete that it is impossible to identify them, let alone modify them. However, it is possible to identify attractors using qualitative research techniques which open a window of analytic opportunity.[7] From the implementation perspective, because complex adaptive systems are unstable and adaptable, it is possible to disrupt them further, catalysing downstream ripple effects as new attractors emerge, and/or existing attractors are modified, as the agents adaptively reorganise around the disruption. During, or after, the submerged reorganisation processes, the shifts in the overall attractor landscape can be monitored and the visible social, or behavioural, emergence associated with each shift in the attractor landscape can be evaluated. Once there is clarity about which attractor/s is/are

influencing preferred social practices and/or promoting cognitive perspectives that contribute to risk reduction, it is then a matter of reinforcing those attractors to expand the impact and, if possible, to simultaneously destabilise the attractors that detract from the project goal. The advantage of this approach is that the intervention is firmly rooted within the functioning of the system, rather than focusing exclusively on the visible characteristics of the system.

Method

In order to identify existing attractors and to create new ones, two catalysing influences were applied: an educational package containing up-to-date information about HIV/AIDS and enabling the participants (n=21) with the autonomy to introduce the content of the educational package into their work in ways that they thought would add value. The findings that are presented were identified using an adapted version of a qualitative research technique called causal layered analysis[7] 12 months after the educational package was introduced.[8]

Findings

Four principal wellness attractors that contributed to reducing the aggregate community viral load were identified during the interven tion pilot: ‘movement from HIV being perceived as a death sentence to a chronic condition’, ‘the viral load’, ‘relating new knowledge about HIV/AIDS to personal experience’ and the ‘origins of HIV’. Each of these wellness attractors was associated with altered social practices and/or cognitive perspectives that contribute to risk reduction, there by reducing the aggregate community viral load (Table 1). The first three wellness attractors have a self-evident logic to them. The fourth was a mystery to the university component of the partnership, but this was explained by WWS. The power of the ‘origins’ attractor, in the context that WWS works, is that it counters localised rumour and myth about the ‘origins of HIV’ which are factors that detract from the ambition of reducing the aggregate community viral load. (Two other pilot studies have been initiated in other parts of the province and preliminary reports indicate that the ‘origins’ and the ‘viral load’ attractors are also emerging in one of them. However, these reports are unsubstantiated at this time.) Examining the same findings in a slightly different way suggests that a combination of wellness attractors influence the same social practices and/or cognitive perspectives that contribute to risk reduction (Table 2). The ‘origins’ attractor remains a mystery from this perspective because it continues to be a source of much positive discussion at WWS, yet its influence remains ambiguous.

Table 1. Attractors and associated shifts in social practices and/or cognitive perspectives associated with risk reduction that contribute to reducing the aggregate community viral load Wellness attractor

Associated changes among clients

Movement from HIV being perceived as a death sentence to a chronic condition

More accepting of status (n=2); disclosure (n=3); testing (n=2); improved client management of HIV (n=9); testing (n=8); improved messaging to clients (n=1)

The viral load

More accepting of status (n=2); understanding false-negative tests (thus the need to return for a second test) (n=5); testing (n=3); understanding co-infections (n=1); disclosure (n=1); understanding serodiscordant couples (n=2); reduction in stigma (n=1)

Relating new knowledge about HIV/AIDS to personal experience

More accepting of status (n=1); understanding the window period (n=2); disclosure (n=2); overcoming the legacy of ABC (n=1); testing (n=3); understanding serodiscordant couples (n=3)

The origins of HIV

Relating HIV to personal experience (n=1); easy to explain with new knowledge (n=8); understanding transmission (n=1)

ABC = Abstain, Be faithful, Condomise. [8] Based on Burman and Aphane.

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Discussion

the participants began the low-cost process of incorporating the new knowledge into their work. The educational package could have acted as a catalyst that produced disproportional changes – the new wellness attractors – and 12 months after the attractors were identified WWS continues to work with them because ‘structure and coherence’ is developing to such an extent that they believe they are the foundations of future prevention and risk-reduction tools.

Partially constrained, patterned instability that contains some nonlinear interactions makes complex adaptive systems prone to emergent incremental change and innovation. For example, zoonosis happens because of the gradual coalescing of the interactions and feedback between novel agents as different systems become compressed into a complex adaptive system, giving rise to emergent possibilities that may adapt into qualitatively new phenomena – such as the emergence of HIV about a century ago.[9] Despite limited numbers, we have demonstrated that during the first pilot study it has been possible to generate emergent social practices and/or cognitive perspectives that contribute to risk reduction and identify the submerged wellness attractors that are associated with the emergence. The partnership is now in the process of reinforcing these attractors to determine if this will increase the impact of the intervention. In the discussion that follows we will only claim abductive plausibility because we believe that further work is required to determine the effectiveness of the intervention design.

Other plausible examples of complex adaptive change processes

The most striking example is the dramatic decline in HIV prevalence – in the absence of widely accessible antiretroviral medication – in Zimbabwe, from 1997 to 2007. In Table 3 an analysis that was pub lished in 2011[10] is re-examined from the perspective of plausibility and complex adaptive systems. It is plausible that a range of discrete feedback loops and relationships gradually altered the attractors on a significant scale in the Zimbabwean HIV landscape that enabled spaces to emerge for a shift in specific social practices and/or cognitive perspectives that contribute to risk reduction that may account for the dramatic, home-grown, biosocial decline in HIV prevalence. One thing is certain, the 2011 account was developed by high-level academics and despite deliberate attempts to identify specific rational causes of the overall decline, none was identified, which goes some way to plausibly suggest that the perspective we have presented may have the potential to be applied on a national scale.

What could have happened in Limpopo?

Many of the WWS participants expressed frustration with the inadequacies of their existing tools and techniques to promote risk-reducing social practices. This could indicate that prior to the intervention dispositional characteristics of the system were: (i) frustration; and (ii) a desire to respond to this frustration by developing new tools to improve the impact of their work. A comprehensive educational package was delivered and

Table 2. Attractors that influenced more than one social practice and/or cognitive perspectives that are associated with risk reduction Wellness attractors Death sentence → chronic

Relating to prior experiences

Viral load

Encourages testing (n=11); including awareness about the implications of the window period (n=18)

✓

Encourages disclosure (n=7)

✓

Accepting status (n=3)

✓

Surface descriptor/characteristic

Understanding serodiscordant couples (n=5)

✓

Messaging to community (n=11) Based on Burman and Aphane.

Tools and techniques

Origins of HIV

✓

[8]

Table 3. A plausible perspective of the dramatic decline in HIV prevalence in Zimbabwe Could complexity explain what happened in Zimbabwe to reduce HIV prevalence from 29% in 1997 to 16% in 2007? An unstable context

A ‘context of severe social, political, and economic disruption’ and the absence of widely available antiretroviral medication

Identified drivers: ‘causal pathways’ (but no proof)

‘Household deaths creating personal experiences that made people fearful of the reality of the consequences of HIV; increased knowledge about transmission routes; less disposable income leading to a reduction in multiple partners and communication about HIV/AIDS at multiple societal levels’

Plausible wellness attractors

‘Personal experience of death’ and ‘increased knowledge about transmission routes’

Emergent social practice

‘Partner reduction’

Reinforced by

‘Mass communication’

Was there a dominant linear (cause-effect) driver? No

‘It was the cumulative exposure to many programs that helped create a ‘‘tipping point’’ leading to changes in behavioural norms’

Similarities to the Limpopo findings? Yes

Plausible wellness attractors in Zimbabwe: ‘personal experience about household deaths’ and ‘transmission route’. Wellness attractors identified in Limpopo: ‘Relating new knowledge about HIV/AIDS to personal experience’ and ‘the viral load’

[10]

Based on Halperin et al.’s

analysis of the Zimbabwean decline in prevalence.

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techniques designed to work with complexity, including electronic monitoring and evaluation tools that could be aligned to SA’s eHealth strategy,[15] to warrant further investigation. This would require further pilots to empirically determine if this style of intervention could contribute to developing one of the biosocial responses that UNAIDS calls for.

Changes in new infections (incidence) – SA Age group

Women (2002 - 2012)

Men (2002 - 2012)

15 - 24 years

Down 60%

Up 67%

25 - 49 years

Up 17%

Up 25%

Conclusion

2012 incidence 15 - 44 years 2.28% 1.21% 2012 1 in 44 women 1 in 83 men incidence: became infected in 2012 became infected in 2012 Fig. 2. HIV incidence 2002 - 2012, South Africa (based on the South African National HIV Prevalence, Incidence and Behaviour Survey, 2012[12]).

Future attractors that are likely to influence the HIV/AIDS landscape

At the moment the SA track record with regard to incidence is not encouraging (Fig. 2), with the exception of prevention of mother-tochild transmission.[11] As the impact of treatment as prevention increases, it is logical to expect this trend to radically alter. However, the downstream effect of this is likely to create instability in systems relating to individual experiences of living with HIV,[13] as well as systems designed to reduce the impact of HIV/AIDS.[14] Both of these downstream challenges represent potential Achilles’ heels to the ambition to end AIDS. Some of this instability is likely to demonstrate some complex characteristics, suggesting that the more we can learn about working with complexity and HIV/AIDS now, the better we will be able to expand the biosocial armamentarium for the future.

What could the implications be for developing a biosocial response to the contemporary epidemic as a contribution to ending AIDS?

It is plausible that this style of intervention could be applied to diverse aspects of the treatment and care continuum that demonstrate complex instability. The process would include identifying instability along the continuum, catalysing the emergence of new attractors that make sense to the target groups and working with the attractors to develop and reinforce appropriate strategies to reduce the aggregate national viral load. The ‘value add’ in this approach is that, when there is instability that is difficult to manage using conventional mechanisms, the identification of relevant attractors and reinforcement of those attractors enables a targeted response that makes sense in different contexts because the process is hard-wired to incorporate localised characteristics of the HIV/AIDS landscape. Despite the limitations of the pilot study in Limpopo, there has been sufficient international growth in management tools and

We have introduced some embryonic findings from Limpopo which suggest that working with HIV risk reduction and prevention using management techniques associated with complex adaptive systems may hold potential to open innovative biosocial spaces that could contribute to the ambition of ending AIDS by 2030. In this instance one educational package, followed by experimental efforts to apply the knowledge, catalysed the emergence of four wellness attractors that influenced biosocial factors that affect the trajectory of the epidemic. By reinforcing these attractors it is plausible that ‘disproportionately major consequences’ that reduce the aggregate community viral load could occur. It is also plausible that this style of intervention could contribute to developing a biosocial response, as called for by UNAIDS. The striking resemblance between the Zimbabwean and the Limpopo attractors could indicate that wellness attractors can influence the epidemic on a national scale. The emergence of HIV was enabled by complex zoonotic processes almost a century ago.[9] It is plausible that complexity can now contribute to reducing its presence in the build-up to 2030. 1. UNAIDS. The Gap Report. Geneva: Joint United Nations Programme on HIV/AIDS, 2014. http:// www.unaids.org/en/resources/campaigns/2014/2014gapreport/gapreport (accessed 12 May 2016). 2. Burman CJ, Aphane M, Mtapuri O, Delobelle P. Expanding the prevention armamentarium portfolio: A framework for promoting HIV-conversant communities within a complex, adaptive epidemiological landscape. J Social Aspects HIV/AIDS 2015;12:18-29. DOI:10.1080/17290376.2015.1034292 3. Sturmberg J, Martin C. Complexity in health: An introduction. In: Sturmberg J, Martin C, eds. Handbook of Systems and Complexity in Health. New York: Springer, 2013. 4. Inayatullah S. Causal layered analysis. Futures 1998;30(8):815-829. DOI: 10.1016/s00163287(98)00086-x. 5. Stacey R. Complexity and Group Processes: A Radical Social Understanding of Individuals. New York: Brunner-Routledge, 2003. 6. Dickinson D. Myths or theories? Alternative beliefs about HIV and AIDS in South African working class communities. Afr J AIDS Res 2013;12:121-130. DOI:10.2989/16085906.2013.863212 7. Bishop BJ, Dzidic PL. Dealing with wicked problems: Conducting a causal layered analysis of complex social psychological issues. Am J Community Psychol 2014;53:13-24. DOI:10.1007/s10464-013-9611-5 8. Burman CJ, Aphane M. Community viral load management: Can ‘attractors’ contribute to developing an improved bio-social response to HIV risk-reduction? Nonlinear Dynamics Psychol Life Sci 2015;20(1):1-36. 9. Sharp PM, Hahn BH. Origins of HIV and the AIDS pandemic. Cold Spring Harb Perspect Med 2011;1:a006841. DOI:10.1101/cshperspect.a006841 10. Halperin DT, Mugurungi O, Hallett TB, et al. A surprising prevention success: Why did the HIV epidemic decline in Zimbabwe? PLoS Med 2011;8:e1000414. DOI:10.1371/journal.pmed.1000414 11. Barker P, Barron P, Bhardwaj S, Pillay Y. The role of quality improvement in achieving effective large-scale prevention of mother-to-child transmission of HIV in South Africa. AIDS 2015;29 (Suppl 2):S137-S143. DOI:10.1097/QAD.0000000000000718 12. Burman CJ, Aphane M, Delobelle P. Reducing the overall HIV-burden in South Africa: Is ‘reviving ABC’ an appropriate fit for a complex, adaptive epidemiological HIV landscape? Afr J AIDS Res 2015;14:13-28. DOI:10.2989/16085906.2015.1016988 13. Vella S. End of AIDS on the horizon, but innovation needed to end HIV. Lancet HIV 2015;2:e74-e5. DOI:10.1016/s2352-3018(15)00023-5 14. Whiteside A, Cohen J, Strauss M. Reconciling the science and policy divide: The reality of scaling up antiretroviral therapy in South Africa. S Afr J HIV Med 2015;16:355. DOI:10.4102/hivmed.v16i1.355 15. Burman CJ, Aphane M, Delobelle P. Weak signal detection: A discrete window of opportunity for achieving ‘Vision 90:90:90’? SAHARA-J: Journal of Social Aspects of HIV/AIDS. 2016;13:17-34. DOI: 10.1080/17290376.2015.1123642

Accepted 20 April 2016.

June 2016, Print edition

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CASE REPORT

A case of biventricular endomyocardial fibrosis complicated by right ventricular outflow tract aneurysms R Gonçalves,1 MB ChB, MMed (Int Med), Cert Card (CMSA); R Meel,2 MB ChB, MMed (Int Med), Cert Card (CMSA) 1 2

epartment of Cardiology, Charlotte Maxeke Johannesburg Academic Hospital and University of the Witwatersrand, Johannesburg, South Africa D Department of Cardiology, Chris Hani Baragwanath Academic Hospital and University of the Witwatersrand, Johannesburg, South Africa

Corresponding author: R Gonçalves (drrgoncalves@gmail.com)

Endomyocardial fibrosis remains a major public health problem worldwide. It is a restrictive cardiomyopathy, of uncertain aetiology, which may lead to right, left or biventricular heart failure. Progress continues to be made in understanding the prevalence and natural history of this disease. Specific treatment, apart from surgery, remains suboptimal. We report a case of advanced, biventricular EMF complicated by right ventricular outflow tract aneurysms. S Afr Med J 2016;106(6):582-584. DOI:10.7196/SAMJ.2016.v106i6.9056

Endomyocardial fibrosis (EMF), despite being the most common restrictive cardiomyopathy worldwide, still remains poorly under stood.[1,2] Although first described in Uganda,[3] this condition has been documented throughout the world, particularly in tropical and subtropical zones in Africa, Asia and South America.[1,2] Its aetiology remains elusive.[1,2] It possibly has different aetiologies in different parts of the world, with a similar final common pathway, although this remains conjecture. Hypotheses ranging from infectious and allergic causes to malnutrition and toxins have been postulated, although none has been rigorously tested. The condition is associated with fibrosis of the endocardium (extending into the myocardium) of the right and left ventricles, involving predominantly the apices and inflow regions, resulting in impaired filling of one or both ventricles.[1,2] Patients may then present clinically with right, left or biventricular failure. Associated mitral and/or tricuspid regurgitation is common owing to frequent involvement of the papillary muscles with tethering to the ventricular wall. Recently, a high prevalence of predominantly asymptomatic cases has been described in Mozambique, suggesting that the disease may be underdiagnosed in neighbouring South Africa (SA).[4] We report a case of advanced biventricular EMF complicated by right ventricular outflow tract (RVOT) aneurysms, with the intention of stimulating clinicians to search for this condition.

Case report

A 49-year-old woman, originally from southern Mozambique, presented with an 8-year history of symptoms and signs of rightsided heart failure. She was initially misdiagnosed as having constrictive pericarditis. She originally presented with symptoms of exertional dyspnoea (grade II New York Heart Association (NYHA)), associated with peripheral oedema, that eventually progressed to anasarca. No history of rheumatic fever was reported. At the time of her assessment she was taking oral spironolactone 25 mg daily, furosemide 80 mg bid, potassium chloride 1200 mg bid, atenolol 25 mg daily, hydrochlorothiazide 25 mg daily (added to address loop diuretic resistance) and warfarin according to her international normalised ratio (INR).

On examination, a raised jugular venous pressure was accompanied by anasarca (with prominent ascites). No jaundice, pallor or clubbing were noted. Pulse was irregular, and of variable volume consistent with atrial fibrillation (AF). The apex beat was undisplaced and normal in character. The heart sounds were normal and no signs of pulmonary hypertension were noted. Murmurs consistent with both tricuspid and mitral regurgitation were noted. The liver was impalpable due to the anasarca. The remainder of the examination was unremarkable. A urine dipstick revealed a trace of protein. An electrocardiogram revealed AF with a ventricular rate of 84 beats/min, slurring of the terminal portion of the R-wave and a prominent R-wave in V2 (R:S ratio was 0.9). Her chest X-ray revealed an increased cardiothoracic ratio (0.7) with a globular heart shadow. This was due to left and right atrial dilation. A bulge was noted on the left heart border. No pleural effusions or pericardial calcification was present. Pulmonary venous congestion or pulmonary artery dilation was absent. Blood results indicated a normal full blood count; urea, creatinine and electrolytes; a therapeutic INR; and mildly deranged liver enzymes in keeping with hepatic congestion. She was HIV-negative. Echocardiography revealed severely dilated atria (left atrial width 5.1 cm and right atrial width 5.3 cm), mildly dilated left ventricle (LV) (LV internal diameter end diastole 5.52 cm, LV internal diameter end systole 3.48 cm) and a normal right ventricle (Fig. 1). LV wall thickness (basal) was within normal limits (interventricular septum end diastolic and LV posterior wall end diastolic diameters were 0.75 cm and 1.29 cm, respectively), although the posterior wall was thicker than the septum. LV ejection fraction was preserved (65%) but the lateral S’-velocity, on tissue Doppler imaging of the mitral annulus, was markedly diminished. Both ventricular apices were obliterated. No thrombi were noted in the atria or the apices. The E:E’ ratios, at both the medial and lateral mitral annulus, were over 10, consistent with diastolic dysfunction. Severe tricuspid regurgitation and moderate mitral regurgitation were noted. The mechanism of regurgitation was due to tethering of the leaflets owing to papillary muscle shortening and annular dilation, as the chordae and leaflets were normal, the jets were central, and there was tip-totip coaptation of the leaflets of atrioventricular valves. The aortic

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Fig. 1. (A) Echocardiogram (apical four chamber views) demonstrating massively dilated atria, small ventricles and obliterated right and left ventricular apices; (B) Calcification (arrow) in the left ventricular apex can be seen on the zoomed-in image.

and pulmonary valves were spared. The estimated systolic pulmonary artery pressure was 37 mmHg. No features consistent with pericardial effusion nor constriction were present. In summary, these findings were in keeping with a restrictive cardiomyopathy, most likely biventricular EMF. Cardiac catheterisation was performed. This revealed a mean right atrial pressure (RAP) of 14 mmHg. Dynamic respiratory manoeuvers did not influence the RAP. The right ventricular (RV) systolic, diastolic and end-diastolic pressures (RVEDPs) were 33, 4 and 15 mmHg, respectively. The systolic, diastolic and mean pulmonary artery pressures were 37, 14 and 23 mmHg, respectively (normal). Mean pulmonary capillary wedge pressure was 20 mmHg and pulmonary arteriolar resistance was 58 dynes.s/cm5 (normal). LV systolic, diastolic and enddiastolic pressures (LVEDPs) were 110, 4 and 14 mmHg, respectively. A dip and plateau sign was seen in both ventricles and LVEDP to RVEDP pressure difference of 1 mmHg was recorded. Ventricular interdependence was absent during deep respiration on simultaneous left and right ventricular pressure measurements. Obliteration of both ventricular apices and distortion of the normal ventricular outline was noted on right and left ventriculography (Figs 2 and 3). An inferior

Fig. 2. A left ventriculogram showing distortion of the left ventricular cavity with an inferior wall aneurysm (arrow) and obliteration of the apex. (A) Diastole; (B) Systole.

wall LV aneurysm was apparent in diastole. Two tubular aneurysms originating from the RVOT were noted, with dilation of the RVOT. These structures did not communicate with another chamber and emptied during systole. Pulmonary artery saturation was 76% and aortic saturation was 96%. The cardiac output was estimated at 4.1 L/min (cardiac index 2.65 L/min). The coronary arteries were normal. An endomyocardial biopsy was not performed. These findings were corroborated by car diac magnetic resonance imaging (MRI) (Fig. 4). Markedly dilated atria and thick ening of the ventricular endocardium, with obliteration of both apices, were noted. Papillary muscle thickening and shortening probably contributed to the tricuspid and mitral regurgitation. No thrombi were noted. After a discussion with the patient, surgery was deferred, given the high surgical risk associated with the procedure. She was continued on the afore-mentioned medical therapy.

Discussion

This case report highlights a unique example of biventricular EMF complicated by RVOT aneurysms. The classically described pathological changes in right-sided EMF include obliteration of the right ventricular

June 2016, Print edition

Fig. 3. A right ventriculogram demonstrating distortion of the right ventricular cavity with obliteration of the apex, dilation of the RVOT and two tubular aneurysms (arrows) originating from the RVOT (both of which empty during systole). (A) Diastole; (B) Systole.

Fig. 4. Cardiac MRI showing bilaterally dilated atria (thick arrows), small ventricles and obliteration of the ventricular apices (thin arrows). Papillary muscle thickening and shortening, a normal pericardium, and the absence of thrombi are noted.

apex by fibrosis, dilation of the RVOT, tricuspid regurgitation and a massively dilated right atrium.[5-8] In left-sided disease, partial LV obliteration by fibrosis occurs. Further extension of the process into the inflow tract causes papillary muscle adhesion to the LV wall leading to subsequent mitral regurgitation. The left atrium is dilated, although frequently less so than the right atrium. Interestingly, early radiological studies occasionally identified a convex bulge, high on the LV border on the chest X-ray,

IN PRACTICE

which was due to diastolic distention of the RVOT based on flouroscopy.[5,6] This feature was present in this case. The presence of focal, tubular aneurysms of the RVOT, however, is unique. These may have arisen owing to high RV diastolic pressures related to reduced RV volume, decreased RV compliance and poor RV relaxation. The RVOT is the most likely region to dilate, given its relatively thin wall and the absence of fibrosis in this region. A similar explanation may account for the LV inferior wall aneurysm that was observed in this case. A recent study performed in Mozambique has contributed significantly to the field.[4] It not only highlighted the prevalence of this disease in that country but also defined a set of echocardiographic criteria that are useful both for diagnosis and assessment of severity. [4] The estimated overall prevalence of EMF was 19.8%, with the highest prevalence among persons 10 - 19 years of age (28.1%), more commonly in males. Biventricular EMF was most common (55.5%), followed by right-sided EMF (28%), and the minority, (16.5%) were left sided. The majority of patients were asymptomatic (77.3%), with most cases diagnosed only on echocardiography. Echocardiography is an essential tool for the diagnosis of EMF. The proposed echocardiographic criteria for diagnosis and assess ment of the severity of EMF are summarised briefly.[4] A definite diagnosis of EMF was made in the presence of 2 major or 1 major and 2 minor criteria. The severity was classified as a total score, with <8 indicating mild disease, 8 - 15 moderate disease and >15 severe disease (the maximum possible score being 35 points). The major and minor criteria follow with the point scores indicated in parentheses. The major criteria were as follows: endomyocardial plaques >2 mm in thickness (2); thin (≤1 mm) endomyocardial patches affecting more than one ventricular wall (3); obliteration of the RV or LV apex (4); thrombi or spontaneous contrast without severe ventricular dysfunction (4); retraction of the RV apex (RV apical notch) (4); and atrioventricular valve dysfunction due to adhesion of the valvular apparatus to the ventricular wall (1 - 4, depending on the severity of regurgitation). The minor criteria were as follows: thin endomyocardial patches localised to one ventricular wall (1); restrictive flow pattern across mitral or tricuspid valves

(2); pulmonary valve diastolic opening (2); diffuse thickening of the anterior mitral leaflet (1); enlarged atrium with normal-size ventricle (2); m-mode movement of the interventricular septum and flat posterior wall (1); and enhanced density of the moderator or other intraventricular bands (1). Based on this scoring system, our patient had a score of least 14, indicating moderate disease. The differential diagnosis includes dilated cardiomyopathy, constrictive pericarditis, tuberculous pericarditis and rheumatic heart disease.[1,2] These conditions have a high prevalence in the areas where EMF is endemic, although a careful clinical and echocardiographic review will usually yield the diagnosis. Ebstein’s anomaly may mimic right-sided EMF. Furthermore, other restrictive cardiomyopathies such as amyloidosis, haemochromatosis and sarcoidosis may pose a diagnostic dilemma. Cardiac MRI would be useful in this regard if the diagnosis remains in doubt. Cardiac malignancies constitute another possible diagnostic group. The treatment has been reviewed elsewhere in detail and will not be discussed.[1]

Conclusion

This case report highlights the importance of considering the diagnosis of EMF, in particular in patients originally from endemic areas. Although EMF is not endemic in SA, SA has a large migrant population from countries where the disease is endemic, in particular Mozambique. For this reason, persistent vigilance is necessary to diagnose and correctly manage this fascinating disease. 1. Mocumbi A, Yacoub S, Yacoub M. Neglected tropical cardiomyopathies: II. Endomyocardial fibrosis: Myocardial disease. Heart 2008;94(3):384-390. DOI:10.1136/hrt.2007.136101 2. Bukhman G, Ziegler J, Parry E. Endomyocardial fibrosis: Still a mystery after 60 years. PLoS Negl Trop Dis 2008;2(2):e97. DOI:10.1371/journal.pntd.0000097 3. Davies J. Endomyocardial fibrosis in Uganda. East Afr Med J 1948;25:10-16. 4. Mocumbi A, Ferreira M, Sidi D, Yacoub M. A population study of endomyocardial fibrosis in a rural area of Mozambique. N Engl J Med 2008;359(1):43-49. DOI:10.1056/NEJMoa0708629 5. Cockshott W, Ŝarić S, Ikeme A. Radiological findings in endomyocardial fibrosis. Circ 1967;35(5):913922. DOI:10.1161/01.CIR.35.5.913 6. Cockshott W. Angiocardiography of endomyocardial fibrosis. Br J Radiol 1965;38:192-200. 7. Connor D, Somers K, Hutt M, Manion W, D’Arbela P. Endomyocardial fibrosis in Uganda (Davies’ disease). Part I. An epidemiologic, clinical, and pathologic study. Am Heart J 1967;74:687-709. 8. Connor D, Somers K, Hutt M, Manion W, D’Arbela P. Endomyocardial fibrosis in Uganda (Davies’ disease). Part II. An epidemiological, clinical, and pathological study. Am Heart J 1968;74:107-124.

Accepted 7 March 2016.

June 2016, Print edition

RESEARCH

Where have all the gun deaths gone? R Matzopoulos,1,2 PhD; P Groenewald,1 MB ChB; N Abrahams,3 PhD; D Bradshaw,1,2 DPhil S outh African Medical Research Council Burden of Disease Research Unit, Cape Town, South Africa School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 3 South African Medical Research Council Gender and Health Research Unit, Cape Town, South Africa 1 2

Corresponding author: R Matzopoulos (richard.matzopoulos@mrc.ac.za)

Background. The low number of firearm assaults and overall assault-related deaths in Statistics South Africaâ&#x20AC;&#x2122;s death notification reports is incongruous with other recently released data, including police crime statistics. Methods. We conducted a review of all gunshot injuries recorded in death notifications from 1997 to 2013, including all cases in which the underlying cause of death was ascribed to cause-specific codes in the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) that referred to a gunshot injury. Results. We identified 105 694 gunshot-related injury deaths over the 17-year period, an average of 6 217 per annum. The total annual number of gunshot injuries increased from 1997 to 2000, at which point firearm-related deaths peaked at 9 540 recorded cases. Thereafter there was a steadily decreasing trend (interrupted only in 2006 and 2008) until 2011, when 3 793 deaths were attributed to gunshot-related injuries as the underlying cause â&#x20AC;&#x201C; a decrease of >60% from the peak in 2000. Conclusion. The cause-specific profile for gunshot injury deaths in this study indicated extensive misclassification, which explained the near-absence of these injuries among assault cases. However, the trend in gunshot-related injury deaths irrespective of intent provides further support for the hypothesis that stricter gun control, coinciding with the implementation of the Firearms Control Act of 2000, accounts for this decrease. S Afr Med J 2016;106(6):589-591. DOI:10.7196/SAMJ.2016.v106i6.10379

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i6.10379

Screening for retinopathy of prematurity in a provincial hospital in Port Elizabeth, South Africa M R Jacoby,1 FCOphth; L du Toit,2 FCOphth epartment of Ophthalmology, Provincial Hospital, Port Elizabeth, South Africa; Department of Ophthalmology, Faculty of Health Sciences, D Walter Sisulu University, Mthatha, Eastern Cape, South Africa 2 D epartment of Ophthalmology, Groote Schuur Hospital, Cape Town, South Africa 1

Corresponding author: M R Jacoby (mark.jacoby@telkomsa.net)

Background. Retinopathy of prematurity (ROP) is an emerging public health problem in many middle-income countries where improved neonatal survival rates coupled with inadequate health resources have created a new epidemic. There are limited available data on the magnitude of the problem, and screening in South African (SA) hospitals has not been uniformly practised. Objective. To describe the results of various interventions implemented over a 6-year period while developing a new ROP screening service in a provincial hospital in Port Elizabeth, SA. Method. A retrospective case folder review of ROP screening at Dora Nginza Hospital, Port Elizabeth, SA, over the 6-year period 2009 2014 was conducted. Results. A total of 919 new cases were seen. Fifteen patients received treatment for type 1 ROP (T1ROP), 223 had type 2 (T2) or earlier ROP, 1 had stage 4 ROP and 6 had stage 5 ROP. The combination of healthcare worker education, improved equipment and human resources and the introduction of dual responsibility for case referrals resulted in an increase in the number of new infants screened from 33 in year 1 to 292 in year 6. The number of infants who were screened late decreased from 33/33 (100%) in year 1, prior to the interventions, to 23/292 in the final year (7.9%). Improved oxygen delivery and adequate oxygen saturation monitoring contributed to a decrease in the incidence of T1ROP from 1.5% to 1% over 1 year and in the incidence of T2 or earlier ROP from 30.3% to 24%.

June 2016, Print edition

RESEARCH

Conclusions. Better management of ROP can be achieved through adequate provision of healthcare professionals and material resources coupled with education and a well-supported referral system. A close working relationship between paediatricians and ophthalmologists results in a more efficient screening programme. S Afr Med J 2016;106(6):598-601. DOI:10.7196/SAMJ.2016.v106i6.10663

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i6.10663

Retinopathy of prematurity screening criteria and workload implications at Tygerberg Children’s Hospital, South Africa: A cross-sectional study E Visser Kift,1 MB ChB, BSc (Med Sci) Hons; N Freeman,2 MB ChB, FCOphth, MMed; C Cook,3 MB ChB, DO, MPH, FCOphth, FRCOphth; L Myer,4 MB ChB, PhD ivision of Clinical Pharmacology, Department of Medicine, Tygerberg Hospital and Faculty of Medicine and Health Sciences, Stellenbosch D University, Tygerberg, Cape Town; Division of Epidemiology and Biostatistics, School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town; Previously affiliated to the Division of Ophthalmology, Department of Surgery, Tygerberg Hospital and Stellenbosch University, Tygerberg, Cape Town, South Africa 2 Division of Ophthalmology, Department of Surgery, Tygerberg Hospital and Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa 3 Division of Ophthalmology, Department of Surgery, Groote Schuur Hospital and Faculty of Health Sciences, University of Cape Town, South Africa 4 Division of Epidemiology and Biostatistics, School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 1

Corresponding author: E Visser Kift (evkift@sun.ac.za)

Background. Screening guidelines for retinopathy of prematurity (ROP) used in high-income countries are not appropriate for middleincome countries, and screening requirements may vary even between units within one city. Objective. To determine optimal ROP screening criteria, and its workload implications, for Tygerberg Children’s Hospital (TCH), Cape Town, South Africa. Methods. This cross-sectional study included premature infants screened for ROP at TCH from 1 January 2009 to 31 December 2014. Logistic regression analysis for prediction and classification was performed. Predictors were birth weight (BW) and gestational age (GA). Endpoints were clinically significant ROP (CSROP) and type 1 ROP (T1ROP). Results. Of 1 104 eligible infants, 33.4% had ROP (CSROP 9.1%, T1ROP 2.5%). All T1ROP infants received laser therapy. The number of screening examinations was inversely correlated with GA and BW. The number needed to screen to identify one infant requiring treatment was 41 (entailing 83 examinations, 4 screening hours, one technician and three doctors). Screening infants with a GA of ≤28 weeks or a BW of <1 000 g would have detected all infants with T1ROP but missed two outliers with CSROP. These outliers would only have been detected with a GA of ≤32 weeks or a BW <1 500 g. Conclusions. Detection of infants with T1ROP is resource intensive. Larger infants require screening to include a few outliers, but they require fewer examinations than smaller infants. Making local screening criteria narrower on the basis of a limited evidence base may be dangerous. Risk factors for CSROP in larger infants need to be researched. S Afr Med J 2016;106(6):602-606. DOI:10.7196/SAMJ.2016.v106i6.10358

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i6.10358

June 2016, Print edition

RESEARCH

HAART in hand: The change in Kaposi’s sarcoma presentation in KwaZulu-Natal, South Africa L Naidoo,1 MB ChB, FCDerm (SA); J S Jacobson,2 DrPH, MPH, MBA, BA; A I Neugut,2 MPH, PhD, MD, BA; N C Dlova,1 MB ChB, FCDerm (SA), PhD; A Mosam,1 MB ChB, FCDerm (SA), MMed, PhD epartment of Dermatology, School of Clinical Medicine, College of Health Sciences, Nelson R Mandela School of Medicine, D University of KwaZulu-Natal, Durban, South Africa 2 Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, USA 1

Corresponding author: L Naidoo (levashni.naidoo@yahoo.com)

Background. HIV/AIDS-related Kaposi’s sarcoma (HIV-KS) is a public health problem in South Africa (SA). It is AIDS defining. There have been no studies evaluating its prevalence since the national roll-out of highly active antiretroviral therapy (HAART). Objective. To evaluate the effect of HAART on the disease profile of HIV-KS in KwaZulu-Natal Province (KZN), SA. Methods. Charts of patients with histologically confirmed HIV-KS were reviewed at an oncology clinic in KZN. The significance of associations of HAART with age, gender, CD4 count, urban/rural residence, fungating lesions, ulceration and lymphoedema, and treatment delay, was determined by t-tests for normally distributed continuous variables and χ2 tests for categorical variables. Logistic regression models were used to analyse the association of HAART with CD4 count. Results. Of 198 patients, 194 were documented as HIV-positive; 168 (86.6%) were on HAART at the time of their KS diagnosis. The mean CD4 count of 266 cells/µL was higher than that in previous studies at this site. The mean age at presentation was 36.6 (standard deviation 10.1) years. Females presented at a younger mean age than males (p<0.001). The mean age of females on HAART was 34.7 years and that of males 39.0 years (p=0.003). HAART-naive patients were three times more likely than those receiving HAART (15.4% v. 4.8%) to have visceral involvement (p=0.03). Conclusions. HAART use has resulted in outcome improvement. Mean age at presentation has increased in the group as a whole and for females in particular. The trend in mean CD4 counts has shown positive growth. Females no longer shoulder a disproportionate burden of disease. S Afr Med J 2016;106(6):611-616. DOI:10.7196/SAMJ.2016.v106i6.10333

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i6.10333

Clinical findings and genetic screening for copy number variation mutations in a cohort of South African patients with Parkinson’s disease A C Mahne,1 MB ChB, MMed (Neurol); J A Carr,2 MB ChB, PhD; S Bardien,3 PhD; C-M Schutte,1 MB ChB, MMed (Neurol), MD epartment of Neurology, School of Medicine, Faculty of Health Sciences, University of Pretoria, South Africa D Division of Neurology, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa 3 Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa 1 2

Corresponding author: C-M Schutte (cschutte@medic.up.ac.za, clara.schutte@up.ac.za)

Background. Parkinson’s disease (PD), with a prevalence of up to 4% in Western countries, appears to be less common in Africa, possibly in part because of genetic factors. African studies investigating the genetic causation of PD are limited. Objective. To describe the clinical and genetic findings in a group of black South African patients with PD. Methods. All black African patients with PD from a tertiary hospital neurology clinic were examined. Symptoms were scored according to the Unified Parkinson’s Disease Rating Scale (UPDRS), and patients were classified according to motor features. Genomic DNA was extracted and multiplex ligation-dependent probe amplification was used for detection of copy number variation (CNV) mutations in the known PD-causing genes.

June 2016, Print edition

RESEARCH

Results. Sixteen patients were identified (ages 56 - 82 years). Three had a family history of PD. Classification into motor subtypes showed 44% mixed, 31% akinetic-rigid, and 25% tremor-dominant subtypes. UPDRS scores ranged from 7 to 88, with dementia in 20%. No patient had G2019S LRRK2 and A30P SNCA mutations, and all except one had no CNV mutations in the known PD-causing genes. A female patient (age of onset 50 years, no family history) had a parkin gene heterozygous deletion of exon 4. She had hyperreflexia, bilateral Hoffmann’s reflexes, normal plantar responses and no dystonia. Conclusion. This group of black African patients showed similar characteristics to patients in Western studies, possibly with a higher proportion having tremor-dominant disease. Genetic analysis showed one parkin gene mutation. The limited knowledge on PD-causing genes and mutations in black populations warrants further studies involving next-generation sequencing approaches. S Afr Med J 2016;106(6):623-625. DOI:10.7196/SAMJ.2016.v106i6.10340

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i6.10340

Identity tags: A vector for cross-infection? S G Cox,1 MB ChB, FCS (SA), Cert Paed Surg (SA); A Burahee;2 A Lucier;3 C Fernando;3 S M Machoki,1 MB ChB, MMed (Surg), FC Paed Surg (SA) Department of Paediatric Surgery, Red Cross War Memorial Children’s Hospital and University of Cape Town, South Africa Medical student, University of Birmingham Medical School, UK 3 Medical student, University of North Carolina, Chapel Hill, USA 1 2

Corresponding author: S G Cox (sharon.cox@uct.ac.za)

Background. Nosocomial infections represent one of the challenging problems of modern medicine. Healthcare providers play an important role in the transmission of these infections on their hands, clothing and equipment. Modern security systems require personnel to wear clearly displayed identity (ID) tags, and to have an easily accessible access disc. These access and ID tags are often worn around the neck on a lanyard, and could possibly harbour bacteria and be a vector for cross-infection. Method. Saline-moistened swabs of the front and back of ID tags of 50 healthcare workers were taken for bacterial culture. Swabs were inoculated onto standard microbiological media. Potential pathogens were subjected to sensitivity testing while organisms resembling normal skin commensals were reported as such. Results. Twenty-eight of the 50 (56%) ID swabs cultured exhibited no bacterial growth. Eighteen (36%) swabs grew primarily skin flora. Neutrophils were observed under microscopy on two (4%) swabs. Seven (14%) swabs grew potentially pathogenic bacteria. Doctors were found to have almost three times the risk of carrying pathogenic bacteria on their ID tags compared with nurses. Recent patient contact also showed a higher incidence of colonisation. There were no statistically significant differences between variables such as ward or area of work, nature of patient contact, time since qualification, level of qualification or length of employment at Red Cross War Memorial Children’s Hospital, Cape Town, South Africa. Conclusions. Prevention of hospital-acquired infections is important in any setting. The ID tag has been identified as a possible source of infection spread in this and previous studies. The ID tag has to date been neglected as a potential source of pathogen spread, and efforts to make staff aware of this potential danger should be considered in every institution. S Afr Med J 2016;106(5):494-496. DOI:10.7196/SAMJ.2016.v106i5.9949

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i5.9949

June 2016, Print edition

CAREERS & CLASSIFIEDS Tel: 012 481 2121 | E-mail: ladinev@hmpg.co.za We accept credit card payments - Visa or MasterCard.

DERMATOLOGIST Durban North Part time and full time position available at established private practice. Option of association is also on offer.

GP LOCUM GP LOCUM REQUIRED FOR NORTHEN CAPE, UPINGTON. DISPENSING PRACTICE

For enquiries contact practice manager Sian (079) 5244385.

SEND CV TO THE FOLLOWING FAX OR EMAIL. FAX: 0543390010 EMAIL: praktyd@telkomsa.net

CLINICAL PATHOLOGISTS / CLINICAL MICROBIOLOGISTS KLERKSDORP/POTCHEFSTROOM/WELKOM/EAST LONDON/VEREENIGING/NAMIBIA/CAPE TOWN We are a dynamic, cutting edge, purpose driven and values based Pathology and Diagnostic laboratory, caring for the health of patients, while offering support and expertise to medical professionals. We are seeking appropriate individuals to assist us in our next phases of growth. We have an opportunity for an Anatomical Pathologist to work at PathCare Namibia and a Clinical Pathologist to work at our East London branch, as well as a vacancy for a Clinical Pathologist to work at our Welkom branch and a Clinical Microbiologist for our Vereeniging branch. We have further vacancies for a Clinical Microbiologist/Clinical Pathologist to work at our Klerksdorp and Potchefstroom branch and a Haematology pathologist to work in Cape Town. If you are a creative, dynamic and passionate professional who adopts a customer-centric approach, is respectful and accountable and possesses a well-developed work ethic, while working with diverse groups of people and excelling within a multi-cultural environment then this opportunity could be what you are looking for. Requirements: • • • •

M. Med or FC Pathology (SA) Current registration with the HPCSA as a Pathologist Relevant working experience High level of ethics and integrity

Interested applicants who meet the criteria and are interested in the post may email a CV to: lindyg@pathcare.co.za Closing date for applications is Friday, 17th June 2016

CAREERS & CLASSIFIEDS

CONSULTANT MICROBIOLOGIST Cape Town This position would suit an energetic Pathologist, who would like to take up an opportunity as a Microbiologist in Cape Town with Drs Du Buisson, Kramer, Swart, Bouwer Inc. (Ampath group) This applicant must be registered with the HPCSA as a Microbiologist. A competitive salary package will be negotiated. Contact: Anli Coetzer (012) 678 1805 or e-mail your CV and references to coetzera@ampath.co.za

MSc Scholarship The Division of Neurology, University of Cape Town, is inviting applications for a MSc Scholarship for 1-2 years to study a complication of myasthenia gravis. Here subjects develop an ophthalmoplegic complication that is resistant to current treatment. Applications are invited to join our laboratory research team.  The candidate will be required to register for a MSc at UCT (potential to upgrade to PhD).  Research methodology includes genetics, molecular biology & bioinformatics.  MBChB or BScHons are eligible Contact Prof Heckmann by 26 Aug 2016 Email: jeanine.heckmann@uct.ac.za Tel: 021 404 3263.

One year old, medically astute and a leader On the 14 April 2016, SMU (Sefako Makgatho Health Sciences University) celebrated its first anniversary as a revitalised institution of health sciences (arising out of the now defunct MEDUNSA), heralding the name of a leader among all leaders – the teacher, politician, pastor and journalist – Sefako Makgatho. On 12 and 13 May 2016, the prowess of this magnificent institution will be demonstrated through a series of inaugural graduations. Is it not time for you to come on board and be part of this success?

MEDICAL SCHOOL DIRECTOR/DEAN

(Associate/Full Professor)

Ref: AP468

Rika Gruss (Assessment Director) is keen to walk you through this outstanding opportunity and help wherever she can – in the first instance, please send her a short letter of motivation, along with your Curriculum Vitae to info@talenting.co.za, or fax the same to 086 631 5571, quoting Ref. AP468. For more info, please visit www.academic-partners.co.za All applications will be treated as strictly confidential. We correspond with all our candidates.

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Your PhD or a professional Master's degree (e.g. MMed) and further credentials giving support to you meeting SMU's qualifying criteria to become either an Associate Professor or Full Professor, will serve as essential criteria, as will your registration with HPCSA as a medical practitioner. Your sound track record as an academic, including a substantial track record in research and proof of capacity to create an environment conducive for optimal research productivity is also essential, as is a minimum of 8 years' experience in tertiary education. You are academically and administratively astute in the field of teaching and learning, especially in respect to the development and implementation of policies. Your commitment to transformation and diversity is unquestionable, as is your ability to lead and manage a diverse staff complement. And, your knowledge and understanding of the challenges facing the higher education sector is exemplary. Other degrees, diplomas or certificates relative to management will put you in an even stronger position for consideration.

Invitation to be placed on the Panel for the Independent Tribunal for Social Assistance Appeals The Minister of Social Development, Ms BO Dlamini, MP, seeks to appoint tribunal members constituted of suitably qualified South African citizens, to form part of the Independent Tribunal for Social Assistance Appeals

5 years post-registration experience in the practise of medicine and must not be in the full-time employ of the public health service or in the full-time or part-time employ of SASSA. Experience in the evaluation of medical

(hereinafter referred to as the Tribunal). Section 18 of the Social Assistance Act, 13 of 2004, makes provision for the Minister of Social Development to appoint an independent tribunal to consider appeals lodged by social grant applicants who are dissatisfied with the decision of the South African Social Security Agency (SASSA).

impairment will be an added advantage.

Applications are hereby invited for consideration and appointment to serve in the Tribunal at the National Office in Pretoria (Gauteng). Applicants should have a broad understanding of social assistance legislation and the social security system in South Africa. The term and deployment of the tribunal members will be determined from time to time by the Minister or her duly authorized delegate. Remuneration is as determined by the Minister of Finance in line with the Service Benefit Packages for Office-Bearers of Certain Statutory and Other Institutions (Category Level A1). Please take note that appointment is on assignment basis and does not guarantee automatic assignment of work.

Enquiries: Dr Jan Olivier (012) 741 6877 Applications: All applications should be submitted with a covering letter, clearly indicating the professional category and must be accompanied by a detailed Curriculum Vitae together with the certified copies of the relevant qualification(s). Applications should be forwarded to: The DirectorGeneral, Department of Social Development, Private Bag X901, Pretoria 0001 and be clearly marked for the attention of the Director-General: The closing date for applications is 20 June 2016. The Tribunal reserves the right not to appoint any applicant and should you not hear from us within 6 months of your application, kindly consider your application unsuccessful.

Medical Practitioners: Requirements: Duly qualified medical practitioner and registered with the Health Professions Council of South Africa. The candidate must be in possession of at least

Building a Caring Society. Together.

www.dsd.gov.za

MEDICAL PROTECTION SOCIETY

Medicolegal Adviser for South Africa Based in Leeds, United Kingdom Attractive Salary + Benefits Package The Medical Protection Society (MPS) is South Africa's leading medical indemnity organisation, dedicated to serving the interests of more than 29,000 doctors and healthcare providers in South Africa and over 300,000 worldwide. As a not-for-profit mutual organisation, MPS offers support to doctors with medicolegal and ethical problems that arise from their professional practice. MPS wish to recruit an additional doctor to join their Medicolegal team in Leeds, in order to enhance their service to members. As a Medicolegal Adviser, you will play a pivotal role in assisting the medical profession in South Africa, and will help members seek assistance on a broad range of issues arising from their professional practice. These may include complaints; clinical negligence claims; HPCSA investigations; inquests; disciplinary inquiries; as well as legal and ethical dilemmas. Additionally, you will also be involved in the educational and risk management activities of MPS. This challenging role represents an opportunity to gain both international perspective and experience in the medicolegal issues wfacing the profession. We are seeking a doctor, who is currently registered in South Africa with substantial clinical postqualification experience and recognised post-graduate qualifications. A proven interest in legal medicine would be valuable, however full training will be provided. Our Medicolegal Advisers receive an extensive induction programme and ongoing training. Applicants will have the ability to think logically and objectively, analyse complex, sensitive situations, write clearly and assess and present members' cases effectively. Excellent communication and interpersonal skills are essential, as is attention to detail, expertise in problem-solving, organisational effectiveness and the ability to deal empathetically with members in stressful situations. The position will require you to work from the Leeds office in the United Kingdom. Registration with the HPCSA and the eligibility to register with the GMC and to reside and work in the UK is desired; all applications will be considered. Benefits will include a pension scheme, 30 days paid holiday in addition to public/bank holidays, private medical insurance and a health care cash plan. If the prospect of an exciting, challenging and rewarding role in legal medicine is attractive, tell us why in a covering letter and send it with your full CV to George Mill, Resourcing Officer, Medical Protection Society, Victoria House, 2 Victoria Place, Leeds, LS11 5PY or email recruitment@medicalprotection.org For further details please visit our website at: www.medicalprotection.org/uk/careers Closing date: 24th June 2016 No Agencies MPS is an equal opportunities employer.

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The REFERENCE MEDICAL REFERENCE ESSENTIAL MEDICAL The ESSENTIAL for professional! healthcare professional! every healthcare for every

The convenient pocket-sized design enables you to fit it comfortably into your hospital bag or coat pocket, so it The convenient pocket-sized design enables you to fit it comfortably into your hospital bag or coat pocket, so it can always be at hand for ready reference. South African Medicines Formulary (SAMF), a joint initiative of the can always be at hand for ready reference. South African Medicines Formulary (SAMF), a joint initiative of the University of Cape Town’s Division of Clinical Pharmacologyyand the Health and Medical Publishing Group, University of Cape Town’s Division of Clinical Pharmacolog and the Health and Medical Publishing Group, publishers for the South African Medical Association, provides easy access to the latest, scientifically accurate publishers for the South African Medical Association, provides easy access to the latest, scientifically accurate information, including full drug profiles, clinical notes and special prescriber’s points. The thoroughly updated information, including full drug profiles, clinical notes and special prescriber’s points. The thoroughly updated 12th edition of SAMF is your essential reference to the rational, cost-effective and safe use of medicines. 12th edition of SAMF is your essential reference to the rational, cost-effective and safe use of medicines.

Go to www.samf12.org to download the order form or contact

Smith DianeSmith Please direct all order queries to:Diane Medical and Health Health and Medical Group Publishing Publishing Group

2069 4812069 012481 Tel:012 Tel: dianes@hmpg.co.za Email:dianes@hmpg.co.za Email: order dispatchofoforder postedonondispatch invoicetotobebeposted Taxinvoice Tax

CPD

JUNE 2016

The CPD programme for SAMJ is administered by Medical Practice Consulting. CPD questionnaires must be completed online at www.mpconsulting.co.za.

True (A) or false (B): SAMJ The role of appropriate diagnostic testing in acute respiratory tract infections: An antibiotic stewardship strategy to minimise diag nostic uncertainty in primary care 1. Most antibiotics for systemic use in adults and children are pre scribed in the community, with acute respiratory tract infections the most common indications. 2. The presence of discoloured sputum is an indicator of bacterial and not viral infection. Emergence of vancomycin-resistant Enterococcus at a tertiary pae diatric hospital in South Africa (SA) 3. Treatment for this resistant organism is limited to the use of linezolid and daptomycin. Where have all the gun deaths gone? 4. From a peak in 2000 until 2011, there was a 60% decrease in firearm assaults in SA. HAART in hand: The change in Kaposi’s sarcoma (KS) presentation in KwaZulu-Natal 5. In developing countries, antiretroviral therapy has been found to improve KS associated with HIV. 6. In Africa, females with KS associated with HIV present at an earlier age and have more extensive cutaneous tumour involvement. Clinical findings and genetic screening for copy number variation mutations in a cohort of SA patients with Parkinson’s disease (PD) 7. It would appear that the prevalence of PD in black Africans is lower than that reported among Americans. 8. Cognitive impairment and dementia may occur in patients with PD, especially after long disease duration.

Delay and poor diagnosis of Down syndrome (DS) in KwaZuluNatal (online only) 9. DS is known to be rare among African population groups. 10. Lack of awareness of DS in black African communities is thought to be due to high infant mortality of affected patients, resulting in a low population prevalence of the disorder. CME Update on adolescent mental health 11. Approximately half of all mental illness and substance-related problems start at the age of 14 years. 12. Suicide remains the second leading cause of death among young people globally. 13. The prevalence of depression ranges from 4% to 8% in adolescents. 14. Acute stress disorder symptoms last from 3 days to 1 month, while post-traumatic stress disorder symptoms are present for >1 month. 15. Panic disorder comprises recurrent panic attacks that are unex pected, as they do not occur in response to an identifiable situation. Addressing adolescent alcohol use in SA 16. Alcohol use in SA is characterised by episodic binge drinking. 17. Despite males generally outnumbering females with regard to lifetime, current and binge drinking, in the recent past females have shown significant increases in binge drinking in SA. 18. Given the length of the Alcohol Use Disorders Identification Test (AUDIT) screening tool, a shorter adaptation (AUDIT-C) is preferred for use in clinical settings. 19. The use of benzodiazepines among adolescents is supported by a body of empirical research. 20. It is better to recommend moderate drinking than total abstinence for adolescents with drinking problems, as studies have found moderate drinking to be beneficial for their health.

Readers please note: articles may appear in summary/abstract form in the print edition of the Journal, with the full article available online at www.samj.org.za

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June 2016, Print edition

When it comes to matters of the heart,

it takes two

COPALIA® - Benefits of a rational and effective fixed-dose combination1 • Greater and sustained BP reductions vs. monotherapies2,3 • Reduced risk of stroke, heart failure and new-onset diabetes, with a neutral effect on MI4 • Consistent efficacy and tolerability, regardless of hypertension stage, age or race2,5 • Simple once-daily dosing1,6,7

References: 1. Waeber B, Ruilope LM. Amlodipine and valsartan as components of a rational and effective fixed-dose combination. Vasc Health & Risk Management 2009;5:165-174. 2. Allemann Y, Fraile B, Lambert M, et al. Efficacy of the combination of amlodipine and valsartan in patients with hypertension uncontrolled with previous monotherapy: The Exforge in Failure After Single Therapy (EX-FAST) study. J Clin Hypertens 2008;10:185-194. 3. Da Silva PM. Efficacy of fixed-dose combination therapy in the treatment of patients with hypertension: focus on amlodipine/valsartan. Clin Drug Investig 2010;30(9):625-641. 4. Bangalore S, Kumar S, Wetterslev J, et al. Angiotensin receptor blockers and risk of myocardial infarction: meta-analyses and trial sequential analyses of 147 020 patients from randomised trials. Br Med J 2011;342:d2234 doi:10.1136/bmj.d2234. 5. Smith TR, Philipp T, Vaisse B, et al. Amlodipine and valsartan combined and as monotherapy in stage 2, elderly, and black hypertensive patients: Subgroup analysis of 2 randomised, placebo-controlled studies. J Clin Hypertens 2007;9(5):355-364. 6. Seedat YK, Rayner BL, Veriava Y. South African hypertension practice guideline 2014. Cardiovascular J of Africa 2014;25(6):288-294. 7. Copalia® approved package insert, June 2015. S3 COPALIA® 5/160 mg tablet. Each film-coated tablet contains amlodipine besylate 6,94 mg (equivalent to amlodipine base 5 mg) and valsartan 160 mg. Reg. No. 45/7.1.3/0850. S3 COPALIA® 10/160 mg tablet. Each film-coated tablet contains amlodipine besylate 13,87 mg (equivalent to amlodipine base 10 mg) and valsartan 160 mg. Reg. No. 45/7.1.3/0851. For full prescribing information refer to the package insert approved by the medicines regulatory authority. 10259624 02/2016. Novartis South Africa (Pty) Ltd. Co. Reg. No. 1946/020671/07. Magwa Cresent West, Waterfall City, Jukskei View, 2090. Tel. +27 11 347 6600 www.novartis.co.za. Marketed by Adcock Ingram Healthcare (Pty) Ltd. Reg. No. 2007/019928/07. Private Bag X69, Bryanston, 2021, South Africa. Tel. +27 11 635 0000 www.adcock.com.

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