VOL. LIX • NO. 10 • 2018

VOLUME LIX • NO. 10 • 2018

Michael Mansour, MD · 2018-19 MSMA President

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VOL. LIX • NO. 10 • OCTOBER 2018

SCIENCE OF MEDICINE

EDITOR Lucius M. Lampton, MD ASSOCIATE EDITORS D. Stanley Hartness, MD Richard D. deShazo, MD

THE ASSOCIATION President Michael Mansour, MD

Tick-Borne Diseases in Mississippi Jerome Goddard, PhD; Lucius M. Lampton, MD

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Hyperbaric Oxygen in vitro against MRSA 301 and P. aeruginosa 19660 Christina D. Jordan, PhD; Amy L. Sullivan, PhD; Mary E. Marquart, PhD; et al.

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President-Elect J. Clay Hays, Jr., MD

Top 10 Facts You Need to Know about Human Papillomavirus-Associated Oropharyngeal Squamous Cell Cancer 458 William H. Replogle, PhD; C. Ron Cannon, MD

MANAGING EDITOR Karen A. Evers

Secretary-Treasurer W. Mark Horne, MD

PUBLICATIONS COMMITTEE Dwalia S. South, MD Chair Philip T. Merideth, MD, JD Martin M. Pomphrey, MD and the Editors

Speaker Geri Lee Weiland, MD Vice Speaker Jeffrey A. Morris, MD Executive Director Charmain Kanosky

JOURNAL OF THE MISSISSIPPI STATE MEDICAL ASSOCIATION (ISSN 0026-6396) is owned and published monthly by the Mississippi State Medical Association, founded 1856, located at 408 West Parkway Place, Ridgeland, Mississippi 39158-2548. (ISSN# 0026-6396 as mandated by section E211.10, Domestic Mail Manual). Periodicals postage paid at Jackson, MS and at additional mailing offices.

CORRESPONDENCE: Journal MSMA, Managing Editor, Karen A. Evers, P.O. Box 2548, Ridgeland, MS 39158-2548, Ph.: 601-853-6733, Fax: 601-853-6746, www.MSMAonline.com.

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The views expressed in this publication reflect the opinions of the authors and do not necessarily state the opinions or policies of the Mississippi State Medical Association.

Copyright © 2018 Mississippi State Medical Association.

Official Publication

MSMA • Since 1959

Top 10 Facts You Need to Know about Arthritis of the Thumb Carolyn A. Cushing, MD

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The Challenges in Anesthetic Management of Patients with Trisomy 18 Semyon Fishkin, MD; Madhankumar Sathyamoorthy, MBBS, MS, MBA; Russel G. Wardlaw, CRNA; John M. Reed, MD

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DEPARTMENTS From the Editor – Creating a Culture of Health Lucius M. Lampton, MD

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President’s Page – Inaugural Address of the 151st President of MSMA Michael Mansour, MD

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MSMA Annual Session Recap

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Letters

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Commentary – Why Marijuana Will Not Fix the Opioid Epidemic Kenneth Finn, MD

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Physician’s Bookshelf – Images in Mississippi Medicine 490 Philip L. Levin, MD Poetry and Medicine –Five Words from Four Letters John D. McEachin, MD

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RELATED ORGANIZATIONS NHLBI Renews Landmark Jackson Heart Study for Six More Years

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Mississippi State Health Officer Retires

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Mississippi Provisional Reportable Disease Statistics

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ABOUT THE COVER Dr. Michael Mansour, a board-certified cardiologist in private practice in Greenville, took the oath of office becoming 2018-19 MSMA president during an inaugural ceremony held at the Old Capital Inn on August 17. The gala was one of many activities held during the 150th Annual Session of the MSMA House of Delegates in Jackson. Dr. Mansour graduated from the University of Mississippi School of Medicine in 1984. He performed his residency training at Ochsner Foundation Hospital in New Orleans. He also completed fellowships at the University of Florida and Harvard Medical School. Dr. Mansour is married to Dr. Kathleen Mansour, also a cardiologist, and they have four children.

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F R O M

T H E

E D I T O R

Creating a Culture of Health M

SMA President Dr. Michael Mansour is a man on a mission: the creation of a culture of health in Mississippi. He rightly perceives that the greatest challenge physicians and patients face is the epidemic of noncommunicable diseases such as diabetes, cardiovascular diseases, cancers, and chronic pulmonary diseases, which shorten the lives of our citizens and negatively impact their ability to live functional lives. Mississippi Lucius M. Lampton, MD of all states possesses the worst milieu to Editor foster this culture change: limited resources and increased disparities.

Despite these hurdles, Mansour hopes to induce this culture change by encouraging the political leadership in our state and nation to end what he calls their “backwards perspective” on health care policy and spending.

This backwards perspective can be seen in most of the policy initiatives from Congress or legislatures, which target the volume of health care delivered. They think that the way to control health care spending is to ratchet down on tests, procedures, or hospitalizations or to limit the

number of medications or office visits allowed. Decreasing access to care is exactly the wrong approach. Rather, the best answer is to increase access to care for those most vulnerable and at risk. Mansour quotes the late health economist Dr. Uwe E. Reinhardt, referring to his “80-20 rule” which reveals the highly skewed distribution of per capita health spending across the country’s population: 20% of any large insured population tends to account for 80% of all health expenditures.

(Reinhardt U. Why are private health insurers losing money on Obamacare?

JAMA. 2016;316(13):1347-1348. doi:10.1001/jama.2016.13743.) Thus, preserving the wellness and health of that 20% is the way to lower the costs of health care and also the way to create a culture of health.

In the recent August JMSMA special “Population Health” issue, Mansour wrote as guest editor: “If we are to promote the very best care for our patients, we must lead the conversation and efforts to transform healthcare in a way that improves access, decreases cost, but also decreases illness.” Mississippi physicians need to rally behind Dr. Mansour’s noble effort to create a culture of health in our state by focusing on the principles of population health and improved access to care. n Contact me at LukeLampton@cableone.net.

— Lucius M. Lampton, MD, Editor

JOURNAL EDITORIAL ADVISORY BOARD ADDICTION MEDICINE Scott L. Hambleton, MD

EMERGENCY MEDICINE Philip Levin, MD

MEDICAL STUDENT John F. G. Bobo, M2

ALLERGY/IMMUNOLOGY Stephen B. LeBlanc, MD Patricia H. Stewart, MD

EPIDEMIOLOGY/PUBLIC HEALTH Mary Margaret Currier, MD, MPH Thomas E. Dobbs, MD, MPH

NEPHROLOGY Harvey A. Gersh, MD

ANESTHESIOLOGY Douglas R. Bacon, MD John W. Bethea, Jr., MD

FAMILY MEDICINE Tim J. Alford, MD Diane K. Beebe, MD Jennifer J. Bryan, MD J. Edward Hill, MD Ben Earl Kitchens, MD James J. Withers, MD

CARDIOVASCULAR DISEASE Cameron Guild, MD Thad F. Waites, MD CHILD & ADOLESCENT PSYCHIATRY John Elgin Wilkaitis, MD CLINICAL NEUROPHYSIOLOGY Alan R. Moore, MD DERMATOLOGY Robert T. Brodell, MD Adam C. Byrd, MD

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GENERAL SURGERY Andrew C. Mallette, MD HEMATOLOGY Vincent E Herrin, MD INTERNAL MEDICINE Daniel P. Edney, MD W. Mark Horne, MD Daniel W. Jones, MD Brett C. Lampton, MD Jimmy Lee Stewart, Jr., MD

OBSTETRICS & GYNECOLOGY Sidney W. Bondurant, MD Darden H. North, MD ORTHOPEDIC SURGERY Chris E. Wiggins, MD OTOLARYNGOLOGY Bradford J. Dye, III, MD PEDIATRIC OTOLARYNGOLOGY Jeffrey D. Carron, MD PEDIATRICS Michael Artigues, MD Owen B. Evans, MD

PLASTIC SURGERY William C. Lineaweaver, MD Chair, Journal Editorial Advisory Board PSYCHIATRY Beverly J. Bryant, MD June A. Powell, MD PULMONARY DISEASE Sharon P. Douglas, MD John R. Spurzem, MD RADIOLOGY P. H. (Hal) Moore, Jr., MD RHEUMATOLOGY C. Ann Myers, MD UROLOGY W. Lamar Weems, MD

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Tick-borne Diseases in Mississippi JEROME GODDARD, PHD; LUCIUS M. LAMPTON, MD

Abstract Ticks and tick-borne diseases continue to be a health issue for persons living in Mississippi, especially for those with environmental exposure from outdoor work or recreation. Mississippi has 18 species of ticks, 5 of which are considered significant medical or veterinary pests. This paper reviews tick-borne diseases occurring in Mississippi, including notes on their vectors and ecology, clinical and laboratory findings for each disease, and the various treatment options.

Tick Biology There are three families of ticks recognized in the world today, 1) Ixodidae (hard ticks), 2) Argasidae (soft ticks), and 3) Nuttalliellidae (a small, curious, little-known group with some characteristics of both hard and soft ticks). The terms hard and soft refer to the presence of a dorsal scutum or “plate” on the back in the Ixodidae, which is absent in the Argasidae. Hard ticks display sexual dimorphism, whereby males and females look obviously different, and the blood-fed females are capable of enormous expansion. Their mouthparts are anteriorly attached and visible from dorsal view. Soft ticks are leathery and nonscutate, without sexual dimorphism. Their mouthparts are subterminally attached in adult and nymphal stages and not visible from dorsal view. Since soft ticks are almost never encountered in southern states, this paper will be limited to the hard ticks responsible for disease transmission in the state of Mississippi.

Hard ticks feed exclusively on blood and begin the process by cutting a small hole into the host epidermis with their chelicerae and inserting the hypostome into the cut, thereby attaching to the skin. Blood flow is maintained with the aid of anticoagulants and vasodilators secreted by the salivary glands. Some hard ticks secure attachment to the host by forming a cement cone around the mouthparts. Two phases are recognized in the feeding of nymphal and female hard ticks: a growth feeding stage characterized by slow continuous blood uptake and a rapid engorgement phase occurring during the last 24 hours or so of attachment.

Hard ticks generally occur in brushy, wooded, or weedy areas containing numerous deer, cattle, dogs, small mammals, or other hosts. Members of each stage (larvae, nymphs, and adults) (Figure 1) climb up on vegetation and attach to passing hosts after which they crawl around looking for a place to feed. Ticks may remain attached to a host for several days while blood-feeding (adults may remain attached 7-10 days).

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Figure 1.

The motile life stages of a hard tick, L-R, larva, nymph, and adult.

(Photo copyright 2014 by Jerome Goddard, PhD)

Figure 2.

Erythema migrans lesion in a patient with Lyme disease.

(Centers for Disease Control photo)

Lyme Disease Introduction Lyme disease (LD), named after a town in Connecticut, is caused by the bacterium Borrelia burgdorferi and is a systemic tick-borne illness which may present with many clinical manifestations such as cardiac, neurologic, and joint problems. Initially, LD presents as a flu-like syndrome with headache, stiff neck, myalgias, arthralgias, malaise, and low-grade fever. Often, a more or less circular, painless, macular

Figure 3.

Clinical and Laboratory Findings The 2017 LD case definition says that a confirmed case is defined by the presence of an EM lesion with exposure in a high incidence state (defined by the CDC), OR a case of EM with laboratory evidence of infection and a known exposure in a low incidence state, OR any case with at least one late LD manifestation that also has laboratory evidence of infection. Laboratory evidence includes: • A positive culture for B. burgdorferi, OR • A positive two-tier test. (This is defined as a positive or equivocal enzyme immunoassay (EIA) or immunofluorescent assay (IFA) followed by a positive Immunoglobulin M (IgM) or Immunoglobulin G (IgG) western immunoblot (WB) for Lyme disease) OR • A positive single-tier IgG WB test for Lyme disease.

Erythema migrans-like lesion after tick bite in Mississippi – not Lyme disease.

(Photo courtesy Jerome Goddard, PhD)

Figure 4.

The case definition requires that EMs be at least 5 cm in diameter; however, smaller and atypical lesions occasionally occur. Not all EM lesions are due to LD4 (Figure 3) and all similar lesions must be distinguished from other manifestations, such as hypersensitivity reactions to tick bites, staph and strep cellulitis, various plant dermatoses, fungal infections, and granuloma annulare.5 EM occurs in 60–80% of LD cases and is often accompanied by mild to moderate constitutional symptoms such as fatigue, fever, headache, mild stiff neck, arthralgias, myalgias, and regional adenopathy. The disease may disseminate within weeks or months, resulting in cardiac, neurologic, and joint manifestations. Symptoms may include Lyme carditis, cranial neuropathy, radiculopathy, diffuse peripheral neuropathy, meningitis, and asymmetric oligoarticular arthritis.

Some labs and university medical centers have capability of detecting B. burgdorgferi DNA molecularly by PCR. Body fluids from patients, such as blood, urine, CSF, and synovial fluid, are good candidates for PCR analysis. However, laboratories conducting PCR may become contaminated, leading to false-positives. The best method of confirming infection with LD at this time is detection of IgM and IgG antibodies with ELISA tests, followed-up with immunoblot (Western blot) analysis.

Western blotting is valuable in distinguishing true-positive from falsepositive ELISA results.

Adult female deer tick, Ixodes scapularis.

(Photo courtesy Dr. Blake Layton and the Mississippi State University Extension Service)

dermatitis is present at the bite site called erythema migrans (EM) (Figure 2). The EM lesion is sometimes said to be pathognomonic for LD, although about 30% of patients do not develop it. EM lesions may steadily increase in size with or without subsequent central clearing. In the United States, there were 38,069 cases of LD reported by the CDC in 2015,1 although an indirect estimate of cases is 300,000 per year.2 Although cases of LD are reported to the Mississippi Department of Health every year, most of these are never confirmed. The vast majority of LD cases occur in the northeastern and north-central United States.

In fact, between 2008-2015, fourteen states in the northeast, midAtlantic, and upper midwest regions accounted for 95.2% of all reported cases and 95.7% of all confirmed cases reported in the United States.3

Ecology of LD In the United States, Ixodes scapularis (Figure 4) is the primary tick vector in the East (including Mississippi) and I. pacificus in the West. Each of the three motile life stages of hard ticks must get on a host, feed, fall off, and then transform into the next stage. If no blood-providing host is available, the ticks will perish. Therefore, an important aspect of vector-borne disease ecology is host availability, and not just availability, but diversity as well. If immature ticks feed on hosts that are refractory to infection with the LD spirochete, then overall prevalence of the disease agent in an area will decline. On the other hand, if an abundant host is available that also is able to be infected with B. burgdorferi producing long and persistent spirochetemias, then prevalence of tick infection increases.

This is precisely the case in the northeastern and upper midwestern states. In those areas, the primary host for immature I. scapularis is the white-footed (WF) mouse, which is capable of infecting nearly 100%

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Figure 5.

Incidence of RMSF in Mississippi versus nationwide. (Note: nationwide case numbers for 2016 not available when graph produced) (Figure courtesy Dr. Wendy C. Varnado and the Mississippi Department of Health)

of larval ticks during feeding. Since infection can be transferred from tick stage to tick stage, this obviously leads to high numbers of infected nymphs and adults. In the West and South, tick infection rates are much lower (and hence, lower numbers of LD cases). This is attributed to the fact that immature stages of I. scapularis and I. pacificus feed primarily on lizards, which are incompetent as reservoirs and incapable of infecting ticks.

Other Lyme-like illnesses have been described in the medical literature and this causes confusion. In the southern United States, there have been reports for years about an LD-like illness6 which other researchers have voiced doubts about — doubts regarding whether or not it is true LD. In fact, the CDC often labels these southern Lyme-like illnesses as Southern Tick-associated Rash Illness (STARI) or Master’s Disease.

Cases of STARI may be due to allergic reactions to tick saliva or other (as yet) unknown causes.7 Treatment Early LD responds readily to oral antibiotics such as doxycycline, amoxicillin, cefuroxime, or azithromycin which are generally prescribed for 2–3 wk.5,8,9 The duration of antibiotic administration should be individualized according to the severity of illness and the rapidity of clinical response. Children younger than 9 may be treated with amoxicillin.9 Individuals with certain cardiac or neurological disease may benefit from intravenous treatment with antibiotics such as ceftriaxone or penicillin. Late-stage LD is a controversial diagnosis and may be more difficult to treat. Consultation with an infectious disease physician is recommended in those cases. Deciding who to treat for LD is frequently a problem since early LD is diagnosed by clinical presentation alone.

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Also, as mentioned above, the disease’s most recognized sign (EM) may be confused with other skin lesions. Finally, in many bona fide cases of LD, patients are initially seronegative and will remain so if antibiotic treatment is begun early.

Rocky Mountain Spotted Fever (RMSF) Introduction Rickettsiae are small, obligate intracellular bacteria. There are many rickettsial species in the spotted fever group (SFG); it contains at least 20 disease agents and another 20 or so with low or no pathogenicity to humans.10 Most produce clinically similar syndromes. For example, American boutonneuse fever cases (next section) are often diagnosed as RMSF in the United States and for that reason the CDC recently changed their reporting category to, “spotted fever rickettsiosis.”

As mentioned, not all SFG rickettsiae are pathogenic, and the role they play in the ecology of human pathogenic rickettsial diseases is complex, such as in the case of RMSF wherein these nonpathogenic species may interfere with the cycle of Rickettsia rickettsii by infecting ticks and thus cross-protecting them from the true R. rickettsii.11 The remainder of this section will be limited to RMSF. Clinical and Laboratory Aspects of RMSF RMSF is the most frequently reported rickettsial disease in the United States with about 4,000 cases reported each year.1 Case numbers in Mississippi have been rising and range from about 150 to 175 each year (Figure 5). RMSF incidence is apparently increasing nationwide, especially among Native Americans. Probably even more cases occur but go unreported. Why? If an unusual febrile illness is treated successfully

Figure 6.

paresis, and peripheral motor neuropathies.12 Laboratory findings include a normal or depressed leukocyte count, thrombocytopenia, elevated serum hepatic aminotransferase levels, and hyponatremia, although these abnormalities are not specific for RMSF.8,13 Specific tests to diagnose RMSF are not widely available (usually only through CDC or some universities). Indirect flourescent antibody (IFA) tests on acute and convalescent sera are fairly accurate and can be used later to confirm the diagnosis. PCR on blood or tissue samples can also be used for diagnosis. RMSF organisms may be visualized in post-mortem samples by immunohistochemistry (IHC).

Adult female American dog tick, Dermacentor variabilis.

(Photo courtesy Dr. Blake Layton and the Mississippi State University Extension Service)

Figure 7.

Adult female brown dog tick, Rhipicephalus sanguineus.

(Photo courtesy Dr. Blake Layton and the Mississippi State University Extension Service)

with doxycyline, there may be little interest in follow-up and reporting.

At the time of initial presentation, there is often the classic triad of RMSF — fever, rash, and history of tick bite. Other characteristics are malaise, severe headache, chills, and myalgias. Sometimes gastrointestinal symptoms, such as abdominal pain and diarrhea, are reported. We have seen the proper diagnosis missed because of GI involvement. The rash, appearing on about the fifth day, usually begins on the extremities and then spreads to the rest of the body. However, there have been confirmed cases without rash. Mental confusion, coma, and death may occur in severe cases. Untreated, the mortality rate is about 20%; even with treatment, the rate is 4%.9 There have been mild to severe neurological sequelae following RMSF infection such as encephalopathy, seizures,

Ecology of RMSF Not all tick species are effective vectors of the rickettsia, and even in the vector species, not all ticks are infected. Therefore, tick infection with R. rickettsii is like a needle in a haystack. Generally, only 1–5% of vector ticks in an area are infected. Several tick vectors may transmit RMSF organisms, but the primary ones are the American dog tick Dermacentor variabilis (Figure 6) in the eastern United States and Dermacentor andersoni in the West. The brown dog tick Rhipicephalus sanguineus (Figure 7) has also recently been shown to be vector in the U.S.14 Adults of both Dermacentor species feed on a variety of medium to large mammals and humans.15,16 Ticks are often brought into close contact with people via pet dogs or cats (dog ticks may also feed on cats). In one case investigated, the mother of the 3-yr-old patient said, “He always carried that puppy around… holding it up next to his face.” Another mode of RMSF transmission may be manual deticking of dogs and subsequent autoinfection via mucosal membranes or eyes. One man contracted RMSF in Mississippi by biting ticks, removed from his dog, between his teeth. That may seem odd, but we have since encountered other persons who claimed to kill ticks by “biting them.”

Prevention and Treatment of RMSF The only sure way of preventing tick-borne diseases is to prevent tick bites. Personal protection techniques for tick bites include avoiding tickinfested woods if possible, tucking pants legs into boots or socks, and using repellents on pant legs and socks. Products containing the active ingredients DEET or picaridin work fairly well in repelling ticks, but permethrin products are more effective. In addition, inspection of the body and removal of attached ticks are more important than many people realize. In most tick-borne diseases, there is a feeding period required before transmission of the disease agent occurs. RMSF organisms generally take 1-3 hours for transmission to occur. Doxycycline is the drug of choice for treatment of suspected or confirmed cases of RMSF in adults and children. Children under eight and pregnant women are sometimes given chloramphenicol, although there is no good reason why children shouldn’t be given doxycycline for RMSF.17,18 Treatment should be initiated on clinical and epidemiologic grounds and never while waiting for confirmation of diagnosis.9,19 American Boutonneuse Fever (ABF) Introduction and Background Several years ago, investigators at the CDC discovered a new tick-borne disease, or more accurately, a “disease within a disease,” because the new clinical entity was apparently hidden within cases diagnosed as RMSF. Over the course of several decades, rickettsiologists speculated

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about the role of supposedly nonpathogenic rickettsiae in human disease, especially Rickettsia parkeri,20-22 which had been shown to cause mild clinical signs in guinea pigs and even eschar-like necrosis at sites of tick attachment.23 Evidence that this species could cause illness in humans was provided when Paddock and associates24 isolated R. parkeri from a patient with suspected rickettsialpox who was evaluated at the Portsmouth Naval Medical Center, Portsmouth, VA . This was the first report of human rickettsiosis caused by R parkeri; many others have followed.25-28 Because of the clinical similarities between disease caused

by R. parkeri and an illness in Europe and Africa termed “boutonneuse fever” (caused by a closely related organism, Rickettsia conorii), a good descriptive moniker for this newly recognized rickettsiosis is “American boutonneuse fever.” 29 Ecology of ABF Many gaps remain in our knowledge about the natural history and ecology of R parkeri. In the U.S., the agent has been identified thus far from only three species of ticks — the Gulf Coast tick, the Lone Star tick, and an obscure rabbit tick30,31 — so any of them could theoretically be a vector, but the Gulf Coast tick (Figure 8) is the primary vector of ABF.28 As for animal reservoirs of R. parkeri, any animal or bird on which the ticks frequently feed could theoretically serve as a reservoir.

Candidates include cotton rats, meadowlarks, and Bobwhite quail.32 Alternatively, the ticks themselves may be the reservoir, with transovarial and transstadial transmission of the agent occurring indefinitely.

Prevention and Treatment of ABF Prevention and treatment of ABF is the same as that for Rocky Mountain spotted fever (see above section).

Ehrlichiosis Introduction Ehrlichia are microorganisms in the family Anaplasmataceae that infect leukocytes. Much of the knowledge gained about ehrlichiae originally came from the veterinary sciences. Canine ehrlichiosis, caused by Ehrlichia canis, wiped out 200 to 300 military working dogs during the Vietnam War.33 The first human case of ehrlichiosis in the United States was a report in March 1986 of a 51-year-old man who had been bitten by a tick in Arkansas and was sick for 5 days before being admitted to a hospital in Detroit.34 He had high titers of E. canis antibodies that fell sharply during convalescence, so physicians assumed he had the dog disease. It turned out not to be the case; he had infection with E. chaffeensis (a hitherto unknown agent). For this reason, there are several reports in the medical literature of human infection in the United States with E. canis, when, in fact, human ehrlichiosis is usually caused by several closely related Ehrlichia organisms. The first one, Ehrlichia chaffeensis, is the most frequently reported and is the causative agent of human monocytic ehrlichiosis (HME), which occurs mostly in the southern and southcentral United States (sporadic cases of HME have also been reported in Europe) and infects mononuclear phagocytes in blood and tissues.35 HME is a significant disease — 1,288 cases were reported to the CDC in 2015.1 There are about 10-20 cases of HME reported to the Mississippi Department of Health each year. The second agent, E. ewingii, mostly a dog and deer pathogen, infects granulocytes and causes a clinical illness similar to HME but thus far has been identified in only a few patients, most of whom were immune-compromised. A recent study

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Figure 8.

Adult female Gulf Coast tick, Amblyomma maculatum.

(Photo courtesy Dr. Blake Layton and the Mississippi State University Extension Service)

suggests that cases of E. ewingii infection are underreported.36 The third Ehrlichia, the E. muris-like agent (sometimes called EMLA or Ehrlichia muris euclairensis), causes fever, malaise, headache, lymphopenia, and elevated liver enzymes.37 Thus far, it has only been reported in a couple hundred patients from the upper midwestern United States (mostly Wisconsin), and the vector is the deer tick, Ixodes scapularis.38 Clinical and Laboratory Findings Clinical and laboratory manifestations of ehrlichial infection are similar.39 Patients usually present with fever, headache, myalgia, progressive leukopenia (often with a left shift), thrombocytopenia, and anemia. Very often, there are moderate elevations in levels of hepatic transaminases.

Sometimes there is a cough, gastroenteritis, or even meningitis. Only about 2 to 40% of the time is there a rash (more common with HME).

Diagnosis depends primarily on clinical findings, although IFA tests may be used to detect antibodies against the respective ehrlichial agents.

As for serologic tests, the gold standard is IFA performed on paired acute and convalescent sera demonstrating a fourfold rise in antibody titers. Antibodies may not be detectable in the first week of illness, so a negative test during that time does not rule out infection. At one time, human anaplasmosis (see next section) was classified as “human granulocytic ehrlichiosis,” and due to this confusion over HGE/HGA terminology, physicians should carefully check what tests they are ordering. Further, due to serological cross-reactivity, tests for ehrlichiosis alone in anaplasmosis-endemic areas may result in an inaccurately high ehrlichiosis incidence and under-recognition of actual anaplasmosis cases.40 Ecology of Ehrlichiosis Ehrlichiosis is transmitted to humans by tick bites, but different ehrlichial agents have different tick vectors. Ehrlichia chaffeensis and E. ewingii are both transmitted by the lone star tick (LST) (Figure 9), while the EMLA has only been found so far in Ixodes scapularis. LSTs generally occur from central Texas east to the Atlantic Coast and north

Figure 9.

Adult female Lone Star tick, Amblyomma americanum.

(Photo courtesy Dr. Blake Layton and the Mississippi State University Extension Service)

to approximately Iowa and Maine. WT deer, possibly along with dogs or other mammals, serve as reservoir hosts for the agent, and LSTs are the most important vectors; however, detection of the HME agent in other tick vectors and a few cases outside the distribution of LST indicates that additional vectors occur.

Treatment and Control of Ehrlichiosis Prevention of ehrlichiosis is essentially the same as that of RMSF. Treatment should be oral or intravenous doxycycline (while doxycycline is no longer absolutely contraindicated in pregnancy, consideration of rifampin is a possible alternative). Treatment should never be delayed while awaiting laboratory confirmation. Fever typically subsides within 24 - 48 hours after treatment when the patient receives doxycycline or another tetracycline during the first 4 -5 days of illness. If a patient fails to respond to early treatment, this response might be an indication that their condition is not a tick-borne rickettsial disease.

Anaplasmosis Introduction Anaplasma phagocytophilum infects granulocytes and causes human granulocytic anaplasmosis (HGA). There is confusion about this terminology because for many years this disease was called human granulocytic ehrlichiosis (HGE) and is often included in the older medical literature under that label. Complicating matters further, sometimes commercial laboratories may still refer to tests for HGA as human granulocytic ehrlichiosis tests. HGA mostly occurs in the upper midwestern and northeastern United States. There were 3,656 cases of HGA reported to the CDC in 2015, a 30% increase over 2014.1 The case fatality rate is 0.3% but may be higher in older patients.41 Only about 5 cases of anaplasmosis are reported from Mississippi each year.

Clinical and Laboratory Findings Clinical and laboratory manifestations of HGA infection include fever, headache, myalgia, progressive leukopenia (with a left shift),

thrombocytopenia, and anemia. Often there are moderate elevations in levels of hepatic transaminases. Sometimes there is a cough, gastroenteritis, or meningitis. Illness due to HGA is somewhat milder than with HME; reported fatality rates are about 1 and 2% for HGA and HME, respectively. Research indicates that both agents alter the patient’s immune system, allowing opportunistic infections such as fungal pneumonia to occur. Diagnosis is made on clinical findings, although IFA tests may detect antibodies against the anaplasmal agent. The gold standard serologic test for anaplasmosis is IFA performed on paired acute and convalescent sera demonstrating a fourfold rise in antibody titers. As is the case with ehrlichiosis, antibodies may not be detectable in the first week of illness, so a negative test during that time does not rule out infection. Due to confusion over HGE/HGA terminology, physicians should carefully check what tests they are ordering. If HGA is suspected, physicians should make sure the test they order detects antibodies to Anaplasma phagocytophilum.

Ecology of Anaplasmosis Anaplasmosis (HGA) is transmitted to humans by the deer tick, Ixodes scapularis. The ecology of HGA is not well known. It has been diagnosed mostly in patients from the upper Midwest, the northeastern United States, and the Pacific Coast area, although cases have also been reported sporadically elsewhere, including Europe and Asia. The tick vector in the United States is Ixodes scapularis which is the same species that transmits the agent of Lyme borreliosis, thus, there is the possibility of co-infection with Lyme borreliosis and HGA (and even babesiosis).42 Animal reservoirs of the HGA agent may be a variety of small rodents and possibly deer.

Treatment and Control of Anaplasmosis Prevention of anaplasmosis is essentially the same as that of other tickborne diseases such as RMSF. Treatment should never be delayed while awaiting laboratory confirmation. Recommended therapy in adults or children is oral or intravenous doxycycline.9,13,43 There is some evidence that treatment of children and pregnant women with rifampin is successful.43 Tularemia Introduction and Medical Significance of Tularemia Tularemia, sometimes called rabbit fever or deer fly fever, is a bacterial zoonosis that occurs throughout temperate climates of the northern hemisphere. Historically, approximately 150–300 cases have occurred in the United States each year, with most cases occurring in Arkansas, Missouri, and Oklahoma.8 There were 314 cases of Tularemia reported in 2015, the highest number since 1964.1 The causative organism, Francisella tularensis, is a highly infectious small, Gram-negative, nonmotile coccobacillus which may be contracted in a variety of ways — food, water, mud, articles of clothing, contact with infected animal tissue, and (particulary) arthropod bites. Arthropods involved in transmission of tularemia include ticks, biting flies, and possibly even mosquitoes. Ticks account for more than 50% of all cases, especially west of the Mississippi River.

Tularemia may present as several different clinical syndromes, including glandular, ulceroglandular, oculoglandular, oropharangeal, pneumonic, and typhoidal.44 In general, the clinical course is characterized by an influenza-like attack with severe initial fever, temporary remission, and a subsequent febrile period of at least 2 weeks. Later, a local lesion with or

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without glandular involvement may occur. Additional symptoms vary depending on the method of transmission and form of the disease (see discussion below). Untreated, the mortality rate for tularemia is as high as 30%; early diagnosis and treatment can reduce that 5% or less.9,45 Clinical and Laboratory Findings Depending on the route of entry of the causative organism, tularemia may be classified in several ways. The most common is ulceroglandular — resulting from cutaneous inoculation — characterized by an ulcer with sharp undermined borders and a flat base. Location of the ulcers may help identify the mode of transmission. Ulcers on the upper extremities are often a result of exposure to infected animals, whereas ulcers on the lower extremities, back, or abdomen most often reflect arthropod transmission. When there is lymphadenopathy without an ulcerative lesion, the classification of glandular tularemia is used. If the tularemia bacterium enters via the conjunctivae, oculoglandular tularemia may result. Oropharyngeal tularemia results from ingestion of contaminated food or water. If airborne transmission of the agent is involved, the pneumonic form occurs. These patients often present with fever, a nonproductive cough, dyspnea, and chest pain. The pneumonic form can be life-threatening. Finally, tularemia may be classified as typhoidal, characterized by disseminated infection mimicking typhoid fever, brucellosis, tuberculosis, or some of the RMSF-type infections.

Patients with tularemia may or may not show abnormal white blood cell counts (WBC), platelet counts, and sedimentation rate. Hyponatremia, elevated serum transaminases, increased creatine phosphokinase, and myoglobinuria have been reported.45 The standard serologic test used to confirm tularemia has historically involved tube agglutination of a bacterial suspension. The test is quite specific for tularemia, although it can cross-react with Brucella. An acute agglutination titer of 1:160 is supportive of a tularemia diagnosis, but definitive evidence of recent infection comes from a fourfold rise in titer between acute and convalescent specimens. In recent years, diagnosis has been aided by detecting Francisella tularensis DNA in blood or tissues by PCR. Treatment The drug of choice for treatment of tularemia is streptomycin, although the recent lack of availability of this drug has forced many healthcare providers to try alternative antimicrobials, such as gentamicin, tetracycline, ciprofloxacin, chloramphenicol, and others.46,47 Unfortunately, controlled studies are lacking to support the efficacy of some of these antibiotics, and some agents are only inhibitory — not bactericidal — thus leading to relapses. A review of the literature found the following cure rate data for some of the most effective agents: streptomycin — 97%; gentamicin — 86%; tetracycline — 88%; and chloramphenicol — 77%.47 Tetracycline was shown to be associated with twice as many relapses as gentamicin. The authors of that study concluded that gentamicin was comparable to streptomycin in efficacy against tularemia.46 Human Babesiosis Introduction and Medical Significance Human babesiosis is a tick-borne disease primarily caused by protozoa in the order Piroplasmidora, family Babesiidae. The most common human agents are Babesia microti and Babesia divergens, although other newly recognized species may also cause human infection.48,49 The

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disease is a malaria-like syndrome characterized by fever, fatigue, and hemolytic anemia lasting from several days to a few months. In terms of clinical manifestations, babesiosis may vary widely from asymptomatic infection to a severe, rapidly fatal disease. The first demonstrated case of human babesiosis in the world was reported in Europe in 1957. In the United States, there have been hundreds of cases of babesiosis (most people with intact spleens) caused by Babesia microti, mostly from southern New England, and specifically Nantucket, Martha’s Vineyard, Shelter Island, Long Island, and Connecticut.50,51 Most cases of babesiosis are caused by bites from the same tick that transmits the agent of Lyme disease, I. scapularis.52 There has been one confirmed case of babesiosis (Babesia microti) in Mississippi53 – a 90-year-old man who lived in a rural area of southwest Mississippi. Collections at the man’s home by one of the authors and Dr. Wendy Varnado from the Mississippi Department of Health yielded 2 adult I. scapularis ticks.

Clinical and Laboratory Findings Babesiosis is clinically very similar to malaria; in fact, confusion between the two diseases is often reported in the scientific literature.54 Headache, fever, chills, nausea, vomiting, myalgia, altered mental status, disseminated intravascular coagulation, anemia with dyserythropoiesis, hypotension, respiratory distress, and renal insufficiency are common to both diseases. However, the symptoms of babesiosis do not show periodicity. The incubation period varies from 1 to 4 weeks. Physical exam of patients is generally unremarkable, although the spleen and liver may be palpable. Lab findings may include hemoglobinuria, anemia, and elevated serum bilirubin and transaminase levels. Diagnosis of babesiosis is usually based on recognition of the organism within erythrocytes in Giemsa-stained blood smears, although PCR with specific Babesia primers is much more accurate and sensitive. The small parasites, several of which may infect a single red blood cell and which appear much like Plasmodium falciparum, can be differentiated from malarial parasites by the absence of pigment (hemozoin) in the infected erythrocytes. IFA can be used to detect specific antibodies in patient serum. Serologic diagnosis can be established by a fourfold or greater rise in the serum titer between the acute phase and the convalescent phase.

Species of Babesia and Their Ecology There are at least 100 species of tick-transmitted Babesia, parasitizing a wide variety of vertebrate animals. Some notorious ones are as follows: Babesia bigemina, the causative agent of Texas cattle fever; Babesia canis and Babesia gibsoni, canine pathogens; Babesia equi, a horse pathogen that occasionally infects humans; Babesia divergens, a cattle parasite that infects humans; and Babesia microti, a rodent parasite that infects humans. Recently, new Babesia species have been recovered from ill humans and have tentatively been variously designated as the WA1 agent, the CA1 agent, or the MO1 agent.55 The WA1 agent, now known as B. duncani, was isolated from a patient in Washington State and was particularly interesting because the man was only 41-year-old, had an intact spleen, and was immunocompetent. Although the parasites were morphologically identical to B. microti, the patient did not develop a substantial antibody to B. microti antigens. Subsequent DNA sequencing of the organism indicated that it was most closely related to the canine pathogen B. gibsoni. Obviously, there is much more to be learned about the many and varied Babesia species, and their complex interactions with animals in nature.

On the other hand, the life cycle of B. microti — the one causing American babesiosis in the northeastern United States — is fairly well known. Rodents serve as natural reservoirs for the parasite. B. microti multiplies readily in hamsters and the white-footed (WF) mouse, Peromyscus leucopus. WF mouse populations are cyclic, depending on food sources, and are more abundant some years compared to others. If ticks happen to feed during those times on an animal (such as a squirrel) that is somewhat refractory to infection with B. microti, then the diversion from reservoir-competent hosts depresses the overall infection rate in ticks and mice. Deer play a role as well — but not as reservoirs — in providing a blood meal for the adult I. scapularis. More deer ultimately lead to more ticks. Therefore, prevalence of B. microti infection in an area depends on the complex interactions of WF mice, the parasite, and deer.

Treatment and Control Standard treatment of symptomatic B. microti infection has been quinine sulfate plus clindamycin; however, a drug regimen consisting of atovaquone and azithromycin has been shown to be effective when clindamycin and quinine fail.9,56 Prevention and control of the disease in the community involve personal protection measures against ticks, searching for and removing promptly any attached ticks, pesticidal treatment of lawns and parks to reduce tick numbers, and possibly host animal management (deer reduction).

Viruses Transmitted by Ticks Introduction People usually associate arboviral encephalitis and dengue-like fevers with mosquitoes. However, ticks may also be involved in the transmission of these type of agents. Tick-borne viral diseases (nonhemorrhagic) have historically been grouped into two categories — the encephalitides group and the dengue fever-like group. The former, containing viral diseases clinically resembling the mosquito-borne encephalitides, includes the tick-borne encephalitis (TBE) subgroup (and its various subtypes). Specific diseases in this subgroup have historically included Central European TBE, Russian spring-summer encephalitis (RSSE), Louping ill, and Powassan encephalitis (POW). The main dengue-like viral disease transmitted by ticks is Colorado tick fever (CTF). In the last decade, new tick-borne viruses have been identified. Heartland virus (a Phlebovirus) is associated with the Lone Star tick, Amblyomma americanum and has been recognized in Missouri, Oklahoma, Kentucky, and Tennessee.57,58 Only about 30 cases of Heartland virus have been identified. A couple of cases of a new Thogotovirus called Bourbon virus have been identified in the Midwest and southern United States with an unknown tick vector.59 Recent evidence suggests the Lone Star tick may be a potential vector of Bourbon virus.60 Tick-Borne Encephalitis (TBE) Clinical and Epidemiologic Features As mentioned, TBE is a general term encompassing several diseases caused by similar flaviviruses spanning from the British Isles (Louping ill), across Europe (Central European TBE), to the Far East (RSSE and similar syndromes). Powassan encephalitis (POW), also part of the TBE serocomplex, is a relatively rare infection of humans that mostly occurs in the northeastern United States, adjacent regions of Canada, and parts of Russia. There were 7 cases of POW reported in the United States during 2015.1 Cases are characterized by sudden onset of fever

with temperature up to 40°C (104°F) along with convulsions. Also, accompanying encephalitis is usually severe, characterized by vomiting, respiratory distress, and prolonged, sustained fever. Only a few dozen cases of POW have been reported in North America,61,62 although its incidence may be increasing.1 Cases have occurred in children and adults, with a case fatality rate of approximately 50%. POW is maintained in an enzootic cycle among ticks (primarily Ixodes cookei) and rodents and carnivores. Ixodes cookei only occasionally bites people, and this may explain the low case numbers. Antibody prevalence to POW in residents of affected areas is generally < 1%, indicating that human exposure to the virus is rare. Another member of this group, deer tick encephalitis, which is closely related to POW, was first discovered in North America in the late 1990s.63 There have only been a few clinical cases ever described, although at least one death has been attributed to this virus.64 The agent has been found along the Atlantic Coast and in Wisconsin, and is primarily found infecting the deer tick, Ixodes scapularis.

Diagnosis and Treatment Definitive diagnosis of TBE is based on isolating the virus from blood or CSF or from postmortem tissues; by PCR; or serologic tests of paired sera; or demonstration of specific IgM in acute serum. Virus isolation is generally an option only at major research hospitals or government institutions. Hemagglutination inhibition is often used to detect antibody rises between early and late serum samples. Enzyme-linked immunosorbent assay (ELISA) tests are used to indicate presence of specific IgM. Treatment is supportive only; no specific antiviral treatment is available.

Tick Paralysis Introduction and Medical Significance Tick paralysis is characterized by an acute, ascending, flaccid motor paralysis that may terminate fatally if the tick is not located and removed.

The causative agent is not a living entity like a bacteria or virus, but instead, a salivary toxin produced by ticks when they feed. In the strictest sense, tick paralysis is not a zoonosis; however, many contend that zoonoses should include not only infections that humans acquire from animals, but also diseases induced by noninfective agents, such as toxins and poisons.65 The disease is more common than one might think. In North America, hundreds of cases have been documented from the MontanaBritish Columbia region.66,67 It occurs in the southeastern United States as well; six cases were seen at the University of Mississippi Medical Center over a 5-yr period.68 Clusters of tick paralysis may occur.69 Tick paralysis is especially common in Australia. However, sporadic cases may occur in Europe, Africa, and South America.

Clinical Features The site of tick bite in a case of tick paralysis looks no different from that in cases without paralysis. There is a latent period of 4–6 days before the patient becomes restless and irritable. Within 24 hours, there is an acute ascending lower motor neuron paralysis of the Landry type. It usually begins with weakness of the lower limbs, progressing in a matter of hours to falling down and obvious incoordination, which is principally owing to muscle weakness, although rarely there may also be true ataxia.70 Finally, cranial nerve weakness with dysarthria and dysphagia leads to bulbar paralysis, respiratory failure, and death. In children, presenting features may include restlessness, irritability, malaise, and sometimes

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anorexia and/or vomiting.70 A tick may be found attached to the patient, often on the head or neck. Some controversy occurs over whether or not severity of symptoms is related to the proximity of the attached tick to the patient’s brain.71 In one study, the case fatality rate in patients with ticks attached to the head or neck was higher than that in patients with ticks attached elsewhere; however, the difference was not statistically significant.67 Although ticks causing paralysis are often attached to the head or neck, it must be noted that cases of paralysis may occur from tick bites anywhere on the body (published examples — external ear, breast, groin, and back70). Once the tick is found and removed, all symptoms usually disappear rapidly.

This happens when ticks (primarily the lone star tick, Amblyomma americanum) feed on mammals, acquiring the carbohydrate, galactoseα-1.3-galactose, or simply “alpha-gal” in their blood meal. After molting to the next stage, if these ticks feed on a human, alpha-gal may be injected via tick saliva. If allergic, the person develops sensitivity to alpha-gal and then days or weeks later, when eating red meat, may develop urticaria, angioedema, or even anaphylaxis 3-6 hours after red meat ingestion.75 Meats known to express alpha-gal and falling into the “red meat” category include beef, pork, lamb, squirrel, rabbit, horse, goat, deer, kangaroo, seal, and whale. Persons sensitive to alpha-gal may still eat chicken, turkey, and fish.75 n

Ticks Involved and Mechanism of Paralysis As many as 43 tick species in 10 genera have been incriminated in tick paralysis in humans, other mammals, and birds.72 In the northwestern United States and British Columbia region of North America, the Rocky Mountain wood tick, D. andersoni, is the principal tick involved.

This tick is an avid human biter and also is known to be a vector of RMSF organisms and CTF virus. In the southeastern United States, a kissing cousin of the Rocky Mountain wood tick, D. variabilis, known as the American dog tick, is the main cause of tick paralysis. This tick, commonly found on dogs, cats, and other medium-sized mammals, is also a common human biter in the summer months.

References

Interestingly, not all feeding female ticks – even of the species known to cause paralysis – produce paralysis. Why, out of hundreds of tick bites, does one result in paralysis? There is some evidence that in cattle, sheep, and dogs numerous ticks feeding simultaneously (to reach a minimum dose) are necessary to elicit paralysis.66 In humans, however, one tick is usually involved.

Most researchers believe that the toxin causing tick paralysis is produced in the salivary glands of the female tick as she feeds. One alternative view would be that the toxin is produced in tick ovaries and subsequently passes to the salivary glands during later stages of tick engorgement.

Although the vast majority of cases are due to female ticks, there are reports of male ticks causing limited paralysis. This fact seems to argue against the ovary toxin theory. There are other theories for the cause of the paralysis, such as host reactions to components of the tick saliva or possibly symbiotic rickettsial organisms commonly found in tick salivary glands.

Prevention and Treatment Since paralysis does not usually develop until late in the feeding phase of the tick (several days), frequent examination of the body and removal of any attached ticks reduce the risk of paralysis. Other than finding and removing the offending tick, treatment is supportive only. In the United States (Dermacentor ticks), after onset of paralysis, removing the tick generally results in rapid improvement — often almost miraculous.

However, patients in deep paralysis should be under constant surveillance even after tick removal, since adverse developments may still rarely occur.

Red Meat Allergy from Ticks Researchers have recently discovered that tick bites may lead to development of allergies to red meat, the so-called “red meat allergy.”73,74

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72. Gothe R, Kunze K, Hoogstraal H. The mechanisms of pathogenicity in the tick paralysis. J Med Entomol. 1979;16:357-369.

73. Commins SP, James HR, Kelly LA, et al. The relevance of tick bites to the production of IgE antibodies to the mammalian oligosaccharide galactose-alpha1,3-galactose. J Allergy Clin Immunol. 2011;127(5):1286-1293.

74. Platts-Mills TA, Schuyler AJ, Tripathi A, Commins SP. Anaphylaxis to the carbohydrate side chain alpha-gal. Immunol Allergy Clin North Am. 2015;35:247260.

75. Ramey K, Stewart PH. Top 10 facts you should know about “Alpha-gal,” the newly described delayed red meat allergy. J Miss State Med Assoc. 2016;57:279-281.

Author Information Extension Professor of Medical and Veterinary Entomology, Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University (Goddard). Associate Clinical Professor of Family and Community Medicine, Tulane University School of Medicine; Adjunct Clinical Professor of Family Medicine, William Carey University College of Osteopathic Medicine; JMSMA Editor; Mississippi State Board of Health; Private Practice Magnolia Clinic, Magnolia, Mississippi (Lampton).

Corresponding Author: Jerome Goddard, PhD, Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, 100 Twelve Lane, Clay Lyle Entomology Building, Mississippi State University, Mississippi State, MS 39762.

E-mail: jgoddard@entomology.msstate.edu.

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M E D I C I N E

Hyperbaric Oxygen in vitro against MRSA 301 and P. aeruginosa 19660 CHRISTINA D. JORDAN, PHD; AMY L. SULLIVAN, PHD; MARY E. MARQUART, PHD; ELGENAID HAMADAIN, PHD; RANDALL S. WILLIAMSON, PHD; LISA A. HAYNIE, PHD; JENNIFER L. BAIN, PHD; ANGELA H. BENTON, MS Abstract Background Hyperbaric oxygen (HBO) aids in bacterial clearance.

This study examined HBO’s effectiveness, measuring the number of colony-forming units (CFU) of P. aeruginosa and MRSA upon exposure to air and oxygen pressures. Methods A stainless steel chamber was refurbished to administer the gases. Linear regression, one-way analysis of variance, and factorial analysis were conducted, followed by Tukey post-hoc for groups with significant differences. Results Significant increases in MRSA quantity were observed following air treatments (R=0.245, P=0.038) but were constant after oxygen treatments (R=0.095, P=0.428). P. aeruginosa quantity decreased insignificantly in air (R= -0.112, P=0.351) but was relatively constant after oxygen treatments (R=0.208, P=0.080). Conclusion Oxygen appears to maintain constant MRSA 301 and P. aeruginosa 19660 quantities. Air treatments may decrease P. aeruginosa quantity after longer applications.

Future studies should explore low-pressure gas combinations in vivo with antibiotic therapies.

Keywords: Hyperbaric oxygen, wound care, MRSA, Pseudomonas aeruginosa Introduction Hyperbaric oxygen therapy (HBO) is a vital asset in the medical armamentarium for its use in expediting wound recovery and is approved for such infectious conditions as necrotizing soft tissue infections,1,2 osteomyelitis,3 and clostridial myonecrosis (or gas gangrene).4 HBO is of recent interest due to its capacity to improve health outcomes associated with conditions such as brain injuries,5 head injuries,6,7 senility,8 stroke,9 myocardial infarction,10 radiation injury,11 and enhancement of survival in free flaps.12 Moreover, a wide consensus of studies consistently support HBO’s capacity to help eradicate a number of opportunistic infections associated with trauma,8,13,14 particularly in diabetic ulcers and burn wounds.4,15 HBO is currently approved for treating arterial gas embolism (AGE) and decompression sickness (DCS).4,16 Though DCS and AGE both affect coastal communities in Mississippi, of far greater incidence in the state are diabetic ulcers and burns where infection is exacerbated by the presence of opportunistic bacteria.

442 VOL. 59 • NO. 10 • 2018

Since evidence-based studies on HBO effectiveness and utilization are rare, physician-authorized HBO treatments are infrequent in wound care. It is arguable that injured individuals who receive HBO treatments observe a remarkable decrease in healing time,17 which is anecdotal at best. The significance and direct influence of HBO on wound healing is difficult to assess because most HBO treatments are administered as adjunct therapies rather than primary ones. For this reason, a direct link to HBO’s impact on patient improvement is difficult to determine.

At present, HBO is clinically approved to treat three conditions caused by invading bacteria: gas gangrene, osteomyelitis, and necrotizing soft tissue infections.4,16 Difficulties in wound healing are due to hypoxic tissues at the center of the wound where the most extreme disruption of tissue integrity is exhibited.18 Systemic HBO treatments yield critical benefits by restoring normal oxygen concentrations throughout the body to help initiate healing.12,18 In the presence of compromised tissues, healing is complicated by single or mixed flora bacteria which invade already compromised cells and perpetuate further tissue damage.

When this occurs, aggressive bacteria, such as Pseudomonas aeruginosa (P. aeruginosa) and methicillin-resistant Staphylococcus aureus (MRSA), may present themselves individually or in mixed combination with the primary cause of gas gangrene, Clostridium perfringens.19 In treating general bacterial infections, HBO therapy is a treatment of choice, but only for such severe complications as necrotizing fasciitis and Wagner Grade III diabetic ulcers.20 Since diabetic ulcers and burns may be complicated by opportunistic infections from a range of pathogens, tailoring HBO dosages appropriately to the type of pathogen is ideal.

However, dosage allocations for individuals remain largely the province of expert opinion rather than evidence-based data. Studies that provide information on the effectiveness of HBO therapy in the context of specific bacteria could serve as an important addition to treatment decisions for patients currently deemed as candidates for HBO therapy.

Previous studies of HBO’s bactericidal effects in treating P. aeruginosa have indicated increased effectiveness when coupled with sulfonamide21 and imipenen22 antibiotics in vitro; however, the former observed bacterial quantities at 0.87, 1.87, and 2.87 atmospheres (atm) while the latter made observations at 3 ATA only. A separate study observed the bactericidal effects of 470 nm of light and 2 atm of hyperbaric oxygen on MRSA, reporting that light alone was more effective than combined therapies.23 The present study measured six air and oxygen pressures on P. aeruginosa and MRSA in an effort to determine the bacterial colony

clearance capacity of HBO. Findings from this study are expected to contribute to improvements in burn and diabetic ulcer treatments for patients in Mississippi as well as to encourage investigations of pathologies arising from these and other bacterial infections.

Methods Bacterium S. aureus strain 301 is a MRSA strain that was originally isolated from a corneal ulcer and was kindly provided by Richard O’Callaghan (University of Mississippi Medical Center). P. aeruginosa ATCC strain 19660, also provided by Richard O’Callaghan, is a human clinical isolate. Both strains of bacteria were maintained as frozen stocks and were routinely isolated on tryptic soy agar (TSA).

Stainless-Steel Chamber A stainless-steel tank was tested with compressed carbon dioxide to ensure it could withstand internal pressures ≥ 50 PSI (equivalent to 3.5 ATAs).

Air and Oxygen Pressure Groups Colonies of each bacterium were suspended in tryptic soy broth (TSB) and grown overnight aerobically at 37oC and 200 rpm, then subcultured in fresh TSB at a 1:100 dilution. An optical density (OD) at 600nm measured cultures of approximately 0.2 and 0.3 for MRSA and P. aeruginosa respectively (equivalent to 10^8 colony forming units per mL, CFU/mL). Cultures were serially diluted and plated on TSA to verify the CFU/mL. One mL of each culture was pipetted into a sterile polypropylene tube for two treatments of air or oxygen. Each bacterial culture was conducted as three (3) independent biological replicates for each treatment parameter. Serial dilutions of each culture were examined for CFU after the first and second treatment of air or oxygen.

Air or oxygen pressure was allocated to each experimental group, where each group received either 0.5 ATA (hypobaric), 1.0 ATA (standard air pressure), or 1.5 ATA incrementally increasing air or oxygen pressure until 3.5 ATA was achieved. Treatment conditions were maintained for 45 minutes, separated by a 10 minute break with no air or oxygen pressure, and then concluding with a final 45 minutes of treatment.

The treatment was administered twice, resulting in samples receiving 200 minutes of air or oxygen pressure overall, including a total of 20 minutes with no air or oxygen pressure. A second iteration of this protocol provided a control where each bacterium received no air or oxygen pressure treatments within the sealed chamber. The goal of this investigation was to analyze changes in the number of P. aeruginosa 19660 and MRSA 301 colonies present on TSA plates after exposing the bacteria to air and oxygen pressures ranging from 0.5 ATA (hypobaric) to 3.5 ATA (hyperbaric), increasing incrementally by 0.5 ATA. Linear regression analysis and multiple linear regression analysis were performed to account for the effects of pressure alone, time alone, and a combination of pressure and time.

before conversion to log base of ten form (Log10 CFU/mL). Data were used to determine descriptive analysis of log10 of P. aeruginosa and MRSA bacteria. Further comparisons were determined using oneway analysis of variance (ANOVA) and factorial analysis, to observe interactions between pressure and time. A multiple comparison test procedure, Tukey post-hoc analysis, was conducted to test for mean differences after ANOVA testing in significant models at P < 0.05. Data analysis was performed using IBM Statistical Package for the Social Sciences Statistics 24 (SPSS Statistics 24) software. This investigation was performed in the Microbiology Department at The University of Mississippi Medical Center.

Results P. aeruginosa 19660 after Air Treatments Overall, P. aeruginosa quantity insignificantly decreased, with the most attenuations in quantity observed at pressures of 1.0, 2.0, and 3.0 ATA. Table 1 displays a comparison of base of 10 logarithmic mean of P. aeruginosa quantity in air (shown in Log10 CFU/mL ± SEM) as pressure increased. Adjusting for pressure alone, bacterial quantity exhibited a weak decrease over the course of treatments (R=-0.112), though not significantly (P=0.351). An R2 value of 0.012 indicates that only 1.2% of the data is close to the regression line: ŷ = 8.264+ -0.022(Pressure)+0.024, when considering pressure alone. Table 2 shows that, adjusting for time, bacterial quantity exhibited a weak increase. Statistical testing shows an increasing trend in the data over Table 1. Descriptive Statistics Log10 mean CFU/mL ± SEM of P. aeruginosa treated with Air

Pressure (ATA)

Log10 Mean (CFU/mL) ± SEM

Control

8.276 ± 0.054

0.5

8.312 ± 0.050

1.0

8.179 ± 0.110

1.5

8.230 ± 0.115

2.0

8.138 ± 0.074

2.5

8.299 ± 0.051

3.0

8.155 ± 0.086

3.5

8.218 ± 0.040

Descriptive log10 mean CFU/mL ± SEM of P. aeruginosa treated with air pressure in 1000µL TSB. Colonies were treated at air pressures ranging from 0.5-3.5 ATA, Samples were collected for analysis at 0, 100, and 200 minutes forCFU/mL a where Descriptive log10 mean ± SEM P. aeruginosa treated with air pressureBacterial in 1000µL TSB. Colonies were treated at air pres theofcontrol received no air treatments. quantity exhibited a weak total of three collections for each group. Bacteria plated fromthe control fromwere 0.5-3.5 ATA, where received treatments.

Bacterial quantity exhibited a weak over the course of decrease over no theaircourse of treatments (R=-0.112), though notdecrease significantly 0.112), though significantly (P=0.351).

(P=0.351). serial dilutions, quantified by count of colony forming unitsnot (CFU),

and converted to colony forming units per milliliter (CFU/mL)

Time (min) 0

Log10 Mean (CFU/mL) ± SEM OCTOBER • JOURNAL MSMA

8.267 ± 0.049

443

P. aeruginosa Quantity with Air

Figure 1. P. aeruginosa Quantity with Air

Log Count of Bacteria (CFU/mL)

10.

7.5

5.

2.5

0.

Control

0.5

1

Before TRT (Inoculum)

Pressure (ATA)

Log10 Mean (CFU/mL) ± SEM

Control

8.276 ± 0.054

0.5

8.312 ± 0.050

1.0

8.179 ± 0.110

1.5

8.230 ± 0.115

2.0

1.5 2 Pressure (ATA) 2.5 After 1st TRT

3.0

2.5

3

8.138 ± 0.074

3.5

8.299 ± 0.051 After 2nd TRT

8.155 ± 0.086

Figure P.baseline aeruginosa Quantity with Pressure1.at (inoculum), after 100Air minutes (1st TRT), and after 200 minutes (2nd TRT). At pressures of 0.5, 2.0, and 3.5 ATA, select points 3.5than at 0 and 100 minutes of treatment.

8.218 ± 0.040 indicate quantity after 200 minutes of air treatment where fewer colonies of bacteria grew

Pressure at baseline (inoculum), after 100 minutes (1st TRT), and after 200 minutes (2nd TRT). At pressures of 0.5, 2.0, and 3.5 ATA, select points indicate quantity after 200 minutes of air treatment where fewer colonies of bacteria grew than at 0 and 100 minutes of treatment.

the course of the three time points (R=0.180), though quantity was Descriptive log10 mean CFU/mL ± SEM of P. aeruginosa treated with air pressure in 1000µL TSB. Colonies were treated at air pressures r Tablereceived 2. Descriptive Statistics indicates thatwhere onlythe control not significant (P=0.131). An R2 value of 0.032from 0.5-3.5 ATA, no air treatments. Bacterial quantity exhibited a weak decrease over the course of treatm mean CFU/mL ± SEM of P. aeruginosa treated with Air 3.2% of the data is close to the regression line: ŷ = 8.276+0.000(Time), 0.112), though not significantlyLog10 (P=0.351). when considering time alone. A coefficient of zero indicates there is no relationship between P. aeruginosa quantity and time after air Time (min) Log10 Mean (CFU/mL) ± SEM treatments. The combined effect of pressure and time did not reveal any significant interactions between pressure and time on bacterial 0 8.267 ± 0.049 quantity (P=0.212). Though correlation greatly increased to reveal a stronger, positive trend in the data (R=0.819), the prediction line, 100 8.264 ± 0.039 ŷ = 8.314+ -0.022(Pressure)+0.000(Time)+0.023, is only capable of fitting 67% of the data to the line of best fit (R2=0.670). Table 3 displays 200 8.157 ± 0.050 information regarding regression data to best predict the log10 value of CFU/mL± SEM of P. aeruginosa bacteria that will grow as air pressure Descriptive log10 mean CFU/mL ± SEM of P. aeruginosa treated with air pressure in increases. Tukey post hoc analysis was not reported since the combined 1000µL TSB at time intervals 0, 100, and 200 minutes. Measurements include values effect of pressure and time did not reveal significantDescriptive interactions.

Figure for the control and show insignificant differences in quantity over the three time log10 mean CFU/mL ± SEM of P. aeruginosa treated with air pressure in 1000µL TSB at time intervals 0, 100, and 200 minutes periods. Statistical testing shows an increasing trend in the data over the course 1 displays P. aeruginosa quantity in air for each pressure group where Measurements include values for and show in quantity three time(P=0.131). periods. Statistical testin of the the control three time pointsinsignificant (R=0.180),differences though quantity wasover notthe significant an 100, increasing in the each line indicates one of the three time points (0, 200trend min).

Atdata over the course of the three time points (R=0.180), though quantity was not significant (P=0.131). pressures of 0.5, 2.0, and 3.5 ATA, select points indicate quantity after 200 minutes of air treatment where fewer colonies of bacteria grew overall, exhibited a moderately strong increase when adjusting for time.

Model Type Statistical testing shows Equation R in the data R2 overSignificance a significantly increased trend than at 0 and 100 minutes of treatment. the course of the three time points (R=0.781, P=0.00). An R2 value of Pressure ŷ = 8.264+ -0.022(Pressure)+0.024 -0.112 0.012line: ŷ 0.351 0.610 indicates that 61.0% of the data is close to the regression MRSA 301 after Air Treatments Adjusting for pressure alone, MRSA quantity exhibited a significantly = 8.067+0.002(Time), when considering time alone. The combined Time ŷ = 8.276+0.000(Time) 0.180 0.032 effect of pressure and time showed significant interactions (P=0.00). 0.131 weak increase in colony count over the course of treatments (R=0.245, P=0.038), with the most attenuations in quantity observed at pressures Also, correlation slightly increased to reveal a moderately strong, ŷ = 8.314+ -0.022 (Pressure)+0.000(Time)+0.023 0.819 line, ŷ0.670 trend in the data (R=0.819). The prediction = 7.971+ 0.212 of 0.5 and 2.5 ATA. Table 4 displays a comparison ofPressure/Time base of 10 positive logarithmic mean of MRSA quantity in air (shown in CFU/mL ± SEM) 0.055(Pressure)+0.002(Time)+0.015, is capable of fitting only 67% of as pressure increased. An R2 value of 0.060 indicates that only 6% of the the data to the line of best fit (R2=0.670). Table 6 displays information data is close to the regression line: ŷ = 8.216+ 0.055(Pressure)+0.026, regarding regression data to best predict the log10 number of CFU/mL ± when considering pressure alone. Table 5 shows that bacterial quantity, SEM of MRSA bacteria that will grow as air pressure increases. Because

444 VOL. 59 • NO. 10 • 2018

of the pressure/time interaction shows an effect on the number of mean CFU/mL ± SEM of P. aeruginosa treated with air pressure in 1000µL TSB at time intervals 0, 100, and 200 minutes.

3. Regression Data differences in quantity over the three time periods. Statistical testing showsCFU/mL in air pressures ranging from 2.3-3.0 and 3.0-3.5 ATA. Figure clude values forTable the control and show insignificant nd in the data over the course of the three time pointsAir (R=0.180), though quantity was not significant (P=0.131).

P. aeruginosa treated with 3 displays a graphic of the pressure and time interaction. Table 7 displays

el Type

Equation

R

R2

Significance

ssure

ŷ = 8.264+ -0.022(Pressure)+0.024

-0.112

0.012

0.351

ime

ŷ = 8.276+0.000(Time)

0.180

0.032

0.131

ŷ = 8.314+ -0.022 (Pressure)+0.000(Time)+0.023

0.819

0.670

0.212

Regression data for P. aeruginosa receiving air treatments show adjustments for pressure, time, and a combination of pressure and time. An R2 value of 0.012 indicates that only 1.2% of the data is close to the regression line: ŷ = 8.264+ -0.022(Pressure), when considering pressure alone. Adjusting for time, bacterial quantity exhibited a weak, insignificant increase (P=0.131). An R2 value of 0.032 indicates that only 3.2% of the data is close to the regression line: ŷ = 8.276+0.000(Time), when considering time alone. The combined effect of pressure and time did not reveal any significant interactions between pressure and time on bacterial quantity (P=0.212). Though correlation greatly increased to reveal a stronger, positive trend in the data (R=0.819), the prediction line, ŷ = 8.314+ -0.022 (Pressure)+0.000(Time), is capable of fitting only 67% of the data to the line of best fit (R2=0.670).

regression data revealed significant differences in MRSA quantity after adjustment pressure, time, and the interaction of pressure and time, Tukey post-hoc analysis was conducted to determine which pressure and time treatment combinations were significantly different. Results

Figure 2. MRSA Quantity with Air

Log Count of Bacteria (CFU/mL)

ure/Time

10.

9.25 8.5 7.75 7.

6.25 5.5 4.75 4.

3.25 2.5 1.75 1.

0.25 -0.5

Control

0.5

significant differences between groups from Tukey post-hoc analysis.

Significant differences between groups indicate that MRSA quantity for controls after receiving 100 minutes of air pressure are significantly different from quantity at 0.5 ATA after 200 minutes of air treatment (P=0.045), 1.0 ATA after 100 min (P=0.008), 1.0 ATA after 200 min (P=0.002), 1.5 ATA after 100 min (P=0.000), 1.5 ATA after 200 min (P=0.000), 2.0 ATA after 100 min (P=0.000), 2.0 ATA after 200 min (P=0.000), 2.5 ATA after and 100 min (P=0.000), 2.5 ATA after 200 min (P=0.000), 3.0 ATA after 100 min (P=0.000), 3.0 ATA after 200 min (P=0.000), and 3.5 ATA after 100 min (P=0.000). Differences were also observed for control groups receiving 200 minutes of air pressure, where significant quantity differences were seen at 1.5 ATA after 200 minutes of air treatment (P=0.001), 2.5 ATA after 100 min (P=0.000), 2.5 ATA after 200 min (P=0.000), 3.0 ATA after 100 min (P=0.000), 3.0 ATA after 200 min (P=0.000), 3.5 ATA after 100 min (P=0.000), and 3.5 ATA after 200 min (P=0.000). Differences also indicate that MRSA quantity for 0.5 ATA after receiving 100 minutes of air pressure was significantly different from quantity at 1.5 ATA after 100 minutes (P=0.018), 1.5 ATA after 200 min (P=0.000), 2.0 ATA after 200 min (P=0.000), 2.5 ATA after 100 min (P=0.000), 2.5 ATA after 200 min (P=0.000), 3.0 ATA after 100 min (P=0.000), 3.0 ATA after 200 min (P=0.000), 3.5 ATA after 100 min (P=0.000), 3.5 ATA after 200 min (P=0.000). Differences also indicate that MRSA quantity for 0.5 ATA after receiving 200 minutes of air pressure was significantly different from quantity at 1.5 ATA after 200 minutes (P=0.006), 2.0 ATA after

MRSA Quantity with Air

1

Before TRT (Inoculum)

1.5 2 Pressure (ATA) After 1st TRT

2.5

3

3.5

After 2nd TRT

Pressure at baseline (inoculum), after 100 minutes (1st TRT), and after 200 minutes (2nd TRT). At pressures of 0.5, 2.0, and 3.5 ATA, select points indicate quantity after 200 minutes of air treatment where fewer colonies of bacteria grew than at 0 and 100 minutes of treatment.

Figure 2. MRSA Quantity with Air Pressure at baseline (inoculum), after 100 minutes (1st TRT), and after 200 minutes (2nd TRT). At pressures of 0.5, 2.0, and 3.5 ATA, select points • JOURNAL MSMA indicate quantity after 200 minutes of air treatment where fewer colonies of bacteria grew than at 0 andOCTOBER 100 minutes of treatment.

445

200 min (P=0.005), 2.5 ATA after 100 min (P=0.002), 2.5 ATA after 200 min (P=0.000), 3.0 ATA after 100 min (P=0.000), 3.0 ATA after Table 4. Descriptive Statistics 200 min (P=0.000), 3.0 ATA after 200 min (P=0.000), 3.5 ATA after Log10 mean CFU/mL ± SEM of MRSA treated with Air 100 min (P=0.000), 3.5 ATA after 200 min (P=0.000). Differences also indicate that MRSA quantity for 1.0 ATA after receiving 100 minutes Pressure (ATA) Log10 Mean (CFU/mL) ± SEM of air pressure was significantly different from quantity at 1.5 ATA Control 8.227 ± 0.063 after 200 minutes (P=0.039), 2.0 ATA after 200 min (P=0.032), 2.5 ATA after 100 min (P=0.012), 2.5 ATA after 200 min (P=0.000), 3.0 0.5 8.205 ± 0.120 ATA after 100 min (P=0.000), 3.0 ATA after 200 min (P=0.000), 3.0 ATA after 200 min (P=0.000), 3.5 ATA after 100 min (P=0.000), 3.5 1.0 8.289 ± 0.078 ATA after 200 min (P=0.000). Differences also indicate that MRSA 1.5 8.313 ± 0.101 quantity for 1.0 ATA after receiving 200 minutes of air pressure was significantly different from quantity at 2.5 ATA after 100 minutes 2.0 8.354 ± 0.098 (P=0.043), 2.5 ATA after 200 min (P=0.000), 3.0 ATA after 100 min (P=0.000), 3.0 ATA after 200 min (P=0.000), 3.5 ATA after 100 min 2.5 8.232 ± 0.062 (P=0.000), and 3.5 ATA after 200 min (P=0.000). Differences also indicate that MRSA quantity for 1.5 ATA after receiving 100 minutes 3.0 8.524 ± 0.056 of air pressure was significantly different from quantity at 3.0 ATA after 3.5 8.345 ± 0.069 200 min (P=0.015) and 3.5 ATA after 100 min (P=0.037). Differences also indicate that MRSA quantity for 2.0 ATA after receiving 100 minutes of air pressure was significantly different from quantity at 2.5 Descriptive log10 mean CFU/mL ± SEM of MRSA treated with air pressure in 1000µL TSB. Colonies were treated at air pressures ranging from 0.5-3.5 ATA, where the ATA after 200 minutes (P=0.004), 3.0 ATA after 100 min (P=0.002), control received no air treatments. Bacterial quantity exhibited a significantly weak Descriptive log10 mean CFU/mL ± SEM in of MRSA pressure 1000µL TSB. Colonies were P=0.038), treated at air pressures rang 3.0 ATA after 200 min (P=0.000), 3.5 ATA after 100 min (P=0.001), increase colonytreated count with overairthe courseinof treatments (R=0.245, with 3.5 ATA, where the control received no air treatments. Bacterial quantity exhibited a significantly weak increase in colony count ove the most attenuations in quantity observed at pressures of 0.5 and 2.5 ATA. and 3.5 ATA after 200 min (P=0.002). Table 7 displays all significant of treatments (R=0.245, P=0.038), with the most attenuations in quantity observed at pressures of 0.5 and 2.5 ATA. interactions between groups. Figure 2 displays MRSA quantity in air for each pressure group, where each line indicates one of the three time points (0, 100, 200 min). At pressures of 0.5, 2.0, and 3.5 ATA, select Table 5. Descriptive Statistics points indicate quantity after 200 minutes of air treatment where fewer Log10 mean CFU/mL ± SEM of MRSA treated with Air colonies of bacteria grew than at 0 and 100 minutes of treatment. (min) ± SEM Log10 MeanTime (CFU/mL)

Time (min)

Log10 Mean (CFU/mL) ± SEM

P. aeruginosa 19660 after Oxygen Treatments 08.062 ± 0.049 8.062 ± 0.049 0 P. aeruginosa quantity remained relatively constant overall with the most attenuations in quantity observed at pressures of 1.0 and 3.5 100 8.321 ± 0.023 100 8.321 ± 0.023 ATA. Table 8 displays a comparison of base of 10 logarithmic mean 200 8.551 ± 0.020 of P. aeruginosa quantity in medical grade oxygen (shown in CFU/mL 200 8.551 ± 0.020 ± SEM) as pressure increased. Adjusting for pressure alone, bacterial quantity exhibited a weak increase over the course of oxygen treatments Descriptive log10 mean CFU/mL ± SEM of MRSA treated with air pressure in 1000µL TSB at time intervals 0, 100, and 200 minutes. Measurements include values for of 100.043 (R=0.208), though not significantly (P=0.080). An Descriptive R2 value log mean CFU/mL ± SEM of Bacterial MRSA treated with airoverall, pressureexhibited in 1000µLaTSB at time intervals 0, 100, and 200 minutes. M the control. quantity, moderately strong, significant includewith values the Bacterial quantity, a moderately strong, Measurements significant increase when adjusting for time indicates that only 4.3% of theCFU/mL data is± close the regression line: ŷ =control.

Descriptive log10 mean SEM oftoMRSA treated airforpressure inincrease 1000µL TSB atadjusting timeoverall, intervals 0, 100, and 200 minutes. when forexhibited time (R=0.781, P=0.00).

P=0.00).exhibited a moderately strong, significant increase when adjusting for time (R=0.781, include values for the control. Bacterial quantity, overall, P=0.00).

Table 6. Regression Data MRSA treated with Air Adjusted For

Equation

R

0.245

0.060

R2

0.245

0.060

0

Equation

Pressure

ŷ = 8.216+0.055 (Pressure) Time

ŷ = 8.067+0.002 (Time)

0.038 0.781

0.610

0

Time

ŷ = 8.067+0.002 (Time) Pressure/Time

0.781 0.610 (Time) ŷ = 7.971+0.055 (Pressure)+0.002

0.000 0.819

0.670

0

Pressure/Time

ŷ = 7.971+0.055 (Pressure)+0.002 (Time)

ŷ = 8.216+0.055 (Pressure)

0.819

Significance

Sign

Adjusted For

Pressure

R2

R

0.670

0.000

*Boldface values indicate significance. Regression*Boldface data for MRSA receiving air treatments show data adjustments pressure, time, and ashows combination values indicate significance.

Regression for MRSAfor receiving air treatments adjustments for pressure, time, and 0.060 indicates 6%0.055(Pressure)+0.026, of the data is close to the regression line: ŷ = 8.216+ combination of 6% pressure anddata time.isAn R2 value of pressure and time. An R2 value of 0.060 indicates that only of the close to theofregression line:that ŷ = only 8.216+ 2 when considering Anregression R value of line: 0.610ŷindicates that 61.0% of the data is close to the regre when considering pressure alone. An R2 value of0.055(Pressure)+0.026, 0.610 indicates that 61.0% of the datapressure is closealone. to the = 8.067+0.002(Time), *Boldface values indicate significance. Regression 8.067+0.002(Time), data for MRSA receiving air treatments showsThe adjustments for pressure, time, when considering time alone. combined effect of pressure andand timeashowed significant interactions (P=0.00 when considering time alone.

The combined effect of pressure and time showed significant interactions (P=0.00).

Also, correlation slightly indicates that only 6% the data is close strong, to the regression line: ŷ =data 8.216+ combination of pressure and time. An R2 value of 0.060 correlation slightly increased to of reveal a moderately positive trend in the (R=0.819). The prediction line, ŷ = 7.971+ increased to reveal a moderately strong, positive trend in the (R=0.819). prediction line, ŷof = 7.971+ 0.055(Pressure)+0.002(Time)+0.015, 0.055(Pressure)+0.002(Time)+0.015, is only capable fitting of data the line of bestline: fit (Rŷ2==0.670).

0.055(Pressure)+0.026, when considering pressure alone.

An data R2 value of 0.610The indicates that 61.0% of the 67% data is the close toto the regression is capable of fittingwhen only 67% of the data the line best fit (R2=0.670).

8.067+0.002(Time), considering timeto alone.

Theof combined effect of pressure and time showed significant interactions (P=0.00). Also, correlation slightly increased to reveal a moderately strong, positive trend in the data (R=0.819). The prediction line, ŷ = 7.971+ 0.055(Pressure)+0.002(Time)+0.015, is only capable of fitting 67% of the data to the line of best fit (R2=0.670).

446 VOL. 59 • NO. 10 • 2018

Table 7. Tukey Analysis Interaction Data MRSA treated with Air

Table 7. Tukey Analysis Interaction Data MRSA treated with Air

Treatment Combination Pressure (ATA)/ Time (min)

Difference Between Groups/ Significance

Pressure (ATA)/ Time (min) Mean Difference ± SE, 0.077

P-value

Control / 0

Control / 100

0.315

0.026

Control / 0

1/0

-0.461

0.000

Control / 0

1.5 / 200

-0.337

0.012

Control / 0

2.0 / 0

-0.372

0.003

Control / 0

2.0 / 200

-0.342

0.009

Control / 0

2.5 / 100

-0.370

0.003

Control / 0

2.5 / 200

-0.487

0.000

Control / 0

3.0 / 0

-0.467

0.00

Control / 0

3.0 / 100

-0.511

0.00

Control / 0

3.0 / 200

-0.552

0.00

Control / 0

3.5 / 0

-0.345

0.008

Control / 0

3.5 / 100

-0.528

0.000

Control / 0

3.5 / 200

-0.528

0.000

Control / 100

0.5 / 200

-0.300

0.045

Control / 100

1.0 / 0

-0.776

0.000

Control / 100

1.0 / 100

-0.348

0.008

Control / 100

1.0 / 200

-0.384

0.002

Control / 100

1.5 / 0

-0.516

0.000

Control / 100

1.5 / 100

-0.538

0.000

Control / 100

1.5 / 200

-0.652

0.000

Control / 100

2.0 / 0

-0.687

0.000

Control / 100

2.0 / 100

-0.438

0.000

Control / 100

2.0 / 200

-0.658

0.000

Control / 100

2.5 / 0

-0.573

0.000

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Table 7. Tukey Analysis Interaction Data MRSA treated with Air Treatment Combination

Difference Between Groups/ Significance

Pressure (ATA)/ Time (min)

Pressure (ATA)/ Time (min)

Mean Difference ± SE, 0.077

P-value

Control Control/ /100 0

2.5 / 100 Control / 100

-0.685 0.315

0.000 0.026

Control Control/ /100 0

2.51//200 0

-0.802 -0.461

0.000 0.000

Control / 100

Control / 0

3.0 / 0 1.5 / 200

-0.782

-0.337

0.000

Control / 100

3.0 / 100

-0.826

0.000

Control / 100

3.0 / 200

-0.867

0.000

Control / 0 Control / 0

Control / 100

2.0 / 0

2.0 / 200

-0.372 -0.342

0.012

0.003 0.009

Control / 0

2.5 / 100

3.5 / 0

-0.661

0.000

Control / 100

3.5 / 100

-0.843

0.000

Control / 0

Control / 100

Control / 0

Control / 200

Control / 0

2.5 / 200

3.5 / 200

3.0 / 0

1.0 / 0

3.0 / 100

-0.370 -0.487

-0.819

-0.467

-0.524

-0.511

0.000

0.000

0.00

0.000

0.00

Control / 200

1.5 / 200

Control / 0

3.0 / 200 2.0 / 0

-0.435

0.000

Control/ 200 /0 Control

3.5/ /100 0 2.5

-0.345 -0.433

0.008 0.000

Control/ 200 /0 Control

3.5//200 100 2.5

-0.528 -0.552

0.000 0.000

Control/ 200 /0 Control

3.5 3.0//200 0

-0.528 -0.530

0.000 0.000

Control Control//200 100

3.0 0.5 / 100 200

-0.574 -0.300

0.000 0.045

Control Control//200 100

3.0 1.0/ /200 0

-0.616 -0.776

0.000 0.000

Control Control//200 100

3.5//100 0 1.0

-0.409 -0.348

0.001 0.008

Control / 200

3.5 / 100

-0.591

0.000

Control / 200

3.5 / 200

-0.567

0.000

0.5 / 0

Control / 100

1.0 / 0

1.5 / 100

-0.611

0.000

0.5 / 0

Control / 100

1.5 / 0

1.5 / 200

-0.352

0.007

0.5 / 0

1.5 / 100

-0.373

0.003

Control / 200

Control / 100 Control / 100

Control / 100

1.0 / 200 1.5 / 0

2.0 / 0

0.5 / 0

1.5 / 200

Control / 100

2.0 / 100

0.5 / 0

Control / 100

2.0 / 0

2.0 / 200

-0.401

0.003

-0.552

-0.384 -0.516

-0.538 -0.652 -0.687

-0.488

-0.438

-0.522

-0.658

0.001

0.00

0.002 0.000 0.000 0.000 0.000

0.000

0.000

0.000

0.000

0.5 / 0

2.0 / 200

-0.493

0.000

Control 0.5 / /0 100

2.5 // 00 2.5

-0.573 -0.408

0.000 0.001

0.5 / 0

2.5 / 100

-0.520

0.000

0.5 / 0

2.5 / 200

-0.637

0.000

448 VOL. 59 • NO. 10 • 2018

Table 7. Tukey Analysis Interaction Data MRSA treated with Air Treatment Combination

Difference Between Groups/ Significance

Pressure (ATA)/ Time (min)

Pressure (ATA)/ Time (min)

Mean Difference Âą SE, 0.077

P-value

0.5 / 0/ 0 Control

3.0 //0100 Control

-0.617 0.315

0.000 0.026

0.5 / 0/ 0 Control

3.01 // 0100

-0.662 -0.461

0.000 0.000

0.5 / 0

Control / 0 0.5 / 0

Control / 0 0.5 / 0

Control / 0 0.5 / 0

Control / 0

3.0 / 200

1.5 / 200 3.5 / 0

2.0 / 0

3.5 / 100

2.0 / 200

3.5 / 200

2.5 / 100

-0.703

-0.337

-0.496

-0.372

-0.678

-0.342

-0.654

-0.370

0.000

0.012

0.000

0.003

0.000

0.009

0.000

0.003

0.5 / 100

1.0 / 0

-0.564

0.000

Control / 0

2.5 / 200

-0.487

0.000

Control / 0 0.5 / 100

3.0 / 0

1.5 / 100

-0.467

Control / 0

3.0 / 100

-0.511

-0.441

0.000

Control /0 0.5 / 100

3.0 / 200 2.0 / 0

-0.552 -0.475

0.000

Control /0 0.5 / 100

3.5//200 0 2.0

-0.345 -0.446

0.008 0.000

Control /0 0.5 / 100

3.5 2.5/ /100 0

-0.528 -0.361

0.000 0.005

0.5 / 100 Control /0

2.5 // 200 100 3.5

-0.473 -0.528

0.000

0.5 / 100 Control / 100

2.5 / 200 0.5

-0.590 -0.300

0.000 0.045

0.5 / 100 Control / 100

3.0 // 00 1.0

-0.570 -0.776

0.000 0.000

0.5 / 100 Control / 100

3.0 / 100 1.0 / 100

-0.614 -0.348

0.000 0.008

0.5 / 100

0.5 / 100

0.5 / 100

Control / 100 0.5 / 100

Control / 100 0.5 / 100

Control / 100

1.5 / 0

1.5 / 200

3.0 / 200

1.0 / 200 3.5 / 0

1.5 / 0

3.5 / 100

1.5 / 100

-0.305 -0.326

-0.656

-0.384

-0.449

-0.516

-0.631

-0.538

0.038

0.00

0.018

0.00 0.00

0.000

0.002

0.000

0.000

0.000

0.000

0.5 / 100

3.5 / 200

-0.607

0.000

Control / 100

1.5 / 200

-0.652

0.000

0.5 / 200

1.0 / 0

-0.476

0.000

Control / 100 0.5 / 200

2.0 / 0

1.5 / 200

-0.687

0.000

Control / 100

2.0 / 100

-0.438

0.000

Control / 100

2.0 / 200

-0.658

0.000

Control / 100 0.5 / 200

2.5//100 0 2.5

-0.573 -0.385

0.000 0.002

0.5 / 200

2.5 / 200

-0.502

0.000

0.5 / 200

3.0 / 0

-0.482

0.000

0.5 / 200 0.5 / 200

2.0 / 0

2.0 / 200

-0.352 -0.387 -0.358

0.006 0.002 0.005

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Table 7. Tukey Analysis Interaction Data MRSA treated with Air Treatment Combination Pressure (ATA)/ Time (min) 0.5 / 200

Difference Between Groups/ Significance

Pressure (ATA)/ Time (min)

Mean Difference ± SE, 0.077

P-value

Control / 0

Control / 100

3.0 / 100

-0.526

0.000

0.5 / 200

3.0 / 200

-0.567

0.000

0.5 / 200

Control / 0

3.5 / 0

1.5 / 200

-0.361

0.005

0.5 / 200

3.5 / 100

-0.543

0.000

0.5 / 200

3.5 / 200

-0.519

0.000

2.0 / 200

-0.342

2.5 / 100

-0.370

Control / 0

Control / 0 Control / 0 1.0 / 0

Control / 0 1.0 / 0

Control / 0

1/0

2.0 / 0

1.0 / 100

1.0 / 200

0.315

-0.461

-0.337 -0.372 0.428 0.393

0.026 0.000 0.012

0.003 0.009

0.000

0.003

0.001

1.0 / 0

2.0 / 100

2.5 / 200

-0.487 0.338

0.011

Control /0 1.0 / 100

3.0/ 200 /0 1.5

-0.467 -0.304

0.00 0.039

Control /0 1.0 / 100

3.0 2.0//100 0

-0.511 -0.339

0.00 0.011

Control /0 1.0 / 100

3.0 // 200 200 2.0

-0.552 -0.309

0.00 0.032

1.0 / 100 Control /0

2.5 3.5/ /100 0

-0.337 -0.345

0.012 0.008

1.0 / 100 Control /0

2.5 3.5 // 200 100

-0.454 -0.528

0.000 0.000

1.0 / 100 Control /0

3.0//200 0 3.5

-0.434 -0.528

0.000 0.000

Control / 100

1.0 / 100

3.0 / 100

0.5 / 200

-0.478

-0.300

0.000

1.0 / 100

3.0 / 200

-0.519

0.000

Control / 100 1.0 / 100

1.0 / 0

-0.776

0.000

0.045 0.000

Control / 100

1.0 / 100

3.5 / 0

-0.312

0.029

1.0 / 100

3.5 / 100

-0.494

0.000

1.0 / 100

3.5 / 200

-0.471

0.000

1.5 / 0

-0.516

Control / 100 Control / 100 1.0 / 200

Control / 100 1.0 / 200

Control / 100 1.0 / 200

Control / 100

1.0 / 200 2.0 / 0

1.5 / 100

2.5 / 100

1.5 / 200

2.5 / 200

2.0 / 0

-0.348 -0.384 0.304

-0.538

-0.302

-0.652

-0.418

-0.687

0.008 0.002 0.000

0.040

0.000

0.043

0.000

0.000

0.000

1.0 / 200

3.0 / 0

-0.399

0.001

Control / 100 1.0 / 200

2.0 // 100 100 3.0

-0.438 -0.443

0.000 0.000

Control / 100 1.0 / 200

2.0 // 200 200 3.0

-0.658 -0.484

0.000 0.000

Control / 100 1.0 / 200

2.5 // 00 3.5

-0.573 -0.277

0.000 0.096

1.0 / 200

3.5 / 100

-0.459

0.000

1.0 / 200

3.5 / 200

-0.435

0.000

450 VOL. 59 • NO. 10 • 2018

Table 7. Tukey Analysis Interaction Data MRSA treated with Air Treatment Combination Pressure (ATA)/ Time (min) 1.5 / 0

Difference Between Groups/ Significance

Pressure (ATA)/ Time (min)

Mean Difference ± SE, 0.077

P-value

3.0 / 100

-0.310

0.032

Control / 0

Control / 100

1.5 / 0

3.0 / 200

1/0

-0.461

-0.351

0.007

1.5 / 0

Control / 0

3.5 / 100

1.5 / 200

-0.326

0.017

1.5 / 0

3.5 / 200

-0.302

0.042

Control / 0

Control / 0

0.315

-0.337

0.026 0.000 0.012

1.5 / 100

3.0 / 200

2.0 / 0

-0.372

0.003

Control / 0

2.0 / 200

-0.342

0.009

Control / 0 2.0 / 100

2.5 / 100

2.5 / 200

-0.370

0.003

Control /0 2.0 / 100

2.5 / 200 3.0 / 0

-0.487 -0.344

0.000 0.009

Control /0 2.0 / 100

3.0/ /100 0 3.0

-0.467 -0.388

0.00 0.002

Control /0 2.0 / 100

3.0 // 200 100 3.0

-0.511 -0.429

0.00 0.000

Control /0 2.0 / 100

3.0 3.5 / 200 100

-0.552 -0.405

0.00 0.001

2.0 / 100 Control /0

3.5 3.5/ /200 0

-0.380 -0.345

0.002 0.008

Control / 0

3.5 / 100

-0.528

0.000

1.5 / 100

3.5 / 100

-0.330 -0.305 -0.364

0.015

0.037 0.004

Significant differences between groups indicate that MRSA quantity for controls after receiving 100 minutes of air pressure are significantly different Significant differences indicates that MRSA quantity1.0 forATA controls aftermin receiving 1001.0 minutes of air pressure are significantly from quantity at 0.5 ATAbetween after 200groups minutes of air treatment (P=0.045), after 100 (P=0.008), ATA after 200 min (P=0.002), 1.5 ATA after different from quantity at 0.5 ATA200 after minutes of air treatment 1.0 ATA after 100 min 1.0 ATA 200 min Control 3.52.0 / 200 -0.528 0.000 100 min (P=0.000), 1.5/ 0ATA after min200 (P=0.000), ATA after 100(P=0.045), min (P=0.000), 2.0 ATA after 200(P=0.008), min (P=0.000), 2.5after ATA after and 100 min (P=0.002), 1.5 ATA after 200 100 min min (P=0.000), (P=0.000), 3.0 1.5 ATA ATAafter after100 200min min(P=0.000), (P=0.000),3.0 2.0ATA ATAafter after200 100min min(P=0.000), (P=0.000), 2.03.5 ATA (P=0.000), 2.5 ATA after and ATAafter after200 100min min(P=0.000), (P=0.000, 2.5 after 100 min (P=0.000), 2.5among ATA after 200 Differences min (P=0.000), ATA after min (P=0.000), 3.0 ATA 200 min SeeATA Figure 3).and Table 7100 shows differences groups. were3.0 observed for100 control groups receiving 200after minutes of air(P=0.000), pressure, and where Control / 0.5 / 200 -0.300 0.045 3.5 ATA after 100 min (P=0.000,were See Figure shows groups.(P=0.001), Differences groups significant quantity differences seen at3).

1.5Table ATA 7after 200differences minutes of among air treatment 2.5were ATA observed after 100 for mincontrol (P=0.000), 2.5receiving ATA after 200 of air pressure, where100 significant quantity weremin seen at 1.5 ATA air treatment 2.5200 ATAmin 200 minutes min (P=0.000), 3.0 ATA after min (P=0.000), 3.0differences ATA after 200 (P=0.000), 3.5after ATA 200 afterminutes 100 minof(P=0.000), and (P=0.001), 3.5 ATA after after 100 min (P=0.000), 2.5 ATA after 200 min (P=0.000), 3.0 ATA after 100 min (P=0.000), 3.0 ATA after 200 min (P=0.000), 3.5 ATA after 100 / 100 1.0 for / 00.5 -0.776 0.000 (P=0.000). Control Differences also indicate that MRSA quantity ATA after receiving 100 minutes of air pressure was significantly different from quantity min (P=0.000), and 3.5 ATA after 200 min (P=0.000). Differences also indicate that MRSA quantity for 0.5 ATA after receiving 100 minutes of air at 1.5 ATA after 100 minutes (P=0.018), 1.5 ATA after 200 min (P=0.000), 2.0 ATA after 200 min (P=0.000), 2.5 ATA after 100 min (P=0.000), 2.5 ATA pressure was significantly different from quantity at 1.5 ATA after 100 minutes (P=0.018), 1.5 ATA after 200 min (P=0.000), 2.0 ATA after 200 Control / 1003.0 ATA 1.0 / 1003.0 ATA -0.348 0.008 after(P=0.000), 200 min (P=0.000), 100 min (P=0.000), min (P=0.000), ATA after min (P=0.000), ATA200 after min 2.5 ATA after 100 after min (P=0.000), 2.5 ATA after 200after min 200 (P=0.000), 3.0 ATA 3.5 after 100 min100 (P=0.000), 3.0 ATA3.5 after min200 min (P=0.000).

Differences also indicate that MRSA quantity for 0.5 ATA after receiving 200 minutes of air pressure was significantly different from quantity (P=0.000), 3.5 ATA after 100 min (P=0.000), 3.5 ATA after 200 min (P=0.000). Differences also indicate that MRSA quantity for 0.5 ATA after at 1.5 ATA200 after 200 /minutes (P=0.006), 2.0significantly ATA after min (P=0.005), 2.5 ATAatafter 100 min (P=0.002), 2.5(P=0.006), ATA after 200 (P=0.000), 3.0 ATA Control 100 1.0200 / different 200 -0.384 0.002 receiving minutes of air pressure was from quantity 1.5 ATA after 200 minutes 2.0 min ATA after 200 min after 100 min 200 min 200 min3.0 (P=0.000), ATA 100 min3.0 (P=0.000), 3.5200 ATAmin after 200 min (P=0.005), 2.5(P=0.000), ATA after 3.0 100ATA minafter (P=0.002), 2.5(P=0.000), ATA after3.0 200ATA minafter (P=0.000), ATA after3.5 100 minafter (P=0.000), ATA after (P=0.000). Differences also indicate that MRSA3.5 quantity for 1.0 receiving3.5 100 minutes of airmin pressure was significantly from quantity (P=0.000), 3.0 ATA after min (P=0.000), ATA after 100ATA minafter (P=0.000), ATA after 200 (P=0.000).

Differencesdifferent also indicate that Control /minutes 100200(P=0.039), 1.5200 / 0min -0.516 0.000 at 1.5 ATA after 2001.0 2.0100 ATAminutes after (P=0.032), 2.5significantly ATA after 100 min (P=0.012), 2.5 ATAatafter 200 after min (P=0.000), 3.0 ATA MRSA quantity for ATA after receiving of air pressure was different from quantity 1.5 ATA 200 minutes after 100 min 200 min 200 min2.5 (P=0.000), ATA 100 min3.0 (P=0.000), 3.5100 ATAmin after 200 min (P=0.039), 2.0(P=0.000), ATA after 3.0 200ATA minafter (P=0.032), 2.5(P=0.000), ATA after3.0 100ATA minafter (P=0.012), ATA after3.5 200 minafter (P=0.000), ATA after (P=0.000), Control / 100 1.5min /for 100 -0.538 0.000 from quantity (P=0.000).

Differences also indicate3.0 that MRSA 1.0 ATA after of air pressure wasafter significantly 3.0 ATA after 200 min (P=0.000), ATA afterquantity 200 (P=0.000), 3.5 receiving ATA after200 100minutes min (P=0.000), 3.5 ATA 200 mindifferent (P=0.000). at 2.5 ATA after minutes 2.5 ATAforafter 200 min after of 100airmin (P=0.000), ATA after different 200 min (P=0.000), 3.5 ATA Differences also100 indicate that(P=0.043), MRSA quantity 1.0 ATA after(P=0.000), receiving 3.0 200ATA minutes pressure was 3.0 significantly from quantity at afterATA 100after min (P=0.000), 3.5 ATA after 200 min (P=0.000).

Differences3.0 alsoATA indicate MRSA quantity for ATA after receiving 100 minutes 2.5 100 minutes 2.5 ATA after 200 min (P=0.000), after that 100 min (P=0.000), 3.0 1.5 ATA after 200 min (P=0.000), 3.5 of Control / 100and(P=0.043), 1.5 / 200 -0.652 0.000 air pressure was significantly quantity 3.0(P=0.000).

ATA after 200 min (P=0.015) and 3.5 ATA 100 min (P=0.037).

Differences also indicate ATA after 100 min (P=0.000),different and 3.5 from ATA after 200atmin Differences also indicate thatafter MRSA quantity for 1.5 ATA after receiving 100 that MRSA quantity forwas 2.0 significantly ATA after receiving 100from minutes of air was significantly differentand from at100 2.5 min ATA(P=0.037). after 200 minutes minutes of air pressure different quantity atpressure 3.0 ATA after 200 min (P=0.015) 3.5quantity ATA after / 100100 2.0 / 200 0after (P=0.004), Control 3.0 ATA after (P=0.002), 3.0for ATA after minreceiving (P=0.000), ATA after 100pressure min (P=0.001), and 3.5 ATA after0.000 200 minquantity (P=0.002).

Differences also indicate thatmin MRSA quantity 2.0 ATA 1003.5 minutes of-0.687 air was significantly different from at 2.5 ATA after 200 minutes (P=0.004), 3.0 ATA after 100 min (P=0.002), 3.0 ATA after 200 min (P=0.000), 3.5 ATA after 100 min (P=0.001), and 3.5 ATA after 200 min (P=0.002).

Control / 100 2.0 / 100 -0.438 0.000

Control / 100 when considering 2.0pressure / 200 alone.

8.237+ -0.040(Pressure)+0.022, Table 9 shows that, adjusting for time, bacterial quantity exhibited a / 100 / 0 increasing weak increase in Control count. Statistical testing shows a 2.5 weak, trend in the data over the course of the three time points (R=0.144), though quantity was not significant (P=0.228). An R2 value of 0.021 indicates that only 2.1% of the data is close to the regression line: ŷ = 8.206+0.000(Time), when considering time alone. A coefficient of

-0.658 0.000P. aeruginosa quantity zero indicates there is no relationship between and time after oxygen treatments. The combined effect of pressure and -0.573 0.000between pressure and time did not reveal any significant interactions time on bacterial quantity (P=0.102). Correlation greatly decreased to reveal a weak, increasing trend in the data (R=0.064), where the prediction line, ŷ = 8.276+ -0.040 (Pressure)+0.000 (Time)+0.022, is capable of fitting only 25.3% of the data to the line of best fit (R2=0.253).

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Table 10 displays information regarding regression data to best predict the log10 number of CFU/mL± SEM of P. aeruginosa bacteria that will grow as medical grade oxygen pressure increases. Tukey post-hoc analysis was not reported, considering the interactions of pressure and time were insignificantly different. Figure 4 displays P. aeruginosa quantity in oxygen for each pressure group, where each line indicates one of the three time points (0, 100, 200 min). Quantity in oxygen pressure at baseline (inoculum), after 100 minutes (1st TRT), and after 200 minutes (2nd TRT) indicates insignificant quantity.

Figure 3. MRSA Quantity Treated with Air Interaction Graph

MRSA 301 after Oxygen Treatments Overall, MRSA quantity remained constant, with the most attenuation in quantity observed at 2.5 ATA. Table 11 displays a comparison of base of 10 logarithmic mean of MRSA quantity in air (shown in CFU/mL ± SEM) as pressure increased. Adjusting for pressure alone, bacterial quantity exhibited an insignificantly weak increase in colony count over the course of treatments (R=0.095, P=0.428).

A low R2 value of 0.009 indicates that only 0.9% of the data is close to the regression line: ŷ = 8.280+0.038(Pressure)+0.048, when considering pressure alone. Table 12 shows that bacterial quantity, overall, exhibited an even weaker increase when adjusting for time (R=0.040). Statistical testing shows that this trend in the data is not significant over the course of the three time points (P=0.737). An R2 value of 0.002 indicates that 0.02% of the data is close to the regression line: ŷ = 8.323+0.000(Time)+0.001, when considering time alone. Line Graph of Mean CFU per milliliter vs. Pressure indicates an interaction between 3. MRSAand Quantity Treated withair Air Interaction Graph pressure time, where treatments after inoculation and after the first air The combined effect of pressure and time showed no significant Figure pressure treatment show an interaction between 2.5-3.0 ATA and between 3.0 and Graph of Mean CFU per milliliter vs. Pressure indicates an interaction between pressure and time, where air treatments after inoculation interactions (P=0.692). Correlation slightly increased to reveal a Line3.5 ATA. weak, positive trend in the data (R=0.103). The prediction line, ŷ = after the first air pressure treatment show an interaction between 2.5-3.0 ATA and between 3.0 and 3.5 ATA. 8.257+0.038(Pressure)+0.000(Time)+0.001+0.048, is only capable of fitting 1.1% of the data to the line of best fit (R2=0.011). Table 13 displays information regarding regression data to best predict the log10 Table 8. Descriptive Statistics number of CFU/mL ± SEM of MRSA bacteria that will grow as 100% Log10 mean CFU/mL ± SEM of P. aeruginosa treated with Oxygen oxygen pressure increases. Tukey post hoc analysis was not reported since pressure and time treatment combinations were insignificantly Pressure (ATA) Log10 Mean (CFU/mL) ± SEM different. Figure 5 displays insignificant decreases in MRSA quantity at 0.5, 1.5, and 2.0 ATA. Control 8.256 ± 0.033 Discussion

0.5

8.262 ± 0.042

Bacterial infections are the most common conditions in wound recovery. Severe bacterial infections may lead to loss of function, mobility, and/or amputation of the infected area, depending on the degree of tissue destruction.

1.0

8.099 ± 0.133

1.5

8.138 ± 0.065

2.0

8.135 ± 0.095

2.5

8.260 ± 0.048

3.0

8.178 ± 0.069

3.5

8.007 ± 0.022

Hyperbaric oxygen therapy (HBO) has exhibited promise in this area, displaying a reduction in bacterial growth for indications due to aggressive infections.21,22,23,24,25,26 Moreover, HBO has exhibited the capacity to reduce wound size and recovery time in patients suffering from severe infections, thereby reducing amputation rates due to infection.27,28,29 Approaches to identify HBO’s clearance effectiveness have shown positive results,21,22,23,24,25,26 while displaying little30 to no effect in others.31,32 The current study provides information on P.

452 VOL. 59 • NO. 10 • 2018

Descriptive log10 mean CFU/mL ± SEM of P. aeruginosa treated with oxygen pressure in 1000µL TSB. Colonies were treated at air pressures ranging from 0.53.5±ATA, where the control received no oxygen for pressure Descriptive log10 mean CFU/mL SEM of P. aeruginosa treated with oxygen pressuretreatments. in 1000µL TSB.Adjusting Colonies were treated at air pressure alone, bacterial quantity exhibited a weak increase over the course of oxygen ranging from 0.5-3.5 ATA, where the control received no oxygen treatments. Adjusting for pressure alone, bacterial quantity exhibited a w aeruginosa that of oxygen treatments (R=0.208), though (P=0.080). increasegroups over the course treatments (R=0.208), thoughnot notsignificantly significantly (P=0.080).

Time (min)

Log10 Mean (CFU/mL) ± SEM

0 mean CFU/mL ± SEM of P. aeruginosa treated with oxygen pressure in 1000µL TSB. Colonies were treated at air pressures 5-3.5 ATA, where the control received no oxygen treatments. Adjusting for pressure alone, bacterial quantity exhibited a weak significant e course of oxygen treatments (R=0.208), though not significantly (P=0.080).

decreases in colony count. Realistically, however, most experimental groups displayed an increase in cell count after adjusting for pressure, time, and the interaction of pressure and time.

Table 9. Descriptive Statistics Log10 mean CFU/mL ± SEM of P. aeruginosa treated with Oxygen Time (min)

Log10 Mean (CFU/mL) ± SEM

0

8.179 ± 0.054

100

8.221 ± 0.033

200

8.101 ± 0.045

At best, the current study identified groups for which bacterial growth insignificantly decreased in count; it also provides information on groups that exhibited a weak increase in cell count for use in selecting groups to examine in future investigations. Data from this study also indicated that using oxygen pressure to assist in the clearance of aerobic MRSA is more effective than air pressure treatments.

The data also supported the use of air pressure treatments as more

Descriptive log10 mean CFU/mL ± SEM of P. aeruginosa treated with oxygen effective in the clearance of aerobic P. aeruginosa than oxygen pressure in 1000µL TSB at time intervals 0, 100, and 200 minutes. Measurements treatments. Neither air nor oxygen pressures decreased bacterial growth include values for the control. Statistical testing shows a weak, increasing trend in the data over the course of the three time points (R=0.144), though growth was significantly; however, oxygen pressure treatments displayed an ability minutes.

0 mean CFU/mL ± SEM of P. aeruginosa treated with oxygen pressure in 1000µL TSB at time intervals 0, 100, and 200 significant (P=0.228). nclude valuesnot for the control. Statistical testing shows a weak, increasing trend in the data over the course of theto three time maintain constant MRSA and P. aeruginosa quantities as pressure ), though growth was not significant (P=0.228).

exhibited a weak increase in colony count after air treatments, allowing for the selection of groups to examine in future investigations. Data from this study also indicated that using oxygen pressure to assist in the clearance of aerobic MRSA is more effective than air pressure treatments.

Data supports the use of air pressure treatments as more effective in the clearance of aerobic P. aeruginosa than oxygen treatments. Neither air nor oxygen pressures decreased bacterial quantity significantly; however, oxygen pressure treatments displayed an ability to maintain relatively constant MRSA 301 and P. aeruginosa 19660 quantities as pressure increased (R=0.095, P=0.428; R=0.208, P=0.080, respectively), while air pressure treatments caused P. aeruginosa 19660 to decrease slightly in count as pressure increased (R=-0.112, P=0.351), with attenuations at 1.0, 2.0, and 3.0 ATA. Ideally, data from this study would reveal

increased (R=0.095, P=0.428; R=0.208, P=0.080, respectively), while air pressure treatments caused P. aeruginosa to decrease slightly in count as pressure increased (R=-0.112, P=0.351), with attenuations at 1.0, 2.0, and 3.0 ATA.

When examining the effects of time for MRSA and P. aeruginosa growth in both air and oxygenated environments, all groups expect MRSA air displayed weak, insignificant increases in colony count (MRSA O2: R=0.040, P=0.737; P. aeruginosa O2: R=0.144, P=0.228; P. aeruginosa Air: R=0.180, P=0.131). MRSA air groups, however, displayed significant increases in colony count when adjusting for pressure (R=0.245, P=0.038), time (R=0.781, P=0.00), and the interaction of pressure and time (R=0.819, P=0.00), with attenuations at 0.5 and 2.5 ATA in the pressure model. MRSA oxygen groups revealed no significant interactions, with a weak increase in colony count (R=0.103, P=0.692). Pressure and time interaction models revealed the strongest correlation for all groups (MRSA O2: R=0.103, P=0.692; MRSA air:

P. aeruginosa Quantity with Oxygen

Log Count of Bacteria (CFU/mL)

Figure 4. P. aeruginosa Quantity with Oxygen 10.

9.25 8.5 7.75 7.

6.25 5.5 4.75 4.

3.25 2.5 1.75 1.

0.25 -0.5

Control

0.5

1

Before TRT (Inoculum)

1.5 2 Pressure (ATA) After 1st TRT

2.5

3

3.5

After 2nd TRT

Pressure (inoculum), after 100Oxygen minutes (1st TRT), and after 200 minutes (2nd TRT) showing insignificant quantities over time. aeruginosa Quantity with Figure 4. atP.baseline

Pressure at baseline (inoculum), after 100 minutes (1st TRT), and after 200 minutes (2nd TRT) showing insignificant quantities over time.

OCTOBER • JOURNAL MSMA

453

Table 10. Regression Data P. aeruginosa treated with Oxygen

Adjusted For

Adjusted For

Equation

R

R2

Pressure

ŷ = 8.237+ -0.040 (Pressure)+0.022

0.208

0.043

0.0

0.021

0.2

0.253

0.1

Equation Time

Pressure

R ŷ = 8.206+0.000 (Time) R

Significance 0.144

2

ŷ = 8.237+ -0.040Pressure/Time (Pressure)+0.022 ŷ = 8.276+ -0.040 (Pressure)+0.000 0.208 0.043 (Time)+0.022

0.080 0.064

Time

ŷ = 8.206+0.000 (Time)

0.144

0.021

0.228

Pressure/Time

ŷ = 8.276+ -0.040 (Pressure)+0.000 (Time)+0.022

0.064

0.253

0.102

Signifi

Regression for P. aeruginosa receiving oxygen shows adjustments for pressure, time,An andR2a combination Regression data for P. aeruginosa receiving oxygen treatments showdata adjustments for pressure, time, treatments and a combination of pressure and time. value of of pressure and ti R2 value of 0.043 indicates that only 4.3% of the data is close to the regression line: ŷ = 8.237+ -0.040 (Pressure), when considering press 0.043 indicates that only 4.3% of the data is close to the regression line: ŷ = 8.237+ -0.040 (Pressure), when considering pressure alone.

An R2 value of 0.021 alone. An R2 value of 0.021 indicates that only 2.1% of the data is close to the regression line: ŷ = 8.206+0.000 (Time), when considering indicates that only 2.1% of the data is close to the regression line: ŷ = 8.206+0.000 (Time), when considering time alone. The combined effect of pressure alone. The combined effect of pressure and time did not reveal any significant interactions between pressure and time on bacterial growth and time did not reveal any significant interactions between pressure and timegreatly on bacterial growth (P=0.102).

Correlation decreased reveal weak, line, ŷ = 8.276+ -0 (P=0.102).

Correlation decreased to reveal a weak, increasing trend greatly in the data (R=0.064),towhere theaprediction increasing trend in the data (R=0.064), where the prediction line, ŷ = 8.276+ -0.040 (Pressure)+0.000 (Time), is capable of fitting only 25.3% of the data to 2 (Pressure)+0.000 (Time), is only capable of fitting 25.3% of the data to the line of best fit (R =0.253). the line of best fit (R2=0.253).

Regression data for P. aeruginosa receiving oxygen treatments shows adjustments for pressure, time, and a combination of pressure and time. An R2 value of 0.043 indicates that only 4.3% of the data is close to the regression line: ŷ = 8.237+ -0.040 (Pressure), when considering pressure alone. An R2 value of 0.021 indicates that only 2.1% of the data is close to the regression line: ŷ = 8.206+0.000 (Time), when considering time alone. The combined effect of pressure and time did not reveal any significant interactions between pressure and time on bacterial growth R=0.819, P=0.00); P. aeruginosa O2: R=0.064, P=0.102; aeruginosatrend air: in the data (R=0.064), where the prediction line, ŷ = 8.276+ -0.040 (P=0.102).

Correlation greatly decreased to reveal a weak,P.increasing (Pressure)+0.000 is only capable of increases fitting 25.3% of the data the line of best (R2=0.253).

Table 11. fit Descriptive Statistics R=0.819, P=0.212)(Time), showing insignificant in colony counttofor

all groups except MRSA air, where growth was significantly different.

Examinations of the data to determine if other correlations exist revealed significant between-group differences for both MRSA and P. aeruginosa. Although no significant differences between these groups were observed for the MRSA samples that received oxygen treatments, differences were observed for the P. aeruginosa samples that received oxygen treatments. Fifty-nine (59) between-group differences were established as significant for MRSA samples(ATA) receiving air treatments, Pressure confirming that air pressure treatments induce significant MRSA growth and are, hence, not beneficialControl clinically in treating MRSA infections.

0.5

Log10 mean CFU/mL ± SEM of MRSA treated with Oxygen Pressure (ATA)

Log10 Mean (CFU/mL) ± SEM

Control

8.194 ± 0.131

0.5

8.300 ± 0.153

Log101.0 Mean (CFU/mL) ± SEM 1.5 2.0

8.194 ± 0.131 8.300 ± 0.153

8.430 ± 0.145 8.311 ± 0.162 8.534 ± 0.142

An opposite trend was observed for the P. aeruginosa samples that 2.5 8.216 ± 0.190 received air pressure treatments, when examining the pressure model 1.0 8.430 ± 0.145 of growth. P. aeruginosa count actually decreased when observing the 3.0 8.300 ± 0.170 effects of pressure, though this phenomenon 1.5 was reversed in time 8.311 ± 0.162 3.5 8.482 ± 0.153 and pressure/time models of growth. Oxygen treatments revealed very weak, insignificant increases in colony 2.0count for all three models, 8.534 ± 0.142 log10 mean CFU/mL ± SEM of MRSA treated with oxygen pressure showing that P. aeruginosa maintains a constant count in oxygen Descriptive in 1000µL TSB. Colonies were treated at air pressures ranging from 0.5-3.5 ATA, treatments overall. In general, air treatments show more promise where the control8.216 2.5 ± 0.190 received no air treatments. Overall, bacterial growth remained Descriptive log10 mean CFU/mL ± SEM with of MRSA oxygen pressure in 1000µL TSB. Colonies were treated at air pressures rangi constant, thetreated most with attenuation in growth observed at 2.5 ATA. Adjusting in P. aeruginosa clearance. The current study also demonstrates that from 0.5-3.5 ATA, where the control received no air treatments. Overall, bacterial growth remained constant, with the most attenuation i for pressure alone, bacterial growth exhibited an insignificantly weak increase in hypobaric exposure to cells is an important3.0 aspect of bacterial clearance growth observed at 2.5 ATA. Adjusting for pressure alone,± bacterial growth exhibited an insignificantly weak increase in colony count ove 8.300 0.170 colony count over the course of treatments (R=0.095, P=0.428). course of treatments (R=0.095, P=0.428). in this strain.

3.5

8.482 ± 0.153

Because this study did not examine the effects of a combination of Limitations oxygen and air treatments as pressure increased from 0.5-3.5 ATA, This investigation was conducted using a range of pressures between future research studies may be aimed at determining if bacterial 0.5-3.5 ATA; therefore, interpretations are limited to oxygen and air clearance improves with this modification. areas of pressures this range.were Other variables also be considered, such Descriptive log10 mean CFU/mL ± SEM of MRSAOther treatedpossible with oxygen pressure in 1000µL in TSB. Colonies treated at airmay pressures ranging from examination 0.5-3.5 ATA, where theacontrol received nostudy air treatments.

Overall, bacterial growth constant, with most attenuation in investigation. future include reiteration of this and the suggested as the strainremained and growth phase of the bacterium used in the growth observed at 2.5 ATA. Adjusting alone,infected bacterialhuman growth exhibited an insignificantly weak increase in colony count over the Additional air/oxygen combination study in vivoforbypressure examining (We used actively replicating bacterium in rich medium.) course of treatments (R=0.095, P=0.428). cells, and/or in an animal model. limitations, besides human error, were dependent on chamber functionality and operability. Weathering of chamber parts contributed

454 VOL. 59 • NO. 10 • 2018

Figure 5. MRSA Quantity with Oxygen

Log Count of Bacteria (CFU/mL)

MRSA Quantity with Oxygen

10.

7.5 5.

2.5 0.

Control

0.5

1

1.5 2 Pressure (ATA)

Before TRT (Inoculum)

After 1st TRT

2.5

3

3.5

After 2nd TRT

Figure 5. Pressure MRSA Quantity with Oxygen at baseline (inoculum), after 100 minutes (1st TRT), and after 200 minutes (2nd TRT). Insignificant decreases in bacteria quantity observed at 0.5, and 2.0minutes ATA. (2nd TRT). Insignificant decreases in bacteria quantity Pressure at baseline (inoculum), after 100 minutes (1st TRT), and1.5, after 200 observed at 0.5, 1.5, and 2.0 ATA.

to the majority of pressure loss observed in this investigation. Internal pressure loss, though momentary, may have resulted in the relatively high mean square errors for groups, as observed for MRSA 301 quantity in oxygen. Also, this in vitro study is not indicative of results that may be obtained from in vivo experiments, as associations observed in the current study may not translate.

References

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Plast Reconstr Surg. 2014;133:208e–15e.

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Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus SE, Weibel S. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2015;6:CD004123.

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Goldman RJ. Hyperbaric oxygen therapy for wound healing and limb salvage: a systematic review. PMR. 2009;1:471–89.

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Weaver, L. Hyperbaric oxygen therapy indications: The HBO committee report.

UHMS. 2014.

A special thanks goes to Mrs. JoAnne Fordham of Jackson State 5.

Yang Y, Zhang YG, Lin GA, Xie HQ, Pan HT, et al. The effects of different University who provided consistent writing assistance and manuscript hyperbaric oxygen manipulations in rats after traumatic brain injury. Neurosci Lett. 2014;563:38-43. preparation. n 6.

Spiegelberg L, Braks JA, Djasim UM, Farrell E, van der Wal KG, et al. Effects of hyperbaric oxygen therapy on the viability of irradiated soft head and neck tissues in mice. Oral Dis. 2014;20(3):e111-9.

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Chen C, Huang L, Nong Z, Li Y, Chen W, et al. Hyperbaric oxygen prevents cognitive impairments in mice induced by d-galactose by improving cholinergic and anti-apoptotic functions. Neurochem Res. 2017;42(4):1240-1253.

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Weixler VH, Yates AE, Puchinger M, Zirngast B, Pondorfer P, et al. Hyperbaric oxygen in patients with ischemic stroke following cardiac surgery: a retrospective 0 8.288 ± 0.088 observational trial. Undersea Hyperb Med. 2017;44(5):377-385.

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Chen C, Chen W, Nong Z, Ma Y, Qiu S, Wu G. Cardioprotective effects of combined therapy with hyperbaric oxygen and diltiazem pretreatment 100 8.416 ± 0.119 on myocardial ischemia-reperfusion injury in rats. Cell Physiol Biochem.

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200 8.334 ± 0.070 11.

Bennett MH, Feldmeier J, Hampson N, Smee R, Milross C. Hyperbaric oxygen therapy for late radiation tissue injury. Cochrane Database Syst Rev. 2012;(5):CD005005.

Descriptive log10 mean CFU/mL ± SEM of MRSA treated with oxygen pressure in Bhutani, Sourabh and Vishwanath, Burusway. Hyperbaric oxygen and wound 1000µL TSB at time intervals 0, 100, and 200 minutes. Measurements include values 12. for the± SEM control.

Bacteria overall, exhibited weaker, log10 mean CFU/mL of MRSA treatedquantity, with oxygen pressure in 1000µLan TSBeven at time intervalsinsignificant 0, 100, and 200 minutes.healing. Ind J Plast Surg. 2012;45(2):316-324.

13.

Eisenbud nts include values for thewhen control.

Bacteria quantity, exhibited an even weaker, insignificant increase when adjusting for time DE. Oxygen in wound healing: nutrient, antibiotic, signaling molecule, increase adjusting for timeoverall, (R=0.040, P=0.737). and therapeutic agent. Clin Plast Surg. 2012;39(3):293-310. =0.737).

usted For

Pressure

Equation

R

R2

Significance

ŷ = 8.280+0.038 (Pressure)+0.048

0.095

0.009

0.428

OCTOBER • JOURNAL MSMA

455

200

8.334 ± 0.070

Descriptive log10 mean CFU/mL ± SEM of MRSA treated with oxygen pressure in 1000µL TSB at time intervals 0, 100, and 200 minutes.

Measurements include values for the control. Bacteria quantity, overall, exhibited an even weaker, insignificant increase when adjusting for time TableP=0.737).

13. Regression Data MRSA treated with Oxygen (R=0.040,

Adjusted For

Equation

R

R2

Significance

Pressure

ŷ = 8.280+0.038 (Pressure)+0.048

0.095

0.009

0.428

Time

ŷ = 8.323+0.000 (Time)+0.001

0.040

0.002

0.737

Pressure/Time

ŷ = 8.257+0.038 (Pressure)+0.000

0.103

0.011

0.692

(Time)+0.001+0.048 Regression data for MRSA receiving oxygen treatments show adjustments for pressure, time, and a combination of pressure and time. A low R2 value of 0.009 indicates that only 0.9% of the data is close to the regression line: ŷ = 8.280+0.038 (Pressure), when considering pressure alone. Bacterial quantity, overall, exhibited an even weaker increase when adjusting for time (R=0.040), though quantity is insignificant thetreatments course of the threeadjustments time pointsfor (P=0.737).

R2 value of 0.002 indicates that 0.02% of the Regression data for MRSA receivingover oxygen shows pressure,An time, and a combination of pressure and time.

A low R2 data is close to the regression line: ŷ = 8.323+0.000 (Time), when considering time alone.

The combined effect of pressure and time alone. value of 0.009 indicates that only 0.9% of the data is close to the regression line: ŷ = 8.280+0.038 (Pressure), when considering pressure showed no significant Correlation slightly increased to reveal a weak, positive trendisininsignificant the data (R=0.103).

Bacterial quantity, overall, interactions exhibited an (P=0.692). even weaker increase when adjusting for time (R=0.040), though quantity over the course 2 value of 0.002 indicates Thethree prediction line, ŷ(P=0.737). = 8.257+0.038 (Time), isthat capable of fitting of the to the line of best (R2=0.011). (Time), of the time points An R(Pressure)+0.000 0.02% of theonly data1.1% is close to data the regression line: ŷ =fit8.323+0.000 when considering time alone. The combined effect of pressure and time showed no significant interactions (P=0.692). Correlation slightly increased to reveal a weak, positive trend in the data (R=0.103). The prediction line, ŷ = 8.257+0.038 (Pressure)+0.000 (Time), is only capable of fitting 1.1% of the data to the line of best fit (R2=0.011).

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Kimmell HM, Grant A, Ditata J. The presence of oxygen in wound healing.

Wounds. 2016;28(8):264-70.

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Selcuk CT, Ozalp B, Durgun M, Tekin A, Akkoc MF, et al. The effect of hyperbaric oxygen treatment on the healing of burn wounds in nicotinized and nonnicotinized rats. J Burn Care Res. 2013;34(4):e237-43.

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Barata P, Cervaens M, Resende R, Camacho O, Marques F. Hyperbaric oxygen effects on sports injuries. Ther Adv Musckuloskelet Dis. 2011;3(2):111-121.

18. Lam G, Fontaine R, Ross FL, Chiu ES. Hyperbaric oxygen therapy: Exploring the clinical evidence. Adv Skin Wound Care. 2017;30(4):181-190.

19. Stephens MB. Gas gangrene: Potential for hyperbaric oxygen therapy. Postgrad Med. 1996;99(4):217-20, 224.

20. Huang ET, Mansouri J, Murad MH, Joseph WS, Strauss MB, et al. A clinical practice guideline for the use of hyperbaric oxygen therapy in the treatment of diabetic foot ulcers. UHM. 2015;42(3).

21. Bumah VV, Whelan HT, Masson-Meyers DS, Quirk B, Buchmann E, et al. The bactericidal effect of 470nm of light and hyperbaric oxygen therapy on methicillinresistant staphylococcus aureus (MRSA). Lasers Med Sci. 2015;30(3):1153-59.

22. Freiberger JJ, Padilla-Burgos R, McGraw T, Suliman HB, Kraft KH, et al. What is the role of hyperbaric oxygen in the management of bisphosphonate-related osteonecrosis of the jaw: A randomized controlled trial of hyperbaric oxygen as an adjunct to surgery and antibiotics. J Oral Maxillofac Surg. 2012;70:1573-1583.

23. Lima FL, Joazeiro PP, Lancellotti M, de Hollanda LM, de Araujo LB, et al. Effects of hyperbaric oxygen on pseudomonas aeruginosa susceptibility to imipenem and macrophages. Future Microbiol. 2015;10(2):179-89.

24. Litwinowicz R, Bryndza M, Chrapusta A, Kobielska E, Kapelak B, et al. Hyperbaric oxygen therapy as additional treatment in deep sternal wound infections - A single center’s experience. Kardiochir Torakochirurgia Pol. 2016;13(3):198-202.

25. Pakman LM. Inhibition of pseudomonas aeruginosa by hyperbaric oxygen. I. Sulfonamide activity enhancement and reversal. 1971;4(4):479-87.

26. Yu WK, Chen YW, Shie HG, Lien TC, Kao HK, et al. Hyperbaric oxygen therapy as an adjunctive treatment for sternal infection and osteomyelitis after sternotomy and cardiothoracic surgery. J Cardiothorac Surg. 2011;6:141.

27. Escobar SJ, Slade JB Jr, Hunt TK, Cianci P. Adjuvant hyperbaric oxygen therapy (HBO2) for treatment of necrotizing fasciitis reduces mortality and amputation rate. Undersea Hyperb Med. 2005;32(6):437-43.

456 VOL. 59 • NO. 10 • 2018

28. Lebel D, Gortzak Y, Nyska M, Katz T, Atar D, et al. Hypebaric oxygen therapy for chronic diabetic wounds of the lower limbs- A review of the literature. Harefuah.

2007;146(3):223-7. Review. Hebrew.

29. Tiaka EK, Papanas N, Manolakis AC, Maltezos E. The role of hyperbaric oxygen in the treatment of diabetic foot ulcers. Angiology. 2012;63(4):302-14.

30. Goldman RJ. Hyperbaric Oxygen Therapy for Wound Healing and Limb Salvage: A Systematic Review. PM R. 2009;1(5):471-89.

31. Jørgensen NP, Hansen K, Andreasen CM, Pederson M, Fuursted K, et al.

Hyperbaric oxygen therapy is ineffective as an adjuvant to daptomycin with rifampicin treatment in a murine model of staphlococcus aureus in implantassociated osteomyelitis. Microorganisms. 2017;5(2).

32. Mutluoglu M, Uzun G, Bennett M, Germonpre P, Smart D, Mathieu D. Poorly designed research does not help clarify the role of hyperbaric oxygen in the treatment of chronic diabetic foot ulcers. Diving Hyperb Med. 2016;46(3): 133134.

Author Information Graduate student, Clinical Health Sciences doctoral program, School of Graduate Studies in Health Sciences and Post-Doctoral Research Fellow, Jackson Heart Study program, University of Mississippi Medical Center (Jordan). Dissertation Committee Chairperson, Professor of Dental Hygiene, School of Dentistry, University of Mississippi Medical Center (Sullivan). Associate Professor, Microbiology and Immunology Department, School of Medicine, University of Mississippi Medical Center (Marquart). Professor of Statistics, Clinical Health Science Program, School of Health Related Professions, University of Mississippi Medical Center (Hamadain).

Assistant Professor, Biomedical Materials Science, School of Dentistry, University of Mississippi Medical Center (Williamson). Professor of Instruction, School Nursing, University of Mississippi Medical Center (Haynie). Assistant Professor, Periodontal and Preventive Science, School of Dentistry, University of Mississippi Medical Center (Bain). Graduate student, Microbiology and Immunology doctoral program, University of Mississippi Medical Center (Benton).

Corresponding author: Christina D. Jordan, PhD, MA, BS; 131 Callaway Circle, Byram, MS 39272.

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Top 10 Facts You Need to Know about Human Papillomavirus-Associated Oropharyngeal Squamous Cell Cancer WILLIAM H. REPLOGLE, PHD; C. RON CANNON, MD

1

5

2

6

3 4

7

Oropharyngeal squamous cell cancer (OPSCC) has shifted from a predominately carcinogen-exposure disease to a virally-mediated disease. Partly associated with a decrease in tobacco use, the incidence of the most common malignancy of the head and neck, squamous cell carcinoma (SCC), has decreased in nearly all subsites over the past 30 years. Likewise, the incidence of human papillomavirus (HPV) negative OPSCC declined 50% from 1988 to 2004 while the incidence of HPV-positive OPSCC more than doubled over the same period. The number of HPV related OPSCC cases is forecasted to surpass the number of HPV-positive cervical cancer cases by 2020.1-3

Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States. There are over 100 HPV subtypes and more than 15 have oncogenic potential.3 The prevalence of any genital HPV among adults aged 18-59 was reported to be 42.5% and the prevalence of an oncogenic-potential genital HPV infection was 22.7%. The prevalence of any oral HPV and oncogenic-potential oral HPV was 7.3% and 4.0%, respectively.4,5 Subtype 16 (HPV-16) is the most prevalent of all oncogenic-potential oral subtypes with a 1% prevalence. HPV-16 is the cause of 90% of HPV-positive OPSCC.6 Transmission of HPV infections occurs mainly by skin-toskin or mucosa-to-mucosa contact.7 Transmission of HPV to the oropharynx can occur via oral sexual behavior or possibly by sexually-associated contact, such as deep kissing.6

HPV appears to be a transient infection.8 The majority of sexually active women will have been infected by one or more genital HPV types during their lifetime9, but 90% or more of newly infected women show no evidence of infection after 18 months.8 Only a very small percentage of women who do not clear the infection will subsequently develop a malignancy,1 with the interval between new infection and invasive cervical cancer estimated to be years or even decades;7 the interval for OPSCC is unknown.

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Patients with HPV-positive OPSCC often have vastly different risk factors compared to patients with HPVnegative OPSCC. Patients with HPV-positive OPSCC are more often white males of a higher socioeconomic status, in the fifth or sixth decade, who have little or no history of tobacco or alcohol use compared to HPV-negative OPSCC patients. The number of lifetime sexual partners has been shown to be related to the development of HPV-positive OPSCC. However, HPV-positive OPSCC is also found among smokers, drinkers, and patients with limited sexual activity; the absence of these factors does not exclude the diagnosis.3,10

The majority of HPV-positive OPSCC patients will present with a mass. The mass will either be an asymptomatic neck mass without a symptomatic primary site or with a symptomatic mass of the palatine or lingual tonsil with possible concurrent lymphadenopathy. Clinical suspicion for OPSCC should remain very high in patients with an asymptomatic neck mass regardless of their history of tobacco or alcohol use. Tenets of the initial evaluation include a careful head and neck exam, including mirror exam or fiber optic endoscopy looking for the primary tumor. Diagnosis is made by fine needle aspiration of the mass; open biopsy is to be avoided. Tissue sampling of the primary tumor confirms the disease. CT, MRI, or PETCT helps determine the extent of disease, lymph node involvement and distant metastasis.1 OPSCC cancers should be tested for HPV status.5

The American Joint Committee on Cancer 2017 eighth edition details changes in the staging of HPV-positive OPSCC. Staging for HPV-negative SCC cancer remains the same.11-12 This new system better differentiates the groups in terms of survival. The new stages in HPV-positive cancer are: Stage IA: T1, N0-N2 Stage IB: T2, N0-N2 Stage II: T1-T2, N3 or T3, N0-N3 Stage III: T4 regardless of node status Stage IV: All tumors with M1 status

Table.15 Recommended number of doses and intervals for human papillomavirus (HPV) vaccine, by age at series initiation and medical conditions — United States, 2016

Population Persons initiating HPV vaccination at ages 9 through 14 years,* except immunocompromised persons†

Recommended number of HPV vaccine doses

Recommended interval between doses

2

0, 6–12 months§

Persons initiating HPV vaccination at ages 15 through 26 years¶ and immunocompromised persons† initiating HPV vaccination at ages 9 through 26 years

3

0, 1–2, 6 months**

Persons initiating HPV vaccination at ages 27 through 45 years18

3

0, 2, 6 months

*ACIP recommends routine HPV vaccination for adolescents at age 11 or 12 years; vaccination may be given starting at age 9 years.

Persons with primary or secondary immunocompromising conditions that might reduce cell-mediated or humoral immunity (see also: Medical conditions) †

§

In a 2-dose schedule of HPV vaccine, the minimum interval between the first and second doses is 5 months.

¶

For persons who were not adequately vaccinated previously, ACIP recommends vaccination for females through age 26 years and for males through age 21 years; males ages 22 through 26 years may be vaccinated.

Vaccination is recommended for some persons aged 22 through 26 years; see Medical conditions and Special populations. ** In a 3-dose schedule of HPV vaccine, the minimum intervals are 4 weeks between the first and second doses, 12 weeks between the second and third doses, and 5 months between the first and third doses. https://www.cdc.gov/mmwr/volumes/65/wr/mm6549a5.htm

8

Surgical and chemoradiation treatment of HPV-positive and negative OPSCC are similar. Treatment of early stage (I or II) HPV-positive OSPSCC comprises either surgery or radiation. For stages III and IV, various combinations of surgery, radiation and chemotherapy are utilized.

9

HPV causes an epidemiologically and clinically distinct form of OSPSCC that is associated with a greater overall survival compared with HPV-negative OSPSCC.2 For example, in the first prospective Phase II trial testing non-surgical, chemoradiation treatment of clinical stage III or IV SCC in oropharynx patients only, HPV-positive versus HPV-negative patients were found to have an overall survival rate at 2 years of 94% and 58%, p=0.004, and progression-free survival at 2 years 85% vs. 50%, p=0.05, respectively.13 Trials are currently underway to identify less intense treatment strategies for HPV-positive OSPSCC that do not compromise survival outcomes.3

10

The CDC’s Advisory Committee on Immunization Practices (ACIP) recommends that both male and female adolescents be vaccinated against HPV.15

Although there has been a HPV vaccine focus on cervical cancer prevention for females, it is notable that males have a higher prevalence of HPV, oral HPV and oral HPV-16 infection compared to females4,6 and are now recognized to be at risk for HPV related cancers as well, especially OPSCC. This underscores the importance of HPV vaccination of both males and females for prevention of HPV related cancer and HPV disease transmission.

Since January 2017 the only HPV vaccine available in the United States is Gardasil 9®. This 9-valent is indicated for HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58 and is approved for males and females. The ACIP recommends that all adolescents aged 11 or 12 years should receive two doses of HPV vaccine six to twelve months apart15 (Table). As outlined in the ACIP recommendations, adolescents should be vaccinated prior to sexual activity/HPV exposure but, if already infected with one or more HPV types, can still be immunized against other HPV types in the vaccine.16 This strategy also applies to both male and female individuals aged 27 to 45 years as the FDA announced in October 2018 a new indication for Gardasil 9 to include this age group.18 A clinician’s recommendation for vaccination is the primary reason

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parents elect to vaccinate their children. Missed opportunities should be avoided by strongly recommending the HPV vaccine to parents of both male and female patients aged 11-12 years on the same day and in the same manner that tetanus-diphtheria and meningococcal vaccines are recommended17 and to adults aged 27 to 45 when corresponding immunizations are reviewed. n References 1. Deschler DG, Richmon JD, Khariwala SS, Ferris RL, Wang MB. The ‘‘new’’ head and neck cancer patient—young, nonsmoker, nondrinker, and HPV positive: evaluation. Otolaryngol Head Neck Surg. 2014, 151(3): 375–380.

2. Chaturvedi AK, Engels EA, Pfeiffer RM, Hernandez BY, Xiao W. Human papillomavirus and rising oropharyngeal cancer incidence in the United States.

J Clin Oncol. 2011; 29(32): 4294–4301.

3. Marur S, D’Souza G, Westra WH, Forastiere AA. HPV-associated head and neck cancer: a virus-related cancer epidemic. Lancet Oncol. 2010; 11(8):781–789.

4. McQuillan G, Kruszon-Moran D, Markowitz LE, Unger ER., Paulose-Ram R. Prevalence of HPV in adults aged 18–69: United States, 2011–2014. NCHS data brief, no 280, 2017. Hyattsville, MD: National Center for Health Statistics.

5. Young D, Xiao CC, Murphy B, Moore M, Fakhry C, Day TA. Increase in head and neck cancer in younger patients due to human papillomavirus (HPV). Oral Oncol. 2015:51:727-730.

6. Gillison ML, Broutian T, Pickard RKL, Tong A, Xiao W, Kahle L, et al.

Prevalence of oral HPV infection in the United States, 2009-2010. JAMA. 2012;307(7):693-703.

7. Schiffman M, Castle PE, Jeronimo J, Rodriguez AC, Wacholder S. Human papillomavirus and cervical cancer. Lancet. 2007; 370: 890–907.

8. Ho GYF, Bierman R, Beardsley L, Chang CJ, Burk RD. Natural history of cervicovaginal papillomavirus infection in young women. N Engl J Med. 1998; 338:423-428.

9.

Baseman JG, Koutsky LA. The epidemiology of human papillomavirus infections. J Clin Virol. 2005; 32S:S16–S24.

10. Dahlstrom KR, Bell D, Hanby D. et al. Socioeconomic characteristics of patients with oropharyngeal carcinoma according to tumor HPV status, patient smoking status, and sexual behavior. Oral Oncol. 2015;51:832–838.

11. AJCC Cancer Staging Manual. In: Amin MB, Edge S, Greene F, et al. (Eds.).

Springer International Publishing, 2017.

12. Hackethal V. New staging system for HPV-positive oropharyngeal cancer.

Available at: https //www.medscape.com/viewarticle/859329. Accessed: January 8, 2018.

13. Fakhry C, Westra WH, Li S, et al. Improved survival of patients with human papillomavirus-positive head and neck squamous cell carcinoma in a prospective clinical trial. J Natl Cancer Inst. 2008; 100(4):261–269.

14. Cancer.gov. Human Papillomavirus (HPV) Vaccines. https://www.cancer.gov/ about-cancer/causes-prevention/risk/infectious-agents/hpv-vaccine-factsheet#q6. Accessed October 28, 2017.

15. Meites E, Kempe A, Markowitz LE. Use of a 2-Dose Schedule for Human Papillomavirus Vaccination — Updated Recommendations of the Advisory Committee on Immunization Practices. MMWR 2016;65:1405–1408. DOI: http://dx.doi.org/10.15585/mmwr.mm6549a5.

16. Center for Disease Control and Prevention. https://www.cdc.gov/hpv/hcp/ need-to-know.pdf Accessed June 6, 2018.

17. Center for Disease Control and Prevention. https://www.cdc.gov/hpv/hcp/ schedules-recommendations.html. Accessed June 6, 2018.

18.

Food and Drug Administration. https://www.fda.gov/downloads/ biologicsbloodvaccines/vaccines/approvedproducts/ucm426457.pdf.

Accessed October 11, 2018.

Author Information Professor, School of Nursing, University of Mississippi Medical Center, Jackson.

(Replogle). Head and Neck Surgical Clinic, Flowood (Cannon).

Corresponding Author: William H. Replogle, University of Mississippi Medical Center, 2500 N. State St., Jackson, MS 39216.

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Top 10 Facts You Need to Know about Arthritis of the Thumb CAROLYN A. CUSHING, MD

Introduction Basal joint (or trapeziometacarpal joint) arthritis is one of the most common presentations of osteoarthritis in the hand. The thumb is the most common location with more than 15% of the population over 30 affected to some degree. The thumb represents nearly 40% of hand function and 25% of the body’s total function; thus dysfunction at this joint can be very disabling to patients. There are many treatment options for basal joint arthritis that can improve both the patient’s function and pain levels.1-4

3

Presenting symptoms are typically pain and visible enlargement of the thumb base. Pain is usually a constant ache that becomes markedly worse with gripping, pinching and twisting. Patients usually report difficulties with sustained activities of pinch and difficulty opening a jar or door.6

4

The thumb trapeziometacarpal (TM) joint has a unique configuration. The thumb TM joint is a saddle joint that is pronated and flexed relative to the other fingers. This allows the prehension (grasping) and opposition (crossing the thumb across the palm) found only in humans but also increases the risk of arthritis.7

1

5

2

6

Basal joint arthritis occurs most commonly in women, the obese and in persons over age 40. Up to 1/3 of postmenopausal women are affected. This may be due to a progressive destruction of the cartilage with normal activities or to a history of high-demand activities or trauma. 2-4 Basal joint arthritis is a progressive disease. Classification of the disease ranges from a simple laxity of the supporting ligaments of the thumb (often seen in young women) to a severe destruction of the entire joint surface with deformity of the thumb itself. Early treatment can markedly improve the progression of pain and disability (Table 1, Figure 1). 5

Diagnosis of basal joint arthritis is made by radiographs, history and physical exam. The history of pain with forceful pinch can be reproduced on exam with axial loading of the joint by pressing the thumb proximal phalanx proximally into the wrist to produce a “grind test”. Tenderness is at the TMC joint most easily accessible dorsally where it is not covered with muscle (Figure 2). 6 Radiographs are very useful in diagnosing basal joint arthritis. X-rays of the affected joint can determine staging of the disease, help to predict outcomes for non-surgical treatments and demonstrate the presence of osteophytes that can impact treatment options. A four-stage classification system is used to categorize the extent of the disease. 5

Table 1. Eaton’s Classification of Basal Joint Arthritis Stage

Radiographs

Clinical Correlate

I

Normal or possible CMC widening due to synovitis

Excessive CMCJ laxity, pain with use; primarily young females

II

Mild narrowing, osteophyte/loose body <2mm diameter

Typically active females 30-40 years old

III

Significant CMCJ narrowing to complete obliteration;

Active adults 40-70 yoa; females affected 5-10x more often

osteophyte/loose body >2mm diameter IV

Same as Stage III plus STT arthritis

(Eaton in Hand Clinics 1987)

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Same as stage III

Figure 1. Eaton classification Stages I-IV (L to R)

(Courtesy of OA Barron)

Figure 2. Grind Test

Figure 3. Thumb Spica Splint

7

Early treatment includes activity modification, splinting and use of nonsteroidal anti-inflammatory medication.

Many patients can modify their activities well enough to control (Courtesy of TheBraceShop.com) their symptoms. A prefabricated or custom made thumb spica splint can be used in combination with NSAIDS full-time for 2-3 weeks and weaned for 3 weeks thereafter (Figure 3). 6

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8

A hand surgeon can also treat the patient with steroid injections if more conservative treatment fails. Though the data are somewhat mixed, patients who are poor surgical candidates or wish to avoid surgery may benefit from corticosteroid injection into the affected joint. This can provide relief to the patient, often in combination with splinting. A need for repeated steroid injections increases the risk of tendon damage and is usually an indication for surgery. 8

9

Patients with continued pain and dysfunction are potential candidates for surgery. There are a variety of surgical techniques for treating basal joint arthritis; most involve removing the trapezium. The primary indication for surgery is pain in the joint that limits daily activities and has failed conservative measures. Some procedures stabilize the thumb metacarpal to the index finger and others place a tendon “spacer” in the void left after the trapezium is removed. All of these procedures have similar outcomes and vary by practitioner. Surrounding wrist joints will also be inspected for arthritic damage that is not always visible on radiographs and may require additional treatment. Deformities in the other thumb joints may also need stabilization. 9

10

Recovery after surgery typically involves splinting, activity limitations and healing with gradual return to normal activities from 3-12 weeks after surgery.

Postoperative protocols vary by technique, patient and practitioner in the amount of time before full return to normal activities. Patients with low-demand occupations should expect recovery within 6-8 weeks whereas heavy laborers may require additional time. A metaanalysis of outcomes show pain and strength continue to improve over the year after surgery. 90-95% of patients have good to excellent results with few complications. 6,9

Conclusion Basal joint arthritis is a common and often debilitating condition that has a variety of nonsurgical and surgical treatments that offer an improved quality of life. Early stages can be managed well with medications, splinting and activity modification. Patients with severe symptoms and loss of function of the joint may be candidates for hand surgery. n References 1. Moran SL, Berger RA. Biomechanics and hand trauma: what you need. Hand Clin. 2003;19(1):17e31.

2.

Armstrong AL, Hunter JB, Davis TR. The prevalence of degenerative arthritis of the base of the thumb in post-menopausal women. J Hand Surg Br. 1994;19(3):340e341.

3. Haara MM, Heliovaara M, Kroger H, et al. Osteoarthritis in the carpometacarpal joint of the thumb: prevalence and associations with disability and mortality. J Bone Joint Surg Am. 2004;86(7): 1452e1457.

4. Sodha S, Ring D, Zurakowski D, Jupiter JB. Prevalence of osteoarthrosis of the trapeziometacarpal joint. J Bone Joint Surg Am. 2005;87(12):2614e2618.

5. Eaton RG, Glickel SZ. Trapeziometacarpal osteoarthritis: staging as a rationale for treatment. Hand Clin. 1987;3(4):455e471.

6. Barron OA, Catalano LW. Thumb basal joint arthritis. In: Wolfe SWW, Hotchkiss RN, Pederson WC, Kozin SH, eds. Green’s Operative Hand Surgery. 6th ed.

Philadelphia, PA: Elsevier, Churchill Livingstone; 2010.

7. Doyle JR, Botte MJ. Surgical Anatomy of the Hand and Upper Extremity.

Philadelphia, PA: Lippincott, Williams & Wilkins; 2003.

8. Meenagh G, Patton J, Kynes C, et al: A randomized controlled trial of intraarticular corticosteroid injection of the carpometacarpal joint of the thumb in osteoarthritis. Ann Rheum Dis. 2004;63:1260.

9. Li YK, White C, Ignacy TA, Thoma A. Comparison of trapeziectomy and trapeziectomy with ligament reconstruction and tendon interposition: a systematic literature review. Plast Reconstr Surg. 2011;128(1): 199e207.

Corresponding Author: Carolyn A. Cushing, MD Plastic and Reconstructive Surgery and Hand Surgery University of Mississippi Medical Center 2500 N. State St. Jackson, MS 39216 (888) 815-2005

Brunini, Grantham, Grower & Hewes, PLLC is pleased to announce that William B. Grete has joined the firm as a Partner in its Jackson office. As the former Vice President and General Counsel of Mississippi Baptist Health Systems Inc., Mr. Grete brings over 20 years of healthcare experience to the firm as an accomplished legal healthcare executive and trusted advisor.

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The Challenges in Anesthetic Management of Patients with Trisomy 18 SEMYON FISHKIN, MD; MADHANKUMAR SATHYAMOORTHY, MBBS, MS, MBA; RUSSEL G. WARDLAW, CRNA; JOHN M. REED, MD

Abstract

Case Report

Infants with Trisomy 18 have multiple complex organ system anomalies and present significant challenges to safe and successful anesthetic management when they present for surgical procedures. In this case report, we describe a child with Trisomy 18 who developed ventricular fibrillation and cardiac arrest soon after anesthetic induction for tracheostomy tube placement in the operating room. This experience triggered our review of the medical literature on this subject. Based on this study, we will discuss possible strategies to reduce the perioperative morbidity and mortality associated with the anesthetic management of these challenging patients.

A 3-month-old male infant weighing 3.38 kg with Trisomy 18 was scheduled for tracheostomy for long-term ventilatory support due to respiratory failure. The child was born at 34 weeks, normal vaginal delivery with Apgar of 4 and 8 and birth weight of 1.62 kg. Trisomy 18 was diagnosed prenatally by amniotic fluid chromosome analysis (47, XY +18 chromosome complement). Fetal ultrasound showed a perimembranous ventricular septal defect (VSD), single umbilical artery, omphalocele and choroid plexus cyst. Other medical issues included cholestasis with liver dysfunction, pulmonary hypertension and hydronephrosis. The infant had a colostomy for the imperforate anus and omphalocele repair at two days of age under general anesthesia without complication. Daily medications included ferrous sulfate and ergocalciferol. Echocardiogram showed patent foramen ovale (PFO) with bidirectional shunting, mild right ventricular hypertrophy, and mild bilateral branch pulmonary stenosis. The child was on palliative supportive care due to his medical condition. His parents were aware of his poor prognosis and wanted all measures taken to extend his life. Since he was unable to tolerate non-invasive positive pressure ventilation, tracheostomy tube placement was planned for comfort and the discharge home from the neonatal intensive care unit (NICU).

Key Words: Trisomy 18, Edward syndrome, anesthesia challenges Introduction Trisomy 18 is the second most common autosomal chromosome disorder after Trisomy 21.1 Live birth prevalence of trisomy 18 is estimated to be 1 in 6,000.2 The overall incidence is higher as most result in fetal loss or prenatal diagnosis resulting in early termination of pregnancy. The prognosis is extremely poor with one-year survival rate ranging between 3% and 12%.3 Those who are genetically heterogeneous with mosaic or partial trisomy 18q have an increased lifespan.1,4 The common factors contributing to mortality in these patients include heart failure, central apnea, upper airway obstruction, aspiration and respiratory failure.5 Many of these patients are treated palliatively. Trisomy 18 patients have dysmorphic craniofacial features, frontal bossing, low set ears, pointed and upturned nose, micrognathia, rocker-bottom feet, clenched fists, overriding fingers and short sternum6 (Figure). They also have congenital malformations affecting the cardiovascular, respiratory, nervous, gastrointestinal, genitourinary and skeletal systems.2 Almost 60 to 80% of them have congenital heart disease and one-third of these patients have complex lesions.7 Anesthetic challenges include difficult airway, complex uncorrected cardiac disease and other organ system dysfunction.

We present anesthetic management of the patient with Trisomy 18 and discuss strategies to improve peri-operative morbidity and mortality of these patients.

466 VOL. 59 â&#x20AC;˘ NO. 10 â&#x20AC;˘ 2018

On examination, he had low set ears, syndactyly of bilateral toes.

He had clear bilateral breath sounds on auscultation, soft abdomen and active bowel sounds. He was on biphasic continuous positive end-expiratory pressure ventilation (SiPAP) with peak pressures of 4cm H20 and inspired oxygen 21% at 8 liters/min. He was in sinus rhythm with a heart rate (HR) 148, respiration rate 43, noninvasive blood pressure (NIBP) 102/63 measured on the left leg and axillary temperature 37.3 C. Electrolyte panel was normal on the day before the procedure and Hemoglobin (Hb) of 10.9 g.dL - 1. In the operating room (OR) after routine monitors were placed, anesthesia induction was carefully performed and titrated with intravenous doses of fentanyl 20 mcg and Propofol 20 mg. He was mask ventilated with 100% O2 and 2-3% Sevoflurane for 2-3 minutes. Direct laryngoscopy with Miller #1 blade showed grade 2b view with visualization of just arytenoids and less than 20% of glottic opening. The two attempts at intubation were unsuccessful. The patient developed bradycardia with his heart rate decreasing to 50s and oxygen desaturation with pulse oximetry

Tables.

Table 1. Reported Cases of Anesthetic Management of Trisomy 18

Table 1. Reported Cases of Anesthetic Management of Trisomy 18

Case 16

Case 2 8

Case 3 9

Case 4 10

Our Case

33 weeks

42 weeks

full term

n/a

34 weeks

n/a

7 years

3 years

11 years

3 months

female

female

female

female

male

Congenital abnormalities

tracheoesophageal fistula

microcephaly, dwarfism, arachnodactyly. severe mental retardation, hypotonia

large occiput, micrognathia, high arched palate, low set ears, hypotonia

n/a

omphalocele, imperforate anus, hydronephrosis, low set ears,

Cardiac problems

ventricular septal defect, pulmonary hypertension

pulmonary stenosis.

ventricular septal defect

aortic stenosis

pulmonary hypertension

bilateral ureteral reimplantation.

bilateral myringotomies

heel cord lengthening

tracheostomy

discharged home

discharged home

discharged home

Gestational age Age at time of procedure Sex

Procedure

Outcome

palliative care with no intervention died at the age of 31 days

intra-operative cardiac arrest/death

n/a: not available

readings in 50s. He recovered quickly after administration of 160 mcg of intravenous atropine and mask ventilation with 100% O2. Soon after, the otolaryngologist (ENT) successfully intubated the trachea using a 2.8 mm 0-degree endoscope with 3.0 uncuffed endotracheal tube. The patient remained stable after intubation and after the team discussion between the surgeon and the anesthesiologist, it was decided to proceed with the tracheostomy since it was a palliative procedure. Soon after the patient was prepped and draped and before the surgical incision, he rapidly desaturated and ventricular fibrillation was noted on EKG monitor. Pediatric advanced life support protocol was initiated starting with chest compressions. The position of the endotracheal tube in the trachea was confirmed by laryngoscopy performed by ENT surgeon. Asynchronous cardiac defibrillation and intravenous epinephrine administered through the femoral central line were not effective in treating the cardiovascular collapse and the patient developed asystole and died.

Discussion Patients with Trisomy 18 have complex physiology and are at the high risk of perioperative morbidity and mortality. Management of these children remains challenging with both medical and ethical issues.

Only a few cases of anesthetic management of Trisomy 18 have been

reported6,8-10 (Table 1). These children have very narrow “window” of acceptable physiology and little reserve – every effort should be made to maintain these patients within this narrow physiologic “window.”

Our recommendations regarding anesthesia management of Trisomy 18 patients describe a “5-star approach”, summarized in Table 2.

The cardiac malformations, especially pulmonary hypertension associated with poor lung development, significantly increase the anesthetic risk. Plans for the anesthetic induction should be based on the cardiopulmonary physiology and airway accessibility. If the child has pulmonary hypertension, maintaining myocardial contractility, systemic vascular resistance and avoiding an increase in pulmonary vascular resistance are the top priorities. Etomidate which has the 7 least effect on the cardiovascular system is a good choice of drug for anesthetic induction. If intravenous (IV) access is not available, intramuscular ketamine can be given in the absence of a history of seizures with subsequent peripheral IV placement. Ketamine does not worsen pulmonary hypertension in children if ventilation is adequately maintained.11 If cardiac physiology is benign, mask induction with 100% O2 and sevoflurane is acceptable. Maintaining spontaneous ventilation in cases of the difficult airway is a safer alternative. Slow titration of intravenous drugs such as fentanyl can be used to attain a deep level of anesthetic before laryngoscopy is attempted to avoid

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Figure.

The phenotype of a patient with Trisomy 18. (A) Triangular hairy face, frontal bossing, pointed and upturned nose, small mouth.

(B) Low-set ears and micrognathia. (C) Camptodactyly (fisting). (D) Rocker-bottom foot. (E) Omphalocele.

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Table 2. Five Star Approach to the Anesthetic Management of Trisomy 18 Table 2. Five Star Approach to the Anesthetic Management of Trisomy 18

1. Pre-anesthetic evaluation

Ø Complete examination including cardiac evaluation, airway assessment Ø Multidisciplinary meeting involving surgeon, anesthesiologist, & intensivist to discuss perioperative plan Ø Open and honest discussion with family about the risks, expectations, and treatment plan

2. Logistics Readiness

Ø Complete anesthesia readiness, including immediate availability of difficult airway equipment and emergency vasoactive drugs Ø Pediatric anesthesiologist with experience in difficult airway management and cardiac anesthesia

3. Intraoperative anesthesia management

Ø “Tight” physiological control during anesthetic, including meticulous attention to ventilation and prevention of the pulmonary hypertensive crisis

4. Immediate post-operative management

Ø Post-operative monitoring in intensive care unit and possible ventilatory support.

5. General risk reduction strategy

Ø Employ “one-stop shopping” strategy: performing more than one procedure under one anesthetic to reduce multiple anesthesia procedures

exacerbating pulmonary hypertension.

Muscle rigidity after use of succinylcholine has been reported in these patients.12 However, there is no known risk for malignant hyperthermia in children with Trisomy 18. Brief surgical procedures such as myringotomies can be managed by laryngeal mask airway (LMA).9 Regional nerve block techniques such as an epidural catheter or single shot caudal can be considered for lower abdominal or extremity procedures in combination with general anesthesia. Pain assessment in older patients in the post-operative period can be challenging due to severe mental retardation.

before proceeding with the planned procedure is imperative. Careful anesthetic management, especially airway management and avoiding a pulmonary hypertensive crisis, is critical. Avoiding multiple procedures and anesthetics may be helpful. n Acknowledgment We would like to thank Khalid Altirkawi, MD, FAAP for giving us permission to use his pictures for the figure.

References 1. Baum VC, O’Flaherty JE. Anesthesia for Genetic, Metabolic, and Dysmorphic Syndromes of Childhood. Third edition. Philadelphia: Wolters Kluwer; 2015.

2. Cereda A, Carey JC. The trisomy 18 syndrome. Orphanet J Rare Dis. 2012;7:81.

3. Meyer RE, Liu G, Gilboa SM, et al. Survival of children with trisomy 13 and trisomy 18: A multi-state population-based study. Am J Med Genet A. 2016 Apr;170A(4):825-37.

4. Banka S, Metcalfe K, Clayton-Smith J. Trisomy 18 mosaicism: report of two cases.

World J Pediatr. 2013;9(2):179-181.

5. Kosho T, Nakamura T, Kawame H, Baba A, Tamura M, Fukushima Y. Neonatal management of trisomy 18: clinical details of 24 patients receiving intensive treatment. Am J Med Genet A. 2006;140(9):937-944.

6. Batees H, Altirkawi KA. Trisomy 18 syndrome: Towards a balanced approach.

Sudan J Paediatr. 2014;14(2):76-84.

7. Boss RD, Holmes KW, Althaus J, Rushton CH, McNee H, McNee T. Trisomy 18 and complex congenital heart disease: seeking the threshold benefit. Pediatrics.

2013;132(1):161-165.

8. Courreges P, Nieuviarts R, Lecoutre D. Anaesthetic management for Edward’s syndrome. Paediatr Anaesth. 2003;13(3):267-269.

9. Bailey C, Chung R. Use of the laryngeal mask airway in a patient with Edward’s syndrome. Anaesthesia. 1992;47(8):713.

10. Miller C, Mayhew JF. Edward’s syndrome (trisomy 18). Paediatr Anaesth.

1998;8(5):441-442.

11. Friesen RH, Twite MD, Nichols CS, et al. Hemodynamic response to ketamine in children with pulmonary hypertension. Paediatr Anaesth. 2016;26(1):102-108.

12. Matsuda H, Kaseno S, Gotoh Y, Furukawa K, Imanaka K. Muscle rigidity caused by succinylcholine in Edwards’ syndrome. Masui. 1983;32(1):125-128.

Author Information

Assistant professor, Department of Anesthesiology, Texas Tech University Health Sciences Center, Lubbock, TX (Fishkin). Associate professor, Department of Anesthesiology, Levine Children's Hospital, Charlotte, NC (Sathyamoorthy). CRNA, Conclusion 8 Department of Anesthesiology, University of Mississippi Medical Center, Jackson, MS (Wardlaw). Professor, Department of Otolaryngology and Communicative Sciences, We propose several strategies for safe perioperative management University of Mississippi Medical Center, Jackson, MS (Reed). The authors report no of these patients. These patients should undergo a thorough pre- financial disclosures or conflict of interest.

anesthetic evaluation and be managed by a pediatric anesthesiologist with experience in managing the difficult airway and cardiac anesthesia.

Detailed discussion with the family about treatment options and risks

Corresponding Author: Semyon Fishkin, MD; Department of Anesthesiology, Texas Tech University Health Sciences Center, 3601 4th Street, STOP 8182, Lubbock, TX 79430. Ph: (806) 743-2981 (semyonfishkin@gmail.com).

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Dr. Michael Mansour (second from left) takes the oath of office while his wife Kathleen, who is also a cardiologist, holds the Bible. Left, Immediate Past President Dr. William Grantham. Board chair Dr. J. Clay Hays, Jr. (right) was elected President-elect.

MSMA Past Presidents line up in support of MSMA’s newest president, Michael Mansour, MD.

“ It is time for physicians to lead the conversation regarding healthcare spending and delivery. It is time for physicians to protect the interest of patients in this battle to control cost. It is time for physicians to promote population health management and prevention.”

– MSMA President Michael Mansour, MD

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P R E S I D E N T ’ S

P A G E

Inaugural Address of the 151st President of MSMA

Michael Mansour, MD, FACP, FACC August 17, 2018 Old Capitol Inn, Jackson

• Groundbreaking surgical and medical treatments have been pioneered here and have resulted in successful kidney, heart, lung, and liver transplants.

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onight I want to give you an overview of healthcare and the practice of medicine in Mississippi over more than 150 years; where we have been, where we are now and where and why we will be going over the next ten 10 to 20 years.

Our colleagues in years past overcame the challenges of cholera, typhoid, tuberculosis, and the influenza pandemic. They saw the rise of the antibiotic era with the discovery of penicillin in 1919 and the polio vaccine with its first use in 1955. The control of infectious diseases has advanced exponentially over the past 150 years.

Nevertheless, even during these great advances in medicine at the same time, in 1921 heart disease became the leading cause of death in the United States. We began the transition from communicable or infectious diseases to non-communicable diseases as the predominant causes of death in the United States.

Despite the pioneering work by many physicians in this state, and around the world, we remain faced with an epidemic of noncommunicable diseases including diabetes, hypertension, obesity, lung disease and even after 100 years, we continue to be plagued by the highest incidence of cardiovascular disease in this country.

Mississippi leads the nation in the incidence of cardiovascular disease and death. Today we have children with adult diseases of hypertension, diabetes, and arthritis due to morbid obesity.

Despite the long-standing ranking as the least healthy state, Mississippi has many bright spots.

Data from the Mississippi State Department of Health show cardiovascular deaths per hundred thousand have decreased more than 19% over a 10-year period with a 25% decrease in African American women.

Many advancements in healthcare have occurred in Mississippi.

• Mississippi is the first State to achieve the trifecta of emergency care with a statewide trauma network, a STEMI network for myocardial infarction, and a statewide stroke network.

Michael Mansour, MD

Today we face a challenge greater than that posed by epidemic illnesses alone. Today our challenge is compounded by the non-sustainable rising cost of healthcare delivery with the national cost equivalent to more than 17% of the Gross Domestic Product.

This non-sustainable financial course has prompted many outside of Medicine to attempt to change this direction. Efforts to control the cost of healthcare have been led by policymakers, economist, and business entities who have wrongly turned to over regulation of healthcare to bend the cost curve.

It is time for physicians to lead the conversation regarding healthcare spending and delivery. It is time for physicians to protect the interest of patients in this battle to control cost. It is time for physicians to promote population health management and prevention.

We must do this because it is the right thing to do. We must do this because it saves lives. We must do this because it saves money.

The burden of non-communicable diseases represents a major public health challenge that undermines the social and economic development in states such as Mississippi with limited resources where large disparities in the total burden of disease persist.

To understand disparities in care, we must understand the determinants of health.

DETERMINANTS OF HEALTH AND WELL BEING: • HEALTHCARE which contributes 10% to overall health • GENETICS contributes 30% to overall health • SOCIAL AND ENVIRONMENTAL FACTORS contribute 20% and • INDIVIDUAL BEHAVIOR contributes 40%.

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Because environmental factors and individual behavior contribute 60% to the health and well-being of individuals, we must broaden our focus and efforts to ensure that these determinants of health do not increase the cost of healthcare.

We thank Dr. Ed Hill, past AMA President and past president of this Association, for his leadership in passage of the Mississippi Healthy Students Act of 2007(MHSA). This Act mandated physical education and also required regulations for child nutrition and defined duties of School Health Councils to oversee these efforts.

Partnering with community organizations and institutions such as schools to address disparities in health may produce lasting results that change the culture contributing to health outcomes.

This idea of creating a culture of health has been promoted and defined by the Mississippi State Health Improvement Plan called UpRoot. UpRoot looks for deep-rooted issues obstructing our efforts to be healthier.

This program seeks to promote a culture of health that begins in our schools, workplaces, and neighborhoods.

The UpRoot program encourages Mississippi work sites to offer employee wellness programs and seeks to increase the percent of School Health Councils in full compliance with the Mississippi Healthy Students Act 2007.

The delivery of healthcare continues to evolve. The physicianpatient relationship has been and will remain the cornerstone of medical care and is essential to the long-term management of chronic disease.

However, to improve cardiovascular health in Mississippi and to address the chronic disease burden we must restructure the way care is organized.

Evidence strongly supports the use of team-based care with protocols for routine disease management. The Hattiesburg Clinic has had great success with this model.

Additionally, telehealth for remote patient monitoring will play an integral role in the future of chronic disease management.

How we practice Preventive Medicine, and Population Health Management will be a major determinant of the future collective health

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and well being of Mississippi.

As physicians, we sometimes find ourselves struggling with these transitions in healthcare. If we are to promote the very best care for our patients, we must lead the conversation and efforts to transform health care in a way that improves access, limits cost, and also decreases illness.

As a profession, we have done a great job of treating illness and prolonging life. Now we must lead in decreasing the incidence of disease so that limited resources can be appropriately used for all to benefit.

The greatest challenge to population health management is that it is of necessity a team endeavor. It will take the best efforts of the medical community and policymakers and the cooperation of the general public to accomplish these goals.

Our imperative to promote health and prevent illness may be the greatest challenge to Medicine in our lifetime. We must move from the science and art of medicine to incorporate the art of engagement, education, and persuasion.

It is apparent that we have many great healthcare leaders in Mississippi taking this issue head-on. The University of Mississippi Medical Center is a national leader with the School of Population Health. We have a vanguard of healthcare innovators around this state seeking to raise Mississippi from the worst to the first in health and economic prosperity.

The Mississippi State Department of Health’s SHIP (State Health Improvement Plan) program is an example of great leadership and thoughtful planning that focuses on addressing Mississippi’s healthcare deficiencies. Perhaps our State will serve as a model to address this predominant global public health challenge of the 21st century.

What can we do in the coming year to answer the challenge of a changing model of health care?

Let me propose five suggestions to those who can lead this transformation of healthcare.

1. Every member of this association can lead in making an impact through education of our families, our communities, and our legislators regarding the importance of prevention as a transformational approach

ABOVE: Dr. Michael Mansour (second from left) with his cardiology friends and guests. Pictured left to right are: Past Chair of the American College of Cardiology Board of Governors Dr. Thad Waites, 2018 ACC Master; Dr. Michael Mansour, 2018-19 MSMA President and Past Chair, ACC Board of Governors; Dr. Andy Miller, Chair of Board of Governors, ACC, Birmingham, and Past President ACC Dr. John G. Harold, who is a Scientific Policy and Advocacy Committee member, World Heart Federation.

OPPOSITE: President Dr. Michael Mansour pins Immediate Past President Dr. William Grantham, a memento of his term as MSMA president.

to controlling the cost of healthcare. I am requesting MSMA provide talking points and PowerPoint slides to any member who wishes to give community talks on Population Health and Prevention.

2. Th is Association can lead by having the Mississippi State Board of Education give biannual updates on the progress of the MHSA 2007 and by allowing this information to be shared with members of this Association, policy makers, and concerned community organizations who are supportive of these efforts.

3. Th e Mississippi Hospital Association can lead by encouraging every hospital to be an example of a healthy work environment by promoting wellness through health screenings, walking spaces in and around the hospital, and healthy choices in hospital cafeterias.

4. O ur Legislature can lead by fully funding the Mississippi Department of Health. To carry out its mission and to improve the health of Mississippi

the MSDH must be fully funded recognizing that small amounts spent on prevention produce major savings compared to the cost of chronic illness.

5. Every citizen of this state can lead by asking their state legislator to pass a Tobacco Tax to discourage non-smokers from starting and to discourage current smokers from continuing. I am asking MSMA to partner with interested parties including the American Heart Association, the American Cancer Society, the American Lung Association to educate the public regarding the importance of passing a tobacco tax to promote wellness and to lower the cost of healthcare delivery.

In conclusion, let me offer this last thought. Partnerships among healthcare providers, the spectrum of government policymakers, and community organizations will be critical to efforts designed to implement programs promoting population health in a way that improves health and lowers the cost of healthcare delivery. n

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Dr. Michael Mansour, the 151st President of the Mississippi State Medical Association, displays the special population health issue of the Journal MSMA, for which he was the guest editor.

Mansour on a Mission: Evolving into a Culture of Health [Each year the Journal interviews the MSMA president to provide members an opportunity to become acquainted with our new leader.

Dr. Michael Mansour, a Greenwood cardiologist, let his voice be heard early when he served as guest editor of the JMSMA's special issue on population health. Dr. Mansour offers the following comments to introduce our membership to his goals as president â&#x20AC;&#x201C; Ed.]

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he coming year in medicine promises to continue with rapid changes in the evolution of the delivery of healthcare both in terms of patient care and in terms of administrative guidelines and reimbursements. Healthcare has now moved from the doctor-patient relationship to include regulatory guidelines that seek to direct the care of patients and reimbursements that seek to lower the cost of patient care through more restrictive services. Physicians must lead in this way to demonstrate that more cost-effective measures can be readily implemented in a way that effectively controls the cost of healthcare while improving the health and outcomes of patients and populations through better preventive measures and the promotion

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of wellness. This will take a community and team based effort to reach the greatest number of people and have the greatest chance of changing from a culture of chronic disease and illness that is a tragedy for the individual and a burden for a state with limited financial resources.

The August 2018 issue of the Journal of the Mississippi State Medical Association combined the works of many of the thought leaders and innovators in population health management around the state and nation. This issue of the Journal presented ideas and developing solutions for our state in the fight against what is recognized as a global epidemic of non-communicable diseases such as heart disease, diabetes, hypertension, and obesity.

Mississippi leads the United States in the incidence and deaths from these diseases and perhaps can also lead in solutions that change us to a culture of wellness that will save lives as well as limited resources.

Since this broader scope of health is to a great extent outside the

AT A GLANCE … Michael Mansour, MD, FACC • Board-certified Cardiologist in private practice, Greenville

• Mississippi Chapter of American College of Cardiology – past president

• MD: University of Mississippi School of Medicine, 1984

• American College of Cardiology Board of Governors – past chair

• Residency: Ochsner Foundation Hospital, New Orleans

• American College of Cardiology Board of Trustees – past secretary and member

• Fellowships: University of Florida and Harvard Medical School • Delta Medical Society – past president and current vice president

• MSMA Secretary-Treasurer for two terms, Council on Legislation, past chair

•C ommunity Activities – Scoutmaster, Boy Scouts of America; annually sponsors YMCA Cotton Classic, Delta Center Stage Community Theater; member, St. Joseph Catholic Church, Greenville •M arried to Dr. Kathleen Mansour (who is also a cardiologist), and they have four children.

Drs. Michael and Kathleen Mansour with three of their four children who were able to attend the inauguration.

the social determinants of health including not only social and environmental factors (race, gender, education, housing, environment, jobs, and violence) but also individual behaviors that influence health and outcomes. Partnering with community organizations, government, employers, and institutions such as schools will help to address these issues in a way that may produce lasting results and change the culture contributing to the disparities in health outcomes.

Clearly, better health leads to more productive and happier lives and greater prosperity. The Mississippi State Medical Association

will continue to educate our communities and policy makers on the benefits of population health management and prevention in a way that seeks to fundamentally change our culture to one of wellness and also helps to control the cost of healthcare. n

Michael Mansour, MD President, Mississippi State Medical Association

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M S M A

2018 Annual Session Recap

2018-19 MSMA BOARD OF TRUSTEES - Seated: Joseph D. Austin, MD - Vice Chair, Vicksburg; Katherine G. Pannel, DO, Oxford; PRESIDENT Michael Mansour, MD, Greenville; PRESIDENT-ELECT J. Clay Hays, Jr., MD, Jackson; Standing L to R: John Cross, MD, YPS, Jackson; SPEAKER Geri Lee Weiland, MD, Vicksburg; John F. Pappas, MD, Gulfport; Chelsea Rick, DO, Resident/Fellow, Fulton; Brett C. Lampton, MD, Oxford; Avani K. Patel, Medical Student, Jackson; Roderick C. Givens, MD, Greenwood; PAST PRESIDENT William M. Grantham, MD, Clinton; SECRETARYTREASURER W. Mark Horne, MD; Laurel; Jennifer J. Bryan, MD, Chair, Jackson; Steven W. Stogner, MD, Secretary, Hattiesburg. Not pictured: J. Lee Valentine, DO, Meridian; Loretta Jackson-Williams, MD, Jackson.

Board of Trustees Dr. Clay Hays (cardiology, Jackson) was voted in as President-elect, in line to take the reins in 2019. The elections were part of MSMA’s 150th Annual Session held August 17-18 at the Westin in Jackson. Dr. Katherine Pannel (psychiatry, Oxford) was elected to represent the northeastern district on the Board of Trustees. Dr. Roderick Givens (radiation oncology, Greenville) was elected to a three-year term representing the Delta district on the Board. Dr. Chelsea Rick (family practice, Tupelo) and Avni Patel were each re-elected to a second one-year term representing residents and students, respectively. The 17-member Board of Trustees elected Dr. Jennifer Bryan (family practice, Flowood) as Chair of the Board, Dr. Joseph Austin (obgyn, Vicksburg) was elected Vice Chair, and Dr. Steven Stogner (pulmonary medicine, Hattiesburg) was elected Secretary of the Board.

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Legislation, Resident Brock Banks Legislation, Student William Buck Medical Education, District 6 Eric Hale Medical Education, District 7 Deidri Ivory Medical Education, District 8 Angela Wingfield Medical Service, District 6 Thomas Dobbs Medical Service, District 7 Carlos Latorre Medical Service, District 8 Erin Dewitt Medical Service, Resident David Green Medical Service, Student Kandice Bailey JOURNAL MSMA Associate Editor Stanley Hartness MSMA ALLIANCE OFFICERS FOR 2018-2019 President: Bo Zimmerman President Elect: Teresa Floyd Secretary: Carol Reeves Treasurer: Angela Abraham Ladner Vice President of Legislation: Nancy Strahan Smith Vice President of Membership: Olivia G White Vice President of Scholarship: Sondra Franks Pinson Vice President of Health: Lauren Reed — with Karen Redd Morris and Donna Stovall Johnson Witty.

Award Recipients Dr. Jennifer Bryan practices family medicine in the Jackson area.

Dr. Amber Colville practices internal medicine on the Gulf Coast.

Dr. Katherine Pannel practices geriatric psychiatry and psychiatry in the Oxford area. In addition to practicing and caring for their patients, these doctors have put their love of advocacy to work in amazingly effective ways.

MSMA Community Service Award recipients – William Grantham, MD with recipients Amber Colville, MD; Katherine Pannell, DO and Jennifer Bryan, MD. The Community Service Award honors members of the Association who have actively engaged in the practice of medicine and have rendered service “above and beyond the call of duty” for the betterment of the community and the state.

The group started Physicians for Mississippians on Facebook. A private forum for sharing insights, ideas and news on advocacy, Physicians for Mississippians now has more than 1,000 members and is active on a variety of subjects every day.

Through this Facebook group, Drs. Bryan, Colville and Pannel have created, nurtured and cultivated a vibrant community of working physicians to share experiences, explore the politics of practice and leverage participation in organized medicine.

President’s Medallion Presentation – Past President William Grantham, MD presents the president’s medallion to Michael Mansour, MD during the 150th Inaugural ceremony.

Mr. Bo Zimmerman made history when he was elected president of the MSMA Alliance, becoming the first man to hold this office.

Interestingly, research from a 2018 Kaiser Family Foundation study of Professionally Active Physicians by Gender in Mississippi shows Females (24%) Males (74%). Data includes currently active allopathic physicians (MDs) and osteopathic physicians (DOs).

Then President Dr. William Grantham presided over the Inaugural Ceremony.

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Timothy Quinn, MD received the MSMA Excellence in Wellness Promotion award. His family accepted this award on his behalf.

Excellence in Wellness Promotion Award Dr. Timothy Quinn is a Family Medicine physician in Jackson and a passionate believer in better health through wellness. Working with a diverse population in his practice, Dr. Quinn sees a wide variety of health issues in patients young and old. He has put his words into action by leading regular fitness walks in the park for his patients and the community. Promoting vigor through healthy lifestyle choices including diet, exercise and preventive screening, Dr. Quinn actively volunteers at health fairs and creates screening opportunities throughout the city. He accepted the challenge to develop a pilot project in conjunction with the AMA Diabetes STAT initiative. The aim of the AMAMSMA initiative is to increase awareness of the dangers of pre-diabetes and stress the importance of screening for pre-diabetes; Dr. Quinn championed the Prediabetes Awareness Campaign in Mississippi in 2017 and 2018. As part of the project, Dr. Quinn visited dozens of churches and reached more than 1,010 congregants with the wellness message encouraging screening for pre-diabetes and urging all to make lifestyle changes that can ensure good health. To take the fitness message to younger Mississippians, Dr. Quinn coordinated a pilot program at Jackson’s Murrah High School in 2017-2018 to promote wellness exams for teenagers. The program included an essay contest where students submitted essays on the importance of wellness exams, cited in a concurrent resolution passed by the State Legislature. The program was a success and is now expanding with replication in additional schools.

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2018 STAT Scholars – Left to Right: Bridget Cheng, Brycen Witcher, Shelby Walters, Taryn Ellis, Wesley Youngblood, Jessie Patel, Megan Fasick, Meghan Case, Alexis Witcher, Lateia Taylor (back row), Shanu Moorthy and John Bobo. The Mississippi State Medical Association Student Advocacy Training program was launched in 2015 to recognize the achievements of medical students who are engaged through the Association in advocacy activities supporting organized medicine. To receive this designation the student must complete at least six of twelve coordinated advocacy activities during medical school. With staff guidance, the student learns about topics and participates in activities that compliments the medical training. Each student completes at least six activities such as: write an article for Journal MSMA, attend MSMA’s Annual Session of the House of Delegates or the AMA Medical Student Section meeting, visit the State Capitol during the legislative session, attend a meeting of the Mississippi State Board of Medical Licensure, join an MSMA legislative update conference call or attend a local medical society activity.

The 2018 Doctors of Distinction – MSMA Physician Leadership Academy Class of 2018 Graduates.

Left to Right: Christy Vowell, DO; Michelle Owens, MD; Shawn McKinney, MD; C. Latoya Mason, MD; Lori Marshall, MD; Tamara Glenn, MD; Corey Jackson, MD; Dedri Ivory, MD; Roderick Givens, MD; Renia Dotson, MD, MPH and John Vanderloo, MD. The MSMA Physician Leadership Academy offers physicians the concepts, tools, and confidence they need to address the daily challenges physicians face. Thus, the graduates of this program are bestowed the Doctor of Distinction Award.

The MSMA Foundation recognizes that the most successful physicians will need to learn about business topics not taught in medical school. Some of these are the skills to influence the medical environment, ways to lead multi-disciplinary teams collaboratively, when and how to advance ideas using communications and media, how regulators affect the practice and ways to convincingly voice the physician’s position with public officials.

Medical students were widespread in attendance at annual session, with 30 UMC and 21 William Carey College of Osteopathic Medicine students registered and 8 resident delegate slots filled. Seen here enjoying the 150th Inaugural Gala are, left to right, WCUCOM students Michael Dillenkofer, George Wilson, Avani Patel (UMC-SOM), Mary Claire Buck (wife), William Buck, William Crim, Lev Shpits, and Amar Patel.

Waites Award Dr. John L. Cross is an Internal Medicine specialist in at Mississippi Baptist Health Systems in Jackson. He graduated cum laude from Mississippi State University with a B.S. in biological engineering. He earned his medical degree at the University of Mississippi School of Medicine in 2006 and served his Internal Medicine residency at UMMC from 2006 to 2009. In addition to his work with Baptist Health Systems, Dr. Cross has worked with University Physicians and the G.V. “Sonny” Montgomery Medical Center.

Dr. John L. Cross (right), recipient of the Dr. James C. Waites Leadership Award at the 150th Inaugural Gala, with Dr. William Grantham (left). The award honors the many contributions of Dr. Waites to his community and to organized medicine by recognizing a physician under the age of 50 who is an outstanding leader in organized medicine and community affairs.

Dr. Cross was a graduate of MSMA’s Physician Leadership Academy in 2015. He was President of Central Medical Society in 2016 and has been a member of MSMA and the AMA since 2002. He is an active participant in organized medicine in the state as a member of Central Medical Society and as the Young Physician Society representative on the MSMA Board of Trustees. Dr. Cross and his wife have three children.

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Grammy recording artist Cassandra Wilson entertained Gala guests with her repertoire of American jazz. Born and reared in Jackson, the vocalist, songwriter, and producer resides in a Sugar Hill (Manhattan) apartment that had periodically belonged to Count Basie, Lena Horne and boxing legend Joe Louis.

Honors Day Awards Additional awards given by MSMA were presented at the University of Mississippi School of Medicine 2018 Honors Day program held May 4, 2018.

• Carl Gustav Evers, MD Award – This award is named for former MSMA President and UMMC Associate Dean of Academic Affairs and is given to medical students who excel in MSMA and AMA activities.

Mary Elizabeth Butts Avani Kishor Patel William Madison Ross

Renowned blues guitarist and singer Jesse Robinson, from Jackson, performed with Raphael Semmes & Friends Jazz Ensemble. Robinson played with Little Milton Campbell from 1979 to 1981 and then led the band for Bobby Rush from 1981 to 1986. He is now known as the front man for the B.B. King’s Blues Band.

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• V irginia Stansel Tolbert, MD Award – Awarded to medical students who have demonstrated superior scholarship and leadership in campus activities.

Kandice Canise Bailey Andrew Stevens Desrosiers Logan Harrison Ramsey Lauren Marie Seal • Wallace Conerly, MD Award – Given to medical students who exemplify the leadership qualities of the former Vice-Chancellor and Dean of the School of Medicine.

Ann Marie Mercier

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M S M A

2018 Annual Session Resolutions Summaries of the resolutions are below: Medical Coverage Expansion MSMA will solicit ideas from physicians across the state on ways to provide medical coverage for the underinsured and uninsured using a survey to include objective inquiry concerning Medicaid expansion as a possible solution and report to the House of Delegates in 2019.

Study of Medical Marijuana The Board of Trustees will form a study committee or assign an existing committee to survey available research on medical marijuana and report back to the House of Delegates in 2019. The committee will look at the ramifications for physicians who recommend/certify its use.

Mobile App for Mississippi Prescription Drug Monitoring Program MSMA will work with the Board of Pharmacy to create a mobile app for the Prescription Monitoring Program.

Standards for the Independent Practice of Medicine MSMA will lead a state Scope of Practice Partnership to promote physicians as leaders of the health care team and to strengthen collaboration between physicians and other members of the team.

Public Awareness to Combat Scope of Practice Infringements Directs MSMA to work with state and national specialty societies on a public awareness campaign promoting physician-led, team-based care.

Building Mid-level Provider Allies Recommends MSMA seek allies on the health care team who don’t seek independent practice and survey those who work with a physician on-site and support the physician-led team.

Cigarette User Fee MSMA will make increasing the tobacco tax a priority to improve public health, offset the costs of smoking-related disease and direct additional revenue to Medicaid.

Access to Mental Health Treatment for Incarcerated Individuals The Association will work with the Mississippi Psychiatry Association

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to require the Department of Corrections to work with Medicaid on enrolling inmates. Also, MSMA will encourage law enforcement to use mental health screening tools for inmates.

Enforcing Trump Regulation Rules to Bloated Medical System The Board of Trustees will study the possibility of extending to the healthcare sector Pres. Trump’s executive order to reduce federal regulations.

Promotion of Healthy Hospital Work Environments The Association will work with the Mississippi Hospital Association to promote healthy work environments, healthy food choices and health screenings in hospitals and in the communities they serve.

Promotion of Healthy School Environments MSMA will work to ensure MDE is complying with the Mississippi Healthy Students Act and its reporting requirements.

Support Increased Physician Workforce in Mississippi Supports adequate funding for the Office of Mississippi Physician Workforce to develop more residency slots.

Two-Year Mississippi Medical License MSMA will explore with the State Board of Medical Licensure the possibility of a two-year medical license for Mississippi physicians.

Survival of Rural Hospitals; and Rural Physician and Patient Access to Hospital Services Critical for State MSMA will communicate to state leaders the importance of rural hospitals and encourage state leaders to find solutions to the rural health care crisis.

Licensing of Genetic Counselors in Mississippi MSMA supports licensing of genetic counselors, and a licensed genetic counselor must be supervised by a collaborating physician medical geneticist.

Physician Non-Compete Agreements The Board of Trustees will consider ways to educate physicians on contracts and seek a legislative policy statement opposing restrictive covenants.

M S M A

2018 Annual Session Resolutions Psychiatric Question by the Mississippi State Board of Medical Licensure MSMA will work with the State Board of Medical Licensure to update reportable conditions on licensure applications so that questions about mental health care consider impairment, not just treatment.

communicate value and increase membership.

Journal of the Mississippi State Medical Association Celebrates 60th Anniversary Recognizes the 60 years of the Journal MSMA and commends the editors for their dedication.

Improving Funding at Department of Health MSMA will work not only for full funding of the Department of Health but also increased funding to address serious matters of population health.

Commending the Career of Charles M. Dunn, III Expresses appreciation for the work of Chuck Dunn of Medical Assurance Company of Mississippi.

Maximizing Medicaid to Improve Health Care in Mississippi MSMA will ask the Medicaid Medical Care Advisory Committee to ask Medicaid to explore creative ways to improve the program that other states have employed.

Health Plan Survey The Association will survey members annually on insurance company policies and claims denial rates to help members make decisions on participation with insurance companies.

Promotion of MSMA via Social Media Resolves that MSMA will enhance its social media marketing to

Increasing Membership Dues MSMA membership will increase to $515 starting in 2019.

PHYSICIANS NEEDED Internists, Cardiologists, Ophthalmologists, Pediatricians, Orthopedists, Neurologists, Psychiatrists, etc. interested in performing consultative evaluations according to Social Security guidelines.

OR Physicians to review Social Security disability claims at the

Mississippi Department of Rehabilitation Services (MDRS) in Madison MS.

Contact us at: Gwendolyn Williams 601- 853-5449

DISABILITY DETERMINATION SERVICES 1-800-962-2230

OCTOBER • JOURNAL MSMA

483

L E T T E R S

Hand Referral System Averts Risk Dr. Cross has recently published in this journal a case report of conservative management of a ring avulsion injury of a ring finger.

The management included preservation of the ring at the site of injury [Cross B. To cut or not to cut: Is waiting the best solution to many of medicine’s problems? J Miss Med Assoc. 2018;59:305].1 While conscientiously undertaken and finally successful, this course of observation is generally very risky. Ring avulsions are a well-studied category of injury. Such injuries fall into two broad categories: injuries with intact or adequate circulation, and injuries with interrupted venous and/or arterial circulation and various degrees of tissue disruption.2 Avulsion injuries with intact circulation can heal with minimal problems. It is very important, however, to keep fingers with intact circulation from developing into fingers with compromised circulation. Any fixed constriction can be a site of increasing tissue pressure related to swelling. This swelling can quickly lead to sufficient pressure to create venous occlusions which can cause further pressure increases capable of compressing digital arteries to occlusion. A finger at this stage of compromise will require complicated microsurgical revascularization or amputation.3 Removal of constriction is therefore a high priority in the initial treatment of a ring avulsion injury. Removal of eschar and loose or deferred closure of avulsion laceration are recognized elements of management.4 Certainly, a ring remaining at the site of injury should be removed. It is easier for a jeweler to repair a ring than it is for a hand surgeon to revascularize a finger.

1. Publication Title

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October 1, 2018

Telephone (Include area code)

601.853.6733

P.O. Box 2548, Ridgeland, MS 39157-2548 9. Full Names and Complete Mailing Addresses of Publisher, Editor, and Managing Editor (Do not leave blank) Publisher (Name and complete mailing address)

Mississippi State Medical Association, P.O. Box 2548, Ridgeland, MS 39158-2548 Editor (Name and complete mailing address)

1. Cross B. To cut or not to cut: Is waiting the best solution to many of medicine’s problems? J Miss Med Assoc. 2018;59:305.

2. Kay S, Werntz J, Wolff T. Ring avulsion injuries: Classification and prognosis. J Hand Surg. 1989;14A:204-213.

3. Adani R, Castagnetti C, Busa R, et al. Ring avulsion injuries: Microsurgical management. J Reconstr Microsurg. 1996;12:189-194.

4. Warwick D, Dunn R, Melikyan E, et al (eds). Hand surgery. Oxford: Oxford University Press; 2009:162-163.

5. Mueller M, Zaydfundim V, Sexton K, et al. Lack of emergency hand surgery. Ann Plast Surg. 2012;68:513-517.

6. Whipple L, Kelly T, Aliu O, et al. The crisis of deficiency in emergency coverage for hand and facial trauma. Ann Plast Surg. 2017;79:345-358.

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Mississippi State Medical Association

William C. Lineaweaver, MD Jackson

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Karen A. Evers

408 West Parkway Place, Ridgeland, MS 39157

Access to emergency hand surgery consultation is limited in many parts of this country.5,6 Recognizing this problem, the Burn and Reconstructive Centers of America practice network has developed a hand referral system in parallel with the practice’s burn referral system.7 Throughout the Southeast, practitioners can call 877-8639595 for hand surgery consultation and, if necessary, transfers and referrals for surgical care.

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While the reported case went on to an uncomplicated resolution, the reported management should not be considered as a standard or a reasonable option.

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484 VOL. 59 • NO. 10 • 2018

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OCTOBER â&#x20AC;¢ JOURNAL MSMA

485

NATIONAL HEART, LUNG, AND BLOOD INSTITUTE OF THE NATIONAL INSTITUTES OF HEALTH

Landmark Jackson Heart Study Renewed for Six More Years The National Heart, Lung, and Blood Institute of the National Institutes of Health has renewed its support of the Jackson Heart Study, expanding the program’s ability to make discoveries about cardiovascular health, translate these findings for the community and train the next generation of biomedical scientists.

The JHS is the largest long-term study of cardiovascular health in a closed, defined group of African-Americans. Since 1998, the JHS has studied more than 5,300 people from the Jackson metropolitan area. Investigators at the University of Mississippi Medical Center, Jackson State University, Tougaloo College and the Mississippi State Department of Health received official notification of the six-year extension August 13.

“The funding is new but the JHS goal remains the same: to figure out what factors can cause and prevent heart disease in African-Americans.

[The partner institutions] will keep working together in the JHS. But the JHS goal can only be reached if you keep participating,” Dr. Adolfo Correa, director of the JHS and UMMC professor of medicine wrote in a letter to the cohort members.

According to the Centers for Disease Control and Prevention, heart disease is the leading cause of death for Americans. Among AfricanAmericans, nearly half of adults have some form of cardiovascular disease, and about one in four dies of heart disease.

“With this new funding, we will do many of the same activities,” Correa said, such as conducting annual follow-up with participants about their health and hosting community events to share study findings.

The first year of funding awards the Jackson Heart Study nearly $8 million. The renewed funding, which will support the study until August 2024, also allows for several new components.

“We are delighted that there will be a new Jackson Heart Study Exam 4 during 2020-2022,” he said.

Like its predecessors, this exam will add to the extensive longitudinal data on cardiovascular disease risk factors, socioeconomic and sociocultural factors, imaging studies and biological samples. Results from the JHS have been published in the Journal of the American Medical Association-Cardiology, Journal of the American Heart Association and Science Translational Medicine, among others.

At UMMC, the NHLBI funding supports the JHS coordinating and field centers which conduct research studies and maintain contact with the JHS cohort.

486 VOL. 59 • NO. 10 • 2018

Dr. Adolfo Correa is director of the Jackson Heart Study.

Dr. Correa and JHS researchers hope that the next phase will also include a component on the relationship between heart health and brain health.

The JHS also gains a new Graduate Training and Education Center at UMMC for students interested in cardiovascular epidemiology and related biomedical research. Led by Dr. Bettina Beech, dean of the School of Population Health, it joins the existing centers for graduate students at JSU and high school and undergraduate students at Tougaloo.

The GTEC at UMMC will provide training in cardiovascular health from a population health perspective to graduate students enrolled in health-, STEM-, or social science-related doctoral and health professional programs at Mississippi colleges and universities.

“Our program is designed to provide students with diverse hands-on experiences in cardiovascular epidemiology, cardiovascular health, minority health and health disparities to encourage them to pursue careers in biomedical science,” Beech said. “We have assembled a team of investigators who are committed to training the next generation of scientists and are senior faculty at the nation’s leading universities in health science including UCLA, Johns Hopkins, University of TexasSouthwestern and Vanderbilt University.”

“The Graduate Training and Education Center provides training in cardiovascular epidemiology that enhances the professional skills of graduate students that will allow them to contribute to the workforce in biomedical sciences and public health,” said Dr. Marinelle

The Jackson Heart Study has been renewed. Since 1998, the NIH-funded project has enabled researchers at UMMC, Jackson State University and Tougaloo College to study cardiovascular health and disease in African-Americans. The study includes physical exams, like the one shown here from 2012 where Dr. Ervin Fox, professor of medicine, monitors as Shari Cook, foreground, and Audrey Samuels, center, take readings from a participant.

Payton, principal investigator of the JSU graduate center.

“Also, this opportunity adds value to scholars’ practical experience in health research to prepare them for careers in biomedical sciences and professions that will greatly impact the Jackson Heart Study community,” said Payton, chair of the department of epidemiology and biostatistics in the School of Public Health at JSU.

Beech

White

“We will promote cardiovascular health in the targeted communities surrounding the Jackson area. These include Madison, Rankin and Hinds counties. However, we will extend our work statewide,” said Dr. Victor Sutton, director of the JHS community center and the Office of Preventive Health at MSDH. “Our team will educate our communities and implement evidence-based activities to support optimal health. We look forward to sharing our work across all centers throughout the nation.”

Outside of the Jackson metropolitan area, the JHS maintains relationships with multiple universities serving as Vanguard Centers and makes its data accessible for ancillary studies.

Dr. Wendy White of Tougaloo College said that thanks to the support of the NHLBI, nearly 200 students have gone through the undergraduate training program, more than half of whom went on to pursue graduate and professional degrees in health-related sciences.

Payton

“The Jackson Heart Study is so important for the community and our students,” said White, principal investigator of the undergraduate center. “It’s profound what we have accomplished. To say that we have been going strong for nearly 20 years speaks to how [the NHLBI] holds us in high regard.”

This year the Mississippi State Department of Health joins the JHS and will manage the new Community Engagement Center.

NHLBI Jackson Heart Study project officer Cheryl Nelson wrote in a letter to participants, Sutton “Your involvement in the study over the past nearly 20 years has helped to advance our knowledge and direction of medical research in this critical area – and, we believe, is saving lives.”

The JHS is funded by the NHLBI and the National Institute on Minority Health and Health Disparities of the National Institutes of Health. n

– UMMC Division of Public Affairs

OCTOBER • JOURNAL MSMA

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C O M M E N T A R Y

Why Marijuana Will Not Fix the Opioid Epidemic Currently, there is no widely available or accepted medical literature showing any benefit for pain with dispensary cannabis in common pain conditions.

Marijuana has been used for reported medical purposes for thousands of years when the plant at that time had THC content of 0.5-3%.

Currently, the most common reported medical use is for pain. As of this writing, 30 states and the District of Columbia have some form of legalized marijuana, with eight states having legalized it for recreational use.

The United States is currently in the grips of an opioid epidemic which has been growing over the last 20 years and began with “pain” being termed the “5th vital sign.” At the time, it was reported that people in pain did not become addicted to opioids, and the number of opioid prescriptions started to increase over time, followed by an increase in 1 opioid overdose deaths.

There has been a lot of discussion about how the use of cannabis 2 will help curb the opioid epidemic. It has been reported that medical cannabis laws are associated with significantly lower opioid overdose mortality rates, and others have suggested that legalization 3 may result in less opioid overdose deaths. Other studies reported medical marijuana laws were associated with a decrease in Medicare 4 prescriptions, saving millions of dollars. The same authors in a later report suggested that medical cannabis laws are associated with significant reductions in opioid prescribing in the Medicare 5 Part D population. Cost savings in this day and age of healthcare is very important, but it was noted that “the researchers themselves cannot say if people switched from opioid prescriptions to using a medical marijuana product.” It is difficult to translate population-level analyses to individual marijuana- opioid substitutions, and this patient population is a rather small percentage of people who may be using opioids and/or medical marijuana. In 2017, Colorado had a record number of opioid overdose deaths from any opioid, including heroin, 6 and Colorado has had a medical marijuana program since 2001.

In the face of the opioid crisis, medical providers should utilize other ways for people to avoid the use of opioids. Treatments such as physical therapy, acupuncture, chiropractic, massage, and cognitive- behavioral therapies are some of the standard treatments in the management of people with pain. Other naturopathic remedies have been suggested 7 and tried but not proven.

There is some evidence that there are components of the marijuana 8 plant which may have therapeutic medical value. Cannabinoid and opioid receptors belong to the rhodopsin subfamily of G-protein-

488 VOL. 59 • NO. 10 • 2018

KENNETH FINN, MD Springs Rehabilitation, PC Board Certified in Physical Medicine and Rehabilitation and Pain Management and Medicine

9

coupled receptors and are synergistic. Both are localized primarily at the presynaptic terminals and, when activated, reduce cellular levels of cyclic adenosine monophosphate (cAMP) by inhibition of adenylyl cyclase, which effects neurotransmission. Receptor activation of both also modifies the permeability of sodium, potassium, and calcium channels, and receptors of both systems coexist in the central nervous system, with overlapping distribution in the brain, brainstem, and 10 spinal cord. Both receptors co-localize on GABA-ergic neurons with potential coupling to second messenger systems, and receptor stimulation can suppress inhibition, suppress excitation, as well as inhibit the release of several neurotransmitters, including L-glutamate, GABA, norepinephrine, serotonin, dopamine, and acetylcholine, therefore modulating pain pathways and potentially providing antinociception. Opioids and cannabinoids share pharmacologic profiles, and both can cause sedation, hypotension, hypothermia, decreased intestinal motility, drug-reward enforcement, and antinociception.

There are several reasons as to why any reported benefit will be outstripped by lack of benefit and increased risk of harm, and why cannabis is contributing to ongoing opioid use and, subsequently, the opioid epidemic. There is evidence in animal models showing adolescent rats exposed to THC will develop enhanced heroin 11 self-administration as adults which may be due to activation of mesolimbic transmission of dopamine by a common mu opioid 11,12 receptor mechanism. More than 90% of heroin users report a prior history of marijuana use compared to a prior history of painkiller use 13 (47%). Prospective twin studies demonstrated that early cannabis 14 use was associated with an increased risk of other drug abuse. This particular study was conducted when the THC content was much lower than today’s products which can reach 95% THC. The currently accepted body of evidence supporting use of cannabis in pain consists of 28 studies comprised of 63 reports and 2,454 15 patients. Additional articles relying on this primary paper are misleading, stating that “there is substantial evidence that cannabis is

16

an effective treatment for chronic pain in adults.” Both articles noted that products typically studied are not available in the United States (nabiximols, Sativex) or were with available synthetic agents (dronabinol, nabilone) and were studied in less common pain conditions: neuropathic and cancer pain.

Currently, there is no widely available or accepted medical literature showing any benefit for pain with dispensary cannabis in common pain 17 conditions. Dispensary cannabis is a generic substance containing multiple components which may have physiologic activity in the body. The College of Family Physicians of Canada outlined potential 18 prescribing guidelines of medical cannabinoids in primary care.

They strongly recommended against use for acute pain, headache, osteoarthritis, and back pain, and also discouraged smoking.

There is currently a large and growing body of evidence showing that cannabis use increases rather than decreases non-medical prescription opioid use and opioid use disorder, based on followup of more than 19 33,000 people. Concurrent use of cannabis and opioids by patients with 20 chronic pain appears to indicate a higher risk of opioid misuse. Closer monitoring for opioid- related aberrant behaviors is indicated in this group of patients and suggests that cannabis use is a predictor of aberrant drug behaviors in patients receiving chronic opioid therapy.

Inhaled cannabis in patients with chronic low back pain does not reduce overall opioid use, and those patients are more likely to meet the criteria for substance abuse disorders and to be non-adherent with 21 their prescription opioids. Findings show patients with chronic pain participating in an interdisciplinary pain rehabilitation program using cannabis may be at higher risk for substance-related negative outcomes and more likely to report a history of an illicit substance, alcohol, and 22 tobacco use. A more recent study of 57,000 people showed that medical marijuana users are more likely to use prescription drugs medically and non-medically, and including pain relievers, stimulants, tranquilizers, and 23 sedatives. There is also evidence that state medical marijuana laws lead 24 to the probability people will make Social Security Disability claims.

There is sufficient and expanding evidence demonstrating that medical marijuana use will not curb the opioid epidemic. There is further evidence that marijuana is a companion drug rather than a substitution drug and that marijuana use may be contributing to the opioid epidemic rather than improving it. Although there are patients who have successfully weaned off of their opioids and use marijuana instead, the evidence that marijuana will replace opioids is simply not there. Medical provider and patient awareness, utilization of prescription drug monitoring programs, widespread availability and use of naloxone, and increasing coverage for atypical opioids and abuse deterrent formulations are only some of the other factors hopefully contributing to any impact on the opioid crisis.

Education and prevention efforts, as well as medication-assisted therapies, will be additional benefits to impact the opioid epidemic. Physicians should continue to monitor their patients closely, perform random drug testing to detect opioid misuse or aberrant behavior, and intervene early

with alternative therapies when possible. Marijuana alone is certainly not the answer. n Kenneth Finn, MD, is with Springs Rehabilitation, PC, Colorado Springs, Colorado. He is Board Certified in Physical Medicine and Rehabilitation and Pain Management and Medicine.

Contact: kfinn@springsrehab.net References 1. National Institute of Drug Abuse, Overdose Death Rates, Revised September 2017.

2. Bachhuber MA. Medical cannabislaws and opioid analgesic overdose mortality in the United States, 1999-2010 JAMA Intern Med. 2014; 174(10):1668-1673.

3. Livingston, M. Recreational cannabis legalization and opioid-related deaths in Colorado, 2000–2015; Am J of Pub Health; 2017; 107(11): 1827-1829.

4. Bradford, AC. Medical marijuana laws reduce prescription medication use in Medicare Part D; Health Aff (Millwood). 2016; 35:1230-1236.

5. Bradford, AC. Association between US state medical cannabis laws and opioid prescribing in the Medicare Part D population. JAMA Intern Med. 2018;178(5):667672.

6. Colorado Department of Public Health and Environment, Vital Statistics Program.

7. Soeken, KL. Selected CAM therapies for arthritis-related pain: the evidence from systematic reviews. Clin J Pain. 2004 Jan-Feb; 20(1); 13-18.

8. Whiting, PF. Cannabinoids for medical use: A systematic review and meta- analysis.

JAMA. 2015; 313(24); 2456-2473.

9. Robledo, P. Advances in the field of cannabinoid--opioid cross-talk. Addict Biol. 2008; 13:213-224.

10. Scavone JL. Cannabinoid and opioid interactions: implications for opiate dependence and withdrawal. Neuroscience. 2013; 284: 637-654.

11. Pickel VM; Chan J, Kash TL, et al. Compartment-specificlocalization of cannabinoid 1 (CB1) and mu opioid receptors in rat nucleus accumbens. Neuroscience. 2004; 127:101–112.

12. Tanda G. Cannabinoid and heroin activation of mesolimbic dopamine transmission by a common µ opioid receptor mechanism. Science. 1997; Jun 27; 276(5321):2048-50.

13. National Survey of Drug Use and Health, 2013 & 2014.

14. Lynskey MT. Early onset cannabis use and progression to other drug use in a sample of Dutch twins. Behav Genet. 2006; 36(2):195-200.

15. W hiting, PF. Cannabinoids for medical use: A systematic review and meta- analysis.

JAMA. 2015; 313(24):2456-2473.

16. National Academies of Sciences, Engineering, and Medicine. The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research. Washington, DC: The National Academies Press 2017. https://doi. org/10.17226/24625.Nugent SM. The Effects of Cannabis Among Adults With Chronic Pain and an Overview of General Harms, A Systematic Review. Ann Intern Med. 2017 Sep 5;167(5):319-331. Epub 2017 Aug 15.

17. Allan GM. Simplified guideline for prescribing medical cannabinoids in primary care.

Can Fam Physician. 2018; 64(2):111-120.

18. Olfson M. Cannabis use and risk of prescription opioid use disorder in the United States.

Am J Psychiatry. 2018; 175(1):47-53.

19. DiBenedetto DJ. The association between cannabis use and aberrantbehaviors during chronic opioid therapy for chronic pain. Pain Med. 2017; 0:1-12.

20. Smaga S. In adults with chronic low back pain, does the use of inhaled cannabis reduce overall opioid use? Evidence-Based Practice. 2017; 20(1),e10.

21. Craner SA. Medical cannabis use among patients with chronic pain in an interdisciplinary pain rehabilitation program: Characterization and treatment outcomes. J Subst Abuse Treat. 2017; 77(6):95-100.

22. Caputi TL. Medical marijuana users are more likely to use prescription drugs medically and nonmedically. J Addict Med. 2018; Jul/Aug;12(4):295-299.

23. National Bureau of Economic Research, February 2018.

Disclosure None reported.

OCTOBER • JOURNAL MSMA

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P H Y S I C I A N ' S

B O O K S H E L F

Philip L. Levin, MD

LAMPTON / EVERS

Images in Mississippi Medicine: A Photographic History of Medicine in Mississippi

Images in Mississippi Medicine MSMA

Lucius “Luke” M. Lampton, MD and Karen A. Evers

Images in Mississippi Medicine: A Photographic History of Medicine in Mississippi; MSMA; Jackson, MS: 2018. $80.00

W

ith a reference to the father of western medicine, Hippocrates, Dr. Luke Lampton and Ms. Karen Evers launch this impressive 266-page coffee-table style expedition into the history of medicine in Mississippi. From Indian tribal techniques through early French colonial physicians onto U.S. territorial regulations, the book explores the path of medicine in our lovely state into the modern age.

Gathering nearly 400 amazing photos, meticulously restored, the book follows the development of the healing arts through the early medical schools, the formation of medical societies, and the founding of regional hospitals. As the book develops, the reader delights in reading the physician biographies, studying the old-time handbills about diseases and quarantines, and delving into the development of

490 VOL. 59 • NO. 10 • 2018

the many medical institutions that formed the foundation of modern Mississippi medical care.

People, places, and things: these make up the substance of our history.

In Images in Mississippi Medicine, the authors pepper the book with a delightful collection of each of these three. Here we read of Dr. William Lattimore, the early 19th-century physician and Congressman who led the creation of, and served on, the first medical licensure board in 1819, which was a rare accomplishment in the United States.

Images include his coat and his elegant signature. Politics of the time come to light as we read of a so-called physician who successfully sued this early board, effectively leaving “the profession in a state of disarray and medical standards in shambles for nearly half a century.”

The biography of Samuel Cartwright, MD, the first president of the Mississippi State Medical Society, reports how his extensive writings on “principal diseases of the Southern states” brought him recognition

IMAGE

AP OF

An old idi words, and the story of medic often can’t con distinctive med influenced by imported disea arduous in the health challeng often-malignan Written b Karen Evers, lo monthly medi A Photographic an extraordina of medicine in latest technolo offers a unique images as well which reveal th history, a large but brilliant m history of the s Over two deca essential to any The story women and th advance their p with fascinatin hospitals and m history of the t of public healt the accomplish

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The books make

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Images in Mississippi Medicine: A Photographic History of Medicine in Mississippi

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This unique collection of rarely seen historic medical images dates from the antebellum period to modern medicine and tells in vivid imagery Mississippi’s important story of the evolution of medicine from horse and buggy days to the current era of high technology and robotic surgery. Also included with the 300-plus images is a comprehensive narrative history of medicine.

Published by the Mississippi State Medical Association (MSMA) under the auspices of the Commemorative Committee for the 150th Anniversary meeting of the MSMA House of Delegates. The work of this Committee is done in honor and memory of Mississippi physicians, without whom this history would not have been possible.

Michael C. Trotter, MD, Chairman Ralph H. Didlake, MD Randy Easterling, MD Hugh A. Gamble, II, MD Bill Grantham, MD Lucius “Luke” Lampton, MD Dwalia S. South, MD J. Martin Tucker, MD Helen Turner, MD, PhD

and handling by

Images in Mississippi Medicine

just in time for the

Karen A. Evers, a native of Jackson, graduated from the University of Mississippi with a B.S. in Journalism and Advertising. Fascinated with graphic design, advertising, publishing and media, she went from Ole Miss to New York City working with such magazines as Better Homes & Gardens, Hippocrates and Health. After 10 years in advertising sales and magazine publishing, she returned home to Mississippi. In 1995, she became managing editor of the Journal of the Mississippi State Medical Association (JMSMA), a position she’s held since, overseeing and coordinating the Journal’s publishing process from content acquisition, writing, editing and production to the printed and online magazine distributed in members’ mailboxes. With her physician editors and the MSMA Committee on Publications, Karen has produced more than 20 bound Journal volumes containing more than 250 issues. She is the recipient of several APEX awards including Best One-Person-Produced Magazine, an Association Trends All-Media Contest Silver Award for Most Improved Magazine, and a Lantern award for a special JMSMA issue “From Doc on Horseback to Managed Care.”

an excellent gift,

LAMPTON / EVERS

Dr. Lucius M. “Luke” Lampton of Magnolia, has served as Editor and Associate Editor of the Journal of the Mississippi State Medical Association for more than two decades, writing thousands of articles on medicine and health care and receiving national awards for excellence in writing and journalism. He also served as Medical Editor of the recently published Mississippi Encyclopedia, authoring multiple entries on the history of medicine in Mississippi. He recently contributed a chapter to America’s leading primary care textbook Conn’s Current Therapy. Dr. Lampton has also served as a member of the Mississippi State Board of Health since 2006 and served as chairman of the Board from 2007-2017. Dr. Lampton specializes in Family Medicine in multiple settings: clinic, hospital, nursing homes, geri-psych, long-term acute care, and hospice. He has been recognized as Mississippi’s “family physician” of the year by the MAFP, alumna of the year by his medical school, professor of the year nominee by his Tulane medical students, and has received national citation for his hospice work.

He serves as Clinical Assistant Professor of Family and Community Medicine at Tulane University School of Medicine, Clinical Instructor in Family Medicine at the University of Mississippi School of Medicine, and as Adjunct Clinical Professor of Family Medicine at William Carey University College of Osteopathic Medicine, Hattiesburg. Dr. Lampton also serves as President of the Foundation of Mississippi History and helped oversee the creation of the Museum of Mississippi History and the Mississippi Civil Rights Museum.

copy today at

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headquarters.

$80.00 ISBN 978-0-692-12459-8

58000>

MSMA

Mississippi State Medical Association 408 West Parkway Place P. O. Box 2548 Ridgeland, MS 39158-2548 www.msmaonline.com

picking up at MSMA

9 780692 124598

as a “specialist in Southern diseases and medicine.” His career in Mississippi was so lucrative, he was able to take his family on an 18-month European tour where he lectured on the inferiority of the “dark-skinned race.”

“Mississippi Institute for the Blind” from the 1920s. These landmark buildings, now all gone, tell of how Mississippi physicians reached out to those suffering from every affliction, determined to bring help to invalids and the medically needy.

The great variety of physicians documented in this book tell tales of the social changes which progressed in our Magnolia state. Felix Underwood’s public health career earned him the title, “The Man Who Saved a Million Lives.” One learns of the research on yellow fever by antebellum physician John Wesley Monette, physician, epidemiologist, author, and historian, one of six physicians in the Mississippi Hall of Fame. Photos of their tombstones decorate biographies, such as of David Phares, MD, naturalist, botanist, and writer. William Henry Holcombe, MD, a homeopath whose treatment of yellow fever was recognized nationally, is also noted. Heroes of medical campaigns tell their stories: Lloyd Tevis Miller, MD, and his fight for AfricanAmerican health access; Dr. B. L. Crawford fighting the White Plague of TB; and Henry Boswell, MD, Mississippi’s “Conqueror of the White Death.”

A kaleidoscope of medical associated items graces the pages of this remarkable book. Hardy’s Invalid Carriage from 1907 was one of the first ambulances in the state. There’s a photo of one of the Board of Health’s 1950s portable chest x-ray machines in a truck parked on a street, encouraging pedestrians roaming the sidewalks to come in and be checked for TB. Posters illustrate Mississippi’s crusades against polio, malaria, and typhoid fever. There’s a photo of a handbill advertising the summer term for the 1904 University of Mississippi School of Medicine across from a photo of the 1904 gross anatomy class.

The history of medical facilities makes for a fascinating read. Tom Franklin Hospital in Columbus, created in 1885, served as the hospital for Mississippi’s first public all-female institution. The 1879 state charity hospital in Vicksburg had 75 beds, with an annex added later for Confederate veterans. A 1904 postcard illustrates the “Jackson Institute for the Deaf and Dumb,” and another postcard the

Santayana said, “Those who cannot remember the past are condemned to repeat it.” Lest we forget, Dr. Lampton and Ms. Evers have brought together this most remarkable photojournalism of the progress of medicine throughout our history. Each page in this spellbinding book brings discovery of a new wonder. At only $80, I urge anyone interested in Mississippi history to urgently order a copy, as only a thousand copies were printed of what is sure to be a collector’s item.

Although it is termed a “Photographic History,” this exemplary book is a full history in every sense of the word. Here is where any study of Mississippi medicine and its history should begin. n

OCTOBER • JOURNAL MSMA

491

M I S S I S S I P P I

S T A T E

D E P A R T M E N T

O F

H E A L T H

Mississippi State Health Officer Retires

T

he end of August, the Mississippi State Department of Health announced the retirement of State Health Officer Dr. Mary Currier, effective November 1, 2018.

needed to continue and further Dr. Currier’s important work. He is a superb choice as our interim State Health Officer,” said Lampton.

Dr. Currier has served in the role of State Health Officer since December 2009, following her time as MSDH State Epidemiologist. With 34 years in government service, Dr. Currier has also worked for MSDH as a staff physician for its prenatal, family planning, STD, and pediatrics programs and as an associate professor at the University of Mississippi Medical Center School of Medicine.

“It has been a privilege to serve in this role for nearly nine years. I have great passion for public health, and I have worked with some of the best people not only in the state but also in the country,” said Dr. Currier. “However, I have three beautiful grandchildren and a wonderful family who need me now. It’s time to pass the baton. I know the field of public health in Mississippi is in great hands.”

Dr. Lucius “Luke” Lampton, MD, FAAFP of Magnolia, Chairman of the Board of Health from 2007-2017 and current Board Member, commented, “Dr. Currier has served our state in an exemplary manner for many decades.

Her leadership even before her most recent role as State Health Officer has been historically important for public health in our state. In 2007, when the reconstituted Board was able to convince him to return as State Health Officer, Dr. Ed Thompson told me, ‘If I return, you will get two for one: Mary is coming with me.’ He recognized her skills and brilliance and knew the department needed her. He certainly was grooming her to be his successor.”

Lampton added, “Her presence at the department with Thompson was critical in restoring the agency to its respected position in the state and nation. Her work as State Health Officer since December 2009 built on Thompson’s accomplishments and, despite the agency’s anemic funding during her almost decade as State Health Officer, she has overseen the modern restructuring of the department in a manner which maintained its scientific competence and its position as the guardian of Mississippi’s public health. Having led the agency to national accreditation status in 2017, she leaves the department both in good shape and in good hands. She will be missed by the agency not only for her skills as a medical leader and public health champion, but also for her personal integrity, bravery, kindness, and empathy for employees and the citizens of the state. She created a culture of civility at the agency during her tenure there.”

Deputy State Health Officer and former State Epidemiologist Dr. Thomas Dobbs will serve as Interim State Health Officer once Dr. Currier retires.

“I was fortunate enough to work with Dr. Currier for several years in my role as a District Health Officer, and then work in tandem with her when I stepped into the State Epidemiologist role in 2012,” said Dr. Dobbs. “Her knowledge of public health and devotion to the people of Mississippi is unmatched. She will be incredibly missed.”

“Dr. Thomas Dobbs has long impressed both Dr. Currier and the Board.

He is an exceptional physician who possesses the leadership and intellect

492 VOL. 59 • NO. 10 • 2018

Dr. Mary Currier Retiring Mississippi State Health Officer

the Public Health Accreditation Board.

Under Dr. Currier’s leadership, the MSDH has attained numerous accomplishments such as the opening of the state-of-the-art Dr. F.E. “Ed” Thompson State Public Health Laboratory, the organizational transition of the agency from nine public health districts to three regions, and most recently, achieving accreditation from

Board of Health Chairman Dr. Ed D. “Tad” Barham said Dr. Currier’s guidance of the agency for nearly a decade has been both steady and compassionate.

“She’s had to make some tough decisions along the way as the public health arena has dramatically changed in the last several years. I admire her fortitude, and she’s been a great leader of this agency,” said Dr. Barham.

Dr. Dwalia South of Ripley, member of the Board of Health, stated, “Dr. Mary Currier’s departure will leave a void that seems to me almost incomprehensible. She has managed through her most remarkable leadership to hold our State Health Department together during the recent horrible and unforgivable budget cuts to this most important state agency.

The Mississippi State Board of Health is the first line of defense against so many diseases and other health threats to all Mississippians, but it needs to be much more appreciated at a governmental level. I think that the Board’s choice of Dr. Thomas Dobbs is the most wonderful choice for State Health Officer at Mary’s departure. Congratulations go to Dr. Currier for a fantastic job well done, and hopeful prayers for Dr. Dobbs in his new role. I for one hope this interim position becomes a permanent one for him. I can think of no one better qualified to step into Mary’s shoes!”

A graduate of the University of Mississippi School of Medicine, Dr. Currier received her master’s degree and preventive medicine residency training in Public Health from the Johns Hopkins School of Hygiene and Public Health. Currier’s bachelor’s degree is from Rice University, and she also attended Trinity College in Dublin.

Currier is a member of the American Medical Association, the Mississippi Central Medical Society, the Association of State and Territorial Health Officials, the American Public Health Association, and is Board certified in General Preventive Medicine and Public Health. She received the Nathan Davis Award for outstanding government service from the American Medical Association in 2016. n

M I S S I S S I P P I

S T A T E

D E P A R T M E N T

O F

H E A L T H

Mississippi Mississippi Mississippi ProvisionalProvisional Reportable Disease Statistics* Reportable Disease Statistics* Provisional Reportable Disease Statistics February 2018 August 20182018 August *Monthly statistics are provisional. Disease totals may change depending on additional reporting

from healthcare providerstotals and public investigation.

Theseon numbers do not reflect the final case *Monthly statistics are provisional.

Disease mayhealth change depending additional reporting counts. from healthcare providers and public health investigation. These numbers do not reflect the final case Public State counts.

Health District

Public I II III Health District

0

Mycobacterial Diseases

Chlamydia

Extrapulmonary TB

Diphtheria

Enteric Diseases

0

2

0

0

0

0

1

2

7

3

0

0 20

1

0

0

0

0

00

Tetanus

0

0

0

0

2 Measles

7

1

2

0

0

0

0

0

0

0

0

0

0

0

0

00

0 1

0

2 2

0

0

0

0

0

0

0

0

0

0 0 West Nile virus

0

0

0 3

0 06

0

00

0

10

0 0 0

0

0 0

10

0 0

03 00 1 1

0

1

Rocky Mountain spotted fever

10

1

1 0

0

2

0

Lyme disease

0

00

0

Animal Rabies (bats)

0

1

0

Invasive H. influenzae disease

0

0

0

E. coli O157:H7/STEC/HUS

0

0

2

1153 1

0 0

Campylobacteriosis

0

99

00

0

Shigellosis

0

VI

0

00

0 0

603

527

8

12

39

6

46 7

37 56

34 502 95

0

115

1

100

1

0

5 1083 6,211 5,548

304 0

0

893

91 6 220 0

0

42,092 3

60

00

0

53 0

2,545 14,142 44 4512,551 81 24

00

0

0

34

1

0

0

1

3

01 00 0 0

0

00

0

0

0

0

0

1

0

20

0

00

1 1

0

0

2

0 0

1 1 0

0

00

0 0 0

0

0

0

00

3

9

3

0

0

0

0 37

0363 0

3130

5

3

10

0

0

0

0

0

0

0 1

5 2

0

23 0

49 0

0

00

00

2

5

2

1 0

47

5

6

10

5

3

3 2

5

7

40

31

1

0 0

01 00 0 0

0

00

0

2

0 13

2 0

40

0

20

0

1

0

0 0

10

0

Totals include reports from Department of Corrections and those not reported from a specific District.

00

0

30

00

00

8

1

0

40

0

16

33

0

0

13 03 0

0

0

00

0

0204 0

2

0

00

0

34077

1

0

0

0

0

954

0

0

0

02

0

00

1

4

2

1274

2452,842210 859 1,633

00

00

0

1

82

39YTD 50 YTD72 2018 2017

0

3

0

1

00

4 0

2

01

0

0

0

0

0

00

0

0

0

IX

0

1 0

43

35 1,529

0

2

31

23196

00

0

20

60

0

7

13

August 16 2017

685 175

VIII

2 362 133 7

0

0

YTD 2017

4

0

0

YTD 2018

21

4

1

Feb

State 2017 Totals**

0

131

0 0

3

Feb 2018

56

VII

1550 126

0

0

Salmonellosis

Hepatitis B (acute) Zoonotic Diseases

Vaccine Preventable Diseases Enteric Diseases Zoonotic Diseases

03

10

Hepatitis A (acute)

*

38

2840 455 9

Poliomyelitis

Hepatitis A (acute)

0

175

0 0 0 0 Invasive Meningococcal disease

Invasive Meningococcal disease

1

0

0

Tetanus

Mumps

0

0

254 156

Invasive H. influenzae disease

Measles

0

106

2

Pertussis

198

71

Hepatitis B (acute)

0

0 August 4 2018

0

V

71

Mumps

1

1

5

Poliomyelitis

5

3

5

Pertussis

1

22

2

Pulmonary Tuberculosis (TB)

1

1 14

7

Diphtheria

2

5

2175 139 3

HIV Disease

IX

57

0

Mycobacteria Other Than TB

VIII

1

0

95

VII

66

4

Extrapulmonary TB

VI

1

IV

Pulmonary Tuberculosis (TB)

V

69

III

HIV Disease

0

IV

61

II

Early Latent Syphilis Gonorrhea

1

3

I

Gonorrhea Chlamydia

Mycobacteria Other Than TB

**

Early Latent Syphilis

Primary & Secondary Syphilis

Vaccine Preventable Diseases

Mycobacterial Diseases

Sexually Transmitted Diseases

Sexually Transmitted Diseases

Primary & Secondary Syphilis

Totals*

21

0

2910 0

1 10

25

14

0

0

7

0

0

0

38

0

78

3

050 3

6

0

6

0

230 0

0

26 8

1

010

20 75

1

24

2157

1

26 4

0

39 0

0 1 0

2 2

0 7 0

10

33

7

22

6

7

4

3

9

101

145

607

672

Shigellosis

1

2

0

0

14

1

1

3

1

23

13

148

100

Campylobacteriosis

5

8

3

2

12

3

0

6

9

48

44

413

328

E. coli O157:H7/STEC/HUS

0

0

0

0

1

0

0

0

0

1

3

63

17

Animal Rabies (bats)

0

0

0

0

0

0

0

0

0

0

0

0

1

Lyme disease

0

0

0

0

0

0

0

0

0

0

0

2

1

Rocky Mountain spotted fever

0

0

0

2

0

2

1

1

3

9

30

90

138

West Nile virus

0

0

2

1

9

1

1

1

1

16

20

35

49

Salmonellosis

Totals include reports from Department of Corrections and those not reported from a specific District.

OCTOBER â&#x20AC;˘ JOURNAL MSMA

493

P O E T R Y

A N D

M E D I C I N E

Edited by Lucius Lampton, JMSMA Editor

Five words from four letters (A poem for 6th graders) [This month, we print a fun poem by John D. McEachin, MD, FAAP, a Meridian pediatrician and the Journal’s unofficial poet laureate. Of his poem “Five words from four letters,” he writes the editor: “Here is a short little fun ditty I put together for a 6th grade grandson. He, not surprisingly, got 4 of the 5 words. One is a little tougher- based on language and literary exposure. This is fun, relaxing material, for composer and hopefully to reader. It is one way to start your day, particularly for retirees. My routine: Prayer of Thanksgiving for another day. Then, oatmeal, orange juice, Cardizem, Miralax –all while working the daily Crossword. Scan ‘Herman’ and ‘Dennis the Menace,’ then on with day’s activities!” He concludes about the poem: “I simply hope it serves as a little diversion.” For more of Dr. McEachin’s wonderful poetry, see past JMSMAs. To contact the poet, email him at mceachinmd@bellsouth.net. Any physician is invited to submit poems for publication in the Journal either by email at lukelampton@cableone.net or regular mail to the Journal, attention: Dr. Lampton.] — Ed.

The Alphabet contains some friends, Four of which are so very tight, They oft play games of hide and seek, Swapping places to test your sight.

Why not “Musical Chairs” for now!

Use only “O,” “P,” “S,” and “T,” Creating five different words.

Think you can do it? Then, let’s see!

The O and P begin the quad; Q and R are simply left out.

The latter pair at the tail end Are S and T without a doubt.

Well, Doc, put a clock on your trial!

And make this your quiz for the day.

Remember, “O,” “P,” “S,” and “T”— 4 letters, only! Make 5 words!?

Now what’s the deal with these four pals?

Name of the game they like to play?

Call it “Ring Around the Roses,” Or “I’ll Make a Move and You Stay!”

494 VOL. 59 • NO. 10 • 2018

— J ohn D. McEachin, MD Meridian

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