Northeast Florida Medicine - Winter 2009 - Travel Medicine by Duval County Medical Society

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From the Editor’s Desk

Our Greatest Gift and Curse “Mankind’s greatest gift, also its greatest curse, is that we have free choice. We can make our choices built from love or from fear” Dr. Elizabeth Kubler-Ross

During the last presidential campaign, the Obama team presented its initial plan on how to provide affordable, accessible health care to all. As part of their multi-faceted approach to improve health care delivery, one stratagem was the promotion of preventive care. At that time, the President stated, “Preventive care only works if Americans take personal responsibility for their health and make the right decisions in their own lives – if they eat the right foods, stay active, and stop smoking”. Since then, the various proposals and formulations on Capitol Hill have focused on controlling the health care industry alone. None of our elected leaders have touched on the subject of how the individual’s role also needs to be reformed. The only time that personal responsibility is mentioned is in reference to the individual’s mandate to purchase health insurance.Unfortunately, having health insurance coverage doesn’t make one healthy. It’s what one does with that coverage and their personal choices that make a difference. Members of Congress should be as concerned about encouraging individual accountability as they are with extending insurance coverage to those without it. There’s little doubt that the majority of this country’s health care costs are self-inflicted. According to a recent study by the Harvard School of Public Health, hypertension, smoking and obesity cause more than 1 million premature deaths annually, with excessive alcohol, hyperglycemia, and physical inactivity not far behind. Government studies have tagged the annual costs for obesity at $147 billion a year, and smoking costs about $193 billion a year in medical expenses and lost productivity. John W. Kilkenny, III, MD Understandably, cost has been the centerpiece in the reform discussion. From an accounting/ Editor-in-Chief objective standpoint, this is rather straightforward. But address the human/subjective aspects of Northeast Florida Medicine equipoise and we run smack into the age-old debate between individual rights and the ‘common good’ of the group. One contentious topic is to levy a user fee on smokers to pay part of the health insurance costs of their habit. Naturally, the habit patterns of those polled can strongly influence their opinions, e.g., 57 percent favoring higher insurance rates for smokers, but only 36 percent saying the same for those who are overweight, in a country where two-thirds of adults are overweight and 20 percent still smoke. One vexing aspect of this dialogue concerns which health problems are the responsibility of the individual, and which are secondary to wider social problems. There is growing unease about increasing taxes to support government health care programs that support a large number of people who seemingly don’t care about their health until they are confronted with a significant illness. Not only should individuals become more responsible for their own good health, but the community must make it easier for this to happen. There is also legitimate concern about where to ‘draw the line’ over penalizing other preventable risky behaviors. In addition to education about prevention, health care reform also needs to provide viable treatment options for those already overweight, already addicted to substance abuse, etc. A number of pilot studies have tried rewarding healthy behavior as well as withholding benefits for detrimental activity, and most have met limited success. In many instances, the individual may not be in a position to make healthier choices, especially with the pressures of a culture in which bad health behaviors are routinely extolled by the advertising industry. The ‘health profession’ is made up of an entire cross section of our society, leading to our physical reflection of its woes. The number of our colleagues who smoke has plummeted, but would this decrease throughout our society have been so successful without laws enacted against it? Again, reflecting our community in general, many health professionals are notably overweight. How can we influence those we care for if many of us obviously do not follow our own advice? There are so many variables that influence one’s views on personal responsibility. As newer and more successful drugs and procedures cure or ameliorate many of our medical maladies, how do we convince our patients that their own free will can be far more powerful, and many times cheaper, than our prescribed remedies? We can simply start addressing these concerns with our patients in a caring and understanding fashion. Keep in mind that in study after study, the primary reason that most patients give for a continuation of medically risky behavior, is that ‘my doctor has never talked to me about it’. “A pessimist, confronted with two bad choices, chooses both” - Jewish Proverb Editor’s Postscript: Thank You for allowing me to guide the growth of this journal for the last three years and to lend some of my thoughts to this page during that time. I confidently hand over these responsibilities to Dr. Joan Huffman and eagerly look forward to more of her already demonstrated wisdom and grace, as she assumes the duties of Editor-in-Chief. (see insert p.6 for more information on Dr. Huffman.)

2 Vol. 60, No. 4 2009 Northeast Florida Medicine

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Northeast Florida Medicine Vol. 60, No. 4 2009 5

DCMS Special Invitation and News You are cordially invited to attend the 2010 Duval County Medical Society Annual Meeting at Jacksonville Municipal Stadium, Touchdown Club - West One Stadium Place, Jacksonville, Florida 32202 Thursday, January 21, 2010 5:45 - 9:00 pm $45.00 per person 5:45 pm - Exhibitor Hall & Reception/One free drink ticket per person (wine, beer, soda or water) 2nd Annual DCMS Scientiﬁc Poster Session

7:15 pm - Dinner & Annual Business Meeting Installation of John W. Kilkenny, III, MD, as the 123rd President of the DCMS Election of DCMS Oﬃcers & Board Members, FMA Delegates & Alternate Delegates Vote on Amendments to DCMS Bylaws Presentation of 2010 DCMS Alliance Representatives DCMS Award Presentations

RSVP by January 14, 2010. Download a reservation form on dcmsonline.org. Refunds will not be issued if reservation is cancelled four (4) days prior to event.

2010 DCMS Annual Meeting Exhibitor List (As of 11/19/2009)

Platinum Sponsors

Exhibitor Sponsors

FPIC

Florida Doctor Magazine Heartland Rehabilitation Services Heritage Publishing, Inc. Jacksonville Jaguars Jacksonville Mobile Imaging Services Jacksonville Sports Medicine Program JW Custom Homes, Inc. Nova SE University PA Program - JAX Prudential Financial Services Ray Howard & Associates The Bittinger Law Firm

Gold Sponsors Baptist Health Blue Cross and Blue Shield of Florida SunTrust Bank University of Florida College of Medicine - Jacksonville

Silver Sponsors Akerman Senterﬁtt Brooks Rehabilitation Clinet Corporation Community Hospice of NE Florida Haven Hospice OptaComp Pﬁzer, Inc. SeaCrest Healthcare Management SunCrest Home Health

Meet these exhibitors and others at the DCMS Annual Meeting Exhibit Hall open 5:45 p.m. - 7:00 p.m.

Giveaways...Key Information...Door Prizes!! 6 Vol. 60, No. 4 2009 Northeast Florida Medicine

2009 DCMS Foundation Donations Please join us in saluting in the following donors whose partnerships in time and ﬁnancial resources make the work of the DCMS Foundation possible and also strengthens organized medicine in NE Florida.

Clarence E. Boudreaux, MD William W. Buckingham, Jr., MD William P. Clarke, MD James W. Clower, III, MD Yank D. Coble, Jr., MD Joe C. Ebbinghouse, MD Walter R. Gilbert, Jr., MD Eugene J. Glenn, MD Kenneth A. Horn, MD R. Stephen Lucie, MD Marianne B. McEuen, MD Charles B. McIntosh, MD George L. Mayer, MD Russell D. Metz, MD Mitchell S. Rothstein, MD Joel P. Schrank, MD Guy T. Selander, MD John W. Wells, MD

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2009 Beals and Shahin Awardees Dr. Mobeen Rathore, (L) and co-authors received the Beals Award for Original Investigation for their article “Continuous Improvement in the Immune System of HIVinfected Children on Prolonged Antiretroviral Therapy”. Dr. Joseph Tepas III, (R) chair of the Beals & Shahin Committees, made all the award presentations. Dr. Andrew Kaunitz received the Beals Award in the Review Category for his article “Hormonal Contraception in Women of Older Reproductive Age.”

Dr. Beston Ahmed received the Shahin Award in the Original Investigation Category for his article “Post-Laparscopic Cholecystectomy Pain: Effects of Intraperitoneal Local Anesthetics on Pain Control - A Randomized Prospective Double-Blinded Placebo-Controlled Trial.”

Dr. Santosh Kale and co-authors received the Shahin Award in the Review Category for their article “A Case and Literature Review of Complicated Gastrointestinal Stromal Tumors” Winners not present at the award ceremony and not pictured are: Dr. Gavan Duﬀy (Beals Award for Clinical Observation) and Dr. Christian Wider (Shahin Award for Clinical Observation).

The Beals Award was begun by Dr. John Beals to recognize outstanding research and publications by a DCMS member. The G. Shahin Awards were created in 1997 by Dr. Shahla Masood in honor of her mother, G. Shahin, whom she considered an exemplary teacher. The Shahin Awards recognize the research and publication eﬀorts of Residents or Fellows training in Jacksonville. Articles submitted for both awards are judged for quality of methods and study design, writing style and data presentation, new ideas and information presented, and overall quality.

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DCMS to Host AMA President-Elect Dr. Cecil Wilson During 2010 AMA Leadership Visit Cecil B. Wilson, MD, the current President-Elect of the American Medical Association (AMA), will visit Jacksonville April 25-27, 2010. Dr. Wilson will become the 164th AMA President in June, 2010. While in the area, Dr. Wilson will speak at a DCMS dinner meeting, be keynoter at the Jacksonville Rotary Club, visit local academic institutions, meet with staff as The Florida Times-Union, BlueCross and BlueShield of Florida, and other area groups. (Watch future DCMS communications for dates and details) The DCMS has been hosting AMA leadership for more than 20 years as a way to broaden the community’s knowledge of organized medicine and to help motivate grassroots advocacy on issues of national importance. A private practice internist from Winter Park, FL, for more than 30 years, Dr. Wilson once served as a Navy flight surgeon, rising to the rank of commander. He interned at the U.S. Naval Hospital, Portsmouth, VA., and completed his residency in internal medicine at the U.S. Naval Hospital, San Diego. He has a distinguished record of service and leadership in organized medicine. At the local level he was president of the Orange County Medical Society. Next he moved to a state position as president of the Florida Medical Association (FMA) and was chair of its Board of Governors and Executive Committee. Dr. Wilson has served in the national arena as an AMA House of Delegates member since 1992, has been an AMA Board of Trustees member since 2002, and served as vice-chair of the AMA Council on Constitution and Bylaws. In addition, Dr. Wilson is past chair of the American College of Physicians (ACP) Board of Regents, has served on the American Society of Internal Medicine’s board. (ASIM), is a board member of COLA (a physician-run organization that accredits physician office labs nationwide), and past president of the Florida Statewide Health Council. Dr. Wilson has received the FMA’s highest award, the Certificate of Merit and the prestigious Laureate Award for service to internal medicine from the Florida Chapter of ACP. He is board-certified in internal medicine and a Master of the American College of Physicians.

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This Issue’s Focus: Travel Medicine

Travel Medicine as an Evolving Specialty “I’ll be bicycling in Thailand…I’m returning to Uganda on vacation to visit family and friends…I have HIV and am planning on going on Safari in Kruger National Park…My medical insurance company is sending me to India for cardiac surgery…I plan to climb Mt. Kilimanjaro.” Pre-travel preparation has become increasingly complex since rapid air travel has opened up access to all but the remotest areas of the world within as little as 48 hours. As a result, Travel Medicine has emerged as a unique specialty, the International Society for Travel Medicine (ISTM) has been formed, and there is now a Certiﬁcate of Knowledge Examination in collaboration with the American Society of Tropical Medicine and Hygiene in the US; as well as training and a Travel Medicine Diploma Examination through the University of Glasgow and the Royal College of Physicians and Surgeons of Glasgow. In addition, there are now at least 10 travel medicine texts, several journals focused on the topic, and a minimum of 1500 articles about travel medicine written in the last ﬁve years that can be found via a Pub Med search.

Michael Sands, MD, MPH & TM, FIDSA UF College of Medicine/ Jacksonville Guest Editor

A travel medicine specialist (A natural ﬁt for an infectious diseases specialist, but it can be any MD, DO, PA, ARNP or RN with specialty training in the area) is tasked with developing an individual plan for each traveler, taking into account their unique combinations of medical co-morbidities, medical and travel history, medications, vaccination history, allergies, sequence of travel destinations and activities agendas. Each travel scenario above has unique associated travel issues. The travel medicine provider must do an individual travel risk assessment and then provide counseling, prophylactic medications and vaccinations as appropriate to minimize the travelers’ risk of morbidity or mortality. Complicating travel medicine further are the growing areas of adventure travel; international adoption; medical tourism; refugees, immigrants and visa workers traveling home to visit friends and relatives (VFR); and the increasing numbers of traveling immunocompromised patients.

In this journal issue you will have a taste of travel medicine, touching on a number of core areas. “Medical Illness During Travel – A Review” by Senthil Meenrajan, MD and Jeﬀ House, DO, give an overview of issues of medical illness during travel, with a focus on preventing DVTs during long distance travel. In “Vaccinations for Travelers,”Nilmarie Guzman, MD, reviews and updates our knowledge on vaccinations for travel. “Travelers’ Diarrhea” by Christina Bailey, MD and Alexander Vandevelde, MD, discusses this common, yet debilitating condition. “An Update on Malaria and Insect Avoidance,” by Rachana Palnitkar, MD, presents core information necessary for decisions on anti-malaria chemotherapy. “High Altitude Travel and Air Craft Cabin Environment by Rebecca Senko, RN, BSN, CTH, discusses altitude associated illnesses, ranging from acute mountain sickness through high altitude cerebral edema. Finally, Levonne Mitchell-Samon, MD, explains the risks associated with “Pregnancy and Travel.” Hopefully journal readers will ﬁnd these articles informative and each will stimulate interest in travel medicine while emphasizing the need for pre-travel specialty assessment, particularly for those travelers venturing to lesser developed areas of the world or engaging in risky activities. Further basic background information can be found in ET Ryan and DC Kain’s review, “Health Advice and Immunizations for Travelers” in the New England Journal of Medicine (2000;342:1716-1725) and the various web sites noted in their article, as well as other references cited in this issue’s articles.

Healthcare and Photography Bring Life Into Focus for Bobi Wall Roberta (Bobi) Wall is a nurse practitioner by vocation, but by avocation she is a photographer. “In my heart I am a photographer,” Bobi says. “I enjoy capturing beauty and time in photos.” She has “dabbled” in photography since the 1970s. Readers will see her photos on the cover of this issue and throughout the clinical section in some special “Traveling Through Photos”. Bobi has two favorite sites to take photos - The Kingdom of Bhutan in South Asia and Africa. She encourages photographers to “Capture the moment you most want to share with others. You cannot go back again.” To see Bobi Wall’s many photo galleries, go online to www.bobiwall.com. www . DCMS online . org

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Medical Illness During Travel - A Review Senthil Meenrajan, MD and Jeﬀ House, DO Abstract:Travel is becoming more common as the number of destinations and the means to get there are expanding. Regardless of the modality, travel has inherent medical risks, even in those who have no pre-existing conditions. Greater awareness of these risks, taking precautions prior to travel and being ready to deal with illnesses when they arise will make for a safe and enjoyable experience.

Introduction Over the last two centuries, great strides have been made in travel technology. Of course, in that same time frame, there have been dramatic changes in the different modes of travel, desired destinations and the number of people traveling. About 60 years ago, approximately 25 million people arrived at different international destinations around the world annually, but in the subsequent 30 years that figure increased to almost 60 million. Today the number of arrivals around the world is thought to be between 1-2 billion each year.1 If domestic travel were included in these figures, the numbers would definitely be astronomical. The reasons for travel are quite variable. It is not always affluent people traveling for pleasure. In fact, until recently the vast majority of mass movement of people occurred as part of immigration out of Europe to America or displacements related to wars and famine, and more recently to trade and for educational purposes.1 Travel brings with it a number of critical considerations for the person traveling and for physicians managing these illnesses. Within the last 15 years there has been a trend toward more illness and deaths occurring during in-flight travel. This may not be merely a reflection of the higher numbers of people traveling but more likely more sick people tend to travel now than ever before. The two broad categories of travel related illnesses are preexisting medical illnesses that have the potential to get worse during travel and new illnesses that are unique to the travel itself. Chronic obstructive pulmonary disease (COPD, diabetes mellitus, and heart disease are examples of illness that will need to be addressed carefully when formulating a travel plan. For this review, however, we focus on medical illnesses that are unique to travel itself. For purposes of simplicity, we will approach illnesses that are more prevalent with air and land travel and cruise travel separately.

first major study addressing this question was the LONGFIT study.2 In this study 355 low risk travelers and 389 high risk travelers with flight travel that lasted an average of 12 hours had ultrasound scans of the lower extremities within 24 hours of completing travel. In the low risk group, no DVTs were noted. In the high risk group, 13 DVTs were noted in 11 individuals in addition to 6 superficial thromboses for a total of 19 (4.9%) thrombotic events. A number of risk factors for the development of DVT during air travel were identified. High risk patients were defined by previous DVT, known coagulation disorder, limitation of mobility or morbid obesity, neoplastic disease within two years, or large varicose veins. Sitting in a center or window seat was also identified as a risk factor. While specific data for long distance travel by land is not available, it is thought that the prevalence and risk factors would likely be the same. Additional modifiable risk factors for DVT include: prolonged immobilization, ‘coach’ position that compresses popliteal veins, duration of travel, alcohol intake, dehydration, hypoxemia and smoking.3 The key to preventing DVT is risk stratification of patients and counseling them on appropriate precautions for long distance travel. LONGFLIT 4 study demonstrated the efficacy of using Kendall travel socks that are knee high, with an ankle pressure of 20-30 mmHg in preventing edema and DVT in low-medium risk as well as high risk travelers.4Anyone that wishes to travel for prolonged periods of time should be encouraged to be adequately hydrated, avoid caffeine and alcohol and ambulate as much as possible or at least exercise their calf muscles while in the seated position. In addition, travelers with higher risk for developing DVT could be considered for prophylaxis with low molecular weight heparin like enoxaparin 40 mgs given subcutaneously a few hours before the journey and repeated in 12 hours if necessary.

High Altitude Illnesses Travel to high altitudes presents a unique set of problems related to the hypoxemia of altitude, dehydration, remote locations, exertion and potentially dangerous terrain. This topic is discussed in detail in an accompanying article by Rebecca Senko. (See “High Altitude Travel and Aircraft Cabin Environment, p. 27)

Deep Venous Thrombosis (DVT)

Motion Sickness

The association between long distance travel and Deep Venous Thrombosis (DVT) formation was made in the 1950s. Subsequent prospective data has been limited. The

Motion sickness is fairly common in all modes of transportation and the exact mechanisms are not completely understood. To some extent this sickness is related to the sensory and vestibular mechanism’s inability to cope with faster rates of travel. Susceptibility varies among diﬀerent individuals with higher rates of occurrence in younger people and in females. Symptoms range from mild nausea, dizziness and headaches to variations in heart rate or blood pressure

Address Correspondence to: Senthil Meenrajan, MD, MBA,University of Florida, College of Medicine-Jacksonville, 653 W 8th Street, 4th Floor LRC, Jacksonville, FL 32209. Email:Senthil.meenrajan@ jax.uﬂ.edu. 10 Vol. 60, No. 4 2009 Northeast Florida Medicine

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with profuse vomiting. For susceptible individuals, a variety of chemoprophylaxis is available with varying degrees of success being reported.5 Commonly used agents are a scopolamine patch applied at the time of travel, dimendydrinate tablets or chewing gum, meclizine, and ginger root. Individual preference, side eﬀect proﬁle and past experience might dictate the choice of agent for any given individual.

Jet Lag Jet lag is the result of asynchrony between the body’s internal clock and the local time. It is typically associated with long distance travel across several time zones. Depending on the distance and number of time zones crossed, symptoms can be mild or severe and they affect up to 94% of travelers.3 Commonly reported symptoms include sleep disturbances, daytime fatigue, decreased cognitive and physical abilities, malaise and irritability2. Specific treatments include bright light exposure, exercise, melatonin, central nervous system (CNS) stimulants and sedatives. Exposure to bright light in the morning causes an internal phase advancement and late afternoon exposure causes a phase delay.6 Bright light is proven to be useful, but it is often impractical and cumbersome. CNS stimulants like caffeine, amphetamines and modafinil and sedatives like temazepam, zolpidem have been tried to alter the sleep cycle. They are generally effective, but there are some concerns for their safety limits. Melatonin appears to be effective taken at 3-5 mg doses at local bedtime for 4-6 days and is useful for travel in both directions. (i.e. east to west and west to east)

Cruise Medicine Every year millions of people will travel all over the world on cruise ships, and roughly 75% of these travelers take North American cruise lines. A myriad of injuries and illnesses can occur on board cruise ships. Most are not unlike those seen in many outpatient clinics. Roughly 69% of illnesses presenting to cruise ship physicians are from general medical conditions, and another 18% are from injuries.7 Over 80% of all visits are due to non-urgent medical problems, 5-10% are for serious injury or illness, and , fortunately, less than 1% require emergent transport to a shore-side hospital. Several maladies are somewhat unique to sea travel and these will be the focus of the remainder of this article. Perhaps the most common illness people associate with sea travel is motion sickness, or “sea sickness.” Fortunately, most cruise ship itineraries are in calm seas and modern cruise ships are equipped with stabilizers to minimize excessive motion. The general principles of motion sickness were covered previously; however there are some features that are unique to sea travel. Although there is variable sensitivity to motion sickness, with enough ship motion virtually everyone has a threshold beyond which they become sea sick.8 The prevalence of motion sickness is higher in women, and other risks include pregnancy, alcohol consumption, and overeating. With continued exposure, adaptation develops and most individuals will experience a progressive reduction in symptoms, although roughly 5% of travelers do not completely adapt.

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Pharmacologic therapy for motion sickness was mentioned previously. Stepping out onto the deck may improve symptoms by providing visual orientation. Staying closer to the center of the ship where motion is decreased, as well as lying supine parallel to the axis of major motion are other commonly recommended maneuvers. Conversely, when finally returning to land, the voyager may experience a “mal de debarquement” phenomenon, which unlike motion sickness, has symptoms that are typically mild and adaptation to land is rapid. After returning to land, the sensation of motion may persist for several days, but there is rarely a need for treatment. As with other forms of travel, crowded ships expose people to a variety of infectious agents with the majority of these being respiratory. Cruise ships have frequently been reported as environments for influenza outbreaks.9-11 Because of the frequent number of outbreaks, influenza programs, including annual vaccination, have been instituted for crew members. Surveillance programs are also present at several major cruise lines to identify outbreaks at an early stage. Although, supportive care and perhaps antivirals can be offered to affected passengers, pre-trip prevention such as taking the vaccine for the current seasons’ influenza and H1N1v should be considered, particularly for high risk patients. Diarrheal illnesses are also quite common on cruise vessels. The most common etiology for infectious diarrhea is the noroviruses. This may spread quickly to involve large numbers of travelers and staff.12 Bacterial causes are rare but include enterotoxogenic Escherichia coli, salmonella, shigella, Staphylococcus aureus, Clostridium perfringens, and campylobacter. Comprehensive cruise ship sanitation programs developed in the 1970s and 80s in conjunction with the Centers for Disease Control (CDC) have significantly reduced outbreaks of diarrheal illnesses by addressing areas such as staff hand hygiene, food preparation standards and quality control of food vendors. (See “Travelers’ Diarrhea” , p. 18)

Conclusion More and more people travel and it is a leisure or business activity for larger groups of people. However, with the threat of DVT, high altitude illnesses, motion sickness, jet lag, and the various conditions one can develop while on a cruise, it is increasing important for a traveler to be prepared physically when taking a trip. If there are doubts about one’s physical condition or the needed precautions before traveling to a certain area, the traveler should consult his/her personal physician. Besides packing clothes, preparations need to be made so the traveler is assured of a pleasant trip and protection from unwanted medical stress.

References 1.

Principles and Practice of Travel Medicine. Edited by Jane N. Zuckerman. 2001 John Wiley & Sons Ltd.UK. Accessed through www.netlibrary.com, July 22, 2009.

Belcaro G, Geroulakos G, Nicolaides AN, Myers KA, Winford M . Venous Thromboembolism from Air Travel: The LONFLIT Study. Angiology 2001;52; 369-374.

Steﬀen, R, Dupont, HL, Wilder-Smith A. Manual of Travel Northeast Florida Medicine Vol. 60, No. 4 2009 11

Medicine and Health. Second edition. Ontario:BC Decker Inc., 2003. pp. 487-489, 503-508. Accessed online Jul 22, 2009 through www.netlibrary.com. 4.

Cesarone MR, Belcaro G, Errichi BM, et.al. The LONFLIT4Concorde Deep Venous Thrombosis and Edema Study: Prevention with Travel Stockings. Angiology 2003; 54:43-154.

Sherman CR. Motion sickness: review of causes and preventive strategies. J Travel Med 2002;9:251–6.

Samel A, Wegman H. Bright light; a countermeasure for jet lag? Chronobiology Int 1997;14:173–83.

Peake DE, Gray CL.Descriptive Epidemiology of Injury and Illness among Cruise Ship Passengers. Ann Emerg Med. Jan 1999; 67-72.

Gahlinger P. Cabin location and the likelihood of motion sickness in cruise ship passengers. J Travel Med. 2000;7:120-124.

Nitsch-Osuch A. Inﬂuenza as a health problem of sea travelers. Int Marit Health. 2008;59(1-4):103-12.

10. Inﬂuenza B virus outbreak on a cruise ship-Northern Europe, 2000. Centers for Disease Control and Prevention (CDC). Morb Mortal Wkly Rep. 2001 Mar 2;50(8):137-40. 11. Brotherton JM, Delpech VC. A large outbreak of inﬂuenza A and B on a cruise ship causing widespread morbidity. Epidemiol Infect. 2003 Apr;130(2):263-71. 12.

Cramer EH, Blanton CJ. Epidemiology of gastroenteritis on cruise ships, 2001-2004. Am J Prev Med. 2006 Mar;30(3):252-7.

Traveling Through Photos An African sunset is striking even in this black and white version of Bobi Wall’s color shot (see www.bobiwall.com) of a peaceful boat ride.

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Vaccinations for Travelers Nilmarie Guzman, MD Abstract It is estimated that approximately 800 million travelers cross international borders every year.1 Americans make approximately 300 million trips to other countries. An increasing number of these trips are to developing countries. According to the Centers for Disease Control (CDC), 30 to 60% of travelers to less developed countries will experience some illness as a result of travel.2,3 This article focuses on the most commonly recommended immunizations for international travel; namely Yellow Fever and Meningococcus.

Introduction Studies show that only a minority of travelers seek pretravel advice.4 Travel may be for a variety of reasons, e.g., for business, tourism, adventure, missionary work, as migrant workers or with the purpose of visiting friends and relatives. It is advised that travelers visiting developing countries seek pre-travel advice with a Travel Medicine practitioner at least one month prior to departure. This pre-travel visit should include individualized recommendations about vaccinations, prophylaxis for malaria, management of traveler’s diarrhea and prevention advice. The pre-travel visit should also be used as an opportunity to update routinely recommended vaccinations, according to US schedules and based on the traveler’s age and underlying health status. The risk of a traveler acquiring a vaccine-preventable illness depends upon his/her itinerary, the duration of travel, activities engaged in during travel, past medical history, medications and vaccination history. For most vaccine-preventable illnesses in travelers, the risk of acquiring infection is low (approximately 1 case per 1000 visits). Vaccines for travelers can be divided into 3 categories: routine preventive health, vaccines mandated for travel in or between specific countries, and those that are recommended according to estimated risk of disease acquisition. Many infectious diseases potentially encountered during travel, such as measles and tetanus, are prevented as part of routine childhood immunization and will not pose a risk if the traveler is up-to-date with routine vaccination. Travelers who deserve special consideration include young children, pregnant travelers, those with chronic medical conditions such as diabetes, chronic renal, cardiac, or pulmonary disease, and persons with HIV infection, malignancy, or other immunodeficiency states. Children should be offered vaccination against the same diseases as adults, taking in consideration that the product, dose and administration may vary. In the United States, the Advisory Committee on Immunization Practices (ACIP) of the CDC creates guidelines for childhood and adult immunization standards in addition to Address Correspondence to: Nilmarie Guzman, MD, 1833 Boulevard, Suite 500, Jacksonville, FL 32206. Email: Nilmarie_Guzman@ doh.state.fl.us.

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guidelines and information for international travelers. The World Health Organization (WHO) delineates the International Health Regulations (IHRs) and recommendations regarding vaccine requirements for travelers. Online documents are published and updated annual by the CDC, e.g., “The Yellow Book” (http://wwwn.cdc. gov/travel/content/yellowbook/home-2010.aspx) and the WHO, e.g., “International travel and health” (http://www. who.int/ith/ITH2009Chapter6.pdf ) to guide the practitioner in the selection of appropriate vaccinations for international travelers. A full review of vaccinology is beyond the scope of this review. Rather, this article focuses on the most commonly recommended immunizations for international travel, beginning with the two potentially mandated vaccines, i.e., Yellow Fever and Meningococcus.

Yellow Fever Vaccine The endemic zones for Yellow Fever (YF) are the Amazonian regions of South America and 15 degrees on either side of the equator in Africa. According to the WHO, approximately 200,000 cases of YF occur each year in endemic populations.5 Clinical manifestations range from subclinical infection to systemic disease including liver, renal failure and hemorrhagic complications. The fatality rate associated with clinical YF is approximately 20%. Travelers visiting areas in Africa or South America where YF has officially been reported must be vaccinated or given a physician letter stating that there is a medical contraindication to vaccination. Yellow Fever clinic vaccination sites are regulated by governmental agencies (CDC and State Health Departments in the United States), as required by IHRs.6 Certain criteria must be met in order to get certified to administer YF vaccine. These include maintenance of the vaccine at the right temperature, prompt administration after reconstitution, the ability to handle anaphylactic reactions, and proper completion of the WHO International Certificate of Vaccination (ICV). State Health Departments provide clinics that administer YF vaccine with a validation stamp that is used when vaccination is recorded in the ICV. Canada, England, South Africa and New Zealand have made it a requirement that health care personnel who wish to administer YF vaccine receive formal training in travel medicine for their clinic to be certified as an official YF vaccinating center. The currently available YF vaccine is a live-attenuated 17D strain and is highly effective. IHRs require that it be administered at least 10 days before departure to allow development of protective antibodies. Boosters are required at 10-year intervals for continued documentation of vaccination. The most common side effects of vaccine administration include low grade fever, headaches and myalgias, often Northeast Florida Medicine Vol. 60, No. 4 2009 13

occurring 7-10 days following vaccination. Severe adverse eﬀects are rare, but include viscerotropic and neurotropic disease. Neurotropic disease is encephalitis following vaccine administration and viscerotropic disease manifests as a febrile multi-organ system failure. These complications are related to altered host response to the vaccine and not to changes in the vaccine itself. Both viscerotropic and neurologic disease are seen at a rate of approximately 1 case per 40,000 doses in the population aged 60 years and older.7 Yellow Fever vaccine can be administered to persons ≥ 9 months of age, traveling to areas in Africa or South America where YF has oﬃcially been reported. Neurotropic disease has been reported in children up to the age of 3 years and the vaccine should be used cautiously in 9 month – 3 year olds.8 For travel to regions without active YF transmission, a physician letter stating a medical contraindication to vaccination might be considered. Yellow Fever vaccine must be avoided in infants < 6 months old, pregnant women, persons allergic to eggs, or patients with an immunosuppressed condition such as HIV/AIDS, leukemia, lymphoma, or long term use of immunosuppressant drugs. Yellow Fever vaccine should not be administered to individuals with a history of thymus disorder or thymectomy.9 It is best for persons in these categories to avoid exposure and to consider altering their travel itinerary. If travel is mandatory, expert advice should be sought to establish whether the individual warrants immunization or should be issued a letter of medical exemption. In any scenario, travelers should strictly adhere to mosquito avoidance measures, particularly at dusk and dawn, which are the maximum biting times of the principle human vector, the Aedes mosquito.

Meningococcal Vaccine Neisseria meningitidis infection can be acquired during travel particularly if travel itinerary includes visiting areas in the so called “meningitis belt” in Africa which extends from Senegal to Ethiopia, where the annual incidence of meningococcal disease is 30 cases per 100,000 people.10 The carrier prevalence is highest in populations living in crowded conditions such as pilgrims on the Hajj and Umra in Saudi Arabia, military recruits and students living in dormitories. There are ﬁve meningococcal serogroups: A,B,C,Y and W-135. Serogroups A and C are most often associated with epidemics but recently serogroup W-135 has emerged as a signiﬁcant strain in Africa and Middle East. Several meningococcal vaccines are available. The bivalent vaccine (A + C) polysaccharide vaccine is used in Europe, Middle East and Africa. The quadrivalent polysaccharide vaccine (A,C,Y,W-135) is used in North America since 1982. In 2005, a conjugated quadrivalent meningococcal vaccine was approved for use in persons aged 11–55 years.11,12 Meningococcal vaccine is recommended for travelers to sub-Saharan Africa, particularly if they are traveling during the dry, winter months from December through June or will have extensive contact with the local population.13 The Saudi 14 Vol. 60, No. 4 2009 Northeast Florida Medicine

Arabian embassy requires proof of immunization before issuing visas for Hajj pilgrims. Routine vaccination is also recommended for first-year college students who will live in dormitories. Microbiologists with frequent exposure to N. meningitidis, military recruits, persons with terminal complement component deficiencies, and individuals with functional or surgical asplenia should also receive vaccine. It should be administered 1 to 2 weeks before departure to ensure maximum antibody response (85 to 90% efficacy). Nonconjugated meningococcal polysaccharide vaccines are poorly immunogenic in children under the age of 2 years. Side effects associated with the vaccine are minimal, including local pain, swelling, erythema at the injection site and on rare occasions, low grade fever.

Hepatitis A Vaccine Acute Hepatitis A is transmitted worldwide. It is acquired by the oral-fecal route manifested by gastrointestinal symptoms. It is usually a self-limited disease and is not associated with chronic infection. It has been estimated that the attack rate is 20/1000 per month of travel for backpackers and budget travelers in highly endemic countries. Prior to the introduction of immune serum globulin (ISG) and inactivated vaccines in the mid-1990s, hepatitis A occurred at an estimated frequency of 1–10 cases per 1000 travelers for 2–3 weeks of exposure, even among those residing in first-class accommodations.14,15 The risk appears to be decreasing secondary to widespread use of vaccines for protection in travelers and changing epidemiology of hepatitis A in destination countries.16-18 Although hepatitis A is self-limited in most patients and is usually asymptomatic in children under the age of 6 years, illness has accounted for the most time lost from work (1 month) in a study of returned travelers and is associated with a 2 to 4% mortality rate among persons > 40 years old.19,20 Persons traveling or working in countries with high or intermediate rates of hepatitis A should be vaccinated.21 Persons traveling from developed countries to undeveloped countries are at high risk for acquiring Hepatitis A. The risk still exists even for travelers in urban areas and those who follow food and water precautions. Hepatitis A vaccine is administered in two doses. The first dose should be administered as soon as travel is considered. Previously, hepatitis A vaccination was recommended to be administered at least 2–4 weeks before departure to an area with intermediate or high rates of hepatitis A. Travelers who were departing in less than two weeks were recommended to receive immune globulin (IG) for short-term protection. However, on the basis of data indicating that immune globulin and vaccine have equivalent postexposure efficacy among healthy persons aged 1-40 years, the ACIP has amended its guidelines for hepatitis A vaccination for travelers. ACIP now recommends that one dose of single-antigen hepatitis A vaccine administered at any time before departure may provide adequate protection for most healthy individuals.22 For optimal protection, older adults, immuno-compromised persons, and persons with chronic liver disease or other chronic medical conditions who are planning to depart in www . DCMS online . org

<2 weeks should receive the initial dose of vaccine and also can simultaneously be administered IG (0.02 mL/kg) at a separate anatomic injection site. Travelers who have an allergy to a vaccine component or who refuse to receive the vaccine can be prophylaxed with a single dose of immune globin (0.02 mL/kg). This dose protects against hepatitis A virus for up to 3 months. If the travel is expected to exceed two months, a 0.06 mL/Kg dose may be administered and repeated if travel schedule exceeds five months. Hepatitis A vaccine is not currently licensed for use in patients less than 12 months of age. Although not approved by the FDA for use in infants, inactivated hepatitis A vaccines are safe, immunogenic and have some protective effect even in infants with circulating maternal antibody. For persons who may have had hepatitis A (individuals who were born or resided in endemic regions or persons who have a history of jaundice), immunity can be assessed by screening for anti-hepatitis A IgG antibodies, avoiding the cost of the vaccine. Duration of protection following the full course of vaccine is likely to be life-long; no booster dose is recommended in immunocompetent hosts.23 The most common side effects associated with Hepatitis A vaccine administration are soreness at the administration site (50%), headache (17%), loss of appetite (more common in children) and fatigue (7%).24

Hepatitis B Vaccine Hepatitis B vaccine is included in the travel vaccines recommended for susceptible adult travelers who are planning to visit endemic areas. Travelers considered at risk include those with exposure to blood or body secretions, unprotected sexual exposure with members of the local population or other travelers, medical conditions that may require hospitalization or blood transfusion, intravenous drug abuse, or activities that include needles.25,26 All individuals with potential exposure to these risk factors should receive Hepatitis B vaccine. In addition, it is recommended for travelers staying longer than four weeks in high risk areas. The widely used Hepatitis B vaccines are the recombinant HBsAg vaccines. The standard dose is administered intramuscularly on days 0,1 and 6 months. For those travelers departing in less than six months, an accelerated schedule can given at 0,2 and 4 months. A more accelerated schedule has been studied in travelers given at 0,7 and 21 days followed by a 12 month booster.27,28 The latter schedule is used when a traveler is leaving in a very short time. An accelerated schedule given at 0, 7 and 21 days is also approved for use with the Hepatitis A/B vaccine, Twinrix®. Side eﬀects associated with Hepatitis B vaccine include pain at injection site, arthralgias, myalgias, and low grade fever.

Typhoid Fever Vaccine Typhoid fever is a life threatening disease caused by Salmonella typhi. It is prevalent worldwide and is associated with poor sanitation practices and contaminated food and water. Approximately 400 cases occur each year in the United States; www . DCMS online . org

70% of those are acquired during travel. It manifests with high fevers, weakness, abdominal pain, headache or loss of appetite. A rash can be present, commonly described as flat, rose-colored spots.29 Acquisition risk is considered highest in travelers visiting Asia, particularly India and Pakistan and lower risk for travelers to Africa and Latin America. There are two main ways of decreasing the risk of acquiring typhoid fever: following careful food and water precautions and being vaccinated. Vaccination is recommended for travelers to endemic areas, particularly Asia, Africa and Latin America, persons with intimate exposure to a S. Typhi carrier, and microbiology laboratorians who work frequently with S. Typhi.30,31 There are two typhoid vaccines available in the United States; Ty21a(Vivotif Berna, Swiss Serum and vaccine Institute) and ViCPS (Typhum Vi, Pasteur Merieux). The Ty21a vaccine is an oral 4-capsule series containing live, attenuated S. Typhi and must be received at least two weeks before departure with revaccination required every five years for continued immunity. The ViCPS is Typhim Vi, a parenteral Vi capsular polysaccharide vaccine, given as a single dose licensed for persons aged > 2 years which must be administered one week before departure and revaccination required in two years. Side effects associated with the Vi polysaccharide vaccine include flu-like symptoms, fever and headache (<1%). Abdominal discomfort, nausea , vomiting, rash ,urticaria and headache occur in 0-5% of Ty21 vaccine recipients.32 Of the two vaccines, Typhim Vi appears to provide better immunity. This may be because of the more complicated dosing and storage requirements of the oral vaccine. It should be refrigerated, taken on alternate days, and antibiotics, antimalarials, or alcohol may inhibit the vaccine if taken simultaneously. A patient must be off antibiotics at least for 24 hours and not receive antibiotics within 72 hrs of vaccine completion. Food and water precautions must be followed even if a traveler receives typhoid fever vaccination.

Rabies Vaccine Rabies has been reported around the globe with certain areas associated with higher endemicity, such as Thailand, Brazil, Guatemala, Bolivia, Colombia, Ecuador and El Salvador. In these countries, transmission occurs primarily by dogs, although other animals are implicated such as cats, monkeys and the mongoose. The rare cases of rabies in travelers have followed a dog bite in areas in which canine rabies is endemic. There are diﬀerent rabies vaccine formulations available. The modern cell culture vaccines (CCV) are considered the safest and most immunogenic. Rabies vaccine is recommended for travelers or expatriates to areas in which rabies is endemic, who will have occupational or recreational exposure, e.g., veterinarians, spelunkers, and others with animal contact, and for children staying in an endemic area for four or more weeks due to their unhindered propensity to pet animals.

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The standard pre-exposure CVV series includes three doses administered intramuscularly in the deltoid on days 0, 7 and 21 or 28. In the setting of continuous occupational exposure, a single booster dose of 1.0mL IM may be given every two years. A course of pre-exposure rabies vaccination eliminates the need for rabies immunoglobulin following a potential exposure. Rabies immunoglobulin of either human or equine origin as well as the vaccine may be very diﬃcult to obtain in resource-poor area.33,34 Adverse events associated with vaccine administration include injection site pain (25%), headache, nausea, abdominal pain, muscle aches and dizziness. Urticaria, pruritus and malaise have been reported in approximately 6% of HDCV booster recipients. It is also recommended that all travelers get counseling about dog avoidance (and avoidance of other animals), thorough cleansing of a wound with soap and water in the event of a bite and the need to obtain prompt post exposure prophylaxis for rabies.

Cholera Vaccine The risk of acquiring cholera during travel is extremely low (.01 to .001% per month of stay) in risk regions.There are no requirements for cholera vaccination prior to travel and no cholera vaccine currently available in the United States.

Japanese Encephalitis Vaccine Japanese Encephalitis is a mosquito borne, viral disease that is prevalent in most countries of Asia and, with limited risk, in some islands of the Western Pacific and in northern Australia. A decision to use the vaccine depends upon the destination and the season of travel. The risk to travelers is for those having prolonged residence in an endemic country, those with shorter visits but with intense rural exposure to rice field mosquitoes during transmission seasons and those engaging in field work or who are camping or bicycling in rural rice field areas. A newly released vaccine, IXIARO, is a purified, inactivated virus product grown in Vero cell cultures. The vaccine is administered intramuscularly on day 0 and 28. Thus far the most common side effects are injection site pain, headache and myalgias occurring in approximately 10% of patients.35

Tick Borne Encephalitis Vaccine Tick borne encephalitis (TBE) is one of the most common tick transmitted Flavivirus central nervous system infections in Europe and Asia. In Europe it has been reported from Belgium to Austria. It is prevalent in Scandinavian countries. TBE occurs in the rural, forested regions, up to 1000 m in altitude. In endemic areas it occurs from May/June to September/October. Symptoms range from meningitis to severe meningoencephalitis with possible residual neurologic sequelae. In general, risk in travelers is low, unless extensive outdoor exposure is anticipated in prevalent areas. In endemic areas, such as Germany and Austria, the vaccine is included in routine childhood immunization schedule. TBE vaccine is not available in the United States, but should be considered for individuals planning to expatriate or live for extended 16 Vol. 60, No. 4 2009 Northeast Florida Medicine

periods in endemic areas and adventure travelers planning extensive outdoor exposure. There are two chick-cell culture derived inactivated vaccines in Europe. The active immunization schedule consists of three doses. First dose of 0.5mL is followed by second dose in 4-12 weeks. A booster dose must be given in 9-12 months. An accelerated schedule can be administered at 0.7 and 21 days with a booster in one year. Common side eﬀects associated with TBE vaccine are local reactions, fever, rash, fatigue, nausea, lymphadenitis, headaches and rarely neuritis may occur. The use of topical DEET and permethrin impregnated clothing for tick bite avoidance should be stressed.

Conclusion Vaccinations are an essential part of safe international travel. Once the region to be visited has been selected, the traveler should schedule a visit to primary care provider or a travel medicine clinic to obtain advice on current immunization recommendations. During the pre-travel evaluation, immunization recommendations are provided based on the risk of acquiring a vaccine-preventable disease, which depends on travel itinerary and style of travel. Past medical history and vaccination history also influence vaccine recommendations. The U.S. Centers for Disease Control and Prevention (CDC) recommends a pre-travel visit 4-6 weeks before an international trip. Modifications of standard recommendations are often needed for the traveler whose departure does not allow completion of the standard immunization schedule. Travel related immunizations are relatively safe and well tolerated. Side effects associated to the various vaccines recommended must be discussed with the traveler along with risks and benefits on a case by case basis.

References 1.

Reed CM. Travel Medicine Recommendations for older adults. Clin Geriatr Med. Aug 2007; 23(3):687-713.

Bhadelia N, Klotman M, Caplivski D. The HIV-positive traveler. Am J Med Jul 2007; 120(7):574-80.

Jong EC, Sanford CA. Travel and Tropical Medicine Manual. 4th ed. Philadelphia, PA: WB Saunders Co; 2008.

Curr Infect Dis Rep. Jan 2009;11(1):51-8. Accessed on Medline, October 30, 2009.

World Health Organization. December 2001.

World Health Organization (WHO). International health regulations (2005). Report no.: A58/55. Geneva: WHO, 2005.

Khromava AY, Barwick Eidex R, Weld LH, et al. Yellow fever vaccine: an updated assessment of advanced age as a risk factor for serious adverse events. Vaccine 2005; 23:3256–63.

Martin S. Cetron, et al. Yellow Fever Vaccine Recommendations of the Advisory Committee on Immunization Practices (ACIP), 2002. Morb Mortal Wkly Rep November 8, 2002; 51(RR17):1-10.

Barwick Eidex R. History of thymoma and yellow fever vaccination [letter]. The Yellow Fever Vaccine Safety Working Group. Lancet 2004; 364:936.

Fact sheet N°100 Revised

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10. Molesworth AM, Thomson MC, Connor SJ, et al. Where is the meningitis belt? Deﬁning an area at risk of epidemic meningitis in Africa. Trans R Soc Trop Med Hyg 2002; 96:242–9. 11.

Campbell JD, Edelman R, King JC Jr, Papa T, Ryall R, Rennels MB. Safety, reactogenicity, and immunogenicity of a tetravalent meningococcal polysaccharide- diphtheria toxoid conjugate vaccine given to healthy adults. J Infect Dis 2002;186:1848-51.

on Immunization Practices (ACIP). MMWR, October 19, 2007;56(41);1080-1084. 23. Van Damme P, Banatvala J, Fay O, et al. Hepatitis A booster vaccination: is there a need? Lancet 2003;362:1065-71. 24. Bell,B.P. Prevention of Hepatitis A Through Active or Passive Immunization. Morb Mortal Wkly Rep, May 19, 2006; 55(RR07);1-23.

12. Pichichero M, Casey J, Blatter M, et al. Comparative trial of the safety and immunogenicity of quadrivalent (A, C, Y,W135) meningococcal polysaccharide-diphtheria conjugate vaccine versus quadrivalent polysaccharide vaccine in two- to ten-year-old children. Pediatr Infect Dis J 2005; 24:57-62.

25. Zuckerman, JN and Steﬀen, R. Risks of Hepatitis B in travelers as compared with immunization status. J Travel Med.2000;7(4):170-174.

13. Pollard AJ, Shlim DR. Epidemic meningococcal disease and travel. J Travel Med 2002; 9:29-33.

27. Engler SH, Sauer PW, Golling M,et al. Immunogenicity of two accelerated hepatitis B vaccination protocol in liver transplant candidates. Eur J of Gastroenterology and Hepatology 2001;13:363-7.

14. Steffen R, Kane MA, Shapiro CN, Billo N, Schoellhorn KJ, van Damme P. Epidemiology and prevention of hepatitis A in travelers. JAMA 1994;272:885–9. 15. Wolfe MS. Hepatitis A and the American traveler. J Infect Dis 1995;171(Suppl 1): S29-32. 16. Tapia-Conyer R, Santos JI, Cavalcanti AM, et al. Hepatitis A in Latin America: a changing epidemiologic pattern. Am J Trop Med Hyg 1999;61:825-9. 17. Teitelbaum P. An estimate of the incidence of hepatitis A in unimmunized Canadian travelers to developing countries. J Travel Med 2004; 11:102-6. 18. Mu¨tsch M, Spicher VM, Gut C, Steffen R. Hepatitis A virus infections in travelers, 1988–2004. Clin Infect Dis 2006; 42:490-7. 19. Steffen R, Rickenbach M, Wilhelm U, Helminger A, Scha¨r M. Health problems after travel to developing countries. J Infect Dis 1987;156: 84-91. 20. Centers for Disease Control and Prevention. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). Morb Mortal Wkly Rep Recomm Rep 2006; 55(RR-7):1-23. 21.

Craig AS, Schaﬀner W. Clinical practice: prevention of hepatitis A with the hepatitis A vaccine. New Engl J Med 2004;350:476-81.

22. Novak R, Williams I. Update: Prevention of Hepatitis A After Exposure to Hepatitis A Virus and in International Travelers. Updated Recommendations of the Advisory Committee

26. Steﬀen R. Risks of Hepatitis B for travelers. Vaccine 1990; (suppl):S31-S32.

28.

Marchou B, Excler JL, Bourderioux C, et al. A 3 weeks hepatitis B vaccination schedule provides rapid and persistent protective immunity: a mulicenter randomized trial comparing accelerated and classic vaccination schedules. J Infect Dis 1995;172:258-60.

29. David A. Pegues, Samuel I.Miller in Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, 7th ed.Chapter 223. 30. Freedman DO, Weld LH, Kozarsky PE, et al. Spectrum of disease and relation to place of exposure among ill returned travelers. New Engl J Med 2006;354:119-30. 31. Centers for Disease Control and Prevention. Measles outbreak in a boarding school -Pennsylvania, 2003. Morb Mortal Wkly Rep 2004;53:306–9. 32. Engels EA, Falagas ME, Lau J, Bennish ML. Typhoid fever vaccines: a meta-analysis of studies on eﬃcacy and toxicity. British Medical Journal 1998; 316: 110–5. 33. Parviz S, Luby S, Wilde H. Postexposure treatment of rabies in Pakistan. Clin Infect Dis 1998;27:751-6. 34. Kositprapa C,Wimalratna O, Chomchey P, et al. Problems with rabies postexposure management: a survey of 499 public hospitals in Thailand. J Travel Med 1998;5:30-2. 35. Duggan, S, Plosker, G. Japanese Encephalitis Vaccine (Inactivated, Adsorbed) [IXIARO®]. Drugs 2009;69 (No.1):115-122(8).

Traveling Through Photos An open air market in Ecuador drew the attention of Bobi Wall’s camera as she captured the many exotic wares on display for tourists and other shoppers. Her color version of this photograph shows a rainbow of hues in all the items for sale.

Go to www.bobiwall.com to see this photograph and many others from around the world.

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Northeast Florida Medicine Vol. 60, No. 4 2009 17

Travelers’ Diarrhea Christina Bailey, MD and Alexander Vandevelde, MD Abstract: Travelers’ diarrhea is the most common infectious illness acquired by travelers. In most cases, it is benign and self-limited, but it can cause significant disruption to travel plans. In this article we review the common etiologies, risk factors and clinical course of the disease. Bacteria remain the most commonly identified causal agents for acute disease. Viruses and protozoa may be more significant in point outbreaks and chronic disease respectively. Although travelers are aware of preventative measures, including safer food and beverage choices prior to departure, they frequently have difficulty adhering to them after embarkation. Prophylactic antimicrobial use is generally discouraged except in select cases. As a result, travelers should be made aware of treatment options. Treatment includes not only supportive care, but also antibiotic therapy in more severe cases. Sometimes chronic diarrhea or post-infectious complications may develop.

Introduction Diarrhea is the most common illness acquired by travelers. Approximately 20% to 50% of international travelers will develop these symptoms.1 Most causative pathogens have been discovered and their epidemiology elucidated, but the frequency of the ailment has not diminished. Travelers’ diarrhea (TD) is defined as three or more loose stools within 24 hours; it usually happens within the first week of travel.1 The diarrhea may be accompanied by fever, nausea, vomiting, abdominal pain or cramping, fecal urgency, tenesmus, and bloody mucus in the stool. Depending on the etiologic agent and the host response, TD can be classified into three broad categories: acute watery diarrhea; acute bloody diarrhea (dysentery); and in a small percentage of patients, chronic, persistent or intermittent diarrhea that can last for months after return from travel.1,2 Most cases of TD, although generally benign and selflimited, cause significant discomfort to the affected person. Additionally, immediate consequences include disruption of travel or business plans, loss of tourist revenue, and decreased combat effectiveness in military troops.2 We will review the epidemiology, etiology, clinical course and options for prevention and treatment.

Epidemiology and Risk Factors While traveling, any consumption of foods that are sanitary but diﬀerent from one’s ordinary menu can upset and partially change the normal gut ﬂora; it causes a certain degree of deranged bowel peristalsis, either with diarrhea or constipation. This cannot be ascribed to an infectious agent and is not related to traveler’s diarrhea.

In contrast, the epidemiology of the agents that cause travel-related gastrointestinal diseases is more complex. The modalities of transmission include not only ingestion of contaminated food or fluids (including ice), but also personto-person contact, hand contamination and the touching of inanimate objects that are covered with hardy microbes, e.g., noroviruses. Flies and rodents have been found to be the vectors of salmonella food contamination.3,4 The destination may be the single most important risk factor for TD. Geographic risk to the traveler for a two-week stay is stratified as low (<8%), intermediate (8% to 20%), or high (20% to 90%).1 Low risk areas include Canada, the United States, Western Europe, Japan, and Australia/New Zealand. Intermediate risk areas include southern and eastern Europe, Russia, China, Israel, the Caribbean, and South Africa. High-risk destinations are the Middle East, Southeast Asia, and most of Africa.1,2 Where you stay, as well as the type of travel, is also important. Adventure tours, safaris, all-inclusive resorts, trekkers, and campers are at higher risk than persons on a beach vacation at a resort or on a cruise ship. Cruise ships, however, are more at risk for point source outbreaks due to viral gastroenteritis.5 Five-star hotels in developing countries actually have a higher rate of infection than four- or three-star hotels, probably due to higher frequency of food preparation by hand by inadequately supervised personnel. Additionally, the travelers’ complacency and feeling of being safe in such high-rated establishments likely contributes to the higher rate of TD.1,2 A traveler from one developing nation to another has a much lower attack rate (2% to 8%) than a traveler from a developed to a developing nation. Younger age (<30 years) may increase risk, possibly due to consumption or exposure to larger numbers of pathogens. No significant sex differences have been seen. Variability in host susceptibility due to genetic factors has been investigated. Persons with blood type O are more vulnerable to Vibrio cholerae. Persons carrying some alleles of interleukin 8 (IL-8) have increase risk for infection with enteroaggregative Escherichia coli (EAEC).6 Diminished gastric acidity from medication or surgery increases the risk for infection by acid-sensitive bacteria such as Salmonella and Campylobacter species. Immunosuppression increases the risk of infection. For example, persons with human immunodeficiency viral infection are particularly vulnerable to protozoal and salmonella bacteremia.1,2

Clinical Features Address Correspondence to: Christina Bailey, MD, Assistant Professor, Division of Infectious and Communicable Diseases, Dept. of Medicine, University of Florida Health Science Center/Jacksonville. 1833 Boulevard, Suite 500, Jacksonville, FL 32206. Email: christina_bailey@doh.state.ﬂ.us.

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Symptoms of TD usually start during the ﬁrst week of travel and are self-limited, lasting 3 to 6 days. Steﬀen et al. subdivided TD into 3 categories of intensity: 1) mild disease with 1-2 bowel movements (BMs) per day with no associated symptoms (cramping, nausea, vomiting, bloody stools, www . DCMS online . org

fever, fecal urgency); 2) moderate disease with 1-2 BMs and associated symptoms or more than 3 BMs with no associated symptoms; and 3) severe, invasive disease with greater than 3 BMs with fever and associated symptoms.1 Many of the afflicted will have to change their itinerary; 20% will be confined to bed for at least one to two days; 5% to 10% will have persistent symptoms for 1 to 2 weeks; 1% to 3% will have chronic diarrhea and 1% will require hospitalization within the visited country. When traveling for an extended period of time, multiple diarrhea attacks are possible. The three patterns of TD, their signs, symptoms and etiologies are depicted in Table I. As a result of severe diarrhea, a traveler may become dehydrated, develop renal insufficiency, have electrolyte disturbances, and have poor absorption of needed medications. Invasive pathogens such as Salmonella, Shigella and Campylobacter species may induce Reiter’s syndrome, Guillain-Barré syndrome, reactive arthritis, or exacerbate inflammatory bowel disease. Bacteremia and other extra-intestinal manifestations are uncommon.2,4 Up to 10% of travelers can develop a post-infectious irritable bowel syndrome (IBS) after TD. This condition seems to be a nonspecific response to the acute enteric infection, resulting in episodic abdominal discomfort and altered bowel habits, not present prior to the infection. Unlike non-infectious IBS, anxiety and depression are less common in post-infectious IBS. Most commonly, the initial symptoms of fever and vomiting resolve, but the abdominal pain, bloating, and diarrhea persist and improve with defecation. The strongest risk factors are the duration and severity of the initial illness. Illnesses lasting greater than three weeks have an 11-fold increased risk.7-9 Tropical sprue is a rare gastrointestinal illness with malabsorption of food causing weight loss and hypovitaminosis

leading to a megaloblastic anemia after several months from the lack of folic acid and vitamin B12. Eventually, the patient will become hypo-albuminemic with peripheral edema.10-12 The syndrome is uncommon among short-time travelers, but much more frequent among expatriates and natives of these countries. Some travelers (1% to 2%) to the Caribbean Isles, particularly to Haiti, or southeast Asia, return home with a diarrheal syndrome of 3 to 4 bulky stools daily. Historically, they had experienced an acute episode of travelers’ diarrhea, however, after a variable period of improvement, the diarrhea returned and persisted. Patients have described a reflex diarrhea after each meal or even any ingestion of food. No etiology was found upon further or renewed diagnostic studies. This history is compatible with tropical sprue.10 No etiology has been determined for tropical sprue. To diagnose tropical sprue, the patient must have lived in or visited an endemic area and have signs of malabsorption. Megaloblastic anemia may be absent early in the disease course. Laboratory tests are nonspecific and only connote a degree of malnutrition (low albumin, calcium, folic acid and vitamin B12, elevated prothrombin time). X-rays (a small bowel follow-through) may give hints when they show segmentation of the barium and dilatation of the bowel lumen. A small bowel biopsy obtained through upper GI endoscopy shows histologic changes that involve the entire small bowel, i.e. blunting of villi with infiltration of mononuclear inflammatory cells in and below the epithelium. This histopathology can also be seen with celiac disease and giardiasis. The D-xylose absorption tests are abnormal in long-standing cases.10-12 Clinical response to tetracycline and folate help differentiate tropical sprue from other etiologies.

Table 1 The Three Patterns of Travelers’ Diarrhea Syndrome

Main Symptoms and Signs

1. Acute watery diarrhea due to cholera-like toxin (non-invasive agents: cholera & some diarrheogenic E. coli)

- Copious, profuse stools - Some vomiting - Dehydration is the main complication. - Symptoms mild to moderate

2. Acute bloody diarrhea/dysentery due to shigella-like toxin (1. invasive agents: some diarrheogenic E. coli, Shigella, Salmonella & Campylobacter 2. Acute amebic dysentery)

- Fevers, systemic malaise and abdominal cramps - Leukocytosis in blood and stools - Stools with mucus and blood - Less acute dehydration - Symptoms moderate to severe

3. Chronic or intermittent diarrhea for at least 2 weeks (Rule out exacerbation or initial presentation of inﬂammatory bowel disease)

- Post-infectious irritable bowel syndrome - Intestinal protozoa (giardiasis & amebiasis) - Tropical sprue - Brainerd diarrhea*

* Brainerd diarrhea is a chronic diarrhea, first described in Brainerd, Minnesota. Raw milk was suspected as the source, but no specific etiologic agent was identified. Other vehicles may be involved. After an incubation period of two weeks, a chronic watery diarrhea develops with urgency and abdominal cramping. The diarrhea can persist for two years. One such epidemic has been reported on a cruise ship.

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Microbiology

Treatment

The causal pathogen is identified in only 40% to 60% of cases in TD. Table II describes the most frequently identified pathogens, the majority (>85%) of which are bacterial in developing countries, and their incidence varies by region.2,4 Contrast this with the situation in developed countries where viruses cause the vast majority of gastrointestinal illness.13 The most commonly identified bacterial pathogens worldwide are the diarrheogenic E. coli, especially enterotoxigenic E. coli (ETEC).1 These bacteria produce both heat-stable and heatlabile enterotoxins.The latter is similar to cholera toxin and is responsible for secretory diarrhea associated with ETEC infection. Enteroaggregative E. coli rates have increased and now account for 10-20% of cases.14 Campylobacter species (up to 30%) may be more common, especially in Asia. Salmonella and Shigella species account for roughly another 15% of infections.15

Treatment is frequently self-administered. In most cases, treatment is supportive. The first step is to prevent dehydration. This is rarely a problem in adults, as long as they have access to safe fluids. The second step is to decrease symptom severity and duration with the use of antimotility and antisecretory agents such as bismuth salicylate or loperamide (Imodium® in trade or generic).17 The latter should only be used with an antibiotic in cases of invasive or severe diarrhea. These agents are very effective, typically reducing stool frequency by 65%, but do not treat the underlying cause.18,19

Viruses are less common in developing countries, accounting for only 10% of cases of TD. In outbreaks, however, viruses such as norovirus (Norwalk-like Calicivirus) have been found to be the cause of explosive gastroenteritides, most notably among passengers of cruise ships.1,4,5 Intestinal protozoa account for a small percentage (0% to12%) of cases of acute TD, but in travelers who have prolonged diarrheal symptoms or don’t respond to antibiotic therapy, they are more significant. These travelers need to be evaluated for Giardia species, Entamoeba histolytica, Cryptosporidia, Cyclospora, microsporidia and isospora.16 If no organism is identified after careful evaluation of multiple stools for bacterial, viral and protozoal pathogens, other diagnoses should be considered. These may include Brainerd diarrhea, Clostridum difficile colitis, inflammatory bowel disease, irritable bowel syndrome and tropical sprue.

Antibiotics are recommended for bacterial TD with moderate to severe symptoms. Fluoroquinolones [ciprofloxacin (Cipro® in trade or generic) or levofloxacin (Levaquin®)] are the current drugs of choice for the majority of travelers. They have high oral bioavailability and achieve high concentrations in the bowel lumen. With treatment, the duration of diarrhea is less than 1½ days in most cases. For non-invasive TD, a single dose may be effective. For bloody mucoid diarrhea, a three-day course of therapy is preferred. Side-effects include rash, photosensitivity, and nausea. There are potential drug interactions with anatacids, certain vitamins, warfarin, phenytoin, cyclosporine, and theophylline. Resistance to the fluoroquinolones is increasing.2-4 Azithromycin (Zithromax®) may be used as an alternative for treatment failures, in children, in pregnant women, and in areas with a high incidence of campylobacter infections i.e. southeast Asia. Trimethoprim/sulfamethoxazole (Bactrim®, Septra® in trade or generic) was the drug of choice for years, but increasing microbial resistance limits its use. It is now recommended only if treatment with both fluoroquinolone and azithromycin fails or in travelers from areas with high rates of cyclospora e.g., Nepal.2-4 Rifaximin (Xifaxan®), a non-absorbable derivative of rifamycin has been studied for both prevention and

Table 2 Etiologies of Travelers’ Diarrhea in Non-Immunocompromised Hosts Viruses Calicivirus (Norwalk-like viruses) Rotavirus Astrovirus Adenovirus, enteric (Types 40 & 41) Other less common viruses: Coronavirus Some Enteroviruses

Bacteria Diarrheogenic E. coli Enterotoxic E. coli (ETEC) Enteroaggregative E. coli (EAEC) Salmonella Shigella Campylobacter Other less common bacteria: Vibrio cholera Halophilic vibrio Aeromonas Yersinia Pleisiomonas Clostridium diﬃcile

20 Vol. 60, No. 4 2009 Northeast Florida Medicine

Parasites/Protozoa Cryptosporidium Giardia Cyclospora Entamoeba histolyticum Other less common intestinal protozoa: Isospora Microsporidia

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treatment of TD. For mild to moderate TD, it is as effective as ciprofloxacin for treatment, but for more severe or invasive disease it is less efficacious and therefore not recommended. The drug does not get into the general circulation and thus has no effect on secondary infections located outside the gastrointestinal tract. Side effects are minimal.20,21 For the treatment of tropical sprue, gluten-free diets are of no help. Patients with tropical sprue are treated with a broad-spectrum antibiotic and vitamin replacements: Rx: Doxycycline 100 mg twice daily for 2 months, followed by 100 mg daily for another 4 months; or, Rx: Tetracycline 250 mg four times daily for 2 months, followed by 250 mg twice daily for another 4 months; and Rx: Folic acid 10 mg PO daily and vitamin B12 1mg IM weekly for the duration of treatment.10-12 The response is fast and impressive. The megaloblastic anemia resolves, and the diarrhea disappears within a few weeks. For patients who do not respond to the above regimen within 4 weeks, an alternate cause of the diarrhea should be pursued. After treatment, however, 1 in 5 patients relapses, and the treatment should be restarted and continued for a few more months.10,11

Prevention Prevention of TD has focused primarily on trying to modify risk behaviors of travelers through education. Travelers are advised to eat only foods that are steaming hot, freshly prepared (avoid buffets), or that they peel/prepare themselves. Dry foods, e.g., breads, are also generally considered safe. Travelers should avoid raw or undercooked meat, especially seafood. Alcohol and citrus, e.g., in seviche, are not bactericidal. Carbonation and boiling are the most effective ways to ensure water is safe. Ice and tap water should be avoided at all times, even on the way back home in the airplane. Remind the traveler that the water in the shower, swimming pool, lakes and rivers is frequently contaminated with sewage.22,23 Compliance to advice may be low. One study of Swiss travelers showed over 70% ate raw vegetables within the first three days of their trip. Other studies have found no correlation between dietary choices and the incidence of TD. This may relate to the background poor sanitation, questionable cleanliness of utensils and dishes, as well as unsafe food preparation and storage.22 No vaccines for ETEC, the most common bacterial etiology of TD are available in the US. For short term travelers, business travelers and those who are immunosuppressed, have severe concurrent disease or have special circumstances, chemoprophylaxis may be considered.18,23,25 The agents should start the day of travel and continue until two days after return. Bismuth subsalicylate has antibacterial, antisecretory, and anti-inflammatory properties. The recommended dose of 2 tablets four times daily provides 62% to 65% protection against TD. The salicylate content is less than aspirin, but concurrent use with warfarin should be avoided. Side effects include tinnitus and blackening of tongue and stools. Use should be limited to www . DCMS online . org

2-3 weeks to avoid the accumulation of bismuth which may cause encephalopathy.17 Trimethoprim/sulfamethoxazole and doxycycline were two antimicrobial treatments studied initially, but now are ineffective due to high levels of bacterial resistance. Azithromycin can be useful due to its long half-life and efficacy against a number of pathogens, including Campylobacter species. Unfortunately, significant resistance does exist and no clinical trials have been done to define appropriate dosing.19,25 Rifaximin given twice daily has been shown to be more than 70% effective for prophylaxis. Side effects were minimal and similar to placebo. No increase in microbial resistance has been seen as yet. However, its efficacy against invasive pathogens such as Salmonella, Shigella, and Campylobacter is limited. Also, the efficacy is short-lived once the drug is stopped.26 Fluoroquinolones have broad coverage of enteropathogens and good safety record. They have up to 90% efficacy for the prevention of TD and until recently were the drugs of choice for most travelers. Increasing fluoroquinolone resistance has already developed in some isolates of Campylobacter, E. coli, and Shigella species. Because of the increasing concern about losing this class of drugs for treatment, use of these agents for prophylaxis is now discouraged.23,27

Conclusion The enjoyment of travel can easily be interrupted by TD. Until sanitation is improved in developing countries, TD will remain a problem for travelers to these regions. Viruses, bacteria and parasites (protozoa) are the most common etiologic agents of travelers’ diarrhea. Many cases of TD could be prevented by a combination of immunization, hand hygiene and the selection of safe food items, although the latter may not be feasible. Chemoprophylaxis should continue to be limited to speciﬁc high-risk travelers and select cases, reserving antibiotics for treatment. Travelers to high-risk destinations will likely need to initiate treatment themselves due to limited medical resources. Continued research for eﬀective, broader range vaccines to include ETEC and the other invasive pathogens would be helpful.

References 1.

Steﬀen R. Epidemiology of travelers’ diarrhea. Clin Infect Dis 2005; 41: S536-40.

Al-abri SS, Beeching NJ, Nye FJ. Traveller’s diarrhea. Lancet Infect Dis 2005;5:349-60.

Fontaine O, Griﬃn P, Henao O, et al. “Acute diarrhea” in Control of Communicable Diseases Manual, 19th ed. Edited by David L. Heymann, 19th ed, Washington, D.C.: American Public Health Association, 2008 pp.179-194.

Fry AM, Braden CR, Griﬃn PM and Hughes JM. “Foodborne Disease” in Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, 6th ed. Edited by Gerald L. Mandell, John E. Bennett, and Raphael Dolin, Philadelphia, PA: Elsevier/Churchill/Livingstone, 2005, Chapter 95, pp.1290-92.

Minooee A, Rickman LS. Infectious diseases on cruise ships. Clin Infect Dis 1999; 29:737-44.

Guerrant RL, Oria R, Bushen OY, Patrick PD, et al. Global

Northeast Florida Medicine Vol. 60, No. 4 2009 21

impact of diarrheal diseases that are sampled by travelers: the rest of the hippopotamus. Clin Infect Dis 2005; 41: S524-30.

16. Okhuysen PC. Traveler’s diarrhea due to intestinal protozoa. Clin Infect Dis 2001; 33: 110-4.

DuPont AW. Postinfectious irritable bowel syndrome. Clin Infect Dis 2008; 46:594-9.

Conner BA. Sequelae of traveler’s diarrhea: focus on postinfectious irritable bowel syndrome. Clin Infect Dis 2005; 41 (8): S577-86.

17. Rao G, Aliwalas MG, Slaymaker E and Brown B. Bismuth revisited: an eﬀective way to prevent travelers’ diarrhea. J Travel Med 2004;11:239-242.

Connor BA. “Persistent Travelers’ Diarrhea” in CDC’s Health Information for International Travel – 2010. The Yellow Book. Edited by Gary W. Brunette, Phyllis E. Kozarsky, Alan J. Magil, David R. Shlim and Amanda D. Whatley, Atlanta, GA: Mosby/Elsevier, 2009 p.281.

10. Ruiz AR Jr. “The Malabsorption Syndromes – Tropical Sprue” in The Merck Manual, 18th ed. Edited by Mark H. Beers and others, Whitehouse Station, NJ: Merck Research Laboratories, 2006, pp. 147-148. 11. Binder HJ. “Tropical Sprue” in Harrison’s Principles of Internal Medicine, 16th ed. Edited by Dennis L. Kasper and others, New York, NY: McGraw-Hill, Medical Publishing Division, 2005. pp.1772-1773. 12. Mansbach CM II. “Diseases Producing Malabsorption and Maldigestion” in ACP Medicine. Edited by David C. Dale and Daniel Federman, Hamilton, Ontario:BC Decker, Inc., 2009, Section 4 –Gastroenterology XI:7-8. 13. Musher DM and Musher BL. Contagious gastrointestinal infections. N Engl J Med 2004; 351: 2417- 2427. 14. Adache JA, Jiang Z-D, Mathewson JJ, Verenker MP, et al. Enteroaggregative Escherichia coli as a major etiologic agent in traveler’s diarrhea in three regions of the world. Clin Infect dis 2001; 32: 1706-1709. 15. Allos BM. Campylobacter jejuni infections: update on emerging issues and trends. Clin Infect Dis 2001:32:1201-6.

18. DuPont HL, Ericsson CD, Farthing MJ, et al. Expert review of the evidence base for self-therapy of travelers’ diarrhea. J Trav Med 2009; 16: 161-171. 19. Ericsson CD. Nonantimicrobial agents in the prevention and treatment of traveler’s diarrhea. Clin Infect Dis 2005; 41: S557-63. 20. Dupont HL, Jiang Z-D, Ericsson CD, Adachi A, et al. Rifaximin versus ciproﬂoxacin for the treatment of traveler’s diarrhea: a randomized, double-blind clinical trial. Clin Infect Dis 2001; 33: 1807-15. 21. Taylor DN. Poorly absorbed antibiotics for the treatment of traveler’s diarrhea. Clin Infect Dis 2005; 41: S564-70. 22. Shlim DR. Looking for evidence that personal hygiene precautions prevent travelers’ diarrhea. Clin Infect Dis 2005; 41: S531-5. 23. DuPont HL, Ericsson CD, Farthing MJ, et al. Expert review of the evidence base for prevention of travelers’ diarrhea. J Trav Med 2009; 16:149-160. 24.

Larson E. Skin hygiene and infection prevention: more of the same or diﬀerent approaches? Clin Infect Dis 1999; 29:1287-94.

25. Rendi-Wagner P, Kollaritsch H. Drug Prophylaxis for Traveler’s Diarrhea. Clin Infect Dis 2002; 34: 628-33. 26. Dupont HL, Jiang Z-D, Okhuysen PC, Ericsson CD, et al. Antibacterial chemoprophylaxis in the prevention of traveler’s diarrhea: evaluation of poorly absorbed oral rifaximin. Clin Infect Dis 2005; 41: S571-6. 27. Sack RB. Prophylactic antimicrobials for traveler’s diarrhea: an early history. Clin Infect Dis 2005; 41: S553-6.

Traveling Through Photos Interesting airport photos taken by Bobi Wall. (Left) A mezzanine walkway brings a diﬀerent perspective to this airport lobby and its artistic tile ﬂoor design. (Right) An intriguing mural in the Jacksonville International Airport in Jacksonville, FL,encourages traveling and taking an adventure.

Go to www.bobiwall.com to see these photographs in color.

22 Vol. 60, No. 4 2009 Northeast Florida Medicine

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Special Insert - CME and News

Children: The Hidden Victims of Intimate Partner Violence

Background - Benefits that Matter! The Duval County Medical Society (DCMS) attempts to provide its members with the benefits that consistently meet your professional needs. One example of how this is being accomplished is by providing to DCMS members free Continuing Medical Education (CME) opportunities in the subject areas mandated/and or suggested by the State of Florida Board of Medicine to obtain and retain medical licensure. The DCMS would like to thank the St. Vincent’s Healthcare (SVHC) Committee on CME for reviewing and accrediting this activity in compliance with the Accreditation Council on Continuing Medical Education (ACCME). Helena Karnani, MD, Chair of the CME Committee; Betsy Miller, Director, Medical Staff, Quality Management; and Cindy Williamson, CME Coordinator, from SVHC deserve special recognition for their work on behalf of DCMS. This issue of Northeast Florida Medicine includes an article, “Children: The Hidden Victims of Intimate Partner Violence” authored by Joan L. Huffman, MD, (see insert, p. 3), which has been approved for 2.0 AMA PRA Category 1 credit(s).™ For a full description of CME requirements for Florida physicians (MD/DO), please visit the DCMS website (http://www.dcmsonline.org/cme_requirements.aspx).

Faculty/Credentials: Joan L. Huﬀman, MD, FACS, is Assistant Professor in the Department of Surgery at the University of Florida, Shands Jacksonville. Objectives for CME Journal Article 1. Deﬁne Intimate Partner Violence and understand the underlying mechanisms that contribute to the abusive behavior patterns.

2. Understand the short and long-term impact of Intimate Partner Violence on children. 3. Screen for Intimate Partner Violence in the families of pediatric patients and make appropriate interventions.

Date of Release: December 7, 2009 Date Credit Expires: December 7, 2011

Estimated time to complete: 2 hrs.

Methods of Physician Participation in the Learning Process 1. Read the “Children: The Hidden Victims of Intimate Partner Violence” article on insert pages 3-5 2. Complete the Post Test and Evaluation on insert page 2 3. Cut out & fax the Post Test and Evaluation to DCMS (FAX) 904-353-5848 OR logon to www.dcmsonline.org & submit test online

CME Credit Eligibility In order to receive full credit for this activity, a minimum passing grade of 70% must be achieved. Only one re-take opportunity will be granted if a passing score is not made on the ﬁrst attempt. DCMS members have two years to submit the post test and earn CME credit. A certiﬁcate of credit/completion will be emailed, faxed or USPS mailed within 4-6 weeks of submission. If you have any questions, please contact the DCMS at 355-6561, ext. 103, or llegacy@dcmsonline.org.

Faculty Disclosure Information Dr. Huffman reports no significant relationships to disclose, financial or otherwise with any commercial supporter or product manufacturer associated with this activity.

Disclosure of Conflicts of Interest St. Vincent’s Healthcare (SVHC) requires speakers, faculty, CME Committee, and other individuals who are in a position to control the content of this educational activity to disclose any real or apparent conflict of interest they may have as related to the content of this activity. All identified conflicts of interest are thoroughly evaluated by SVHC for fair balance, scientific objectivity of studies mentioned in the presentation and educational materials used as basis for content, and appropriateness of patient care recommendations.

Joint Sponsorship Accreditation Statement This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of St. Vincent’s Healthcare and the Duval County Medical Society. St. Vincent’s Healthcare is accredited by the Florida Medical Association to provide continuing medical education for physicians. The St. Vincent’s Healthcare designates this educational activity for a maximum of 2.0 AMA PRA Category 1 credit(s) .TM Physicians should only claim credit commensurate with the extend of their participation in the activity.

Insert

Northeast Florida Medicine

Vol. 60, No. 4 2009

Children: The Hidden Victims of Intimate Partner Violence

CME Questions & Answers (Circle Correct Answer) Free-DCMS Members/$50.00 charge non-members*

(Return prior to December 7, 2011 by FAX: 353-5848, by mail: 555 Bishopgate Lane * Jacksonville, FL 32204 OR online: www.dcmsonline.org) b. You must submit an oral report to the Florida Department of Children and Family Services (DCFS). c. Hope the abuser doesn’t ﬁnd out you know and slits the tires on your Jaguar. d. Recommend family counseling for the family unit: the victim, the abuser and the child.

1. Intimate partner (IPV) violence is: a. Rare in upper socioeconomic classes b. Usually a single unrepeated event c. A repetitive cyclical pattern of power and control d. Not inﬂuential on childhood development 2. Which increased risks exist for children who live with IPV? a. Neglect b. Indirect or direct abuse c. Losing one or both parents d. Exposure to traumatic emotional events e. All of the above

6. Children exposed to IPV may display all the maladaptive responses EXCEPT: a. Emotional responses b. Cognitive responses c. Desire to play team sports d. Biologically-based responses e. Behavioral responses

3. Children who repeatedly witness IPV are at risk for: a. Type I Trauma b. Type II Trauma c. Neither 4. Signs and symptoms of children exposed ti IPV include all of the below EXCEPT: a. Large peer groups b. Cruelty to pets c. Bullying d. Bed-wetting e. Food addictions 5. If as a Florida physician, you have knowledge of reason able cause to suspect abuse, abandonment or neglect of a child: a. Try not to worry about it. It’s none of your business what goes on inside a private family home.

7. Children need the following to grow up emotionally healthy EXCEPT: a. Safe and secure home environment b. Numerous expensive toys c. Routine and normalcy d. Non-violent role models 8. Factors that influence the effect of IPV on children: a. Emotional effects are worse the older the child is when exposed. b. Distantly occurring IPV is more detrimental than recent events c. Kids with good social supports are harmed the worst d. The more intense and frequent the violence the greater the impact

Evaluation questions & CME Credit Information (Please evaluate this article. Circle one number using this scale: 1= Strongly Agree to 5= Strongly Disagree)

The article met the stated objectives: 1 2 3 4 5 The article was appropriate to my practice: 1 2 3 4 5 The topic was current and well presented: 1 2 3 4 5 Comments:_______________________________________________________________________ __________________________________________________________________________________________ _________________________________________________________________________________________ Name (Print)___________________________________________Email__________________________ Address/City/State/Zip_________________________________________________________________ Phone__________________________Fax_____________________DCMS Member (circle)

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Insert

Children: The Hidden Victims of Intimate Partner Violence Joan L. Huﬀman, MD, FACS Abstract: Intimate Partner Violence (IPV), a repetitive cyclic pattern of power and control, is pervasive in our society today. Many resources on assessing, identifying and referring adult IPV victims are available to the Florida Practitioner.1, 2, 3 Unfortunately, adults and their partners are not the only victims of IPV. Tragic as IPV is, it aﬀects not only the individual victim but also the children in the home who are unwitting observers and as such may be either primary or secondary victims as well. The impact of IPV on children can have both short and long-term implications. Physicians must learn to screen for IPV in the families of pediatric patients and know how to make appropriate interventions. As correctly stated by Herbert Ward, “Child abuse casts a shadow the length of a lifetime.” 4

Background on Intimate Partner Violence Intimate partner violence (IPV) is a pattern of repeated assaults and/or coercive behavior that one intimate partner imposes upon another. The abuses can take many forms; from physical, to sexual, and/or psychological. The perpetrator utilizes these behaviors to maintain power and control through a cyclic chain of events beginning with a buildup of tension, leading to an outbreak of violence and then receding in a honeymoon phase. The awful cycle repeats, often becoming more and more vicious. Anyone can be a victim of IPV regardless of ethnic, cultural, social, religious or sexual orientation.3, 5

Statistical Scope The scope of the problem is enormous. In the US, onequarter to one-third of women and 11% of men experience domestic violence from their intimate partner, and 90% of children in those homes witness the events. At least 10-20% of all American children witness IPV, therefore, 3.3 -10 million children see violence in their homes. Worldwide, 275 million children observe IPV at home. A survey of a single day in 2007 found that because of IPV, greater than 13,000 children were living in a transitional housing facility or domestic violence shelter. Greater than 5,000 used services of a non-residential program.6, 7, 8, 9 In one-half to one-third of families where the woman is abused, children are abused, too. Girls in those families are at 6.5 times greater risk for sexual abuse by the male batterer. All children in those homes are of victims of abuse and neglect at a rate greater than 15 times that of other families. Women IPV victims are twice as likely as non-victims of IPV to abuse a child. Children can be injured by several means in the IPV home: indirect violence, e.g., the victim is holding the child when she is assaulted, the child accidentally gets caught in the middle of an altercation between adults or

Address Correspondence: Joan L. Huffman, MD, FACS, University of Florida @ Shands Jacksonville, 655 West 8th Street, 8th Floor Clinical Center, Jacksonville, FL 32209. Email:joan.huffman@ jax.ufl.edu. Insert

tries to intervene to protect the victim; or direct violence, the abuser purposefully hurts or sexually assaults the child to cause emotional harm to the victim. All these data lead to a serious conclusion: IPV can lead to child neglect, child physical and sexual violence, and even death, and as such is a critical public health concern.5, 10

Impact of the Problem Four increased risks exist for children who live with IPV: neglect, indirect or direct abuse, losing one or both parents, and exposure to traumatic emotional events. Any or all of these risks can cause negative outcomes for children in the realm of safety, stability and well-being and lead to associated childhood problems. Adverse childhood experiences influence health and well-being throughout the lifespan from conception to death. One may think of this as a developmental pyramid, with each phase building upon the prior stage. If an infant is exposed to IPV there may be interrupted neurodevelopment, which can lead to social, emotional and cognitive impairment, adoption of health-risk behaviors, disease, disability and social problems and even early death.6, 10 Because IPV is classically ongoing, with traumatic events of repeated or prolonged exposure, it meets criteria as Type II trauma. This trauma involves extreme or severe threatening events that may be unpredictable and uncontrollable and overwhelm normal coping skills. Specific patterns of avoidance and hyper-arousal occur. Due to the threat to safety and security in a persistent manner, Type II trauma has a great impact on long term individual functioning, with a sense of helplessness maintained. Children who are victims of Type II trauma may develop Posttraumatic Stress Disorders (PTSD) with associated maladaptive behaviors. 5, 6, 10 (Table 1, p.4) Extreme resiliency and protective factors, e.g., intelligence, strong peer and sibling relationships, social competence, outgoing temperament, high self-esteem and/or a relationship with a supportive adult, may lead some fortunate children to overcome the adverse effects of witnessing IPV. Additional issues that impact the influence of IPV on children are the nature of the violence (intensity and frequency), individual coping skills, strategies and networks, child age at exposure (worse in younger children), presence of concurrent child sexual/physical abuse and time since the IPV occurred.6

Signs and Symptoms of Exposure to IPV Various age groups display a wide range of reactions in response to exposure to IPV. Preschool and kindergarten children do not understand what is happening when they see IPV and may feel “I must have done something wrong”, and exhibit self-blame. Regressive behaviors may surface, like clinging, whining, and bed-wetting. They may withdraw and become non-verbal, have problems eating and sleeping, experience anxiety, or lack concentration. They may have more Northeast Florida Medicine

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Table 1 Maladaptive Responses in Children Exposed to IPV

Emotional

Cognitive

Shock Terror Guilt Horror Irritability Anxiety Hostility Depression

Concentration impairment Confusion Self-blame Intrusive thoughts Flashbacks Decreased self-eﬃcacy Fears of losing control Fear of recurrence of trauma

Biologically Based Insomnia Nightmares Exaggerated startle response Psychosomatic symptoms

allergies, asthma attacks, gastrointestinal problems or the flu due to the stress on their immune systems.5, 6, 10, 11 Grade school kids tend to lose respect for the victim and identify with the aggressor, equating anger with violence and justifying the violence; some however, will become very dependent or protective. Male roles are identified as dominant, female roles as subordinate.10 Pre-adolescent youngsters are more verbal about the events of IPV, but they too may display symptoms of anxiety and avoid social activities and peer relationships.Traditionally, male children display aggressive externalized behaviors, becoming abusers or victimizers, having tantrums, bullying, fighting, threatening, treating pets cruelly, destroying property, or exhibiting violent attention-getting maneuvers. Female children exhibit internalized effects of depression or withdrawal; self-destructing to become victims themselves. Sadly, a quiet withdrawn child may not be noticed as a child in need of significant help.5 Risks for adolescents are failing academically, dropping out of school, falling into delinquency or substance abuse. These kids may run away, develop food addictions, or be victims of sexual assault/date rape/ teen pregnancy. Depressed teens may attempt or succeed at suicide. Approximately 20-33% of teenagers abuse or are abused by their dating partners; 30-50% of these abusive relationships may re-create the same escalating violence as their adult role models. Thus, a new generation of violent families begins. 5

Behavioral Avoidance Social withdrawal Decreased intimacy in relationships Decreased trust Substance abuse

of IPV are reluctant to disclose abuse, and so too, are the children that witness IPV. They may have been threatened or warned about talking to strangers about the events that occur at home. At risk children should be referred to counselors or social workers. Other resources are relatives and teachers. Certainly children should be encouraged to verbalize their feelings and concerns, but if they are not comfortable with that level of personal emotional exposure, there are other therapies like art or journaling to facilitate expression. Older pre-adolescents and teens may feel more open about talking. Give them permission to share their experiences. In that case, warm, non-judgmental, genuine listening and unconditional acceptance will be most eﬀective.5, 10 If real abuse, neglect or abandonment is identiﬁed, by Florida law the standard for reporting for all doctors, dentists, nurses, mental health and social workers is “knowledge of reasonable cause to suspect abuse, abandonment or neglect”. The mechanism is an oral report to the Florida Department of Children and Family Services (DCFS).12

What Children Need

Practice Implications

Children need a safe, secure home environment where adults will listen, believe and shelter them in a home that provides routine and normalcy. They also need child-focused support services that teach IPV is wrong and then guide them to learn non-violent conﬂict resolution by role-modeling. One place where these services are oﬀered is at Hubbard House in Jacksonville, FL. (see www.hubbardhouse.org) There are other local domestic violence shelters in other locations. Doing an online search will provide contact information.

First, physicians must identify the problem. Just as all adult patients must be screened for IPV by utilizing the RADAR (Table 2, p.5) method and Partner Violence Screen, (Table 3, p.5) so too must parents and children be screened for evidence that children are witnesses to violence in the home.1, 2, 3 Victims

In order for the necessary role-modeling and teaching to occur, children need courageous adults and healthcare providers to break the silence and speak out, to create laws and policies that protect children and to raise the social awareness of the impact of IPV on children.13, 14, 15

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Table 2 RADAR Acronym for IPV Intervention

R = Routinely ask about Domestic Violence A = Ask direct questions D = Document your ﬁndings A = Assess patient readiness & safety R = Respond, review options & refer References 1.

Domestic Violence: The Florida Requirement. Course #9787. CME Resource. August 2009; 135:1:13-24. Sacramento, CA or www.NetCE.com.

Domestic Violence and Abuse Screening and Counseling (Level III). Health Care Guideline: Preventive Services for Adults. Institute for Clinical Systems Improvement (ICSI) pp 4, 33. http://www.icsi.org/preventive_services_for_adults/ preventive_services_for_adults_4.html. 14th Ed. Oct.2008.

Huﬀman JL. Intimate Partner Violence Update. Northeast Florida Medicine. 2007; 58:4:31-36.

http://thinkexist.com/common/cite.asp? dit-http://einstein/ /einstein/quotes/herbert_ward/&name-Herbert%20Ward %20&name=Herbert%20Ward%20quotes.

Volpe JS. Eﬀects of Domestic Violence on Children and Adolescents: An Overview. The American Academy of Experts in Traumatic Stress, Inc. http://www.aaets.org/article8.htm 1996.

Children and Domestic Violence. Bulletin for Professionals. Child Welfare Information Gateway. http://www.childwelfare. gov/pubs/factsheets/domestic violence.pdf August 2003.

The Facts on Children and Domestic Violence. Family Violence Prevention Fund. http://endabuse.org/userﬁles/ﬁle/ Children_and_Families/Children.pdf August 2008.

The Facts on Preventing Violence against Women and Children. Family Prevention Fund. http://endabuse.org/userﬁles/ﬁle/ Children_and_Families/Prevention.pdf.

Fact Sheet: Intimate Partner Violence and Healthy People 2010 Fact Sheet. Family Prevention Fund. http://endabuse. org/userﬁles/ﬁle/HealthCare/pediatric.pdf.

Table 3 IPV Screen Patient Interview Questions

1. “Have you been hit, kicked, punched, or otherwise hurt by someone in the past year?” 2. “Do you feel safe in your current relationship?” 3. “Is there a partner from a previous relationship who is making you feel unsafe now?” 10. Fact Sheet: Domestic Violence and Young Children. Action Alliance for Children. July-August 1997. ttp://www.4children. org/issues/1997/july_august/fact_sheet_domestic_violence_ and_young_children. 11. Kyra Gottesman Evans. If Mom’s Battered Children Suffer. Action Alliance for Children. July-August 1997. http:// www.4children.org/issues/1997/july_august/fact_scheet_ domestic_violence_and_young_children. 12. Groves BA, Augustyn M, Lee D and Sawires P. Identifying and Responding to Domestic Violence. Consensus Recommendations for Child and Adolescent Health. The Family Violence Prevention Fund. http://endabuse. org/userfiles/file/HealthCare/pediatric.pdf. First Printing: September 2002; Updated: August 2004. 13. Behind Closed Doors: The Impact of Domestic Violence on Children. UNICEF Child Protection Section http://www. unicef.org/media/files/BehindClosedDoors.pdf & the Global Stop the Violence in the Home Campaign by The Body Shop. www.bodyshop.com 2006. 14. Taggart, S. Child and Family Service Review Outcomes: Strategies to Improve Domestic Violence Responses in CFSR Program Improvement Plans. August 2009. http://endabuse. org/userfiles/file/Children_and_Families/CFSR%202009. pdf. 15. Healthcare Guideline: Domestic Violence. Institute for Clinical Systems Improvement (ICSI) pp 1-47. http://www. icsi.org/domestic_violence/domestic_violence_2589.html. Tenth Edition, September 2006. Note: All Web sites cited accessed on October 14, 2009.

“Physicians must learn to screen for intimate partner violence (IPV) in the families of pediatric patients and know how to make appropriate interventions.” Insert

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A Special Thank You WE CARE Jacksonville gives a special thank you to specialty and primary care physicians who volunteer their time to provide access to health care for the low income, uninsured residents of Duval County. We also thank those physicians who serve on the WE CARE Jacksonville Board

Physician Specialty Groups Anesthesia Consultants Borland-Groover Clinic ECG Associates of Jacksonville Emergency Medical Specialists Emergency Resources Group First Coast Cardiovascular Institute Florida Anesthesia Associates ICON Jacksonville Anesthesia Providers Jacksonville Heart Center Jacksonville Orthopaedic Institute Jacksonville Pathology Consultants Drs. McClow, Clark and Berk Drs. Mori, Bean and Brooks North Florida Anesthesia Consultants North Florida Surgeons N.E. Florida Endocrine & Diabetes Associates St. Vincent’s Pathology Associates

Legacy of Care Health Clinic Mission House Clinic Oasis Medical Clinic River City Health Clinic St. Vincent’s Mobile Health Van Trinity Rescue Mission

WE CARE Jacksonville Physician Board Members: Dr. Gary Bowers Dr. James Burt Dr. William Cody Dr. Leonardo Del Rosario Dr. Javier Herrera Dr. Daniel Lestage Dr. Stanton Longenecker Dr. Charles McIntosh Dr. David Moomaw Dr. Todd Sack Dr. Sue Nussbaum, Executive Director

Individual Physician Participants Dr. Scot Ackerman Dr. Curtis Bleau Dr. Paul Coley Dr. Cynthia Flanders Dr. Kay Holmes Dr. John Kartsonis Dr. William Knauer Dr. Jeﬀrey Levenson Dr. Lawrence Lisska Dr. Robert Loper Dr. Frank McDonald Dr. Raul Moreno Dr. Paul Ossi Dr. Ryan Perkins Dr. Matthew Robertson Dr. Hemant Shah Dr. Rajesh Shetty Dr. Walter Smithwick Dr. Leonard Spillert Dr. James Staman Dr. George Trotter Dr. Amit Vijapura

We Care Jacksonville A Voluntary Health Care Program in Service to the Community 900 University Boulevard North, Suite 200-E Jacksonville, FL 32211 Phone: (904) 253-2269 Fax: (904) 253-2457 Website: www.WeCareJacksonville.org

Volunteer Primary Care Health Clinics Christ the Clinic Medical Clinic City Rescue Mission Healing Hands Clinic The Help Center Health Clinic I.M. Sulzbacher Healthcare for Homeless I.M. Sulzbacher Beaches Community Healthcare Clinic

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An Update on Malaria and Insect Avoidance Rachana M. Palnitkar, MD Abstract: Malaria remains endemic in many parts of the world. Physicians providing pre-travel services must understand the geographic distribution of malaria, its drug sensitivity in the travel area and the appropriate chemoprophylactic choice. The adjunctive use of insect bite prevention measures maximizes the travelers’ protection against acquiring malaria. A discussion of management of malarial infection is beyond the scope of this review.

Introduction Each year millions of United States (U.S.) travelers visit malaria endemic areas. About 800 returning travelers are diagnosed with malaria each year. Of those, 73% of malaria cases diagnosed in the U.S. are found in travelers who went to Africa. Between 1985 and 2002, 78 U.S. travelers died from malaria.1 Knowledge of the geography of malaria and the means of protection against infection; both through insect bite avoidance and anti-malarial chemoprophylaxis are essential to protect the potentially exposed traveler.

Epidemiology Although malaria has been eradicated from many areas of the world, like North America and Western Europe, it remains endemic in many tropical countries in sub-Saharan Africa, Asia and Central and South America.1 Malaria occurring in non-endemic countries is usually imported from an endemic area by travelers, often those returning to their country of origin to visit friends and relatives (VFR). Malaria due to Plasmodium falciparum is most commonly acquired in the African region (70%), followed by South East Asia (25%).2 Infection due to P.vivax can be acquired in India (17%), Indonesia (12.1%), South America (11.4%) and Western Africa (11.4%).3 “Airport malaria” occurs when an infected mosquito from an endemic area arrives in a non-endemic area in an aircraft and bites local residents.4

The Pathogen – Mosquito Relationship Plasmodium species, the causative agents of malaria, are protozoan parasites belonging to the group Apicomplexa.4 Four species of Plasmodium infect humans i. e. Plasmodium falciparum,, Plasmodium vivax, Plasmodium malariae and Plasmodium ovale. The infection is transmitted to humans by the bite of an infected female Anopheles mosquito. The plasmodium species has a developmental period in the mosquito to reach the infective stage. This pre-patent period may range from ﬁve days to two weeks depending on the ambient temperature and humidity. It follows then that a newly infected mosquito is not immediately infectious to the next person bitten. Address correspondence to: Rachana M. Palnitkar, MD,Department of Infectious Disease, University of Florida College of Medicine, Jacksonville, FL 32206. Email: rachana.palnitkar@jax.uﬂ.edu.

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Life Cycle in Man The life cycle of Plasmodium species in the human host is divided into an exo-erythrocytic and an erythrocytic phase. When the mosquito has a blood meal on a human host, sporozoites, the infective plasmodia form, are injected into the persons’ bloodstream. The sporozoites travel to the liver, mature into schizonts, which rupture and release merozoites., a process that takes about 1-2 weeks for P.falciparum and P.malariae.4 In P.vivax and P.ovale life cycles hypnozoites (dormant stages) persist in the liver, which can release merozoites into the blood stream weeks or even years later, causing relapses. This is the exo-erythrocytic phase of the malarial life cycle. The merozoites infect the red blood cells (RBCs) and mature to form trophozoites, then schizonts, which further mature into multiple merozoites. RBC rupture results in release of the merozoites and infection of new red cells. This is the erythrocytic phase of the life cycle. Each cycle of red cell rupture (48 hrs in P.falciparum, P. vivax, P. ovale and 72 hrs in P.malariae) releases pyrogenic metabolic products of the schizont causing the fever and rigors typical of malaria. This red cell lysis results in anemia.5 Some of the trophozoites in the RBCs diﬀerentiate into sexual forms, i.e., microgametocytes (male) and macrogametocytes (female), which are taken in by the Anopheles mosquito during a human blood meal. The microgamete penetrates the macrogamete resulting in development of zygotes in the stomach of the mosquito. These mature and migrate to the mosquitos’ salivary glands and rupture to release sporozoites, which then are injected into humans during a blood meal.1

Pathophysiology The classic malaria paroxysm is chills and rigors followed by high fevers, profuse sweating and then fatigue.4 These paroxysms coincide with rupture of the RBCs containing matured schizonts as mentioned earlier. Plasmodium falciparum causes the most acute, severe and potentially fatal malaria. Many mechanisms are responsible for the diﬀerence between falciparum and other plasmodium species. P. falciparum infects red cells of all ages, as opposed to P. vivax which infects only young RBCs. This accounts for the very high parasitemias in P. falciparum infections. Infected RBCs have decreased deformability and increased surface stickiness leading to sequestration in the microcapillary circulation of many organs, including the spleen, brain and lungs with microinfarction and tissue hypoxemia. Cytoadherence, rosetting and immune complex deposition on RBCs are the various mechanisms involved in the pathogenesis of this disease.4,6,7

Northeast Florida Medicine Vol. 60, No. 4 2009 23

Clinical Presentations The malaria paroxysm is characterized by fever (>92% cases), chills (79%), diaphoresis (64%) and occurs due to rupture of the schizont and erythrocyte destruction. Physical examination could reveal fever, tachycardia, jaundice, pallor, hepatosplenomegaly.8 Severe malaria is commonly caused by P.falciparum, but rarely other species such as P.vivax, P.ovale can cause severe relapses and death. Severe malaria generally includes cerebral malaria, which can present as confusion, coma, seizures, hallucinations, psychosis. Other manifestations such as acute lung injury, severe anemia, hypoglycemia, acidosis, renal failure, thrombocytopenia contribute to increased morbidity and mortality in infected patients especially children. The fatality rate due to falciparum malaria in returning travelers is 0.6-3.8% and up to 20% for severe malaria.8 Due to the potential severity and mortality of the infection, malaria should always be considered as an etiology of fever after recent travel to endemic country. A suspicion of malaria should prompt consultation with an expert in infectious diseases and/or tropical medicine to aid in the diagnosis and therapy.

Malaria Chemoprophylaxis Basics Agents used for malaria prophylaxis are not 100% effective, but in conjunction with insect avoidance measures can be successful in preventing the majority of episodes of malaria related to travel. Chemoprophylactic agents must be taken at variable times before travel, continued throughout the stay and then ongoing for variable periods after completion of travel for maximum efficacy. To select an appropriate anti-malarial chemoprophylactic regimen, attention must be given to the geographic area of travel, antimalarial drug resistance in that travel area, the traveler’s allergy, medical and medication histories. Chemoprophylactic agents can be divided into those that kill intra-erythrocytic schizonts , the blood schizonticides; those that kill hepatic schizonts and hypnozoites, the tissue schizonticides and those that have both modes of activity. Chemoprophylaxis with agents having tissue schizonticidal activity, e.g. malarone, can be completed with seven days of therapy after the exposure versus four weeks of post exposure therapy for agents with only erythrocytic schizonticidal activity eg chloroquine or mefloquine. Refer to Table 1 for drug dosages and duration.9 Chloroquine remains the chemoprophylactic drug of choice only for travelers going to areas of known chloroquine sensitivity. These areas include Dominican Republic, Haiti, Central America west of the Panama Canal and some countries in the Middle East.1 Adverse effects of chloroquine include nausea, vomiting, itching, and dizziness. It is safe to use in pregnancy and children. It is a blood stage schizonticide and hence therapy needs to be continued for four weeks after travel completion. Atovaquone – proguanil (Malarone®) has become the combination agent of choice for travelers to areas with chloroquine resistance that remain atovoquone-proguanil sensitive. At this 24 Vol. 60, No. 4 2009 Northeast Florida Medicine

time resistance is rare. It is contraindicated in pregnancy, breast feeding, children <11 kg, and renal dysfunction. It is a blood and tissue stage schizonticide and hence therapy needs to be continued only for seven days after travel completion.9 Mefloquine (Lariam®, also available in a generic) is an alternative to atovaquone – proguanil in areas of chloroquine resistance. Mefloquine resistance has been reported along the Thailand borders with Cambodia and Myanmar. Adverse reactions include psychoses, seizures, vomiting, vivid dreams and headache. It is contraindicated in anyone with psychoses, active depression or history of seizures. It can be used in pregnancy and children. It is a blood stage schizonticide and hence therapy needs to be continued for four weeks after travel completion.9 Doxycycline is an option in travelers going to endemic areas with chloroquine or mefloquine resistance; travelers with a contraindications to the use of mefloquine or those requesting a less expensive option to malarone. Doxycycline is taken daily and since it is a blood stage schizonticide, therapy needs to be continued for four weeks after travel completion. Adverse effects include gastrointestinal side-effects such as heartburn and nausea, photosensitization and mucosal candidiasis. It is contraindicated in children <8yrs due to staining of dental enamel and pregnancy due to teratogenicity. Primaquine is a tissue stage schizonticide and hypnozoiticide and is used as prophylaxis against late relapses due to P. vivax for travelers to hyper-endemic areas eg the Solomon Islands. It rarely has been used as a primary prophylactic agent, however, this is generally not recommended. Hemolysis in glucose 6 phosphate dehydrogenase (G6PD) deficiency limits its broad use.9

Insect avoidance Insect avoidance is an important adjunct to chemoprophylaxis in preventing malaria in travelers and in any strategy to control malaria transmission. N, N-diethyl-meta-toluamide (DEET) has a good safety profile and efficacy in preventing mosquito bites. The female Anopheles mosquito feeds on the human host typically from dusk to dawn. Application of DEET to exposed areas during this time period effectively prevents bites. DEET can be used in various concentrations, 30-35% being the most commonly used. Protection can last from a few to 8-10 hours depending on the DEET preparation and ambient conditions. Toxicity is minimal and is usually from incorrect application. Neurotoxicity and local allergic reactions have been reported. It can be used with caution and in low concentration on infants as well as pregnant women after the first trimester. Care should be exercised when used on infants and children to avoid application around the eyes and on parts of their hands, which could be inserted in their mouths. Other insect repellants include citronella, lavender oil, Skin So Soft and Bite Blocker. Most of these do not provide protection beyond minutes to a few hours and are not as effective as DEET. The safety profiles of these have not been well studied.10 www . DCMS online . org

Picaridin (2-(2-hydroxyethyl)-1-piperidinecarboxylic acid 1-methylpropyl ester) is a recently approved insect repellant in the United States. It is a safe, eﬀective and odorless non-greasy product. It can be used on children older than 2 years of age. It is available as a 7% solution under the trade name Cutter Advanced®. Picaridin is the recommended insect repellant for mosquitoes transmitting malaria according to World Health Organization proclamation in 2000.11

10. Stauﬀer WM, Kamat D, Magill AJ. Traveling with infants and children. Part IV: insect avoidance and malaria prevention. J Travel Med. 2003 Aug ;10(4):225-240. 11. Katz TM, Miller JH, Hebert AA. Insect repellents: historical perspectives and new developments. J. Am. Acad. Dermatol. 2008 May ;58(5):865-871.

Permethrin is a synthetic pyrethroid that acts as a contact insecticide. It is not for use on skin, but used to saturate clothing and bed nets. The effect lasts for a minimum of two weeks despite laundering. The safety and efficacy profile are remarkable. Together with topically applied 35% DEET, permethrin impregnated clothing provides 99% protection against bites for a period of 8 hours.10

Conclusion Travel related malaria is a signiﬁcant cause of morbidity and in some instances mortality, which can be eﬀectively prevented by a combination of insect avoidance strategies and chemoprophylaxis.

Resources Tan KR, Mali S, Arguin PM. Malaria risk information and prophylaxis by country. 2010 CDC Health information for international travel – Yellow Book. Chapter 2. http://wwwn.cdc. gov/travel/yellowbook/2010/chapter-2/malaria-risk-informationand-prophylaxis.aspx. Accessed August 13, 2009. 2009 WHO International travel and health. Chapter 7. Malaria http://www.who.int/ith/ITH2009Chapter7.pdf. Accessed August 13, 2009.

References 1.

CDC-malaria [Internet]. Available from: http://www.cdc. gov/malaria/ Accessed August 13, 2009.

Snow RW, Guerra CA, Noor AM, Myint HY, Hay SI. The global distribution of clinical episodes of Plasmodium falciparum malaria. Nature. 2005 Mar 10;434(7030):214-217.

Mühlberger N, Jelinek T, Gascon J, et al. Epidemiology and clinical features of vivax malaria imported to Europe: sentinel surveillance data from TropNetEurop. Malar. J. 2004 Mar 8;35.

Mandell G, Bennett J, Dolin R. Mandell, Douglas, and Bennett’s: Principles and Practice of Infectious Diseases, 6th ed. Philadelphia, PA:Elsevier; 2005, pp. 3121-3144.

5. Ghosh K et al: Pathogenesis of anemia in malaria: a concise review. Parasitol Res. 2007 Nov.; 101(6):1463-9 Epub 2007 Sep 16. 6.

Ringwald P, Peyron F, Lepers JP, Rabarison P, Rakotomalala C, Razanamparany M, Rabodonirina M, Roux J, Le Bras J. Parasite virulence factors during falciparum malaria: rosetting, cytoadherence, and modulation of cytoadherence by cytokines. Infect. Immun. 1993 Dec ;61(12):5198-5204.

Anstey NM, Russell B, Yeo TW, Price RN. The pathophysiology of vivax malaria. Trends Parasitol. 2009 May ;25(5):220-227.

Trampuz A, Jereb M, Muzlovic I, Prabhu RM. Clinical review: Severe malaria. Crit Care. 2003 ;7(4):315–323.

Freedman DO. Clinical practice. Malaria prevention in shortterm travelers. N. Engl. J. Med. 2008 Aug 7;359(6):603-612.

www . DCMS online . org

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High Altitude Travel and Aircraft Cabin Environment Rebecca Senko, RN, BSN, CTH Abstract:This article examines the risks associated with the hypoxia caused by travel to high altitude settings. Although travel to high altitudes has long been explored by man, much about the physiological aﬀects of hypoxia are still unknown.1, 2 Key in promoting safe and healthy travel to high altitude is education about protective measures, signs and symptoms of high altitude illness and actions to take in order to prevent this catastrophic illness.2 This article provides the reader with practical advice for those seeking to travel to higher altitudes.

Introduction Whether trekking the Himalayas at 18,000 ft. or traveling in an aircraft at 40,000 ft., with a 6500 foot relative cabin pressure, altitude presents challenges to the traveler to avoid potentially fatal high altitude illness. The travel medicine provider needs to assess ﬁtness for altitude travel and educate those who are ﬁt for such travel about the risks involved.2 A study done with trekkers in the Himalayas to assess their knowledge of altitude illness showed that there is a strong need for educational improvement.3

Physiology and Pathophysiology As altitude increases, barometric pressure decreases, thus reducing the partial pressure of ambient oxygen. At sea level the oxygen concentration is 21%. In Denver, Colorado at 5,331 ft. (1,610 m) above sea level, the oxygen concentration is 17%, inspired pO2 approximately 120 mm Hg and alveolar PO2 approximately 80 mm Hg in a healthy traveler.2 At 5,000 ft. (1500 m) the first physiologic effects occur. Arterial hypoxia is sensed by the carotid body signaling the respiratory center in the medulla to increase ventilation. As respiration increases, this produces alkalosis. The kidneys then attempt to normalize this imbalance by excreting bicarbonate thus bringing the pH back to near normal, although normal values are never quite reached. Ventilation continues to increase reaching a maximum at 4-7 days at the same altitude when “ventilatory acclimatization” is reached. After this time altitude sickness is unlikely, but may occur as more ascent is attempted.2 This chain of events increases oxygen delivery and is described as the Hypoxia Ventilatory Response (HVR). HVR is most likely determined by genetics but also can be influenced by respiratory depressants, such as alcohol and certain drugs. Physical fitness and age do not seem to be factors in determining HVR.4 Those travelers with a slow HVR are more prone to altitude-related illness. The affects of increased altitude normally cause some symptoms with which every trekker should be familiar. Those symptoms are hyperventilation, fatigue, dyspnea on exertion (not at rest), increased urination, periodic breathing during Address Correspondence to: Rebecca Senko,1833 Boulevard, Suite 500, Jacksonville, FL 32206 Email: rebecca_crouse@doh. state.fl.us.

www . DCMS online . org

sleep and insomnia. Awakening during one of these episodes of periodic breathing may cause the traveler to panic if he/she is not aware of these symptoms.5, 6 In view of this physiology, what medical conditions might prohibit travel to high altitudes? Generally even persons with mild to moderate lung disease can safely travel to moderately high altitudes of 6,000-8,000 ft. (2,000-2,500m). Obviously persons who are on oxygen at home will need to increase FiO2 on ascent to high altitudes.2 Some persons with asthma and chronic bronchospasm report easier breathing at high altitudes due to lower air density and cleaner air.2 However, altitude often is accompanied by exercise and colder temperature. So those asthmatics with exercise induced asthma may have problems.4 Older patients with coronary artery disease are not at greater risk for acute mountain sickness. One study showed that active older travelers with preexisting pulmonary and cardiovascular disease could ascend without compromising their conditions.5 Hypertension is not a contraindication to travel to high altitudes. Blood pressure does increase slightly, but generally not dramatically. Diabetics are able to safely travel to high altitude but need to be made aware that ketoacidosis may be aggravated by altitude illness and is more difficult to treat when the diabetic is taking acetazolamide. It is also important for the diabetic to know that the accuracy of glucose meters may be affected by high altitude.7 Sickle cell crisis has often been reported at high altitudes. High altitude has even been the cause of the first sickle cell crisis for some patients previously unaware of their condition.4,8 Patients who have experienced sickle cell crisis are advised to avoid altitude of more than 1,800 ft. (500 m) unless taking supplemental oxygen.8 Women with normal uncomplicated pregnancies can safely ascend to 9,000 ft. (3,000 meters). The importance of a slow ascent is important in preventing altitude illness especially high altitude pulmonary edema which could compromise oxygen delivery to the fetus.2 Absolute contraindications to active and passive ascent are unstable neurological conditions such as patients with stroke or transient ischemic attack within the last 90 days. Those persons with multiple sclerosis and severe diabetic neuropathy can safely tolerate passive ascent, but should avoid active ascent.9 Trekkers with snoring, sleep apnea, and sleep disordered breathing who become hypoxic at sea level will become severely hypoxic at high altitudes. Acetazolimide may be considered to assist with the acclimation of these persons to altitude.4

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Acute Mountain Sickness (AMS) AMS occurred within 36 hours in 25% of travelers to Colorado mountain resorts at altitudes between 6300 – 9700 ft.2,5 The statistics for children are similar to that of adults.10,11 Individuals with a past history of AMS have twice the incidence of AMS compared to those who are non-susceptible regardless of the rate of ascent. The incidence is directly influenced by altitude of permanent residence, rate of ascent, underlying lung disease, previous AMS and obesity.2, 4, 5 The symptoms of AMS are headache plus one or more of four other symptoms: GI upset, fatigue/weakness, dizziness/lightheadedness, and/or insomnia.2,4,5 In preverbal children, the symptoms include fussiness, lack of playfulness, anorexia, nausea, vomiting and sleep disturbances.10,11 These symptoms are something all travelers to high altitude should recognize along with the fact that no further ascent should be attempted until symptoms have resolved. If the symptoms worsen, descent should be immediate.5 An AMS headache is bilateral, generalized, dull, increases with exertion, most commonly occurs at night, responds well to non-steroidal anti-inflammatory drugs, and resolves within 24 - 48 hours of ascent.4 Aspirin or Ibuprofen may be used as a pretreatment or treatment for altitude headache.12 An AMS associated headache is a benign condition and does not have any related neurological changes. If there is confusion or ataxia, this signals a more severe condition i.e. high altitude cerebral edema and demands immediate descent as discussed later in this article. A slow gradual climb is the best prevention for altitude associated illness. When climbs are to over 3000 M. (9800 ft.), a standard 1000 ft. (300m) sleeping elevation gain per night should be the maximum. The actual climb for the day may safely exceed 1000 ft., but the climber then needs to return to the previous 1000 ft. gain mark for sleeping. Individuals without experience should not ascend and sleep above 10,000 ft. (3,000 m) and should spend two or three nights at 8,000-10,000 ft. (2,500 -3,000m) before ascending further, with an extra night of rest for each subsequent 2,000-3,000 ft. (600-900 m). Abrupt increase of more than 2,000 ft. (600m) of sleeping altitude should be avoided over 8,000 ft. (2,500 m).12 It is not always possible to make a measured slow ascent due to preset travel plans and tours. Flights into La Paz, Bolivia 12,000 ft. (3658m) or Lhasa, Tibet 12,090 ft. (3685m) are two additional common destinations where a slow gradual ascent is not possible.2 When rapid ascent cannot be avoided, acetazolamide (DIAMOX®) can be useful to rapidly acclimate the body to altitude, thus preventing AMS. Acetazolamide is useful in treating AMS as well. The drug acts by inducing the kidneys to excrete bicarbonate, which is followed by acidification of the blood and hyperventilation. The dosage for treatment and prevention is the same-125-250 mg q 12 hours for adults. For children, the dosage is 1.25mg/kg/dose q 12hrs with a maximum 125mg/dose.10,11 Prophylaxis for both adults and children is started 24 hours before ascent and continued for 48-72 hours after arrival.13 28 Vol. 60, No. 4 2009 Northeast Florida Medicine

Acetazolamide will not mask symptoms of AMS and relapse will not occur after it is discontinued. Side eﬀects of acetazolamide may include paresthesis of the hands and feet, taste alterations and tinnitus. Since acetazolamide is a derivative of sulfonamides, those patients with sulfa drug allergies should not be given this drug.5 Generally AMS is self limiting and symptoms will subside in 24-48 hours provided there is no further ascent.

High Altitude Cerebral Edema (HACE) HACE is almost always fatal if left untreated.12 Patients with HACE have gait ataxia and/ or mental status changes distinguishing this syndrome from the headache associated with AMS.12 HACE is largely preventable. The prescription for treatment for HACE is descent, descent, and descent.12 Descent should be immediate and should be to the altitude at which the trekker last slept and awoke symptom free. If that information is unknown, the descent should be to the altitude at which the trekker slept two nights previously. HACE can result in death in a matter of hours. Although HACE usually occurs at night, the descent should not be delayed. Trekkers have died with HACE at 11,330 ft. waiting for a helicopter pick up.12 When descent is not immediately possible due to weather conditions, terrain, or patient condition, dexamethasone, hyperbaric treatment and oxygen may be life saving. Unfortunately, even though gross mental status symptoms resolve quickly, the ataxia may persist for days or weeks and there may be long term neurocognitive defects.12

High Altitude Pulmonary Edema (HAPE) HAPE is caused by patchy hypoxic vasoconstriction in the pulmonary vascular bed. Blood flow is consequently forced through limited number of vessels causing a high pressure leak. Pulmonary hypertension is always present.2 Symptoms include at least two of the following: dyspnea at rest, cough, weakness or decreased exercise performance, and chest tightness. Signs include at least two of the following: crackles or wheezing in lung field, central cyanosis, tachycardia, tachypnea, and fever may be present.5 Many deaths have occurred when HAPE was missed and mistreated as pneumonia. AMS and HACE can be present at the same time. Subtle prodromal symptoms may be displayed as dyspnea on exertion progressing to dyspnea at rest and a nonproductive cough.4 Treatment is emergent descent.6 The mortality rate for HAPE victims is 10-15%. Nifedipine (PROCARDIA®, ADALAT®) may also aid in the treatment of HAPE by causing pulmonary vasodilation and thus relieving pulmonary hypertension causing the capillary leak. Trekkers who have a history of HAPE should consider carrying nifedipine 20mg to be taken orally three times daily or 30mg-60mg slow release every 12 hours for prevention of HAPE when started on the day of ascent and continued for 72 hours at higher altitudes.13 Additional possibilities for treatment or prevention of HAPE are sidenafil (VIAGRA®) and tadalafil (CIALIS®). A study in 2004 showed that sildenafil suppressed altitude induced pulmonary hypertension, assisted with cardiac www . DCMS online . org

adaptation to exercise and did not alter acclimatization.12, However, until more studies are done, nifedipine remains the drug of choice. Salmeterol (SEREVENT®) used in treatment of asthma has also shown promise in the management of HAPE associated pulmonary edema.13,15

Hypobaric Hypoxia and Aircraft Travel Modern aircraft often fly at altitudes above 41,000 ft. Cabin atmospheric pressure is required to be maintained below the equivalent of 8,000 ft. (2,500 m). This produces a PaO2 of about 70 mm Hg in a healthy individual. Most passengers will tolerate this atmosphere, although, a recent study, showed that protracted periods of time at cabin altitude tended to increase passenger discomfort.16 Some travelers with underlying medical conditions will be mildly to severely affected by the cabin altitude. The increase in altitude and resulting drop in air pressure can cause a 25% increase of expansion of gases within body cavities causing pain, discomfort, injury and possibly pathology.17 Flying is contraindicated for those with a history of pneumothorax, incarcerated bowel, persons who are <10 days post chest or abdominal surgery, infants< than 7 days old, and children prone to otitis media. Passengers with heart and lung diseases, blood disorders, such as anemia, may travel safely if they are evaluated prior to flying and the necessary preparations are made.

a lay over in a terminal while waiting to board another plane. The National Home Oxygen Patient’s Association provides a brochure, Airline Travel with Oxygen, which can be helpful in assisting passengers who need to travel with oxygen. The brochure can be obtained through the website http://. homeoxygen.org/airtrav.html.18

Conclusion Even with all the risks high altitudes present, it is possible for many travelers to withstand these challenges. It is important that the patient be aware of these risks and how to mediate them. As with all types of preparation for travel, the medical preparation is only part of the necessary preparation. The patient must be encouraged to arm himself with the knowledge of the protective measures that are the first line of defense. The health care provider should be prepared to share basic concepts about altitude and the affects on the body, and resources for further education before high altitude travel is attempted especially for the first time. Websites, published articles, and books for the lay public abound. A list of these in a handout would be a great start for the traveler to become knowledgeable about safe travel to high altitudes.

Suggested reading: West JB. The physiological basis of high altitude diseases. Ann Intern Med 2004;141:789-800.

References

Generally, those who have previously traveled without symptoms by plane or to an elevation of over 8,000 ft. (2,500 m) should have no problem flying, unless their condition has worsened since they were last at that altitude. Patients with an arterial pO2 of 80 should also be able to fly without any supplementary oxygen. Patients with pO2 of less than 60 at sea level on room air will need supplementary oxygen. Patients with elevated pCO2 at sea level in addition to hypoxemia should be discouraged from flying without pre-travel evaluation and simulation testing.

Appenzelle O. Altitude and the nervous system. ARCH Neurology 1998;55:1007-9. Available from: http://www. archneurol.com. Accessed March 18, 2009.

Hackett, PH. “Medical Problems of High Altitude: in Textbook of Travel Medicine Edited by Dupont HL, Steﬀen R. Hamilton, Ontario: Decker BC, Inc.,1997, pp.51-62.

Paz A, Steinfeldt I, Potasman I. Are we doing our best to educate travelers about the risk of acute mountain sickness? An onsite prospective study in the Himalayas. Journal of Travel Medicine 2007;14:168-72.

Patients with a nonstable medical condition such as acute exacerbations of bronchospasm or bronchitis, respiratory infection, pneumothorax, pulmonary hypertension, unstable angina or uncompensated congestive heart failure should not fly. Even ambulation to the lavatory can cause lower oxygen levels in 80% of these passengers.18 Other medical conditions which maybe affected by hypobaric hypoxia are asthma, cystic fibrosis, heart failure, severe angina, and sickle cell disease (not including sickle cell trait). These patients should be carefully evaluated prior to departure for fitness to fly.17

Freer L, Hackett PH. “High Altitude Medicine” in Expedition and Wilderness Medicine. Edited by Bledsoe G, Manyak M, Townes D. New York, New York: Cambridge Press 2009.pp. 240-261

Altitude Illness Clinical Guide for Physicians. http//www. highaltitudemedicine.com/AMS-medical.html. Accessed March 12, 2009.

Gill S, Walker N. Severe facial edema at high altitudes. Journal of Travel Medicine 2008; 15:130-2.

Shlim DR. ‘Altitude Illness” in CDC Health Information For International Travel 2008. Edited by Arguin P, Kozarsky P, Reed C. Philadelphia, Pennsylvania: Mosby/Elsevier 2008. pp.455-60.

Cook, A. A case of splenic infarction at high altitude in sickle cell trait. http://www.expeditionmedicine.wordpress.com. Posted 4/22/08. Accessed April 28, 2009.

Aurerbach P. Going to high altitude with a pre-existing neurological condition.http://www.healthline,com/blog/ outdoor_health/2007/09. Accessed March 3, 2009.

Patients who need oxygen supplementation must arrange with a commercial provider for oxygen as early as possible prior to their flights. Some airlines will not service those who need supplemental oxygen. Most airlines require a minimum of 48-72 hour pre-notification before flying. However, airlines vary and some require several weeks notice. Federal Regulations forbid the use of the passenger’s personal oxygen equipment on board. Passengers are responsible also for making their own arrangements for oxygen while on the ground, such as during

www . DCMS online . org

10. Yaron M, Niermeyer S. Travel to high altitudes with young

Northeast Florida Medicine Vol. 60, No. 4 2009 29

children: an approach for clinicians. High Altitude Medicine and Biology 2008; 9:265-69. 11. Yaron M, Waldman N, Honigman B. The diagnosis of acute mountain sickness in preverbal children. ARCH Pediatric Adolescent Medicine1998;152:683-87.

Encourage DCMS Membership

12. Dietz T. An Altitude Tutorial. http://www.ismmed.org/np_ altitude_ tutorial. htm. Accessed March 9, 2009.

Organized medicine must remain uniﬁed during the ongoing Health System Reform debate. It is crucial as physicians work to improve, not completely reinvent, the world’s greatest healthcare delivery system.

13. Rose S. Altitude illness. In: “Traveling Healthy”. http//www. travmed.com. Accessed February 26, 2009. 14. Richalet J, Gratadour P, Robach, et al. Sildenaﬁl inhibits altitude-induced hypoxemia and pulmonary hypertension. American Journal of Respiratory and Critical Care Medicine 2005;171:275-81. 15. Sartori C, Alleman Y, Deplain H. Salmenterol for the prevention of high-altitude pulmonary edema. The New England Journal of Medicine 2002; 346:1631-36. Available from: http://www. nejm.org. Accessed April13, 2009. 16. Dawson A. “Travel-related illness” (motion sickness, jet lag, thrombosis, other) in Textbook of Travel Medicine. Edited by Dupont H., Steﬀen R. Hamilton, Ontario: Decker BC, Inc. 1997, pp.265-71.

Talk to a colleague TODAY about becoming a DCMS member and joining the eﬀort to postively inﬂuence Health System Reform.

Contact Barbara Braddock, membership@dcmsonline.org or 904- 355-6561 x107

17. Muhm M, Rock P, Mc Mullin D, et al. Eﬀect of air-cabin altitude on passenger discomfort. New England Journal of Medicine 2007; 357:18-27. Available from:http://www.nejm. org. Accessed March 24, 2009. 18. Mac Kenzie W, Gallagher N. “Air travel, including disinsection” in CDC Health Information for International Travel 2008. Edited by Arguin P, Kozarsky P, Reed C. New Yo r k , N Y: Mosby/Elsevier 2008, pp.496-501.

Traveling Through Photos This Ecuadorian bird seems to be showing oﬀ for Bobi Wall’s camera. See this colorful fowl on the journal’s cover or go to www.bobiwall.com.

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Pregnancy and Travel Levonne Mitchell-Samon, MD Abstract:Traveling while pregnant raises concern for potential disease exposure which may have significant adverse effects on the expectant mother, as well as the fetus. Having a pre-travel medical evaluation and educating the pregnant traveler on specific disease preventive measures, appropriate chemoprophylaxis and vaccines is essential for the safety and well-being of both the expectant mother and unborn child.

Introduction The decision to travel during pregnancy requires careful planning and consideration to optimize the safety of the mother and the unborn child. Pregnancy alone poses an increased risk of travel- related illnesses, and when the travel destination presents multiple potential disease risks, the clinician may choose to advise cancelling or postponing the trip. If postponement is not possible, the clinician is asked to provide the education, vaccines and medical prophylaxis necessary to minimize the pregnant traveler’s risks, which is best accomplished through a multidisciplinary care approach. This article reviews some of the potential infectious and non-infectious causes of travel-related diseases facing the pregnant traveler. Human immunodeﬁciency virus (HIV) and tuberculosis are beyond the scope of this article and are reviewed in the literature.1,2

Preparing to Travel The second trimester is considered the safest time for traveling. The risk of spontaneous abortion and pre-term labor is very low and the pregnant woman generally is feeling more comfortable at this stage.3 At least one month prior to departure, the travel plans should be discussed with the patient’s travel medical provider(s). The pre-travel assessment should include questions regarding the mode of travel, destination(s), duration of travel, length of stay, and planned activities. Most commercial airlines will allow travel up to the 36th week gestation for domestic flights and the 35th week for international flights for an uncomplicated pregnancy.3 Many airlines require a letter from the doctor confirming absence of complications for women flying after the 28th week of gestation. Past medical history should be reviewed to identify pregnant women who are at higher risk for complications during travel. Pregnant women over age 35, multiple gestation, hypertension, diabetic pregnancies and intrauterine growth retardation are at higher risk for placental hypo-perfusion in the hypoxic conditions which may occur during a long flight. In theory, there is a potential for intra-uterine fetal death or premature labor under these conditions. It is not recommended for Address Correspondence to Levonne Mitchell-Samon, MD, Duval County Health Department, Disease Control Division, 1833 Boulevard, Suite 500, Jacksonville, Florida 32206. Email: Levonne_Mitchell-Samon@doh.state.fl.us. www . DCMS online . org

these women to fly after 32 weeks gestation. The potential for thrombosis (DVT/PE) during prolonged air, car or rail trips also needs to be assessed. Women with thrombophilia, such as antiphospholipid syndrome, are at excessive risk for venous thromboembolism (VTE) during a long-haul flight.4 People tend to increase their level of activity during vacation. The American College of Obstetrics and Gynecology recommends at least 30 minutes of daily exercise for women with a normal pregnancy.5 Pregnant travelers need to be aware of certain limitations with common vacation activities. Due to an altered center of gravity; pregnant women are at greater risk of falling with some common vacation activities such as skiing, hiking, mountain climbing and horseback riding. Snorkeling is considered safe during pregnancy, but scuba diving is contraindicated due to the fetal risk of decompression disease that may result in malformation and gas embolism.1 If traveling to high altitudes, sufficient time must be taken to acclimatize and exercise should be kept to a minimum, as well as maintaining hydration to avoid altitude sickness. Acetazolamide, a drug commonly used to prevent altitude sickness, is not advised in pregnancy due to reports of fetal metabolic problems associated with its use.6 International travel brings with it the added risk of acquiring infectious and communicable diseases that are endemic to the region of planned travel. The role of the clinician is to offer the appropriate travel advice, immunizations and medical prophylaxis. Emphasis should be on personal protective measures to minimize the risk of infection, including food and water precautions, protection from insect bites, safe sexual practices and avoiding large crowds. The clinician should be aware that individuals who will be long-term visitors or are returning to visit family or friends may perceive themselves to be less at risk, which may increase the possibility of poor compliance with appropriate prophylactic measures. The expectant female traveler should also have knowledge of local medical resources, should medical care become necessary, take copies of medical records, as well as a plan and insurance for medical evacuation should an emergency arise. Travel during pregnancy should be relatively safe if adequate preparations are made and precautions adhered to; however, for some patients, the best advice is to postpone travel if effective preventive measures cannot be performed and access to medical care is uncertain.

Travel-related Thrombosis Seating conditions, ﬂight duration and cabin atmospheric pressure play a role in increasing the risk of deep venous thrombosis (DVT) and venous thromboembolism (VTE). Travel- related thrombotic events on long-distance ﬂights occur in 1/6,000. The hypercoagulable state of pregnancy increases the risk of VTE by 5-10-fold. Pregnant women Northeast Florida Medicine Vol. 60, No. 4 2009 31

with thrombophilia are at excessive risk of thrombotic events during and following long-haul flights. Unfortunately, to date, there is insufficient research study to guide the clinician in prophylaxis and management of thrombosis in this group of travelers. Prophylactic measures that are applicable for all passengers, such as performing frequent exercise, should be advised. Elastic stockings have been shown to reduce DVT risk by almost 90 % in normal risk patients. The use of pharmacologic agents is controversial; however, low-molecular weight heparin has been suggested as the drug of choice for travelers at high risk for VTE. Self-injection of LMWH (0.5 mg/kg enoxaparin) one hour prior to take-off should cover a long-haul flight with duration of at least 16 hours.4 For car travel, it is advised to stop every two hours to allow some walking and no more than six hours of travel per day is recommended.6

Preventive Measures For many travel-related insect borne infections that pose significant risk to the expectant mother and fetus, the only preventive measure available is insect avoidance. Insect bites are the mode of transmission for malaria, yellow fever, leishmaniasis, filariasis, dengue fever, trypanosomiasis and a large number of other arboviruses. The traveler should be advised to wear long sleeves and pants, as well as full-coverage footwear; minimize time spent outdoors during the biting times of dusk and dawn, apply a permethrin-containing spray or solution to clothing and bed nets, and insect repellant, i.e. DEET or Picaridin-containing cream to exposed skin. Food and water contamination is a common source of infection in travelers and may transmit hepatitis A, hepatitis E, toxoplasmosis, typhoid fever, leptospirosis and enterotoxigenic E. coli, a common cause of traveler’s diarrhea. The traveler should be advised to refrain from ingesting unpasteurized milk and milk products, eating salads, consuming uncooked vegetables and undercooked meats. It is best the traveler eat only fruits that she herself has peeled, and she should limit beverages to hot tea or coffee, or drinks that are canned or bottled, keeping in mind alcohol avoidance. She should also be advised to avoid ice-containing drinks, tap water at hotels and if a personal water purification system is used, it should be nonchemical to avoid exposure to iodine in chemically treated water.7 Vaccination during pregnancy causes concern for many clinicians, however, the risk to the fetus is for the most part, theoretical with no clear-cut evidence of adverse events.8 Vaccines for tetanus/diphtheria, hepatitis A, hepatitis B and inactivated polio are considered safe during pregnancy and can be administered if needed for the planned travel destination. Live virus vaccines such as measles, mumps, rubella, varicella and yellow fever should be avoided during pregnancy, unless the risk of disease exposure is significant and unavoidable.6 The ability of the pregnant woman to mount an immune response to vaccines is questionable. In one study, up to 50% of pregnant women who were given a yellow fever vaccine failed to show an adequate antibody response.9 32 Vol. 60, No. 4 2009 Northeast Florida Medicine

Traveler’s Diarrhea Traveler’s diarrhea, one of the most common illnesses to aﬀect travelers, may be even more severe in pregnancy due to decreased gastric acidity and slower intestinal transit. Dehydration and ketosis may result, which can lead to premature labor or sudden fetal death. Fluoroquinolones, which are commonly prescribed for treatment, are not recommended. Trimethoprim-sulfamethoxizole may be used, but may be ineﬀective in some areas due to bacterial resistance patterns. Bismuth subsalicylate is contraindicated in pregnancy. The medical provider should advise on strict hygiene and food and water precautions, as well as vigorous oral hydration if symptoms should develop.10

Malaria Malaria is found worldwide with its highest incidence in returning travelers from Africa (W. Africa predominantly), accounting for 72% of the cases. The remaining cases reported are travelers to Asia (mostly the Indian subcontinent), Central America and the Caribbean. Of the cases diagnosed in the US in 2002, thirty-two (7%) were in pregnant women, 28% of whom reported taking a recommended prophylactic regimen. Malaria infection during pregnancy has been associated with preterm birth and low birth weight. Infants born to infected mothers are more likely to suffer from dehydration, seizures, splenic rupture, thrombocytopenia and neonatal death. The potential for stillbirths and abortion is also a concern. Pregnant women are more attractive to Anopheles mosquitoes perhaps due to increased respiratory production of carbon dioxide or an increase in body surface temperature. Transmission to the fetus may occur transplacentally or during delivery with mixing of maternal and neonatal blood.6,7 There are no preventive measures against malaria infection that are 100% effective and prevention during pregnancy is extremely important. Insecticide treated bed nets and insect repellants containing 20% N,N-diethyl-3-methylbenzamine (DEET) are safe and effective. Medical prophylaxis with chloroquine is safe; however, chloroquine-resistant malaria is widespread and chloroquine may only be effective in Mexico, Central America (west of the Panama Canal), the Caribbean, East Asia, and a few Middle Eastern countries.11 Mefloquine is safe during the second and third trimesters. Atovaquone-proguanil (Malarone, GlaxoSmithKline, Research Triangles Park, NC) is not recommended by the Centers for Disease Control (CDC) for use in pregnancy due to insufficient data.8 A small number of women in the US Army who received mefloquine during various stages of pregnancy all had healthy infants at birth with no congenital abnormalities. Doxycycline increases the risk of altered bone growth and dental staining if used during pregnancy and is not recommended. Primaquine may induce hemolysis in babies with G6PD deficiency. If proguanil, dapsone, or pyrimethamine is used, folic acid supplementation is necessary, as these drugs are folate antagonists.6 The World Health Organization (WHO) and the CDC both recommend that pregnant women not travel to areas www . DCMS online . org

that are endemic for malaria.10 The best advice may be to postpone travel, or change the itinerary. If the pregnant woman is not able or willing to delay or change her travel plans, then meﬂoquine is the drug of choice for chloroquineresistant malaria, but there is limited data of its safety during the ﬁrst trimester.

Yellow Fever The risk of acquiring yellow fever in travelers to endemic regions is low (0.4-4.3 cases per million). There are two forms of yellow fever, urban and sylvatic (jungle). The vector for the urban form, the Aedes aegypti mosquito has been eradicated from many parts of the world. The vector mosquito for the sylvatic form is found in the forest-savannah tropical zones of Africa and humans can be infected while traveling to the jungle in parts of Africa within 15°N to 10° S of the equator. Infection rates are highest at the end of the wet season or the beginning of the dry season. Yellow fever is also endemic in the Americas in certain South American countries, Panama, Trinidad and Tobago, with the highest rates occurring in the rainy season. Individuals who have previously received a single dose of vaccine are protected for at least 10 years and possibly a lifetime. In general, live-attenuated vaccines are avoided in pregnancy and the absolute safety of the yellow fever vaccine remains unknown. There has been one case of congenital yellow fever after vaccination during pregnancy. A small case-control study in pregnant women in Brazil showed a twofold increased risk of spontaneous abortion, which was not statistically significant. In Nigeria, 101 pregnant women at various stages of pregnancy received the vaccine during a yellow fever outbreak. The children were followed prospectively for four years and no adverse effects were noted.7 If travel to an endemic area is required for a pregnant woman, and exposure to yellow fever is likely and unavoidable, the evidence suggests to offer the vaccine. If it is a travel requirement for entry to the country and disease exposure is unlikely, then, providing a waiver to the pregnant traveler is preferred.10 Educating the traveler on mosquito avoidance measures is absolutely essential.

Hepatitis Hepatitis A, B, C, and E can cause illness in pregnant travelers. The vaccines for hepatitis A and B are considered safe in pregnancy. The hepatitis A virus is spread by fecaloral contamination. Hepatitis A has been associated with placental abruption and premature delivery. Hepatitis B is more likely to be transmitted at delivery due to blood exposure and intrauterine transmission is rare. The vertical transmission rate of hepatitis C is less than 5%, with higher rates in HIV- co-infected women. Hepatitis E infection in pregnancy has a case fatality rate of 15-30%.6 Transmission to the fetus may be intrauterine or perinatal. Pregnant travelers should receive hepatitis A and B vaccines if appropriate and should be advised on food and water hygiene to prevent hepatitis E virus infection. They should also be instructed to avoid unsterile tattoo needles and ink as well as infected body ﬂuids to prevent hepatitis C infection.7 www . DCMS online . org

Japanese Encephalitis Japanese encephalitis is endemic in rural areas of Southeast Asia and the Indian subcontinent. The Japanese encephalitis virus (JEV) is transmitted by the Culex mosquito from pigs and birds to humans, usually in the evening hours. The mortality rate for this infection is as high as 30%. In one reported case, transplacental infection resulted in the fetus being aborted and the virus was isolated from the brain, liver and placenta. A new vaccine against Japanese Encephalitis, Ixiaro, a puriﬁed, inactivated virus product has recently become available. There are no large scale studies of safety in pregnancy. Mosquito avoidance should be emphasized.

Rubella The eﬀects of congenital rubella infection can be severe, including deafness, cataracts, cardiovascular defects and mental retardation. Routine immunization in the United States began in 1969 but is still endemic in many parts of the world. The risk of transplacental infection is highest in the ﬁrst and third trimester. Premature delivery and intrauterine growth retardation occurs frequently. It is contraindicated to give this vaccine during pregnancy and women of child-bearing age who receive the vaccine should avoid getting pregnant for at least 28 days post-immunization. Transmission occurs from human to human through nasopharyngeal secretions containing the rubella virus.

Typhoid Fever The incidence of typhoid fever in US travelers is low at 2.6 cases per million travelers each year. When it occurs during pregnancy, complications in the mother such as hepatic dysfunction, gastrointestinal bleeding, intestinal perforation and death may occur. The causative organism, Salmonella typhi can cross the placenta and cause chorioamnionitis, miscarriage or fetal/neonatal infection.7 The newer Vi capsular vaccine has very little data in pregnancy, however, it is preferred by some experts over the live vaccine.10 In addition, the clinician should advise travelers on food and water precautions to prevent infection.

Leptospirosis Leptospirosis mainly occurs in tropical and subtropical climates with heavy rainfall, but can occur worldwide. Humans can become infected by transmission of the Leptospira spirochetes through open waters or soil contact contaminated with body ﬂuids of infected wild and domesticated animals. Infection during pregnancy may result in spontaneous abortion, fetal death or congenital leptospirosis. Preventive measures include avoiding potentially contaminated water, vaccination of animals and wearing waterproof clothing. Doxycycline, an eﬀective chemoprophylaxis is contraindicated during pregnancy.7

Dengue Fever Dengue is a mosquito-borne virus with a similar distribution to malaria, mostly in the tropics. The A. aegypti mosquito is most active in the daytime and mosquito avoidance is essential. Congenital infection does occur, although the exact

Northeast Florida Medicine Vol. 60, No. 4 2009 33

mechanism is unclear. The risk of morbidity in the infant increases with gestational age at the time of infection.12 There is no eﬀective chemoprohylaxis or vaccine. Insect bite avoidance is necessary.

African Trypanosomiasis (Sleeping Sickness) This infection is caused by the parasite Trypanosoma brucei transmitted by the tsetse fly found in African countries between 15°N and 20° S latitude. The risk to US travelers is very low with approximately one case reported per year. Congenital infections have been reported in the literature, however, in most cases, no infection was identified in the mother and the route of transmission is unclear. Tsetse flies bite through clothing, mostly in the daytime. Common insect repellants may be ineffective but they are killed by contact with permethrin.7

American Trypanosomiasis (Chagas Disease) Chagas disease is caused by the protozoan parasite, Trypanosoma cruzi, endemic to Mexico, and Central and South America. The vector is the triatomine “kissing bug” and the trypapnosomes excreted enter through mucosal surfaces or broken skin. Congenital infection occurs in 2%- 10% of newborns born to infected mothers via parasites crossing the placenta. Insect repellants and bed nets are the only available measures of prevention.7

Summary Travel-related diseases in the pregnant female have the potential for causing harm not only to the mother but the fetus or neonate. The reasons for travel to areas endemic for potential pathogens are varied and sometimes, despite knowing the risks, the expectant mother has compelling reasons to proceed with the travel plans. The pregnant woman’s medical provider should provide education needed regarding the potential risks, disease prevention, as well as, appropriate chemoprophylaxis and vaccines. While there may be hesitancy on the part of medical providers to immunize a pregnant woman, it is stated by the American College of Obstetricians and Gynecologists that the beneﬁts of immunization to the pregnant woman and neonate usually outweigh the theoretic risks of adverse

effects. The risk of disease exposure to the pregnant woman and fetus must be balanced against the efficacy and benefits of the vaccine.10 The overall goal of the pre-travel medical visit is to have a well-informed pregnant traveler, armed with the necessary preventive measures needed for safe travel.

References 1.

Shetty AK, Maldonado Y. Preventing mother-to-child transmission of human immunodeﬁciency virus type 1 in resourcepoor countries. Pediatr Infect Dis J, 2003; 22:553-555.

Smith KC. Congenital tuberculosis: a rare manifestation of a common infection. Curr Opin Infect Dis, 2002;15:269-274.

Walentiny C. Pregnancy and traveling. Dtsch Med Wochenschr, 2009; Mar; 134(12): 594-8. Epub 2009 Mar 10.

Brenner B. Prophylaxis of travel-related thrombosis in women. Thrombosis Research 2009; 123 Suppl. 3:, S26-S29

American College of Obstetricians and Gynecologists Education Pamphlet AP119- Exercise During Pregnancy http://www.acog.org/publications/patient_education/bp119. cfm. Accessed October 29, 2009.

Carroll ID, Van Gompel A. The pregnant wilderness traveler. Travel Medicine and Infectious Disease, 2005; 3:225-238

McGovern LM, Boyce T, Fischer P. Congenital Infections Associated With International Travel During Pregnancy. Journal of Travel Medicine, 2007;14 Issue 2:117-128.

D’Acremont V, Tremblay S, Genton B. Impact of Vaccines Given During Pregnancy on the Oﬀspring of Women Consulting a Travel Clinic: A Longitudinal Study. Journal of Travel Medicine, 2008; 15 Issue 2:77-81.

Nasidi A. Yellow fever vaccination and pregnancy: a four-year prospective study. Trans R Soc Trop Med 1993; 87(3):337-9.

10. Carroll D, Williams, D. Pre-travel vaccination and medical prophylaxis in the pregnant traveler. Travel Medicine and Infectious Disease, 2008; 6:259-275. 11. Freedman D. Malaria Prevention in Short-Term Travelers. N Engl J Med, 2008;359:603-12. 12. Carroll D, Toovey S, Van Gompel A. Dengue fever and pregnancy- A review and comment. Travel Medicine and Infectious Disease, 2007; 5:183-188.

Traveling Through Photos This majestic mountain range in the Kingdom of Bhutan draws Bobi Wall’s camera to its majesty and grandeur.

Go to www.bobiwall.com to see color Bhutan photographs from Bobi’s recent trip to this mystical place.

34 Vol. 60, No. 4 2009 Northeast Florida Medicine

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Special Case Study

An Unusual Case of Hepatitis and Polyserositis Mohammad A. Khan, MD, MRCP; Atman Shah, MD; and Fauzia Rana, MD Editor’s Note: Due to production constraints, Images 1 & 2 and Figure 1 are not printed in the journal. They are available online at dcmsonline.org.

Case Presentation A 34-year-old Caucasian female presented to the emergency room with symptoms of nausea, vomiting and low grade fever. She had ﬂu like symptoms for four days, which progressively increased in severity. She then developed right upper quadrant abdominal pain and shortness of breath unrelieved by any over-the-counter medication. Her shortness of breath progressively increased to the extent that she was unable to carry out her activities of daily living. She denied chest pain, cough, phlegm or any changes in bowel and bladder habits. The rest of the review of system was within normal limits. She denied any major medical or surgical problems in the past. She also denied alcohol, tobacco or drug use. She was sexually active in a monogamous relation. She denied using any medication on a regular basis. There was no history of recent travel. Family history was unremarkable as well.

Physical Examination Physical examination revealed a white female who looked appropriate for her age and was in no apparent distress. Her blood pressure was 110/65 mmHg, pulse of 112 beats/min and regular. Her respiratory rate was 18 breaths per minute with temperature of 99.8F. Her oxygen saturation was 92% on room air. She was icteric with no pallor. Pupils were equal and reacting to light, bilaterally. She had no jugular venous distension, thyroid enlargement or carotid bruit on neck exam. Cardiovascular examination revealed distant heart sounds, no murmur, rubs or gallops. Examination of her chest was signiﬁcant for dullness to percussion in both lung bases, decreased air entry on auscultation and no egophony. She had a soft abdomen with no tenderness, negative Murphy’s sign with no palpable masses or organo megaly and normal bowel sounds. The rectal examination was unremarkable and stool was negative for occult blood. The neurological exam was within normal limits. Evaluation of extremities revealed good capillary reﬁll with no evidence of edema, calf tenderness, clubbing or cyanosis.

Laboratory Data Laboratory investigation revealed Hemoglobin of 12.4 g/dL, white cell count of 8.9 and normal chemistry. Serum bilirubin was 2.9 mg/dl (Normal <1.2), Indirect bilirubin of 2.7, ALT of 226U/L (Normal <31), ALT of 224 U/L (Normal <31), Alkaline Phosphatase of 137 U/L (normal 40-130) and INR of 1.6.

Address correspondence to: Atman Shah, MD, Department of Internal Medicine, University of Florida, College of Medicine, Jacksonville, FL. Email: atman.shah@yahoo.com www . DCMS online . org

A CT scan of the chest, abdomen and pelvis showed pericardial effusion, moderate pleural effusion bilaterally (Image 1, dcmsonline.org), ascites (Image 2, dcmsonline.org) and mild hepatomegaly. There was no evidence of lymphadenopathy on the CT. The echocardiogram suggested moderate pericardial effusion without tamponade physiology. Blood cultures and viral serology were sent on admission.

Clinical Course The patient was admitted with diﬀerential diagnosis of acute hepatitis and bilateral pleural eﬀusion of unknown cause. Her initial workup included the following: • •

•

Acute hepatitis panel and HIV tests were negative. Blood cultures were all negative for any growth. Serological markers for connective tissue disorders, including anti nuclear antibodies, anti neutrophilic cytoplasmic antibodies, anti-double stranded and anti-Smith antibodies were negative which ruled out connective tissue disease. Diagnostic thoracocentesis revealed transudate ﬂuid which was negative for malignant cells.

The patient remained hemodynamically stable throughout her stay in the hospital. On day four of her admission, viral serology revealed positive IgG against CMV with negative IgM. Both IgM and IgG Antibodies were strongly positive against EBV (titers 1.34 and 5.8 respectively). The antibody to EBV nuclear antigen (anti-EBNA) was also positive with high titers of more than 5.0, conﬁrming acute Epstein-Barr virus infection. Her transaminases and INR normalized on day 6 of admission, and she was discharged to home. A repeat chest X-Ray and a follow-up appointment with her primary care physician were arranged in a week’s time. Another chest X-Ray in a week showed complete resolution of both pleural and pericardial eﬀusions.

Discussion Epstein-Barr virus (EBV) is a member of the Herpes virus family with a characteristic herpetic envelope and a double stranded DNA.1 It was discovered 32 years ago by Epstein, Achong and Barr by using electron microscopy of cells cultured from Burkett’s lymphoma.2 Two strains, type A and type B infect humans, and both strains are equally prevalent in the United States.3 Infection with EBV usually occurs by contact with oral secretions. The virus replicates in cells of the oropharynx, and nearly all seropositive people shed the virus in their saliva.4 Transmission via blood transfusion or bone marrow transplant is rare.5 The IM syndrome is deﬁned as a clinical triad of fever, sore throat, and generalized lymphadenopathy in over 50% of the patients.6 EBV is an ubiquitous virus that infects lymphoid and epithelia tissue (Figure 1, dcmsonline.org) and causes a spectrum of clinical conditions, including Infectious mononucleosis (IM), Burkett lymphoma, nasopharyngeal carcinoma, non-Hodgkin’s B-cell lymphoma and many Northeast Florida Medicine Vol. 60, No. 4 2009 35

lymphoproliferative disorders in people with congenital or acquired cellular deficiencies. IM, the paradigmatic disease associated with EBV, is discussed in detail since other diseases are out of focus of this specific case. Spleno megaly, hepato megaly and palatal petechiae are present in less than 10% of patients.7 Pleural effusions remain a common finding in EBV infections.8 Pericardial involvement is rare and the prevalence is unknown. Other rare presentations include headache, myalgia, nausea, chills, arthralgia, and jaundice. CMV, HIV, syphilis and Toxoplasma gondii may mimic mononucleosis-like illness.9 IM can occur in all age groups, but most cases occurs in adolescence and early adulthood. Diagnosis of acute EBV is predominantly clinical with supportive lab findings. The majority of patients have leukocytosis with absolute increase in peripheral mononuclear cells, Paul-Bunnell heterophile antibodies, elevated transaminases, and atypical T-lymphocytes on peripheral smear. IgM antibodies to EBV viral capsid antigen disappear in 4-6 weeks, thus their detection is presumptive evidence of recent infection. Measurement of IgG antibody is not useful except in diagnosis and management of nasopharyngeal carcinoma.10 Anti-EBNA appears relatively late after onset of symptoms and its absence in a previously healthy person with strong clinical suspicion doesn’t rule out IM.11 Infectious mononucleosis is a self-limiting disease and is usually managed with supportive care and by addressing the patient’s anxiety provoked by adenopathy. Complications are rare and depend on the immunopathologic response to the virus.12,13 (Table 1) Unless symptoms and signs progress well beyond the period of acute illness, no further work-up is needed. In the oropharynx, EBV directly infects resting B cells or infects epithelial cells, which in turn infect B cells. During primary infection, EBV-infected B cells undergo lytic infection with production of virus or they express the full complement of latent viral proteins. The latter cells are kept in check by natural killer cells and cytotoxic T cells. After convalescence, EBV is present in the peripheral blood in latently infected memory B cells that express latent membrane protein (LMP) 2 and possibly EBV nuclear antigen (EBNA). The latter cells can undergo EBV reactivation and express other latent viral proteins, resulting in their recognition and destruction by cytotoxic T cells. Some latently infected cells undergo lytic replication in the oropharynx, resulting in production of virus with shedding of virus into the saliva or infection of epithelial cells with release of virus.

recipient and recovery of same strain of virus from recipient’s blood. Blood 1996;87: 812-17. 6.

Andreoli, T., Carpanter C., Griggs R., Loscalzo J. Cecil Essentials of Medicine 6th Edition, Philadelphia, Pa, WB Saunders, 2004:829-33.

Cohen JI. Epstein - Barr virus Infection. NEJM 2000;343:481-92.

Collins TR, Sahn SA. Thoracocentesis. Clinical value, complications, technical problems, and patient experience. Chest 1987; 91: 817–822.

Schooley RT, Dolin R. Epstein-Barr virus (infectious mononucleosis).In: Mendell GL, Bennett JE, Dolin R. Principles and Practices of Infectious Disease. 5th edition. Churchill Livingston, New York. 2000:1599-1612.

10. Straus SE, Cohen JI, Tosato G, Meier, J. Epstein-Barr Virus Infections: Biology, Pathogenesis, and Management. Annals of Int Med 1993;118:45-57. 11. Epstein - Barr virus and Infectious Mononucleosis. National Center for Infectious Diseases. www.cdc.gov. Accessed 08/01/2009. 12. Straus SE. Acute Progressive Epstein-Barr virus infections. Annu Rev Med. 1992 :43:437-49 13.

Cohen, Jeﬀrey I, MD. Epstein - Barr virus and the Immune System: Hide and Seek. JAMA Vol 278(6), 13 August 97, 510-513.

Table 1 Complications of Infectious Monomucleosis RESPIRATORY

RENAL

HEPATIC

CARDIAC

Murray PR, Lennette, E, et al. Manual of Clinical Microbiology. 6th edition ASM Press, Washington.1995:905-910.

Epstein MA, Achong BG, Barr YM. Virus particles in cultured lymphoblast from Burkett’s lymphoma. Lancet 1964;1:702-703.

Sixby J, Shirley P, Chesny P. Detection of a second widespread strain of Epstein-Barr virus. Lancet. 1989;2:761-5.

Yao QY, Rickinson AB, Epstein MA. A re-examination of the EB virus carrier state in healthy seropositive individuals. Int J Cancer 1985;35:35-42.

Alﬁeri C, Tanner J, Carpanteri L, Perpetta C, Anik S. EBV transmissions from a blood donor to an organ transplant

36 Vol. 60, No. 4 2009 Northeast Florida Medicine

GN, Interstitial nephritis

Hepatitis, Hepatic necrosis

Myocarditis, Pericarditis

HEMOTOLOGIC

Hemolytic anemia, Thrombocytopenia, Aplastic anemia.

NEUROLOGIC

Encephalitis, Transverse mylitis, The Gullian-Barre’ syndrome, Bell’s palsy, Optic neuritis.

SKIN

Rash (Ampicillin-associated), Oral hairy leukoplakia, Urticaria, Vacuities.

References 1.

Pleuritis, Interstitial pneumonitis, Nasopharyngeal carcinoma, Pneumonia, Impending airway obstruction due to massive tonsillar swelling .

IMMUNOGENIC

X-linked and non X-linked lymphoproliferative syndromes, Burkett’s and Non-Hodgkin’s lymphoma, T-cell lymphoma.

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DCMS Membership Applications These physicians’ applications for membership in the Duval County Medical Society are now being processed. Any information or opinions you may have concerning the eligibility of the applicants listed here may be directed to John M. Montgomery, MD, MPH, DCMS Membership Committee Chair (904-860-4683) or Barbara Braddock, Membership Director (904-355-6561).

Medical Degree: University of South Alabama College of Medicine Residency: University of Virginia Medical Center Fellowship: University of South Alabama College of Medicine Nominated by: Todd Sack, MD; Renard Rawls, MD; M. Akin Cabi, MD

Ashraf Andrawis, MD Pain Management/Anesthesiology Premier Spine & Pain Center 554 Kingsley Ave. #5 Medical Degree: Zagazig Medical School Residency: MetroHealth Medical Center Case Western Reserve Fellowship: University of Pittsburgh Medical Center Nominated by: Farid Hakim, MD; Kamal Bohsali, MD; Fady Bahri, MD

Daniel Castillo, MD Anesthesiology UF Anesthesiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: Colombian School of Medicine Internship: Boston University School of Medicine Residency: Brigham & Women’s Hospital Fellowship: Brigham & Women’s Hospital, Jackson Memorial Hospital Nominated by: UFJP

Luis F. Anez, MD Family Medicine 9765 San Jose Blvd. #102 Medical Degree: Xaveriana University Internship/Residency: University of Florida College of Medicine Nominated by: Terry Hashey, DO; Timothy Lucey, DO

Perry Jon Cole, MD Anesthesiology/Pain Management The Cole Clinic 7999 Philips Hwy. #303 Medical Degree: Eastern Virginia Medical School Residency/Fellowship: University of Florida College of Medicine Nominated by: Orlando Florete, MD; Hernando DeSoto, MD; Jyoti Patel, MD

Indermeet S. Bhullar, MD Trauma/Critical Care Surgery UF Trauma Surgery 655 W. 8th St. 8th FL Clinical Center Medical Degree: University of Alabama at Birmingham School of Medicine Residency: University of California School of Medicine Fellowship: Emory University Hospital, Baylor University Medical Center Nominated by: UFJP Qammer A. Bokhari, MD Administrative Medicine Blue Cross Blue Shield of Florida 4800 Deerwood Campus Parkway Medical Degree: Rawalpindi Medical College, Pakistan Residency: Holy Family Hospital & District Headquarters Hospital, Pakistan Nominated by: John Montgomery, MD; Raed Assar, MD; Allen Seals, MD Monique D. Bosque-Perez, DO Family Medicine Commonwealth Family Practice Center 761 Edgewood Ave. N. Medical Degree: Chicago College of Osteopathic Medicine Residency: St. Vincent’s Family Medicine Program Nominated by: UFJP Andrew R. Brown, MD Gastroenterology Borland Groover Clinic 3 Shircliﬀ Way, #400

Chirag V. Desai, MD Psychiatry UF Psychiatry Center 580 W. 8th St. Tower II #6005 Medical Degree: Albany Medical College Residency: Westchester County Medical Center Fellowship: New York Presbyterian Hospital Nominated by: UFJP Diana L. Edgar, MD Breast Imaging/Radiology UF & Shands Radiology 655 W. 8th St. C90 Medical Degree: University of Texas Health Science Center San Antonio Residency: Ochsner Foundation Fellowship: Tulane Medical Center Nominated by: Richard White, MD; Susan Snodgrass, MD; Derek Hamlin, MD Anne T. Egan, MD Pediatrics The Carithers Pediatric Group 2121 Park St. Medical Degree: Yale School of Medicine Residency: Children’s Hospital of Pittsburgh Nominated by: Robert Colyer, MD; Julie Baker, MD; James Cheek, MD Mohammad Farooque, MD Psychiatry UF Psychiatry Center

38 Vol. 60, No. 4 2009 Northeast Florida Medicine

580 W. 8th St. Tower II #6005 Medical Degree: Allama Iqbal Medical College Residency: University of Missouri Medical School Nominated by: UFJP Ulysses D. Findley, MD Family Medicine 1660 Blanding Blvd. Medical Degree: Meharry Medical School Residency: St. Vincent’s Residency Program Nominated by: Fred Porcase, DO; John Montgomery, MD; Vincent Galiano, MD CAPT Bruce L. Gillingham, MD Orthopedics/Pediatric Orthopedics Naval Hospital Jacksonville 2080 Child St. Medical Degree: Uniformed Services University of Health Sciences Residency: Hospital for Sick Children, Toronto Nominated by: Paul Kaufman, MD; CAPT Terry McGee, MD Zachary A. Goldman, MD Emergency Medicine UF Emergency Medicine 655 W. 8th St. 1st FL Clinical Center Medical Degree: University of New Mexico Medical School Residency: University of Florida Health Science Center Nominated by: UFJP Reetu Grewal, MD Family Medicine Anchor Plaza Family Medicine & Pediatrics 5480 Blanding Blvd. #3 Medical Degree: UMDNJ-Robert Wood Johnson Medical School Residency: Spartanburg Regional Medical Center Fellowship: Mayo Clinic Jacksonville Nominated by: UFJP Ian M. Heger, MD Neurosurgery UF Pediatric Neurosurgery Center 836 Prudential Dr. #1005 Medical Degree: SUNY Downstate Medical Center College of Medicine Internship: SUNY Downstate Medical Center College of Medicine Residency/Fellowship: SUNY Downstate Medical Center College of Medicine Fellowship: The Children’s Hospital of Philadelphia and Children’s Hospital Boston Nominated by: UFJP Steven E. Hodgett, MD General Surgery North Florida Surgeons 836 Prudential Dr. #1107 Medical Degree: Medical College of Wisconsin www . DCMS online . org

Residency: University of South Florida School of Medicine Fellowship: Washington University School of Medicine Nominated by: Theodore Felger, MD; Gordon Polley, MD; John Crump, MD Kelly K. Jago, MD OB-GYN North Florida OBGYN St. Vincent’s 1 3 Shircliﬀ Way, Ste. 200 Medical Degree: Jeﬀerson Medical College School of Medicine Residency: Naval Medical Center San Diego Nominated by: D. Scott Wells, MD; William Long, MD; Thomas Virtue, MD Yazan Khatib, MD Interventional Cardiology, Cardiovascular Disease, Vascular Medicine, Endovascular Medicine First Coast Cardiovascular Institute PA 3900 University Blvd. S. Medical Degree: Damascus University School of Medicine Residency: Cleveland Clinic Foundation Fellowship: Loyola University Medical Center Maywood/Indiana Heart Institute/ Alexian Brothers Mercy Hospital Nominated by: Majdi Ashchi, DO; Sumant Lamba, MD Diana C. Maccario, MD Family Medicine First Coast Family Medicine 9191 RG Skinner Pkwy. #603 Medical Degree: St. George’s University Medical School Residency: St. Vincent’s Medical Center Residency Program Nominated by: Terry Hashey, DO; Robert Raspa, MD; Maria Mahmoodi, MD; Richard Peterson, MD Jennifer Manuel, MD Hand Surgery/Orthopedics Jacksonville Orthopaedic Institute 1325 San Marco Blvd. #200 Medical Degree: Boston University School of Medicine Residency/Fellowship: Brown University School of Medicine Michael E. Menefee, MD Medical Oncology Mayo Clinic 4500 San Pablo Rd. Medical Degree: Meharry Medical College Residency: Mayo Clinic Fellowship: National Cancer Institute, NIH Nominated by: Candido Rivera, MD; Gerardo Colon-Otero, MD; Alvaro Morena-Aspitia, MD Iman Naseri, MD Otolaryngology UF Otolaryngology 655 W. 8th St. 2nd FL Faculty Clinic

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Medical Degree: Medical University of South Carolina Residency: Emory University Hospital Fellowship: Mount Sinai Hospital Nominated by: UFJP Leonard J. Newton, MD Otolaryngology/Administrative Medicine Blue Cross Blue Shield of Florida 4800 Deerwood Campus Pkwy. Bldg. 9-5 Medical Degree: Albert Einstein School of Medicine Residency: New York Presbyterian Hospital/Monteﬁore Medical Center Nominated by: John Montgomery, MD Chrysoula Pappa, MD Rheumatology UF Southside Specialty Care Center 4555 Emerson Exwy. #200 Medical Degree: Aristotle University of Thessaloniki Residency/Fellowship: Albany Medical College Nominated by: UFJP Trishna Y. Patel, MD Diagnostic Radiology Drs. Mori Bean & Brooks PA 3599 University Blvd. S. Bldg. 300 Medical Degree: Albany Medical College Residency: New York Medical College Fellowship: Massachusetts General Hospital Nominated by: Christine Granﬁeld, MD; Shannon Beardsley, MD; John McKenzie, MD William C. Rupp, MD Medical Oncology Mayo Clinic 4500 San Pablo Rd. Medical Degree: University of Minnesota Medical School Residency/Fellowship: University of Cincinnati Medical Center Nominated by: Stephen Lange, MD; William Maples, MD; Floyd Willis, MD Louis S. Russo, MD Neurology The Neuroscience Institute at Shands 580 W. 8th St. 9th FL Tower I Medical Degree: New York University School of Medicine Internship: Mayo Clinic Residency: Mount Sinai Medical Center Nominated by: UFJP Haritha Sakhamuri, MD Nephrology UF Nephrology 655 W. 8th St. Basement Clinical Center Medical Degree: PSG Institute of Medical Sciences Residency/Fellowship: University of Florida College of Medicine Jacksonville Nominated by: UFJP

Christopher B. Scuderi, DO Family Medicine New Berlin Family Medicine Center 3122 New Berlin Rd. Medical Degree: Lake Erie College of Osteopathic Medicine Internship: Naval Medical Center Portsmouth Residency: St. Vincent’s Family Medicine Program Nominated by: UFJP Sunil K. Sharma, MD Surgery/Surgery Oncology UF Surgery 655 W. 8th St. 3rd FL Faculty Clinic Medical Degree: Mahatma Gandhi Memorial Medical College Residency: Monmouth Medical Center Fellowship: Newark Beth Israel Medical Center & University of Pittsburgh Medical Center Nominated by: UFJP Leslie V. Simon, DO Emergency Medicine UF Emergency Medicine 655 W. 8th St. 1st FL Clinical Center Medical Degree: Nova Southeastern University College of Osteopathic Medicine Internship: Naval Hospital NAS Jacksonville Residency: Naval Medical Center San Diego Nominated by: UFJP Stephen S. Topp, MD Emergency Medicine UF Emergency Medicine 655 W. 8th St. 1st FL Clinical Center Medical Degree: University of South Florida College of Medicine Residency: University of Florida Health Science Center Nominated by: UFJP Karen V. Toronczyk, MD Pathology UF Pathology 655 W. 8th St. 1st FL Clinical Center Medical Degree: University of Buenos Aires Residency: Berkshire Medical Center Fellowship: MD Anderson Cancer Center Nominated by: UFJP Danny H. Vo, MD Vascular Surgery UF Surgery 655 W. 8th St. 3rd FL Faculty Clinic Medical Degree: Medical College of Wisconsin Residency: University of Chicago Hospitals Fellowship: Mayo Clinic Nominated by: UFJP

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