Travel-Acquired Illnesses

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48

Travel-Acquired Illnesses

Sources of Information

The Centers for Disease Control and Prevention (CDC) publishes several authoritative sources of information on travel medicine. Health Information for International Travel (the “yellow book”) is updated annually. Two other periodicals, the weekly Morbidity and Mortality Weekly Report (MMWR) and Summary of Health Information for International Travel (the “blue sheet,” published biweekly), provide updated information on the status of immunization recommendations, worldwide disease outbreaks, and changes in health conditions. A reliable way to obtain current travel health information, including vaccine requirements, malaria chemoprophylaxis, and disease outbreaks for various regions of the world, is to consult the CDC Travelers’ Health website at http://wwwnc.cdc.gov/travel/. See Chapter 49 for more information on immunizations for travel. For nonmedical information of interest to the traveler, the U.S. State Department can be accessed at http://travel.state.gov/. Additional resources for travel medicine information are listed at the end of the chapter.

Aside from traveler’s diarrhea (see Chapter 44), traffic-related accidents, and purified protein derivative conversion, the major travel-acquired illnesses in descending order from most to least common are as follows:

These disorders are often preventable if the traveler takes specific precautions or prophylactic agents. Influenza, acute HIV infection, Legionella, and poliomyelitis are not discussed in this chapter because they are generally preventable with standard immunizations, or their medical management is similar to that in developed countries. Travelers at risk for HIV exposure should consider bringing 72 hours of postexposure prophylaxis medication, because many developing countries do not have access to HIV drugs.

Dengue Fever

Dengue virus is a single-stranded ribonucleic acid (RNA) flavivirus that is transmitted by the day-biting urban mosquito Aedes aegypti or the jungle mosquito Aedes albopictus. A. aegypti is the principal vector for dengue viruses worldwide. Viral transmission is maintained through a mosquito-human cycle without a major animal reservoir.

Signs and Symptoms (Compare Dengue With Malaria in Table 48-1)

Table 48-1

Clinical Illness in Malaria and Dengue Fever

SIGNS AND SYMPTOMS MALARIA DENGUE FEVER
Fever +++ +++
Chills +++ ++
Headache +++ +++
Malaise   ++
Anorexia   ++
Nausea, vomiting ++ ++
Abdominal pain ++  
Myalgia ++ ++
Arthralgia   ++
Backache +  
Dark urine +  

+++, >90% of patients; ++, >50% of patients; +, <10% of patients.

1. Clinically, may range from undifferentiated viral symptoms with fever and mild respiratory/gastrointestinal symptoms to dengue hemorrhagic fever

2. Incubation period: 4 to 6 days, although may be as long as 14 days

3. Early prodromal symptoms of fever (temperature usually greater than 39° C [102.2° F]), myalgias, headache, arthralgias, and rash. May also have gastrointestinal symptoms of nausea and vomiting

4. After several days, often maculopapular or morbilliform rash spreading outward from chest

5. Dengue can progress to severe forms, referred to as dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). Severe DHF/DSS may progress to circulatory failure with shock and spontaneous bleeding from almost any site, most commonly the skin, nose, and gastrointestinal tract

6. After infection, patients often develop extreme fatigue persisting for weeks or months

7. DHF/DSS is unlikely in travelers not previously infected with dengue

8. Awareness of the local epidemiology of DHF/DSS is important in establishing the diagnosis. Definitive diagnosis of all forms requires serologic examination (antibody identification via enzyme-linked immunosorbent assay [ELISA] or polymerase chain reaction [PCR]) or viral isolation from serum

9. Predictors of more severe disease manifestations, including DHF/DSS, include serotype (DEN-2 is the most severe), prior exposure, age, malnutrition, and genetic factors such as human leukocyte antigen (HLA) type

Yellow Fever

Yellow fever is one of the viral hemorrhagic fevers. It is caused by a single-stranded RNA flavivirus that is transmitted by mosquitoes. The liver is the principal target organ. All recent cases of American yellow fever were acquired in the jungle environment; however, urban transmission continues to occur in Africa.

Signs and Symptoms

1. May appear as an undifferentiated viral syndrome

2. Specific diagnosis in the wilderness is extremely difficult; clinical suspicion is based on immune status, geographic distribution of the disease, travel history, and characteristic triphasic fever, as follows:

a. Infection phase: After 3 to 6 days of incubation period, onset of headache, photophobia, fever, malaise, back pain, epigastric pain, anorexia, and vomiting. May also have “Faget sign” (bradycardia occurring at the height of the fever), conjunctival injection, and a coated tongue with pink edges

b. Remission phase: The 3 to 4 days of infection phase is followed by up to 48 hours of brief remission

c. Intoxication phase (up to 15% of individuals infected with yellow fever virus): Onset of jaundice, fever, encephalopathy, and in severe cases, hypotension, shock, oliguria, coma, and multiorgan failure. Hemorrhage usually manifested as hematemesis, but bleeding from multiple sites possible

d. Signs of a poor prognosis include early onset of the intoxication phase, hypotension, severe hemorrhage with disseminated intravascular coagulation, renal failure, shock, and coma

Rabies Exposure

Rabies exists almost everywhere in the world with the exception of Antarctica and a few island nations. Most cases of human disease in the developing world result from multiple, deep bites to the face, scalp, or upper extremities from an unimmunized canine. In more developed countries, however, the majority of rabies transmission occurs from wild animal carriers (see Chapter 42). Travelers who plan on spending more than 1 month in regions at high risk for rabies should consider preexposure rabies immunization. CDC recommendations for rabies prophylaxis can be found at http://www.cdc.gov/diseases/rabies.html. Rabies is almost universally fatal within a few weeks of symptom onset. If a potential rabies exposure occurs, immunized patients will require only two subsequent rabies immunization boosters on days 0 and 3 post exposure with close follow up. Patients without preexposure immunizations should receive rabies immune globulin and rabies immunization as outlined in Chapter 43.

Hepatitis Viruses

The causes of hepatitis may be divided into two groups. First, the lettered viruses now include hepatitis A to G. These are associated with defined clinical syndromes and elevated liver function test results. Second, other organisms that cause hepatitis as part of a more systemic infection include Epstein-Barr virus, cytomegalovirus, toxoplasmosis, and leptospirosis.

Hepatitis A

Hepatitis A virus (HAV) is transmitted mainly through the fecal-oral route, either by person-to-person contact or by ingestion of contaminated food or water. Occasional cases are associated with exposure to nonhuman primates. HAV is endemic worldwide, but developing regions have a significantly higher prevalence. In most instances, resolution of the acute disease is permanent, but rare cases of relapse have been noted. Death from HAV is rare. After natural infection, HAV antibodies confer immunity. HAV patients are infectious for approximately 2 weeks before the onset of symptoms. Viral shedding declines with the onset of jaundice. The patient is typically not infectious 1 to 2 weeks after the onset of clinical disease.

Signs and Symptoms

1. Incubation period ranging from 2 to 7 weeks

2. Infection is often asymptomatic or mild, especially in children

3. Classic syndrome: early onset of anorexia, followed by nausea, vomiting, fever, and abdominal pain

4. Symptoms possibly accompanied by hepatosplenomegaly

5. Jaundice after gastrointestinal syndrome by several days to a few weeks; resolution of jaundice lasting another 3 to 4 weeks

6. Although rare, HAV sometimes follows a fulminant course (0.5% to 1% of patients), resulting in hepatic necrosis, hepatic encephalopathy, and death. The incidence of fulminant hepatitis increases with age

7. Clinical presentation is often milder than with other types of viral hepatitis, but not distinctive enough to allow clinical differentiation

8. A number of laboratory tests are available to confirm the diagnosis, but diagnosis in the field is clinical

Hepatitis B

With the widespread use of serologic markers for hepatitis B disease, it became apparent that spread occurs through exchange of blood, semen, or, rarely, saliva of infected people. Although spread is possible from persons with acute disease, the primary sources of viral particles are chronic carriers. The carrier state follows acute infection in up to 90% of infected infants and 10% of adults. In many areas of the developing world, most infections occur in infancy or childhood, and chronic carriers may constitute as much as 10% to 20% of the total population; thus travelers are more likely to be exposed to carriers than is the nontraveling population. The risk is higher in persons regularly exposed to body fluids, including medical personnel and persons with many sexual partners.

Hepatitis C

This syndrome was previously termed non-A, non-B (NANB) hepatitis and was thought to be caused by a heterogeneous group of causes. It is now clear that a majority of such cases were due to hepatitis C. Risk factors for hepatitis C include IV drug use and, before routine testing, transfusion of blood products. Nonparenteral routes of infection are less important for hepatitis C than for hepatitis B. Hepatitis C is a global problem. Approximately 80% of exposed individuals develop chronic infection, which may lead to cirrhosis in 20% of subjects and hepatocellular carcinoma in up to 5% of this subset of infected persons. Rates of infection vary from 1% to 5% in most Western countries to 20% in parts of the Middle East, such as Egypt.

Hepatitis E, F, and G

1. Hepatitis E is an RNA virus and is the second most common cause of viral hepatitis transmitted via the enteric route.

2. The epidemiologic characteristics are similar to hepatitis A. However, hepatitis E has animals (pigs and deer) as its reservoir.

3. This group of infections is especially important in the Indian subcontinent, the Middle East, and Africa.

4. The incubation period is 2 to 6 weeks.

5. The disease is usually self-limited but may be associated with severe illness in pregnant women.

6. Diagnosis in travelers from endemic areas can be made on the basis of IgM antibody to hepatitis E in serum or testing of stool for viral antigen.

7. Vaccines are not available. Prophylaxis is appropriate advice for travelers and involves counseling with respect to precautions regarding ingestion of food and water in endemic areas.

8. Hepatitis F is a putative hepatitis virus of uncertain significance, first described in France.

9. Hepatitis G is a member of the flavivirus family with limited homology to hepatitis C. Its significance as a cause of hepatitis is unclear.

Typhoid and Paratyphoid Fever

Typhoid fever occurs worldwide, but its prevalence and attack rates are much higher in developing countries. It is estimated to cause 26 million cases and 200,000 deaths annually. Humans are the only host for Salmonella typhi, the most common cause of the typhoid fever syndrome. Nearly all cases are contracted through ingestion of contaminated food and water. The risk for transmission is relatively high in Mexico, Peru, India, Pakistan, Chile, sub-Saharan Africa, and Southeast Asia.

Salmonella species are gram-negative enteric bacilli. S. typhi is the prime cause of typhoid fever, but other species may cause a typhoid fever–like syndrome. The term enteric fever is used to describe a severe systemic infection with Salmonella paratyphi (paratyphoid fever). The clinical appearance of S. paratyphi infection is similar to that seen with typhoid (see Signs and Symptoms), but typically S. paratyphi infection runs a shorter course.

Signs and Symptoms

1. Onset of illness is usually 10 to 14 days after exposure to the pathogen.

2. Gastroenteritis is possible early in the course of the disease with associated abdominal pain and constipation. Diarrhea is more common in younger children.

3. Fever

4. Headaches, malaise, anorexia

5. “Rose spots” (2- to 4-mm maculopapular blanching lesions) classically described on the trunk, although not seen in most patients

6. Hepatomegaly, splenomegaly in many patients

7. Uncomplicated, untreated typhoid fever usually resolves spontaneously in 3 to 4 weeks.

8. Life-threatening complications:

9. Definitive diagnosis possible by bacterial culture

10. Possible for patients to remain asymptomatic carriers and continue to shed organisms for years

Treatment

1. Give antibiotics:

2. Make certain that the patient has adequate nutrition and food support.

3. High-dose steroids are not recommended for those with mild to moderate disease but may be used cautiously in those with severe disease. The current recommendation in severe disease is dexamethasone 3 mg/kg for the first dose, followed by 1 mg/kg every 6 hours for eight more doses.

4. Be aware that relapse can occur after 2 weeks of therapy and necessitates retreatment with the same regimen.

Cholera

Cholera is a potentially lethal diarrhea disease in adults and children caused by Vibrio cholerae O1. Occasionally causing pandemic outbreaks, cholera is spread by contaminated water and food supplies in areas of poor sanitation. Cholera can be transmitted in crustaceans or survive in a dormant state in brackish water. Death usually occurs following voluminous diarrhea, dehydration, hypovolemia, and shock.

Treatment

1. Aggressive oral, IV, or intraosseous (IO) fluid replacement in two phases: (1) rapid rehydration of existing fluid deficits over 2 to 4 hours, and (2) maintenance hydration for duration of illness.

2. Severe dehydration is typically 10% to 15% of patient’s body weight; 30% of the estimated fluid losses should be replaced in the first 30 minutes in adults, and first hour in children, following fluid initiation.

3. After rehydration has been achieved, measure fluid losses over a 4-hour period and replace on top of maintenance fluids over the next 4 hours. Oral hydration should be attempted first, with IV or IO hydration reserved for significant ongoing fluid losses and inadequate oral hydration alone.

4. Oral hydration can be achieved with homemade or commercially available oral rehydration solution (ORS) (see Chapter 44) or parenterally with lactated Ringer’s solution with 20 mEq of KCl added to every 1 L of solution. Alternatively, normal saline with 20 mEq of KCl added to every 1 L of solution can be used if lactated Ringer’s solution is not available.

5. If IV or IO access is unobtainable and the patient is not taking adequate volume of ORS, a nasogastric tube can be placed with administration of ORS at the same rate. Be sure to elevate the head of the bed 30 degrees to prevent aspiration.

6. Initiate antibiotic therapy with tetracycline 500 mg PO q6h in adults and 50 mg/kg/day PO divided q6h in children older than 8 years for 3 to 5 days. Alternatively, use doxycycline 300 mg PO once daily in adults and 4 to 6 mg/kg PO once daily in children older than 8 years for 3 to 5 days. In pregnant women, children younger than 8 years, or in tetracycline/doxycycline-resistant areas, use azithromycin 1 g as a single dose in adults or 20 mg/kg as a single dose in children, or ciprofloxacin 500 mg PO once daily for 1 to 3 days in adults or 20 mg/kg PO once as a single dose in children.

7. Transport or evacuate the patient as soon as possible to definitive medical care while continuing rehydration and antibiotic therapy.

Japanese B Encephalitis

1. Japanese encephalitis is a viral infection transmitted by Culex mosquitoes. Transmission takes place year-round in tropical and subtropical areas and during the late spring, summer, and early fall in temperate climates. This disease occurs primarily in rural areas, often associated with pig farming.

2. Encephalitis is caused by a neurotropic flavivirus.

3. After initial replication near the mosquito bite, viremia occurs and may seed infection to the brain.

4. The virus causes central nervous system nerve cell destruction and necrosis.

5. Most infections in endemic areas involve children, but this disease may occur in any age-group.

6. Japanese encephalitis virus is the leading cause of viral encephalitis in Asia, with recent expansion into northern Australia.

7. There have been rare reported outbreaks in U.S. territories and in the western Pacific.

Meningococcal Disease

Meningococcal disease is caused by Neisseria meningitidis, a gram-negative diplococcus. Meningococcal meningitis classically attacks children and young adults and is often seen in epidemic form. Despite effective antibiotic therapy and immunization, this disease remains problematic in many parts of the world. Epidemic situations pose the greatest health problem to both travelers and resident populations. Since 1970, large outbreaks have occurred in Brazil; China; sub-Saharan Africa; New Delhi, India; and Nepal.

Transmission of the organism occurs through respiratory secretions, so close contact is believed to be important in the spread of the disease.

Signs and Symptoms

1. Variety of forms, including but not limited to the following:

2. Sustained meningococcemia may lead to severe toxemia with hypotension, fever, and disseminated intravascular coagulation.

3. Meningitis caused by N. meningitidis is marked by the classic triad of fever, headache, and stiff neck and possibly accompanied by bacteremia and any of several skin manifestations including petechiae, pustules, or maculopapular rash.

4. Severe meningitis may progress to mental status deterioration, hypotension, congestive heart failure, disseminated intravascular coagulation, and death.

5. During an epidemic a presumptive diagnosis can be made on the basis of clinical presentation.

6. Definitive diagnosis requires culture of the organism from cerebrospinal fluid or blood.

7. Several commercial kits for measuring meningococcal antigen are now available for use on cerebral spinal fluid or blood samples.

Treatment

1. Be aware that meningococcal meningitis, or sepsis, is a medical emergency, with suspected patients requiring immediate evacuation to an appropriate medical facility.

2. Note that, fortunately, the organism remains sensitive to many antibiotics, such as the following:

3. Give supportive care, including close monitoring for hypotension and cardiac failure (will necessitate ICU-level care) and IV fluid support.

4. Dexamethasone may be of value for patients in a coma or with evidence of increased intracranial pressure.

5. Make sure that close contacts receive prophylaxis to eradicate the organism (ciprofloxacin 500 mg PO as a single dose, or rifampin 600 mg PO q12h for four doses).

Travel Medicine Information Resources

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