Non–North American Travel and Exotic Diseases

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Chapter 85 Non–North American Travel and Exotic Diseases

Travelers to tropical and subtropical areas of the world where hygienic conditions are poor and ecologic conditions are permissive may encounter infectious agents that are no longer endemic or have never existed in temperate regions of the world. Although economic development and industrialization of developing countries of the tropics have resulted in a decreased health burden of many tropical infectious diseases, it is important to realize that there is still a risk for exposure for the traveler who is unaware of appropriate measures to prevent or treat such conditions. The most important consideration in the management of this problem, which is increasing as international travel expands, is appropriate preventive measures through counsel with a travel medicine specialist and prophylaxis using safe drugs and vaccines. This topic has recently been reviewed in several excellent publications.*

This chapter is concerned with infectious diseases that are uncommon or do not exist in North America and with which most health professionals in North America have scant familiarity. Other chapters give specific details relevant to malaria (Chapter 49), tick-borne diseases (Chapter 51), infectious diarrheas (Chapter 68), and travel medicine (Chapter 84). The infectious diseases considered in this chapter should not be considered a complete listing. This is especially important to keep in mind in an era when diseases once thought to be eliminated or nonexistent in North America are emerging or reemerging coincidental with large-scale movements of human and vector populations.

Major Viral Infections

This section describes select viral infections that may be acquired outside North America. Emphasis is placed on viral infections that have recently been recognized as being highly pathogenic and endemic in select tropical areas, such as those due to filoviruses, and those for which there are effective preventive or therapeutic measures, such as viral hemorrhagic fever due to the yellow fever virus, select types of viral hepatitis, and Japanese B encephalitis.

Yellow Fever

European physicians did not recognize until the late 1490s the clinical syndrome now known as yellow fever. Initially described by Columbus in the West Indies, large-scale epidemics were later observed throughout the Americas and tropical Africa in the 1700s and 1800s. After epidemic yellow fever in Texas, Louisiana, and Tennessee caused 20,000 deaths in the 1880s, the Yellow Fever Commission was organized to study the problem. Identification of the mosquito vector, Aedes aegypti, and definitive studies conducted by the U.S. military under the leadership of Walter Reed were followed by massive campaigns to eradicate mosquito breeding sites. This led to virtual elimination of urban yellow fever from the Americas. The last case of yellow fever acquired in the continental United States was reported in 1911. Because it is difficult if not impossible to eliminate jungle reservoirs, there continue to be cases reported annually from South America and tropical Africa. Larger outbreaks secondary to resurgent vector populations have occurred in recent years in tropical West Africa.14,35,38,70

Ecology and Epidemiology

In the Americas, primates in the forest canopy serve as hosts for the yellow fever virus. Mosquitoes of the genus Haemagogus transmit infection. Because this vector does not travel far from the forest, jungle yellow fever occurs when humans enter jungle areas or the forest border zones. Urban yellow fever involves a different vector, A. aegypti. This mosquito is highly anthropophilic, lives in and around human habitations, and prefers domestic water storage containers for breeding. The presence of a large population of A. aegypti breeding sites in an urban area is a significant risk for epidemic spread of yellow fever once the virus is introduced from a nearby forest area. In Africa the presence of larger numbers of mosquito species that can serve as vectors has hindered complete understanding of the ecology of the disease.

Currently, both the Americas and Africa have a constant low level of jungle yellow fever because of inability to control either the monkey reservoir or the mosquito vector. Overall there are about 200,000 cases per year, resulting in approximately 30,000 deaths, occurring primarily in sub-Saharan Africa.79 Some suggest that these rates are underestimated by at least 10-fold. Persons at risk include workers or travelers in or near the tropical rainforest canopy. Urban yellow fever had been reduced in the western hemisphere through massive campaigns to control breeding and spread of the Aedes vector. However, the benefits of these campaigns have declined, and there is currently an increased threat of further outbreaks of disease. Introduction of Aedes albopictus, an aggressive anthropophilic dengue vector from Southeast Asia, and reemergence of A. aegypti into the Americas raise the specter of increased yellow fever transmission in the western hemisphere.65 Less-intense vector control measures and a more complex ecology have made elimination of urban yellow fever in Africa even more difficult.

Clinical Presentation

Although yellow fever may appear as an undifferentiated viral syndrome, classic disease is characterized by a triphasic pattern. The infection phase begins with sudden onset of headache, fever, and malaise, often accompanied by bradycardia and conjunctival suffusion. After approximately 3 to 4 days, victims often experience brief remission. Within 24 hours, however, the intoxication phase develops, characterized by jaundice, recrudescent fever, prostration, and, in severe cases, hypotension, shock, oliguria, and obtundation. Hemorrhage is usually manifest as hematemesis; however, bleeding from multiple sites may occur. Signs of a poor prognosis include early onset of the intoxication phase, hypotension, severe hemorrhage with disseminated intravascular coagulation (DIC), renal failure, shock, and coma. Death occurs in one-quarter to one-half of all cases. Diagnosis in the infection phase is difficult. With development of the classic syndrome, the differential diagnosis narrows somewhat, but still includes malaria, leptospirosis, typhoid fever, typhus, Q fever, viral hepatitis, and other viral hemorrhagic fevers. The standard means of diagnosis is evaluation for neutralizing antibodies in acute and convalescent sera (available through the Centers for Disease Control and Prevention [CDC] and state health departments in the United States). Several new systems for early detection of immunoglobulin M (IgM) or viral antigen are now being evaluated for more rapid diagnosis. A specimen of whole blood (at −70° C [−94° F] on dry ice) should be sent to the state health laboratory for isolation. Growth of the virus is possible in a number of systems, including Vero cells and infant mice. The virus is most easily isolated during the first 4 days of fever.

Prevention

Avoidance of this potentially fatal infection is possible through use of yellow fever vaccine. The vaccine strain 17D is an attenuated live virus grown in chicken embryos. Greater than 95% of persons vaccinated achieve significant antibody 1evels. Repeat vaccinations are recommended every 10 years, although persistent antibody titers have been detected as long as 30 to 40 years after vaccination. Yellow fever vaccine is generally well tolerated, with headache or malaise occurring in less than 10% of those vaccinated. Rare allergic side effects occur primarily in persons with hypersensitivity to eggs. Other serious adverse events, including death, have been reported, with the greater risk being associated with age older than 60 years.5,49,66,81 Vaccination is not recommended in the first 6 months of life or in other situations where live virus vaccines are contraindicated. Although pregnant women have received the vaccine without adverse effect to themselves or their infants, it is not recommended for use in this group because of possible teratogenic effects. Other means of reducing the risk for yellow fever (and any mosquito-borne infectious disease) include liberal use of mosquito repellent and netting in endemic areas. Outbreak control in endemic countries is primarily through focused vaccination campaigns.

Treatment of severe yellow fever is difficult and often unsuccessful, with a mortality rate of approximately 50%. Avoidance through mosquito protection measures and administration of the highly effective vaccine before entry into endemic areas are of utmost importance.

Dengue fever

Dengue fever has been reported since the late 1700s. Since World War II, increased attention has focused on the dengue virus, largely as a result of recognition of dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). First noted in Southeast Asia, DHF and DSS have attained worldwide distribution in the last 30 years.34,53,67,86 Dengue is the most common insect-borne viral infection in the world. The infection has been reported in more than 100 countries, with 50 to 100 million dengue infections each year resulting in approximately 500,000 cases of life-threatening disease (DHF and DSS) annually.36,37

Clinical Presentation

Most dengue infections appear after an incubation period of 2 to 14 days, either as an undifferentiated viral syndrome with fever and mild respiratory or gastrointestinal symptoms or as dengue (“break-bone”) fever with bone pain, generalized myalgia, severe headache, and retroorbital pain. Febrile illnesses that appear more than 2 weeks after putative exposure to dengue virus are unlikely to be due to this virus. After 1 to 3 days, a quiescent period may ensue. There may be a subsequent second episode of fever accompanied by a patchy maculopapular or morbilliform rash that spreads outward from the chest and that ultimately desquamates. Lymphadenopathy and leukopenia occur during this phase of the illness. The distinct severe forms of dengue disease referred to as either DHF or DSS may occur around the usual time of recovery. These are due to the development of capillary leak syndrome with associated hemorrhagic manifestations (Figure 85-1). The advanced forms have the unique feature that the platelet count decreases to less than 100,000 per mm3 and hematocrit increases by more than 20%. The severity is classified as grade I to IV, according to World Health Organization guidelines. In cases of grade I DHF, the only hemorrhagic manifestation is a positive tourniquet test, in which inflation of a tourniquet to midway between systolic and diastolic blood pressure for 5 minutes leads to development of 20 or more petechiae per square inch distal to the tourniquet. A complete blood cell count classically shows decreased platelet and leukocyte counts and increase in hematocrit value. Grade II DHF is defined as the above with hemorrhage from any site (e.g., gingiva, nares, conjunctivae). Grade III DSS includes clammy skin, hypotension, or a narrow pulse pressure (<20 mm Hg) in a patient with DHF. An undetectable blood pressure defines grade IV DHF and DSS. Most studies have noted DHF and DSS primarily in infants and young children, usually with a history or serologic evidence of previous heterologous dengue infection, but there is an increasing trend of cases in adults.

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FIGURE 85-1 Hemorrhagic manifestations of dengue hemorrhagic fever or dengue shock syndrome.

(From Ryan ET, Wilson ME, Kain KC: Illness after international travel, N Engl J Med 347:505, 2002.)

Lassa Fever

Four viral hemorrhagic fevers—Lassa, Marburg, Ebola, and Crimean-Congo—have been associated with outbreaks of fatal person-to-person spread. Although the overall number of clinical cases in travelers caused by these viruses is small, they represent potentially significant threats as emerging diseases. They have also achieved notoriety as a group as a result of media interest and their potential use as agents of bioterrorism. Lassa fever was first recognized in 1969, when several nurses caring for febrile patients at a mission hospital in Nigeria became ill. Since that time, seroepidemiologic studies have established a large area of endemicity and a broad spectrum of clinical manifestations of infection.

Clinical Presentation

Most seroconversions to Lassa virus are not accompanied by obvious symptoms.63,64,69 Only 5% to 14% of seroconverters experienced a febrile illness. The incubation period is between 3 and 21 days. Patients hospitalized with Lassa fever show a distinct clinical syndrome. Fever, malaise, and purulent pharyngitis often develop after the insidious onset of headache. Retrosternal chest pain, possibly a result of pharyngitis and esophagitis, suggests the diagnosis. The combined presence of retrosternal chest pain, fever, pharyngitis, and proteinuria is the best predictor of Lassa fever.62 Hemorrhagic complications (hematemesis, vaginal bleeding, hematuria, lower gastrointestinal bleeding, and epistaxis) were seen in fewer than 25% of patients with Lassa fever. Nonfatal disease usually begins to resolve in 8 to 10 days. The combined presence of fever, sore throat, and vomiting was associated with a poor prognosis (relative risk for death = 5.5). Terminal stages of fatal disease were accompanied by hypotension, encephalopathy, and respiratory distress caused by stridor (presumably secondary to laryngeal edema). The most common complication after recovery from Lassa fever is sensorineural hearing loss, presumably due to host immune response reactions against elements of the inner ear.

Management

Ribavirin has been used with success in patients with Lassa fever. It is most effective if started early in the course of the illness. For adults, a 2-g loading dose, followed by 1 g every 6 hours for 4 days, then 0.5 g every 8 hours for 6 days is recommended. Additional supportive care with maintenance of appropriate fluid and electrolytes, ventilation and blood pressure support, and treatment with broad-spectrum antibiotics for concomitant bacterial superinfections are often necessary.

Lassa fever has been associated with outbreaks of fatal person-to-person spread. Secondary infection occurs through direct contact with infected persons or their secretions. The role of aerosols in person-to-person spread is unclear. Blood and body fluids should be considered infectious. In light of the potentially fatal outcome of Lassa fever and the relative ease of transmission, the CDC has published specific recommendations for management of possible or confirmed cases. If a person has (1) a compatible clinical syndrome (especially pharyngitis, vomiting, conjunctivitis, diarrhea, and hemorrhage or shock); (2) a relevant travel history, including time spent in an endemic area; and (3) prior contact within 3 weeks of presentation with a person or animal from an endemic area suspected of having a viral hemorrhagic fever, he or she should be isolated and local, state, and federal health officials contacted. Ideally, an isolation unit with negative air pressure vented outside the hospital should be used. However, lack of a negative-pressure room alone is not a reason for transfer to another medical care facility.

The probability of transmission of Lassa fever virus to medical and nursing staff can be reduced by routine blood and body fluid precautions as well as strict barrier nursing. Barrier nursing includes wearing gloves, gown, mask, shoe covers, and, if there is risk for splashing fluids, goggles whenever entering the patient’s room. Decontamination of solid articles and rooms may be accomplished with 0.5% sodium hypochlorite solution. Recommendations for the management of patients with viral hemorrhagic fever have been published.17,11

There is no vaccine available. Prevention is through avoidance of contact with rodents, especially in geographic areas where outbreaks occur.

Ebola and Marburg Viruses

Ebola and Marburg viruses are closely related large-RNA viruses known as filoviruses. They cause severe viral hemorrhagic fever syndromes with some of the highest case fatality rates (approximately 90%) of any known infectious disease. Both are endemic in focal areas of central and southern Africa.73 Ebola virus seropositivity has been noted in Sudan, Democratic Republic of the Congo, the Central African Republic, Côte d’Ivoire, and Kenya. A strain of Ebola known as Ebola Reston has been found in monkeys imported into the United States from the Philippines. More recently, there have been outbreaks with fatalities in Gabon, the Democratic Republic of Congo, and Angola. Marburg disease is found in South Africa, Zimbabwe, and Kenya. In 2005, there was an outbreak that caused over 300 deaths in Angola.18 Although there is not definitive evidence indicating the animal reservoir that maintains these filoviruses in nature, current evidence strongly suggests that bats are involved. Person-to-person transmission has been well documented, primarily through contaminated needles and contact with the secretions of infected individuals.72,74

Crimean-Congo Hemorrhagic Fever

Pathophysiology and Clinical Presentation

Pathophysiologic mechanisms are presumably similar to those of other hemorrhagic fevers.28 One in five infections results in clinical disease with a case fatality rate ranging from 10% to 50%. The incubation period is approximately 1 week with initial symptoms of fever, severe headache, myalgias, vomiting, and diarrhea. Various forms of hemorrhage, including petechiae, large ecchymoses, melena, and hematemesis, are more pronounced in CCHF than in other hemorrhagic viral diseases. Severe cases progress rapidly to DIC, shock, and death.

Hemorrhagic Fever with Renal Syndrome and Hantavirus Pulmonary Syndrome

Hantaviruses, when transmitted from rodent reservoirs, cause two significant human diseases, hemorrhagic fever with renal syndrome (HFRS) in Asia and Europe, and hantavirus pulmonary syndrome (HPS) in the Americas. HFRS first came to the attention of Western medical science during the Korean conflict, when febrile illness accompanied by bleeding and renal failure developed in 3000 United Nations troops and was ultimately found to be caused by the hantavirus species Hantaan virus.40 Mortality ranged from 5% to 10%. A similar, less severe syndrome (nephropathia epidemica) had been recognized in Scandinavia since the 1930s. HPS was first recognized in a cluster of deaths in the southwestern United States in 1993. A nonspecific febrile illness is followed by shock and alveolar pulmonary edema caused by the hantavirus species Sin Nombre virus.23

Japanese B Encephalitis

Japanese B encephalitis (JE) has been recognized in Japan since the 19th century. It is the only arboviral encephalitis for which an effective inactivated vaccine has been developed. Vaccine use in Japan and elsewhere since the 1960s has resulted in a significant decrease in the disease rate; however, the inactivated mouse brain–derived JE vaccine (JE-VAX) is no longer being produced because it was associated with adverse reactions, usually with the third dose. An inactivated Vero cell–derived JE vaccine (Ixiaro) has been licensed for use in adult travelers (safety and efficacy data in children are not yet available). This vaccine is recommended to be given if adults are traveling to an endemic region for greater than 30 days.

Epidemiology

JE is the most common cause of encephalitis in Asia. Of the estimated 35,000 to 50,000 cases annually, 20% to 30% of infected individuals die and of those that recover, 30% to 50% have neurologic sequelae.30,46 Transmission correlates with monsoon rains in the tropics and in the summer and fall seasons in temperate regions. Rice field–breeding and other culicine mosquitoes serve as the vectors. In addition to humans, birds and pigs can be infected. Pigs play an important role as amplifying hosts because they develop high-grade viremia from which large numbers of mosquitoes may be infected. Most infections in endemic areas occur in children, whereas all age-groups of previously unexposed populations are at risk. Transmission of JE currently occurs in India, Southeast Asia, China, Korea, Indonesia, and the Western Pacific region.30 Routine use of JE vaccine in Japan has been eliminated because of low risk in this country. Recent outbreaks and case reports of JE in islands of the Torres Strait, which runs between Northern Australia and Papua New Guinea, indicate that the virus spread southward from Asia, presumably by migratory ardeid birds.39

Named Hepatitis Viruses

Although infectious hepatitis has been a well-known clinical entity for hundreds of years, it is only in the last few decades that identification of specific viral pathogens has been possible. The causes of hepatitis may be divided into two groups. First, the so-called named, or more accurately, lettered viruses, now include hepatitis A to G. These are associated with defined clinical syndromes and elevated liver function tests. Second, other organisms that cause hepatitis as part of a more systemic infection include Epstein-Barr virus, cytomegalovirus, toxoplasmosis, and leptospirosis. Only select examples in the former group are discussed here.

Hepatitis A

Epidemiology

Hepatitis A virus is transmitted primarily by the fecal–oral route by either person-to-person contact or ingestion of contaminated food or water. Food items commonly associated with outbreaks are raw or undercooked clams and shellfish. Risk factors include contact with a hepatitis A–infected person, international travel, household or personal contact with a child who attends a child care center, foodborne outbreaks, male homosexual activity, and use of illegal drugs.3,59 Occasional cases are associated with exposure to nonhuman primates. Transmission by blood transfusion has been reported, but this is an uncommon source of infection. Hepatitis A is endemic worldwide, but underdeveloped nations have a higher prevalence than those in North America. Most persons in these areas show serologic evidence of past infection with hepatitis A virus. Hepatitis A is a common viral infection occurring in travelers, but rates are declining with increased use of hepatitis A vaccine

Diagnosis

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