Of returning travelers who become ill, many have neither serious nor exotic illnesses.¹ The most likely causes of acute symptoms are common problems such as upper respiratory infections, diarrheal illnesses, or reactions to stress, fatigue, or new medications. The ED physician often does not confirm the final diagnosis, but rather protects the health of the public from potentially communicable diseases, begins diagnostic and therapeutic interventions, and provides appropriate referral. Local or regional international health clinics are good resources for referral of patients who need more advanced evaluation, serologic testing, and long-term follow-up (see http://www.travelersvaccines.com/).

Key points for the initiation of ED care are the following:

1. 
   

   Isolate and use personal protective precautions early when evaluating patients with suspected travel-related infections.

   
   
2. 
   

   Most travelers do not have exotic diseases; think of common causes.

   
   
3. 
   

   Malaria lurks in the febrile patient returning from travel, even in the presence of prophylaxis.

RISK ASSESSMENT

Of travelers, 64% report one or more illnesses during travel, 26% are ill upon return, and 56% of those ill upon return develop symptoms after arrival in the United States.² Many disease incubation times are longer than the transit times.

Most travelers on vacation or business are abroad for <20 days, and <5% spend extended time overseas. Some travelers originate from disease-endemic nations, as tourists or newly arrived immigrants; these people are at risk of illness due to transit and exposure to areas with high rates of endemic infectious disease. Others at risk include nonvoluntary travelers, such as refugees and displaced persons, as well as landed immigrants returning from visiting their homeland. In all extended-duration travelers, consider endemic illnesses, even if they lived in the area previously. Travelers also have a risk of tropical illness due to increasing adventure-type travel to areas that were previously inaccessible (Table 161-1).

Diseases such as malaria are uncommon in the United States but are leading causes of mortality overseas. Other parasitic agents, such as helminths and rickettsia, also occur with increased frequency and severity in the tropics (see chapters 158 and 160, “Malaria” and “Zoonotic Infections”). Diagnosis of a tropical infection requires a unique set of tests, and therapy is organism specific.

Think of a potential bioterrorist agent as a cause of disease when factors suggest intentional release, such as divergence of the disease presentation from the typical epidemiology of the community and an atypical number of patients presenting with similar clinical syndromes. Examples of diseases that could be weaponized include anthrax, plague, viral hemorrhagic fevers, and tularemia (see chapters 9, “Bioterrorism” and 160).

INCUBATION PERIOD

The approximate incubation period (the time between exposure and signs and symptoms) can be helpful in assessing illness risk. For example, if fever begins >21 days after return or infected patient contact, yellow fever, viral hemorrhagic fevers (including Ebola, covered elsewhere), and other arboviruses (e.g., dengue fever) are unlikely, irrespective of the exposure history (Table 161-2). In comparison, schistosomiasis may cause symptoms 5 weeks after exposure. Many diseases have variable incubation depending on factors such as host immunity and the use of chemoprophylaxis and antipyretics.

HISTORY

Suspect imported disease in recent world travelers, and direct the history appropriately (Table 161-2 and Table 161-3). Note previous medical conditions because immunosuppression, age <5 years, advanced age, pregnancy, and diabetes often render the patient less tolerant of tropical infections.

Ask about the duration of travel (suggesting specific disease incubation periods) and destination or origin (suggesting possible cause), which can focus the differential diagnosis (Table 161-4). Other important considerations are the living conditions and locale of the traveler (rural areas have greater infectious risks of certain diseases), type of accommodation, and travel-related activities (suggesting possible exposure, Table 161-5).

Review any pretravel immunizations and preventive medications, high-risk behaviors, and prior medical conditions. Immunization history is relevant because proper vaccination against hepatitis A, hepatitis B, and yellow fever can effectively rule these out as causes of illness. Adherence to appropriate chemoprophylaxis reduces the risk of acquiring malaria—which is the most important tropical emergency—yet it cannot eliminate the possibility. Because of increasing malaria resistance, assume that the febrile returning traveler has malaria even if chemoprophylaxis was correctly taken.

A history of medications, herbs, and traditional medicines consumed is also useful information, because these may contain antipyretics that can alter disease presentation. If altered mental status exists, suspect cerebral malaria or meningitis and consider early empirical treatment for both until the diagnosis is confirmed.

PHYSICAL EXAMINATION

When assessing vital signs, consider that antipyretics can mask fever. Evaluate the abdomen for hepatosplenomegaly or focal abdominal discomfort. Examine for lymphadenopathy and inspect the skin for rashes, lesions, or pallor. Ophthalmologic examination for scleral icterus, conjunctival injection, or petechiae helps detect causes. Imported diseases should be suspected in the presence of high fever, signs of hemorrhage, diarrhea, shortness of breath, skin lesions, and neurologic disturbances. Table 161-6 lists other signs of tropical illness.³

Usually one or more hallmark symptoms or signs are associated with specific infections, allowing categorization. These include fever, CNS complaints, abdominal pain, diarrhea, skin and eye complaints, and respiratory symptoms. It is important to identify diseases that may be rapidly fatal, easily treatable, and/or potentially contagious.

LABORATORY TESTING

Initial studies include a CBC with differential and platelet count, hepatic function tests, and urinalysis; thick and thin blood smears for malaria (and rapid antigen detection test); blood cultures, urine cultures, stool cultures, and stool analysis for WBCs, ova, and parasites; and a chest radiograph for fever and cough. The absolute eosinophil count is often elevated to >500/mm³ in parasitic diseases caused by worms. In a clinically well-appearing patient in whom malaria treatment is not begun but malaria is suspected, obtain blood for smear every 12 to 24 hours. Specific serologic tests are deployed selectively, such as erythrocyte sedimentation rate, purified protein derivative, syphilis test, human immunodeficiency virus test, and serology for arboviruses or rickettsiae.

Consult an infectious disease specialist early in the evaluation to optimize testing and follow-up. It is also wise to obtain an extra vial of serum in a red-top tube (for serology and immunology) during the initial evaluation. This specimen can be used later for comparison with convalescent-stage specimens.

Although fever is nonspecific, it raises the suspicion for a serious infection (Table 161-7).^4,5 Patients with fever after tropical travel have malaria until proven otherwise. Other common serious infections are listed in Table 161-8.^6,7

MALARIA

The classic clinical triad for all species of malaria is fever, splenomegaly, and thrombocytopenia.^8,9 Fever is typically irregular for the first week and later may demonstrate periodicity. Patients usually have continuous symptoms initially followed by episodic pyrexia every 2 to 3 days, depending on the infecting species. Periodicity is unusual with falciparum malaria. Serious malaria infections occur primarily in young children, pregnant women, the elderly, individuals never previously infected, and patients with comorbid medical problems. Because associated symptoms such as headache, cough, and GI problems mimic other conditions, malaria is a consideration in all febrile travelers.

Diagnosis is based on clinical presentation and confirmed with laboratory evidence of bloodborne protozoa. Patients with fever >38.5°C (101.4°F) of unclear origin and recent or past travel to an endemic area should be screened by blood smears and rapid antigen detection tests when available. Refer to chapter 158 for a detailed discussion of malaria diagnosis and treatment.

DENGUE FEVER

Dengue is the most serious febrile tropical disease after malaria. The World Health Organization reported a 30-fold increase in incidence of dengue in from the 1960s to the 2010s, with up to 50 million cases occurring annually worldwide.¹⁰ Suspect dengue fever among travelers with fever developing within 2 weeks of travel. Dengue may be contracted more than once because each of the four strains offers no cross-protective immunity. Many cases are self-limiting, and the illness is not reporTable in the United States.¹¹

Dengue fever occurs in urban environments in most tropical nations and is transmitted by the peridomestic day-biting Aedes aegypti mosquito. Urban dengue in the Americas, Africa, and the Indian subcontinent is usually classical dengue fever, whereas in Southeast Asia, it manifests as hemorrhagic fever and shock. Classic dengue fever presents after a typically short incubation period of 4 to 7 days with sudden high fever, headache, nausea, vomiting, myalgias, and rash usually lasting several days. Facial flushing, conjunctival injection (although uncommon), and retro-orbital pain can occur. After defervescence, a fine, pale, morbilliform rash develops on the trunk and spreads to the extremities and face. Small children may only present with a mild upper respiratory infection, and classic dengue may be confused with influenza, measles, or rubella. Although other causes of fever can present with a similar clinical picture, such as West Nile fever (transmitted by the Culex mosquito), West Nile fever causes lymphadenopathy, which is usually absent in dengue. Dengue can also cause petechial hemorrhages indistinguishable from meningococcemia.

Dengue hemorrhagic fever preferentially occurs among infants of immune mothers, children >1 year old, and those with second and subsequent infections. It begins as classical dengue with fever and myalgias. After 2 to 7 days, as pyrexia improves, lassitude, fatigue, and shock develop with an ensuing mortality that is >10%. Clinical features include pleural effusions and bleeding diathesis with epistaxis, purpura, petechia, and marked thrombocytopenia with elevated hematocrit because of vascular permeability. Dengue hemorrhagic fever may rapidly evolve into dengue septic shock, which is often fatal. Dengue septic shock is heralded by abdominal pain, severe emesis, mental status changes, and alternating severe pyrexia and hypothermia.

Diagnosis of dengue is based on clinical findings; although serology is confirmatory, cross-reactivity often occurs with other flaviviruses. Enzyme-linked immunosorbent assay provides rapid confirmation of infection by day 6 of the illness. Laboratory abnormalities include leukopenia, thrombocytopenia, and hepatic dysfunction. In uncomplicated dengue fever, treatment is supportive and consists of fluids and analgesics. Only acetaminophen is recommended for managing pain and fever because aspirin and other nonsteroidal anti-inflammatory drugs are contraindicated due to anticoagulant properties.

TYPHOID FEVER

Enteric fever, or typhoid fever, is a serious infection diagnosed in roughly 400 travelers annually returning to the United States, with an additional 100 cases of paratyphoid. Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi, respectively.¹² Once malaria is excluded, typhoid fever is commonly the cause of a febrile illness lasting >10 days.¹³ Imported cases occur in visiting friends and relatives and travelers from Mexico, Indonesia, Peru, and the Indian subcontinent. Vaccination before travel helps thwart acquisition, although protection wanes with time and revaccination is required.

The disease is transmitted in a dose-related fashion after food contamination by feces or urine from actively infected cases or healthy disease carriers. Incubation times and disease severity vary from 1 to 3 weeks. After ingestion, bacteria adhere to the small bowel mucosa, invade lymphoid tissues, and disseminate by lymphatics to the bone marrow, gallbladder, and spleen to reproduce in macrophages. Most pathology occurs in the gut as a consequence of inflammation, necrosis, and ulceration. Typhoid fever classically begins with fever and headache, and then progresses to high fever with chills, headache, cough, abdominal distention, myalgias, constipation, and prostration. The differential diagnosis includes malaria, typhus, viral hepatitis, amebic liver abscess, and other types of infective enteritis. In epidemics, patients can present with acute diarrhea and vomiting, headache, and meningeal signs. Most patients, however, present with constipation rather than diarrhea. Bradycardia relative to fever is classic (but may be absent); after several days of fever, a pale red macular rash may appear on the trunk (rose spots) among fair-skinned individuals. As the disease progresses, splenomegaly develops. Patients may develop leukopenia and elevated liver enzymes, although most cases have nonspecific laboratory values. Complications include small bowel ulceration, anemia, disseminated intravascular coagulopathy, pneumonia, meningitis, myocarditis, cholecystitis, and renal failure. Sequelae include deafness, and neurologic involvement including psychosis, ataxia, and seizures can occur.¹⁴

Diagnosis is clinical and confirmed by culturing blood, urine, or stool (during the second week) or by rapid antigen testing. Although most cultures have a moderate yield, bone marrow culture is most sensitive, and organism identification is possible after antibiotic treatment.

Current treatment recommendations for typhoid fever include fluoroquinolones (ciprofloxacin), cephalosporins (cefixime and ceftriaxone), or azithromycin, with duration of treatment dependent on severity of illness. Currently, ampicillin, trimethoprim-sulfamethoxazole, and chloramphenicol are unreliable due to resistance. Nalidixic acid–resistant S. typhi strains are also associated with fluoroquinolone resistance; these organisms are found in both India and Southeast Asia. If typhoid meningitis is suspected, administer dexamethasone, 3 milligrams/kg IV loading dose over 30 minutes, followed by 1 milligram/kg IV every 6 hours for eight doses in addition to antibiotics. Supportive treatment includes IV rehydration and blood transfusion (if needed from GI losses). Untreated, mortality is 10% to 15%, mostly in young children.

RICKETTSIAL SPOTTED FEVERS

Rickettsial spotted fevers are transmitted by the bite, body fluid, or feces of ixodid arthropod ticks, and the ticks are widely globally distributed. Fleas and mites also transmit rickettsial infections. Among the eight major rickettsial infections, there is great variation in severity. Mortality without treatment approaches 25%, which is lowered to 5% with treatment (see chapter 160). Suspect scrub typhus (Rickettsia orientalis) after rural travel in the Asia-Pacific region and maritime Russia and African tick typhus (Rickettsia conorii var. pijperi) after travel to sub-Saharan Africa or the West Indies.

Scrub Typhus and African Tick Typhus

The mite bite, in the case of scrub typhus, or tick bite, with African tick typhus, may go unnoticed. After 3 to 14 days of incubation, patients develop fever, malaise, myalgias, severe headache, rash, nausea, and vomiting. The rash may be absent. Scrub typhus is characterized by a papule at the bite site. The papule later becomes necrotic and forms a crusted black “tache noire” eschar. As organisms disseminate, patients develop fever, malaise, headache, lymphadenopathy, and splenomegaly. African tick typhus presents like scrub typhus, but with much less severe symptoms and localized lymphadenopathy associated with an eschar. Diagnosis is clinical, and serologic tests are confirmatory. Doxycycline, 100 milligrams PO twice daily for 7 to 10 days, is the empirical treatment of choice, and chloramphenicol is an alternative. African tick typhus requires only 3 days of therapy and is often self-limited even without treatment. In severe cases of scrub typhus, death occurs from a multiorgan toxemia within 1 to 2 weeks of illness onset if untreated. Continue treatment for at least 5 days and for 48 hours after defervescence.

Typhus (Epidemic Louse-Borne Typhus)

Typhus is a rickettsial louse-borne disease caused by Rickettsia prowazekii. Typhus is a different disease from the bacterial disease due to S. typhi, typhoid fever (see above). Epidemic louse-borne typhus is transmitted by the arthropod body louse. Typhus is widespread and found in Central Africa, Asia, and Central, North, and South America. It is also common in cold mountainous regions affected by famine, war, or mass population movement, where adequate clothing exists to harbor the louse or lice. Louse-borne disease occurs after louse body fluids and feces are rubbed into abrasions or after bites. Infection results in high fevers after an 8- to 12-day incubation period. Severe headache is common, and a maculopapular rash appears between days 4 and 7, generally sparing palms and soles. The rash may be hemorrhagic. Diagnosis starts on clinical grounds and is confirmed with serologic testing. Treatment is doxycycline (100 milligrams PO twice daily) or chloramphenicol (50 milligrams/kg/d PO in four divided doses) for 7 days and until 48 hours after defervescence. Untreated, mortality is as high as 60%.

LEPTOSPIROSIS (WEIL’S DISEASE)

Leptospirosis, or Weil’s disease, follows mucous membrane or percutaneous exposure to freshwater contaminated by Leptospira interrogans. Infected animals excrete the spirochete in their urine. Infected patients typically have had contact with dogs; swam, rafted, or waded in contaminated surface water; or farmed or gardened in contaminated areas. Outbreaks commonly occur after flooding. Although the risk to most routine travelers is low, recent ecotourists and adventure travelers have become infected after intense water exposure.

The clinical course can be asymptomatic, but often symptoms illustrate a biphasic pattern. After an incubation of 2 to 20 days, high fever, severe headache, chills, myalgias, hepatitis (with or without jaundice), and nonspecific influenza-like symptoms develop. NoTable is conjunctival injection without purulent discharge.

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