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the spirochetes die. Doxycycline can be used in older patients with milder disease. Contact precautions are
recommended.

Tick-borne Diseases
Rickettsial diseases in the returned traveler may include Rickettsia africae (African tick typhus), Rickettsia conorii
(causing varying clinical syndromes in different geographic regions, and called by a number of names:
Boutonneuse fever; or Mediterranean, Israeli, Kenyan, or Indian tick typhus), and Orientia tsutsugamushi (scrub or
bush typhus in Japan and Russia). These are all arthropod transmitted from game and cattle ticks, dog ticks, and
mites (“chiggers”), respectively. Symptoms are similar to endemic rickettsial diseases: fever, headaches, myalgia,
and rashes. A painless eschar can sometimes be found at the site of the bite. Risk factors include hiking, camping,
or traveling on safari in grassy or scrubby regions. Examination findings may include localized lymphadenopathy
and a petechial or nonpetechial rash (African tick typhus typically presents without rash, or with a few macular or
vesicular lesions). Laboratory findings include leukopenia and thrombocytopenia. The diagnosis is usually clinical
and treatment with doxycycline should not await confirmatory serologies or PCR-based diagnostics. Standard
precautions are recommended.

Plague
Plague is caused by a gram-negative coccobacillus, Yersinia pestis, a zoonotic infection of rodents and fleas. It can
be transmitted by respiratory droplet from person-to-person. Plague cases are consistently recorded throughout
several countries in Africa, Asia, and the Americas with a vast majority of these cases occurring in Africa. In the
United States, the main risk factor is contact with prairie dogs, and it is most common in the upper Midwestern
states. The most common form is bubonic plague, characterized by an initial brief prodrome of fever, anorexia, and
headache followed by the development of tender regional adenopathy (often in the inguinal area after flea bites to
the lower extremities). These nodes develop a reddish discoloration and proceed to necrosis. More severe forms
include pneumonic and septicemic plague. Most patients have a rapidly progressive course characterized by fever;
initial symptoms mimic influenza. If untreated, pneumonic and septicemic plague is almost uniformly fatal and
bubonic plague has a mortality rate approaching 50%. The proximate causes of death are disseminated
intravascular coagulation, respiratory failure, and renal failure. The diagnosis is made by culture; Gram stain
demonstrates a bipolar appearance to the bacillus that appears like a safety pin with clustering of the stain at the
poles with relative central clearing. The treatment of choice is an aminoglycoside. Alternative agents include
fluoroquinolones or chloramphenicol for plague meningitis, tetracyclines, or doxycycline. Cephalosporins are not


effective. TMP-SMZ is not recommended as monotherapy. The disease must be reported to public health
authorities. Droplet precautions should be used for patients with pneumonic plague.

CENTRAL/PERIPHERAL NERVOUS SYSTEM
There are numerous processes that may cause fever and neurologic manifestations; however, special consideration
should be given to specific etiologies in the returning traveler. Malaria, tuberculosis, typhoid fever, rickettsial
infections, leptospirosis, poliomyelitis, rabies, and the viral encephalitides (including Japanese encephalitis, West
Nile encephalitis, and tick-borne encephalitis) are possible infections that affect the CNS. Travelers to the
“meningitis belt” regions in Africa (during the months of December to June) and those who travel to the Arab
world around the time of the annual pilgrimage to Mecca for the Hajj are at increased risk for developing
meningococcal meningitis. CNS involvement with eosinophilia should also raise the possibility of
coccidioidomycosis and angiostrongyliasis (the latter caused by the rat lungworm Angiostrongylus cantonensis ).

Neurocysticercosis
Cysticercosis is caused by the pork tapeworm, Taenia solium, commonly found throughout central and South
America, South Asia, and China. Human cysticercosis is acquired via fecal–oral transmission by ingestion of
tapeworm eggs from a human tapeworm carrier or by autoinfection. The incubation period may be several years.
Morbidity is almost entirely due to infection of the CNS; most commonly, seizures (partial seizures with or
without secondary generalization) due to larval cysts in the brain parenchyma serving as a seizure focus. Other
manifestations can include gait dysfunction from cerebellar involvement, ocular disease with visual loss, or
encephalitis. One study in Chicago found that neurocysticercosis was a common cause of new-onset afebrile
seizures in Latino children. Subcutaneous cysts are primarily only of cosmetic significance and produce painless
palpable nodules.



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