hepatitis and may be either early-onset (within first eight weeks) or late-onset (8 to
12 weeks) after jaundice develops (112–115). Hepatitis B accounts for 30% to 60% with
coinfection with delta virus in 30% to 40% that has been demonstrated to increase disease
severity (116). Hepatitis A only accounts for<0.1% of causes of fulminant hepatitis,
although overall Hepatitis A represents the most commonly acquired agent of viral
hepatitis (50% to 60% in most series) (113). Hepatitis C association with fulminant non-A,
non-B hepatitis has been reported in Japan but is very uncommon in Western countries
(117,118). Hepatitis E, a virus transmitted via an enteric route, has an increased fatality
rate in pregnant women (119). Early indicators of a poor prognosis and the potential
need for liver transplantation in viral hepatitis include age<11 years or>40 years,
duration of jaundice before onset of encephalopathy less than seven days, serum bilirubin
300 mmol/L, and prothrombin time>50 seconds (120). Early diagnosis of acute hepatitis
is important, given evidence of specific benefit from antiviral therapies including
lamivudine in acute Hepatitis B and interferon therapy for Hepatitis C (121–125). Other
less common causes of fulminant hepatitis include Yellow fever virus and leptospirosis.
Yellow fever virus–endemic zones are updated on a regular basis and available (as are
cholera- and plague-endemic zones) through the weekly CDC publication (theBlue Sheet).
A resurgence in yellow fever in Africa and South America emphasize the continued threat
from this agent for unvaccinated travelers (126). Severe yellow fever is fatal in>50% of
cases and continues to be a cause of deaths in returning travelers (127–130). Leptospirosis
has widespread distribution and is usually transmitted to humans through contact with
surface water contaminated with urine from infected animals (131). Travelers returning
with leptospirosis typically present with a mild or moderate illness. The spectrum of
disease includes fulminant hepatitis, meningoencephalitis, hemorrhagic manifestations,
pulmonary manifestations including ARDS, and renal failure (131–136). Leptospirosis
should be considered in most severely ill returning travelers. A recent randomized
controlled trial demonstrated equal efficacy of seven-day intravenous therapy with
ceftriaxone (1 g daily) and penicillin G (1.5 million U every six hours) in severe
leptospirosis (137). However, case fatality was 5.8% with 10% requiring dialysis and 22%
experiencing respiratory failure.
Fever with Eosinophilia
Eosinophilia in the returning traveler is not uncommon and requires an initial assessment of
the absolute eosinophil count (eosinophilia >450/mm^3 ), consideration if travel-related
(i.e., check pretravel differential white blood cell counts) and the most likely parasite based
on travel destination, duration of stay, and exposure history (138). Critically important is a
determination of whether the eosinophilia is related to the patient’s current symptoms since
most causes of eosinophilia in travelers result in either asymptomatic or mild disease; although
the predictive value of peripheral eosinophilia has limitations (139). A tenet of tropical
infectious diseases is that patients may present with multiple infections, an acutely ill traveler
with moderate eosinophilia may have malaria as the cause of the symptoms and asymptomatic
hookworm infection as the etiology of the eosinophilia. Infectious etiologies of fever and
eosinophilia that may present with potentially life-threatening illnesses include acute
schistosomiasis (acute serum sickness-like disease termed Katayama fever or acute neurologic
sequelae of myelitis or encephalitis), visceral larva migrans, tropical pulmonary eosinophilia,
acute fascioliasis, and acute trichinosis (138). Schistosomiasis is the most common of these
infections with reported high infection rates (mean 77%) in groups of travelers exposed to fresh
water in endemic regions occasionally resulting in severe acute infection approximately four to
eight weeks postexposure (140–142). Definitive diagnosis of schistosomiasis requires identi-
fication of the ova in stool, urine, or tissue specimens. The acute hypersensitivity syndromes of
schistosomiasis occurring prior to ova deposition or ectopic distribution of the schistosome ova
(such as in the CNS) necessitate the use of sensitive serologic methods for diagnosis (143).
Specific therapy with praziquantel is highly efficacious in the low worm density infections
seen in travelers (143). The acute hypersensitivity syndromes often require adjunctive
corticosteroid therapy.
Tropical Infections in Critical Care 331