GASTROINTESTINAL/GENITOURINARY
Amebiasis
Amebiasis, caused by the parasite E. histolytica, is responsible for approximately
55,000 deaths/yr globally; it is the third most frequently isolated pathogen
among returning travelers with infectious diarrhea. Amebiasis is transmitted via
fecal–oral contact with amebic cysts; humans are the only reservoir. High-risk
groups include foreign travelers, migrant workers, immunocompromised
individuals, children in daycare centers, and prisoners. Less than 20% of persons
who consume infected cysts develop symptoms. The spectrum of infection
ranges from asymptomatic carriers to intestinal amebiasis, hepatic abscesses, or
amebomas. Intestinal amebiasis typically has an insidious onset consisting of
weight loss, abdominal pain, and initially nonbloody progressing to dysentery.
Fever is rare. Complications include intestinal ulcers, fulminant colitis, and
perforation. Hepatic amebic abscesses present clinically as fever, cough,
tachypnea, hepatomegaly, and right upper quadrant pain with referred shoulder
pain (the latter is more common in adults). Liver abscesses are the most common
extraintestinal form of amebiasis. Rupture of the abscess with peritoneal seeding
can be fatal. While drainage may be adjunctive to medical therapy, percutaneous
drainage under controlled circumstances is optimal to prevent peritoneal seeding.
Other extraintestinal manifestations are rare, but may include pericardial,
pleuropulmonary, cerebral, genitourinary, and cutaneous amebiasis. Amebomas
are annular lesions of cecum or colon that can mimic cancer or pyogenic
abscesses. These usually can be managed medically.
Diagnosis is made via visualization of cysts or trophozoites in stool (for
colitis) or serum enzyme immunoassay (EIA) testing (for extraintestinal
disease). PCR can differentiate E. histolytica from related, nonpathogenic
species. CT can help identify extraintestinal manifestations. Ancillary testing
may reveal leukocytosis, anemia, or transaminitis. Treatment of asymptomatic
carriers is with paromomycin (25 to 35 mg/kg/day in three divided doses for 7
days) or diloxanide furoate (20 mg/kg/day in three divided doses [maximum:
500 mg/dose] for 10 days). Treatment of colitis is with metronidazole (35 to 50
mg/kg/day divided into three doses for 7 to 10 days; maximum: 750 mg/dose).
Treatment of liver abscesses, ameboma, or moderate/severe intestinal amebiasis
is with metronidazole and paromomycin. Surgical intervention may be needed
for patients with hepatic abscesses unresponsive to medical management or
those with toxic megacolon. Contact precautions are recommended.
Giardia
Giardiasis is caused by Giardia intestinalis, a protozoan spread by fecal–oral
transmission. While humans are the primary reservoir, domesticated and wild
animals can also be infected. Most U.S. outbreaks have been associated with
contaminated drinking water, daycare facilities, and food handlers. One-half to
three-quarters of infections are asymptomatic. Symptoms include malodorous
watery, nonbloody diarrhea, flatulence, abdominal pain, and weight loss. Anemia
may be noted. Children with humoral immunodeficiencies can develop chronic
symptomatic infection. The diagnosis is based on EIA or direct fluorescent
antibody (DFA) assays, which have sensitivity and specificity far superior to
identification of organisms in the stool. Treatment is not needed for self-limited
infections in normal hosts, and treatment of asymptomatic carriers is not
recommended unless they live in the home with an immunocompromised person.
For patients requiring treatment, metronidazole (5 mg/kg every 8 hours
[maximum: 250 mg/dose for 5 to 7 days]), tinidazole (single dose, licensed for
children 3 years of age and older: 50 mg/kg [maximum: 2 g]), or nitazoxanide
(3-day course for children 1 year of age and older: 1 to 3 years: 100 mg twice
daily, 4 to 11 years: 200 mg twice daily, ≥12 years: 500 mg twice daily) are
options. Standard and contact precautions should be used for the incontinent
child.
Cryptosporidium
Cryptosporidiosis is caused by C. parvum and C. hominis, protozoal species
spread by fecal–oral transmission. Humans, cattle, and other animals are
reservoir species. In the United States, almost 8,000 cases occur annually, so a
travel history is not a prerequisite for infection. Risk factors include swallowing
contaminated water (including at hotel swimming pools), hiking and drinking
unfiltered water, daycare attendees, workers, and the families of children who
attend day care, and travelers. Asymptomatic infection can be seen. Most
patients will develop low-grade fever, watery, nonbloody diarrhea with crampy
abdominal pain, vomiting, and weight loss. Symptoms last 1 to 2 weeks,
although more severe and chronic symptoms can be seen in HIV-infected
patients
and
other
immunocompromised
hosts.
In
addition,
immunocompromised children can develop extraintestinal manifestations: biliary
tract and pneumonitis. DFA and EIAs are more sensitive than detection of
oocytes in stool. Self-limited illness in immunocompetent hosts usually does not
require treatment. Nitazoxanide is approved for children 1 year of age and older
(3-day course for children 1 year of age and older: 1 to 3 years: 100 mg twice
daily, 4 to 11 years: 200 mg twice daily, ≥12 years: 500 mg twice daily). Longer
treatment courses may be needed in HIV-infected children and other
immunocompromised hosts. Standard and contact precautions should be used for
the incontinent child.
Gram-negative Enterics: Vibrio, E. coli, Campylobacter,
Shigella
Several gram-negative enteric pathogens are more common in developing
nations than in industrialized countries. These include Vibrio cholera,
enterotoxigenic, enteropathic, enteroinvasive, and enteroaggregative E. coli, and
Campylobacter ( e-Table 94.22 ). Cholera is characterized by painless watery
diarrhea, and persons most at risk are those with low gastric acidity. It can be
easily spread in congregate settings, and is a major cause of diarrhea in camps
for displaced persons. The character of diarrhea varies based on E. coli type, and
some types produce a Shiga-like toxin. Campylobacter is also a cause of
dysentery (bloody stools with fecal leukocytes) in the United States, but is more
common internationally. The most at-risk group for Shigella domestically is the
child in daycare. In addition to the acute symptoms (which are more severe in
immunocompromised hosts), patients with Campylobacter can also have
postinfectious sequelae with Guillain–Barré syndrome, including the Miller
Fisher variant (ataxia out of proportion to sensory loss, areflexia, and
ophthalmoplegia). All three pathogens can be cultured on routine stool culture
media. The mainstay of therapy is rehydration. Adjunctive antibiotic treatment is
recommended to decrease symptom duration, decrease fecal shedding, and
decrease secondary transmission. Standard and contact precautions are
recommended.
Schistosomiasis
Schistosomiasis is caused by mammalian blood trematodes (flukes) in the
Schistosoma genus. Freshwater snails transmit the infection through penetration
of intact skin. Schistosomiasis is endemic in more than 75 countries worldwide
including in Africa, the Middle East, China, Southeast Asia, Brazil, Venezuela,
and the Caribbean. Adult worms can live as long as 30 years, causing disease
decades after patients have left an endemic area. The clinical manifestations of
the most common syndromes caused by schistosomes are summarized in
eTable 94.23 . The severity of chronic illness is associated with worm burden.
Those with low to moderate burden may never develop significant illness, while
those with significant worm burden may develop mucoid bloody diarrhea and
tender hepatomegaly. Severe infection with the intestinal form of the disease
may result in development of portal hypertension, ascites, esophageal varices,
and hematemesis. The drug of choice is praziquantel (dosing varies depending
on the species) and the treatment must be repeated approximately 1 to 2 months
later due to failure of the medication to kill developing worms. Schistosomal
dermatitis (swimmer’s itch) does not require therapy. Paradoxical inflammation
after antiparasitic therapy is common and can be treated with systemic
corticosteroids. Standard precautions exist for isolation of infected patients.
Soil Helminthic Infections
A number of helminthic infections cause human disease. Most are transmitted
through the fecal–oral route, though in some cases helminths can penetrate intact
skin. The most common helminthic infections are Enterobius vermicularis
(pinworms), Trichuris trichiura (whipworm), Ascaris lumbricoides
(roundworm), Ancylostoma (hookworm), cutaneous larva migrans (CLM)
(sandworm), and Strongyloides. Most infected individuals are asymptomatic.
Clinical manifestations are strongly related to the intensity of the infection and
worm burden. Some infections result in anemia or impaired growth and
cognition. Diagnosis is usually made via visualization of larvae in the stool. The
clinical manifestations, diagnosis, and treatment are summarized in
e-Table
94.24 . Most can be treated with either albendazole or mebendazole; albendazole
is typically more tolerable for patients in terms of taste and side effects. The
albendazole dose is 400 mg for both children and adults. A single-dose regimen
is the recommended treatment for Ancylostoma, Ascaris, and Enterobius,
whereas Trichuris requires a 3-day course and Strongyloides a 7-day course with
twice-daily dosing.
SKIN/SOFT TISSUE INFECTIONS
Dermatologic conditions are common among persons who have recently traveled
( Table 94.21 ). Urticaria is common, and can be caused by Strongyloides
stercoralis, scabies, schistosomiasis, onchocerciasis, or insect bites. Insect bites
(such as bedbugs and fleas) are the most common cutaneous finding in the
returning traveler. The most common cause of ulcers is pyoderma, caused by
streptococci and staphylococci, but can also be caused by cutaneous
leishmaniasis. Eschars may be seen in rickettsial disorders such as
Mediterranean spotted fever, scrub typhus, and African tick typhus. Burrowing
lesions can be caused by botflies (myiasis) and fleas (tungiasis).
Leishmaniasis