Tropical Medicine 4: Gastrointestinal and Abdominal Manifestations
As with fever, virtually any infection or noninfectious disease may present with nausea or other abdominal complaints. This chapter presents those diseases for which abdominal symptoms are the hallmark.
Bowel Trouble—Diarrhea and Dysentery
Cholera
Cholera is a bacterial infection that, via its toxin, causes
severe diarrhea and
death by water and electrolyte depletion. Cholera is spread via the fecal-oral
route directly or through contamination of food and water. After an incubation
period of just a few days, profuse, watery diarrhea develops. Fever is rare; hypoglycemia is common.
Diagnosis is clinical for severe cases; few other etiologies exist for this clinical picture. Mild cases may be misdiagnosed as rotavirus or other viral gastroenteritis. Microscopy (dark field) of stool in severe cases can aid in diagnosis, as can culture.
Treatment is based on rehydration. Initial rehydration may require rates of 4 L/h IV for adults with lactated Ringer’s the solution of choice. Once stabilized, ensuring that inflow equals loss (may be over 20 L/day) is essential. Use of glucose-electrolyte oral rehydration solution should replace IV fluids when the patient is able to maintain appropriate intake. Tetracycline (500 mg PO every 6 hours for 3 days), or doxycycline (300 mg PO once) may be helpful in severe cases, but should be avoided in mild forms to prevent resistance.
Traveler’s Diarrhea
This syndrome is common (affecting 50% to 70% of travelers) 1,2
and usually self-limiting. It presents as watery diarrhea, cramps,
nausea, mild fever, and malaise. Traveler’s diarrhea is usually caused
by enterotoxigenic Escherichia coli
(E coli), but
may also be
due to
Campylobacter, Salmonella, Shigella, and
other bacterial pathogens as well as
protozoan and viral agents.
Diagnosis is clinical. If prolonged or severe symptoms are present, consider additional diagnoses beyond simple traveler’s diarrhea.
To treat, hydrate the patient and administer the presumptive antibiotic ciprofloxacin (Cipro) 500 mg twice daily for 3 days (other quinolones may also be used for 3 days) or azithromycin 500 mg PO day 1, 250 mg PO day 2 through resolution of symptoms. Antimotility agents should not be given without also using antibiotics.
Tropical Sprue
Often following acute diarrheal illness, a malabsorption syndrome
may develop. It is characterized by non-bloody diarrhea and steatorrhea, bloating, and weight
loss. Duodenal biopsy shows villous atrophy similar to celiac sprue. The
underlying mechanism is not known. The course may be prolonged with
significant morbidity associated with it. Tetracycline and folic acid is often
effective at reversing the symptoms.
Giardiasis
Giardia is a protozoan
acquired by ingestion of cysts. This organism may produce
a malabsorptive diarrhea manifest as explosive gas emissions and a remarkably
foul odor. Often, the patient appears otherwise healthy.
Diagnosis is identification of the organism in the stool; serological and antigenic tests are also available.
Giardiasis responds well to metronidazole 500 mg twice daily for 5 days.
Coccidian Infections
Cryptosporidium, Cyclospora, Isospora, and
Microspora are all protozoan parasites
that cause prolonged
watery diarrhea, cramps, fever, and fatigue. Often
asymptomatic, they are of significance mainly for the immunocompromised.
Diagnosis is often missed. Identification of the organism in the stool is the mainstay. If suspected, specifically instruct the lab to look for these organisms.
Treatment is variable. Use paromomycin for HIV patients with cryptosporidiosis; Bactrim is effective for Isospora and Cyclospora.
Dysentery
Dysentery differs from diarrhea in that there is significant blood and mucous in
the stools. This may be caused by a variety of
organisms.
Bacterial
Shigellae
is the most common cause of bacillary dysentery, and is acquired
through the fecal-oral
route. Following ingestion and an incubation of around a week, disease
develops, ranging from (1) asymptomatic to (2) mild, self-limiting
to (3) possibly fatal, fulminate gangrenous enterocholitis with serious
blood loss, sepsis, and hemolytic uremic syndrome. Complications may
include toxic
megacolon, strictures, and even neuropathy and Reiter’s syndrome. In
more
severe cases, the stool is described as
currant jelly in appearance, contains pus, and may number 20 to 60 per day.
Diagnosis is clinical, though culture may be helpful.
Management is primarily supportive, especially in regard to fluid and electrolytes. Blood transfusion and dialysis may be required in some cases. Drug resistance is common, and quinolones or macrolides may be used in more severe cases. There is some evidence, however, that use of antibiotics in children may increase risk of development of HUS (hepatic uremic syndrome).
Enterohemorrhagic E coli O157:H7 is similar in presentation, course, and treatment.
Protozoan
Amoebic dysentery, caused by Entamoeba histolytica, is acquired through ingestion of the cysts. Incubation ranges from days to years, and the majority of infections remain asymptomatic. Invasive colitis seems to be triggered by other infection or immunocompromise. Onset of symptoms is insidious and variable in severity. Fever is uncommon. Complications may include peritonitis, hemorrhage, ulcerative colitis, extra-intestinal abscess formation, or an amoeboma (a mass of granulation tissue arising from a localized colonic infection), which may present as a tender palpable mass, bowel obstruction, or intussusception.
Diagnosis is identification of the organism in the stools. Serology, antigenic and DNA testing, and endoscopy may be helpful.
A 5-day course of metronidazole 500 mg twice daily is often adequate to treat dysentery. Extralumenal abscesses require more aggressive treatment.
Helmintic
The geohelminth, Trichuris,
may present with
a dysentery-like clinical picture, occasionally associated with rectal
prolapse. It is acquired via the fecal-oral route. Diagnosis is
by identification of the ova or
the worms in the stool, and treatment
with a single dose of mebendazole 500 mg PO (100 mg PO twice daily for
3 days
in severe cases).
Bowel Trouble—Parasites
Parasitic infestation may manifest itself as diarrhea, constipation, abdominal mass, or a combination of the above; thus they will be presented by organism rather than symptom.
Ascariasis
The life cycle of
Ascaris explains its clinical presentations, and is worth
reviewing. In addition, it serves as a representative of the
other geohelminths.
The nematode parasite is acquired via the fecal-oral route. Its ova can persist in the environment for extended periods of time. Once within the human host, the larvae emerge and migrate to the lungs where they undergo maturation steps. They are then coughed up in phlegm; if this is swallowed, they complete their maturation back in the digestive tract. (See figure.) Adult worms are pencil-sized, and their eggs pass in the stool to the next host.
Clinical manifestations may include significant pulmonary symptoms and asthma as the result of these highly allergenic larvae passing through the lungs. The adult worms may form large tangled boluses in the bowel, obstructing it; they may also obstruct the biliary tree and present as colicky pain, or even migrate out of the digestive system and trigger sepsis by the bowel flora.
Diagnosis is via identification of the ova in stool samples; occasionally, larvae may be seen in sputum samples as well. Adult worms may be passed per rectum and can be as long as 6 to 8 inches.
Ivermectin, mebendazole, and thiabendazole are used in treatment (see Vol III—TM13 Antiparasitic Primer).
Hookworms
Hookworms have a lifecycle similar to that of
Ascaris, with the notable exception
that, rather than being
acquired through the ingestion of ova, its ova “hatch” in
the soil, and the larvae penetrate
the new host’s bare foot from which they
migrate to the lungs and ultimately the bowel. There, instead of absorbing
nutrients in competition with the host, it latches on and sucks
its blood.
Pulmonary and gastrointestinal manifestations of this infestation are less common than ascariasis. Rather, severe microcytic hypochromic anemia is the symptom most often recognized.
Diagnosis is identification of the ova in the stool, and treatment is similar to that
for ascariasis.
Strongyloidiasis
This geohelminth is acquired through the skin like hookworms, only it doesn’t
cause anemia, instead
competing with its host for nutrients like
Ascaris.
Again, pulmonary or gastrointestinal symptoms are unusual. However, these worms are prone to venture beyond the lumen of the bowel and trigger a polymicrobial sepsis (that prompts the astute clinician to order a stool specimen for ova and parasites). Diagnosis is visualization of the worms on microscopy. It is the only human helminth normally passed as live worms, not ova, in the stool (if the stool specimen is not fresh, hookworm ova may hatch, and their larvae will mislead the microscopist into misdiagnosing the worm).
Treatment agents mirror those used for Ascaris.
Pinworm
These worms are acquired by the ingestion of
ova from the environment. They
hatch and the larvae mature in the bowel. Adult worms then migrate out the
anus, adhering their ova to
the perianal skin before returning from
whence they came. As the adhesive
dries, the eggs slough
off and may be carried throughout
the house on air currents.
The main clinical symptom is severe pruritis ani, resulting from the allergenic worm slime used to adhere the eggs in place. Diagnosis is by tape test, whereby Scotch tape is stuck to the perianal region and then gently removed, placed on a microscope slide, and examined. Treatment is mebendazole or ivermectin.
Tapeworm
Tapeworms have a lifecycle that includes
both tissue- and lumen-dwelling
stages. The host acquires the tapeworm by ingesting meat containing the
tapeworm cysts (cysticerci). From this, the adult worm develops within the
bowels, producing many packets of eggs (proglottids), which are passed in the
stool while the head (scolex) remains embedded within the host. The second host
acquires cysticerci by ingesting eggs. This cycle typically involves passing the
parasite between a herbivore and its predator. (See figure.)
Taenia are parasites of domestic cattle and pigs. Humans may acquire the tapeworms by eating undercooked meat. Clinical symptoms are nonspecific, and infection is usually recognized after passing proglottids in the stool. Treatment of the tapeworm stage is the use of praziquantel (Vol III—TM13 Antiparasitic Primer). If humans ingest the ova, cysticercosis develops (Vol III—TM6 Muscular Manifestations), which is most serious if the cysticerci develop within the central nervous system (Vol III—TM7 Neurological Manifestations).
Ecchinococcus normally infects dogs and sheep (or other canine-predator-prey relationships such as wolves, deer, coyotes, and dingos). These organisms form hydatid cysts instead of cysticerci when humans are infected. These large cysts, in contrast to cysticerci, cause trouble wherever they form. Though they may affect the central nervous system, they are most commonly seen intra-abdominally. They generally present as rapidly growing masses. Ultrasonography and other imaging modalities are useful in the diagnosis. Treatment is challenging, for surgical excision is complicated by the fact that the contents of the cyst are highly allergenic and can trigger anaphylactic reactions if spilled intraoperatively. In addition, the hydatid sand includes brood capsules, which may form multiple new cysts if they are spilled. Albendazole has been shown to be reasonably effective medical therapy.
Diphyllobothrium is acquired by ingesting cysticerci in fish and may grow to extraordinary lengths. It is significant in that its tremendous surface area competes for vitamin B12 and its clinical presentation may well be pernicious anemia. Diagnosis is identification of ova in stool. Praziquantel is the agent of choice.
Other tapeworms may affect humans, including Dipylidium, and Hymenolepis, but are usually asymptomatic and self-limiting.
Biliary Trouble—Jaundice, Hepatomegaly, or Colic
Viral Hepatitis
Acute
viral hepatitis A, B, D, and E are virtually indistinguishable
clinically
(acute hepatitis C is usually so mild that care isn’t sought).
Jaundice, nausea, vomiting, and malaise are common, and ascites and
coagulopathies
may occur. The food-
and water-borne hepatitis A and E
have no long-term consequences, but the body-fluid-borne hepatitis B,
C, and D do.
Diagnosis of viral hepatitis is clinical; distinguishing the particular type relies on serological studies. No drugs have demonstrated efficacy in treatment of acute viral hepatitis, and treatment is supportive. Pharmacological intervention in chronic viral hepatitis may be beneficial, but is beyond the scope of this chapter.
Kala-Azar
Visceral leishmaniasis
is a protozoan parasitic infection transmitted by the sand
fly bite. The promastigote form injected by the bite is phagocytized by
macrophages in which they convert to amastigotes and multiply by binary
fission.
This infection is also called dumdum
fever. (See Vol III—TM5 Dermatological Manifestations).
Clinically, the onset is insidious with low-grade fever, hepatosplenomegaly, and anorexia. Low-grade abdominal pain may develop as the result of splenic infarcts. Fatality is up to 50% in treated patients and 90% in those untreated.3
Serological tests are useful in diagnosis, as is demonstration of the intramacrophagal amastigotes in splenic aspirates, bone marrow, buffy coat, or lymph nodes.
Treatment consists of toxic drugs, see Vol III—TM13 Antiparasitic Primer Noteworthy is the occurrence of post-kala-azar dermatitis in 10% of patients following treatment.3 Initially a maculopapular rash, this may progress to the appearance of lepromatous leprosy and may last many years. Longer courses of pentavalent antimonials may be necessary to clear this up.
Liver and Bile Flukes
Fasciola, Opisthorchis, and
Clonorchis are acquired by consuming the infective
metacercarial cysts on raw vegetable (watercress), upon
which they were
deposited by snails. These trematodes mature and migrate to
the liver and bile
ducts. Acute symptoms include fever, fatigue, abdominal pain, anorexia, and
respiratory symptoms. Chronically, recurrent biliary colic may be present, as can
hepatomegaly, and in heavy infections, bleeding into the biliary system may
result.
Diagnosis is the identification of ova in the stool; serological tests are also available, and a fecal antigen test looks promising.
Praziquantel readily treats these infections.
Visceral Larval Migrans
Toxocara, an infection of dogs and cats, may infect humans, though they do not mature beyond the larval stage in the wrong host. Acquired via the fecal-oral route (imagine children playing in the sandbox), the larva migrate, searching unsuccessfully for their proper habitat. As they migrate, they cause local damage and elicit significant host responses. Pneumonitis, myalgia, hepatosplenomegaly, and neuropsychiatric disturbances may occur, depending on the tissue through which the larvae are passing.
Diagnosis is via serology (or clinical, especially in the case of cutaneous larval migrans); a variety of anthelmintics are effective. (See Vol III—TM13 Antiparasitic Primer).
Schistosomiasis, also known as bilharziasis, causes substantial morbidity throughout the world. The larval form, cercariae, is shed by freshwater snails (who in turn were infected by metacercariae-hatched eggs passed in human feces). These penetrate the skin of their swimming or wading host and migrate to the liver by way of the lungs, and ultimately the mesenteric veins (or bladder plexus in the case of Schistosoma haematobium [S haematobium], which will be discussed in Vol III—TM10 Urogenital Manifestations. There, they lay eggs in terminal venules, which slowly erode their way to the lumen of the bowels and are passed in the feces.
Acute illness may include swimmer’s itch from the invasion of the cercariae, and Katayama fever (fever, urticaria, eosinophilia, diarrhea, hepatosplenomegaly, bronchospasms, and cachexia). Chronically, the constant irritation may lead to pseudopolyposis of the colon. Of greatest significance is Symmers’ pipestem fibrosis, which is the result of the countless eggs which get swept away by circulation into the liver rather eroding to the bowels. The granulomatous reaction to this leads to portal hypertension with sparing of hepatocellular function (until the very end) and presents with hepatosplenomegaly, esophageal varices, and caput medusae. Occasionally, the worms may wander and conditions such as neuroschistosomiasis may develop.
Diagnosis is identification of the ova in sedimented stool (not just a smear), or in rectal biopsy. It is important to wait an adequate period (3 months) for egg-laying to begin. Serological testing is not reliable.
The treatment of choice is praziquantel; once the egg-laying ceases, the granulomas tend to regress.
Yellow Fever
Covered in TM3 (Vol III—TM3 Fever and Systemic Manifestions), yellow fever got its name for
the jaundice it produces.
Ascariasis
Covered earlier in this chapter, these large worms may cause biliary obstruction.
Cancer
Neoplasms may also cause symptoms referable to the hepatobiliary system. Of
significance, cancer of the gall bladder is associated with the carrier
state in
typhoid, and risk for cholangiocarcinoma is increased in the setting of infection
by bile flukes.
Other Causes
A variety of other infectious diseases may cause jaundice, including
leptospirosis, Q fever, and malaria, all of which were discussed in the previous
chapter.
Another potential cause of jaundice is mildly (or not mildly) hepatotoxic or cholestatic traditional herbal medicines or teas used abroad. Although this cause is relatively common among the locals, it is less common among expatriates and is discovered by taking a complete history. Not only traditional medicines, but also the Western medicines prescribed for travelers may cause liver enzyme anomalies (eg, mefloquine, acetaminophen).
References
- Steffen R, Lobel HO. Epidemiological basis for the practice of travel medicine. J Wilderness Med. 1994;4:56-66.
- Castelli F, Saleri N, Tomasoni LR, Carosi G. Prevention and treatment of travelers’ diarrhea. Digestion. 2006;73:109-118.
- Gill GV, Beeching NJ. Lecture notes in tropical
medicine, 5th ed. Malden, MA: Blackwell Science, 2004.