A 26-year-old woman has persistent diarrhea and dehydration. She recently returned from a two-week vacation in Thailand. Before her trip, she had been immunized with tetanus and diphtheria toxoids, oral poliovirus vaccine, immune globulin, and typhoid vaccine; she also took mefloquine HC1 to prevent malaria.
Not All Trips To Thailand End Well
Trip To Thailand and Chiang Mai
The patient attempted to follow strict food and water precautions to prevent traveler’s diarrhea. Several days after returning to the United States, however, she experienced watery, nonbloody diarrhea (6-8 times per day) associated with nausea and vomiting. Over the next few days, her condition worsened, and she had abdominal cramps, anorexia, and lightheadness on standing. She felt feverish and was unable to ingest fluids without vomiting.
Her medical history and a review of systems were unremarkable. Vomiting precluded her taking mefloquine after returning home. She denied having any allergies, a history of drug abuse, or significant alcohol intake.
At examination, she was not in acute distress. Her temperature was 100.8 [degrees]F (38.2 [degrees]C), respiratory rate was 16 breaths per minute, pulse rate was 104 beats per minute, and blood pressure was 105/60 mmHg while lying down. On sitting, the patient’s heart rate increased to 130 beats per minute, and her blood pressure dropped to 85/55 mmHg. Her sclerae were nonicteric. Her mouth was dry. Lung and cardiac examination findings were normal except for a sinus tachycardia. There was no abdominal tenderness or organomegaly, and her stool was negative for occult blood. The remainder of the examination was normal.
Laboratory values were a white blood cell count of 8,600/[unkeyable]L with a normal differential. Thick and thin malarial smears were negative. Blood urea nitrogen and creatinine levels were 28 mg/dL and 1.0 mg/dL, respectively. The electrolyte concentrations and liver function tests were within normal limits.
* What would you do now?
* What is the differential diagnosis?
* What will confirm the diagnosis?
* What is the treatment of choice?
The patient was admitted to the hospital for treatment of dehydration and evaluation of her diarrhea. Stool samples were obtained for a fecal leukocyte count, culturing, and examination for parasites. A diagnosis of traveler’s diarrhea was made pending identification of an etiologic agent.
* Traveler’s diarrhea By far the most common health problem encountered by Americans venturing to developing countries is traveler’s diarrhea (also known as Delhi belly, Montezuma’s revenge, and la turista, among others). It often develops 5-15 days after arrival in an underdeveloped country, but it may occur at any time during or even after the trip.
The incidence of traveler’s diarrhea is 4-51%, depending on the countries visited and the duration of the trip; in general, the rate approaches 50% for a stay of two weeks or longer. In persons older than 25 years, the attack rate decreases, perhaps reflecting the more adventurous itineraries and eating habits of younger people. The most important determinant for acquiring traveler’s diarrhea is destination: High-risk areas include Africa, Asia, the Middle East, and South and Central America. Less risky areas are southern Europe and a few of the Caribbean islands.
The typical symptoms of traveler’s diarrhea are malaise, anorexia, nausea, abdominal cramps, and watery diarrhea. About one third of patients have low-grade fever. Vomiting occurs in approximately 15% of patients and patients and bloody stools or high fevers in 2-10%. Diarrhea usually lasts 1-5 days but may extend over 10 days.
Traveler’s diarrhea is acquired through ingestion of fecally contaminated food or water. Salads, uncooked vegetables, and raw meat and seafood are particularly risky. Tap water, ice, and unpasteurized milk or other dairy products may also be associated with increased risk.
The etiology of traveler’s diarrhea usually involves an infectious agent (see Table 1). The most common pathogen, found in about 50% of cases, is enterotoxigenic Escherichia coli. Salmonella may cause gastroenteritis or dysentery, characterized by the passing of small stools containing bloody mucus. Likewise, shigellae may cause dysentery and, in a small number of individuals, watery diarrhea. Campylobacter jejuni is another cause of traveler’s diarrhea, as is Vibrio cholerae, the etiologic agent in cholera. Cholera was rarely a serious problem for travelers from the United States in the past. With the recent epidemic in South America, however, you should consider it in any patient with watery diarrhea, especially if they are returning from Latin America.
Viruses, most frequently rotaviruses and the Norwalk virus, and enteric parasites, such as Giardia lamblia and Entamoeba histolytica, are also occasional causes of diarrhea in returning travelers. Of note is that patients with malaria may also have gastrointestinal symptoms that suggest traveler’s diarrhea.
of traveler’s diarrhea
Bacterial enteric pathogens
Vibrio cholerae (non-O1)
Viral enteric pathogens
Parasitic enteric pathogens
Traveler’s diarrhea can be treated with a variety of medications while patients are still overseas. Antimotility drugs such as diphenoxylate HC1/atropine sulfate (Lomotil) and loperamide HCl (Imodium) offer prompt symptomatic but temporary relief of uncomplicated traveler’s diarrhea. They should not be used when patients have high fever or bloody stools. Antimicrobial treatment with such agents as trimethoprim/sulfamethoxazole (Bactrim, Cotrim, Septra, etc.), doxycycline hyclate (Doryx, Vibramycin, Vibra-Tabs, etc.), or ciprofloxacin HCl (Cipro) may also be helpful. In addition, bismuth subsalicylate (Pepto-Bismol) has been shown to decrease the duration and severity of traveler’s diarrhea. Travelers should seek medical help if their diarrhea does not respond to these standard approaches, is severe, or is associated with high fever or bloody stools.
In this case, a modified acid-fast stain of a stool smear demonstrated numerous oocysts of the parasite Cryptosporidium. No other enteric pathogens were identified. Results of stool cultures and fecal leukocyte examinations were negative. The patient was given intravenous fluids. Over the next several days, her vomiting and diarrhea diminished, and she was able to tolerate oral fluids. She was discharged, and two weeks later a stool examination was negative for cryptosporidial oocysts.
* About cryptosporidiosis Cryptosporidium parvum is a small, coccidian protozoan that causes enteric infection in animals as well as humans. More than 30 species of animals are known to be infected with this parasite, and before 1976 Cryptosporidium was considered exclusively a veterinary pathogen. After that date, it was recognized as a sporadic cause of disease in immunocompromised humans.
In 1982, Cryptosporidium was found to be a significant cause of diarrhea in patients with AIDS. The Centers for Disease Control estimate that 34% of AIDS patients have cryptosporidial enteritis, and some centers report rates as high as 10-20%. The infection in these patients is characterized by protracted, voluminous diarrhea with nausea, vomiting, and abdominal pain. Profound weight loss and malnutrition may lead to death.
Diarrhea due to infection with this pathogen is also seen in immunocompetent patients. Examples include children in day-care centers, members of communities with contaminated public water supplies, animal handlers, health care workers, and residents of developing countries.
As in our patient, diarrhea secondary to infection with Cryptosporidium may develop in travelers to underdeveloped countries. Infection may be acquired in most underdeveloped countries worldwide, but the precise epidemiology remains undefined and the frequency of diarrhea induced by Cryptosporidium in travelers is unknown.
Contaminated food and water has been implicated as an infection source–no contact with animals is necessary. The onset of illness is within several weeks of a trip abroad, at which time watery diarrhea, anorexia, crampy abdominal pain, malaise, and, occasionally, fever develop. In an immunocompetent individual, the illness is self-limited, with symptoms typically present for 10-14 days (although they may last longer). Fecal clearance of the oocysts lags behind resolution of the clinical illness by 1-3 weeks.
* Diagnosis and treatment Establishing the diagnosis of Cryptosporidium infection is by identification of oocysts in the stool (see Figure 1). Staining techniques include various acid-fast techniques (cold Kinyoun modified, hot Kinyoun, and Ziehl-Neelsen methods), the fluorescent auramine-rhodamine stain, and periodic acid-Schiff’s and carbofuchsin stains. Stool concentration techniques often improve the diagnostic yield in immunocompetent patients.
At present, no therapy is available for the treatment of cryptosporidiosis. This patient did not have any risk factors for infection with the human immunodeficiency virus (HIV), and an HIV-1 antibody titer was negative. For travelers with an intact immune system, the disease is self-limited, and only supportive therapy, such as electrolyte and fluid replacement and lactose avoidance, is necessary. The role of nonspecific antidiarrheal medications is unclear.