Travelers' diarrhea: an overview.

The diarrhea of travelers is a syndrome and not a disease; its history is reviewed here. Dysentery is caused by agents that damage the epithelium of the intestinal tract; diarrhea results from the response of intact intestinal cells to toxins that stimulate enzymatic processes to release liquid and ions. Toxigenic Escherichia coli, the most frequent pathogen in diarrhea, produces a recognizable, benign syndrome; however, other agents of disease, including viruses, bacteria, and protozoa, are responsible for a significant proportion of cases of diarrhea. Hygienic precautions are generally advised, despite the lack of evidence supporting their efficacy. Antibiotic prophylaxis is effective in reducing the incidence of diarrhea caused by E. coli but may not be desirable because of toxicity and the possibility of complicating the diagnostic process. Diagnosis requires better laboratory methods than are usually available but can be made with limited accuracy by a clinician acquainted with the various manifestations of potential causes. Treatment after diarrhea has started should be limited to fluid and ion replacement, with the possible addition of drugs that reduce intestinal motility, although some advocate the use of antibiotics at this time. The number of people traveling, especially to developing countries, continues to increase. This trend would expand enormously if the fear of diarrhea were removed.

Epidemic of amoebiasis and giardiasis in a biased population.

Of 126 homosexual men in a selected population in New York City, 31.7% were infected with Entamoeba histolytica, 18.3% with Giardia lamblia, and 39.7% with one or both on a single stool examination. Of 5885 clinic and hospital patients examined in the same laboratory by the same methods, 1.3% were infected with E. histolytica, 2.1% with G. lamblia, and 3.3% with one or both. Evidence indicates that an epidemic of intestinal protozoan infection exists in the homosexual male population in New York City. The difficulty in making a diagnosis, inadequate therapy, failure to alert potential victims, and official neglect of the epidemic have combined to create a dangerous situation.

The complement-fixation test in the diagnosis of congenital toxoplasmosis.

We present serologic results on 26 patients with congenital toxoplasmosis and on 22 of their mothers. The infection was severe (central nervous system involvement) in 12 patients, 12 had only ocular manifestations, and two were asymptomatic. The dye test results were positive on all specimens, and were positive at a titer of 1:1,024 or higher if collected from patients younger than 2 years of age. The complement-fixation test (CFT) results were positive on all specimens from patients younger than 2 years of age and on 69% of specimens collected from older patients. These serologic results are contrasted with those obtained on two control groups: (1) 46 uninfected infants followed up after birth because of substantial antibody titers in their mothers during pregnancy; and (2) 190 infants and children tested because toxoplasmosis was tentatively included in the differential diagnosis of the current illness. In both control groups the positive results on the CFT were limited almost exclusively to cord blood specimens or specimens collected during the first 2 weeks of life. Lower CFT titers in follow-up specimens suggested that the antibodies were maternal in origin. These two tests are valuable in providing laboratory support for the diagnosis of congenital toxoplasmosis, particularly the test for the comparatively short-lived complement-fixing antibody.

Malaria - the mime. Recent lessons from a group of civilian travellers.

Clinical data on 24 civilian patients hospitalized for malaria in The New York Hospital were analyzed. Of 16 patients infected with Plasmodium falciparum, 14 acquired the disease in West Africa. Only three of the 24 had taken recommended courses of prophylaxis. Diagnosis was invariably, and often dangerously, delayed because physicians often made diagnoses of viral syndromes or used antibiotics; only one patient had a blood smear taken by a personal physician. Although all patients had fever and chills, classic malarial fever was seen in only seven patients; nausea, vomiting and diarrhea were common. Hepatomegaly and splenomegaly occurred in about half the patients. Blood smears stained in routine fashion by Wright's stain were positive in 23 of 24 patients. A normal leukocyte count was present in 19 of the 24 patients and thrombocytopenia in 16 of 23. The most frequent complications were those of central nervous system involvement. Therapy consisted mainly of chloroquine phosphate but other drugs, including quinine, pyrimethamine, sulfonamides and primaquine, were used in special situations. Suggestions for prophylaxis, diagnosis and therapy were made.

Travelers' diarrhea and toxigenic Escherichia coli.

In a group of 133 United States students studied for 18 days after arriving in Mexico, diarrhea developed in 38 (29 per cent). Diarrhea rarely began before the fourth day, and the mean onset was 13 days after arrival. Symptoms lasted an average of 3.4 days but persisted in 21 per cent of sick students. Heat-labile enterotoxin-producing Escheria coli was found in the stools of 72 per cent of sick and 15 per cent of healthy students. None had heat-labile Esch. coli when they entered Mexico. The incubation period was short, generally 24 to 48 hours, and the carrier state was five days or less in 82 per cent of students surveyed. Entamoeba histolytica was found in 6 per cent of cases of diarrhea, but not salmonella, shigella or penetrating Esch. coli. These studies suggest that approximately 70 per cent of travelers' diarrhea in Mexico is associated with heat-labile toxigenic strains of Esch. coli.