TRAVELER'S DIARRHOEA

Travelers' diarrhea (TD) is the most common illness affecting travelers. When travelers from the developed western countries visit developing nations where the sanitary measures are poor, they develop diarrhoeal disease. The onset of TD usually occurs within the first week of travel but may occur at any time while traveling, and even after returning home.

Risk factors:  
Developing countries such as Latin America, Africa, the Middle East, and Asia are the high-risk destinations. Persons at particular high-risk include young adults, immunosuppressed persons, persons with inflammatory-bowel disease or diabetes and persons taking H-2 blockers or antacids.

Etiology:  
The most common causative agent isolated is enterotoxigenic Escherichia coli (ETEC). Besides ETEC and other bacterial pathogens, a variety of viral and parasitic enteric pathogens also are potential causative agents. Other common bacterial causes include Campylobacter jejuni, Shigella, Salmonella, Aeromonas and Yersinia species, Plesiomonas shigelloides and Vibrio parahaemolyticus.

Pathogenesis:  
Infection is acquired by ingestion of food or water contaminated with ETEC. Contamination of water with human sewage may lead to contamination of foods. Infected food handlers may also contaminate foods. The infective dose is 10⁶-10¹⁰ bacilli. With high infective dose, diarrhea can be induced within 24 hours. Infants may require fewer organisms for infection to be established.
The bacteria colonize the GI tract by means of a fimbrial adhesin (CFA I and CFA II). These fimbrial adhesins adhere to specific receptors on enterocytes of the proximal small intestine. The symptoms of diarrhoea are due to ETEC strains produce enterotoxins. Enterotoxins produced by ETEC include the LT (heat-labile) toxin and or the ST (heat-stable) toxin, the genes for which may occur on the same or separate plasmids. LTs are similar to cholera toxin in structure and mode of action. Like cholera toxin, LTs are holotoxin consisting of A subunit and B subunit. The B subunit of LTs binds to specific ganglioside receptors (GM1) on the epithelial cells of small intestine and facilitates the entry of A subunit where it activates adenylate cyclase. Stimulation of adenylate cyclase causes an increased production of cAMP, which leads to hypersecretion of water and electrolytes into the lumen and inhibition of sodium reasborption. LT are divided into two antigenic types LT-I and LT-II. While LT-I is plasmid encoded, LT-II is chromosomally encoded. STs are of two types, ST-I and ST-II. Following colonization, the cells produce ST-I, which binds to glycoprotein receptor and stimulates guanylate cyclase. This results in increased production of cGMP that is followed by hypersecretion of water and electrolytes. The mechanism of ST-II is independent of cGMP activation and has not been found on strains affecting humans.
In several strains, the plasmids carry genes for both enterotoxin and colonization factor production. The enterotoxin production is limited to following O serotypes: O6, O8, O15, O25, O63, O78, O148 and O159.

Signs and symptoms:  
Symptoms ETEC infections include diarrhea without fever. Typically, a traveler experiences four to five loose or watery bowel movements each day. Other commonly associated symptoms are nausea, vomiting, abdominal cramping and bloating. Most cases are benign and resolve within few days without treatment.

Laboratory diagnosis:  
Since TD is self-limiting laboratory diagnosis is not mandatory. Whenever required, the sample of feces is cultured on McConkey's agar. The ETEC stains are indistinguishable from the resident E.coli by biochemical tests. These strains are differentiated from nontoxigenic E.coli present in the bowel by a variety of in vitro immunochemical, tissue culture, or DNA hybridization tests designed to detect either the toxins or genes that encode for these toxins. With the availability of a gene probe method, foods can be analyzed directly for the presence of enterotoxigenic E.coli, and the analysis can be completed in about 3 days.
Detection of LTs: Ligated rabbit ileal loop test, morphological changes in Chinese hamster overy cells and Y1 adrenal cells, ELISA, immunodiffusion, coaglutination etc.
Detection of STs: Infant mouse assay, ELISA

Prevention:  
Risk of RD can be minimized by avoiding eating of foods or drinking beverages purchased from street vendors or other establishments where unhygienic conditions are present, avoiding eating raw or undercooked meat and seafood and avoiding tap water, ice, unpasteurized milk, and dairy products. Use of antibiotics for chemoprophylaxis is not justified.