Most ingested typhoid bacilli are killed by stomach acid. Factors that reduce stomach acid (antacids) and speed transit time through the stomach (infancy, surgery, water rather than food as a bacterial vehicle) enhance the chances of infection.

Once in the small intestine, the bacilli penetrate the mucosal lining and are ingested by white cells located in gut lymph nodes. Perhaps because of its protective envelope (Vi antigen), S. typhi resists intracellular digestion and proceeds to multiply within the cells that normally destroy bacteria. Bacteria multiply and pass into the bloodstream. Initially, they are cleared from the blood by white cells located in the liver and spleen, but there, too, the bacilli multiply intracellularly, and reenter the bloodstream. It is during this second period of bacteremia that the clinical symptoms of typhoid begin.

Lymph nodes in the small intestine become particularly laden with bacilli, occasionally to such an extent that they and the surrounding tissues die, leading to intestinal hemorrhage or perforation-the major causes of mortality in typhoid. The biliary tract is infected, and the patient may begin shedding S. typhi in the stool. Delirium, inflammation of the heart, and shock may occur and are caused not by direct infection but, rather, by toxins released either by the bacilli or by the white cells. Over a period of weeks, the body's intracellular immune system recognizes the typhoid bacillus, permitting the host to destroy the invader.

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