Salmonellosis - Pathogenesis

Pathogenesis

An infectious process can only begin after living salmonellae (not only their toxins) reach the gastrointestinal tract. Some of the microorganisms are killed in the stomach, while the surviving salmonellae enter the small intestine and multiply in tissues (localized form). By the end of the incubation period, the macro-organisms are poisoned by endotoxins that are released from the dead salmonellae. The local response to the endotoxins is enteritis and gastrointestinal disorder. In the generalized form of the disease, salmonellae pass through the lymphatic system of the intestine into the blood of the patients (typhoid form) and are carried to various organs (liver, spleen, kidneys) to form secondary foci (septic form). Endotoxins first act on affected organs' vascular and nervous systems, manifested by increased permeability and decreased tone of the vessels, upset thermal regulation, vomiting and diarrhea. In severe forms of the disease, enough liquid and electrolytes are lost to upset the body's water-salt metabolism, to decrease the circulating blood volume and arterial pressure, and to cause hypovolemic shock. Septic shock may develop. Shock of mixed character (with signs of both hypovolemic and septic shock) is more common in severe salmonellosis. Oliguria and azotemia develop in severe cases as a result of renal (kidney) involvement due to hypoxia and bacteremia.