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Chapter: Medical Microbiology: An Introduction to Infectious Diseases: Enterobacteriaceae

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Enteric ( Typhoid ) Fever ( Salmonella sero type Typhi )

Typhoid is the fever of the phrase “she died of a fever,” as in Victorian novels or the street ditty of sweet Molly Malone.

ENTERIC ( TYPHOID ) FEVER

Salmonella sero type Typhi )

Typhoid is the fever of the phrase “she died of a fever,” as in Victorian novels or the street ditty of sweet Molly Malone. Typhoid fever has a slow, insidious onset and if untreated, lasts for weeks. It ends either by a gradual resolution or in death due to complications (eg, rupture of the intestine or spleen). Family members may note only the extended fever, although physicians may observe a subtle rash or feel an enlarged spleen. Diarrhea may occur once or twice during the course but is not a consistent feature.

EPIDEMIOLOGY

Typhoid is a strictly human disease. Chronic carriers of serotype Typhi are the primary reservoir. Some patients become chronic carriers for years (hence the famous “typhoid Mary” Mallon), typically because of chronic infection of the gallbladder and the biliary tract when stones are present. All cases should be traced back to their human source. If a patient with typhoid has not traveled to an endemic area, the source must be a visitor or someone else who prepared food. The pathogen can be transmitted in the water supply in developing endemic areas or where defects in any system allow sewage from carriers to contaminate drinking water. Transmission is by the fecal – oral route. The infecting dose of 105 to 106 bacteria is intermediate between Shigella and most S. enterica and decreases in the presence of the capsular Vi antigen.

Typhoid fever is still an important cause of morbidity and mortality worldwide. In the United States and most other industrialized nations, it is mostly seen in travelers to en-demic areas such as Latin America, Asia, and India. Visitors from these areas who are carriers are often the source of isolated cases. The decline in disease in industrialized na-tions largely reflects the availability of clean water supplies and improved disposal of fe-cal waste.

PATHOGENESIS

As there is no animal model for the strictly human Typhi, the details of the cellular events are inferred from studies of Typhimurium, which in mice produces a disease similar to ty-phoid (thus the name). The invasion and killing of intestinal M cells and macrophages are presumed to follow the same pattern as S. enterica. Two differences are the surface poly-saccharide Vi antigen and the extended multiplication of Typhi in macrophages. In the submucosa, the Vi antigen retards polymorphonuclear neutrophil (PMN) phagocytosis by interfering with complement deposition in a manner similar to other bacterial surface polysaccharides. This may favor uptake by macrophages where at least some Typhi cells establish a privileged niche. Like other serotypes of Salmonella, the typhoid bacteria re-main within a membrane-bound vacuole and replicate, leading in many cases to macrophage death.

The primary difference between Typhi and the other serotypes is its prolonged intra-cellular survival in macrophages. This is due to the organism’s ability to inhibit the oxida-tive metabolic burst and continue to multiply. As the bacteria proliferate in macrophages, they are carried through the lymphatic circulation to the mesenteric nodes, spleen, liver and bone marrow, all elements of the reticuloendothelial system (RES). At the RES sites, Typhi continues to multiply, infecting new host macrophages, but eventually the bacteria begin to spill into the bloodstream. This seeding of Gram-negative bacteria and their LPS endotoxin starts the fever, which increases and persists with the continuing bacteremia, sometimes resulting in infection of the urinary tract and other organs. Spread to the bil-iary tree leads to reinfection of the bowel. This cycle beginning and ending in the small intestine takes approximately 2 weeks to complete.

IMMUNITY

The immune response to enteric fever is both humoral and cell mediated. In nonfatal cases, humoral antibody and activated macrophages eventually subdue the untreated in-fection over a period of about 3 weeks. Reinfection is rare unless the course was short-ened by early administration of antimicrobics. Which antigens stimulate this immunity is not clearly understood. The Vi antigen is usually credited, but various surface proteins are also candidates.

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