Typhoid fever pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Innoculation Orofecal transmission Infective dose 1000 to 1 million

Gastrointestinal Infection Stomach Enters stomach High tolerance for acid Survives PH as low as 1.5 Small intestine Adherence to mucosal cells Invade mucosal M cells overlying payers patches Internalisation in M cells Translocation to underlying lymphoid tissue and draining lymph nodes

Systemic spread Dissemination of S.typhi to reticuloendothelial system Spreads via lymph and blood Replication within reticuloendothelial system Evades immune system

Chronic carrier state Resides and multiplies in gall bladder Excretion in urine and stool

Heterozygous advantage

It is thought that cystic fibrosis may have risen to its present levels (1 in 1600 in UK) due to the heterozygous advantage that it confers against typhoid fever. The CFTR protein is present in both the lungs and the intestinal epithelium, and the mutant cystic fibrosis form of the CFTR protein prevents entry of the typhoid bacterium into the body through the intestinal epithelium.