Typhoid fever pathophysiology: Difference between revisions
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== Pathophysiology == | == Pathophysiology == | ||
<br><br> | |||
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{{Family tree | | | | A01 | | | |A01= '''Innoculation''' | |||
:*Orofecal transmission | |||
:*Infective dose 1000 to 1 million | |||
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{{Family tree | | | | B01 | | | |B01= '''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 | |||
:* | |||
}} | |||
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{{Family tree | | | | B01 | | | |B01= '''Systemic spread'''}} | |||
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{{Family tree | | | | B01 | | | |B01= '''Chronic carrier state'''}} | |||
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== Heterozygous advantage == | == Heterozygous advantage == |
Revision as of 20:13, 30 August 2016
Typhoid fever Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Innoculation
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Gastrointestinal Infection
Stomach
Small intestine
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Systemic spread | |||||||||||||||||||
Chronic carrier state | |||||||||||||||||||
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.