Bacterial pathognesis I

===Lecture Details===
Julian Rood; Week 5 MED1022; Microbiology
===Lecture Content===
Most deaths from infectious diseases: pneumonia, diarrhoeal diseases, HIV/AIDS, TB, malaria, measles. Koch's postulates: bacteria must be associated with a disease lesion, bacterium must be isolated in pure culture, isolated bacterium must produce disease in host, same bacterium should be re-isolated. Does not take host factors into account, emphasis on culturing which is not always possible. Organism may lose virulence in a lab, changing when cultured. Disease may not require organism to infect a host such as clostridium botulinim where the toxins are sufficient to cause damage. Koch's postulates also require an animal model to be tested.
Molecular Koch's postulates are that a gene will only be found in strains causing disease, gene should be expressed by bacterium when in animal or human host, mutating gene should reduce virulence, complementation of mutated gene should restore virulence
Pathogenesis is the process where an organism causes disease, virulence is ability of organism to cause disease. Virulence factor is required to cause disease.
Transmission is generally from exogenous source. Bacterium must enter the body, overcome human defences, grow and spread. Once in the body they cause cell and tissue damage, then may spread to other members of the population. Few present with typical disease picture. Most have less severe presentation of disease, and can be asymptomatic.
Normal flora can cause disease if there is a change in ecological niche, they gain entry to a body cavity or if the host is immunosuppressed. Resp tract, GIT tract and urogenital tract are part of the external environment. Bacteria must enter through a break in the skin or altering the mucus membranes.
Bacteria have virulence factors to cause disease. Secretin systems act on host response. Iron-binding proteins act on metabolism. Polysaccharide capsules are anti-phagocytosis. LPS act on host response.
Pili, fimbriae, non-fimbrial adhesins and capsules allow adherence to body surfaces and cells to prevent being passed through the system. Pili and fimbriae are rod, hollow structures that are helical arrays of pilin protein subunits. The tip mediates adhesion, may be pilin or another protein determining host specificity. They can be all over the cell (petricious) or polar. Non fimbrial adhesins form close associations with host cells as some form of surface protein or carbohydrate that can attach to host cell membranes. Polysaccharide capsules are sticky and allow to attach to surfaces such as teeth.
E coli produces toxins and pili; causes traveller's diarrhoea. Bordetella percussis has non-fimbrial adhesins (filamentous haemagglutinin). Bartonella spp. (endocarditis or cat scratch disease) has non-fimbrial adhesins, binds to epithelial cell and extracellular matrix.
Tetanus: clostridium tetani; plague: Yersinia pestis; cholera: vibrio cholerae; gas gangene: clostridium perfringens; TB: mycobacterium TB; dysentery: shigella spp. typhoid fever: salmonella typhi; endocarditis: Bartonella spp; endocarditis: Coxiella burnetti; Lyme's disease: Borrelia burgdorferi; gastro- campylobacter jejuni; Legionnaire's disease- legionella spp.; pseudomembranous colitis: clostridium difficile
===Readings===