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Level 7

Bacterial RT/GIT Infections


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Bacterial pneumonia
symptoms include chest pain, pain on breathing, purulent sputum, cough and breathlessness. Lung consolidation evident on xrays.
Extracellular elementary bodies
of chlamydia are inhaled in droplets, bind to resp. epithelial cell receptors and mediate endocytosis. They prevent lysosome binding and maintain pH to survive intracellularly.
Intracellular reticulate bodies
are metabolically active chlamydial EBs that use host ATP to proliferate (more EBs) that are released upon cell lysis.
2 host and 2 bacterial membranes
need to be penetrated in order for antibiotics to clear intracellular bacteria in chlamydial pneumonia
Toxin-producing strains
of cornyebacterium diphtheriae colonise URT (+ UT, skin) and produce toxins blocking protein synth., destroying epitherlial cells, causing ulcers, "bull neck" and resp. obstruction.
Elongation factor 2
is blocked by fragment A of the diphtheria toxin thus inhibiting protein synth., after binding to epithelial cells with fragment B
IV anti-toxin
is administered along with Abx in order to treat C. diphtheriae infections
Exogenous GIT pathogens
include Salmonella, Shigella, Campylobacter, Vibrios, and Aeromonas and are never part of normal flora.
Normal GIT gram-negative bacilli
are glucose fermenting, catalase +ve (reduce H2O2), oxidase -ve (anaerobic) bacilli with LPS as a major cell wall antigen
Serous or Watery diarrhea
E. coli or V. cholerae infect sml intestine without tissue invasion leading to copious amounts of watery stools with no pus or blood.
Dysentry
Shigellae or E. histolytica invade large intestine leading to scant amount of stools with blood, pus and mucus.
Hemorrhagic colitis
E. coli (EHEC strains) infect large intestine without tissue invasion causing copious amounts bloody stools with no leukocytes.
Bloody watery diarrhea
Salmonella, Campylobacter or Y. enterocolitica invade ileum/colon causing copious amounts of bloody or blood-tinged stools, sometimes with pus.
Lipopolysaccharide
induces release of clotting factors, kinins, as well as IL-1 and TNF from macrophages, activates complement and fibrinolysis, leading to significant host tissue damage and vasogenic shock.
Enterotoxigenic
E.coli causes most diarrhea cases as heat stable and labile toxins activate cGMP and cAMP signals, respectively, to cause hypersecretion of H2O and ions from GIT epithelia.
Enteroinvasive
E. coli causes fever and diarrhea (identical to shigellosis) as bacteria bind and enter intestinal cells, producing no toxins but causing severe damage by mechanical cell destruction
Enteropathogenic
E. coli causes diarrhea (particularly pediatric) by employing many adhesins (bundle forming pili, intimin, afimbrial adhesins) to colonize the small intestine and produce lesions on intestinal enterocytes.
Enterohemorrhagic
E. coli causes initially non-bloody and then bloody diarrhea as bacteria produces shiga-like toxin (verotoxin) that inactivates vascular epithelia ribosomes, degrading the vessels and leading to hemorrhage.
Enteroaggregative
E. coli causes persistent diarrhea in children as fimbrial adhesins (=aggregative adherence fimbria) and a heat stable enterotoxin (EAST1) causes mucosal damage.