University:
University of Wolverhampton
Course:
4PY019 | Pharmacy
Academic year:

2023
Views:

113

Pages:

2
Author:

Carisma

GRAM NEGATIVE ORGANISMS: Cell wall provides structure as cell has no cytoskeleton -multilayered cell envelope with layers,thin peptidoglycan layer in periplasm between cytoplasmic and outer membrane. Outer membrane-lipopolysaccharide membrane LPS: Poring contained within allowing diffusion of molecules within and out of, other surface proteins such as Braun’s lipoprotein linking layers together outer membrane and peptidoglycan LPS molecules found on the outer part of outer membrane Made up of 3 regions: lipid A. Fatty acids connected to disaccharide, Core polysaccharide: various sugars consisting I.e. ketodeoxyoctonate KDO, O-polysaccharide. Repeating side chain sugars LPS endotoxins: Endotoxins: not secreted but released upon destruction of cell to cause damage within the host, heat stable associated with outer membrane LPS or lipid A toxin part I.e. salmonella, ecoli for food poisoning symptoms such as diarrhoea and vomiting These cannot be destroyed by sterilisation, they remain toxic to cells Small quantities may cause mild fever and immune response stimulation Large quantities of the toxic may cause low blood pressure, increased heart rate, organ failure, tissue necrosis, death, systematic inflammatory responses I.e. due to cytokine production Pathogenesis: Of most infections is multi factorial from a wide range of virulence factors by the bacterium 3 stages- exposure.& adherence to host cells, invasion colonisation & infection, host damage & disease Particular bacteria determinants of virulence mediate each of these stages Endobacteriaceae/ enteric: I.e. salmonella, escherichia coli, yersinia pestis, kleibsiells sp, shigella sp Rod-shaped facultatively anaerobes with movement via flagella. No spores produced Fermentation of sugars to produce lactic acid, oxidase negative catalase positive Normal p;art of gut flora & one of the most common pathogens to infect humans Virulence factors: 3 distinct stages: exposure & adherence to host, invasion colonisation & infection, host damage & disease .LPS endotoxin, antigens O H K, capsules, fimbriae, exotoxins, siderophores, haemolysins, type 111 secretion system producing needle like projections to be injected into host cells Escherichia coli: I.e. intestinal tracks of animals humans, soil & plants May cause UTI, food poisoning gastroenteritis, meningitis, septacaemia Pathogenicity multi factorial & strain dependant on adhesions, endotoxins & enterotoxins may cause nausea & diarrhoea due to loss of iron in cells ( specific endotoxin type) . O157:H7 Most prevalent strain in developed countries most commonly in ingestion of contaminated food as few as 10 cells needed for the disease to occur May cause severe abdominal plain, bloody diarrhoea, severe fatal haemorrhagic colitis, haemolytic uraemia syndrome HUS causing renal function Virulence mechanisms: adherence to intestinal epithelial cells using flagella producing shiga-like toxins. Injecting proteins to distrust cell metabolism & act as receptors for further adhesion.