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MVST 1B (Subject) / BOD - Microbiology (Lesson)

BOD - Microbiology

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  • Streptococcus pyogenes Causative agent of pharyngitis, other acute suppurative infections, necrotising fascitis, Toxic Shock Like Syndrome Ag-AB complexes → post-infection glomerulonephritis Spread, survival, damage? M protein binding complement factor H??   Identification Medium colonies, complete beta-haemolysis facultative anaerobe Gram-(+)-ve cocci in pairs or chains Lancefield group A throat infections  
  • Streptococcus pneumoniae Causative agent of pneumonia, (meningitis) colonises nasopharynx, adhesins, streptolysin, IgA protease migrates to lower respiratory tract, avoids phagocytosis lung damage by pneumolysin and inflammation Identification Medium colonies, greenish incomplete haemolysis facultative anaerobe Gram-(+) cocci in pairs or chains Capsule stain
  • Legionella pneumophila Causative agent of Legionnaire's disease Facultative intracellular parasite of microbae Survives in air conditioning water
  • Bordatella pertussis Causative agent of Whooping Cough; Diphtheria-Pertussis-Tetanus vaccine Aerosol inhalation, adhesins, multiply in mucosa LPS Lipid A (→ inflammation), exotoxins (pertussis toxin, AC toxin) → destruction of ciliated epithelial / mucosal cells Fever, bronchitis, paroxysms of coughing
  • Yersinia pestis Causative agent of pneumonic plague Highly virulent
  • Meningitis Inflammation of meninges caused by LPS Lipid A Neisseria meningitidis haemophilus influenzae type B Strep. pneumoniae E. coli Adhesins, IgA proteases, polysaccharide capsules
  • Pseudomonas aeruginosa Drug resistant opportunist in CF, burns, wounds, UTI   Identification Large colonies, green pigment on nutrient agar, acrid aerob Gram-(-)-ve bacilli
  • Mycobacterium tuberculosis Causative agent of tuberculosis [TB], live BCG vaccine Intracellular pathogen myolic acid, waxy coat chronic inflammation type IV hypersensitivity caseous necrosis through TH1 immune response Treatment Isoniazid Rifampin ? ?
  • Food intoxications Clostridium botulinum → flaccid paralysis Staphylococcus aureus → super-antigens Clostridium perfringens → toxins (→ Nagler plate) interact with mucose, superAg's? → point source outbreaks
  • Vibrio cholerae Causative agent of cholera AB5 cholera toxin → GM1-ganglioside host receptor → ADP-ribosylation of αs → ion imbalance, copious diarrhoea Identification Gram (-)-ve comma-shaped facultative anaerobe
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  • Shigella Causative agent of dysentery Intracellular in mucosal cells Shiga toxin -→ glycosidase to modify rRNA HUS
  • Salmonella spp Food-borne gastroenteritis: S. enteritidis, S. typhimurium Intracellular pathogen → S. typhi → typhoid fever   Identification Large irregular colonies, pale on MacConkey's Facultative anaerobe Gram-(-)-ve bacilli H & O antigen serotypes
  • E. coli ETEC EPEC EHEC UPEC neonatal meningitis
  • Clostridium difficile Causative agent of anti-biotic associated diarrhoea and pseudomembraneous colitis; problem in hospitals direct damage: exotoxins → glycosylation of GTPases in signalling pathways indirect damage: inflammation, pseudomembrane
  • Helicobacter pylori Associated with gastric/duodenal ulcers flagella, adhesions, urease mucosal inflammation / ulceration: induced IL-8, vacuolating cytotoxin Treatment: (metronidazole), clarithromycin
  • Campylobacter Food-borne gastro-enteritis ~ dysentery (shigella), salmonellosis
  • Outbreaks Point source food poisoning Legionnaire's nosocomial Continous source typhoid (carrier) travellers' diarrhoea hospital staph's food-borne infections Propagated Whooping cough TB gonorrhoea dysentery cholera typhoid
  • Bacterial exotoxins ADP-ribosylating enzymes CTX, ELT → αs PTX → αi DTX → EF2 adenylate cyclases Bordatella pertussis Bacillus anthracis glycosidases Shiga toxin (shigella dysenteriae) → rRNA glucosilases clostridium difficile → small GTPases neurotoxins TeNT BoNT
  • Staphylococcus aureus Pyogenic pathogen, opportunistic infections, e.g. nosocomial MRSA, TSS; commensal skin, pathogenic most areas Identification very opaque cream colonies facultative anaerob Gram-(+)-ve cocci, grape-like clusters Catalase (+), coagulase (+)
  • Typhoid Food-borne infection; Salmonella enterica serovar typhi multiple burst or propagated outbreaks
  • Staphylococcus epidermydis Identification Very opaque white colonies, facultative anaerob Gram-(+) cocci in grape-like clusters Catalase-(+), coagulase-(-) commensal skin
  • Streptococcus viridans Identification Tiny colonies, greenish incomplete haemolysis facultativ anaerobe Gram-(+) cocci in pairs or chains dental caries
  • Enterococcus faecalis Gut commensal Identification White clear edge colonies, non-haemolytic, RED on MacConkey's facultative anaerobe Gram-(+) cocci in pairs or chains
  • Neisseria pharyngis Commensal throat Identification Gram-(-) cocci, mostly diplococci
  • Neisseria gonorrhoeae Pathogenic genital mucosa, gonorrhoea Identification Gram-(-)-ve cocci, mostly diplococci Oxidase reaction stains
  • Clostridium perfringens Wounds "gas gangrene" identification Volcano colonies, haemolytic (alpha toxin) obligate anaerobe Nagler plate for alpha toxin
  • Clostridium sporogenes Wounds "gas gangrene" identification "Medussae" colonies, non-toxic, foul, may spore Obligate anaerobe Gram-(+)-ve bacilli Malachite stain for terminal spores
  • Escherichia coli Commensal gut Identification Large irregular colonies, red on MacConkey's (enteric organisms) facultative anaerobe Gram-(-)-ve bacilli EHEC, ETEC, EPEC, UPEC
  • Bacteroides fragilis Commensal gut, post-OP infecitons Identification very opaque white colonies obligate anaerobe Gram-(-)-ve bacilli
  • Acute vs chronic bacterial infections Acute Whooping cough (B. pertussis) Cholera (V. cholerae)   Chronic TB (m. tuberculosis) Syphillis (T. pallidum) Lepra (M. leprae) H. pylori
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  • Viral transmission Horizontal vs vertical Factors Virion stability duration of shedding (acute → high, persistent → low) virus concentration availability of susceptible hosts
  • Identification of viruses Inclusion bodies etc ??
  • ELEK plate Phage-dependent diphtheria toxin
  • Nagler plate Clostridium perfringens alpha-toxin produces insoluble diglyceride clood from egg lecithin.
  • Epstein-Barr virus Causative agent of glandular fever & Burkitt lymphoma Latency in B cells and epithelial cells
  • Babesia spp Protozoa Tick-borne disease in cattle
  • Fungi Yeast & moulds, eukaryotic Cell wall Ergosterol Polysaccharides (chitin, ...)   Toxins, beta-lactam antibiotics (penicillin)
  • Bacteria Prokaryotes, ~ 4000 genes, 3μm long Transduction, conjugation, transformation
  • Bacteria host defence evasion phase variation avoid phagocytosis survive within macrophages destroy antibody
  • Systemic viral infections Longer incubation, more severe, e.g. ectromelia virus Entry → amplification → exit; 1ary and 2ary viraemia spread via lymph, blood, nerves (e.g. rabies)
  • Haemostasis platelets activation: ECM, collagen adhesion to collagen (vW factor), morphological changes, secretion (TXA2, 5-HT, ADP) → vasconstriction, aggregation → 1ary haemostatic plug contraction, apposition, fusion (JAM, ESAMs, eph/-rin) Coagulation cascade Factor X activated by intrinsic (factors VIII / IX) & extrinsic (factor VII / tissue factor) Xase; factor V → activation of thrombin → fibrin → 2ary haemostatic plug Fibrinolysis: plasminogen activator → plaminogen → plasmin Endothelium (intact) - physical / chemical / enzymatic NO, PGI2 antithrombin tissue factor pathway inhibitor --| extrinsic Xase thrombomodulin → ↑protein C / ↓ fibrin (via thrombin) --| factors V, VIII protein S: cofactor of protein C Endothelium (damaged) underlying tissue exposed von Willbrand factor → platelet activation tissue factor → extrinsic Xase   HMW kinin → XII → XI → IX → intrinsic Xase
  • Artherosclerosis Molecular pathogenesis endothelial dysfunction / injry monocyte migration smooth muscle cell activation lipoprotein infiltration T-lymphocyte migration platelet adherence Spectrum of lesions Outcome
  • Ischaemia Definition Causes Shock Susceptibility of cells / organs results, affecting factors infarction - coagulative necrosis reperfusion injury specific examples
  • p53 pathway Oncogenes → ARF --| Mdm2 DNA damage → AT-PK --| Mdm2; → p53 Mdm2 --| p53 → p21, Bax p21 --| cyclin/CDK → G1/S, G2→ Bax → apoptosis
  • Rb pathway p16INK4 --| cyclinD/CDK4-6 → pRb → E2F → G1-S → proliferation deregulation: mutation, amplification, methylation, deletion integration with p53 via p21
  • Wnt pathway Wnt → Frizzled → dishevelled --| GSK3 GSK3 & APC & ...--| beta-catenin (phosphorylation → degradation) beta-catenin →nucleus → tcf-4 → growth   mutation in APC → constitutively switched on beta-catenin with e-cadherin in adherens junctions or in cytosol
  • Apoptosis Death receptor (Fas, TNFR) + ligand → death complex → enzyme cascade → apoptosis Stress → cyt c → death complex   pro-apoptotic: p53 → Bax, PUMA, NOXA anti-apoptotic: Bcl-2
  • Recessively inherited cancers Somatic heterozygotes express tumour phenotype Rb APC LiFraumeni - p53 HNPCC / Lynch - MLH1/MSH2 Breast/ovary - BRCA-1,2 Basal cell naevus - Ptch Gene functions!
  • Dominantly inherited cancer Somatic monozygotes express cancer phenotype Ataxia telangiectasia Blooms Fanconi's anaemia Xeroderma pigmentosum   gene function!
  • Viral immune evasion Physical barriers: physical resistance Innate immunity interfering with inteferon,e.g. poxviruses stopping activation of PRR-induced signalling → no INFβ produced release of soluble IFN binding proteins inhibition of JAK/STAT to block induction of ISGs block action of ISG proteins (PKR, OAS, Mx) Apoptosis: block caspases, inactivate Bcl-2 Cyto-/chemokines: secret binding proteins; EBV: vIL-10→TH2 NK-cells: MHC-I analogues Adaptive immunity: interfere with Ag presentation

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