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29 Cards in this Set
- Front
- Back
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What are streptococci |
Gram positive cocci that grow in pairs or chains facultative or obligate anaerobes Often cause a variety of suppurative infections and immunologically mediated post-streptococcal syndromes |
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Name some of the different types of streptococci and give examples of diseases they cause |
Alpha haemolytic - s. pneumonia - pneumonia, meningitis, endocarditis strep viridans - endocarditis Beta haemolytic group A: Strep pyogenes - pharyngitis, impetigo, erysipelas, scarlet fever - Rh fever group B: Strep agalactiae - neonatal sepsis/meningitis |
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What post infectious syndromes do streptococci cause? |
Glomerulonephritis Rheumatic fever Erythema nodosum |
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What factors in streptococci contribute to their virulence? |
capsule: polysaccharide capsule prevents phagocytosis Surface molecules: M protein inhibits phagocytosis Secretes enzymes: c5a peptidase, degrades c5a, lyses target cells Production of toxins: fever + rash |
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Describe the aetiology and pathogenesis of post-streptococcal glomerulonephritis |
Group A beta haemolytic strep 90% typically occurs post pharyngeal/skin infection immunologically mediated, Type 2/3 Immune complex deposition in the glomeruli, leads to leaky glomeruli - complement activation |
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Describe the clinical features of post streptococcal GN |
Occurs 1 - 4 wks post strep infection (pharynx/skin) Malaise, fever, oliguria + haematuria Red cell casts, mild proteinuria + oedema w/ HTN Most recover w/in 1 - 3 wks 95% 4% chronic 1% severe renal failure |
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Describe the virulence factors of staph aureus |
Surface molecules: receptors that bind to host endothelial cells Secrete enzymes: lipase degrades skin lipis, tissue induction Secrete toxins: haemolytic toxins, enterotoxins, exfoliative toxins, toxic shock syndrome toxins |
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What infections do the different species of staphylococci cause? |
S. aureus - skin (impetigo, wound infx, scalded skin, toxic shock), pneumonia, osteomyelitis, IE in IVDU S. epidermidis - IE prosthetic valves S. saprophyticus - UTI |
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What are the 2 clinically significant Neisseria? |
N. meningitidis N. gonorrhoea |
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Describe the pathogenesis of N. meningitidis infection |
Respiratory droplet spread Common coloniser of the oropharynx (10% population at any one time) In a small proportion the organism crosses resp. epithelium and enters the blood stream. x BBB into CSF Neisseria have a capsule which reduces opsonisation + protects against destruction by complement proteins |
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What are the microbiological features of neisseria? |
Aerobic, gram -ve diplococci coffee-bean shaped Chocolate blood agar |
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What type of organisms are the clostridia? |
Gram +ve, anaerobic, spore forming bacilli |
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Name the organisms and the diseases they cause in humans |
C. tetani - tetanus C. perfringens - gas gangrene C. botulinum - botulism C. difficile - pseudomembranous colitis |
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How does botulism toxin cause disease? |
eaten in contaminated food binds to gangliosides on motor neuron and is transported into cell Toxin cleaves protein, synaptobrevin, this prevents release ACh at NMJ = flaccid paralysis |
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What is the pathogenesis of gas gangrene? |
C. perfringens releases enzymes and toxins in particular alpha toxin degrades membranes, muscle, RBC release of prostglandins Causes derangements in cell metabolism and cell death |
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Describe the structure of the influenza virus |
Single stranded RNA virus |
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What are the types and subtypes? |
type: neuroprotein - A, B, C Subtype: lipid bilayer containing - haemoglutinin - neuroaminidase |
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What is the pathological basis of pandemics and epidemics? |
Only in influenza A Antigenic shift = pandemic Ag replaced by recombination of RNA segments with those of animal viruses Antigenic drift = epidemic H+N Ag allow escape from most host Ab |
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How does the influenza virus cause pneumonia? |
Virus attaches to upper resp tract epithelium necrosis of cells followed by inflammation interstitial inflammation w/ outpouring of fluid into alveoli secondary infection by staph/strep |
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How does the human body clear a primary influenza infection? |
2 mechanisms: cytotoxic T cells + macrophages cytotoxic T cells kill virus infected cells antiinfluenza protein is induced in macrophages by cytokines IFN Future infection prevented by haemogluttinin Ab and neuroaminidase Ab |
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Describe the pathogenesis of measles |
RNA paramyxovirus (single stranded) Transmitted by resp droplet spread Multiplies in upper resp tract epithelial cells, spreads to lymphoid tissue where it replicates to mononuclear cells -> haematogenous spread |
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What type of immune response occurs in measles |
T - cell mediated immunity: controls infx + rash Ab mediated: protects against re-infection |
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Describe some of the systemic features of measles infection |
Fever Rash - maculopap spread face, neck, down Coryza/cough Conjunctivitis Koplik spots Enlarged LN Secondary infx: pneumonia, encephalitis |
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What are the 2 clinical conditions associated with varicella zoster virus? |
Chicken pox Shingles |
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Describe the pathogenesis and clinical course of infection with this virus |
Aerosol or droplet spread Haematogenous dissemination Vesicular skin lesions, rupture and crust over then heal Some virus lies dormant in dorsal root ganglion and reactivates during immunosuppresion |
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What are the complications of chicken pox? |
Pneumonia Encephalitis, transient myelitis Shingles, secondary bacterial infection Necrotising gut visceral lesions |
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Describe the pathogenesis of glandular fever |
EBV Transmitted by close contact/saliva Colonises naso-oropharyngeal lymphoid tissues ie. tonsils -> submucosal lymphoid tissue B-cell infection - Lysis infected cells + virion release - Latent infection Reactive T cell proliferation in lymphoid tissues - lymphadenopathy + splenomegaly Atypical lymphocytes present IgM Ab and later IgG |
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What are the clinical features of glandular fever |
Fever, sore throat, lymphadenitis, splenomegaly atypical: lethargy/fatigue, lymphadenopathy, haepatitis, rash |
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What are the outcomes of glandular fever? |
4 - 6 wks most resolve, may have fatigue going longer Hepatic dysfunction Splenic rupture Transformation -> lymphomas |
