Immunology* Flashcards
Definitions and factors needed to be named of/a pathogen and commensals?
Pathogen is an organism which can cause disease (needs to be found in all cases of disease, cultured out of the body and reproduce the disease)
Commensal is an organism which is part of the flora (normal flora site, pathogenicity and clinical context)
Definition of pathogenicity and the requirements?
Capacity of a microorganism to cause an infection
Requirements such as infectivity and virulence
Definition of infectivity and actions for infectivity?
Ability to become established on or within a host
Attachment of E. coli via P-fimbriae and receptor on uroepithelial cells
Acid resistance of H. pylori via urease making ammonia from urea (reduces acidity)
Definition of virulence and actions of virulence factors? (specificity?)
Capacity to cause harmful effects once established
Conferred by virulence factor:
- invasiveness, toxin prod and immune evasion
Specific to strains, not species
S. aureus - specific virulence factor? clin signs? coagulase negative staph location?
Coagulase +ve staphylococci
Formation of purulent abscesses
Can become systemic
Attracted to the prosthetics, can cause problems
Virulence factors - invasiveness? toxin production - c. tetani, c. difficile, c. perfringens, cholera and E. coli?
- clinical signs?
Invasiveness from strep pyogenes can cause necrotising fasciitis, cellulitis caused by CT breakdown via hyaluronidase and collagenase
Fibrinolysis via streptokinase
Toxins such as exotoxins released extracell by microorganisms. enterotoxins are exotoxins act on GI and endotoxins part of gram -ve cell wall
Tetani - tetanus, uncontrolled muscle spasms, immunisation via modified toxin
Difficile - can be commensal, diarrhoea, spreads via spores and detected by ELISA
Perfringens - soil or commensal, cause food poisoning (enterotoxins) and can cause gas gangrene
Cholera - SI, increases cAMP, inhibits Na/Cl-, stims Cl- and HCO3- causing dehydration
E. coli - pili, capsule and toxins, ferments lactose and causes UTI and diarrhoea
Virus pathogenic mechanisms - cell destruction and virus-induced changes?
Cell destruction via death of CD4 by HIV
Virus-induced changes causing tumour viruses
Sites of viral entry?
Conjunctiva Arthropod Capillary Skin Resp tract Alimentary tract Urogenital tract
Types of viral infection progression, examples and pathophysiology?
Acute - fast peak and drop (influenza A - infect and destroy resp and altered cytokine exp leading to fever - antigenic drift and shift)
Latent - fast peak and drop, but re-emergence later on (HSV1/2 - prim infection via epith, migrates to ganglia and lays latent in nuc, migrates to epith and released)
Chronic - fast peak and drop, with continuous low level virus
Tumour - v low level virus causing tumour and increased levels (papillomavirus - cervical carcinoma, HTLV - 1 - blood transmission, infects T causes leukemia/lymphoma)
Innate immunity - physical and immune cell examples?
Skin, gastric acid and mucociliary escalators
Phago cells:
- polymorphs (neutrophils, eosinophils and basophils) and macrophages (previous monocytes)
Process of phagocytosis and opsonisation?
Organism held in phagosome
Fusion with lysosome
Phagolysosome
Intra-cell killing
Opsonisation - coating with abs or complement
Phagocytic cell receptor for both
Increases phagocytosis efficiency
Acquired immunity - definition? antibodies and function?
Specific response to antigen, split into humoral (abs) and cellular (cells) causing memory cells
Primary - IgM
Secondary - IgG
Mucosal - IgA
Allergy - IgE
Neutralises bacterial toxins, viruses, prevents adherence and aids opsonisation
B-lymph to plasma produce abs (need T-cell help)
Complement process?
C1 - C9
Combo of antibodies and its specific antigen trigger the cascade reactions
End have a variety of action
Cell mediated immunity - definition, controlled by, and immune cells?
Macrophages present antigens and stim T-cells
Cytokines produced and control response
CD4 - Th1 (act macrophages) and Th2 (B cell)
CD8 - suppressor and cytotoxic cells (killer)
