Clinical ID Flashcards
Classes of bacterial pathogens
Viruses
Chlamydiae
Rickettsiae
Mycoplasmas
Bacteria, spirochetes, mycobacteria
Fungi imperfecti
Protozoa
Helminths
Table 8.1
Host barriers to infection
Skin and mucosal surfaces
Secretory products: lysozyme int tears and acid in stomach
Mechanisms of bacterial induced injury
Bacterial virulence: ability to adhere, invade, and deliver toxic moietites
Bacterial adherence
Adhesion on surface molecules; lipoteichoic acids, M proteins, fimbriae/pili (gram-)
Bacterial invasion
Entry into macrophages via complement or antibodies
Entry into epithelial cells; epithelial cell receptors ie intregrin
Bacterial toxins
Endotoxin: LPS, structural component in gram-, induces cytokine release to cause fever, activate macrophages and B cells
Exotoxins: toxins released that interfere with cellular metabolism and allow bacteria to outgrow competing bacteria
Antigenic variation
Mechanism by which an infectious agent alters its surface proteins in order to evade a host immune response (resisting complement/phagocytosis, varying/shedding antigens, causing immunosuppression)
Ex pathogens:
Rhinoviruses (colds)
Influenza virus (flu)
Neisseria gonorrhoeae (gonorrhea)
Borrelia hermsii (relapsing fever)
Borrelia burgdorferi (lyme disease)
Trypanosoma brucei (african sleeping sickness)
Giardia lamblia (giardiasis)
Plasmodium falciparum (malaria)
Suppurative inflammation
Pus-forming
Incresed vscular permeability and leulocytic infiltration by neutrophils
Pyogenic bacteria
Mononuclear and granulomatous inflammation
Mononuclear interstitial infiltrates form (lymphocytes, macrophages)
Granulomatous inflammation occurs when aggregates of macrophages form or fuse to make giant cells
Syphilis & Mycobacterium
Cytopathic-cytoproliferative inflammation
Characteristic of virus-mediated damage in absence of host inflammatory responses
Result in inclusion bodies, blisters, lesions, sysplastic changes and cancers
CMV, measles, herpesvirus, venereal warts/HPV
Necrotizing inflammation
Rapid and severe tissue damage with cell death in absence of inflammatory inflitrates
Caused by uncontrolled viral infections, secreted bacterial toxins, or cytolysis of host cells in protozoa infection
Necrotizing fasciitis caused by Group A streptococcus
Chronic inflammation and scarring
Chronic inflammation can lead to either complete healing or to extensive scarring
Schistosome eggs can cause scarring response