unit 2 microbio

virulence

ability of a microorganism to cause disease, measured by numbers of microorgan needed to cause infection in host (infective dose), low infective dose means more virulent

virulence factors

allow the pathogen to escape host defenses by resisting phagocytosis, biofilm formation, bacterial structure (adherence, capsule, protein A, lipid A)

adherence

adhesions or receptors allowing for adherence of pathogens, mutations affect pathogen attachment to host

capsule

polysac, most common phagocytosis evasion tech, steptococcus pneumoniae, haemophilus influenzae

protein A

interferes with activation of host antibodies blocking phagocytosis, staphylococcus aureus

lipid A

endotoxin on the lipopolysac LPS (cell wall of gram neg)

intracellular survival of pathogens

ability to avoid phagocytosis and replicate

microbial toxins- exotoxin

heat labile, proteins excreted by living pathogenic cells, usually gram pos, specific targets killing host cells, aid in spreading, interfere with intracellular activities

microbial toxins- endotoxin

heat stable, LPSs, gram neg, effective after cell death/lysis, disrupt clotting, fever, activate complement and immune system, circulattory changes, septic or endotoxic shock

microbial toxins- entertoxin

specific for intestinal mucosa, exotoxin

microbial toxins- neurotoxin

destruction of nerve tissue, exotoxin

microbial toxins- cytotoxin

destruction of cells, exotoxin

extracellular enzymes- proteases

can act as an exotoxin, destroys extracellular structures

extracellular enzymes- hyaluronidases

spreading factor, breaks down hyaluronic acid (structural component of hosts extracellular matrix), increases tissue permeability allowing escape of pathogens, deeper invasion means faster spread

host defenses-

physical barrier, chemsing mechansims, antimicrobial substances (fatty acids, HCl in stomach, lysozymes, IgA), indigenous normal flora, phagocytosis, inflammation

cleansing mechanisms

skin shedding of epithelium, tears, resp tract (nasal hairs, ciliary epithelium, musous membranes), urine, GI tract (acidic pH),

normal flora

competes with path for nutrients and space, some produce bacteriocins to inhibit the growth of closely related bacteria

arthropods

transmission from bugs

local infection

Organism enters the body and remains confined to specific tissue

systemic infection

spreads to several sites and tissue fluids

acute infection

appear rapidly, severe symptoms, rapidly vanishes

chronic infection

less severe symptoms but persists for long periods of time

epidemiology

study and analysis of the distribution, patterns, and determinants of health and disease in the population

pathogens are classified by

area of body, clinical significants (path vs normal), bacterial requirements and type, characteristic infections associated

normal flora types

resident (normal throughout life), transient (same location as resident but limited time)

role of normal flora

isolated in the absence of disease, colonizers, protect host from infection of pathogenic organisms

normal flora protects infection of pathogenic organisms by

competing for the same nutrients and receptor sites on host cells, bacterial products toxic to other organisms, natural antibodies, primes immune system for rapid response

normal flora maintains a balance of organisms

limits the quantity and predominance of any one organism

opportunistic pathogens- normal flora balance interrupted

compromised immune system, changes in normal flora, normal flora enters sterile site, due to antibiotic therapy (chemo)

opportunistic pathogens- compromised immune system

HIV, malnutrition, stress, age, chemotherapy

opportunistic pathogens- changes in normal flora

after antibiotic use (clostridium difficile infection) or after chemotherapy (candida species infection)

opportunistic pathogens- normal flora into sterile body site

burns, surgery

definite pathogens

always cause disease, NOT normal flora, bacillus anthracis (anthrax), yersinia pestis (bubonic plague), vibrio cholera (cholera)

nosocomial acquired infection NI

infection caused by patient during a hospital stay after being admitted due to another reason, within 48hrs, 3 days of discharge, 30 days of an operation

healthcare acquired infection HAI

infection acquired by patient in any healthcare setting

staphylcoccis aureus is

potential from non sterile site

neisseria ginorrhoeae is

primary from any source

sterile body site source/ specimen type

csf, pleural fluid, synovial fluid

sterile body site but can be contaiminated with normal during collection source/ specimen type

blood, sputum, urine

contamination

degree determined by procedure/facility, increases in epithelial cells, poor quality of squamous epithelial cells and no wbcs in skin wound= contaminated

sterile specimen

blood, suprapubic urine (needle from bladder), csf, all fluid, bone marrow, abscess, tissue, wound

synovial fluid

joints

pleural fluid

lining of lungs

peritoneal fluid

lining of abdominal organs

bronchoalveolar lavage BAL

fluid squirted into lungs than collected

sputum

mixture of saliva and mucus