pathogenesis of bacterial infection Flashcards
what are commensals
do not cause disease/not pathogenic however can become pathogenic if they enter the wrong places in body e.g. sterile areas. commensals live all other the body- human skin and mucosae
examples of commensal flora
- s aureus (nose)
- s epidermidis (skin)
- anaerobes (gut, vagina)
- s. pneumoniae (upper resp tract)
- escherichia coli (gut)
when can the listed commensal floras become pathogenic
- wound (s. aureus)
- prosthesis (s. epidermidis)
- lower respiratory tract (s. pneumoniae)
- urinary tract (e. coli)
- gut perforation/other mucosal lesion ( e coli and anerobes)
what are some bacteria which are never commensal (always bad)
- strep pyogenes
- mycobacterium tb
- neisseria gonorrhoea
- bordetella pertussis
what are low virulence bacteria
- only cause harm to immunocomprimised/ hospatilised patients
-pseudomonas aeruginosa (very common)- oppurtunistic pathogen
what are primary pathogens
- inherent ability to breach host defences
opportunistic pathogens
- require some underlying defect or alteration in host defences
what is a polymicrobial infection
- multiple pathogens working together facilitating each others survival, one pathogen wouldn’t cause disease
- community in mouth
-anaerobes often involved forms a wet gangrene and abdominal abscess
how to microorganisms reach their unique niche in sufficient numbers
- motility
- chemotaxis
- adhesions- bind to specific receptors on the substrate and must compete with the resident microflora. adhesions located on surface of bacterial cells organised structures fimbriae
how does bacteria defend themselves from host immune system
- evade host defences via:
- antiphagocytic capsule
- toxins and enzymes ( destroy anatomical barriers and immune cells, avoid/manipulate immune system
what are some of the features of s.pyogenes which allow it to survive and efend itself from host immune
- m protiens on surface, immunopathology ( rheumatic disease, scarlett fever)
- streptolysin s,o ( break down red blood cells)
- streptokinase
- exotoxin a,b,c - superantignes= toxic shock syndrome
- C5a and Ig binding proteins
-hyaluronidase, collagenase, DNAse- local invasion and ssti
what are streptococal pyrogenic exotoxins
- released from s. pyogenes
- also known as erythrogenic toxins
- A and C are superantigens
- unspecifically activated a third of t cells which result in cytokine release and a cytokine storm- leads to toxic shock syndrom which is presented as having low bp
- exotoxin pyrogenic is also responsible for scarlet fever
- phage encoded ( coded by viral genome not dna)
what are the different group of toxins of bacteria
- endotoxin. (gram negative bacteria, lipid A found in lipopolysacharide on outer membrane)
- gram positive bacteria cell wall components e.g. peptidogylcan and teichoic acid in s. pneumoniae
- exotoxin ( enterotoxin, cytotoxin, neurotoxin, tss toxin)
what are endotoxins
- gram negative bacteria has lipopolysacharides on outer membrane
- lipopolysacharides have a lipid A component which acts as the endotoxin
- triggers cytokine release specifically interleukin 1 and tumour necrosis factor from tH1
- leads to septic shock, multiple organ failure
- at this point using antibiotics to kill bacteria has limited uses/benefits
what are cytotoxins
- type of exotoxin released by bacteira
- two examples include shiga and diptheria
- shiga causes destruction of ribosomes and diptheria caues inhibition of elongation factor in transcription (leads to cell death) so both inhibit protien synthesis
- shiga> bloody diarrhoea (gut epithelium), haemolytic uraemic anaemia (endothelium)
- diptheria > damges pharynx, myocardium and axons
