pathogenesis of bacterial infection

Question 1

what are commensals

Answer 1

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

Question 2

examples of commensal flora

Answer 2

• s aureus (nose)
• s epidermidis (skin)
• anaerobes (gut, vagina)
• s. pneumoniae (upper resp tract)
• escherichia coli (gut)

Question 3

when can the listed commensal floras become pathogenic

Answer 3

• wound (s. aureus)
• prosthesis (s. epidermidis)
• lower respiratory tract (s. pneumoniae)
• urinary tract (e. coli)
• gut perforation/other mucosal lesion ( e coli and anerobes)

Question 4

what are some bacteria which are never commensal (always bad)

Answer 4

• strep pyogenes
• mycobacterium tb
• neisseria gonorrhoea
• bordetella pertussis

Question 5

what are low virulence bacteria

Answer 5

• only cause harm to immunocomprimised/ hospatilised patients
  -pseudomonas aeruginosa (very common)- oppurtunistic pathogen

Question 6

what are primary pathogens

Answer 6

• inherent ability to breach host defences

Question 7

opportunistic pathogens

Answer 7

• require some underlying defect or alteration in host defences

Question 8

what is a polymicrobial infection

Answer 8

• 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

Question 9

how to microorganisms reach their unique niche in sufficient numbers

Answer 9

• 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

Question 10

how does bacteria defend themselves from host immune system

Answer 10

• evade host defences via:
• antiphagocytic capsule
• toxins and enzymes ( destroy anatomical barriers and immune cells, avoid/manipulate immune system

Question 11

what are some of the features of s.pyogenes which allow it to survive and efend itself from host immune

Answer 11

• 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

Question 12

what are streptococal pyrogenic exotoxins

Answer 12

• 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)

Question 13

what are the different group of toxins of bacteria

Answer 13

• 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)

Question 14

what are endotoxins

Answer 14

• 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

Question 15

what are cytotoxins

Answer 15

• 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

Question 16

what is neurotoxin and give examples, and treatment

Answer 16

• neurotoxin type of exotoxin- affect neurotransmitter activity
• example include tetanus and botulinum
• tetanus causes spastic paralysis (overactivartion)
• botulinum causes flaccid paralysis - interfering with neural transmission
• treated using antitoxins not antibiotics to neutralise the toxins preventing the inteference of neurons

Question 17

what are enterotoxin

Answer 17

• type of exotoxin
• examples include cholera
• cholera causes over activation of adenylate cyclase so increased amount of cyclic AMP formed- affects ion channels which distrupts ion balance and can cause dehydration and watery diarrhoea
• enterotoxin- overactivity of secretary mechanisms

Question 18

what are examples of toxic shock syndrome toxins

Answer 18

• branch of exotoxin
• released by s. pyogenes and s.aureus
• s pyogenes theres include A and c pyrogenic exotoxins which are super antigens
• activate 1/3 of t cells non specifically- leading to cyotkine release and therefore cytokine storm
• results in toxic shock syndrome
  -symptoms include hypotension, fever rash

Question 19

what are examples of post infection syndromes

Answer 19

• rheumatic fever (s. pyogenes)
• glomerulonephritis ( s.pyogenes- 10-14 days after)
• reactive arthritis ( salmonella, neisseria gonorrhea)

Question 20

rheumatic fever

Answer 20

• caused by m proteins on s. pyogenes which have similar chemical properties and structure to other host cells/ structure in the body
• host cell mistakes are own cells for s. pyogenes
• immunopathology- attacks are own cells leading to rheumatic disease- lead to rheumatic heart disease which can particularily affect are heart valves
• develops 2-3 week after infection particularily if infection not treated
• cross reaction between host tissue
• molecular mimicry
• symptoms include rash, swollen or inflammed joint, narrowing valve