16. pathogenicity of bacteria Flashcards
1
Q
what is bacterial pathogenicity? 6
A
- pathogenicity/virulence is the capacity to cause disease
- bacteria vary in their pathogenicity
- commensals in normal flora in normal, healthy host never cause disease
- opportunistic pathogens - colonization does no harm until immunosuppressed, then can be fatal
- these pathogens are usually commensal
- highly virulent pathogens always cause disease
2
Q
What are opportunistic pathogens? 5
A
- pseudomonas aeruginosa is a gram negative rod found in plants and soil
- infects those with third degree burns as immune defences in the form of skin and lymphatic system are burnt away
- also found in CF patients as their mucocilliary escalators do not function, mucus is too thick
- this mucus makes a goof breeding ground for the bacteria, leading to lung infections
- staphylococcus epidermis is a gram positive coccoid that lives on skin and infects catheters
3
Q
What is the danger with catheter biofilms? 6
A
- upon piercing of skin, S, epidermis cells attach to catheter
- blood plasma proteins coat catheter, forming a conditioning film
- this provides anchorage for binding and growth of bacteria
- s. epidermis multiplies and forms a biofilm community on catheter
- this is antiobiotic resistant because the biofilm contains gelatinous mucopolysaccharide
- these polymers prevent antibiotics contacting the bacteria
4
Q
Describe Neisseria meningitidis. 6
A
- Causes meningitis and sceptisceamia, and is a commensal of nasopharynx, 10-20% of the population carries this bacteria
- disease is transmitted through repiratory droplets or close, prolonged contact
- incubation period of 4 days and symptoms include stiff neck, fever, light sensitivity, confusion, headaches and vomiting
- if it reaches the bloodstream, it causes meningococcal septicaemia, a systemic infection
- rash casued by growth of organisms at skin surface where capilarries have burst, leading to amputation or entry of bacteria into cns
- 10-20% of survivors have brain damage or hearing loss due to cns infection
5
Q
Describe the highly virulent pathogen, mycobacterium tuberculosis. 6
A
- TB not a major probelm in developed world but is common in aids patients and prisoners
- gram positive bacterial rods which are spread by respiratory route - resist dessication very well
- grow inside macrophages in the lung, primary tb is usually resolved by the immune system
- slow process, tubercules form and bacteria live inside, this is dead lung tissue surrounded by cells, which can spread if immunosupressed after many years
- can be treated with antibiotics but many are now resistant
- some strains resistant to all antibiotics, so lung must be removed
6
Q
Describe the highly virulent treponema pallidum, which casues syphilis. 6
A
- big 19thc STD where only treatments were dangerous and could be spread to unborn child
- flexible, helical bacteria which causes a primary lesion (chancre) at site of entry in 2 weeks
- in this ulcer, bacteria grow and divide, it resolves itself, then bacteria migrate into bloodstream
- this is the secondary stage (10 wks). cells spread to eyes, joints, bones and skin, causing rash
- rash resolves and symptoms go - latent phase. Some people are never bothered by the disease again
- years later, 40% develop tertiary syphilis, infection spreads to CNS and cells grow in brain, leading to insanity and death
7
Q
what is the immune response to tb? 6
A
- tubercule, aka ghon complex, is made of necrotic tissue containing pus
- surrounded by macrophages and other immune cells
- the immune cells wall off the live bacteria and prevent it from spreading
- macrophages interlock and some can fuse to form giant, multinucleate cells
- T and B cells around the outside create immune response
- if this is unsuccessful and granule bursts, bacteria spreads and causes secondary tb
8
Q
What are koch’s postulates? 5
A
- devised in 1882 to prove cause and effect on microbial infections
- organism must be found in lesions eg. B. anthrax
- organism grown outside body in lab, however this is sometimes impossible
- Organism must reproduce disease when infected, eg. sheep, or dr marshall for h. pylori, which proved it could survive in the stomach
- organism must be re-isolated from test animal and proven to be the same
9
Q
What problems are there with Koch’s postulates? 6
A
- some cultures eg. mycobacterium leprae (leprosy) can’t grow in lab, only grows in humans or on armadillo footpads (below 37 degrees)
- ethical problems make some tests impossible eg. AIDS and ebola only grow in humans
- lab workers have developed aids by mistake
- some mild illness eg. old viruses get human volunteers
- sometimes there is no suitable animal model eg. gonorrhoea
- Gonococcus was unethically tested in 60s, participants didn’t know what they were doing.
10
Q
What measures of virulence do we use? 6
A
- one method is minimum infectious dose
- very virulent - 10 bacteria cause disease eg. streptococcus pneumoniae
- 10-100 eg. shigella flexeneri, which casues dysentry - food and water borne pooey disease
- can also be measured by LD50 - dose required to kill 50% of animals/cells in a given time
- also used to quantify relative toxicity of toxins
- its hard to establish ethically so we don’t know ld50 for a lot of bacteria
11
Q
What are virulence determinants? 6
A
- required by bacteria to cause disease and protect themselves from immune system and colonize host
- its more the immune response that is harmful than the bacteria
- pathogens produce multiple virulence factors
- capsule of mucus like poly-d-glutamic acid, which inhibits phagocytosis and complement deposition, creating muccoid colonies
- toxins supress immune activation and cytokine production. if infection becomes systemic and toxins are injected into blood, it can cause TSS and death
- If capsule or toxins lost, strains become attenuated.
12
Q
How do commensal bacteria adhere to the host? 5
A
- all commensals living on the epithelium adhere to the host
- eg ecoli attach by type 1 peritrichous fimbriae
- omposed of protein subunits,carrying a tip adhesin (protein H)
- specifically attaching to mannose receptors in the colon on epithelial cells
- these are also abundant in the bladder, causing UTIs
13
Q
How do pathogens adhere to the host? 5
A
- pathogens adhere selectively to epithelial surfaces
- fimbriae carry adhesins - pathogenic ecoli strains carry different fimbriae, 40+ types
- eg. pathogenic e.coli use CFA (colonization factor antigen) fimbriae to attach to duodenal mucosa
- Release toxins at critical mass
- this can be viewed by staining with immunogold - gold flecks with antibodies attached
14
Q
what are non-fimbrial adhesins?4
A
- protein structures used by come bacteria eg. stroptococcus pyogenes (sore throat and impetigo rash)
- S. pyogenes can also cause rhematic fever - cells bind to respiratory tract receptors by m protein if cells reach blood stream
- M protein covers bacterial surface like a capsule, not hair like
- mediates attachment to epithelial cell
15
Q
What stages are there in the disease process? 5
A
- enter host
- adhere by specific mechanisms
- sometimes penetrate tissue
- eg. listeria monocytogenes leads to food poisoning, misscarriage and death when it enters host cells
- found in unpasteruised dairy products and unwashed veg
