28: Staph Aureus Flashcards
characteristics of staphylococcus aureus
cocci (round)
non-motile
- don’t have a flagellum
non-spore forming
opportunistic pathogen
how common is staph aureus?
inhibits nasal passages of 10-40% of humans without causing disease
staphylococcus aureus toxins
disease-causing because of toxins
virulence factors released by bacteria to provide better survival for the bacteria in the host
common toxins include hemolysin, leukotoxin, exfoliative toxin, enterotoxin and toxic-shock syndrome toxin 1
what else does staph aureus have apart from toxins?
enzymes and surface proteins considered as virulence factors
how does staph aureus replicate?
extracellularly, using fast replication and toxins to survive in host
however, it can still invade and survive in human cells
- evasion from the immune system, antibiotic treatment and allows bacterial proliferation
invasion of skin and blood
bacteria can get across the skin membrane, then get inside, forming an abscess
- area with inflammation, pus and bacteria
once attached to endothelial/epithelial cells, activation of inflammatory cytokines and interferons
diseases caused by staphylococcus aureus
local site of skin infection
- boils, pimples, impetigo
* leading cause of acne alongside strep
diseases from skin infections (toxin-related)
- staphylococcal scalded skin syndrome
- menstrual/non-menstrual toxic shock syndrome
- staphylotoxin-mediated food poisoning
diseases caused by staphylococcus aureus in healthcare settings
serious and rare events
bacteremia/sepsis when bacteria gets into the blood
- systemic inflammatory disease
pneumonia
- typically in patients with underlying lung disease or on mechanical ventilators
- bacteria comes in opportunistically after immunosuppression, and then patients die of infection
endocarditis where heart valves are infected
- leads to heart failure or stroke
osteomyelitis where bones get infected
local impetigo with staph aureus
relatively harmless skin infection in children
treated with antibiotics
staphylococcal scalded skin syndrome
disease mediated by exfoliation toxins
primarily kills skin cells in children
no vaccine
history of toxic shock syndrome
first used in 1978 to describe staph outbreaks in children
- bacteria could not be isolated, indicating a toxin might be involved
emerging disease since no one had seen this before and no one recorded systemic toxic shocks
in 1980, appearances of TSS in menstruating women
- common risk factor identified as users of rely tampons
toxic shock syndrome symptoms
unexplained acute fever
vomiting
rash
high number of deaths
TSS and tampons
rely tampons made with polyester and carboxymethyl cellulose
high absorbency tampons mean lack of liquid access so bacteria grows better and toxin crosses mucosal membrane
excessive absorbency leads to altered microbial ecosystem in the vagina
bacteria preventing the viscosity of vaginal fluids, which increased and got thicker
deaths from TSS
208 deaths from 5296 cases from 1979-1996
- not all were menstrual TSS
not causing a high number of deaths
menstrual TSS
starts within 2 days of beginning or end of menses
associated with high absorbency tampons
TSST-1 isolated from >95% of cases
- bacteria produces toxin and causes disease by leaking into the bloodstream
- bacteremia is not required for TSS
non menstrual TSS
similar to menstrual TSS but caused by colonisation of various sites (lung, skin, surgery)
wounds are not inflamed
- can be just a boil
caused by TSST-1 (<50%) or other toxins/superantigens
mortality for menstrual and non-menstrual TSS
<5% with proper treatment
complicated with antibiotic resistance
superantigens
toxins responsible for TSS and staph-mediated food poisoning
very powerful antigen that activates T cells to make cytokines, and activates macrophages to make more cytokines and inflammation
bind to the side of MHC and T cell receptor, so it will activate T cells to make cytokines as if you were infected with the antigen the T cell normally recognises
super antigens that nonspecifically glue the TCR to the MHC, regardless of the peptide present
nonspecific activation of a large percentage of T helper cells results in excessive inflammatory cytokine production by macrophages
- highly toxic
staphylotoxin-mediated food poisoning
one of the main causes of food poisoning where super antigens are enterotoxins
viable bacteria not necessarily found in contaminated food
toxins are heat-stable
no fever but severe nausea and vomiting
- no bacteria replicating
