B4.068 Staphylococcus Aureus Flashcards
pyogenic
pus forming
common gram neg pyogenic bacteria
Neisseria
E.coli
pseudomonas aeruginosa
common gram pos pyogenic bacteria
strep pyogenes staph aureus (80% of pus forming infections)
suppuration
formation of pus
what is pus
mixture of living and dead neutrophils, bacteria, and cellular debris
usually forms in an area of persistent infection
abscess
circumscribed collection of pus
relatively inaccessible to antibodies and antibiotics
may have to be drained to relieve pressure or to resolve infections
preliminary immune response to pyogenic bacteria
activation of macrophages and other innate immune cells
chemotactic factors produced by resident cells to mount and acute phase response
activation of adaptive immunity and Th17 cells
acute inflammation (neutrophil infiltration, production of lysosomal enzymes)
how does an abscess form?
inflammatory area contained within a thick walled fibrous cap
from the hosts point of view, it has contained the invading organism
describe the overarching features of staph aureus
gram pos coccus grow in irregular grapelike clusters nonmotile, non spore forming catalase positive coagulase positive
why is the coccus shape important?
highly resistant shape/size can survive: high temp high salt concentrations drying
how does staph aureus react on blood agar
colonies are golden
strongly hemolytic
B hemolytic
how many individuals in the US are colonized with s. aureus?
as many as 80%
most only intermittently
20-30% colonized persistently
who has high rates of colonization?
health care workers
persons with diabetes
patients on dialysis
main site of colonization
anterior nares
other sites of colonization
axilla
rectum
perineum
vaginal (higher during menses)
what can happen after abscess formation with s. aureus?
organisms can disseminate hematogenously
largely due to bacterial proteolytic enzymes
what are some signs of s. aureus dissemination?
pneumonia, bone and joint infections, infection of heart valves
pneumonia: infants, young children, debilitated
endocarditis: janeway lesions, oslers nodes, roth’s spots
mortality rate of untreated s. aureus
80%
mortality rate of staph TSS
3-5%
TSS diagnostic criteria
fever 102 or higher
rash resembling scarlet fever
desquamation of skin 1-2 weeks after onset
hypotension
clinical/lab abnormalities in 3 organ systems
what cell type is a major player against staph aureus
neutrophils
what is the difference between colonization and non-colonization pathways
colonization: ClfB binding, micro-invasion, upregulation of IL-10
non-colonization: bacterial clearance rather than ClfB binding, upregulation of IL-17, neutrophil infiltration
what is ClfB and what opposes it?
clumping factor B, allows for adhesion
hBD-3 = human B-defensing 3 blocks binding
most common cause of septicemia following surgical procedures
staph aureus
common pathology of MRSA
mild to severe skin infections resulting in death if not treated promptly
common manifestations of staph infections
skin (folliculitis, furuncles/carbuncles, impetigo)
wound
scalded skin syndrome
folliculitis
tender pustule involving a hair follicle
furuncle
small abscess that exudes purulent material from a single opening
carbuncle
aggregate of furuncles with several openings
septic arthritis
warmth, erythema, and tenderness of the joint together with constitutional symptoms and fever
nearly always unilateral
osteomyelitis
fever and bony tenderness/a limp
endocarditis due to s. aureus
usually acute course
most present with high fever
common in IV drug users
what bacteria causes many catheter associated infections?
staph epidermidis
what does staph saprophyticus cause
UTIs in sexually active young girls
dysuria and pyuria
responds to many antibiotics
examples of s. aureus virulence factors
cell surface: 1. protein A 2. fibronectin binding protein 3. clumping factor 4. other MSCRAMMs secreted: 1. superantigen 2. cytolysins (toxins) 3. exoenzymes 4. polysaccharide intracellular adhesion
function of capsule
inhibits phagocytosis
function of protein A
binds to the H chain of Ab and can inhibit Ab opsonization, preventing phagocytosis
can activate classical complement pathway with Ab/protein A complex
how does s. aureus form a fibrin barrier around infectious loci?
coagulates plasma with coagulase
binds fibrinogen and causes production of fibrin
how can s.aureus break down clots and why?
enzymes like staphylokinase break down fibrin and clots
breaks out of walled off areas to colonize rest of body
function of toxins
toxic for many blood cells (aka cytotoxins, lysins)
panton valentine leucocidin (PVL)
exotoxin
occurs in <5% of strains
phage derived
causes leukocyte destruction and necrosis, especially in skin and lungs
exfoliatin toxins
consist of ETA and ETB
result in scalded skin syndrome (SSSS)
what is SSSS
fever, erythema, blisters
blisters eventually rupture and leave a red base
positive nikolskys sign (bullae moves under skin)
bullous impetigo
localized SSSS
culture positive (unlike disseminated SSSS)
nikolskys sign not present
primarily occurs in infants and young children
which virulence factors are responsible for food poisoning with s. aureus
enterotoxins A-E and G-I
superantigens that stimulate certain T cells
stimulate production of cytokines such as IFN-y and TNF causing inflammation of the tissues
symptoms of enterotoxins
often localized to gut, but can be fatal is systemic
often occur from skin of food handlers
cause vomiting and watery diarrhea 2-6 hours after ingestion
usually self limited
characterize toxic shock syndrome
caused by a superantigen
first described in kids
most frequently associated with tampons, but at least half of cases not associated with menstruation
which exotoxins are associated with TSS
TSST-1
enterotoxin B and C
how to diagnose s. aureus
obtain cultures as appropriate for site of infection
blood cultures from patients with serious infections
who is more susceptible to s. aureus infections?
neutropenic patients
important factors in defense against s. aureus
- neutrophils
- opsonization w Ab and complement
- T cells, Th17 recently implicated
- IL-1
- recognition by TLR-2
what can defend against toxins?
antibody
characterize coagulase negative staph
s. epidermidis most common
lack many virulence factors
cause problem in artificial heart valves
