a brief description on morphology and pathogenesis caused by Staphylococcus Aureus, Staphylococcus Epidermidis, Staphylococcus Saprophyticus, toxic shock syndrome toxin (tsst) and it's treatment, enterotoxin , exfoliatin , pyogenic infections, abscess etc
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7. • Microscopically grape like structure
• CATALASE
important virulence factor
enable bacteria (staphylococcus) to survive killing effect within
neutrophil
not produced by STREPTOCOCCUS
CATALASE +
• Ferments MANITOL
H2O2 H2O O2
8. • COAGULASE
produced only by S. aureus
causes plasma to clot
PROTHROMBIN THROMBIN
FIBRINOGEN FIBRIN
coagulase
9. • STAPHYLOXANTHIN
carotenoid pigment
impart golden color to colonies
enhance pathogenicity
inactivates effect of ROS( H2O2 )
• HEMOLYSIN
only produced by S. Aureus
hemolyse RBCs source of IRON
used to produce CYTOCHROME
Generates energy
10. • BETA- LACTAMASE
produced by plasmid present in 90% of S. Aureus
resists many but not all penicillin i.e. METHICILLIN NAFCILLIN
some strains of S. Aureus are resistant even to beta lactamase resistant
penicillin
due to mutations in PBPs
MRSA
NRSA
11. IMPORTANT STRUCTURES
OF S. AUREUS• Protein A
major protein in cell wall
imp. Virulence factor
bind the Fc portion of IgG at complement binding site
preventing activation of complement cascade
no C3b produced
opsonization is reduced
phagocytosis is reduced
• TECHOIC ACID
polymer of ribitol phosphate
mediate adherence of S. Cocci to mucosal membranes
• LIPOTECHOIC ACID has role in production of septic shock by
producing CYTOKINES i.e. IL-1 TNF
12. • MICROCAPSULE small amount of polysaccharide capsule around S. aureus
poorly immunogenic difficult to form effective vaccines
• PEPTIDOGLYCAN of S. Aureus
has endotoxin like property
produces CYTOKINES
activation of coagulase and
complement cascade
can cause clinical finding of
septic shock yet not posses endotoxin
13. HUMAN RESERVOIR
FOR S. AUREUS
• Nose is main site of colonization
• Skin common site of S. aureus esp. in hospital personnel and patients
hand contact imp. Mode of transmission
• Vagina in 3% of women
predisposes Toxic shock syndrome
• Additional sources are human lesion
fomites contaminated by
these lesions i.e. towel
14. CONDITIONS WHICH
PREDISPOSES TO S.
AUREUS INFECTIONS• Reduced humoral immunity
including low level of antibodies
neutrophils
complement
• Diabetes
• Intravenous drug usage
• CGD ( chronic granulomatous disease )
defected neutrophils unable to kill bacteria
16. PYOGENIC
INFLAMMATION• Typical lesion of S. aureus infection is an ABSCESS
• Abscess undergoes
central necrosis
usually drain to outside FRUNCLES and BOILS
organism may disseminate via blood stream as well
• Foreign bodies are important predisposing factor
sutures
intravenous catheter
17. ENTEROTOXIN• Causes food poisoning
watery and non bloody diarrhea
prominent vomiting caused by cytokines released by lymphoid cells
stimulates action of enteric nervous system to
activate vomiting center of brain
• Act as super antigen within GIT
stimulates release of large amount of IL-1, IL-2
• Fairly heat resistant
not inactivated by brief cooking
• Resistant to acid and enzyme of stomach and jejunum
• Six immunologic types of enterotoxin from A-F
18.
19. TOXIC SHOCK SYNDROME
TOXIN (TSST)
• Is a super antigen
• Cause toxic shock syndrome
in individuals with wounds
patients with nasal packing
release of large amount of IL-1 and TNF
• Locally produced by S. aureus present in vagina , nose and other infected sites
• Toxic enters in blood stream TOXEMIA
• Occurs in people who don’t have antibody against TSST
TREATMENT
• Correction of shock by using fluid pressor drugs , inotropic drugs
• Administration of beta lactamase resistant penicillin i.e. Methicillin
• pooled serum globulin which contain antibody against TSST
20.
21. EXFOLIATIN
• Cause scalded skin in young children
• Is epidermolytic
• Act as a protease cleaves desmoglein present in
• desmosomes
separation of epidermis
from granular cell layer
22. TREATMENT
• 90% or more of S. Aureus strains are resistant to penicillin
• I can be treated with Beta lactamase resistant penicillin
vancomysin
cephalosporin
• 20% of S. aureus strains are
MRSA methicillin resistant
NRSA nafcillin resistant
resistance is due to mutations in PBPs
drug of choice vancomysin + gentamysin ( some times added)
daptomycin
24. • S. epidermidis is coagulase negative
• Doesn’t produces exotoxin
• Doesn’t cause food poisoning
toxic shock syndrome
• Causes pyogenic infections
particularly on intravenous catheter
prosthetic implants heart valves
prosthetic joint
(hip joint)
vascular graft
25. • Part of normal human flora on skin and mucous membrane
• can enter blood streams BACTEREMIA
can cause metastatic infection
esp. at the site of an implant
• Infections are almost always hospital acquired
• Major cause of sepsis in neonates
• Cause of peritonitis in patient with renal failure
who are under going
peritoneal dialysis
26. • Most common bacterium to cause CSF shunt infection
• Produce glycocylex which enables to adhere to
prosthetic implant materials
• Doesn’t produce hemolysin Non Hemolytic
• Doesn’t produce STAPHYLOXANTHINE white colonies
28. • S. saprophyticus is coagulase negative
• Doesn’t produces exotoxin
• Doesn’t cause food poisoning
toxic shock syndrome
• Found in mucosa of genital tract in young women
• Infection almost always Community acquired
29. • 2nd to E. coli as a cause of community acquired UTI in young women
• Doesn’t produce staphyloxanthin white colonies
• Doesn’t produce hemolysin non hemolytic
• Causes pyogenic infections
esp. Urinary tract infection in young
CYSTITIS women
30. PREVENTION
• No vaccine against staphylococci
• Control of S. aureus spreading by
frequent hand washing
aseptic management of lesion
cleanliness
• Nasal colonies of S. aureus is reduced by
oral antibiotics CIPROFLOXACIN etc.
intranasal mupirocin
but difficult to eliminate completely
• CEFAZOLIN often used preoperatively to prevent staphylococcal surgical
wound infections
31.
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