Transcript Gram Positive Cocci: STAPHYLOCOCCUS

Gram Positive Cocci:
STAPHYLOCOCCUS
EDWARD-BENGIE L. MAGSOMBOL, MD,
FPCP, FPCC
Department of Microbiology
Fatima College of Medicine
Staphylococci: General
Characteristics
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Greek: “staphyle”= bunch of grapes
arranged in clusters, divides in many
planes
Gram positive
Catalase positive
Grow best in aerobic conditions but may
behave as facultative anaerobes
Grow in 7.5% NaCl
Gram Positive cocci in clusters
Staphylococci: Classification
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S. aureus: most important pathogen
responsible for most human infections
S. epidermidis: opportunistic infections
S. saprophyticus: opportunistic infections,
UTI in sexually active females
Staphylococci: Structure
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Cell wall teichoic acid
S. aureus= ribitol teichoic acid
S. epidermidis= glycerol teichoic acid
Peptidoglycan
tetrapeptides attached to muramic acid
residues and linked by pentaglycine
bridges
sensitive to lysostaphin (S. staphylolyticus)
Staphylococci: Determinants of
Pathogenicity
1.
Exotoxins
a. pyrogenic exotoxins= interacts with
both MHC-II of macrophages and
specific variable regions on T-cells
“superantigens”
release IL-1, TNF alpha, IL-6
fever, capillary leak, circulatory collapse
and shock
Staphylococci: Determinants of
Pathogenicity
2.
Types
a. Enterotoxins= in 33% of S. aureus;
heat stable CHONs
(1) Enterotoxin A= most common;
vomiting and diarrhea
(2) Enterotoxin B-F= structure and
function same with A
Staphylococci: Determinants of
Pathogenicity
2.
Types
b. TSST-1= fever, multiple organ
dysfunction and shock
structurally identical to enterotoxin
F
Staphylococci: Determinants of
Pathogenicity
b.
c.
Leucocidin: kills PMNs and
macrophages
Exfoliatins: cleave stratum corneum
coded by chromosomal gene or
plasmid
immunogenic
Staphylococci: Determinants of
Pathogenicity
2. Hemolysins alpha, beta, gamma and
sigma: lyse RBCs; facilitates tissue
destruction
3. Protein A: surface CHON
covalently bound to peptidoglycan
in >90% of isolates
MOA: binds to Fc portion of IgG,
prevents Abs from binding to bacteria,
hinders opsonization
massive complement activation--shock
Staphylococci: Determinants of
Pathogenicity
4.
Enzymes
B-lacamase (penicillinase)
fibrinolysin (staphylokinase)
DNAse
phospholipase
hyaluronidase
Staphylococci: Clinical Disease
1.
Superficial infections
a. Pyoderma (impetigo)
b. Folliculitis, furuncles (boils) and
sties
c. Abscesses and carbuncles
Folliculitis
Carbuncle
Staphylococci: Clinical Disease
2.
Deep infections
a. Osteomyelitis
b. Pneumonia
c. Acute endocarditis
d. Arthritis
e. Bacteremia, septicemia
f. Deep organ abscesses (brain,
kidney, lungs)
Brain abscess
Acute infective endocarditis
Staphylococci: Clinical Disease
3.
Staphylococcal toxin diseases
a. Scalded skin syndrome (SSS)
(1) bullous impetigo
(2) staphylococcal scarlet fever
b. Staphylococcal food poisoning
c. Toxic shock syndrome (TSS)
Bullous impetigo
Staphylococci: Epidemiology
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Colonizes skin and mucous
membranes of 30% of normal humans
Anterior nares: most common site
Human to human transmission
Nosocomial infectious agent
Contamination of food by handlers
Phage typing used to trace the source
Staphylococci: Laboratory Diagnosis
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Microscopic: gram (+) cocci in
clusters
Culture: BAP, aerobic conditions
7.5% NaCl, 40% bile,
polymyxin
mannitol salt agar
Identification: coagulase test
mannitol fermentation
Gram Positive cocci in clusters
S. epidermidis culture
Coagulase test
Staphylococci: Treatment
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Most isolates now resistant to penicillin
Penicillinase-resistant penicillin
(methicillin, oxacillin, nafcillin)
First generation cephalosporin
Vancomycin: for MRSA
Erythromycin, clindamycin, 1st gen
cephalosporin: for penicillin allergic pts
Staphylococci: Treatment
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Both superficial and deep infections
need to be given antibiotics but deep
infections need higher doses, IV route,
and prolonged treatment
Debridement or drainage may be
needed
Staphylococci: Control and
Prevention
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Suppress the carrier state
Diligent aseptic practices
No vaccine available