4. INTRODUCTION
• Staphyloccocci - derived from Greek
“stapyle” (bunch of grapes)
• Gram positive cocci arranged in clusters
• Hardy organisms surviving many non
physiologic conditions
• Include a major human pathogen and skin
commensals
5. Gram Stain of Staphylococcus Culture
Gram-positive cocci predominately in clusters
6. Spread of Hospital Strain of Staphylococcus aureus
Nurse
(Carrier)
Doctor:
Boil
Salesman:
Carrier
and
Paronychia
Son:
Impetig
o
7. Properties of Staphylococcus species
Species
S. aureus
Catalase Coagulase
positive
S. epidermidis positive
Mannitol Novobiocin
positive
positive
sensitive
negative
negative
sensitive
S. saphrophyticus positive negative
negative resistant
9. A. Staphylococcus aureus
• Major human pathogen
• Habitat - part of normal flora in some humans and
animals
• Source of organism - can be infected human host,
carrier, or environment
10. 2. Staphylococcus epidermidis
• Skin commensal
• Infection of an implanted device such as
heart valve, intravenus catheter.
• Ass. With infection of prosthetic
• Causes urinary tract infection in
cathetarised patients
• Usually resistant to many drugs.
11. 3. Stapylococcus saprophyticus
• Skin commensal
• Imp. Cause of UTI in sexually active young
women
• UTI in men (usually after age 50)
• Cystitis, pyelonephritis
12. Resistance to antibiotics
– β- lactamase production - plasmid mediated
Has made S. aureus resistant to penicillin group
of antibiotics - 90% of S. aureus
• Resistance to Naficillin-OxacillinMethicillin
• (Chromosomal mediated)
• Tolerance
• Resistance to Tetracyclin- ErythromycinAminoglycosides ( plasmid mediated )
13. • Tested in lab using methicillin
• Referred to as methicillin resistant S. aureus
(MRSA)
• Emerging problem in the world
• In Sri Lanka prevalence varies from 20- 40%
in hospitals
• Drug of choice - vancomycin
• In Japan emergence of VIRSA(vancomycin
intermediate resistant S. aureus)
• No effective antibiotics discovered -We
might have to discover
15. Staphylococcus Structural Virulence Factors
= peptidoglycan
= capsule
= PNSG (biofilm)
= clumping factor
= fibronectin binding protein
= protein A
= collagen binding protein
= teichoic acid
16. Structural Carbohydrates and Virulence
Peptidoglycan
Inflammatory
Teichoic Acid
Inflammatory & allergen
Capsule*
Anti-phagocytic
PNSG*
Biofilm
* - Antibodies to these carbohydrates are protective
17. Staphylococcal binding sites
• The binding sites allow staphylococci to
persist in areas where these substances
abound.
• Fibronectin,
• C1q
• Lamanin (glycoprotein in mammalian
basement membranes)
• Colagen
18. S. aureus Exoproteins and Virulence
Hemolysins:
alpha-hemolysin
beta-hemolysin
gamma-hemolysin
delta-hemolysin
Proteases
Coagulase
Hyaluronidase(s)
Staphylokinase
Lipase(s)
Protease V8
tissue damage at
site of infection
tissue damage
correlates with virulence
spreading factors
destroy host defense
20. Toxins
- Cytotoxins (α , β ,γ)
- Leukocidin
- Exfoliative toxins (ETA , ETB)
- Enterotoxins (A-F , G-I and three subtype
C)
- SEB (super Ag)
- Toxic Shock Syndrom toxin-1 (super Ag)
21. α , β ,γ -hemolysin
•
•
•
•
Toxic for :
leukocytes , erythrocytes,
macrophages and platelets
Lymphocytes
22. DISEASES
• Due to direct effect of
organism
– Local lesions of
skin
– Deep abscesses
– Systemic infections
• Toxin mediated
– Food poisoning
– toxic shock
syndrome
– Scalded skin
syndrome
24. Conditions Leading to S. aureus Infections
Skin damage: burns, cuts, sutures
Reduced Chemotaxis: burns, diabetes, cancer
Reduced Phagocytosis: diabetes, complement
deficiency, immunoglobulin
deficiency, genetic defect
in phagocytes
Age: very young or very old
25.
26. Staphylococcus aureus Pyodermas
Impetigo - crusting vesicle formation of the skin
Folliculitis - hair follicles infected
Furnuncles - boil
Carbuncle - multiple skin lesions connected by sinuses
in the connective tissue
Paronychia - infection of the nail bed
Cellulitis - spreading connective tissue infection
Eye Infections -
41. Carbuncle
• Extensive infection of a group of contagious follicles
• Staph. aureus
• Middle or old age
• Predisposing factors
– Diabetes
– Malnutrition
– During prolonged steroid therapy
42. • Painful, hard lump
• Suppuration begins after 5-7 days
• Pus discharge from multiple follicular
orificies
• Large deep ulcer
52. B. TOXIN MEDIATED
DISEASES
• 1. Staphylococcal food poisoning
–
–
–
–
Due to production of entero toxins
(A-F, G-I, K-M) SEB (super Ag)
heat stable entero toxin acts on gut
produces severe vomiting following a very
short incubation period
– Resolves on its own within about 24 hours
53. Causes of Food Poisoning - - circa 1980
Parasitic
Viral
Chemical
UNKNOWN
Other
C. botulinum
Shigella Salmonella
Staphylococcus
C. perfringens
54. 2. Toxic shock syndrome
• High fever, diarrhoea,vomiting, shock and
erythematous skin rash which desquamate
• Mediated via ‘toxic shock syndrome toxin’
• 10% mortality rate
• Described in two groups of patients
– ass. With young women using tampones
during menstruation
– Described in young children and men
59. Toxic Shock Syndrome: Cutaneous and
Soft Tissue Involvement
Woman’s side
showing extensive
tissue rash due to
TSST.
60. 3. Scalded skin syndrome
• Disease of young children
• Mediated via exfoliative toxins
• Mild erythema and blistering of skin
followed by shedding of sheets of epidermis
• Heals 7 - 14 day
• Don’t grow staph. from blister fluid
65. Scalded-Skin Syndrome: S. aureus Exfoliative Toxin
Toxin produced during
rather limited infection
from either plasmid or
chromosomal toxin gene.
This condition is
typically reversible with
antibiotic therapy.