Download STAPHYLOCOCCUS GRAM POSITIVE SPHERICAL BACTERIA

STAPHYLOCOCCUS
GRAM POSITIVE SPHERICAL BACTERIA THAT OCCUR
IN GRAPE-LIKE CLUSTERS.
IN 1884 ROSENBACH DESCRIBED TWO PIGMENTED
COLONY TYPES:
S.aureus (YELLOW/GOLDEN) COLONIZES NASAL
PASSAGES. HAEMOLYTIC ON BLOOD CULTURES
S.albus (WHITE) COLONIZES THE SKIN AND IS NOW
CALLED S.epidermidis.
THE BACTERIA ARE CATALASE POSITIVE OXIDASENEGATIVE
ALL S.aureus PRODUCE COAGULASE AND SHOULD
BE REGARDED AS PATHOGENIC
S.epidermidis ARE NON-PATHOGENIC, PLAY A
PROTECTIVE ROLE IN THEIR HOST AS NORMAL
FLORA. IN CERTAIN CIRCUMSTANCES MAY BE
PATHOGENIC IN HOSPITALS.
PATHOGENESIS: TENDS TO BE MULTIFACTORIAL
S.aureus CAUSES:
SUPPURATIVE (PUS FORMING) CONDITIONS
BOILS
STYES
FURUNCULOSIS
PNEUMONIA
MASTITIS
PHLEBITIS
URINARY TRACT INFECTIONS
MENINGITIS
OSTEOMYELITIS
ENDOCARDITIS
NOSOCOMIAL INFECTIONS
TOXINOSES
FOOD POISONING
TOXIC SHOCK SYNDROME, DUE TO
SUPERANTIGENS
VIRULENCE FACTORS
1) SURFACE PROTEINS THAT PROMOTE
COLONIZATION OF HOST TISSUES
2) INVASINS THAT PROMOTE SPREAD OF BACTERIA IN
TISSUES. (LEUKOCIDIN, KINASE, HYALURONIDASE).
3) SURFACE FACTORS THAT INHIBIT PHAGOCYTIC
ENGULFMENT (CAPSULE PROTEIN A)
4) BIOCHEMICAL PROPERTIES THAT ENHANCE
SURVIVAL IN PHAGOCYTES (CAROTENOIDS,
CATALASE PRODUCTION)
5) IMMUNOLOGICAL DISGUISES (PROTEIN A,
COAGULASE, CLOTTING FACTOR)
6) MEMBRANE DAMAGING TOXINS THAT LYSE
EUKARYOTIC CELL MEMBRANES
7) (HAEMOLYSINS, LEUKOTOXIN, LEUKOCIDINS).
8) EXOTOXINS THAT DAMAGE HOST TISSUES OR
PROVOKE SYMPTOMS OF DISEASE (SEA-G, TSST,
ET).*
*SE A-G = STAPH ENTEROTOXINS A.B.C.D.E.&G. CAUSE
DIARRHOEA AND VOMITING. THESE TOXINS WHEN
EXPRESSED SYSTEMICALLY CAN CAUSE TSS.
*TSST-1= TOXIC SHOCK SYNDROME. TOXIN
RESPONSIBLE FOR 75% OF TSS INCLUDING ALL
MENSTRUAL CASES.
*ET=EXFOLIATING TOXIN (ETA) & (ETB), CAUSE
SCALDED SKIN SYNDROME IN NEONATES. BLISTERING
AND LOSS OF EPIDERMIS. TOXINS CONTAIN ESTERASE
AND PROTEASE ACTIVITY TARGET PROTEIN INVOLVED
IN MAINTAINING INTEGRITY OF EPIDERMIS.
9) INHERENT AND ACQUIRED RESISTANCE TO
ANTIMICROBIAL AGENTS.
CHARACTERISTICS OF INFECTION:
HUMAN STAPH INFECTIONS ARE USUALLY LOCALIZED AT
THE PORTAL OF ENTRY BY THE HOST’S IMMUNE SYSTEM.
INFLAMMATION AND WALLING OFF OF THE INFECTION BY
WBC. OFTEN RESULTS IN BOIL OR ABSCESS.
HENCE THE ENTRY MIGHT BE A HAIR FOLLICLE, NEEDLE
STICK, SURGICAL WOUND AND SUTURE LINE OR THE
RESPIRATORY SYSTEM.
SEPTICAEMIA OCCURS IF THE ORGANISM GETS INTO THE
BLOOD STREAM. INTERNAL ABSCESSES AND INFECTIONS
IN THE LUNGS, KIDNEY, HEART, MENINGES, MUSCLES.
ADHERENCE TO HOST CELL PROTEIN
SURFACE PROTEINS CAN ATTACH TO HOST CELL
PROTEINS SUCH AS LAMININ, FIBRONECTIN THAT FORM
THE EXTRACELLULAR MATRIX OF EPITHELIAL AND
ENDOTHELIAL SURFACES
HAVE A FIBRIN/FIBRINOGEN BINDING PROTEIN THAT
ALLOWS THEM TO ATTACH TO BLOOD CLOTS AND
TRAUMATIZED TISSUE.
AN ADHESIN THAT PROMOTES ATTACHMENT TO
COLLAGEN HAS BEEN FOUND IN THE STRAIN THAT
CAUSES OSTEOMYELITIS AND SEPTIC ARTHRITIS. IT MAY
ALSO PROMOTE ATTACHMENT TO DAMAGED TISSUES.
INVASION
1) MEMBRANE DAMAGING TOXINS:
ALPHA HAEMOLYSIN, ATTACHES TO PLATELETS,
MONOCYTES CAUSE THE CELLS TO LEAK.
BETA-TOXINS, ATTACK LIPIDS AND ARE NOT ACTIVE IN
HUMANS.
DELTA-TOXINS. THEIR ROLE IS NOT KNOWN.
LEUKOCIDINS. DAMAGE THE MEMBRANES. ONLY 2% Staph
aureus EXPRESS THIS TOXIN UNLESS IT IS CAUSING
DERMONECROTIC LESIONS
2) COAGULASE AND CLUMPING FACTOR:
ROLE IS NOT CLEAR BUT THOUGHT TO CAUSE CLOTTING
AND PREVENT PHAGOCYTOSIS.
STAPHYLOKINASE, THIS LYSES FIBRIN AIDS BACTERIAL
SPREAD.
PROTEASE, LIPASE, DEOXYRIBONUCLEASE (DNASE) AND
FATTY ACID MODIFYING ENZYME (FAME). THE FIRST
THREE HELP THE BACTERIUM UTILIZE NUTRIENTS, WHILE
FAME IS IMPORTANT IN ABSCESS FORMATION AND
MODIFYING ANTI-BACTERIAL LIPIDS.
AVOIDANCE OF HOST DEFENSES
CAPSULAR POLYSACCHARIDE: IMPEDES PHAGOCYTOSIS
IN THE ABSENCE OF COMPLEMENT.
PROTEIN ‘A’: BINDS IgG BY THEIR Fc REGION DISRUPTS,
PHAGOCYTOSIS AND OPSONIZATION.
LEUKOCIDIN: TOXIN THAT ACTS ON PMN LEUCOCYTES ,
DESTROYING PHAGOCYTES.
SUPERANTIGENS & IMMUNITY
STIMULATE ‘T’ LYMPHOCYTES NON-SPECIFICALLY
WITHOUT NORMAL ANTIGENIC RECOGNITION
1 IN 5 LYPHOCYTES ARE STIMULATED WHEREAS ONLY 1
IN 10,000 ARE STIMULATED IN NORMAL ANTIGEN
PRESENTATION.
SUPERANTIGENS BIND DIRECTLY TO CLASS 11 MHC
COMPLEXES OF APC OUTSIDE OF THE CONVENTIONAL
ANTIGEN BINDING GROVE/
CAUSES POTENT STIMULATION OF IMMUNE SYSTEM
MASSIVE RELEASE OF IL1, IL-2, IL6.
TUMOUR NECROSIS FACTOR
Gamma INTERFERON
CAUSES:
HYPOTENSION
FEVER
PHYSIOLOGICAL SHOCK
See figure 4 SUPER ANTIGENS.
RESISTANCE OF STAPHYLOCOCCI TO ANTIMICROBIAL
DRUGS:
HOSPITAL STRIANS ARE RESISTANT TO MOST
ANTIBIOTICS . DUE TO MUTATION, PLASMIDS,
TRANSPOSONS, TRANSDUCING PARTICLES.
MRSA ( Methicillin resistant Staphylococcus aureus) IS VERY
WIDESPREAD IN BOTH HOSPITALS AND THE COMMUNITY
IN THE PAST THE LAST LINE OF ANTIBIOTIC DEFENCE
WAS VANCOMYCIN.
A PLASMID ASSOCIATED WITH VANCOMYCIN RESISTANCE
IN Enterococcusfaecalis CAN BE TRANSFERRED TO STAPH
aureus.
THE ORGANISM IS ALSO RESISTANT TO ANTISEPTICS AND
DISINFECTANTS AND THIS AIDS THEIR SURVIVAL IN
HOSPITALS.