Lecture 2 Staphylococcus 2023 PDF

Gram positive bacteria – Topic 3 Staphylococcus The Firmicutes- Actinobacteria – Low GC gram-positive bacteria the high GC gram positive bacteria Non Spore forming bacteria The lactic acid bacteria Streptomyces Streptococcus Lac...

Gram positive bacteria – Topic 3 Staphylococcus The Firmicutes- Actinobacteria – Low GC gram-positive bacteria the high GC gram positive bacteria Non Spore forming bacteria The lactic acid bacteria Streptomyces Streptococcus Lactobacillus Nocardia Staphylococcus Corynebacteria Listeria Mycobacteria Mycoplasma The spore forming bacteria Clostridium Bacillus  STAPHYLOCOCCI Gram+ non-motile cocci (>30 species) Facultative anaerobe capable of both fermentation and respiration Ferment sugars with the formation of lactic acid as one of the major products. G + C (30 - 40%) content similar to lactic acid bacteria - less restrictive growth requirements.  Grape like-clusters of cocci staphyle – Greek, bunch of grapes  Staphylococci Catalase positive (distinguishes from Streptococcus) 3% H2O2  Staphylococcus aureus Beta-hemolysis on blood agar Coagulase positive -distinguishes from S. epidermidis and micrococcus) -causes plasma to clot by conversion of fibrinogen to fibrin Used to be performed in a tube or on a slide now usually performed using latex bead agglutination Only S.aureus is coagulase positive  Staph. aureus diseases: Major components of normal flora –skin -nose Pneumonia and septicaemia in new-born and immunocompromised patients (also a problem in burns units). Skin infections. Organism invades subcutaneous tissue with the aid of lipases - inflammation -> white blood cells -> organisms release toxins that kill cells - > pus -> organisms releases coagulase - > fibrin barrier -> boils, carbuncles. Also impetigo. Furuncle Carbuncle Skin infections Impetigo  Staph. aureus diseases: Pneumonia and septicaemia in new-born and immunocompromised patients (e.g. burns units). Skin infections. Organism invades subcutaneous tissue with the aid of lipases - inflamation -> white blood cells -> organisms relesaes toxins that kill cells - > pus -> organisms releases coagulase - > fibrin barrier -> boils, carbuncles. Also impetigo. Septic arthritis Osteomyelitis Endocarditis Wound infections, absesses. Common hospital acquired infection - can be transmitted by hospital personnel, but usually patient. Major cause of nosocomial infections. Coag+ staphs carried by 20-30% population but approx. 50% hospital staff (unless “decolonised”).  Septic arthritis Staphylococcal septic arthritis - babies and young children- older individuals could be many different bacteria Serious – damage to bones and cartilage Bacteria gain access – Via the bloodstream. – From an injury that cuts into the joint – During surgery.  Osteomyelitis Direct inoculation OR Bacteria introduced during trauma or surgery Hematogenous osteomyelitis  Scalded skin syndrome (SSSS) A toxin produced by phage group 2 Staphylococcus aureus (usually) Initial infection in the mouth, nasal cavities, throat, or umbillicus A lytic toxin (exfoliatin A or B, usually) is produced which affects the skin at remote Sites leading to desquamation Mostly in young children particularly neonates It heals up in a matter of weeks  Staph. aureus diseases: Pneumonia and septicaemia in new-born and immunocompromised patients (e.g. burns units). Skin infections. Organism invades subcutaneous tissue with the aid of lipases - inflamation -> white blood cells -> organisms relesaes toxins that kill cells - > pus -> organisms releases coagulase - > fibrin barrier -> boils, carbuncles. Also impetigo. Septic arthritis Osteomyelitis Endocarditis Wound infections, absesses. Common hospital acquired infection - can be transmitted by hospital personnel, but usually patient. Major cause of nosocomial infections. In an unscreened health setting,Coag+ staphs carried by 20-30% pop but 50-70% hospital staff.  Pathogenicity: hemolysins - (lyse erythrocytes) - toxins - will damage a large number of cell types. leukocidin - toxin acts on polymorphonuclear leukocytes and macrophages. exfoliatin - plasmid encode skin toxin – produces wrinkling and peeling of epidermis. enterotoxins A,B & D - exotoxins that cause a food poisoning - severe diarrhoea and vomiting. Heat stable - resist boiling. TSST-1 - superantigen. Stimulates T-cells to activate macrophages to release TNF -> shock. lipases - lipid hydrolysing enzymes - allows organisms to invade tissues fibrolysin - disolves fibrin clots -> spread extracellular coagulase - may be involved in forming fibrin wall of abscess Panton Valentine Leukocidin produced by strains carrying the lukF and lukS genes on a phage Associated with community acquired infections in the young and healthy. Occasionally hospital outbreaks Acts with other leukocidins to lyse host cell membranes. Invasive soft tissue infections  Pathogenicity: hemolysins - (lyse erythrocytes) - toxins - will damage a large number of cell types. leukocidin - toxin acts on polymorphonuclear leukocytes and macrophages. exfoliatin - plasmid encode skin toxin – produces wrinkling and peeling of epidermis. enterotoxins A,B & D - exotoxins that cause a food poisoning - severe diarrhoea and vomiting. Heat stable - resist boiling. TSST-1 - superantigen. Stimulates T-cells to activate macrophages to release TNF -> shock. lipases - lipid hydrolysing enzymes - allows organisms to invade tissues fibrolysin - disolves fibrin clots -> spread extracellular coagulase - may be involved in forming fibrin wall of abscess  Food poisoning not a human infection caused by ingestion of preformed toxin food contaminated from humans – bacterial growth – enterotoxin production onset and recovery both occur within few hours – Very rapid - acts on emetic receptor site -> vomiting Inhibits water absorption → ‘explosive’ diarrhoea. Toxin is not destroyed by normal cooking.  Pathogenicity: hemolysins - (lyse erythrocytes) - toxins - will damage a large number of cell types. leukocidin - toxin acts on polymorphonuclear leukocytes and macrophages. exfoliatin - plasmid encode skin toxin – produces wrinkling and peeling of epidermis. enterotoxins A,B & D - exotoxins that cause a food poisoning - severe diarrhoea and vomiting. Heat stable - resist boiling. TSST-1 – toxic shock syndrome toxin is a superantigen. Stimulates T-cells to activate macrophages to release TNF -> shock. S. aureus treatment and resistance Standard Treatment Produces penicillinase (-lactamases). Usually sensitive to synthetic (beta-lactamase resistant) penicillins such as oxacillin, methicillin. MRSA Vancomycin  Methicillin resistant S. aureus - MRSA In UK, many hospitals have been colonised with methicillin drug resistance S. aureus (MRSA) due to production of altered penicillin binding proteins and penicilinase - plasmid mediated. First MRSA strains isolated in 1960s Rates of MRSA infection in hospitals increased greatly in the 1990’s but have since stabilised. Many MRSA strains are resistant to multiple antibiotics - aminoglycosides, tetracyclines, chloramphenicol, fluoroquinolones – can presently be treated with the glycopeptide antibiotic, vancomycin. So far vancomycin-resistance appears to be holding. However, vancomycin-resistant enterococci (streps) are becoming common – transfer? → nightmare????. And it has happened! A VRSA strain was isolated from a dialysis patient with a foot ulcer in Detroit (2002). Strain had acquired resistance genes from a vancomycin-resistant E. faecalis strain that was also isolated from the woman’s foot.  Community acquired MRSA (C-MRSA) “Community acquired MRSA (C-MRSA) are defined as MRSA occurring in a healthy person who we would not normally expect to acquire MRSA ; for example, a person who hasn't been recently hospitalised, or undergone surgical procedures or prolonged antibiotic treatment.” “most of the UK cases identified have been seen in injecting drug users. Several other countries have encountered more serious problems with C- MRSA. Risk factors in these countries have included massage parlours and close-contact sports such as rugby or wrestling. “ Government source: Public Health England  Staphylococcus epidermidis Non-hemolytic, coagulase negative staphylococcus major component skin flora, also in gut and respiratory tract opportunistic infections less common than S.aureus Major cause of nosocomial infections e.g. infection in catheters, shunts and prosthetic heart valves.