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  1. 1. STAPHYLOCOCCI Dr Kamran Afzal Asst Prof Microbiology
  2. 2. Introduction Staphylococcus genus Two groups on the basis of their ability to clot blood plasma ( Coagulase reaction ) Coagulase-positive - Staphylococcus aureus Coagulase-negative staphylococci ( CNS ) are now known to comprise over 30 species Staphylococcus epidermidis Staphylococcus saprophyticus
  3. 3. Staphylococcus - derived from Greek “stapyle” (bunch of grapes) Gram positive cocci arranged in grapelike clusters Cell division occurs along different planes, daughter cells remain attached to one another
  4. 4. Properties Salt-tolerant: allows them to tolerate the salt present on human skin Tolerant to desiccation: allows survival on environmental surfaces A major human pathogen and skin commensal Habitat - part of normal flora in some humans and animals Many neonates, children, adults - intermittently colonised by S. aureus Usual sites - skin, nasopharynx, perineum
  5. 5. Staphylococcus aureus
  6. 6. Staphylococcus aureus Reservoir – Humans Carriage sites – Anterior nares, intertriginous areas of hands, perineum, axillae and groins 30-50% of healthy adults colonized Colonizers – Both MRSA and MSSA Leading cause of abscesses, nosocomial pneumonia and SSI
  7. 7. GPC arranged in grape-like clusters Catalase +ve Coagulase +ve DNAse +ve Ferments Mannitol Haemolysis of RBCs Produces carotenoid pigment that gives its colonies golden color Characteristics
  8. 8. Factors predisposing to S. aureus infections Host factors Breach in skin Chemotaxis defects Opsonisation defects Neutrophil functional defects Diabetes mellitus Presence of foreign bodies Pathogen Factors Catalase (counteracts host defences) Coagulase Hyaluronidase Lipases (important in disseminating infection) B-lactamase (assoc. with antibiotic resistance)
  9. 9. Pathogenicity
  10. 10. Virulence Factors
  11. 11. Clinical Manifestations Due to direct effect of organism Local lesions of skin and wound Deep abscesses Systemic infections Toxin mediated Food poisoning Scalded skin syndrome (SSS) Toxic shock syndrome (TSS)
  12. 12. A. Due to direct effect of organism 1. Skin lesions Boils Styes Furuncles (infection of hair follicle) Carbuncles (infection of several hair follicles) Wound infections Impetigo (skin lesion with blisters that break and become covered with crusting exudates )
  13. 13. 2. Deep abscesses Breast abscess in 1-3% of nursing mothers in puerperium Single or multiple Other sites - kidney, lung, brain from septic foci in blood
  14. 14. 3. Systemic Infections a. With obvious focus Osteomyelitis , septic arthritis b. No obvious focus Heart (infective endocarditis ) Brain (brain abscesses ) c. Assoc. with predisposing factors Multiple abscesses, septicaemia (IV drug users) Staphylococcal pneumonia (Post viral)
  15. 15. B. Toxin mediated diseases 1. Staphylococcal food poisoning Due to production of entero-toxins Heat stable entero-toxin acts on gut Produces severe vomiting following a very short incubation period - 6 hrs Resolves on its own within about 24 hours
  16. 16. 2. Scalded skin syndrome Disease of young children Mediated through minor Staphylococcal infection by ‘epidermolytic toxin’ producing strains Mild erythema and blistering of skin followed by shedding of sheets of epidermis Children are otherwise healthy and most eventually recover
  17. 17. 3. Toxic shock syndrome High fever, diarrhea, shock and erythematous skin rash which desquamate Mediated via ‘toxic shock syndrome toxin’ Young women using tampons during menstruation 10% mortality rate
  18. 18. Superantigens Superantigens stimulate T cells non-specifically without normal antigenic recognition Bind directly to class II major histocompatibility complexes (MHC) of antigen-presenting cells outside the conventional antigen-binding grove Cytokines are released in large amounts, causing the symptoms of TSS
  19. 19. Lab Diagnosis In all pus forming lesions Gram stain and culture of pus In all systemic infections Blood culture In infections of other tissues Culture of relevant tissue or exudates
  20. 20. Methods Specimens Pus, pus swab, tissue, body fluids, blood, sputum, urine, catheter tips and tubes Processing of specimens Blood agar and MacConkey agar Incubation: 24-48 hours at 37º C Identification of Staphylococcus aureus Gram stain Catalase, Coagulase and DNAse tests
  21. 21. Gram +ve (purple/blue) cocci Catalase +ve (clusters) Staphylococcus Catalase –ve (chain) streptococcus Coagulase Coagulase +ve S. aureus Coagulase –ve S. epidermidis OR S. saprophyticus S. saprophyticus sensitive S. epidermidis resistant Novobiocin or Colistin (Polymyxin) Catalase test HAEMOLYSIS
  22. 22. Blood Agar
  23. 23. Isolation Selective medium - Mannitol Salt Agar Contains 7.5% sodium chloride Staphylococcus aureus
  24. 24. Identification Gram stain Catalase and Coagulase production Deoxyribonuclease (DNAse) Rapid Identification Agglutination with latex particles Staphaurex Quantitative Polymerase Chain Reaction (PCR)
  25. 25. Test system to identify Staphylococcus
  26. 26. Treatment Drain infected area Antibiotic treatment Deep/metastatic infections Semi-synthetic penicllins, combination Cephalosporins Erythromycin Clindamycin Fluoro-quinolones Endocarditis Semi-synthetic penicillin + an aminoglycoside
  27. 27. Antibiotic Resistance Mechanisms β - lactamase production (Plasmid mediated) β - lactamase stable penicillins (cloxacillin, oxacillin, methicillin) used Alteration of penicillin binding proteins (Chromosomal mediated) Has made S. aureus resistant to β - lactamase stable penicillins Vancomycin is the drug of choice
  28. 28. Historical Progression Of Antibiotic Resistance Of S. aureus Antibiotic Year introduced Reports of resistance Penicillin 1941 1940s Streptomycin 1944 mid-1940s Tetracycline 1948 1950s Erythromycin 1952 1950s Methicillin 1959 late 1960s Gentamicin 1964 mid-1970s Ciprofloxacin 1988 late 1980s Vancomycin 1958 1997
  29. 29. Understanding MRSA MRSA is a type of the Staphylococcus, sometimes called a “Superbug” that is resistant to certain antibiotics Methicillin and other more common antibiotics such as oxacillin, penicillin and amoxicillin This makes MRSA much harder to treat
  30. 30. Problems with MRSA Multi-drug resistant Resistant to all β-lactam drugs Penicillins Cephalosporins Carbapenems Resistant to β-lactamase inhibitors Augmentin, Tazocin, Unasyn
  31. 31. MRSA Treatment Options FDA-approved Vancomycin Linezolid Daptomycin Tigecycline Not FDA-approved, but sometimes used TMP-SMX Clindamycin Tetracyclines Investigational agents Telavancin Dalbavancin Oritavancin PBP-2a–targeted  -lactams (eg, ceftobiprole, ceftaroline)
  32. 32. Key Prevention Strategies
  33. 33. Prevention of MRSA Infection MRSA Protocol Proper hygiene, segregation of carrier from highly susceptible individuals Proper sterilization of instruments Good aseptic techniques when handling surgical instruments Control of hospital infections The most effective way to prevent the spread of MRSA is frequent hand washing
  34. 34. Staphylococcus epidermidis
  35. 35. Staphylococcus epidermidis Skin commensal Has predilection for plastic material Assoc. with infection of IV lines, prosthetic heart valves, shunts Bacteremia and septicemia in susceptible patients Urinary tract infection in catheterized patient
  36. 36. Staphylococcus saprophyticus
  37. 37. Stapylococcus saprophyticus Skin commensal Imp cause of UTI in sexually active young women Usually sensitive to wide range of antibiotics
  38. 38. Case History A 25 year old female , previously in excellent health, presents with a sudden onset of fever, chills, sore throat and myalgias on the 4th day of her menstrual period . Two days later as the fever continues, she develops diarrhea , abdominal pain and becomes disoriented and drowsy . On exam she is hypotensive and has a generalized “sunburn” type rash. Any ideas?