MEDI2003 Week 7 - Gram Positive Cocci Flashcards
(35 cards)
Gram positive cocci
Staphylococcus Streptococcus Enterococcus
Staphylococcus
88 species, Staph = bunches or grapes-like shape/clusters. Clusters -> only in clinical smears not from colonies. Single cells, pairs or tetrads. Catalase +ve, non-motile, most are facultative anaerobes (with or w/o O2) and attacks sugars fermentatively (anaerobe fermentation of glucose) Divided into coag +ve and coag -ve species.
Staphylococcus aureus
Most virulent + clinically significant pathogen among staphs. (all isolates are considered significant) -Most colonies are creamy yellow in colour “golden staph” -Slide AND Tube coag +ve. NF in humans: -> Anterior nares (nostrils) in 20-40% of population. -> Nasopharynx, perineal area, skin. -> Can colonise various epithelial + mucosal surfaces. -> 60-70% of people in hospitals are carriers. Significant cause of nosocomial infection.
Staphylococcus aureus resistance
MRSA - methicillin resistant S. aureus nmMRSA - non-multi resistant MRSA mrMRSA - multi-resistant MRSA nmMSSA - non-multi resistant methicillin susceptible S. aureus mrMSSA - multi-resistant methicillin susceptible S. aureus
Infection of S. aureus
1) Wound infections (post surgical or foreign object damage) 2) Bacteraemia, endocarditis, pericarditis. 3) Meningitis 4) Pulmonary infections 5) Osteomyelitis and septic arthritis 6) Food poisoning - consuming food containing heat stable enterotoxins (diarrhoea, vomiting, abdominal cramping 2-6hrs after ingestion) 7) Scalded skin syndrome - sloughing of the superficial skin layers, usually seen in infants and neonates. 8) Toxic shock syndrome - multi-system illness, fever, hypotension, rash, dizziness, vomiting, diarrhoea, renal failure etc. 9) Folliculitis, Furuncle, Carbuncle, Impetigo
Virulence factors of S. aureus
1) Polysaccharides 2) Protein A 3) Enzymes: catalase, coagulase, fibrinolysins, hyaluronidase, lipases, nuclease + B-lactamases (confer resistance against penicillin, ampicillin and other B-lactam AB) 4) Haemolysins - toxic to variety of host cells, different to haemolysins produced by steptococci. 5) Toxins: -> Epidermolytic toxins/exfoliatins - proteolytic activity on skin + causes scalded skin syndrome -> Enterotoxins - A to D, E, H, I - assoc with food poisoning - heat stable. A, D, H, and I toxic shock syndrome (TSS)
Coagulase test
Staphylococcal coagulase enzyme converts fibrinogen protein in plasma into insoluble fibrin threads, which results in the formation of a clot in the tube
Two forms of coagulase tests
- Bound coagulase (cell wall) is detected by the slide coagulase test. - Free coagulase (secreted) is detected by the tube coagulase test. Use EDTA plasma
Slide coagulase test
“Clumping factor” Mix a heavy suspension of organism in saline until milky, then add plasma (straight wire dipped in plasma). (Careful: 5% of S. aureus are slide coag neg, and some CoNS are slide coag pos!) All negative results should be checked by the tube method since strains deficient in clumping factor may produce free coagulase.
Tube coagulase test
detects free coagulase (extracellular proteins) Emulsify 2-3 colonies in 0.5ml of plasma. Incubate at 35ºC for 4 hours and check for clot formation. If -ve after 4hrs, incubate at RT overnight: - some strains produce fibrinolysin during prolonged incubation at 35ºC (lead to a false -ve result)
Staphylococcus epidermidis
Common CoNS. 50-80% of all CoNS isolates, 90% of all skin flora. Almost all truly significant infections are nosocomial origin: -> Practices + procedures esp. implantation of medical devices. -> Surgery, instrumentation allows invasion of organism. -> Organism produce a biofilm on artificial surfaces (R to Tx + therapy IR) -> Readily acquires resistance from other bacteria. Clinical relevance should be substantiated before ID and reporting: - Purity of growth - Quantity of growth - SIte of infection - Clinical Hx
Staphylococcus saprophyticus
Commonly assoc with UTI (especially in young sexually active females) UTI + urethritis in men, Prostatitis (elderly men) Commensal of rectum, urethra and cervix (part of NF) CoNS, very bright white glossy colonies + resistant to NV.
Virulence factors of S. saprophyticus
Adherence to epithelial cells (uroepithelial, urethral and periurethral cells) Urease production - contributes to bladder tissue invasion. Produces a slime layer in the presence of urine + urease: -> therefore is very sticky in urinary system - not flushed out. -> Slime layer also gives resistance to AB, phagocytosis.
Plasma vs serum
Plasma has clotting factors serum doesn’t
Infections of Staphylococcus epidermidis
Intravascular Catheter Infections. Infectious Endocarditis. Cardiac Devices, Prosthetic Joints, and CNS Shunt Infection.
catalase negative GPC
Streptococcus and Enterococcus. - Facultative anaerobes (w/ or w/o O2) - Attack sugars fermentatively - breakdown glucose w/o O2. - Begin ID with haemolysis and/or growth characteristics on various media. Streptococci - pairs and chains (clinical smears only)
Lancfield groups
Antigenic structure Grouping based on cell wall carbohydrate “C” antigens/C substances. Groups A-H, K-V. Streptococci from groups A,B,C,D,F,G commonly isolated. - ABCFG antigens are cell wall polysaccharides. - D antigen in Group D enterococci and streptococci are lipoteichoic acids. Rapid + useful for identifying beta-haemolytic strains.
Streptococcus pyogenes (Group A)
Skin + mucous membranes of the URT. Humans are the only known reservoir. 5-15% in the throat for NF of population. Transmitted by direct contact or via secretions and aerosols. All isolates are clinically significant.
Infections of Streptococcus pyogenes
Pharyngitis/tonsilitis Erypsipelas - acute soft tissue infection by erythema + oedema. Cellulitis - inflammatory process involving large areas of skin. Impetigo (school sores) Puerperal sepsis - infection of upper genital tract post-partum. Post partum infection of neonate. Streptococcal toxic shock syndrome.
Pharyngitis/tonsillitis
2-4 day incubation before getting symptoms. Abrupt onset of fever, sore throat, headache, malaise. Grey/white exudate on tonsils. Concurrent red rash over the body Suppurative complications - sinusitis, otitis media, bacteriaemia, abscess tonsils, pharynx. Non-suppurative complications (sequelae) - acute + chronic rheumatic fever. - glomerular nephritis.
Rheumatic fever
1-5 weeks post S. pyogenes pharyngitis infection (only) Sudden onset of fever + joint pain. Cardiac murmurs, enlargement, congestive heart failure. Cross reaction of abys (antibodies) produced against strep antigens with own tissue = autoimmune response to own heart. (3-6months)
Acute glomerulur nephritis
URT infection/scarlet fever or skin/wound infection. onset 10days after pharyngitis onset 3-6weeks after skin infection deposition of abys/ag complexes in kidney - damages glomeruli. malaise, weakness, anorexia, oedema, headache, hypertension.
S. pyogenes virulence factors
- M protein: surface antigens (group A antigen, adherence to epithelial cells + resistant to phagocytosis) - streptokinase (hydrolysases fibrin barriers at the periphery of a spreading infection) - hyaluronic acid capsule (resists phagocytosis, assists the bacterial cell to adhere to host tissue + antigenically invisible) - hemolysins (O is responsible for B-haemolysis + is immunogenid in vivo, S is non-immunogenic, both are toxic to various host cells.) - Streptococcal pyrogenic exotoxins (SPE) types ABC (strep. TSS, hypotension, shock and scarlet fever)
Identification of S. pyogenes
Small colony with large zone of strong B-haemolysis. -> May have a “Hockey-puck” effect on BA. -> Fastidious - required enrichment (BA/CHOC media) Lancefield group A - agglutination tests. Bacitracin sensitive - any zone around = sensitive. PYR Test - +ve (but not usually used) S to penicillin or erythromycin. Treat with clindamycin if allergic to Pc and resistant to erythromycin.