MEDI2003 Week 7 - Gram Positive Cocci Flashcards

(35 cards)

1
Q

Gram positive cocci

A

Staphylococcus Streptococcus Enterococcus

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2
Q

Staphylococcus

A

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.

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3
Q

Staphylococcus aureus

A

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.

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4
Q

Staphylococcus aureus resistance

A

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

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5
Q

Infection of S. aureus

A

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

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6
Q

Virulence factors of S. aureus

A

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)

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7
Q

Coagulase test

A

Staphylococcal coagulase enzyme converts fibrinogen protein in plasma into insoluble fibrin threads, which results in the formation of a clot in the tube

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8
Q

Two forms of coagulase tests

A
  • Bound coagulase (cell wall) is detected by the slide coagulase test. - Free coagulase (secreted) is detected by the tube coagulase test. Use EDTA plasma
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9
Q

Slide coagulase test

A

“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.

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10
Q

Tube coagulase test

A

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)

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11
Q

Staphylococcus epidermidis

A

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

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12
Q

Staphylococcus saprophyticus

A

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.

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13
Q

Virulence factors of S. saprophyticus

A

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.

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14
Q

Plasma vs serum

A

Plasma has clotting factors serum doesn’t

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15
Q

Infections of Staphylococcus epidermidis

A

Intravascular Catheter Infections. Infectious Endocarditis. Cardiac Devices, Prosthetic Joints, and CNS Shunt Infection.

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16
Q

catalase negative GPC

A

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)

17
Q

Lancfield groups

A

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.

18
Q

Streptococcus pyogenes (Group A)

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.

19
Q

Infections of Streptococcus pyogenes

A

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.

20
Q

Pharyngitis/tonsillitis

A

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.

21
Q

Rheumatic fever

A

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)

22
Q

Acute glomerulur nephritis

A

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.

23
Q

S. pyogenes virulence factors

A
  • 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)
24
Q

Identification of S. pyogenes

A

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.

25
Group B Streptococcus
Streptococcus agalactiae NF in URT, GIT, Genital tract (10-35% women carry it vaginally) Neonatal disease - neonates acquire organism in utero before delivery, during birth or after birth, 1 in 2 infants from colonised mothers become colonised, pregnant women screened for group B prior to delivery. (36/40) -> Septicaemia, pneumonia meningitis in newborn Elderly/immunocompromised at risk of various infections including systemic infection and wounds.
26
Virulence factors of S. agalactiae
1) Capsular polysaccharide 2) Enzymes - hyalurodinase + C5a peptidase (interferes with immune response) 3) Beta haemolysin - toxic to lung endothelial cells. 4) Lipoteichoic acid - adherence
27
S. agalactiae characteristics
Large colony with a narrow zone of B or gamma haemolysis. (hazy edge to colonies) Lancefield Group B. R to bacitracin Bile tolerant, aesculin negative. Hippurate + Can treat infections with penicillin. Some R to erythromycin and clindamycin. Can also use ampicillin, cefotaxime or ceftriaxone.
28
Group C, F and G streptococci
NF (GIT, vagina, skin and oropharynx) Infections: septicaemia, cellulitis, pneumonia, tonsillitis/pharyngitis, meningitis, endocarditis, abscess. B-haemolytic, similar colony morphology to group A. ID first by agglutination + only report group if no APISTREP, VITEK or MALDI-TOF available. Treat w/ penicillin, ampicillin, erythromycin, cephalosporins.
29
Streptococcus pneumoniae
NF in the URT of 5-10% adults. Infections: pneumonia, septicaemia, meningitis, sinusitis, otitis media + mastoiditis. Predisposing factors to infection: bronchopulmonary disease, compomised humoral immunity (decreased abys 65yrs) + viral infection of the lungs. GP diplococcus w/ lancet shape (one side flattened when joined) Fastidious (BA/CHOC), Two colony types (mucoid- smooth, draughtsman- rough) Alpha haemolytic - narrow zone NOT TYPEABLE by Lancefield grouping. Optochin sensitive, Bile soluble. treat w/ cephalosporins, erythromycin + tetracycline.
30
Virulence factors of streptococcus pneumoniae
polysaccharide capsule, alpha haemolysin Enzymes: hyalurodinase, neuraminidase (cell adherence) + IgA1 proteases. Increasing resistance to penicillin.
31
Viridans streptococci
NF of the mouth, GIT and Urogenital tract. Can cause - dental caries + endocarditis especially sub-acute bacterial endocarditis = septicaemia. Virulence factors - produce hydrolytic enzymes in the mouth = plaque build up + also have capsules. Sensitive to Tx with penicillin. Alpha or non-haemolytic, small colonies (grey-white), R to Optochin disc + R to 10% desoxycholate (Bile solubility test)
32
Group D streptococcus
Normal GIT flora. Non-enterococcal Group D streptococci. Lancefield group D antigen (glycerol-teichoic acid is the D antigen) Group D streptococci ARE NOT 6.5% salt tolerant and are PYR neg. Group D enterococci are 6.5% salt tolerant and are PYR pos. Streptococcus bovis (lac fermenter on MAC), Streptococcus equinus (non-lactose fermenting on MAC)
33
PYR test
1. Purpose of test is to look for a particular ENZYME a. L-PYRROLIDONYL ARYLAMIDASE b. Used for identification of GROUP A STREPTOCOCCI (S. PYROGENES) and ENTEROCOCCI L-pyrrolidonyl-B-naphthylamide -enzyme--> B-naphthylamine. B-naphtylamine + p-dimethylaminocinnamaldehyde reagent --> bright red colour (pos)
34
Enterococcus Group D
NF in the gut + vaginal flora. Found in soil, water and food = poor human hygiene if contracted. E. faecalis most common 70-90% of human clinical isolates. E. faecium 5-25% of human isolates. Other species 1-5% Group D antigen pos, usually grey, non-haemolytic, SOME B + A haemolytic. ALL ARE BILE TOLERANT (MAC+) and aesculin POS. Propensity to acquire AB resistance - difficult to Tx, VRE thought to be due to industrial Avoparcin usage.
35
Enterococcus infections
UTI (most are caused by enterococci, nosocomial origin or there's a Hx urinary structural abnormalities or instrumentation of the urinary tract. Abdominal infections, peritonitis, endometritis, endocarditis, septicaemia + meningitis.