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Gram Positive Cocci - Strep & Staph Flashcards

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1
Q

Streptococci vs Staphylococci

A
  1. Chains vs clusters (grape-like granules)

2. Catalase negative vs catalase positive (degrades H2O2 into O2 & H2O, bubbles show a positive reaction)

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2
Q

Classification of streptococci

A

hemolytic reaction on BLOOD AGAR

Alpha-hemolytic streptococci - partial RBC hemolysis - greenish zone

  1. Streptococcus pneumoniae - optochin sensitive
  2. Other/viridans - S. oralis, S. mitis, S. mutans - optochin resistant

Beta-hemolytic streptococci - full RBC hemolysis - secrete exotoxins (hemolysins), lyse RBCs

  • Lancefield groups - diff carb Ags detected on the surface
    1. Group A: Streptococcus pyogenes
    2. Group B: Streptococcus agalactiae
    3. Group C & G
    4. Group D:
    • Enterococci (alpha/beta/non-hemolytic)
    • Streptococcus bovis

Gamma/Non-hemolytic streptococci - no RBC hemolysis

Anginosus group (alpha/beta/non-hemolytic, Group A/C/F/G/none)

Abiotrophia spp (nutritionally variant streptococci)

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3
Q

Classification of staphylococci

A

Coagulase positive
1. Staphylococcus aureus

Coagulase negative

  1. Staphylococcus lugdunensis
  2. Staphylococcus saprophyticus
  3. Staphylococcus epidermidis
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4
Q

Epidemiology of strep pneumoniae

A
  • not normal flora but carried in throat
  • more common in the presence of predisposing factors (age, chronic disease, immunosuppression)
  • dangerous in patients unable to produce immunoglobulin/have no spleen/hyposplenism
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5
Q

Transmission of strep pneumoniae

A

Respiratory droplets

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6
Q

Virulence factors of strep pneumoniae (2)

A
  1. Anti-phagocytic capsule - different strains have different capsule types & confer type-specific immunity - capsule Ags are vaccine targets
  2. Pneumolysin - membrane damaging toxin
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7
Q

Clinical presentations of strep pneumoniae (4)

A
  1. Pneumonia - common, lobar consolidation, complications: lung abscess, empyema
  2. Meningitis - high mortality, deafness common
  3. Bacteremia & Septicemia - seeding to other organs eg meninges, joints, pericardium
  4. URTI, sinusitis, otitis media
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8
Q

Diagnosis of strep pneumoniae (2)

A
  1. Culture - blood & site specific samples eg sputum & CSF for pneumonia & meningitis - colonies w central depressions & raised rims - draughtsman colonies
  2. Antigen detection in urine
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9
Q

Treatment & prevention of strep pneumoniae

A
  1. RTIs - IV benzylpenicillin/oral amoxycillin - but often treated empirically with wider spectrum antibiotics (cephalosporins, fluoroquinolones), but disrupts normal flora - increasing resistance due to PBP mutations
  2. Meningitis - ceftriaxone + vancomycin - penicillins do not penetrate BBB as well
  3. Pneumococcal vaccines
    - Older vaccine: polysaccharide capsule from 23 strains of pneumococci
    - Newer vaccine: conjugate vaccine (capsule polysaccharide + protein carrier)
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10
Q

Transmission & clinical presentations of viridans streptococci (3)

A

Normal flora of GIT, mouth
1. Dental procedures, chewing

  1. Dental caries (S. mutans)
  2. Mucosa associated infections
  3. Infectious endocarditis
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11
Q

Transmission of strep pyogenes

A
  1. Respiratory droplets

2. Direct contact

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12
Q

Virulence factors of strep pyogenes (4)

A
  1. M protein - surface component which prevents phagocytosis & killing
  2. Streptococcal pyrogenic exotoxins - SPEs types A, B, C cause fever; A & C - erythrogenic toxins - cause scarlet fever; A is assoc w severe invasive disease & streptococcal toxic shock syndrome
  3. Streptolysins O & S - responsible for beta-hemolysis & damage certain host cells eg leukocytes
  4. Hyaluronidase - breaks down intercellular cement, allowing for spread through tissues
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13
Q

Clinical presentations of strep pyogenes (7)

A
  1. Pharyngitis/tonsillitis
    - complications: peritonsillar abscess (quinsy), sinusitis, otitis media, mastoiditis, pneumonia (unusual, may follow viral infections eg influenza)
  2. Scarlet fever - generalized rash & circumoral pallor (around the mouth)
  3. Necrotizing fasciitis
  4. Streptococcal toxic shock syndrome - acute illness w fever, hypotension, multi organ failure (SPE A)
  5. Non-suppurative complications - not due to direct spread but due to self-limiting autoimmunity, attacks body tissues
  6. Acute glomerulonephritis (AGN) - may develop acute renal failure
  7. Acute rheumatic fever (ARF)
    - leading cause of childhood heart disease - recurrent attacks & cumulative damage to heart valves - rheumatic heart disease
    - occurs after pharyngeal infection by strep pyogenes, assoc w particular M types
    - Revised Jones Criteria for diagnosis: 2 major/1 major + 2 minor, with evidence of recent strep infection (maj: carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules; min: fever, arthralgia, elevated acute phase reactants, prolonged P-R interval
    - symptomatic treatment + eradicate strep (IM benzathine penicillin or 10d course oral penicillin)
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14
Q

Diagnosis of strep pyogenes (2)

A
  1. Serology: Anti-streptolysin O (ASO), Ab to hyaluronidase, DNAse B
  2. Gram stain & clinical picture, grows well in culture
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15
Q

Treatment of strep pyogenes

A
  1. Penicillin, erythromycin
  2. Clindamycin for severe infection w necrotizing fasciitis - inhibits protein synthesis - toxin production + removal of dead/infected tissue
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16
Q

Virulence factors & clinical presentations of strep agalactiae (2)

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A

Normal flora of vagina & colon
1. Different capsular polysaccharide types

  1. Neonatal sepsis
    - early onset - likely septicemia, pneumonia, meningitis
    - late onset - usually meningitis
  2. Maternal post-partum infections
17
Q

Treatment & prevention of strep agalactiae (1+2)

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A
  1. Penicillin + gentamicin in severe infections
  2. Prophylactic penicillin
  3. Research into vaccines
18
Q

Associations & clinical presentations of group C & G strep (3)

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A
  • Group C pharyngitis associated with unpasteurised milk
  • Group G cellulitis associated with pre-existing lymphedema
  1. Sore throat
  2. Soft tissue infections + other forms of invasive sepsis
  3. Occasionally AGN (C) & scarlet fever (G)
19
Q

Clinical presentations of enterococci (group D) (4)

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A
  1. UTI
  2. Intra-abdominal infections
  3. Endocarditis
  4. Impt cause of nosocomial infection
20
Q

Treatment of enterococci (group D) (3)

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A
  1. RESISTANT to cephalosporins - those receiving broad spectrum antibiotics are highly susceptible to enterococci (damage of normal flora)
  2. Penicillin/ampicillin/vancomycin
    - E. faecalis is sensitive, E. faecium is increasingly resistant to ampicillin, VRE are becoming more common
  3. Endocarditis - cell wall active agent (ampicillin, vanco) + aminoglycoside (gentamicin)
21
Q

Clinical presentations of strep bovis (3)

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A

Normal flora in the colon

  1. Hepatobiliary sources
  2. Endocarditis
  3. Bowel carcinoma, colon cancer
22
Q

Treatment of strep bovis (2)

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A
  1. Penicillin

2. Cephalosporins

23
Q

Transmission of staph aureus

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A

Not normal flora, but carried by ~30% of the population

  • Direct/indirect (fomites, prostheses, lines) contact from sites of colonization to skin/mucous membranes
  • commonly carried in ant nares, axilla, groin, perineum & transient carriage on the hands/heavy carriage by those w chronic skin diseases eg eczema
24
Q

Virulence factors of staph aureus (3)

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A
  1. Cell wall components - contribute to binding to host molecules (adhesion) - most strains produce protein A which binds Fc portion of IgG, inhibits opsonisation
  2. Extracellular proteins (enzymes)
    - degradative enzymes break down host molecules & provide nutrients, some have leukocidins that specifically destroy phagocytes
  3. Extracellular proteins (toxins)
    (A) Enterotoxins A-E: heat stable, cause food poisoning
    (B) Toxic shock syndrome toxin-1 (TSST-1): superantigen, links MHCII on Ag presenting cell to T lymphocytes - activating T cells - massive cytokine release - toxic shock syndrome
    (C) Epidermolytic exotoxins A & B: cause intra-epidermal blisters (Bullous Impetigo) locally near site of infection, if absorbed & spread systematically - Staphylococcal scalded skin syndrome, Ritter’s disease/pemphigus neonatorum
25
Clinical presentations of staph aureus ( 6)
Localised infections 1. Skin infections: boil (furuncle) - hair follicle/sebaceous gland invaded by bacterium; carbuncle - multiple sites in 1 area; impetigo - superficial; stye - infection of sebaceous gland; cellulitis - deeper subcut tissue; folliculitis - often results in pus formation Internal sites 2. Deep abscesses (muscles, kidney, brain, lung) - common cause of osteomyelitis & septic arthritis, deep tissue accessed via blood stream (hematogenous spread) or trauma/surgery (post operative wound inf) 3. Endocarditis 4. Line infections eg intravascular catheters - bacteremia 5. Pneumonia - sec to influenza/assoc w R sided endocarditis esp IV drug abusers - cannonball lesions 6. SSSS, TSS, food poisoning (due to toxins)
26
Diagnosis of staph aureus (3)
1. Typing (phage typing, PFGE, MLST - compare genome seq) 2. Specimens eg tissues, pus - culture on blood agar - catalase & coagulase positive 3. Mass spectrometry
27
Treatment of staph aureus (5)
1. I+D - debridement of devitalised tissue, drain pus, remove foreign material 2. Penicillin - beta-lactamase producing strains - beta-lactamase stable cloxacillin - penicillin allergic - erythromycin 3. Co-amoxiclav, cephalosporins - active, but damages flora 4. MRSA - does not respond to penicillins, cephalosporins, carbapenems except - Ceftaroline & Ceftobiprole - MRSA is due to mutation in mecA gene of PBP2A, drugs cannot bind well - MRSA is resistant to multiple antibiotics - need more toxic drugs - vanco, linezolid, daptomycin 5. Mupirocin - topically for superficial infections, eradicate nasal carriage
28
Virulence factors of staph lugdunensis, saprophyticus, epidermidis
Normal flora (skin, perineal) 1. Produces slime - large amounts of extracellular material - insulation from infections & adhesion to materials introduced into the body - slime + bacteria = biofilm
29
Clinical presentations of staph lugdunensis (4)
1. Perineal/buttock wound infections 2. Endocarditis 3. Vertebral osteomyelitis 4. Infection related to prosthetic material eg prosthetic valve endocarditis, replacement artificial joints, plastic lines, line related sepsis
30
Clinical presentations of staph saprophyticus
1. UTI esp sexually active young women
31
Treatment & prevention of staph lugdunensis, saprophyticus, epidermidis
1. Remove foreign material if necessary 2. Vancomycin (frequently multi resistant) 1. Surgical theatres with HEPA filters & laminar flow air systems - keep air clean - reduce infections inoculated by accident during surgery

microb - bacteria (11 decks)

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