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microb - bacteria > Gram Positive Cocci - Strep & Staph > Flashcards

Gram Positive Cocci - Strep & Staph Flashcards

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)

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)

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)

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)

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

Treatment of enterococci (group D) (3)

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)

A

Normal flora in the colon

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

Treatment of strep bovis (2)

A
  1. Penicillin

2. Cephalosporins

23
Q

Transmission of staph aureus

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)

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
Q

Clinical presentations of staph aureus ( 6)

A

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

  1. 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)
  2. Endocarditis
  3. Line infections eg intravascular catheters - bacteremia
  4. Pneumonia - sec to influenza/assoc w R sided endocarditis esp IV drug abusers - cannonball lesions
  5. SSSS, TSS, food poisoning (due to toxins)
26
Q

Diagnosis of staph aureus (3)

A
  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
Q

Treatment of staph aureus (5)

A
  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
Q

Virulence factors of staph lugdunensis, saprophyticus, epidermidis

A

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
Q

Clinical presentations of staph lugdunensis (4)

A
  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
Q

Clinical presentations of staph saprophyticus

A
  1. UTI esp sexually active young women
31
Q

Treatment & prevention of staph lugdunensis, saprophyticus, epidermidis

A
  1. Remove foreign material if necessary
  2. Vancomycin (frequently multi resistant)
  3. 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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