Gram Positive Cocci - Strep & Staph Flashcards
Streptococci vs Staphylococci
- Chains vs clusters (grape-like granules)
2. Catalase negative vs catalase positive (degrades H2O2 into O2 & H2O, bubbles show a positive reaction)
Classification of streptococci
hemolytic reaction on BLOOD AGAR
Alpha-hemolytic streptococci - partial RBC hemolysis - greenish zone
- Streptococcus pneumoniae - optochin sensitive
- 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)
Classification of staphylococci
Coagulase positive
1. Staphylococcus aureus
Coagulase negative
- Staphylococcus lugdunensis
- Staphylococcus saprophyticus
- Staphylococcus epidermidis
Epidemiology of strep pneumoniae
- 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
Transmission of strep pneumoniae
Respiratory droplets
Virulence factors of strep pneumoniae (2)
- Anti-phagocytic capsule - different strains have different capsule types & confer type-specific immunity - capsule Ags are vaccine targets
- Pneumolysin - membrane damaging toxin
Clinical presentations of strep pneumoniae (4)
- Pneumonia - common, lobar consolidation, complications: lung abscess, empyema
- Meningitis - high mortality, deafness common
- Bacteremia & Septicemia - seeding to other organs eg meninges, joints, pericardium
- URTI, sinusitis, otitis media
Diagnosis of strep pneumoniae (2)
- Culture - blood & site specific samples eg sputum & CSF for pneumonia & meningitis - colonies w central depressions & raised rims - draughtsman colonies
- Antigen detection in urine
Treatment & prevention of strep pneumoniae
- 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
- Meningitis - ceftriaxone + vancomycin - penicillins do not penetrate BBB as well
- Pneumococcal vaccines
- Older vaccine: polysaccharide capsule from 23 strains of pneumococci
- Newer vaccine: conjugate vaccine (capsule polysaccharide + protein carrier)
Transmission & clinical presentations of viridans streptococci (3)
Normal flora of GIT, mouth
1. Dental procedures, chewing
- Dental caries (S. mutans)
- Mucosa associated infections
- Infectious endocarditis
Transmission of strep pyogenes
- Respiratory droplets
2. Direct contact
Virulence factors of strep pyogenes (4)
- M protein - surface component which prevents phagocytosis & killing
- 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
- Streptolysins O & S - responsible for beta-hemolysis & damage certain host cells eg leukocytes
- Hyaluronidase - breaks down intercellular cement, allowing for spread through tissues
Clinical presentations of strep pyogenes (7)
- Pharyngitis/tonsillitis
- complications: peritonsillar abscess (quinsy), sinusitis, otitis media, mastoiditis, pneumonia (unusual, may follow viral infections eg influenza) - Scarlet fever - generalized rash & circumoral pallor (around the mouth)
- Necrotizing fasciitis
- Streptococcal toxic shock syndrome - acute illness w fever, hypotension, multi organ failure (SPE A)
- Non-suppurative complications - not due to direct spread but due to self-limiting autoimmunity, attacks body tissues
- Acute glomerulonephritis (AGN) - may develop acute renal failure
- 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)
Diagnosis of strep pyogenes (2)
- Serology: Anti-streptolysin O (ASO), Ab to hyaluronidase, DNAse B
- Gram stain & clinical picture, grows well in culture
Treatment of strep pyogenes
- Penicillin, erythromycin
- Clindamycin for severe infection w necrotizing fasciitis - inhibits protein synthesis - toxin production + removal of dead/infected tissue
Virulence factors & clinical presentations of strep agalactiae (2)
Normal flora of vagina & colon
1. Different capsular polysaccharide types
- Neonatal sepsis
- early onset - likely septicemia, pneumonia, meningitis
- late onset - usually meningitis - Maternal post-partum infections
Treatment & prevention of strep agalactiae (1+2)
- Penicillin + gentamicin in severe infections
- Prophylactic penicillin
- Research into vaccines
Associations & clinical presentations of group C & G strep (3)
- Group C pharyngitis associated with unpasteurised milk
- Group G cellulitis associated with pre-existing lymphedema
- Sore throat
- Soft tissue infections + other forms of invasive sepsis
- Occasionally AGN (C) & scarlet fever (G)
Clinical presentations of enterococci (group D) (4)
- UTI
- Intra-abdominal infections
- Endocarditis
- Impt cause of nosocomial infection
Treatment of enterococci (group D) (3)
- RESISTANT to cephalosporins - those receiving broad spectrum antibiotics are highly susceptible to enterococci (damage of normal flora)
- Penicillin/ampicillin/vancomycin
- E. faecalis is sensitive, E. faecium is increasingly resistant to ampicillin, VRE are becoming more common - Endocarditis - cell wall active agent (ampicillin, vanco) + aminoglycoside (gentamicin)
Clinical presentations of strep bovis (3)
Normal flora in the colon
- Hepatobiliary sources
- Endocarditis
- Bowel carcinoma, colon cancer
Treatment of strep bovis (2)
- Penicillin
2. Cephalosporins
Transmission of staph aureus
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
Virulence factors of staph aureus (3)
- Cell wall components - contribute to binding to host molecules (adhesion) - most strains produce protein A which binds Fc portion of IgG, inhibits opsonisation
- Extracellular proteins (enzymes)
- degradative enzymes break down host molecules & provide nutrients, some have leukocidins that specifically destroy phagocytes - 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
Clinical presentations of staph aureus ( 6)
Localised infections
- 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
- 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)
- Endocarditis
- Line infections eg intravascular catheters - bacteremia
- Pneumonia - sec to influenza/assoc w R sided endocarditis esp IV drug abusers - cannonball lesions
- SSSS, TSS, food poisoning (due to toxins)
Diagnosis of staph aureus (3)
- Typing (phage typing, PFGE, MLST - compare genome seq)
- Specimens eg tissues, pus - culture on blood agar - catalase & coagulase positive
- Mass spectrometry
Treatment of staph aureus (5)
- I+D - debridement of devitalised tissue, drain pus, remove foreign material
- Penicillin
- beta-lactamase producing strains - beta-lactamase stable cloxacillin
- penicillin allergic - erythromycin - Co-amoxiclav, cephalosporins - active, but damages flora
- 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 - Mupirocin - topically for superficial infections, eradicate nasal carriage
Virulence factors of staph lugdunensis, saprophyticus, epidermidis
Normal flora (skin, perineal)
- Produces slime - large amounts of extracellular material - insulation from infections & adhesion to materials introduced into the body
- slime + bacteria = biofilm
Clinical presentations of staph lugdunensis (4)
- Perineal/buttock wound infections
- Endocarditis
- Vertebral osteomyelitis
- Infection related to prosthetic material eg prosthetic valve endocarditis, replacement artificial joints, plastic lines, line related sepsis
Clinical presentations of staph saprophyticus
- UTI esp sexually active young women
Treatment & prevention of staph lugdunensis, saprophyticus, epidermidis
- Remove foreign material if necessary
- Vancomycin (frequently multi resistant)
- Surgical theatres with HEPA filters & laminar flow air systems - keep air clean - reduce infections inoculated by accident during surgery
