Streptococcus Classification, S. pyogenes, OmpathStudy

--- STREPTOCOCCUS — CLASSIFICATION Classified primarily by haemolytic properties : alpha (partial/green haemolysis), beta (complete haemolysis), non-haemolytic (gamma) This — not Lancefield grouping — is the single most important method for classifying/speciating streptococci (tested directly) Streptococcus pneumoniae (pneumococci) — alpha-hemolytic, can be serotyped based on their polysaccharide capsule Enterococci — group D streptococci, classified by ability to grow in 6.5% sodium chloride and 45% bile ; most strains sensitive to penicillin, sulfonamides, cephalosporins, gentamicin, streptomycin (NOT resistant, as a distractor claims) Viridans streptococci — alpha-hemolytic; NOT identified by Lancefield grouping (that's the wrong statement in the "except" question) — Lancefield grouping is based on the C-carbohydrate in the cell wall and applies to other groupable streptococci Pneumococci vs viridans streptococci — both alpha-hemolytic but differentiated by bile solubility test and susceptibility to optochin (pneumococci are bile-soluble and optochin-sensitive; viridans strep are not) Group B Streptococcus ( S. agalactiae ) — part of normal vaginal flora, but can cause neonatal meningitis — a key exception to "normal flora doesn't cause disease" STREPTOCOCCUS PYOGENES — VIRULENCE FACTORS AND PATHOGENESIS (5–20 marks, appears repeatedly) Toxins: Streptolysin O and S (hemolysins) — responsible for hemolysis and leukocidal activity (kill white blood cells) Pyrogenic/erythrogenic toxin (scarlet fever toxin) — a superantigen, causes the scarlet fever rash and anti-inflammatory/immune-inhibiting effects Enzymes (spreading factors): Streptokinase — promotes lysis of fibrin by converting plasminogen to plasmin DNase (streptodornase) — depolymerizes DNA, liquefying pus Hyaluronidase — breaks down hyaluronic acid in connective tissue, aiding spread through tissue Lipase — degrades lipids/phospholipids on host cell membranes Cell wall components: Capsule — antiphagocytic (protects from being engulfed by phagocytes) M protein — major virulence factor, gives rigidity, resists phagocytosis, and is the antigen basis for immune classification (also key in rheumatic fever pathogenesis via molecular mimicry) Pili — mediate attachment to host cells Clinical complications caused by S. pyogenes : pharyngitis, scarlet fever, rheumatic fever — "all of the above" is the typical MCQ answer Complication of streptococcal pharyngitis specifically: rheumatic fever (not pseudomembrane formation, not meningococcemia — those belong to other organisms) RHEUMATIC FEVER vs ACUTE GLOMERULONEPHRITIS (post-streptococcal complications — 10 mark comparison, repeated) Site of infection that precedes each: Glomerulonephritis — can follow either skin or throat infection Rheumatic fever — follows throat infection only Latent period before onset: Glomerulonephritis — 1–3 weeks Rheumatic fever — 2–5 weeks Prior sensitization needed: Glomerulonephritis — not essential Rheumatic fever — essential Repeated attacks: Glomerulonephritis — absent; one heals completely, doesn't recur from the same episode pattern Rheumatic fever — repeated attacks are common Serotypes responsible: Glomerulonephritis — nephritogenic strains, associated with skin and throat serotypes Rheumatic fever — associated with throat serotypes specifically Clinical manifestation: Glomerulonephritis — hematuria, albuminuria, edema; pathology at the base of the glomerulus Rheumatic fever — swelling of joints, inflammation of heart muscle (myocarditis, pericarditis, endocarditis) Pathogenesis: Glomerulonephritis — antibody-antigen immune complex deposition at the glomerulus (type III hypersensitivity) Rheumatic fever — antibody against the streptococcal antigen cross-reacts with heart tissue antigen (molecular mimicry, type II hypersensitivity) --- STAPHYLOCOCCUS Coagulase test — differentiates S. aureus (coagulase-positive) from S. epidermidis (coagulase-negative) Nose is the most likely source of S. aureus in an outbreak of neonatal nursery sepsis (normal flora reservoir) Toxin-mediated diseases from S. aureus : Scalded skin syndrome — caused by exfoliative toxin (exfoliatin) Toxic shock syndrome — caused by TSST-1 (a superantigen); classic scenario: nasal tampon left in place post-surgery, fever, hypotension, diffuse erythematous rash including palms/soles, elevated liver enzymes, renal failure Food poisoning (food intoxication, not infection) — caused by a preformed enterotoxin in food; rapid onset (~2 hours), vomiting-predominant Biofilm-related infection (e.g., long-term central venous catheter with S. epidermidis ): The complex molecular interactions within the biofilm make it difficult to provide effective antimicrobial therapy — catheter often needs removal to cure infection Biofilm does NOT wash off easily, and bacteria in it are NOT more susceptible to antibiotics from slowed metabolism (both are wrong distractors) Associated with formation of a bacterial biofilm: classic examp