Streptococci Flashcards
What are streptococci
Gram positive cocci, chains
Pneumoniae usually in pairs
What are the classifications of streptococci by haemolysis?
Blood agar plate - horse blood contains in tact RBCs
Alpha haemolysis - some bacteria can only partially break down RBCs, not really able to utilise nutrients as fully as beta- tend not to be frequent causers of invasive disease - most frequent = endocarditis - viridans streptococci e.g. streptococcus pneumoniae (Capsule - Thick sugar coating over surface of cells - pneumoniae, Capsule choke neutrophils)
Beta haemolysis - some bacteria break the RBCs down completely by haemolysin - bacteria can take up the iron and utilise it for bacterial growth = beta e.g. streptococcus pyogens (pus forming)
Non-haemolytic (gamma) - e.g. enterococcus faecalis
What are the classification schemes for streptococci
• Lancefield, 1933 – Serological classification of beta-haemolytic streptococci, based on cell wall antigens
• Sherman, 1937 – pyogenic, viridans, enterococcal, lactic streptococci
• 16S ribosomal RNA sequences
See slide for table
What is streptococcus pyrogenes
Lancefield group A beta-haemolytic streptococcus
See slide for agar image
What are the streptococcus pyrogens virulence factors and their actions
Hyaluronic acid capsule - Action/s Inhibits phagocytosis by neutrophils and macrophages. Poor immunogen because of similarity to human connective tissue hyaluronate
M protein - Resistance to phagocytosis by inhibiting activation of alternative complement pathway on bacterial cell surface. > 150 antigenically different serotypes as a consequence of nucleotide variants of emm gene.
Adhesins, including lipoteichoic acid, M protein, fibronectin binding proteins - Adherence is first step in colonisation/infection
Streptolysins O and S - Lysis of erythrocytes, neutrophils, platelets
Dnases A, B, C and D - Degradation of DNA
Hyaluronidase - Degradation of hyaluronic acid in connective tissue
Streptokinase - Dissolution of clots through conversion of plasminogen to plasmin - bacteria can invade
Streptococcal pyrogenic exotoxins - Cleaves Ig G bound to Group A strep. Member of superantigenic. Spe family (clonal T-cell proliferation)
What are streptococcus pyrogens M proteins?
-
What is streptococcal pharyngitis?
• Streptococcus pyogenes
• Peak incidence 5-15 years
• Droplet spread - relatively large particles
- aerosols - few microns in diameter - spread very widely
• Association with over- crowding
• Untreated patients develop M protein specific antibody - they will be unlikely to get this strain of infection again - benefit of no treatment
Clinical features
Abrupt onset sore throat, Malaise, fever, headache, Lymphoid hyperplasia, Tonsillopharyngeal exudates, Throat swab -> Group A strep
What is scarlet fever?
A complication of streptococcal pharyngitis - Scarlet fever
• Due to infection with streptococcal pyrogenic exotoxin strain of S.pyogenes
• Local or haematogenous spread
• High fever, sepsis, arthritis, jaundice
• 1800’s epidemics with 20% mortality
What are the suppurations complications of streptococcal pharyngitis?
Suppurative complications - pus forming • Peritonsillar cellulitis/abscess • Retropharyngeal abscess • Mastoiditis, sinusitis, otitis media • Meningitis, brain abscess - Can spread from lateral pharyngeal space into carotid artery - bacteria can spread into brain
Tonsil abscess can burst and rupture into lateral pharyngeal space - downed spread through the neck - thoracic infection
Can also spread to bone
What are immunological complications of streptococcal pharyngitis?
Both are immune reaction - both follow group a strep infection
Body produces antibodies which cross react with host tissues - antibody response causes these manifestations
Acute rheumatic fever - antibiotics have no effect - management aimed at reducing inflammatory response • Inflammation of heart, joints, CNS • Follows on from pharyngitis • Rheumatogenic M types • Possible mechanisms: – Auto-immune – Serum sickness – Binding of M protein to collagen – ASO, ASS induced tissue injury
Acute post-streptococcal glomerulonephritis - some group A streps
• Acute inflammation of renal glomerulus
• M type specific but NOT same as ARF M types
• Antigen-antibody complexes settle in glomerulus - produce inflammatory response
What are streptococcus pyogens skin infections?
Impetigo, erysipelas, cellulitis, necrotising fasciitis
What is impetigo
Impetigo
– Childhood infection, 2-5 years
– Initial skin colonisation, followed by intradermal innoculation
– No ARF but impetigo is most common cause of glomeruonephritis
- honey coloured lesions around mouth
- superficial infection with group A strep
- usually self resolving
What is erysipelas?
• Erysipelas
– Dermis infection with lymphatic involvement
– Face, lower limbs
– Facial lesions (red raised swollen hot - see slide) frequently preceded by pharyngitis
– Lower limb infection usually secondary to invasion of skin via trauma, skin disease or local fungal infection
What is cellulitis?
Cellulitis
– Skin and subcutaneous tissue infection
– Impaired lymphatic drainage and illicit injecting drug use important risk factors
- one limb
- make sure they are drying off properly etc
What is necrotising fasciitis?
• Necrotising fasciitis
– Infection of deeper subcutaneous tissues and fascia.
– Rapid, extensive necrosis
– Usually secondary to skin break - group A strep got in
– Severe pain, even before gross clinical changes
– High fever, fulminant course, high mortality (20-70%)
- deepest subcutaneous tissues and fascia tissues, even muscle,
- extensive surgery to remove necrotic tissue, limb amputation,
- intravenous immunoglobulin - give antibodies against streptococci -
