streptococcus / streptococcal infections

see also:

• clinically important bacteria
• VicHealth patient information sheet Group A Strept infections

• Streptococcal bacteria are Gram +ve cocci belonging to the phylum Firmicutes and the order Lactobacillales (lactic acid bacteria) and are a common cause of infection
• they grown in pairs or in chains hence the name of the genus
• there are over 50 species and most are oxidase-negative and catalase-negative, and many are facultative anaerobes
• alpha-haemolytic species produce hydrogen peroxide which lyses RBCs and these include Str. pneumoniae and Str. viridans
• beta-haemolytic species have a Streptolysin exotoxin which lyses RBCs and these include Str. pyogenes
  • two types of Streptolysin:
    • Streptolysin O:
      • an oxygen-sensitive cytotoxin, secreted by most Group A streptococcus (GAS) which affects cholesterol on cell membranes of most eukaryotic cells but especially RBCs and WBCs.
      • detecting in serum via the antistreptolysin O titre (ASOT) test which is evidence of recent infection
    • Streptolysin S:
      • an oxygen-stable cytotoxin also produced by most GAS strains which results in clearing on the surface of blood agar and which affects immune cells impairing the immune response and also is a cardiotoxic exotoxin
  • Streptokinase fibrinolytic was discovered in 1933 from beta haemolytic strept.

• see also https://en.wikipedia.org/wiki/Lancefield_grouping
• Group A Strept include S. pyogenes which is the the predominant species harboring the Lancefield group A antigen, but S. dysgalactiae can also be group A
• Group B Strept (GBS) include S. agalactiae
• Group C Strep include S. equi and S. zooepidemicus which affect horses and cattle, and S. dysgalactiae which can cause pharyngitis and pyogenic infections in humans
• Group D Strept include enterococci and S. bovis and S. equinus
• Group F Strept include the S. milleri group
• Group G Strept include S. dysgalactiae, S. phocae and S. canis
• Group H Strept include canine species which rarely infect humans unless there are dog bites

• is defined by the isolation of GAS from a normally sterile site but generally excludes cellulitis and pharyngitis
• Group A streptococcal (GAS) infection is caused by a Group A (beta-haemolytic) Streptococcus - usually Str. pyogenes (see below)
• this may be life threatening if untreated or delays to treatment and is responsible for 0.5 million deaths worldwide each year
• no vaccines are available
• risk factors:
  • age < 1 yr or age > 65 yrs
  • chickenpox
  • immunosuppressed people including systemic corticosteroid use, immunosuppressants or chemotherapy
  • burns victims
  • elderly with cellulitis, diabetes, vascular disease, or cancer
  • intravenous drug users (IVDU) or injection drug use (IDU)
  • pregnant and post-partum women have 20x risk (a cause of puerperal fever)
  • retained vaginal tampon may cause toxic shock syndrome
  • there is increased risk to household contacts of also developing iGAS and antibiotic prophylaxis such as cephalexin should be considered
    • see RCH guideline on Mx of household contacts
• example infections:
  • sepsis / septicaemia
  • Streptococcal Toxic Shock Syndrome (STSS)
  • necrotizing fasciitis
  • pneumonia / Empyema
  • Retropharyngeal abscess
  • osteomyelitis / Septic arthritis
  • meningitis
• early symptoms include:
  • high fevers, severe muscle aches, sore throat, cellulitis, erysipelas, or “sunburn-like” rash, diarrhoea or vomiting, or severe headache
• diagnosis can be confirmed by isolating group A streptococcus by culture from a normally sterile site, such as blood, cerebrospinal fluid, or pleural fluid

• see also https://en.wikipedia.org/wiki/Streptococcus_pyogenes
• Group A beta haemolytic streptococcus commonly colonises the skin, nasopharynx or anogenital tract.
• transmission by skin contact of nasal discharge or impetiginous lesions or respiratory droplets
• impetigo / school sores is highly contagious (may also be caused by Staph. aureus)
• can also be spread from cattle to humans through raw milk and contaminated foods (salads, milk, eggs)
• It can cause a wide range of clinical disease, from mild illnesses such as pharyngitis, tonsilitis, impetigo, scarlet fever, and cellulitis, to severe, life-threatening invasive infections (referred to as iGAS - see above)
• it may produce Streptococcal pyrogenic exotoxin which may cause the rash of scarlet fever or toxic shock syndrome
  • scarlet fever
    • sore throat, fever, circum-oral pallor, a bright red tongue (known as ‘strawberry tongue’)
    • classical rash: pink-red rash spreading across the abdomen, side of the chest and in the skin folds. The rash may feel like sandpaper when touched.
• treatment:
  • fortunately, this bacteria remains acutely sensitive to penicillin (unless other local commensal organisms produce β-lactamase which may result in Rx failure)
  • certain strains have developed resistance to macrolides, tetracyclines, and clindamycin
• return to social contacts such as schools or childcare
  • impetigo or pharyngitis: child can return to school after 24 hrs of antibiotic treatment. Make sure all exposed sores are covered with a watertight dressing. Ensure full course of antibiotics is taken. *
• some people will develop auto-immune diseases following these infections resulting in either:
  • rheumatic_fever
  • acute post-infectious glomerulonephritis
  • paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)
    • see https://en.wikipedia.org/wiki/PANDAS
• virulence factors:
  • a recent increase in severe infections by S. pyogenes-caused epidemic has been linked to horizontal gene transfer event that resulted in the acquisition of an allele-variant of a gene encoding an enzyme, nicotinamide adenine dinucleotide (NAD)-glycohydrolase (NADase) that controls the expression of the operon encoding the pore-forming toxin streptolysin O (SLO).
    • these pores allow S. pyogenes to enter the host cell where:
      • 1) NADase within the host cells depletes NAD, which deprives cells of adenosine triphosphate (ATP), which, in turn, leads to cell death
      • 2) enzymatically active bacterial NADase within the cell also suppresses c-di-AMP-induced and STING-mediated type I IFN (IFNβ) production to increase the virulence of humans-infecting S. pyogenes strains. There is a dynamic host-pathogen interplay between human STING genotype and bacterial NADase activity that regulates disease outcome. STING-HAQ or STING-R232H variants – exhibiting reduced c-di-AMP-binding capacity – and bacterial strains expressing high NADase activity promote poor outcome. Proficient STING-mediated type I IFN production conversely protects against host-detrimental inflammation ¹⁾

• see https://en.wikipedia.org/wiki/Streptococcus_pneumoniae
• an encapsulated, lancet-shaped diplococcus which may be alpha-haemolytic or beta-haemolytic under anaerobic conditions with a polysaccharide capsule which is a virulence factor
• more than 90 serotypes are known
• a vaccine is available
• typically colonizes the respiratory tract, sinuses, and nasal cavity
• it may become invasive when the immune system is suppressed, especially in patients who have had a splenectomy
• a common cause of:
  • community acquired pneumonia
  • otitis media
  • sinusitis
  • meningitis in children and the elderly, cerebral abscesses
  • septicaemia in immunocompromised patients such as those with HIV / AIDS
  • and may cause peritonitis

• a common cause of urinary tract infections (UTIs) / cystitis
• see Enterococci

• see also https://en.wikipedia.org/wiki/Viridans_streptococci
• normal oral commensals which may cause dental caries, and, sbe in patients with endocardial lesions
• They possess no Lancefield antigens
• are either α-haemolytic, producing a green coloration on blood agar plates (hence the name viridans), or non-haemolytic
• rarely, may cause purpuric rash with Strept Toxic Shock Syndrome eg. S. gordonii and plantar purpura ²⁾

• Group B Strept
• normally,a harmless commensal bacterium colonizing the gastrointestinal and genitourinary tracts
• a cause of neonatal meningitis and sepsis as well as meningitis in the elderly, and also bovine mastitis
• risk factors for neonates include:
  • Preterm labour (<37 weeks)
  • Prolonged rupture of membranes (>18 hours)
  • Intrapartum fever (>38C)
  • Prior GBS affected infant
  • GBS bacteriuria during this pregnancy
  • positive vaginal swab prior to normal vaginal delivery

• haematogenous spread infections usually arise from GIT and often in association with colonic carcinoma (hence all adults with GDS infection should undergo colonoscopy to Ix for occult neoplasm) or advanced liver disease (especially hep C related)
  • GDS accounts for 2-6% of infective endocarditis cultures
  • septic arthritis
  • osteomyelitis
  • prosthetic joint infection
  • vertebral discitis
  • endophthalmitis
  • adult meninigitis if immunocompromised
• may cause neonatal sepsis +/- meninigitis