Streptococcus and enterococcus Flashcards
Streptococcus meaning
Streptos = chainm coccus = grain or berry
Obligate anearobe
Killed by atmospheric oxygen
Streptococcus metabolism
General strong fermenters of carbohydrates (makes lactic acid and changes pH)
Name the six clusters of the streptococcus genus:
1) Pyogenic (pus generating) includesmost of the pathogens
2) Mitis (pneumonia) - oral commensals
3) Anginosus (commensal oral)
4) Salivarius (commensal oral)
5) Bovis (colon)
6) Mutans (colonises tooth surfaces - some are dental caries)
Almost all are opportunistic pathogens if they gain acces to blood stream.
Haemolytic activity in streptococci
Investigations have shown that the pyogenic strains posses bacterial haemolysins that can break of red blood cells (this process is called beta haemolysis) - this gives clear area around pyogenic strains grown on blood agar.
Commensal streptococci don’thave this but causes oxidation of haemoglobin by hydrogen peroxide (alpha hemolysis). This is green (viridis in latin - viridans streptococci)
Lancefield grouping
The different species of the pyogenic streptococci has been shown to have different cell wall components called lancefield grouping. (see images).
Streptococcus Pyogenes
Lancefield group A. Respiratory tract, skin and soft tissue infections.
Virulence factors of streptococcus pyogenes:
1) F-protein interacts with fibronectin in connective tissue and on cells mediating cell internalisation.
2) M-protein - binds host protein and thereby masks the bacterialo cell from phagocytosis.
3) Some strains produce hualrounic acid capsule that disguises the bacterium
4) C5a peptidase
5) Streptolysin O (oxygen) and S (serum soluble) - lysis of blood cells.
6) pyrogenic exotoxins (generates fever) -SPE-A to C
7) Hyaluronidase - degrades connective tissue
8) Streptokinase - Plasmin activating (breaks down fibrin) which makes invasion easier.
Most normal non-invasive strep. pyogenes infections:
1) Pharyngitis (inflammation in the pharynx, enlarged tonsils, sore throat) - strep throat
2) Scarlet fever - after pharyngitis a red rash is seen usually in chest region and the mucuos membrane of tongue and mouth
3) Skin infections - makes pus filled regions - enters through small craks in skin
Most normal invasive strep. pyogenes infections:
1) Necrotising fascitis - enters through skin but colonises fat or fascia (bindevæv) and kills it
2) Streptococcal toxic shock syndrome - fever diarrhea etc from toxins produced by strep. pyogenes.
3) Bacteraemia - bacteria in blood
Sequalae from pyogenes:
1) Rheumatic fever - inflammtion of joints, heart mm. Autoimmune from cross reactive antibodies.
2) Acute poststreptococcal glomerulonephritis - coffee coulered urine and edema.
Streptococcus agalactiae
Group B lancefield and beta-hemolysis - exists in the colon and sometimesin the vagina.
2 different neonatal agalactiae infections:
1) Early onset - 12 hours after birth - from vagina into amniotic fluid - initially causes tiredness, low blood oxygen and apnoea - then septicimea (bloodstream infection)follws which can lead to meningitis or other stuff.
2) late onset 7 days to 3 months after birth. - purulent meningitis
Can alsoinfect non-pregnant people.
Streptococcus pneumoniae
Diplococcus (two) In the respiratory microbiota.
Strep. pneu. virulence factors
1) Anti-phagocytotic capsule
2) IgA1 protease
3) Pneumolysis - autolysid toxin that damges membranes and through that
- Neutrophil chemotaxis
- Phagocytosis
- lymphocyte proliferation
4) autolysin - cuts up own cell wall and causes massive reaction.