Streptococcus, Enterococcus Flashcards
1
Q
What are the microbiological characteristics of Streptococcus?
A
- gram (+) cocci
- aerobic or facultatively anaerobic
- commonly grouped by: (hemolysis (a, B, gamma); Lancefield group (surface antigens identified serologically)
- can be fastidious - requires blood or serum in media to grow
- differentiate from Staphylococcus (other Gram (+) cocci) using catalase test (also staph forms clusters where strep forms chains)
2
Q
What is the biocontainment level of Streptococcus?
A
2
3
Q
What is Streptococcus’s/ Enterococcus’s natural host or habitat?
A
- host associated, part of the normal microbiota (mucous membranes & respiratory tract (Streptococci); intestinal tract (Enterococci))
- carriers of these organisms are the primary source
- environmental contamination w/ Enterococcus sp associated w/ nosocomial infections
4
Q
What are options for biochemical identification?
A
- commercial biochemical strip test (each well of the strip contains a reagent that the bacteria can react with producing a colourimetric change
- CAMP test
5
Q
What is Lancefield grouping?
A
- named after Rebecca Lancefield who developed this
- Groups A, B, C, F, & G are polysaccharides
- Group D is a lipoteichoic acid
- some organisms fail to group w/ Lancefield antisera (S. suis)
6
Q
What virulence factors does Streptococcus have?
A
- MSCRAMMs
- exotoxins (superantigen - Streptococcus pyogenes)
- phage mediated superantigen (some Streptococcus canis)
- capsule (prevents phagocytosis, some capsules composed of hyaluronic acid are indistinguishable from some host tissues - may explain post-infection autoimmunity)
- hemolysins (cytotoxic to eukaryotic cells)
- CAMP factor (pore forming toxin)
7
Q
How may Mozart have died?
A
- Dec 5, 1791
- evidently, he was working on his Requiem on his death bed
- records from the time describe a localized epidemic of deaths involving “edema”
- Mozart reportedly had an “inflammatory fever” earlier that fall
- speculation that Mozart may have suffered from Strep throat (Streptococcus pyogenes), followed by post-streptococcal glomerulonephritis (infection may stimulate production of cross-reactive antibodies)
8
Q
What is the clinical significance of Streptococcus agalactiae?
A
- contagious mastitis (infected cows are the source)
- mainly subclinical disease w/ bouts of illness (not systemically ill)
- disease suggests breakdown of biosecurity (teat hygiene, cleaning milk equipment, handwashing)
- intra-mammary antibiotics (unlike staph, many strep remain penicillin susceptible)
9
Q
What is the clinical significance of Streptococcus dysgalactiae?
A
- environmental mastitis (contamination of teats from environment/bedding)
- often subclinical
- suggests management issue (improve cleanliness, better bedding, access to shelter)
- treatment (dry cow treatment & teat sealer)
10
Q
What is the clinical significance of Streptococcus equi subsp equi?
A
- normal inhabitant of upper respiratory tract
- strangles (abscessation of submandibular & retropharyngeal lymph nodes)
- transmitted by contact w/ nasal secretions/discharge from abscesses; either direct contact or fomites; very contagious (high morbidity, low mortality) - ISOLATION IS KEY - prevent transmission)
- 2-6 day incubation period
- penicillin is treatment of choice
- long term sequelae following infection possible: metastatic abscesses “bastard strangles” (hematogenous spread to lung, liver, mesentery, spleen, kidneys, & brain); purpura hemorrhagica (vasculitis secondary to deposition of immune complexes (type III hypersensitivity)); guttural pouch empyema
- transfer of immunity in colostrum - protects foals until weaned
- vaccines are available
11
Q
A