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BACTERIOLOGY > 7 – Streptococcus, Enterococcus > Flashcards

7 – Streptococcus, Enterococcus Flashcards

1
Q

Microbiology Characteristics

A
  • Biocontainment level 2
  • Gram-positive cocci
  • Aerobic or facultatively anaerobic
  • Can be fastidious
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2
Q

Commonly grouped by

A
  • Hemolysis
  • Lancefield group (surface antigens IDed serologically)
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3
Q

Fastidious

A
  • Requires blood or serum in media to grow
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4
Q

How do you differentiate Streptococcus+Enterococcus from Staphylococcus

A
  • Using catalase test
  • Staphy=positive
  • Strept+Entero=negative
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5
Q

Sterp vs. Entero: 2 tests

A
  • Aesculin test
  • Growth in NaCL
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6
Q

Streptococcus on agar

A
  • Chains
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7
Q

E. faecalis on blood agar

A
  • blue/grey colonies
  • non-hemolytic
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8
Q

Natural host or habitat

A
  • Host associated, part of normal microbiota
    o Mucous membranes and respiratory tract: Strept
    o Intestinal tract: Entero
  • Carriers are primary source
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9
Q

Environmental contamination with Enterococcus species associated with

A
  • Nosocomial infections
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10
Q

Taxonomy

A
  • Biochemical ID
  • Lancefield grouping
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11
Q

Biochemical ID

A
  • CAMP test
    o Looking at enhancing of hemolysis of one organism due to the presence of another
    o Positive=enhances it
  • Commercial biochemical strips
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12
Q

Lancefield grouping

A
  • Groups A, B, C, F, G are polysaccharides
  • Group D is a lipoteichoic acid
  • *if antigen present=glandular appearance
  • **some don’t group well (S. suis)
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13
Q

Virulence factors

A
  • MSCRAMMs
  • Exotoxins
  • Phage mediate superantigen
  • Capsule
  • Hemolysins
  • CAMP factor
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14
Q

Capsule

A
  • Prevents phagocytosis
  • Some composed of hyaluronic acid indistinguishable from some host tissues (may explain post-infection autoimmunity)
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15
Q

Hemolysins

A
  • Cytotoxic to eukaryotic cells
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16
Q

CAMP factor

A
  • Pore forming toxin
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17
Q

Mozart’s death

A
  • Epidemic of deaths involving edema
  • Previous to death: inflammatory fever
  • *may have suffered Strept throat
    o Had post-streptococcal glomerulonephritis
    o *infection may stimulate production of cross-reactive antibodies
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18
Q

Clinical significance: S. pyogenes

A
  • Humans
  • Ex. strept throat, necrotizing fascilitis
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19
Q

Clinical significance: S. pneumoniae

A
  • Humans: opportunistic and skin infections
  • Horses: pneumonia
  • Guinea pigs: pneumonia
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20
Q

Clinical significance: S. agalactiae (mastitis)

A
  • CONTAGIOUS mastitis
  • Source=infected cows
  • Mainly subclinical (not systematically ill)
  • Disease suggests breakdown of biosecurity
  • Intra-mammary antibiotics (*many remain penicillin susceptible)
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21
Q

Breakdown of biosecurity: S. agalactiae

A
  • Teat hygiene
  • Cleaning milk equipment
  • Hand washing
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22
Q

Clinical significance: S. dysgalactiae (mastitis)

A
  • ENVIRONMENTAL mastitis
  • Contamination of teats from environment/bedding
  • Often subclinical
  • Suggests management issues
  • Treatment: dry cow treatment and teat sealer
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23
Q

Management issues: S. dysgalactiase

A
  • Improve cleanliness
  • Better bedding
  • Access to shelter
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24
Q

Clinical significance: S. uberis in bovine milk

A
  • CHAINS of gram-positive cocci
25
Q

Clinical significance: S. equi subsp.equi (strangles)

A
  • Normal inhabitant of upper respiratory tract
  • 2-6 day incubation period
  • High morbidity: 100%
  • Low mortality: 10%
  • *PENICILLIN is treatment of choice
  • 75% who survive=resistance
  • Transfer of immunity in COLOSTRUM
  • Vaccines available
26
Q

‘stangles’

A
  • Abscessation of submandibular and retropharyngeal lymph nodes
27
Q

S. equi subsp. Equi: strangles transmitted by

A
  • Contact with nasal secretions form abscesses
  • Direct contact or fomites
  • Very contagious
  • ISOLATION IS KEY: prevent transmission
28
Q

Long term sequale following infection of S. equi subsp equi is possible

A
  • Metastatic abscesses (‘bastard strangles’): spread throughout body
  • Purpura hemorrhagica: vasculitis (Type III hypersensitivity)
  • Guttural pouch empyema
29
Q

Clinical significance: S. canis

A
  • Infections not limited to particular anatomical site
  • *penicillin is treatment of choice
  • Necrotizing fasciitis and toxic and toxic shock syndrome (TSS)
30
Q

Clinical significance: S. canis in kittens

A
  • Respiratory
  • Skin and soft tissue infections
  • Abscessation
31
Q

Clinical significance: S. canis in dogs

A
  • Opportunistic pathogens (urinary, wounds, mammary)
32
Q

Necrotizing fasciitis and TSS

A
  • Phage superantigens expressed following exposure to FLUROQUINOLONES
    1. Lysogenic phage into bacteria chromosome
    2. When treat S. with fluroquionlones (interfere with DNA metabolism)=SOS response and get lytic phase of phage=bacteria burst
    3. Phages interact with T-cells OUT of control=massive release of cytokines=shock=hypovolemia=death
33
Q

Clinical significance: S. suis is cause of

A
  • Meningitis
  • Arthritis
  • Septicemia
  • Sudden death
  • *high case fatality rate
  • *early treatment may be effective
34
Q

Clinical significance: S. suis

A
  • Affects nursery pigs, but can affect any age
    o Acquire from sow and environment at farrowing
  • Associated with moving pigs, over-crowding and poor ventilation
  • *enters body through TONSILS
  • *discoloured ears and snout
35
Q

Clinical significance: S. suis grouped by serotype

A
  • Defined by capsular antigens
  • Currently 33 serotypes
36
Q

Clinical significance: S. suis, zoonotic infections primarily associated with serotype 2

A
  • Most commonly people with animal contacts
    o Pig farmers, vets, workers, abattoir workers, meat inspections
  • High fever
  • Malaise
  • Vomiting
  • Meningitis
  • Toxic shock
  • Coma
  • *human outbreak in China in 2005
  • *enters through cuts/scratches (also nasopharynx, GIT)
37
Q

Clinical significance: S. bovis

A
  • D group, easily mistaken for Enterococcus or Viridans Strept
  • Included in some probiotic cultures
  • *role in rumen acidosis (grain overload)
38
Q

Clinical significance: S. bovis, if isolated from suspect infection

A
  • Should consider CLINCALLY SIGNIFICANT
    o Wide variety of infections in people
    o Opportunistic infections in dogs/cats
39
Q

Clinical significance: S. bovis lactic acid producer

A
  • Increase lactic acid produced with high fermentable diets
  • Other rumen microbiota can’t metabolize lactate efficiently enough
  • Rumen pH falls below 5=kills other organisms
  • High lactate concentrations in rumen=water osmotically flows in from circulation=DEHYDRATION
  • Absorption of lactate leading to SYSTEMIC ACIDOSIS
40
Q

Chemical rumenitis causes

A
  • Damage
    o Allows organism translocation into portal vasculature and hepatic abscessation
41
Q

Clinical significance: Enterococcus spp. (chickens)

A
  • Mortality in chickens
    o *fecal contamination of eggs
  • Management is key (prevent stress, cleaning, disinfect)
  • Treat with antibiotics if catch early
  • MUST be based on susceptibility test results
42
Q

Clinical significance: Enterococcus spp. (chickens), acute

A
  • Septicemia (depression, ruffled feathers)
  • Some causes: only dead birds, first sign=death
43
Q

Clinical significance: Enterococcus spp. (chickens), subacute to chronic

A
  • Depression
  • Loss of condition
  • pyrexia
44
Q

Clinical significance: Enterococcus spp. (dog and cat)

A
  • opportunistic infections (nosocomial infections)
  • *antimicrobial resistance
    o Intrinsic and aquired
45
Q

Clinical significance: Enterococcus spp. (dogs and cats) most commonly reported

A
  • systemic infections: bacteremia, endocarditis
  • localized infections: abdominal cavity, genitourinary tract, soft tissue, respiratory tract
46
Q

Clinical significance: Enterococcus hirae(dog and cat)

A
  • associated with GI infections in dogs/cats
47
Q

Clinical significance: Enterococcus spp. (dog and cat), uncommonly causes URINARY tract INFECTIONS

A
  • frequently encountered in uninfected animals
  • ‘sub-clinical bacteriuria’
  • *are there clinical signs consistent with infection?
48
Q

Specimens to collect

A
  • Mastitis: milk
  • Dermatitis/surface: swabs, pus, exudates
  • Sepsis/deat whole animal, culture brain for S. suis meningitis
  • Respiratory: trans-tracheal wash fluid
49
Q

Sample handling

A
  • Stept susceptible to desiccation
  • Entero generally pretty tough
  • Swaps sent with transport media
  • Do NOT freeze samples (except milk)
50
Q

Laboratory ID

A
  • Easily grown on ‘standard’ lab culture
    o Most readily grow on blood agar (some better on chocolate agar)
    o May improve growth with CO2 enriched atmosphere
  • Growth may take 48hrs
  • Commercial biochemical test panels=helpful
  • MALFI-TOF
  • NAAT+DNA sequencing
  • May want to ID S. suis serotypes
51
Q

Zoonotic transmission: S. suis

A
  • Primarily associated with pig contact
  • Serotype 2
  • TSS, meningitis, sepsis, deafness on recovery
52
Q

Zoonotic transmission: S. equi subsp. Zooepidemicus

A
  • From dogs and horses
  • Drinking unpasteurized milk
53
Q

Zoonotic transmission: S. canis

A
  • From dogs
  • May be underrecognized
54
Q

Treatment options: Enterococcus spp

A
  • MUST be guided by susceptibility testing
  • *all are intrinsically resistance to cephalosporins
  • Some intrinsically resistance to vancomycin (NOT VRE)
55
Q

Treatment options:

A
  • Streps and enterococci don’t tend to produce beta-lactamase (amox+clav offers no advantage over amox)
  • Intrinsic resistance is important consideration (particularly for Enterococcus spp.)
  • Strep: often think penicillin
56
Q

Sequelae

A
  • Negative after affect
57
Q

Glomerulonephritis

A
  • Inflammation that involves the capillaries of the renal glomeruli
58
Q

Bacteriophage (phage)

A
  • Virus that infects bacteria

BACTERIOLOGY (19 decks)

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