Strep and Staph Flashcards

1
Q

What are the characteristics of streptococci

A
  • gram (+)
  • cocci
  • ~<2um
  • Singly/pairs/chains
  • Faculative anaerobe
  • Fastidious
  • Commensal in upper resp and low urogenital
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2
Q

Define fastidious

A
  • Fastidious: require additional blood or serum to grow
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3
Q

What are 2 ways to classify streptococci

A
  • Groups
    o Hemolysis – alpha, beta, gamma
     Beta hemolytic = most pathogenic
    o Lancefield group – A, B, C, D
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4
Q

What is the primary pathogenic mechanism of strep? 2 examples

A
  • Pyogenic = abscess and suppuration
  • S. suis and pneumoniae
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5
Q

Define Abscess

A
  • Abscess: pus (dead leukocytes and living/dead bacteria) surrounded by intact phagocytes and fibrin
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6
Q

Explain the levels of hemolysis

A

Hemolysis
* Alpha: incomplete lysis of RBC and oxidation of iron = greenish
o Commensal/opportunistic
* Beta: complete lysis: clear zone of inhibition
o Pathogenic
* Gamma: no ability to lyse RBC
o Non-pathogenic

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7
Q

List 6 virulence factors that strep has. What is their function

A
  • exotoxins: superantigen
  • Capsular polysaccharide – prevent phagocytosis
  • Hemolysis – cytotoxic
  • CAMP – pore forming
  • M-protein – antiphagocytic
  • Streptokinase – evade host immune system
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8
Q

List the common pathogens causing bovine mastitis

A
  • Common pathogens:
    o Strep agalactiae, Staph aureus (contagious)
    o Strep dysgalactiae, uberis (environmental or contagious)
    o Klebsiella/E. coli (environmental pathogens)
     Cause severe mastitis
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9
Q

How to diagnose bovine mastitis

A
  • Use California mastitis test
    o Healthy: <200,000 cell/ml
    o Allowable: <400,000 cell/ml (in USA <750,000 cell/ml)
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10
Q

What are the clinical signs of bovine mastitis

A
  • Clinically: can be subclinical
    o Swelling/heat/red/fever/anorexia/shock
  • Can cause atrophy of the alveolus
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11
Q

What are the features of Strep. Agalactiae

A

Strep. Agalactiae: mastitis
* Lancefield group B
* Obligate pathogen of mammary glands in cow
* Commensal in human GI (but it is a different strain than in cows)
* Contagious: direct spread (milking machine)

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12
Q

What is the pathogenesis of Strep. Agalactiae causing mastitis

A
  • Contagious: direct spread (milking machine)
    o Milk back flow due to improper use (not complete seal) or teat damage
    o Keratin plug expelled in milking so backflow or damage can allow entry
    o Bacterial invasion
    o Bacteria adhere via pillus
    o Colonize teat cistern and ducts – causing inflammation > fibrosis
    o Without treatment it can persist in udder
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12
Q

What type of bovine mastitis does Strep. Agalactiae cause

A
  • Causes subclinical mastitis (high SCC/reduced production)
  • Can eradicate from herd = low prevalence in CA
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13
Q

What are the virulence factors associated with Strep. Agalactiae and bovine mastitis

A
  • Virulence: type 3 capsular polysaccharide preventing C3 opsonization (avoid phagocytosis) = most important virulence factor
    o Toxins: sphingomyelinase/neuramindase/hemolysin/lipoteichoic acid
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14
Q

What are the features of Strep. Uberis and what kind of bovine mastitis does it cause

A
  • Commensal in tonsil and intestine
  • Environmental pathogen (enter teat canal and colonize mammary mucosa)
  • Clinical mastitis: severity depends on strain and dose
    o Migrate to LN
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15
Q

What are the virulence factors associated with Strep. uberis and bovine mastitis

A
  • Virulence: type 3 capsular polysaccharide preventing C3 opsonization (avoid phagocytosis) = most important virulence factor
    o Toxins: sphingomyelinase/neuramindase/hemolysin/lipoteichoic acid
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16
Q

What are the subspecies of Strep. dysgalactiae

A
  • Subspecies: dysgalactiae
  • Subspecies: equisimilis
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17
Q

What are the features of Strep. dysgalactiae dysgalactiae? What kind of bovine mastitis does it cause

A

o Lancefield group C
o Alpha hemolytic
o Mastitis in cows
o Contagious and environmental
o Acute and clinical mastitis
o Sporadic in herds
o Associated with teat injury

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18
Q

What are the virulence factors of Strep. dysgalactiae dysgalactiae?

A

o Virulence factors
 Hyaluronidase – spreading factor
 M-like protein/fibrinolysin – colonization
 Lipoteichoic acid
 capsule

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19
Q

What are the features of Strep. dysgalactiae equisimilis ? What kind of disease does it cause

A

o Lancefield group A, C, G, or L
o Beta hemolytic
o Disease in many species

o Clinically:
 Puppy and kitten pneumonia
 Horse: metritis and placentitis
 Piglet: septicemia/arthritis/meningitis/endocarditis

o Not zoonotic – species specific strain

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20
Q

What are the virulence factors of Strep. dysgalactiae equisimilis ?

A

o Virulence: streptokinase (convert plasminogen to plasmin = break fibrin)
 Prevent walling off of bacteria

21
Q

What is the pathogenesis of Strep. dysgalactiae equisimilis in pigs

A

o Pigs: commensal in tonsil and repro – shed in nasal cavity/mammary gland/vaginal and preputial secretions
 Common to infect piglet during birth = bacteremia/septicemia

22
Q

What are the features of Strep suis? What species? What bacterial type?

A
  • Lancefield group D
  • Pigs: spread in resp secretions
    o Common in weaners and growing pigs
  • Many serotypes = many pathogenicity
    o Serotype 2 most pathogenic
  • Zoonotic
23
Q

What are the virulence factors of Strep suis?

A
  • Virulence: capsular polysaccharide (block opsonization) + suilysin (cytotoxic exotoxin = create hole in target cell membrane)
24
What are the gross lesions of Strep suis in pigs and humans? how do humans get it?
* Gross: o Swollen hock o Lung petechiae o Polyserositis * In humans: sepsis/meningitis/hearing loss/renal failure/endocarditis/pneumonia o Via eating contaminated/raw pork, pork blood oral or skin infections
25
What are the features of Strep. Equi subsp. Equi? What does it cause? What are the clinical signs
* Lancefield group C – beta hemolytic * Obligate pathogen * Clinically: strangles (high morbidity/low mortality) o Clinical signs within 3-11d  Fever > lymphoid abscess  Can cause dyspnea or guttural pouch empyema/chondroids (dry pus) * Very contagious * Mainly only horses * Can survive in environment: water trough reservoir (live up to 6wks)
26
What is the pathogenesis of Strep. Equi subsp. Equi?
o Inhale/ingest from acutely infected or carrier horse o Strep equi M-proteins. = adhesions that attach to lingual tonsils o access LN (sublingual and retropharyngeal) o proliferate in LN o enlarge LN
27
What is the virulence factors of Strep. Equi subsp. Equi?
o Hyaluronic acid capsule – prevent phagocytosis o Iron acquisition – equibactin / heme binding system o Streptolysin S – cytotoxic exotoxin o Streptokinase- invasion o IgG endopeptidase – interfere with Ig binding o M protein – antiphagocytic o SeeI/SeeL/SeeM (+/-SeeM) = superantigen (pyrogenic mitogens)  Stimulate overzealous immune reaction – draw a large number of neutrophils
28
What are 4 complications of strangles
o Guttural pouch disease o Persistent carriers o Metastatic abscessation: bastard strangles o Purpura hemorrhagic
29
Explain persistence carriers of strangles
o Persistent carriers  Rupture of retropharyngeal LN into guttural pouch = guttural pouch empyema = chondroid formation = aspiration pneumonia  Can be clinically normal and shed  Require culture or PCR  Can be carriers for years if chondroids present
30
Explain metastatic abscessation of strangles
o Metastatic abscessation: bastard strangles  Colonize any other organ  Clinically: depend on where they colonize * Abdomen – peritonitis/colic * Brain – neuro  2-20% cases
31
Explain Purpura hemorrhagic of strangles
o Purpura hemorrhagic  Type 3 HS: immune mediated vasculitis  Rarely after vaccination for strangles or exposed to disease  Petechiae or ecchymosis hemorrhage on skin/mucosa/kidney
32
What are the features of Strep. Equi subsp. zooeepidemicus? What species does it affect? What does it cause?
* Commensal * Opportunistic * Zoonotic * Horse: joint infection/lymphadentitis/pneumonia/metrtritis/mastitis * Pig: septicemia
33
What are the virulence factor of Strep. Equi subsp. zooeepidemicus?
* Virulence factors: protase o No M protein/variable capsule/less superantigen
34
What are the features of Strep. canis? What species does it affect? What does it cause?
* Lancefield group G * Beta hemolytic * Colonize mucus membranes * Opportunistic * Cause skin infection/LN abscess/metritis/kitten septicemia
35
What are the characterisitics of staphylococci
* Gram (+) cocci * 0.8-1um * Single/pair/tetrad/irregular or grape clusters * Facultative anaerobes * Main organism of microflora = opportunistic
36
List 3 main staphylococci infections. List the species and main clinical manifestation for each
* 3 main: o S. aureus  Rabbit: pododermatitis  Chicken: pododermatitis  Cow: mastitis o S. pseudointermedius  Dog: pyoderma o S. hyicus  Pig: exudative epidermitis
37
What is the pathogenesis of staphylococci infections
* Pyogenic = suppurative lesion * More virulent strains = invasive causing bacteremia/hematogenous spread * Require predisposing factors for infection
38
List the virulence factors of staphylococci infections
* Coagulase = most important * Enterotoxins * Clumping factor * catalase * Exfoliatins – skin damage * Hemolysins – lyse RBC * Toxic shock – inflammation
39
How does coagulase act as a virulence factors? Provide examples
* Coagulase = most important o Associated with virulence/pathogenicity o Adherence to prothromobin – transforms fibrinogen to fibrriin o Coag (+) = S. aureus/pseudointermedius o Coag (-) = opportunisitic o S. hyicus has variable coagulase
40
How does hemolysins act as a virulence factors?
* Hemolysins – lyse RBC o Alpha toxin: pore forming o Beta toxin: sphingomyelinase = damage cell membrane o Gamma toxin = pore forming o Delta toxin = cytolytic (promote pro-inflam cytokines)
41
How does Toxic shock act as a virulence factors?
* Toxic shock – inflammation o Emesis – due to mast cell degranulation o Infectious disease – due to superantigens
42
What does S. aureus cause in cattle
* Chronic/subclinical infection * Contagious * Colonize mammary epithelium due to teat injury * Gangrenous/necrotizing mastitis * Can also cause metritis/abscess/pneumonia/umbilical infection
43
What does S. aureus cause in poutlry
* Poultry o Commensal on skin and mucous membranes o Septicemia in joints/tendon sheaths o Clinical: arthritis/synovitis/chondronecrosis/osteomyelitis  Gangrenous dermatitis  Omphalitis  Lameness/fever  Pododermatitis – abscesses covered by scab
44
What does S. aureus cause in horse
* Horse o Neonatal septicemia o Secondary: wound/surgical site infection/tenosynovitis/septic arthritis
45
What does S. hyicus cause? What are the manifestations
* Pig * Commensal * Exudative epidermitis: greasy pig disease o Acute to chronic o Young pig – generalized dermatitis with sebaceous secretion/exudate/exfoliation o Death if lots of exudation and dehydration
46
What is the pathogenesis of S. hyicus in pigs?
* Pathogenesis: damage skin = exfoliative toxin = epidermal necrolysis * Typically you see pigs up to 7 weeks with brown/black scab on shoulder/neck – spread * Transmit: contact with older pigs
47
What are the virulence factors of S. hyicus in pigs?
* Virulence o Exotoxin o Adhesion o Capsular polysaccharide/protein A
48
What does S. psuedointermedius cause? What are the manifestations
* Dog * Skin and ear infection * Opportunistic – predisposing factors * Clinically: pyoderma o UTI/surgical site infection/orthopedic implants/discospondylitis
49
What is a relevant AMR mechanism for staph
Antibiotic Resistance: Methicillin (MRSA/MRSP) * Common in: surgical site infection/pyoderma/otitis/UTI * Due to mecA gene = general beta lactam resistance * Transmissible between pets and humans
50
What type of sample should you take
Specimens * Depend on pathological condition o Exudate/aspirate/pus/milk/skin scraping/CSF/urine/tissue
51
How do you isolate and identify the pathogen
* Isolate and ID o Direct microscopy (diffQuik/gram) o Culture  Blood agar o PCR – Strep equi * Abx susceptibility testing