Strep equi Flashcards

1
Q

What is the most common agent identified in horses in the United States, 6 to 10 years old?

A

Strep. equi

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2
Q

What are the first signs of Strep equi infection occurring 3 to 14 days after exposure and before most horses are contagious?

A

Pyrexia with lethargy

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3
Q

What clinical signs of strangles are present that may accompany horses reluctant to eat or drink?

A

significant pharyngitis

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4
Q

Squeezing the larynx in horse with strangles causes what clinical signs?

A

marked pain
stridor
gagging followed by coughing

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5
Q

Which lymph nodes are typically involved in Strangles?

A

submandibular
retropharyngeal
LNs

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6
Q

When do abscesses typically develop and rupture in Strangles?

A

-lymphaenopathy is a typical C/S
-abscess develop a thick fibrous capsule
-rupture in 7 days and 4 weeks after infection

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7
Q

What percentage of horses with guttural pouch empyema exhibit an intermittent unilateral nasal discharge and cough?

A

approximately 50%

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8
Q

What neurologic signs can be seen with strangles?

A

-neuropraxia (external trauma) resultign in temporary laryngeal hemiplegia, dysphagia or both
-recurrent laryngeal nerve damage– difficulty breathing
-dysphagia

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9
Q

Not all infections are with S. equi are confined to the upper respirtory tract with abscesses reported in multiple sites referred to as:

A

bastard strangles

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10
Q

Upon entering the mouth or nose, S. equi attaches to the cells located where?

A

w/in crypts of lingual and palatine tonsils & to follicular assoc epithelium of the pharyngeal and tubal tonsils

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11
Q

Why, are nasal and nasopharyngeal samples culture negative in the early stages of infection?

A

b/c a few hours after infection, a few hours after infection, the organism is difficult to detect on mucosal surface, but visible within epithelial cells and subepithelial tonsillar follicles

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12
Q

Visible abscessation after S. equi infection occurs in what time frame after S. equi enters the lymph nodes?

A

3 to 5 days

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13
Q

How does Strep equi resist phagocytosis?

A

hyaluronic acid capsule
anti-phagocytic SeM protein
H factor binding Se 18.9
Mac protein

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14
Q

When does nasal shedding occur after infection with S. equi?

A

2 to 3 days after onset of fever and persists for 2 to 3 weeks in most animals

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15
Q

Systemic and mucosal immune responses are evident within what time frame after infection and coincide with mucosal clearance of strangles?

A

2 to 3 weeks after infection

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16
Q

If not treated with antibiotics, what percentage of horses with strangles develop long-term convalescent immunity as a result of individual immune response as well as natural exposure to disease over time contributing to reboosting and herd immunity?

A

approximately 75%

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17
Q

Approximately what percentage of horses become susceptible to a second attack of strangles within several months? and due to what?

A

approximately 20 to 25%
– failiure to produce or maintain adequate mucosal & systemic antibodies
–ongoing exposure to S. equi

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18
Q

Which horses can develop catarrhal or atypical strangles (mild form)?

A

-older horses with residual immunity
-foals with waning maternal antibody protection
-vaccinated animals have limited susceptibilty

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19
Q

What animals shed virulent S. equi that will produce severe disease in more susceptible, often young, horses?

A

horses with catarrhal or atypical strangles

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20
Q

milk from mares that have recovered froms trangles contains which immunoglobulins?

A

-IgGb and Iga specificities

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21
Q

When does shedding of strangles occur?

A

not until 1 or 2 days after onset of pyrexia

**makes it possible to isolate new cases before they can transmit infection

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22
Q

nasal shedding of strangles typically persists for how long?

A

2 to 3 weeks in most animals

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23
Q

Horses can be infectious for at least how many weeks after their purulent discharges have dried up?

A

at least 6 weeks

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24
Q

Persistent guttural pouch infection with strangles may result in intermittent shedding for how long?

A

**persist intermittent shedding for years

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25
Q

How is Strep equi transmitted?

A

-direct (nose to nose contact) or indirect (contam housing, water sources, feed or feeding utensils, twitches, tack, etc). transfer of purulent discharges between affected & susceptible horses

26
Q

How long does S. equi remain viable in water?

A

for 4 to 6 weeks, but not in feces or soil

27
Q

How quickly does S. equi live on fencing and soil?

A

rapid death (1-3 days)
**S. equi is sensitive to bacteriocins from environmental bacteria & does not readily survive in the presence of other soil-borne flora

28
Q

What bloodwork abnormalities are seen with S. equi?

A

leukocytosis characterized by neutrophilia
– hyperfibrinogenemeia

29
Q

What is the optimal sample for confirmation of S. equi infection?

A

A needle aspirate from an enlarged or asbcessed lymph node

30
Q

Which diagnostic for S. equi has increased sensitivity to nasal swabs?

A

nasopharyngeal swabs

31
Q

The presence of which bacteria may complicate interpretation of culture of S. equi?

A

other beta hemolytic streptococci, esp S. zooepidemicus

32
Q

In what situations, are culture of S. equi unsuccessful?

A

during incubation, early clinical phases & when bacterial count is low during convalescence

33
Q

At what time period is S. equi present on mucosa?

A

until 24 ro 48 hours after osnet of fever

34
Q

What is the gene in S. equi for antiphagocytic M protein?

A

SeM sequence

35
Q

What is the caveat of Strep equi positive PCR?

A

PCR does not distinguish between dead and live organisms
– technically false pos reaction potentially undermine its absolute diagnostic value with respect to detection of actual infection

36
Q

At what titer level indicates horses are at greater risk for developing purpura hemorrhagica, if vaccinated?

A

> /= 1: 3200

37
Q

What SeM titer level is supportive of diagnosis of existing S. equi associated purpura hemorrhagica?

A

titer >/= 12,800

38
Q

What SeM titer level supports diagnosis of metastatic abscessatoin (baster strangles)?

A

titer >/= 12,800

39
Q

An indirect ELISA (iELISA) for S. equi has been developed to overcome the problem of cross-reactivity with S. zoopeidemicus, uses what proteins?

A

using N-terminal portion of SeM

40
Q

Strep equi ELISA can be used in what scenerios?

A
  • to identify recent infection as early as 2 weeks

-to identify exposed animals without signs that may still be harboring S. equi, (carriers) and which may pose an otherwise unsuspected infectious risk to other horses

41
Q

Strangles Extract vaccine with purified M protein antigen extract is available, and booster is recommended how often?

A

once annually

**naive horses have a 3 doses at interval of 3 weeks

42
Q

With the Strangle extract vaccine, can be administered to pregnant mares at what time period?

A

a month before expected date of foaling

43
Q

Strep equi extract vaccines, a reduction in clinical attack rate of what percent was reported?

A

50% reduction in clinical attack rate

44
Q

What safety issues exist with the attenuated live Strep equi vaccine?

A

-residual virulence with formation of mandibular abscesses in a proportion of vaccinates
-nasald ischarge
-occasional cases of immune-mediated vasculitis (purpura)

45
Q

in attenuated, live intranasal vaccine for Strep equi is not recommended in what age range?

A

foals less than 1 year of age d/t risk of significant clinical disease (fevers & lymph node enalrgement)
-increased shedding of the vaccine strain

46
Q

Horses that have received the Strep equi intranasal vaccine test positive on PCR for how long?

A

for up to 6 weeks

47
Q

Resistance of foals to strangles within the first few months of life is mediated by which immunoglobulin?

A

IgGb
**not IgA

48
Q

What is the best preventative measure for strangles?

A

limiting exposure still remains the best method to prevent S. equi infections

49
Q

What percentage of horses in strangles outbreaks experience apparent failure of the guttural pouch drainage mechanism resulting in persistent GP empyema?

A

–average of 10%

50
Q

Both topical and prolonged systemic administraiton of what improves treatment success rate of S. equi?

A

benzylpenicillin administration (10 days)

51
Q

What is the mechanism fo acetylcysteine instillation in strep equi guttural pouch?

A

Denaturing the solubilizing activity by disrupting disulfide bonds in mucoprotein molecules, decreasing mucus viscosity & facilitating natural drainage

52
Q

Disinfection of pastures occurs over what time period with S. equi?

A

prolonged survival of S. equi on pastures, used to hold infectious animals should be rested for several weeks after animals are removed to allow denaturation of S. equi through drying and direct sunlight
**cultured S. equi shown to survive less than 24 hours on wood, rubber & metal surfaces

53
Q

What is the zoonotic risk of S. equi?

A

Cases are shown in debilitated humans
** rare in humans

54
Q

When are antibiotics indicated in the treatment of Strangles?

A

-acutely infected with high fever & malaise before abscess formation

-horses with profound lymphadenopathy & respiratory distress

-horses with metastatic abscessation

-cases of purpura hemorrhagic treated with corticosteroids

-guttural pouch infections treated locally & systemically to eliminate the carrier state

-Antibiotics should NOT be used as a preventative in animals that may have been exposed

55
Q

What is the drug of choice for treatment of strangles?

A

penicillin: 22-44,000 unites/kg bwt IM q12h or IV q6h

56
Q

What is the overall case fatality rate for strangles on large farm outbreaks?

A

8.1- 9.7%
**can be as high as 20%

57
Q

What are potential complications of Strangles?

A

-spread of infection from head & neck region
-immune-mediated processes, including purpura hemorrhagica & myopathies
-extension of infection to the sinuses
-others: anemia, agalactia, myocarditis, endocarditis, panophthalmitis, periorbital abscesses, ulcerative keratitis, paravertebral abscesses, meningitis, funiculitis, septic arthritis, tenosynovitis

58
Q

Purpura hemorrhagica is an aseptic necrotizing vasculitis is caused by

A

deposition of immune complexes in blood vessel walls

59
Q

What are clinical signs of purpura hemorrhagica?

A

-subcutaneous edema– most freq involving head, limbs, trunk or both
-petechiation & ecchymoses of mucous membranes
+/- oozing from skin surfaces/ sloughing of skin

– other organ involvement– may see colic, respiratory difficulties & mm soreness

60
Q

What is seen on histological exam with purpura hemorrhagica?

A

leukocytoclastic vasculitis

61
Q

What is the primary treatment for purpura hemorrhagica?

A

corticosteroids
– dexmethasone at 0.1-0.2 mg/kg, following a tapering dose regime over 2 to.4 weeks, reducing by 15% every 2 days

62
Q

What is seen with muscle infarction in horses as a complication for strep equi?
**+/- rhabdomyolysis

A

-mild inc serum CK
-titers of SeM specific ab may exceed 1: 6,400
-C/S: muscle stiffness, lameness, abdominal pain