Streptococcus equi Flashcards

1
Q

What lymph nodes are most commonly affected with Strep equi subsp equi?

A

Submandibular, retropharyngeal commonly

Parotid and cranial cervical occasionally

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2
Q

What gives infection with Strep equi subsp equi the name strangles?

A

Inflammation assoc. with pharyngitis and lymph node abscess formation/rupture can cause obstruction of the upper respiratory tract. Neuropraxia can result in temporary laryngeal hemiplegia, dysphagia or both.

Damage to the recurrent laryngeal nerve and the subsequent paralysis of the arytenoid cartilage may contribute to the difficulty in breathing, assoc. with upper airway inflammation/swelling.

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3
Q

What happens after Strep equi subsp equi enters the mouth or the nose?

A

S. equi attaches to the cells within the crypts of lingual and palatine tonsils and to the follicular-associated epithelium of the pharyngeal and tubal tonsils.

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4
Q

What initiates the formation of abscesses in Strep equi subsp equi?

A

The bacterial peptidoglycan interacts with complement, generating complement-derived chemotactic factors. These factors attract large numbers of polymorphonuclear neutrophils. The neutrophils oft fail to phagocytose and kill the streptococci due to a combination of the hyaluronic acid capsule, antiphagocytic SeM protein, H factor binding Se18.9, Mac protein and other undetermined antiphagocytic factors released by the organism.

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5
Q

How soon does nasal shedding begin, after infection with Strep equi subsp equi?

A

Nasal shedding usually begins 2-3 days after onset of fever and persists for 2-3 weeks in most animals.

The larger the intranasal inoculum of cultured S. equi, the shorter the incubation period and the more severe the disease.

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6
Q

Which groups of horses have limited susceptibility and can develop a mild form of strangles, often termed “catarrhal or atypical strangles?”

A

Older horses with residual immunity, foals with waning maternal antibody protection and vaccinated animals.

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7
Q

Who contributes to the maintenance of increased levels of immunity and extended strangles-free status within isolated herds of previously infected horses?

A

Ongoing exposure to S. equi due to the presence of guttural pouch carriers contributes to continued spread

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8
Q

List the different types of transmission of Strep equi subsp equi.

A

Direct - horse-to-horse, nose-to-nose

Indirect - contaminated housing, water sources, feed or feeding utensils, twitches, tack and other less obvious fomites such as the clothing and equipment of handlers and veterinarians

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9
Q

How persistent in the environment is Strep equi subsp equi?

A

Strep equi subsp equi can live in water for 4-6 weeks, but not in feces or soil. Rapid death (1-3 days) of bacteria on fencing and soil has been shown.

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10
Q

Describe the four ways testing of Strep equi subsp equi can occur, as well as any details.

A

Culture - however, the presence of other beta hemolytic bacteria can complicate the interpretation of cultures. Zoocins produced by S. zooepidemicus will kill S. equi.; may be unsuccessful during the incubation, early clinical phases and when the bacterial count is low during convalescence.

PCR - quantitative, detects “seel,” a superantigen-encoding gene; does not distinguish between dead and ive organisms; should be used on endoscopically guided guttural pouch lavage

SeM ELISA - Ab titers to SeM peak about 5 weeks after exposure and remain high for at least 6 months; paired titers showing a 4-fold or greater increase, 10 days apart; titer >/= 12,800 can support diagnosis of purpura hemorrhagica or metastatic abscessation

Combined Ag A and Ag C - this is an indirect ELISA to a portion of SeM that is unique to Strep equi subsp equi that has been developed to overcome the problem of cross-reactivity with S. zooepidemicus; to be used (if no vax have been used) to identify recent infection as early as 2 weeks, identify carriers

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11
Q

What are the two types of vaccines against Strep equi subsp equi?

A

Extract - single purified M-protein Ag extract vax, elicits serum Ab responses 7-10 days later; pregnant mares can be boostered a month before date of foaling; EFFICACY BEEN DISAPPOINTING

Attenuated live - only given to healthy nonfebrile animals free of nasal discharge; safety issues include: residual virulence with formation of slowly developing mandibular abscesses in a proportion of vaccinates, nasal discharge and occasional cases of purpura; can test positive on PCR for up to 6 weeks; animals with previous strangles should not use vax; lacks differentiating infected from vaccinated animals capability

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12
Q

What kind of titers are found in foals from vaccinated mares?

A

Foals have higher titers of SeM-specific IgGb but not IgA in mucosal washes during the first 2 months of life.

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13
Q

What role does acetylcysteine solution play in treatment of Strep equi subsp equi?

A

Acetylcysteine has a denaturing and solubilizing activity by disrupting disulfide bonds in mucoprotein molecules, reducing mucous viscosity and theoretically facilitating natural drainage.

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14
Q

How susceptible is Strep equi subsp equi to disinfectants?

A

Strep equi subsp equi is relatively susceptible, hypochlorites, quaternary ammonium compounds, phenolic compounds, potassium peroxymonosulfate and accelerated hydrogen peroxides

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15
Q

Describe the development of purpura hemorrhagica assoc. with Strep equi subsp equi.

A

Purpura hemorrhagica is an aseptic necrotizing vasculitis characterized primarily by edema and petechial or ecchymotic hemorrhage. Appears to be caused by deposition of immune complexes in blood vessel walls.

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16
Q

List the clinical disease that occurs with purpura hemorrhagica assoc. with Strep equi subsp equi.

A

Purpura hemorrhagica ranges from a mild, transient reaction to a severe, fatal disease. Typical signs are a result of vasculitis, including SQ edema, most frequently involving the head; limbs, trunk or both; petechiation and ecchymoses of the mm.

Histology shows leukocytoclastic vasculitis on skin biopsy.

17
Q

Three types of myopathies have been documented in horses after exposure to Strep equi subsp equi. List and describe.

A

Muscle infarction - likely a severe manifestation of purpura hemorrhagica, immune-mediated vasculitis within muscle and mild muscle necrosis; can develop a severe vasculopathy characterized by infarction of skeletal muscle, skin, GI tract and lungs; acute coagulative necrosis of muscle with infarctions

Rhabdomyolysis with acute myonecrosis - acute severe rhabdomyolysis, stiff gait and can become recumbent; large multifocal pale, friable areas in muscle at necropsy; hypothesized that rhabdomyolysis is due to either an inflammatory cascade similar to streptococcal toxic shock syndrome or potentially direct toxic effects of Strep equi subsp equi in muscle tissue

Rhabdomyolysis with progressive atrophy - some of these horses had underlying polysaccharide storage myopathy; muscle biopsies revealed chronic active rhabdomyolysis with regeneration, prominent macrophage infiltration, atrophy of fast twitch fibers and lymphocytic vasculitis