Texas Equine Veterinary Association

www.texasequineva.com | 21 peri-inguinal, perianal (commonly inside the dorsal rectum causing obstruction), internally (abdominal lymph nodes and pneumonia), limb lymphangitis, brain, periarticular, and percutaneous on the back. Abscesses typically rupture between 7 – 28 days aer exposure. Severity of disease varies greatly depending on the immune status of the patient, infectious dose, and bacterial strain. Young horses are more likely to exhibit the worst signs due to their naïve immune system. Older horses that have had the disease or proper vaccination develop mild symptoms and recover quickly or have no clinical signs at all. Pyrexia is the first sign found 3-14 days aer exposure. Fevers are persistent until sufficient abscess rupture and commonly exceed 103˚F. Lethargy usually accompanies the high fevers and is typically the first sign observed in an outbreak of the most vigilant caretakers. Many times, an outbreak is first noted when the horses already have draining abscesses. Pathogenesis S. equi enters the mouth or nose, settles in the lymph tissue around the tongue, palate, and pharynx. Translocation to the associated lymph nodes occurs within hours and gross abscessation is evident within 3-5 days. Nasal shedding does not begin until 1-3 days aer onset of pyrexia. erefore, the horse is not contagious during the incubation period. During an outbreak, potentially exposed horses can be checked frequently for fevers and moved to an isolation stall or pasture before exposing other horses. A horse with adequate immunity may never shed the bacterium. Systemic and mucosal immune responses are apparent 2-3 weeks aer infection and when infection is cleared from the mucosal surfaces. While most horses shed for 2-3 weeks, some can stay persistently infected in the guttural pouches or sinus and shed intermittently for years. All horses that develop disease will shed. Approximately 75% of horses develop a long-term convalescent immunity. Giving antibiotics can greatly reduce this percentage. e remaining 20- 25% of horses are susceptible to disease within months due to an inadequate initial immune response or failure to maintain production of mucosal and systemic antibodies. Suckling foals are protected by colostrum and milk antibodies from mares that have recovered from S. equi or are adequately vaccinated. Epidemiology Transmission occurs primarily through direct and indirect transfer from horses shedding in the time periods discussed above. Another important initiator of an outbreak are the outwardly healthy horses harboring bacteria in their guttural pouches or sinuses. e convalescent horse can also appear healthy and shed bacteria for 6 weeks or longer. S. equi needs moisture for it to persist in an environment. It remains viable for 4-6 weeks in water. Without water, S. equi will die within 1-3 days on fencing, soil, and feces due to bacteriocins from other bacteria. Diagnosis Most of the time diagnosis is easy. Classic clinical signs give you the diagnosis of S. equi 99% of the time. It's the other presentations of S. equi that warrant more probing. Bloodwork reveals leukocytosis characterized by neutrophilia, hyperfibrinogenemia, and significantly increased serum amyloid A. e best sample for testing is the purulent material directly aspirated from an abscess. is obviously is in a progressed state of disease. Other sampling techniques are nasal swab, nasopharyngeal swab, nasopharyngeal wash, and guttural pouch lavage. ese techniques can produce false negative results if sampled in the early non-shedding stage of disease. e nasopharyngeal wash was found to be more sensitive than a nasopharyngeal swab because it samples more surface area. e best detection of the carrier state is performing a guttural pouch lavage, but this technique requires experience entering the guttural pouch and is time consuming. Culture was once the gold standard test for S equi. It still works well if there is purulent material and fever present. e test is widely available and usually cheaper. e test usually takes 2-3 days for results once the laboratory has the sample. Specimens are plated on Columbia CNA agar with 5% sheep or horse blood added. Colonies are small white mucoid pin-point beta hemolytic colonies and look very similar to Strep zoo, which can dominate and kill S. equi via zoocins. is complicates the interpretation of cultures and requires more testing to differentiate. Abscesses that have been open and draining can become colonized by Strep zoo easily. Culture of S. equi is not successful if in the early non- shedding clinical stage, incubation, or when bacterial counts drop during convalescence. Polymerase Chain Reaction (PCR) is a frequently used test for detection of S. equi at all stages of disease. It can be performed in 1-2 hours; therefore, results are received same day as testing. e PCR test is most useful in detecting horses in the carrier state or subclinical convalescent stage of disease via guttural pouch lavage sampling. Serology is best used for detection of horses with internal abscesses (bastard strangles), S. equi associated purpura hemorrhagica, and determining if vaccination is warranted or contraindicated. e only ELISA available in the United States measures antibodies against the SeM surface protein. Prevention Vaccination S. equi vaccines are administered on a risk-based approach. Horses living in or moving into endemic areas benefit from vaccination. Horses at no risk to exposure do not need vaccinated. Vaccinating in the face of an outbreak is not recommended. It will significantly increase the risk of developing purpura hemorrhagica. Horses predisposed to purpura hemorrhagica typically have a SeM titer >1:3200. erefore, SeM titers can be performed in valuable horses to determine if vaccination is warranted. Horses with SeM titers >1:3200 are not vaccinated. A killed M-protein extract vaccine is available in the United States and elicits a serum antibody response 7-10 days later. Naïve horses require a 3-dose series, 3 weeks apart and a booster annually to follow. Horses are still susceptible to contracting disease, but as with most vaccines, the hope is to decrease severity and duration of disease. Mares are vaccinated along with other pre-foaling shots. Foals can be given this vaccine with the usual vaccine series starting at 4-6 months.

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