Bacterial disease in horses caused by Streptococcus equi subsp equi (a Lancefield group C streptococcus and the agent of strangles) is evident throughout the world. It is highly contagious and was first recognized in medieval Europe.1 The organisms infect the oropharynx and adjacent lymph nodes of equids.2 The disease progresses with fever, swelling of local lymph nodes, and formation of abscesses and purulent nasal discharge. Typical hematologic abnormalities in horses with clinical strangles include leukocytosis (approx 30,000 cells/μL) with a neutrophil count 25,000 cells/μL and a plasma fibrinogen concentration > 600 mg/dL.3 Mature abscesses rupture externally through the overlying skin and subcutis or internally into the ventral diverticulum of the auditory tube (guttural pouch). Compression of the trachea by swollen lymph nodes can cause respiratory distress, and the name strangles derives from recognition of this clinical sign. Although strangles is usually limited to the retropharyngeal or submandibular lymph nodes, it can spread (presumably via the hematogenous route) to distant sites, including the lungs, tracheobronchial lymph nodes, mesenteric lymph nodes, muscles, and brain. Convalescent horses may continue to harbor bacteria in the guttural pouch and may act as a reservoir of the disease.4 Because S equi is fragile in the environment, the development of carrier animals is fundamental to the survival of the bacteria between outbreaks.5,6 Strangles is often accompanied by loss of condition with the potential for visible scarring, and serious complications can arise in 20% of affected animals, with a case fatality rate of approximately 8%.6 The economic impact of this disease on the equine industry is profound because of the high prevalence of disease, with estimates of approximately 30% of infections in horses throughout the world attributable to S equi.7
Outbreaks of strangles at breeding facilities and racetracks in the United States have become increasingly problematic, which has resulted in strict requirements by some establishments for extensive testing before movement of horses between facilities. In 2004, there was an increase in the number of samples obtained from horses with clinical signs of strangles and submitted to the University of Illinois Veterinary Diagnostic laboratory. Many of these horses had a history of recent or prior vaccination with a commercially available modified-live S equi vaccine. Isolates of S equi with a dry colony morphology, which is characteristic of the acapsular MLV strain, were recovered from these samples. Dry morphology colonies were also recovered in combination with mucoid (encapsulated) S equi colonies. It was determined by use of a 96-well microbial identification and phenotyping system that regardless of the colony morphology (dry or mucoid), several of these clinical isolates had a vaccine-like carbon source utilization phenotype. Many of these isolates also had a vaccine-like genotype as determined by means of pulsed-field gel electrophoresis.a These findings, in combination with a mucoid colony phenotype in isolates cultured directly from the reconstituted vaccine, prompted the study reported here, which was a modification of a traditional safety and efficacy study for vaccine challenge exposure. The purpose of the study reported here was to test several hypotheses that attempt to explain the increase in apparent vaccine failures. These hypotheses included that the commercially available vaccine will not cause clinical signs of strangles in vaccinated ponies, will result in increased concentrations of serum anti-S equi IgG, will not be recovered at > 3 days after vaccination or administration of a booster vaccination, and will not result in reversion or recombination events after vaccination.
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Criteria used to assign a clinical score for the severity of clinical disease caused by Streptococcus equi susp equi in ponies.*
|Rectal temperature (°C)||≤ 38.0||38.0–39.4||≤ 39.5|
|Lymphadenopathy||Mild enlargement||Mild enlargement; warm or causes signs of pain||Mild enlargement; warm or causes signs of pain; abscess formation (with or without rupture)|
|Nasal discharge||Slight or serous||Moderate suppurative||Copious suppurative|
|Hematologic analysis||Within reference limits for a stress leukogram||Neutrophilia; plasma fibrinogen concentration ≤ 600mg/dL||≥ 30,000 WBCs/mL or ≤ 25,000 neutrophils/mL; plasma fibrinogen concentration > 600mg/dL|
|Endoscopy of the ventral diverticulum of the auditory tube (guttural pouch)||Mild swelling of retropharyngeal lymph nodes||Moderate swelling of retropharyngeal lymph nodes or mucopurulent discharge||Abscesses in retropharyngeal lymph nodes or copious purulent discharge|
|Miscellaneous clinical signs (anorexia, coughing, neck extended, dyspnea, dysphagia, and increase in lung sounds)||1 sign||2 signs||≥ 3 signs|
In the present study, any pony with a score > 9 was euthanized immediately.