Laboratory Diagnosis of Strangles

Laboratory Diagnosis of Strangles

Highly contagious equine strangles is transmitted by inhalation or ingestion of Streptococcus equi originating from discharges of the nose of abscess of an infected horse.

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Highly contagious equine strangles is transmitted by inhalation or ingestion of Streptococcus equi originating from discharges of the nose of abscess of an infected horse. Nasal shedding begins approximately four to 16 days after initial infection and continues for two to three weeks in most horses.

However, survival of the organism in pus located in the guttural ouch could continue for months or years and be associated with periodic escape of the organism through the nasal passages. Persistent carrier animals can therefore serve as long-term sources of infection for naive, susceptible horses with which they have contact. Some carrier horses can be recognized by an intermittent unilateral (one-sided) nasal discharge, cough, or have palpable swelling in the throatlatch area below the larynx. Numbers of viable S. equi in infected guttural pouches become very few and detection of carrier horses generally requires direct endoscopic examination and sampling of the pouch.

Bacteriologic Culture

Nasal swabs and nasopharyngeal washes collected two to three days after fever onset in the acute phase of strangles and pus from abscesses usually contain abundant S. equi. The characteristic watery colonies are easy to recognize on appropriate selective culture media within 18 hours of incubation. Sugar fermentation assays can then be completed in three hours to confirm identity. The wide availability, low cost, and diagnostic certainty provided by demonstration of the pathogen argue strongly for inclusion of culture in strangles outbreak diagnosis. Ideally, three to five horses in a nascent outbreak should be cultured to establish presence of the pathogen and mitigate effects of poor sample quality. In contrast to its value in acute phase diagnosis, culture has low sensitivity in detection of chronic carrier horses (sensitivity refers to the probability that the test will be positive when the horse is affected). This is explained by massive S. equi die-off in pus-filled guttural pouches in combination with infrequent drainage into the nasopharynx.

Polymerase Chain Reaction (PCR)

A variety of formats and gene targets based on PCR have been shown to be at least three times more sensitive that culture in detection of S. equi in diagnostic samples from the nasopharynx and guttural pouch. PCR will detect S. equi DNA in numbers too few to be detectable by culture and is effective in the presence of background contaminants. However, in addition to cost and limited local availability, a positive PCR reaction is not proof of presence of viable S. equi and, hence, there is risk of false positive reactions. Also, PCR is vulnerable to accidental contamination during collection and in the laboratory. Nevertheless, PCR is, by far, the most sensitive diagnostic aid in detecting possible guttural pouch farrier horses.

Detection of Serum Antibody

S. equi-specific antibody responses are detectable in serum two to three weeks following exposure, persist at high levels in most horses for 10 to 12 weeks, and—with the exception of SeM antibodies—decline to near baseline by 30 weeks. Ideally, antibody responses to two or three proteins of S. equi should be measured in combination for greatest sensitivity and allow for differences in responses of individual horses. A positive level of antibody could indicate infection or vaccination within the previous six months or possibly of persistent guttural pouch carriage. Serology is especially helpful in diagnosis of occult (bastard) strangles abscesses and S. equi-associated immune mediated vasculitis (purpura). Affected horses usually have very high antibody levels to S. equi proteins. Serology is also helpful in deciding whether to vaccinate. Horses with a preexisting positive level of antibody are likely to have protective immunity and a few of these will be at risk of developing purpura if vaccinated.

CONTACT—John F. Timoney, DSc, MVB, MS, PhD—jtimoney@uky.edu—859/218-1106—University of Kentucky Maxwell H. Gluck Equine Research Center, Lexington, Kentucky


This is an excerpt from Equine Disease Quarterly, funded by underwriters at Lloyd’s, London.

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Equine Disease Quarterly

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