Strangles: Fighting an age-old disease

Strangles: Fighting an age-old disease

Early detection, hygienic practices can help curb the spread of strangles
Jan 01, 2008

It was described in veterinary literature as far back as 1251, more than 750 years ago, yet it remains one of the most commonly diagnosed infectious diseases in horses worldwide.

It's called strangles because symptomatic lymph-node enlargement can compress the pharynx, larynx or trachea of infected horses, causing them literally to strangle and die from asphyxia.

In today's environment, careful attention and proper management of the disease can help more horses than ever to survive. Farm operators who pay special attention to testing and isolating asymptomatic carriers eventually can reintroduce those horses back into the general population.

Meanwhile, progress continues to be made toward a vaccination for strangles.

"There's certainly reason to be optimistic," says Corrine R. Sweeney, DVM, Dipl. ACVIM, professor of medicine, associate dean and chief operating officer and executive director of the George D. Widener Hospital for Large Animals at the University of Pennsylvania School of Veterinary Medicine's New Bolton Center.

As data on the bacterial genome sequence evolve, along with other findings, a vaccine seems to be on the horizon. Additional progress is being made on detecting asymptomatic carriers by means other than culture, washes, etc. The goal is a simple blood test that could determine whether a horse is a carrier.

"Are those things done and available yet? No, but those are the directions so that we can prevent the disease. Until it's prevented, we can have a simpler, effective method to detect carriers to prevent the spread," Sweeney says.

Clinical signs

Caused by Streptococcus equi, strangles is characterized by a sudden fever (>103° F), followed by upper respiratory catarrh, mucropurulent nasal discharge and acute swelling with subsequent abscess formation in submandibular and retropharyngeal lymph nodes.

Fever persists as the disease progresses. Lymph glands swell and the abscess matures. Infected horses often become depressed, listless and anorexic. Lymphadenopathy is a major clinical sign. The lymph glands of the jaw and neck become painful and swollen within one week after infection. Edema accompanied by serum oozing at the skin surface eventually ruptures and drains to the outside of the neck and into the guttural pouch. Often discharge is noted periorbitally, with severe swelling of the eyelids.

"Nasal shedding of S. equi usually begins two to three days after onset of fever and persists for two to three weeks in most animals," Sweeney says.

"Purulent discharges from horses with active and recovering strangles are an important and easily recognizable source of new S. equi infections among susceptible horses."

Not only is horse-to-horse contact a concern, but also indirect transmission via contaminated equipment and personnel who handle infected animals.

"S. equi can remain viable in frozen mucoid discharges, but survival in the environment requires water, protection from sunlight and protection from other organisms," says Robert Holland, DVM, PhD, a Lexington, Ky., practitioner.

"Bacteria survive in the environment in dirt or on a fence for up to a week, and in water (troughs, etc.) for up to 30 days," Holland says.

Asymptomatic carriers

"A recovered horse may be a potential source of infection for at least six weeks after its clinical signs of strangles have been resolved," Sweeney explains.

Horses recently recovered from the disease may shed bacteria for several weeks after clinical signs have disappeared, even though the organism is no longer detectable.

Asymptomatic subclinical S. equi carrier horses are potentially infectious for prolonged periods via periodic shedding.

"The majority of those horses at one time had some symptoms, but they are probably why strangles has continued to be perpetuated," Sweeney says.

The carrier state may result either from incomplete drainage of exudates from the guttural pouches, empyema, and/or sinuses following rupture of abscesses. In some affected horses there is no shedding, while in others, especially those with contamination of the guttural pouches, shedding may persist for some time. Those with guttural-pouch chondroid formation may act as asymptomatic carriers for months or even years.