Infectious Myopathies in Horses: Myopathies in Horses: Merck Veterinary Manual

Infectious Myopathies in Horses: Myopathies in Horses: Merck Veterinary Manual

West Nile Virus (WNV) encephalitis is a viral disease that is relatively new to the United States. Later in life VZV can reactivate to cause herpes zoster. Equine herpesvirus II was previously known as “equine CMV (cytomegalovirus)”. doi:10.1006/jmbi.1995.0314. equine industry.2 An outbreak of EHV-1 at the Hawthorne Race Course in suburban Chicago in October 2012 resulted in four confirmed cases, two horse deaths and numerous quarantines, prompting officials to cancel a day of racing. At the same time, itching and irritation are also clear signs of the beginnings of conjunctivitis and these symptoms may appear before others symptoms arrive. A direct toxic effect of A phagocytophilum on muscle cells is postulated.

Three of these — EHV-1, EHV-3, and EHV-4 — pose the most serious health risks for domesticated horses and can have significant economic impacts on the equine industry. Common triggers for headshaking are bright light, heat, spring/summer season, and exercise. Once a horse is infected with a herpes virus that virus stays in the horse’s system for life. The best protection is to limit movement of horses and avoid mixing horses from various locations. EHV are specific to the horse and are not contagious to people. According to Cesare, an autopsy performed by the state could not definitely state that his ill horse had herpes. Further, we propose that this newly described disease develops in association with infection by the equine γ-herpesvirus, EHV-5.

At postmortem, large, pale areas of necrotic muscle are evident in hindlimb and lumbar muscles. Mares that abort after EHV-1 infection seldom display premonitory signs. Sublumbar muscles often show the most severe and chronic necrosis, as indicated by greater macrophage infiltration of myofibers. The virus is transmitted by mosquitoes who acquire it from infected birds. Appropriate therapy includes IV penicillin combined with an antimicrobial that inhibits protein synthesis, such as rifampin. Virol. NSAIDs and possibly high doses of short-acting corticosteroids may diminish the inflammatory response.

Infectious Myopathies in Horses: Myopathies in Horses: Merck Veterinary Manual
Voices. Constant-rate infusion of lidocaine, detomidine, or ketamine may provide better anxiety and pain relief than periodic injections of tranquilizers. Horses should be placed in a deeply bedded stall and moved from side to side every 4 hr if they are unable to rise. Aphis acknowledges that the increase in EHV-1 outbreaks is worrying, because they likely fit the criteria of a disease that is evolving and changing in virulence and behavior. Treatment is aimed at minimizing triggers and reducing the horse’s pain response. Young, old, weak, high exposure, immune challenged, and stressed horses are more likely to get sick. “It’s the same with horses; disease can crop up again later.

Neurologic disease appears suddenly and is rapidly progressive reaching its peak intensity in 2-3 days. These horses are restricted from shipping into the Churchill Downs barns of their trainers. All tissue sections were stained with hematoxylin and eosin. Myocardial damage occurs in some horses. Otherwise, the diagnosis is presumptively based on clinical signs and CSF analysis (xanthochromia, albuminocytologic dissociation)[5]. Serum CK and AST are usually moderately increased; however, they often do not reflect the toxicity of clostridial myonecrosis. The clinical signs of the disease may be indistinguishable from other equine encephalitides including rabies, equine herpes virus-1, equine protozoalmyeloencephalitis, and Eastern, Western, or Venezuelan equine encephalomyelitides.

Aspirates of affected tissues examined via direct smears or fluorescent antibody staining should show characteristic rod-shaped bacteria. Anaerobic bacterial culture of freshly acquired samples may also be of value. Cut tissue from the affected area may reveal abundant serosanguineous fluid with an odor of rancid butter. At postmortem, swelling, crepitus, and autolysis are rapid, and bloodstained fluid is often seen discharging from body orifices. Wound fenestration and aggressive surgical debridement over the entire affected area is required for successful treatment. Additional treatment includes high doses of IV potassium penicillin every 2–4 hr until the horse is stable (1 to 5 days), combined with or followed by oral metronidazole along with supportive fluid therapy and anti-inflammatory agents. Consistent, basic biosecurity practices play an important role in reducing risk of exposure to diseases such as influenza, strangles, pigeon fever, or equine herpes virus, CDFA said.

Therefore, surgical treatment is reserved as a last resort in most cases. Initially there is an ill-defined cellulitis, which may heal or progress to a well-defined abscess. An abscess may heal, expand, or fistulate, usually to the skin surface with potential for a chronic granuloma with intermittent discharge. Veterinary care for suspect horses should be performed on the farm as much as possible to prevent spread of the disease. Deep abscesses are more difficult to manage successfully. The formalin-fixed tissue was digested by addition of 200 μl of ATL buffer, followed by the addition of 20 μl of proteinase K solution (DNeasy tissue kit; QIAGEN Inc., Valencia, CA). Ultrasonography and culture of aspirated fluid are the best means of diagnosis in superficial sites.

If horses with EHV-1-associated neurologic disease remain ambulatory, or are recumbent for only 2-3 days, the prognosis is usually favorable. There may be an increased fibrinogen and nucleated WBCs. Diagnosis of WNV can be determined by submitting dead birds to the ADDL or the Indiana Department of Health. Treatment consists of poulticing, lancing, flushing, and draining. Occasionally, surgical removal may be required for complete excision. If antimicrobial therapy is used, it should be continued for several weeks.

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