Expert Q & A

Managing equine botulism

By Adam Marcus

Botulism may no longer be as dreaded by humans as it was in the days before sterile canning and botulinum antitoxin, but the bacterial disease remains a rare yet potentially lethal problem around farms. Horses are particularly susceptible to botulism, typically through contaminated feed, wounds or even ingestion of the Clostridium botulinum microbe. Compared with mice—the reference animal for studying botulinum toxin—horses are as much as 10,000 times more sensitive to the deadly toxin that the bacteria release.

In a recent review article, Kali Slavik, DVM, DACVIM, of the University of Pennsylvania New Bolton School of Veterinary Medicine, in Kennett Square, and her colleagues discuss the current understanding of equine botulism and how to manage the condition in horses. The Modern Equine Vet spoke with Dr. Slavik about her paper. This interview has been edited for clarity and length.

MEV: Given the rapid progression often seen in adult horses, do you have any red flag clinical markers that indicate the antitoxin’s efficacy is likely to be negligible, and at what point does its administration become a poor use of client resources?

Dr. Slavik: Botulinum antitoxin is the only specific treatment for botulism in horses. Antitoxin works by binding to circulating free (unbound) botulinum toxin within the horse’s body. This means that the antitoxin cannot reverse the effects of botulinum toxin that has already bound within the nerves, and therefore, it cannot cause immediate improvement in the horse’s clinical signs. Horses often have some degree of progression of clinical signs for up to 24 hours after administration of antitoxin, before their clinical signs plateau.

Without treatment, the mortality rate for horses with botulism is roughly 90%, while this number drops to 30% with botulinum antitoxin treatment. Severe clinical signs such as prolonged recumbency and respiratory distress carry a worse prognosis than milder cases and often require significant supportive care, leading to expensive hospitalization bills—often exceeding $10,000; however, these cases may still recover with appropriate care if given time.

MEV: What are some indicators of equine botulism that differentiate it from other diseases that lead to weakness, such as myeloencephalopathy or West Nile virus?

Dr. Slavik: Equine botulism is characterized by a neuromuscular blockade resulting in a flaccid paralysis of skeletal muscles, and distinctly lacks any effect on the central nervous system. Early signs of botulism in horses often include difficulty eating due to weak tongue tone, weak tail tone, exercise intolerance, and trembling of the large anti-gravity muscle groups, such as the triceps and gluteal muscles, due to fatigue.

Unlike the encephalitides—West Nile virus, equine herpes myeloencephalopathy and the equine encephalitis viruses—botulism does not alter the horse’s mentation, nor does it typically present with fever. Horses with equine protozoal myeloencephalitis may present with similar poor tongue tone or dysphagia, but they typically have a characteristic asymmetric multifocal-to-diffuse distribution of neurologic signs with prominent proprioceptive ataxia and muscle atrophy not seen in botulism cases.

MEV: You note that certain antibiotics—specifically aminoglycosides, tetracyclines, and procaine penicillin—can potentiate neuromuscular blockade and worsen paralysis. In cases in which a horse has already developed secondary aspiration pneumonia due to dysphagia, what is the recommended empiric antimicrobial protocol that provides adequate coverage for oral flora and gram-negative bacteria without further compromising the neuromuscular junction?

Dr. Slavik: Horses with evidence of secondary aspiration pneumonia should be treated with broad-spectrum antibiotics to provide coverage for both gram-positive and gram-negative bacteria, while avoiding antibiotics that may potentiate botulism’s neuromuscular blockade, including aminoglycosides, tetracyclines, and penicillin preparations such as procaine. Treatment of pneumonia or other secondary infections in botulism cases can be achieved with a combination therapy of a penicillin (without procaine) and a fluoroquinolone, or with a single broad-spectrum antibiotic preparation, such as a cephalosporin or a potentiated sulfonamide.

MEV: Testing for botulinum toxin has various tradeoffs. The mouse bioassay—the historical gold standard—has a sensitivity as low as 53% in foals. While polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) are more sensitive tests, their results can be delayed. Should clinicians move toward a treat-on-suspicion model in endemic areas? And do you think of the “tongue stress test” or “grain test” as semi-quantitative measures to justify the high cost of antitoxin?

Dr. Slavik: The mouse bioassay is the gold-standard confirmatory test for botulism in horses and the only test currently readily available for clinical veterinary samples in the United States; however, the turnaround time for results can range from 24 hours to more than 4 days. Although PCR and ELISA testing boast markedly decreased turnaround times compared with the mouse bioassay, they are not currently available for clinical veterinary samples in the United States.

With equine botulism cases, time is of the essence with treatment, and delaying treatment until test results are confirmed could significantly increase the morbidity and mortality rate of clinical cases. Therefore, in clinical cases, testing for botulinum toxin is often not elected, and prompt empiric therapy with botulinum antitoxin should be pursued if botulism is suspected. Clinical tests, including the tongue stress test and grain test, when combined with compatible clinical signs, support a clinical suspicion of botulism, especially in endemic areas, and should prompt treatment.

MEV: Management of a recumbent adult horse is notoriously difficult and often carries a grave prognosis. How strong is the evidence for the use of slings or repositioning schedules to reduce the risk for compartment-syndrome–like myopathy and pressure sores while the horse waits for new motor endplates to regenerate?

Dr. Slavik: Horses that are completely recumbent are difficult to manage regardless of the underlying disease process. Recumbent horses are prone to developing pressure sores, myopathies and neuropathies. In botulism cases, sling assistance to stand recumbent horses is contraindicated as this encourages the horse to utilize the minimal muscular strength they possess, further depleting their acetylcholine stores, which could lead to worsening of their condition and progression to respiratory failure in severe cases.

In recumbent botulism cases, round-the-clock nursing care to provide deep, cushioned bedding, padding over bony prominences, and rotation of recumbency with minimal stimulation is recommended. Some horses’ temperaments allow them to tolerate recumbency and the associated nursing care well with minimal struggling, while other horses can become anxious and panicked. If horses become anxious, sedation can be used to facilitate recumbency changes and treatments, but should be used sparingly to not further depress the horse’s respiratory condition.

MEV: While “Shaker Foal Syndrome” is the classic presentation for neonates, C. botulinum colonization within the adult gastrointestinal tract also occurs. What is the prevalence of this form of equine botulism, and what should its clinical management entail?

Dr. Slavik: Toxicoinfectious botulism occurs when C. botulinum bacteria colonize the intestinal tract and actively produce botulinum toxins. As with human infants, this disease is more common in foals than in adult horses due to the foal’s immature gastrointestinal tract, which has a higher gastric pH than adults, an immature mucosal barrier and an immature gastrointestinal microbiome, all of which can lead to favorable conditions for C. botulinum growth and toxin production.

In addition, foals with necrotic duodenal ulcers are at increased risk of toxicoinfection due to the anaerobic environment produced. In adult horses, a low gastric pH, intact mucosal barrier and diverse gastrointestinal microbiome are protective against C. botulinum proliferation, making toxicoinfection much less common, although cases do occasionally occur. In cases of suspected toxicoinfectious botulism in an adult horse, treatment should be as with wound botulism cases—including administration of botulinum antitoxin to bind circulating toxin and treatment with high-dose penicillins to resolve the bacterial infection. MeV