12/12/2022
https://www.facebook.com/108942262476613/posts/5682859415084842/?mibextid=Nif5oz
INFECTIOUS DISEASE ALERT
Dr. Nathan Slovis our infectious disease chairman has been consulting with several of his colleagues in Texas and Louisiana about a PRESUMPTIVE botulism outbreak associated with Hay Cubes manufactured in Colorado.
Both Farms used the same source for the hay cubes.
We have heard that other states that MAY have farms affected as well.
The hay cubes appear to have been contaminated with dead animal carcasses (Images Attached from one of the farms affected that used the hay cubes)
Botulism
Definition/Overview
Botulism is a neuromuscular disease characterized by flaccid paralysis that is caused by neurotoxins produced by strains of Clostridium botulinum. Horses are one of the most susceptible species, with both individual and group outbreaks reported.
Etiology
Clostridium botulinum is a Gram positive, spore forming anaerobic bacterium. Spores are found in the soil throughout most of the world with the distribution of strains dependent on temperature and soil pH. Eight serotypes of botulinum neurotoxin exist and are labeled A, B, C1, C 2 , D, E, F and G, all of which have similar toxicity. There is geographic variation in the predominant serotypes. In North America, botulism in horses is most often caused by type B toxin and less often by toxin types A and C1.
Pathophysiology
There are two main forms of botulism. Toxicoinfectious botulism, also known as ‘shaker-foal syndrome’ occurs almost exclusively foals as a result of overgrowth of C. botulinum in the intestinal tract, followed by production of neurotoxins. The disease most often affects fast growing foals from 1-2 months of age, although cases outside this age range have been seen. The mature, protective gastrointestinal microflora of adult horses typically prevents overgrowth of C. botulinum following ingestion.
In adult horses, botulism occurs following ingestion of pre-formed toxins in feed. Spoiled hay or silage are most commonly implicated in botulism caused by types A and B. Silage with a pH greater than 4.5 is favorable for sporulation and toxin production. This is known as “forage poisoning”. It has also been suggested that birds may be able to carry preformed toxin from carrion to the feed of horses. Type C botulism is associated with ingestion of feed or water contaminated by the carcass of a rodent or other small animal. Less commonly, botulism can occur when neurotoxins are produced in wounds infected with C. botulinum. Proliferation of C. botulinum type B organisms in gastric ulcers, foci of hepatic necrosis, abscesses in the navel or lungs and wounds in skin and muscle have been associated with toxicoinfectious botulism.
The third less common form of botulism is associated with the infection of wounds with C. botulinum
Botulinum neurotoxins bind to presynaptic membranes at neuromuscular junctions, irreversibly blocking the release of the neurotransmitter acetylcholine resulting in flaccid paralysis. Botulinum neurotoxin has also been linked to equine grass sickness.
Clinical presentation
The clinical picture of symmetrical flaccid paralysis is consistent, with the onset and rate of progression dependent on the amount of toxin that is absorbed. The initial clinical signs include dysphagia with apparent excess salivation, weak eyelid tone, weak tail tone and exercise intolerance. Affected animals also spend increased amounts of time resting due to generalized muscle weakness, which is also associated with tremors, carpal buckling and ataxia. Pharyngeal and lingual paralysis causes marked dysphagia and predisposes to aspiration pneumonia. The affected animals tend to quid their food. Paralysis of the diaphragm and intercostal muscles results in an increased respiratory rate and decreased chest wall expansion. Severely affected animals die from respiratory paralysis and cardiac failure.
Differential Diagnosis
Differential diagnoses for botulism include viral causes of encephalitis, protozoal causes of encephalomyelitis, and toxic causes of sudden death or neurologic dysfunction.
Diagnosis
Botulism should be suspected in animals with flaccid paralysis displaying the above clinical signs. Botulinum toxin does not affect the central nervous system but does affect the cranial nerves; thus symmetrical cranial nerve deficits in an animal with normal mentation can help differentiate botulism from other disorders. Botulism is often a clinical diagnosis. Definitive diagnosis can be achieved by the mouse inoculation test using serum or gastrointestinal contents. However, horses are extremely sensitive to the toxin and this test is often negative. The traditional mouse bioassay identifies Clostridium botulinum in only about 30% of f***s collected from adult horses with clinical disease. If the toxin is demonstrated with mouse inoculation, the serotype can be determined through inoculation of mice passively protected with different serotypes of antitoxin. Detection of antibody titers in a recovering unvaccinated horse is also evidence for the diagnosis of botulism. Demonstration of spores in the intestine is not diagnostic, as they can be ingested and observed as contaminants.
Quantitative real-time PCR (qPCR) test for the detection of Clostridium botulinum neurotoxins in equine diagnostic samples (F***s or Food Samples) are available. . This assay tends to be more economical, time efficient and sensitive than the traditional mouse bioassay
Management
Immediate treatment with a polyvalent antitoxin prevents binding of the toxin to presynaptic membranes. However, antitoxin cannot reactivate neuromuscular junctions that have already been affected. Thus, antitoxin administration may have little effect in animals that are severely affected. Generally, only one dose (200ml of antiserum to foals (30,000 IU) or 500ml (70,000 IU) to adults of antitoxin is needed and provides passive protection for up to two months.
Antibiotics should be administered if toxicoinfectious botulism is suspected or if here is secondary lesions such as aspiration pneumonia or decubital ulcers. Antibiotics that can cause neuromuscular blockade and possibly exacerbate clinical signs such as aminoglycosides should be avoided and neurostimulants such as neostigmine should not be used. Good nursing care including the provision of a deep bed and a quiet environment are essential. Frequent turning of recumbent animals, nasogastric feeding and fluid support for animals with pharyngeal and lingual paralysis, frequent catheterization of the urinary bladder, application of ophthalmic ointments and ventilatory support may all be required.
If botulism is suspected to have been caused by ingestion of preformed toxin in feed, an alternate feed source should be provided while the origin is investigated. Potentially contaminated feeds.
Prognosis
A survival rate of 88% has been reported in foals with toxicoinfectious botulism that were provided with intensive nursing care (including mechanical ventilation and botulism antitoxin). However, this type of treatment is not available in all areas and is quite expensive. Without aggressive supportive care, the mortality rate is high, with death usually occurring 1-3 days after the onset of clinical signs.
The prognosis is variable in adult horses that have ingested pre-formed toxin, depending on the amount of toxin absorbed and the severity of clinical signs. Mildly affected animals may recover with minimal treatment while severely affected animals that become recumbent have a poor prognosis. The mortality rate has been reported to be as high as 90% in recumbent adult horses, with death occurring within hours of the appearance of signs. In animals that survive, complete recovery is most common. Development of full muscular strength takes weeks to months. Persistent tongue weakness not affecting the ability to eat has been reported.
Prevention
Type B toxoid is available and should be used in areas in which type B botulism is Vaccination is particularly important in areas where neonatal botulism occurs. Widespread vaccination of mares in certain high-risk areas has dramatically decreased the incidence of neonatal botulism. An initial series of three vaccinations a month apart followed by annual boosters has been recommended. Pregnant mares should receive a booster four weeks prior to foaling to ensure adequate antibody levels in colostrum. Type B vaccine only provides protection against type B toxin. There is no cross protection against type C toxin and type C toxoid is not licensed for use in North America.
Silage, haylage and other fermented feeds should not be fed to horses because of the risk of botulism.
REFERENCES
1) Wilkins PA, Palmer JE. Botulism in foals less than 6 months of age: 30 cases (1989‑2002).J Vet Intern Med;(2003);17;5:702‑707
2) Wilkins PA, Palmer JE. Mechanical ventilation in foals with botulism: 9 cases (1989‑2002). J Vet Intern Med;(2003);17;5:708‑712
3) Junaine M. Hunter, DVM, Barton W. Rohrback, VMD, MPH et at. Round Bale Grass Hay: A Risk Factor for Botulism in Horses Compend Contin Educ Pract Vet;(2002);24;2:166‑166
4) Schoenbaum MA, Hall SM, G***k RD, Grant K, Jenny AL, Schiefer TJ, Sciglibaglio P, Whitlock RH. An outbreak of type C botulism in 12 horses and a mule. J Am Vet Med Assoc;(2000);217;3:365‑8
5) S. H. GUDMUNDSSON. Type B botulinum intoxication in horses: case report and literature review. Equine Vet Educ;(1997);9;3:156‑159
6) H. Kinde et al. Clostridium botulinum type‑C intoxication associated with consumption of processed alfalfa hay cubes in horses. J Am Vet Med Assoc;(Sept 15, 1991);199;6:742‑746
