Common neurological diseases in food animal (Proceedings)


Common neurological diseases in food animal (Proceedings)

Nov 01, 2010


Maybe this doesn't really fit "common" but it is always interesting to hear about cases. The main thing about rabies in cattle (and other species) is that signs are quite variable and inconsistent. Certain signs should be "red flags" for bovine rabies. Oftentimes cattle with rabies will have some history of hindlimb ataxia, weakness, or paralysis (this in itself is typical of many bovine diseases but for cattle exhibiting these signs, rabies should be considered). Constant straining with or without rectal prolapse is a red flag. Don't expect to find bite wounds because of the length of the incubation period. Three forms are described and include 1) cerebral or furious: aggressive behavior, photophobia, hyperesthesia, straining, and convulsions), 2) brainstem or dumb form: depression and dementia with ataxia, excessive drooling and pharyngeal paralysis and 3) spinal cord or paralytic form: progressive ascending paralysis. Common cattle signs in order of most common are salivation, bellowing, aggressiveness, paresis or paralysis and straining. A 5-year-old cow died of rabies 4 days after being presented with persistent unrelenting rectal straining. The rectal straining was controlled with caudal epidurals. Occasional yawning and bilateral rear limb knuckling developed and got progressively worse. This cow did not appear to have a serious change in mentation (not aggressive nor more docile) and was not ever seen attempting to eat or drink.

Diagnosis is via brain FA. Histopathology may show eosinophilic intracytoplasmic Negri bodies in neurons. If only spinal cord disease is present, virus and Negri bodies may not be found in the brain (only the spinal cord). Thus, premature euthanasia may not be prudent. The incubation period varies from 2 weeks to 6 months depending on site of inoculation. A bite on the rear foot may take 6 months before clinical signs appear whereas a bite on the nose may only take a couple of weeks. Once clinical signs appear, most animals die by 10 days. I have heard of a couple of cases surviving > 15 days. The rabies virus passes along neurons within the nervous system to the brain. Initially, there may be hyperactivity of affected neurons with signs such as hyperesthesia, tremor, straining, and salivation. Eventually the neurons die; resulting in flaccid paralysis, dysphagia, and anesthesia. Treatment is not a practical option. Vaccines are available but not routinely used in cattle due to expense and relatively low incidence.


Listeriosis is defined as an acute bacterial meningoencephalitis of ruminants characterized by circling and cranial nerve deficits. The clinical signs typically relate to caudal cranial nerves (V thru XII)....thus affected cattle can usually see. General signs of fever (last 2-4 days), anorexia, depression, excessive salivation may be seen as well. Neurological signs include proprioceptive deficits, head-pressing, depressed consciousness (due to lesions of the reticular activating system), constant or sporadic walking or circling (the latter due to lesions of the basal ganglia). Sometimes the affected animal, because of the desire to circle, gets stuck against a wall or gets stuck in the corner. Spinal reflexes may show mild to moderate hypertonia and hyperreflexia in the limbs contralateral to the lesion. Lesions of the cerebellar peduncles may result in a head tilt opposite of the direction of circling. The primary cranial deficits (many or none may be present) include: dropped jaw and or facial anesthesia (CN V), medial strabismus on the ipsilateral side of the lesion (CN VI), ptosis, loss of menace, absent palpebral reflex, drooped ear, loss of levator nasolabialis muscle function (one open, one semi-closed nostril), decreased lip tone (CN VII), nystagmus (any type and inconsistent) that changes as the position of the head is altered and head tilt to the ipsilateral side of the lesion, a tendency to circle to the side with the lesion (CN VIII), stertorous breathing, dysphagia and paresis or paralysis of the tongue (cranial nerves IX, X, and XII). With unilateral lesions, the tongue may protrude from the side of the mouth ipsilateral to the lesion. If not treated in time, signs will progress to convulsions, coma and death. Diagnosis is presumptive and based on clinical signs and response to therapy. There is usually NOT an inflammatory leukogram. A CSF tap can be helpful. The CSF tends to be a mononuclear pleocytosis (> 12 cells/ul) with a mildly elevated protein (> 40 mg/dl). The organism can be cultured from CSF or microabscesses but requires refrigeration, enrichment and a long incubation time.

Treatment can be successful but may take from 1 week to 1 month. Fluids are necessary for those that cannot swallow or have difficulty swallowing. Fluids should be alkalizing because of salivary bicarbonate loss (due to persistent drooling in those that can't swallow). Several different antibiotics are effective with the standard oxytetracycline @ 10 mg/kg BID IM, IV, or SQ or procaine penicillin G @ 40,000 IU/kg IM 3-4 x day for 1 week followed by half this dose SID for another 1-2 weeks being the drugs of choice. Under hospital conditions, we will use potassium penicillin @ 44,000 IU/kg IV 3-4 x day for 3-5 days and then follow with one of the antibiotics above on valuable and pet animals. The disease agent is the gram-positive bacterium Listeria monocytogenes. This is probably one of the two most common neurologic diseases of ruminants. Cases are mostly sporadic but occasional outbreaks occur (outbreaks usually point to a common feedstuff). CNS infection may occur hematogenously or by ascension of a cranial nerve (some evidence points toward CN V). Silage is the most commonly implicated source but cases certainly occur without the presence of silage. Properly ensiled silage is not supportive of Listeria growth (proper silage should be anaerobic and have a pH < 5.4). Listeria may be shed in the feces of carriers and may be found in rotting vegetation. It may survive in soil up to 2 yrs and is very resistant to environmental factors. Commercial vaccines are not available. The mortality rate for untreated cases is nearly 100%. Most livestock treated properly and in a timely manner survive though some may have permanent neurologic deficits.