BSE is defined as a slow developing neurodegenerative disease of cattle that begins insidiously with subtle signs progressing to terminal recumbency. This is a cerebral disease thus signs are consistent with abnormal mentation. Slight changes in behavior include increased apprehension and tactile and auditory hyperesthesia.
Bovine Spongiform Encephalopathy (BSE)
BSE is defined as a slow developing neurodegenerative disease of cattle that begins insidiously with subtle signs progressing to terminal recumbency. This is a cerebral disease thus signs are consistent with abnormal mentation. Slight changes in behavior include increased apprehension and tactile and auditory hyperesthesia. The cattle aren't really "mad" but increased aggression may occur. One of the major differences between this disease and other bovine neurological diseases is that BSE typically progresses much slower, over a period of 6 months (can be shorter or longer) whereas most other neurologic diseases of cattle have acute onsets and clinical signs progress rapidly. Government authorities should be notified if cases are suspected. Diagnosis is confirmed by histological examination of brain tissue showing vacuolation and spongiform degeneration of neurons; currently a definitive diagnosis cannot be performed antemortem because there is no apparent immune response. There is no treatment for this disease. The majority of reported cases are between 2 and 6 years old with greater than 50% of cases being 4-5 years old. Less than 0.02% of cases are younger than 3 years old. The disease agent (a prion) has not been found in milk. There is no conclusive evidence of direct transmission. Three cases of BSE have been detected in the US. The first was a Canadian dairy cow that had been moved to Washington State. The second and third cases were atypical BSE and were found in Texas and Alabama. The ban of feeding ruminant meat and bone meal in the UK resulted in a dramatic drop in the incidence.
This is a relatively rare neurologic disease often caused by Arcanobacterium pyogenes in ruminants. Clinical signs are acute and progress rapidly over a 7-10 day period. General signs include ataxia, head and neck extension, inappetence, depression, and bradycardia (< 60 bpm). Neurologic signs include a base-wide stance, ataxia, head-pressing, asymmetric cranial nerve deficits with dysphagia, blindness, anisocoria, lack of papillary light reflexes, mydriasis, lack of tongue tone, nystagmus, facial paralysis, ventrolateral strabismus, and head tilt. Like many neurological diseases there is eventually recumbency, coma, and death. Diagnosis is challenging and a definitive diagnosis probably requires advanced radiographic imaging. A CSF analysis may reveal a neutrophilic pleocytosis with an elevated protein, both mild to greatly elevated. The most suggestive signs include bradycardia, blindness and a pyogenic CSF process. Treatment is not usually attempted because of poor prognosis but would include long term antibiotics and supportive care. The epidemiology is interesting. The infectious agent reaches the pituitary via hematogenous spread and may infect the rete mirabile (a complex of vessels surrounding the pituitary). A pyogenic infection of the head (e.g. face abscess) may predispose to pituitary abscesses. The disease is most commonly seen in yearlings and older stock and has been associated with nose rings. The prognosis is poor.
A 3-year-old Guernsey cow was presented as an emergency to the University of Tennessee College of Veterinary Medicine for open-mouth breathing and depression of 12 hour duration in August. This was the only cow on the farm. The owners used the milk from this cow for their own consumption. Ten days prior to presentation, the cow had been treated (antibiotics and anti-inflammatory drugs) by field services veterinarians for fever (105.2°F), anorexia, depression, dyspnea, and decreased milk production. The presumptive diagnosis was pneumonia. The cow was re-evaluated by field service 6 days after the first visit and retreated with antibiotics. Emergency examination findings included a 5 inch thorny stick in the right nasal passage, a normal thoracic ultrasound, and a 30 day pregnancy. It was thought that the heat (August) and the stick in the nose were the cause of the open-mouth breathing. The morning after the emergency presentation, the cow was bright and alert, defecated and urinated normally but would periodically extend her head and neck and open-mouth breathe. At other times, the cow would appear normal. In the afternoon, the cow began to demonstrate head pressing and nose pressing. At this time, a neurologic examination was performed. The cow appeared to have decreased papillary light reflexes (PLR); the speed of which differed between the right and the left pupils. There seemed to be a subtle unilateral facial droop on the left side that was most apparent with the left eyelid which drooped and remained partially closed. Although very subtle, the left nare appeared more flattened than the right and the tongue would remain hanging from the left side of the mouth for short periods of time. These signs seemed to indicate cranial nerve deficits suggestive of Listeriosis. Despite these findings, the cow still had a good appetite and appeared bright and responsive. Endoscopy was performed to rule out foreign bodies in the nasal passages, esophagus, pharyngeal region or trachea. No foreign bodies or evidence of trauma/inflammation were found. Lungs auscultation did not reveal anything abnormal. Results of a CBC were suggestive of an inflammatory process as neutrophils (56%) were a higher percentage than lymphocytes (38%) and the fibrinogen was 800 mg/dl (normal range: 100-500 mg/dl). At this point, we believed the cow's problem to be more of an inflammatory neurologic condition rather than pneumonia or foreign body related. Because of the subtle cranial nerve abnormalities, the cow was treated with antibiotics and anti-inflammatory drugs for Listeriosis. Other less common neurologic differentials were considered (mostly tongue in cheek because either didn't really fit or are quite rare) at this time as well (brain abscess, brain neoplasia, head trauma, aberrant parasite migration, neurologic toxins, polioencephalomalacia and Histophilus somni). On day 2 of hospitalization, the cow was still bright and alert and interested in eating however she began to drop her cud; possibly suggestive of other cranial nerve deficits. She also began drooling. Examination of the eyes revealed a total absence of PLRs in both eyes, the left eye may have been bulging out more than the right and the ophthalmology specialists thought that the cow was blind in the right eye. Because of the increased evidence of cranial nerve deficits, the cow was treated more aggressively with potassium penicillin IV. The following day, the cow appeared much better (day 3). On day 4, the cow was less active and less interested in eating. A CSF analysis collected on day 3 showed 35 nucleated cells/μl (normal: 0-3 cells μl), predominately mononuclear cells represented primarily by small lymphocytes. Small lymphocytes are most suggestive of a viral or listeria infection. CSF protein was 102 mg/dl (normal < 40 mg/dl) and no microbes were seen. The CSF interpretation was "consistent with non-suppurative inflammation". On day 5, the cow was more depressed and had developed a fever (104.2°F). On day 6, the cow's appetite had returned but the neurologic signs were more constant or severe (head pressing, head and neck stretching with tongue extended). The cow collapsed later on day 6 and the owners elected euthanasia. Necropsy revealed a pituitary abscess.
Pituitary abscess signs usually are acute and progress rapidly. Once this cow was in the clinic, signs did eventually progress rapidly but there were days when the cow seemed to be improving. Some pituitary abscess signs were present (head and neck extension, head pressing, asymmetric CN deficits with dysphagia, anisocoria, PLR absence, lack of tongue tone) and some were never seen (ataxia, bradycardia, base-wide stance, nystagmus, head tilt). The CSF analysis was somewhat misleading in this case as we would have expected suppurative inflammation. Although speculative, the disease process may have started with the thorny twig that was found in the nasal cavity. The venous return from the nasal septum flows by the rete mirabile. Thus, it is possible that upon the initial field service visit, the thorny stick was present in the nasal passage (giving the appearance of a cow with pneumonia). It had penetrated the nasal mucosa allowing A. pyogenes to spread hematogenously to the pituitary. Arcanobacterium pyogenes was the predominate organism cultured from this pituitary abscess.
Nervous Coccidiosis (NC)
Nervous coccidiosis is a neurologic disease thought to be associated with a neurotoxin released in some cases of coccidial infection. Clinical signs include mild ataxia and tremor along with the more common seizures (intermittent or continuous). A typical seizure consists of the calf becoming recumbent with opisthotonos, tonic-clonic movement, medial strabismus, and snapping of the eyelids. A key sign of this condition is that the animal may be perfectly normal for long periods between seizures. Stress and handling may precipitate seizures. Blindness and hyperexcitability occur and most that become recumbent die. There is usually evidence of intestinal coccidiosis preceding the neurologic form. There is no means of definitive diagnosis. Many theories have been put forth as to the pathophysiology but none are proven. There are no definitive pathological or histopathological lesions.
Treatment consists of sulfonamides (sulfamethazine @ 110 mg/kg for 5 days) or an anti-coccidial drug (amprolium @ 50 mg/kg/day for 7 days) to treat the coccidia. Fluid and electrolyte therapy should be administered as needed. Try to provide a warm, dark, and quiet environment to help reduce seizure activity. Anticonvulsant drugs (diazepam, sodium pentobarbital or phenobarbital) should be used as needed. Calves and young cattle especially feedlot cattle are most often affected. The disease occurs most frequently during cold weather. A heat labile neurotoxin has been identified in the serum of affected calves but is not present in CSF or at least at detectable levels. No additional research has been published since the publication of the neurotoxin discovery in 1987. The frequency of the disease is not known but seems to be relatively rare thus control measures to control coccidiosis should be done. The prognosis of clinically affected cattle is poor with a 70-100% case-fatality rate. Death usually occurs within 5 days of neurologic signs.
A 2-year-old 2-week postpartum Dexter cow was admitted as an emergency to the UT veterinary hospital for bloody diarrhea of 2 days duration. The owners had treated the cow with probiotics and an unknown anti-diarrhea drug. The accompanying calf was normal and showed no evidence of illness during the stay. Physical examination revealed a fever (105.4°F), normal heart and respiratory rates, evidence of dehydration (PCV 54; high normal 44), and a low plasma protein (5.7 mg/dl; normal 6-8.5 mg/dl). A closer examination of the bloody diarrhea revealed that the caudal 12-18 inches of the rectum were roughened compared to the more cranial rectum (possibly due to loss of mucosa). The bloody diarrhea was not foul smelling. Abdominal ultrasound findings were normal but ultrasound of the rectum revealed thickened walls. No abnormalities were found associated with the urogenital tract. Rectal trauma, Type II BVD and salmonellosis were the primary differentials for a 2-year-old cow with bright red bloody diarrhea. Coccidiosis was not initially considered because most cattle experience coccidiosis at less than 1 year of age. The cow was administered fluids, antibiotics and flunixin meglumine the first night. The fluids administered resulted in a PCV of 44 and a plasma protein of 3.9 mg/dl. Because the owners greatly valued this cow, one unit of plasma was given to replenish the low protein. A CBC on day 2 was normal and the fibrinogen was only 300 mg/dl. The findings so far were not consistent with our initial differential list. Salmonellosis typically presents with a foul smelling diarrhea and the CBC and fibrinogen levels should indicate inflammation. Type II BVD was still thought possible but a careful and thorough examination of the oral mucosa did not reveal any lesions. A rectal endoscopy was performed and trauma was considered unlikely because visually all of the caudal portion of the rectum was affected.....whereas with a foreign body we would expect severe lesions in some places while other areas of the rectum would be unaffected. Various toxins were considered but again should not result in this regional but diffuse pattern of rectal damage. Had this been a 5 month old calf, coccidiosis would have been the first thing considered. A fecal was submitted to parasitiology and numerous oocysts were found. The cow was then administered amprolium at 10 mg/kg every 24 h for 5 days. The following days the cow improved considerably to the point that the manure was back to normal and ready to be discharged. While attempting to load the cow on the owner's trailer, the cow was reported to have become extremely ataxic. The cow was kept at the clinic and administered thiamine. No other neurologic signs were seen during the night or the following day, even when moving the cow around. The next day, the cow appeared very ataxic when walking although she appeared normal at times; she so began licking the walls but was still eating and drinking. On the fourth day after pseudodischarge, the cow was normal until forced to make a quick turn. She became extremely ataxic and fell over. Several attempts were made to repeat the ataxic episode but the majority of the time, we were unsuccessful. The majority of the time the cow appeared normal and content. Differentials considered for a periodic ataxic were: polioencephalomalacia (possibly due to the amprolium) but improvement was not continuing with the thiamine, a brain abscess or neoplasia but we wouldn't expect normalcy most of the time, Listeriosis was unlikely because there were no obvious cranial nerve deficits and nervous coccidiosis. There is no definitive test for NC. Diagnosis is based on clinical signs and history of enteric coccidiosis. Most of the clinical signs mentioned above were not present in this cow. In addition, NC is reported to occur more commonly during cold weather. This case occurred in August. In addition, stress and handling is supposed to precipitate seizures but we were largely unsuccessful in stimulating seizures. One seizure was seen but it lasted less than 1 minute. During the seizure the cow developed extensor rigidity, opisthotonus, and snapping of the eyelids. The only sign that was consistent with NC was that ataxia and rare seizure activity was intermittent. Periods of normalcy are the characteristic of NC that separates it from most other neurologic diseases. It very well may have been that the ataxia was actually a seizure. Treatment for NC was discussed above. We did administer magnesium but do not know if it had any affect. We did not try to create a dark and quiet environment. We had anti-convulsant therapy available but no seizure lasted long enough to allow us to give it (although it should be available, just in case). The case-fatality rate is supposed to be > 70% but this cow made a complete recovery. The cow is still in the herd and has had no other incidents. We do believe that this was a case of NC in a Dexter cow. The case was atypical because it occurred in an adult animal during the summer and the cow survived.
Vitamin A Deficiency
Clinical signs are mostly seen in calves and consist of blindness, ill thrift, diarrhea, dermatitis, and pneumonia. In calves an absent menace with absent PLRs and sometimes dilated pupils (severe cases) may be seen. A "star-gazing" stance may also develop. Vitamin A and carotene levels (normal is 150 ug/ml) in plasma and feed can be diagnostic. Vitamin A @ 440 IU/kg parenterally is the treatment but blindness is often permanent. The condition occurs most often when livestock does not have access to succulent plants. Succulent plants contain beta-carotene, which is converted to vitamin A in the liver. Other feedstuffs that are low in vitamin A are dry pastures and cereal grains other than corn. Activity of carotene decreases in feed and hay after prolonged storage. About 80% of vitamin A of hay is lost during field curing. Retinal and optic nerve degeneration occur and are thought due to decreased CSF absorption and increased intracranial pressure causing hydrocephalus and optic nerve compression. Cattle fed a vitamin A deficient diet take about 180 days before clinical signs become evident.
Signs at birth include ataxia, opisthotonos, base-wide stance, intension tremors, hypermetria, hyperreflexia and abnormal nystagmus or strabismus. Mentation is usually normal. A calf was presented with a typical sawhorse stance and other than intension tremors was quite healthy. The owner reported that when attempting to nurse the calf would often fall over head first. The long-term prognosis is poor but antemortem diagnostics would include advanced radiology (necropsy is definitive). No treatment but affected animals may survive and grow normally but would need good footing and special care. Bovine viral diarrhea (infection between 100-150 gestation) is the major agent of this condition and the affected could be persistently infected or have other more serious congenital defects. Control by vaccination of female cattle prior to breeding.