Accidental poisoning of a group of yearling cattle by the organophosphate insecticide trichloronat

Eight yearling cattle were accidentally poisoned with the agricultural organophosphate insecticide trichloronat. One animal showed signs of acute organophosphate poisoning and died. The others showed signs of chronic organophosphate poisoning (organophosphate-induced delayed neuropathy) after 2-3 weeks and one animal died from renal failure at 12 weeks. High levels of trichloronat were measured in fat samples at 6 1/2 weeks. The remaining animals still showed signs of ataxia, possibly due to distal axonopathy, 1 year later but no trichloronat was detected in fat samples at this time.     

Accidental poisoning of a group of yearling cattle by the organophosphate insecticide trichloronat

Eight yearling cattle were accidentally poisoned with the agricultural organophosphate insecticide trichloronat. One animal showed signs of acute organophosphate poisoning and died. The others showed signs of chronic organophosphate poisoning (organophosphate-induced delayed neuropathy) after 2–3 weeks and one animal died from renal failure at 12 weeks. High levels of trichloronat were measured in fat samples at 6 1/2 weeks. The remaining animals still showed signs of ataxia, possibly due to distal axonopathy, 1 year later but no trichloronat was detected in fat samples at this time.     

Congenital Cerebellar Cortical Degeneration in Holstein Cattle in Southern Brazil

A congenital progressive cerebellar disorder is described in Holstein calves. The clinical signs were progressive and were characterized by ataxia, hypermetria, a wide stance and fine head tremors. When the affected cattle were forced to run, the signs were exacerbated, leading to epileptiform attacks. Histological lesions consisted of a very selective cerebellar cortical degeneration, almost exclusively affecting the Purkinje cells. The disease affected 6 out of 200 Holstein calves from the same bull. However, results of mating tests of the bull with his daughters and granddaughters suggested that it was not hereditary (p = 0.0062) although an environmental–genetic interaction could not be ruled out.     

Chlorpyrifos (Dursban 44r) toxicity in dairy bulls

The toxicity of Dursban 44 (chlorpyrifos) in dairy bulls in two large Northeastern A.I. bull centers is reported. One hundred eighty-five (185) bulls were treated at the first center and two hundred thirty-two (232) at the second. The application of this product resulted in the death of seven and one bulls, respectively. The knowledge and experience gained at the first center resulted in rapid diagnosis and specific treatment at the second and was felt to be a significant reason for the lower death rate. Typical, clinical signs of organophosphate poisoning were not exhibited in these two outbreaks. Specific diagnosis, treatment and the course of chlorpyrifos poisoning in Holstein bulls are discussed.     

Cerebellar abiotrophy in crossbred cattle

Cerebellar abiotrophy affected 9 of 74 calves sired by a Poll Hereford bull over 2 successive calving seasons. The disease was characterised by episodes of recumbency and ataxia, with hypermetria and wide base stance. Clinical signs commenced between birth and 8 months of age. Two calves which were affected first at 8 months of age recovered clinically 9 months later. Histological lesions were found in the cerebellar cortex of 7 calves and consisted of segmental degeneration and loss of Purkinje cells, and axonal swellings. The clinical signs and pathological findings were consistent with bovine familial convulsions and ataxia, which has not been described previously in Australia. The clinical signs were not attributable to the lesions observed in the cerebellum and an underlying electrophysiological abnormality is proposed. The aetiology of the condition is probably genetic and appears to have a multifactorial basis.     

Susceptibility of Selected Inland Salmonids to Experimentally Induced Infections with Myxobolus cerebralis,the Causative Agent of Whirling Disease

Abstract

Laboratory exposures to the infectious stages (triactinomyxons) of Myxobolus cerebralis demonstrated a range of susceptibility to whirling disease among four species of inland salmonids. Replicate groups of each species were exposed to two concentrations of triactinomyxons, a low dose (100–200 per fish) and a high dose (1,000–2,000 per fish). Exposed fish were evaluated for clinical signs, for severity of microscopic lesions at 35 d, 2 and 5 months, and for spore concentrations in the head cartilage at 5 months. A standard strain of rainbow trout Oncorhynchus mykiss matched for age served as a susceptible species control. Rainbow trout, westslope cutthroat trout O. clarki lewisi, Yellowstone cutthroat trout O. clarki bouvieri, and bull trout Salvelinus confluentus were susceptible to M. cerebralis infections. Clinical signs, including radical swimming (“whirling”) and black tails, were observed at 7 weeks postexposure among rainbow and cutthroat trout challenged at 3 weeks of age. Clinical signs were rare among bull trout exposed at an age of 4 weeks and absent among rainbow and cutthroat trout exposed at 3 months posthatch. Most rainbow, cutthroat, and bull trout were found to be infected when examined at 5 months postexposure. The most severe microscopic lesions among infected fish at 5 months postexposure were found among rainbow trout. Cutthroat trout had less severe lesions, bull trout had mild infections, and no evidence of infection was found among Arctic grayling Thymallus arcticus. Mean spore concentrations among infected fish correlated with the severity of microscopic lesion scores. Rainbow trout had mean concentrations of spores in head cartilage reaching 10⁶, whereas more resistant species such as bull trout had 10⁴ spores; no spores were found among Arctic grayling at 5 months postexposure.     

Localized diseases of the bovine brain and spinal cord

Localized lesions of the central nervous system do occur in cattle. Those affecting the cranial nerves and focal lesions of the spinal cord are most easily recognized by careful neurologic examination. Once the lesion has been anatomically localized, likely etiologic causes can be pursued. Probably the most common cause of cranial nerve deficits in cattle is listeriosis. Important differential diagnoses include brain and pituitary abscesses and extensions of ear infections. Other possible causes include PEM, TEME, hypovitaminosis A, and several rare, sporadic causes. In young cattle, spinal trauma and vertebral body abscesses are the most common causes of progressive paresis resulting from spinal cord lesions. Congenital abnormalities must be considered in the differential diagnoses for very young calves. Non-neurologic conditions, including fractures of the limbs and especially nutritional muscular dystrophy, must be ruled out. In older cattle, compressive neoplasms, most notably lymphosarcoma, are primarily responsible for progressive paresis. Differential diagnosis should include other neurologic conditions such as delayed organophosphate neurotoxicity; early progressive diffuse neurologic diseases such as rabies, pseudorabies, and botulism; plant toxicities; and non-neurologic conditions resulting in recumbency, such as hypocalcemia and musculoskeletal trauma.     

Bilateral laryngeal paralysis in the horse

Four two-year-old Thoroughbreds suffered an acute gastrointestinal illness shortly after dosing with mineral oil which was thought to have been contaminated with an organophosphate compound. Three weeks later all four were noted to be dyspnoeic and endoscopic examination showed that they had developed bilateral laryngeal paralysis. Two of the horses died during severe bouts of dyspnoea six and eight months later and the third was killed shortly thereafter. Examination of the left and right recurrent laryngeal nerves from these horses showed a severe loss of myelinated fibres distally, especially in the left nerve. A similar but less severe lesion was seen in other long peripheral nerves, including the phrenic and digital nerves of the third horse. The spinal cord in two horses showed evidence of mild axonal degeneration which was not related to a particular tract or location. The fourth horse had bilateral laryngeal paralysis two years later. The acute clinical signs and delayed neurological sequelae seen in these horses were strongly suggestive of accidental organophosphate toxicity.     

Progressive paresis in sheep due to delayed neurotoxicity of triaryl phosphates

This report describes the history, signs, histopathology, and diagnosis of a delayed neurotoxicity in Suffolk sheep caused by transmission oil. The signs of toxicity included hyperexcitability, a stiff gait, tetraparesis and inability to maintain sternal recumbency. The circumstances involved in exposure to the transmission oil were determined. Histopathology revealed widespread degeneration of axons in the spinal cord, especially their more distal portions.     

The occurrence of dermatosparaxis in a commercial Drakensberger cattle herd in South Africa

Dermatosparaxis is a heritable collagen dysplasia causing skin extensibility and fragility. In Belgian Blue cattle this mutation has been described as a 3 base pair (bp) change followed by a 17bp deletion in the gene coding for procollagen 1 N-Proteinase (pNPI). An outbreak in a commercial Drakensberger herd in South Africa followed the introduction in late 2000 of a 3-year-old bull that developed skin lesions in 2001 and was culled in 2002. Some of his offspring were similarly affected, 1 of which was kept as a breeding bull after his sire's death. Two affected calves were referred to the Onderstepoort Veterinary Academic Hospital in October 2005. Detailed examination revealed only skin abnormalities limited to the lateral extremities of the thorax, abdomen and pelvis, viz. either acute lacerations of varying sizes, slow healing defects or thin scars in chronic cases. During a subsequent farm visit, 13 animals with similar wounds were seen in the herd of 146 animals. Electron microscopic examination of skin biopsies revealed haphazard arrangement and loose packing of dermal collagen fibrils within collagen fibres. The fibrils showed size variation and slightly irregular outlines on cross-section, consistent with mild dermatosparaxis. DNA samples of affected calves were analysed using primers designed to amplify the region of the pNPI gene that contained the mutation described in Belgian Blue cattle, but this mutation could not be demonstrated in any of the animals tested. It is concluded that a form of dermatosparaxis with a different gene mutation from that described in Belgian Blue cattle exists in Drakensberger cattle in South Africa. This possibly also explains the milder and more delayed clinical signs and the milder dermal collagen ultrastructural abnormalities.     

A congenital bovine epidermolysis resembling epidermolysis bullosa simplex of man

Twenty-five of 72 calves sired by a Simmental bull were affected with a congenital skin disease which appeared to be inherited as an autosomal dominant trait. The affected calves showed hypotrichosis, erythema and breaks in the integrity of the skin. The distribution of the lesions and the ease with which excoriations occurred suggested an abnormal vulnerability to trauma. Mortality was high but in affected survivors the clinical signs moderated with age. Histopathologically, dermoepidermal separation and cytolysis of the germinal cell layer of the epidermis were seen. The name bovine epidermolysis is proposed and a relationship with epidermolysis bullosa simplex of man is suggested.     

Anomalous development of the spinal cord in a calf.

A full term Friesian bull calf was born unable to stand. The dam had no signs of illness during pregnancy. In the thoracic spinal cord there was anomalous development of the central canal and a dorsally placed fusiform and longitudinal dilatation. Mild inflammatory lesions were seen in some body organs and central nervous system where they were suggestive of viral infection. Several skeletal muscles had an extended range of muscle cell cross sectional areas and some cells had numerous internal nuclei.     

Effects of social stress on the toxicity of malathion in young chickens

Thirty-eight 7-week-old white leghorn chickens of two strains (high and low antibody response to sheep erythrocytes) were divided into groups for exposure to high and low levels of social stress. They were then challenged orally with a toxic dose of the organophosphate insecticide malathion (250 mg/kg body weight) and evaluated 60 min later for muscarinic signs (diarrhea, lacrimation, respiratory secretions), nicotinic signs (muscle weakness), plasma cholinesterase activity, and brain acetylcholinesterase activity. A significant correlation was shown between clinical and biochemical indices of organophosphate toxicity. The correlation between social stress and malathion toxicity was less well defined. Chickens with low antibody response preexposed to high social stress were most resistant to organophosphate toxicity.     

Patent ductus arteriosus in Murrah buffalos

Two cases of patent ductus arteriosus are described in 2 Murrah buffalos, a 7.5-month-old heifer calf and a 5-month-old bull calf. The main clinical signs consisted of exercise intolerance, dyspnea, and tachycardia. At necropsy, lesions were consistent with congestive heart failure as indicated by dependent subcutaneous edema, body cavity effusions, and nutmeg liver. The lungs were extensively atelectatic. The heart was enlarged and had a globous shape. The ductus arteriosus, measuring 0.8 cm in length and 0.4 cm in caliber, was patent. The proximal pulmonary artery had an approximately 50-mm-long aneurysm. Eccentric cardiac hypertrophy was evident primarily in the right but to a lesser degree also in the left ventricle. Additionally, there was diffuse subendocardial fibrosis in the left and right ventricle. To the best of the authors' knowledge, patent ductus arteriosus was not previously described in buffalos. Since both calves were sired by the same bull, it is possible that this cardiac anomaly has a hereditary basis.     

Hereditary neuraxial oedema in a Poll Hereford herd

Cases of neuraxial oedema in a Poll Hereford herd were investigated and the pedigrees of affected calves determined. In all cases, and over no more than 3 generations, the pedigree led back to a common bull. Analysis of the herd breeding records supported an autosomal recessive mode of inheritance of the disease. Fractures of the femoral heads, acetabular cartilage and/ or bone, or both, were seen in some affected calves. This lesion was probably induced during birth or soon after, and the suggestion is made that such hip lesions could be regarded as highly suggestive of hereditary neuraxial oedmea of Herefords. The majority of calves showed clinical signs at birth, but 2 calves did not develop clinical signs until they were 2 days old.     

Hind limb skeletal lesions in 12-month-old bulls of beef breeds

In the present study, right hind limb bones from 46 12-month-old bulls with no clinical signs were examined to identify and describe lesions that could predispose the stifle and tarsal joints to osteoarthritis. The bulls came from a performance testing station and were slaughtered due to a low index at the end of the testing period 1996-97. Differences in frequency of lesions among breeds as well as the relationship between lesions and growth rate were evaluated. Forty-five (97.8%) of the 46 bulls had lesions in the joints and/or growth plates. Prevalence of lesions was 100% in the Charolais (22/22), the Hereford (8/8), and the Limousin (4/4) breeds, and 85.7% (6/7) in the Simmental breed. The stifle was affected in 37, the tarsus in 33, and the growth plates in 34, of the 46 bulls. Lesions found in the stifle joint were: osteochondrosis of the articular-epiphysical cartilage complex (AECC) (25), subchondral bone cyst of the distal femur (1), fragmentation of the medial intercondylar eminence of the tibia (20), cleft in the distal part of the patellar groove (28), and an avulsion fracture of the lateral condyle together with a partial tear of the cranial cruciate ligament (1). Lesions found in the tarsal joint were: osteochondrosis of the AECC (23), ulcerative lesions of the articular cartilage of the talus (25), and fracture of the medial malleolus (4). Twenty-eight bulls had lesions of osteochondrosis at the AECC and 37 at the growth plates. When osteochondrosis at the AECC and thickening of the growth plates were combined, 44 of the 46 bulls had at least one lesion at the AECC and/or the growth plate. Prevalence of bulls with at least one lesion was similar between breeds, but the number of lesions per bull was significantly higher in Charolais followed by Simmental, Hereford, and Limousin. Number of lesions per bull was significantly correlated with daily weight gain, carcase weight, and the width of the proximal tibial epiphysis. Lesions were statistically independent, indicating that local biomechanical factors within the joints are important in the pathogenesis. In conclusion, we suggest that the high incidence of hind limb osteoarthritis reported in the Swedish beef bull population can be explained by the high prevalence of skeletal lesions found in the present material. The lesions appeared to be related to high growth rate and to the breed.     

Beef herd poisoning due to ingestion of tansy ragwort in southwestern Ontario

Deaths attributed to Senecio jacobaea were investigated. The animal presented was a mature bull that was lethargic and dragging its feet. The bull was euthanized and 3 other cows died. Significantly, this disease has not been documented in Ontario before, and clinical signs of icterus or hepatoencephalopathy were not observed.     

Chlorpyrifos Toxicosis in Two Cats

Organophosphate compounds are widely employed for control of external parasites in cats and for control of insects in homes and yards. Chlorpyrifos is a long-acting organophosphate (OP) available for use as a systemically and topically acting parasiticide and insecticide in cattle. Its use on cats is not recommended, and no previous clinical cases of toxicosis have been described. Two cases of chronic chlorpyrifos toxicosis in cats are presented and pathophysiology as well as treatment are discussed. The cats had been showing signs of chronic organophosphate toxicosis before diazepam administration. Signs of acute organophosphate toxicosis were precipitated after diazepam was given. Treatment with pralidoxime chloride (2-PAM) and atropine was attempted. Response to treatment was dramatic and complete recovery was achieved with six injections of pralidoxime and atropine administration.     

Oak leaf (Quercus pyrenaica) poisoning in cattle

Three experiments were conducted to study the clinical and pathological findings associated with poisoning in cattle due to ingestion of young oak leaves (OL) and the main factors responsible for toxicosis. In Experiment 1, six 1.4 year-old bulls were fed up to 5 kg of young OL per animal per day and showed no signs of toxicity, apart from a slight proteinuria. In Experiment 2, another six 1.4 year-old bulls were first subjected to severe feed restriction for eight days and then fed a higher amount of OL (approx. 10 kg) daily. A marked increase of serum creatinine and blood urea (BUN) was detected in urine as well as clinical signs consistent with renal failure. At necropsy, animals showed gastrointestinal ulcers and kidney tubular necrosis. Since these results suggested a crucial role of the feed restricting period, a third experiment was conducted administering the same amount of young OL as in Experiment 1, but adding the severe feed restricting period as in Experiment 2. There was a wide variation in clinical signs, with one bull showing clinical signs and lesions, another recovering after showing mild clinical signs and high levels of creatinine and BUN, and the third appearing clinically normal. The relevance of restriction access to food in the development of OL toxicosis appears to be critical because the intoxication was only elicited when the OL administration was preceded by a severe feed restricting period.