Neuraxial oedema of Hereford calves with and without hypomyelinogenesis

The clinical and pathological features of 11 Hereford calves with neuraxial oedema with and without hypomyelinogenesis are described. Calves were affected at birth, recumbent and showed intermittent extensor spasm and hyperaesthesia. Nystagmus was noted in six cases. Pathologically, vacuolation of the central nervous system was seen in all cases. In two calves of horned Hereford stock this was restricted to white matter areas, while in the remaining calves of polled Hereford origin it was distributed in both white and grey matter. Hypomyelinogenesis was also a feature of this latter group of calves.     

Maple syrup urine disease as a cause of spongiform encephalopathy in calves

Estimates of branched chain amino acid concentrations in plasma and, or, serum, urine, cerebrospinal fluid, formalin-fixed cerebral tissue and the associated formalin, provided evidence for a diagnosis of branched chain keto acid decarboxylase deficiency in five polled Hereford calves. The similarity of the clinical signs of dullness, recumbency and opisthotonos, and the observation of severe status spongiosus within the central nervous system, indicated that this condition had probably affected seven other newborn calves. It is suggested that this condition is analogous to branched chain keto acid decarboxylase deficiency or maple syrup urine disease of children.     

Maple syrup urine disease in five hereford calves in ontario

Five newborn grade horned or polled Hereford calves in Ontario exhibited the clinical signs characteristic of hereditary neuraxial edema, namely, inability to rise, and hyperesthesia with extensor spasms upon tactile or auditory stimulation. Histologically, there was widespread spongy vacuolation in both white and gray matter in the brains of all five calves, especially in the midbrain, brain stem, and cerebellum. Amino acid analysis of formalin-fixed cerebral tissue of three calves demonstrated an amino acid composition consistent with a diagnosis of branched chain keto acid decarboxylase deficiency. This condition has been recently reported in Hereford calves in Australia; it is characterized by the delayed onset of neurological signs and severe lesions of status spongiosus, and has been considered analogous to maple syrup urine disease of children.     

Maple syrup urine disease in calves: a clinical, pathological and biochemical study

The clinical, pathological and biochemical findings of a study of 30 Poll Hereford, Hereford, Poll Hereford cross or Hereford cross calves affected with branched chain ketoacid dehydrogenase (BCKAD) complex deficiency or maple syrup urine disease (MSUD) are presented. In breeding studies, 6 of 21 calves from obligate heterozygote matings were affected with MSUD, suggesting the disease is inherited in an autosomal recessive manner. Calves were clinically affected from birth, but there were variations in the subsequent course of progressive deterioration of central nervous system function. Concentrations of the branched chain amino acids and keto acids were elevated in pre-suckle plasma and cerebellar water content was higher in affected calves. Activity of BCKAD complex was minimal in fibroblasts cultured from an affected calf. Spongiform encephalopathy and elevated ratios of the branched to straight chain amino acids in formalin fixed cerebral tissue were found in a stillborn foetus and a 3-month-old Hereford calf. These findings suggest the disease occurs prenatally and that a delayed form may exist.     

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.     

Case report: congenital myoclonus in a German Holstein calf

A female German Holstein calf was not able to stand up after birth. Resting the animal was lying in normal position and could lift its head. Sensory stimuli like auditory or tactile impulses induced myoclonic jerking of the whole body. Afterwards it calmed down quickly. The signs observed correspond to the clinical findings of congenital myoclonus in poll Hereford calves. The pathological examination revealed no indications for changes in organs. The inbreeding coefficient of the calf was 1.56 %. The present type of congenital myoclonus in the calf examined is likely to be genetically determined, even if the point mutation in exon 2 of the glycin receptor alpha 1 gene was not confirmed.     

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.     

Clinicopathology of meningoventriculitis due to Streptococcus bovis infection in neonatal calves.

Three neonatal calves ranging in age from 4 to 14 days were examined pathologically and bacteriologically. The calves showed depression, anorexia, pyrexia, and difficulty or inability to stand followed by cloudiness of the ocular aqueous humor or cornea. Autopsy revealed congestion, petechiae, and cloudy areas in the meninges. Histologically, the central nervous system (CNS) lesions were prominent and limited to the meninges where fibrinous exudate and infiltrations of neutrophils, macrophages, and lymphocytes were present. There were mild or slight degrees of choroid plexitis and ependymitis. Endophthalmitis was seen as a concurrent lesion in all cases. Fibrinous or fibrinopurulent changes were found in the peritoneum and epicardium as well as in several other organs. Numerous Gram-positive cocci were detected in affected areas of the whole body. Bacteriologically, Streptococcus bovis was isolated from all examined materials consisting of the brain, cerebrospinal fluid, ocular aqueous humor, and several other organs. These results suggest that the lesions were associated with infection of the organism and that the present cases were in the process of septicemia.     

Prenatal occurrence and mode of inheritance of neuraxial oedema in Poll Hereford calves

Breeding experiments were conducted in 1981, 1982 and 1983 using bulls and cows that were obligatory heterozygotes for neuraxial oedema. Fifty-six calves were born in the herd, 14 of which were diagnosed as cases of neuraxial oedema. The mean gestation length for affected calves born in 1983 was nine days shorter than that for unaffected calves. Observations were made of the birth of three affected calves. In one calf spasms of the forelimbs were observed during an unassisted delivery, and in this and two others, typical clinical signs were observed within two minutes of birth. Radiological and, or, pathological examination of each of the eight affected calves born in 1983 revealed lesions in the coxae, some of which predated parturition. These observations are consistent with the calves being affected with neuraxial oedema while in utero.     

Suspected levamisole intoxication in calves

CASE HISTORY: A group of 32 Friesian and four Hereford calves, 3–4 months old with body weights between 100–120?kg, were purchased from a weaner sale. On arrival at the property the Hereford calves were treated with a combination anthelmintic containing 2?g/L abamectin and 80?g/L levamisole hydrochloride. Shortly afterwards they developed tremors and frothing from the mouth, and two died overnight. The Friesian calves were treated with the same anthelmintic on the following day, when some showed hypersalivation and frothing from the mouth.

CLINICAL FINDINGS: Examination of the three most severely affected Friesian calves revealed severe nicotinic-type symptoms including hypersalivation, frothing from the mouth, muscle tremors, recumbency, rapid respiration, hyperaesthesia, and central nervous system depression. Other calves showed mild to moderate signs of intoxication including restlessness, tail switching, salivation, tremors, frequent defaecation, mild colic and jaw chomping. Two calves died shortly afterwards. An adverse drug event investigation revealed that the formulation and quality of the anthelmintic was within the correct specification, and that the drench gun was functioning correctly.

DIAGNOSIS: Suspected levamisole intoxication due to a combination of possible overdosing, dehydration, and stress caused by transportation and prolonged yarding.

CLINICAL RELEVANCE: Susceptibility to levamisole toxicity in New Zealand calves can be increased if factors like dehydration or stress are present. Levamisole has a narrow margin of safety, and overdosing in calves can easily occur if the dose rate is not based on their actual weight or health status.     

Variability in limb malformations and possible significance in the pathogenesis of an inherited congenital neuromuscular disease of Charolais cattle (syndrome of arthrogryposis and palatoschisis)

Limb abnormalities in 30 calves with an inherited congenital neuromuscular disorder known as syndrome of arthrogryposis and palatoschisis were classified according to the range of severity of joint deformity in either flexion or extension, and restricted joint movement. Joint movement was variably affected; it was either normal, lax, restricted in the range of mobility, or occasionally, fixed. The characteristic findings were: bilateral hyperextension of the hind fetlock, flexion deformity of the forelimb that particularly involved the fetlock and the carpus, with restricted articular movement and complete rigidity in some cases. One-third of calves also had medial deviation of the forelimb due to angular deformity of articular surfaces in the carpus. All nine live calves were floppy due to marked generalized muscular hypotonia. Birth weight of deformed calves was reduced. In some calves muscle development was impaired as judged by muscle weight, and histological examination. In some calves the gross appearance, muscle weight and histological examination revealed no abnormal development and indicated that the effects on skeletal muscle were secondary. No lesions were found in the spinal cord of 23 of 24 calves examined histologically. The remaining calf had a localized cavitation in the dorsal white matter at T2-3. Based on the observations in calves in this study it is proposed that both primary and secondary factors contribute to the phenotypic expression of this congenital deformity. The primary lesion is considered to be a neurogenic abnormality of differentiation in the central nervous system. Cytogenetic analysis of 16 carrier cows and two deformed calves showed normal karyotypes. Serology for Akabane virus in 16 carrier cows was negative.     

An outbreak of congenital hydranencephaly and cerebellar hypoplasia among calves in South Kyushu, Japan: a pathological study

An outbreak of congenital hydranencephaly and cerebellar hypoplasia occurred between November 1985 and May 1986 in Miyazaki, South Kyushu, Japan. Seventy-three calves had nervous signs of varying severity such as inability to stand, locomotor difficulties, defective vision and difficulty in sucking. At necropsy, 62 calves had macroscopic lesions in the central nervous system: hydranencephaly accompanied by cerebellar hypoplasia in 47; hydranencephaly alone in eight; and dilatation of the lateral ventricle in seven; none had arthrogryposis. Microscopically, all 62 cases involved various degrees of hypoplasia of neural components, such as total or partial thinning of the cerebral or cerebellar laminae. Heterotopia, such as abnormal islands of granule cells or Purkinje cells was also observed. Fourteen of these animals had other lesions such as non-purulent encephalitis, focal gliosis, neuronal degeneration, calcification or pseudocalcification, and cholesterol deposits, activation of vascular endothelial cells and haemorrhage. From the findings, these cases were considered to represent mainly hypoplasia of nerve tissue due to infection with a virus different from Akabane virus.     

Hyperextension of fetlock joints in German Holstein and German Holstein-Limousin crossbred calves

In two different dairy farms six calves exhibiting bilateral flexion of the fetlock joints in front or rear legs were born in 2000 to 2002. Four of the affected calves from the same farm were crossbred between German Holstein cows with red and white coat colour and a bull of the breed Limousin. The other two affected calves born on another farm were purebred German Holsteins with a black and white coat colour. The tests for BVD virus antigen and antibodies were negative in all affected calves. Three of the calves showed a lower selen and a higher glutamate dehydrogenase concentration in the analyses of blood metabolites. Two crossbred calves showed a degeneration of the liver with a progressive periportal fibrosis in a histological examination. In one calf an edema of astrocytes of the central nervous system was seen. The analysis of the pedigrees revealed for the four crossbred calves the Limousin bull as common ancestor and the mothers of the calves as relatives. For the affected purebred German Holstein calves also a sire was identified as a common ancestor. The pedigrees support inheritance through a monogenic autosomal recessive locus or more recessive gene loci with variable expressivity. However, the analysis could not clarify whether different gene loci are responsible for the congenital anomalies observed in the calves from the two farms and thus, the observed anomalies may be different genetic entities. Obvious environmental reasons were not found.     

MENINGEAL HAEMORRHAGE AND CONGESTION ASSOCIATED WITH THE PERINATAL MORTALITY OF BEEF CALVES

Thirty Angus, Hereford and Shorthorn term calves dying before, during or within 7 days of birth in a large beef herd were autopsied. Selected specimens were examined histologically. Two carcasses were classified in the category of ante-parturient death, 24 as parturient, and 4 were classified in the post-parturient death category. Three of the latter showed evidence of starvation. Eight of the calves in the parturient death category were assisted during delivery, and 16 were not assisted. The incidence of nulliparous dams among assisted parturient deaths was significantly higher than among the unassisted group. A high incidence of meningeal haemorrhages and congestion were observed at single or multiple sites, within and around the cranial and spinal meninges. The lesions comprised subdural and epidural haemorrhages, bloodstained cerebrospinal fluid and leptomeningeal haemorrhage and congestion. They were seen in calves in both parturient and post-parturient death categories but not in the ante-parturient group. All calves classified in the parturient death category which were assisted during delivery showed haemorrhages involving the cranial and/or spinal meninges. Additional birth injuries, including separation of the costo-chondral junctions, fractured ribs, haemorrhage into the hip joints, inter-vertebral fibrocartilages and axillae, and rupture of the liver, were frequently present. Ten of the calves in the parturient death category which were unassisted during delivery showed meningeal haemorrhage and congestion. Two of the 4 calves in the post-parturient death category showed similar lesions and both showed evidence of starvation. The meningeal haemorrhages and congestion were similar to those observed in perinatal lamb mortality. They are considered manifestations of injury to the CNS arising from trauma and/or hypoxia during birth. Gross or microscopic evidence of infection was present in 2 calves in the post-parturient death category. Calves which had starved showed subcutaneous oedema of the distal limbs, congestion and focal haemorrhage of the adrenal cortex and red-brown fat depots. It is suggested that these changes are evidence of cold injury, and that fat in newborn calves responds to cold and starvation in a manner similar to the brown fat of newborn lambs.     

Prickly paddy melon (Cucumis myriocarpus) poisoning of cattle

Twenty-six Hereford heifers died after eating mostly ripe fruit of Cucumis myriocarpus growing in a fallowed cultivation paddock. Four affected cattle were dehydrated and apparently had abdominal pain. Necropsy of three revealed intense congestion with haemorrhage of the alimentary tract, numerous C. myriocarpus seeds in ruminal contents, pulmonary congestion and oedema and, in two, swollen livers. Midzonal swelling and vacuolation of hepatocytes occurred in these two. C. myriocarpus fruit (83% by weight ripe) were dosed to two calves at 60 g wet weight/kg live weight. Both collapsed with tachycardia and dyspnoea and died within 6 h. Their packed cell volumes just before death had increased to 0.7. They had hydropic degeneration and necrosis of the ruminal mucosa, intense congestion and oedema of the rumen, abomasum and intestines, swollen and vacuolated hepatocytes and foci of myocardial degeneration and necrosis. Two other calves were dosed daily with 20 g fruit/kg for three days, then 40 g/kg for three days. One calf received a further 40 g/kg next day. Both calves developed persistent diarrhoea and neutrophilia, and their plasma gamma glutamyltransferase and bilirubin concentrations increased. Necropsy revealed necrosis and oedema of the rumen and swollen degenerate hepatocytes.     

Crooked calf disease: a histological and histochemical examination of eight affected calves

Macroscopic, histopathologic, and histochemical investigations were made on a group of eight neonatal Angus X Hereford calves, selected from an ongoing outbreak of crooked calf disease among calving heifers. Arthrogryposis of the forelimbs was seen to varying degrees in all eight animals, and torticollis was present in six calves. Histopathology, using hematoxylin and eosin stain, did not reveal any striking or consistent lesion in the affected animals; the majority of the tissues sampled were normal. Muscle samples were processed for adenosine triphosphatase (ATPase) and NADH-tetrazolium reductase (NADH-tr) histochemistry, and the data suggest that a primary myopathy is not responsible for the congenital anomalies in the affected calves.     

Neural changes in vaccinated calves challenge exposed with virulent infectious bovine rhinotracheitis virus

Recurrent infection in calves vaccinated with infectious bovine rhinotracheitis-(IBR) modified live virus was induced by dexamethasone (DM) treatment given 49 days after challenge exposure with virulent IBR virus. Nonchallenge-exposed IM and intranasally vaccinated calves did not excrete the virus after DM treatment; however, IM and intranasally vaccinated and subsequently challenge-exposed calves excreted the challenge-exposure virus into the nasal secretions 5 to 11 days and 6 to 10 days after the DM treatment, respectively. The calves were killed 15 to 18 days (experiment 1) and 14 days (experiment 2) and DM treatment was started and then were examined by histopathologic and fluorescent antibody techniques. All DM-treated calves that were inoculated with the vaccinal virus and challenge exposed with the virulent virus developed nonsuppurative trigeminal ganglionitis and encephalitis. On the contrary, the DM-treated nonchallenge-exposed vaccinated calves did not have lesions in the peripheral nervous system and CNS. Infectious bovine rhinotracheitis virus antigens were not observed in tissues of any of the calves examined (experiments 1 and 2) by fluorescent antibody techniques. These observations indicated that the modified live IBR virus neither produced lesions nor induced latent infection and that modified live IBR virus vaccination did not protect the calves against the establishment of a latent infection after their exposure to large doses of the virulent IBR virus.     

Experimental Bovine Pneumonic Pasteurellosis II. Genesis and Prevention

Two experiments were conducted. In the first, 16 crossbred Hereford calves were divided into two equal groups. The first group was vaccinated intranasally with a commercial vaccine against bovid herpesvirus 1 and the second group was unvaccinated. The calves were later exposed to an aerosol of bovid herpesvirus 1 (strain 108) for five minutes. Four calves from each group were subjected to transportation and four calves from each group were kept in an environmental chamber for four days. Four days after viral aerosol all calves were exposed to an aerosol of Pasteurella haemolytica and the same subgroups were again transported or held in the chamber for a further four days.

The calves that did not die from pneumonia were necropsied ten days after the final day of transport. Pulmonary lesions were present in both vaccinated and control animals but were less extensive in the vaccinated calves. Six of eight vaccinated but none of the eight control calves survived.

In the second experiment, eight crossbred Hereford calves were divided into two equal groups. One group was vaccinated with bovid herpesvirus 1 (strain 108) and the other acted as controls. Four weeks later all calves were sequentially exposed to aerosols of bovid herpesvirus 1 (strain 108) and P. haemolytica four days apart. Three of the four controls but none of the vaccinates died from pneumonia. Every lobe of the lungs in all the controls was affected by pneumonia while no pulmonary lesions were found in the vaccinated calves. The differences in efficacy of the modes of vaccination and the possible role of transport stress are discussed.

     

Heterosis retention for birth and weaning characters of calves in the third generation of a five-breed diallel.

Data were 876 birth records and 727 weaning records of straightbred and F3 crossbred calves produced in the third generation of a five-breed diallel. Among straightbreds at birth, Holstein calves were heaviest and widest at the shoulders and hips. Jersey calves were lightest and narrowest at the hips, and Brahman calves were narrowest at the shoulders. Holstein crosses tended to be larger at birth than crosses among other breeds. Among straightbreds at weaning, Holstein calves were heaviest and tallest, and Hereford calves were lightest and shortest. Angus calves had the highest survival to weaning rate, and Holstein calves had the lowest survival rate. Among crossbred calves, Holstein crosses tended to be larger at weaning. Estimates of average heterosis retained for birth characters were not significant. Significant breed mean heterosis retention was observed for birth weight, shoulder width, and hip width of Hereford calves and for shoulder width and hip width of Holstein calves. Estimates of average heterosis retained for weaning weight and height were 6.1 kg (P less than .01) and 1.02 cm (P less than .05), respectively. In general, estimates of specific and average heterosis retained for survival to weaning were nonsignificant. Significant breed mean heterosis was observed for weaning weight and height of Brahman, Hereford, and Holstein calves and for survival to weaning of Hereford, Holstein, and Jersey calves.     

Experimental transmission of chronic wasting disease agent from mule deer to cattle by the intracerebral route.

This communication reports final observations on experimental transmission of chronic wasting disease (CWD) from mule deer to cattle by the intracerebral route. Thirteen calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated 6 years after inoculation. During that time, abnormal prion protein (PrP(res)) was demonstrated in the central nervous system (CNS) of 5 cattle by both immunohistochemistry and Western blot. However, microscopic lesions suggestive of spongiform encephalopathy (SE) in the brains of these PrP(res)-positive animals were subtle in 3 cases and absent in 2 cases. Analysis of the gene encoding bovine PRNP revealed homozygosity for alleles encoding 6 octapeptide repeats, serine (S) at codon 46, and S at codon 146 in all samples. Findings of this study show that although PrP(res) amplification occurred after direct inoculation into the brain, none of the affected animals had classic histopathologic lesions of SE. Furthermore, only 38% of the inoculated cattle demonstrated amplification of PrP(res). Although intracerebral inoculation is an unnatural route of exposure, this experiment shows that CWD transmission in cattle could have long incubation periods (up to 5 years). This finding suggests that oral exposure of cattle to CWD agent, a more natural potential route of exposure, would require not only a much larger dose of inoculum but also may not result in amplification of PrP(res) within CNS tissues during the normal lifespan of cattle.