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.     

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.     

Bovine citrullinaemia: a clinical, pathological, biochemical and genetic study

Calves affected with citrullinaemia are clinically normal immediately after birth. In the majority of calves the clinical course of the disease was similar. Within 24 hours of birth they become depressed; then within 3 to 4 days were observed to wander aimlessly or stand with their head pressed against a wall or fence. By day 4 to 5 they become recumbent, developed convulsions, followed by collapse and death. Oedema of the cerebral cortex is a consistent histological lesion. Citrulline concentration in blood, cerebrospinal fluid, eye fluid and cerebral tissue is greatly elevated. Information gathered from pedigrees of affected calves indicate that the defect is widely disseminated throughout the Australian Friesian population.     

Dwarfism in Hereford cattle: a genetic morphological and biochemical study

A study of 40 Hereford cattle dwarfs in New Zealand confirmed that dwarfism in this country was morphologically the same as that described in North American Herefords and that its mode of inheritance was as an autosomal recessive trait. The histological architecture of growth plates was essentially normal but palisading columns were shorter and more irregular than in controls. A small proportion of chondrocytes in dwarf cartilage showed increased areas of cytoplasmic metachromasia, which probably coincided with increased cystic dilations of endoplasmic reticulum containing granular material as noted by electronmicroscopy. The above growth-plate abnormalities were neither prominent nor consistent enough to be of diagnostic significance; nor do they currently help understanding of the underlying pathogenic mechanism of dwarfing. Histological and mucopolysaccharide excretion studies unequivocally demonstrated that this disease is not a mucopolysaccharidosis as had previously been reported.     

Dwarfism in Hereford cattle: a genetic morphological and biochemical study

A study of 40 Hereford cattle dwarfs in New Zealand confirmed that dwarfism in this country was morphologically the same as that described in North American Herefords and that its mode of inheritance was as an autosomal recessive trait. The histological architecture of growth plates was essentially normal but palisading columns were shorter and more irregular than in controls. A small proportion of cbondrocytes in dwarf cartilage showed increased areas of cytoplasmic metachromasia, which probably coincided with increased cystic dilations of endoplasmic reticulum containing granular material as noted by electronmicroscopy. The above growth-plate abnormalities were neither prominent nor consistent enough to be of diagnostic significance; nor do they currently help understanding of the underlying pathogenic mechanism of dwarfing. Histological and mucopolysaccharide excretion studies unequivocally demonstrated that this disease is not a mucopolysaccharidosis as had previously been reported.     

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.     

Acute lead poisoning in calves: clinical, pathological and toxicological findings]

We present a case of acute lead poisoning in 10 calves. All calves died with few or no clinical signs prior to death. The clinical signs included neurologic and gastrointestinal symptoms but were of an unspecific nature. Several painted iron girders, stored on a field close to the farm, were determined as the source of the poisoning. Postmortem findings were minimal. Some animals presented acid-fast, intranuclear inclusion bodies in the renal tubules. A chemical analysis of some frozen parts of the liver and kidney revealed levels of lead as high as 12 ppm in the liver and 63 ppm in the kidney on a wet-weight basis. This article discusses the etiology, clinical signs, postmortem findings and diagnosis of lead poisoning in calves with special emphasis on the chemical analysis.     

Congenital dyserythropoiesis and progressive alopecia in Polled Hereford calves: hematologic, biochemical, bone marrow cytologic, electrophoretic, and flow cytometric findings.

Congenital dyserythropoiesis with dyskeratosis is a slow, progressive, and often fatal disease in Polled Hereford calves. Affected calves have a macrocytic normochromic anemia with a mild reticulocytosis. Studies indicate that calves are hyperferremic with increased saturation of serum total iron binding capacity, which rules out iron deficiency as a cause. Other secondary causes of dyserythropoiesis, including cobalamin and folate deficiencies, are unlikely because serum cobalamin and folate levels of affected calves were normal. Virus isolation was negative, and failure to identify bovine retroviral antigens or antibodies from several calves suggested that viral agents were not involved. Bone marrow cytologic findings were similar to those in congenital hereditary dyserythropoiesis in humans and included occasional multinucleate cells, internuclear chromatin bridging between nuclei of partially divided cells, and, more frequently, irregular nuclear shapes and chromatin patterns. DNA content and cell cycle distribution of erythroid cells appeared normal, and no electrophoretic abnormalities were detected in erythrocyte membrane proteins. The Polled Hereford syndrome is similar in many ways to type I congenital dyserythropoiesis in humans and may be an appropriate biomedical model for studying erythroid proliferation during dyserythropoiesis.     

Feline dysautonomia (the Key-Gaskell syndrome): a clinical and pathological study of forty cases

Feline dysautonomia is a dysfunction of the autonomic nervous system, the main features of which are dilated pupils, dry mucous membranes, mega-oesophagus and constipation. The clinical and pathological features, treatment and follow-up details of 40 cases seen at the University of Glasgow Veterinary School are described. The pathology was demonstrated to be mainly restricted to the autonomic ganglia and neurons in selected cranial nerve nuclei. Less marked changes were also found in neurons of the spinal cord and dorsal root ganglia. Nine cases recovered but this required up to one year and, in some, mild clinical signs persisted. Viral, toxicological and epidemiological studies were unrewarding and the aetiology is presently unknown. The similarities between this condition, grass sickness of horses and dysautonomia in the dog and man are discussed.     

Sarcoids in two captive tapirs (Tapirus bairdii): clinical, pathological and molecular study

This case report describes for the first time sarcoids in tapirs (Tapirus bairdii), namely, a 2-year-old male and a 3.6-year-old female born and housed at the same facility. The male presented with a 3-cm nodular, red, pedunculated, hairless, ulcerated mass on the inner surface of the left pinna. No recurrence or additional growths were present during the 3 years following surgical excision of the mass. The female presented with a similar 2-cm mass on the inner surface of the right pinna, which recurred 2 months following surgical excision, but was subsequently successfully treated locally with liquid nitrogen with no further recurrence during a 2-year follow-up period. Histologically, these two masses closely resembled equine sarcoids. Similarly, an association with bovine papillomavirus 1 was demonstrated using polymerase chain reaction and in situ hybridization.     

Clinical, biochemical and pathological study of perinatal lambs in a commercial flock

The birth and fate of 818 lambs born to 571 ewes on a low-ground farm in the Scottish Borders with a history of substantial perinatal mortality were monitored with a range of physiological, biochemical and pathological measurements. In lambs which survived, the rectal temperature, birthweight and plasma concentrations of fructose, insulin, thyroxine and the third component of complement at birth, and the weight at four months of age, decreased with litter size. One hundred and thirty-seven lambs were stillborn or died within four days and seven others died later. The mothers of 77 per cent of these lambs had low condition scores, but the lamb deaths did not correlate significantly with the condition scores. From data relating to birthweight, temperature, packed cell volume and plasma composition it was deduced that placental insufficiency was involved in 24 per cent of these deaths; acute hypoxaemia at birth accounted for 35 per cent, inadequate thermogenesis for 12 per cent and starvation for 13 per cent. The remaining 16 per cent of dead lambs could not be assigned to any of these categories. Using only clinicopathological criteria, 37 per cent of the lamb deaths were attributed to antenatal influences which included immaturity, developmental anomalies, and degenerative or inflammatory changes. Thirty-three per cent of the deaths were due to post natal factors which included, in declining order of frequency, starvation, enteritis, misadventure, pneumonia, navel infections and septicaemia. No conclusions could be drawn from the pathological examinations alone in the remaining 30 per cent, although almost half of these had low rectal temperatures after birth, death being attributed to hypothermia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Membranous nephropathy in the cat: a clinical and pathological study

A series of 13 cases of feline membranous nephropathy is presented. Two groups were distinguished clinically; eight cats had the nephrotic syndrome and five others were in renal failure but not nephrotic. The definitive diagnosis was based on histological, immunofluorescence and ultrastructural examinations of renal tissue obtained at renal biopsy or necropsy. Glomerular lesions were classified according to the degree of glomerular change into three distinct groups; mild, moderately severe and advanced. A relationship was established between the mild and moderately severe groups and cats with the nephrotic syndrome, and the advanced group and cats in renal failure. Diuretic therapy was satisfactory in initial control of oedema in the nephrotic cases. Monitoring of previously nephrotic cats for up to three years indicated that the disease is progressive, although in some cases it is sufficiently slow for a cat to live a relatively normal life without continuing treatment. The prognosis for cats presented in renal failure is hopeless.     

Behavioural, biochemical, and pathological responses of possums (Trichosurus vulpecula) poisoned with phosphorus paste

AIM: To investigate the behavioural, biochemical and pathological responses of possums following poisoning with phosphorus paste, in order to assess the implications for the welfare of possums. METHODS: After ingestion of phosphorus paste by wild-caught possums (18 high dose, nine low dose, and 12 non-poisoned controls), behavioural observations were made at 15-min intervals for 24 h or until death. Serum biochemistry, and gross and microscopic pathology were assessed at 3-hourly intervals in a further 21 possums. RESULTS: Possums that ingested phosphorus paste developed an abnormal posture (high incidence of crouching after 4-8 h), mild congestion of the gastric mucosa, and elevated levels of creatine kinase (CK) in serum after 3-6 h. Retching was observed in 67% possums, and 44% vomited at least once. Possums were prostrate from about 18 h after eating the poison, and the response to handling, an indicator of consciousness, was lost at about 24 h, followed by death at 25 h. CONCLUSION: The main welfare concern was the possibility of discomfort or pain caused by the congestion of the gastric mucosa, as indicated by the crouched posture adopted by poisoned possums. Retching and vomiting may also have caused pain and distress. The degree of pain or discomfort would depend on the degree of congestion of the gastric mucosa, which was typically mild, and on the duration and severity of retching and vomiting, which were typically short and mild. Possums remained conscious until 1 h before death, implying that they were able to experience pain and distress from the effects of ingestion of phosphorus for almost the entire period of illness, which lasted for approximately one day.     

Relationships between clinical and pathological signs of disease in calves infected with Mannheimia (Pasteurella) haemolytica type A1.

Respiratory disease was induced in 16 calves, and the terminal clinical signs of disease and postmortem pathological observations were recorded. By Spearman's correlation coefficient, the respiratory rate, rectal temperature and clinical scores of the calves were significantly correlated with the extent of lung consolidation. The respiratory rate was the clinical sign most consistently correlated with the other clinical and pathological signs of respiratory disease.