Biomedical subjects

J A Coetzer

Publications and source records attributed to J A Coetzer.

At least 37 records · Page 2Linked to original sources

PubMed1982

The pathology of Rift Valley fever. II. Lesions occurring in field cases in adult cattle, calves and aborted foetuses.

Since the original description of Rift Valley fever in sheep, cattle and man in the Rift Valley in Kenya in 1931, very little has been published on the disease in cattle. This report deals with the macroscopic and microscopic pathology of field cases of Rift Valley fever in 22 adult cattle, 8 calves and 8 aborted foetuses. The microscopic liver lesions in 13 adult cattle were characterized by marked centri- and midzonal eosinophilic necrosis, involving almost 2/3 of the lobules, and accompanied by sparsely distributed primary foci of necrosis. In 3 animals, however, the hepatic lesions were more focal in nature, while a massive hepatic necrosis was evident in 6 others. In calves, the lesions in the liver ranged from cases showing numerous haphazardly scattered primary foci of necrosis to cases where the latter were accompanied by eosinophilic necrosis of the remaining hepatocytes in the lobules. Vascular lesions, thrombosis and sinusoidal fibrin deposits were sometimes seen in the livers of both calves and adult cattle. Although the aborted foetuses were in a fairly advanced state of autolysis, it was still possible to make a diagnosis of Rift Valley fever from the characteristic lesions which were similar to those reported for new-born lambs. Other noteworthy lesions in adult cattle and calves included pyknosis and karyorrhexis of lymphocytes in the spleen and lymph nodes, widespread serosal and visceral haemorrhages which were sometimes accompanied by copious free blood in the gastrointestinal tract, and a nephrosis.

Animals↗

PubMed1982

Studies on Parafilaria bovicola Tubangui, 1934 III. Pathological changes in infested calves.

More lesions were found in the carcass of an animal that has been naturally infested with Parafilaria bovicola than in one artificially infested with a single subcutaneous injection of infective larvae of this species. This may be because natural infestations are either more frequent or more successful. Similarities in the distribution of lesions in naturally and experimentally infested animals suggest that certain predilection sites may be used by the intermediate fly hosts. Subcutaneous areas infiltrated with eosinophils are more conspicuous during the first 20 days after infestation and during the patent phase of the life cycle of P. bovicola. Yellowish discolorations caused by oedema are usually present in all lesions. When these are combined with eosinophil infiltrations, the lesions become yellowish-green. After the appearance of bleeding spots the green colour of lesions is dominated by the appearance of a brown pigment (haemosiderin) in numerous macrophages. The histopathological changes in the dermis, subcutis and superficial muscles bordering the affected areas are described.

Animals↗

PubMed1982

Oak (Quercus rubor)poisoning in cattle.

Two outbreaks of oak poisoning in cattle in the Republic of South Africa are described. In the first outbreak 22 out of 80 head of cattle were severely affected while 40 out of a herd of 135 cattle were affected in the second outbreak. Of these 40, only one survived after 9 months despite vigorous treatment. Only young cattle under 2 years were affected during both outbreaks in spite of an average herd age of approximately 6 years in the second group of cattle. Clinical signs included severe weakness with a swaying gait, diarrhoea and dehydration. Some were pot bellied while others were emaciated and remained stunted. The most prominent macroscopic and microscopic lesion present in 3 animals autopsied, was a non-suppurative interstitial nephritis which was accompanied by oedema and ulceration of the caecum and colon. Histochemical studies were carried out on pigment granules observed in kidney sections.

Animals↗

PubMed1982

Sequential development of the liver lesions in new-born lambs infected with Rift Valley fever virus. I. Macroscopic and microscopic pathology.

Ten new-born lambs were necropsied at various intervals after artificial infection with Rift Valley fever virus for the study of the sequential development of the hepatic lesions. During the late stage of the disease, the livers were slightly to moderately swollen and mottled yellow, orange-brown and red. Greyish-white foci, approximately 0,25-0,5 mm in diameter, were also scattered throughout the parenchyma. Microscopically, the liver lesions progressed from sparsely distributed acidophilic bodies and hepatocytes, revealing acidophilic degeneration and necrosis 6-12 h post-inoculation, to small randomly scattered primary foci of necrosis 12-24 h after infection. At 30-36 h, these primary foci were larger and more circumscribed. In addition, numerous acidophilic bodies and necrotic hepatocytes were dispersed throughout the markedly degenerated parenchyma. The terminal stage of the disease (48-53 h after inoculation), was characterized by massive hepatic necrosis in which primary foci of necrosis could still be recognized as dense aggregates of cytoplasmic and nuclear debris.

Animals↗

PubMed1982

Sequential development of the liver lesions in new-born lambs infected with Rift Valley fever virus. II. Ultrastructural findings.

The macroscopic and microscopic lesions in livers of new-born lambs experimentally infected with Rift Valley fever virus and killed at various intervals between 6-53 h after inoculation, were described in a previous paper. This communication gives an overview of the ultrastructural changes affecting hepatocytes, sinusoids and spaces of Disse, biliary tree and portal triads as well as observations on the morphology and morphogenesis of the virus. Hepatocytes were those primarily affected, while inflammatory and architectural changes were secondary. The changes included prominent nuclear alterations, fragmentation or disintegration of necrotic hepatocytes, focal cytoplasmic degradation and sequestration, and the presence of acidophilic bodies. The ultrastructure and origin of the intranuclear inclusions are discussed.

Animals↗

PubMed1982

Observations on the clinical, cardiac and histopathological effects of fluoroacetate in sheep.

Fluoroacetate was dosed per stomach tube to 17 Merino sheep at the rate of 0,05-1,0 mg/kg/day. The clinical signs, haemodynamic changes, chemical pathology and pathology of acute, subacute and chronically intoxicated cases are described. Tetanic convulsions were seen in acutely intoxicated animals and in them respiratory failure, occurring concomitantly with cardiac failure, may have been the cause of death. Subacute intoxication resulted in less conspicuous clinical signs when the sheep were at rest, but they developed apparent nervous signs on being handled, and later tended to lie down. Chronically intoxicated animals were only mildly affected. At all levels of intoxication changes in the chemical pathological parameters were either absent or were mild and transient. The microscopic lesions in the hearts of acutely intoxicated sheep included degeneration as well as necrosis of individual or small groups of myocardial fibres. In the subacutely and chronically intoxicated animals the multifocal myocardial lesions were more widespread and in various stages of development or resolution.

Animals↗

PubMed1980

Wesselsbron disease: virological and serological studies in experimentally infected sheep and goats.

Adult sheep and goats and new-born lambs and kids were experimentally infected with a Wesselsbron disease virus. The viraemia in lambs commenced approximately 27 h after infection and lasted on the average for 50 h. A febrile reaction, which was mostly biphasic, commenced several hours after the viraemia and outlasted it by 50 h. The viraemia in adult animals began about 50 h after infection and lasted for 30 h. The fever usually commenced several hours after the viraemia and, as in 3 cases out of 4 in lambs, it outlasted the viraemia by at least 30 h. The virus could be reisolated in mice from every tissue examined in lambs, although it has previously been shown that pathological lesions are restricted to the liver and lymphatic tissues.

Animals↗

PubMed1980

[Brain teratology as a result of transplacental virus infection in ruminants].

Various viruses relating to congenital brain teratology in ruminants are discussed. These include: bluetongue which may be responsible for porencephaly and hydranencephaly; Akabane disease, Rift Valley fever (mouse brain attenuated virus) and Wesselsbron disease (wild-type and mouse brain attenuated viruses) which can give rise to porencephaly, hydranencephaly, micrencephaly and cerebellar hypoplasia, and bovine viral diarrhoea-mucosal disease which results only in cerebellar hypoplasia. Certain foetal, maternal and virological factors that might have an effect on the pathogenesis of viral teratogenesis are briefly reviewed. Mention is also made of the different diagnostic procedures that can be used such as, gross and histopathological examination, virus isolation and serology.

Animals↗

PubMed1980

Photosensitivity in South Africa. II. The experimental production of the ovine hepatogenous photosensitivity disease geeldikkop (Tribulosis ovis) by the simultaneous ingestion of Tribulus terrestris plants and cultures of Pithomyces chartarum containing the mycotoxin sporidesmin.

The mycoflora of toxic pastures were surveyed during a number of outbreaks of ovine hepatogenous photosensitivity in South Africa. Pure cultures of several isolates were dosed to sheep, but only those of Pithomyces chartarum and Myrothecium verrucaria proved to be toxic. Photosensitization was induced in sheep by dosing them with cultures of a P. chartarum isolate (GA10) obtained from Tribulus terrestris plants collected during an outbreak of geeldikkop in the Karoo. Thus for the first time a mechanism whereby T. terrestris plants can contribute to the causation of ovine hepatogenous photosensitivity was demonstrated. When cultures of GA10 equivalent to approximately 0,75--4,0 mg/kg sporidesmin were dosed at Onderstepoort Veterinary Research Institute to Highveld and Karoo sheep on a diet of lucerne, facial eczema was produced. Dosing the same cultures at levels equivalent to c. 1,0 mg/kg of sporidesmin in the Karoo resulted in lesions characteristic of both facial eczema and geeldikkop. Typical hepatic lesions of geeldikkop could be elicited by dosing GA10 at levels equivalent to c. 0,25--0,7 mg/kg of sporidesmin to Karoo sheep grazing on predominantly T. terrestris pastures in the Karoo. In the latter experiment geeldikkop was induced in the sheep on T. terrestris pastures, while those receiving identical doses on veld with little T. terrestris developed facial eczema. Geeldikkop, therefore, can be brought about by the ingestion of T. terrestris plants together with toxic cultures of P. chartarum. The plant appears not only to act as a vehicle for ingestion of spores, but also to interact with sporidesmin to induce lesions typical of geeldikkop, whereas sporidesmin alone results in facial eczema. Indications are that it can enhance the ability of sporidesmin to cause photosensitivity or, possibly, vice versa. The histopathological findings of these experiments are described in detail.

Animals↗

PubMed1979

Subcutaneous and pulmonary emphysema as complications of bovine ephemeral fever.

Subcutaneous and pulmonary emphysema was observed in some cattle on farms on which outbreaks of bovine ephemeral fever (BEF) occurred. BEF virus was isolated in baby hamsters from one of the cases and cattle were injected with blood from this animal. Although the experimental animals developed typical BEF symptoms, no signs of emphysema could be detected by clinical and pathological examinations. The histopathological changes in the skeletal muscle and synovial membranes of the natural case resembled those of BEF described by Basson, Pienaar & Van der Westhuizen (1970). The lumina of the terminal and respiratory bronchioles in the lungs were obliterated by cellular debris and the muscular portion of some of these bronchioles was necrotic. The possible pathogenesis of pulmonary emphysema is discussed.

Animals↗

PubMed1979

Wesselsbron disease: a cause of congenital porencephaly and cerebellar hypoplasia in calves.

Fifteen pregnant cows were inoculated subcutaneously and intravenously between 101-147 days of gestation with the wild-type Wesselsbron disease virus. In addition, 2 foetuses were injected directly through the uterine wall after surgical exposure of the pregnant horn. The clinical symptoms, viraemia and serology in the cows are reported, as also the gross- and histopathology and the virological and serological results of the calves and foetuses. Abortion was not an important manifestation of experimental Wesselsbron disease in cows, as it occurred in 3 animals only. Apart from a short temperature reaction in some cows no other clinical symptoms were recorded. A viraemia was not always present in these cows and, when detected, was of low magnitude and short duration. One cow, in which the foetus was ioculated at 115 days of gestation, aborted at 231 days. The foetus showed marked porencephaly and cerebellar hypoplasia.

Animals↗

PubMed1978

[Infectious causes of perinatal mortalities in ruminants (author's transl)].

The advantages and disadvantages of the different diagnostic techniques e.g. pathological and microbiological studies, immunoglobulin and specific antibody determinations and fluorescent antibody studies in relation to these mortalities are discussed. The most important pathological lesions in the placentas and foetuses are described.

Abortion, Veterinary↗

PubMed1978

Wesselsbron disease, pathological, haematological and clinical studies in natural cases and experimentally infected new-born lambs.

This is a report on the clinical signs of Wesselsbron disease in 37 lambs and the pathology of 4 natural and 12 experimental cases. Generally the symptoms were ill-defined. At autopsy 13 of the 14 lambs revealed a mild to severe icterus and a slight to moderate hepatomegaly with discoloration of the liver. No foci of hepatic necrosis were observed macroscopically and, except for petechial and ecchymotic haemorrhages in the mucosa of the abomasum and generalized lymphadenopathy, no other obvious macroscopic lesions were noted. Perforation of the abomasum occurred in one lamb only. Microscopy on the liver showed mild to extensive necrosis of the parenchyma. Degenerated and necrotic hepatocytes were diffusely scattered throughout the liver, but no definite well-circumscribed foci of necrosis were seen. Mitotic figures and hepatocytes with large nuclei indicated that active regeneration of parenchymal cells had occurred in some of the livers. Other changes, for example, Kupffer cell proliferation, sinusoidal leucostasis, bile duct proliferation and infiltration of mononuclear cells in the portal triads, were frequently encountered. Moderate to severe cholestasis was a feature in 66% of the livers examined, while intranuclear inclusions and intracytoplasmic acidophilic or Councilman-like bodies were frequently observed. A complete haematological study was carried out on 4 experimentally produced cases. The gross and histopathological lesions in the liver are compared with those of Rift Valley fever in the new-born lamb.

Animals↗

PubMed1978

Amicarbalide: a therapeutic agent for anaplasmosis.

When administered subcutaneously in 2 equal daily doses at a total dosage rate of 20 mg/kg, amicarbalide was found to be an effective agent for controlling acute infections of Anaplasma marginale and A. centrale in intact and splenectomized cattle. Attempts to sterilize patent and latent Anaplasma infections, however, were unsuccessful. At total dosage rates of 40 mg/kg and higher, amicarbalide exhibited potent hepato- and nephrotoxic tendencies.

Amidines↗

PubMed1978

A chronic wasting syndrome in a horse associated with granulomatous enteritis.

A case of granulomatous enteritis in a 2 year-old Thoroughbred colt is reported. Clinically the horse showed chronic wasting and subcutaneous oedema of the ventral parts of the body and legs. Grossly the wall of the jejunum and ileum was uniformly thickened. Microscopically the lamina propria, submucosa and the tunica muscalaris of the small intestine were infiltrated with lymphocytes, plasma cells, epithelioid cells and occasional multinucleated giant cells. The granulomatous reaction was most marked in the muscular layers of the gut wall.

Animals↗

PubMed1978

The pathology of an inherited lysosomal storage disorder of calves.

The clinical symptoms, gross and histopathological, as well as the ultrastructural appearance of a condition in cross-bred Aberdeen Angus calves resembling the inherited lysosomal storage disease, alpha-mannosidosis, are reported. The neurones and perithelial cells in the brain and the reticuloendothelial cells in the lymph nodes and spleen were extensively vacuolated. The vacuoles were filled with a sparse, flocculated to granular material within which membranous structures were frequently seen. No specific substance could be identified within the vacuoles, either histochemically or ultrastructurally. Besides the vacuolation, cystic tubular structures were seen in the kidneys. The lining epithelial cells of the thyroid follicles were vacuolated while some of the follicles contained no colloid.

Animals↗

PubMed1977

Hydrops amnii in sheep associated with hydranencephaly and arthrogryposis with wesselsbron disease and rift valley fever viruses as aetiological agents.

During the 1974/75 lambing season numerous reports were received from various parts of the Republic of South Africa and South West Africa of severe abdominal distension in ewes after vaccination with the attenuated Rift Valley fever and/or attenuated Wesselsbron disease vaccine. The ewes were vaccinated at different stages of gestation in spite of recommendations to the contrary, the syndrome being especially obvious in ewes immunized with one or both of these vaccines during the first trimester of pregnancy. In some of the flocks hydrops amnii was recorded in as many as 15% of the ewes. Many of the ewes so affected showed a prolonged gestation of up to 6-7 months and, towards the end of gestation, were unable to rise or walk. They eventually died of ketosis, hypostatic pneumonia and complications due to dystocia. The foetuses examined were malformed and larger than normal with a mass of 3,6-6,7 kg. They usually showed arthrogryposis, brachygnathy inferior, hydranencephaly, hypoplasia or segmental aplasia of the spinal cord and neurogenic muscular atrophy. The amnion contained 8,0-18,0 1 of amniotic fluid, the endometrium was oedematous, and cystic tube-like dilatations, 1-10 mm in diameter, filled with a clear fluid, were scattered in the endometrium. No definite conclusions as to the aetiology of the syndrome could be drawn from serological tests performed on the ewes, lambs or foetuses. Preliminary experimental work confirmed previous observations that the attenuated Wesselsbron disease vaccine virus is responsible for this syndrome and that the wild-type virus is also implicated. In addition, the attenuated Rift Valley fever vaccine virus was found to the responsible for arthrogryposis and hydranencephaly without hydrops amnii and for micrencephaly and arthrogryposis associated with hydrops amnii in the ewe.

Anencephaly↗

PubMed1977

The pathology of Rift Valley fever. I. Lesions occurring in natural cases in new-born lambs.

A widespread epizootic of Rift Valley fever occurred in the Republic of South Africa and South West Africa during 1974--75. This is a report on the gross pathology of 34 new-born lambs and the histopathology of 93 new-born lambs that died during this outbreak. The liver was affected in every case and showed the most pronounced lesions. The organ was grossly enlarged in most cases, with scattered greyish-white necrotic foci 1--2 mm in diameter and haemorrhages of varying size throughout. Haemorrhages were also frequently seen in the mucosa of the abomasum. The massive diffuse necrosis of hepatocytes (pannecrosis) associated with well-demarcated foci of primary coagulative necrosis, present in 100% of the cases examined, was characteristic of the histopathology of the new-born lamb. Bile thrombi were noticed in the livers of 31% of the lambs and intranuclear inclusions in 49% of the cases. The diagnostic significance of the microscopic liver lesions is discussed. Focal necrosis and haemorrhages were frequently seen in the adrenal cortex while generalized destruction of lymphocytes in the lymph nodes and spleen occurred in many of the animals. In addition, the following hitherto undescribed or previously not well-documented lesions are recorded: (i) mineralization of single or groups of necrotic hepatocytes in 62% of the livers: (ii) pyknosis and karyorrhexis of the cellular elements in the glomeruli and a hyalinized appearance of many of these affected glomeruli; and (iii) necrosis of the tips of the villi in the small intestine in some of the animals.

Animals↗