The pathology of Johne''s disease in sheep

The clinical, gross and histopathological findings in 50 sheep affected with Johne's disease are described. Clinically 90% were emaciated and 20% showed severe diarrhoea. On necropsy there was thickening of the walls of the intestines, particularly of the ileum, caecum and less frequently the jejunum, but in 36% of sheep the changes were only mild. Histologically there was a granulomatous enteritis, typhlitis and colitis, with the most severe changes in the terminal ileum. High numbers of acid-fast organisms were present in the terminal ileum in over 70% of sheep. Mycobacterium paratuberculosis was cultured from only 8% of the sheep examined.     

TSE pathogenesis in cattle and sheep

Many studies have been undertaken in rodents to study the pathogenesis of transmissible spongiform encephalopathies (TSE). Only a few studies have focused on the pathogenesis of bovine spongiform encephalopathy (BSE) and scrapie in their natural hosts. In this review, we summarize the most recent insights into the pathogenesis of BSE and scrapie starting from the initial uptake of TSE agents and crossing of the gut epithelium. Following replication in the gut-associated lymphoid tissues (GALT), TSE agents spread to the enteric nervous system (ENS) of the gut. Infection is then carried through the efferent fibers of the post-ganglionic neurons of the parasympathetic and sympathetic nervous system to the pre-ganglionic neurons in the medulla oblongata of the brain and the thoracic segments of the spinal cord. The differences between the pathogenesis of BSE in cattle and scrapie in sheep are discussed as well as the possible existence of additional pathogenetic routes.     

The pathology and pathogenesis of Salmonella stanley infection in experimental chicks

Experimental infection with Salmonella stanley was produced by oral, intravenous and intramuscular routes in day-old chicks. The earliest evidence of the presence of the organisms was in duodenal mucosa six hours after oral infection. Following oral infection the organisms were detected in the duodenum from six hours to five days, in the caecum from 12 hours to nine days, liver, spleen and blood from 24 hours to seven days. The resistance to infection was found to be significant after 10 days old, but not up to six days old. The work confirmed that the survival time of birds given S stanley by the intravenous or intramuscular routes was inversely proportional to the dose up to a maximum beyond which the survival time was not further decreased by dose increase. The presence of S stanley in tissues and blood was detected by isolation and by the fluorescent antibody technique.     

The pathology and pathogenesis of Trypanosoma vivax infection in the goat.

Acute and chronic forms of disease can be distinguished in Trypanosoma vivax infection in the goat. The main difference between the acute and chronic form seems to be the presence of microthrombi in the acute stage of infection; these consist of platelets, trypanosomes, monocytoid cells and some fibrin. This thrombus formation seems directly related to the high parasitaemia in acute trypanosomiasis and may result in ischaemia which could also explain the haemorrhages, the oedema of the lungs and other tissues, and the necrotic changes found in several organs. The anaemia, associated with erythrophagocytosis, haemosiderosis, extramedullary haemopoiesis and hyperactivity of the bone marrow, seemed to be of haemolytic origin. The factors leading to emaciation seemed to be degenerative atrophy of muscular tissue and loss of protein in the urine caused by a possible immune complex glomerulonephritis.     

The pathogenesis of excessive wear in the deciduous teeth of sheep

The teeth and various supporting and ancillary tissues were examined post mortem from two flocks of sheep, one of which had previously shown high deciduous incisor wear. Sheep were killed in groups selected on clinical signs at equivalent ages from birth to 116 weeks of age. At the end of this time the lengths of clinical crowns of the remaining deciduous incisor teeth in the high wear flock were not measurable, whereas the other flock had up to 5.5 mm in visible crown. Using the cingulum as a marker, measurements were made from extracted teeth of the attrition of the crown and size of the root. The tooth root did not grow substantially longer after the 13th week of the sheep;s life. Wear facets were just visible in some sheep at six weeks. More rapid wear occurred three times in the high wear flock. The first of these was relatively small and occurred between the 13th and 27th week of age in I1 and I2. The second was larger and occurred between the 38th and 57th week of age in the winter/spring period. A third period of wear, which was not measured from the cingulum, because this structure had by then been worn away, was seen in the remaining deciduous teeth between the ages of 91 and 110 weeks of age, i.e., during the second winter and spring. In the low wear flock the first of these periods of wear did not occur, the second was of shorter duration and smaller size, and the third equivocal. Eruption of the teeth after the 6th week was principally passive. There was no difference in the degree of wear of the molar teeth from the two flocks. Histological examination showed that the wear was compensated for by the deposition of reparative dentine in the pulp cavity. This usually gave the appearance of an ordered process. However, when wear was excessively rapid, a different, less orderly form of reparative dentine was laid down. In a few cases the reparative process was not fast enough, and a connection developed between the mouth and the pulp causing pulpitis. There was no histological evidence that the supportive tissues of the teeth, or the upper dental pad, contributed to the excessive wear.     

The pathogenesis of excessive wear in the permanent teeth of sheep

The two central pairs of permanent incisor teeth (l1P, I2P) were compared post mortem in sheep from two flocks, one of which showed excessive wear. Sheep were usually killed in groups of six. Excessive wear occurred during the winter and spring after the eruption of l1P. When l1P erupted at an early age it was also subject to that season;s wear but when it erupted at a later age, it was subject to less wear according to the amount of time it was in apposition with the dental pad during the high wear season. A small amount of compensatory growth at the root of the tooth occurred in some sheep when cementum was deposited on the apex. Apparent eruption of the crown of the tooth was actually due to gum recession. Normal reparative dentine was laid down in the pulp cavity of the crown of the tooth in anticipation of wear, but where wear was excessive unstructured dentine was deposited. In two cases the rate of wear was so great that the reparative dentine could not keep up and infection was able to gain access to the pulp cavity. There was no evidence of difference in the rate of wear of the molar teeth between the two flocks.     

The pathogenesis of Babesia motasi (Wales) infection in sheep

Studies on the pathogenesis of Babesia motasi (Wales) infection following blood transfusion of infected blood to normal or splenectomised recipients showed that the intact animal is refractory to infection but that infection in splenectomised animals caused weight loss, fever, anorexia, lassitude and a macrocytic hypochromic anaemia which coincided with the peak of parasitaemia. There was an initial leucocytosis, largely due to a neutrophilia. The prepatent period following blood transfusion was 2-3 days. Unconjugated and conjugated (direct) bilirubin levels increased from pre-infection levels to peaks of 1.43 and 0.70 mg/100 ml of blood, respectively. Serum glutamic pyruvic acid transaminases (SGPT) increased slightly but serum glutamic-oxaloacetic acid transaminases (SGOT) and blood sugar (glucose) levels did not show significant changes after infection. Total serum protein levels increased temporarily and then returned to normal. Blood urea nitrogen levels increased, with biphasic peaks (76.32 and 86.29 mg/100 ml) on Days 2 and 8 post-patency. Clinical infections even in splenectomised sheep, were mild and of short duration, although recovered sheep remained carriers.     

The pathogenesis of the nervous syndrome of Phalaris aquatica toxicity in sheep

The clinical signs displayed by 96 sheep affected by the nervous syndrome of Phalaris aquatica toxicity and 10 normal sheep injected intravenously with the phalaris alkaloid, 5-methoxy dimethyltryptamine (dose range 0.01 to 5.0 mg/kg), were observed. The distributions of phalaris indole-like cytoplasmic pigments in nuclei of the brains and spinal cords of 9 naturally affected sheep were determined microscopically. Based on the relationship between clinical signs and the central nervous system nuclei involved in their production, the distribution of phalaris indole-like pigments, and the pharmacology of dimethylated tryptamines, it is suggested that the nervous syndrome induced by Phalaris aquatica results from a direct action of phalaris alkaloids upon serotonergic receptors in specific brain and spinal cord nuclei.     

Clinical signs and pathology of accidental monensin poisoning in sheep

The clinical signs and postmortem findings in sheep from two flocks accidentally poisoned with monensin are described. Clinical signs began within 24 hours of exposure to monensin. In the acute stages they consisted of lethargy, stiffness, muscular weakness, a stilted gait and recumbency. Feed refusal was seen in one flock but not in the second. Subacute to chronic clinical signs were decreased muscle volume of the rump and thigh. When forced to run, chronically affected sheep had a stilted, stiff legged, rocking horse gait.

Gross postmortem changes were not always visible. Where visible, they affected skeletal muscles and consisted of pale streaking, with atrophy in the chronic stages. Lesions were most severe in muscles of the rump and hind limbs. Microscopically myofiber swelling and hyalinization were seen with interstitial mononuclear cell reaction and extensive sarcoplasmic mineralization in some cases. Chronic lesions consisted of fibrosis and myofiber atrophy. In lambs less than one month old, diffuse gastrointestinal hemorrhage was the only finding.

     

The pathology of natural and experimentally induced Campylobacter jejuni abortion in sheep

We describe here the gross and microscopic lesions in 18 experimentally induced and 120 natural Campylobacter abortions. In natural Campylobacter abortions, gross lesions were reported infrequently; placentitis was recorded in 6% and hepatic lesions in 4% of our field cases. Placentitis was the microscopic lesion identified most consistently in natural abortions (93%) and was often observed in association with abundant bacterial colonies in chorionic villi (54%) and less often with placental vasculitis (13%). In natural abortions, suppurative fetal pneumonia (48%), necrosuppurative hepatitis (16%), and purulent meningitis (7%) were also observed. The better-preserved specimens from experimentally induced abortions were utilized to define placental changes more precisely. Placentitis was identified in all 18 experimentally induced abortions and was observed most consistently in the chorionic villus stroma (100%), often accompanied by suppurative surface exudate (89%). An inflammatory infiltrate was less commonly identified in the cotyledonary hilus (39%) and intercotyledonary placenta (22%). Bacteria were visualized in H&E-stained sections in 89% of placentas from experimentally infected ewes, primarily as well-demarcated bacterial colonies within subtrophoblastic, sinusoidal capillaries (89%), in the cotyledonary villus stroma (89%), and within the cytoplasm of trophoblasts (22%). Transmission electron microscopy and immunohistochemistry confirmed that the vast majority of the well-demarcated bacterial colonies characteristic of Campylobacter abortion were within subtrophoblastic sinusoidal capillaries. The most characteristic microscopic lesions identified in cases of Campylobacter abortion in sheep were placentitis with placental bacterial colonies, placental vasculitis, and fetal pneumonia.     

甘南州羊泰勒虫病临床症状及病理变化观察

对近百例羊泰勒虫病自然感染病例和人工感染病例的临床症状、病理变化进行了详细的观察。主要表现为高热，呈典型的稽留热，体表淋巴结肿胀；病的中后期，在羊的尾根、腋下、股内侧等部位有散在的出血点；病羊严重贫血，血液检查，红细胞数量减少，血红蛋白含量降低；病死羊的全身实质脏器及淋巴结出血。     

The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep.

The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep.     

Gross pathology and histopathology of haemonchosis in sheep and goats in Iraq

The response of Awassi sheep and a local breed of goats to H. contortus, the prevalent ovine and caprine strongyloid species in Iraq, was studied. A dose of 500 H. contortus (sheep origin) larvae kg-1 body wt. induced clinical and pathological changes of haemonchosis. Although the percentage recovery of worms was higher in sheep, the pathological (gross and microscopic) changes were more marked in infected goats. The extensive abomasal changes noted in goats were, in general, accompanied by a higher density or larvae in the gastric wall; the pathology did not necessarily depend upon parasite count alone and a definite relationship could not be established. The tissue changes in the goats are possibly of immunological origin, although a genetic resistance may operate, primarily at the level of worm establishment.     

Enzootic calcinosis in sheep: clinical signs and pathology.

Enzootic calcinosis in Corriedale sheep was characterized by degeneration and mineralization of elastic connective tissue of aorta, arteries, lung, and kidney and by ulceration of cartilage of joints of limbs. Results of serum chemical analysis revealed low Ca X P value and significantly low, but inconsistent magnesium concentration and normal inorganic phosphorus content. The Ca:P ratio in bone was low in affected sheep. Clinicopathologically, calcinosis of sheep at Mattewara, India, appeared to be similar to the disease described as Enteque seco in South America, Naalehu disease in Hawaii, Manchester wasting disease in Jamaica, and calcinosis in central Europe, Israel, and South Africa. The disease might be due to complex mineral imbalance, although the possibility of a plant poisoning has not been ruled out.     

The etiology and pathogenesis of ovine pulmonary carcinoma (sheep pulmonary adenomatosis)

Ovine pulmonary carcinoma (OPC, sheep pulmonary adenomatosis, jaagsiekte) occurs naturally as a contagious bronchioloalveolar carcinoma of sheep in the Americas, Europe, Africa and Asia. The disease is endemic and economically important in Peru and apparently more common than previously suspected in the U.S.A. The tumor is a result of transformation of type II alveolar epithelial cells or non-ciliated bronchiolar cells of the lung. Clinically affected sheep develop dyspnea, tachypnea and often a watery nasal discharge that originates from tumor secretions. The course is progressive and death usually occurs within a few weeks. To study the viral etiology and pathogenesis of OPC in the U.S.A., the disease was experimentally transmitted to neonatal or young lambs with a success rate of 69%. Ovine lentivirus (OvLV), present in the inocula, was concurrently transmitted and induced lymphoid interstitial pneumonia in most animals. While morphological, immunological and other studies implicate a type D or type B retrovirus as the etiologic agent of OPC, this virus has not yet been cultured and the role of ovine lentivirus in the disease remains unknown.     

Clinical pathology of experimental Schistosoma curassoni infections in sheep and goats

The clinical pathology of Schistosoma curassoni infection in sheep and goats was studied for 22 weeks following experimental infection with 7000 and 4000 cercariae, respectively. Excretion of eggs began at week 7 after infection: in goats the numbers increased to 30 to 50 eggs per gram faeces (epg) at weeks 8 to 18, followed by a reduction. In a pregnant goat, epg values increased markedly before and after parturition. The mean faecal egg counts in sheep were lower than in goats, increasing to a maximum level of 30 epg at weeks 16 and 17 after infection. Infected sheep maintained growth rates roughly comparable with controls, whereas infected goats failed to gain as much weight as the controls. Infected goats and sheep produced eosinophil counts of about 3 x 10(3) mm-3, five and eight weeks after infection, respectively. Sheep developed a progressive anaemia from week 11 after infection, in goats blood values remained within normal limits. Differences in serum protein concentration were observed between infected and uninfected goats about nine weeks after infection, but not in sheep. Increased total protein values, hyperglobulinaemia and lowered albumin to globulin ratios were features of infected goats. Serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, gamma-glutamyl transferase, total lactate dehydrogenase and bilirubin were not significantly changed. The mean recovery in sheep was 608 worms, in goats 428 worms, but the total tissue egg counts were higher in the latter. Of the total eggs deposited in the goats 92 per cent were found in the liver with 51.5 per cent in the ovine liver. The histopathological changes were studied.     

A syndrome of dental abnormalities of sheep: II. The pathology and radiology

Histological and radiographic examination of 23 ewe heads has revealed that mandibular osteopathy is a feature of the ovine dental abnormality syndrome described by Bruère et al.⁽³⁾ The bone changes consisted of excessive irregular remodelling of bone with osteoporosis. Developmental faults were also demon-strated. The most dramatic of these were dentigerous cysts involving unerupted permanent incisors, although malposition-ing of permanent incisors was also observed.

A histological feature of the excessive incisor wear was chronic pulpitis, perhaps a. result of the rate of wear exceeding the rate at which protective secondary dentine could be de-posited in the pulp cavity.

A number of nutritional deficiencies is known to cause gener-alised osteoporosis. Recognition of the osteopathy described here thus supports the clinical evidence of Bruère et al.⁽³⁾ that a nutritional disorder could be a major factor in the pathogenesis of this syndrome.