Psychosis and sexual abuse: An interpretative phenomenological analysis.

OBJECTIVES: This study aimed to investigate the first-person perspective of psychosis sufferers who survived childhood sexual abuse. METHODS: Interpretative phenomenological analysis was employed to explore the experiences of 7 women with a history of sexual abuse and psychosis. RESULTS: Analysis generated six themes: (a) degradation of self, interlinking shame, guilt, and sometimes disgust; (b) body-self entrapment, experiencing bodily constraint and distortion; (c) a sense of being different to others, involving interpersonal problems; (d) unending struggle and depression, a pervasive sense of defeat; (e) psychotic condemnations and abuse, describing psychotic phenomena related to harm and sexual abuse; and (f) perception of links to the past, the links made from past abuse to current functioning. CONCLUSION: Participants suffered extreme psychological, physical, and interpersonal difficulties past and present. Psychotic experiences reported exhibited themes of condemnation by external entities and reflected the topic of sexual abuse. Participants did not generally link psychosis to their past abusive experiences.

Cardiomyopathy of ruminants induced by the litter of poultry fed on rations containing the ionophore antibiotic, maduramicin. II. Macropathology and histopathology.

This report contains an account of the gross and histopathological lesions of 20 cattle and four sheep in 15 field outbreaks of poultry litter toxicity, one steer fed ad lib. and six sheep dosed with toxic poultry litter, and ten sheep fed experimental rations containing c 2,5 ppm and 5 ppm maduramicin. The principle macroscopic lesions in most cattle that died in field outbreaks were indicative of congestive heart failure. The lesions in sheep were similar, but generally milder. Cardiac dilatation was observed in both sheep and cattle. Microscopically, the cardiac lesions were more pronounced in cattle and comprised varying degrees of atrophy, hypertrophy, degeneration, necrosis of myocardial fibres, and interstitial fibrosis. Skeletal muscle lesions were usually more severe in sheep, particularly in the muscles of the hindquarters which appeared pale, oedematous and mottled. One of the sheep in the poultry litter dosing trial developed signs of congestive heart failure and the hearts of two others were dilated. Extensive hypertrophy and atrophy of myocardial fibres were evident in the steer fed ad lib. with this material. As in field cases, the myocardial lesions of the sheep were less severe than those of the steer. Mild cardiac dilatation was present in four of the seven sheep in the maduramicin feeding trial. Diffuse hypertrophy of myocardial nuclei was present in all seven cases, myocardial fibre atrophy in six, multifocal fibrosis and necrosis in six and two cases, respectively, and focal endocardial thickening in two. The skeletal muscles revealed granular degeneration and foci of necrosis and regeneration. The cardiac and skeletal lesions in the field outbreaks, poultry litter feeding trials and maduramicin feeding trials, were highly comparable. This suggests that this form of poultry litter intoxication is a chronic form of ionophore toxicity the pathology of which is characterized by a dilated cardiomyopathy with congestive heart failure and mild (cattle) to severe (sheep) skeletal muscle lesions.

Spinal cord degeneration in adult dairy cows associated with the feeding of sorghum beer residues.

A neurological syndrome in a herd of Friesland cows (n = 100) on a diet including sorghum beer residues is described. Over a period of 8 months, 76 cows developed weakness of the hindquarters, progressively worsening ataxia and, eventually, paralysis and permanent recumbency. The course of the disease varied from 2 to 8 weeks. The lesions were significant in the 2 cows necropsied and included extensive, bilaterally symmetrical dilation of myelin sheaths, axonal swelling and loss with Wallerian degeneration, and depletion of myelin in both ascending and descending tracts at all levels of the spinal cord. Focal neuronal degeneration in the spinal cord grey matter and dorsal root ganglia, and focal loss of axons and ovoid formation in the spinal nerve roots and ischiatic nerves were also evident. The pathogenesis of the spinal lesions appears to involve a primary axonopathy with secondary myelin loss. The epidemiology, clinical signs and pathology suggest that the disease was associated with the fungus Aspergillus clavatus.

Experimentally-induced Cestrum laevigatum (Schlechtd.) poisoning in sheep.

Dried, milled Cestrum laevigatum plant material was drenched to 6 ewes at doses ranging from 2,5 to 10 g/kg/day for 1 to 47 days. The most noticeable clinical signs were depression, anorexia and ruminal stasis. These signs were accompanied by clinical pathological changes indicative of liver involvement such as increases in the serum activities of aspartate transaminase, lactate dehydrogenase and gamma-glutamyltransferase. Hepatosis characterized by accentuated lobulation, and centrilobular to midzonal coagulative necrosis, haemorrhage and congestion occurred in 2 of the 3 ewes given high doses of plant material. Liver lesions in the other animals included disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas. Spongy changes in the cerebral white matter were evident in the ewes of the high-dose group. Ultrastructural changes in the liver comprised degeneration and necrosis of hepatocytes and occasionally endothelial cells, and disruption of sinusoidal walls.

Cardiomyopathy of ruminants induced by the litter of poultry fed on rations containing the ionophore antibiotic, maduramicin. I. Epidemiology, clinical signs and clinical pathology.

The epidemiological, clinical and clinical pathological findings in 20 cattle and 4 sheep from 15 outbreaks of poultry litter toxicity in South Africa over the past 6 years are documented. In 6 outbreaks, the litter emanated from batteries where maduramicin had been incorporated into rations of broilers. According to circumstantial evidence the litter involved in the 9 other outbreaks was also derived from broilers which had been fed on rations containing an ionophore. The litter was fed ad libitum to the affected stock or constituted 30-80% by volume of their rations. The principal sign manifested was sudden mortality of up to 70% of the herd or flock, usually within 20-40 days of commencement of feeding of poultry litter. A few cattle developed signs of congestive heart failure, and stiffness was commonly seen in sheep. In a dosing trial with poultry litter involving 1 steer and 6 sheep, the steer and a sheep died suddenly and a second sheep was destroyed in extremis. Tachycardia and/or cardiac arrythmia were recorded in 5 sheep, and the activity of aspartate transaminase (AST) and/or lactate dehydrogenase (LD) in the sera of 4 was elevated. Since the cardiac lesions in field cases were similar to those of ionophore poisoning and broiler rations containing maduramicin was a common factor in several outbreaks, toxic litter from some of these outbreaks were tested for the presence of this compound. Analysis by high performance liquid chromatography of litter from 2 specimens of outbreaks revealed that they contained 2.5 ppm and 6.1 ppm maduramicin.(ABSTRACT TRUNCATED AT 250 WORDS)

The pathology of Cestrum laevigatum (Schlechtd.) poisoning in cattle.

The clinical features and pathological findings of 6 steers drenched with dried plant material of Cestrum laevigatum are described. Doses ranging from 0.5 to 10 g/kg/day were given intraruminally for 1 to 38 days. Animals that received 5 to 10 g/kg/day showed nervous signs including ataxia, muscle tremors, hypersensitivity and intermittent chewing. Clinical signs in the steers which received 0,5 to 4 g/kg/day were mild. High doses induced moderate to severe hepatosis characterized by centrilobular to midzonal coagulative necrosis, haemorrhage and congestion. At lower rates only mild hepatic lesions, characterized by disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas were evident. Ultrastructural changes were primarily limited to the hepatocytes and comprised degeneration, necrosis and fatty change. Degeneration and necrosis of endothelial cells and disruption of sinusoidal walls were occasionally observed.

Concurrent babesiosis and ehrlichiosis in the dog: blood smear examination supplemented by the indirect fluorescent antibody test, using Cowdria ruminantium as antigen.

Giemsa-stained, peripheral blood smears of 67 dogs, showing clinical signs typical of babesiosis or reminiscent of concurrent babesiosis and ehrlichiosis, were examined for the presence of Babesia canis and Ehrlichia canis. Since Cowdria ruminantium cross-reacts with Ehrlichia, the sera of these dogs were also subjected to the indirect fluorescent antibody (IFA) test in which C. ruminantium was used as antigen. Fifty-five per cent of these dogs had mixed infections of B. canis and E. canis, as judged by blood smear examination and serology. The serum of 32% of these dogs with mixed infections reacted positively in the IFA test. Six out of 9 dogs, the blood smears of which were negative for both B. canis and E. canis, were serologically positive for E. canis. Furthermore, sero-conversion from a negative in the initial serum sample to titres of up to 1:160 in a subsequent sample was recorded in 9 out of 13 dogs with suspected mixed infection on blood smear.

A field outbreak in Ile-de-France sheep of a cardiotoxicosis caused by the plant Pachystigma pygmaeum (Schltr) Robyns (Rubiaceae).

A field outbreak of Pachystigma pygmaeum intoxication in sheep is described. Noteworthy clinical signs were: respiratory distress, apathy and subcutaneous oedema of mainly the head. Gross changes included cardiomegaly, centrilobular hepatic necrosis and effusion of body cavities. Microscopically myocardial fibrosis, affecting predominantly the endocardium of the apex, left free ventricular wall and interventricular septum, was most striking in the majority of animals, whilst myofibre atrophy was present in 1 sheep.

Acute Lantana camara toxicity in cattle.

An outbreak of acute Lantana camara poisoning in cattle is described in which 10 out of 91 animals died. The affected cattle became icteric and voided soft, black faeces. Necropsies were performed on three steers, and the macro- and microscopical changes in their livers and kidneys were compatible with those of L. camara poisoning. Changes were similar in two steers that developed typical signs after being dosed with fresh L. camara collected in the toxic camp. Clinical pathological changes in experimental animals included elevated serum urea and creatinine concentrations.

Cardiac glycoside poisoning in sheep caused by Urginea physodes (Jacq.) Bak. and the isolated physodine A.

Urginea physodes (Jacq.) Bak., a species closely related to or possibly synonymous with U. pusilla, is described and its distribution given. Four bufadienolides were isolated from U. physodes and the approximated LD50 and cumulative effect of some of them determined in guinea pigs. The most toxic one proved to be mildly cumulative. Typical signs of acute cardiac glycoside poisoning, involving the locomotory, gastro-intestinal, respiratory and cardiac system, were seen in the field cases and/or were experimentally induced by the plant. Similar signs could also be induced by injecting the isolated bufadienolide, physodine A, to a sheep.

A haemorrhagic syndrome in recently weaned pigs ascribed to hypovitaminosis K.

An outbreak of a haemorrhagic syndrome involved recently weaned, mixed-breed pigs in a large piggery. The pigs were fed a pelleted complete ration containing antibacterial drugs. Affected pigs failed to grow, became pale and developed large, subcutaneous haematomas. Some pigs became lame and one had epistaxis. The monthly mortality rate in the weaner house, which was previously less than 2%, exceeded 6% during the outbreak. Coagulation time, activated partial thromboplastin time and prothrombin time were prolonged in blood from some of the pigs. The outbreak resolved promptly after supplementation of the diet with vitamin K3.