Endoscopic findings in children born with oesophageal atresia in an academic unit in South Africa.

BACKGROUND: Oesophageal atresia (OA) is one of the most common congenital gastrointestinal (GI) abnormalities. Due to advances in multidisciplinary care, early prognosis has improved with emphasis shifting to the long-term impact of this disease. Literature suggests a higher incidence of Barrett's and eosinophilic oesophagitis in these children, with an increased risk of oesophageal carcinoma. Guidelines for adults born with OA include routine endoscopy and lifelong screening of the upper gastrointestinal tract (GIT). Despite this, uncertainty remains regarding the necessity and frequency of endoscopic surveillance for children born with OA. We describe our endoscopic findings in children born with OA. METHODS: A prospective analytic cohort study was undertaken, which included all children born with OA, that were followed-up in our unit between 2020 and 2022. History regarding feeding and GI symptoms were documented after which an endoscopy was performed. RESULTS: During the study period, 37 endoscopies were performed in patients born with OA at a median age of 25 months. The most common clinical appearance on endoscopy was anastomotic strictures followed by oesophagitis. Twelve patients had biopsies taken, with abnormal histology in all but one patient. The most common histological finding was oesophagitis with lymphocytes and chronic gastritis. Two patients had Helicobacter Pylori infection, and one had findings suggestive of eosinophilic oesophagitis. CONCLUSION: All patients with a clinical indication for an endoscopy had abnormal clinical or histological findings, thus concurring with the literature in highlighting the need for regular endoscopy. We recommend regular clinical follow-up and endoscopic surveillance if clinically indicated for children born with OA.

Outcomes for open and laparoscopic appendicectomy for complicated appendicitis in children.

BACKGROUND: The study aimed to compare the outcomes of paediatric laparoscopic appendectomy (LA) with open appendectomy (OA) for complicated appendicitis (CA). All trainees could perform OA without supervision. METHODS: This is a single-centre, retrospective, non-randomised review of children 4-12 years of age, who had either an OA or LA for CA. The data was collected from August 2012 to June 2016. Nineteen surgical trainees were initially supervised by a consultant until deemed able to perform LA safely. The on-call surgeon decided on operative approach. Intra- and postoperative complications were analysed. Primary endpoint was comparison of infection rates between groups, simultaneous differences between the two procedures performed by surgical trainees and consultants were evaluated. RESULTS: One hundred and fifty-five patients had appendicectomy for CA during the study period. Fourteen patients with incomplete information were excluded. Ninety had OAs and 51 LAs. Both groups were well matched demographically. Postoperative infective complications occurred in 13/51 (25.5%) of the LAs, and in 23/90 (25.6%) of the OA (p = 0.159). Fourteen trainees performed 27 LAs without consultant supervision by the conclusion of the study. The mean duration of LA surgery for surgical trainees was 110.35 minutes (IQR 22.5) and for consultants 93.87 minutes (IQR 35, p = 0.497). CONCLUSION: There is no difference in intra- and postoperative complications between LA and OA for CA. Duration of surgery between surgical trainees and consultants were comparable. This indicates that surgical trainees acquire LA skill over a short period of time and that LA as a laparoscopic teaching procedure merits consideration.

A study of the pathology and pathogenesis of the myocardial lesions in gousiekte, a plant-induced cardiotoxicosis of ruminants.

Myocardial lesions were studied in sheep in which gousiekte was induced by experimental dosage of Pachystigma pygmaeum, Fadogia homblei or Pavetta harborii. The single most consistent diagnostic histological feature in 33 animals was hypertrophy of myocardial fibres in the subendocardial region. Fibrosis in the subendocardial region of the apex or left ventricular wall was often scarce or absent in animals with a short latent period, and was not always prominent even in sheep with an intermediate or long latent period. The presence or absence of fibrosis cannot therefore be used to confirm or exclude gousiekte, particularly in cases with shorter latent periods. Light microscopical and ultrastructural lesions in sheep with gousiekte correspond to a large extent to changes reported in humans with dilated cardiomyopathy of unknown cause. It appears that the myocardial lesions in gousiekte represent a final common pathway of cellular damage rather than a manifestation of a specific type of heart disease. The predilection for hypertrophy of myofibres in the subendocardial region is probably related to diminished perfusion that potentiates the primary myocardial dysfunction.

Effect of pavetamine on protein synthesis in rat tissue.

Pavetamine, the active principle of plants causing gousiekte in ruminants, was found in this study to be an inhibitor of protein synthesis in the rat heart. Sprague-Dawley rats were injected intra-peritoneally with 8-10 mg/kg pavetamine and the levels of protein synthesis in different organs determined utilizing L-[4-3H]phenylalanine incorporation. In contrast to the more than 23% inhibition found in heart tissue at 4, 24 and 48 h after administration of pavetamine, the effect on the kidney, liver, spleen, intestine and skeletal muscle was minimal or returned to pretreatment levels within 48 h. These results may offer an explanation for the clinical signs observed in ruminants with gousiekte, where the heart only is affected.

The distribution, diagnoses and estimated economic impact of plant poisonings and mycotoxicoses in South Africa.

Maps are provided showing the national and provincial distributions of many plant poisonings and mycotoxicoses in South Africa. The various poisonings are briefly described and criteria for their diagnoses are given. The annual mortalities of cattle from plant poisonings/mycotoxicoses in South Africa were calculated as c. 37 665 head with a current cash value of c. R57 627 450, and that of small stock as c. 264851 head with a value of c. R46 878 627. The annual total cost of plant poisonings/mycotoxicoses to the livestock industry of South Africa is conservatively estimated at R104 506 077. These figures do not include hidden losses such as diminished production, reproductive failure, the cost of not utilizing toxic pastures and the fall in price of infested land.

Poisoning of wildlife in South Africa.

Over a period of 7 years the Toxicology Diagnostic Laboratory at the Onderstepoort Veterinary Institute investigated 370 suspected incidents of poisoning of wildlife. A diagnosis was made in 166 of the outbreaks. Synthetic organic pesticides were responsible for 82.5% of the poisonings. More than 90% of the poisonings were maliciously intended and monocrotophos was the chemical most often used. The data were derived from authenticated outbreaks of poisoning and indicate the chemicals most often incriminated in acute poisoning of wildlife. Of all wild animals, birds are the most frequent victims of poisoning. Uncommon toxicities such as ionophore, cardiac glycoside poisoning and chronic fluorosis are also described.

A tremorgenic mycotoxicosis in cattle caused by Paspalum distichum (l.) infected by Claviceps paspali.

This is the first reported outbreak of paspalum staggers in cattle following ingestion of Paspalum distichum (L) infected by Claviceps paspali in South Africa. A day after starting to graze on an ergotised paspalum field, 43 animals exhibited various degrees of generalised tremors and ataxia. Four animals became paretic and went into sternal recumbency. All affected animals recovered. The condition was reproduced by feeding ergotised grass to a calf. Signs of intoxication were observed 48 h after ingestion of c. 30 g/kg of the semi-dry plant material. The calf developed tremors and a slight ataxia, which became more pronounced following light exercise.

A chronic cardiomyopathy in feedlot cattle attributed to toxic levels of salinomycin in the feed.

The clinical signs and pathology in an outbreak of toxicity in feedlot cattle attributed to the ingestion of toxic levels of the ionophore antibiotic salinomycin over an extended period of 11 weeks are described. Thirty-nine out of 380 cattle developed signs consistent with cardiac failure and 8 of these died. Clinical signs included dyspnoea, tachypnoea, tachycardia and exercise intolerance. Two cattle were necropsied and in one there were macroscopic lesions suggestive of congestive heart failure, namely pulmonary oedema, hydrothorax and hepatomegaly. Histopathology revealed a chronic cardiomyopathy characterised principally by extensive myocardial fibre atrophy with multifocal hypertrophy and interstitial and replacement fibrosis. Hepatic and pulmonary lesions were consistent with those of congestive cardiac failure. The myocardial lesions in this outbreak were similar to those encountered in cases of a chronic toxicity associated with the ingestion of litter derived from poultry rations containing ionophores (ionophore-associated poultry litter toxicity). Hence, the clinical and pathological findings in this outbreak indicate that in cattle, the prolonged ingestion of ionophores over several weeks may result in the development of chronic myocardial lesions comparable to those of IAPLT but significantly different from those encountered in the more traditional acute outbreaks of ionophore toxicity as described in the literature.

Isolation of the toxin responsible for gousiekte, a plant-induced cardiomyopathy of ruminants in southern Africa.

Gousiekte was induced in sheep and goats by the oral and intravenous (i/v) administration of methanolic and ethanolic precipitates of aqueous extracts of Pavetta harborii. Further purification of the toxic principle was carried out by dialysis and ion-exchange chromatography. The toxin was eluted from the cation-exchange resin with 1 mol/l of ammonium acetate and finally purified on Sephadex G-10 and silica gel. Spots on thin-layer chromatographic plates (TLC) were visualized with ninhydrin. Gousiekte was induced with the pure toxin after i/v administration in goats. The yield of pure toxin was about 10 mg/kg of dried leaves.

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.

A nervous disorder in cattle, caused by the plants Ficus ingens var. ingens and Ficus cordata subsp. salicifolia.

Two outbreaks of neurotoxicoses are reported in cattle browsing on the leaves of Ficus spp. In the first outbreak, three animals died and one became ill. A sheep developed severe nervous signs, including tetanic spasms, when dosed with the leaves of Ficus ingens var. ingens from the toxic camp where the cattle had died. The second outbreak resulted in the death of 12 heifers within 48 h of ingestion of the leaves of F. cordata subsp. salicifolia. Clinical signs included hyperaesthesia, ataxia, muscle tremors and padding motions while in lateral recumbency. Similar signs were reproduced by drenching the incriminated leaves to a steer. The sheep dosed with F. ingens var. ingens and two cattle, one of which had died during the second outbreak and the steer drenched with F. cordata subsp. salicifolia, were necropsied. Light microscopical examination consistently revealed oedema of the central nervous system. In the steer, focal demyelination was evident in localized areas of the brain and spinal cord. Liver lesions ranged from mild degeneration to focal disseminated necrosis of hepatocytes.

An outbreak of narasin poisoning in swine.

An outbreak of narasin poisoning in swine is described. Forty nine out of 108 lactating sows died over a period of one month after being fed a ration accidentally contaminated with narasin. Clinical signs included anorexia, respiratory distress, lethargy and posterior paresis, progressing to lateral recumbency and death. Necropsy examination in 3 pigs revealed extensive myocardial and skeletal muscle damage. Analysis of the feed confirmed the presence of high concentrations of narasin.

Galenia africana L. poisoning in sheep and goats: hepatic and cardiac changes.

Lesions in 4 field cases (3 sheep and 1 goat) of 'waterpens' or water belly, caused by the plant Galenia africana, are described. The clinical pathological and pathological findings in 7 sheep which were drenched with toxic plant material are also reported. Inappetence, ruminal stasis and apathy as well as tachycardia were noticed in some of the sheep towards the end of the dosing period. The most prominent clinical pathological change in the experimental animals was an increase in the activity of gamma-glutamyltransferase which in some animals occurred within days after commencement of dosing. This indicates liver involvement in the early stages of the intoxication, and at this stage no heart abnormalities were detected clinically, clinical pathologically or with cardiac function tests. Decrease in cardiac function were recorded in 2 sheep towards the end of the dosing period. Liver and heart lesions were present in all the animals. In some cases hepatic changes were mild and characterized by dilation of central veins and sinusoids and, less commonly, centrilobular fibrosis. More advanced lesions included centrilobular fibrosis and bridging between neighbouring lobules with adjacent areas of coagulative necrosis, lysis and ballooning degeneration of hepatocytes. Myocardial changes occurred in the free ventricular walls and interventricular septum and comprised hypertrophy of myocytes with consequent degeneration and necrosis and fibrosis. In cases of longer duration myocytes were diffusely atrophic with scattered groups of remaining hypertrophic fibres. The clinical pathological and pathological features suggest that G. africana is primarily hepatotoxic with myocardial involvement occurring only in the terminal stages of the intoxication.

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)

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.

Clinical pathological changes in gousiekte, a plant-induced cardiotoxicosis of ruminants.

Twenty sheep were dosed with either Pachystigma pygmaeum or Fadogia homblei belonging to the Rubiaceae. The experimentally-induced cardiotoxicoses were monitored by various clinical pathological parameters and heart function tests. Elevated AST (aspartate transaminase) activity in the serum proved to be a more reliable indicator of cardiac damage in gousiekte than either LD (lactate dehydrogenase) or CK (creatine kinase). Persistent increases of AST activity were recorded from c. 14 days after commencement of dosing, and this activity sometimes peaked as late as 30 days after the dosing had ceased. Tachycardia and diminished heart function were registered only terminally. Lesions of gousiekte were present in all the sheep that were exposed to the plants. In a field outbreak of P. pygmaeum, where 60 out of 90 sheep died, 14 out of the 15 animals examined had increased AST levels compared with none of the 15 controls. These results indicated that increased enzyme levels can be of use to identify affected animals during latency in a natural outbreak of gousiekte.

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.