Hydatid disease in goats in Bangladesh

A total of 12 344 goats of different ages from various localities of Bangladesh were examined for the presence of hydatid disease and 1024 (8.29%) were found to be infected. The incidence of infection by organ was: liver 36.72%, lungs 32.03%, spleen 4.69%, heart 3.13%, kidney 1.56%, omentum 0.78%, and both liver and lungs 21.09%. The severity of infection was: weak (84.56% and 86.55%), medium (13.32% and 11.87%) and heavy (2.12 and 1.58%) in the liver and lungs respectively. Of the 1792 cysts examined, 175 (9.76%) were fertile, 1342 (74.89%) were sterile, 206 (11.50%) were calcified, 47 (2.62%) were supporative and 22 (1.23%) were undeveloped. The incidence of infection by age of host was: 0.63% between 0 and 1 year, 2.48% between 1 and 2 years, 5.53% between 2 and 3 years, 16.80% between 3 and 5 years and 21.64% for 5 years old and above.     

Abscess disease in goats in the Sudan

The "abscess disease" was described in naturally infected goats for the first time in Sudan. An anaerobic respiratory deficient staphylococcus was isolated in pure form. The biochemical properties were studied. The disease was successfully reproduced in experimental goats.     

Epidemiological features of Morel's disease in goats

Morel's disease caused by Staphylococcus aureus subsp. anaerobius was diagnosed for the first time in Poland in October 2006 in a goat flock. A second infected flock was found two months later. The course of the disease in both flocks was observed for 15-17 months. Clinical manifestation was confined to abscesses located near major superficial lymph nodes, mostly: superficial cervical, subiliac, parotid and mandibular. At necropsy no other lesions were found. The incubation period was estimated at 3 weeks. Clinical signs were seen both in young and adult goats and up to 7 abscesses in one animal were noted. Abscesses tended to persist for 1 to 5 months, then rupture and heal completely. The initial high in-flock point prevalence in both flocks (93.6% and 84.4%) dropped to approximately 10-30% during next 3-4 months. Until the end of the observation period the in-flock point prevalence remained at this level and only single abscesses were observed, mainly in young animals. No influence of the concurrent caprine arthritis encephalitis virus (CAEV) infection on the clinical course of Morel's disease was noticed. It is to be concluded that the clinical course of Morel's disease in a goat flock resembles caseous lymphadenitis (CLA). However, in Morel's disease abscesses occur more frequently in young goats and are located near, not inside, the lymph nodes, as in the case with CLA. Also, the incubation period of Morel's disease seems to be shorter (3 weeks versus 2-6 months in CLA).     

Foot and mouth disease in sheep and goats

Small ruminants play an important role in the epidemiology and transmission of Foot-and-Mouth Disease (FMD). The main reasons therefore are: FMD is difficult to diagnose as infected sheep not always show typical clinical symptoms or as the cardinal signs mimicked other diseases. Sheep and goats may be carriers. Infected herds which practice transhumance or are nomadic can spread the infection to other herds long before diagnose of the disease is established. Shipping and trade with live sheep and goats is much more common world wide than in other FMD susceptible species. Lack of registration of all sheep and goat herds (especially of small hobby herds) and lack of individual identifications signs (ear tags) may result in incomplete control measurements under FMD conditions. Basing on published experiences with the actual FMD epidemic in the UK and basing on the own experiences with the restrictions to prevent from spreading of the FMD from the UK to Germany suggestions for future disease control are made.     

关于当前蛋鸡群中流行的白冠病

当前蛋鸡群中流行一种以鸡冠、脸发白的疾病,暂称为“白冠病”。这个“白冠病”不完全是卡氏住白细胞原虫病,而是包括卡氏住白细胞原虫病在内的贫血病。能够引起鸡冠、脸发白的病因很多。那么,当前蛋鸡群中流行的白冠病的病因是什么呢?不少禽病门诊一古脑儿诊断为卡氏住白细胞原虫病,而笔者认为,有的白冠病确是卡氏住白细胞原虫病,但有的是马立克氏病,或以马立克氏病为主的贫血综合征。在临床症状上,卡氏住白细胞原虫病冠、脸表现苍白,但鸡冠不萎缩,青年鸡呈急性发病,暴发死亡,而成年鸡则能耐过成为带虫者,死亡零星,似散发。因此,死亡鸡能保…     

Lysosomal storage disease caused by Sida carpinifolia poisoning in goats

A neurologic disease characterized by ataxia, hypermetria, hyperesthesia, and muscle tremors of the head and neck was observed for 2 years in a flock of 28 Anglo-Nubian and Saanen goats on a farm with 5 ha of pasture. Six newborns died during the first week of life, and five abortions were recorded. The predominant plant in the pasture was Sida carpinifolia. The disease was reproduced experimentally in two goats by administration of this plant. Three goats with spontaneous disease and the two experimental animals were euthanatized and necropsied. No significant gross lesions were observed. Fragments of several organs, including the central nervous system, were processed for histopathology. Small fragments of the cerebellar cortex, liver, and pancreas of two spontaneously poisoned goats and two experimentally poisoned goats were processed for electron microscopy. Multiple cytoplasm vacuoles in hepatocytes, acinar pancreatic cells, and neurons, especially Purkinje cells, were the most striking microscopic lesions in the five animals. Ultrastructural changes included membrane-bound vacuoles in hepatocytes, Kupffer cells, acinar pancreatic cells, Purkinje cells, and the small neurons of the granular cell layer of the cerebellum. Paraffin-embedded sections of the cerebellum and pancreas were submitted for lectin histochemical analysis. The vacuoles in different cerebellar and acinar pancreatic cells reacted strongly to the following lectins: Concanavalia ensiformis, Triticum vulgaris, and succinylated Triticum vulgaris. The pattern of staining, analyzed in Purkinje cells and acinar pancreatic cells coincides with results reported for both swainsonine toxicosis and inherited mannosidosis.     

Post-mortem examination in the diagnosis of Johne's disease in goats.

Post-mortem examinations play an important role in Johne’s disease programmes in Norway. The results of such examinations of samples of viscera from 2997 goats carried out during the 5-year period 1972–1976 are given. The investigations show that the demonstration of macroscopical changes in mesenteric lymph nodes and small intestine has only limited value as a guideline in the post-mortem diagnosis of Johne’s disease in goats. Often macroscopical changes were not seen or they were non-specific. Caseous and/or calcified foci in mesenteric lymph nodes in infected animals were demonstrated quite often whilst observed intestinal changes were strikingly few. Corrugation of the mucosa was rare. However, in sections of macroscopically unchanged intestine marked epithelioid cell infiltrations and abundant acid-fast bacilli were not uncommon. In sporadic cases productive inflammation with tubercle formation was seen in lymph nodes in infected animals.Bacteriological culture was by far the most reliable post-mortem diagnostic method. By this method 92% of the infected goats were detected. The corresponding figures for histological examination and microscopy were 54% and 47%, respectively.     

Interstitial lung disease in West Highland White Terriers

Progressive respiratory failure and pulmonary fibrosis in West Highland White Terriers (WHWT) is an apparently genetic disorder of unknown pathogenesis. This study characterizes the light microscopic, ultrastructural, and immunohistochemical features of affected WHWT in comparison with lesions in usual interstitial pneumonia (UIP) of humans. Lesions in WHWT were confined to the expansion of the interstitial space of alveolar septa by extracellular matrix (ECM) determined to be mixtures of type-I and -III collagens. Features of UIP such as intra-alveolar fibroblastic foci, subpleural distribution, and honeycombing were not observed in six WHWT. Comparison with normal dogs showed no apparent increase in septal myofibroblasts. Ultrastructually, the ECM in alveolar septa consisted of large aggregates of periodic collagen filaments underlying alveolar capillaries that were surrounded by thick bands of amorphous to fine fibrillar matrix. This study suggests that chronic pulmonary disease of WHWT is a result of aberrant collagen regulation.