June 2015
Case A
History
Tissue from a heifer that had shown clinical weight loss and dyspnoea.
Example Histopathological Description
A single rectangular section of lung tissue (without pleura) is presented. Extensive areas of lung parenchyma are effaced by coalescing areas of eosinophilic coagulative necrosis with an outer zone of mild fibroplasia. A hypercellular infiltrate is rich in degenerate and non-degenerate neutrophils, macrophages and scattered lymphocytes. Fibrillar and homogenous eosinophilic material (fibrin and proteinaceous fluid) are abundant. Intralobular arteries show expanded walls and infiltrating inflammatory cells indicating vasculitis. Interlobular septae are markedly expanded by similar inflammatory cells, fibrin and fluid. Markedly ectatic lymphatics contain fibrin, fibrin thrombi and eosinophilic fluid (lymphangitis). In the centre of the section a bronchiole has a moderate mixed cellular infiltrate signifying bronchiolitis with markedly hyperplastic bronchiole associated lymphoid tissue (BALT). The bronchiolar epithelium is hyperplastic. Surrounding alveoli are flooded with mixed inflammatory cells and mild fibroplasia.
Morphological Diagnosis
Bronchopneumonia; fibrinonecrotic, severe, coalescing, with vasculitis, lymphangitis and BALT hyperplasia.
Comments
The extent of testing for aetiological agent(s) would depend on the prevalence rate in the herd, severity of disease and the possibility of a pathogen exotic to Australia. Based on the histopathological findings, mycoplasmas and a range of other bacterial and viral agents should be considered. Mycoplasma mycoides subspecies mycoides (small colony) and M. bovis should be included in the differential diagnosis.
This is a case of Contagious Bovine Pleuropneumonia (CBPP) from Botswana, Africa. Mycoplasma mycoides subspecies mycoides (small colony) was identified in lung smears by an indirect fluorescent antibody test and seroconversion was confirmed by complement fixation test and cELISA. CBPP was widespread in Australia until eradicated in 1973. This was a chronic active lesion. The animal was emaciated and dyspnoeic.
This case is in the AAPSP Digital Slide Collection, in the AFIP Wednesday Slide Conference folder, case 61. It is also in the AFIP collection as case 2, conference 14 of 2000.
June 2015
Case B
History
This Beagle pup had shown progressive hind limb ataxia from 12 weeks of age. It developed a head tilt, then seizures and was submitted for euthanasia.
Example Histopathological Description
The tissue presented is a coronal section of half the cerebellum and medulla at the level of the cerebellar peduncles. Multiple folia, particularly those in the vermis are variable in thickness and cellularity. In severely affected areas folia show non-uniform thinning with marked reduction of the inner granular layer with mild thinning of the granular layer. Purkinje cells are missing in some areas and sparse and misplaced in other areas. When present they are often shrunken or swollen, hypereosinophilic and angular. Affected Purkinje cells are sometimes associated with swollen axons (spheroids). When Purkinje cells are absent they are replaced with clear spaces or spaces filled with eosinophilic fibrillary material (empty baskets). Multifocal astrogliosis of Bergmann’s glia and occasional apoptotic bodies are present in some areas of the Purkinje cell layer. There are foci of neuropil vacuolation in the vicinity of the cerebellar nuclei, and cerebellar peduncle.
In the medulla there are scattered spheroids and focal neuropil vacuolation. Sparse Gitter cells are present. Some nerve bodies contain fine granular brown pigment in their cytoplasm, presumed to be lipofuscin.
Morphological Diagnosis
Cerebellar atrophy and abiotrophy with prominent Purkinje cell loss; multifocal to coalescing, moderate to severe.
Comments
The history, clinical signs, breed, age of onset and preferential loss of Purkinje cells are consistent with inherited autosomal recessive cerebellar abiotrophy. Canine parvovirus and possibly canine herpesvirus 1 can cause similar lesions. In-utero and neonatal infections usually produce clinical signs at or near birth. Toxic causes such as organomercury poisoning should also be considered.