Case A
History
A four month old Bull Mastiff dog with onset of hindquarter paresis progressing to paralysis over two-three days. Nothing abnormal was seen on X-ray and the animal was unresponsive to treatment. Euthanasia was performed.
Example Histopathological Description
There is one transverse and one longitudinal section of spinal cord and some spinal nerves. In both cord sections there are large, multifocal to coalescing, hypercellular areas of inflammation primarily within the white matter and extending into the grey matter, meninges and nerve roots, with changes centred on hypertrophic vessels. These areas are infiltrated predominantly by macrophages, plasma cells, lymphocytes and occasional granulocytes, including eosinophils, with moderate associated astrocytosis. Much of the white matter neuropil in affected areas is swollen and vacuolated, with multiple linear vacuoles frequently containing cellular debris or macrophages (digestion chambers) and scattered swollen, eosinophilic axons (spheroids). Vacuolar changes are also prominent throughout the white matter of the dorsal funiculi associated with astrocytic hypertrophy, but with minimal inflammatory cell infiltration. Scattered through the areas of inflammation are occasional large ovoid structures (40-70 μm in diameter) containing multiple, small, basophilic, oval organisms (2-4 μm in diameter) but without a discrete capsule (protozoan tissue cysts). In one area a group of zoites lie free within the neuropil. The spinal nerves are swollen, oedematous and have axonal swellings, scattered digestion chambers and are infiltrated by small numbers of lymphocytes.
Morphological Diagnosis
Myelitis; granulomatous, lymphoplasmacytic, chronic-active, multifocal to coalescing and severe, with intralesional apicomplexan protozoan organisms.
Radiculoneuritis; nonsuppurative, chronic, diffuse, mild.
Comments
Neospora caninum infection is the preferred diagnosis rather than Toxoplasma gondii infection, although definitive identification of the organism requires immunohistochemical (IHC) staining. How dogs become infected with Neospora caninum in nature is not fully understood.1 The possible modes of transmission causing CNS infection in a four-month-old pup are vertical (congenital transmission of tachyzoites from its dam) or horizontal (from ingestion of cattle tissue containing bradyzoites in tissue cysts – meat, foetal membranes). The second mode would normally result in intestinal sexual reproduction within the dog as the primary definitive host, yielding oocysts in faeces (for exogenous infection of cattle, the usual intermediate host). However, dogs can also act as intermediate hosts, with tachyzoites from the gut causing systemic infection, including CNS infection, via infected leukocytes (leukocytic trafficking) and CNS endothelial tropism and consequent injury and CNS inflammation. That dogs can become infected by ingesting infected tissues has been amply demonstrated, but whether they can be infected by the ingestion of sporulated oocysts (which are shed only by dogs and dingoes as definitive hosts) is unknown.1
Also, re-activation of a transplacentally-acquired, but dormant infection of bradyzoites within tissue cysts, in a puppy can be triggered by immunosuppression (including, it is suggested, transient immunosuppression associated with the first or second dose of combination modified live virus vaccines containing canine distemper virus (CDV): CAV-1 or CAV-2)2.
Dogs are an intermediate host for T gondii and become infected by ingestion of feed, water or material contaminated with sporulated oocysts (containing sporozoites) from cats or by ingestion of bradyzoites in tissue cysts in tissues of other intermediate hosts. The organism can spread systemically in blood or lymph as free organisms or intracellularly via leukocytic trafficking.
- Dubey JP, Schares G, Ortega-Mora LM. Epidemiology and control of neosporosis and Neospora caninum. Clin Microbiol Rev. 2007 Apr;20(2):323-67.
- The American Animal Hospital Association 2011 Canine Vaccination Guidelines.
June 2013
Case B
History
Lactating Holstein dairy cow found dead. It was one of 10 that died over the last six weeks.
Example Histopathological Description
Heart: There is diffuse congestion and mild to moderate, multifocal epicardial, endocardial and myocardial haemorrhage associated with mild to moderate epicardial and interstitial oedema. Unassociated with any inflammatory change, there are two intracellular, round or oval, 100-150 µm diameter, protozoal cysts containing large numbers of closely-packed fusiform bradyzoites (Sarcocystis spp), which was interpreted as an incidental finding.
Spleen: The capsule is intact and the red pulp:white pulp ratio is approximately 9:1. The red pulp is uncongested and therefore appears moderately cellular. Diffusely distributed throughout the red pulp are large numbers of macrophages with cytoplasm distended with light brown granules (haemosiderin), and occasional megakaryocytes. The white pulp has mildly congested marginal zones and densely cellular, periarteriolar lymphoid sheaths (PALS) and splenic lymphoid follicles; the latter have well-developed germinal centres, which contain occasional macrophages with intracytoplasmic haemosiderin granules.
Morphological Diagnosis
Cardiac haemorrhage; acute, multifocal, mild to moderate (non-specific agonal change).
Splenic haemosiderosis; chronic diffuse moderate (incidental finding).
Aetiological Diagnosis
Agonal myocardial change
Comments
Epicardial and endocardial haemorrhages are common agonal changes, unrelated to the cause of death. In view of the history, the possibility of a peracute cardiotoxicosis (e.g. due to polyether ionophore antibiotics – Monensin; or cardiac glycosides – fluoracetate/1080) should be followed up with the submitter.
Splenic haemosiderosis, although prominent in this section, is a common incidental finding in cattle.