December 2013

Case A

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Well grown six-month-old crossbred lambs were moved into a paddock of annual ryegrass, autumn phalaris and broadleaf weeds. There were 12 deaths in the first two days.

Example Histopathological Description

This section of kidney is wedge shaped and includes capsule, cortex and proximal medulla. Renal pelvis is not present. The main changes are in the tubules of the cortex with milder changes in the medulla. In the cortex there are multiple foci of mildly dilated proximal convoluted tubules with swollen vacuolated and or hypereosinophilic granular epithelial cells (tubular degeneration). Intracytoplasmic eosinophilic droplets are present in some cells indicating hyaline degeneration. Other foci have flattened attenuated epithelium suggesting early repair.  Multiple small foci show epithelial separation, pyknosis and detachment (necrosis and cellular casts). Some tubules contain granular to amorphous eosinophilic material (granular and hyaline casts) in scattered cortical and medullary tubule lumina. Randomly scattered in the tubules of some of these areas are small aggregates of brown/grey translucent refractile acicular material typical of oxalate crystals.

There are multiple foci of interstitial congestion at the corticomedullary junction and sparse small interstitial aggregates of mononuclear cells, predominantly lymphocytes and plasma cells. Rare scattered small refractile basophilic deposits occur in the interstitium of the medulla indicating mineralisation. Bowman’s space in some glomeruli is expanded by homogenous eosinophilic material. Multiple Bowman’s capsules show mild but consistent cuboidal metaplasia of the parietal epithelium.

Morphological Diagnosis

Nephrosis; mild to moderate, subacute and multifocal with intralesional oxalate crystals.

Aetiological Diagnosis

Oxalate nephrosis


Oxalate nephrosis is likely to have been caused by ingestion of oxalate containing plants. In Australia these can include docks and sorrel (Rumex spp), soursob (Oxalis pes-caprae), pigweed (Portulaca spp) and Amaranthus spp; however, this is not a complete list.  It can also be caused by the ingestion of mouldy feed caused by Aspergillus niger. However, the lesions in this lamb are only mild to moderate and the tubules show evidence of repair. This suggests that the lesions did not occur in the two days of grazing in the most recent paddock. Oxalate nephrosis could be a contributing cause of mortality, but not necessarily the only cause. Further investigations to confirm oxalate toxicity could include: examination of additional animals for blood or eye fluid for hypocalcaemia, oxalate containing plants in the rumen, rumenitis and pulmonary oedema in affected animals; a history of oxalate-unadjusted animals and the presence in paddocks of oxalate-containing plants with evidence of them having been grazed.

Because this may not be a simple oxalate toxicity problem, the clinician and farmer should be advised to consider the possibility of additional diagnoses. Hungry lambs can eat indiscriminately and acute phalaris poisoning (caused by cardiotoxic alkaloids and sometimes producing no gross or histologic lesions) should be considered. In addition, annual ryegrass toxicity (use ELISA to detect Rathayibacter toxicus in faeces), and nitrate poisoning (test for methaemoglobinaemia) should also be considered.

In the meantime, it would be wise to remove lambs from the current pasture, not return them to recently grazed paddocks and supply ad lib good quality water.  Consider symptomatic treatment of lambs showing staggers and musculoskeletal weakness with subcutaneous calcium borogluconate to correct suspected hypocalcaemia. Inspect paddocks for potentially toxic plants and reintroduce animals gradually and in small numbers to demonstrate safety.

Case B

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This was the 16th pigeon to die in this loft over the last three weeks. It was found dead.

Example Histopathological Description

There are two sections of pancreas, with similar changes. There is moderate congestion and multifocally extensive areas of mild parenchymal pallor and glandular disruption in the exocrine pancreas. This is most severe in sub-capsular areas. Affected acinar cells are shrunken, separated, and often have vacuolated pale cytoplasm. Zymogen granules are pale or absent in affected cells. Nuclei of affected cells are sometimes karyorrhexic or pyknotic. The pattern of single cell necrosis extends to cell loss (“dropout”) in places. There is a fine network of fibrosis associated with areas of cell dropout. Sparse to moderate numbers of lymphocytes and fewer plasma cells are present throughout the organ with some concentrated in perivascular locations. Islets of Langerhans are sparse but of normal appearance. Autolytic changes are present, most obviously in the sloughing of ductular epithelium. Occasional cells show suspicious chromatin margination with possible intranuclear eosinophilic inclusions. Other cells show suspicious variably-sized eosinophilic intracytoplasmic inclusions. It is not clear whether these are viral inclusion bodies or non-specific changes in secretory cells.

Morphological Diagnosis.

Pancreatic necrosis; multifocal, mild to moderate, with acinar degeneration, single cell necrosis and lymphoplasmacytic infiltration.

Aetiological Diagnoses.

Pigeon Paromyxoviral pancreatic necrosis.


Avian Influenza, Newcastle disease, pigeon herpes virus, avian encephalomyelitis virus, Se deficiency, Zn toxicity and various vitamin B deficiencies should be considered in the differential diagnosis.

Pigeon paramyxovirus (PPM1) can be confirmed by PCR from cloacal and tracheal swabs and tissues from dead or in-contact birds. Paramyxovirus (PMV1) cross reacts with some Newcastle disease genes in routine NDV PCRs. This can be useful if PMV1 PCRs are not available. Avian influenza is a notifiable disease in Australia and should be excluded by PCR or other means. Serology of cohorts may be useful if the flock has not been vaccinated for PMV1. The other causes listed above should be considered as alternatives or co-factors.