A Review of Canine Pseudocyesis

The purpose of this article is to review the most relevant features of the physiology, clinical signs, diagnosis, treatment and prevention of canine pseudocyesis (PSC). This is a physiological syndrome, characterized by clinical signs such as: nesting, weight gain, mammary enlargement, lactation and maternal behaviour, which appears in non‐pregnant bitches at the end of metaoestrus. PSC is a frequent finding in domestic dogs. Although it is generally admitted that prolactin (PRL) plays a central role in the appearance of PSC, its precise aetiophysiology is not completely understood yet. A number of clinical studies suggest that at some point of metaoestrus circulating PRL levels rise in overtly pseudopregnant bitches. Individual differences in sensitivity to PRL as well as the existence of molecular variants of canine PRL with different bioactivity versus immunoreactivity ratios may help clarify the aetiopathology of PSC. Diagnosis of PSC is based on the presence of typical clinical signs in metaoestrous non‐pregnant bitches. Considering that PSC is a self limiting physiological state, mild cases usually need no treatment. Discouraging maternal behaviour and sometimes fitting Elizabethan collars to prevent licking of the mammary glands may suffice in these cases. Sex steroids (oestrogens, progestins and androgens) have been traditionally used to treat PSC but the side‐effects usually outweigh the benefits of these medications. Inhibition of PRL release by ergot derivatives [ bromocriptine (10–100 μg/kg per day for 10–14 days], cabergoline (5 μg/kg per day during 5–10 days), metergoline (0.2 mg/kg per day during 8–10 days) has proved to be effective for the treatment of canine PSC. Although some of these ergot derivatives present some untoward side‐effects, they are transient and can usually be managed. Predisposed bitches not intended for breeding should be spayed as ovariectomy is the only permanent preventive measure.     

Reduced growth of Lucilia cuprina larvae fed serum from sheep treated with anthelmintics

The effect of three commonly used anthelmintics, levamisole hydrochloride, ivermectin and closantel, on the development of the sheep blowfly, Lucilia cuprina, was determined. Sheep were treated with each anthelmintic using the manufacturers' recommended dose for helminth control. Both ivermectin and closantel significantly (p < 0.05) reduced the growth rate of larvae of L cuprina cultured in vitro on serum from these sheep. Levamisole hydrochloride had no effect. Ivermectin was effective for less than 6 days after treatment, whereas closantel significantly reduced larval growth 21 days after treatment. Dose-response experiments showed that lower concentrations of both ivermectin and closantel were not as effective in reducing larval growth.     

Spironucleosis in Australian king parrots (Alisterus scapularis)

OBJECTIVE: To describe a syndrome of wasting, diarrhoea and mortality in Australian king parrots (Alisterus scapularis). DESIGN: Field observations and laboratory examinations. Procedure Pathological examinations were performed on 50 Australian king parrots with wasting and diarrhoea. Wet preparations of intestinal contents were examined by light microscopy. Tannins were extracted from acorns (Quercus sp) and tested for toxicity in mice. CLINICAL SIGNS AND EPIDEMIOLOGY: A syndrome of wasting, diarrhoea and mortality was observed in wild juvenile Australian king parrots in eastern Australia from 1984 to 2000. Sporadic cases and outbreaks of disease occurred from May to September in New South Wales, the Australian Capital Territory and Victoria. Outbreaks in the Australian Capital Territory in 1990 and 1991 were associated with parrots congregating to feed on acorns. Most affected birds failed to respond to treatment with dimetridazole and died 1 to 14 days after hospitalisation. Selected cases recovered following treatment with metronidazole. PATHOLOGY: Affected birds were emaciated, with faecal matting of feathers around the cloaca and yellow-green fluid, foamy intestinal contents. Abundant motile Spironucleus trophozoites were observed in wet preparations of faeces of clinically affected birds and intestinal contents of birds examined within 1 h of death. Protozoa were detected histologically in crypts of Lieberkühn in the intestine in association with exudation of mucus (catarrhal enteritis) or lymphoplasmacytic enteritis. Toxicology Tannin extracts from acorns induced periacinar hepatic necrosis in mice. CONCLUSION: Wasting, diarrhoea and mortality in wild juvenile Australian king parrots were associated with Spironucleus-like protozoa in the intestine. Acorns were not considered to be the cause of the syndrome.     

Cerebellar ataxia in sheep grazing pastures infested with Romulea rosea (onion grass or Guildford grass)

There have been anecdotal reports since 1962 of 'staggers' in sheep grazing Romulea rosea infested pastures, but this is the first detailed account. In September 2005, a locomotor disorder developed in 12 of 120 Merino wethers that had grazed R. rosea infested pasture at Albury, New South Wales, over several months. Affected sheep displayed signs that included limb paresis, knuckling over in the fetlocks, fine head tremor, incoordination, and an equilibrium disturbance characterised by frequent falling. The microscopic examination of brain and spinal cord tissues from two affected sheep revealed mild vacuolation, occasional lymphocytic cuffing around blood vessels, mild Wallerian degeneration, and occasional glial cells that contained honey-brown cytoplasmic pigments. The most significant changes were found in the cerebellum, where there were decreased numbers of Purkinje cells, increased numbers of glial cells, scattered vacuoles and occasional swollen axons. Previous reports of cerebellar toxicoses in ruminants have involved goats and cattle and have been associated with the ingestion of six Solanum spp. The Purkinje cell loss in this type of disorder is ultimately extensive and consequently affected animals may survive, but will remain permanently disabled. Aust Vet J 2008;86:354 -356.