The role of Penicillia in ryegrass staggers

Tremorgenic strains of Penicillium verrucosum var cyclopium, P canescens, P janthinellum, P novaezeelandiae and P estinogenum were isolated from the faeces of 15 of 23 affected sheep and cattle in eight of nine field outbreaks of ryegrass staggers. One tremorgenic strain of P griseofulvum was isolated from the faeces of one of 25 sheep grazing in unaffected flocks. Tremorgenic strains of P verrucosum var cyclopium, P canescens, P janthinellum and P estinogenum were also isolated from the A horizon of New Zealand soils. Since a large proportion of experimentally dosed live P verrucosum var cyclopium died during passage through the gut, the faecal evidence from naturally staggering animals suggests that at least some outbreaks of ryegrass staggers are caused by tremorgenic Penicillia and that their source may be soil.     

The occurrence of phalaris staggers in sheep

Extract

Typical cases of the “staggers” syndrome associated with Phalaris tuberosa poisoning occurred at Invermay Research Station in October, 1954. It is being recorded because detailed records of pasture management and climatic conditions are available for the period when symptoms were seen, also the pasture composition of the Phalaris plot.     

Isolation of Salmonella dublin from a sheep in New Zealand

Extract

On March 8, 1964, formalinized samples of liver, kidney and lung and fresh samples of mesenteric lymph nodes and lung from a ram hogget were submitted to the Wallaceville Animal Research Centre. The animal had died suddenly and post-mortem examination revealed intense reddening of the intestinal and abomasal mucosa and enlarged mesenteric lymph nodes, with some consolidation and pleural adhesions. Small red spots were observed on the liver surface. The possibility of salmonellosis was considered and appropriate cultures were made of the fresh material in addition to aerobic cultures on blood agar.     

Enzootic pneumonia of sheep in New Zealand

Extract

Enzootic pneumonia of sheep is a specific condition confined to southern Otago and the Southland district and is commonly referred to as “Southland Pneumonia.” It has been recognized as a distinct clinical entity for many years in that area, heavy losses being reported in the Gore district of Southland in 1924.     

Isolation of Parainfluenza type 3 virus from sheep in New Zealand

Extract

Bovine virus diarrhoea (BVD) and infectious bovine rhinotracheitis (IBR) viruses are commonly thought on clinical grounds to be widespread in the. New Zealand cattle population, and records of virus isolation and serology from this laboratory support this assumption. To date, however, few reports have been published on the prevalence of these two diseases in New Zealand.     

Scrapie in imported sheep in New Zealand

Extract

The disease known as Scrapie was diagnosed in New Zealand for the first time in June, 1952. Two positive cases and, one suspected case occurred in Canterbury in Suffolk sheep which were imported from England early in 1950. The disease appeared after a typiqally long incubation period and ran a characteristic course in the affected sheep. The outbreak of Scrapie in New Zealand and the drastic measures necessary to control it have placed new emphasis on the difficulty of preventing the introduction of this and other diseases which develop insidiously after a long incubation period, and for which no biological test is available. The same factors have also been responsible for the peculiar difficulties encountered by overseas workers in investigating Scrapie and in establishing clearly the facts of its etiology and transmission.     

Flow-mediated K+ secretion in horses intoxicated with lolitrem B (perennial ryegrass staggers)

AIM: To investigate the effects of lolitrem B intoxication on renal K⁺ secretion in response to increased tubular flow rates.

METHODS: Results are derived from a repeated measure pilot study of seven horses fed non-perennial ryegrass feed for a week prior to exposing them to perennial ryegrass seed and hay that contained an average of 2 ppm lolitrem B. At the end of the control and treatment period frusemide (1 mg/kg I/V) was administered and serial fractional excretion of K⁺(FEK⁺) and fractional excretion of Na⁺(FENa⁺) calculated. Baseline concentration of aldosterone in plasma, serum K⁺concentration and feed K⁺ concentration were also compared.

RESULTS: Key findings included a reduced change in FEK⁺ from 0 to 15 minutes in response to frusemide administration (p=0.022, Wilcoxon signed-rank test) and a reduced baseline concentration of aldosterone in plasma (p=0.022, Wilcoxon signed-rank test) during the treatment period compared with the control.

CONCLUSIONS: Results suggest that lolitrem B intoxication reduced flow-mediated K⁺ secretion and interfered with aldosterone production or secretion. However, further investigation is required to validate these findings and to further elucidate the underlying pathophysiology.

CLINICAL RELEVANCE: Lolitrem B intoxication in horses may cause disruption to electrolyte handling in addition to neurological deficits.     

Multifocal retinitis in New Zealand sheep dogs

Thirty-nine percent of 1,448 working sheep dogs were affected with varying degrees of multifocal retinal disease on ophthalmoscopic examination. Lesions consisted of localized areas of hyperreflexia in the tapetal fundus, often associated with hyperpigmentation. Severely affected animals had widespread hyperreflexia with retinal vascular attenuation. Only 6% of 125 New Zealand dogs raised in urban environment were similarly affected. Both eyes of 70 dogs from New Zealand were examined histologically. Forty-seven of 70 dogs had ocular inflammatory disease. Ten other dogs had noninflammatory eye disease, and 13 dogs had normal eyes. Histologically, eyes with inflammatory disease were divided into three categories: Dogs 3 years of age or less with active inflammatory disease of the retina, uvea, and vitreous. Four dogs in this group had migrating nematode larvae identified morphologically as genus Toxocara. Diffuse retinitis and retinal atrophy in conjunction with localized retinal necrosis and choroidal fibrosis. Dogs in this category were severely, clinically affected. Chronic, low-grade retinitis with variable retinal atrophy. Most dogs in this category were over 3 years of age, and many were visually functional. The existence of a definable spectrum of morphological changes associated with inflammation, suggests that Toxocara sp. ocular larva migrans may be the cause of a highly prevalent, potentially blinding syndrome of working sheep dogs in New Zealand.     

Segmental axonopathy of Merino sheep in New Zealand

AIM: To investigate an axonopathy of Merino sheep that caused progressive hindlimb ataxia and slight to moderate paresis, with the purpose of understanding its pathogenesis. METHODS: Tissues were fixed in buffered paraformaldehyde or paraformaldehyde and glutaraldehyde, processed into wax and epoxy resin, respectively, and examined by light and electron microscopy. Fresh frozen spinal cord and trigeminal nerve roots were subjected to homogenisation, centrifugation and two-dimensional electrophoresis. Selected protein spots were identified using matrix-assisted laser desorption ionisation (MALDI) mass spectrometry. RESULTS. By light microscopy, there were large pale foamy spheroidal axonal swellings affecting peripheral as well as central axons. By electron microscopy, these were shown to contain many membrane-bound vesicles. The main abnormalities in expressed proteins involved cytoskeletal elements and myosin heavy chain, the latter interpreted as associated with the molecular motor myosin Va. CONCLUSIONS: The disorder is the same as that described in Merinos in Australia as segmental axonopathy, and believed to have an inherited aetiology. The lesions and protein changes indicate abnormalities of the cytoskeleton, its relationship with the myelin sheath, and myosin Va molecular motor. The consequence appears to be abnormal axonal transport and inability to maintain the integrity of axons and their myelin sheaths.     

Nematode burdens of alpacas sharing grazing with sheep in New Zealand

Sheep and alpacas of similar age groups (6, 18 and 36+ months) were grazed for 16 weeks on pasture contaminated by lambs. Faecal egg counts, bulked larval cultures, lungworm larvae in faeces, dag scores, liveweight changes and nematode larvae on pasture were measured. Chabertia, Oesophagostomum, Cooperia, Ostertagia and Haemonchus and Trichostrongylus larvae were cultured from both the sheep and the alpacas. For the respective age groups, the alpacas had lower liveweight gains (10, 32 and 47 g/d vs 88, 84 and 120 g/d), peak faecal egg counts (384, 50 and 60 epg vs 1500, 500 and 140 epg) and faecal contamination of the perineum than the same ages of sheep. These results suggest alpacas became less affected with gastrointestinal nematodes than sheep.     

Characterization of two strains of adenovirus isolated from New Zealand sheep

Two strains of adenovirus were isolated from a flock of lambs sampled regularly for 10 months. The first strain was isolated in January from nasal secretions. The second strain was isolated in May and June from nasal secretions, faeces and lung tissue. Representative isolates were identified as adenoviruses on the basis of their morphology, physico-chemical characteristics and the presence of the adenovirus group-specific antigen. The two isolates selected for characterization were serologically dictinct by cross-neutralization tests. They also differed in their behaviour in tissue culture and in their ability to agglutinate chicken erythrocytes.     

Segmental axonopathy of Merino sheep in New Zealand

AIM: To investigate an axonopathy of Merino sheep that caused progressive hindlimb ataxia and slight to moderate paresis, with the purpose of understanding its pathogenesis.

METHODS: Tissues were fixed in buffered paraformaldehyde or paraformaldehyde and glutaraldehyde, processed into wax and epoxy resin, respectively, and examined by light and electron microscopy. Fresh frozen spinal cord and trigeminal nerve roots were subjected to homogenisation, centrifugation and two-dimensional electrophoresis. Selected protein spots were identified using matrix-assisted laser desorption ionisation (MALDI) mass spectrometry.

RESULTS. By light microscopy, there were large pale foamy spheroidal axonal swellings affecting peripheral as well as central axons. By electron microscopy, these were shown to contain many membrane-bound vesicles. The main abnormalities in expressed proteins involved cytoskeletal elements and myosin heavy chain, the latter interpreted as associated with the molecular motor myosin Va.

CONCLUSIONS: The disorder is the same as that described in Merinos in Australia as segmental axonopathy, and believed to have an inherited aetiology. The lesions and protein changes indicate abnormalities of the cytoskeleton, its relationship with the myelin sheath, and myosin Va molecular motor. The consequence appears to be abnormal axonal transport and inability to maintain the integrity of axons and their myelin sheaths.     

Amino acid polymorphisms of PrP gene in Mongolian sheep

To characterize amino acid polymorphisms in sheep prion protein (PrP), we analyzed the PrP genes from 271 sheep of 4 breeds (Khalkh, Yeroo, Orkhon and Khangai) raised in central Mongolia (Tuv, Uvurkhangai and Selenge prefectures). A total of 16 genotypes and 8 allelic variants of the PrP gene at codons 112, 136, 154 and 171 were found. At codon 171, 1.8% of the sheep had arginine/arginine (R/R) (resistant to scrapie) and 66.8% had glutamine/glutamine (Q/Q) (susceptible to scrapie). Several Yeroo and Orkhon sheep raised in Selenge prefecture had valine at codon 136 (136V) (highly susceptible to scrapie). Several Yeroo, Orkhon and Khangai sheep raised in Selenge prefecture had histidine at codon 154 (154H). Novel polymorphisms of valine (V) and serine (S) at codon 127, lysine (K) at codon 171, and leucine (L) and arginine (R) at codon 189 were also found in Khalkh, Yeroo and Orkhon sheep. It is not known whether these novel polymorphisms affect scrapie susceptibility.