Early neonatal lamb mortality: postmortem findings.

An investigation of stillbirth and early neonatal lamb mortality was conducted in sheep flocks in Norway. Knowledge of actual causes of death are important to aid the interpretation of results obtained during studies assessing the risk factors for lamb mortality, and when tailoring preventive measures at the flock, ewe and individual lamb level. This paper reports on the postmortem findings in 270 liveborn lambs that died during the first 5 days after birth. The lambs were from 17 flocks in six counties. A total of 27% died within 3 h after birth, 41% within 24 h and 80% within 2 days. Most lambs (62%) were from triplet or higher order litters. In 81% of twin and larger litters, only one lamb died. The most frequently identified cause of neonatal death was infectious disease (n=97, 36%); 48% (n=47) of these died from septicaemia, 25% (n=24) from pneumonia, 22% (n=21) from gastrointestinal infections and 5% (n=5) from other infections. Escherichia coli accounted for 65% of the septicaemic cases, and were the most common causal agent obtained from all cases of infection (41%). In total, 14% of neonatal deaths resulted from infection by this bacterium. Traumatic lesions were the primary cause of death in 20% (n=53) of the lambs. A total of 46% of these died within 3 h after birth and 66% within 24 h. Severe congenital malformations were found in 10% (n=27) of the lambs, whereas starvation with no concurrent lesions was the cause of death in 6% (n=17). In 16% (n=43) of the lambs, no specific cause of death was identified, lambs from triplet and higher order litters being overrepresented among these cases. In this study, the main causes of neonatal lamb mortality were infection and traumatic lesions. Most neonatal deaths occurred shortly after birth, suggesting that events related to lambing and the immediate post-lambing period are critical for lamb survival.

Characterization of amyloid in equine recurrent uveitis as AA amyloid.

Two horses with chronic uveitis and histological lesions consistent with equine recurrent uveitis (ERU) were examined. Microscopical findings in the ciliary body included deposits of amyloid lining the non-pigmented epithelium, intracytoplasmic, rod-shaped, eosinophilic inclusions and intraepithelial infiltration of T lymphocytes. Ultrastructural examination of the ciliary body of one horse confirmed the presence of abundant extracellular deposits of non-branching fibrils (9-11 nm in diameter) consistent with amyloid. Immunohistochemistry revealed strong positive labelling for AA amyloid and mass spectrometry showed the amyloid to consist primarily of serum amyloid A1 in both cases. The findings suggest that localized, intraocular AA amyloidosis may occur in horses with ERU.

Pancreatitis in hyperlipemic mink (Mustela vison).

In both man and animals, inflammatory changes in the pancreas often occur with disturbances in lipid metabolism, including hypertriglyceridemia and an excess of free fatty acids. Hyperlipoproteinemia type I is a human condition caused by a deficiency of lipoprotein lipase. A similar metabolic disturbance that occurs in mink is of considerable comparative interest, as it is also followed by pancreatitis. Pancreatic lesions in hyperlipoproteinemic mink included overt variably sized nodules with hemorrhage and necrosis. These lesions began as intralobular necrosis of exocrine cells and progressed to total lobular destruction, with eventual involvement of interlobular tissue. Remnants of epithelial cells and lipid-filled macrophages were seen in necrotic areas, along with other types of inflammatory cells scattered in a lipid-rich exudate. Granulation tissue developed rapidly in necrotic areas. Additional observations included ductal proliferation, replacement of epithelial cells with fat, and mural arterial thickening, most conspicuously with vacuolated cells and endothelial proliferation. Extravasation of lipid-rich plasma is thought to be a major intensifier of the inflammatory response.

Fibrotic contracture of the canine infraspinatus muscle: pathophysiology and prevention by early surgical intervention.

Fibrotic contracture of the canine infraspinatus muscle (FCIM) is considered a rare musculotendineous disorder mainly affecting hunting dogs. After an acute onset of a painful non-weight bearing lameness, the initial pain and lameness improve over a period of one to four weeks, after which a characteristic circumducted gait abnormality develops in the forelimb. The initial injury to the infraspinatus muscle is not fully recognized or correctly interpreted in most cases, at least not with regard to its potential as a precursor of myopathy and FCIM. A mixed breed hunting dog developed an acute and extremely painful swelling of the infraspinatus muscle. The injury was easily recognized during clinical examination. The clinical signs were interpreted as an osteo-fascial compartment syndrome (OFCS) of the infraspinatus muscle. Immediate surgical decompression of the osteo-fascial compartment to prevent development of FCIM was undertaken. The histopathological and immunohistochemical examinations of the injured infrapinatus muscle revealed tissue changes that indicated acute muscle rupture, without any signs of an initiating degenerative process. On the day following surgery the dog was fully weight bearing. Restriction of activity for four weeks was recommended. Eight months after the initial injury, the dog had completely recovered and had full days of vigorous exercise and hunting activity without any apparent lameness. The findings in this case suggested that the infraspinatus muscle may be considered to be an osteo-fascial compartment in dogs and must be added to the list of compartments that may pose a potential risk for OFCS in the canine extremity.

Filter function and immune complex trapping in splenic ellipsoids.

The role of splenic ellipsoids in the trapping of particulate material and immune complexes was investigated in mink (Mustela vison). The ellipsoids were prominent, with typical features such as a permeable endothelium and a discontinuous basement membrane surrounded by a sheath of macrophages and reticular cells. Ellipsoidal trapping of circulating particles was demonstrated 10 min after intracardiac injection of colloidal carbon and fluorescent microspheres. Preformed peroxidase-antiperoxidase immune complexes were detected in ellipsoids 10 min and also 1 h after intracardiac injection. Erythrocytes were frequently observed in the ellipsoidal sheath, and many phagocytized fragments of erythrocytes were found in the ellipsoidal macrophages. It was concluded that mink ellipsoids are effective blood filters with a role in retention of circulating particulate material, and that mammalian splenic ellipsoids also have the ability to trap immune complexes.

Kinetics of glycosaminoglycan deposition in splenic AA amyloidosis induced in mink.

The kinetics of splenic glycosaminoglycan (GAG) expression in mink has been investigated during the course of AA amyloid induction, i.e. at 3 to 6 weeks of lipopolysaccharide (LPS) treatment. Splenic amyloid was demonstrated by means of Congo red staining in five of 19 LPS-treated mink. Chondroitin/dermatan sulfate (CS/DS), as well as heparan sulfate proteoglycans (HSPG), was extracted from amyloid and control spleens. Independently of the presence of amyloid, the total amount of splenic GAGs increased with the duration of LPS treatment, and an HSPG population was found confined to the LPS-treated spleens. The differential expression of various PG and GAG epitopes in mink spleen was investigated with the help of immunohistochemistry. The amyloid deposits were shown to contain GAG chains of CS and HS, and the core proteins of DSPG decorin and the HSPGs perlecan and agrin. Decorin and perlecan were shown in normal spleens localized to the splenic ellipsoids, an early target for AA amyloid deposition. The constitutive expression of PGs at predilection sites for amyloid deposition and their increased expression in the tissues developing amyloidosis at these early stages show that PGs are available for the formation and deposition of AA amyloid.

The role of the defective interfering particle DI9c in mucosal disease in cattle.

Mucosal disease occurs in cattle persistently infected with a noncytopathogenic strain of bovine viral diarrhoea virus (BVDVnc) following in utero infection. The disease can be initiated by superinfection with a cytopathogenic biotype (BVDVc) of the virus with antigenic "homology" to the persisting virus. A BVDVc isolated from a clinical case of mucosal disease has been discovered to consist of a defective interfering particle, DI9, and an associated BVDVnc helper virus. A defective virus corresponding to DI9 was recently recovered from an infectious cDNA clone and was named DI9c. To evaluate the role of DI9 in the pathogenesis of mucosal disease a two-part experimental study was carried out which included clinical, haematological, pathological and virological investigations. Eight of nine calves persistently infected with BVDVnc were experimentally inoculated with DI9c. The defective virus was propagated in cells preinfected with the same strain of virus used to persistently infect the calves in utero. The calves were euthanased on days 4, 7, 14, 21, 28, 40, 40 or 87 post inoculation. None of the inoculated animals developed classical mucosal disease, neither clinically nor pathologically. DI9c was not found in serum, nasal swab or tissue samples from the calves by observing cytopathogenic effect and/or using a polymerase chain reaction after reverse transcription (RT-PCR) of viral RNA. DI9c did not replicate to a detectable extent in these assays, and its participation in the pathogenesis of mucosal disease could not be proven.

Comparison of oral and intraperitoneal toxicity of yessotoxin towards mice.

Currently, yessotoxin is regulated among the toxins in the diarrhetic shellfish poisoning (DSP) complex. Yessotoxin is equally acutely toxic towards mice upon intraperitoneal injections as those algal toxins giving diarrhea, but is not diarrheagenic. Its presence in mussels may therefore lead to overestimation of risk of DSP in consumers when the standard mouse bioassay is used. Arguments are presented for the use of analytical methods instead of the mouse bioassay for the diarrheagenic DSP toxins and yessotoxin. Yessotoxin was found to be more than ten times less toxic to mice via the oral route, compared with intraperitoneal injections. Even at 10mg/kg body weight, the highest dose ever tested orally, yessotoxin did not kill the mice. By means of light microscopy of several organs, moderate changes were only observed in the heart. Ultrastructural studies revealed swelling of heart muscle cells leading to separation of the organelles. Effects were most pronounced close to the capillaries. The pathological changes were clearly dose dependent, and the lowest oral dose where any effects were seen was 2.5mg yessotoxin per kg.