H Thompson

Clinical and pathological findings in feline immunodeficiency virus experimental infection

n Abstractn n A study is described of the clinical and pathological findings in 20 specific pathogen free cats infected when 1 year old with feline immunodeficiency virus and monitored over 12 months. Cats were divided into two groups (A and B). The clinical and clinicopathological features were studied in Group A. In Group B, at 1, 2, 4, 9 and 12 months post infection two cats were necropsied. Clinically all cats developed generalised lymphadenopathy, six cats were neutropenic and five cats lymphopenic. Three cats became febrile with conjunctivitis and anterior uveitis and one of these cats ultimately developed jaundice. Postmortem examinations confirmed a generalised lymphadenopathy involving peripheral and visceral lymph nodes with concurrent stimulation of splenic white matter and mucosal lymphoid tissue of the digestive tract and conjunctiva. Within the lymph nodes there was a reactive follicular hyperplasia accompanied by a paracortical hyperplasia with an increased paracortical vascularity. Unusual features were the presence of lymphoid follicles in the bone marrow, thymus and parathyroid tissue. In addition, aggregates of lymphoid cells were found within salivary glands, kidneys, sclera and choroid of the eye. One cat developed a lymphosarcoma affecting the liver and kidneys at 36 weeks post infection. The cat with jaundice had a cholangitis with marked biliary epithelial hyperplasia.n n

Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals

REASONS FOR PERFORMING STUDYnGastric ulceration is now widely recognised as an important disease in high performance horses. Little is known about gastric histopathology in healthy or diseased animals; a comprehensive assessment would enhance interpretation of gross findings through assessment of their accuracy and allow for identification of lesion variety and pathogenesis in different anatomical regions of the stomach.nnnOBJECTIVESnTo investigate the true extent and variety of gastric lesions in a mixed population of mature horses at post mortem.nnnMETHODSnStomachs were removed from a mixed population of 21 horses at post mortem. Mucosal abnormalities were recorded in photographic and written form. Representative samples from all gross lesions were taken for histopathology and processed routinely. Special stains including Gram, PAS and Warthin Starry, were used when appropriate. Pathological classification of lesion type using both gross and histological appearances was performed.nnnRESULTSnClassification of lesions within the squamous region included hyperkeratosis, punctate scars, diffuse erosions/ ulcerations and margo injuria; and within the glandular region, hyperaemia, focal erosions and ulcerations. Glandular metaplasia was recognised for the first time in the equine stomach. No Helicobacter-like organisms were detected in association with lesion development.nnnCONCLUSIONS AND POTENTIAL RELEVANCEnThis study used gross and histological examination to highlight the large variety of naturally occurring gastric lesions in a mixed population of horses. Analysis of the pathogenesis of lesion development is now possible. Further research regarding the range of pathology in larger, more diverse groups of horses is required.

Pathology of gastritis and gastric ulceration in the horse. Part 2: A scoring system

REASONS FOR PERFORMING STUDYnHigh numbers of racehorses in training are reported to have gastric ulceration. Gross lesion scoring systems exist, but there is no fixed protocol with which to record gastric microscopic findings. In man, the histological classification of stomach lesions helps in the identification of recognised and emerging aetiologies of gastric disease and aids accurate comparison of findings between studies. In horses, the development of such a system would therefore be of benefit.nnnOBJECTIVESnTo develop a pathological scoring system that can be applied to examine samples of the equine stomach at biopsy and post mortem.nnnMETHODS AND RESULTSnThe equine gastritis grading (EGG) system was developed initially using horse stomachs at post mortem. The protocol involved sampling tissue from 5 fixed locations within the squamous and glandular regions. Histological examination recorded both type and degree of inflammatory infiltrate and the presence of erosions, ulceration or any other reactive change in each slide. These results were combined and an overall diagnosis of gastritis type given for each stomach.nnnCONCLUSIONS AND POTENTIAL RELEVANCEnThis is the first example of a complete pathological scoring system developed specifically for recording gastric lesions in the horse. It provides a thorough and repeatable method with which to examine the equine stomach in microscopic detail. It can be used in diagnostic or research situations and the consistency of the information gathered will enable accurate comparison of data between different studies. It aims to give an indication as to the currently undetermined pathological variations seen in the stomach of healthy and diseased horses, as well as increasing the understanding of the pathogenesis of gastritis and gastric ulceration. Using this information, interpretation of biopsy samples is improved.

Canine Nephrotoxic Glomerulonephritis: A Combined Light, Immunofluorescent, and Ultrastructural Study

The sequential pathology of canine nephrotoxic glomerulonephritis was studied by light microscopy, immunofluorescence and electron microscopy. The disease was induced by intravenous administration of antiglomerular basement membrane serum, and experimental animals were examined from 4 h up to 60 days after administration of nephrotoxic serum. During the first few days there was extensive glomerular capillary necrosis and infiltration by neutrophils. This was followed by mesangial proliferation and glomerular scarring. Using immunofluorescence, nephrotoxic (rabbit) serum and host IgG and complement (C3) were detected in damaged glomeruli.

Central diabetes insipidus associated with primary focal B cell lymphoma in a dog

CENTRAL diabetes insipidus is an uncommon condition characterised by polyuria due to a deficiency in the secretion of antidiuretic hormone from the posterior pituitary gland. The causes of central diabetes insipidus in dogs include intracranial tumours, such as craniopharyngioma, meningioma,

Idiopathic hepatic veno-occlusive disease causing Budd-Chiari-like syndrome in a cat

Budd‐Chiari‐like syndrome (BCLS) is a rare clinical entity characterised by portal hypertension and ascites. This report describes a case of BCLS in a cat due to obstruction at the level of the hepatic veins. The diagnosis was based on the clinical findings and a histopathological assessment of the liver demonstrating perivenular fibrosis around the central and sublobular veins. Although these lesions are similar to those observed in man with BCLS, the aetiology in this case remains unknown.

Cloning, sequence analysis and expression of the cDNAs encoding the canine and equine homologues of the mouse double minute 2 (mdm2) proto-oncogene

The mdm2 oncogene is amplified and overexpressed in a variety of human tumours and the oncogenic potential of MDM2 is partly due to its ability to inactivate tumour suppressor p53 function. In the present communication we describe the cloning, sequence analysis and expression of the complete wildtype canine and equine mdm2 cDNAs. The encoded full-length canine and equine cDNAs show strong sequence homology with MDM2 proteins from other species and both cDNAs generate recombinant proteins of approximately 90 kDa. These data will allow for the role of this oncogene to be established in companion animal oncology.

Arrhythmogenic right ventricular cardiomyopathy secondary to adipose infiltration as a cause of episodic collapse in a horse

A 15-year-old Clydesdale cross gelding was investigated and managed over a 2-year period for intermittent collapse. The horse presented initially after an observed episode of collapse at rest, and had a resting tachycardia, elevated Cardiac Troponin I and polycythaemia. Multiple dysrhythmias were detected on telemetric electrocardiography. Vital parameters, cardiac rhythm and red cell count returned to reference range with prolonged rest but further resting syncopal episodes were observed, and due to safety concerns and limited treatment options the horse was euthanased. Post mortem evaluation identified extensive infiltration and replacement of right and left ventricular myocardial fibres with adipose and fibrous tissue, consistent with arrhythmogenic right ventricular cardiomyopathy. This report provides further information regarding the clinical and pathological features of this rarely reported condition.

Analysis of Campylobacter jejuni infection in the gnotobiotic piglet and genome-wide identification of bacterial factors required for infection

To investigate how Campylobacter jejuni causes the clinical symptoms of diarrhoeal disease in humans, use of a relevant animal model is essential. Such a model should mimic the human disease closely in terms of host physiology, incubation period before onset of disease, clinical signs and a comparable outcome of disease. In this study, we used a gnotobiotic piglet model to study determinants of pathogenicity of C. jejuni. In this model, C. jejuni successfully established infection and piglets developed an increased temperature with watery diarrhoea, which was caused by a leaky epithelium and reduced bile re-absorption in the intestines. Further, we assessed the C. jejuni genes required for infection of the porcine gastrointestinal tract utilising a transposon (Tn) mutant library screen. A total of 123 genes of which Tn mutants showed attenuated piglet infection were identified. Our screen highlighted a crucial role for motility and chemotaxis, as well as central metabolism. In addition, Tn mutants of 14 genes displayed enhanced piglet infection. This study gives a unique insight into the mechanisms of C. jejuni disease in terms of host physiology and contributing bacterial factors.

LYMPH NODE PATHOLOGY IN EXPERIMENTAL FIV INFECTION

Feline immunodeficiency virus (FIV) was first isolated in 1986 from a colony of cats in California exhibiting multiple, and often chronic, infections (Pedersen et al, 1987). The virus was characterised as a T-lymphotropic lentivirus morphologically similar but antigenically distinct from human immunodeficiency virus (HIV), the cause of acquired immunodeficiency syndrome (AIDS) in man (Barre-Sinoussi et al, 1983; Gallo et al, 1984). Subsequently the virus was isolated throughout the world (Harbour et al, 1988; Ishida et al, 1988) and analysis of stored serum samples indicated that FIV infection has been present since at least the 1960s in cat populations (Gruffydd-Jones et al, 1988; Shelton et al, 1990). It is likely that biting is the most common means of transmission of the virus (Yamamoto et al, 1989). Infection is persistent and can be detected by the demonstration of infectious virus in activated T cells from peripheral blood (Pedersen et al, 1987), by amplification of FIV nucleic acid sequences in blood or other cells by the polymerase chain reaction (PCR) (Dandekar et al, 1992) or by the demonstration of anti-FIV antibodies in the serum or plasma (Pedersen et al, 1987; Hosie & Jarrett, 1990).