G. R. Pearson

Oesophageal strictures in cats associated with doxycycline therapy.

Four cases of oesophageal stricture subsequent to doxycycline administration are reported. All cases were young to middle age (median age 3 years; range 1–7 years), and either domestic shorthair or domestic longhair breed. In all cases the predominant clinical sign was regurgitation, which developed at variable times after doxycycline administration. In all cases the reason for doxycycline use was treatment or prophylaxis of suspected infections (Mycoplasma haemofelis, Chlamydophila felis or Bordetella bronchiseptica), and the duration of therapy was variable. In one case the stricture was definitively diagnosed at post mortem examination, in the three other cases, definitive diagnosis was by endoscopy. Balloon dilation was successful in the three cases that were treated. This is the largest case series, to date, of oesophageal disease in cats associated with doxycycline administration. Caution should be exercised when administering oral medication to cats, especially doxycycline, and should be accompanied either by a water or food swallow.

Attaching-effacing bacteria in animals

Summary Enteric bacteria with a demonstrable or potential ability to form attaching-effacing lesions, so-called attaching-effacing (AE) bacteria, have been found in the intestinal tracts of a wide variety of warm-blooded animal species, including man. In some host species, for example cattle, pigs, rabbits and human beings, attaching-effacing Escherichia coli (AEEC) have an established role as enteropathogens. In other host species, AE bacteria are of less certain significance. With continuing advances in the detection and typing of AE strains, the importance of these bacteria for many hosts is likely to become clearer. The pathogenic effects of AE bacteria result from adhesion to the intestinal mucosa by a variety of mechanisms, culminating in the formation of the characteristic intimate adhesion of the AE lesion. The ability to induce AE lesions is mediated by the co-ordinated expression of some 40 bacterial genes organized within a so-called pathogenicity island, known as the “Locus for Enterocyte Effacement”. It is also believed that the production of bacterial toxins, principally Vero toxins, is a significant virulence factor for some AEEC strains. Recent areas of research into AE bacteria include: the use of Citrobacter rodentium to model human AEEC disease; quorum-sensing mechanisms used by AEEC to modulate virulence gene expression; and the potential role of adhesion in the persistent colonization of the intestine by AE bacteria. This review of AE bacteria covers their molecular biology, their occurrence in various animal species, and the diagnosis, pathology and clinical aspects of animal diseases with which they are associated. Reference is made to human pathogens where appropriate. The focus is mainly on natural colonization and disease, but complementary experimental data are also included.

A retrospective study of 286 cases of neurological disorders of the cat.

Abstract Archive central nervous tissue from 286 cats with neurological disorders was reviewed for histological evidence of feline spongiform encephalopathy (FSE), which may have occurred before it was first recognized in 1990. The following six categories of disease were identified: congenital; degenerative; inflammatory; neoplastic; FSE; lesion-free. The largest category (inflammatory) contained 92 cats, of which 47 were considered to be consistent with infection by feline infectious peritonitis (FIP) virus. Six cats showed evidence of more than one disease process; thus, one cat with FIP also had toxocara infection of the lateral ventricles and five cats with FSE also showed perivascular cuffing suggestive of concurrent viral infection. In only two cases did the diagnosis on review differ significantly from the original interpretation. There was no evidence of FSE before the original case was recognized in April 1990.

Non-toxigenic Escherichia coli O157:H7 strain NCTC12900 causes attaching-effacing lesions and eae-dependent persistence in weaned sheep

Ruminants are regarded as a primary reservoir for Escherichia coli O157:H7, an important human pathogen. Intimin, encoded by the Locus of Enterocyte Effacement by E. coli O157:H7 organisms, has been cited as one bacterial mechanism of colonisation of the gastrointestinal tract. To confirm this and to test whether a non-toxigenic E. coli O157:H7 strain would colonise and persist in a sheep model, E. coli O157:H7 strain NCTC12900, that lacks Shiga toxin (stx) genes, was evaluated for use in a sheep model of persistence. Following oral inoculation of six-week-old sheep, persistent excretion of NCTC12900 was observed for up to 48 days. E. coli O157-associated attaching-effacing (AE) lesions were detected in the caecum and rectum of one six-week-old lamb, one day after inoculation. This is the first recorded observation of AE lesions in orally inoculated weaned sheep. Also, mean faecal excretion scores of NCTC12900 and an isogenic intimin (eae)-deficient mutant were determined from twenty-four six-week-old orally inoculated sheep. The eae mutant was cleared within 20 days and had lower mean excretion scores at all time points after day one post inoculation compared with the parental strain that was still being excreted at 48 days. Tissues were collected post mortem from animals selected at random from the study groups over the time course of the experiment. The eae mutant was detected in only 1/43 samples but the parental strain was recovered from 64/140 samples primarily from the large bowel although rumen, duodenum, jejunum, and ileum were culture positive especially from animals that were still excreting at and beyond 27 days after inoculation.

Attaching and effacing lesions in the large intestine of an eight-month-old heifer associated with Escherichia coli O26 infection in a group of animals with dysentery.

Escherichia coli O26:K60, with genetic attributes consistent with a potentially human enterohaemorrhagic E coli was isolated from the faeces of an eight-month-old heifer with dysentery. Attaching and effacing lesions were identified in the colon of a similarly affected heifer examined postmortem, and shown to be associated with E coil 026 by specific immunolabelling.

Attaching and effacing lesions caused by Escherichia coli O157:H7 in experimentally inoculated neonatal lambs

Four 6-day-old conventionally reared lambs were inoculated orally with a total of 10(9) cfu comprising equal numbers of four enterohaemorrhagic Escherichia coli (EHEC) O157:H7 strains. All animals remained clinically normal. Tissues were sampled under terminal anaesthesia at 12, 36, 60 and 84 h post inoculation (hpi). EHEC O157:H7 was cultured from most gastrointestinal tract sites. Small, sparse attaching and effacing (AE) lesions were found in the caecum at 12 and 36 hpi and in the terminal colon and rectum at 84 hpi. Organisms in the lesions were labelled specifically by an O157 antiserum. The results indicate that the well-characterised mechanisms for intimate attachment encoded by the locus for enterocyte effacement (LEE) of EHEC O157:H7 may contribute to the initial events, at least, of colonisation of sheep.

Ageing changes in cat brains demonstrated by β-amyloid and AT8-immunoreactive phosphorylated tau deposits

The life expectancy of domestic pet cats is increasing, along with the occurrence of geriatric-onset behavioural problems, such as cognitive dysfunction syndrome (CDS). While the cause of CDS is unclear, it has been suggested that it may result from age-related neurodegeneration. In aged and in particular senile human beings, histopathological changes may include the extracellular accumulation of plaque-like deposits of β-amyloid (Aβ) protein and the intracellular accumulation of an abnormally hyperphosphorylated form of the microtubule-associated protein, tau. In severe cases, the latter may form into neurofibrillary tangles. Brain material was assessed from 19 cats, aged from 16 weeks to 14 years; 17 of which had clinical signs of neurological dysfunction. Immunohistochemical methods were used to detect Aβ and its intracellular precursor protein (amyloid precursor protein (APP)) and hyperphosphorylated-tau. APP was constitutively expressed, with diffuse staining of neurons and blood vessels being detected in all cats. More intense staining and diffuse extracellular Aβ staining deposits were found within the deep cortical areas of the anterior- and occasionally mid-cerebrum of seven cats, all of which were over 10 years of age. Neurons staining intensely positive for AT8-immunoreactivity were seen in two cats, aged 11 and 13 years. However, no mature neurofibrillary tangles were detected. This study demonstrated that extracellular Aβ accumulation and AT8-immunoreactivity within neurons are age-related phenomena in cats, and that they can occur concurrently. There are similarities between these changes and those observed in the brains of aged people and other old mammals.

Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy.

Feline spongiform encephalopathy (FSE), a transmissible spongiform encephalopathy or prion disease of cats, first reported in Great Britain in 1990, is believed to result from the consumption of food contaminated by the agent of bovine spongiform encephalopathy (BSE). The accumulation of PrP in non-neural tissues of cats diagnosed as suffering from FSE was investigated by immunohistochemistry. In the majority of the cats no disease-specific PrP was detected in lymphoid tissues. Small amounts of PrP were detected in the spleen of only two of 13 samples examined, in Peyers patches of one of the two cases for which suitable material was available, but in the myenteric plexus of all four cats in which sections of intestine were examined. In addition PrP immunostaining was found in the kidney of all the cats with FSE whose kidneys were examined.

Infection of gnotobiotic calves with Escherichia coli O157 : H7 strain A84

Six colostrum-deprived, hysterotomy-derived calves were maintained under sterile conditions and fed a milk replacer diet. At five days of age, five of the calves were dosed orally with 109 cfu of Escherichia coli 0157: H7 strain A84. They were killed after, one, two, six, 12 and 24 days, and samples were taken for bacteriological and pathological examination. The sixth uninfected control calf was killed at seven days of age and matched samples were taken for pathological comparison. The animals remained normal throughout the observation period. Bacteriological data indicated a heavy bacterial load of strain A84 throughout the gastrointestinal tract but the bacterium was not found in liver, kidney or muscle. No evidence of ‘attaching and effacing’ lesions in the small or large intestine was found although there was a mild inflammatory response in the intestinal tract consisting mainly of infiltrating eosinophils.

Immunohistochemical demonstration of Wilms tumour gene product WT1 in a canine ''neuroepithelioma'' providing evidence for its classification as an extrarenal nephroblastoma

An intradural extramedullary tumour, surgically removed from the spinal canal of a young dog with paraplegia, had the histological appearance of a nephroblastoma. Subsequent necropsy revealed no evidence of a renal primary tumour or of any other tumour. Similar tumours of the spinal canal have been described previously under a variety of names, in particular neuroepithelioma. With an antibody to the human Wilms tumour (nephroblastoma) gene product WT1, labelling of glomeruloid bodies, similar to glomerular podocytes in human fetal kidney, was demonstrated in the tumour. This finding strengthened the suggestion that it was a nephroblastoma.