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Canine granulomatous colitis (histiocytic ulcerative colitis) is an uncommon disease, predominantly of young French Bulldogs and Boxer dogs, that manifests from a dysregulated immune response, primarily to adherent-invasive Escherichia coli (AIEC). In conjunction with histopathology and periodic acid-Schiff staining, the diagnosis of granulomatous colitis currently relies on fluorescence in situ hybridization (ISH) or immunohistochemistry to identify and localize AIEC organisms within macrophages in the mucosa and/or submucosa. We investigated the utility of ISH for E. coli using formalin-fixed, paraffin-embedded specimens collected from 29 cases of suspected granulomatous colitis. Most confirmed cases of granulomatous colitis were in French Bulldogs (12 of 20; 60%) and Boxers (3 of 20; 15%), and the mean age was 25 ± 6 mo with no sex predilection. E. coli ISH signal localized bacterial genetic material within the mucosa in 20 of 29 (69%) cases, supporting the diagnosis. ISH signal was limited to the lumen in 8 of 29 (28%) cases, which did not support the identification of these organisms as AIEC. The remaining case had no hybridization signal, and the diagnosis of granulomatous colitis was not supported. Our results revealed that ISH is a quick and specific detection method that can effectively confirm the diagnosis of canine granulomatous colitis., Competing Interests: Declaration of conflicting interestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

This case report describes a case of granulomatous colitis (GC) associated with adherent-invasive Escherichia coli (AIEC) with extension to cecum and ileum and dissemination to multiple lymph nodes, the spleen, and brain in a 10-year-old, male Sphynx cat. The cat had an episode of diarrhea 4 months prior to consultation due to sudden blindness. Signs rapidly progressed to ataxia, seizures, and death. Gross and histologic findings were consistent with granulomatous inflammation in all affected organs. In situ hybridization confirmed the presence of intracellular E. coli within enterocytes and infiltrating macrophages, and whole genome sequencing identified virulence traits commonly linked to AIEC strain. This is the first characterization of GC in a cat associated to AIEC resembling the metastatic form of Crohn's disease in humans and GC of dogs. Extraintestinal involvement might provide evidence of the ability of AIEC to promote granulomatous inflammation beyond the gut.

Granulomatous colitis in dogs can be associated with infection of the colonic mucosa by invasive strains of Escherichia coli . To date, fluorescence in situ hybridization (FISH) is the gold-standard method to assess intramucosal and intracellular bacterial invasion. However, FISH requires expensive fluorescence microscopy equipment and is therefore not widely available. We investigated the use of immunohistochemistry (IHC) as an alternative method to detect invasive E. coli in dogs with granulomatous colitis. Archived paraffin-embedded blocks were selected from 26 dogs with colitis, in which FISH had been performed by an outside laboratory. Using a polyclonal antibody, IHC for E. coli was performed on sections cut from the same blocks, and the presence of invasive E. coli was recorded. All 11 specimens in which FISH had detected E. coli were also positive on IHC, with strong immunolabeling in the cytoplasm of macrophages and extracellularly in the lamina propria; all 15 specimens that were negative for invasive bacteria on FISH were also negative on IHC. We found that IHC is a sensitive technique for the detection of invasive E. coli in dogs with granulomatous colitis.

Objectives: To describe the clinical characteristics and long-term outcome of Escherichia coli-associated granulomatous ileocolitis in dogs., Methods: Retrospective review of medical records from dogs with periodic acid-Schiff positive (PAS+) granulomatous ileocolitis and mucosally invasive E. coli in the ileum and colon. Initial bacterial colonisation was evaluated using fluorescence in situ hybridization (FISH) in all dogs and corroborated with colonic and/or ileal culture, when performed., Results: Four boxer dogs and 1 French Bulldog with PAS+ granulomatous ileocolitis (GIC) were evaluated. All dogs had chronic diarrhoea refractory to empirical therapy. Ileocolonoscopy revealed mucosal haemorrhage and ulceration in the ileum (3/4) and colon (5/5). E. coli were visualised as clusters within the ileal and colonic mucosa. Complete (CR, 4/5) or partial (PR, 1/5) clinical response to fluoroquinolones was noted in all dogs within 30 days. CR was sustained in three of four dogs (median disease-free interval 40 months, range 16 to 60). Two dogs relapsed while receiving fluoroquinolones. Repeat biopsy isolated multidrug-resistant, mucosally invasive E. coli in the ileum (1/2) and colon (2/2). Targeted antimicrobial therapy was associated with long-term PR (78 months) in both dogs., Clinical Significance: Concurrent E. coli-associated granulomatous inflammation in the ileum and colon did not impart a poor clinical outcome or lack of response to the conventional standard of care for granulomatous colitis in dogs that were aggressively diagnosed and treated. Clinical outcome was influenced by antimicrobial resistance, with response dependent upon antimicrobial therapy informed by susceptibility testing., (© 2021 British Small Animal Veterinary Association.)

A 6-month-old French bulldog was presented due to chronic large intestinal diarrhea of 4 months duration. The diagnostic procedures initiated by the referring veterinarian had resulted in a tentative diagnosis of chronic enteropathy, however treatment consisting of elimination diet as well as antibiotic, anthelmintic, anti-inflammatory and immunosuppressive medication had been unsuccessful. By means of endoscopy and histological examination, pronounced erosions and ulcerations of the colonic mucosa were detected. Fluorescence in situ hybridization enabled the identification of invasive Escherichia coli within the colonic mucosa and colonic macrophages, allowing for the diagnosis of granulomatous colitis. The dog showed complete remission of clinical signs following 8 weeks of treatment with enrofloxacin. This case report describes the first successful treatment of granulomatous colitis with enrofloxacin in a French bulldog puppy in Germany and is intended to sensitize the reader to this disease in (young) dogs., Competing Interests: Der Autor A. Moritz erhielt in den letzten 3 Jahren Forschungsunterstützung durch die Firmen IDEXX, Bayer, MSD, Scil und Ushio. Die Autoren bestätigen, dass kein Interessenkonflikt vorliegt., (Thieme. All rights reserved.)

Background: Eradication of intramucosal Escherichia coli correlates with remission of periodic acid-Schiff-positive E coli-associated granulomatous colitis (GC). Treatment failures attributed to multidrug resistant (MDR) bacteria necessitate alternative approaches., Hypothesis/objectives: Determine clinical outcome of E coli-associated GC in dogs treated based on antimicrobial susceptibility profiling and characterize E coli phylogeny and resistance mechanisms., Animals: Twenty Boxers and 4 French Bulldogs with E coli-associated GC., Methods: Culture, antimicrobial susceptibility profiling, and molecular characterization of E coli were performed and response to treatment was evaluated., Results: Initial biopsy sample culture yielded fluoroquinolone-sensitive (FQ-S) E coli from 9/24 dogs and fluoroquinolone-resistant (FQ-R) E coli from 15/24. All but 1 FQ-R E coli were MDR with susceptibility to macrophage-penetrating antimicrobials restricted to carbapenems in 13/15 dogs. Of 22/24 treated based on susceptibility profiling, 8/9 FQ-S dogs had complete initial clinical response (CR) during fluoroquinolone (FQ) treatment, whereas 9/13 FQ-R dogs had complete or partial response (PR) during meropenem or doxycycline treatment. In 5/9 FQ-S and 12/13 FQ-R dogs with follow-up ≥3 months, CR was sustained in 5/5 FQ-S (median, 25 months; range, 4-46) whereas 6/12 FQ-R had long-term CR (median, 59 months; range 15-102), 4/12 PR (median, 19 months; range, 5-65), and 2/12 had no response (NR). Four dogs with long-term follow-up died within 4 years of diagnosis, including 2 euthanized for refractory colitis. Escherichia coli were genetically diverse. Fluoroquinolone resistance was associated with mutations in gyrA and parC, with plasmid-mediated resistance less common., Conclusions and Clinical Importance: Antimicrobial treatment guided by susceptibility profiling was associated with positive long-term outcomes in >80% of cases. Fluoroquinolone-resistance was widespread and not clonal. Further study is required to optimize treatment for dogs with MDR E coli-associated GC., (© 2020 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC. on behalf of the American College of Veterinary Internal Medicine.)

A 10-month-old male Rhodesian Ridgeback was presented to the Clinic of Small Animal Medicine, LMU, Germany, with a 6-month history of chronic diarrhea and hematochezia. The dog lived in Germany and had never traveled abroad. Complete blood count and serum biochemistry performed by the referring veterinarian revealed neutrophilia, hyperkalemia, and hyponatremia, with a basal cortisol of 4.3 µg/dl, which excluded hypoadrenocorticism. Since antibiotic treatment had not resulted in any improvement, a 2 week course of prednisolone administration had been initiated, leading to a marked deterioration of intestinal signs and a significant weight loss of 6 kg. At the time of referral, the patient was markedly emaciated, dehydrated, hypovolemic and had a rectal temperature of 39.6 °C. Abdominal ultrasound showed a thickened and irregular colonic wall. On colonoscopy, an irregular colonic mucosa with ulcerations was observed. Histopathologic examination revealed an ulcerative granulomatous colitis, and on Periodic acid-Schiff reaction (PAS) numerous organisms consistent with Prototheca spp. were identified. Prototheca zopfii infection was confirmed by culture and MALDI-TOF MS. In order to test for an underlying immunodeficiency, immunoglobulin levels in serum were determined. IgM was decreased, while IgG and IgA levels were within the reference interval. Due to deterioration of general condition, grave prognosis and costs of a treatment trial, the patient was euthanized one week later, and necropsy was performed. Prototheca spp. were detected on histopathologic examination in the lymphnodes, however not in the eyes or the central nervous system. Protothecosis should be considered an differential diagnosis in dogs with chronic diarrhea and ulcerative granulomatous colitis even in dogs living in Germany. Histopathologic examination of colonic biopsies with special stains such as PAS is recommended in every dog with signs of chronic large bowel disease in order to avoid missing this rare infectious disease., Competing Interests: Die Autoren bestätigen, dass kein Interessenkonflikt besteht., (Thieme. All rights reserved.)

This study investigated morphological changes associated with soya bean meal-induced enteritis (SBMIE) in distal intestine (DI) of rainbow trout (Oncorhynchus mykiss) fed a soya bean meal (SBM)-based diet and exposed to normoxia or hypoxia created by optimal and low water flow rates, respectively. A 28-day adaption period was followed by a 42-day challenge period where 600 fish were subjected to dietary challenge and/or hypoxia. Twelve tanks each containing 50 juvenile trout were assigned randomly in triplicate to each treatment. Histopathological and immunohistochemical evaluation revealed pathological features that have not previously been described in association with SBMIE. Vacuolar degeneration of epithelial cells mainly at the base of mucosal folds, epithelial cysts, epithelial dysplasia, necrosis, shedding of necrotic cells, and granulomatous inflammation including infiltration of enlarged, sometimes finely vacuolated or "foamy" macrophages, multinucleated giant cells and increased proliferation of fibroblasts were observed. Acid-fast bacteria were not detected in enlarged macrophages; however, these cells contained AB-PAS- and sometimes cytokeratin-positive material, which was interpreted to be of epithelial/goblet cell origin. Hypoxia did not affect the morphological changes in DI. These results suggest that SBM was associated with a granulomatous form of enteritis in DI of rainbow trout regardless of water oxygen level., (© 2017 John Wiley & Sons Ltd.)

Since World War II, several factors such as an impressive industrial growth, an enhanced environmental bioavailability and intensified food consumption have contributed to a significant amplification of human exposure to aluminum. Aluminum is particularly present in food, beverages, some drugs and airbone dust. In our food, aluminum is superimposed via additives and cooking utensils. Therefore, the tolerable intake of aluminum is exceeded for a significant part of the world population, especially in children who are more vulnerable to toxic effects of pollutants than adults. Faced with this oral aluminum influx, intestinal tract is an essential barrier, especially as 38% of ingested aluminum accumulates at the intestinal mucosa. Although still poorly documented to date, the impact of oral exposure to aluminum in conditions relevant to real human exposure appears to be deleterious for gut homeostasis. Aluminum ingestion affects the regulation of the permeability, the microflora and the immune function of intestine. Nowadays, several arguments are consistent with an involvement of aluminum as an environmental risk factor for inflammatory bowel diseases., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

Two young female Beagle dogs in a laboratory colony with clinical signs of loose stools and fecal blood were confirmed to have histiocytic ulcerative colitis by histologic evaluation. This syndrome is well recognized in other dog breeds such as Boxers and related French Bulldogs, Mastiffs, Alaskan malamutes and Doberman Pinschers. Formalin-fixed paraffin sections of large intestine from one dog demonstrated the presence of Escherichia coli strain LF82 by immunohistochemistry and 16S ribosomal RNA gene sequencing. E coli strain LF82 has been implicated in the pathogenesis of Crohn's disease and similar bacteria have been cultured from cases of histiocytic ulcerative colitis in Boxer dogs. Spontaneous histiocytic ulcerative colitis must be differentiated from test article-related findings in nonclinical toxicity studies in Beagle dogs., (Copyright © 2014 Elsevier GmbH. All rights reserved.)

Background: French Bulldogs develop a form of granulomatous colitis (GC) with histopathological resemblance to GC of Boxer dogs (GCB). GCB is associated with mucosally invasive Escherichia coli whose eradication correlates with clinical remission., Hypothesis/objectives: To characterize the clinical and histopathological features, presence or absence of invasive colonic bacteria, and response to fluoroquinolones in French Bulldogs with GC., Animals: A total of 6 French Bulldogs with a histological diagnosis of GC., Methods: Retrospective study of medical records. Bacterial colonization was evaluated using 16S rRNA probes for eubacteria and E. coli. Biopsy specimens from 3 dogs were cultured for bacteria. Clinical response to fluoroquinolone antimicrobials was determined., Results: All dogs were ≤1 year of age with hematochezia that was refractory to empirical therapy. Clinicopathologic and fecal analysis did not reveal abnormalities. Abdominal ultrasound revealed patchy thickening of the colon in 4/5 dogs and regional lymphadenopathy in 5/5. Colonoscopic abnormalities included irregularly thickened and ulcerated mucosa, hyperemia, and overt bleeding in 4/6 cases. Multifocal accumulations of PAS-positive macrophages and intramucosal E. coli were present in colonic biopsies of all 6 dogs. Administration of enrofloxacin (5/6) or marbofloxacin (1/6) at 4.4-10 mg/kg (median 10 mg/kg) PO q24h for 6-10 weeks was associated with clinical improvement within 5-14 days. All dogs remained in remission over a 3-30 month follow-up period., Conclusions: Granulomatous colitis in young French Bulldogs is associated with the presence of invasive E. coli and closely parallels GCB. Treatment with fluoroquinolone antimicrobials can induce lasting clinical remission., (Copyright © 2012 by the American College of Veterinary Internal Medicine.)

Granulomatous colitis (GC) is a rare, breed-specific inflammatory bowel disease of young Boxer dogs. GC has been refractory to treatment and associated with high mortality rates, but culture-independent molecular analysis has transformed therapy and prognosis by uncovering a correlation between GC and Escherichia coli invasion within colonic mucosal macrophages. GC-associated invasive E coli are similar to a newly identified E coli pathotype, "adherent and invasive E coli," that are increasingly associated with Crohn's disease in humans. Successful treatment of GC requires antimicrobials that are effective against E coli and penetrate intracellularly. Enrofloxacin is widely regarded as the antibiotic of choice., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Granulomatous colitis of Boxer dogs is characterized by mucosal and submucosal infiltration by abundant large macrophages and lymphocytes and plasma cells. Involved intestine is thickened, corrugated and ulcerated. The macrophages that occur in colon, cecum and regional lymph nodes are PAS-positive, lipid-rich, contain cholesterol, and some of the time can be seen to hold bacteria. Paraffin tissue blocks of formalin-fixed colon and colic lymph nodes from 10 cases were cut at 5 microm and immunostained by a streptavidin-biotin immunoperoxidase technique, employing primary antibodies against Escherichia coli, E. coli 0157: 2, Campylobacter, C. jejuni-coli, Yersinia pseudotuberculosis, Salmonella, Shigella, Pseudomonas and Lawsonia intracellularis. The macrophages in the lamina propria and submucosa, as well as those in aggregates in regional lymph nodes, showed immunoreactivity with polyclonal E. coli antibody in all 10 cases. Tissues lacking granulomas were negative, as were those reacted with the other eight antibodies, with the exception that there was rare focal staining for Campylobacter, Lawsonia and Salmonella in a few dogs. We believe these results identify the causative agent of this granulomatous disease of Boxer dogs, a disease with great histologic and etiologic similarity to granulomatous leptomeningitis of Beagle dogs, and malacoplakia and xanthogranulomatous cholecystitis of man. Macrophages that are immunopositive for E. coli antigen occur in Crohn's disease as well, where their significance is less well understood.

Ileocolitis associated with spiral bacteria identified as an Anaerobiospirillum sp. was found in six cats. Two cats had acute onset of gastrointestinal signs characterized by vomiting and diarrhea in one cat and vomiting in another cat, one cat had chronic diarrhea that was refractory to medical therapy; one cat had acute onset of anorexia and lethargy, and two cats had clinical signs that were not related to the gastrointestinal tract. The presence of an Anaerobiospirillum sp. was demonstrated on the basis of ultrastructural morphology of spiral bacteria associated with intestinal lesions and PCR amplification of a genus-specific 16S rRNA gene from affected tissues from each cat. The colons of three clinically healthy cats without lesions and one cat with mild colitis not associated with spiral bacteria were negative for Anaerobiospirillum spp. in the same assay. Comparative nucleotide sequence analysis of cloned PCR products from three affected cats further suggested that the spiral bacteria were closely related to Anaerobiospirillum succiniciproducens.

Five tamarins (four Saguinus mystax and one S. labiatus) died with wasting syndrome characterized by chronic diarrhea at the Center for Reproduction and Conservation of Non-Human Primates in Iquitos, Peru. At necropsy, the terminal ileum of all affected tamarins was found to be markedly thickened. Histologically, the terminal ileal mucosa was completely ulcerated, and effaced by debris and mononuclear inflammatory cells. The submucosa and serosa were thickened by fibroplasia, mononuclear cell infiltrates and variable edema. No infectious agent was observed. The lesions were similar to those described previously for Crohn disease. This is to our knowledge the first report of terminal ileitis resembling Crohn disease in non-human primates.

Intestinal samples and/or lymph nodes of two Iberian pigs from two different farms were submitted for histopathologic examination. Both pigs had proliferation of ileal and/or cecal crypts with almost complete absence of goblet cells. Infection by Lawsonia intracellularis was demonstrated by immunohistochemistry and polymerase chain reaction assay. The mesenteric lymph node of one pig had moderate lymphocyte depletion with granulomatous inflammation of the lymph node parenchyma. Histiocytes and multinucleated giant cells from the lymph node of one pig contained L. intracellularis antigen within the cytoplasm. This pig had also porcine circovirus type 2 (PCV-2) infection, but nucleic acid and antigen of this virus were not demonstrated in the lymph node. The second pig had lymphocyte depletion and marked granulomatous inflammation in Peyer's patches. Histiocytes and multinucleated giant cells in areas of granulomatous inflammation contained L. intracellularis antigen; no PCV-2 nucleic acid or antigen was detected in the tissues of this pig. This is the first description of granulomatous ileitis and lymphadenitis associated with L. intracellularis infection.

In recent years, a substantial number of baboons died at the Southwest Foundation for Biomedical Research following protracted intractable diarrheas. The histopathologic diagnosis at autopsy was chronic colitis. The diarrhea could last for more than one year and occurred in infants, juveniles or young adult baboons, i.e. < or = 8 years of age (a healthy baboon may live up to 27 years). The aim was to assess the histopathologic subtype of chronic colitis in a relatively large number of colonic specimens obtained at autopsy (n = 132). In 88 out of 132 baboons with chronic diarrhea, the colonic mucosa was well preserved for histological examination. At review, various histological phenotypes of chronic colitis were disclosed in 86 of the 88 baboons. Chronic lymphocytic-plasmacytic colitis was found in 54.6% (47 out of 86), chronic ulcerative colitis in 15.1% (13 out of 86), Crohn's colitis in 12.8% (11 out of 86), superficial lymphocytic colitis in 10.5% (9 out of 86), cryptal lymphocytic colitis in 5.8% (5 out of 86) and collagenous colitis in 1.2% (1 out of 86). Chronic ulcerative colitis, Crohn's colitis, superficial lymphocytic colitis and collagenous colitis in baboons closely mimic corresponding histological phenotypes of chronic colitis in humans. Recently, cryptal lymphocytic colitis has also been found in humans. The awareness that chronic colitis in baboons is not one disease but a series oi chronic inflammatory changes, having common clinical symptoms and similar gross appearance, may lead to the correct diagnosis of the subtype of the disease. Only then would it be feasible to systematically initiate the search for the corresponding etiologic agent(s), aiming to tailor specific therapeutic strategies in those animals.

A review of reported cases of inflammatory bowel diseases (IBDs) of horses for which no etiology was identified included cases of granulomatous enteritis (GE), multisystemic eosinophilic epitheliotropic disease (MEED), lymphocytic-plasmacytic enterocolitis (LPE), and idiopathic eosinophilic enterocolitis (EC). The terms EC and MEED were both used to describe a disease in horses characterized by infiltration of intestine and extraintestinal tissues with eosinophils. We use EC to describe IBD characterized by only intestinal infiltration by eosinophils. Horses with GE, MEED, or LPE are usually examined because of weight loss and depression, but horses with EC are usually examined because of signs of abdominal pain. Typically, horses with IBD have low concentrations of serumal proteins, especially albumin, and fail to adequately absorb glucose or xylose. Antemortem diagnosis of IBD can only be made by histologic examination of affected intestine. In some cases, antemortem diagnosis is made from histologic examination of rectal mucosa obtained by biopsy. Suspected causes of IBD in the horse include abnormal immune response to bacterial, viral, parasitic, or dietary antigens. Most horses with IBD do not survive, but horses with EC are more likely than those with LPE, MEED, or GE to respond to treatment. Successful treatments of horses with IBD include resection of grossly affected intestine and administration of corticosteroids.

A cluster of 6 cases of equine granulomatous enteritis is described. Aluminium was demonstrated in the tissues and lesions of these horses and in the intimal bodies of intestinal vessels. The relationship between granulomatous lesions, aluminium, acidity and invading microorganisms, particularly parasites, is presented and discussed.

Regional enteritis was diagnosed in an 11-year-old, spayed female German shepherd dog with a history of intermittent vomiting and anorexia. Segmental, transmural granulomatous enteritis involved the pylorus, jejunum, and ileum. The jejunal lesions were excised. The remaining lesions completely resolved subsequent to long-term prednisone and sulfasalazine therapy.

A 5-year-old Quarter Horse mare was examined because of weight loss of 2 months' duration. The horse was anemic and in poor body condition, and had several areas of cutaneous ulceration, including areas on the muzzle and distal portion of the limbs. Histologic examination of a rectal mucosa biopsy specimen revealed a lymphoplasmacytic infiltrate in the lamina propria mucosa. Results of a glucose absorption test were suggestive of malabsorption. Histologic examination of a biopsy specimen from the cutaneous lesions revealed pronounced arteritis, and weak, patchy immunofluorescent staining for immunoglobulins at the basement membrane. The horse was treated with prednisone, but did not improve, so the horse was humanely destroyed. Necropsy revealed granulomatous enteritis. This case identified an unusual combination of clinical problems and suggests further evidence for similarities between equine granulomatous enteritis and regional enteritis in human beings.

Granulomatous enteritis was diagnosed in a 4-year-old Standarbred mare suffering from chronic weight loss, depression, dependent oedema but not diarrhoea. There was hypoproteinaemia (hypoalbuminaemia), lymphocytopaenia and neglibible carbohydrate absorption from the small intestine. Pathological changes in almost the entire small intestine included proprial infiltration resulting in partial villous atrophy, and granuloma formation beneath the muscularis which was most severe in the ileum. Slight infiltration occurred in the stomach and the colon. The cells were predominantly lymphocytes and histocytes. No acid-fast organisms were found.

Catalase-negative vibrios can be isolated in large numbers from the affected intestinal mucosa of pigs suffering from a range of porcine enteropathies in which the mucosa has an adenomatous component. These vibrios cannot be distinguished from strains of Campylobacter sputorum subsp. mucosalis. The resemblance between these bacteria strengthens the case already made on morphological evidence that these enteropathies have a common origin. Catalase-negative vibrios have also been isolated from the mouth and faeces of pigs. Some of these conform to the criteria established for the mucosalis subspecies but others can be differentiated from it. An antigenic analysis shows that strains of the mucosalis subspecies are closely related antigenically, but that differences may allow separation of strains.

A morphological study on equine granulomatous enteritis (EGE) in 13 horses is presented. All horses were young (1 to 5 years old) standardbreds. Based on gross pathology, cases were classified into those with diffuse (11 cases) and those with localized (2 cases) small bowel lesions. The granulomatous reaction in the gut was marked by diffuse and patchy infiltrates and distinct granulomas, composed of epithelioid cells, macrophages and lymphoid cells, and was devoid of necrosis. Salient accompanying features of the small bowel included lymphoid hyperplasia, peri-lymphatic and transmural inflammation, lymphangiectasia, villous atrophy, mucosal ulcerations and crypt abscesses. Granulomatous changes were often demonstrated in alimentary tract tissues beyond the small bowel and its lymph nodes and were in some cases shown to occur multi-systemically. The morphology and epidemiological features of the condition suggest a specific aetiology. The histology indicated that an immune reaction was operative and that inflammation of the lamina propria was an early event in the pathogenesis of the gut lesion. No conclusive evidence of a specific infectious cause was found. It is suggested that the disease might be associated with intrinsic disturbances of inflammatory defence mechanisms.

The jejunal mucosa of 4 cases of equine granulomatous enteritis and 2 control horses was investigated by light microscopy and by scanning and transmission electron microscopy. Attention was focused upon changes in mucosal topography and enterocyte morphology in the inflamed mucosa. Structural changes ranged in severity from only a slight thickening and shortening of villi to the appearance of a virtually flat mucosa, upon which crypts opened directly or through shallow cavities encircled by collars of epithelial cells. Between these extremes, the mucosa showed a variety of patterns, all characterized by distinctly abnormal villus projections. These were often united by epithelial bridges and were commonly markedly short, broad and irregular. Enterocytes of mildly changed mucosae showed a normal histology and fine structure, whereas more severely changed specimens displayed a flattened surface epithelium with ultrastructural abnormalities, the most consistent being a pronounced shortening of microvilli. In particular, greatly flattened cells showed evidence of cellular injury, such as prominence of cytolysosomes and degenerative changes of the rough endoplasmic reticulum, while other cells were chiefly characterized by an abundance of non-membrane-bound ribosomes and other features signifying an immature state. Cell-membrane-tight junctions of the surface epithelium appeared to be intact. No intracellular micro-organisms were detected. It is suggested that several factors are involved in the creation of the abnormal mucosal topography in this disease, including excessive enterocyte loss, crypt cell destruction, inflammatory distension of villi and villus fusions.

Morphological and histological changes were described in regional ileitis of pigs, which constitutes one of the forms of the complex of diseases referred to as intestinal adenomatosis of pigs. The most pronounced changes were concentrated on the ileum and were characterized, from the morphological point of view, by a distention of the intestinal wall and from the histological point of view, by proliferation of the epithelial cells of ileum, proliferation of the lymphatic tissue of tunica mucosae and submucosae, and hypertrophy of tunica muscularis. This disease has not been described in Czechoslovakia up to now.

Thirteen cases of granulomatous colitis of Boxer dogs were studied by electron microscopy to define the contents of macrophages and to seek infectious agents. Macrophages were of three types. The most numerous were distended with residual bodies composed of membranes and parallel pairs of membranes, many arranged in circular patterns. A second common form had heterogeneous cytoplasm distended with phagosomes containing numerous small granular spheres of various sizes and electron densities. The least common were "young" macrophages containing phagocytic vacuoles. Rare macrophages in four of 13 dogs contained bacteria. Macrophages in five of the dogs contained abundant coccoid, coccobacillary of lobulated granular structures, 100-500 nm in diameter, resembling chlamydia. Transition from phagocytic particle to phagosome to residual body was apparent. Granulomatous colitis of Boxer dogs is probably caused by a lipid-rich, ribosome-rich, coccoid to coccobacillary organism that possesses a cell membrane and sometimes a nucleoid, and ranges from 100 to 500 nm in size.

A newly recognized syndrome characterized by an acute focal ulcerative ileocolitis, anemia and thrombocytopenic purpura in five juvenile cotton-top tamarins is described. The presentation and morphology of this syndrome is distinct from any other reported gastrointestinal disease reported in tamarins. Traditional etiologies such as viruses, ingested toxins, Campylobacter, Salmonella and Yersinia and Clostridium difficile are not considered likely etiologic agents. Nontraditional etiologies such as anaerobes or pathologic strains of Escherichia coli are now being considered. This syndrome is of potential significance to ongoing research into the etiology of idiopathic tamarin colitis.

Horses presented with chronic weight loss are difficult to manage clinically. A diagnosis of granulomatous colitis due to mucosal stages of cyathostomes (small strongyles) should be considered in those cases exhibiting weight loss, intermittent diarrhea, hypoalbuminemia, increased serum globulins, and low fecal egg counts. Treatment can be attempted with larva-cidal doses of fenbendazole or ivermectin. Clinical and necropsy findings in one such case are presented.

Clinical and pathological features of a variety of forms of feline colitis or enterocolitis were examined and classified into 9 separate entities: Salmonella enterocolitis, the colitis of feline infectious peritonitis, mycotic enterocolitis, acute angiopathic colitis, acute angiopathic colitis with ischaemic ulcers, feline granulomatous colitis, the colitis of feline panleucopenia, feline histiocytic colitis, and feline ulcerative, lymphocytic mucosal-submucosal colitis.

Granulomatous enteritis was diagnosed in 9 horses between 1 and 11 years of age. The complaint in all cases was persistent weight loss. Four of the horses had chronic diarrhea. Two consistent diagnostic features were hypoalbuminemia and decreased phagocytic activity of mesothelial cells in the peritoneal fluid. In 2 cases the diagnosis was confirmed by biopsy of the rectal mucosa. Remaining cases were definitively diagnosed by exploratory laparotomy and biopsy or at necropsy.