J Vet Intern Med 2016;30:996–1001
Campylobacter Species and Neutrophilic Inflammatory Bowel Disease in Cats C.L. Maunder, Z.F. Reynolds, L. Peacock, E.J. Hall, M.J. Day, and T.A. Cogan Background: Inﬂammatory bowel disease (IBD) is a common cause of signs of gastrointestinal disease in cats. A subset of cats with IBD has neutrophilic inﬂammation of the intestinal mucosa. Hypothesis: Neutrophilic enteritis in cats is associated with mucosal invasion by microorganisms, and speciﬁcally Campylobacter spp. Animals: Seven cats with neutrophilic IBD and 8 cats with lymphoplasmacytic IBD. Methods: Retrospective review of duodenal biopsy specimens that were collected endoscopically for histologic examination. Cases were identiﬁed and selected by searching the histopathology archive for cats with a diagnosis of neutrophilic and lymphoplasmacytic IBD. Fluorescence in situ hybridization (FISH) targeting either all eubacteria or individual Campylobacter spp. was performed on archived samples. Neutrophils were detected on the same samples using a FISH probe for neutrophil elastase. Results: Campylobacter coli was present in (6/7) cats with neutrophilic IBD and in (1/8) cats with lymphoplasmacytic IBD (P = .009). Cats with neutrophilic IBD had signiﬁcantly higher number of C. coli (median bacteria 0.7/hpf) in the mucosa than cats with lymphoplasmacytic IBD (median bacteria 0/hpf) (P = 0.002). Colocalization of neutrophils and C. coli was demonstrated, with C. coli closer to the neutrophils than any other bacteria (P < .001). Conclusions and clinical importance: Identiﬁcation of C. coli associated with neutrophilic inﬂammation suggests that C. coli is able either to produce compounds which stimulate neutrophils or to induce feline intestinal cells to produce neutrophil chemoattractants. This association should allow a directed therapeutic approach in cats with neutrophilic IBD, potentially improving outcome and reducing any zoonotic risk. Key words: Duodenum; Endoscopy; Enteritis; FISH; Histopathology.
nﬂammatory bowel disease (IBD) is a common cause of chronic signs in cats with gastrointestinal disease.1 Intestinal biopsies are needed to conﬁrm intestinal inﬂammation, but cases are deemed idiopathic if no underlying cause is found.1–3 Typically, lymphoplasmacytic inﬂammation is found in biopsy specimens, but a subset of cats with IBD has neutrophilic inﬂammation of the intestinal mucosa. The clinical relevance of neutrophilic inﬁltration is unclear. It might be secondary to bacterial infection, but neutrophilic colitis is seen with Tritrichomonas foetus infection4 and a case of suppurative colitis in a cat was described5, where no bacterial infection could be identiﬁed. Mucosal friability and erosions might also induce neutrophilic inﬁltrates because of the loss of mucosal barrier integrity. If no etiological agent is identiﬁed, directed or appropriate treatment is
From the School of Veterinary Sciences, University of Bristol, Langford, UK (Maunder, Reynolds, Peacock, Hall, Day, Cogan). The work in this study was performed at the School of Veterinary Sciences, University of Bristol and supported by a grant from the Langford Trust. The abstract from this paper was presented at the European College of Veterinary Internal Medicine Congress in Lisbon, Portugal 2015. Corresponding author: C. Maunder, Small Animal Hospital, School of Veterinary Sciences, University of Bristol, Langford House, Langford, Bristol, BS40 5DU, UK; e-mail: [emailprotected]
Submitted October 21, 2015; Revised February 19, 2016; Accepted June 11, 2016. Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. DOI: 10.1111/jvim.14374
Abbreviations: 12-LOX AIEC DNA FCEAI FISH H&E HPF IBD IL-8 NF-jB PCR rRNA WSAVA
12-lipoxygenase attaching and invasive E. coli deoxyribonucleic acid feline chronic enteropathy activity index ﬂuorescence in situ hybridization hematoxylin and eosin high-powered ﬁeld inﬂammatory bowel disease interleukin 8 nuclear factor kappa beta polymerase chain reaction 16S ribosomal ribonucleic acid World Small Animal Veterinary Association
unclear and empirical antibacterial treatment might be prescribed. Using more traditional diagnostic techniques, the evidence for infectious agents causing neutrophilic intestinal inﬂammation is poor. The clinical relevance of identifying bacteria in fecal samples is unclear as they might be found in the feces of healthy cats as well as in those with diarrhea.6–9 The use of ﬂuorescent in situ hybridization (FISH) has enabled detection and visualization of intact bacteria within tissues and their localization as part of understanding the ecology of a disease process.10 In small animal gastrointestinal research, FISH has been used to demonstrate gastric Helicobacter spp. infections and clearance of these bacteria with treatment,11 and that attaching and invasive E. coli (AIEC) are associated with granulomatous colitis in Boxers and can be eradicated with prolonged antibiotics,12,13 Janeczko14 used FISH and showed higher number of mucosa-associated
Neutrophilic IBD in Cats
Enterobacteriaceae in cats with gastrointestinal signs compared with healthy cats, although it was not clear whether this association was the cause of the inﬂammation or a consequence of the mucosal disruption and altered environment selecting for bacterial dysbiosis. The aims of this study were: (1) to determine the presence, and identity of intact bacteria within feline intestinal biopsy specimens using FISH and (2) to determine the location of neutrophils and their proximity to any bacteria to demonstrate an association and possible bacterial etiology.
Materials & Methods Study Population Cases from which there was histopathologic assessment of endoscopic intestinal biopsy specimens at the University of Bristol, School of Veterinary Sciences, were identiﬁed from the pathology archive and the biopsy specimens were reviewed. The inclusion criteria were that duodenal biopsy specimens had a diagnosis of neutrophilic or lymphoplasmacytic inﬂammation and were of adequate quality and size for FISH to be performed requiring at least 3 well-oriented villi with subvillus lamina propria extending to the muscularis mucosa in each section. Samples from 15 cats (7 with neutrophilic IBD and 8 with lymphoplasmacytic IBD) met the inclusion criteria for the study and also had suﬃcient intestinal tissue archived as formalin-ﬁxed and paraﬃn wax-embedded material. The signalment of these cats was documented, but the clinical severity and response to treatment was not uniformly reported. Ethical approval for the study was granted by the University of Bristol Ethics Committee. Samples from all cats were retrospectively analyzed for intestinal bacterial pathogens by PCR as detailed below.
Histopathologic Analysis In every case, hematoxylin and eosin-stained sections of the duodenal biopsy specimens were reviewed, without knowledge of the case history, by a Board-certiﬁed veterinary pathologist (MJD). The histopathologic changes were graded according to the scoring system developed by the World Small Animal Veterinary Association (WSAVA) Gastrointestinal Standardization Group.15 Five parameters of inﬂammation (ie, intraepithelial lymphocytes, lamina propria lymphocytes, plasma cells, eosinophils and neutrophils, and other inﬂammatory cell types within the lamina propria) were evaluated. Morphologic features of mucosal inﬂammation (villus stunting, epithelial injury, crypt dilatation/distortion, lacteal dilatation, and mucosal ﬁbrosis) were also evaluated. Changes in morphological features were noted, but there was
no appreciable diﬀerence between groups, with a range of none– moderate within each group. The ﬁnal diagnosis was categorized as 1 of 8 diﬀerent histopathologic diagnoses: no abnormalities detected (NAD), lymphoplasmacytic inﬂammatory, eosinophilic inﬂammatory, neutrophilic inﬂammatory, lymphangiectasia, lymphoma, mucosal atrophy/ﬁbrosis (noninﬂammatory) and other. Only samples from cats with lymphoplasmacytic inﬂammatory histopathologic changes and neutrophilic inﬂammatory histopathologic changes were included in the study.
Fluorescence In Situ Hybridization—Bacteria Fluorescence in situ hybridization (FISH) was performed on formalin-ﬁxed and paraﬃn wax-embedded duodenal biopsy specimens using a method slightly modiﬁed from that previously reported in the literature, in that hybridization buﬀer containing 25% formamide was used as opposed to buﬀer containing 30% formamide in the previous study.16 16S ribosomal RNA (rRNA)-directed ﬂuorescence-labeled oligonucleotide probes were used (Table 1). Successive sections from each biopsy specimen were analyzed in steps, each employing a different probe mix. Steps one and two were general probes for Eubacteria and Firmicutes using three diﬀerent probes for each bacterial group. A mixture of probes with slight base variations were used to maximize the spectrum of coverage of each probe mix. The third step used speciﬁc probes for Campylobacter species. These were used in combination with one probe labeling C. upsaliensis, another probe for C. jejuni, and a ﬁnal probe labeling all thermophilic Campylobacter spp. Bacteria labeled solely by this last probe could either be C. lari or C. coli and were speciated by subsequent polymerase chain reaction (PCR). We did not examine the sections for E. coli and would not, using these methods, have been able to detect AIEC. Processed slides were mounted with glass cover slips with hardset Vectashield mounting medium containing DAPI. Once set, slides were examined with a Leica DMR-A Microscope equipped with a monochrome Hamamatsu 8-bit digital camera. Bacterial cells in the epithelium and lamina propria were counted at 9400 magniﬁcation by a single blinded observer across 10 ﬁelds of view, and an average count was obtained. Fields of view were chosen as being central to a biopsy and including epithelium and so that not more than 2 were viewed for a single biopsy.
Polymerase Chain Reaction (PCR) DNA was extracted from pooled multiple sections of tissue using a DNeasyTM blood and tissue kit (Qiagen, Manchester, UK). This was screened by Langford Veterinary Services (Bristol, UK) for the presence of Salmonella, pathogenic E. coli, Campylobacter spp., and Clostridium spp. A 153-bp DNA fragment unique to Campylobacter was ampliﬁed by PCR17 and sequenced to conﬁrm the Campylobacter species present.
Table 1. FISH oligonucleotide probes. Details of sequences of oligonucleotide probes used for in situ localization of bacterial species within duodenal biopsy tissues. Probe name
Sequence (50 ->30 )
EUB338 EUB338-II EUB338-III LGC354A LGC354B LGC354C Catherm Cajej CaUp
Eubacteria Eubacteria Eubacteria Firmicutes Firmicutes Firmicutes Thermophilic Campylobacter Campylobacter jejuni Campylobacter upsaliensis
GCTGCCTCCCGTAGGAGT GCAGCCACCCGTAGGTGT GCTGCCACCCGTAGGTGT TGGAAGATTCCCTACTGC CGGAAGATTCCCTACTGC CCGAAGATTCCCTACTGC GCCCTAAGCGTCCTTCCA AGCTAACCACACCTTATACCG CTCTACAGAATTTGTTGGAT
FITC FITC FITC Texas Red Texas Red Texas Red Texas Red FITC AF350
Step Step Step Step Step Step Step Step Step
1 1 1 2 2 2 3 3 3
Maunder et al
Fluorescent In Situ Hybridization—Colocalization of Bacteria and Neutrophils Campylobacter jejuni and thermophilic Campylobacter spp. probes were used in combination with a FISH probe designed to detect feline neutrophil elastase mRNA. The feline neutrophil elastase probe 50 CAGAGGCTGCTGAACGACATCGTGATTCTC CAGCTCAAT30 was used concurrently with Campylobacter spp. probes (Thermophilic Campylobacter spp. 50 GCCCTAAGCGTCC TTCCA 30 and C. jejuni 50 AGCTAACCACACCTTATACCG 30 ). Slides were viewed under ﬂuorescence using a DMRB microscope (Leica) equipped with a Retiga EXi camera (QImaging) and Volocity imaging software (PerkinElmer) and searched for the expression of feline neutrophil elastase and Campylobacter. Images were taken when a ﬁeld of view (9400 objective) contained a neutrophil elastase expressor and one or both of the Campylobacter expressors. A record was made of any neutrophil elastase expressors that did not have a Campylobacter expressor in the same ﬁeld, as well as the overall presence of C. jejuni and thermophilic Campylobacter. Image J software (http:// rsb.info.nih.gov/ij) was used after images had been captured to allow automated measurement of the distance between two points selected by the user—neutrophil and Campylobacter. The distance was measured in pixels on the digital images. The maximum ﬁeld size used was 1850 pixels. The use of this software allowed multiple accurate measurements to be taken and compiled for statistical analysis.
Diﬀerences between the group with neutrophilic inﬂammation and the group with lymphoplasmacytic inﬂammation in the number of bacteria of diﬀerent species found in tissue were analyzed using a Mann-Whitney U-test. Similarly, diﬀerences in the pixel distance between C. jejuni and neutrophils or C. coli and neutrophils were analyzed using the same test.
Results Fifteen cats met the inclusion criteria: 8 were domestic short hair (DSH), 1 was domestic long hair (DLH), and 5 were pure breeds (Maine Coon, Birman, Oriental, and 2 Siamese). There was no breed recorded for one of the biopsy specimens. The age range was 2–15 years (median 9 years). There were 11 male cats and 4 female cats. Bacterial DNA extraction results for all the cats showed than none were positive for Salmonella or pathogenic genotypes of E. coli (a deﬁnition which excludes AIEC). One animal in each group was positive for Clostridium spp. All were Campylobacter positive. Sequencing for Campylobacter to separate the thermophilic species showed that C. lari and C. upsaliensis could not be detected in tissues (data not shown). Only the species C. coli and C. jejuni were present in tissues. The PCR speciation results concurred with FISH results (Fig 1).
Statistics Analysis was performed using statistical software; GraphPad Prism version 5.03. The presence of bacteria in the cats with neutrophilic and lymphoplasmacytic IBD was compared and tested for statistical signiﬁcance using Chi-squared testing.
Presence of Bacteria in the Cats with Neutrophilic IBD and the Cats with Lymphoplasmacytic IBD Bacteria were identiﬁed within the mucosa of cats with either neutrophilic or lymphoplasmacytic
Fig 1. A Shows the number of C. jejuni within the mucosa of the cats with neutrophilic inﬂammatory bowel disease (IBD) and the cats with lymphoplasmacytic IBD. B Shows the number of C. coli within the mucosa of the cats with neutrophilic IBD and the cats with lymphoplasmacytic IBD. C Frequency of ﬁnding C. jejuni within the mucosa of the cats with neutrophilic IBD and the cats with lymphoplasmacytic IBD. D Frequency of ﬁnding C. coli within the mucosa of the cats with neutrophilic IBD and the cats with lymphoplasmacytic IBD
Neutrophilic IBD in Cats
inﬂammation. There was no signiﬁcant diﬀerence in the number of Eubacteria seen in specimens from either of the two groups. There were few C. upsaliensis and further statistical analysis was not possible. C. jejuni and C. coli were present in greater number and so the distribution of these organisms between the neutrophilic group and lymphoplasmacytic group of cats was compared. There was no signiﬁcant diﬀerence between the presence of C. jejuni within the mucosa of the cats with neutrophilic or lymphoplasmacytic inﬂammation. However, C. coli was more prevalent in the mucosa of cats with neutrophilic inﬂammation (6/7) compared with cats with lymphoplasmacytic inﬂammation (1/8) and this distribution was signiﬁcant (P = .009) (Fig 1).
Number of Bacteria in the Cats with Neutrophilic IBD and the Cats with Lymphoplasmacytic IBD The number of C. jejuni and C. coli within the mucosa of the cats with neutrophilic inﬂammation and cats with lymphoplasmacytic inﬂammation were then compared. For C. jejuni the numbers were similar in both groups and there was no signiﬁcant diﬀerence in distribution. However, for C. coli the numbers were greater within the cats with neutrophilic inﬂammation (median number of bacteria per high-powered ﬁeld of view [9400 magniﬁcation] was 0.7) compared to the cats with lymphoplasmacytic inﬂammation (median number of bacteria per high-powered ﬁeld of view was 0) and this diﬀerence was signiﬁcant (P = 0.002). (Fig 1).
Coocalization of Bacteria with Neutrophils There was an insuﬃcient number of neutrophils within the mucosa of cats with lymphoplasmacytic inﬂammation to investigate the association with microorganisms, as 62 of the 63 ﬁelds of view examined did not show Campylobacter and a neutrophil in the same ﬁeld of view. Within the mucosa of cats with neutrophilic inﬂammation, only 6 of the 63 ﬁelds of view examined did not show Campylobacter and a neutrophil in the same ﬁeld of view. Cells expressing neutrophil elastase had typical PMN morphology on light microscopy. Within the mucosa of cats with neutrophilic inﬂammation the colocalization of C. jejuni and C. coli was analyzed; C. upsaliensis numbers were again too few for statistical analysis. For C. jejuni there was no evidence of an association between location of the bacteria and that of the neutrophils and often no organism was seen within the same ﬁeld of view as a neutrophil (>1850 pixels). For C. coli, there was an association between the location of the organism and that of the neutrophils (P < .001) (Fig 2).
Fig 2. Proximity of Campylobacter coli is closer to neutrophils as compared to C. jejuni. Data show pixel distance of neutrophils to Campylobacter as measured by ImageJ software. The maximal pixel distance per ﬁeld is 1850 pixels; when a ﬁeld of view did not contain both a Campylobacter and a neutrophil distance was recorded as 1850 pixels.
parasitic). Cases with histopathologic changes consistent with neutrophilic inﬂammation may result from mucosal invasion by microorganisms, develop secondary to mucosal defects, or Tritrichomonas foetus infection or be idiopathic. The aims of this study were to use FISH to elucidate the presence of mucosal bacterial invasion in feline IBD, and to identify any association between Campylobacter invasion and neutrophilic inﬂammation (Picture 1). Bacteria were identiﬁed within the mucosa of cats with both neutrophilic and lymphoplasmacytic inﬂammation, suggesting mucosal disruption. There was no clear pattern to their localization (mucosa/submucosa/ lamina propria) within the tissue. The total numbers of bacteria did not diﬀer between groups and for two
Discussion Inﬂammatory bowel disease is one cause of chronic signs of gastrointestinal disease in cats, others include adverse food reactions, antibiotic responsive enteropathy, and infection (virus, fungi, bacterial, protozoal, or
Picture 1. Fluorescence in situ hybridization (FISH) demonstrating red ﬂuorescence for a thermophilic Campylobacter species (C. coli) and blue ﬂuorescence for neutrophil elastase. Not all bacteria are highlighted in a single sectional view as organisms outside the plane of focus are not visible in a single image.
Maunder et al
bacterial species (C. jejuni and C. upsaliensis) there was also no diﬀerence in distribution between the two groups. A signiﬁcant diﬀerence was found between the two groups regarding the presence of C. coli. This in itself is simply an observation and merely demonstrates an increased presence of C. coli in cats with neutrophilic inﬂammation. However, FISH neutrophil elastase probes demonstrated close proximity to neutrophils and conﬁrmed the possible association with C. coli. No association between neutrophil location and other species of bacteria was demonstrated. This association supports the hypothesis that C. coli is particularly associated with a speciﬁc neutrophilic form of inﬂammation in the duodenal mucosa of cats with enteric disease compared with other microorganisms. Campylobacter species are known to be powerful chemoattractants for neutrophils. Previous in vitro studies with porcine and human epithelial cells have shown that C. jejuni and C. coli induce neutrophilic intestinal inﬂammation via activation of NF-jB and subsequent production of the neutrophil chemokine IL-8 and also induce migration of neutrophils across the epithelium via the production of chemotactic n-formyl peptides in concert with metabolites of 12-LOX.18,19 In the present retrospective study there was evidence that C. coli, but not C. jejuni, appears to colocalize with neutrophils and therefore might be acting as the etiological agent in this particular subset of feline inﬂammatory bowel disease, although other cell types and mechanisms could be involved. In vitro studies using feline neutrophils similarly to previous work on porcine neutrophils18,19 would be necessary to determine a mechanism for chemoattraction. Limitations of the study mostly relate to its retrospective nature and the lack of clinical data. Once the inclusion criteria were met, the numbers recruited to each group were small because samples had to be of suﬃcient quality for histopathological review and of adequate volume for the subsequent molecular diagnostic tests to be performed. We were unable to document any diﬀerences in clinical presentation between the two groups or to assess data relating to treatment and outcome as the cases were not always treated in our hospital; these were drawn from a pathology archive so the remit of this study is speciﬁcally to associate bacteria with pathology. The lack of clinical data means we are unable to determine if any of the cats received antibiotic treatment before endoscopic biopsy collection. This is a potential confounding eﬀect but prior antibiotic treatment would be expected to reduce bacterial numbers and the likelihood of ﬁnding a signiﬁcant difference between the groups, except in the unlikely event that all the cats with lymphoplasmacytic IBD were treated with antibiotics and none of the cats with neutrophilic IBD were. Fecal analysis from each cat might also have been useful to determine whether Campylobacter spp. had been identiﬁed on culture. A prospective study based on the ﬁndings of this work would be necessary to evaluate clinical and treatment factors.
The histopathologic classiﬁcation and subsequent analysis was performed on duodenal biopsy specimens and these may not reﬂect the nature of the inﬂammatory changes elsewhere in the gastrointestinal tract. A previous study20 showed that in dogs with enteropathy that there was poor agreement between histopathologic ﬁndings in ileal and duodenal biopsy specimens. Another study21 also showed poor agreement on diagnosis between duodenal and ileal biopsy specimens in cats; although this distinction, between lymphoplasmacytic inﬂammation and small cell lymphoma, is more problematic than simply identifying neutrophilic inﬂammation. Although it is possible that inﬂammatory changes elsewhere in the gastrointestinal tract were different to the duodenum, our hypothesis related to an infectious etiology for the localized neutrophilic inﬂammation and so our ﬁndings remain valid. The preliminary ﬁndings from this retrospective study highlight a need for prospective investigation to understand the relevance of the C. coli tissue localization. This would allow investigation into whether this subset of cats have a diﬀerent clinical presentation and FCEAI score or diﬀerent endoscopic lesions identiﬁed on endoscopy. Identiﬁcation of C. coli as a potential etiological agent for this subset of cats would allow directed treatment and would potentially improve the outcome and also reduce any zoonotic risk.8,22 Further in vitro molecular studies would also help determine by what means C. coli induces the neutrophilic response: whether it produces compounds which stimulate neutrophils or induces feline intestinal cells to produce neutrophil chemoattractants. A prospective study would also allow an epidemiological study of risk factors and the interaction of these cats with their owners.
Acknowledgments Conﬂict of Interest declaration: Authors declare no conﬂict of interest. Oﬀ-label Antimicrobial Declaration: Authors declare no oﬀ-label use of antimicrobials.
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Neutrophilic IBD in Cats 7. Hill SL, Cheney JM, Taton-Allen GF, et al. Prevalence of enteric zoonotic organisms in cats. J Am Vet Med Assoc 2000;216:687–692. 8. Marks SL, Rankin SC, Byrne BA, et al. Enteropathogenic bacteria in dogs and cats: Diagnosis, epidemiology, treatment and control. ACVIM Consensus statement. J Vet Intern Med 2011;25:1195–1208. 9. Rossi M, H€ anninen ML, Revez J, et al. Occurrence and species level diagnostics of Campylobacter spp., enteric Helicobacter spp. and Anaerobiospirillum spp. in healthy and diarrheic dogs and cats. Vet Microbiol 2008;129:304–314. 10. Simpson KW. Bacteria and inﬂammatory bowel disease: causes and consequences. Proceedings of the 33rd World Small Animal Veterinary Association Congress Dublin, Ireland 2008. Available at: http://www.vin.com/members/cms/project/defaultadv1.aspx?pId=11268&meta=VIN&catId=32729&id=3866515. Accessed April 15, 2015. 11. Jergens A, Pressel M, Crandell J, et al. Fluorescence in situ hybridization conﬁrms clearance of visible Helicobacter spp. associated with gastritis in dogs and cats. J Vet Intern Med 2009;23:16–23. 12. Simpson KW, Dogan B, Rishniw M, et al. Adherent and invasive Escherichia coli is associated with granulomatous colitis in boxer dogs. Infect Immun 2006;74:4778–4792. 13. Mansﬁeld CS, James FE, Craven M, et al. Remission of histiocytic ulcerative colitis in Boxer dogs correlates with eradication of invasive intramucosal Escherichia coli. J Vet Intern Med 2009;23:964–969. 14. Janeczko S, Atwater D, Bogel E, et al. The relationship of mucosal bacteria to duodenal histopathology, cytokine mRNA and clinical disease activity in cats with inﬂammatory bowel disease. Vet Microbiol 2008;128:178–193.
15. Day MJ, Bilzer T, Mansell J, et al. Histopathological standards for the diagnosis of gastrointestinal inﬂammation in endoscopic biopsy samples from the dog and cat: A report from the World Small Animal Veterinary Association gastrointestinal standardization group. J Comp Pathol 2008;138(Supplement 1):S1– S43. 16. Jennings JL, Sait LC, Perrett CA, et al. Campylobacter jejuni is associated with, but not suﬃcient to cause vibrionic hepatitis in chickens. Vet Microbiol 2011;149:193–199. 17. Van Doorn LJ, Verschuuren-van Haperen A, Burnens A, et al. Rapid identiﬁcation of thermotolerant Campylobacter jejuni, Campylobacter coli, Campylobacter lari, and Campylobacter upsaliensis from various geographic locations by a GTPase-based PCR-reverse hybridization assay. J Clin Microbiol 1999;37:1790– 1796. 18. Murphy H, Cogan T, Hughes R, et al. Porcine intestinal epithelial responses to Campylobacter infection. Comp Immunol Microbiol Infect Dis 2011;34:489–495. 19. Murphy H, Cogan T. Humphrey. Direction of neutrophil movements by Campylobacter-infected intestinal epithelium. Microbes Infect 2011;13:42–48. 20. Casamian-Sorrosal D, Willard MD, Murray JK, et al. Comparison of the histopathologic ﬁndings in biopsies from the duodenum and ileum of dogs with enteropathy. J Vet Intern Med 2010;2010:80–83. 21. Scott KD, Zoran DL, Mansell J, et al. Utility of endoscopic biopsies of the duodenum and ileum for diagnosis of inﬂammatory bowel disease and small cell lymphoma in cats. J Vet Intern Med 2011;25:1253–1257. 22. Fox JG. Enteric bacterial infections: Campylobacter. In: Greene CE, ed. Infectious Diseases of the Dog and Cat, 3rd ed. St.Louis, MO: Elsevier Saunders; 2006:339–343.
A subset of cats with IBD has neutrophilic inflammation of the intestinal mucosa. Hypothesis: Neutrophilic enteritis in cats is associated with mucosal invasion by microorganisms, and specifically Campylobacter spp. Animals: Seven cats with neutrophilic IBD and 8 cats with lymphoplasmacytic IBD.
There are several known causes, but the most common way that a cat comes into contact with campylobacter bacteria is from kennels, which may allow animals to come into direct contact with contaminated feces. Ingestion of contaminated food or water is another mode of transmission.
Recovery of Campylobacteriosis Infection in Cats
Full recovery from a Campylobacteriosis infection may take several weeks or even months although the worst symptoms generally pass within three to seven days.
Although there is no cure for IBD in cats, symptoms can often be managed, allowing your cat to live comfortably for many years. That said, if your cat is not responding to the treatments above your vet may recommend further diagnostic testing to see if there is an underlying disease causing the symptoms.