Clostridium spiroforme-associated enteric disease in domestic rabbits: a retrospective study of 32 cases in California, 1992-2019, and literature review.

Clostridium spiroforme has been associated with spontaneous and antibiotic-associated enteric disease (C. spiroforme-associated enteric disease, CSAED) in rabbits, which is clinically characterized by anorexia, diarrhea, or sudden death. Diagnosis is usually based on gross and microscopic lesions, coupled with finding the characteristic coiled bacteria in intestinal smears. Isolation of C. spiroforme is often challenging, and a PCR protocol has been developed. We reviewed 32 cases of CSAED submitted for autopsy to the Davis, Tulare, and Turlock laboratories of CAHFS between 1992 and 2019. The reported gross findings were soiling of the perineum, tail, and/or hind legs with diarrhea (16 of 32); gastric (16 of 32), small intestinal (6 of 32), cecal (15 of 32), and/or colonic (4 of 32) distention with brown-to-green, watery content; and serosal hemorrhages in the cecum (15 of 32). The most common microscopic finding was necrotizing enteritis (19 of 32), followed by cecal mucosal or submucosal edema (8 of 32), necrotizing or pleocellular typhlitis (6 of 32), necrotizing or heterophilic typhlocolitis (6 of 32), and cecal transmural hemorrhages (5 of 32). In all 32 rabbits, typical helically coiled, gram-positive bacilli were observed in fecal or intestinal smears. C. spiroforme was isolated from the intestinal content of 2 of 24 rabbits and detected by PCR assay in 8 of 8 rabbits.

Pathological lesions associated with avian schistosomes (Digenea: Schistosomatidae) in the freshwater snail Chilina dombeiana (Gastropoda: Chilinidae) from Southern Chile.

Avian schistosomes inhabit the blood stream of domestic and wild birds with aquatic snails as their intermediate hosts. In the Neotropics there is an emerging effort to describe species from these hosts, including Chile, although the knowledge about their pathological consequences is mostly understudied. This study aimed to describe the pathological changes associated with the parasitism of a native schistosomatid restricted to the Southern Cone of Neotropics. To achieve this, a total of 401 Chilina dombeiana snails (Chilinidae) were collected in two locations from Southern Chile. All of them were disposed to cercarial release procedure for three consecutive days. Furcocercariae released were stained and characterized by microscopic evaluation. Then, all snails were dissected under stereomicroscope and preserved in 10 % buffered formalin until histopathological analysis was performed. Eight out 401 (P = 2 %) snails were found parasitized with avian schistosomes. The released furcocercariae were identified as Schistosomatidae gen. sp. Lineage II which was previously reported in the same host. The main pathological change was an atrophy of ovotestes and an absence or mild infiltration of hemocytes in the surrounding tissues. Besides, a co-infection with echinostomes was found which was associated with a moderate hemocyte infiltration, granuloma-like lesion, and a reduced presence of schistosome' sporocysts. The latter would suggest an antagonistic interaction between these two digeneans, as has been proposed in the Echinostoma spp.-Schistosoma mansoni model. Despite the above, the release of furcocercariae was present but reduced, in contrast with the non-release of echinocercariae. This interaction requires further attention. This study represents the first attempt to characterize the pathological consequences of parasitism by a native, yet undescribed, avian schistosome in an endemic snail. Future studies should consider experimental infections to understand the dynamics of single infections in other Chilina species, including inter- and intra-specific parasitism as previous studies have found, including this study.

Identification of orphan histidine kinases that impact sporulation and enterotoxin production by Clostridium perfringens type F strain SM101 in a pathophysiologically-relevant ex vivo mouse intestinal contents model.

When causing food poisoning or antibiotic-associated diarrhea, Clostridium perfringens type F strains must sporulate to produce C. perfringens enterotoxin (CPE) in the intestines. C. perfringens is thought to use some of its seven annotated orphan histidine kinases to phosphorylate Spo0A and initiate sporulation and CPE production. We previously demonstrated the CPR0195 orphan kinase, but not the putative CPR1055 orphan kinase, is important when type F strain SM101 initiates sporulation and CPE production in modified Duncan-Strong (MDS) sporulation medium. Since there is no small animal model for C. perfringens sporulation, the current study used diluted mouse intestinal contents (MIC) to develop an ex vivo sporulation model and employed this model to test sporulation and CPE production by SM101 CPR0195 and CPR1055 null mutants in a pathophysiologically-relevant context. Surprisingly, both mutants still sporulated and produced CPE at wild-type levels in MIC. Therefore, five single null mutants were constructed that cannot produce one of the previously-unstudied putative orphan kinases of SM101. Those mutants implicated CPR1316, CPR1493, CPR1953 and CPR1954 in sporulation and CPE production by SM101 MDS cultures. Phosphorylation activity was necessary for CPR1316, CPR1493, CPR1953 and CPR1954 to affect sporulation in those MDS cultures, supporting their identity as kinases. Importantly, only the CPR1953 or CPR1954 null mutants exhibited significantly reduced levels of sporulation and CPE production in MIC cultures. These phenotypes were reversible by complementation. Characterization studies suggested that, in MDS or MIC, the CPR1953 and CPR1954 mutants produce less Spo0A than wild-type SM101. In addition, the CPR1954 mutant exhibited little or no Spo0A phosphorylation in MDS cultures. These studies, i) highlight the importance of using pathophysiologically-relevant models to investigate C. perfringens sporulation and CPE production in a disease context and ii) link the CPR1953 and CPR1954 kinases to C. perfringens sporulation and CPE production in disease-relevant conditions.

Clostridial diarrheas in piglets: A review.

Clostridium perfringens type C and Clostridioides difficile are the main enteric clostridial pathogens of swine and are both responsible for neonatal diarrhea in this species. The role of Clostridum perfringes type A is under discussion. History, clinical signs, gross lesions and histological findings are the basis for a presumptive diagnosis of C. perfringens type C or C. difficile infection. Confirmation is based upon detection of beta toxin of C. perfringens type C or toxin A/B of C. difficile, respectively, in intestinal contents or feces. Isolation of C. perfringens type C and/or C. difficile is highly suggestive of infection by these microorganisms but it is not enough to confirm a diagnosis as they may be found in the intestine of some healthy individuals. Diagnosis of C. perfringens type A-associated diarrhea is more challenging because the diagnostic criteria have not been well defined and the specific role of alpha toxin (encoded by all strains of this microorganism) and beta 2 toxin (produced by some type A strains) is not clear. The goal of this paper is to describe the main clostridial enteric diseases of piglets, including etiology, epidemiology, pathogenesis, clinical signs, pathology and diagnosis.

Equine abortion and stillbirth in California: a review of 1,774 cases received at a diagnostic laboratory, 1990-2022.

Reproductive failure represents an important cause of economic loss for the equine industry. We reviewed the cases of equine abortion and stillbirth submitted to the California Animal Health and Food Safety Laboratory System, University of California-Davis from 1990 to 2022. A total of 1,774 cases were reviewed. A confirmed cause of abortion was determined in 29.2% of the cases. Abortion or stillbirth was attributed to infectious agents in 18.7% of the cases, with Streptococcus spp., equine herpesvirus 1, and Leptospira spp. being the most prevalent. Noninfectious causes of abortion were established in 10.5% of the cases, with umbilical cord torsion being the most common. In 70.8% of the cases, a definitive cause of abortion could not be established. Our study demonstrated the difficulties in establishing an etiologic diagnosis, even when following a standard diagnostic work-up. New diagnostic approaches are needed to improve the likelihood of reaching a final diagnosis in cases of equine abortion and stillbirth.

Tyzzer disease in 19 preweaned orphaned kittens.

Clostridium piliforme, the agent of Tyzzer disease, has traditionally not been considered a major pathogen of cats. We queried the database of the Pathology Service of the Veterinary Medical Teaching Hospital, University of California-Davis, for kittens <6-mo-old autopsied between 2000-2021 that had colitis, hepatitis, and/or myocarditis; 37 cases met the search criteria. Sections of colon, liver, and heart from these 37 cats were stained with modified Steiner; 19 of 37 (51%) cases had intraepithelial, Steiner-positive rods compatible with C. piliforme in at least one organ, confirming Tyzzer disease. The affected age range was 7-42 d (median: 17.5 d). Eighteen were orphaned kittens. Colitis was the major lesion (18 of 19) followed by random hepatitis (11 of 19). Perianal dermatitis with intraepithelial stacked rods was seen in 2 of 19. Myocarditis was not evident in any of the cases. A PCR assay for C. piliforme on 10 selected cases using formalin-fixed, paraffin-embedded (FFPE) blocks was positive or suspected in colon (5 of 10), liver (5 of 10), and heart (1 of 10). The modified Steiner stain was more sensitive in the detection of bacteria than PCR on FFPE samples. Fifteen kittens had comorbidities. A weakened immune state caused by maternal, environmental, infectious, and/or nutritional causes is speculated to have contributed to disease onset. We found that Tyzzer disease is more common than previously believed in orphaned kittens and should be considered in kittens with colitis and/or hepatitis.

Paeniclostridium sordellii-associated peripartum metritis in goats.

Paeniclostridium sordellii is involved in enteric and histotoxic infections in several animal species. In humans, P. sordellii has been linked to gynecological disease, an association not previously investigated in animals. To unveil a potential association of P. sordellii with veterinary reproductive disease, a retrospective search of the database of the California Animal Health and Food Safety Laboratory System (1990-2020) was conducted and identified 9 cases of goats with P. sordellii-associated metritis or endometritis that were confirmed by immunofluorescence antibody test and/or bacterial isolation, and often co-colonized by Escherichia coli. Six of 9 does were also copper deficient. Polymerase chain reaction (PCR) on formalin-fixed, paraffin-embedded uterine tissue identified the sordellilysin gene in all 9 cases, and the lethal toxin gene in 4. Our findings suggest goats could be predisposed to P. sordellii-associated endometritis/metritis and toxemia when co-infected with E. coli. The role of mineral deficiencies influencing vulnerability to puerperal bacterial infections in goats is possible but remains undetermined. To our knowledge, this is the first report documenting the association of P. sordellii with veterinary gynecological disease.

Characterizing the Contributions of Various Clostridium perfringens Enterotoxin Properties to In Vivo and In Vitro Permeability Effects.

Clostridium perfringens enterotoxin (CPE) is thought to cause lethal enterotoxemia when absorbed from the intestinal lumen into the circulation. CPE action sequentially involves receptor-binding, oligomerization into a prepore, and pore formation. To explore the mechanistic basis by which CPE alters permeability, this study tested the permeability effects of several recombinant CPE (rCPE) species: rCPE and rCPEC186A (which form pores), rC-CPE and rCPED48A (which bind to receptors but cannot oligomerize), rCPEC186A/F91C (which binds and oligomerizes without pore formation), and rCPEY306A/L315A (which has poor receptor-binding ability). On Caco-2 cells, i) only rCPE and rCPEC186A were cytotoxic; ii) rCPE and rCPEC186A affected transepithelial resistance (TEER) and 4 kDa fluorescent dextran (FD4) transit more quickly than binding-capable, but noncytotoxic, rCPE variants; whereas iii) rCPEY306A/L315A did not affect TEER or FD4 transit. Using mouse intestinal loops, rCPE (but not noncytotoxic rC-CPE, rCPED48A or rCPEY306A/L315A) was lethal and caused intestinal histologic damage within 4 h. After 2 h of treatment, rCPE was more strongly absorbed into the serum than those noncytotoxic rCPE species but by 4 h rC-CPE and rCPED48A became absorbed similarly as rCPE, while rCPEY306A/L315A absorption remained low. This increased rC-CPE and rCPED48A absorption from 2 to 4 h did not involve a general intestinal permeability increase because Evans Blue absorption from the intestines did not increase between 2 and 4 h of treatment with rC-CPE or rCPED48A. Collectively, these results indicate that CPE receptor binding is sufficient to slowly affect permeability, but CPE-induced cytotoxicity is necessary for rapid permeability changes and lethality. IMPORTANCE Clostridium perfringens enterotoxin (CPE) causes lethal enterotoxemia when absorbed from the intestines into the bloodstream. Testing recombinant CPE (rCPE) or rCPE variants impaired for various specific steps in CPE action showed that full CPE-induced cytotoxicity causes rapid Caco-2 monolayer permeability alterations, as well as enterotoxemic lethality and rapid CPE absorption in mouse small intestinal loops. However, receptor binding-capable, but noncytotoxic, rCPE variants did cause slow-developing in vitro and in vivo permeability effects. Absorption of binding-capable, noncytotoxic rCPE variants from the intestines did not correlate with general intestinal permeability alterations, suggesting that CPE binding can induce its own uptake. These findings highlight the importance of binding and, especially, cytotoxicity for CPE absorption during enterotoxemia and may assist development of permeability-altering rCPE variants for translational purposes.

Colonic mucinous adenocarcinoma in a tufted deer: differential diagnosis and literature review.

An 18-y-old female tufted deer (Elaphodus cephalophus) had a short history of chronic diarrhea, progressive weight loss, and hindlimb instability. Given the poor prognosis, the deer was euthanized and submitted for postmortem examination. The most significant gross finding was segmental and multinodular mural thickening of the proximal colon. On cut surface of the affected colonic segments, 0.5-2-cm diameter, intramural, multiloculated, cystic structures containing gray, translucent, gelatinous material elevated the edematous mucosa. Microscopically, the intramural cystic structures were filled with mucinous matrix admixed with foamy macrophages, and lined by discontinuous segments of well-differentiated columnar, pancytokeratin-positive epithelium with basilar nuclei. Multifocally, transition was observed from hyperplastic mucosal crypt epithelium to dysplastic or neoplastic columnar and flattened epithelium lining submucosal and serosal cysts. Cyst lumina were irregularly disrupted by polypoid ingrowths of collagenous tissue covered by attenuated epithelium. Based on these findings, we diagnosed a well-differentiated mucinous adenocarcinoma. Although intestinal adenocarcinomas have been described in humans and animals, they are considered uncommon in most domestic species, except for sheep, for which genetic and environmental factors appear to influence occurrence. Our report addresses the knowledge gap regarding intestinal adenocarcinomas affecting cervids and specifically the tufted deer, a less-studied, near-threatened Asian cervid.

A review of cardiac blackleg in cattle, and report of 2 cases without skeletal muscle involvement in Argentina.

Blackleg is an infectious disease caused by Clostridium chauvoei. Cardiac blackleg has been reported in ruminants as an uncommon presentation of the disease; its pathogenesis is not understood completely. We include here a literature review of cardiac blackleg and a description of 2 cases in 12-15-mo-old feedlot steers in Argentina. Fourteen of 1,190 steers died suddenly over a period of 10 d. Postmortem examinations were performed on 5 of these animals. Grossly, severe, diffuse, fibrinous pericarditis and pleuritis, multifocal necrohemorrhagic myocarditis, diffuse pulmonary congestion, mild splenomegaly, and moderate congestion of meningeal vessels were observed. No significant gross lesions were observed in the skeletal muscles of any animal. Histology was performed on 2 of the steers. The main microscopic features were necrotizing myocarditis with myriad intralesional gram-positive rods with subterminal spores plus fibrinosuppurative pericarditis and pleuritis. C. chauvoei was detected by immunohistochemistry and PCR in the myocardium of both animals. These findings confirm a diagnosis of cardiac blackleg in these 2 steers and presumptively in the other affected animals.

Clostridium piliforme and canine distemper virus coinfection in 2 domestic dog littermates and a gray fox kit.

Concurrent Clostridium piliforme and canine distemper virus (CDV) infection was diagnosed in 2 canine littermates and 1 gray fox kit from Texas, USA. In all 3 animals, intracytoplasmic, filamentous bacteria, consistent with C. piliforme, were present along the margins of foci of hepatic necrosis. Additional histologic findings included intracytoplasmic and intranuclear inclusion bodies in bile duct and bronchial epithelial cells of the fox kit, and mild intestinal necrosis in 1 puppy. PCR assays confirmed the presence of C. piliforme in all 3 animals, CDV in both puppies, and canine parvovirus in 1 puppy. Fluorescent antibody testing confirmed the presence of CDV in the fox kit. Concurrent canine distemper and Tyzzer disease in canine littermates and the gray fox has not been reported previously, to our knowledge.

Necrotizing Salpingitis by Fowl Adenovirus in a Backyard Hen.

A 3-yr-old Ameraucana hen was received for postmortem examination following a 1-day history of lethargy and death. Gross lesions observed during necropsy were limited to pulmonary congestion and a small clump of egg yolk material in the oviductal lumen. On histopathology, there was a necrotizing salpingitis of the infundibular and isthmus mucosa with amphophilic, intranuclear inclusion bodies in superficial epithelial cells. Transmission electron microscopy identified the intranuclear inclusions as aggregates of adenovirus virions. Fowl adenovirus (FAdV) type A was identified with PCR and sequencing. Although the cause of death was not determined in this case, this is the first report of FAdV type A-associated salpingitis in a hen.

Reporte de caso- Salpingitis necrotizante por adenovirus en una gallina de traspatio. Una gallina de tres años fue recibida para examen post-mortem después de sufrir letargia por un día y la muerte. Las lesiones macroscópicas observadas durante la necropsia se limitaron a congestión pulmonar y pequeñas cantidades de yema de huevo en el lumen del oviducto. A través del examen histopatológico se observó una salpingitis necrotizante en la mucosa del infundíbulo e istmo con cuerpos de inclusión intranucleares y anfofílicos en las células epiteliales superficiales. Con el uso de microscopía electrónica de transmisión se determinó que las inclusiones intranucleares consistían en agregados de viriones de adenovirus. Se identificó adenovirus del pollo tipo A (FAdV) mediante PCR y secuenciación. Aunque la causa de muerte no fue determinada en este caso, este es el primer reporte de salpingitis asociada a la infección por adenovirus del pollo tipo A en una gallina.

Clostridial Diseases of Horses: A Review.

The clostridial diseases of horses can be divided into three major groups: enteric/enterotoxic, histotoxic, and neurotoxic. The main enteric/enterotoxic diseases include those produced by Clostridium perfringens type C and Clostridioides difficile, both of which are characterized by enterocolitis. The main histotoxic diseases are gas gangrene, Tyzzer disease, and infectious necrotic hepatitis. Gas gangrene is produced by one or more of the following microorganisms: C. perfringens type A, Clostridium septicum, Paeniclostridium sordellii, and Clostridium novyi type A, and it is characterized by necrotizing cellulitis and/or myositis. Tyzzer disease is produced by Clostridium piliforme and is mainly characterized by multifocal necrotizing hepatitis. Infectious necrotic hepatitis is produced by Clostridium novyi type B and is characterized by focal necrotizing hepatitis. The main neurotoxic clostridial diseases are tetanus and botulism, which are produced by Clostridium tetani and Clostridium botulinum, respectively. Tetanus is characterized by spastic paralysis and botulism by flaccid paralysis. Neither disease present with specific gross or microscopic lesions. The pathogenesis of clostridial diseases involves the production of toxins. Confirming a diagnosis of some of the clostridial diseases of horses is sometimes difficult, mainly because some agents can be present in tissues of normal animals. This paper reviews the main clostridial diseases of horses.

Phlegmonous gastritis in 2 yearling horses.

Phlegmonous gastritis was diagnosed in 2 yearling fillies that were presented with a 1-wk history of fever, lethargy, and hypoproteinemia, associated with a previous diagnosis of equine proliferative enteropathy based on clinical signs and PCR assay detection of Lawsonia intracellularis in fecal samples. Abdominal ultrasound revealed enlargement of the stomach and expansion of its submucosal layer with hypoechoic fluid, as well as thickened hypomotile small intestinal segments. Given the poor prognosis and poor response to treatment, both horses were euthanized, one on the day of presentation and the other after 3 wk of intensive medical management including a combination of antimicrobials, analgesics, and intravenous colloids. At autopsy, acute mural gastritis characterized by severe submucosal edema with suppurative inflammation (i.e., phlegmonous gastritis) and necroulcerative enteritis compatible with the necrotizing form of equine proliferative enteropathy were identified in both horses. The gastric inflammation was associated with thrombosis and mixed bacterial populations, including Clostridium perfringens, that were confined to the submucosa without evidence of mucosal involvement; toxin genes compatible with C. perfringens type C were identified in one case. Human phlegmonous gastritis is an uncommon, often-fatal pyogenic infection that is often associated with mucosal injury, bacteremia, or immunocompromise. Our finding of this unusual gastric lesion in 2 horses with similar signalment, clinical disease, and spectrum of postmortem lesions suggests a similar etiopathogenesis that possibly involves local, regional, or distant hematogenous origin, and should be considered a potential complication of gastrointestinal mucosal compromise in horses.

Gut microbiota and age shape susceptibility to clostridial enteritis in lorikeets under human care.

BACKGROUND: Enteritis is a common cause of morbidity and mortality in lorikeets that can be challenging to diagnose and treat. In this study, we examine gut microbiota in two lorikeet flocks with enteritis (Columbus Zoo and Aquarium-CZA; Denver Zoo-DZ). Since 2012, the CZA flock has experienced repeated outbreaks of enteritis despite extensive diet, husbandry, and clinical modifications. In 2018, both CZA and DZ observed a spike in enteritis. Recent research has revealed that the gut microbiota can influence susceptibility to enteropathogens. We hypothesized that a dysbiosis, or alteration in the gut microbial community, was making some lorikeets more susceptible to enteritis, and our goal was to characterize this dysbiosis and determine the features that predicted susceptibility. RESULTS: We employed 16S rRNA sequencing to characterize the cloacal microbiota in lorikeets (CZA n = 67, DZ n = 24) over time. We compared the microbiota of healthy lorikeets, to lorikeets with enteritis, and lorikeets susceptible to enteritis, with "susceptible" being defined as healthy birds that subsequently developed enteritis. Based on sequencing data, culture, and toxin gene detection in intestinal contents, we identified Clostridium perfringens type A (CZA and DZ) and C. colinum (CZA only) at increased relative abundances in birds with enteritis. Histopathology and immunohistochemistry further identified the presence of gram-positive bacilli and C. perfringens, respectively, in the necrotizing intestinal lesions. Finally, using Random Forests and LASSO models, we identified several features (young age and the presence of Rhodococcus fascians and Pseudomonas umsongensis) associated with susceptibility to clostridial enteritis. CONCLUSIONS: We identified C. perfringens type A and C. colinum associated with lorikeet necrohemorrhagic enteritis at CZA and DZ. Susceptibility testing of isolates lead to an updated clinical treatment plan which ultimately resolved the outbreaks at both institutions. This work provides a foundation for understanding gut microbiota features that are permissive to clostridial colonization and host factors (e.g. age, prior infection) that shape responses to infection.

The comparative pathology of enterocolitis caused by Clostridium perfringens type C, Clostridioides difficile, Paeniclostridium sordellii, Salmonella enterica subspecies enterica serovar Typhimurium, and nonsteroidal anti-inflammatory drugs in horses.

To determine if there were significant differences produced by 5 of the most prevalent causes of equine enterocolitis, we studied retrospectively the gross and microscopic pathology of 90 cases of enterocolitis submitted to the San Bernardino laboratory of the California Animal Health and Food Safety Laboratory. Included were cases caused by Clostridium perfringens type C (CP; n = 20), Clostridioides difficile (CD; n = 20), Paeniclostridium sordellii (PS; n = 15), Salmonella enterica subspecies enterica serovar Typhimurium (ST; n = 20), and NSAID intoxication (NS; n = 15). Grossly, necrotizing hemorrhagic typhlocolitis was seen most frequently in cases of CD, ST, and NS disease. Cases of CP and PS had enteritis or colitis in similar percentages. Congestion, hemorrhage, and pleocellular inflammatory infiltrates followed by mucosal and submucosal necrosis were the main lesions found in horses with enteritis or colitis produced by any of the etiologic agents investigated. Severe lesions were more frequent in cases of CD and CP than in cases associated with any of the other 3 etiologies. Pseudomembranes were observed with similar prevalence in the small intestine and colon affected by all agents studied. Thrombosis of the lamina propria and/or submucosa was observed in ~50% of the cases of enteritis and colitis by all etiologies, except for PS, in which the majority of the cases had thrombosis. Gross and microscopic lesions of enterocolitis were not sufficiently specific for any of these etiologic agents to enable these enteritides to be distinguished by gross and/or histologic examination.

Clostridium piliforme infection (Tyzzer disease) in horses: retrospective study of 25 cases and literature review.

Tyzzer disease (TD) is caused by Clostridium piliforme, a gram-negative and obligate intracellular bacterium. The disease occurs in multiple species. A triad of lesions, namely colitis, hepatitis, and myocarditis, is described in cases of TD in some species, such as rats and mice. We carried out a retrospective analysis of 25 equine cases with a diagnosis of TD; 24 of 25 cases occurred in foals <45 d old; the remaining foal was 90 d old. There were 12 males and 12 females; no sex information was available for one foal. The affected breeds were Quarter Horse, Thoroughbred, Arabian, Paint, and Hanoverian. Most of the cases (19 of 25) occurred in the spring. There were 9 cases of sudden death; the remaining animals had diarrhea, fever, distended abdomen, depression, weakness, non-responsiveness, and/or recumbency. Gross findings included icterus, hepatomegaly with acinar pattern, serosal hemorrhages, pulmonary edema, and/or fluid content in small and large intestine. Microscopically, all foals had severe, multifocal, necrotizing hepatitis. Necrotizing lymphohistiocytic colitis was observed in 10 of 25 foals, and multifocal necrotizing myocarditis was found in 8 of 25. Gram-negative, Steiner-positive, intracytoplasmic filamentous bacteria were observed in hepatocytes, enterocytes, and myocardiocytes, respectively. PCR detected C. piliforme DNA in the liver (24 of 24), colon (20 of 24), and heart (5 of 25). Our results indicate that necrotic hepatitis is the hallmark of TD in horses; the so-called triad of lesions is not a consistent characteristic of the disease in this species.

Leukocyte numbers and intestinal mucosal morphometrics in horses with no clinical intestinal disease.

Healthy horses and other animals have large numbers of resident leukocytes in the intestinal wall, but there is scant information regarding which and how many leukocytes are normally present in the equine intestinal wall. Our aim was to provide a reference range of leukocytes in the intestinal mucosal and submucosal propria of normal horses. We included in our study intestinal tissues from 22 Thoroughbred racehorses with no clinical intestinal disease, which had been euthanized because of catastrophic musculoskeletal injuries. Neutrophils, lymphocytes, eosinophils, macrophages, and plasma cells were counted in 5 random 17,600-µm2 areas of villus lamina propria of the duodenum, jejunum, and ileum, and deep lamina propria of the duodenum, jejunum, ileum, right ventral colon, left ventral colon, left dorsal colon, right dorsal colon, and small colon. Other features investigated in the same intestinal segments included villus height and width (small intestine), presence of ciliated protozoa, Paneth cells number, subcryptal leukocyte layers (number of leukocyte layers between the bottom of the crypts and the muscularis mucosae), and submucosal leukocytes. Lymphocytes were the most numerous cells in all segments analyzed, followed by plasma cells, eosinophils, macrophages, and neutrophils. Eosinophil numbers were significantly higher in both lamina propria and submucosa of the large intestine than in the small intestine. The duodenum had shorter and thinner villi than either jejunum or ileum. The data provided from our study will be useful for diagnosticians examining inflammatory processes in the intestinal tract of horses.

Bacterial and viral enterocolitis in horses: a review.

Enteritis, colitis, and enterocolitis are considered some of the most common causes of disease and death in horses. Determining the etiology of these conditions is challenging, among other reasons because different causes produce similar clinical signs and lesions, and also because some agents of colitis can be present in the intestine of normal animals. We review here the main bacterial and viral causes of enterocolitis of horses, including Salmonella spp., Clostridium perfringens type A NetF-positive, C. perfringens type C, Clostridioides difficile, Clostridium piliforme, Paeniclostridium sordellii, other clostridia, Rhodococcus equi, Neorickettsia risticii, Lawsonia intracellularis, equine rotavirus, and equine coronavirus. Diarrhea and colic are the hallmark clinical signs of colitis and enterocolitis, and the majority of these conditions are characterized by necrotizing changes in the mucosa of the small intestine, colon, cecum, or in a combination of these organs. The presumptive diagnosis is based on clinical, gross, and microscopic findings, and confirmed by detection of some of the agents and/or their toxins in the intestinal content or feces.