Immunohistochemical localisation of alpha 2-macroglobulin in the horse

A peroxidase antiperoxidase technique was used to identify alpha 2-macroglobulin in formalin-fixed sections of normal equine lung and liver and in tissue sections and bronchoalveolar lavage fluid from horses with various lung diseases. Equine peripheral blood leucocytes and bronchoalveolar lavage samples from clinically normal horses were negative for alpha 2-macroglobulin. It was concluded that liver and pulmonary macrophages may be potential sources of alpha 2-macroglobulin. Although alpha 2-macroglobulin may play a role in various chronic bronchointerstitial pneumonias of the horse, it is doubtful that it is of importance in equine chronic small airway disease.     

Immunohistochemical localisation of alpha-1-protease inhibitor in the horse

Using a peroxidase anti-peroxidase technique alpha-1-protease inhibitor (alpha-1-PI) was identified in normal equine hepatocytes in formalin-fixed liver sections, and in airway secretions and macrophages in formalin-fixed lung sections of horses with chronic small airway disease and chronic bronchointerstitial pneumonia. In addition, it was identified occasionally in macrophages in bronchoalveolar lavage samples from clinically healthy horses and from horses with chronic small airway disease. Equine peripheral blood leucocytes and formalin-fixed lung sections with normal histology were negative for alpha-1-PI.     

Pericarditis in horses: six cases (1982-1986)

Records of 6 horses with pericarditis were reviewed. Septic pericarditis was suspected in all horses, based on historic and clinical findings. In horses 1, 2, and 4, cytologic examination of the pericardial effusion revealed acute inflammation with severe neutrophil degeneration. In horses 3 and 5, cytologic examination of pericardial fluid revealed subacute inflammation with degenerated neutrophils, and in horse 6, chronic active inflammation, with well preserved neutrophils. In horses 1 and 3, bacteria were identified on cytologic examination of pericardial fluid. Results of microbiologic cultures of pericardial fluid were positive in horse 3. All horses were treated with broad-spectrum antibiotics. An indwelling pericardial catheter was used to lavage and directly administer antibiotics into the pericardial sac. Horses 1, 4, 5, and 6 survived, horse 2 died of unrelated causes, and horse 3 was euthanatized at the owner's request. Surviving horses returned to athletic performance.     

Ubiquitin expression in muscle from horses with polysaccharide storage myopathy

Serial sections of formalin-fixed, paraffin-embedded muscle biopsy specimens from 28 Quarter Horse, Paint, and draft-related breeds, aged 0.5-23 years, were treated with periodic acid-Schiff (PAS) stain for glycogen and were immunostained to detect ubiquitin expression. On the basis of findings in PAS-stained sections, a diagnosis of equine polysaccharide storage myopathy (EPSSM) was made in 22 horses aged 2-23 years (mean, 9.4 years); samples from 6 horses aged 0.5-15 years (mean, 7.3 years) had a normal PAS staining pattern, with no relevant lesions. Ubiquitin expression was detected in all but a 2-year-old EPSSM-affected horse and was not detected in the non-EPSSM-affected horses. Ubiquitin expression was greater than the degree of PAS-positive, amylase-resistant material, and ubiquitin was detected in aggregates of amylase-sensitive glycogen as well as in aggregates of amylase-resistant material. Results suggest that glycogen aggregates develop and are ubiquitinated prior to development of amylase-resistant inclusions. Ubiquitin immunostaining may be most useful for confirming the diagnosis of EPSSM in horses with only amylase-sensitive glycogen aggregates and in horses with early amylase-resistant inclusions. However, ubiquitin immunostaining is no more sensitive than is PAS staining for diagnosis of EPSSM.     

Role of bacteria in the pathogenesis of recurrent uveitis in horses from the southeastern United States

OBJECTIVE: To determine the role of intraocular bacteria in the pathogenesis of equine recurrent uveitis (ERU) in horses from the southeastern United States by evaluating affected eyes of horses with ERU for bacterial DNA and intraocular production of antibodies against Leptospira spp. SAMPLE POPULATION: Aqueous humor, vitreous humor, and serum samples of 24 clinically normal horses, 52 horses with ERU, and 17 horses with ocular inflammation not associated with ERU (ie, non-ERU inflammation). PROCEDURES: Ribosomal RNA quantitative PCR (real-time PCR) assay was used to detect bacterial DNA in aqueous humor and vitreous humor from clinically normal horses (n = 12) and horses with chronic (> 3-month) ERU (28). Aqueous humor and serum were also evaluated for anti-Leptospira antibody titers from clinically normal horses (n = 12), horses with non-ERU inflammation (17), and horses with confirmed chronic ERU (24). RESULTS: Bacterial DNA was not detected in aqueous humor or vitreous humor of horses with ERU or clinically normal horses. No significant difference was found in titers of anti-Leptospira antibodies in serum or aqueous humor among these 3 groups. Only 2 horses, 1 horse with ERU and 1 horse with non-ERU inflammation, had definitive intraocular production of antibodies against Leptospira organisms. CONCLUSIONS AND CLINICAL RELEVANCE: In horses from the southeastern United States, Leptospira organisms may have helped initiate ERU in some, but the continued presence of the organisms did not play a direct role in the pathogenesis of this recurrent disease.     

Kinetics of equine neutrophil elastase release and superoxide anion generation following secretagogue activation: a potential mechanism for antiproteinase inactivation

Man and horses both suffer from neutrophil mediated pulmonary diseases however there are striking species differences in the underlying pathology. In particular while pulmonary emphysema is a common pathological sequel to human respiratory disease it is not a major feature of the common equine neutrophil mediated condition, chronic obstructive pulmonary disease (COPD). The proposed reason for this difference is that equine neutrophils contain less elastase than equivalent human cells and therefore there is a reduced risk of excess and/or uninhibited elastase activity, which is considered the major cause of pulmonary emphysema in man, in the horse lung. In previous studies equine neutrophil elastase (ENE) has been assayed by measuring elastinolytic activity whereas human neutrophil elastase content has been determined using immunological techniques. Neutrophils contain several intracellular protease inhibitors therefore measurement of elastase activity may underestimate the total NE content. The aim of the current study was to develop immunological techniques to allow investigation of the cellular content, distribution and release of ENE from purified equine neutrophils. Equine neutrophil elastase 2A (ENE 2A), the most abundant elastase in equine neutrophils, and equine alpha-1-proteinase inhibitor (API), the main inhibitor of elastase were found to be present at 0.813 pg +/- 0.179 and 0.021 pg +/- 0.003 (mean +/- SEM, n = 11 individual horses) per neutrophil, respectively. This represents twice as much elastase as previously found in the equine neutrophil and a comparable amount to that reported in human neutrophils. Immunolocalisation demonstrated that ENE 2A has a granular distribution within the cytosol of neutrophils, whereas API exhibits a uniform non-granular cytoplasmic appearance. In addition the kinetics of simultaneous generation and release of superoxide anions (SOA) and release of ENE 2A from equine neutrophils, stimulated in vitro by zymosan-activated serum (ZAS) in the presence and absence of the cation chelator ethylene glycol-N,N,N',N'-tetraacetic acid (EGTA), showed a close relationship between total SOA generation and total ENE 2A release during the initial 90 min post-ZAS stimulation and the dependence of both events on extracellular cations. In conclusion these studies have shown that horse and human neutrophil elastase content and mediator release functions are more closely matched than was previously thought. This suggests that the species differences in pathology resulting from neutrophil-mediated respiratory disease are determined by other factors such as differences in the abundance and function of intra- and extra-cellular protease inhibitors.     

Effect of antigen challenge on the activation of peripheral blood neutrophils from horses with chronic obstructive pulmonary disease

The effect of antigen challenge on the state of activation of peripheral blood neutrophils from horses with chronic obstructive pulmonary disease ( ) has been determined by measuring neutrophil superoxide anion formation. Prior to a seven-hour antigen challenge superoxide anion production by neutrophils from asymptomatic horses with and normal horses in response to platelet activating factor ( ) (with and without cytochalasin B), serum treated zymosan ( ) and phorbol myristate acetate ( ) was similar. Agonist-induced superoxide production by neutrophils from symptomatic and normal horses remained unchanged five and 24 hours after antigen challenge. Interestingly, however, superoxide production by neutrophils from symptomatic horses was significantly increased 24 hours after antigen challenge in the control samples for each agonist (basal superoxide production), a five-fold increase being measured in the presence of cytochalasin B. There was a small increase in superoxide production by neutrophils from normal horses but this only reached significance in one set of control samples. The change in activation state of circulating neutrophils during antigen challenge may facilitate the lung neutrophilia and subsequent tissue damage which occur in .     

Interaction of transforming growth factor-beta-1 with alpha-2-macroglobulin from normal and inflamed equine joints.

Binding between equine plasma alpha-2-macroglobulin (alpha 2M) and several cytokines known to participate in inflammatory reactions in other species was initially examined. Plasma was obtained from 5 horses with various abnormalities. Samples, both untreated and after reaction with methylamine, were incubated with exogenous, radiolabeled, porcine-derived transforming growth factor-beta-1 (125I-TGF-beta 1), recombinant human interleukin-1-beta (125I-IL-1 beta), and recombinant human tumor necrosis factor-alpha (125I-rhTNF-alpha). They were then subjected to nondenaturing polyacrylamide gel electrophoresis (PAGE). Binding of the native (slow) and activated (fast) forms of alpha 2M to each cytokine was subjectively evaluated with autoradiography. Equine alpha 2M bound 125I-TGF-beta 1. However, poor or no binding was observed between alpha 2M and either of 125I-rhTNF-alpha or 125I-IL-1 beta. Synovial fluid was then obtained from 6 normal horses, 6 horses with septic arthritis, and 6 horses with degenerative joint disease. Untreated and methylamine-reacted samples were quantitatively examined for binding with 125I-TGF-beta 1, using the autoradiographic techniques described above and densitometry. Native and activated alpha 2M were also quantified by densitometry of PAGE gels. Native alpha 2M was significantly elevated in septic arthritis (6.4% to 29.5% of total protein detected) and degenerative joint disease (2.8% to 12.3%), compared to normal joints (0.9% to 4.2%). Activated alpha 2M, however, was not detected in untreated synovial fluid samples. In all plasma and joint fluid samples, whether untreated or reacted with methylamine, 125I-TGF-beta 1 bound predominantly to alpha 2M, and preferentially to the activated form of alpha 2M. In synovial fluid, the amount of 125I-TGF-beta 1 binding was proportional to the quantity of alpha 2M present. These results indicate that: 1) equine alpha 2M binds TGF-beta 1; 2) the native form of alpha 2M is present in both equine plasma and synovial fluid, and 3) alpha 2M is a major binding protein for TGF-beta 1 in equine synovial fluid. Therefore, alpha 2M may play a role in regulating this mediator of inflammation in equine joints.     

Cytology of tracheobronchial aspirates in horses.

Tracheobronchial aspirates were obtained from 27 normal horses and from 57 horses with respiratory disease. Aspirates from normal horses contained mainly ciliated columnar epithelial cells, mononuclear cells, a few neutrophils and mucus. Aspirates from horses with acute suppurative bronchopneumonias or chronic bronchiolitis had predominantly neutrophils and usually large amounts of mucus; in severe suppurative inflammatory diseases, many of the cells were degenerated, and there were coils of fibrinous material resembling Curschmann's spirals. Eosinophils were rarely found, even from horses with histories suggestive of allergic respiratory disease. Aspirates from horses with epistaxis frequently had macrophages with intracytoplasmic green globules (hemosiderin). Tracheobronchial aspirates occasionally revealed subclinical lung disease. Four horses with no clinical signs of lung disease and lungs that were unremarkable on percussion and normal on auscultation had adpirates suggestive of inflammation; histologic examination confirmed bronchiolitis.     

Myosin heavy chain composition in normal and atrophic equine laryngeal muscle

The myosin heavy chain (MHC) composition of a given muscle determines the contractile properties and, therefore, the fiber type distribution of the muscle. MHC isoform expression in the laryngeal muscle is modulated by neural input and function, and it represents the cellular level changes that occur with denervation and reinnervation of skeletal muscle. The objective of this study was to evaluate the pattern of MHC isoform expression in laryngeal muscle harvested from normal cadavers and cadavers with naturally occurring left laryngeal hemiplegia secondary to recurrent laryngeal neuropathy. Left and right thyroarytenoideus (TA) and cricoarytenoideus dorsalis (CAD) were obtained from 7 horses affected with left-sided intrinsic laryngeal muscle atrophy and from 2 normal horses. Frozen sections were evaluated histologically for degree of atrophy and fiber type composition. MHC isoform expression was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of muscle protein. Histologic atrophy was seen in all atrophic muscles and some right-sided muscles of 3 affected horses, as well as the left TA of 1 normal horse. Fiber type grouping or loss of type I muscle fibers was observed in the left-sided laryngeal muscles in all but 1 affected horse, as well as in the right muscles of 2 affected horses, and the left TA of 1 normal horse. SDS-PAGE showed 2 bands corresponding to the type I and type IIB myosin isoforms in the CAD and TA of the 2 normal horses. Affected horses demonstrated a trend toward increased expression of the type IIB isoform and decreased expression of the type I isoform in atrophic muscles. This study confirmed the presence of histologic abnormalities in grossly normal equine laryngeal muscle, and it demonstrated an increased expression of type IIB MHC with a concurrent decreased expression of type I MHC in affected muscles. Evaluation of muscle fiber changes at the cellular level under denervated and reinnervated conditions may aid in assessing future strategies for reinnervation or regeneration of atrophic laryngeal muscle.     

Arachidonate metabolites in bronchoalveolar lavage fluid from horses with and without COPD.

Arachidonate metabolites were measured in bronchoalveolar lavage fluid (BALF) from horses with (N = 4) and without (N = 7) chronic obstructive pulmonary disease (COPD). Prostaglandin (PG) D2, leukotriene (LT) B4 and LTC4 were present in highest concentrations in BALF from clinically normal horses. Concentrations of PGE2 and PGF were significantly higher in BALF from horses with COPD than in BALF from normal horses, but no differences were detected in thromboxane B2, 6-keto-PGF1 alpha, PGD2, LTB4 or LTC4.     

Inhibition of interleukin-1 activity by equine synovial fluid.

The presence, in equine synovial fluid, of inhibitors of interleukin-1 (IL-1) activity has been investigated by means of an assay involving IL-1-mediated production of PGE2 by synovial cells. Inhibitors of IL-1 alpha and IL-1 beta were identified in normal synovial fluid and synovial fluid from two horses with early joint disease. Inhibitors of IL-1 alpha were also present in synovial fluid from two horses with long-standing joint disease. However, IL-1 beta inhibitory activity was not present in fluid from the horses with more chronic joint disease. The effect appeared to be specific for IL-1, and not a direct action on PGE2 production, as synovial fluid had no effect on lipopolysaccharide-mediated PGE2 production. It is suggested that the inhibitory activity may be involved physiologically in the control of IL-1 activity in the joint, and the loss of IL-1 inhibition may be at least as important biologically as increased production of IL-1.     

Use of scintigraphy for the determination of mucociliary clearance rates in normal, sedated, diseased and exercised horses.

Mucociliary clearance rates from the trachea were determined in normal, sedated, diseased and exercised horses from scintigraphs obtained after an injection of technetium-99m sulphide colloid into the tracheal lumen. The group mean tracheal clearance rate of eight clinically normal horses during 42 trials was 2.06 +/- 0.38 cm/min. Significant between horse differences were found (p less than 0.05). When six and seven of these horses were given xylazine and detomidine hydrochloride, respectively, mean group tracheal clearance rates dropped significantly (p less than 0.05). The decreases from each normal horse's mean tracheal clearance rate ranged from 18 to 54%. There did not appear to be a difference between the tracheal clearance rates (TCRs) of the normal horses and those with chronic respiratory disease. Postexercise evaluations were not significantly different from the pre-exercise TCRs in three clinically normal horses and three horses with chronic obstructive pulmonary disease (p greater than 0.05). This minimally invasive scintigraphic technique for determining TCRs has proved to be useful and reliable.     

Temporomandibular joint cytokine profiles in the horse

It has been suggested that dental abnormalities lead to temporomandibular joint inflammation and pain that may be mitigated by regular dental care. There is considerable literature on the pathophysiology of equine joint disease including studies on cytokine profiles in diseased appendicular joints. This study examined the effects of age and dental malocclusions summarized as a dental pathology score on equine temporomandibular joint cytokine (IL-1, IL-6, IL-8, TNF alpha and TGF-beta1, -beta2, -beta3) concentrations. TGF-beta3 was not detected in any joint sample. IL-1, IL-6 and TNF alpha were not influenced by age. Foals had significantly lower concentrations of lL-8 and TGF-beta1, and higher levels of TGF-beta2 compared with older horses. Age did not effect cytokine concentration in older horses although there was a trend towards increasing 1L-8 with age. The dental pathology score increased with age in mature horses, however there was no effect of dental pathology score on cytokine concentration. There was no effect of incisor eruption, and presence or number of periodontal lesions on temporomandibular joint cytokine concentration. Our findings indicate that age but not dental pathology affected temporomandibular joint proinflammatory cytokine concentration in this population of horses.     

Equine multinodular pulmonary fibrosis: a newly recognized herpesvirus-associated fibrotic lung disease

Pulmonary fibrosis and interstitial lung disease are poorly understood in horses; the causes of such conditions are rarely identified. Equine herpesvirus 5 (EHV-5) is a gamma-herpesvirus of horses that has not been associated with disease in horses. Pathologic and virologic findings from 24 horses with progressive nodular fibrotic lung disease associated with EHV-5 infection are described and compared with 23 age-matched control animals. Gross lesions consisted of multiple nodules of fibrosis throughout the lungs. Histologically, there was marked interstitial fibrosis, often with preservation of an "alveolar-like" architecture, lined by cuboidal epithelial cells. The airways contained primarily neutrophils and macrophages. Rare macrophages contained large eosinophilic intranuclear viral inclusion bodies; similar inclusion bodies were also found cytologically. The inclusions were identified as herpesviral-like particles by transmission electron microscopy in a single horse. In situ hybridization was used to detect EHV-5 nucleic acids within occasional macrophage nuclei. With polymerase chain reaction (PCR), the herpesviral DNA polymerase gene was detected in 19/24 (79.2%) of affected horses and 2/23 (8.7%) of the control horses. Virus genera-specific PCR was used to detect EHV-5 in all of the affected horses and none of the control horses. EHV-2 was detected in 8/24 (33.3%) of affected horses and 1/9 (11.1%) of the control horses. This disease has not been reported before, and the authors propose that based upon the characteristic gross and histologic findings, the disease be known as equine multinodular pulmonary fibrosis. Further, we propose that this newly described disease develops in association with infection by the equine gamma-herpesvirus, EHV-5.     

Serum lipids and lipoproteins in equine colic and grass sickness

Serum total lipids, lipoprotein fractions, triglycerides, cholesterol, phospholipids and free fatty acids were measured in horses with acute, subacute and chronic grass sickness (equine dysautonomia) and in colic cases. The values were compared with those of normal grazing and stabled horses. A marked individual variation occurred, but total lipids, triglycerides and free fatty acids were significantly higher than normal in grass sickness and colic cases with cholesterol was significantly higher than normal in grass sickness cases only. Pre-beta lipoprotein was significantly increased in colic and subacute grass sickness although all abnormal groups showed this fraction which was absent from normal horses. The percentage of alpha 2b lipoprotein was significantly higher in colic and grass sickness. The changes described are typical of those occurring in fat mobilisation in the horse and are considered to be due to a number of factors including decreased food intake, cortisol and catecholamine release and insulin resistance.     

Characterization of alpha-adrenoceptor subtypes in smooth muscle of equine ileum

OBJECTIVE: To determine the concentration and binding characteristics of alpha-adrenoceptor subtypes in smooth muscle cell membranes of equine ileum. SAMPLE POPULATION: Segments of longitudinal and circular smooth muscle from the ileum of 8 male and 8 female adult horses. PROCEDURE: Distribution of alpha-adrenoceptor subtypes was assessed by use of radioligand binding assays incorporating [3H]-prazosin and [3H]-rauwolscine, highly selective alpha1- and alpha2-adrenoceptor antagonists, respectively. Characterization of adrenoceptor subtypes was performed by use of binding inhibition assays. RESULTS: On the basis of binding affinity for specific radioligands, low- and high-affinity alpha1- and alpha2-adrenoceptors were detected. Concentration of low-affinity alpha2-adrenoceptors was significantly greater in male horses, compared with females. Competition studies confirmed the specificity of the radioligands used in the binding assays. Alpha1-adrenoceptors of both subtypes in male and female horses had a higher affinity for prazosin than phentolamine, whereas yohimbine did not compete with the radioligand for binding. For alpha2-adrenoceptors regardless of subtype, potency of inhibition elicited by each drug varied between sexes. In males, yohimbine was a more potent inhibitor than phentolamine, which was more potent than prazosin. In females, yohimbine was more potent than prazosin, which was more potent than phentolamine. CONCLUSIONS AND CLINICAL RELEVANCE: High- and low-affinity alpha1- and alpha2-adrenoceptors were detected in smooth muscle of equine ileum. Because alpha-adrenoceptor subtypes, particularly alpha2-adrenoceptors, are involved in the regulation of gastrointestinal tract function, characterization of these receptors may represent the basis for development of new therapeutic strategies for the control of gastrointestinal disturbances in horses.     

Treatment of inflammatory airway disease in young standardbreds with interferon alpha

The effect of oral treatment with natural or recombinant human interferon alpha (HIA) on inflammatory airway disease in young standardbreds was assessed in a double-blind, randomized clinical trial. A total of 34 horses with nasal discharge, excess mucus in the trachea, and a persistent cough of at least 2 weeks' duration that interfered with training completed the trial. Horses were rested for 1 week and received oral treatment with either a saline placebo, recombinant human interferon alpha (rHIA; 90 U/horse/day), or natural human interferon alpha (nHIA: 50 U/horse/day) for 5 days. There was a significant decline in nasal discharge and cough scores in all groups and the apparent response rate was similar. However, significantly fewer horses relapsed within 2 weeks once treatment was ceased when interferon rather than placebo was used (P = 0.012). Seventeen of 22 horses treated with rHIA or nHIA were cough-free 4 weeks after treatment, compared with only 4 of 12 after treatment with the placebo. Treatment with oral interferon is a useful adjunct to rest in standardbreds with inflammatory airway disease.     

Fibrin/fibrinogen in lungs and respiratory secretions of horses with chronic pulmonary disease

The concentration of soluble fibrinogen derivatives (SFD) and protease and procoagulant activities were determined in cell-free supernatants of equine respiratory secretions obtained from horses with chronic pulmonary disease. The concentration of neutrophils was estimated from direct smears of the secretions. Lung specimens and smears of the secretions were evaluated for the presence of fibrin or fibrinogen by use of immunohistochemical methods. Thirty-five of 80 specimens tested contained SFD. Respiratory secretions from horses with moderate or severe chronic pulmonary disease contained SFD more frequently than did secretions from mildly affected horses (P less than 0.05). Respiratory secretions with vast numbers of neutrophils had significantly (P less than 0.05) higher SFD concentrations than respiratory secretions with fewer neutrophils. Protease and procoagulant activities in respiratory secretion specimens were positively correlated with neutrophil content, clinical diagnosis, and SFD concentration. Immunohistochemically, macrophages that stained for fibrin or fibrinogen were observed in direct smears of respiratory secretions from horses with moderate and severe chronic small airway disease, but not in smears from mildly affected horses. Fibrin or fibrinogen was detected in a few thickened alveolar septa from 10 horses with moderate or severe chronic small airway disease, but not in lungs from horses with mild or no evidence of chronic small airway disease. Fibrin or fibrinogen was detected in alveolar septa, granulomas, and on alveolar macrophages in lungs of all horses with chronic granulomatous and chronic bronchointerstitial pneumonia. The presence of SFD in equine respiratory secretions may be an indicator of pulmonary inflammation.     

Idiopathic muscular hypertrophy of the equine small intestine: 11 cases (1980-1991).

The medical records of 11 horses with idiopathic muscular hypertrophy (MH) of the small intestine were reviewed to determine the clinical and pathological features of the disease. The median age of affected horses was 10.0 years (range 5-18 years). No breed or sex predisposition was apparent. Ten horses (91%) had chronic (23 days to 2.4 years) signs of mild, intermittent colic, and 1 horse had signs of severe colic of only 3 days' duration. Partial anorexia and chronic weight loss of variable duration (1-6 months) were prominent historical findings in 5 (45%) horses. Diagnostic tests, with the exception of exploratory caeliotomy, were ineffective for definitive diagnosis of intestinal MH as a cause of colic. In 2 horses, however, a thickened, rigid ileum was detected by palpation per rectum, and in 5 horses, multiple loops of distended small intestine were detected by palpation per rectum. Hypertrophy of both the circular and longitudinal layers of muscularis was determined as the cause of intestinal thickening in all horses. Muscular hypertrophy of the ileum was present in 9 (82%) horses. Two horses (18%) had MH of a section of jejunum only, and 4 (36%) horses had MH of the ileum in combination with MH of other sections of small intestine. Two (18%) horses had MH of the entire small intestine. In 9 (82%) horses, intestinal MH resulted in narrowing of the luminal diameter at the site of MH. Small diverticula were present on the mesenteric border of the hypertrophied ileum of 5 (45%) horses. Five linear (up to 150-cm) diverticula were present in the hypertrophied jejunum of 1 (9%) horse. Haemomelasma ilei was present on the antimesenteric serosal surface of affected intestine of 8 (73%) horses. Full-thickness rupture of the ileum with subsequent diffuse, septic peritonitis occurred in 3 (27%) horses.