A 16-year-old, 473-kg, Thoroughbred mare was referred to the Cornell University Hospital for Animals with a 1-year history of chronic cough, halitosis, weight loss, and lethargy. Nine months earlier, the mare had been treated for a bacterial or viral respiratory infection with a course of potentiated sulfonamides. During the 6-week treatment period, the owner reported that the horse had decreased appetite and had lost weight but that the respiratory signs seemed improved. More recently, over the last 2–3 months, the mare exhibited intermittent respiratory signs, inappetence, and weight loss. On presentation, the mare (body condition score 4/9) was alert and responsive and had a normal rectal temperature (100.6°F) and heart rate (40 beats/min), but was tachypneic (32 breaths/min). Her mucous membranes were pink and capillary refill time was normal (<2 seconds). During the examination, a nonproductive cough occurred intermittently and was associated with foul-smelling breath. Cardiothoracic auscultation was normal and a rebreathing examination disclosed decreased lung sounds in the cranioventral lung fields. Auscultation of abdomen was normal. Clinical laboratory tests identified the presence of mature neutrophilia (7.2 × 103/μL; reference range, 2.7–6.6 × 103/μL), hyperproteinemia (9.7 g/dL; reference range, 5.7–7.7 g/dL), hyperglobulinemia (7.1 g/dL; reference range, 2.4–4.4 g/dL), hyperfibrinogenemia (400 mg/dL; reference range, 0–200 mg/dL), and hypoalbuminemia (2.8 g/dL; reference range, 3–3.7 g/dL). Red cell indices (HCT, RBC numbers, MCV, RDW) were within normal limits. Serum electrolyte concentrations (sodium, potassium, chloride, calcium, and phosphorus) were normal, and CK and AST activities were decreased (95 and 161 U/L, respectively; reference range CK, 142–548 U/L; reference range AST, 199–374). Serum creatinine concentration, hepatic enzyme activities (SDH, GLDH, GGT), and serum bilirubin (indirect, direct) concentrations also were within the reference range. Thoracic radiography disclosed the presence of 3 lesions: Cranio-ventrally, there was lung consolidation and air bronchograms consistent with pneumonia. Caudo-dorsally, there was a single, oval, well-margined, soft tissue opacity that spanned 4 intercostal spaces and silhouetted with the diaphragm. Because this lesion silhouetted with the diaphragm, its abdominal extension could not be confirmed by radiography. Cranio-dorsally, within the abdomen and close to the diaphragm, were 2 well-marginated structures with fluid–gas interfaces that spanned 4 intercostal spaces (Fig 1). Based upon the radiographic findings, the gas accumulations were considered to represent abscesses within the liver or gas-filled segments of bowel. Thoracic sonography confirmed the presence of bilateral ventral lung consolidation consistent with pneumonia. The caudo-dorsal lung lesion, visible on radiographs, was not observed on ultrasound examination because it was surrounded by aerated lung. Sonography of the right cranio-dorsal abdomen confirmed that the liver contained an encapsulated, well-marginated, multi-loculated mass (or multi-focal masses) containing gas and a complex echogenicity fluid consistent with abscessation (Fig 2). Sonography was not able to determine the association between the liver abscess, which spanned the 13th through 16th intercostal spaces, and the focal craniodorsal lung lesion because the deeper and cranial aspects of the diaphragm and liver were obscured by aerated lung. Aspiration of the mass or biopsy of the hepatic tissue was not considered because of the potential risk of spreading the infection into the peritoneal or pleural cavities. Measurement of serum bile acids, although potentially helpful in cases of extensive hepatic abscessation, was not performed. A rectal examination was performed but no abnormalities were detected on palpation. An abdominocentesis failed to yield any peritoneal fluid. A transtracheal aspirate yielded degenerative neutrophils, moderate numbers of intracellular and extracellular Gram-negative rods, and occasional Gram-positive cocci indicative of a septic suppurative inflammation. Aerobic and anaerobic culture of the aspirate yielded Actinobacillus equuli and Peptostreptococcus asaccharolyticus, respectively. Blood culture yielded no bacterial growth. The mare was hospitalized for 5 days and treated with potassium penicillin1 22,000 IU/kg IV q6h, gentamicin sulfate2 6.6 mg/kg IV q24h, and metronidazole3 25 mg/kg per rectum q8h. She was nebulized4 q8h with a 25-mL solution containing 5 mL of acetylcysteine,5 1 mL of albuterol sulfate solution,6 and 19 mL of 0.9% saline.7 While hospitalized, the mare showed mild clinical improvement in her demeanor and appetite. At the time of her discharge, the client was instructed to administer chloramphenicol8 (50 mg/kg PO q8h) and omeprazole9 (1.1 mg/kg PO q24h) and to have the horse re-evaluated in 3 weeks. On the return visit, laboratory evaluation disclosed a persistent hyperproteinemia (8.6 g/dL), hyperglobulinemia (6.4 g/dL), hypoalbuminemia (2.4 g/dL), and neutrophilic leukocytosis (10,900/μL). Thoracic and abdominal ultrasound examination demonstrated an increase in the size of the hepatic abscesses within the right dorsal liver. Because of the poor response to treatment, the owner elected to euthanize the mare. A complete postmortem examination was performed approximately 20 hours after euthanasia. On gross examination, an encapsulated 18 × 15 × 5 cm abscess was found in the left caudo-dorsal lung. The mass communicated transdiaphragmatically with the left lateral liver lobe; the liver and lung were adhered to the diaphragm at the location of the mass. The abscess contained approximately 500 mL of white-tan thick liquid and an accumulation of inspissated material. An aseptic aspirate of the hepatic abscess subsequently yielded Fusobacterium necrophorum and Bacteroides vulgatus. Other findings included diffusely thickened and hypertrophic ileal musculature (1 cm wall thickness) containing approximately a dozen diverticula present in the antimesenteric border ranging in size from 1 mm3 to 2 × 1 × 1 cm, some of which were impacted with feed whereas others contained purulent material (Fig 3). There was evidence of moderate, diffuse peritonitis with fibrin strands present throughout the abdomen. No lesions consistent with cranioventral pneumonia were identified. All tissues were fixed in 10% neutral-buffered formalin, processed routinely for histopathology, and stained with hematoxylin and eosin (H&E). The hepatic abscess was characterized by a central area of liquefactive necrosis, fibrin, cellular debris, degenerate and nondegenerate neutrophils, lymphocytes, and extracellular bacterial rods surrounded by a fibrovascular capsule. The ileal musculature was diffusely hypertrophied except in areas of the diverticula. These diverticula were formed by layers of the longitudinal and circular ileal muscles forming serosal outpouchings. The lumina of the the diverticula were lined by variably inflamed mucosa and submucosa. Several diverticula contained a neutrophilic, lymphoplasmacytic inflammatory cell population that dissected through the muscular layers extending to within 1 mm of the serosal surface (Fig 4). To the authors' knowledge, this is the first reported case of a transdiaphragmatic hepato-pulmonary abscess in a horse. In contrast to cattle, hepatic abscessation in horses is uncommon and most often is a sequela to Streptococcus equi or Corynebacterium pseudotuberculosis infections1 or secondary to bacterial translocation from the gastrointestinal tract.2 Hepatic abscesses also develop secondary to penetrating foreign objects within the gastrointestinal tract.2-5 As occurs in cattle, caudal vena caval phlebitis and secondary embolic pneumonia may result from hepatic abscessation in horses.2, 6 However, neither sequelae were apparent in this case. Given the microbiologic results of a mixed anaerobic infection along with the presence of ileal diverticulitis, it is likely that translocation of bacteria through the compromised ileal wall either via the peritoneum or the portal circulation caused the hepatic abscess. In humans, diverticulitis of the small intestine or large colon has been associated the development of hepatic abscesses.7, 8 The virulence factors of F. necrophorum, which include leukotoxins, lipopolysaccharide, hemolysins, dermonecrotic toxins, and extracellular enzymes9, 10 likely resulted in tissue necrosis and subsequent extension of the hepatic abscess through the diaphragm and into the adjacent lung in this horse. A primary pulmonary abscess originally was considered possible, but the discrete and caudo-dorsal location of the affected lung along with the presence of intestinal diverticulitis made this less likely to be a primary event. The discrepancy between the imaging of the liver abscess and the location at necropsy is considered to have occurred because the left liver lobe extends to the right of the caudal vena cava in the horse. Small intestinal muscular hypertrophy typically is a condition of mature horses, and there is no reported breed or sex predisposition.11 The lesion often is found incidentally at postmortem examination. Suggested predisposing factors for small intestinal muscular hypertrophy include Anoplocephala perfoliata at the ileocecal junction, mucosal inflammation, uncontrolled peristalsis, and intestinal sand accumulation. An association between ileal muscular hypertrophy and ileal diverticula has been suggested.12, 11, 13-18 In contrast to the current case report, the most common clinical presentation of horses with small intestinal diverticula is chronic colic. In a retrospective study of 11 horses with idiopathic muscular hypertrophy, 10 horses presented with chronic colic, from 1 to 6 months duration, and a single horse presented with acute colic. Of these horses, 45% had small diverticula present in the ileum. Intestinal rupture and subsequent peritonitis also have been reported secondary to jejunal diverticulosis in 2 horses.16 In humans, the relationship between intestinal muscular hypertrophy and diverticula has been more defined. Most intestinal diverticula are thought to be acquired pulsion lesions. Luminal pressure is increased secondary to distorted smooth muscle contractions leading to formation of diverticula.19 Antemortem diagnosis of diverticula is difficult in veterinary medicine. The large size of horses, extensive nature of the gastrointestinal tract, and relatively small proportion of the intestine that may be affected make noninvasive diagnosis difficult. In human medicine, computed tomography is the diagnostic test of choice, but the finding of a diverticulum often is serendipitous during abdominal surgery. This case represents an unusual combination of clinical and postmortem findings and is the first report of a transdiaphragmatic abscess in a horse. Intestinal diverticulum should be considered in horses with nonspecific abdominal signs, peritonitis, or hepatic abscessation with atypical culture results. Conflict of Interest: Authors disclose no conflict of interest.