West Nile Virus Infection in a Pekin Duck ( Anas platyrhynchos domesticus ) Developer Flock.

Developer ducks are ducks being reared for breeding. Like breeder candidate chickens, they are raised with appropriate light and feed programs. A commercial Pekin duck (Anas platyrhynchos domesticus) developer flock experienced an extraordinary, elevated mortality event at 6 wk of age. Weekly mortality rate that week was 162 ducklings out of a flock of 6420 (2.5%). Mortality jumped to 988 (15.4%) ducklings the next week. On first elevated mortality, six dead ducks from that flock were submitted for diagnostic investigation at Michigan State University Veterinary Diagnostic Laboratory. Myocarditis, pale striping or diffuse pallor of the epicardium, was grossly evident in five of the six submitted ducklings. All of the ducklings had hydropericardium, three had ascites, and three had congested meninges. Histology confirmed myocarditis with myocardial necrosis. Cerebrum and brainstem had lymphocytic vasculitis with rare neuronal necrosis in affected areas, as well as Purkinje cells in the cerebellum. West Nile virus was confirmed by PCR the day after submittal and by immunohistochemistry soon thereafter.

Reporte de caso- Infección por el virus del Nilo occidental en una parvada en desarrollo de patos Pekin (Anas platyrhynchos domesticus) reproductores. Los patos reproductores en desarrollo son patos que se crían para la reproducción. Al igual que los pollos candidatos para reproducción, se crían con programas de iluminación y alimentación adecuados. Una parvada comercial en desarrollo de pato Pekín (Anas platyrhynchos domesticus) experimentó un evento de mortalidad elevada y extraordinaria a las seis semanas de edad. La tasa de mortalidad semanal de esa semana fue de 162 patitos de una parvada de 6420 (2.5%). La mortalidad se elevó a 988 (15.4%) patitos la semana siguiente. En el primer aumento de mortalidad, seis patos muertos de esa bandada fueron enviados para una investigación de diagnóstico en el Laboratorio de Diagnóstico Veterinario de la Universidad Estatal de Michigan. La miocarditis, caracterizada por rayas pálidas o palidez difusa del epicardio, fue evidente en cinco de los seis patitos presentados. Todos los patitos mostraron hidropericardio, tres tenían ascitis y tres tenían meninges congestionadas. La histología confirmó miocarditis con necrosis miocárdica. El cerebro y el tronco del encéfalo tenían vasculitis linfocítica con rara necrosis neuronal en las áreas afectadas, así como de las células de Purkinje en el cerebelo. El virus del Nilo Occidental se confirmó mediante PCR el día después de la llegada al laboratorio y mediante inmunohistoquímica poco tiempo después.

Amdoparvovirus-associated disease in striped skunks (Mephitis mephitis).

Disease caused by the archetypical amdoparvovirus (APV), Aleutian mink disease virus (AMDV), has been well studied, but APV infections in other carnivores are poorly understood. Skunk amdoparvovirus (SKAV), one of a handful of newly discovered APVs, is apparently species-specific in striped skunks (Mephitis mephitis) and has a high prevalence across North America. We have evaluated the infection status and viral tissue distribution in a cohort of 26 free-ranging California skunks from a single rehabilitation facility who were euthanized due to poor prognosis for recovery from neurologic disease. SKAV was detected in the majority of this cohort, and virus was associated with a spectrum of lesions including tubulointerstitial nephritis, meningoencephalitis, myocarditis, and arteritis. Affected tissue and patterns of inflammation were partially overlapping with those of AMDV infection but were notably distinct in the kidney.

Neurologic and cutaneous infection by Clostridium piliforme in a kitten with systemic Tyzzer disease.

Tyzzer disease (TD) is a highly fatal condition of animals caused by Clostridium piliforme and characterized pathologically by enteritis, hepatitis, myocarditis, and occasionally encephalitis. Cutaneous lesions have been reported only rarely in animals with TD, and infection of the nervous system has not been described in cats, to our knowledge. We describe here neurologic and cutaneous infection by C. piliforme in a shelter kitten with systemic manifestations of TD and coinfection with feline panleukopenia virus. Systemic lesions included necrotizing typhlocolitis, hepatitis, myocarditis, and myeloencephalitis. The cutaneous lesions consisted of intraepidermal pustular dermatitis and folliculitis, with necrosis of keratinocytes and ulceration. Clostridial bacilli were identified within the cytoplasm of keratinocytes by fluorescence in situ hybridization, and a PCR assay was positive for C. piliforme. C. piliforme can infect keratinocytes leading to cutaneous lesions in cats with the location suggesting direct contact with contaminated feces as a route of infection.

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.

Clinical-pathological findings induced by Histophilus somni isolated in subacute cardiac death in feedlot cattle.

The purpose of this report is to provide information about the different presentations of cardiac and extra-cardiac histophilosis and, to assess the antimicrobial (ATM) susceptibility of Histophilus somni isolated from these cardiac lesions to different ATM agents commonly used for treating bovine bacterial respiratory pathogens. Eight feedlot calves, which died after suffering from food rejection, apathy, hyperthermia, cough and nasal mucous discharge, and lack of response to ATM therapy, were studied. Cardiac lesions observed at necropsy included valvular/mural endocarditis, myocardial infarction, and necrotizing myocarditis, miliar non-suppurative myocarditis, myocardic necrotic sequestrum, and/or pericarditis. Histopathological, bacteriological and molecular studies confirmed the presence of a fastidious microorganism in the affected organs. H. somni showed no resistance to most ATM tested (ceftiofur, gamithromycin, enrofloxacin, florfenicol, tilmicosin). The results obtained in this study confirmed that H. somni was the main cause of the subacute cardiac lesions associated with hyperthermia, apathy and respiratory signs observed in cattle examined in this research. These presentations must be considered by veterinary practitioners in order to establish a rational therapeutic.

Curcumol inhibits EMCV replication by activating CH25H and inhibiting the formation of ROs.

BACKGROUND: Zedoary turmeric oil extracted from the roots of curcuma (Curcuma aeruginosa Roxb.) is used for the treatment of myocarditis in China. EMCV infection causes abortion in pregnant sows and myocarditis in piglets. Our previous studies demonstrated that curcumol significantly increased the expression of IFN-ß in EMCV infected HEK-293T cells. The present results showed that curcumol inhibits EMCV replication by interfering the host cell cholesterol homeostasis and reducing ROs production through activation of the JAK/STAT signaling pathway. METHOD: This study was designed to explore whether curcumol can inhibit the replication of encephalomyocarditis viruses (EMCV) in cell culture. The expression level of JAK1, IRF9, STAT2, P-STAT2, CH25H, PI4KA and OSBP in EMCV-infected HEK-293T cells treated with curcumol, ribavirin or hydroxypropyl-ß-CD (HPCD) were determined by Western blotting (WB). The cholesterol level in EMCV infected HEK-293T cells treated with curcumol and HPCD were detected using Amplex™ Red Cholesterol Assay Kit. The antiviral effects of curcumol and HPCD on EMCV were also quantitatively detected by real-time fluorescence quantitative PCR (q-PCR). The amount and morphology of ROs were observed by transmission electron microscopy (TEM). RESULTS: The results demonstrated that curcumol significantly (P < 0.05) increased the expression of JAK1, IRF9, P-STAT2 and CH25H proteins, while that of STAT2, PI4KA and OSBP were remained unchanged. Compared with virus group (0.134 µg.µg-1 proteins), the total cholesterol level was significantly (P < 0.05) reduced by curcumol (0.108 µg.µg-1 proteins) and HPCD (0.089 µg.µg-1 proteins). Compared with virus group (88237 copies), curcumol (41802 copies) and HPCD (53 copies) significantly (P < 0.05) reduced EMCV load. Curcumol significantly reduced the production of ROs in EMCV-infected HEK-293T cells and activated CH25H through the JAK/STAT signaling pathway. CONCLUSION: Curcumol inhibited EMCV replication by affecting the cholesterol homeostasis and the production of ROs in HEK-293T cell.

Eosinophilic Granulomatous Myocarditis in Two Pigs.

Eosinophilic myocarditis is a human condition that has been rarely documented in animals. We now report two unrelated porcine cases of idiopathic eosinophilic granulomatous myocarditis that resembled the human disease and which were associated with sudden death. The most relevant gross finding in both cases was marked cardiomegaly, accompanied by raised, multifocal to coalescent small white nodules (1-2 mm) and poorly demarcated multifocal pale areas in the epicardium. Histologically, there were multifocal to coalescent areas of cardiomyocyte loss with replacement by an intense inflammatory infiltrate of eosinophils and epithelioid macrophages, and proliferation of fibrous connective tissue. Immunohistochemistry for porcine circovirus type 2 (PCV2) and Toxoplasma gondii, in-situ hybridization and quantitative polymerase chain reaction tests for PCV2 and porcine circovirus type 3 and aerobic bacterial culture on myocardium samples were negative.

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.

Myocardial Iba1, MHC class II, and CD3 are diffusely increased in canine myocarditis: A step toward antemortem myocarditis diagnostics.

Canine myocarditis is a rare but serious health concern, potentially causing heart failure and death. Antemortem diagnosis is hampered by the numerous causes, nonspecific course, and dearth of diagnostic criteria. Currently, definitive diagnosis can only be made after death. The current human diagnostic gold standard is endomyocardial biopsy pairing cardiac histopathology with immunohistology to enhance detection of often-multifocal disease. We evaluated immune response markers in the canine heart to establish similar immunohistologic criteria. We hypothesized that myocardial major histocompatibility complex class II (MHCII), cluster of differentiation 3 (CD3), and ionized calcium binding adapter molecule 1 (Iba1), markers increased in human myocarditis, would be increased in canine myocarditis cases. Archived paraffin-embedded myocardial tissue from 22 histopathologically confirmed cases of adult and juvenile myocarditis and 23 controls was analyzed by immunohistochemistry for MHCII, CD3, and Iba1, and the fraction of myocardium with labeling was determined. All 3 markers were significantly increased compared with controls across the entire section: Iba1, 10.1× (P < .0001, Mann-Whitney U test); MHCII, 3.04× (P = .0019); and CD3, 4.4× (P = .0104). To mimic off-target biopsy, samples from 2 mm2 outside of inflammatory foci were analyzed, and these showed significant increases in Iba1 by 3.2× (P = .0036, Mann-Whitney U test) and CD3 by 1.2× (P = .0026). These data show diffusely increased immune response markers with canine myocarditis, with detection potentially independent of tissue sampling. Thus, endomyocardial biopsy and immunohistochemical detection of MHCII, CD3, and Iba1 may permit sensitive antemortem diagnosis of canine myocarditis.

Histopathological Findings in the Cardiovascular System of Psittacidae in Routine Diagnostics.

Samples of 363 Psittacidae were included in this study with a focus on cardiovascular diseases. These were identified in 28.9% of the animals, with pericarditis and/or epicarditis and myocarditis representing approximately half of all lesions and bacteria being the most common infectious cause. Cardiac lymphoma was only seen in 5 birds, whereas degenerative vascular lesions were diagnosed in 26.7% of the cases. Histopathology in the context of clinical findings and complementary examination results is the most useful tool for the evaluation of cardiac diseases.

Pancarditis as the sole clinical manifestation of protothecosis in a Boxer dog.

A 4.2-year-old, male castrated Boxer was diagnosed with a dilated cardiomyopathy phenotype, complex arrhythmias and left-sided congestive heart failure, but died suddenly shortly after initial diagnostics were complete. Ultrasensitive cardiac troponin I was markedly elevated (9.345 ng/mL [reference range: 0-0.06 ng/mL]), and a Trypanosoma cruzi immunofluorescent antibody titer was positive at 1:80. Necropsy revealed a severe, necrotizing, histiocytic, lymphoplasmacytic pancarditis with intralesional algae consistent with protothecosis, as well as evidence of left-sided congestive heart failure. Algal organisms were found only in the heart. Acute Chagas disease was not thought to play a role given the lack of T. cruzi amastigotes on postmortem and negative reverse transcription polymerase chain reaction testing on formalin fixed, paraffin embedded myocardium, however a possible contribution of chronic Chagas disease to the clinical picture could not be ruled out. Canine protothecosis is typically a disseminated disease. This case represents the first report of canine protothecosis limited solely to the heart.

Hypereosinophilic syndrome with cardiac infiltration and congestive heart failure in a cat.

Hypereosinophilic syndrome is an uncommon disorder in the cat. It is a heterogeneous group of conditions defined by a persistent hypereosinophilia associated with organ damage directly attributable to tissue hypereosinophilia. A seven-year-old castrated domestic shorthair cat presented to the emergency service for dyspnea. Initial physical examination identified the presence of a grade III/VI systolic left parasternal murmur with no gallop or arrhythmia. A snap N-terminal-pro hormone brain natriuretic peptide was abnormal, and a point-of-care ultrasound revealed mild pleural effusion, scant pericardial effusion, and an enlarged left atrium. There was leukemia (72.35 K/uL, reference range 4.5-15.7 K/uL) predominated by eosinophilia (33.84 K/uL; reference range 0-1.9 K/uL). On echocardiogram, there was concentric hypertrophy of the left ventricular walls with irregular endocardial borders. The left atrium was enlarged with evidence of spontaneous echogenic contrast. The mitral valve was thickened with a vegetative lesion on the anterior leaflet. Despite treatment, the patient experienced cardiopulmonary arrest, and cardiopulmonary resuscitation was unsuccessful. Complete necropsy with histopathology revealed eosinophilic infiltrates in multiple organs and the presence of a severe, acute-on-chronic, fibrinous, and eosinophilic-granulomatous endomyocarditis with mural thrombosis and marked endocardial fibrosis. This case represents an unusual presentation of the hypereosinophilic syndrome in the cat with cardiac involvement and congestive heart failure as a primary clinical sign.

Fatal Toxoplasma gondii myocarditis in an urban pet dog.

A 70-day-old Boxer dog from a household in Montevideo, Uruguay, died after presenting neurologic, respiratory, and gastrointestinal signs for 6 days. Autopsy findings included lymphadenomegaly, ascites and hepatomegaly. Histopathology revealed severe widespread lymphohistiocytic and plasmacytic myocarditis with cardiomyocyte necrosis, mineralization and numerous intrasarcoplasmic protozoa immunoreactive with anti-Toxoplasma gondii antisera on immunohistochemistry. The protozoa were ultrastructurally confirmed as T. gondii by transmission electron microscopy. Other lesions included diffuse centrilobular hepatocellular necrosis, multifocal lymphohistiocytic portal hepatitis and interstitial nephritis. Other causes of myocarditis, including Neospora caninum, Trypanosoma cruzi, Sarcocystis neurona, canine distemper virus, and canine parvovirus were ruled out by immunohistochemistry. Toxoplasma gondii infections in dogs are usually subclinical; however, clinical disease with fatal outcome can occur. To our knowledge, this is the first report of fatal toxoplasmosis in a dog in Uruguay. This case raises awareness for dogs as sentinels and possible sources of human toxoplasmosis in urban settings in Uruguay.

Myocarditis caused by Listeria monocytogenes in a dog.

BACKGROUND: Canine myocarditis can result from infection with bacteria Listeria monocytogenes. CASE REPORT: A 14-week-old female entire Staffordshire Bull Terrier was assessed for lethargy, inappetence and dyspnoea. Radiographs and echocardiography revealed fluid within the pericardial space, a plaque of marked hyperechogenicity within the right ventricular free wall, marked right atrial dilation and myocardial systolic dysfunction. Histopathology of the myocardium was consistent with severe pyogranulomatous myocarditis, with gram stain revealing gram-positive bacilli, consistent with a Listerial infection. Bacterial culture of the myocardium yielded a light growth of Listeria monocytogenes. CONCLUSION: To the best of the authors' knowledge, this is the first case of canine myocarditis caused by Listeria monocytogenes to be described and should be included as a differential diagnosis of myocarditis. Further, it prompts the consideration of potential zoonotic risks for veterinarians treating dogs with pericardial effusions.

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.

Acquired myasthenia gravis with concurrent polymyositis and myocarditis secondary to a thymoma in a dog.

Background: Canine thymomas are associated with multiple paraneoplastic syndromes, among which myasthenia gravis (MG) is the most common. Acquired MG is an autoimmune disease characterized by the presence of antibodies against acetylcholine receptors (ACHRs). ACHRs antibodies are the most commonly formed, but the production of antistriational antibodies binding to skeletal and cardiac muscle proteins has also been recorded both in humans and dogs. An association between the occurrence of antistriational antibodies and a severe form of myocarditis, giant cell myocarditis, has been described in humans. Case Description: A 4-year-old mixed-breed dog was referred because of 1 month history of exercise-induced weakness, hypersalivation, and regurgitation. The neurologic examination was indicative of a neuromuscular junction disease, and MG was suspected. A computed tomographic scan examination showed the presence of a megaoesophagus and a thymic mass. Serum antibodies against ACHRs confirmed the diagnosis of MG. Treatment with pyridostigmine was started, and the thymic mass was surgically excised, and a diagnosis of thymoma was confirmed by histology. 24 hours after surgery, the dog developed a third-degree atrioventricular block. Severe arrhythmia and increased troponin serum levels suggested myocarditis which rapidly led to cardiopulmonary arrest. Histopathologic examination of the heart, esophagus and diaphragm revealed a lymphocytic and macrophagic infiltration, consistent with myocarditis and polymyositis. Scattered rare giant multinucleated cells were also detected in the myocardium. Conclusion: To the author's knowledge, this is the first report of thymoma-associated MG with concurrent polymyositis and giant cell-like myocarditis in a dog.

Infection with SARS-CoV-2 variant B.1.1.7 detected in a group of dogs and cats with suspected myocarditis.

BACKGROUND: Domestic pets can contract severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; however, it is unknown whether the UK B.1.1.7 variant can more easily infect certain animal species or increase the possibility of human-to-animal transmission. METHODS: This is a descriptive case series reporting SARS-CoV-2 B.1.1.7 variant infections in a group of dogs and cats with suspected myocarditis. RESULTS: The study describes the infection of domestic cats and dogs by the B.1.1.7 variant. Two cats and one dog were positive to SARS-CoV-2 PCR on rectal swab, and two cats and one dog were found to have SARS-CoV-2 antibodies 2-6 weeks after they developed signs of cardiac disease. Many owners of these pets had developed respiratory symptoms 3-6 weeks before their pets became ill and had also tested positive for COVID-19. Interestingly, all these pets were referred for acute onset of cardiac disease, including severe myocardial disorders of suspected inflammatory origin but without primary respiratory signs. CONCLUSIONS: These findings demonstrate, for the first time, the ability for pets to be infected by the B.1.1.7 variant and question its possible pathogenicity in these animals.

Acute Late-Stage Myocarditis in the Crab-Eating Macaque Model of Hemorrhagic Smallpox.

Hemorrhagic smallpox, caused by variola virus (VARV), was a rare but nearly 100% lethal human disease manifestation. Hemorrhagic smallpox is frequently characterized by secondary bacterial infection, coagulopathy, and myocardial and subendocardial hemorrhages. Previous experiments have demonstrated that intravenous (IV) cowpox virus (CPXV) exposure of macaques mimics human hemorrhagic smallpox. The goal of this experiment was to further understand the onset, nature, and severity of cardiac pathology and how it may contribute to disease. The findings support an acute late-stage myocarditis with lymphohistiocytic infiltrates in the CPXV model of hemorrhagic smallpox.

[Reversible left ventricular hypertrophy and congestive heart failure due to suspected myocarditis in a cat in the course of FLUTD]. / Reversible linksventrikuläre Muskelhypertrophie und Herzversagen durch vermutete Myokarditis bei einer Katze im Zuge einer FLUTD.

A 2.5-year-old castrated male domestic shorthair cat with a past pertinent history of FLUTD treatment 8 days earlier was presented during the night due to apathy and anorexia. Radiographs, ECG, blood pressure measurement and echocardiography revealed left-sided congestive heart failure, left ventricular concentric hypertrophy, left atrial dilation, severe diastolic dysfunction, hypotension, and vagotonus-associated sinus bradycardia with a first degree AV-block as well as a right bundle brunch block. NT-ProBNP and troponin I concentrations were elevated (NT-ProBNP > 1500 pmol/l, Troponin I 32.87 ng/ml). Presumptive diagnosis was acute myocarditis. Bartonella henselae PCR and Toxoplasma gondii IgM titer were negative. Initial IgG titer amounted to 1:32 (reference range: < 1:32) and on later testing this was negative. FeLV and FIV tests exhibited negative results. Coronavirus testing was not performed because the cat was vaccinated accordingly. A metastatic infection with Proteus mirabilis, which had been isolated from the urine, appeared possible. Alternatively, a hypersensivity reaction to drugs or a stress-induced myocarditis was taken into consideration. The hospitalized cat was treated with furosemide (initialy and in the course of further treatment), theophyllin (initially), continuous infusion with lactated Ringer's solution, pimobendan, and the addition of enrofloxacin to the ongoing amoxicillin/clavulanic acid administration. After 4 days, the cat's general condition improved satisfactorily and blood pressure returned to normal range. Left ventricular hypertrophy resolved, however, diastolic dysfunction as well as left atrial dilation persisted. Within the next 8 weeks, echocardiographic findings and cardiac biomarkers returned to near normal values. All medication was tapered and finally discontinued. During the last recheck examination 7 months following initial presentation, no cardiac changes were apparent.

ACUTE NECROTIZING AND EOSINOPHILIC MYOCARDITIS IN A CHIMPANZEE (PAN TROGLODYTES).

Cardiac disease is of importance in captive chimpanzee (Pan troglodytes) health. Here we report an eosinophilic and necrotizing myocarditis in a 17-y-old chimpanzee with no previous history of cardiac disease that progressed to death within 48 h. Toxic and infectious causes were ruled out. The chimpanzee had eosinophilia at different occasions in previous years. The animal had a severe, diffuse, and acute monophasic necrotizing myocarditis, with a moderate lymphoplasmacytic infiltrate that was rich in eosinophils. Ante- and postmortem investigations are compatible with an unusual eosinophilic myocarditis with clinical evolution and morphology comparable with human eosinophilic myocarditis secondary to hypereosinophilic syndrome.