Leukoencephalomyelopathy of mature captive cheetahs and other large felids: a novel neurodegenerative disease that came and went?

A novel leukoencephalomyelopathy was identified in 73 mature male and female large captive felids between 1994 and 2005. While the majority of identified cases occurred in cheetahs (Acinonyx jubatus), the disease was also found in members of 2 other subfamilies of Felidae: 1 generic tiger (Panthera tigris) and 2 Florida panthers (Puma concolor coryi). The median age at time of death was 12 years, and all but 1 cheetah were housed in the United States. Characteristic clinical history included progressive loss of vision leading to blindness, disorientation, and/or difficulty eating. Neurologic deficits progressed at a variable rate over days to years. Mild to severe bilateral degenerative lesions were present in the cerebral white matter and variably and to a lesser degree in the white matter of the brain stem and spinal cord. Astrocytosis and swelling of myelin sheaths progressed to total white matter degeneration and cavitation. Large, bizarre reactive astrocytes are a consistent histopathologic feature of this condition. The cause of the severe white matter degeneration in these captive felids remains unknown; the lesions were not typical of any known neurotoxicoses, direct effects of or reactions to infectious diseases, or nutritional deficiencies. Leukoencephalomyelopathy was identified in 70 cheetahs, 1 tiger, and 2 panthers over an 11-year period, and to our knowledge, cases have ceased without planned intervention. Given what is known about the epidemiology of the disease and morphology of the lesions, an environmental or husbandry-associated source of neurotoxicity is suspected.

IL-4(-/-) mice with lethal Mesocestoides corti infections--reduced Th2 cytokines and alternatively activated macrophages.

Protection against Mesocestoides corti, a cestode that invades vital organs, is dependent on the production of IL-4, as IL-4(-/-) mice were found to have higher parasite burdens when compared with wild-type mice. The goal of this study was to investigate the role of IL-4 in immunity to M. corti, focusing on the immunological profile and on potential mediators of pathology. IL-4(-/-) mice infected with M. corti showed 100% mortality by 32 days, whereas wild-type mice survived for approximately 1 year. Parasite burdens were significantly increased in the liver, peritoneal, and thoracic cavities of IL-4(-/-) mice, associated with impaired recruitment of inflammatory cells and a reduction in monocytes and macrophages. IL-5 production by splenocytes and expression in liver tissue was decreased in infected IL-4(-/-) mice compared with wild-type mice. In contrast, IL-4(-/-) mice produced increased amounts of IFNgamma and TNFalpha. Alternatively activated macrophages were a major feature of liver granulomas in wild-type mice evidenced by Arginase I expression, while livers from infected IL-4(-/-) mice showed impaired alternative macrophage activation without increased classical macrophage activation. Thus, lethality during M. corti infection of IL-4(-/-) mice is associated with decreased Th2 cytokines, increased Th1 cytokines and impairment of alternatively activated macrophages.

Polymicrogyria in standard poodles.

BACKGROUND: Polymicrogyria is a disorder of cerebrocortical migration resulting in increased numbers of small, disorganized gyri. This disorder occurs in Standard Poodles and in cattle. OBJECTIVES: To describe the clinical, electroencephalographic, imaging, and histopathologic features in poodles with polymicrogyria. ANIMALS: Five Standard Poodles with histologically confirmed polymicrogyria. METHODS: Retrospective case series. Cases were obtained by personal communication with 1 of 2 authors (TJVW, DPO). RESULTS: All dogs had cortical blindness and other neurologic abnormalities including gait and behavioral changes. Magnetic resonance imaging of 3 dogs showed multiple disorganized gyri, which were especially apparent on T2-weighted dorsal plane images. Electroencephalogram (EEG) of 1 dog revealed epileptiform discharges, including both spike and spike and wave discharges with voltage maximum potentials over the parietal/occipital region. The EEG supported that the repetitive behavior displayed by the dog was a complex partial motor seizure. One dog had concurrent hydrocephalus. All dogs had occipital lobe involvement and 2 dogs had involvement of other lobes. CLINICAL IMPORTANCE: The cases presented here demonstrate a larger age range (7 weeks to 5 years) and a decreased frequency of associated hydrocephalus when compared with the previous report.

Secondary intracranial neoplasia in the dog: 177 cases (1986-2003).

BACKGROUND: This study investigates the frequency, location, and clinical findings associated with 177 secondary brain tumors in dogs. HYPOTHESIS: Secondary intracranial neoplasia is more common than primary intracranial neoplasia in dogs during the time period studied, and hemangiosarcoma (HSA) is the most common secondary intracranial tumor. ANIMALS: One hundred and seventy-seven client-owned dogs presented to the Matthew J. Ryan Veterinary Hospital between 1986 and 2003. METHODS: Medical records were searched for a diagnosis of intracranial neoplasia in dogs who underwent complete postmortem examination. Of these dogs, those with a diagnosis of primary intracranial neoplasia were excluded. RESULTS: Of the 177 secondary brain tumors, 51 (29%) were HSAs, 44 (25%) were pituitary tumors, 21 (12%) were lymphosarcomas, and 21 (12%) were metastatic carcinomas. The average age at diagnosis was 9.6 +/- 3.0 years. Most tumors were located in the cerebrum, and a mentation change was the most common presenting clinical sign. On postmortem examination, the same tumor that was in the brain was also present in the lung in 84 cases (47%), in the kidney in 62 cases (35%), and in the heart in 55 cases (31%). CONCLUSIONS AND CLINICAL IMPORTANCE: Secondary intracranial neoplasia in dogs was more common than primary intracranial neoplasia during the time period studied. Many of these dogs had related disease in other body systems that was apparent on diagnostic tests such as thoracic radiography.

Interobserver Agreement Using Histological Scoring of the Canine Liver.

BACKGROUND: Grading schemes for the assessment of hepatic fibrosis and necroinflammatory activity in humans previously have been applied to dogs with chronic hepatitis. Interobserver agreement is a desirable characteristic for any histological scoring scheme. HYPOTHESIS/OBJECTIVES: To assess interobserver agreement associated with pathologists using a previously published histological scoring scheme to assess hepatic fibrosis and necroinflammatory activity in dogs and to compare fibrosis scores assigned to serial sections stained with hematoxylin & eosin (H&E) and picrosirius red. ANIMALS: Histological sections of liver from 50 dogs with variable degrees of hepatic fibrosis and necroinflammatory activity were selected from institutional tissue archives. METHODS: Six board-certified veterinary anatomic pathologists assigned fibrosis and necroinflammatory activity scores to the histological sections. The multiuser kappa statistic was calculated to assess interobserver agreement. Fibrosis stage assigned to serial sections stained with picrosirius red and H&E was compared using the Wilcoxon signed-rank test. RESULTS: Multiuser kappa statistics for assessment of fibrosis and necroinflammatory activity from H&E-stained sections were 0.35 and 0.16, respectively. There was no difference in median fibrosis scores assigned to serial section stained with H&E and picrosirius red (P = .248). CONCLUSIONS AND CLINICAL IMPORTANCE: There was fair interobserver agreement when pathologists assessed fibrosis and poor agreement when they assessed necroinflammatory activity. This suboptimal agreement must be taken into account by clinicians making decisions based on histology reports of the liver and in the design of studies evaluating these findings. To decrease this variability, ideally >1 pathologist should evaluate each section.

Magnetic resonance imaging observations of blood-brain-barrier permeability in an animal model of brain injury.

RATIONALE AND OBJECTIVES: Knowledge of the in vivo relaxivity of paramagnetic contrast agents is important in the accurate measurement of the permeability of the blood-brain barrier (BBB). This study was aimed at developing an animal model for the magnetic resonance (MR) imaging investigation of injuries to the BBB. METHODS: MR imaging (1.9 T) was performed in 18 rats with acute, stable injuries to the brain caused by freezing. After injection of gadodiamide (0.05-0.20 mmol/kg), estimates were made of BBB permeability, leakage space, and relaxivity (also measured in saline). RESULTS: The BBB was always disrupted at the injured site (permeability = 0.038 min-1 +/- 0.0006). The central area of necrosis and the periphery of edema showed substantial differences in leakage space and relaxivity. The relaxivity of gadodiamide was much greater at the injured site than in saline. CONCLUSION: The in vivo relaxivity at a site of pathologic change in the brain may be substantially greater than that measured in aquo.

Clinicopathological and immunophenotypical features of canine intravascular lymphoma (malignant angioendotheliomatosis).

Intravascular lymphoma (IVL) is a rare angiotropic large-cell lymphoma in which neoplastic lymphocytes proliferate within the lumina of blood vessels in the absence of a primary extravascular mass or leukaemia. A retrospective review of veterinary medical records identified 17 cases of canine IVL. Spinal cord ataxia (seven dogs), posterior paralysis (one dog), seizures (four dogs) and vestibular disease (three dogs) dominated the clinical presentation. Haemorrhage, ischaemia, and occasional foci of vascular proliferation were found in tissue sections from affected dogs. Vessels, predominantly veins, throughout the body were frequently filled with neoplastic lymphocytes. Splenic involvement occurred in only one of 10 cases examined and bone marrow involvement was absent in four cases examined. Formalin-fixed paraffin wax-embedded tissues from 15 cases were examined immunohistochemically with streptavidin-biotin-horseradish peroxidase and a catalysed signal amplification system. The neoplastic cells were classified in eight cases as T cells (CD3+/IgG-/CD79a-), in one case as B cells (CD3-/CD79a.dim/IgG+), and in the remaining six cases as non-T, non-B (CD3-/IgG-/CD79a-). The clinical and pathological features of canine IVL closely resembled those of the human disease. In striking contrast to human cases, which are most often B-cell lymphomas, the immunophenotypes of the canine IVLs in this series were heterogeneous. The canine IVLs were derived primarily from T cells and non-T, non-B lymphocytes, B cells being found in only a single instance.

Retrovirus-like activity in an immunosuppressed dog: pathological and immunological findings.

A putative retrovirus was isolated from a dog with a severe, acquired immunodeficiency-like syndrome. The haematological abnormalities and immunological deficiencies included anaemia, leucopenia (lymphopenia and neutropenia), thrombocytopenia, decreased humoral immunity, and ineffective T-cell responses in-vitro. The necropsy findings included generalized lymphoid depletion, severe bone marrow hypoplasia, plasmacytic infiltrates in lymphoid and non-lymphoid organs, and severe secondary infections. Supernates of peripheral blood mononuclear cell cultures from the affected dog contained an agent with manganese-dependent reverse transcriptase (RT) activity that sedimented at a density of 1.122 g/ml. RT activity was also found post-mortem in extracts prepared from the bone marrow, lymph nodes, and small intestine. The lymph nodes and small intestine expressed a 3.8 kb mRNA that was recognized by a bovine leukaemia virus (BLV) pol DNA probe by Northern blotting. DNA isolated from the lymph nodes and small intestine from the affected dog showed distinct band patterns by Southern analysis, suggesting an exogenous retrovirus. The retrovirus could be propagated in normal canine peripheral blood mononuclear cells or short-term canine lymphocyte cell lines in-vitro, and was cytopathogenic for cells of canine, but not human, origin. These results suggest the existence of a pathogenic canine retrovirus capable of producing disease of the type associated with retroviruses in other species.

Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976-1989).

Medical records and histologic sections of 40 cats with acute pancreatitis were reviewed. Two distinct groups of cats with pancreatitis were established by histologic analysis of tissue. Group 1 (32 cats) had acute pancreatic necrosis (APN). Group 2 (8 cats) had suppurative pancreatitis. Ages of affected cats ranged from 3 weeks to 16 years. The majority consisted of indoor cats of the Domestic Short-Haired breed but Siamese cats were over-represented relative to the general population (P < 0.05). Twenty-two percent of cats were obese and 57% were underweight. Thirty-eight percent of cats had acute disease. In the other cats, two stages in the progression of the disease were evident: (1) anorexia, weight loss, and lethargy, followed by (2) acute deterioration, development of shock, and a moribund state, despite fluid therapy. The most common clinical signs were severe lethargy (100%), reduced appetite (97%), dehydration (92%), and hypothermia (68%). The initial hemogram occasionally showed a neutrophilia (30%) and anemia (26%) but packed cell volume (PCV) decreased markedly to the extent that 55% of cats were anemic terminally. Serum biochemical abnormalities included increased activities of ALT (68%) and ALP (50%), and increased concentrations of bilirubin (64%) and cholesterol (64%). Cats with APN were hyperglycemic (64%), glycosuric (60%) and ketonuric (20%), whereas cats with suppurative pancreatitis tended to be hypoglycemic (75%). Renal failure and electrolyte abnormalities were mild or infrequent except for hypokalemia (56%). This study characterizes a severe necrotizing pancreatitis in the cat similar to that reported in other species, and a histologically distinct suppurative pancreatitis.

Cerebellar Purkinje's cell degeneration and coat color dilution in a family of Rhodesian Ridgeback dogs.

A syndrome of cerebellar Purkinje's cell degeneration and coat color dilution was diagnosed in a family of Rhodesian Ridgeback dogs. One male and 1 female from the same litter and 1 female from a different litter were evaluated for growth retardation, inability to ambulate, and progressive ataxia. On physical examination, lateral recumbency, severe ataxia, tremors, and diluted coat color were identified. Littermates with nondiluted coat color were neurologically normal. Results of routine laboratory tests, urine metabolic screenings, and karyotype analyses were normal. Histopathologic abnormalities at necropsy included cerebellar Purkinje's cell degeneration, reduced granular cell layer thickness, and uneven distribution of macromelanosomes within hair shafts. Pedigree analysis suggested an autosomal recessive mode of inheritance. This is the first description of a genetic syndrome affecting the central nervous system and associated with coat color dilution in dogs.

Study of long-term survival after transsphenoidal hypophysectomy in clinically normal dogs.

Experimental hypophysectomies were performed in 7 clinically normal dogs, using a new modification of the transsphenoidal approach. This approach facilitated centering of the sphenoid bone trephination and allowed safe exposure of the hypophysis regardless of the size or shape of a dog's skull. Complications did not occur during surgery and all dogs recovered well from surgery. Growth hormone secretory capacity was measured over a 3-month period to assess completeness of hypophysectomies. One dog was euthanatized 2 months after surgery, 4 dogs were euthanatized at 3 months after surgery, and 2 dogs were allowed to survive and their progress was followed for 2.5 years. Soft palate dehiscence and keratoconjunctivitis sicca developed in 2 of the dogs. The technical deficiencies responsible for these complications were corrected shortly after the beginning of the study. In 4 of the 5 necropsied dogs, minute remnants of adenohypophyseal tissue were found in the sellae turcica. Measurement of in vivo growth hormone secretory capacity revealed that these remnants had an altered stage of functional activity. Although complete hypophysectomy was not achieved consistently, the main technical obstacle of hypophysectomy, the reliable identification and the avoidance of the vascular structures surrounding the hypophysis, has seemingly been overcome. The surgical technique proved to enhance the safety of hypophysectomy, and the procedure can be recommended to treat clinical cases of canine pituitary-dependent hyperadrenocorticism. The clinical significance of potential subtotal hypophysectomy remains yet to be evaluated.

Cryptosporidiosis in young artiodactyls.

Cryptosporidium was found in the intestinal tract of 10 blackbuck, 2 scimitar-horned oryx, 2 fringe-eared oryx, 2 addax, and 1 sable antelope that had diarrhea. Cryptosporidia were most numerous in the small intestine, but also were found in the cecum, spiral colon, and colon. The small intestine had minimal inflammation in association with the cryptosporidia. Salmonella typhimurium was isolated from 10 of the 51 animals evaluated, with extensive inflammation of the cecum, spiral colon, and colon observed in these animals.

Clinical manifestations and associated disease syndromes in dogs with cranial vena cava thrombosis: 17 cases (1989-1996).

OBJECTIVE: To characterize cranial vena cava thrombosis in dogs with regard to signalment, clinical manifestation, potential inciting causes, treatment, and outcome. DESIGN: Retrospective study. ANIMALS: 17 dogs with a cranial vena cava thrombus. PROCEDURE: Medical and necropsy records were reviewed for signalment, potential causes of thrombus formation, diagnosis, clinicopathologic findings, treatment, and outcome. RESULTS: A signalment predisposition was not found. Ten dogs had cranial vena cava syndrome, and 10 had a pleural effusion. Ten dogs were dyspneic, and 5 had palpable jugular thrombi. Predisposing conditions identified were presumed immune-mediated hematologic disease and corticosteroid administration (6 dogs), sepsis (6), protein-losing nephropathy (2), neoplasia (2), and cardiac disease (1). Central venous catheterization was implicated as a contributing cause. Thrombocytopenia was the most consistent clinicopathologic finding, and ultrasonography was helpful in confirming the diagnosis. Treatment varied, but 15 of the 17 dogs died or were euthanatized within 20 days of clinical manifestation of the thrombus. At necropsy, thrombi were found in other organs, mainly the right atrium, jugular veins, and pulmonary arteries. CLINICAL IMPLICATIONS: Prognosis is poor for dogs with cranial vena cava thrombosis associated with clinical signs. Use of central venous catheters should be avoided in dogs with predisposing diseases such as immune-mediated disease, sepsis, protein-losing nephropathy, neoplasia, and cardiac disease.

Concurrent disorders in dogs with diabetes mellitus: 221 cases (1993-1998).

OBJECTIVE: To characterize concurrent disorders in dogs with diabetes mellitus (DM). DESIGN: Retrospective study. ANIMALS: 221 dogs with DM. PROCEDURE: Medical records were reviewed, and clinical signs, physical examination findings, and results of clinicopathologic testing, urinalysis, aerobic bacterial culture of urine samples, coagulation testing, endocrine testing, histologic evaluation, diagnostic imaging, and necropsy were recorded. RESULTS: For most dogs, CBC results were normal. Common serum biochemical abnormalities included hypochloremia (127 dogs, 60%) and high alanine aminotransferase (163, 78%), aspartate aminotransferase (78, 71%), and alkaline phosphatase (188, 90%) activities. Venous pH and serum ionized calcium concentration were measured in 121 and 87 dogs, respectively, and were low in 56 (46%) and 41 (47%) dogs. Lipemia was observed in 92 (42%) dogs. Urine samples from 159 (72%) dogs were submitted for aerobic bacterial culture, and 34 (21%) yielded bacterial growth. Escherichia coli was the most commonly isolated organism. Thirty-six (16%) dogs had dermatitis or otitis. Hyperadrenocorticism was diagnosed in 51 (23%) dogs on the basis of clinical signs and results of a low-dose dexamethasone suppression test (41 dogs), an adrenocorticotropic hormone stimulation test (5), both tests (4), or histologic evaluation of necropsy specimens (1). Acute pancreatitis was diagnosed in 28 (13%) dogs. Eleven (5%) dogs had tumors for which a histologic diagnosis was obtained. Eight (4%) dogs were hypothyroid. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that dogs with diabetes mellitus may have many concurrent disorders. The most commonly identified concurrent disorders included hyperadrenocorticism, urinary tract infection, dermatitis, otitis, acute pancreatitis, neoplasia, and hypothyroidism.

Myocardial infarction in dogs and cats: 37 cases (1985-1994).

OBJECTIVE: To determine the incidence of acute and subacute myocardial infarction on postmortem examination, identify associated diseases, and evaluate clinical or diagnostic indicators of myocardial infarction in dogs and cats. DESIGN: Retrospective study. ANIMALS: 32 dogs and 5 cats. PROCEDURE: Records from the necropsy service from December 1985 through August 1994 were searched for dogs and cats in which acute or subacute myocardial infarction was diagnosed on postmortem examination. Clinical records were reviewed for signalment, initial owner complaint, medical history, results of physical examination, electrocardiography, radiography, echocardiography, CBC, serum chemistry analysis, urinalysis, and coagulation profile as well as clinical course, outcome, necropsy findings, and results of histologic evaluation. RESULTS: Initial owner complaints and physical examination findings were consistent with associated diseases. Electrocardiographic abnormalities in dogs included ventricular tachycardia (16%), atrial fibrillation (9%), and premature ventricular contractions (6.5%). Premature ventricular contractions were noticed in 2 cats. Echocardiography revealed dilated, poorly contractile hearts (n = 3) and thickened mitral valves (2) in dogs, and ventricular hypertrophy (3) in cats. Ninety-seven percent of dogs had infarction of the left ventricle as well as other other portions of the heart. Infarctions in cats were found in all parts of the myocardium including the right ventricle (n = 3), left ventricle (3), and interventricular septum (1). CLINICAL IMPLICATIONS: Myocardial infarction is rare in dogs and cats. It is associated with a number of common diseases and may contribute to morbidity and mortality in those dogs and cats that are critically ill.

Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986-1995).

OBJECTIVE: To determine clinical, clinicopathologic, radiographic, ultrasonographic, and coagulation abnormalities in dogs in which acute pancreatitis was fatal. DESIGN: Retrospective study. ANIMALS: 70 dogs. PROCEDURE: History, clinical signs, and physical examination findings at the time of initial evaluation at the veterinary teaching hospital; results of pretreatment laboratory tests, abdominal radiography, and ultrasonography; and histologic abnormalities were obtained from medical records. RESULTS: Clinical signs included anorexia, vomiting, Weakness, diarrhea, polyuria and polydipsia, neurologic abnormalities, melena, weight loss, hematemesis, and passage of frank blood in feces. At the time of initial examination at the veterinary teaching hospital, 68 (97%) dogs were dehydrated, 18 (26%) were icteric, 22 (32%) were febrile, 40 (58%) had signs of abdominal pain, and 30 (43%) were classified as overweight or obese. Most dogs had leukocytosis, neutrophilia with a left shift, and thrombocytopenia. Various serum biochemical abnormalities were identified, including hypoglycemia, azotemia, hypercalcemia and other electrolyte abnormalities, hypoalbuminemia, high hepatic and pancreatic enzyme activities, hypercholesterolemia, and lipemia. For 17 of 28 (61%) dogs, results of coagulation function tests were abnormal. Results of abdominal ultrasonography and radiography were consistent with a diagnosis of acute pancreatitis in 23 of 34 (68%) and 10 of 41 (24%) dogs, respectively. For 2 dogs, results of abdominal ultrasonography were not suggestive of acute pancreatitis, but results of abdominal radiography were. CLINICAL IMPLICATIONS: Clinical signs and results of clinicopathologic tests are inconsistent. Abdominal ultrasonography may be valuable in the diagnostic evaluation of dogs suspected to have acute pancreatitis.

Clinical and clinicopathologic findings in dogs with acute respiratory distress syndrome: 19 cases (1985-1993).

OBJECTIVE: To describe clinical and clinicopathologic findings from dogs with histologic pulmonary lesions consistent with human adult respiratory distress syndrome and to identify potential factors. DESIGN: Retrospective study. ANIMALS: 19 dogs with acute respiratory distress. PROCEDURE: Medical records of dogs were reviewed. Signalment, physical examination and clinicopathologic findings at admission, and thoracic radiographic and necropsy findings were recorded. RESULTS: The most common clinical sign was dyspnea. Respiratory rate ranged from 36 to 140 breaths/min and abnormal breathing patterns were detected. Crackles were auscultated in 7 dogs. Severe diffuse interstitial and alveolar infiltrates were observed on thoracic radiography in 9 dogs shortly after arrival and developed later in 4 dogs. Four dogs were leukopenic and neutropenic. Disseminated intravascular coagulation was diagnosed in 2 dogs, and hypoalbuminemia was found in 8 dogs. Respiratory status deteriorated rapidly in all dogs, and 10 dogs were mechanically ventilated. Death was attributed solely to respiratory failure in 8 dogs. In the other 11 dogs, severe lesions in nonpulmonary organs, sepsis, or both may have contributed to death. The most common associated conditions that may have contributed to acute respiratory failure were microbial pneumonia, sepsis, aspiration pneumonia, and shock, with more than 1 factor found in 11 of 19 dogs. CLINICAL IMPLICATIONS: The index of suspicion for acute respiratory distress syndrome should be high in dogs with bilateral pulmonary infiltrates and acute respiratory distress that rapidly progresses to failure.

Respiratory function and treatment in dogs with acute respiratory distress syndrome: 19 cases (1985-1993).

OBJECTIVE: To characterize respiratory function and treatment in dogs with findings compatible with those of human adult respiratory distress syndrome (ARDS) and to evaluate the application in dogs of clinical for diagnosis of ARDS. DESIGN: Retrospective review of medical records. ANIMALS: 19 dogs with acute respiratory distress syndrome. RESULTS: Arterial blood pH was 7.30 +/- 0.59 (mean +/- SD). Nine dogs had metabolic acidosis. In nonmechanically ventilated dogs, PaCO2 was 15.0 to 54.9 mm of Hg. Respiratory acidosis developed in 2 mechanically ventilated dogs. Hypoxemia was observed in 4 of 5 dogs breathing room air. In 4 mechanically ventilated dogs, oxygenation was inadequate, despite use of > 60% inspired O2 and positive end-expiratory pressure in 3 dogs. Alveolar-to-arterial oxygen tension gradients were widened in 4 dogs breathing room air and in 6 dogs ventilated with 100% O2. Ten dogs were mechanically ventilated; ventilatory rate was 18 to 60 breaths/min. Tidal volume was 12 +/- 3.8 ml/kg of body weight in 4 dogs, minute ventilation > 400 ml/kg/min in 2 dogs, and peak airway pressures > 25 cm of H2O in 6 dogs. Positive end-expiratory pressure was used in 8 dogs. Pneumothorax was detected in 5 ventilated dogs. Human clinical criteria for diagnosis of ARDS were fulfilled in 7 dogs. Fluid treatment consisted of IV crystalloids and synthetic colloids. Drugs most often administered were antibiotics and loop diuretics. CLINICAL IMPLICATIONS: Human clinical criteria for identification of ARDS may be helpful in diagnosis of acute respiratory distress syndrome in dogs.

Severe sepsis in cats: 29 cases (1986-1998).

OBJECTIVE: To document the clinical, clinicopathologic, and pathologic findings in cats with severe sepsis, identify abnormalities unique to this species, and identify criteria that could be used antemortem to diagnose the systemic inflammatory response syndrome in cats. DESIGN: Retrospective study. ANIMALS: 29 cats confirmed to have severe sepsis at necropsy. PROCEDURE: Pertinent history, physical examination findings, and results of hematologic and biochemical testing were extracted from medical records. RESULTS: Clinical diagnoses included pyothorax, septic peritonitis, bacteremia secondary to gastrointestinal tract disease, pneumonia, endocarditis, pyelonephritis, osteomyelitis, pyometra, and bite wounds. Physical examination findings included lethargy, pale mucous membranes, poor pulse quality, tachypnea, hypo- or hyperthermia, signs of diffuse pain on abdominal palpation, bradycardia, and icterus. Clinicopathologic abnormalities included anemia, thrombocytopenia, band neutrophilia, hypoalbuminemia, low serum alkaline phosphatase activity, and hyperbilirubinemia. Necropsy findings included multi-organ necrosis or inflammation with intralesional bacteria. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that severe sepsis in cats is characterized by lethargy, pale mucous membranes, signs of diffuse abdominal pain, tachypnea, bradycardia, weak pulses, anemia, hypoalbuminemia, hypothermia, and icterus. Recognition of this combination of clinical findings should facilitate the diagnosis of severe sepsis in cats.

Evaluation of risk factors for fatal acute pancreatitis in dogs.

OBJECTIVE: To identify risk factors associated with fatal acute pancreatitis in dogs. DESIGN: Case-control study. ANIMALS: 70 case dogs with clinical evidence and histopathologic confirmation of fatal acute pancreatitis and 104 control dogs that had trauma, underwent necropsy, and did not have histologic evidence of acute pancreatitis. PROCEDURE: Information on signalment, weight, body condition, medical history, concurrent disease, and results of histopathologic examination was obtained by reviewing medical records. Logistic regression analysis included calculation of univariate and multivariate (adjusted) odds ratios and 95% confidence intervals. RESULTS AND CLINICAL IMPLICATIONS: Dogs with fatal acute pancreatitis were largely middle- to older-aged dogs. Risk of developing fatal acute pancreatitis was increased by overweight body condition, diabetes mellitus, hyperadrenocorticism, hypothyroidism, prior gastrointestinal tract disease, and epilepsy. Additionally, Yorkshire Terriers were at increased risk, and Labrador Retrievers and Miniature Poodles were at decreased risk, of developing fatal acute pancreatitis. Males and neutered females appeared to have an increased risk of developing fatal acute pancreatitis, compared with sexually intact females. Thrombus formation was more likely in dogs that developed fatal acute pancreatitis than in control dogs.