Objective-To establish an immortalized cell line and transplantable xenograft of feline bronchioloalveolar lung carcinoma (BAC). Sample Population-Pleural effusion from a 12-yearold Persian male cat with BAC. Procedure-Tumor cells from the pleural effusion were grown in monolayer cell culture and injected into severe combined immunodeficient (SCID) mice to establish an immortalized cell line as well as a transplantable xenograft. Results-Both the primary lung carcinoma, the derived cell line, and the transplantable xenograft had evidence of a type-II pneumocyte origin expressing lamellar bodies ultrastructurally and thyroid transcription factor-1 and surfactant immunocytochemically. All 3 also expressed nuclear p53 immunoreactivity. A metaphase spread of the cell line (SPARKY) probed with fluorescein-labeled genomic feline DNA gave evidence of its feline origin. Flow cytometric studies indicated aneuploidy with a DNA index of 1.6. An R-banded karyotype revealed a modal number of 66 including the feline Y chromosome. The cell line had a doubling time of 16 hours. The xenograft (SPARKY-X) reached a diameter of 1 cm in 3 weeks in SCID mice. Deoxyribonucleic acid fingerprint analysis revealed that SPARKY and SPARKY-X were novel and strongly matched each other, except for the murine component found in SPARKY-X. Interestingly, SPARKY-X manifested the characteristic lepidic growth pattern of pulmonic BAC. Conclusions-Both the cell line and xenograft retained their autochthonous BAC phenotype, making them useful for the subsequent dissection of molecular abnormalities in feline BAC and in vitro screening of chemotherapeutic agents.

Objective-To determine whether cats exposed at a residence were infected with Mycobacterium bovis, whether the tuberculin skin test can identify cats infected with M bovis, and whether an ELISA could identify tuberculosis-infected cats. Animals-20 domestic cats exposed to a cat with laboratory-confirmed disseminated M bovis infection. Procedure-Cats were administered a tuberculin skin test and monitored for 72 hours. Blood and fecal samples were collected. Cats were then euthanatized, and postmortem examinations were performed. Tissues were examined grossly and histologically for signs of mycobacteriosis. Pooled tissue samples and fecal samples were submitted for mycobacterial culture. Blood samples were examined for evidence of tuberculosis by use of a comparative ELISA. Results-4 cats had positive responses for the ELISA, and 2 cats had suspicious responses. All tuberculin skin tests yielded negative results. No gross or histologic lesions of tuberculosis were detected in any tissues, and mycobacteria were not isolated from tissues or feces obtained from the 20 cats. Conclusions and Clinical Relevance-All cats that had positive or suspicious responses for the ELISA were offspring of the cat with tuberculosis. Evidence of tuberculosis was not seen in other cats at the residence, the owner, or the attending veterinarian. The most likely source of tuberculosis for the infected cat was through the consumption of M bovis-infected wildlife carcasses or offal. Because M bovis is endemic in wildlife in northeastern Michigan, there is a risk of exposure to tuberculosis in companion animals, their owners, and attending veterinarians.

Objective-To determine whether Haemobartonella canis and Mycoplasma haemofelis (formerly known as H felis [large form]) can be differentiated by use of comparative analysis of gene sequences. Sample Population-Blood samples obtained from 3 dogs infected with H canis and 2 cats infected with M haemofelis. Procedure-The partial 16S rDNA and ribonuclease P RNA (RNase P) genes were amplified, cloned, and sequenced in blood samples obtained from H canis-infected dogs and M haemofelis-infected cats. The DNA sequences were subjected to comparative analysis. Results-The 16S rDNA sequences of H canis and M haemofelis were nearly identical (homology of 99.3 to 99.7%). In contrast, RNase P gene sequences had a lower degree of sequence homology between the 2 organisms (94.3 to 95.5%). Conclusions and Clinical Relevance-Haemobartonella canis and M haemofelis are not identical organisms. Molecular differentiation of H canis and M haemofelis is more clearly evident by use of comparative analysis of RNase P gene sequences than by comparative analysis of 16S rDNA gene sequences.

Objective-To determine tracheal mucociliary clearance rate (TMCCR) by use of a standard protocol in healthy anesthetized cats and to determine the effect of theophylline on TMCCR in healthy anesthetized cats. Animals-6 healthy cats. Procedure-Cats were anesthetized with propofol, and a droplet of the radiopharmaceutical technetium Tc 99m macroaggregated albumin was placed endoscopically at the carina. Dynamic acquisition scintigraphic imaging was performed, using the larynx as the end point. The TMCCR was determined by measuring the distance the droplet traveled by frame rate. Each cat was imaged 6 times as follows: 3 times following placebo administration and 3 times following the administration of sustained release theophylline (25 mg/kg, PO). Serum theophylline concentrations were assessed during imaging to ensure therapeutic concentrations. Results-The TMCCR in healthy adult cats anesthetized with propofol was 22.2 +/- 2.8 mm/min. Tracheal mucociliary clearance rate in cats receiving theophylline was 21.8 +/- 3.5 mm/min. Theophylline administration did not significantly alter TMCCR. Conclusion and Clinical Relevance-Theophylline has been shown to increase TMCCR in humans and dogs. In our study, we determined TMCCR in healthy anesthetized cats and found that it was not accelerated by the administration of theophylline.

Objective-To determine total glutathione (GSH) and glutathione disulfide (GSSG) concentrations in liver tissues from dogs and cats with spontaneous liver disease. Sample Population-Liver biopsy specimens from 63 dogs and 20 cats with liver disease and 12 healthy dogs and 15 healthy cats. Procedure-GSH was measured by use of an enzymatic method; GSSG was measured after 2-vinylpyridine extraction of reduced GSH. Concentrations were expressed by use of wet liver weight and concentration of tissue protein and DNA. Results-Disorders included necroinflammatory liver diseases (24 dogs, 10 cats), extrahepatic bile duct obstruction (8 dogs, 3 cats), vacuolar hepatopathy (16 dogs), hepatic lipidosis (4 cats), portosystemic vascular anomalies (15 dogs), and hepatic lymphosarcoma (3 cats). Significantly higher liver GSH and protein concentrations and a lower tissue DNA concentration and ratio of reduced GSH-to-GSSG were found in healthy cats, compared with healthy dogs. Of 63 dogs and 20 cats with liver disease, 22 and 14 had low liver concentrations of GSH (µmol) per gram of tissue; 10 and 10 had low liver concentrations of GSH (nmol) per milligram of tissue protein; and 26 and 18 had low liver concentrations of GSH (nmol) per microgram of tissue DNA, respectively. Low liver tissue concentrations of GSH were found in cats with necroinflammatory liver disease and hepatic lipidosis. Low liver concentrations of GSH per microgram of tissue DNA were found in dogs with necroinflammatory liver disease and cats with necroinflammatory liver disease, extrahepatic bile duct occlusion, and hepatic lipidosis. Conclusions and Clinical Relevance-Low GSH values are common in necroinflammatory liver disorders, extrahepatic bile duct occlusion, and feline hepatic lipidosis. Cats may have higher risk than dogs for low liver GSH concentrations.

Objective-To provide an epidemiologic investigation of the seroprevalence of antibodies to Toxoplasma gondii in populations of cats and wild rodents in Rhode Island and to address the possible epidemiologic role of wild rodents in the spread of toxoplasmosis. Animals-200 cats and 756 small wild rodents. Procedure-Serum samples were obtained from 84 cats in animal shelters and 116 cats in veterinary hospitals. Serum samples were also obtained from 756 small wild rodents from multiple sites in Rhode Island. Sera from rodents and cats were assayed for antibodies to T gondii by use of the modified agglutination test Results-Overall, 42% (84/200) of cats had serum antibodies to T gondii. Seroprevalence was not significantly different between stray (50%; 42 /84) versus client-owned (36%; 42/116) cats, between male (43%; 40/94) versus female (42%; 39/93) cats, or between indoor (26%; 7/27) versus outdoor (39%; 35/89) cats. Seroprevalence rate of trapped rodents was 0.8% (6/756). Six rodents captured in Washington County accounted for of the seropositive rodents. Four of 6 of the seropositive rodents were trapped at a single site in Washington County (an abandoned barn). Five stray cats, known to have resided at the same site in Washington County as 4 of the seropositive rodents, were also found to be seropositive for antibodies to T gondii. Conclusions and Clinical Relevance-Seroprevalence rate in rodents was not correlated with the seroprevalence rate in cats. Stray cats, especially those known to be feral, may be more likely to perpetuate the cat-mouse cycle of T gondii than clientowned cats.

Objective-To evaluate splenic mast cell tumors (MCT) of cats for activating mutations in the protooncogene c-kit. Sample Population-10 formalin-fixed, paraffinembedded splenic MCT from cats in the pathology database of the Veterinary Medical Teaching Hospital at the University of California, Davis. Procedure-Genomic DNA was isolated from tumor specimens, and the polymerase chain reaction (PCR) procedure was performed for exons 11, 12, and 17. The PCR products were analyzed by use of agarose gel electrophoresis and then directly sequenced. Results-We did not identify mutations in the juxtamembrane domain (encoded by exons 11 and 12) or catalytic domain (encoded by exon 17) of c-kit in any of the splenic MCT specimens. Conclusions and Clinical Relevance-Although mutations in the proto-oncogene c-kitoccur frequently in naturally developing MCT in dogs and aggressive mastocytosis in humans, the data reported here documented that dysregulation of Kit function through activating mutations is unlikely in splenic MCT of cats. Therapeutic strategies aimed at inhibiting Kit signaling (ie, kinase inhibitors such as imatinib [STI571]) may not be of benefit for the treatment of this disease in cats.

Objective- To determine the hemodynamic effects of IM administration of romifidine hydrochloride in propofol-anesthetized cats. Animals-15 adult domestic shorthair cats. Procedure-Cats were randomly assigned to receive romifidine (0, 400, or 2,000 µg/kg, IM). Cats were anesthetized with propofol and mechanically ventilated with oxygen. The right jugular vein, left carotid artery, and right femoral artery and vein were surgically isolated and catheterized. Heart rate; duration of the PR, QRS, and QT intervals; mean pulmonary artery pressure; mean right atrial pressure; systolic, diastolic, and mean arterial pressures; left ventricular systolic pressure; left ventricular end-diastolic pressure; and cardiac output were monitored. Systemic vascular resistance, rate of change of left ventricular pressure, and rate pressure product were calculated. Arterial and venous blood samples were collected anaerobically for determination of pH and blood gas tensions (PO2 and PCO2). Results-Administration of romifidine at 400 and 2,000 µg/kg, IM, decreased heart rate, cardiac output, rate of change of left ventricular pressure, rate pressure product, and pH. Arterial and pulmonary artery pressures, left ventricular pressure, left ventricular end-diastolic pressure, and right atrial pressure increased and then gradually returned to baseline values. Arterial blood gas values did not change, whereas venous PCO2 increased and venous PO2 decreased. Significant differences between low and high dosages were rare, suggesting that the dosages investigated produced maximal hemodynamic effects. Conclusion and Clinical Relevance-Romifidine produces cardiovascular effects that are similar to those of other α2-agonists. High dosages of romifidine should be used with caution in cats with cardiovascular compromise.

Objective-To determine whether opioids with varying interactions at receptors induce a reduction in minimum alveolar concentration (MAC) of isoflurane in cats. Animals-12 healthy, female, spayed cats. Procedure-Cats were anesthetized with isoflurane and instrumented to allow collection of arterial blood and measurement of arterial blood pressure. Each drug was studied separately, and for each drug cats were randomly allocated to receive 2 doses. The drugs studied were morphine (0.1 or 1.0 mg/kg), butorphanol (0.08 or 0.8 mg/kg), buprenorphine (0.005 and 0.05 mg/kg), and U50488H (0.02 and 0.2 mg/kg). All drugs were diluted in 5 ml of saline (0.9% NaCl) solution and infused IV for 5 minutes. The MAC of isoflurane was determined in triplicate, the drug administered, and the MAC of isoflurane redetermined for a period of 3 hours. Results-All drugs had a significant effect on MAC over time. With morphine only, the effect on MAC over time was different between doses. The greatest mean (+/- SD) reductions in MAC of isoflurane in response to morphine, butorphanol, buprenorphine, and U50488H administration were 28 +/- 9, 19 +/- 3, 14 +/- 7, and 11 +/- 7%, respectively. Conclusions and Clinical Relevance-Morphine (1.0 mg/kg) and butorphanol (0.08 and 0.8 mg/kg) induced significant reductions in MAC of isoflurane that were considered clinically important. Although significant, reductions in MAC of isoflurane induced by morphine (0.1 mg/kg), buprenorphine (0.005 and 0.05 mg/kg), and U50488H (0.02 and 0.2 mg/kg) were not considered clinically relevant because they fell within the error of the measurement technique. Administration of morphine or butorphanol decreases the need for potent inhalant anesthetics in cats and could potentially be beneficial in combination with inhalants.

Objective-To investigate the effects of preexisting FeLV infection or FeLV and feline immunodeficiency (FIV) coinfection on the pathogenicity of the small variant of Haemobartonella felis (Hfsm, California variant) in cats. Animals-20 FeLV infected, 5 FeLV-FIV coinfected, and 19 retrovirus-free cats. Procedure-A client-owned cat, coinfected with FeLV and Hfsm, was the source for Hfsm. Inoculum 1 (FeLV free) was obtained by passage of source Hfsm through 4 FeLV-resistant cats. Inoculum 2 was obtained by further passage of Hfsm (inoculum 1) through 2 specific pathogenfree cats. Results-A mild-to-moderate anemia started 21 days after inoculation, with its nadir occurring at 35 to 42 days after inoculation. Infection with Hfsm induced greater decrease in hemoglobin concentration in FeLV infected cats, compared with retrovirus free cats. Reticulocytosis, macrocytosis, and polychromasia of erythrocytes developed in anemic cats regardless of retrovirus infection status. Mean neutrophil counts decreased during the hemolytic episode. For most cats, the anemia was transient. Four FeLV infected cats, 1 of which was also FIV infected, developed fatal FeLV-associated myeloproliferative diseases. Of the surviving cats, 8 died over the next 24 months from other FeLV-related diseases. Hemolysis did not recur after the initial episode. Inoculum 1 induced more severe anemia than inoculum 2. Conclusions and Clinical Relevance-Our results support the clinical observation that cats coinfected with FeLV and H felis develop more severe anemia than cats infected with H felis alone. Infection with Hfsm may induce myeloproliferative disease in FeLV infected cats. The small variant of H felis may lose pathogenicity by passage through FeLV-free cats.