Objective-To correlate tissue distribution with development of lesions after experimental infection with a virulent strain of noncytopathic bovine viral diarrhea virus (BVDV) type 2 in calves. Animals-Ten 14-day-old and two 2-month-old colostrum-deprived calves. Procedure-Calves were intranasally inoculated with BVDV type-2 strain 1373 from an outbreak of clinically severe bovine viral diarrhea (BVD). Two 14-day-old calves served as noninfected controls. Two calves each were euthanatized on postinoculation days 3, 6, and 12, and 1 each on days 8, 9, 13, and 14. Tissues were collected for immunohistologic and histologic examination. Results-Inoculated calves developed nonspecific clinical signs characterized by high fever and decreased numbers of leukocytes and thrombocytes. Viral antigen was detected focally in lymphoid tissues on day 3. On days 6, 8, 9, 12, and 14, viral antigen became increasingly widespread throughout organs and tissues. Viral antigen in lymphoid tissues was associated with severe depletion of all compartments. Lesions in other tissues were not well correlated with distribution of viral antigen. Depletion of lymphoid tissues was observed in a calf on day 13, but viral antigen had been cleared from most tissues and was detected in vascular walls only. Conclusions and Clinical Relevance-Infection with a virulent BVDV strain resulted in wide dissemination of viral antigen in host tissues. Severe lymphoid depletion developed in lymphoid tissues, whereas viral antigen was generally not associated with lesions in other tissues. Findings suggest that development of lesions in acute BVD is not solely a function of viral replication and is also attributable to host reaction to infection.

Cells infected with bovine coronavirus (BCV) were solubilized with Triton X-100 to yield a cell lysate (CL) antigen having high hemagglutinating (HA) titers. The antigen gave high HA titers using rat erythrocytes, suggesting that it contained large amounts of hemagglutinin esterase (HE) antigen. The CL antigen, combined with an oil adjuvant, was tested for protective and antibody-inducing activities in cattle. Four groups (2 cattle/group) of cattle were inoculated with CL antigen having HA titers of 16 000, 4000, 1000, and 250. Another group served as untreated controls. Two intramuscular inoculations were given at an interval of 3 wk. The animals were challenged with virus 1 wk after the second inoculation. The groups immunized with the CL antigen having an HA titer of 4000 or 16 000 produced hemagglutination inhibition (HI) antibody titers of > 320 and serum neutralizing (SN) antibody titers of > 1280. These groups of animals showed no clinical abnormalities after challenge. In the groups immunized with CL antigen at an HA titer of 1000 or 250, HI antibody titers were 40 to 160 and SN titers were 80 to 640. The cattle with HI antibody titers of > or = 160 and the SN titers of > or = 640 showed no clinical signs, but the cattle with the HI antibody titer < 80 and the SN antibody titer < 160 developed watery diarrhea and fever after challenge. These results indicate that CL antigen with high HA titer induces antibody production in cattle that provides effective protection against winter dysentery.

The effect of a passive heat and moisture exchanger on tracheal and large airway temperature, as reflected by esophageal temperature at the thoracic inlet, was determined for 12 anesthetized and ventilated tumor-bearing dogs undergoing whole-body hyperthermia at 42 C. Delivered thermal dose to the esophagus and rectum during 120 minutes of whole-body hyperthermia was quantified as the thermal dose summary measure EQ43. The heat and moisture exchanger significantly increased esophageal EQ43 from 7.3 minutes to 12.1 minutes. Esophageal EQ43, however, remained lower than rectal EQ43. Although use of a heat and moisture exchanger improved esophageal temperature during whole-body hyperthermia, presumably through improved airway temperature, additional methods will be necessary to increase esophageal and airway temperature to the target value of 42 C.

We tested the hypothesis that lymphocytes from swine with susceptibility to malignant hyperthermia (MH) had calcium extrusion activity higher than unaffected swine. Cytoplasmic concentration of ionized calcium was determined by use of dual emission spectrofluorometry and measurement of the ratio of free to calcium-bound form of the fluorescent calcium dye indo-1. Net calcium accumulation and unidirectional calcium extrusion rate were dependent on intracellular calcium concentration. Calcium extrusion from calcium-loaded lymphocytes was monitored while calcium influx was inhibited by suspending the cells in calcium-free medium with a calcium chelator. Net calcium accumulation of untreated lymphocytes was monitored in calcium-replete medium. A novel method of calculation of ionized calcium was used. This method confirmed our previous findings of lower ionized calcium concentration (86 +/- 40 and 370 +/- 216 nmol/L; P < 0.01) and slower rates of calcium accumulation (39 +/- 16 and 127 +/- 52 nmol/L/min) in untreated lymphocytes from MH-susceptible swine compared with controls. These changes were attributable to calcium extrusion activity two- to three-fold higher in lymphocytes of MH-susceptible swine (154 +/- 36 and 408 +/- 47 nmol/L/min at 175 nmol/L; 972 +/- 111 and 1,690 +/- 505 nmol/L/min at 425 nmol/L). These data were compatible with our model of higher calcium extrusion activity being a compensatory adaptation of MH-susceptible swine lymphocytes to their hypersensitivity to stimuli that increase cytoplasmic calcium concentration.

A rare case is presented of a 58-year-old woman who developed ahepatic-bronchopleural fistula following a hydatid hepatic cyst complication. The hepatic-bronchopleural fistula was diagnosed when patient complained of severe repetitive attacks of productive cough of brown yellow to dark colour sputum biliptysis (bile in cough) with vomiting associated with night sweating and fever, for the past one month. She also complained of right side chest and abdominal pain for the past 3 years. This paper describes a unique case of hepatic-bronchopleural fistula caused by hydatid disease, emphasising the clinical feature and its surgical management. Hydatid disease is a zoonotic infection dueto the damage caused by Echinococcus granulosus. E. granulosus, also called the hydatid worm, hyper tape-worm or dog tapeworm, is a cyclophyllid cestode that parasitises the small intestine of canids as an adult, but which has important intermediate hosts such as livestock and humans, where it causes cystic echinococcosis, also known as hydatid disease. It is hoped thatthis case report will add to the meagre case management reports of hepaticbronchopleural fistula in literature.

A comprehensive study was conducted on the clinical observationsincluding clinical history, physical examination along with haematobiochemical alteration on 41 naturally occurring cases of canine babesiosis from Punjab state, India. Examination of 964 dogs revealed 4.25 percent (41/964) prevalence of the disease including 3.84 percent (37) B. gibsoni and 0.41 percent (4) B. canis infected cases. Clinical and parasitological diagnosis was finally confirmed by polymerase chain reaction. A large variation of clinical anifestations including rare findings of paraplegia, blindness, ocular bleeding, immune mediated haemolytic anaemia (IMHA), ascites and skin lesions were observed among the affected animals. Bloodfilms showed anisocytosis and nucleated erythrocytes indicating regenerative anaemia. Blood parameters of the affected dogs revealed significant decrease in Hb, TEC, PCV and thrombocytes. Significantdecrease in lymphocytes was found in B. gibsoni affected animals. The affected dogs showed significant increase in serum bilirubin, ALT, AKP, BUN and creatinine. Haemato-biochemical observations wereindicative of severity of babesiosis in dogs.

OBJECTIVE To determine clinical effects of CT-guided lumbosacral facet joint, transforaminal epidural, and translaminar epidural injections of methylprednisolone acetate in healthy dogs. ANIMALS 15 healthy Beagles. PROCEDURES Dogs were randomly assigned to 3 groups (5 dogs/group) and received a single CT-guided lumbosacral facet joint, transforaminal epidural, or translaminar epidural injection of methylprednisolone acetate (0.1 mg/kg). Contrast medium was injected prior to injection of methylprednisolone to verify needle placement. Neurologic examinations were performed 1, 3, 7, and 10 days after the injection. In dogs with neurologic abnormalities, a final neurologic examination was performed 24 days after the procedure. RESULTS Methylprednisolone injections were successfully performed in 14 of the 15 dogs. In 1 dog, vascular puncture occurred, and the methylprednisolone injection was not performed. No major or minor complications were identified during or immediately after the procedure, other than mild transient hyperthermia. During follow-up neurologic examinations, no motor, sensory, or postural deficits were identified, other than mild alterations in the patellar, withdrawal, cranial tibial, and perineal reflexes in some dogs. Overall, altered reflexes were observed in 11 of the 14 dogs, during 27 of 65 neurologic examinations. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that CT-guided lumbosacral facet joint, transforaminal epidural, and translaminar epidural injections of methylprednisolone acetate were associated with few complications in healthy dogs. However, the number of dogs evaluated was small, and additional studies are needed to assess clinical efficacy and safety of these procedures.

Objective: To determine whether increased gene expression of a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4) in laminae of horses with starch gruel–induced laminitis was accompanied by increased enzyme activity and substrate degradation. Sample: Laminae from the forelimb hooves of 8 healthy horses and 17 horses with starch gruel–induced laminitis (6 at onset of fever, 6 at onset of Obel grade 1 lameness, and 5 at onset of Obel grade 3 lameness). Procedures: Gene expression was determined by use of cDNA and real-time quantitative PCR assay. Protein expression and processing were determined via SDS-PAGE and quantitative western blotting. Protein distribution and abundance were determined via quantitative immunofluorescent staining. Results: ADAMTS-4 gene expression was increased and that of versican decreased in laminitic laminae, compared with expression in healthy laminae. Catalytically active ADAMTS-4 also was increased in the tissue, as were ADAMTS-4–cleavage fragments of versican. Immunofluorescent analyses indicated that versican was depleted from the basal epithelia of laminae of horses at onset of Obel grade 3 lameness, compared with results for healthy laminae, and this was accompanied by regional separation of basal epithelial cells from the basement membrane. Aggrecan gene and protein expression were not significantly affected. Conclusions and Clinical Relevance: Changes in gene and protein expression of ADAMTS-4 and versican in the basal epithelium of laminitic laminae indicated a fundamental change in the physiology of basal epithelial cells. This was accompanied by and may have caused detachment of these cells from the basement membrane.

Objective-To determine the comparative virulence of 5 isolates of bovine viral diarrhea virus (BVDV) type II by inoculating 6- to 9-month-old beef calves with isolates originating from the tissues of cattle affected with naturally occurring, transient, acute, nonfatal infections or naturally occurring, peracute, fatal infections. Animals-22 calves that were 6 to 9 months old. Procedure-The study used BVDV isolates 17011, 713, and 5521 that originated from fetuses aborted from cows with transient, nonfatal, acute BVDV infections and isolates 23025 and 17583 that originated from the tissues of cattle with peracute, fatal BVDV infections. Calves were allotted to 6 groups (1, mockinfected control calves [n = 2]; 2, inoculated with BVDV 17011 [4]; 3, inoculated with BVDV 713 [4]; 4, inoculated with BVDV 5521 [4]; 5, inoculated with BVDV 23025 [4]; and 6, inoculated with BVDV 17583 [4]). Rectal temperatures and clinical signs of disease were recorded daily. Total and differential WBC and platelet counts were performed. Histologic examination and immunohistochemical analysis were conducted to detect lesions and distribution of viral antigens, respectively. Results-Calves inoculated with BVDV 23025 or 17583 developed more severe clinical signs of disease (fever and diarrhea), more severe lymphopenia, and more severe lesions (alimentary epithelial necrosis, lymphoid depletion, and BVDV antigen deposition in lymphatic tissues), compared with calves inoculated with BVDV 713, 5521, or 17011. Conclusions and Clinical Relevance-Relative severity of experimentally induced infections corresponded to severity of clinical signs of naturally occurring infections with respective BVDV isolates.

The heart rate (HR) induced by maximal beta-adrenergic activation, which was elicited by infusion of isoproterenol, was studied in 8 healthy horses before (control) and after hyperthermia was induced by IV administration of 2,4-dinitrophenol (DNP). Isoproterenol was administered IV at 1.0 micrograms.kg-1.min-1 for 3 minutes and the HR was determined during the final 30 seconds of the infusion. As the rectal temperature increased (P < 0.001) from 38.2 +/- 0.1 C (mean +/- SEM; normothermic control) to 40.1 +/- 0.1 C at 60 minutes after DNP administration, the isoproterenol-induced HR also increased from 198 +/- 4 beats/min (control) to 214 +/- 4 beats/min (P < 0.001). It appeared that the values of HR achieved with maximal beta-adrenergic activation were augmented by the hypermetabolic, hyperthermic state induced by DNP.