Failure to spread bovine virus diarrhoea virus infection from primarily infected calves despite concurrent infection with bovine coronavirus

Previous reports on the spread of bovine virus diarrhoea virus (BVDV) from animals primarily infected with the agent are contradictory. In this study, the possibility of transmission of BVDV from calves simultaneously subjected to acute BVDV and bovine coronavirus (BCV) infection was investigated. Ten calves were inoculated intranasally with BVDV Type 1. Each of the 10 calves was then randomly allocated to one of two groups. In each group there were four additional calves, resulting in five infected and four susceptible calves per group. Virulent BCV was actively introduced in one of the groups by means of a transmitter calf. Two calves, susceptible to both BVDV and BCV, were kept in a separate group, as controls. All ten calves actively inoculated with BVDV became infected as shown by seroconversions, and six of them also shed the virus in nasal secretions. However, none of the other eight calves in the two groups (four in each) seroconverted to this agent. In contrast, it proved impossible to prevent the spread of BCV infection between the experimental groups and consequently all 20 study calves became infected with the virus. Following infection, BCV was detected in nasal secretions and in faeces of the calves and, after three weeks in the study, all had seroconverted to this virus. All calves, including the controls, showed at least one of the following clinical signs during days 3-15 after the trial started: fever (> or =40 degrees C), depressed general condition, diarrhoea, and cough. The study showed that BVDV primarily infected cattle, even when co-infected with an enteric and respiratory pathogen, are inefficient transmitters of BVDV. This finding supports the principle of the Scandinavian BVDV control programmes that elimination of BVDV infection from cattle populations can be achieved by identifying and removing persistently infected (PI) animals, i.e. that long-term circulation of the virus without the presence of PI animals is highly unlikely.     

Studies on the pathogenesis of chicken infectious anaemia virus infection in six-week-old SPF chickens

The pathogenesis of chicken infectious anaemia virus (CAV) infection was studied in 6-week-old and one-day-old SPF chickens inoculated intramuscularly with graded doses of Cux-1 strain (10(6)-10(2) TCID50/chicken). Viraemia, virus shedding, development of virus neutralizing (VN) antibodies and CAV distribution in the thymus were studied by virus isolation, polymerase chain reaction (PCR), immunocytochemistry (IP) and in situ hybridization until postinfection day (PID) 28. In 6-week-old chickens infected with high doses of CAV, viraemia and VN antibodies could be detected 4 PID and onward without virus shedding or contact transmission to sentinel birds. However, virus shedding and contact transmission were demonstrated in one-day-old infected chickens. In the 6-week-old groups infected with lower doses, VN antibodies developed by PID 14, transient viraemia and virus shedding were detected. The thymus cortex of all 1-day-old inoculated chickens stained with VP3-specific mAb. Cells with positive in situ hybridization signal were fewer and scattered throughout the thymus tissue of the one-day-old inoculated chickens as compared to IP-positive cells. These results suggest that early immune response induced by high doses of CAV in 6-week-old chickens curtails viral replication and prevents virus shedding.     

RADIOGRAPHIC ANATOMY OF THE CRIBRIFORM PLATE (LAMINA CRIBROSA)

The radiographic appearance of the cribriform plate was investigated in 16 canine cadaver heads. The cribriform plate appeared as a "V"-shaped multilinear bone-opaque stripe in the caudal nasal region in projections perpendicular to the hard palate in 6 dogs with a skull index between 50.00 and 54.00. In 9 dogs with a skull index between 55.40 and 74.40, the cribriform plate had a more "C"-shaped and sharp appearance. In vertically oblique projections with an obliquity greater than 20 degrees, the cribriform plate lost its sharp outline and finally (40 degrees) disappeared. In lateral projections the cribriform plate appeared as a "C"-shaped interrupted bone-opaque stripe in all 16 dogs. In more brachycephalic dogs frontal bone structures superimposed on the cribriform plate on ventrodorsal and dorsoventral views and accentuated the radiographic appearance of the plate. Vertically oblique views separated both structures to produce two lines.     

Baclofen intoxication in a dog successfully treated with hemodialysis and hemoperfusion coupled with intensive supportive care

Objective: To describe a case of confirmed baclofen intoxication in a dog that was successfully treated with hemodialysis and hemoperfusion (HD/HP) and to report the serum baclofen kinetics. Case summary: A 2.5‐year‐old, 23 kg, spayed female Brittany Spaniel‐mix was treated after ingesting 21‐52 mg/kg of baclofen. The dog was comatose and was receiving manual ventilation at the time of presentation. Extracorporeal HD/HP was started 10 hours after admission. Within 3 hours of starting HD/HP the dog began initiating breaths and was extubated 18 hours after admission. Serial serum samples that were obtained during the first 24 hours of hospitalization were later analyzed for baclofen concentrations. The dog had elevated creatine phosphokinase and liver enzymes that correlated with an agitated recovery period. The dog had thrombocytopenia that resolved by 10 days after presentation. New or unique information provided: HD/HP shortened the baclofen serum elimination half‐life from 5 to 1.5 hours in the initial 2 hours of treatment. The intrinsic elimination rate constant (K_intr) for this dog was 0.138/hour and the total elimination rate constant (K_tot) during the first 2 hours of HD/HP treatment was 0.458/hour. In this dog, HD/HP was an effective method for rapidly decreasing serum baclofen concentration after an acute overdose.     

Plasma atrial natriuretic peptide concentration in warmblood horses with heart valve regurgitations

ObjectivesThis study measured plasma atrial natriuretic peptide (ANP) concentration in horses with heart valve regurgitations (HVR) with and without atrial and ventricular dilatation.BackgroundIn humans and small animals, plasma ANP concentration is increased in heart disease and correlates with the severity of clinical signs and heart enlargement.Animals, materials and methodsTen healthy horses (control) and 36 horses with HVR were evaluated by auscultation, electrocardiography, echocardiography, and determination of plasma ANP.ResultsControl horses demonstrated mean plasma ANP concentration of 21 ± 5.4 pg/mL. Of the 36 horses with HVR, 17 horses possessed normal echocardiographic heart size (group 1), 10 horses had a left atrial dilatation (group 2) and 9 horses had both left atrial and ventricular dilatation (group 3). Mean plasma ANP concentration of groups 1, 2 and 3 was 20.1 ± 5.6 pg/mL, 22.9 ± 11.0 pg/mL and 27.6 ± 17.4 pg/mL, respectively. The plasma ANP concentrations of HVR and control horses were not significantly different. The highest ANP concentrations were observed in horses with atrial and ventricular dilatation. No correlation between left atrial or ventricular size, weight, or sex and the plasma ANP concentration was found.ConclusionsNo significant differences in plasma ANP concentration was observed between groups. Further study, especially in horses with clinical signs of heart failure is needed.     

提高猪群繁殖效率的策略与方法

一、诱导母猪发情与发情检测 发情是后备母猪受胎能力和筛选的标记，是经产母猪受胎能力的标记，以及输精时间的标记。[第一段]     

News from the Scientific Organising Committee Learning new tricks to treat old dogs

Treating elderly pets and maximising your practice returns will be in focus at this year's AVA Annual Conference. The Scientific Organising Committee is delighted that such distinguished international and local speakers have agreed to give presentations in the Small Animal (Geriatric Medicine and Surgery) and Practice Management streams at the conference.
The AVA Conference will be at Hobart's Wrest Point Conference Centre from May 21–26, 2006. To see the full program and to register online visit www.ava.com.au/avaconference.