A Computed Tomographic Study of the Molar Teeth of Babyrousa spp.

A photographic and computed tomography (CT) scanning study was carried out on 295 molar teeth of 18 adult male Babyrousa babyrussa skulls and 8 skulls of Babyrousa celebensis including seven adult males and one adult female. The occlusal morphology of the permanent maxillary and mandibular molar teeth of B. babyrussa was very similar to that of B. celebensis. Most B. babyrussa maxillary molar teeth had six roots, with small numbers of teeth having four, five or seven roots. A similar pattern was suggested in B. celebensis. Mandibular molar teeth had between four and eight roots. Tooth roots of maxillary and mandibular first and second molar teeth were largely tapering, rod-like structures. The roots of the right and left maxillary third molar teeth had a more complex arrangement; some were inserted almost vertically into the maxilla; others were orientated in a more distal direction. The mesial and distal roots were splayed in appearance. The right and left mandibular third molar tooth roots retained elements of the open 'C' shape and were generally orientated distally. The pulp chambers were arched to fit under the main cusps in all molar teeth. Pulp canals were variable in number.

Myocardial injury in dogs with snake envenomation and its relation to systemic inflammation.

OBJECTIVE: To investigate the presence of myocardial injury in dogs hospitalized for snake envenomation and to examine its relationship with systemic inflammation. DESIGN: Prospective case-control study. SETTING: University teaching hospital and small animal referral hospital. ANIMALS: Dogs naturally envenomed by the European viper (Vipera berus; n = 24), African puff adder (Bitis arietans; n = 5), or snouted cobra (Naja annulifera; n = 9). INTERVENTIONS: Blood was collected from dogs envenomed by V. berus at admission, 12-24 hours postadmission, and 5-10 days postadmission. Blood was collected from dogs envenomed by B. arietans or N. annulifera at admission, and 12, 24, and 36 hours postadmission. MEASUREMENTS AND MAIN RESULTS: Concentrations of cardiac troponin I (cTnI), a marker of myocardial injury, and C-reactive protein (CRP), a marker of systemic inflammation, were measured in each blood sample. Evidence of myocardial injury was found in 58% of dogs envenomed by V. berus at one or more time points. A significant correlation between cTnI and CRP concentrations was found at all time points. Evidence of myocardial injury was found in 80% of dogs envenomed by B. arietans at one or more time points; however, no correlation was found between cTnI and CRP concentrations. Evidence of myocardial injury was found in 67% of dogs envenomed by N. annulifera at one or more time points. A significant correlation between cTnI and CRP concentrations was found at admission, but not at other time points. CONCLUSIONS: Myocardial injury frequently occurred in dogs with snake envenomation. While the degree of systemic inflammation was significantly correlated with degree of myocardial injury in V. berus envenomation at all time points, this was not the case in dogs envenomed by N. annulifera or B. arietans. This could be due to differences in the toxic substances of the snake venoms or to differences in the cytokines induced by the venom toxins.

Efficacy of enalapril for prevention of congestive heart failure in dogs with myxomatous valve disease and asymptomatic mitral regurgitation.

We evaluated the long-term effect of early angiotensin-converting enzyme (ACE) inhibition (enalapril maleate) as monotherapy to postpone or prevent congestive heart failure (CHF) in asymptomatic dogs with mitral regurgitation (MR) attributable to myxomatous valvular disease (MVD) in a prospective, randomized, double-blinded, placebo-controlled multicenter trial involving 14 centers in Scandinavia. Two hundred twenty-nine Cavalier King Charles (CKC) Spaniels with MR attributable to MVD but no signs of CHF were randomly allocated to treatment with enalapril 0.25-0.5 mg daily (n = 116) or to placebo groups (n = 113). Each dog was evaluated by physical examination, electrocardiography, and thoracic radiography at entry and every 12 months (+/-30 days). The number of dogs developing heart failure was similar in the treatment and placebo groups (n = 50 [43%] and n = 48 [42%], respectively; P = .99). The estimated means, adjusted for censored observations, for the period from initiation of therapy to heart failure were 1,150 +/- 50 days for dogs in the treatment group and 1,130 +/- 50 days for dogs in the placebo group (P = .85). When absence or presence of cardiomegaly at the entrance of the trial was considered, there were still no differences between the treatment and placebo groups (P = .98 and .51, respectively). Multivariate analysis showed that enalapril had no significant effect on the time from initiation of therapy to heart failure (P = .86). Long-term treatment with enalapril in asymptomatic dogs with MVD and MR did not delay the onset of heart failure regardless of whether or not cardiomegaly was present at initiation of the study.