Unusual outcome of in utero infection and subsequent postnatal super-infection with different PCV2b strains / 中国病毒学·英文版

VC2002, isolated from postweaning multisystemic wasting syndrome (PMWS)-affected pig, is a mixture of two porcine circovirus genotype 2b (PCV2b) viruses, K2 and K39. Preliminary experiments disclosed short-term adverse effects of K39, but not K2, on porcine foetuses. These findings led to the hypothesis that infection of immuno-incompetent foetuses with K2 confers a status of immunotolerance, and postnatal super-infection with K39 triggers PMWS. To explore this hypothesis, nine 55-day-old foetuses were inoculated in utero (three with K2-104.3TCID50, three with K39-104.3TCID50 and three with medium), and foeto-pathogenicity examined. At 21 days post-inoculation (dpi), K2 did not induce pathology, whereas pathological effects of K39 were evident. Twenty-four 45-day-old foetuses were subsequently inoculated to examine the long-term effect of K2, including six with K2-high dose-104.3TCID50, six with K2-low dose-102.3TCID50 and 12 mock-inoculated controls. Both doses resulted in ifve mummiifed foetuses and one live-born piglet each (69dpi). K2 was recovered from all mummies. K2 and K2-speciifc antibodies were not detected in serum of the two live-born piglets at birth, indicating full control of K2 infection. The K2-low dose-infected piglet was immunostimulated at day 2, but not the K2-high dose-infected piglet. Both non-stimulated and stimulated K2-infected piglets were super-inoculated with K39 at day 6 or 8 (taken as 0 days post super-inoculation). Low viral replication was observed in the non-stimulated K2-K39 piglet (up to 103.3 TCID50/g;identiifed as K39). In contrast, viral replication was extremely high in the stimulated K2-K39 piglet (up to 105.6TCID50/g) and identiifed as K2, indicating that K2 infection is controlled during foetal life, but emerges after birth upon immunostimulation. However, none of the piglets showed any signs of PMWS.

Pulmonary function profile in chronic congestive heart failure and the effect of ipratropium bromide.

Twenty-five symptomatic patients of chronic heart failure were subjected to spirometry to detect abnormalities of pulmonary function and to assess the effect of ipratropium bromide in reversing or minimising these abnormalities. All the patients exhibited abnormal pulmonary function manifesting as obstructive (15/25) or restrictive (10/25) ventilatory defect. There was overall improvement in lung functions with ipratropium bromide especially in those with obstructive ventilatory defects and mostly comprised of smokers. Forced expiratory volume in one second increased by 47.7 percent (p < 0.02), forced expiratory volume in one second/forced vital capacity ratio by 14.1 percent (p < 0.001) and maximal voluntary ventilation by 40.6 percent (p < 0.05) in these patients. It is concluded that ipratropium bromide can prove as a promising adjunctive therapeutic intervention in improving quality of life in patients of chronic congestive heart failure who are incapacitated by dyspnoea and have clearly documented ventilatory defects.

Immune response in acute coronary syndromes.

Inflammatory response in the atherosclerotic lesions of coronary artery disease, mediated by cellular immune mechanisms is well appreciated. The significance of the immuno-inflammatory processes for the development of acute ischaemic sequelae of these lesions remains unsettled. Fifty patients of acute coronary syndromes were studied for complement components and immunoglobin levels by single radial immunodiffusion method. Twenty-eight patients of acute myocardial infarction showed significantly lower levels of complement components C3 and C4 at admission (C3--69.19 +/- 12.91 mg% compared to 82.40 +/- 9.26 mg% in controls, p < 0.01; C4--14.56 +/- 2.46 mg% compared to 18.53 +/- 2.69 mg% in controls, p < 0.01). Twenty-two patients of unstable angina did not show any significant change (C3--83.14 +/- 8.01 mg% and C4--19.07 +/- 4.47 mg%). Sixteen patients of acute myocardial infarction who were thrombolysed with streptokinase showed a steep rise in the levels of complement components immediately after thrombolysis (C3--69.19 +/- 12.91 mg% before and 100.56 +/- 17.09 mg% after thrombolysis, p < 0.001; C4--14.56 +/- 2.46 mg% before and 21.48 +/- 4.78 mg% after thrombolysis, p < 0.001). Plasma C3 and C4 levels in acute myocardial infarction showed no relationship with peak CPK levels. Plasma immunoglobulins remained unchanged in patients of acute coronary syndromes.

Silent myocardial ischemia and cardiac autonomic neuropathy in diabetics.

OBJECTIVE: To evaluate the association of silent myocardial ischemia (SMI) with cardiac autonomic neuropathy in asymptomatic diabetic patients. MATERIAL AND METHODS: Two hundred asymptomatic patients of diabetes mellitus were assessed for evidence of cardiac autonomic neuropathy. Of these, 30 (15 males, 15 females; mean age 44.7 +/- 8.8 years) were found to have cardiac autonomic neuropathy. Thirty (30) age and sex matched diabetic patients (mean age 42.4 +/- 7.6 years) who had no evidence autonomic neuropathy were included in the study as control group. Both the groups of patients were evaluated for SMI by 24 hour ambulatory electrocardiographic (ECG) monitoring. RESULTS: Incidence of SMI was significantly higher in patients with autonomic neuropathy 12/30 (40%) compared to those without 3/30 (10%) p < 0.001. Duration of diabetes was more (13 +/- 1.59 years) in patients with autonomic neuropathy compared to the control group (8.66 +/- 1.55 years) p < 0.001. Serum cholesterol and triglyceride levels were significantly higher in patients with autonomic neuropathy in comparison to control group < 0.05 and < 0.01, respectively. There was no difference in the pattern of SMI in the two groups (p = N.S). CONCLUSION: Cardiac autonomic neuropathy predisposes patients with diabetes mellitus to SMI. Twenty four hour ambulatory ECG monitoring provides useful diagnostic information in early detection and evaluation of SMI in asymptomatic diabetic patients.

Clinical spectrum of infective endocarditis: 15 years experience.

Four hundred and sixty-six patients (277 males, 189 females; mean age 23.2 years) diagnosed as cases of infective endocarditis during the past 15 years were retrospectively analysed. Two-thirds of patients belonged to the 15 to 35 years age group. The most common predisposing cardiac lesion was rheumatic heart disease seen in 73.4 percent patients. Mitral valve prolapse and right-sided endocarditis were infrequent, seen in four patients each. Blood culture positivity was 28.7 percent in adults and 61 percent in children. Commonest organism isolated was staphylococcus aureus in adults (39.3%) and streptococcus viridans in children (48%). Salmonella typhi was detected in 17 patients and showed excellent response to ciprofloxacin and gentamycin. Overall mortality was 13.9 percent and resistant heart failure was the leading cause of death. Our study presents the clinical spectrum of infective endocarditis and highlights the comparison with western studies.