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PubMed2006

The 2000 canine distemper epidemic in Caspian seals (Phoca caspica): pathology and analysis of contributory factors.

More than 10,000 Caspian seals (Phoca caspica) were reported dead in the Caspian Sea during spring and summer 2000. We performed necropsies and extensive laboratory analyses on 18 seals, as well as examination of the pattern of strandings and variation in weather in recent years, to identify the cause of mortality and potential contributory factors. The monthly stranding rate in 2000 was up to 2.8 times the historic mean. It was preceded by an unusually mild winter, as observed before in mass mortality events of pinnipeds. The primary diagnosis in 11 of 13 seals was canine distemper, characterized by broncho-interstitial pneumonia, lymphocytic necrosis and depletion in lymphoid organs, and the presence of typical intracytoplasmic inclusion bodies in multiple epithelia. Canine distemper virus infection was confirmed by phylogenetic analysis of reverse transcriptase-polymerase chain reaction products. Organochlorine and zinc concentrations in tissues of seals with canine distemper were comparable to those of Caspian seals in previous years. Concurrent bacterial infections that may have contributed to the mortality of the seals included Bordetella bronchiseptica (4/8 seals), Streptococcus phocae (3/8), Salmonella dublin (1/8), and S. choleraesuis (1/8). A newly identified bacterium, Corynebacterium caspium, was associated with balanoposthitis in one seal. Several infectious and parasitic organisms, including poxvirus, Atopobacter phocae, Eimeria- and Sarcocystis-like organisms, and Halarachne sp. were identified in Caspian seals for the first time.

Animals↗

PubMed2002

[Physical training as interval or continuous training in chronic heart failure for improving functional capacity, hemodynamics and quality of life--a controlled study].

We conducted a three-week randomized trial comparing the improvement of functional capacity by exercise training in chronic heart failure by the steady-state (EF 27.3%, n = 20) and the interval modus (EF 29.3%, n = 20) with a control group (EF = 26.6%, n = 10). Minimal EF was 10%, the lowest maximal oxygen consumption was 9.3 ml/kg/min and the lowest cardiac output was 1.9 l/min; 9 patients had been evaluated for HTX. VO2 at the anaerobic threshold and at maximal exercise increased in the continuous exercise group by 1.4 or 1.6 ml/kg/min, respectively, corresponding to an increase of 13.7% (p < 0.05) and 9.3% (p < 0.05). In the interval training group the increase was 1.3 and 1.5 ml/kg/min corresponding to 14% (p < 0.05) and 8.1% (p < 0.05). Continuous short-term exercise had no impact to central hemodynamics as pulmonary artery pressure (PA), capillary wedge pressure (pc), cardiac index (CI) or stroke volume index (SVI), whereas after interval training a significant increase at maximal exercise could be seen in CI (p < 0.05) and SVI (p < 0.01) with a concomitant drop in systemic peripheral resistance (p < 0.05) compared to the steady-state modus. Interval training was further characterized by a higher short-term but lower mean work load with a significantly smaller increase in lactate. Quality of life was improved according to the SF-36 questionnaire in both training groups but the psychologic sum factor was three times as high, increasing to 24.2% in the steady-state exercise group. It can be concluded that clinically stable patients with heart failure and even those already having been evaluated for cardiac transplantation profit from short-term physical training. Both training modalities seem equally suited to improve functional capacity. However interval training leads to more pronounced improvement in hemodynamics compared to the steady-state exercise, whereas the later had a greater impact on psychological well-being and quality of life. Patients with heart failure and severe peripheral deconditioning tolerate higher workloads with more peripheral stress by an interval training modus. Long-term training modalities need to be established to further improve and stabilize functional status.

Activities of Daily Living↗

PubMedDate not supplied

Mass die-Off of Caspian seals caused by canine distemper virus.

Thousands of Caspian seals (Phoca caspica) died in the Caspian Sea from April to August 2000. Lesions characteristic of morbillivirus infection were found in tissue specimens from dead seals. Canine distemper virus infection was identified by serologic examination, reverse transcriptase- polymerase chain reaction, and sequencing of selected P gene fragments. These results implicate canine distemper virus infection as the primary cause of death.

Animals↗