Bovine Tuberculosis in Swedish Farmed Deer: Detection and Control of the Disease

Bovine tuberculosis (BTB) was introduced into Swedish farmed deer herds in 1987. Epidemiological investigations showed that 10 deer herds had become infected (July 1994) and a common source of infection, a consignment of 168 imported farmed fallow deer, was identified (I). As trace-back of all imported and in-contact deer was not possible, a control program, based on tuberculin testing, was implemented in July 1994. As Sweden has been free from BTB since 1958, few practicing veterinarians had experience in tuberculin testing. In this test, result relies on the skill, experience and conscientiousness of the testing veterinarian. Deficiencies in performing the test may adversely affect the test results and thereby compromise a control program. Quality indicators may identify possible deficiencies in testing procedures. For that purpose, reference values for measured skin fold thickness (prior to injection of the tuberculin) were established (II) suggested to be used mainly by less experienced veterinarians to identify unexpected measurements. Furthermore, the within-veterinarian variation of the measured skin fold thickness was estimated by fitting general linear models to data (skin fold measurements) (III). The mean square error was used as an estimator of the within-veterinarian variation. Using this method, four (6%) veterinarians were considered to have unexpectedly large variation in measurements. In certain large extensive deer farms, where mustering of all animals was difficult, meat inspection was suggested as an alternative to tuberculin testing. The efficiency of such a control was estimated in paper IV and V. A Reed Frost model was fitted to data from seven BTB-infected deer herds and the spread of infection was estimated (< 0.6 effective contacts per deer and year) (IV). These results were used to model the efficiency of meat inspection in an average extensive Swedish deer herd. Given a 20% annual slaughter and meat inspection, the model predicted that BTB would be either detected or eliminated in most herds (90%) 15 years after introduction of one infected deer. In 2003, an alternative control for BTB in extensive Swedish deer herds, based on the results of paper V, was implemented.

On the Ecology and Distribution of Echinococcus spp. (Cestoda: Taeniidae), and Characteristics of Their Development in the Intermediate Host. II. Comparative Studies on the Development of Larval E. multilocularis Leuckart, 1863, in the Intermediate Host

This paper reports the results of a comparative study of the development of the larval Echinococcus multilocularis Leuckart, 1863), and associated tissue reaction in naturally and experimentally infected mammals representing 31 species. The histogenesis of the larval cestode was traced in detail in arvicoline rodents of several species, and interspecific differences were defined. In arvicoline rodents, the developing larva exhibited host-specific characteristics within about a month after infection was established. The tissue reaction in Microtus oeconomus was characterized by the production of a large quantity of detritus around the larva, and by the formation of a thick epithelioid zone. In one subspecies, M. oeconomus innuitus, development of the larva was retarded, and the detrital mass was often calcified; in another, M. oeconomus operarius, the detritus rarely became calcified and the larva proliferated more rapidly. In M. pennsylvanicus, the tissue reaction was minimal, and little detritus was present. The characteristics of the tissue reaction in M. montebelli placed it in an intermediate position between the aforementioned species. In Clethrionomys rutilus, a thin epithelioid zone and an outer zone of loose collagenous fibers composed the adventitial layer; exogenous budding was retarded in this vole. A minimal tissue reaction occurred in Lagurus curtatus. In Lemmus spp., larger cysts were characteristic, but areas of small-cystic proliferation were always present. Similar differences in species or subspecies of Citellus and Dicrostonyx were described. Lesions of alveolar bydatid disease in man also were studied. The invasive growth of the larval cestode in the human liver involves a process comparable to small-cystic proliferation in the natural intermediate hosts. Although the later stages of development of the larval cestode are inhibited in man, exogenous proliferation of vesicles continues for the life of the host. The lesion in man was compared with a morphologically similar formation produced by anomalous development of the larval E. granulosus in the bovine liver. The latter is distinguished by the absence of areas of small-cystic proliferation. Non-echinococcal lesions found in the tissues studied, some of which resembled foci caused by the larval E. multilocularis, were briefly discussed.