The causes of embryonic mortality in Hermann’s tortoises (Testudo hermanni) during artificial incubation were determined. Total egg failure at the end of the hatching period was investigated. The hatching artefacts represented 19.2% (N = 3557) of all eggs (N = 18,520). The viability rate of incubated eggs was 80.8%. The eggs, i.e., embryos, were sorted according to the cause of unsuccessful hatching and subsequently analyzed. Some of the eggs were divided into two or more groups. Unfertilized eggs were confirmed in 61.0%, infected eggs in 52.5%, and eggs in various stages of desiccation in 19.1%. This group also included mummified embryos. Pseudomonas aeruginosa, Bacillus sp., Purpureocillium lilacinum, and Escherichia coli were frequently confirmed in infected eggs. Embryos were divided into three groups: embryos up to 1.0 cm—group 1 (2.2%), embryos from 1.0 cm to 1.5 cm—group 2 (5.4%) and embryos longer than 1.5 cm—group 3 (7.3%) of all unhatched eggs. Inability of embryos to peck the shell was found in 1.3%. These tortoises died shortly before hatching. Embryos still alive from the group 2 and group 3 were confirmed in 0.7% of cases. Dead and alive deformed embryos and twins were detected in the group 3 in 0.5% and 0.1% of cases, respectively. For successful artificial hatching, it is important to establish fumigation with disinfectants prior to incubation and elimination of eggs with different shapes, eggs with broken shells, and eggs weighted under 10 g. Eggs should be candled before and periodically during artificial incubation, and all unfertilized and dead embryos must be removed. Heartbeat monitor is recommended. Proper temperature and humidity, incubation of “clean” eggs on sterile substrate and control for the presence of mites is essential. Monitoring of the parent tortoises is also necessary.

After cannibalism had appeared in the reproductive units of a white mouse colony, treatment against confirmed Hymenolepis nana, a tapeworm with zoonotic potential, was performed on 67 mice in the reproductive and nursery units. Faecal droppings were evaluated by flotation and sedimentation methods. The sedimentation method revealed a higher number of positive results before, during and after the treatment, but the flotation method yielded some additional positive cases. In the reproductive unit, H. nana eggs were confirmed in 50% of the tested mice by the flotation and in 70% by the sedimentation method. In the nursery units, H. nana eggs were detected in 10.5% of the tested mice by the flotation and in 24.6% by the sedimentation method. A colony of mice was treated against the tapeworm H. nana with praziquantel and emodepside in doses of 2.574 mg praziquantel/100 g body mass and of 0.642 mg emodepside/100 g body mass. The content of the original pipettes (Profender^®) was applied as a spot-on on the back of the neck in the area between the shoulders. The application was repeated three times at 14-day intervals. Seven days after the third therapy no H. nana was found in any of the tested mice in the reproductive or the nursery units. After the treatment, cannibalism was no longer observed. This treatment represented one of the steps aimed at improving animal welfare and preventing potential zoonotic disease. The public health significance of this cestode should receive more attention, especially among people who take care of mice, have them as pets, or feed them to reptiles.

This study describes experiences obtained with microchipping of Hermann’s tortoises in Slovenia. Over a period of three years, a total of 5,128 Hermann’s tortoises from parental breeding stock were microchipped. Microchips were implanted subcutaneously in the left inguinal region. During the application of microchips, males were bleeding in 2.6% and females in 1.4% of the cases. Bleeding frequency was related to sex, animal size and environmental temperature at the time of microchipping. The presence of microchips was followed up over a period of several years. At the control check conducted a few years later, all previously microchipped tortoises were included. Out of the entire parental breeding stock, 235 (4.6%) had lost their microchips, thus 63 males (5.7%) and 172 females (4.3%) were unmarked. The possible reasons for microchip loss are migration or inactivity of the implanted microchips.