Multiple freeze-thaw cycles are common in alpine, polar and temperate habitats. We investigated the effects of five consecutive cycles of approx. -5 degrees C on the freeze-tolerant larvae of Pringleophaga marioni Viette (Lepidoptera: Tineidae) on sub-Antarctic Marion Island. The likelihood of freezing was positively correlated with body mass, and decreased from 70% of caterpillars that froze on initial exposure to 55% of caterpillars that froze on subsequent exposures; however, caterpillars retained their freeze tolerance and did not appear to switch to a freeze-avoiding strategy. Apart from an increase in gut water, there was no difference in body composition of caterpillars frozen 0 to 5 times, suggesting that the observed effects were not due to freezing, but rather to exposure to cold per se. Repeated cold exposure did not result in mortality, but led to decreased mass, largely accounted for by a decreased gut mass caused by cessation of feeding by caterpillars. Treatment caterpillars had fragile guts with increased lipid content, suggesting damage to the gut epithelium. These effects persisted for 5 days after the final exposure to cold, and after 30 days, treatment caterpillars had regained their pre-exposure mass, whereas their control counterparts had significantly gained mass. We show that repeated cold exposure does occur in the field, and suggest that this may be responsible for the long life cycle in P. marioni. Although mean temperatures are increasing on Marion Island, several climate change scenarios predict an increase in exposures to sub-zero temperatures, which would result in an increased generation time for P. marioni. Coupled with increased predation from introduced house mice on Marion Island, this could have severe consequences for the P. marioni population.
In a retrospective survey, the epidemiological characteristics of nursing sickness in Standard Black and Pastel mink (Mustela vison) were examined in a Danish fur research farm. Based on the clinical diagnosis of the disease, the overall morbidity in a total of 1774 lactating females amounted to 14.4% and the case fatality rate to 7.8%. Apparently healthy females weaned an average of 5.0 kits per litter, while dams suffering from nursing sickness raised and weaned an average of 5.4 kits per litter (p less than 0.01). Based on logistic regression analysis, the increasing age of the lactating dam, followed by littersize and female weight loss, appeared to be major determinants for the development of nursing sickness. The impact of additional covariates such as litter weight gain and female color type were remarkably low. At weaning (day 43) the mean individual live weight of the kits of either sex did not differ between healthy and sick dams. In Standard Black, the total biomass of the offspring raised by sick dams was significantly larger than that of the healthy controls (p less than 0.01). During the final two weeks of lactation, apparently healthy dams lost on average 14% of their body mass, whereas those affected by nursing sickness had a mean weight loss of about 31% (p less than 0.001). Postmortem examination of 25 dams with severe nursing sickness verified the clinical findings of progressive dehydration and emaciation. The gastrointestinal tract was empty and gastric ulcers and melaena were frequently present. Other common findings included small livers,enlarged adrenals and pitted kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
The incidence of AIDS in Denmark is the highest reported among the countries of Western Europe. This preliminary account is a report of the autopsy findings in 10 patients, 9 homosexual men and 1 woman. Our aim is to provide a detailed description of the patho-anatomical findings, as well as to compare these with corresponding results reported from the United States, with a view to establishing possible geographical differences in the disease picture. The results of the patho-anatomical studies correspond in all essentials to those from the United States. However, it must be stated that no malignant lymphomas were demonstrated in our patients, although the disease can give rise to very pronounced, possibly transitory, lesions in the lymphatic tissue, easily misinterpreted as malignant. Further features that should be emphasized are the often widespread mycobacterial infection found in the intestinal wall in protracted cases, the occurrence of CMV vasculitis, particularly in the adrenal cortex and medulla, and thromboembolic lesions, often demonstrated in a variety of tissues. The studies made so far emphasize the importance of autopsy in AIDS deaths, as it has extended our detailed knowledge of the patho-anatomical lesions associated with certain opportunistic infections. Further, the autopsy findings have been demonstrably significant either for confirming or for rejecting the clinical diagnosis. On the basis of an analysis of the cellular immunological profile in AIDS, parallels can be drawn to the conditions in certain lymphoproliferative diseases. In autopsied AIDS cases, we recommend a standard scheme covering the tissue specimens to be obtained for histological examination. Strict safety precautions should be observed against infection during autopsy.
Obligatory findings in 42 postmortem observation of anthrax were hemorrhagic alterations of the intrathoracic lymph nodes and mediastinum. Hemorrhagic alterations in the respiratory organs, digestive tract, brain and meninges were also found macroscopically.
Histologic studies of 42 cases of anthrax revealed that serous-hemorrhagic, hemorrhagic and hemorrhagic-necrotic inflammation was a substrate of macroscopic changes. Morphological characteristics of alterations in the respiratory organs, lymph nodes and mediastinum, digestive tract and liver, spleen, kidneys, brain and meninges are presented.
Hemorrhagic lymphadenitis of the intrathoracic lymph nodes and mediastinitis are shown to be the primary septical focus, this indicating an inhalation route of the contamination with development of pulmonary anthrax. The alterations in the gastrointestinal tract and central nervous system are considered to be secondary resulting from lymphohematogenic generalization of the anthraxic sepsis. The attention is drawn to the morphological signs of the immunodepression and the inhibition of granulocytic reaction. It is noted that the epidemic outburst of the pulmonary anthrax is without analogs and its development may be the result only of a massive penetration of bacteria into the atmosphere.