Toxoplasma gondii infection in the mountain hare (Lepus timidus) and domestic rabbit (Oryctolagus cuniculus). I. Pathology.

Mountain hares and domestic rabbits infected experimentally with Toxoplasma gondii were compared in respect of pathological changes and distribution of organisms in the tissues. Seven hares and nine rabbits were each inoculated orally with 50 oocysts of the T. gondii Tg-SweF1 isolate and killed after one week to avoid adverse clinical effects. The only clinical sign observed was respiratory distress in a single hare. At necropsy, gross lesions, which occurred only in the hares, were found in the mesenteric lymph nodes and occasionally the liver. Histologically, the hares showed extensive necrotic areas in the small intestine, mesenteric lymph nodes and liver, and less prominent foci of necrosis in various other organs. Immunohistochemically, T. gondii was identified in all organs examined, large numbers of organisms being associated with the lesions. These findings were analogous to those seen previously in naturally infected hares. In the rabbit, the pathological changes consisted mainly of accumulations of mononuclear cells in the liver and heart, and T. gondii was found only in the heart and skeletal muscle of two rabbits. Thus, the hares developed severe acute toxoplasmosis, but the rabbits showed few organisms and no major tissue damage one week after inoculation.

Pathological findings indicative of distemper in European seals.

The first recorded cases of the recent epizootic were harbour seals observed at the Danish island of Anholt, 12 April 1988. The disease then spread throughout the sea waters of north-western Europe. The total mortality in Europe up to November 1988, was estimated to be at least 17,000 seals. The mortality rate in Danish-Swedish waters was about 60%. Autopsies including sampling for histology of most organs were performed on 37 harbour seals and 12 grey seals, collected mainly at the Swedish west coast and in the southern Baltic. In most of the harbour seals and in three of the grey seals we found histological changes in the upper and lower respiratory tracts, in the lower urinary tract and in the lymphatic system consistent with those diagnostic of distemper viral infection in the canine. These diagnostic criteria were: presence of intracytoplasmic eosinophilic inclusion bodies of epithelial cells of the trachea and the urinary bladder, interstitial pneumonia, and atrophy of lymphatic organs due to depletion of lymphocytes. Our findings in pathology of a canine distemper-like disease in the seals were presented in late August 1988, together with the Dutch findings in virology by Dr. Osterhaus and collaborators.

The cause of Kaposi's sarcoma: an avian retroviral analog.

Changes in the epidemiologic patterns of Kaposi's sarcoma prior to and during the epidemic of acquired immunodeficiency suggest that a virus transmitted similarly to the human immunodeficiency virus (HIV) may be responsible. We propose a natural avian model for Kaposi's sarcoma. Hemangiomatosis of fowls corresponds clinically and pathologically to the human disease, with characteristics including predilection for distal skin, multicentricity with organ involvement, bleeding and recurrence after excision. Pathologic stages are also similar and include initial dissection of collagen by benign endothelial cells, the formation of large blood-filled spaces, spindle cell growth, and progression to fibrosarcomalike tumors. Avian hemangiomatosis is induced by a retrovirus of the lymphoid leukosis group and has been associated with laboratory transmission of lymphomatosis. An etiopathologic parallel should be sought in man.

Distribution and ultrastructure of mast cells in the duck.

The distribution and ultrastructure of mast cells in the duck were studied. Carnoy's fluid was found to be the best fixative, and Padawer's method was found to be useful in demonstrating the metachromasia. Mast cells were seen in many of the organs and were most numerous in the proventriculus. Perivascular location was frequently seen. The ultrastructure resembled that of the chicken mast cell. The cell contained different types of membrane-bound granules, some of which were electron-dense and mottled.

Life span and organ pathology in rats after life-long noise exposure.

The role of ambient sound level in longevity, cause of death, and incidence of disease was investigated in rats. Two hundred twenty-seven rats (154 Sprague-Dawley (N), 73 spontaneously hypertensive Wistar (SH)), were housed in three sound isolated boxes and subjected to controlled acoustic milieus from approximately three months of age until their natural death. Thirty-nine of the N rats were kept as external controls in a regular animal room. In one of the boxes, no noise was introduced (control). In the other two, the rats were exposed, respectively, to a frequency-modulated, chopped noise with an equivalent level of 80 dB Leq and 100 dB Leq, ten hours daily. It was found that the SH animals had a shorter life span and a higher incidence of cardiovascular disease than the N rats but a lower rate of malignant tumors. No measurable effects on life span or total incidence of disease were seen. Minor differences in incidence of various disease entities were observed but were not consistent across groups. The results do not support the hypothesis that physical sound environment represents a significant cause of somatic disease.