We examined the mortality rates and causes of death of harbor seal (Phoca vitulina) pups in three regions of the inland waters of Washington (USA) in 1984. One hundred eight pups were collected during 239 searches of the shoreline areas near harbor seal haulout sites or through public reports. Minimum neonatal (up to 1 mo after birth) mortality rates at these regions ranged from 12% to 26% of the pups born. Neonatal mortality was highest in the Strait of Juan de Fuca; 33 of the estimated 105 (31%) pups born at the primary site died. Causes of death varied by location. In southern Puget Sound predation by coyotes (Canis latrans) was the primary cause of death, accounting for eight of 43 (19%) of the dead pups examined; starvation was the next most common cause of death. Mortality at study sites in the Strait of Juan de Fuca was related to premature parturition; 19 of 49 (39%) of the pups found dead were born prematurely. Nine species of bacteria were identified in samples taken from 42 pups; Proteus sp. and Escherichia coli were the most common.

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Abstract. Twelve Rhesus monkeys were inoculated intravenously with about 500 000 malaria parasites, Plas~nodiwn kriowlesi. Acute hemolysis occurred 5 days later, and all animals died on the 6th or 7th day after inoculation. All organs were gray-green to graybrown because of deposition of hemoglobin and malaria pigments. This deposition was particularly striking in the lung, brain, abdominal fat and serous surfaces. Microscopic changes indicative of acute hypoxia were found in the liver (centrilobular necrosis) and kidneys (acute tubular necrosis). Terminal intravascular coagulopathy was evidenced by widely distributed, recently formed, fibrin thrombi.Plasmodium knowlesi, a simian parasite o f quotidian periodicity, is indigenous to the jungle and swamp forests of Malaysia. Its range extends from the East Indian Archipelago to the Philippines. where Macaca fascicularis is the natural host and the Anopheline mosquito is the primary vector (4, 6, IS]. Contact with the vector can result in human infection 141. Experimentally induced infections in the Rhesus monkey (Macaca mulatta) are rapidly and uniformly fatal and have been used as a model for the human disease.The parasite has a life cycle similar to that of other malarial organisms. During the asexual (intraerythrocytic) phase, the outer membrane of the trophozoite acquires a digestive function, which results in the degradation of hemoglobin to hematin (hemozoin or "malaria pigment") [6]. The distribution of this compound is responsible for the gray-brown discoloration of affected organs and serous membranes.Reports on the pathology of simian malaria have appeared sporadically in the literature [6. 16, 20, 221. These studies included a number of different malarial parasites and primate species and in general, concentrate on the description of a single organ system. As a result, documented discussion of pathological features of the disease is fragmentary. The pathology of P. falciparum malaria in owl monkeys has been reported recently 191, but pathological changes were sparse.This report describes and documents the range of pathological changes in 12 Rhesus monkeys inoculated experimentally with P. knowlesi. 83

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Abstract. Thrombosis, sometimes with infarction, occurred in 20 of 52 dogs with renal amyloidosis. Pulmonary thrombosis was most commonly encountered, although the heart, kidneys, intestine, and other tissues were occasionally affected. Recent thrombi and older, organized thrombi occurred, sometimes in the same animal. The possible role of dehydration, hemoconcentration, hyperfibrinogeneniia, hyperglobulinemia, and clot-promoting factors in producing a hypercoagulable state is discussed.