Annie K. Prestwood

Intramuscular Sarcocystis sp. in two cats and a dog.

Sarcocystis sp. was diagnosed in the skeletal muscle of a cat and myocardium of a dog and cat. The cysts were similar in size and structure when examined by light and transmission electron microscopy. The 3 animals were debilitated and probably immunocompromised due to pancytopenia or terminal neoplasia.

A dot-ELISA mimicry western blot test for the detection of swine trichinellosis

A dot enzyme-linked immunosorbent assay (dot-ELISA) using antigens purified by monoclonal antibody affinity chromatography was developed for detecting Trichinella spiralis infection in swine. The test was as sensitive as an ELISA using excretory-secretory products as antigen and western blot analysis, and nearly as specific as the western blot. The dot-ELISA detected all of 20 low infections (0.08-4.74 larvae per gram of diaphragm), most of them by 5-6 wk postinfection. Sera from 1,960 farm-reared swine were tested by conventional ELISA, dot-ELISA, and western blot. Of the 1,960 sera, 262 (13.4%) were considered positive on conventional ELISA, 16 (0.82%) by dot-ELISA, and 15 (0.77%) by western blot. The improved specificity was achieved by employing species-specific denatured antigens. More importantly, the dot-ELISA was much simpler to perform than western blot analysis. The principles employed in this test can be adapted to other infectious diseases, such as AIDS.

THE 1971 OUTBREAK OF HEMORRHAGIC DISEASE AMONG WHITE-TAILED DEER OF THE SOUTHEASTERN UNITED STATES1

Hemorrhagic disease (HD) caused by bluetongue and epizootic hemorrhagic disease viruses occurred in white-tailed deer (Odocoileus virginianus) of seven southeastern states during the late summer and early fall, 1971. The disease first appeared in South Carolina and then erupted almost simultaneously in Florida, Georgia, Kentucky, North Carolina, Tennessee, and Virginia. Peracute, acute, and chronic forms of HD were distinguished. Few gross lesions were observed in peracute HD but hemorrhage and edema commonly were seen in acute HD. Stomatitis and laminitis characterized the chronic disease. Mortality rate appeared to be related to the number of deer on the area.

An Update on the Distribution of Parelaphostrongylus tenuis in the Southeastern United States

An update is presented on the distribution of the meningeal worm (Parelaphostrongylus tenuis) of white-tailed deer (Odocoileus virginianus) in the southeastern United States. The parasite is widely distributed and common in all or much of Arkansas, Kentucky, Louisiana, Maryland, North Carolina, Tennessee, Virginia and West Virginia. It is also common in the northern half of Alabama and Georgia. In contrast, it is rare or absent along the Atlantic and Gulf coastal plains of Alabama, Georgia, Mississippi and South Carolina. It has been collected from a single deer in Florida.

Repeated low-level infection of white-tailed deer with Parelaphostrongylus andersoni.

Two white-tailed deer (Odocoileus virginianus) were given 5 infective larvae of Parelaphostrongylus andersoni each weekday for 13 weeks. At 23 weeks one of these deer and a control were challenged with single doses of 200 third-stage larvae. Repeated low-level infection of P. andersoni resulted in a sustained leukocytosis with an absolute eosinophilia which declined only after administration of larvae ceased, partial failure of worms to become established in the musculature, reduced numbers and reduced viability of eggs in the lungs, and an apparent active immunity which enabled the deer to resist challenge. The results of this study suggest that wild deer become infected with P. andersoni by isolated chance encounters with infected gastropods.

Experimental infection of mule deer with Parelaphostrongylus tenuis.

Six adult and three fawn mule deer (Odocoileus hemionus) were experimentally infected with a range of 75-100 infective larvae of Parelaphostrongylus tenuis. Five of the six adult deer developed clinical signs of neurologic disease that terminated in paralysis between 35 and 80 days. The sixth deer developed slight signs of neurologic disease for 10 days, but recovered. All three mule deer fawns developed neurologic disease. Adult meningeal worms were recovered from the subdural space of the spinal cord of two fawns. Eggs were observed on the cranial dura mater of one of these fawns, indicating that P. tenuis can complete its life cycle provided mule deer can survive the damage resulting from the infection. Neither eggs nor larvae of P. tenuis were recovered from the feces or lungs of infected mule deer. Clinical signs and histologic lesions observed in experimentally infected mule deer resembled those reported in infected moose (Alces alces americana). Two critical periods were apparent in mule deer infected with P. tenuis: nematode migration through the spinal neural parenchyma, and penetration of the adult nematodes into the cranial neural parenchyma. While most adult deer were unable to survive the first critical period, fawns survived the first but succumbed to infection during the second critical period.

Experimental Parelaphostrongylus andersoni Infections in White-Tailed Deer

Gross and microscopic lesions caused by Parelaphostrongylus andersoni were studied in white-tailed deer (Odocoileus virginianus) infected with large (1000 or 5000) and moderate (200–356) numbers of third-stage larvae. In heavy infections, adult worms caused eosinophilic myositis in the loin and thigh. Masses of eosinophils underwent caseous necrosis surrounded by a granulomatous border. Adult worms, eggs, and larvae were in the lesions. Muscle damage caused by moderate doses was slight. One deer given a moderate dose maintained a patent infection for more than 1 year and was reinfected. Gross lung damage caused by eggs and larvae occurred with both degrees of infection and consisted of firm miliary nodules. Microscopically, the main changes were granulomatous encapsulation of eggs and first-stage larvae in alveolar capillaries, accumulations of eosinophils and mononuclear inflammatory cells in the adjacent alveolar septa, congestion, and interstitial pneumonia.

SEVERE PARASITISM IN AN OPOSSUM

Chronic debilitation and anemia were observed in a free-living opossum (Didelphis marsupialis) heavily parasitized by Physaloptera turgida, Brachylaima virginianum, and Cruzia americana. Chronic interstitial pneumonia associated with Capillaria aerophila and a metastrongyloid nematode also was present.

Distribution of Meningeal Worm (Pneumostrongylus tenuis) in Deer in the Southeastern United States

Pneumostrongylus tenuis was found in the meninges of 1,197 (49.7%) of 2,409 white-tailed deer collected in Alabama, Arkansas, Florida, Georgia, Kentucky, Louisiana, Maryland, Mississippi, North Carolina, Tennessee, Virginia, and West Virginia. Infected deer were not found in South Carolina and St. Croix of the U. S. Virgin Islands. In the southeastern United States, meningeal worm appears to occur mainly in deer of oak-pine subclimax and climax deciduous forest types. It was not found in areas having a sandy soil and a predominantly pine forest. During the past few years considerable attention has been given to the biology of Pneumostrongylus tenuis Dougherty, 1945, the meningeal worm of white-tailed deer (Odocoileus virginianus). This helminth, apparently restricted to eastern North America, is noteworthy because it is a neurotropic form which generally produces a silent infection in the normal host (Anderson, 1963, 1965b; Anderson and Strelive, 1967; Lankester and Anderson, 1968) but can cause neurologic disturbances including paralysis in unusual hosts. Neurologic disease caused by P. tenuis has been produced experimentally in moose (Anderson, 1964), wapiti and mule deer (Anderson et al., 1966), woodland caribou (Anderson and Strelive, 1968), sheep (Anderson and Strelive, 1966b), and guinea pigs (Anderson and Strelive, 1966a; Spratt and Anderson, 1968). Neurologic disease associated with naturally acquired infections of meningeal worm has been reported in domestic sheep (Kennedy et al., 1952; Whitlock, 1952, 1959; Nielson and Aftosmis, 1964), moose (Smith et al., 1964; Anderson, 1965a; Kurtz et al., 1966; Karns, 1967a; Smith and Archibald, 1967; Behrend and Witter, 1968), and caribou (Behrend and Witter, 1968). The same disease probably occurs in wild wapiti in certain Received for publication 15 April 1969. * This study was supported by an appropriation from the Congress of the United States. Funds were administered and research coordinated under the Federal Aid in Wildlife Restoration Act (50 Stat. 917) and through Contract Nos. 1416-0008-676 and 14-16-0008-777, Bureau of Sport Fisheries and Wildlife, U. S. Department of the Interior. parts of eastern North America (Anderson et al., 1966). Although P. tenuis occurs rather extensively in eastern North America, precise data concerning its abundance and distribution have not been available. In view of rapidly expanding white-tailed deer populations throughout this section of North America and the proven pathogenicity of P. tenuis to other animals which come into contact with deer, it is essential that more information be obtained on its distribution. This article presents results of an extensive survey to determine the distribution of meningeal worm among white-tailed deer of the southeastern United States. MATERIALS AND METHODS From 1960 through early 1969 heads of 2,409 white-tailed deer were examined for P. tenuis. Animals originated from 137 counties in 13 southeastern states and St. Croix of the U. S. Virgin Islands (Fig. 1). Most deer heads were from animals killed by hunters during annual harvests in each state but some were obtained from deer dying of natural causes or collected for research purposes. Approximately two-thirds of the deer were females. Since hunters were reluctant to donate heads of mature bucks, does and immature bucks were most prevalent in the samples. Heads from hunter-killed animals were frozen prior to examination, while others were examined within 12 hr following death. After thawing, frozen and fresh heads were examined similarly. For individual examination, the head was skinned and freed of extraneous tissue. Horizontal cuts were made immediately posterior to the eyes and at the external occipital protuberance, with care taken not to damage the meninges. Frontal bones were opened along the sagittal crest, and bones lifted with a screwdriver. Bits of bone were removed with needle-nosed pliers until the brain with intact meninges was exposed. The olfactory bulb was grasped with a large pair of forceps, and tissue severed adjacent to the cribriform plate.

Trichinella spiralis (T1) and Trichinella T5 : A comparison using animal infectivity and molecular biology techniques

We compared Trichinella T5 of bobcat (Lynx rufus) origin with Trichinella spiralis (T1) by using animal infectivity and molecular biology techniques. Swine, SD rats, and CF1 mice were highly resistant to infection with Trichinella T5 but sensitive to T. spiralis, whereas deer mice (peromyscus maniculatus) had similar sensitivity to both parasites. The fecundity of Trichinella T5 in deer mice was 10-35-fold higher in comparison to the fecundity in laboratory rodents (SD rats and CF1 mice). Fecundity of T. spiralis was approximately the same in both groups. A western blot, using excretory-secretory proteins (ESP) from first-stage larvae of T. spiralis as antigen, showed similar banding patterns in the pigs infected with either T. spiralis or Trichinella T5, however, the homologous reaction was stronger than the heterologous reaction. Antibodies were detectable in swine sera commencing 3 or 5 wk postinfection with T. spiralis or Trichinella T5, respectively. Complementary DNAs encoding the 46-, 49/43-, or 53-kDa ESP showed 3.54, 1.94, and 5.91% differences, respectively, between the 2 parasites. Deduced amino acid sequences of the 3 cDNAs were different at 7.20, 5.08, and 8.55%, respectively. All recombinant proteins of the 3 cDNAs from both parasites could detect antibodies in positive sera. The sequences of cDNAs encoding the 46-, 49/43-, or 53-kDa ESP from T. spiralis are also compared to the previously reported sequences, and the differences are discussed.