Biology and pathogenesis of the coccidium Eimeria funduli infecting killifishes.

Epizootics of Eimeria funduli involved estuarine killifishes (Fundulus grandis, F. pulvereus, F. similis, and F. heteroclitus) in Mississippi, Alabama, and Virginia. All of more than 500 specimens examined of F. grandis from Mississippi during 1977 though 1979 had infections, regardless of age, sex, or season collected. Oocysts occurred primarily in the liver and pancreas, replacing up to 85% of both those organs. Infrequent sites of infection were fatty tissue of the body cavity, ovary, intestine, and caudal peduncle. Living fish did not discharge oocysts. Eimeria funduli is the first known eimerian to require a second host. To complete the life cycle, an infective stage in the grass shrimp Palaemonetes pugio had to be eaten. In 6-mo-old killifish reared in the laboratory at 24 C, young schizonts were first observed in hepatic and pancreatic cells 5 days postfeeding, followed by first generation merzoites by day 10, differentiation of sexual stages during days 15 to 20, fertilization between days 19 and 26, sporoblasts from days 25 to 30, and sporozoites about day 60. Unique sporopodia developed on sporocysts by day 35 when still unsporulated. Temperatures of 7 to 10 C irreversibly halted schizogony. Both schizogony and sporogony progressed slower as age of host increased. When infective shrimp in doses ranging from 1 to 10% of a fish's body weight were eaten, the level of intensity of resulting infections did not differ significantly. Pathogenesis followed a specific sequence, with the host response apparently unable to contend with extensive infections as seen typically in nature and in our experiments. Premunition was indicated. When administered Monensin orally, infected fish exhibited a reduction in oocysts by 50 to 70% within 20 days as compared with untreated fish. Furthermore, infected killifish exclusively on a diet of TetraMin for 3 mo completely lost their infections.

A new and unusual eimerian (protozoa: Eimeriidae) from the liver of the Gulf killifish, Fundulus grandis.

Oocysts and sporocysts of Eimeria funduli sp. n. are described from the Gulf killifish, Fundulus grandis, on the basis of light microscopy, transmission and scanning electron miscroscopy, and location in the liver of infected hosts. The spherical sporulated oocysts of E. funduli isolated from liver tissue measure 20-31 (25) micrometer across with ovoid sporocysts 9-11 X 5-7 (10 X 6) micrometer. A micropyle, polar granule, and oocyst residuum are absent, but sporocysts have Stieda and substieda bodies, a few residual granules, and 10-25 (15) unique projecting structures with expanded distal portions that we term "sporopodia". Sporopodia 1-3 (2) micrometer high support a transparent membrane that completely surrounds the sporocyst. Sporozoites have one large posterior refractile body. Ultrastructurally, the oocyst wall consists of two thin layers of granular material: an electron-dense outer layer with a rough external surface and an electron-lucent inner one of approximately equal thickness. One or two unit membranes line the inner surface of the inner layer. Each layer is 40-60 (55) nm thick. The sporocyst wall, 78-130 (110) nm thick, consists of an electron-lucent material with the outer surface being more electron dense and giving rise to osmiophilic sporopodia; closely associated with these and the outer surface are one or two unit membranes. A thin osmiophilic layer of fine granular material lines the inner surface.

Vertebral osteomyelitis and suspected diskospondylitis in an Atlantic bottlenose dolphin (Tursiops truncatus).

A 21-yr-old male Atlantic bottlenose dolphin (Tursiops truncatus) was performing at an aquatic park when it developed a soft tissue swelling anterior to the flukes. Subsequent radiographic evaluation revealed the animal to have vertebral osteomyelitis and suspected diskospondylitis. The case was successfully managed with long-term antibiotic therapy.

Selenium toxicosis in three California sea lions (Zalophus californianus).

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.