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 through 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 post feeding, followed by first generation merozoites 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 maintained exclusively on a diet of TetraMin® for 3 mo completely lost their infections.

Introduction [to Biology of the Acanthocephala]

Introduction to Biology of the Acanthocephala, edited by D.W.T. Crompton and Brent B. Nickol; Cambridge University Press, 1985.

Epizootiology: [Chapter 9 in Biology of the Acanthocephala]

In practice, epizootiology deals with how parasites spread through host populations, how rapidly the spread occurs and whether or not epizootics result. Prevalence, incidence, factors that permit establishment of infection, host response to infection, parasite fecundity and methods of transfer are, therefore, aspects of epizootiology. Indeed, most aspects of a parasite could be related in sorne way to epizootiology, but many of these topics are best considered in other contexts. General patterns of transmission, adaptations that facilitate transmission, establishment of infection and occurrence of epizootics are discussed in this chapter. When life cycles are unknown, little progress can be made in understanding the epizootiological aspects of any group of parasites. At the time Meyer's monograph was completed (1933), intermediate hosts were known for only 17 species of Acanthocephala, and existing descriptions are not sufficient to permit identification of two of those. Laboratory infections of intermediate hosts had apparently been produced for only two species. Study at that time was primarily devoted to species descriptions, host and geographical distribution, structure and ontogeny. Little or nothing was known about adaptations that promote transmission and the concept of paratenic hosts was unclear. In spite of the paucity of information, Meyer (1932) summarized pathways of transmission among principal groups of hosts, visualized the relationships among life cycle patterns for the major groups of Acanthocephala, and devised models for the hypothetical origin of terrestrial life cycles from aquatic ones. Nevertheless, most of our knowledge regarding epizootiology has been recently acquired.