Parasitic Protozoa

Parasitic Protozoa

Volume 4

Second Edition

Julius P. Kreier

Professor Emeritus, Department of Microbiology, The Ohio State University, Columbus, Ohio

ACADEMIC PRESS, INC.

Harcourt Brace Jovanovich, Publishers

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Table of Contents

Cover image

Title page

Copyright page

Contributors

Preface to the Second Edition

Preface to the First Edition

Chapter 1: Avian Coccidosis

I Introduction: Significance of the Avian Coccidia

II Taxonomy and Nomenclature

III Basic Life Cycles

IV The Coccidia of Avian Hosts

V Genetics of Coccidia

VI Host Specificity of Coccidia

VII Site Specificity off Coccidia

VIII Viability of Coccidial Oocysts

IX Metabolism of Coccidia

X Pathophysiological Changes Induced by Infection with Coccidia

XI Effects of Dose and Frequency of Dosing of Oocysts on Coccidial Disease

XII Effects of Age of Host on Coccidiosis

XIII Effects of Enteric Bacteria and Nutritional Status of the Host on Coccidiosis

XIV Interactions with Viruses

XV Interaction between Species of Eimeria

XVI Immunity against Eimeria Infections

XVII Immunization against Coccidiosis

XVIII Control by Chemotherapy

Chapter 2: Coccidia of Mammals

I Introduction

II Life Cycles

III Coccidiosis of Man and Domestic Animals

IV Ultrastructure and Cell Penetration

V Development in Vitro

VI Immunity

VII Caryospora: Unusual Coccidians

VIII Summary and Conclusions

Acknowledgments

Chapter 3: The Gregarines

I Introduction

II Life Cycle of an Eugregarine and the Different Types of Trophozoites

III Cellular and Molecular Organization of the Different Stages

IV Host–Parasite Interactions: Exuberance of Gregarines

V Schizogony and Taxonomy of Gregarines

VI Conclusion

Acknowledgments

Chapter 4: The Haemogregarinidae and Lankesterellidae

I Introduction

II The Haemogregarinidae

III The Lankesterellidae

IV Concluding Remarks

Chapter 5: The Genera Leucocytozoon, Haemoproteus, and Hepatocystis

I Introduction

II The Taxonomy of the Haemosporina/Haemospororida

III leucocytozoon, Sambon, 1908

IV Haemoproteus, Kruse, 1890

V The Prevalence and Epizootiology of Avian Haematozoa with Special Reference to Leucocytozoon and Haemoproteus

VI Hepatocystis, Levaditi and Schoen, 1932, emend, Garnham, 1951

VII Summary

Index

Contents of Future Volumes

Copyright

Copyright © 1993, 1978 by ACADEMIC PRESS, INC.

All Rights Reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher.

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United Kingdom Edition published by

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Library of Congress Cataloging-in-Publication Data

(revised for vol. 4)

Kreier, Julius P.

 Parasitic protozoa.

 Includes bibliographical references and index.

 1. Protozoa, Pathogenic. I. Baker, John R. (John Robin). II. Title.

QR251.K74     1992  593.1'045249  91-19635

ISBN 0-12-426014-4

PRINTED IN THE UNITED STATES OF AMERICA

93 94 95 96 97 98 OW 9 8 7 6 5 4 3 2 1

Contributors

Numbers in parentheses indicate the pages on which the author’s contributions begin.

Gordon F. Bennett (273)     International Reference Centre for Avian Haematozoa, Memorial University of Newfoundland, St. John’s, Newfoundland, Canada A1B 3X9

Sherwin S. Besser (247, 273)     Department of Zoology, University of Toronto, Toronto, Ontario, Canada M5S 1A1

David S. Lindsay (89)     Department of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, Alabama 36849

Peter L. Long (1)     Department of Poultry Science, College of Agriculture, University of Georgia, Athens, Georgia 30602

Michel Philippe (133)     Museum National d’Histoire Narurelle, URA CNRS, 75271 Paris, France

Joseph Schrevel (133)     Laboratoire de Biologie Cellulaire, URA CNRS, 86022 Poitiers, France, and Museum National d’Histoire Narurelle, 75271 Paris, France

Kenneth S. Todd, Jr. (89)     Department of Pathobiology, College of Veterinary Medicine, University of Illinois, Urbana, Illinois 61801

Preface to the Second Edition

Julius P. Kreier; John R. Baker

The second edition of Parasitic Protozoa follows the first edition by approximately 14 years. During this time new information about the parasitic protozoa has accumulated. This edition attempts to accommodate the new information without missing the goal of the first edition, which was to present a balanced review of the status of parasitic protozoa with solid information not likely to become quickly outdated.

All of the chapters have been completely rewritten, some by the original authors. In some cases new authors have been chosen because previous authors and dear friends have died, among whom are R. H. Whittaker, A. Zuckerman, and Earl H. Fife, Jr. In other cases, the original authors were not available for a variety of reasons: some have retired, some changed fields, some no longer wished the task, and regrettably we have simply lost track of some.

Some changes have been made in coverage. There has been some expansion in the coverage of the protozoa affecting animals in the aquatic environment, and the reviews of the rickettsial organisms in the Anaplasmataceae, Bartonellaceae, and Ehrlichieae are no longer included. The introductory chapters on broad classification and taxonomy are very different from those in the first edition. A new chapter entitled The Nature of Protozoa has been added. The chapter on broad classification is based on cladistics and takes a very different view of the biological system from the corresponding chapter in the first edition. The chapter on systematics of parasitic protozoa has also been much changed and reflects the state of flux in protozoan taxonomy that exists today. In many respects a better grasp of the areas of taxonomy and systematics can be gained by a comparative reading of the chapters in the first and second editions than by just reading the new chapters in the second edition.

We wish to thank the staff of Academic Press for their valuable aid in preparation of these volumes, and we wish to give special thanks to Edna Chandler who faithfully transformed much editorial scratching into clear, correct, and legible transcript.

Preface to the First Edition

Julius P. Kreier

The parasitic protozoa are a large and diverse group. Many are of interest to physicians and veterinarians because they produce disease in man and his livestock. Others, which seldom produce disease, should be familiar to the practitioner of medicine and to the research scientist because they are present in the animal body and thus must be recognized to avoid a misdiagnosis, while still others, such as the intestinal and rumen protozoa, perform a useful function in the animal’s economy, and their presence is an indication of health rather than disease.

I have included in these volumes protozoa parasitic in animals, such as fish and insects, which are not usually included in books on pathogenic protozoa. I did this because I believe veterinary medicine should concern itself with all species of animals, excepting man, whose care falls to the physician. From a more practical standpoint, I feel the inclusion of parasites of diverse species is appropriate in a book on protozoa of veterinary and medical interest because no matter how we set ourselves off from nature we remain a part of it, and thus we inevitably share parasites with the other species with which we live.

Because of the wide range of parasites and the volume of material available, no single author could hope to be qualified to write on all of them; thus I have chosen to have each chapter written by someone qualified in that area. This course of action, while it avoids the problems of the limitations of a single author, has problems of its own, the most serious being the variability in the authors’ styles and attitudes which produces unevenness in the treatment of the contributions. For this I accept responsibility as editor. For all that is good and useful in these volumes I thank the authors of the chapters and the staff of Academic Press who have aided in the production of these volumes. I also wish to thank the Army Malaria Project, whose support of my research has made it possible for me to continue my interest in protozoology.

Chapter 1

Avian Coccidosis

Peter L. Long

I Introduction: Significance of the Avian Coccidia

Under natural conditions, most birds pass small numbers of coccidial oocysts in their feces without apparent ill effects. Coccidiosis becomes important as a disease when animals live, or are reared, under crowded conditions that permit the buildup of infective oocysts in the environment and their ingestion by susceptible birds. Because today poultry are often kept in large numbers under crowded conditions, exposure to coccidial oocysts in large numbers may occur easily and thus intestinal coccidiosis is an important disease of poultry throughout the world.

The parasites are transmitted as sporulated oocysts. Broiler chickens are kept in houses with litter floors (usually wood shavings) 10,000 to 30,000/house at a density of 0.6 to 0.8 square foot per bird. The houses are kept warm and well ventilated, and fecal matter builds up on the floors. These conditions are ideal for sporulation and survival of oocysts and reinfection is sure.

Intestinal coccidiosis, caused by Eimeria spp., is important enough to warrant the widespread use of continuous medication given in the food. Without such medication, the poultry industry as we know it would probably not exist.

II Taxonomy and Nomenclature

The coccidia belong to the phylum Apicomplexa, a diverse group of obligate intracellular protozoa infecting mainly vertebrates. Most species of coccidia infecting vertebrates are homoxenous (one host in the life cycle) and most develop within epithelial cells of the intestine. Some species of coccidia causing disease in man and domesticated animals are, however, obligatory heteroxenous parasites, having an intestinal phase of development (asexual and sexual, or sexual only) in one host and extraintestinal development (usually asexual) in an intermediate host (Levine, 1970).

The coccidia of avian hosts are found within three of the more than nine families constituting the true coccidia (suborder Eimeriorina) (Figure 1.1). The coccidia of medical and veterinary importance are also contained in the same three families of the suborder Eimeriorina (the true coccidia).

Figure 1.1 Taxonomic relationships of coccidia affecting man and domestic animals.

The majority of species of coccidia within the family Eimeriidae of the suborder Eimeriorina are intestinal parasites. Most belong to one or the other of the two genera Eimeria and Isospora. Many Eimeria and some Isospora are found in avian hosts.

Research published from 1965 to 1967 initiated a change in our knowledge of the coccidia and the relationship of these parasites to the other organisms classified as Sporozoa, an unnatural assemblage of diverse groups of protozoan parasites. Electron microscopy, for example, revealed that the extraintestinal merozoites (zoites) of Toxoplasma gondii and Sarcocystis were structurally similar to those of the intestinal-dwelling eimerian species, suggesting that these two genera were coccidia. Hutchison’s (1965) work was a watershed. He was able to transmit Toxoplasma by inoculating mice with feline feces. It was already known that consumption of infected meat would transmit toxoplasmosis. In 1970, just 5 years after Hutchison’s discovery, our knowledge of the life cycle of T. gondii was completed by the finding of sexual stages of the parasite in the gut of the cat and the finding of oocysts in their feces. As a result of these studies it became apparent that coccidia were not just homoxenous, strictly enteric pathogens transmitted only by passage of oocysts as previously thought but were also heteroxenous parasites with life cycle stages distributed in many organs of the host and with transmission of infection by carnivorism.

Approximately 10 years after the recognition that both T. gondii and Sarcocystis were coccidial parasites, another coccidian, Cryptosporidium, was recognized as an important pathogen of man and domestic animals. This recognition caused our view of Cryptosporidium to change from that of a rare organism infecting mammals to that of an important, widespread cause of diarrheal illness in several animal species, including birds. The family Cryptosporidiidae is represented by small homoxenous coccidia assigned to a single genus, Cryptosporidium. One species, C. parvum, is now recognized as an important cause of diarrheal illness in several mammalian hosts, including man. Another species, C. baiłeyi, can produce severe respiratory disease in chickens and turkeys. Other species, including C. meleagridis, may cause enteritis and diarrhea in commercially reared poultry (Current and Blagburn, 1990).

The taxonomy of coccidia has been the subject of considerable controversy and change during the past two decades as new information concerning the morphology, life cycles, and genetics of these organisms became available. It was as a direct result of the rapid advances in our understanding of the fine structure of parasitic protozoa that occurred in the early 1960s that Levine (1970) created the phylum Apicomplexa. He recognized that as the Sporozoa contained diverse groups of protozoan parasites revision of the group was required. The phylum Apicomplexa, which he created, brings together all protozoa that possess an apical complex. This complex is an assemblage of organelles at the anterior end of coccidia in certain stages of development that facilitates attachment to and entry into host cells. A variety of organelles are included in the apical complex. There are one or more electron-dense polar rings; a conoid formed by several spirally coiled microtubules inside the polar ring; a number of rhoptries, which are electron-dense, tubular or saccular organelles often enlarged posteriorly, extending back from the anterior region inside the conoid; a number of micronemes, which are elongate, electron-dense organelles extending longitudinally in the anterior part of the cell, perhaps attached to the rhoptries; and a number of subpellicular microtubles, which are slender, electron-dense hollow structures extending back just beneath the pellicle from a polar ring (Figure 1.2).

Figure 1.2 Diagrammatic representation of a merozoite. (a) Longitudinal section of a merozoite. (b) Transverse and longitudinal section of a micropore, (c) The conoid. (From Scholtyseck, 1979.)

As a result of a grouping based on possession of an apical complex, the Apicomplexa as we now know it includes not only the true coccidia (suborder Eimeriorina) but also the Toxoplasms, Sarcocysts, and malarial parasites (suborder Haemosporina) of man and other animals, as well as the piroplasms of domesticated and wild animals, the heteroxenous hemogregarines, and the gregarines of invertebrates.

The history of development of our knowledge of the coccidia has been reviewed extensively. Books by Hammond and Long (1973) and Long (1982) provide an excellent introduction to the history of development of knowledge of coccidia. A thorough treatment of the taxonomy and biology of the more than 4000 named species and over 300 named genera in the Apicomplexa can be found in books by Levine (1988a,b).

III Basic Life Cycles

A STAGES IN THE LIFE CYCLE

Coccidia have life cycle stages that occur inside the host, termed endogenous stages. They also have exogenous stages that occur outside the host. Maturation of oocysts (sporogony) is the major exogenous stage. Some species of coccidia are homoxenous, with all endogenous stages occurring within one host. Other species are heteroxenous, with some endogenous stages occurring within the definitive host and other stages occurring within another host. Coccidia of economic importance in poultry are generally homoxenous.

Development of all true coccidia proceeds through a series of life cycle stages that ultimately results in the formation of oocysts. The oocysts are very resistant to adverse environmental conditions and may survive for long periods of time. Differentiation of coccidia into six genera can be made based on the structure of the sporulated oocysts (Figure 1.3).

Figure 1.3 Diagram showing morphology of five genera of coccidia affecting man and domestic animals. Original diagram.

1 Sporogony, Excystation, and Entry into Host Cells

Oocysts are exogenous stages that are usually shed unsporulated in the feces of a definitive host. The unsporulated oocysts need moisture and a favorable temperature to reach the infective sporulated stage (Figures 1.4a and 1.4b). The process of maturation is called sporogony and is the process by which a one-celled sporont (zygote) within the oocyst wall undergoes a series of divisions to form sporozoites, which may lie free within the oocyst wall or which may be contained within sporocysts. Development requires oxygen, moisture, and an optimum temperature (25–30 °C). Only sporulated oocysts, those containing fully formed sporozoites, are infective to the definitive and intermediate hosts.

Figure 1.4 (a) Photomicrograph of unsporulated oocysts of Eimeria tenella. (b) Photomicrograph of sporulated oocysts of E. tenella. (c) Photomicrograph of E. dispersa sporozoites (interference phase contrast), (d) Sporozoite of E. tenella in cecal epithelium of a chicken 1½ hours after inoculation with oocysts by mouth (hematoxylin and eosin). (e) Sporozoite of E. tenella in crypt of Lieberkuhn of the ceca 24 hours after inoculation of oocysts of mouth (hematoxylin and eosin). Original photomicrograph.

After being ingested by a host, the sporulated oocysts undergo the process of excystation, which is the release of infective sporozoites (Figure 1.4c). Excystation can occur in vitro if oocysts or sporocysts are exposed to conditions that occur in the gastrointestinal tract of the host, i.e., exposure to reducing conditions to adequate CO2, to temperatures equivalent to the host body temperature, and to solutions containing bile salts and trypsin.

Some investigators have suggested that there are two major steps in excystation. They suggest that the first step, an alteration of oocyst wall permeability, can be triggered by exposure to temperatures equal to those occurring in the host body and by exposure to elevated levels of CO2. This step may also be accomplished by treatment with sodium hypochlorite or by physical manipulations such as grinding in a tissue grinder, a process similar to that which occurs in the gizzard of an avian host. They suggest that the second step is the breakdown of the oocyst wall with release of the sporozoites from sporocysts. This may result from the action of pancreatic enzymes and bile salts.

Sporozoites of eimeriid coccidia may also escape without complete degradation of the sporocyst. They may do this through an opening in one pole of the sporocyst that is formed by degradation of a plug, the Stieda body. It is believed that trypsin degrades the Stieda body and that bile salts stimulate sporozoite motility.

The whole question of the excystation mechanism is now being reexamined since excystation has been shown to occur without the action of the gizzard and without exposure of oocysts and sporocysts to the enzymes of the upper intestine (Guyonnet, et al., 1989).

Once free in the intestinal lumen, the motile sporozoites (Figure 1.4d) actively penetrate into a host cell. It is believed that organelles of the apical complex of the invasive stages (sporozoites and merozoites) are involved in the penetration of host cells. The invasion process is illustrated in Figure 1.5.

Figure 1.5 Electron micrograph of a sporozoite of Eimeria papillała invading an epithelial cell of the mouse intestine. (Reproduced by the kind permission of B. Chobotar, H. Danforth, and R. Entzeroth.)

The cells of the reticuloendothelial system, particularly the macrophage, have long been considered to be involved in passage of sporozoites to appropriate host cells. Early studies suggested that after initial invasion of the intestinal mucosa, the sporozoites of E. necatrix (Van Doomink and Becker, 1957), E. tenella (Pattilo, 1959), and E. acervulina (Doran, 1966) are transported by macrophages to their sites of development. Unfortunately, the authors offered no definitive evidence that the transporting cells were indeed macrophages. They identified the cells as macrophages solely on the basis of their possessing large, densely staining nuclei. There is evidence that the cells that transport sporozoites to their sites of development are not macrophages but rather intraepithelial leukocytes (Lawn and Rose, 1982). In the study by Lawn and Rose, unlike the earlier studies, the investigators identified the cell using light and electron microscopy. Rose et al. (1984) further showed that after the sporozoites are transported to the deep glands of the intestinal epithelium within IELs, they leave these cells and enter epithelial cells for their development into first-generation meronts.

Lee and Al-Izzi (1981) have provided further evidence that the cells involved in sporozoite transport are not macrophages. These workers treated chickens prior to inoculation with E. tenella with carrageenan, a polygalactose selectively toxic to macrophages. The severity of infection increased rather than decreased, suggesting that cells other than macrophages were responsible for sporozoite transport. Other explanations are, of course, possible for the results obtained. Macrophages are responsible for many facets of the immune response. If they are absent, the immune response to the infection may be lacking and that may have been the factor responsible for the enhancement of the infection.

Thus, at least in chickens infected with E. necatrix, E. tenella, and E. acervulina, transport of sporozoites from the villus epithelium to the deep glands is known to occur and is probably mediated by IEL. The first-generation meronts of E. maxima as well as E. mitis also occur in the deep glands and are probably transferred there by IELs (Millard et al., 1972; Novilla et al., 1987). In chickens infected with E. praecox and E. brunetti, however, first-generation meronts develop in the superficial villi and along the sides of the villi and transport by IELs may not be important for their development (Long, 1967; Ryley et al., 1972).

2 Merogony (Schizogony)

After penetration of the mucosa the sporozoites of some species of coccidia such as E. tenella may, as just noted, be taken up by IELs and transported to their sites of development such as the crypts of Lieberkuhn (Lawn and Rose, 1982). Once in the crypts, the sporozoites leave the IELs and enter crypt epithelial cells (Figures 1.4d and 1.4e). Once inside the crypt epithelial cells, sporozoites round up and transform into uninucleate meronts. A photomicrograph of sporozoites undergoing the rounding-up process is shown in Figure 1.6b. The rounding-up process initiates merogonic development. As soon as the sporozoites begin to transform into meronts, there is an increase in the size of the nucleus and nucleolus of the host cell. This conclusion is supported by the observation of Marquardt et al. (1984), who found a positive correlation between the area of the nucleolus and the size of the parasite in fixed and stained tissues.

Figure 1.6 (a) Second generation meronts of Eimeria tenella (5) in a single host cell. Note enlarged host cell nucleus (HN). Hematoxylin and eosin. Magnification × 500. (b) Second generation merozoites of E. tenella freshly released from a meront. Note stages of rounding up (1–4) in a tissue-cultured CAM cell. Hematoxylin and eosin. Magnified × 900. (c) Microgametocyte of E. tenella in a tissue-cultured CAM cell. Stained hematoxylin and eosin. Magnification × 2000.

Merogonic development is followed by merogony, the asexual proliferative phase. This process is initiated when mitotic nuclear division occurs and is completed when elongate merozoites are released from the surface of the meront. After maturation the merozoites leave the host cell to enter other cells to start another meront generation. It has been generally accepted that coccidia of most species produce a fixed number of merozoites in each meront generation and that most coccidia have a fixed number (usually two to four) of asexual generations.

Some researchers have suggested that merogony is not really intracellular because the meront is separated from the cell cytoplasm by a parasitophorous vacuole (Figure 1.7c). This is not a common opinion.

Figure 1.7 (a and b) Unsporulated oocysts of Eimeria truncata from the feces of a gosling, (a) Magnification × 700. (b) Magnification × 1800. (c) Developing second generation meront of E. dispersa in an epithelial cell from the small intestine of a turkey poult. Spine-like structures (Sp) protrude from the membrane of the parasitophorous vacuole (pV). (From Long et al., 1979.)

The E. dispersa meront shown in Figure 1.7c appears to be anchored to the cytoplasm by a series of spines. Such a system of attachment has not been observed in host cells of chickens infected with other species of Eimeria, but has been seen in host cells from the bobwhite quail infected with E. dispersa (B. J. Millard, unpublished results).

There are questions about the validity of some aspects of the generally accepted version of the asexual cycle of Eimeria. It was always thought for example that the endogenous life cycle of E. tenella must proceed through second-generation merogony before gametocytes were formed. McDonald and Rose (1987), however, provided evidence that gametogony of E. tenella is normally initiated by merozoites of third-generation meronts. McDougald and Jeffers (1976) working with a particular strain of E. tenella showed that gametogony could also be initiated by merozoites from first-generation meronts. These observations are important because many scientists doing studies on the effect of antiparasitic substances on the gametogony of E. tenella assumed that chickens given second-generation merozoites immediately formed gamonts. Long and Jeffers (1982), for example, reported that sulfaquinoxaline was effective against gametogony because medication initiated after inoculation of second-generation merozoites prevented oocyst production. In view of the McDonald and Rose (1987) findings, it is possible that sulfaquinoxaline could have affected third-generation merogony not gametogony.

A glance at oocyst output data for any species of Eimeria in chickens shows that gametogony is initiated early, reaches a peak within 48 hours, and continues for several days. Gametogony and associated oocyst production can be extended by administering immunodepressant drugs (Long and Rose, 1970).

The results of these various studies all suggest that the numbers of asexual generations that may occur are not as rigorously defined as has been commonly believed.

3 Gamogony

Merozoites of the final generation of merogony enter host cells and initiate the sexual portion of the endogenous cycle (gamogony). In this process the merozoites develop into male or female gamonts, which are called microgamonts and macrogamonts, respectively. The microgamonts undergo repeated nuclear division followed by cytoplasmic division. As a result several thousand microgametes are formed. All known coccidian microgametes, except those of the genus Cryptosporidiums, are fusiform. They contain a nucleus (some may have two) and have two or three flagella for locomotion. Microgametes of Cryptosporidium do not have flagella and move by gliding. The macrogamonts, which remain uninucleate, grow to 15–50 μm in diameter. During growth of the macrogamont, there is proliferation of various organelles, including the wall-forming bodies that are involved in the subsequent formation of an oocyst wall. After the macrogamont matures it may be fertilized by a microgamete and then develop into a zygote. Maturation of the zygote into an oocyst includes formation of a protective wall. The oocyst when surrounded by its protective wall is released from its host cell and shed into the environment.

B SUMMARY OF THE LIFE CYCLE OF A TYPICAL EIMERIA: A HOMOXENOUS LIFE CYCLE

A diagram of the life cycle of a typical Eimeria of poultry is shown in Figure 1.8. Most species of Eimeria infecting poultry are homoxenous and have an endogenous intestinal cycle with asexual stages that proliferate by multiple division (merogony) and with sexual stages (gamogony) that produce oocysts. There is generally a limit to the number of asexual generations that may occur. Unsporulated oocysts are passed from the host and after passage undergo sporogony to form sporulated oocysts. Eimerian oocysts contain four sporocysts, each with two sporozoites. The life cycle of Eimerian coccidia is completed when a susceptible host ingests the infective, sporulated oocysts. Most species of Eimeria develop in the intestines of their hosts but some species of Eimeria develop in extra-intestinal sites such as the liver, gall bladder, and kidneys, and more rarely in the placenta, peritioneal cavity, and uterus.

Figure 1.8 A diagram of the life cycle of Eimeria tenella from the chicken. Original diagram.

C THE UNIQUE ASPECTS OF THE LIFE CYCLE OF CRYPTOSPORIDIUM: A HOMOXENOUS PARASITE CAPABLE OF AUTOINFECTION OF ITS HOST

Species of Cryptosporidium studied to date have life cycles that differ in four basic respects from the life cycles of Eimeria. Perhaps the biggest difference is the presence in some species of Cryptosporidium of thin-walled, autoinfective oocysts that allow prolonged infections in the absence of repeated oral exposure to the thick-walled, environmentally resistant oocysts. Another difference is the ability of some meronts of Cryptosporidium to recycle through an indefinite number of cycles thus producing large numbers of asexual organisms. A third difference is that cryptosporidial oocysts may sporulate within the host, resulting in production of oocysts that can initiate an autoreinfection or an infection in a susceptible host immediately after passage. The fourth difference is that development of several species of Cryptosporidium (e.g., C. parvum, C. baileyi) is much less rigidly confined to the gastrointestinal tract than development of Eimeria. Cryptosporidial development may occur in a variety of sites, including the gut epithelium, respiratory epithelium, biliary epithelium, and conjunctival epithelium.

IV The Coccidia of Avian Hosts

A THE CLASSIC COCCIDIA

1 Eimeria of Chickens

Coccidiosis in chickens may be caused by any one of seven species of coccidia, i. e., E. acervulina, E. brunetti, E. maxima, E. mitis, E. necatrix, E. praecox, and E. tenella. Each of these species causes distinctly different forms of intestinal coccidiosis. These species have been described extensively by Long et al. (1976) and Reid et al. (1984) and are almost certainly valid. Two additional species of Eimeria which have been reported to be parasites of the domestic chicken are probably not valid. One of these species, E. hagani, has not been studied since it was isolated in 1938 and has not been found outside the United States. In addition to my doubts about the validity of E. hagani, I now consider E. mivati not to be a true species. I therefore recognize as valid only the seven species E. acervulina, and E. necatrix, E. brunetti, E. maxima, E. mitis, E. acervulina, and E. praecox. A simple key by which organisms of these species can be identified is given in Table 1.1.

Table 1.1

Simple Key for the Identification of Eimeria Species in the Chicken

As coccidiosis of the chicken may be caused by any one of seven different species of Eimeria, it is often necessary to distinguish between them. The identification of the various species may be made using some or all of the following criteria: the location of the parasite in the host tissues and the characteristics of the lesions produced; the timing of the parasite’s patent and prepatent periods; the morphology of the oocysts and other developmental stages of the parasites; and the parasite’s immunological specificity. The characteristics of the seven valid species of Eimeria from the chicken are given in Table 1.2.

Table 1.2

Characteristics of the Seven Species of Eimeria of the Chicken