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Sulfaquinoxaline played an important part in the demotion of roast chicken from vaunted Sunday-dinner status to an unrespected position on the everyday menu of the Western world. It had its origins in the chemical synthetic program that sprang from the introduction of sulfonamide drugs into human medicine in the 1930s. The program was sustained through the years of World War II despite declining clinical use of that chemical class. Several sulfa drugs were known to be active against the sporozoan parasite (Plasmodium spp.) that causes malaria, but were not satisfactory in clinical practice. A sulfonamide that had a long plasma half-life would ipso facto be considered promising as an antimalarial drug. Sulfaquinoxaline, synthesized during the war, was such a compound. It proved too toxic to be used in human malaria, but was found to be a superior agent against another sporozoan parasite, Eimeria spp., the causative agent of coccidiosis in domestic chickens. In 1948 sulfaquinoxaline was introduced commercially as a poultry coccidiostat. It was not the first sulfonamide found active against Eimeria spp. in poultry, but its practical success in disease control firmly established the routine incorporation of anticoccidial drugs in poultry feed. In this way, the drug exerted a major impact on the worldwide production of poultry meat. Although it has long been eclipsed by other drugs in poultry management, it continues to be used in other host species. This article describes the discovery of sulfaquinoxaline as a practical therapeutic agent, and examines the way in which the discovery arose from a partnership between industry and academia.

Although earlier investigators experimented with anticoccidial vaccines, the world's first commercially successful product was developed by Prof. S. A. Edgar of Auburn University, Auburn, AL. This product contained live, nonattenuated Eimeria tenella oocysts and was first marketed by Dorn and Mitchell, Inc., in 1952. Under the trade names of DM® Cecal Coccidiosis Vaccine, Coxine®, NObiCOX®, and CocciVac®, it went through several formulations containing various Eimeria species that parasitize chickens, and a further product containing turkey Eimeria species was also developed. After many product and company changes, one turkey and two chicken formulations of CocciVac® are still marketed worldwide by Schering-Plough Animal Health, Inc. Chicken and turkey formulations of Immucox®, a similar type of vaccine, were developed by Dr. E.-H. Lee and first marketed in 1985 in Canada by Vetech Laboratories, Inc. In 1974, Dr. T. K. Jeffers of Hess and Clark, Inc., Ashland, OH, published his discovery of precocious lines of coccidia, which facilitated the development of the first attenuated anticoccidial vaccine. For commercial reasons, Jeffers was unable to do this himself, but this first attenuated vaccine was designed by Dr. M. W. Shirley and colleagues at the Houghton Poultry Research Station (HPRS) in the United Kingdom. The vaccine was commercially developed under license in the United Kingdom by Glaxo Animal Health Ltd. and then Pitman-Moore, Inc., and launched in The Netherlands during 1989 under the trade name Paracox®. After further changes in company ownership, two formulations for chickens are now marketed worldwide by Schering-Plough Animal Health, Inc. Attenuation of coccidia by embryo adaptation was reported in 1972 in the United Kingdom by Dr. P. L. Long, who originally worked at the HPRS and later became a professor at the University of Georgia, Athens, GA. An embryo-adapted line of E. tenella was included with precocious lines of other species in a series of three attenuated vaccines for chickens under the trade name Livacox®, developed by Dr. P. Bedrník and launched in the Czech Republic in 1992 by Biopharm. The formulations of all other commercially available live anticoccidial vaccines for poultry are currently based upon the scientific principles established for the CocciVac®, Paracox® or Livacox® vaccines.

Oocysts attributable to Eimeria macusaniensisGuerrero et al. 1971, were found in coprolites and in archaeological sediments dating to the Holocene of Patagonia, Argentina. By means of a nonparametric regression using a generalized additive model, a significant relationship was found between the size of the oocysts and their antiquity. Specifically, a reduction in oocyst size over time was discovered, probably due to a parasite response to host replacement, to an extinct eimeriid species common during the Pliestocene–Holocene transition, or to environmental changes known for the Holocene. Explanations regarding coevolution between parasites, hosts, and paleoenvironmental conditions are discussed herein.

In 1910, H. B. Fantham described the life cycle of a coccidian parasite in birds. Fantham was a parasitologist at Cambridge University in the United Kingdom working for an enquiry into diseases affecting the red grouse. Despite the growing importance of the poultry industry and the realization that coccidiosis was an important disease of the fowl, little further work was carried out in the United Kingdom until coccidiosis research was initiated at the Veterinary Laboratory, Weybridge almost 30 yr later. Further progress depended upon research carried out at academic and agricultural institutions in the United States. E. E. Tyzzer at Harvard University provided the solid foundation upon which our present knowledge of coccidiosis, and the species of Eimeria involved in the disease, is based. Agricultural experiment stations (AESs) throughout the nation played an important role in communicating advances to the agricultural community. W. T. Johnson at Western Washington and, subsequently, Oregon AES made significant contributions to our understanding of the disease, as did C. A. Herrick and coworkers at Wisconsin AES, J. P. Delaplane and coworkers at Rhode Island AES, and P. P. Levine at Cornell University. Abbreviation: AES = agricultural experiment station

Albany was a prosperous town having 2 military bases (1 Air Force and 1 Marine) and several factories. If I liked the teacher or the class I could apply myself and make an A or B. I can remember taking literature classes and never reading an assigned story. In my final year at Troy State I was fortunate enough to take Invertebrate Biology, Embryology, Microscopical Techniques, and Parasitology from Dr. Raymond Kisner. Once I had worked out the life cycle of I. suis, I returned to Auburn to discuss it with Dr. Ernst.

This history addresses some of the developments in coccidiosis control that have permitted the poultry industry to expand and still live with this disease complex. Only a limited number of the hundreds of papers, reviews, or presentations made at numerous coccidiosis conferences can be cited in this history.

Cystoisospora belli is a coccidian parasite of humans, with a direct fecal–oral transmission cycle. It is globally distributed, but mainly found in tropical and subtropical areas. Many cases of C. belli infections have been reported in patients with HIV, and in patients undergoing immunosuppressive therapy for organ transplants or those treated for tumours worldwide. Unsporulated or partially sporulated oocysts of C. belli are excreted in feces. When sporulated oocysts in contaminated water or food are ingested, asexual and sexual stages of C. belli are confined to the epithelium of intestines, bile ducts and gallbladder. Monozoic tissue cysts are present in extra-intestinal organs (lamina propria of the small and large intestine, lymph nodes, spleen, and liver) of immunosuppressed humans. However, a paratenic host has not been demonstrated. Cystoisospora belli infections can be persistent, lasting for months, and relapses are common; the mechanism of relapse is unknown. Recently, the endogenous stages of C. belli were re-examined and attention was drawn to cases of misidentification of non-protozoal structures in the gallbladder of patients as C. belli. Here, we review all aspects of the biology of C. belli, including morphology, endogenous stages, prevalence, epidemiology, symptoms, diagnosis and control.

Most of the major contributions of Americans to knowledge of poultry parasites have been made in the last 100 years. Factors responsible for this tardiness differed somewhat according to the disease. The first parasitic diseases to receive attention were usually those with distinctive characteristics as well as serious consequences, such as \"gapes\" and lousiness. Since helminths could usually be readily observed, whereas protozoa could be observed only by persons skilled in microscopy, disorders attributable to the former usually received attention earlier than did protozoan diseases. The control of ectoparasites, before the use of modern insecticides, became vastly simplified as mechanical incubators and brooders replaced the hen, and as the birds were provided with better housing. The major contributions of Americans to our understanding of parasitic diseases of poultry are detailed for five disorders attributable to helminths, and two attributable to protozoa. The latter are histomoniasis of turkeys and coccidiosis of chickens. No attempt has been made to evaluate the impact of contemporary research.

Background Knowledge about parasitic infections is crucial information for animal health, particularly of free-ranging species that might come into contact with livestock and humans. Methods We investigated the seroprevalence of three tissue-cyst-forming apicomplexan parasites ( Toxoplasma gondii , Neospora caninum and Besnoitia besnoiti ) in 506 individuals of 12 wildlife species in Namibia using in-house enzyme linked immunosorbent assays (indirect ELISAs applying purified antigens) for screening and immunoblots as confirmatory tests. We included six species of the suborder Feliformia, four species of the suborder Caniformia and two species of the suborder Ruminantia. For the two species for which we had most samples and life-history information, i.e. cheetahs ( Acinonyx jubatus , n  = 250) and leopards ( Panthera pardus , n  = 58), we investigated T. gondii seroprevalence in relation to age class, sex, sociality (solitary, mother-offspring group, independent sibling group, coalition group) and site (natural habitat vs farmland). Results All but one carnivore species (bat-eared fox Otocyon megalotis , n  = 4) were seropositive to T. gondii , with a seroprevalence ranging from 52.4% (131/250) in cheetahs to 93.2% (55/59) in African lions ( Panthera leo ). We also detected antibodies to T. gondii in 10.0% (2/20) of blue wildebeest ( Connochaetes taurinus ). Adult cheetahs and leopards were more likely to be seropositive to T. gondii than subadult conspecifics, whereas seroprevalence did not vary with sex, sociality and site. Furthermore, we measured antibodies to N. caninum in 15.4% (2/13) of brown hyenas ( Hyaena brunnea ) and 2.6% (1/39) of black-backed jackals ( Canis mesomelas ). Antibodies to B. besnoiti were detected in 3.4% (2/59) of African lions and 20.0% (4/20) of blue wildebeest. Conclusions Our results demonstrate that Namibian wildlife species were exposed to apicomplexan parasites at different prevalences, depending on parasite and host species. In addition to serological work, molecular work is also needed to better understand the sylvatic cycle and the clear role of wildlife in the epidemiology of these parasites in southern Africa.