Coccidiosis

David A. Stevens , in Encyclopedia of Immunology (Second Edition), 1998

Vaccines

Vaccination, as a means of controlling coccidiosis, is an attractive alternative to prophylactic medication which is, inevitably, accompanied by the emergence of drug-resistant strains of the parasite. Until recently the only type of 'vaccine' commercially available (for chickens) consisted of wild-type, fully virulent organisms. Now there are two vaccines whose constituents have been attenuated by selection for abbreviated developmental cycles, or by adaptation to growth in developing chicken embryos. These are being successfully used in various types of flocks but, in view of their cost, are likely to be most useful for breeders and layers. The possibility of deriving live, attenuated strains suitable for vaccinating rabbits or sheep is being pursued.

Although live vaccines are effective, for reasons of cost, convenience (e.g. shelf-life) and safety, the ultimate goal of immunoprophylaxis for coccidiosis must be the availability of subunit vaccines, produced by recombinant DNA technology. Crude parasite extracts (primarily of sporozoites), given parenterally or orally, are capable of inducing protection against subsequent homologous challenge infection, but the results are influenced by the resistance phenotype of the host. Various purified candidate peptide antigens have afforded partial protection, either when given directly or via the hen (above).

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A Selective Review of Advances in Coccidiosis Research

H. David Chapman , ... Fiona M. Tomley , in Advances in Parasitology, 2013

Abstract

Coccidiosis is a widespread and economically significant disease of livestock caused by protozoan parasites of the genus Eimeria. This disease is worldwide in occurrence and costs the animal agricultural industry many millions of dollars to control. In recent years, the modern tools of molecular biology, biochemistry, cell biology and immunology have been used to expand greatly our knowledge of these parasites and the disease they cause. Such studies are essential if we are to develop new means for the control of coccidiosis. In this chapter, selective aspects of the biology of these organisms, with emphasis on recent research in poultry, are reviewed. Topics considered include taxonomy, systematics, genetics, genomics, transcriptomics, proteomics, transfection, oocyst biogenesis, host cell invasion, immunobiology, diagnostics and control.

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Biology and Diseases of Ruminants: Sheep, Goats, and Cattle

Margaret L. Delano , ... Wendy J. Underwood , in Laboratory Animal Medicine (Second Edition), 2002

Etiology.

Coccidiosis is an important acute and chronic protozoal disease of ruminants. In young ruminants, it is characterized primarily by hemorrhagic diarrhea. Adult ruminants may carry and shed the protozoa, but they rarely display clinical signs. Intensive rearing and housing conditions and stress increase the severity of the disease in all age groups.

Coccidia are protozoal organisms of the phylum Apicomplexa, members of which are obligatory intracellular parasites. There are at least 11 reported species of coccidia in sheep, of which several are considered pathogenic: Eimeria ashata, E. crandallis, and E. ovinoidalis (Schillhorn van Veen, 1986). At least 9 species of Eimeria have been recognized in the goat (Foreyt, 1990). Eimeria ninakohlyakimovae, E. arloingi, and E. christenseni are regarded as the most pathogenic. Eimeria bovis and E. zuernii (highly pathogenic), and E. auburnensis and E. alabamensis (moderately pathogenic), are among the 13 species known to infect cattle. Eimeria zuernii is more commonly seen in older cattle and is the agent of "winter coccidiosis."

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Japanese Quail as a Laboratory Animal Model

Janet Baer DVM , ... Kimberly Cheng PhD , in Laboratory Animal Medicine (Third Edition), 2015

3 Protozoa Agents

Coccidiosis, caused by coccidian protozoa, Eimeria spp., has been diagnosed in Japanese quail (Teixeira et al., 2004). In young quail chicks, infection is characterized by weight loss and diarrhea; it can be fatal or leave the bird with compromised digestion leading to malnutrition. Sulfonamides are an effective treatment.

Cryptosporidiosis, a diarrheal disease caused by infection with Cryptosporidium sp. has been reported in commercial quail colonies. Infected quail may have respiratory and intestinal involvement similar to chickens. The parasite is protected by an outer shell that allows survival outside the body for long periods and resistance to chlorine and many other disinfectants; however, it is killed by exposure to temperatures greater than 65°C.

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Biology and Diseases of Ferrets

Joerg Mayer Dr. med.vet., MSc, Dipl. ACZM, Dipl. ECZM (small mammal), Dipl. ABVP (ECM) , ... James G. Fox DVM, MS, DACLAM , in Laboratory Animal Medicine (Third Edition), 2015

Clinical Signs

Coccidiosis in ferrets is usually subclinical but has been reported to be associated with diarrhea, lethargy, and dehydration in one ferret ( Blankenship-Paris et al., 1993). Clinical signs are often seen in young, newly acquired ferrets and are more common after a stressful event (Rosenthal, 1994). Rectal prolapse can also develop in association with coccidial infection (Rosenthal, 1994). Severe clinical signs were reported in a recent outbreak in which morbidity rate was high, including an appreciable number of deaths, and ferrets of all ages were affected (Sledge et al., 2011). One case of biliary infestation with Eimeria furonis has been reported in the scientific literature (Williams et al., 1996).

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Introduction

Donald W. Duszynski , Lee Couch , in The Biology and Identification of the Coccidia (Apicomplexa) of Rabbits of the World, 2013

Coccidiosis: Disease, Symptoms, Perpetrators

Coccidiosis in rabbits primarily is a disease of young animals, while adults most often act as carriers by discharging oocysts into the environment. Rabbits become infected by ingesting sporulated oocysts with their food or water. The severity of the disease depends upon the number of infective oocysts ingested, upon the coccidian species involved and its preferred habitat and cell type within the rabbit, and upon each rabbit's own immune and nutritional status. Disease occurs most often in intensively managed animals, but it appears also in well-cared-for rabbits ( van Praag, 2011). Feces may contain blood and threads of mucus. Young rabbits present with retarded growth, due mainly to side effects on the kidney and the liver. In general, during both intestinal and hepatic coccidiosis, the normal function of infected cells is inhibited, the cells are hypertrophied, and they eventually die.

Intestinal coccidiosis mainly affects youngsters from age 6 wks to 5 mo. Clinical symptoms may include a rough coat, dullness, depression, diminished appetite and poor feed conversion, abdominal pain, dehydration, loss of weight, pale watery mucous membranes, and (sometimes profuse) diarrhea, 4 to 6 days post-infection (PI). Within intestinal enterocytes, when numerous cells are infected the villi will atrophy, leading to malabsorption of nutrients, electrolyte imbalance, anemia, hypoproteinemia, and dehydration due to erosion and ulceration of the epithelium. If weight loss reaches 20%, death may follow within 24 hr and can be preceded by convulsions or paralysis. In intestinal coccidiosis, disturbances in water and electrolyte balance occur in parasitized parts of the intestine before the appearance of the macroscopic lesions and are characterized by a loss of water and sodium (Bhat et al., 1996). The loss of sodium is compensated by the exchange of potassium from the blood, thereby leading to hypokalemia, and may cause death (Lebas et al., 1986). The majority of intestinal species develop in the small intestine, while only E. flavescens and E. piriformis complete their development in the caecum and colon, respectively. Upon necropsy, inflammation and edema will be found in the most heavily infected portions of the gastrointestinal tract (dependent on the coccidian species), sometimes accompanied by bleeding and mucosal ulcerations (Oncel et al., 2011; van Praag, 2011). Intestinal coccidia species can be classified into four groups based on clinical parameters (weight loss, diarrhea, mortality): non-pathogenic to slightly pathogenic: E. exigua, E. irresidua, E. matsubayashi, E. perforans, E. piriformis; moderately pathogenic: E. coecicola, E. media; very pathogenic: E. flavenscens, E. intestinalis, E. magna; and unknown pathology: E. nagpurensis, E. oryctolagi, E. roobroucki, E. vejdovskyi (numerous authors; see Chapter 6).

Hepatic coccidiosis, caused only by E. stiedai, affects rabbits of all ages when the parasite develops in the bile ducts of the liver, which become enormously enlarged, and thereby interferes with liver function. In hepatic coccidiosis, white nodules or cords develop on the liver, which later tend to coalesce; infected animals may have diarrhea and their mucous membranes may be icteric. Other symptoms include listlessness, thirst, wasting of the back and hindquarters, and enlargement of the abdomen caused by an enlarged liver and gall bladder. This infection can take either a chronic course during several weeks, or it may turn acute and end in death within 10 days, preceded by coma and sometimes diarrhea. At necropsy, liver, gall bladder, and the bile duct will be found to be distended and enlarged with white nodules covering the surface. Secondary bacterial infection, in particular with Escherichia coli, can lead to bacterial presence in the nervous system (Abdel-Ghaffar et al., 1990; Bhat et al., 1996; Yakchali and Tehrani, 2007; Freitas et al., 2010; van Praag, 2011).

Finally, hematological studies of rabbits infected with either intestinal or hepatic eimerian species (or both) demonstrate numerous changes in blood parameters including, but not limited to: reduced hemoglobin and RBC count, accompanied by a significant increase in packed cell volume (PCV) and total white blood cell (WBC) count; decreased levels of liver lipids and of sodium and chloride, but increased levels of total protein, globulin, cholesterol, low-density lipoproteins (LDL-c), triacylglycerols, and potassium. Electrolyte imbalance is likely attributed to diarrhea. Serum calcium, iron, copper, zinc, and glucose are usually slightly lower than in healthy animals and may indicate malnutrition due to intestinal damage or secondary bacterial infection. Liver coccidiosis is accompanied by significant elevation of serum bilirubin, alkaline phosphatase (ALP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and gamma glutamyl transpeptidase (GGT) (Licois et al., 1978a, b; Peeters et al., 1984; Abdel-Ghaffar et al., 1990; Bhat and Jithendran, 1995; Jithendran and Bhat, 1996; Kulišić et al., 1998, 2006; Tambur et al., 1998a, b, c, 1999; Freitas et al., 2010). When animals return to normal after appropriate treatment, values return to normal levels (van Praag, 2011).

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Zebra Finches in Biomedical Research

Mary M. Patterson MS, DVM, DACLAM , Michale S. Fee PhD , in Laboratory Animal Medicine (Third Edition), 2015

Coccidiosis

Coccidiosis occurs frequently in passerine birds. Isospora spp. (two sporocysts with four sporozoites) are more prevalent than Eimeria spp. (four sporocysts with two sporozoites) (Dorrestein, 2009a), but specific identification can be difficult. An older report describes the death of 7/24 zebra finches in a zoological park (Helman et al., 1984). At necropsy, most of the dead birds exhibited splenomegaly and two birds had hepatomegaly. Microscopic lesions, consisting of necrosis and granulomatous inflammation, were most severe in the liver and spleen. Macrophages contained oval to crescent-shaped organisms undergoing extraintestinal schizogony; however, oocysts were not visible in fecal examinations of the affected zebra finches. The authors attributed the mortalities to an Isospora or Toxoplasma gondii infection. Laboratory birds with coccidiosis can be administered coccidiostats such as amprolium (50–100   mg/l of drinking water for 5 days), if desired; cages should be changed near the end of the treatment period.

Cryptosporidiosis is rare in passerines. Fecal samples from 434 pet birds in China revealed 35 samples (8.1% prevalence) with Cryptosporidium oocysts (Qi et al., 2011). Out of 40 zebra finch samples, two were positive (5% prevalence); these were genotyped as Cryptosporidium baileyi. Among other passerines and psittacines, zebra finches could be infected with Sarcocystis sporocysts obtained from experimentally infected opossums (Box and Smith, 1982); in contrast, zebra finches resisted infection with Neospora caninum tachyzoites (McGuire et al., 1999).

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Foods, Materials, Technologies and Risks

A. Anadón MR Martínez-Larrañaga , in Encyclopedia of Food Safety, 2014

Coccidiosis

Coccidiosis is a parasitic disease, which can occur wherever animals are housed in small areas that are contaminated with coccidial oocysts. Coccidiosis has affected historically all species of wild and domestic birds. The nature of the parasitic infestation is present in all poultry farms, even in the presence of high sanitary standards and good management, with a high potential impact on animal welfare. Coccidia are without question the most important parasites of poultry in terms of distribution, frequency, and economic losses. Coccidiosis is an important enteric disease often caused by highly host-specific intestinal protozoan intracellular parasites which belong to the genus Eimeria (phylum Apicomplexa), and is characterized by high mortality. Some species tend to be more pathogenic in terms of the inoculation dose required to produce measurable effects, but all species of avian Eimeria produce weight loss, increased feed conversion ratios, loss of skin pigment, and decreased egg production. Avian coccidia of the genus Eimeria are extremely host specific. Chickens, turkeys, pheasants, and Japanese and bobwhite quails all have their own species. Each poultry species may be infected with several different Eimeria species (Eimeria necatrix, Eimeria tenella, Eimeria acervulina, Eimeria brunetti, Eimeria maxima, and Eimeria mivati in broiler chickens or chickens for fattening; Eimeria meleagrimitis, Eimeria gallopavonis, Eimeria adenoides, and Eimeria dispersa in turkeys; Eimeria duodenalis, Eimeria colchici, and Eimeria phasiani in pheasants). Although there are no exact prevalence and incidence data on clinical and subclinical coccidiosis in commercial poultry, it is widely acknowledged that the parasites are present in all commercial flocks.

The life cycle of the coccidium is complex (Figure 1). It begins when a susceptible bird ingests sporulated oocysts from the environment in contaminated litter, feed, and water. After ingestion, the sporozoites are released from the oocysts, and actively penetrate the host cells (intestinal mucosa or epithelial cells lining the gut wall), and develop intracellularly into multinucleate schizonts (also called meronts). The sporozoite transforms into trophozoite, which undergoes multiple karyokinesis and eventually produces numerous merozoites. This sequence of developmental events occurs a predetermined number of times (reinfective cycle), and each cycle is called a generation. Eventually the merozoites produced by the terminal generation of merozoites transform into sexual gametes. Some merozoites become differentiated into male and female gametes and the sexual part of the cycle is initiated. Immature sexual forms are known as gametocytes. The male gametocytes divide into a large number of mobile microgametocytes, whereas the development of macrogametocytes (female) leads to the production of a single microgametocyte. The male and female gametocytes unite resulting in the production of a zygote, which secretes a cyst wall and becomes an oocyst. The oocyst is excreted in the feces, usually in the nonsporulated condition. Sporulation occurs in the environment. Each oocyst ingested by the host may give rise to hundreds of thousands of infective oocysts in the feces within 7–12 days. Transmission from one farm to another is facilitated by the movement of personnel and equipment, and even new farms will have the parasite present within a few weeks after poultry are introduced.

Figure 1. Life cycle and reproduction of Coccidia.

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Biology and Diseases of Ruminants (Sheep, Goats, and Cattle)

Wendy J. Underwood DVM, MS, DACVIM , ... Adam Schoell DVM, DACLAM , in Laboratory Animal Medicine (Third Edition), 2015

Clinical Signs and Diagnosis

Coccidiosis is an important protozoal disease of young ruminants characterized primarily by hemorrhagic diarrhea. Diarrhea develops 10 days to 3 weeks after infection. Fecal staining of the tail and perineum will be present. Animals will frequently display tenesmus and rectal prolapses may develop. Anorexia, weight loss, dehydration, anemia, fever (infrequently), depression, and weakness may also be seen in all ruminants. The diarrhea is watery and malodorous and will contain variable amounts of blood and fibrinous, necrotic tissues. The intestinal hemorrhage may subsequently lead to anemia and hypoproteinemia. Concurrent disease with other enteropathogens may also be part of the clinical picture.

The disease is usually diagnosed by history and clinical signs. Numerous oocysts will be observed in fresh fecal flotation (salt or sugar solution) samples as the diarrhea begins. The pre-patent period for Eimeria is from 2 to 3 weeks and usually coincides with the development of clinical signs.

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Summary and Conclusions

Donald W. Duszynski , Lee Couch , in The Biology and Identification of the Coccidia (Apicomplexa) of Rabbits of the World, 2013

Pathology

Coccidiosis is one of the most frequent and prevalent parasitic diseases of domesticated food animals, including rabbits, and is accompanied by weight loss, mild intermittent to severe diarrhea, feces containing mucus or blood, dehydration, and decreased (rabbit) breeding ( Peeters et al., 1984; Bhat and Jithendran, 1995; Jithendran and Bhat, 1996).

Coudert et al. (1995) classified E. exigua, E. perforans, and E. vejdovskyi as slightly pathogenic. The pathogenicity may be connected, at least partially, to the localization of these coccidia, in most instances, in the upper parts of the villi (Streun et al., 1979; Pakandl and Coudert, 1999). In contrast, the most pathogenic rabbit coccidia, E. intestinalis and E. flavescens, parasitize the crypts of the lower part of the small intestine or cecum, respectively (Norton et al., 1979; Licois et al., 1992c; Pakandl et al., 2003). The intestinal epithelium is apparently more heavily damaged if the parasite destroys its stem cells located in the crypts (Jelínková et al., 2008). Endogenous development also causes desquamation of intestinal mucosa, capillary rupture, and bleeding into the intestinal lumen with catarrhal or hemorrhagic enteritis (Peeters et al., 1984; Bhat and Jithendran, 1995). Besides damaging intestinal mucosa, coccidia may cause a general reaction of the host with consequent changes in blood, urine, and feces (Licois et al., 1978a, b; Jithendran and Bhat, 1996; Kulišić et al., 1998; Tambur et al., 1998a, b, c, 1999). Blood taken from rabbits experimentally infected with coccidia revealed significant changes in the activity of GOT and alkaline phosphatase, and in the amount of bilirubin (Sherkov et al., 1986).

Kulišić et al. (2006) infected 52-day-old chinchilla rabbits (O. cuniculus) with a mixture of either 2 × 105 or 4 × 105 sporulated oocysts of E. flavescens (7%), E. matsubayashii (9%), E. magna (12%), E. neoleporis (19%), E. perforans (21%), and E. media (32%); rabbits were bled immediately before inoculation (day 0) and on days 4, 7, and 10 PI. During their infection, rabbits developed what they termed "mild coccidiosis," and presented symptoms that included polydipsia, bristling hair, decreased appetite, and moderate body weight loss. In their infected rabbits, the number of white blood cells (WBCs) never increased significantly over uninfected controls. Neutrophils in both infected groups increased significantly over control values on days 4, 7, and 10 PI, apparently because of the inflammation. Percentages of basophils and eosinophils remained at mostly similar levels throughout the experiment. Monocytes rose significantly only on day 10 PI. Lymphocyte numbers decreased significantly in infected rabbits. They (2006) suggested that the inflammatory process locally recruited leukocytes (lymphocytes?) that were lost through the damaged intestinal mucosa, and this was the probable reason for their count decrease. The count increase in the later phase of infection was attributed to hemoconcentration as a result of fluid loss (Kulišić et al., 2006).

Finally, it is difficult to find any brood of rabbits without also finding coccidian oocysts in their feces. These infections attack young rabbits more severely, especially those from 2 to 6 mo old (Gres et al., 2003). Older animals having recovered from any disease-related symptoms acquire immunity, but they are still important as carriers.

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