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Infections by Sarcocystis in cattle are ubiquitous worldwide. There is considerable debate concerning the identity of Sarcocystis spp. in cattle. Proper diagnosis of Sarcocystis spp. is important to assess their economic and public health importance. Currently there are seven named species: Sarcocystis hirsuta, Sarcocysti cuzi, Sarcocysti hominis, Sarcocysti bovifelis, arcocysti. heydorni, Sarcocysti bovini and Sarcocysti rommeli. Additionally, there are unnamed Sarcocystis spp. Two species, S. hominis and S. heydorni, are zoonotic. One out of seven species (S. hirsuta, contracted from cats) forms macroscopic cysts which can be visible during carcass inspection. Current molecular characterization is based on DNA extracted from sarcocysts from naturally infected cattle because DNA was not characterized from tissues of experimentally infected cattle or feces of experimentally infected definitive hosts. Sarcocystis cruzi (transmitted via canids) is recognized as the most pathogenic species and it causes abortion, low milk yield, poor body growth, and outbreaks of clinical sarcocystosis and death. Additionally, Sarcocystis infections have been linked to an inflammatory condition of striated muscles termed bovine eosinophilic myositis (BEM). Cattle affected by BEM appear clinically normal. Diagnosis of BEM at slaughter occurs when inspecting the carcass surface, or once the carcass has been divided into prime cuts or quarters. Sex and breed have no apparent influence on prevalence of BEM. The condition evidently occurs with equal frequency in steers, cows, and heifers. Virtually all striated muscles can be affected including skeletal muscles, the muscles of the eye, larynx, and the heart. In the USA, regulations require condemnation of BEM-affected parts, or (in severe cases) the entire carcass. These aesthetic considerations result in economic losses. Cattle experimentally infected with Sarcocystis have not shown BEM at slaughter. Here, we review the status of Sarcocystis spp. and BEM in cattle including prevalence, lesions, epidemiology, and association of BEM with different species of Sarcocystis.

Emerging infectious diseases are frequently zoonotic, often originating in wildlife, but enteric protozoa are considered relatively minor contributors. Opinions regarding whether pathogenic enteric protozoa may be transmitted between wildlife and humans have been shaped by our investigation tools, and have led to oscillations regarding whether particular species are zoonotic or have host-adapted life cycles. When the only approach for identifying enteric protozoa was morphology, it was assumed that many enteric protozoa colonized multiple hosts and were probably zoonotic. When molecular tools revealed genetic differences in morphologically identical species colonizing humans and other animals, host specificity seemed more likely. Parasites from animals found to be genetically identical - at the few genes investigated - to morphologically indistinguishable parasites from human hosts, were described as having zoonotic potential. More discriminatory molecular tools have now sub-divided some protozoa again. Meanwhile, some infection events indicate that, circumstances permitting, some “host-specific” protozoa, can actually infect various hosts. These repeated changes in our understanding are linked intrinsically to the investigative tools available. Here we review how molecular tools have assisted, or sometimes confused, our understanding of the public health threat from nine enteric protozoa and example wildlife hosts (Balantoides coli - wild boar; Blastocystis sp. - wild rodents; Cryptosporidium spp. - wild fish; Encephalitozoon spp. - wild birds; Entamoeba spp. - non-human primates; Enterocytozoon bieneusi - wild cervids; Giardia duodenalis - red foxes; Sarcocystis nesbitti - snakes; Toxoplasma gondii - bobcats). Molecular tools have provided evidence that some enteric protozoa in wildlife may infect humans, but due to limited discriminatory power, often only the zoonotic potential of the parasite is indicated. Molecular analyses, which should be as discriminatory as possible, are one, but not the only, component of the toolbox for investigating potential public health impacts from pathogenic enteric protozoa in wildlife., Graphical abstract Image 1, Highlights • Wildlife is a potential reservoir of disease agents that may infect humans. • The public health threat from enteric protozoa in wildlife is poorly understood. • Molecular tools may help in understanding this threat, but may also confuse. • We use nine enteric protozoa-wildlife host examples to review the current position. • Data accumulate, but more discriminatory tools and other approaches are important.

Toxoplasma gondii infections are common in humans and animals worldwide. Wild and domestic avian species are important in the epidemiology of T. gondii infections because felids prey on them and excrete millions of oocysts in the environment, disseminating the infection. Herbivorous birds are also excellent sentinels of environmental contamination with T. gondii oocysts because they feed on the ground. Toxoplasma gondii infections in birds of prey reflect infections in intermediate hosts. Humans can become infected by consuming undercooked avian tissues. Here, the authors reviewed prevalence, persistence of infection, clinical disease, epidemiology and genetic diversity of T. gondii strains isolated from turkeys, geese, ducks, ratites and avian species (excluding chickens) worldwide 2009-2020. Genetic diversity of 102 T. gondii DNA samples isolated worldwide is discussed. The role of migratory birds in dissemination of T. gondii infection is discussed.

Neospora caninum, Toxoplasma gondii, and Sarcocystis spp. are related Apicomplexan parasites that have 2 hosts in their life cycles. The definitive hosts excrete unsporulated (Neospora caninum, T gondii) or sporulated (Sarcocystis spp.) oocysts in their feces after ingesting tissue cysts from the tissues of ruminant intermediate hosts. These coccidians can cause abortion and neonatal mortality in ruminants. T gondii and Sarcocystis hominis (from cattle) are zoonotic. This article reviews information on the etiology, life cycle, diagnosis, control and prevention of these parasites and the diseases they cause in ruminants.

Cyclospora cayetanensis is the only species of the genus Cyclospora known to infect humans. The main risk factors for cyclosporiasis in industrialized countries include international travel to cyclosporiasis-endemic areas and domestic consumption of contaminated food, mainly fresh produce imported from the regions. In the developed world, cyclosporiasis has been observed in the general population regardless of age. Cyclosporiasis is common in impoverished endemic areas where water and food sanitation are poor or nonexistent, particularly affecting children. Most cases of cyclosporiasis reported in Europe and Australia have been acquired by visitors in regions where the parasite is endemic. The identification of food items that serve as vehicles in cyclosporiasis outbreaks represents a major challenge. Cyclospora cayetanensis outbreaks have been mostly reported in North America, probably due to better detection methods and disease surveillance that have helped in tracking outbreaks. A modified heated safranin stain was reported to uniformly stain Cyclospora oocysts a brilliant reddish-orange color.

The water buffalo is important to the economy of several countries in Asia and South America, and there are also isolated herds in Europe. This chapter reviews in detail history, taxonomy, and biology of coccidia and coccidiosis in buffaloes and summarizes the essential information concerning the biology of bubaline coccidiosis. Eleven or more Eimeria species, originally described from cattle, have been reported in buffalo. In experimentally infected buffaloes, endogenous development occurred in jejunum and ileum. Clinical coccidiosis has been reported in 3-week-old to 4-month-old buffaloes from India, Brazil, and the Netherlands. Gamonts and oocysts of Eimeria bareillyi have also been noted in ileum of naturally infected buffaloes in samples obtained at a slaughter in Mathura, India. Epidemiological investigations revealed that buffaloes can acquire Eimeria infection soon after birth. Several anticoccidial drugs are effective in treating coccidiosis in buffaloes. Sulfadimidine and amprolium prophylaxis were effective against experimentally induced Eimeria bareillyi coccidiosis.

This chapter presents essential information of coccidiosis in dogs. There are four species of Cystoisospora considered to be valid in dogs, C. canis, C. ohioensis, C. burrowsi, and C. neorivolta. Extraintestinal stages of C. canis, C. neorivolta, and C. burrowsi in tissues of dogs are unknown; however, biological evidence indicated that C. ohioensis invaded the spleens and mesenteric lymph nodes of dogs fed oocysts; dogs fed individual extraintestinal tissues excreted oocysts. Dog’s experimentally infected with C. burrowsi remained asymptomatic. Mice and rats were shown to be paratenic hosts based on feeding tissues to naive dogs. Coccidia are prevalent in dogs worldwide. The ingestion of food and water contaminated with oocysts is the major mode of transmission of Cystoisospora infections in dogs. Toltrazuril and ponazuril are most commonly used; medication with the compounds reduced or stopped oocyst excretion both in naturally exposed and experimentally infected dogs.

Coccidiosis is a common disease of livestock, including water buffaloes. Reports discussing the prevalence and identity of coccidian parasites in water buffaloes from Egypt are few, and nothing is known concerning the most pathogenic species

Coccidiosis is a common disease of camels, and camels are important for the economy of Asia and the Arabian Peninsula. Little is known regarding the prevalence of coccidian parasites in camels in Egypt. Fecal samples collected from the rectums of 200 camels at the Cairo slaughterhouse were processed using the sucrose flotation technique.

Toxoplasmosis in wild turkeys (

The coccidian parasite

Here, we report confirmation of sarcocysts of Sarcocystis jamaicensis in an experimental intermediate host, IFN-γ gene knockout (KO) mice orally inoculated sporocysts from its natural definitive host, a red-tailed hawk ( Buteo jamaicensis) (RTH). A RTH submitted to the Carolina Raptor Center, Huntersville, North Carolina, was euthanized because it could not be rehabilitated and released. Fully sporulated sporocysts from intestinal scrapings of the RTH were orally fed to 2 laboratory-reared outbred Swiss Webster mice (SW; Mus musculus) and to 2 KO mice. The sporocysts were infective for KO mice but not to SW mice. Both SW mice remained asymptomatic, and neither schizonts nor sarcocysts were found in their tissues when euthanized on day 54 post-inoculation (PI). The KO mice developed neurological signs and were necropsied 38-54 days PI. Schizonts/merozoites were found in both KO mice euthanized and they were confined to the brain. The predominant lesion was meningoencephalitis. Microscopic sarcocysts were found in muscles of both KO mice. When viewed with light microscopy, the sarcocyst wall appeared thin (1 μm thick) and smooth. Ultrastructural details of sarcocysts are described.

The life cycle of Sarcocystis species is heteroxenous (2-host), with carnivores being the definitive host and herbivores serving as intermediate hosts in predator-prey relationships. Raptors (eagles, hawks, falcons, and owls) are apex predators and are not consumed routinely by other carnivores, making the occurrence of sarcocysts in their muscles unusual. Recent reports of sarcocysts in eagles and owls with Sarcocystis encephalitis suggests that this condition may be becoming more frequent, and Sarcocystis falcatula has been implicated as the agent of encephalitis in golden ( Aquila chrysaetos) and bald eagles ( Haliaeetus leucocephalus) as well as great horned owls ( Bubo virginianus). The present study was done to determine the prevalence of sarcocysts of Sarcocystis species in the muscles of raptors from the southeastern United States. Pectoral and heart muscle from 204 raptor patients from the Carolina Raptor Center, Huntersville, North Carolina were tested for the presence of Sarcocystis species using histology. Only a few sarcocysts were seen in sections of pectoral muscle from 39 of 204 raptors (19.1%) and heart muscle from 9 that also had sarcocysts in their pectoral muscle. Two structural types of sarcocysts, thin-walled (1 μm; 62%) or thick-walled (2 μm, 38%), were seen. Statistical analysis of raptor age and gender was done by Fisher's exact test on samples from raptors with 20 or more samples per group. The prevalence of sarcocysts by age (2 yr or more) was significant for red-shouldered hawks ( Buteo lineatus) ( P = 0.022) and Cooper's hawks ( Accipiter cooperii) ( P = 0.028). Sarcocyst prevalence in male raptors from these groups evaluated statistically were always less than in females. Prevalence in female red-tailed hawks ( Buteo jamaicensis) (42.1%) was significantly greater than in males (6.7%) using Fisher's exact test ( P = 0.047). Examination of case histories from the 39 sarcocyst-positive raptors did not reveal an association with sarcocysts in raptor pectoral or heart muscle and in a diagnosis of encephalitis. Additional studies are needed to determine the epidemiology and relationships of Sarcocystis spp. that use raptors as intermediate hosts and the importance of Sarcocystis spp. in the overall wellbeing of raptors in their natural environments.

The coccidian parasite Cystoisospora canis (syn. Isospora canis) can cause clinical disease in dogs. Three generation of schizonts have been reported in the small intestine of dogs before oocysts are excreted 9-11 days post inoculation (PI). Here, we re-evaluated asexual development of C. canis in 2 dogs necropsied 10 days after oral inoculation with 100,000 C. canis oocysts; both dogs had excreted oocysts 9 days PI. Asexual and sexual stages were seen in the lamina propria throughout the small intestine. Merozoites of different sizes were present, often in the same vacuole. They were arranged singly, in pairs, and many within a single parasitophorous vacuole. The maximum number of nuclei within developing merozoites in a group was 8, but it could not be discerned if they were individual nuclei or parts of merozoites. Findings of abundant asexual stages 1 day after dogs had started excreting oocysts indicated continued asexual multiplication beyond the prepatent period. The stages found resemble the 3 generations reported previously. The mode of division of the asexual generations remains unclear. The results of the present study indicate that there are many generations that are difficult to determine because of the multiplication of merozoites in the original host cell without leaving it to enter new host cells. From the literature, it is evident that cat and dog coccidia ( Cystoisospora spp.) divide by more than 1 type of division, including endodyogeny. In the past, the schizont/meront groups containing more than 1 generation have been called "cysts." However, cyst is not an accurate term because it is best used for an orally infective stage of coccidia; monozoic tissue cysts of C. canis can occur in paratenic hosts in extraintestinal organs. We recommend the term "types" as originally proposed for intestinal stages of Toxoplasma gondii and used for the original description of the life cycle of C. suis of swine when describing endogenous stages of the Sarcocystidae. Ultrastructural studies are needed to determine the precise form of multiplication of canine Cystoisospora species.