The Sarcocystis-cyst containing beef and pork as the sources of natural intestinal sarcocystosis in Thai people.

BACKGROUND: Human intestinal sarcocystosis is a zoonotic disease caused by two coccidians, i.e. Sarcocystis fusiformis (syn. S. bovihominis, S. hominis) due to consumption of raw infected beef and Sarcocystis meischeriana (syn. S. suihominis) due to consumption of infected raw pork. In 1987, survey of the macroscopic S. fusiformis cysts in market beef mainly from old water buffalos aged more than 15 years were commonly observed in Bangkok. In 2005, the macroscopic cyst was no longer seen in beef of cattle and water buffalo aged less than three years. OBJECTIVE: The epidemiological investigation of Sarcocystis spp. infected meat in Bangkok and Lampang. MATERIAL AND METHOD: Samples for each of the tongue and beef of cattle and water buffalo, pork from Bangkok markets and pork of domestic swine from some remote villages in various subprovinces (Ampurs) in Lampang were obtained for microscopic examination by H and E and selectively by PAS staining. RESULTS: The microscopic S. fusiformis cysts were seen in all five specimens of tongues and ten specimens of muscles of cattle and water buffalo obtained from fresh-food markets in Bangkok. Ten samples of pork from Bangkok markets revealed no coccidian infection. The microscopic S. meischeriana cysts were seen in three specimens of swine muscles collected from two subprovinces in Lampang. CONCLUSION: The present merozoites in coccidian cysts retrieved from beef and pork are similar to those previously observed in human intestine. This may histologically indicate an invasive sarcocystosis by both species leading to a condition presently known as chronic inflammation of undetermined etiology in man.

Utilization of stress in the development of an equine model for equine protozoal myeloencephalitis.

Neurologic disease in horses caused by Sarcocystis neurona is difficult to diagnose, treat, or prevent, due to the lack of knowledge about the pathogenesis of the disease. This in turn is confounded by the lack of a reliable equine model of equine protozoal myeloencephalitis (EPM). Epidemiologic studies have implicated stress as a risk factor for this disease, thus, the role of transport stress was evaluated for incorporation into an equine model for EPM. Sporocysts from feral opossums were bioassayed in interferon-gamma gene knockout (KO) mice to determine minimum number of viable S. neurona sporocysts in the inoculum. A minimum of 80,000 viable S. neurona sporocysts were fed to each of the nine horses. A total of 12 S. neurona antibody negative horses were divided into four groups (1-4). Three horses (group 1) were fed sporocysts on the day of arrival at the study site, three horses were fed sporocysts 14 days after acclimatization (group 2), three horses were given sporocysts and dexamethasone 14 days after acclimatization (group 3) and three horses were controls (group 4). All horses fed sporocysts in the study developed antibodies to S. neurona in serum and cerebrospinal fluid (CSF) and developed clinical signs of neurologic disease. The most severe clinical signs were in horses in group 1 subjected to transport stress. The least severe neurologic signs were in horses treated with dexamethasone (group 3). Clinical signs improved in four horses from two treatment groups by the time of euthanasia (group 1, day 44; group 3, day 47). Post-mortem examinations, and tissues that were collected for light microscopy, immunohistochemistry, tissue cultures, and bioassay in KO mice, revealed no direct evidence of S. neurona infection. However, there were lesions compatible with S. neurona infection in horses. The results of this investigation suggest that stress can play a role in the pathogenesis of EPM. There is also evidence to suggest that horses in nature may clear the organism routinely, which may explain the relatively high number of normal horses with CSF antibodies to S. neurona compared to the prevalence of EPM.

Risk factors associated with the presence of Sarcocystis neurona sporocysts in opossums (Didelphis virginiana).

Sarcocystis neurona is the most important cause of equine protozoal myeloencephalitis (EPM) in horse in the Americas. The only known definitive host for this parasite in the United States is the opossum (Didelphis virginiana); however, despite the importance of the disease, the epidemiology of the parasite in the definitive host is poorly understood. To begin addressing these data gaps, potential risk factors were evaluated for their association with the presence of sporocysts of S. neurona in opossums live-trapped in March 1999 and November 1999 to May 2000. Sporocysts of S. neurona were found in 19 of the 72 animals examined. Potential risk factors evaluated were locality, trap date, age, gender, the presence of young in the pouch of females, and body condition score. Variables that were associated with the presence of S. neurona sporocysts were used in logistic regression analysis. Of the factors examined, season and body condition score were associated with increased odds of an animal harboring sporocysts.

Analysis of risk factors for the development of equine protozoal myeloencephalitis in horses.

OBJECTIVE: To investigate risk factors for development of equine protozoal myeloencephalitis (EPM) in horses. DESIGN: Case-control study. ANIMALS: 251 horses admitted to The Ohio State University Veterinary Teaching Hospital from 1992 to 1995. PROCEDURE: On the basis of clinical signs of neurologic disease and detection of antibody to Sarcocystis neurona or S neurona DNA in cerebrospinal fluid, a diagnosis of EPM was made for 251 horses. Two contemporaneous series of control horses were selected from horses admitted to the hospital. One control series (n = 225) consisted of horses with diseases of the neurologic system other than EPM (neurologic control horses), and the other consisted of 251 horses admitted for reasons other than nervous system diseases (nonneurologic control horses). Data were obtained from hospital records and telephone conversations. Risk factors associated with disease status were analyzed, using multivariable logistic regression. RESULTS: Horses ranged from 1 day to 30 years old (mean +/- SD, 5.7 +/- 5.2 years). Risk factors associated with an increased risk of developing EPM included age, season of admission, prior diagnosis of EPM on the premises, opossums on premises, health events prior to admission, and racing or showing as a primary use. Factors associated with a reduced risk of developing EPM included protection of feed from wildlife and proximity of a creek or river to the premises where the horse resided. CONCLUSIONS AND CLINICAL RELEVANCE: Development of EPM was associated with a number of management-related factors that can be altered to decrease the risk for the disease.

Diarreas parasitarias no amebianas / Non amoebian parasitary diarrheas

Se analiza un conjunto de infecciones parasitarias que se traducen por diarreas agudas altas, hipersecretoras, de evolución más arrastrada que las bacterianas; de curso inicialmente febril y que comprometen el estado general debido a alteraciones hidroelectrolíticas y trastornos de la absorción intestinal. Estos cuadros, producidos por protozoos esporulados (Isospora belli, Sarcocystis hominis, Cryptosporidium, Cyclosporidium y Mycrosporidium), afecta de preferencia los pacientes inmunodeprimidos y no tienen tratamiento reconocidamente eficaces. En los sujetos no inmunodeprimidos son autolimitados

Instar susceptibility of the monarch butterfly (Danaus plexippus) to the neogregarine parasite, Ophryocystis elektroscirrha.

The susceptibility of the monarch butterfly (Danaus plexippus) larvae to the neogregarine parasite, Ophryocystis elektroscirrha, was tested in the laboratory. Spore loads recovered from infected monarch butterflies were directly related to the inoculum level, larval stage of the host, and spore age. There was a linear relationship between spores ingested by first instar larvae and spore concentration. Larvae feeding on leaves treated with 0, 50, 500, 5000, or 50,000 spores averaged 0, 0, 193, 457, or 1,255 spores, respectively, on the abdomens of the adult butterflies. When first, third, and fifth instar larvae were given 14.5 spores/mg of body weight, there was no significant difference in the spore load of the adults resulting from the first and third instars. However, there were significant differences in the spore load from adults resulting from the first and third instars versus the fifth instar. In addition, 1-year-old spores were not as infectious as fresh spores. Our findings indicate that under field conditions, the first instar is most likely to become infected because one spore appears sufficient to produce a detectable spore load in the adult. Older instars are less susceptible and have fewer opportunities to encounter sufficient viable spores for infection to occur. Thus, vertical transmission appears to be the primary mode of parasite maintenance in natural populations of monarch butterflies.

Studies on pathogenesis, tissue infection and congenital transmission in cows experimentally infected with Sarcocystis cruzi by various routes.

A group of nine cows, naturally infected with Sarcocystis, were challenged with Sarcocystis cruzi: three intrarumenally with sporocysts, two intrarumenally with water (controls), two intravenously with merozoites grown in vitro and two intravenously with saline solution (controls). The animals intrarumenally challenged with sporocysts developed acute sarcocystiosis and produced stillborn calves, whereas those intravenously challenged with merozoites suffered from subclinical sarcocystiosis with premature births. No parasites were found in calves from cows challenged with sporocysts; however, a meront of Sarcocystis was found within a macrophage in the cerebrospinal fluid of a calf from a cow intravenously inoculated with merozoites of S. cruzi. This is the first time that merozoites of S. cruzi grown in vitro have been demonstrated to retain the ability to infect their natural intermediate host and complete their life cycle.

Sarcocystis sp. en el diafragma de un gato doméstico de Valdivia, Chile / Sarcocystis sp. in a domestic cat diaphragm at Valdivia, Chile

During 1987, diaphragm of 24 domestic cats from the city of Valdivia, Chile, were examined. In one (3,7 percent) cat infection by cysts of Sarcocystis sp. was observed. This is the first report of feline muscular infection by Sarcocystis sp. in Chile

Identification of opossums (Didelphis virginiana) as the putative definitive host of Sarcocystis neurona.

Sarcocystis neurona is an apicomplexan that causes equine protozoal myeloencephalitis (EPM) in North and South America. Horses appear to be an aberrant host, because the merozoites continually divide in the central nervous system, without encysting. The natural host species has not previously been identified. The small subunit ribosomal RNA (SSURNA) gene of S. neurona was compared to those of Sarcocystis muris, Sarcocystis cruzi, Toxoplasma gondii, and Cryptosporidium parvum to identify a unique region suitable for a species-specific amplification primer. The S. neurona SSURNA primer was used in a polymerase chain reaction (PCR) assay for the purpose of identifying this organism in feces and intestinal digest of wildlife specimens. Sporocysts were isolated from 4 raccoons (Procyon lotor), 2 opossums (Didelphis virginiana), 7 skunks (Mephitis mephitis), 6 cats (Felis catus), 1 hawk (Accipiter sp.), and 1 coyote (Canis latrans). The S. neurona SSURNA PCR assay and a control PCR assay using protist-specific primers were applied to all sporocyst DNA samples. All sporocyst DNA samples tested positive on the control assay. The SSURNA PCR assay yielded a 484-bp product only when applied to opossum samples. The SSURNA gene of both opossum sporocyst samples was sequenced to determine its relationship to the S. neurona SSURNA gene. The sequence had 99.89% similarity with S. neurona. This suggests that opossums are the definitive host of S. neurona.

Muscle disorders in the horse: a retrospective study.

Case records of horses with muscle disorders presenting to the Veterinary Medical Teaching Hospital of the University of California, Davis, over a nine year period were evaluated. The objectives of the review were to identify the common myogenic muscle problems and their clinical features. Muscle disease of idiopathic aetiology following exercise was by far the most common condition noted. Other causes of myogenic muscle disorders included congenital, infectious, immune-mediated and nutritional factors.

Pathology of experimental Sarcocystis falcatula infections of canaries (Serinus canarius) and pigeons (Columba livia).

Sarcocystis falcatula is an apicomplexan parasite with a broad range of avian intermediate hosts. The pathology and pathogenesis of infection with this parasite has been studied experimentally in the budgerigar (Melopsittacus undulatus). The present study quantitatively examines the pathology of this parasite in canaries (Serinus canarius) and pigeons (Columba livia) and compares it with that found in budgerigars. The general progression of merogony and cyst formation is similar qualitatively to that seen in budgerigars, but it differs quantitatively. The principal site of precystic merogony is in pulmonary endothelial cells. The magnitude of pulmonary meront burdens (at similar inoculated dosages) varies in different intermediate host species. Merogony is less persistent than in budgerigars. Among the various species of birds, the magnitude of precystic merogony correlates differently with the magnitude of skeletal muscle cyst burdens. The distribution of cyst burdens among various muscles also differs. The composition of inflammatory cells differs among various avian species' response to S. falcatula. Pathologic changes quantitatively parallel tissue meront burdens (except possibly in the liver of canaries), resulting in an interstitial pneumonitis, hepatitis, and mild inflammatory lesions of other organs.

Effects of Sarcocystis miescheriana infection on carcass quality and on the water-binding capacity of the meat of halothane-tested fattening pigs.

Ten halothane-positive pigs (stress sensitive, group A) and ten halothane-negative pigs (stress insensitive, Group C) with a mean body weight of 36 kg were each inoculated orally with 50,000 sporocysts of Sarcocystis miescheriana. Twelve halthane-positive pigs (Group B) and ten halothane-negative pigs (Group D) served as non-infected controls. Thirteen weeks post infection (p.i.) the lean: fat ratios of the pigs of the infected groups A and C were lower (A, 1:0.41 +/- 0.09; C, 1:0.50 +/- 0.10) than those of the pigs of the non-infected groups B and D (B, 1:0.50 +/- 0.08; D, 1:0.55 +/- 0.08). The back-fat thickness, the fat thickness 'A' and the fat thickness 'B' were thinner in infected pigs than in non-infected pigs. The difference in Lendenstärkespeckquotient (Loin Fat Thickness Quotient) (LSQ) between infected and non-infected pigs was not statistically significant. The values of the water-holding capacity were lower in infected pigs than in non-infected pigs, the difference being statistically significant only in the halothane-negative groups (C, 0.45 +/- 0.02; D, 0.48 +/- 0.04). The water-absorbing capacity was significantly higher in the infected groups (A, 5.92 +/- 3.99%; B, 2.26 +/- 1.08%; C, 8.96 +/- 2.90%; D, 4.97 +/- 2.51%). In conclusion, it can be said that there was a slight tendency towards a better carcass quality and a better water-binding capacity in infected pigs, although this was combined with reduced growth rates.

The effects of Sarcocystis miescheriana infections on blood enzymes and weight gain of stress-sensitive and stress-insensitive pigs.

The effects of mild Sarcocystis miescheriana infection on blood enzymes and body weight were compared in stress-sensitive (halothane positive) and in stress-insensitive (halothane negative) pigs. Ten halothane-positive pigs (Group A) and ten halothane-negative pigs (Group C) with a mean body weight of 36 kg were each inoculated orally with 50,000 sporocysts of S. miescheriana. Twelve halothane-positive pigs (Group B) and ten halothane-negative pigs (Group D) served as non-infected controls. Five days before infection (a.i.) and 58 days post infection (p.i.) all pigs were myostress challenged (creatine kinase test). During the whole period of the experiment (3 weeks a.i. to 13 weeks p.i.) body weights were determined and blood samples taken at weekly intervals. Creatine kinase (CK), aspartate aminotransferase (ASAT) and Sarcocystis antibody titres were determined. The infection induced slightly elevated temperatures (max. 42.8 degrees C) and transient reduced food intake during the 2nd and 3rd week p.i. The CK values of the infected pigs in Groups A and C increased from Day 28 p.i. onwards, and were significantly higher than those of the pigs of the non-infected controls (Days 35-77 p.i.). The ASAT values of the infected groups (A and C) increased from Day 21 p.i. onwards, and were significantly higher than those of the non-infected controls from Days 28-77 p.i. The myostress injection at 5 days a.i. (1st CK test) resulted in significantly higher CK and ASAT values in stress-sensitive pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenesis of infection with Sarcocystis rauschorum (Apicomplexa) in experimentally infected varying lemmings (Dicrostonyx richardsoni).

This study describes the sequential formation of lesions associated with the endogenous development of Sarcocystis rauschorum (Apicomplexa: Sarcocystidae) in varying lemmings, Dicrostonyx richardsoni. Lethal doses of sporocysts (greater than 500) were orally administered to lemmings examined 1-6 days postinoculation (DPI) whereas sublethal doses were administered to lemmings examined subsequently. Transient necrosis and purulent inflammation, in association with precystic merogony, occurred in the liver by 4.5 DPI, peaked at 6 DPI and subsided beginning at 11 DPI with the liver returning to normal by 15 DPI. Cyst formation in skeletal and cardiac muscle was associated with purulent inflammation and sarcolemmal proliferation beginning at 9 DPI. These lesions persisted to 42 DPI. In addition, multifocal nonsuppurative meningoencephalitis was present in six of 11 infected lemmings examined between 11 and 15 DPI.