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Objective: To describe clinical signs, treatment, and outcome for California sea lions (Zalophus californianus) with Sarcocystis-associated polyphasic rhabdomyositis., Animals: 38 free-ranging juvenile to adult California sea lions examined at a rehabilitation center in California between September 2015 and December 2017., Procedures: Medical records at The Marine Mammal Center were reviewed to identify sea lions in which sarcocystosis had been diagnosed., Results: Clinical signs were highly variable and associated with polyphasic rhabdomyositis attributed to Sarcocystis neurona infection. Generalized severe muscle wasting, respiratory compromise, and regurgitation secondary to megaesophagus were the most profound clinical findings. Respiratory compromise and megaesophagus were associated with a poor prognosis. Eight of the 38 sea lions were treated and released to the wild, and 2 subsequently restranded and were euthanized. Two additional animals received no targeted treatment and were released. The remaining 28 animals were either euthanized or died during treatment., Conclusions and Clinical Relevance: Results suggested that unlike other marine mammals, which typically develop encephalitis, California sea lions with sarcocystosis often have polyphasic rhabdomyositis with highly variable clinical signs and that extensive diagnostic testing may be required to confirm the diagnosis. Treatment with an antiprotozoal drug in combination with corticosteroids may resolve clinical disease, but the prognosis is guarded.

An ante-mortem diagnosis of equine protozoal myeloencephalitis (EPM) is presently based on clinical presentation, immunodiagnostics performed on serum and cerebrospinal fluid (CSF), and ruling out other neurological disorders. Molecular techniques introduce a novel and promising approach for the detection of protozoal agents in CSF. Hypothesizing that real-time PCR (rtPCR) can be a useful complement to EPM diagnostics, 210 CSF samples from horses suspected of neurological disease with EPM included as a differential diagnosis were tested using rtPCR to detect Sarcocystis neurona DNA and immunodiagnostics targeting antibodies against the same pathogen, performed on serum and CSF samples. Molecular and immunological results were compared with respect to origin of the horse, time of the year, signalment, clinical signs and treatment history. Twenty-five horses tested positive in CSF for S. neurona by rtPCR only, while 30 horses had intrathecally-derived antibodies to S. neurona only (serum to CSF ratio ≤ 64 by indirect fluorescent antibody test - IFAT), and 13 horses tested rtPCR-positive in CSF with evidence of intrathecally-derived antibodies to S. neurona. Previous treatment for EPM was the only variable presenting statistical difference between the two testing modalities, highlighting that animals with history of anti-protozoal treatment were more likely to test positive solely in IFAT, while horses without treatment were more likely to test positive by rtPCR only. The results support the use of molecular diagnosis for EPM caused by S. neurona as a complement to immunodiagnostics. The use of rtPCR in CSF for the detection of S. neurona may improve the diagnostic work-up of neurologic disease suspected horses, especially in animals without previous anti-protozoal treatment., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: Infection by 2 or more protozoa is linked with increased severity of disease in marine mammals with protozoan encephalitis., Hypothesis/objectives: To assess whether horses with equine protozoal myeloencephalitis (EPM) caused by Sarcocystis neurona also have evidence of infection with Neospora hughesi or Toxoplasma gondii. We hypothesized that horses with EPM would be more likely than horses with cervical vertebral stenotic myelopathy (CVSM) to be positive for antibodies to multiple protozoan parasites., Animals: One hundred one horses with neurologic disease: 49 with EPM and 52 with CVSM., Methods: Case review. Archived serum and cerebrospinal fluid (CSF) from 101 horses were examined. Inclusion criteria included neurologic disease, antemortem or postmortem diagnosis of EPM or CVSM, and availability of serological results or archived samples for testing. Additional testing for antibodies was performed on serum for T. gondii, as well as serum and CSF for N. hughesi., Results: Horses with EPM were more likely than horses with CVSM to have positive immunologic results for S. neurona on serum (95.9% versus 76.9%, P = .0058), CSF (98.0% versus 44.2%, P < .00001), and serum : CSF titer ratio (91.8% versus 0%, P < .00001). Positive results for Neospora and Toxoplasma were uncommon, with total seroprevalence rates of 12.9% and 14.9%, respectively. The proportions of EPM cases testing positive for Neospora and Toxoplasma (16% and 12%) were not different from the proportions of CVSM cases testing positive (10% and 17%, P = .31 and .47, respectively)., Conclusion: Results do not indicate an important role for protozoal coinfection in EPM in the eastern United States., (Copyright © 2018 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.)

Typically, carnivores are the definitive and herbivores the intermediate hosts for protozoan Sarcocystis spp. In the definitive host, the parasite has sexual multiplication in the intestine. Asexual phases occur in the musculature of different intermediate hosts. Although intestinal sarcocystosis is common in dogs, muscular symptomatic sarcocystosis is rarely reported. Here we report a fatal dual Sarcocystis spp. infection in a dog. The dog had acute onset of non-ambulatory tetraparesis. While neurological findings suggested a generalized neuromuscular disease with peripheral neuropathy concordant with the neurological deficits, the highly elevated muscle enzymes were more suggestive of a myopathy. Despite supportive therapy, the dog died three days after the onset of clinical signs. Necropsy revealed severe monophasic multifocal myodegeneration with severe pyogranulomatous inflammation. Histology revealed multiple sarcocysts in skeletal muscles and a smaller number in the heart. In light microscopy, both thin-walled and very thin-walled sarcocysts were found in skeletal muscles. Transmission electron microscopy confirmed the presence of two types of mature sarcocysts. Morphologically, cysts were indistinguishable from Sarcocystis caninum and Sarcocystis svanai, which were previously reported in a dog from USA. A region of the 18S rRNA gene sequence confirmed the presence of one species, S. arctica/caninum, without evidence for a dual infection. This is the first report of muscular sarcocystosis in a dog in Europe and, intriguingly, revealed morphologically similar species across the Atlantic., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Muscular sarcosporidial infections by Sarcocystis lutrae (Apicomplexa: Sarcocystidae) from the otter (Lutra lutra) and badger (Meles meles) (Carnivora: Mustelidae) were found in the Czech Republic. As part of a diversity evaluation of Sarcocystis in wild carnivores during 2016-2017, samples of diaphragm, tongue and hind-limb muscles were collected from nine districts, examined by compression and characterized molecularly. Cyst walls were thin, with no visible protrusions, and histological sections of infected muscle tissue showed no host responses. Fourteen of 17 badgers (82% prevalence) and one otter (100% prevalence) were positive for sarcocysts. Sequence analyses at four loci (18S rRNA, 28S rRNA, ITS1 and cox1) confirmed the identity as S. lutrae. This is also the first report of a co-infection with muscular sarcocystosis and Trichinella in badger. The finding of Trichinella is important from the zoonotic point of view, since badgers are used for meat consumption. Similar and future monitoring of both parasitic taxa are needed.

Canine distemper virus commonly infects free-ranging, terrestrial mesopredators throughout the United States. Due to the immunosuppressive effects of the virus, concurrent opportunistic infections are also common. Among these, secondary systemic protozoal infections have been described in a number of species. We report an unusual presentation of necrotizing encephalitis associated withSarcocystissp in four raccoons and one skunk concurrently infected with canine distemper virus. Lesions were characterized by variably sized necrotizing cavitations composed of abundant mineral admixed with inflammatory cells and protozoa.Sarcocystissp was confirmed via immunohistochemistry using a monoclonal antibody toSarcocystis neurona The pathologic changes are similar to lesions in human AIDS patients infected withToxoplasma gondii., (© The Author(s) 2015.)

Toxoplasma gondii and Sarcocystis neurona are protozoan parasites with terrestrial definitive hosts, and both pathogens can cause fatal disease in a wide range of marine animals. Close monitoring of threatened southern sea otters (Enhydra lutris nereis) in California allowed for the diagnosis of dual transplacental transmission of T. gondii and S. neurona in a wild female otter that was chronically infected with both parasites. Congenital infection resulted in late-term abortion due to disseminated toxoplasmosis. Toxoplasma gondii and S. neurona DNA was amplified from placental tissue culture, as well as from fetal lung tissue. Molecular characterization of T. gondii revealed a Type X genotype in isolates derived from placenta and fetal brain, as well as in all tested fetal organs (brain, lung, spleen, liver and thymus). This report provides the first evidence for transplacental transmission of T. gondii in a chronically infected wild sea otter, and the first molecular and immunohistochemical confirmation of concurrent transplacental transmission of T. gondii and S. neurona in any species. Repeated fetal and/or neonatal losses in the sea otter dam also suggested that T. gondii has the potential to reduce fecundity in chronically infected marine mammals through parasite recrudescence and repeated fetal infection.

Recent reports of Sarcocystis fayeri-induced toxicity in people consuming horse meat warrant investigation on the prevalence and molecular characterization of Sarcocystis spp. infection in horses. Sarcocysts in skeletal muscle of horses have been commonly regarded as an incidental finding. In this study, we investigated the prevalence of sarcocysts in skeletal muscle of horses with neuromuscular disease. Our findings indicated that S. fayeri infection was common in young mature horses with neuromuscular disease and could be associated with myopathic and neurogenic processes. The number of infected muscles and number of sarcocysts per muscle were significantly higher in diseased than in control horses. S. fayeri was predominantly found in low oxidative highly glycolytic myofibers. This pathogen had a high glycolytic metabolism. Common clinical signs of disease included muscle atrophy, weakness with or without apparent muscle pain, gait deficits, and dysphagia in horses with involvement of the tongue and esophagus. Horses with myositis were lethargic, apparently painful, stiff, and reluctant to move. Similar to humans, sarcocystosis and cardiomyopathy can occur in horses. This study did not establish causality but supported a possible association (8.9% of cases) with disease. The assumption of Sarcocysts spp. being an incidental finding in every case might be inaccurate., (Copyright © 2015 Elsevier B.V. All rights reserved.)

A 3-yr-old captive-born California sea lion (Zalophus californianus) developed Sarcocystis neurona-induced myositis and rhabdomyolysis that led to acute renal failure. The sea lion was successfully managed with fluid therapy, antiprotozoals, antibiotics, anti-inflammatories, antiemetics, gastroprotectants, and diuretics, but developed severe delayed hypercalcemia, a syndrome identified in humans after traumatic or exertion-induced rhabdomyolysis. Treatment with calcitonin was added to the management, and the individual recovered fully. The case emphasizes that animals with rhabdomyolysis-induced renal failure risk developing delayed hypercalcemia, which may be life threatening, and calcium levels should be closely monitored past the resolution of renal failure.

Acalculous cholecystitis and cholangitis are increasingly being recognized as complications of AIDS. The opportunistic parasites that have been most commonly associated with these disorders are Cryptosporidium species, Isospora belli, Cyclospora cayetanensis and Enterocytozoon bieneusi. The authors performed a parasitological survey on the gallbladder tissue sections of patients underwent cholecystectomy due to chronic acalculous cholecystitis at the Shiraz University of Medical Sciences, Iran. Light microscopic investigation in more than three hundred archived histopathological slides revealed the presence of sexual stages (i.e., mature sporocysts) of a coccidial protozoan in a patient with AIDS who developed acalculous cholecystitis as confirmed by histological, parasitological and molecular tests in which Sarcocystis species was the only identifiable pathogen in gallbladder sections. In the best of our knowledge it's the first documented case of chronic non-calculous cholecystitis due to Sarcocystis parasite in an Iranian AIDS patient from worldwide.

Sarcocystis neurona is an unusual species of the genus Sarcocystis. Opossums (Didelphis virginianus, D. albiventris) are the definitive hosts and several other species, including dogs, cats, marine mammals, and horses are intermediate or aberrant hosts. Sarcocysts are not known to form in aberrant hosts. Sarcocystis neurona causes fatal disease in horses (Equine Protozoal Myeloencephalitis, EPM). There are numerous reports of fatal EPM-like infections in other species, usually with central nervous system signs and associated with the schizont stage of S. neurona. Here, we report fatal disseminated S. neurona infection in a nine-week-old golden retriever dog from Mississippi, USA. Protozoal merozoites were identified in smears of the cerebrospinal fluid. Microscopically, lesions and protozoa were identified in eyes, tongue, heart, liver, intestines, nasal turbinates, skeletal muscle and brain, which reacted intensely with S. neurona polyclonal antibodies. Mature sarcocysts were seen in sections of muscles. These sarcocysts were ultrastructurally similar to those of S. neurona from experimentally infected animals. These data suggest that the dog is another intermediate host for S. neurona. Data suggest that the dog was transplacentally infected., (Copyright © 2014 Elsevier B.V. All rights reserved.)

To date, sarcocystis has been considered an asymptomatic infection in humans. Even though cases with glomerulonephritis have been reported in animals with sarcocystis, there have been no reports of a similar occurrence in humans. We report a case of acute proliferative glomerulonephritis and leukocytoclastic vasculitis in a patient with sarcocystis infestation.

Experiments have established that the first target for echinococcus is the liver and lung and that for pathogenic fungi and protozoa is the heart. Adult patients with hepatic hydatid disease complicated by paecilomycosis have been found to have atypical paecilomycosis-associated myocarditis, the treatment of which was developed by the authors, by using antibiotics, fungicides, and homeopathic remedies.

Background: Dogs are definitive hosts for numerous species of the intracellular protozoan parasite Sarcocystis. Reports of sarcocysts in muscles of dogs most often represent incidental findings., Hypothesis/objectives: To report the clinicopathologic, ultrastructural, and molecular findings in 2 dogs with myositis associated with Sarcocystis spp. infection, as well as the response to treatment with antiprotozoal drugs., Animals: Two dogs with severe myositis in association with massive sarcocystosis., Methods: Retrospective case review. Affected dogs were identified by a diagnostic laboratory. Attending clinicians were contacted, and the medical records reviewed. Immunostaining and electron microscopy were performed on muscle biopsies. Biopsies also were subjected to 18S rRNA gene PCR., Results: Both dogs had fever, lymphopenia, thrombocytopenia, and increased serum alanine aminotransferase (ALT) activity when first evaluated. One dog developed hyperbilirubinemia. Subsequently, both dogs had increased serum creatine kinase activity and clinical signs of myositis, with reluctance to move, generalized pain, and muscle wasting. Histopathology of muscle biopsies showed severe inflammatory and necrotizing myopathy with numerous sarcocysts. Ultrastructural studies and 18S rRNA gene sequence results were consistent with infection with a Sarcocystis spp. other than Sarcocystis neurona. Both dogs initially were treated unsuccessfully with clindamycin and anti-inflammatory drugs. One dog died. The other dog subsequently responded to treatment with decoquinate., Conclusions and Clinical Importance: Sarcocystis spp. infection should be included in the differential diagnosis for dogs that develop fever, thrombocytopenia, increased liver enzyme activities, and clinical and biochemical evidence of myositis. Although additional studies are required, decoquinate holds promise as an effective treatment for the disease., (Copyright © 2011 by the American College of Veterinary Internal Medicine.)

A free-living, young adult, male Japanese raccoon dog (Nyctereutes procyonoides viverrinus) was rescued in Gifu, Japan in March 2009. The animal was weak and emaciated with neurological signs that included head tilt, tremor and tic. The brain showed no gross abnormality at necropsy, but microscopically there was severe meningoencephalitis associated with protozoa, which were morphologically consistent with the asexual developmental stage of Sarcocystis spp. The protozoa were immunohistochemically negative for Toxoplasma gondii and Neospora caninum, but reacted weakly with antiserum specific for Sarcocystis cruzi. Analysis of the partial 18S rRNA gene sequence revealed that the protozoa were most closely related to an unidentified Sarcocystis species that was isolated from the white-fronted goose (Anser albifrons)., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Sarcosporidian cysts in the skeletal muscle of domestic pigeons (Columba livia f. domestica) have previously been attributed to infection with Sarcocystis falcatula, which is shed in the faeces of the opossum (Didelphis virginiana). Here, we describe fatal spontaneous encephalitis and myositis associated with Sarcocystis infections in three flocks of racing pigeons with 47 of 244 animals affected. The clinical course was characterized by depression, mild diarrhoea, torticollis, opisthotonus, paralysis and trembling. Histopathological examination of 13 pigeons revealed generalized severe granulomatous and necrotizing meningoencephalitis and myositis with sarcosporidian cysts. Light and transmission electron microscopy identified cysts in heart and skeletal muscle of 1 to 2 mm in length and 20 to 50 microm in width. These were subdivided into small chambers by fine septae and filled with lancet-shaped cystozoites (7.5 x 1.5 microm) and dividing metrocytes, which is characteristic for Sarcocystis. The cysts had smooth walls and were devoid of protrusions typical of S. falcatula. Polymerase chain reaction amplification and sequencing of the internal transcribed spacer region (ITS-1) and the complete 28S rRNA identified a novel Sarcocystis species with only 51% ITS-1 nucleotide sequence similarity with S. falcatula. A phylogenetic comparison of the 28S rRNA revealed close sequence homologies with Frenkelia microti, Frenkelia glareoli and Sarcocystis neurona. The clinical, histopathological, electron microscopic and genetic data are unlike any previously described protozoan infections in pigeons, suggesting a novel, severe disease due to an as yet undescribed Sarcocystis species.

The prevalence of Sarcocystis spp. was investigated by gross and histopathological examinations in 250 camels (Camelus dromedarius) slaughtered from 2002 to 2005 in the Mashhad Slaughterhouse, eastern Iran. Samples were taken from the diaphragm, heart, tongue, esophagus and masseter muscles for histopathological studies. No macroscopic sarcocysts were found in the samples at gross inspection. Sarcocysts were detected in 209 of 250 (83.6%) examined camels at histopathological level. The infection rate of the esophagus, heart, masseter muscles, diaphragm, and tongue was 58.8%, 48.0%, 46.8%, 41.6%, and 28.0%, respectively. There was no significant difference in the rate of infection between male (85.8%) and female (81.0%) camels. The tissue response to vital cysts was minimal; however, reaction to the degenerating cysts was severe and caused tissue damages resulting in hyperemia, hemorrhages, mononuclear cell infiltration, necrotic changes, and fibrosis. The wild and domestic carnivores especially dogs may be the final hosts of Sarcocystis spp. in this area.

The aim of the study was to diagnose Sarcocystis sp. infections in cattle and to detect coinfections by Toxoplasma gondii and/or Neospora caninum. Blood, diaphragm, esophagus, and myocardium from 90 beef cattle from Argentina were collected. Histopathological, immunohistochemical, polymerase chain reaction assays, and direct microscopical examination were carried out. Sarcocysts from myocardium were measured and counted. Indirect fluorescent antibody test (IFAT) for the three protozoans was performed. Sarcocystis cruzi sarcocysts were found in 100% of myocardium samples. Sarcocysts per gram ranged from 8 to 380 with higher values found in adult cattle (p < 0.001). T. gondii and N. caninum were not detected by immunohistochemistry. T. gondii DNA was found in myocardium of 2/20 seropositive animals, while N. caninum DNA was not found. Antibodies against S. cruzi were detected in all samples, those against N. caninum in 73% and against T. gondii in 91% of the samples (IFAT titer > or =25). It is concluded that serology by IFAT is a suitable method to diagnose these protozoan infections due to its specific IgG detection; therefore, IFAT may be a useful tool to evaluate the impact of each protozoan infection in coinfected animals.

Objective: To confirm existence of Sarcocystis suihominis and possible transmission cycle between human and pigs., Methods: Based on the human-pig-human infection cycle of Sarcocystis suihominis, feces of naturally infected pigs were collected and over 10,000 sporocysts were received by flotation technique, which were mixed with fodder to infect a normal pig. Fresh pork meat containing mature sarcocysts was chopped into pieces and swallowed by a volunteer (the first author of this paper) with about 71,000 sporocysts. Symptoms and development of the parasites after infection were observed., Results: The volunteer showed abdominal distension in about 5 hours after infection, with watery diarrhea 13 times from the 8th to 36th hour, vomiting 4 times, chilling and fever with a temperature of 38.5 degrees C, dizziness, headache, joint and muscle ache, epigastralgia, and anorexia. Un-sporized sporocysts were found in the faces 10 days after infection and sporocysts appeared on the 12th day. The average size of sporocysts was 11.9 (8.8-14.5) microm x 9.2 (7.5-12.5) microm. The infected pig showed a slight anorexia, fatigue, constipation, hair loosen in 5-8 days after infection, and returned normal on the 17th day. The average size of the sarcocysts was 299.2 (175-575 ) microm x 62.3 (30-102.5) microm. Size of bradyzoites was 11.5 (9.5-13.5) microm x 4.1 (2.8-5.0) microm. The volunteer was treated with acetylspiramycin for 15 days (0.2 g/time, 4 times/d) after 46 days of infection, and fecal examination turned negative 30 days later., Conclusion: There is a man-pig cycle for Sarcocystis suihominis in Guangxi.

A 2-year-old, captive-born, clinically healthy male, rhesus macaque, was euthanatized as part of an experimental study. At necropsy, diffuse pale streaking of the trunk, lumbar, and limb muscles were noted macroscopically. On histology, numerous elongated cysts that contained crescent-shaped basophilic spores were found in the fibers of skeletal muscles. Scattered affected myofibers were degenerate and accompanied by eosinophilic-to-granulomatous inflammation. Sarcocysts had prominent villus-like projections with the morphology of a type 11 sarcocyst wall similar to Sarcocystis neurona but possessing many more villus microtubules than is reported for S. neurona. In addition, bradyzoites were very long, up to approximately 12 microm in length. The protozoa were consistent with a Sarcocystis sp., based on histology and ultrastructure, however, a definitive identification of the species was not possible. Nonspecific immunohistochemical crossreaction with Sarcocystis cruzi antisera was observed. The 18S ribosomal deoxyribonucleic acid sequence showed 91% similarity to Sarcocystis hominis, 90% similarity to Sarcocystis buffalonis, and 89% similarity to Sarcocystis hirsuta. Interestingly, the ITS1 sequence showed very little homology to any sequence in GenBank, suggesting that this is possibly a unique Sarcocystis sp. Sarcocystosis is often considered an incidental finding, particularly in wild-caught animals, with little clinical significance. However, as demonstrated in this report and others, disseminated sarcocystosis can occur in captive-born rhesus macaques with or without clinical signs. In some cases interference with research results can occur; including death in fulminant cases.

A case of eosinophilic myositis (EM) in an 8-year-old beef cow was investigated. The animal originated from a herd in which a high incidence of the disease had been observed in slaughtered adult females over a period of 2 years. Histologically, the lesions in the muscles were characterized as granulomas with a central core of degenerate eosinophils and remnants of necrotic muscle fibres, surrounded by a rim of epithelioid cells and fibrous tissue with an infiltrate consisting predominantly of eosinophils radiating outwards. Degenerate sarcocysts with a thick (7-9 microm) wall were present in the suppurative centre of most lesions. Intact sarcocysts with similar morphology were present in adjacent muscle fibres but without an associated inflammatory reaction. By transmission electron microscopy the sarcocysts were identified as Sarcocystis hominis, based on the morphology of villar protrusions of the sarcocyst wall, which were broad-based and cylindrical, with a blunt distal end, and contained numerous long microfilaments. Circumstantial evidence indicated a human source of infection, human faecal material having been spread on the pasture grazed by the cattle. The findings supported a causal relationship between S. hominis infection and EM in cattle.

Sarcocystis neurona is an apicomplexan parasite that is the primary etiologic agent of equine protozoal myeloencephalitis in horses. Protective immune responses in horses have not been determined, but interferon-gamma (IFN-gamma) is considered critical for protection from neurologic disease in mice. The role of adaptive and innate immune responses in control of parasites was explored by infecting BALB/c, IFN-gamma knockout (GKO), and severe combined immune deficient (SCID) mice with S. neurona (10(4) sporocysts/mouse). Immune competent BALB/c mice eliminated parasites within 30 days, with no sign of neurologic disease, whereas GKO mice developed fulminant neurologic disease. In contrast, SCID mice remained healthy throughout the experimental period despite the persistence of parasite at low levels in some mice. Treatment with anti-IFN-gamma antibody resulted in neurologic disease in infected SCID mice. Although SCID mice lack adaptive immune responses, they have natural killer (NK) cells capable of producing significant quantities of IFN-gamma. Therefore, SCID mice were infected with sporocysts of S. neurona and treated with anti-asialo GM1. Depletion of NK cells, confirmed by flow cytometry, did not result in neurologic disease in SCID mice. These results indicate that IFN-gamma mediates protection from neurologic disease in SCID mice. Protective levels of IFN-gamma may originate from a low number of nondepleted NK cells or from a non-T cell, non-NK cell population.

Canine distemper and pulmonary sarcocystosis were diagnosed in a 10-week-old Rottweiler with 4-day history of diarrhea, vomiting, and weakness. Microscopic examination of the lung revealed bronchointerstitial pneumonia typical of morbillivirus infection. Also, numerous apicomplexan parasites were scattered in the alveolar walls. This protozoan infection was first thought to be toxoplasmosis but immunoperoxidase staining revealed large numbers of Sarcocystis canis. This is the first case of canine sarcocystosis reported from Latin America that further emphasizes the importance of immunohistochemistry in the differential diagnoses of apicomplexan infections in dogs.

Sarcocystis neurona is an important cause of equine protozoal myeloencephalitis (EPM) in horses in the Americas. An EPM-like neurological disease also has been reported from other mammals but it is difficult to induce this disease in the laboratory. A 4-month-old male domestic cat developed neurological signs 3 days following castration. The cat was euthanized 12 days later because of paralysis. Encephalomyelitis was the only lesion and was associated with numerous Sarcocystis schizonts and merozoites in the brain and spinal cord. The protozoa reacted positively with S. neurona-specific polyclonal rabbit antibody. Two unidentified sarcocysts were present in the cerebellum. It may be possible that stress of surgery triggered relapse of S. neurona infection in this cat.

A serum indirect fluorescent antibody test (IFAT) was compared with a Western blot (WB) and a modified Western blot (mWB) for diagnosis of equine protozoal myeloencephalitis (EPM). Using receiver-operating characteristic (ROC) analysis, the area under the curve of the IFAT was greater than the areaunder the curves of the WB and the mWB (P = 0.025 and P = 0.044, respectively). There was no statistically significant difference between the areas under the curves of the WBs (P > 0.05). On the basis of an arbitrarily chosen cut-off titer for a positive test result of 1:80 for the IFAT and interpreting weak positive WB results as positive test results, the sensitivities and 95% confidence intervals (CI) of all 3 tests were identical and equal to 88.9% (51.8-99.7%). The specificities and 95% CIs of the IFAT, WB, and mWB test were 100% (91-100%), 87.2% (72.6-95.7%), and 69.2% (52.4-83%), respectively. The overall accuracy of the IFAT was shown to be better than that of the WBs and, therefore, the test has potential for use in the diagnosis of EPM caused by Sarcocystis neurona.

A two-month-old Appaloosa colt developed neurological signs shortly after birth involving deficits affecting cranial nerves IV, VII, VIII, IX, X and XII, and possibly nerve VI. The most likely differential diagnoses were congenital anomalies, meningoencephalitides, trauma or nutritional causes. The foal was investigated by the analysis of cerebrospinal fluid (CSF), electromyelography (EMG), brain auditory evoked responses, magnetic resonance imaging (MRI), peripheral nerve biopsy, and Western blot analysis for the presence of intrathecal antibodies to Sarcocystis neurona, the causative agent of equine protozoal myeloencephalitis. Significantly abnormal EMG findings included spontaneous electrical activity of the tongue, suggesting denervation. The MRI was useful in ruling out masses, congenital anomalies and focal abscessation. The cytology of CSF revealed mild mononuclear reactivity. Western blot testing of CSF was positive, indicating the intrathecal presence of antibodies to S neurona. The foal was treated with pyrimethamine and trimethoprim-sulphadiazine for two months and returned to nearly normal neurologic status.

Sarcocystis neurona associated granulomatous encephalitis was found in 2 of 84 adult raccoons. Both raccoons also had an extensive nonsuppurative myocarditis and one had S. neurona schizonts and merozoites in the myocardium. Only the asexual stages (schizonts and merozoites) of S. neurona are found in tissues of naturally infected animals (horse, mink, raccoons, cats, skunk, pony, seals, sea otters) and since these have not been reported outside the central nervous system, the presence of concurrent myocarditis in raccoons with the presence of S. neurona in the current study is of interest. Pathologists should consider the possible association of S. neurona with myocardial inflammation in other S. neurona susceptible animals.

A 13-yr-old female Canada lynx (Felis lynx canadensis) died after a short clinical illness, and necropsy revealed multifocal, nonsuppurative encephalitis with protozoal schizonts present in cerebral vascular endothelial cells. The schizonts stained immunohistochemically with antiserum to Sarcocystis neurona. This is the first report of Sarcocystis encephalitis in the Canada lynx.

An 8-yr-old intact male Grant's zebra (Equus burchelli bohmi) was referred to the Veterinary Medical Teaching Hospital of the University of California-Davis after being found in the owner's pasture obtunded and in lateral recumbency. The animal was hypothermic, weak, and unwilling to rise. There was no evidence of trauma, and the zebra had seemed normal the preceding evening. There was no extensor rigidity, and cranial nerve reflexes were normal. Flexor and extensor reflexes were weak upon initial examination. A complete blood count and serum biochemistry analysis revealed a mild leukocytosis, hyperfibrinogenemia, hypoglycemia, hyponatremia, hypochloremia, hypocalcemia, and hypoalbuminemia. Urinalysis was normal, and a urine toxicology screen for alkaloids was negative. No toxic substance was found in the hay or pasture grasses although the owner reported the presence of yellow star thistle and mushrooms in the pasture. The cerebrospinal fluid cytologic and biochemical analyses were normal, but antibodies to Sarcocystis neurona were detected. The zebra died despite aggressive supportive therapy over a 4-day period. The necropsy demonstrated severe gastrointestinal nematodiasis that could account for hypoalbuminemia and electrolyte abnormalities. Histopathologic examination of the nervous system revealed focal areas of perivascular cuffing in the brainstem that were comprised mainly of lymphocytes, monocytes, and plasma cells. Immunohistochemical staining identified the presence of S. neurona merozoites associated with the lesions. This zebra probably died from severe endoparasitism that resulted in malabsorption, weakness, and recumbency rather than from encephalitis associated with S. neurona merozoites. Equine protozoal myeloencephalitis has not been reported previously in nondomestic equids.

Disseminated eosinophilic myositis was diagnosed in an alpaca that had been imported to the USA from Peru 5 years earlier. The myositis was associated with macroscopically visible large sarcocysts that were characterized histologically by septate compartments containing bradyzoites, and ultrastructurally by cyst walls composed of anastomosing villous protrusions. Two hours before death, the alpaca aborted an 8-month-gestation fetus, but no lesions were found in the uterus, placenta or fetus. Additional macroscopical findings included haemoabdomen and myofibre haemorrhage, degeneration and necrosis. It is believed that this is the first described case of clinical disease associated with a Sarcocystis sp. (probably S. aucheniae) in camelids., (Copyright 1999 Harcourt Publishers Ltd.)

This paper describes acute visceral and neural sarcocystosis in four dogs. One animal was simultaneously infected with distemper virus, and another with Blastomyces dermatitidis. Schizonts and merozoites of Sarcocystis canis were found in the lesions. 1999 W.B. Saunders and Company Ltd.

The effects of experimental infection of calves with Sarcocystis cruzi on the blood coagulation cascade were investigated. Calves were inoculated orally with 1 x 10(5) sporocysts (group S1, n = 6) or with 5 x 10(5) sporocysts of S. cruzi (group S2, n = 3). A group of eight calves served as non-infected controls (group C). The animals were bled once during the first 4 weeks of infection and twice a week thereafter until day 40 p.i. The following parameters were measured: activated partial thromboplastin time, prothrombin time, thrombin time, reptilase time, thrombin coagulase time, factors XII, XI, X, IX, VIII:C, VII, V, prekallikrein, fibrinogen, alpha 2-antiplasmin, antithrombin III, alpha 1-antitrypsin, alpha 2-macroglobulin, haematocrit, haemoglobin, numbers of erythrocytes and thrombocytes. The infected calves developed acute sarcocystiosis from 25 (S1) or 29 (S2) days p.i. onwards. During the acute disease, antiproteases tended to elevated values and thrombocyte counts were generally reduced. In group S1 prolonged prothrombin time and reduced activities of factors VII or V were found. In group S2 accelerated prothrombin time and activated partial thromboplastin time, as well as elevated factor X activities, were recorded even before the onset of clinical disease at 19 days p.i. While prothrombin time returned to normal levels thereafter, activated partial thromboplastin time remained short. Activities of factor V, factor VII and factor X were significantly reduced in group S2 at the onset of acute sarcocystiosis, and one of the three calves died at 29 days p.i. The other parameters were not significantly affected by either dose of infection. No evidence for a classical disseminated intravascular coagulation syndrome could be found; however, it was demonstrated that S. cruzi alters plasma coagulation in a dose-dependent way.

A multistage protozoan parasitic disease was used as a cachexia model to study the effects of daily administration of bovine growth hormone (GH) on endocrine and body composition changes of young calves from the onset of the acute phase response (APR). Male calves averaging 127.5 +/- 2.0 kg body weight were assigned to control, ad libitum fed, noninfected (C); ad libitum fed, infected (250,000 oocysts Sarcocystis cruzi, per os, I); noninfected, pair-fed (PF) to matched I-treatment calves and these respective same treatments in calves injected daily with GH (USDA-bGH-B1), 12.5 mg/calf/day, im) designated as CGH, IGH and PFGH. GH injections were initiated on Day 20 postinfection (PI), 3 to 4 d before the onset of clinical signs of APR, and continued to Day 56 PI, at which time animals were euthanized for tissue collections. Abrupt increases in rectal temperature commensurate with up to 70% reduction in voluntary feed intake were observed in I and IGH beginning 23-25 d PI. For the trial period between Days 20 and 56 PI, average daily carcass protein gains were 123, 52, 109, 124, 48, and 67 g/d and average daily carcass fat gains were 85, 11, 43, 71, -23, and 29 g/d for C, I, PF, CGH, IGH, and PFGH, respectively. Effects of GH were significant for fat accretion and plasma urea depression. Rectus femoris was highly refractory to catabolic effects of infection while psoas major was significantly catabolized during infection. Plasma concentrations of insulin-like growth factor-I (IGF-I) increased significantly in all GH-treated calves between Day 20 and 23 PI. Plasma IGF-I declined well below Day 20 values in all infected calves from the onset of the APR through the end of the study. The decrease in plasma IGF-I concentrations in I and IG was highly correlated with the magnitude of the fever response. Hepatic mRNA for GH receptor and IGF-I was decreased in infected calves. Hepatic microsomal membrane binding of 125I-GH did not differ between groups. The data suggest that effects of GH and parasitism on tissue metabolism during disease may vary among different specific tissue pools. The data demonstrate that daily GH administration in young calves does not prevent lean tissue losses and may accelerate fat depletion associated with cachectic parasitism. Furthermore, the onset of APR overrode the capacity for GH to maintain elevated plasma concentrations of IGF-I, an effect not readily explained through changes of GH-receptor binding.

Equine protozoal myeloencephalitis (EPM) is a common neurologic disease of horses in the Americas. Horses with EPM most commonly have abnormalities of gait, but they also may present with signs of brain disease. The disease ranges in severity from mild lameness to sudden recumbency, and clinical signs usually are progressive. A causative agent, Sarcocystis neurona, has been isolated from affected horses, and serologic surveys suggest that approximately 50% of horses in the United States have been exposed. EPM is considered a treatable disease, although the response to antimicrobial treatment often is incomplete. This article highlights new information about the life cycle of S. neurona and reviews the literature regarding diagnosis, clinical signs, and treatment of the disease.

Four mature ewes developed mild neurological symptoms. Histological examination revealed a nonsuppurative encephalitis and myelitis associated with protozoan cysts identified as Sarcocystis spp. by immunoperoxidase. The mild clinical signs and apparent recovery of 1 ewe suggest that neurological disease caused by Sarcocystis spp. may be more common than indicated by the infrequency of reports.

Muscle sarcocystosis is a parasitic infection acquired by ingestion of sporocysts of Sarcocystis species. A case is described where symptoms of fever, chronic myositis and eosinophilia were present. Diagnosis was made via muscle biopsy. Improvement and cure coincided with treatment with cotrimoxazole. A limited review of human muscle sarcocystosis and an outline of the gaps in the knowledge of this infection is presented.

Sarcocystis-associated encephalitis was diagnosed in a backyard chicken flock that had nervous manifestations. The main histopathologic lesion was necrotizing encephalitis characterized by a large focal area of necrosis infiltrated and surrounded by mononuclear cells, heterophils, and multinucleated giant cells. Schizonts and merozoites were observed in the lesion. Immunohistochemical staining of the brain lesion revealed positive reaction to Sarcocystis antiserum. The ultrastructural characteristics of the parasite were typical of Sarcocystis, including the presence of a nucleus, a conoid, numerous micronemes, and lack of rhoptries. Medication with amprolium and sulfamethazine or with chlortetracycline was not effective in controlling the mortality. Trapping of opossums on the farm and relocating the chickens to clean, new premises seemed to reduce mortality from this infection.

Protozoan parasites are a significant cause of abortion and infertility in domestic ruminants. Toxoplasma gondii, a widespread cause of abortion in sheep and goats, and Sarcocystis spp., which cause a common, frequently asymptomatic infection of domestic ruminants, both have a two-host life cycle. Carnivorous definitive hosts spread the infection through their feces and domestic ruminants are intermediate hosts. A similar, recently recognized protozoa, Neospora sp., has emerged as an important cause of reproductive disease, especially as an abortifacient in dairy cattle. Neospora is presumed to also have a two-host life cycle, although the definitive host(s) has not been identified. The venereally transmitted Tritrichomonas foetus is an important cause of pregnancy loss in naturally bred cattle throughout the world. In the absence of effective methods for vaccination or treatment, control of these parasites is based on management procedures to reduce infection and transmission.

Extensive brain pathology attributed to Sarcocystis is described in a heifer and a 2- to 4-month-old calf. These appear to be the first recorded cases of naturally occurring acute sarcocystosis in cattle in sub-Saharan Africa. The heifer became recumbent and had convulsions before dying, while clinical signs in the calf included loss of body mass, diarrhoea, nervousness and opisthotonus. Disseminated haemorrhages were noted in the brains of both animals at necropsy. Microscopically, the grey and white matter contained multiple areas of necrosis associated with haemorrhage, fibrinoid vasculitis, perivascular cuffing and gliosis. A multifocal meningitis was also present. First-generation Sarcocystis schizonts were evident in, or adjacent to endothelial cells of several arterioles and small arteries. The association of first- (as opposed to second-) generation schizogony with overt and fatal bovine sarcocystosis, has not previously been reported.

A captive-born rhesus monkey (Macaca mulatta) experimentally infected with simian immunodeficiency virus developed neurologic abnormalities approximately seven months postinoculation. A chronic necrotizing encephalomyelitis with intralesional protozoal schizonts was diagnosed histologically. The protozoa was identified as Sarcocystis neurona based on its morphologic characteristics by light and electron microscopic examination, the developmental stages of the schizonts, and positive staining with antisera against Sarcocystis cruzi by immunocytochemical techniques. Although S. neurona may be confused with Toxoplasma gondii by light microscopy, the former lacks rhoptries, is in direct contact with the host cell cytoplasm, and divides by endopolygeny. Sarcocystis neurona has recently been identified as an etiologic agent of encephalomyelitis in horses, raccoons, and mink.

Three of six wild dogs (Lycaon pictus) which died of rabies, and one Alsatian dog which died of adenocarcinoma, were found to harbour sarcocysts in their cardiac and/or skeletal muscles. The bradyzoites and metrocytes of the cysts were smaller than those seen in a lion infected with Microbesnoitia leoni and the common Sarcocystis spp. found in ruminants. It is proposed that Lycaon pictus is the natural intermediate host of the unidentified Sarcocystis-like species.

The first two out of an experimental group of 17 sheep assigned for orthopaedic surgery died during inhalation anaesthesia with halothane-nitrous oxide-oxygen before the arthrotomy of the knee joint could start. Further casualties could be prevented by the use of epidural anaesthesia. Each of the 17 sheep underwent a pathologic-anatomical, histological, bacteriological and parasitological examination. It was found that all of them were infected with sarcosporidia-oocysts with myocarditis of different intensity. Possible infections with sarcosporidia-oocysts in animals, which could have had contact to carnivora, and which are taken for therapeutic surgery or for an experiment should be taken into consideration, because the lesion in the heart due to sarcosporidia-oocysts can be the cause of sudden death.