Pathogenes Inc.
Pathogenes Inc.
PO Box 970, Fairfield, Fl. 32634
15471 NW 112th Ave, Reddick, Fl. 32686
ph: 352-591-3221
fax: 352-591-4318
sellison
Sarcocystis fayeri
Sarcocystis fayeri in horses
Sarcocystis fayeri may be self limiting in normal horses but devestating in malnourished animals. This paper describes a case of S. fayeri as well as highlights the issue of misidentification of sarcocystis in horses.
Sarcocystis calchasi in birds
Follow this link to a paper that describes lethal neurologic disease in domestic pigeons in Germany.
It is interesting that they conclude: "among the experimentally infected pigeons, different diseases were caused by different infectious doses. Pigeons infected with high doses died 7–12 days after infection and had massive parasite-induced liver necroses; those infected with lower doses had central nervous signs, which did not develop until 8 weeks after infection. The late occurrence of brain lesions and the absence of parasitic stages from the brain suggest an indirect, currently unknown, mechanism of encephalitis that awaits further clarification."
Sarcocystis calchasi-associated neurologic disease in a pigeon in North America. DEC. 2011 REPORT OF S. CALCHASI IN MINNESOTA
Genetic Analysis of S. falcatula
Sarcocystis falcatula is a pathogen that cycles between the opossum and bird intermediate hosts. This organism can be isolated from tissues using its ability to infect budgies. This ability distinguishes it from S. neurona a common contaminant of oocyst and tissue samples used in the study of EPM in horses. We have been able to identify genes from S. falcatula that vary between strains that can infect budgies but are antigenically similar to S. neurona. The antigens Sn SAG 2, 3, and 4 are expressed genes that are highly similar in both falcatula and neurona. We have been unable to identify highly similar genes at the SnSAG 1 allele but have identified highly similar genes at SnSAG 4, 5, and 6 that may define cross-reactions between these species.
A Case for S. neurona toxins
Sarcocystis falcatula is very closely related to S. neurona, so close in fact it was mistaken for the etiologic agent of EPM in the horse. This strain of sarcocystis is carried by the opossum, commonly infects birds, and can produce antibodies in horses detected by Western Blot and IFAT tests. What is interesting is that scientists that study sarcocystis sp. interpret delayed neurological signs and the absence of parasites in the brains of diseased birds as a different "disease" that is dependent on the dose of infections. See the above link to this interesting German paper.
Lower doses of parasites presumably induced neurological disease in the host that is seen later in the course of the disease. This could indicate the virulence factor is a toxin, possibly a stage related protein, expressed by the developing merozoite or the degenerating cyst.
This research supports our hypothesis that a toxin produced by S. neurona may be responsible for neurological signs in horses. A toxin was identified from S. cruzi (cow-dog cycle; does not infect opossums) and the purified toxin caused pathology in rabbits including paralysis and death.
Intuitively the best prevention for the toxic effect of Sarcocystis may be a toxoid vaccination once the toxin is identified. Anti-protozoal drug therapy will not treat the effects of a toxin. It remains unknown if prophylactic drug therapy would prevent the neurologic stage/dose of parasites that cause disease.
Sarcocystis fayeri can be detected by IFAT
The Journal of parasitology 2004;90(6):1487-91.
Experimental infection of ponies with Sarcocystis fayeri and differentiation from Sarcocystis neurona infections in horses.
Saville W J A; Dubey J P; Oglesbee M J; Sofaly C D; Marsh A E; Elitsur E; Vianna M C; Lindsay D S; Reed S M infected ponies with S. fayeri to determine if this common infection could be misdiagnosed as S. neurona using IFAT.
"Sarcocystis neurona and Sarcocystis fayeri infections are common in horses in the Americas. Their antemortem diagnosis is important because the former causes a neurological disorder in horses, whereas the latter is considered nonpathogenic. There is a concern that equine antibodies to S. fayeri might react with S. neurona antigens in diagnostic tests. In this study, 4 ponies without demonstrable serum antibodies to S. neurona by Western immunoblot were used. Three ponies were fed 1 x 10(5) to 1 x 10(7) sporocysts of S. fayeri obtained from dogs that were fed naturally infected horse muscles. All ponies remained asymptomatic until the termination of the experiment, day 79 postinoculation (PI). Using indirect immunofluorescence antibody tests (IFATs), 7 serum samples were found to be positive for S. neurona antibodies from 1:25 to 1:400 dilutions. Sarcocystis fayeri sarcocysts were found in striated muscles of all inoculated ponies, with heaviest infections in the tongue. All sarcocysts examined histologically appeared to contain only microcytes. Results indicate that horses with S. fayeri infections may be misdiagnosed as being S. neurona infected using IFAT."Sarcocystis falcatula is highly similar to SAG2, 3, and 4 of S. neurona
J.M. Wendte M.A. MillerP.A. Conrad A. K. Nandra S. M. Peat P. R. Crosbie M. E. Grigg used molecular tools to study S. neurona in sea otters and determined that the "limited genetic diversity among southern sea otters precludes distinction between marine and terrestrial islolates". In their study thye found that the differences previously reported by Howe which was based on western blot analysis was due to cross reactions of polyclonal antibodies to conserved regions of other proteins. Grigg et. al also reported that "SnSAG2, 3, and 4
in the closely related species finding that has implications for the specificity of diagnostic tests based on PCR and antibodies for these proteins."
Sarcocystis falcatula
Sarcocystis falcatula
Extrapulmonary disease
The definitive and intermediate host life cycles for Sarcocystis falcatula, as well as the pathogenesis of disease in each host, have been well documented. This organism serves to understand the pathogenesis of cyst formation and can shed light on the extrapulmonary disease in other avian, and perhaps equine, sarcocystis. The sarcocystis literature is full of important observations that portend significant discoveries.
An interesting caveat presented by Schneider et al (73rd annual meeting of the American Society of Parasitologists) after discussing the genetic DNA banding analysis of S. falcatula, and related protozoa, using AFLP stated that the DNA banding patterns derived from the S. falcatula sporocyst populations differed significantly from banding patterns for S. falcatula merozoites maintained in vitro. Perhaps a clue that oocysts that were identified as S. falcatula were mixed with unidentified oocysts found in the opossum or that there are several falcatula organisms that have genetic differences. MORE...
Sarcocystis fayeri can be detected by Western blot tests
Clinical and Diagnostic Laboratory Immunology, September 2005, p. 1050-1056, Vol. 12, No. 9
Enzyme-Linked Immunosorbent Assays for Detection of Equine Antibodies Specific to Sarcocystis neurona Surface Antigens
Jessica S. Hoane, Jennifer K. Morrow, William J. Saville, J. P. Dubey, David E. Granstrom, and Daniel K. Howe assessed the antibody cross-reactivity of antibodies from horses challenged with S. fayeri. They determined that "the Western blot analysis clearly demonstrated that S. fayeri-infected horses produce antibodies that cross-react with multiple S. neurona antigens." see the figure 4A.
SAG1 ELISA will not detect S. fayeri infections in the horse.
The ELISA that uses SAG1 won't bind antibodies to the SAG2, 3, and 4 protein of S. fayeri or S. falcatula. This test is of no value to detect muscle cysts in the horse due to these infections. These infections do not cause disease in the horse but are commonly present in muscle tissues.
Link to Sarcocystis in a Cockatoo. The authors found that the inflammation (in muscle) related to myocyte degeneration and weakly to meront burden. The statements are similar to Smith et. al. (J. Parasit. Vol 75, No 2. April 1989). Smith and co-workers found that although only 1/3 of the birds in their study demonstrated meronts, all birds had some perivascular microgliosis by the fourth week PI, suggesting that some encephalitis was sustained by all.
Pathogenes Inc.
PO Box 970, Fairfield, Fl. 32634
15471 NW 112th Ave, Reddick, Fl. 32686
ph: 352-591-3221
fax: 352-591-4318
sellison
