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
New Topics
This Weeks Topic is S. neurona SAG Titer
>In our experimental cases we learned that there was no statistical correlation with titer and disease.>There is a statistical difference when titer is examined over time, the longer the duration of infection, the higher the titer.>The change in titer in 2 to 4 weeks is diagnostic for disease (active parasite).>A protective titer using recombinant SAG 1 is statistically significant at >256 against SAG 1 challenge.Because each horse responds differently and the "immune background" (if the horse has seen the organism before) is different for each horse, the titer will be somewhat different for each animal. Although the titers for a group of animals, say 75, will follow a bell shape curve, if you look at each horse at 30 days post challenge, or 45 days post challenge there is no statistical correlation for a single point test. For example, you can't say with 95% confidence that all horses will have a titer of 32. What you can say is that when the group of 75 is examined over time there is a statistical difference because the longer the infection goes on, the higher the titer will be in the horses. Also, for the group of 75, the titer was measured at 32 when clinical signs appeared in most of the horses. A less virulent organism will produce less of a response.What was diagnostic for disease was neurological exam and titer when a change in titer was recorded. For the 75 horses the change in titer was sufficient to identify the sick horses. That said, drug use can delay the increase in titer (for diclazuril and toltrazuril ,Marquis) but the effect lasts about 30 days in most animals. If an animal is on these drugs then the titer can be delayed. Most likely there is threshold to the number of live organisms (and the antigens they produce) that is affected by the drug that causes this delay. There will be an immune response and a rise in titer indicating that not all the parasites are killed.Vaccination is protective and statistically the trend (more horses are necessary to have statistical significance) is that a protective titer was 256 or greater. It is unlikely that a field case will have a titer that high without significant disease because the antigen make up of the organism wouldn't stimulate that kind of response quickly enough, but a high titer will be apparent after 60-90 days. This is well beyond the stage that an owner would recognize disease. To get a titer of 256 or greater in the field the horse would have to have a large parasite load for more than 45 days.At this time the significance of SnSAG 6 isn't known. We do know that we have tested horses with ataxia that only have a titer to this antigen. We also have normal horses with a titer indicating that more is going on and neurological exam and testing go hand in hand.Phenotypes strains of S. neurona differ in their pathogenicity
The SAG 1 ELISA detects specific antibodies to SAG1, the immunodominant protein of S. neurona, etiologic agent of EPM in the horse. Response to treatment is a strong indicator of disease, with response to treatment the antibody titer usually decreases. An increase in titer (2 to 4 weeks apart) accompanied by clinical signs of EPM are strong indicators of disease. Antibody is detected between 17 and 30 days post exposure and follows the appearance of clinical disease. It is recommended to recheck the serum in 2 to 4 weeks for a rise in titer if you suspect disease. We used a highly virulent strain for our studies in which a titer of 32 coincided with clinical signs of EPM.
The SAG 5 ELISA detects specific antibodies to SAG 5. Sarcocystis neurona SnSAG5 strains of S. neurona have been rarely isolated from horses with clinical EPM. Experimental induction of disease with SAG5 phenotypes has not been successful in horses and exposure may elicit transient infections only. We have found clinical cases documenting ataxic in horses that only have SAG 5 antibody. A change in titer 2 to 4 weeks apart is important to determine active disease. An increase in titer (2 to 4 weeks apart) accompanied by clinical signs of EPM are strong indicators of disease.
Sarcocystis neurona SnSAG6 strains have not been recognized in horses. We can identify S. falcatula and S. neurona antibodies in horses because it is antigenically identical at the SAG 6 antigen. Experiments show that, so far, S. falcatula does not cause EPM in horses. The only way to differentiate infections with these organisms that display SAG 6 is because the SnSAG 6 horse has clinical signs of EPM while the S. falcatula infected horse does not. An increase in titer (2 to 4 weeks apart) accompanied by clinical signs of EPM are strong indicators of disease. We don’t know yet if antibodies elicited by SfSAG6 are protective against SnSAG6 phenotypes. Our research would suggest that it is.
Genotype markers can seperate S. neurona into three antigenic groups. These groups are the finest resolution afforded by antibody testing. The groups are SAG 1, SAG 5 and SAG 6. These groups can be divided into 12 sub-groups or genotypes. The markers that are used to genotype the sub-groups are not useful in antibody assays because they can't distinguish other species of Sarcocystis. To distinguish the species the full ITS gene sequence is necessary.
Pathogenes Inc.
PO Box 970, Fairfield, Fl. 32634
15471 NW 112th Ave, Reddick, Fl. 32686
ph: 352-591-3221
fax: 352-591-4318
sellison
