Equine protozoal myeloencephalitis (EPM) is a potentially serious neurologic disease of horses caused by infection with the protozoan parasite Sarcocystis neurona. This parasite has a complex life cycle involving multiple host species. Opossums are the definitive host, meaning the parasite reproduces sexually in the opossum gastrointestinal tract. Horses are intermediate hosts, meaning they can be infected by ingesting S. neurona spores shed in the feces of opossums, but the parasite does not reproduce sexually in horses. EPM occurs when S. neurona migrates to and damages the central nervous system of infected horses. Given this complex life cycle involving multiple hosts, a logical question is: can birds also act as intermediate hosts or transmitters of S. neurona to horses?
Birds as Intermediate Hosts
There is limited evidence that some bird species can serve as intermediate hosts and harbor S. neurona infections. A few studies have detected S. neurona DNA in tissues of wild birds, suggesting natural exposure and infection. Experimentally, several bird species have been shown to develop detectable S. neurona infections when fed sporocysts from opossum feces. However, the parasite does not appear to multiply extensively or cause clinical disease in these avian hosts. Overall, the current evidence suggests birds do not play a major role as intermediate hosts for S. neurona. They may harbor low-level infections, but are likely “dead-end” or “incidental” hosts that do not propagate the parasite life cycle.
Birds as Mechanical Vectors
While not biologically important intermediate hosts, there is more evidence that birds could act as mechanical vectors spreading S. neurona spores. Birds commonly feed on grains and insects present in horses’ feces, ingesting any S. neurona spores shed by infected horses. These spores may then pass through the digestive tract intact and be deposited in new areas via defecation. Several studies have detected S. neurona DNA in the feces of wild birds, confirming they can mechanically transport spores. Furthermore, areas with high populations of grain-eating birds have been associated with higher EPM rates in horses. Therefore, while they do not propagate the parasite life cycle, birds may contribute to dispersal and horse exposure through mechanical transmission of S. neurona spores.
Role of Bird Feathers
In addition to ingesting spores while foraging, bird feathers may provide another route of mechanical S. neurona transmission. Spores clinging to muddy feathers could potentially be brushed off onto feed or pasture and infect horses through oral ingestion. A few studies have detected S. neurona DNA on the feathers of wild birds. However, the viability and infectivity of spores on feathers has not been proven. More research is needed to determine if contact with contaminated feathers poses a significant risk of EPM transmission. Overall, the ingestion of spores from feces or feed sources is likely the primary route of mechanical transmission by birds.
Evidence that Birds Transmit EPM
While the potential is there, direct evidence linking birds to EPM transmission in horses remains limited. Here is a summary of the key research to date:
S. neurona Infection in Birds
| Study | Findings |
| Fenger et al. 1995 | Detected S. neurona antibodies in 2/52 wild birds tested |
| Cummings et al. 2005 | Detected S. neurona DNA in tissues of naturally exposed crows |
| Mansfield et al. 2008 | Experimentally infected multiple bird species with S. neurona sporocysts from opossum feces |
These studies show wild and experimentally infected birds can harbor S. neurona infection, but disease and propagation of the parasite life cycle within avian hosts was very limited.
S. neurona in Bird Feces/Feathers
| Study | Findings |
| Fenger et al. 1995 | Detected S. neurona DNA in feces from 2/52 wild birds |
| Dame et al. 1995 | Detected S. neurona antibodies in 12% of passerine birds on a farm with high EPM rate |
| Sturbaum et al. 2001 | Detected S. neurona DNA on feathers from 3/55 wild birds |
These studies show birds can mechanically pass viable S. neurona spores in feces and on feathers, supporting their potential role in transmission.
Bird Density and EPM Risk
| Study | Findings |
| Duncan et al. 2005 | Observed higher EPM rates in horses on pastures with more abundant bird and wildlife activity |
| Fayer et al. 2006 | Saw positive correlation between bird density near barns and number of horses affected with EPM |
These observational studies associate increased wild bird populations with higher EPM occurrence, indirectly linking birds with greater transmission risk. However, direct transmission was not proven.
Conclusion
Overall, current evidence suggests wild birds may contribute to EPM transmission through mechanical transportation of S. neurona spores in feces or on feathers. However, their role as propagators of the parasite life cycle appears very limited. More targeted research is still needed to directly quantify the risk of transmission from contact with wild birds. For now, horse owners should still take reasonable precautions like discouraging abundant bird activity in barns and pastures, keeping feed covered, and picking up feces promptly. But major actions to exclude or reduce wild bird populations do not appear warranted based on existing information. With further research, we can better define evidence-based guidelines for managing bird activity on farms to balance transmission risks against environmental impact.
Key Points Summary
- EPM is caused by a parasite, S. neurona, shed in opossum feces
- Horses are infected by ingesting spores, often from pasture or feed contamination
- Birds do not play a major role as intermediate hosts but may transmit spores mechanically
- Some evidence links birds to higher EPM risk, but direct transmission has not been proven
- Current precautions to limit bird contact and manure exposure are reasonable
- More research needed to quantify actual transmission risk from birds
