EPM Flashcards
1
Q
What was the initial name for EPM identified by Rooney in 1970?
A
Segmental Myelitis
2
Q
What is the primary cause of EPM?
A
Sarcocystis neurona
3
Q
Which protozoan is less commonly implicated in EPM cases compared to S. neurona?
A
Neospora hughesi
4
Q
Who are the definitive hosts for Sarcocystis neurona?
A
Opossums in North America and various South American opossums
5
Q
Name some intermediate hosts for Sarcocystis neurona.
A
Skunks, raccoons, armadillos, and cats.
6
Q
Where does sexual reproduction of Sarcocystis neurona occur in opossums?
A
In the intestinal epithelium.
7
Q
What do sporozoites form in intermediate hosts?
A
Latent sarcocysts in muscle tissue
8
Q
How do horses become infected with Sarcocystis neurona?
A
By ingesting food or water contaminated with feces from an infected opossum
9
Q
Why are equine carcasses seldom accessible to opossums?
A
To reduce the likelihood of horses contributing to the parasite’s life cycle.
10
Q
Is vertical transmission of Sarcocystis neurona common in horses?
A
No, it is considered uncommon despite antibodies being detected in foals before suckling.
11
Q
How does Sarcocystis neurona likely enter the CNS?
A
Through infection of endothelial cells or leukocytes.
12
Q
Is the complete life cycle of Neospora hughesi known?
A
No, it remains poorly understood.
13
Q
Are dogs confirmed definitive hosts for Neospora hughesi?
A
No, it has not been established.
14
Q
Can Neospora hughesi be transmitted transplacentally in horses?
A
Yes, recent studies suggest it can be transmitted transplacentally.
15
Q
Are all horses susceptible to EPM?
A
Yes, but not all infected horses develop clinical disease.
16
Q
What have studies in mice and horses shown about the immune response to Sarcocystis neurona?
A
They demonstrated a critical role for the immune response in preventing disease.
17
Q
Do all horses with EPM show the same immune response?
A
No, some show altered immune responses which are sometimes antigen-specific.
18
Q
What factors may influence the progression to severe neurologic disease in EPM?
A
Variations in protozoal inoculum and stress-induced immune suppression.
19
Q
Did efforts to increase stress and treatment with immunosuppressive steroids consistently lead to increased disease severity?
A
No, they did not consistently lead to increased disease severity.
20
Q
Has genetic variation been observed among strains of Sarcocystis neurona?
A
Yes, some strains may be particularly virulent, though not confirmed in horses.
21
Q
What percentage of EPM cases occurred in horses aged 4 years or less?
A
61.8%.
22
Q
What was the mean age of affected horses?
A
3.6 ± 2.8 years.
23
Q
Which breeds are most commonly affected by EPM?
A
Thoroughbreds, Standardbreds, and Quarter Horses.
24
Q
Was there any significant sex or seasonal bias found in EPM cases?
A
No significant sex or seasonal bias was established.
24
What is the range of Sarcocystis neurona seroprevalence in the United States?
15% to 89%.
24
How common is Neospora hughesi seroprevalence in horses?
Generally low, with more than 10% in some regions but less than 3% in others.
24
What is the annual incidence of EPM in horses aged 6 months or older according to NAHMS?
Approximately 14 ± 6 cases per 10,000 horses.
25
Is the proportion of EPM cases attributable to N. hughesi known?
No, it is uncertain.
26
Does EPM usually occur sporadically or in clusters?
Sporadically, but clusters of cases can occur.
27
What age groups have a higher risk of developing EPM?
Young horses (1-5 years) and older horses (>13 years).
28
When is the risk of EPM the least?
In winter.
29
What environmental factor increases the risk of EPM by 2.5-fold?
Presence of opossums on the premise.
30
What effect does the presence of a creek or river have on the risk of EPM?
Reduces the likelihood of EPM by one-third.
31
What stressful events can increase the risk of EPM?
Heavy exercise, transport, injury, surgery, or parturition
32
How much more likely are horses treated with an anticoccidial drug to improve compared to untreated horses?
10 times more likely to improve.
33
How can EPM present in horses?
EPM can present acutely or chronically with insidious onset, showing focal or multifocal signs affecting the brain, brainstem, or spinal cord.
34
What may severely affected horses experience?
Difficulty standing, walking, or swallowing, with potential for rapid disease progression.
35
Can EPM clinical signs stabilize and relapse?
Yes, clinical signs may stabilize but relapse days or weeks later.
36
What parts of the CNS does EPM affect?
Both white and grey matter at multiple CNS sites.
37
What are signs of gray matter involvement?
Focal muscle atrophy and severe muscle weakness.
38
What are signs of white matter involvement?
Ataxia and limb weakness caudal to the infection site.
39
What are early signs of EPM?
Stumbling and frequent limb interference, which can be mistaken for lameness.
40
How do EPM clinical signs progress?
There is a gradual progression in severity and range of clinical signs, sometimes leading to sudden exacerbation causing recumbency.
41
What are the usual vital signs in EPM-affected horses?
Usually normal; affected horses appear bright and alert.
42
How might the physical condition of EPM-affected horses appear?
Some horses may appear thin and mildly obtunded.
43
What kind of weakness is observed in EPM?
General weakness, often involving all four limbs.
44
What is asymmetric ataxia?
Uncoordinated movement affecting one side more than the other.
45
What types of sensory loss may be present?
Areas of hyporeflexia (reduced reflexes), hypoalgesia (reduced pain sensation), or complete sensory loss.
46
What are common signs of brain/brainstem involvement in EPM?
Reduced alertness (obtundation), tilted head posture (head tilt), facial nerve paralysis, and difficulty in swallowing (dysphagia).
47
Are clinical signs limited to the brain or brainstem?
No
48
Why do the clinical signs of EPM vary widely?
Due to the diverse areas of the CNS that can be affected by the infection.
49
What is required for the definitive diagnosis of EPM?
Postmortem examination of CNS tissues to confirm protozoal infection by identifying the presence of Sarcocystis neurona or Neospora hughesi within CNS lesions.
50
What is the first step in antemortem diagnosis of EPM?
Conduct a thorough neurologic examination to identify abnormalities and localize lesions.
51
What are key signs to look for during a neurologic examination?
Asymmetric ataxia, focal muscle atrophy, and spasticity.
52
What diagnostic tools can be used to exclude other potential causes of neurologic signs?
Cervical radiography to rule out cervical vertebral stenotic myelopathy (CVSM) or trauma.
53
What is assessed in serum and CSF testing for EPM?
The ratio of antibodies in serum to CSF to identify intrathecal production, differentiating between passive transfer and active infection.
54
What tests are used for cases with equivocal ELISA results or suspected blood-brain barrier compromise?
Goldman-Witmer coefficient (C-value) or the antigen-specific antibody index (AI).
55
Which commercially available tests provide information regarding intrathecal antibody production?
SnSAG2, 4/3 ELISA serum titer ratio and NhSAG1 ELISA serum titer ratio.
56
What clinical signs suggest EPM should be considered as a differential diagnosis?
Asymmetric gait and focal muscle atrophy.
57
Do horses affected by EPM typically exhibit pain or fever?
No, they typically do not exhibit pain or fever unless there are comorbid conditions.
58
How does Cervical Vertebral Stenotic Myelopathy (CVSM) typically present?
With symmetric signs, more severe in pelvic limbs than thoracic limbs, without focal muscle atrophy.
59
What should be considered as a cause of spinal cord damage presenting abnormal neurologic signs?
Trauma
60
What are the signs of Equine Herpesvirus-1 (EHV-1) neurologic disease?
Symmetric pelvic limb weakness, ataxia, bladder distention, perineal hypoalgesia, and cranial nerve deficits.
61
How does Equine Motor Neuron Disease (EMND) present in early stages?
With severe limb weakness, muscle fasciculations, and tremors. Chronic EMND presents with profound muscle atrophy.
62
What other spinal cord diseases should be considered in the differential diagnosis?
Other than EHV, EMND, CVSM, trauma
Extradural and spinal cord tumors, epidural abscess, migrating metazoan parasites, rabies, West Nile viral encephalomyelitis, equine degenerative myeloencephalopathy, lead poisoning, creeping indigo toxicity, Lyme neuroborreliosis, vascular malformations, and discospondylopathies.
63
How is EPM confirmed postmortem?
By demonstrating protozoa in CNS lesions through histological examination.
64
What increases the sensitivity of detecting organisms in H&E sections?
Immunohistochemical staining increases sensitivity from 10-36% to 20-51%.
65
What other method may assist in detecting parasites in CNS tissues postmortem?
PCR, although it has not been demonstrated experimentally.
66
Are immunodiagnostic tests the primary diagnostic method for EPM?
No, they are adjuncts to clinical diagnosis.
67
Why is performing serology as part of a general health screen discouraged?
Due to low positive predictive value in non-neurologic horses.
68
When does testing for serum antibodies against S. neurona have diagnostic value?
When results are negative, indicating the horse has not been infected or resides in a low-exposure area.
69
What is the significance of positive results for S. neurona serology?
They have low positive predictive value due to common exposure among horses.
70
Why does detection of serum antibodies against N. hughesi have higher positive predictive value in neurologic horses?
Due to lower seroprevalence.
71
What do negative results for N. hughesi serology suggest?
The horse has not been infected and alternative diagnoses should be pursued.
72
When is repeated serologic testing indicated?
For horses with recent development of compatible clinical signs before seroconversion.
73
Why is detection of antibodies in CSF more informative?
Because it can indicate active infection, although it is not definitive due to passive transfer of antibodies.
74
What can cause false-positive results in CSF testing?
Blood contamination of CSF samples.
75
What do Goldman-Witmer Coefficient (C-value) and Antigen-Specific Antibody Index (AI) assess?
Whether the amount of pathogen-specific antibody in the CSF is greater than expected from passive transfer across the BBB.
76
What did an initial study with 29 clinical cases show about minor blood contamination of CSF and its effect on C/ AI value?
It does not confound assay results if up to 10,000 red cells per µL are present.
77
Should the serum titer ratio method be effective for diagnosing EPM caused by N. hughesi?
Yes, although an optimal serum titer ratio cut-off for N. hughesi needs to be established.
78
Is calculation of A/ AI value always necessary?
No, a simple serum antibody titer ratio is sufficient for accurate diagnosis of EPM caused by S. neurona.
79
What is the current status of WB in EPM diagnosis?
It has largely been supplanted by more quantitative tests.
80
What does IFAT test for?
Antibodies against culture-derived whole merozoites.
81
Why has recent research focused on SAG ELISAs?
Due to their high level of expression in the parasite and their immunogenicity in infected horses.
82
Which SnSAG tests are recommended?
2 and 4/3
83
Why is the utility of SnSAG1 ELISA limited?
Because this antigen is not expressed by all strains of S. neurona.
84
What is unclear about SnSAG1, 5, 6 ELISA?
Its reliability in detecting antibodies to S. neurona due to lack of validation.
85
What tests are avilable for N. hughesi?
ELISA (NhSAG1 ELISA), IFAT
86
Which test for N. hughesi is more sensitive?
IFAT (up to 100%), but is not fully validated
87
What is the mechanism of action for Ponazuril?
Targets the parasite's apicoplast organelle, disrupting its reproduction (Benzeneacetonitrile drug).
88
How can the bioavailability of Ponazuril be increased?
By up to 15% with concurrent administration of vegetable oil (1/2 cup).
89
What is the mechanism of action for Diclazuril?
Similar to Ponazuril, targets the parasite's apicoplast organelle (Benzeneacetonitrile drug).
90
Does vegetable oil increase the bioavailability of Diclazuril?
No, vegetable oil does not increase its bioavailability.
91
What is the mechanism of action for Sulfadiazine/Pyrimethamine?
Interferes with folic acid metabolism and the biosynthesis of purine and pyrimidine nucleotides necessary for the parasite's survival.
92
What administration considerations should be noted when treating with Sulfadiazine/Pyrimethamine?
Avoid feeding hay 2 hours before or after treatment to prevent dietary folate interference.
93
What is the efficacy of Sulfadiazine/Pyrimethamine?
Clinical improvement in 60-70% of treated horses.
94
What are the toxic effects of Sulfadiazine/Pyrimethamine?
BM suppression, anorexia, urticaria, self-limiting diarrhea, progressive mild anemia, neutropenia, thrombocytopenia, and teratogenic effects.
95
What additional supportive treatments may be warranted?
NSAIDs, corticosteroids (if brain involvement or risk of recumbence, DMSO, Vit E)
96
What biological response modifiers have been suggested?
Levamisole, killed proprionibacterium acnes, mycobacterial wall extract, inactivated parapox ovis virus, transfer factor 4. These are not validated
97
How can the risk of EPM be reduced through environmental management?
By reducing exposure to opossums, preventing wildlife access to feed, maintaining clean water sources, storing feed securely, and cleaning up spilled feed promptly.
98
How can stress reduction help prevent EPM?
By minimizing stressors like heavy exercise, transport, and ensuring proper rest and recovery periods for performance horses.
99
Why is regular monitoring important in preventing EPM?
To detect signs of neurologic disease early and seek veterinary evaluation if symptoms are observed. Implement routine health checks and maintain detailed records.
100
Is there a vaccine for EPM?
No, but maintaining overall health and immunity through appropriate vaccination schedules and deworming protocols is essential.
101
What other pharmacological methods may be used for prevention?
Prophylactic doses of ponazuril or diclazuril. Shown to reduce but not eliminate seroprevalence.
