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ECEIM consensus statements > EPM > Flashcards

EPM Flashcards

1
Q

What was the initial name for EPM identified by Rooney in 1970?

A

Segmental Myelitis

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2
Q

What is the primary cause of EPM?

A

Sarcocystis neurona

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3
Q

Which protozoan is less commonly implicated in EPM cases compared to S. neurona?

A

Neospora hughesi

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4
Q

Who are the definitive hosts for Sarcocystis neurona?

A

Opossums in North America and various South American opossums

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5
Q

Name some intermediate hosts for Sarcocystis neurona.

A

Skunks, raccoons, armadillos, and cats.

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6
Q

Where does sexual reproduction of Sarcocystis neurona occur in opossums?

A

In the intestinal epithelium.

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7
Q

What do sporozoites form in intermediate hosts?

A

Latent sarcocysts in muscle tissue

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8
Q

How do horses become infected with Sarcocystis neurona?

A

By ingesting food or water contaminated with feces from an infected opossum

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9
Q

Why are equine carcasses seldom accessible to opossums?

A

To reduce the likelihood of horses contributing to the parasite’s life cycle.

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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.

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11
Q

How does Sarcocystis neurona likely enter the CNS?

A

Through infection of endothelial cells or leukocytes.

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12
Q

Is the complete life cycle of Neospora hughesi known?

A

No, it remains poorly understood.

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13
Q

Are dogs confirmed definitive hosts for Neospora hughesi?

A

No, it has not been established.

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14
Q

Can Neospora hughesi be transmitted transplacentally in horses?

A

Yes, recent studies suggest it can be transmitted transplacentally.

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15
Q

Are all horses susceptible to EPM?

A

Yes, but not all infected horses develop clinical disease.

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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.

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17
Q

Do all horses with EPM show the same immune response?

A

No, some show altered immune responses which are sometimes antigen-specific.

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18
Q

What factors may influence the progression to severe neurologic disease in EPM?

A

Variations in protozoal inoculum and stress-induced immune suppression.

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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.

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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.

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21
Q

What percentage of EPM cases occurred in horses aged 4 years or less?

A

61.8%.

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22
Q

What was the mean age of affected horses?

A

3.6 ± 2.8 years.

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23
Q

Which breeds are most commonly affected by EPM?

A

Thoroughbreds, Standardbreds, and Quarter Horses.

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24
Q

Was there any significant sex or seasonal bias found in EPM cases?

A

No significant sex or seasonal bias was established.

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24
Q

What is the range of Sarcocystis neurona seroprevalence in the United States?

A

15% to 89%.

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24
Q

How common is Neospora hughesi seroprevalence in horses?

A

Generally low, with more than 10% in some regions but less than 3% in others.

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24
Q

What is the annual incidence of EPM in horses aged 6 months or older according to NAHMS?

A

Approximately 14 ± 6 cases per 10,000 horses.

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25
Q

Is the proportion of EPM cases attributable to N. hughesi known?

A

No, it is uncertain.

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26
Q

Does EPM usually occur sporadically or in clusters?

A

Sporadically, but clusters of cases can occur.

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27
Q

What age groups have a higher risk of developing EPM?

A

Young horses (1-5 years) and older horses (>13 years).

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28
Q

When is the risk of EPM the least?

A

In winter.

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29
Q

What environmental factor increases the risk of EPM by 2.5-fold?

A

Presence of opossums on the premise.

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30
Q

What effect does the presence of a creek or river have on the risk of EPM?

A

Reduces the likelihood of EPM by one-third.

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31
Q

What stressful events can increase the risk of EPM?

A

Heavy exercise, transport, injury, surgery, or parturition

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32
Q

How much more likely are horses treated with an anticoccidial drug to improve compared to untreated horses?

A

10 times more likely to improve.

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33
Q

How can EPM present in horses?

A

EPM can present acutely or chronically with insidious onset, showing focal or multifocal signs affecting the brain, brainstem, or spinal cord.

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34
Q

What may severely affected horses experience?

A

Difficulty standing, walking, or swallowing, with potential for rapid disease progression.

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35
Q

Can EPM clinical signs stabilize and relapse?

A

Yes, clinical signs may stabilize but relapse days or weeks later.

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36
Q

What parts of the CNS does EPM affect?

A

Both white and grey matter at multiple CNS sites.

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37
Q

What are signs of gray matter involvement?

A

Focal muscle atrophy and severe muscle weakness.

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38
Q

What are signs of white matter involvement?

A

Ataxia and limb weakness caudal to the infection site.

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39
Q

What are early signs of EPM?

A

Stumbling and frequent limb interference, which can be mistaken for lameness.

40
Q

How do EPM clinical signs progress?

A

There is a gradual progression in severity and range of clinical signs, sometimes leading to sudden exacerbation causing recumbency.

41
Q

What are the usual vital signs in EPM-affected horses?

A

Usually normal; affected horses appear bright and alert.

42
Q

How might the physical condition of EPM-affected horses appear?

A

Some horses may appear thin and mildly obtunded.

43
Q

What kind of weakness is observed in EPM?

A

General weakness, often involving all four limbs.

44
Q

What is asymmetric ataxia?

A

Uncoordinated movement affecting one side more than the other.

45
Q

What types of sensory loss may be present?

A

Areas of hyporeflexia (reduced reflexes), hypoalgesia (reduced pain sensation), or complete sensory loss.

46
Q

What are common signs of brain/brainstem involvement in EPM?

A

Reduced alertness (obtundation), tilted head posture (head tilt), facial nerve paralysis, and difficulty in swallowing (dysphagia).

47
Q

Are clinical signs limited to the brain or brainstem?

A

No

48
Q

Why do the clinical signs of EPM vary widely?

A

Due to the diverse areas of the CNS that can be affected by the infection.

49
Q

What is required for the definitive diagnosis of EPM?

A

Postmortem examination of CNS tissues to confirm protozoal infection by identifying the presence of Sarcocystis neurona or Neospora hughesi within CNS lesions.

50
Q

What is the first step in antemortem diagnosis of EPM?

A

Conduct a thorough neurologic examination to identify abnormalities and localize lesions.

51
Q

What are key signs to look for during a neurologic examination?

A

Asymmetric ataxia, focal muscle atrophy, and spasticity.

52
Q

What diagnostic tools can be used to exclude other potential causes of neurologic signs?

A

Cervical radiography to rule out cervical vertebral stenotic myelopathy (CVSM) or trauma.

53
Q

What is assessed in serum and CSF testing for EPM?

A

The ratio of antibodies in serum to CSF to identify intrathecal production, differentiating between passive transfer and active infection.

54
Q

What tests are used for cases with equivocal ELISA results or suspected blood-brain barrier compromise?

A

Goldman-Witmer coefficient (C-value) or the antigen-specific antibody index (AI).

55
Q

Which commercially available tests provide information regarding intrathecal antibody production?

A

SnSAG2, 4/3 ELISA serum titer ratio and NhSAG1 ELISA serum titer ratio.

56
Q

What clinical signs suggest EPM should be considered as a differential diagnosis?

A

Asymmetric gait and focal muscle atrophy.

57
Q

Do horses affected by EPM typically exhibit pain or fever?

A

No, they typically do not exhibit pain or fever unless there are comorbid conditions.

58
Q

How does Cervical Vertebral Stenotic Myelopathy (CVSM) typically present?

A

With symmetric signs, more severe in pelvic limbs than thoracic limbs, without focal muscle atrophy.

59
Q

What should be considered as a cause of spinal cord damage presenting abnormal neurologic signs?

A

Trauma

60
Q

What are the signs of Equine Herpesvirus-1 (EHV-1) neurologic disease?

A

Symmetric pelvic limb weakness, ataxia, bladder distention, perineal hypoalgesia, and cranial nerve deficits.

61
Q

How does Equine Motor Neuron Disease (EMND) present in early stages?

A

With severe limb weakness, muscle fasciculations, and tremors. Chronic EMND presents with profound muscle atrophy.

62
Q

What other spinal cord diseases should be considered in the differential diagnosis?
Other than EHV, EMND, CVSM, trauma

A

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
Q

How is EPM confirmed postmortem?

A

By demonstrating protozoa in CNS lesions through histological examination.

64
Q

What increases the sensitivity of detecting organisms in H&E sections?

A

Immunohistochemical staining increases sensitivity from 10-36% to 20-51%.

65
Q

What other method may assist in detecting parasites in CNS tissues postmortem?

A

PCR, although it has not been demonstrated experimentally.

66
Q

Are immunodiagnostic tests the primary diagnostic method for EPM?

A

No, they are adjuncts to clinical diagnosis.

67
Q

Why is performing serology as part of a general health screen discouraged?

A

Due to low positive predictive value in non-neurologic horses.

68
Q

When does testing for serum antibodies against S. neurona have diagnostic value?

A

When results are negative, indicating the horse has not been infected or resides in a low-exposure area.

69
Q

What is the significance of positive results for S. neurona serology?

A

They have low positive predictive value due to common exposure among horses.

70
Q

Why does detection of serum antibodies against N. hughesi have higher positive predictive value in neurologic horses?

A

Due to lower seroprevalence.

71
Q

What do negative results for N. hughesi serology suggest?

A

The horse has not been infected and alternative diagnoses should be pursued.

72
Q

When is repeated serologic testing indicated?

A

For horses with recent development of compatible clinical signs before seroconversion.

73
Q

Why is detection of antibodies in CSF more informative?

A

Because it can indicate active infection, although it is not definitive due to passive transfer of antibodies.

74
Q

What can cause false-positive results in CSF testing?

A

Blood contamination of CSF samples.

75
Q

What do Goldman-Witmer Coefficient (C-value) and Antigen-Specific Antibody Index (AI) assess?

A

Whether the amount of pathogen-specific antibody in the CSF is greater than expected from passive transfer across the BBB.

76
Q

What did an initial study with 29 clinical cases show about minor blood contamination of CSF and its effect on C/ AI value?

A

It does not confound assay results if up to 10,000 red cells per µL are present.

77
Q

Should the serum titer ratio method be effective for diagnosing EPM caused by N. hughesi?

A

Yes, although an optimal serum titer ratio cut-off for N. hughesi needs to be established.

78
Q

Is calculation of A/ AI value always necessary?

A

No, a simple serum antibody titer ratio is sufficient for accurate diagnosis of EPM caused by S. neurona.

79
Q

What is the current status of WB in EPM diagnosis?

A

It has largely been supplanted by more quantitative tests.

80
Q

What does IFAT test for?

A

Antibodies against culture-derived whole merozoites.

81
Q

Why has recent research focused on SAG ELISAs?

A

Due to their high level of expression in the parasite and their immunogenicity in infected horses.

82
Q

Which SnSAG tests are recommended?

A

2 and 4/3

83
Q

Why is the utility of SnSAG1 ELISA limited?

A

Because this antigen is not expressed by all strains of S. neurona.

84
Q

What is unclear about SnSAG1, 5, 6 ELISA?

A

Its reliability in detecting antibodies to S. neurona due to lack of validation.

85
Q

What tests are avilable for N. hughesi?

A

ELISA (NhSAG1 ELISA), IFAT

86
Q

Which test for N. hughesi is more sensitive?

A

IFAT (up to 100%), but is not fully validated

87
Q

What is the mechanism of action for Ponazuril?

A

Targets the parasite’s apicoplast organelle, disrupting its reproduction (Benzeneacetonitrile drug).

88
Q

How can the bioavailability of Ponazuril be increased?

A

By up to 15% with concurrent administration of vegetable oil (1/2 cup).

89
Q

What is the mechanism of action for Diclazuril?

A

Similar to Ponazuril, targets the parasite’s apicoplast organelle (Benzeneacetonitrile drug).

90
Q

Does vegetable oil increase the bioavailability of Diclazuril?

A

No, vegetable oil does not increase its bioavailability.

91
Q

What is the mechanism of action for Sulfadiazine/Pyrimethamine?

A

Interferes with folic acid metabolism and the biosynthesis of purine and pyrimidine nucleotides necessary for the parasite’s survival.

92
Q

What administration considerations should be noted when treating with Sulfadiazine/Pyrimethamine?

A

Avoid feeding hay 2 hours before or after treatment to prevent dietary folate interference.

93
Q

What is the efficacy of Sulfadiazine/Pyrimethamine?

A

Clinical improvement in 60-70% of treated horses.

94
Q

What are the toxic effects of Sulfadiazine/Pyrimethamine?

A

BM suppression, anorexia, urticaria, self-limiting diarrhea, progressive mild anemia, neutropenia, thrombocytopenia, and teratogenic effects.

95
Q

What additional supportive treatments may be warranted?

A

NSAIDs, corticosteroids (if brain involvement or risk of recumbence, DMSO, Vit E)

96
Q

What biological response modifiers have been suggested?

A

Levamisole, killed proprionibacterium acnes, mycobacterial wall extract, inactivated parapox ovis virus, transfer factor 4. These are not validated

97
Q

How can the risk of EPM be reduced through environmental management?

A

By reducing exposure to opossums, preventing wildlife access to feed, maintaining clean water sources, storing feed securely, and cleaning up spilled feed promptly.

98
Q

How can stress reduction help prevent EPM?

A

By minimizing stressors like heavy exercise, transport, and ensuring proper rest and recovery periods for performance horses.

99
Q

Why is regular monitoring important in preventing EPM?

A

To detect signs of neurologic disease early and seek veterinary evaluation if symptoms are observed. Implement routine health checks and maintain detailed records.

100
Q

Is there a vaccine for EPM?

A

No, but maintaining overall health and immunity through appropriate vaccination schedules and deworming protocols is essential.

101
Q

What other pharmacological methods may be used for prevention?

A

Prophylactic doses of ponazuril or diclazuril. Shown to reduce but not eliminate seroprevalence.

ECEIM consensus statements (11 decks)

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