Disease Of the Nervous System p917-1014

Question 1

How long can xanthochromia be present after the introduction of blood?

A) 1 week
B) 10 days
C) 2 weeks
D) 18 days

Answer 1

B) 10 days

Question 2

Normal CSF should contain less than how many WBCs/dL?

A) 6
B) 10
C) 20
D) 50

Answer 2

A) Less than 6 WBCs/dL

Question 3

What should the protein concentrations be in the CSF of normal ruminants and horses?

A) < 50 mg/dL, < 75 mg/dL
B) < 75 mg/dL, < 50 mg/dL
C) < 50 mg/dL, < 100 mg/dL
D) < 100 mg/dL, < 50 mg/dL

Answer 3

C) Ruminants [protein] in CSF < 50 mg/dL

Equine [protein] in CSF < 100 mg/dL

Question 4

What does the albumin quotient measure?

Answer 4

Measures the blood brain barrier permeability. Elevated levels indicate BBB leakage or contamination of CSF with blood.

= (CSF albumin/serum albumin)x100

Question 5

What does the IgG index measure when evaluating the CSF?

Answer 5

IgG index measures intrathecal production of IgG and an elevated index can support infectious disease of the CNS.

= (CSF IgG/Serum IgG)x(Serum albumin/CSF albumin)

Question 6

Discuss the three steps in the progression of clinical signs in a horse infected with EEE, WEE, or VEE. Which of these three diseases is the most severe and rapidly progressive?

Answer 6

1) Inoculation —> viral proliferation in regional lymph nodes —> low-grade viremia and fever 2 days after inoculation
2) Viral proliferation in various body organs after spread from LN —> febrile, anorexia, depression, tachycardia, diarrhea
3) Clinical encephalomyelitis, with onset of neurologic signs about 5 days after infection and death 2-3 days later

EEE is the most severe and rapidly progressive

Question 7

Which of the following DOES NOT describe an ideal time or condition for the encephalitides (EEE, WEE, VEE) to occur?

A) Summer and early fall
B) Warmth and humidity
C) Dry, cool
D) Rainfall in excess

Answer 7

C) Dry, cool times typically are not ideal times for mosquito breeding or bird activity

Standing surface water for mosquito larval development, bush cover for wild hosts and immune status of various hosts affect timing and magnitude of equine epizootics.

Question 8

What is the most common, primary clinical sign seen in cases of EEE, WEE, and VEE?

A) CN deficits
B) Dementia
C) Obtundation
D) Ataxia

Answer 8

C) Obtundation is the c/s most recognized by owners. This is followed by dementia and CN deficits. Further progression leads to asymmetrical ataxia, paresis, and finally recumbency.

Question 9

The CSF analysis for horses with EEE are quite distinctive. List those abnormalities.

Answer 9

Hyperproteinemia, high NCC, neutrophilic pleocytosis (can be lymphocytic as well)

Question 10

What is the method of choice for testing for viral encephalitis and why?

Answer 10

IgM Ab capture ELISA because a titer of > 1:400 can distinguish between vaccinal (IgG) and viral infection induced (IgM and IgG) titers.

Question 11

List some supportive treatments for viral encephalitis and what their aims are.

Answer 11

DMSO 1 g/kg as 10% soln IV or IG
Flunixin 1.1 mg/kg q12IV for 3 day
Dexamethasone 0.5-1.0 mg/kg IM or IV for 3 days then taper
Mannitol 0.25-1.0 g/kg IV at 20% soln
Hypertonic saline at 2 ml/kg 4-6 times during the first day

These are aimed at reducing brain edema and inflammation

Question 12

When is it recommended to vaccinate for EEE, WEE and VEE?

Answer 12

For foals, start at 4-6 mths, inoculate 4-6 weeks later and booster at 10-12 mths. No earlier than 4 mths.

For regularly vax horses, start in Jan or Feb - May or June, with q6mths

Pregnant mares should get booster 4-6 weeks prior to foaling

Question 13

Describe how Fusarium verticilliodes and F. proliferatum cause CNS intoxication? What are the types of toxins that are produced from these bacteria?

Answer 13

Fusarium bacteria produce B1, B2 and B3 toxins, of which B1 was the most common and most studied. These toxins are responsible for CNS intoxication of the CNS by interfering with sphingolipid metabolism, disrupting endothelial cell walls and basement membranes.

Question 14

What other organ system, other than the CNS, is routinely involved with equine leukoencephalomalacia?

Answer 14

Hepatic involvement occurs in many cases, as evidenced by high serum liver enzymes. Failure is uncommon, and fatal outbreaks of liver disease without brain involvement has been reported.

Question 15

What are trigger factors for horses with head shaking?

Answer 15

Bright lights, sun, heat, cold, stress, extreme neck flexion, riding on narrow roads, hearing people’s voices, riding near trees or waters

Half of the cases are partially or completely seasonal with signs beginning suddenly or getting worse in spring and ending in the late summer or fall.

Question 16

What nerves are thought to be involved with the etiology of headshaking in horses?

Answer 16

Proximal aspect of the infraorbital nerve and maxillary nerve. 24/27 horses stopped headshaking when the posterior ethmoidal nerves (branches of the ophthalmic nerve).

Some headshaking appears to represent optic-trigeminal summation of stimuli arriving via both nerves.

Whatever the inciting cause, idiopathic headshaking appears to be a nasal/facial pain syndrome assoc with hyperactivity of trigeminal pain pathway.

Question 17

There are three forms of treatment in attempts to try to curb headshaking in horses. What are the three and how efficient are they?

Answer 17

Physical - use of a muzzle net, about 30% improved ~70%; contact with the nose area or upper forehead may px nerve from firing

Surgical - interruption of pain pathways in the trigeminal nerve or its branches; two approaches infraorbital neurectomy, and caudal infraorbital nerve compression; often provides temporary remission only to relapse weeks to months later

Medical - unlikely that complete and permanent remission can be achieved medically; cyproheptadine 0.3 mg/kg PO BID has had some success, this is an anti-histamine; melatonin is advocated as a way to suppress the neurologic responses to increasing photoperiod but should be started before seasonal onset

Question 18

What are the two small ruminant lentiviruses? A

Answer 18

Ovine progressive pneumonia virus

Caprine arthritis encephalitis virus

Question 19

What are some clinical signs seen with ovine progressive pneumonia virus? How common are neurologic signs?

Answer 19

Neurologic signs are rare. Nervous system signs represent a diffuse encephalitis —> ataxia, gradual progressive limb weakness.

Other signs are emaciation, nonsuppurative, progressive arthritis, and enlargement of the mammary gland.

Question 20

In what ways are maedi-visna virus spread?

Answer 20

Ingestion of infected milk, in-utero and horizontal throughout the herd

Question 21

Ovine progressive pneumonia virus affects the body by :

A) Being idiopathic, unknown pathophysiology
B) Being immunosuppressive
C) Causing autoimmune destruction
D) Being hemolytic

Answer 21

B) Immunosuppressive, leading to secondary bacterial infections

Diffuse, non-suppurative, perivascular inflamm throughout the neuroaxis, demyelination, gliosis, lymphocytic choriomeningitis and local necrotic areas

Question 22

When do the different clinical manifestations of caprine arthritis-encephalitis present in goats?

Answer 22

Leukoencephalomyelitis predominantly seen in < 1 year of age. Polysynovitis-arthritis can be recognized in goats as young as 6 mths, but generally seen in mature adults.

Question 23

How is CAE tested for? What does a positive mean to a producer?

Answer 23

AGID using OPPV Ag, if positive, means that this animal has a lifelong infection.

Question 24

What are tissues of importance when it comes to CAEV localization? What is causing the granulomatous inflammation in these tissues?

Answer 24

Synovium, mammary gland and CNS are important. Within the tissues can be found immune complexes generated by interaction of non-neutralizing Ab produced by lymphocytes and assoc. virus-infected macrophages.

Question 25

What disease causes the following: abortion, infertility, deformed lambs with abnormal hair coat, arthrogryposis, uncontrollable tremors? A) Ovine progressive pneumonia virus B) Bovine viral diarrhea virus C) Transmissible spongiform encephalopathy D) Border disease

Answer 25

D) Border disease is a togovirus, genus Pestivirus, related to classical swine fever and BVDV

Question 26

If an adult sheep becomes infected with border disease, how will it deal with re-infection? How is a lamb in utero infected?

Answer 26

If an adult sheep becomes infected with border disease, it has a short-term viremia and is immune to reinfection. If lambs in utero are infected, they can become immunotolerant and be viremia for life. Once lambs are infected in early gestation < 50 d, the CNS, skin and skeleton are the most seriously affected. Tetragenic effects are most observed when dam is infected between 50-90 d. Abortions are generally seen around 63 d.

Question 27

What is the most accurate method of diagnosing border disease? What tissues most consistently contain viral Ag?

Answer 27

Identifying viral Ag in abomasum, pancreases, kidney, thyroid and testicles are the most accurate for diagnosing border disease.

Question 28

What are three reasons proposed for hypomyelination in sheep with border disease?

Answer 28

1) Virus-induced degeneration of oligodendroglial cells 2) Persistent viral infection 3) Diminished secretion of thyroid hormones due to direct inhibition of the thyroid gland This disease is also immunosuppressive by depressing blastogenic activity of lymphocytes, decreasing T-helper cell function and increasing T-suppressor cell function.

Question 29

What is a prion and how does it cause a progressive neurologic dysfunction?

Answer 29

A host encoded membrane protein that does not carry any nucleic acid (PrP) has an altered confirmation, to PrP-BSE for instance, and then replicates by inducing a posttranslational confirmational change. After a prolonged incubation period, the accumulation of the abnormal isoform occurs in the CNS, causing progressive neurologic dysfunction.

Question 30

Other then the CNS tissue, where else might the prion in BSE be found?

Answer 30

The prion is also thought to undergo propagation in the distal ileum, by moving through the gut-associated lymphoid tissue. The skeletal muscles and lymphatic tissues are unaffected.

Question 31

What is the causative agent of scrapie? What are some clinical signs of this disease?

Answer 31

PrP-Sc is the prion responsible for scrapie. Pruritus, secondary wool loss, dermatitis, skin infections, bruxism, ptyalism, tremors, convulsions, death

Question 32

What tissues can the prion in scrapie be identified?

Answer 32

Lymphoreticular system, kidneys, placenta

Question 33

How is scrapie transmitted? Once in the body, how does scrapie get to the CNS?

Answer 33

Scrapie is most likely transmitted via infected placenta, oral entry is the most common. Once ingested, the agent travels via the vagus nerve to vagal nucleus of the brainstem

Question 34

The genetic makeup of the host controls the susceptibility and resistance to scrapie in various breeds. Polymorphisms of which codons of the PrP gene are the main determinants of susceptibility? What genotype is most susceptible and what genotype is highly resistant?

Answer 34

Most importantly codon 171, with 136 and 154 playing a small role. Codon 171 can be RR, QR, or QQ. With QQ being susceptible. VV136, RR154, QQ171 (or AA136,RR154, QQ171) thought to be most susceptible AA136, RR154, RR171 thought to be highly resistant

Question 35

Diagnosing scrapie occurs how ante- and post-mortem?

Answer 35

Ante-mortem IHC of nictitating membranes, retropharyngeal LN, tonsils, etc have limited sensitivity. After death, microscopy of the brain and spinal cord are classic. Looking for neuronal vacuolation and PrP-Sc deposits

Question 36

The suid herpesvirus type 1 is responsible for a disease that manifests as what in cattle, sheep, cats, dos, goats, wildlife, and, rarely, horses?

Answer 36

Pseudorabies, Aujeszky Disease, Mad Itch, or Bulbar paralysis presents with paresthesia, acute and severe pruritis, depression, excessive licking of the nose, vocalization, convulsions, ending in death

Question 37

What is the United State’s status with Aujeszky disease?

Answer 37

As of Dec 2006, all states are classified as free of pseudorabies in domesticated swine, though some remains present in feral pigs.

Question 38

What routes of transmission occur with pseudorabies?

Answer 38

Nose-to-nose, fecal oral, venereal Indirect transmission occurs by inhalation of aerosolized virus. The virus can travel up to 2 km (1.2 miles)

Question 39

Any unexplained, acute, rapidly progressive, intracranial disease, with autonomic instability, dysphagia, hydrophobia, paresis, or parethesis should have WHAT as its primary differential?

Answer 39

RABIES!!!!

Question 40

The incubation period varies greatly for rabies, depending on the pathogenicity of the inoculum and what?

Answer 40

The distance of the bite, from the brain, in cases of rabies can cause variation in the incubation period of rabies. Bites to the head have shorter incubation periods vs bites on the extremities.

Question 41

There are three manifestations of rabies. What are they?

Answer 41

Furious rabies - hyperexcitability, fearful, enraged Dumb rabies - mentally depressed Paralytic rabies - dumb rabies with flaccid paraparesis, tetraparesis, and/or tetraplegia

Question 42

What postmortem changes are seen with rabies?

Answer 42

Nonsuppurative meningoencephalomyelitis, Negri bodies on histology of the brain

Question 43

Once an animal is bitten, how does the the rabies virus progress to cause clinical signs?

Answer 43

Once infected, the virus binds to Ach of the peripheral nerves and migrates retrogradely to the CNS through peripheral nerves, spinal rootless and the spinal cord. Once in the CSF, it spread along the rootlets of the CN, to the salivary glands, and the nasal epithelium. Certain signaling proteins for helping cells respond to infection are blocked, allowing propagation of rabies.

Question 44

If a vaccinated animal is bitten by an animal suspected to have rabies, what happens next?

Answer 44

Vaccinate the animal again, and closely monitor for 90 days.

Question 45

This disease is caused by Chlamydophila pecorum, and can affect multiple body systems. List three of those and the disease that does this.

Answer 45

Sporadic bovine encephalitis is rare but infected cattle can have pneumonia, polyarthritis, and peritonitis. Once meningoencephalitis occurs, animals can die within 4-10 days.

Question 46

When diagnosing sporadic bovine encephalitis (SBE), what samples can be collected and the finding of ___ can be highly suggestive of SBE?

Answer 46

Since SBE often causes a peritonitis or a pleuritis, a sample of effusion can be collected and the finding of reticulate bodies in the exudate cells is highly suggestive of SBE.

Question 47

What can sporadic bovine encephalitis or Chlamydophila pecorum, be treated with?

Answer 47

Early cases can be treated with 20 mg/kg of oxytet, for a minimum of 7days.

Question 48

Define meningitis, meningoencephalitis and meningoventriculitis.

Answer 48

Meningitis - inflammation of the meninges, surrounding the brain and/or spinal cord that results from bacterial invasion of these tissues Meningoencephalitis - if the infectious process spreads to the brain tissues Meningoventriculitis - if the infectious process spreads to the ventricles

Question 49

What is the definition of polioencephalomalacia?

Answer 49

Softening or necrosis (malacia) of regions of gray matter of the brain

Question 50

What are possible etiologies for polioencephalomalacia?

Answer 50

1) Excessive sulfur consumption 2) Altered thiamine metabolism 3) Salt poisoning or water deprivation 4) Amprolium administration 5) Rations of molasses and urea 6) Lead intoxication

Question 51

If ruminal gas-cap gas was measured in a case of polioencephalomalacia, what levels of H2S would indicate excessive sulfur consumption?

Answer 51

H2S > 1000 ppm in the ruminal gas cap would indicate excessive sulfur consumption.

Question 52

What are several ways that thiamine deficiency can be measured?

Answer 52

1) Determining total blood thiamine concentration using a thiamine dependent Lactobacillus bioassay 2) Determining transketolase activity by comparing active (holoenzyme) and inactive (apoenzyme) forms with activity of the two forms AFTER addition of thiamine; large increase in specific transketolase activity suggest a thiamine deficiency

Question 53

In polioencephalomalacia, the primary lesion is neuronal edema with necrosis. What is postulated to be the cause of this edema and subsequent necrosis?

Answer 53

The bony calvarium limits expansion and neuronal swelling leads to pressure necrosis. The edema occurs from insufficient function of the sodium-potassium pump in cortical cells, due to ATP depletion.

Question 54

ATP depletion contributes to the edema causing polioencephalomalacia. What largely contributes to this ATP depletion in the brain?

Answer 54

The brain relies on glucose and oxygen for ATP production. While the brain only has about 10 minutes worth of glycogen, the ECF contains approx 100x as much glucose as the oxygen required for complete aerobic glycolysis. Oxygen delivery is rate limiting for ATP production and factors that inhibit oxygen utilization (H2S, lead) could contribute.

Question 55

Where does a ruminant get thiamine from and how is it utilized?

Answer 55

Thiamine is produced by rumen microbes and is important to the glycotic pathways. Thiamine diphosphate is an important coenzyme for transketolase, the rate-limiting enzyme in the hexose monophosphate pathway of glycolysis and the alpha-ketoacid dehydrogenases of the Krebs cycle.

Question 56

What are factors that might decrease production, absorption or function of thiamine?

Answer 56

1) Production of ruminal thiaminases 2) Production or ingestion of inactive thiamine analogs 3) Ingestion of preformed plant thiaminases 4) Decreased intake of preformed thiamine by preruminants 5) Impaired absorption or phosphorylation of thiamine by rumen bacteria 6) Increased fecal output of thiamine 7) Decreased ruminal production of thiamine diphosphate

Question 57

What are some examples of man-made or natural thiaminases?

Answer 57

Amprolium, Bacillus thiaminolyticus, Clostridium sporogenes, bracken fern (Pteridium aquilinum), horsetail (Equisetum arvense), Nardoo fern (Marsilea drummondii), Bacillus aneurinolyticus

Question 58

There are two pathways of sulfur in the rumen. What are they, how do they work and which one produces a potential cause of polioencephalomalacia?

Answer 58

1) The assimilatory pathway - reduction of sulfate to sulfides —> incorporation into sulfur-containing organic compounds —> incorporated into microbial crude protein 2) The dissimilatory pathway - energy producing pathway in which microorganisms use sulfate as a terminal e- acceptor, with end product being a sulfide ion This dissimilatory pathway can contribute to polioencephalomalacia, as a high sulfur diet can cause a high surge in ruminal sulfide generation. This can ultimately lead to overwhelming of hepatic detoxification capacity and sulfide then affects e- transport, and impairs ATP production.

Question 59

While the brain is only ___% of body weight, it accounts for ___ - ___% of body glucose utilization and ___% of oxygen utilization in adults? A) 10%, 40-50% and 20% B) 2%, 20-30% and 20% C) 5%, 40-50% and 10% D) 10%, 20-30% and 10%

Answer 59

B) 2%, 20-30% and 20%

Question 60

What is the reported oral toxic dose of sodium chloride for cattle, horses and sheep?

Answer 60

Cattle and horses 2.2 g/kg toxic dose of NaCl | Sheep 6 g/kg toxic dose of NaCl

Question 61

Once an animal has ingested toxic concentrations of NaCl (> 7000 ppm), has had water deprivation, or the CSF sodium concentration is greater than 160 mEq/L, they are undergoing salt poisoning. What is the pathophysiology that causes CNS edema and acute encephalopathy?

Answer 61

Ionic sodium accumulates into the brain cells by passive diffusion. This hyperosmolarity reduces energy-dependent sodium transport. Once an animal is permitted to drink, the ECF expands and there is an abrupt reduction in ECF osmolarity. Water will then diffuse down its osmolar gradient and into the hyperosmolar CSF, contributing to CNS edema, increased cranial pressure and acute encephalopathy.

Question 62

If an animal has severe hypernatremia, a high sodium crystalloid solution (HSCS) can be made. What level of sodium is recommended fo this solution, how fast should it be administered and what is the optimal reduction of serum sodium concentration?

Answer 62

1) The level of sodium in a HSCS should be no lower than 10-15 mEq/L less than the patient’s serum sodium concentration. 2) It should be administered at 1-2 mL/kg/hr 3) An optimal sodium reduction should be 0.5-1 mEq/L/h

Question 63

What are precursors of Vitamin A that are provided in cattle rations, and where are these used to synthesize Vitamin A, in the body?

Answer 63

Vitamin A, or retinol, is synthesized in the liver from plant carotenoid precursors. Cattle rations will have beta-carotene or retinoids as precursors.

Question 64

What life situations require more Vitamin A and animals during these are at risk for developing deficiencies.

Answer 64

Growing animals, animals not having forages provided, or immune compromised animals require more Vitamin A and are at risk for developing deficiencies.

Question 65

Vit A deficiency can cause anorexia, ill-thrift, blindness, diarrhea and pneumonia, as well as intermittent tonic-clonic convulsions. What are further ocular changes that occur, as well as reproductive disturbances?

Answer 65

1) Pupils become dilated and unresponsive. Optic disc becomes pale, borders indistinct. Retinal vessels become tortuous and occluded as they course over the disc. 2) Reproductive disturbances include malformation of fetuses, abortions, loss of libido, testicular degeneration and decreased sperm counts. Calves that are born to deficient dams are blind, domed foreheads, thickened carpal bone joints and are weak at birth.

Question 66

Why is Vit A so important for vision? There are three ways Vit A has been assoc. with blindness. What are those and are they reversible?

Answer 66

Vit A is necessary for regeneration of rhodopsin. 1) Night blindness is caused by decreased formation of Vit A aldehyde in the regeneration of visual pigment rhodopsin; REVERSIBLE 2) Degenerative changes in the outer retinal layers; can be reversible if treated in early stages 3) Stenosis of the optic foramen and compression of the optic nerve; IRREVERSIBLE

Question 67

There is a seasonal difference in the levels of Vit A, depending on the seasons. Destruction of carotene is also hastened by several environmental factors. What are those?

Answer 67

Heat, sunlight, trace mineral supplements and humidity; pelleting and exposure to rancid fat can destabilize Vit A

Question 68

What causes secondary deficiencies in Vit A?

Answer 68

Interference with Vit A absorption, inhibition of the conversion of beta-carotene to retinol in the SI, increases requirement in the face of inadequate intake (fever, lactation, high ambient temp and inadequate dietary energy can increase the daily requirement for Vit A)

Question 69

What recommended treatment for cattle with Vit A deficiency?

Answer 69

440 IU/kg of Vit A parents rally and then 6000 IU/kg parentally every 50-60 d until the diet has been enriched better.

Question 70

What is the difference between hydranencephaly and hydroencephaly?

Answer 70

Hydranencephaly is caused by normotensive hydroenephaly, due to failure of cell growth or cellular necrosis. Hydroencephaly is a hypertensive process, caused by occlusion or compression of the ventricular system, or decreased CSF absorption. Sites of obstruction include lateral apertures, mesencephalic aqueduct, lateral ventricles, interventricular foramina and fourth ventricle.

Question 71

What are causes of hydranencephaly and when does this generally occur?

Answer 71

Hydranencephaly is typically acquired in utero, by virus infections such as: BVDV, Schmallenburg, Aino, Cache Valley, bluetongue, akbane & border disease

Question 72

What are causes of hydroencephaly and when do these typically occur?

Answer 72

Hydroencephaly can be both acquired or congenital. Acquired examples are cerebral abscesses, cholesteatoma, EIA, Coenurus cerebralis infestation, meningitis, lymphosarcoma Congenital hydroencephaly is a hereditary condition seen in Herefords, Charolais, Ayrshire, Dexter, Holstein and Jersey calves. This has also been recognized in Arabian foals.

Question 73

How does lead poisoning present differently between ruminants and equine?

Answer 73

Ruminants - acute encephalopathy | Equine - chronic polyneuritis

Question 74

If livestock have been chronically poisoned with lead, how might lead toxicity be diagnosed?

Answer 74

Animals that have been chronically poisoned with lead may have normal plasma levels but high concentration in the bone. This can be diagnosed with administration of EDTA, which will solubilize bone lead and increase plasma concentrations.

Question 75

What else can be measured in blood to diagnose lead toxicity?

Answer 75

Erythrocyte porphyrins and erythrocytes concentrations of alpha-aminolevulinic acid (ALA) can be measured if lead plasma concentrations are normal.

Question 76

While hematologic abnormalities of lead toxicity are subtle, if they are present, what is the most common abnormality?

Answer 76

Normocytic, normochromic hemolytic anemia

Question 77

What happens to lead after it is absorbed from the GI tract?

Answer 77

Lead is bound to erythrocyte proteins, and once these erythrocytes have died, the lead is deposited in the bone as triphosphate salt.

Question 78

With lead toxicity, enzymes of heme synthesis are susceptible to injury. What process does lead interfere with?

Answer 78

Lead interferes with ferrochelatase which inhibits formation of heme from protoporphyrin. This results in a buildup of unmetabolized porphyrins.

Question 79

How does lead cause an encephalopathy in ruminants?

Answer 79

Capillary dysfunction leads to cerebellar hemorrhage and edema. Microvascular damage, cellular necrosis, brain swelling, neurotransmitter dysfunction and decreased glucose uptake all contributes to manifestations of encephalopathy.

Question 80

What is the treatment for lead toxicity?

Answer 80

Removal of the lead from the digestive tract, chelation therapy with calcium disodium EDTA, as well as fluid and nutritional support. EDTA should be dosed at 66 mg/kg/day, divided into several doses, daily for 3-5 days. 2 day non-treatment period for soft tissue and bone lead reequilibration. Then again daily for 5 days.

Question 81

EHV-1 has been associated with what disease manifestations?

Answer 81

Late-term abortion, death of neonatal foals, spinal cord disease

Question 82

How soon after infection does EHV-1 usually start having C/S? A) 2 weeks B) Immediately C) 6-10 days D) 1-2 months

Answer 82

C) In 6-10 days after infection with EHV-1, acute onset of ataxia and tetraparesis can occur

Question 83

What are the neurologic signs of equine herpes myeloencephalopathy?

Answer 83

Signs reflect damage to white and grey matter —> truncates ataxia and paresis, bladder distention, urinary incontinence, weakness of the tail and anus, reduced perineal sensation Hind end tends to be more severely affected than the fore limbs

Question 84

Ocular lesions can occur with equine herpes myeloencephalopathy. What are those?

Answer 84

Mydriasis, hypopyon, uveitis, optic neuritis,

Question 85

Which of the following findings are consistent with a horse that equine herpes myeloencephalopathy? (More than one answer may apply) A) Monocytic pleocytosis B) Xanthochromia C) Low protein concentration D) Severely elevated nucleated cell count

Answer 85

B) Xanthochromic fluid, with a high protein count and a normal to mildly elevated nucleated cell count is almost pathopneumonic for EHM. Normal protein concentration and/or a mononuclear pleocytosis can occur occasionally.

Question 86

What is the diagnostic technique of choice for equine herpes myeloencephalopathy? A) Virus isolation from biopsied tissue B) PCR amplification in nasal swabs or blood C) Convalescent serum virus neutralizing titers D) Complement-fixation antibody titers

Answer 86

B) PCR amplification in nasal swabs or blood Convalescent serum virus neutralizing or complement-fixation Ab titers taken 7-21 days apart, showing a fourfold or greater increase, can be presumptive evidence of an EHV-1 infection. However, these do not distinguish between EHV-1 or EHV-4.

Question 87

If PCR is positive for equine herpes myeloencephalopathy, the sample can be analyzed for a single nucleotide variant, where and for what purpose?

Answer 87

EHM is caused by a nucleotide variant in the viral DNA polymerase gene, DNApol, D752, which defines the best known and most important neuropathic strain of EHV-1.

Question 88

Once EHV-1 has colonized the upper respiratory tract, where and how does it disseminate next?

Answer 88

EHV-1 spreads and amplifies in the regional lymph nodes before circulating in the blood within the lymphocytes.

Question 89

How does EHV-1 get into endothelial cells of small arterioles?

Answer 89

After attaching to MHC-1 receptors, EHV-1 enters the endothelial cells of small arterioles, where vasculitis and widespread arterial microthrombosis occur.

Question 90

When and how do horses become infected with EHV-1? Do they all show clinical signs?

Answer 90

Horses typically become infected with EHV-1 prior to 1 y of age, when they come in contact with infected fomites or aerosolized droplets. The latent virus can live in the trigeminal ganglia or lymphoid tissue around the head. More than 50% of normal horses have latent infections of EHV-1.

Question 91

How are mules and donkeys affected with EHV-1?

Answer 91

They can become infected and shed the virus, but do not develop EHM.

Question 92

What can be used as treatment for equine herpes myeloencephalopathy? What is the most important aspect of treating this disease?

Answer 92

Supportive care is the most important when it comes treating EHM. Acyclovir, a guanosine analog, can be used in horses, but is extremely expensive.

Question 93

What are the four steps when managing premises with EHM cases? How long should quarantine continue?

Answer 93

1) Isolate affected horses 2) Monitor temperatures twice daily on all quarantined horses 3) Submit diagnostic samples 4) Implement robust biosecurity AAEP recommends a 28 day quarantine continuing AFTER last bout of fever.