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NSB II > Parasitic Diseases of the Brain, Spinal Cord, and Eyes > Flashcards

Parasitic Diseases of the Brain, Spinal Cord, and Eyes Flashcards

1
Q

describe neospora caninum (3)

A
  1. tissue cyst forming coccidian with worldwide distribution
  2. indirect life cycle:
    -DH: canids, sexual stage in intestinal epithelium
    -IH: most mammals (cattle, ungulates), asexual stage in tissue-cysts
  3. NOT zoonotic
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2
Q

describe clinical presentation of neospora caninum (3)

A
  1. infectious inflammatory myopathy in dogs
  2. if adults develop disease (neuromuscular): muscle atrophy, rigid hyperextension, paralysis, head tilt, gait abnormality, dysphagia, seizure, cerebellar atophy
  3. congenital disease in puppies: myositis and polyradiculitis of lumbosacral spinal nerve roots
    -ascending paralysis, muscle atrophy, fibrous muscle contracture with joint contracture, hyperextension of the pelvic limbs

(abortion in cows, rigid paralysis in puppies)

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3
Q

describe diagnosis, prevention and treatment of neospora caninum

A

diagnosis:
-serology, ID, or PCR in biopsy, aspirate, CSF, blood
-finding an oocyst in the feces often not enough bc looks like a lot of other guys, often PCR is necessary

prevention: no raw meat diets!
-cattle: cull or bulk milk test

treatment: +/- sulfa drugs

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4
Q

describe sarcocystis neurona (3)

A
  1. tissue forming coccidian and causative agent of EPM
    -+/- neospora hughesi: may also cause EPM
  2. indirect life cycle:
    -DH: opossum, sexual stage in intestinal epithelium
    -IH: variety of mammals, asexual stage in tissue cysts
    -Aberrant/dead-end host: horses
  3. not zoonotic?
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5
Q

describe clinical presentation of sarcocystis neurona in horses (EPM)

A

3 As!

  1. asymmetry
  2. atrophy: rump and face (frequently can’t eat due to facial muscle atrophy)
  3. ataxia: most frequent sign is gait abnormality related to CNS disease
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6
Q

describe diagnosis, treatment, and prevention of EPM

A

high seroprevalence but low clinical disease in horse population!!
-80-90% horses seropositive
-<1% develop neurologic disease

diagnosis:
SAG 4/3/2 on serum AND CSF
-serum:CSF ratio <100 suggests EPM

treatment:
1. antiprotozoals:
-ponazuril (Marquis): treat for at least 1 month
2. anti-inflammatory therapy
3. neuro-supportive therapy

prevention: keep possums out!!

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7
Q

describe toxoplasma gondii (3)

A
  1. ZOONOTIC, tissue cyst forming coccidian with worldwide distribution
  2. indirect life cycle:
    -DH: felids only; asexual and sexual reproduction in enterocytes (ONLY CATS SHED OOCYSTS)
    -IH: SO MANY
    -all IH can have tissue stages; we get toxo from ingesting tissue stages
  3. major cause of abortion in small ruminants, significant morbidity in marsupials, and ocular disease in humans
    -congenitally infected kittens can be clinical
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8
Q

describe the life cycleS of toxoplasma gondii

A
  1. direct: cat to cat
    -transplacental, or ingesting sporulated oocysts from environment
  2. facultative indirect life cycle:
    -cat to paratenic host
    -paratenic host to cat
  3. paratenic host to paratenic host

all these life cycles plus lack of host specificity is why so successful and widespread

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9
Q

describe toxoplasma gondii in cats (clinical signs, diagnosis, treatment, and control)

A

clinical signs:
1. intestinal/acute disease: usually no complaint
-10-20% of cats develop self-limiting small bowel diarrhea
2. systemic disease (non-specific):
-pneumonia (esp FIV+ cats)
-fever, anorexia, vomiting, diarrhea, myositis, uveitis, enlarged lymph nodes, encephalitis, nephritis, death

diagnosis:
1. intestinal/acute disease: oocysts in feces (fecal float centrifugation)
-but only shed for 2 weeks!!
2. systemic disease: serologic tests (IgG and IgM antibodies)
3. definitive: detection of tachyzoites in effusions, tissue aspirates, or biopsy samples

treatment:
1. intestinal/acute disease (shedding oocysts): pyrimethamine plus triple sulfa drugs, clindamycin, or ponazuril
-hospitalize cat during oocyst shedding to reduce zoonosis
2. systemic disease (clinically ill): clindamycin for at least 4 weeks, supportive treatment depending on clinical signs

control:
1. clean litter box daily: environmental sporulation in 1-3 days
-pregnant women no touch litter box!
2. no raw meat
3. don’t let cats outside to defecate or hunt

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10
Q

describe toxoplasma gondii in dogs (4)

A
  1. systemix toxoplasmacosis
  2. less commonly develop clinical disease
  3. fever, neurological, ocular, or respiratory signs
  4. rule out neospora caninum infection
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11
Q

describe toxoplasma gondii in sheep and goats (4)

A
  1. systemic and congenital toxoplasmosis
  2. systemic: CNS signs (circling, etc.)
  3. congenital: abortion
  4. toxovac S48 live vaccine available!
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12
Q

describe toxoplasma gondii in cattle and horses

A

very rarely develop clinical disease!

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13
Q

describe toxoplasma gondii in rodents (3)

A
  1. systemic toxoplasmosis
  2. decreased fear of cats
  3. major source of infection for cats and pigs
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14
Q

describe toxoplasma gondii in swine (4)

A
  1. systemic toxoplasmosis
  2. fever and respiratory signs
  3. highly prevalent in free range pigs
  4. important sources of human infections!!
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15
Q

describe toxoplasma gondii in poultry (3)

A
  1. systemic toxoplasmosis
  2. prevalent in free-range and backyard chickens
  3. important source of infection for humans!!
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16
Q

describe transmission of toxoplasma gondii (3)

A
  1. food borne (ingestion)
    -cysts from undercooked/underpasteurized food: free range pork and chicken, goat and cow milk
    -oocysts on unwashed vegeetables
  2. ingestion of oocysts from cat feces/unclean hands
  3. blood transfusions and organ transplants (rare)
17
Q

describe parelaphostrongylus tenius

A
  1. metastrongylid nematode/brain worm/meningeal worm
  2. indirect life cycle:
    -DH: white tailed deer; adults in meninges and subdural spcae
    -IH: terrestrial gastropods
  3. clinical disease in accidental hosts
  4. NOT zoonotic
18
Q

describe P. tenius presentation

A
  1. little to no disease in white tailed deer
  2. clinical signs in accidental hosts
    -asymmetric spinal cord disease: ascending, UMN lesions, hypermetria, ataxia, truncal sway
    -cerebral/brainstem signs reported (worse prognosis): seizures, depression
  3. differential diagnoses:
    -cervical spinal cord disease: trauma, DJD, fracture, abscessation; diskospondylitis
    -neoplasia
19
Q

describe life cycle of P. tenius (5)

A
  1. adult worm lays eggs on dura mater of deer brain
  2. worm larvae hatch, migrate to deer lungs, are swallowed, and coughed back up
  3. worm larvae enter deer’s alimentary canal and are passed through feces
  4. larvae are picked up by slug or snail (gastropod) through their foot

5a. deer inadvertently eats snail or slug and larvae penetrate deer stomach and migrate to spinal cord OR

5b. accidental host inadvertently eats infected slug or snail, worm larvae travel to spinal cord and brain, get lost, dig tracts, and accidental host shows signs of abnormal behavior and then dies

20
Q

describe diagnosis, treatment, and clinical signs of P. tenius

A

diagnosis:
1. clinical signs
2. eosinophilia in CSF
-not where parasite wants to be so won’t see in poop

treatment:
1. anthelmintics and anti-inflammatories
-fenbendazole: 50mg/kg every 24 hours for 5 days
-macrocylic lactones are ineffective for parasites within CNS (don’t cross BBB) but may have some benefit for parasites in tissues outside CNS

prevention:
1. minimize contact with WTD and snail/slug
2. monthly administration of anthelmintics
-ivermectin or doramectin
-begin 1 month after last frost, stop after first frost

21
Q

what are differential diagnoses to rule out for P. tenuis?

A
  1. cervical spinal cord disease: trauma, DJD, fracture, abscessation; discospondylitis
  2. neoplasia
22
Q

describe thelazia sp.

A
  1. spirurid nematodews (eyeworms) with adult stages in the orbital cavities and large animals
  2. indirect life cycle:
    -DH: many mammalian hosts; dogs and cattle; female worms are ovoviviparous
    -IH: nonbiting dipteran muscid flies or drosophila fruit flies; transmission while flies feed on lacrimal secretions
  3. clinical signs may vary: may predispose cattle to Moraxella bovis infection
  4. ZOONOTIC
23
Q

describe clinical signs of thelazia sp.

A

small animals:
1. excessive lacrimation and epiphora
2. ocular pruritis, conjunctivitis, keratitis with corneal opacity and ulceration
3. hyperemia
4. blindness (rarely)

large animals
1. aysmptomatic OR
2. mild conjunctivitis, excessive lacrimation
3. localized edema
4. keratitis, corneal clouding
5. occasionally subconjunctival cysts

affected animals may be particularly attractive to flies, enhancing transmission

24
Q

describe diagnosis, treatment, and prevention of thelazia sp.

A

diagnosis:
-recovery of adult worms
-larvae recovery from lacrimal secretions

treatment:
-mechanical removal after local anesthetic
levamisole, macrocyclic lactones (ivermectin, doramectin)

prevention:
-fly control measures
-good stable hygiene

25
Q

describe tick paralysis

A

acute, progressive, symmetrical, ascending motor paralysis due to salivary neurotoxins produced by certain species of ticks

-dermacentor andersoni (rocky mountain wood tick) and dormacentor variabilis (american dog tick)

26
Q

describe clinical signs, diagnosis, treatment, and prevention of tick paralysis

A

clinical signs:
-rapidly progressing, usually starts with hindlimb incoordination
-death rates approx 7% in domestic species

diagnosis:
-compatible clinical signs
-history of tick bit exposure or known tick area

treatment:
-tick removal!!
-drastic clinical improvement within 24 hours, complete recovery within 72 hours

prevention: tick prevention and tick checks

27
Q

describe myiasis (2)

A
  1. parasitic infection of the body by fly larvae (maggots); 3 classifications

-accidental: ingestion of contaminated items

-facultative: opportunistic, exploiting living tissues

-obligatory: fly REQUIRES living in host

  1. examples with CNS; ocular migration
    -hypoderma bovis: cattle, spinal canal
    -oestrus ovis: sheep, paranasal sinuses
    -cuterebra sp.: companion animals, eyes/brain

NSB II (17 decks)

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