Parasitic Diseases of the Urogenital System Flashcards

1
Q

describe neospora caninum

A
  1. tissue cyst forming coccidian with worldwide distribution
  2. indirect lifecycle
    -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 congenital and transgenerational transimission of neospora caninum

A
  1. IH to IH
  2. parasite able to cross placenta and infect fetus; most exposed in utero!
  3. can have a healthy uninfected calf or
  4. aborted, premature, or impaired calf or
  5. calf with persistent infection with bradyzoites that can be a later source of infection if establish in tissue
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3
Q

describe the clinical disease of N. caninum in cattle

A

infertility and abortion!

  1. abortions: 2nd to 3rd trimester
    -usually with post 1st infection pregnancy, autolysis of fetus
    -later pregnancies usually go to term, but calves are infected = maintenance of disease in herds
  2. transgenerational infections:
    -seropositive calves eventually give birth to seropositive calves without reinfection via sporocyst ingestion! (IH to IH transmission)
  3. decrease in milk production and decrease in weight gain
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4
Q

describe diagnosis of N. caninum

A

dogs:
-puppy: classic flaccid hind limb paralysis
-serology, molecular tests (PCR)
-organism on biopsy, necropsy of litter mates
-usually negative oocysts on fecal (TINY)

cattle:
-diagnostic test for multiple abortion infectious agents (cows and fetuses)
-serology, PCR, histology
-antibody tests for whole milk

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5
Q

describe treatment of N. caninum

A

dogs:
-no drugs available to kill tissue form
-clindamycin and TMS (static) or ponazuril (-cidal) MAY help with clinical signs
-the earlier treatment starts the better!

cattle:
no drug therapy available

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6
Q

describe epidemiology, control, and zoonosis of N. caninum

A

epidemiology:
-risk factors: presence of dogs on farm
-pure breed/immunosuppressed dogs at higher risk for neosporosis

control:
-limit cattle exposure to wild and domestic canids
-farm hygiene (remove abortus! dogs could eat and continue life cycle)
-cull seropositive cows? cull cows with midterm abortions?
-don’t let dogs have access to raw meat, raw food, or dead animals
-spay female dogs with infected litters

zoonosis: NOT zoonotic

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7
Q

describe toxoplasma gondii

A
  1. ZOONOTIC tissue cyst forming coccidian with worldwide distribution
  2. indirect life cycle:
    -DH: felids only; asexual and sexual repro in enterocytes
    -IH: so so many
  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 toxoplasma gondii in non-felid peratenic hosts

A

dogs:
-systemic toxoplasmosis
-less commonly develop clinical disease
-fever, neurological, ocular, or respiratory signs
-rule out N. caninum infection

sheep and goats:
-systemic and congenital toxoplasmosis
-systemic: CNS signs (circling)
-congenital: abortion
-toxovac S48 live vaccine available

cattle and horses: very rarely develop clinical disease

rodents:
-systemic toxoplasmosis
-decreased fear of cats
-major source of infection for cats and pigs

swine:
-systemic toxoplasmosis
-fever, respiratory signs
-highly prevalent in free-range pigs
-important source of infection for humans!

poultry:
-systemic toxoplasmosis
-prevalent in free-range and backyard chickens
-important source of infection for humans!!

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9
Q

describe congenital toxoplasmosis

A
  1. transmission:
    -infection of mother: ingestion of oocysts or tissue cysts
    -infection of fetus: transplacental transmission
  2. fetal toxoplasmosis:
    -severe disease: congenital malformation, intellectual disability, death
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10
Q

describe testing for T. gondii antibodies just prior to pregnancy or newly pregnant

A

T. gondii seronegative:
-the mother-to-be has not been previously exposed to T. gondii
-no protective antibodies
-HIGH risk of congenital toxoplasmosis if mother exposed for first time during pregnancy

T. gondii seropositive:
-represents previous exposure
-antibodies are protective (if immunocompetent)
-LOW risk of congenital toxoplasmosis if mother exposed again during preg

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11
Q

describe veterinary advice to pregnant cat owners

A
  1. get antibody tested: mother AND cat
    -if seropositive, low worries
    -cats usually only shed oocysts once
  2. avoid cat feces (sporulation 1-3 days)
  3. avoid uncooked meat, unclean hands/veggies/knives/cutting boards
  4. casual contact with cats is very low risk:
    -indoor cats< outdoor cats
    -old cats < young cats
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12
Q

describe tritrichomonas foetus and T.blagburni

A
  1. obligate parasites; exist only as trophozoites
  2. urogenital and GI tracts
  3. specific host-pathogen interactions
    -bovine trichomoniasis: colonize urogenital tract, venereal disease, causes infertility, abortions in cows and hiefers, economic loss
    -feline trichomoniasis: colonize large intestine, large bowel diarrhea
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13
Q

describe the life cycle of T. foetus bovine genital trichomonas

A

primary hosts: cows/bulls

transmission:
-sexual: bulls to cows and cows to bulls
-artificial insemination

stages:
-trophozoite
-no cyst stage

reproduction: binary fission in urogenital tract

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14
Q

describe T. foetus bovine pathology

A

not well understood

cows/heifers:
-trophozoites cause indirect damage to epithelial cells in repro tract
-vaginits and endometritis: abortion, infertility, pyometra
-infection is self limiting: clearance approx 20 weeks post infection

bulls:
-trophozoites attach to epi cells lining penins, prepuce, and distal portion of urethra
-no damage to cells, no change in semen quality or sexual behavior
-essentially serve as reservoirs (persistently infected)

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15
Q

describe clinical signs of bovine genital trichomoniasis

A

main complaints:
1. abortions (early to mid term)
2. failed pregnancy, infertility suspect
3. more open and late cows

pathological findings:
-vaginitis, cervicitis, pyometra, endometritis, mummified fetus

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16
Q

describe diagnosis of bovine genital trichomoniasis

A

most diagnostis in bulls!

cows: history of abortion
bull: preputial wash or scrapings

  1. microscopic exam of fresh wet mounts for trophozoite
  2. culture kits
  3. PCR

testing method based on state requirements

positive results = reportable!

17
Q

describe control and treatment of bovine genital trichomoniasis

A

control: good farm management and biosecurity!
1. strict surveillance of bulls/closed herds/no commingling
2. cull all positive bulls
3. replace bulls >4 years
4. hygienic AI: can survive semen freezing process!
5. vaccines available but not complete protection

treatment: none

18
Q

describe epidemiology/risk factors of bovine genital trichomoniasis

A
  1. bulls at or older than 4 years
  2. grazing on public land/commingling herds
  3. herds with at least 500 cows
  4. large sire herds
19
Q

describe dioctophyme renale (giant kidney worm)

A
  1. adult worms in renal parenchyma
    -minks are normal host
    -dogs can become infection
  2. adult worms (35-105cm) in RIGHT kidney
    -after destroy kidney, make way into abdominal cavity (non-patent)
    -may find free in abdominal cavity on spay
  3. destroys kidney tissue, may cause perotinitis
20
Q

describe clinical signs, diagnosis, and control of kidney worm

A

clinical signs:
-usually asymptomatic (other kidney compensates)
-dysuria. hematuria, and lumbar pain
-uremia with destruction of both kidneys, obstructed ureters

diagnosis:
-usually incidental finding in abdominal cavity
-eggs in urine sediment

treatment/control:
-can remove surgically if needed
-don’t allow dogs to eat raw fish

21
Q

describe kidney worm of swine/stephnaurus dentatus

A
  1. strongyle parasite of renal, perirenal, and hepatic tissues
  2. found in warm and tropical climates
  3. large, stout nematodes (2-4cm long)
    -size and site are diagnostic
  4. symptom: failure to gain weight
  5. life cycle: direct (optional earthworm IH)
    -swine ingest free living L3 larvae of infected earthworms; larvae penetrate stomach wall and migrate to liver
    -larvae migrate to perirenal tissue and become patent at month 6-19; shed in urine