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Parasitology > Nematode II - Details > Flashcards

Nematode II - Details Flashcards

1
Q

Strongylida

General Characteristics

A
  • Very large order.
  • Economically very important.
  • Important in human and vet medicine.
  • Almost all have large copulatory bursa on posterior end of males.
  • Most are parasites of intestines of vertebrates.
  • Most have direct life cycle.
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2
Q

Trichostrongyloidea

General Characteristics

A
  • “hair worms” of ruminants.
  • Very large group
  • Especially common and pathogenic in grazing ruminants.
    • most common nematodes found in fecal floats of ruminants.
    • annual loss in US, $90 million cattle, $20 million sheep.
  • Also infects pigs, horses, cats, and birds.
  • Mostly infect stomach/abomasum and small intestines.
  • Small in size (up to 1”) and hair-like with copulatory bursa.
  • Direct life cycle.
  • No migration within definitive host.
  • Infection by ingestion of infective J3.
  • HYPOBIOSIS is important
    • seasonal arrested development.
    • important in controlling infection.
    • J3’s survive the winter in soil and become infective in spring.
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3
Q 
Trichostrongylus spp. (axei)
Which animal(s) does it infect?
A

Ruminants, Horses

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4
Q

Trichostrongylus spp. (axei)

Life Cycle

A
  1. Infective J3’s overwinter (hypobiosis), ensheathed.
  2. Ruminants infected in spring when they begin to graze and ingest infective J3.
  3. When weather gets warm, the J3’s in pasture die off, but now new adults are growing inside newly infected animals.
  4. Eggs are in feces of contaminated animals.
    • ”strongyle-type eggs”
    • thin smooth shells, ellipsoid in shape.
  5. In the pasture in the summer/fall eggs develop to J3 larvae.
  6. These larvae undergo hypobiosis in winter and infect new animals in spring.
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5
Q

Trichostrongylus spp. (axei)

Symptoms and Disease

A
  • Light infection: may be asymptomatic.
  • Heavy infection: causes illness.
  • Serious and debilitating diarrhea.
    • ”black scours”
    • often watery and black in color.
    • fecal lumps often attach to hind quarter due to diarrhea.
  • Can be fatal, due to severe diarrhea.
  • On necropsy:
    1. often see nodular lesions containing worms in digestive system.
    2. worms are so tiny, often must use magnification to see them.
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6
Q

Trichostrongylus spp. (axei)

Diagnosis

A

Based on a combination of factors:

  • clinical signs / symptoms.
  • seasonal occurrence of disease.
  • eggs in feces.
  • necropsy results.
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7
Q 
Ostertagia ostertagi
Which animal(s) does it infect?
A

Cattle, Sheep, Goat

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8
Q

Ostertagia ostertagi

General Characteristics

A
  • Small, about 10mm.
  • Adults are reddish-brown (difficult to see at necropsy).
  • Pathogenic effects are due to growth of developing larvae in gastric glands of stomach.
  • Very important in cattle, much less so in sheep and goats.
  • Can be devastating
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9
Q

Ostertagia ostertagi

Life Cycle

A

See Trichostrongylus, except:

  1. Develops into infective J3 in pasture (~2 weeks).
  2. J3’s invade gastric glands of stomach and develop into J5’s
    • J4’s may undergo hypobiosis, may survive up to 6 months in stomach.
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10
Q

Ostertagia ostertagi

Symptoms and Disease

A

There are two forms of disease:
Type I Ostertagiosis (“summer ostertagiosis”)
-J3’s hypobiotic in pasture over winter.
-Young cattle infected by J3’s in spring.
-Cows appear sick in late summer (peak season: Aug-Oct).
-Most common in Southern US (warmer climate).

Type II Ostertagiosis (“winter ostertagiosis”)

  • J4’s hypobiotic in stomach of cow over winter.
  • Outbreaks of disease occur late winter (peak season: Feb-May).
  • Most common in Northern US (colder climate).

Young Cattle

  • Chronic abomasitis, watery diarrhea, anemia, bottle jaw.
  • Looks emaciated but has good appetite.
  • Animal starves to death due to lack of function of the abomasum.
    • death within weeks of infection.
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11
Q 
Haemonchus contortus
Which animal(s) does it infect?
A

Cattle, Sheep, Goat

-abomasum

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12
Q

Haemonchus contortus

General Characteristics

A
  • Common but very pathogenic.
  • White egg-filled uterus (gravid) wraps around blood filled gut.
  • Thrives in warm weather (tropical regions = major problem).
  • Adult worm is a blood-sucker.
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13
Q

Haemonchus contortus

Life Cycle

A

See Trichostrongylus, except:

*NO hypobiosis

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14
Q

Haemonchus contortus

Symptoms and Disease

A
  • Severe anemia.
    • parasite injects hemolytic enzymes into host.
  • Principle symptom: Pallor of skin and mucous membranes.
  • A lamb may loose up to 1/5 of its circulating erythrocytes per day.
    • probably fatal
  • May have “bottle jaw” (submaxillary edema).
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15
Q

Haemonchus contortus

Diagnosis

A
  • Anemia, pale gums, and mucous membranes.
  • Eggs in feces:
    • yellowish in color.
    • otherwise, eggs similar to Trichostrongylus.
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16
Q 
Cooperia spp.
Which animal(s) does it infect?
A

Ruminants

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17
Q

Cooperia spp.

General Characteristics

A
  • Small, adults less than 9mm long.
  • Male has copulatory bursa.
  • Adult body is coiled like a watch spring (easy to id).
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18
Q

Cooperia spp.

Life Cycle

A

See Trichostrongylus.

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19
Q

Cooperia spp.

Symptoms and Disease

A
  • Considered mild pathogens.
  • Usually are secondary pathogens to more serious infections with Haemonchus or Ostertagia.
  • Diarrhea, weight loss, anorexia.
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20
Q

Cooperia spp.

Diagnosis

A
  • Eggs in feces.

- Rarely seen alone in feces.

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21
Q 
Nematodirus spp.
Which animal(s) does it infect?
A

Ruminants, mostly sheep.

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22
Q

Nematodirus spp.

General Characteristics

A
  • Species vary greatly in size.
  • Infections usually do not lead to serious clinical disease.
  • Some infections can be very serious and fatal in lamb flocks.
    • up to 30% mortality.
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23
Q

Nematodirus spp.

Life Cycle

A
  • Differs from other Trichostrongyles.
    1. Larva develops into infective J3 within the egg.
    2. Hatching of infective larvae is very concentrated in spring.
    3. Reproduction may be limited to one generation per year.
    • single wave of infection and disease in late spring.
      1. Severity of infection is totally dependent on previous year’s contamination of pasture.
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24
Q

Nematodirus spp.

Symptoms and Disease

A
  • Usually a secondary pathogen in a mixed Nematode infection.
  • May not cause serious disease in adult sheep.
  • May be fatal to lambs.
  • Very severe and debilitating diarrhea.
  • Whole flock may show sudden loss of thrift and severe diarrhea.
  • Death begins 2 days to 2 weeks after onset of symptoms.
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25
Q 
Hyostrongylus rubidus
Which animal(s) does it infect?
A

Swine

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26
Q

Hyostrongylus rubidus

General Characteristics

A

-Very small, less than 1cm, hairlike.

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27
Q

Hyostrongylus rubidus

Life Cycle

A

See Trichostrongylus, except:

  1. May overwinter, but usually die in winter.
  2. In the pasture, develop into infective J3 (~1 week).
  3. Adults invade gastric glands and suck blood.
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28
Q

Hyostrongylus rubidus

Symptoms and Disease

A
  • Anemia due to hemorrhagic gastritis.
  • Loss of appetite.
  • Severe gastritis with ulceration and sometimes hemorrhage.
  • Secretion of mucus in feces.
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29
Q

Hyostrongylus rubidus

Diagnosis

A
  • Eggs in feces.

- Necropsy (worms are almost microscopic).

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30
Q 
Dictyocaulus viviporus 
Which animal(s) does it infect?
A

Cattle

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31
Q

Dictyocaulus viviporus

How does it differ in the predilection site from other Trichostrongyloids?

A

It infects the air passages instead of the stomach / abomasum / small intestine.

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32
Q

Dictyocaulus viviporus

General Characteristics

A
  • Common and economically important.

- Sometimes called “husks” or “hoose” in grazing cattle.

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33
Q

Dictyocaulus viviporus

Life Cycle

A
  1. Adults in lungs lay eggs w/J1 larvae.
  2. Eggs hatch in lungs or feces.
  3. Some eggs may overwinter.
  4. Eggs usually hatch before being excreted (J1).
  5. Develop into infective larvae in environment.
  6. Infective J3 ingested by new host.
  7. Migrate to lungs of new host.
  8. Develop into adults in lungs.
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34
Q

Dictyocaulus viviporus

Symptoms and Disease

A
  • Prepatent Period: 4 weeks
  • Chronic bronchitis (blockage of bronchioles by worms).
  • Light Infections: can be fairly mild.
  • Heavy Infections: can cause death du to emphysema/respiratory failure.
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35
Q

Dictyocaulus viviporus

Diagnosis

A
  • Clinical signs.
  • Presence of J1’s in feces (Baerman).
  • Bronchoscopy and radiography may be used.
  • Transbracheal wash.
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36
Q

Superfamily Strongyloidea

General Characteristics

A
  • Often called “strongyloids”.
  • Adults are larger and wider than trichostrongyloids.
  • Large mouth and buccal cavity.
  • Well developed copulatory bursa.
37
Q

Superfamily Strongyloidea

General Life Cycle

A
  1. Direct
  2. Ensheathed J3 is infective stage.
  3. Females lay “strongyle type” eggs.
    a. smooth surface
    b. ellipsoid (oval shaped).
    c. contain an embryo in morula stage.
    ~morula is a mass of embryonic cells (~10 to 20).
    ~see mass of cells inside eggs.
    d. passed out in feces, usually.
38
Q

Subfamily Strongylinae

General Characteristics

A
  • Chiefly parasites of large intestine of equines.
  • Predilection sites primarily: cecum, colon, lg intestine.
  • Readily seen at necropsy (lg. size).
39
Q

Subfamily Strongylinae

Importance

A
  • Some of the most dangerous & destructive parasites of horses & donkeys.
  • Common in the environment.
  • Can be fatal.
40
Q

Subfamily Strongylinae

Pathogenicity

A

a. Juveniles migrate extensively throughout the host.
-migration is very damaging, esp in foals and yearlings.
b. Mucosal feeders that result in blood sucking.
c. pathogenic effects due to 2 things:
1. mucus sucking by adults that results in blood sucking.
~lg worms with lg mouths and buccal cavities.
~aggressive feeders.
~suck on one spot, then move to another.
*necropsy: see small bleeding ulcers, granulations, & scars where feeding occurred.
2. juvenile (larval) migrations
~extensive migrations through mesenteric arterial sys.
~damages walls of important mesenteric arteries.
~inflammatory arthritis and thickening of artery wall.
~some arteries may become completely occluded.
d. Death usually due to infarction or necrosis of organs supplied by mesenteric blood vessels.

41
Q

Subfamily Strongylinae

Persistance in the Environment

A
  • Ensheathed, can overwinter in envrio and dried hay.

- Any pasture that has held a horse w/in the last year can be contaminated.

42
Q

Strongylus vulgaris

Life Cycle

A
  1. Eggs excreted in feces.
  2. Develops into infective form in environment.
  3. Horse or donkey ingests J3.
  4. J3 enters wall of colon and/or cecum.
  5. Develops into J4 in the wall.
  6. J4’s enter arteries and circulate through mesenteric arteries.
  7. J4’s eventually stop in arterioles of colon and cecum.
  8. Mature into j5s in nodules in intestinal wall.
  9. Nodule rupture and release adults in lumen of intestine.
  10. Adults in lumen of intestine begin to feed & reproduce.
43
Q

Strongylus vulgaris

Symptoms and Disease

A
  • Prepatent period: 6-7 months.
    • does its most damage before adult stage is reached.
    • prolonged (at least 4 mo) & extensive larval migrations in mesenteric arteries.
44
Q

Strongylus edantatus

General Characteristics

A

Same as vulgaris, except:

  • Juveniles migrate through liver.
  • Mature into J5’s in nodules in liver.
  • See liver nodules and fibrosis on necropsy.
45
Q

Strongylus equinus

General Characteristics

A

Very similar to S. edantatus.

46
Q

Subfamily Cyathostominae

General Characteristics

A
  • Parasites of lg intestines of horses (& some other animals).
  • Predilection site cecum and colon.
  • Adults are 1/8 to 1 inch and often red.
  • Greatly outnumber lg strongyles in numbers.
    • 75% or more of eggs in horse feces may be small strongyles while 10% may be lg strongyles.
    • may find 15-20 different species of small strongyles at one time in one horse.
  • Less pathogenic than large strongyles
    • no migration in host.
47
Q

Subfamily Cyathostominae

Life Cycle

A
  1. Eggs in feces.
  2. Develops into infective form in environment.
  3. Horse ingests J3.
  4. J3’s develop into J4’s in cecum and colon (occurs in nodules).
  5. Mature to adults in lumen of cecum and colon.
  6. Prepatent period is 6-14 weeks.
48
Q

Subfamily Cyathostominae

Pathogenicity

A
  • Larvae do NOT penetrate the wall of the intestine very deeply.
  • Juveniles (J4) become encapsulated in small nodules on lining of intestines.
  • Nodules are seen on necropsy.
  • Low levels of infection may be asymptomatic.
  • High levels of infections may cause:
    • persistent diarrhea.
    • progressive emaciation.
    • rough coat (failure to shed).
  • Most severe in horses under 2 yrs old.
49
Q

Subfamily Cyathostominae

Diagnosis and Prevention

A
  • May be no fecal egg shedding during illness
    • makes dx difficult.
  • Many infections are resistant to anti-helmintic drugs.
    • larvae in nodules are not affected.
    • often use steroid therapy.
    • normal anti-helmintics may not be highly effective in prevention either.
50
Q 
Oesophagostomum dentatum
Which animal(s) does it infect?
A

Pigs and other ruminants.

51
Q

Oesophagostomum dentatum

General Information

A

Predilection site: lg intestine.
Pathogenicity
-Mostly du to inflammation caused by larvae (J4) in nodules penetrating the mucosa of the intestines.
-Nodules progress into hemorrhagic lesions in intestine.
*often fill with puss.

52
Q

Oesophagostomum dentatum

Life Cycle

A
  1. Strongyle type eggs passed in feces.
  2. Develops into infective form in environment.
  3. J3 ingested by host.
  4. J3’s become enclosed in nodules in colon.
    • penetrate mucosa.
  5. Mature into J4’s in nodules
  6. J4’s emerge from nodules and develop into adult stage.
53
Q

Oesophagostomum dentatum

Symptoms and Disease

A
  • Prepatent period: 32-45 days.
    • can be nonpatent

Heavy Infection

  • Lining of intestine completely covered with lg nodules.
  • Intestines severely inflamed.
  • Fetid, watery, dark diarrhea.
  • Weight loss with rapid emaciation.
  • Can be fatal.
  • Usually no eggs in feces (nonpatent).

Chronic Infection

  • ”Thin Sow Syndrome” (weight loss).
  • Eggs seen in feces.
54
Q

Oesophagostomum dentatum

Diagnosis

A
  • Very difficult in heavy infection.
  • May be few adults in infected animal so little or few eggs in feces.
  • Diagnosis may be based on symptoms.
55
Q 
Stephanurus dentatus
Which animal(s) does it infect?
A

Swine, Sometimes Cattle

56
Q

Stephanurus dentatus

General Information

A

Predilection Sties:

  • Kidney (major site)
  • Walls of ureter
  • Perirenal fat (around Kidney instead of inside)
  • Liver

Found mostly in Southern US
-do not survive cold well.

57
Q

Stephanurus dentatus

Life Cycle

A

May be direct, earthworms may serve as intermediate hosts.
Three Modes of Infection:
1. Ingestion of free-living J3’s.
2. Ingestion of earthworms carrying J3’s.
3. Skin penetration by J3’s.

Life Cycle

  1. Ingested J3’s exsheath in intestine.
    • those that enter through skin travel to intestines.
  2. Enter lymphatic sys & travel to liver.
  3. Spend several months destructively wandering around in the liver.
  4. Some eventually migrate to kidneys and ureters.
  5. Eggs are excreted in urine.
    • may persist in urine for 3+ years.
  6. Piglets may be infected in utero.
58
Q

Stephanurus dentatus

Symptoms and Disease

A

Prepatent Period: 9-16 months.

Pathogenicity:

  • Extensive migrations lead to extensive damage.
  • May cause severe destruction in liver.
  • May migrate through other organs (ex: pancreas) and cause damage.
  • Death is usually due to liver damage.
    • cirrhosis, emaciation

Clinical Signs

  • Not very distinctive.
  • Appetite loss.
  • Blood in urine.
  • Weight loss.
  • Can be very serious and lead to death.
59
Q

Stephanurus dentatus

Diagnosis

A
  • Usually eggs not found in urine of pigs less than 2 years old.
    • due to long prepatent period.
  • Eggs in urine of adult animals.
  • Infections are commonly diagnosed at necropsies / meat inspections.
    • may find liver nodules.
    • may find muscle tissue damage due to migration.
    • cause for condemnation of meat.
60
Q

Superfamily Metastrongyloidea

General Information

A

General Characteristics

  • Infect respiratory, vascular, and nervous system of mammals.
  • Most require a snail, slug, or earthworm as intermediate host.
  • Diversity of structure and biology within the superfamily.
61
Q 
Aelurostrongylus abstrusus
Which animal(s) does it infect?
A

Cats

62
Q

Aelurostrongylus abstrusus

General Information

A

Most common in cats that hunt.

Prevention: keep cats from hunting.

63
Q

Aelurostrongylus abstrusus

Life Cycle

A
  1. Infected intermediate host containing J3 is ingested by cat.
  2. Larvae migrate to cat lungs and mature to adults.
  3. Female deposits “nests of eggs” in cat lungs.
  4. J1’s hatch from eggs in lung nodules.
  5. J1’s travels up to mouth and are swallowed
  6. Juveniles (larvae) are excreted in cat feces (J1).
  7. The J1’s in feces enter a snail, slug, or earthworm.
  8. Develop into infective J3 in slimy thing.
  9. Encyst in snail & when eaten by cat, develop into reproductive adults.

*Slimy thing can be eaten by mouse/ bird, & cat eats mouse/bird.

64
Q

Aelurostrongylus abstrusus

Symptoms and Disease

A
  • Chronic coughing.
  • Anorexia and weight loss.
  • Sometimes fatal.
65
Q

Aelurostrongylus abstrusus

Diagnosis

A
  • J1 larvae in fecal floatation (Baerman)

- Eggs in sputum, but mostly J1 larvae.

66
Q 
Parelaphostrongylus tenuis
Which animal(s) does it infect?
A

Definitive Host:
White Tailed Deer

Aberrant Hosts:
Sheep, Goats, Llamas, Alpacas
Rarely, Cows, Horses

67
Q

Parelaphostrongylus tenuis

General Information

A

Prevention:

  • Deer control.
  • Removal of thick ground cover, vegetation free buffer zones.
  • Prophylactic antihelmintics.
68
Q

Parelaphostrongylus tenuis

Life Cycle

A

The same as Aelurostrongylous abstrusus, except:

  1. in abomasum of new host migrate to spinal cord & mature there (20-30 days).
  2. Adults migrate to subdural space then travel up to brain.
  3. Adults lay eggs in meninges of deer.
  4. Eggs enter venous circulation and travel to lungs.
  5. Slimy thing is ingested by new host while grazing.

In aberrant hosts:

  • Does not migrate to brain.
  • Invades the spinal cord & often blocks it.
  • May migrate all over the body subcutaneously.
  • Does NOT reach adulthood, migrating juveniles.
69
Q

Parelaphostrongylus tenuis

Symptoms and Disease

A

Prepatent Period: 82-92 Days
White Tailed Deer:
-No real symptoms, never penetrates the brain.
-Up to 85% of deer in NYS may be infected.

Aberrant Hosts:
Neurological
-leg dragging (esp. hind legs), major 1st symptom.
-ataxia
-head tilt
-circling
-blindness, etc

Other Symptoms

  • intense itching, hard nodules on skin.
  • Usually fatal, esp to Alpaca & Llama.
70
Q

Parelaphostrongylus tenuis

Diagnosis

A

White Tailed Deer:
-Larvae in feces.

Aberrant hosts:

  • Definitive diagnosis only possible at necropsy.
  • Symptoms
  • Serological (ELISA) tests not highly accurate.
71
Q 
Superfamily Ancylostomatoidea
Which animal(s) does it infect?
A

Dogs, Cats

Foxes, and Humans

72
Q

Superfamily Ancylostomatoidea

General Information

A

“Plumber’s Itch”

  • Hookworms of dogs and cats.
  • One of the MOST common intestinal parasites of dogs and cats.
    • especially puppies and kittens.
  • Predilection Site: Small Intestines
  • Infective Stage: ensheathed J3
  • All adults feed by sucking blood through wall of sm intestine.
  • Strongyle type eggs containing morula stage.
  • 2 Major genera of veterinary importance.
    • Ancylostoma spp.
    • Uncinaria spp.

Adult Worms:

  • Small (¼ to ¾ inch)
  • Rarely detected in stool.
    • size & firmly attached to intestinal wall.
  • Each female lays thousands of eggs per day.
  • Buccal cavity has oblique opening.
    • gives mouth hook shape.
    • some species are more hook shaped than others.
  • Buccal cavity has “teeth” or cutting plates.
    • different species have different # of pairs of teeth.
    • used for attachment to host intestines.
73
Q

Superfamily Ancylostomatoidea

Life Cycle

A
  1. Eggs pass in feces.
  2. Develop into ensheathed J3 in envrio.
  3. J3’s taken into host:
    By Skin Penetration
    • Extensive migration through tissue to reach blood or lymph vessel.
      -Carried to lungs.
      -Come out of blood in lungs.
      -Coughed up and swallowed.
      -Reach small intestine.
    By Ingestion:
    • Travel through digestive sys to sm intestine.
  4. In sm intestine, mature into adults.
  5. Adults can live up to 2 years.
74
Q

Superfamily Ancylostomatoidea

Methods of Infection

A
  • Ingestion of larvae in food & water.
  • eating an infected transport host.
  • larvae penetrating skin.
  • transplacental or transmammary.
75
Q

Superfamily Ancylostomatoidea

Symptoms and Disease

A

Pathology:
-Suck blood from host through sm intestine wall.
-One adult of A. caninum can suck 0.8mL of blood per day.
-Produce anticoagulant in saliva.
*prevents clot to prolong worm’s meal.
*when hookworm moves to new feeding site, original continues to bleed.
Depends on:
-The number of hookworms infecting host.
-Virulence of hookworm.
*A. caninum more virulent than other hookworms.
-Resistance of host:
*Adults get more resistant as they get older.
*Puppies & kittens least resistant.
~pups infected in utero or transmammary can die w/in 2 weeks after birth.
~50 to 100 worms can be fatal in pups.

Symptoms:

  • Can be chronic asymptomatic to rapidly fatal.
  • Anemia (can be rapid & severe).
    • pale gums, weakness.
  • Stunted growth in young animals.
  • Poor coat, dull & dry.
  • Diarrhea (often black & tarry)
76
Q

Superfamily Ancylostomatoidea

Diagnosis

A
  • Eggs in feces.
  • Fecal sample MUST be fresh.
    • less than 48 hrs, eggs hatch very quickly.
  • In very young animals, may get severe disease before eggs are present in feces.
  • Strongyle type eggs.
77
Q

Superfamily Ancylostomatoidea

Zoonosis

A

How Humans Get Infected:

  • Skin Penetration.
  • Usually in feet.

CLM (cutaneous larval migrans)

  • Hookworms migrate in dermis of human skin.
  • Leave red, very itchy tracks in skin.
  • Eventually the larvae die & infection goes away.
  • Larvae do NOT develop into adults.

Enteric Hookworm Infection

  • Rare
  • Hookworms may reach sm intestine & rarely may mature to adult stage there.
    • do NOT produce eggs.
  • Sudden onset severe abdominal pain.
  • Treated with antihelmintics.
  • Some infections may be sulbclinical.

Prevention of Zoonosis

  • Good hygiene (esp w/children).
  • Do not let children play where dogs & cats defecate.
  • Cover sandboxes.
  • Do not walk barefoot.
  • Remove feces from enviro daily.
  • Train pets to defecate in 1 place in yard.
    • preferably concrete, in direct sunlight, in dry place
  • Plumbers and Electricians
    • crawl on ground a lot, should use tarp.
    • ”plumber’s itch”.
78
Q

Superfamily Ancylostomatoidea

Which organisms are in this superfamily and which animal(s) do they infect?

A

Ancylostoma caninum
*dog, fox

Ancylostoma braseiliense
*dog, cat, fox

Uncinaria stenocephala
*dog, cat, fox

Ancylostoma tubaeforme
*cat

79
Q 
Order Rhabditida
Which animal(s) does in infect?
A

Dog, Horse, Goat, Swine

ALL zoonotic!

80
Q

Order Rhabditida

General Information

A

Very large group of small nematodes.

  • Most are free living and nonparasitic.
  • A few are parasitic to domestic animals.

Pathology

  1. Most infections of adult animals are moderate and asymptomatic.
  2. Is almost universally present in adult ruminants.
  3. Most serious disease occurs in heavily infected young animals. (esp. Newborns)
  4. Mostly causes diarrhea and stunted growth in young animals.
81
Q

Order Rhabditida

Life Cycle

A
  1. Alternates between parasitic and free living forms.
  2. Only the FEMALE is parasitic.
  3. Life cycle is complex and involves hermaphroditism and parthenogenesis.
  4. J3’s are infective stage.
    a. usually enter the host by skin penetration.
    b. transmammary transmission is most common in domestic animals.
    - most important route of infection
    - very dangerous infection in newborns
  5. Once inside the host, can migrate to deeper body tissue.
  6. Main predilection site is small intestine.
    • female lives deep in mucosal crypts of small intestine.
82
Q

Order Rhabditida

Diagnosis and Symptoms

A
  1. Eggs in feces in pigs and ruminants.
  2. In dogs and cats:
    a. egg hatches in intestine
    b. find J1’s in feces (Baerman).
83
Q

Order Rhabditida

Zoonosis

A
  1. Strongyloides stercoralis infects dogs and cats and can be contracted by humans.
  2. Usually transmitted to humans by skin penetration.
    • usually the feet from fecal contaminated soil.
    • can also be ingested, fecal-oral route.
  3. Usually causes a cutaneous larval migrans type of infections.
  4. May also cause a chronic and persistent (auto) infection.
    • abdominal cramping and pain.
    • sporadic diarrhea.
    • can last many years.
  5. Very important and dangerous for AIDS and immunocompromised (can be rapidly fatal).
84
Q

Order Rhabditida

Which organisms are in this order, and which animal(s) do they infect?

A

Strongyloides stercoralis
*Dog

Strongyloides westeri
*Horse

Strongyloides papillosus
*Ruminants (mainly goat [kids])

Strongyloides ransomi
*Swine

85
Q

Strongyloides stercoralis

Symptoms and Disease

A

IF symptomatic:

  • watery or mucous diarrhea.
  • brohchopneumonia in severe cases.
86
Q

Strongyloides westeri

Symptoms and Disease

A

In infected foal:
-”foal-heat” diarrhea
-have diarrhea ~2 weeks after birth.
Transmammary
-mother may not be producing eggs in feces.
-infected foal begins to shed eggs after ~2 weeks.

87
Q

Strongyloides papillosus

Symptoms and Disease

A

Usually only causes disease w/heavy infection.

  • exception is severe diarrhea in goats w/ light infection.
  • only a few thousand worms can be fatal to kids.
88
Q

Strongyloides ransomi

Symptoms and Disease

A

Piglets:

  • acute enteritis.
    • bloody diarrhea, rapid emaciation, anorexia, stunted growth, sometimes fatal.

Parasitology (14 decks)

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