Nematodes Part 1 Flashcards

1
Q

Toxocara Canis

  • Adult characteristics
  • egg characteristics
A

Adults: are large nematodes. Remember ascarid said are the largest worms and are very heavy bodied.

Eggs - will FLOAT

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2
Q

Life cycle of Toxocara Canis

What is the infective stage of T. Canis?

A
  1. Adults found in the SI of the DH; non-embryonated eggs leave DH via feces.
  2. Eggs embryo ate to L1-L2 in environment.

Infective stage: egg with L2 larvae inside of it

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3
Q

Possible routes of transmission for the Toxocara Canis to its DH

A
  1. Direct transmission (ingestion)
  2. Prenatal/transuterine transmission
  3. Colostral/lactogenic transmission
  4. Ingestion of a paratenic host
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4
Q

Describe the life cycle of Toxocara Canis via direct transmission in a dog LESS THAN 3 months old?

A

They ingest infective egg with L2 larva and then undergo “tracheal migration.”

  • egg hatches in duodenum
  • penetrates intestine and migrates to mesenteric LN
  • migrates to liver, heart, lungs
  • molts to L3 in alveoli
  • L3 is coughed up and swallowed into the stomach.
  • molts to L4/L5 in SI - a mature adult
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5
Q

Describe the life cycle of Toxocara Canis via direct transmission in a dog that is GREATER THAN 3 months old?

A

ingest infective egg with L2 larva and then undergoes “somatic migration.”

  • larva hatches from egg in duodenum
  • penetrates intestine - migration, enters systemic circulation
  • L2 larvae encyst (hypo biotic) in various tissues - liver, lungs, etc.
  • NO MATURATION OCCURS
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6
Q

Toxocara Canis: lifecycle of prenatal/transuterine transmission

A
  • hypobiotic L2 larvae mobilize day 42 or later of pregnancy
  • L2s migrate to fetuses and enter the liver of the fetus where they molt to L3
  • L3s migrate to lungs at birth. They are eventually coughed up and swallowed to the stomach.
  • L4/L5 in SI mature to adults in approx. 2 weeks.
  • eggs will be found in puppy feces by 23 - 40 days old.
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7
Q

Lifecycle of Toxocara Canis via Colostral/lactogenic transmission

A
  • hypobiotic L2 larvae in mammary tissues
  • L2 passed to puppies via colostrum
  • L2 go directly to the stomach
  • NO migration
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9
Q

Name two ascarids that have very similar looking eggs and name their differences.

A

Toxocara cati

  • equivalent of Toxocara Canis; only it is found in the SI of cats
  • their eggs have a dark center with a rough she’ll

Toxascaris leonine

  • found in SI of BOTH cats and dogs
  • eggs have a hyaline center (clear) with a smooth shell
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9
Q

Identify the life cycle differences of Toxascaris leonina by transmission type

A

With direct transmission they undergo NO MIGRATION at all.

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10
Q

Lifecycle of Toxocara Canis via paratenic host

A
  • ingest a paratenic host (rodents) with encysted L2s
  • L2s go directly to the stomach
  • NO MIGRATION
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11
Q

Pathogenicity of ascarids

A
  • generally a problem with younger animals (puppies and kittens)
  • heavy infections resulting in death are rare.
  • clinical signs would include: pneumonia, vomiting, diarrhea, pot-bellied appearance, focal lesions in CNS (migrations) - neuro disorder
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12
Q

Identify the life cycle differences of Toxocara cati by transmission type

A

With direct transmission you get “tracheal migration” often from ingestion of a paratenic host.

Will undergo lactogenic transmission but NOT prenatal/transuterine transmission like Toxocara Canis does

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13
Q

Why are all ascarids easy to identify?

A

Bc they have 3 huge lips on anterior end that you can see grossly.

All their eggs are sticky so in a float you will often see debris stuck to the edges of them

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13
Q

Name 2 unique characteristics of ascarids that are used for identification

A

Alae
- an extension of the cuticle; each species has a different pattern

Eggs
- can be differentiated by color and size

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15
Q

How are ascarids diagnosed?

A

Fecal FLOTATION

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16
Q

Treatment of ascarids

A
  • dogs and cats: fenbendazole, milbemycin oxime, moxidectin, pyrantel pamoate
  • cats (T. Cati): selamectin, emodepside
  • treat nursing dams with litter: 2, 4, 6, 8 and 12 weeks, then monthly to 6 months
  • treat pregnant bitches with fenbendazole and ivermectin
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17
Q

Control of ascarids

A
  • remove the poop
  • bleach
  • rodent control
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18
Q

Why is there a debate about whether or not you can have a Toxocara free dog?

A

Because no drug can touch the hypobiotic larvae once they are encysted.

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19
Q

Zoonotic condition associated with Toxocara Canis in humans

A

Visceral Larval Migrans (VLM)

  • chronic granulomatous lesions due to larval migrations (seen in liver, lungs, brain, eye)
  • will have enlarged liver
  • loss of weight, appetite, persistent cough
  • human is considered a paratenic host - children that are “dirt eaters”
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20
Q

Baylisascaris procyonis

  • worm type
  • where is it found and in what species? Who is its DH?
  • geography
  • adult and egg characteristics?
A
  • Ascarid
  • found in dogs; raccoons are the DH
  • very common in northeast and Midwest and thought to be less common in southeast though we are starting to see cases
  • adults are large and white in color
  • eggs are ellipsoidal, dark brown
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21
Q

Baylisascaris procyonis : DH

- meaning of DH

A
  • raccoons, dogs, kinkajous

- DH meaning hosts that contain sexually mature adults and will produce eggs in the feces

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22
Q

Baylisascaris procyonis: Life cycle via direct transmission

A
  • ingestion of paratenic host (mice, rabbit, etc).
  • direct transmission of egg containing L2 larva
  • eggs released by DH
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23
Q

How ascarids are transmitted to humans

A
  • ingestion of larvated eggs thru contaminated food/water or via hay, straw, bedding
  • geophagy (eating dirt)
  • consumption of raw meat
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24
Q

Baylisascaris infections: clinical signs seen in definitive hosts

A
  • usually none seen in raccoons or dogs

- heavy infections in raccoons have been associated with intestinal obstruction

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25
Q

Baylisascaris infections: clinical signs seen in paratenic hosts

A

Visceral larval Migrans - many will develop neurological disease.
Severity varies with species and number of larvae - rodents and birds have high susceptibility, small ruminants have low susceptibility.

Been found in more than 90 species of mammals and birds

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26
Q

Baylisascaris infections: clinical signs and lesions seen in paratenic hosts

A
  • respiratory distress: high numbers of larvae in lungs
  • granulomas: large numbers of worms migrate thru tissues
  • invasion of spinal cord or brain: cause hemorrhage, necrosis and inflammation
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27
Q

Diagnosis of Baylisascaris infections in definitive hosts

A

FLOATATIONS for eggs. Will be auburn brown in color and may be larvated inside. Once you see the larvae you know they are infected.

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28
Q

Baylisascaris infection management

A
  • keep food/bedding away from raccoons that could defecate in product
  • infected definitive hosts (raccoons) should not be relocated to non-endemic areas
  • don’t keep raccoons as pets
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29
Q

Spirocerca Lupi

  • common name
  • where it’s found and in what species
  • IH and any paratenic hosts
  • geography
A
  • esophageal worm
  • found in caudal esophagus of dogs, foxes and both wild and domestic cats
  • IH = dung beetle
  • paratenic hosts = amphibians, reptiles, birds
  • geography = worldwide, particularly tropical/subtropical areas
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30
Q

Spirocerca Lupi

  • adult characteristics
  • egg characteristics
A
  • adults are coiled and BRIGHT RED

- larvated, have a thick shell

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31
Q

Life cycle of spirocerca Lupi

A
  1. Larvated eggs found in lumen of esophagus make their way to the intestine out via feces
  2. Eggs ingested by dung beetle (IH) where it develops to L3
  3. If a Paratenic host ingests the dung beetle - in which case the L3 encysts
  4. IH or paratenic host are ingested by the DH. The L3 migrates from the stomach via gastric arteries to the aorta.
  5. Remain in aorta for awhile and eventually migrate to esophagus where it forms a nodule and matures to an adult.
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32
Q

Spirocerca Lupi: clinical signs and pathogenicity

A

Clinical signs arise from 2 things: larval migration and adults.
Larval migration
- hemorrhage, inflammatory reactions, necrosis
- roughened aorta, aneurysm, death
- nodules in aorta or esophagus
- spondylitis of vertebrae via aberrant migration

Adults
- nodule formation - may lead to hemorrhage
- granulomas may form around nodule and develop into a sarcoma (this happens fairly often)
- obstruction of esophagus, vomiting, emaciation
- mild anemia
-

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33
Q

Spirocerca Lupi: diagnosis

A
  • floatation: high specific gravity

- radiography: caudal esophageal mass, undulant border of aortic wall, spondylitis

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34
Q

Spirocerca Lupi: treatment

A
  • ivermectin (may need to repeat)
  • ivermectin + prednisolone
  • doramectin
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35
Q

Spirocerca Lupi - control

A
  • prevent hunting (and ingesting paratenic host)
  • removal of feces
  • controlling coprophagous beetles is NOT feasible
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36
Q

Physaloptera praeputialis and pysaloptera rara

  • common name
  • where it’s found and in which species
  • IH and paratenic hosts if any
A
  • the stomach worm
  • found in the stomach of dogs and cats
    P. Praeputialis = cats
    P. Rara = dogs
  • IH: coprophagous beetles, cockroaches, grasshoppers
  • paratenic hosts: snake, rats, frogs
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37
Q

P. Praeputialis and P. Rara

  • adult characteristics
  • egg characteristics
A
  • adults are small

- eggs are small, oval, thick shelled, and larvated

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38
Q

Lifecycle for P. Praeputialis, and P. Rara

A
  1. Larvated eggs pass out of DH via feces
  2. Eggs ingested by IH: beetles, cockroaches, grasshoppers and develop into L3
  3. Paratenic host may or may not be utilized - snake, rat, frog. If they are, the L3 encysts in them
  4. IH or paratenic host is ingested by DH and L3s are released into the the stomach where they attach to mucosa and mature.
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39
Q

Physaloptera spp. Clinical signs and pathogenicity

A
  • usually asymptomatic
  • adults: can cause edematous wounds in stomach, inflamed mucosa, increased mucus production, chronic vomiting, weight loss.
  • can see worms in vomitus.
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40
Q

Physaloptera spp. Diagnosis

A
  • fecal or vomitus exam: must use high specific gravity
  • dark, tarry feces
  • endoscopy
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41
Q

Physaloptera spp. Treatment

A
  • mebendazole
  • pyrantel pamoate
  • fenbendazole
  • ivermectin
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42
Q

Ollulanus Tricuspis

  • common name
  • where it’s found and in what species
  • IH and paratenic hosts if any
  • adult characteristics
  • egg characteristics
A
  • stomach worm of cats
  • found in the stomach of cats, foxes, pigs, rarely dogs
  • none! They have a direct lifecycle
  • adults: very small, have cusps on posterior end.
  • eggs: they don’t make any! The female produces and releases an l3
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43
Q

Physaloptera infective stage

A

L3

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44
Q

Spirocerca Lupi infective stage

A

L3

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45
Q

Ollulanus tricuspis: lifecycle

A
  1. L3 in lumen of stomach (adults burrow into mucosa)
  2. Enter environment as L3 via parasite-induced vomitus
  3. DH ingests L3, matures to adults in stomach

They have a direct life cycle

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46
Q

Ollulanus tricuspis: clinical signs

A

When they vomit, the feed will look undigested, they will vomit right after eating.

Chronic gastritis

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47
Q

Toxocara Canis

  • common name
  • where it’s found and in what species
A
  • canine ascarid = ROUNDWORMS

- small intestine of dogs

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48
Q

S. Stercoralis and tumefaciens

  • adult characteristics: what is unique?
  • egg characteristics
A

Adults

  • pathogenic females are long, thread-like and entwined in mucosa
  • free-living males and females are small, thick, have a rhabditiform esophagus
  • something unique about the free-living males and females is its rhabditiform esophagus which contains a corpus, isthmus and bulb

Egg characteristics
- ellipsoidal, thick shelled, embryonated

49
Q

Ollulanus tricuspis: diagnosis & treatment

A
  • L3, L4 or adults in vomitus
  • Baermann: funneling and centrifuging vomitus then putting under the microscope
  • stomach irrigation

Treatment: fenbendazole

50
Q

Life cycle of s. Stercoralis and s. Tumefaciens

A

Life cycle is dependent on environmental conditions.
1. Embryonated eggs are passed in feces and develop into an L1. In case of s. Stercoralis L1s are directly passed in feces.

  1. If conditions are good, they will enter a heterogonic cycle where free living males and females mate. Eggs hatch and develop into an L3. If conditions are bad, they enter a homogonic cycle where 3N females survive and larvae develop to an L3.
  2. Infective 3N larvae (L3) infect vertebrate host - they penetrate skin or are ingested (ingested via milk or colostrum).
  3. They then migrate to lungs, trachea, descend to esophagus and intestine.
  4. Mature from L4 to L5 to adult parthenogenic females (3N)
51
Q
Strongyloides Stercoralis
Strongyloides tumefaciens
- common name
- where it's found and in what species
- describe the 2 forms of worms
A

= THREADWORMS

  • S stercoralis found in the SI of dogs, primates and humans
  • S. tumefaciens found in the SI of cats
  • there are two forms - a free living normal male and female worm and a parasitic stage which is all parthanogenic females in which she will produce her offspring on her own.
52
Q

The infective stage of the s. Stercoralis and tumefaciens

A

The 3N Larvae

53
Q

Clinical signs and pathogenicity of strongyloides spp. (Aka s. Stercoralis and tumefaciens)

  • what is the most common clinical sign?
A
  • usually asmptomatic
  • if young animal or large number of worms will see erosion of mucosa, diarrhea, weight loss and inappetence
  • the most common clinical sign is diarreha and it smells horrible!

Can also be autoinfectious: meaning they can just stay in their host, they dont need to be passed into the environment in order to become an adult. Will see this with immunocompromised animals. Then they will develop pneumonia. This is the worst case scenario with this parasite.

54
Q

Diagnosis and treatment of strongyloides spp.

A
  • fecal exam: look for eggs of S. Tumefaciens and larve for both s. Stercoralis and s. Tumefaciens
  • diagnostic feature is the larva have a fork on the tail that looks like a “Y”
  • treat with ivermectin and fenbendazole.
55
Q

Ancylostoma caninum

  • common name
  • where its found and in what species
A

= HOOKWORMS

- found in the SI of dogs

56
Q

Ancylostoma caninum

Adult and egg characteristics

A

Adults

  • have two pairs of teeth or 3 pairs of teeth
  • medium sized nematodes and may be red in color
  • male has copulatory bursa on posterior end - looks like fingers

Eggs
- wil larvate

57
Q

Differences bteween ancylostoma tubaeformae and Ancylostoma braziliense

A

A. Tubaeformae

  • SI of cats
  • 3 pairs of teeth

A. Braziliense

  • SI of dogs and cats
  • 2 pair of teeth
58
Q

Unicaria stenocephala

  • what type of worm is it? (Big group)
  • where is it found and in what species?
  • identifying characteristics?
  • geographic distribution?
A
  • HOOKWORM (ancylostoma)
  • found in SI of dogs
  • they have large buccal cavity with cutting plates
  • found in N. America
59
Q

What is the difference between an ancylostoma caninum and an ancylostoma braziliense?

A

A. Caninum has 3 pairs of teeth.

A. Braziliense has 2 pairs of teeth

60
Q

Lifecycle of a. Caninum and infective stage

A
  1. Adults in SI are attahced to mucsa. Non-larvated eggs leave DH via feces.
  2. Eggs embryonate in environment - they like moisty sandy soil
  3. In 24hrs, L1 develops in the egg and hatches.
  4. L1 molts to an L2 which then matures to an L3 and remains ensheathed. This is the infective stage of the worm.
  5. Then infects the DH
61
Q

Name the 5 ways the a. Caninum can infect its DH:

A
  1. Oral - ingestion of L3
  2. Skin penetration by L3
  3. Prenatal/transplacental infeciton
  4. Lactogenic infection
  5. Ingestion of paratenic host (just like toxocara)
62
Q

Describe DH infection of a. Caninum via oral infection

A
  • ingestion of L3 larvae
  • rare; not found in nature
  • no larval migration; adults mature in SI
63
Q

Describe DH infection of a. Caninum via skin penetration in dogs

A
  • L3s penetrate skin via paw pads or oral mucus membranes
  • undergo extensive migration: reach systemic circulation, carried to heart or lungs, pass into alveoli, swallowed, mature to adults in SI
64
Q

Describe DH infection of a. Caninum in dogs > 3 months old

A
  • L3s penetrate skin
  • undergo extensive migration: reach systemic criculation and follow a “somatic route” where they become dormant (hypobiotic) and encyst in muscle and remain there until pregnant if female.
65
Q

Describe DH infection of a. Caninum via transplacental transmission, lactogenic transmission and paratenic host transmission

A

Transplacental

  • rare
  • L3s enter bloodstream, pass to placenta and enter fetus

Lactogenic

  • hypobiotic larvae migrate to mammary glands
  • L3s recovered from milk up to 20d after whelping
  • adults mature in SI; no migration

Paratenic hosts

  • ingest host that harbors encysted hypobiotic L3s (mice and rats)
  • adults migrate in SI; no migration
66
Q

Identify hookworm lifecycle differences in ancylostoma tubaeformae and unicaria stenocephala

A

In a. Tubaeformae, they are only acquired after birth via environmental contamination

In unicaria stenocephala, oral infection is most successful

67
Q

Clinical signs of ancylostoma spp.

A
  • diarrhea with blood (mucus-y, black or tarry)
  • poor appetite
  • poor growth/hair coat
  • weak
  • pale mucus membranes
  • hemorrhagic pneumonitis
  • moist eczema (skin penetration)
68
Q

Ancylostoma pathogenciticy

Which ones are most pathogenic?

A
  • anemia: attachment sites continue to bleed, puppies are the hardest hit
  • A. Caninum, A. Tubaeformae are most pathogenic - they are voracious bloodsuckers
69
Q

What are the 4 clinical forms of disease from hookworms (ancylostoma)?

A
  1. Peracute hookworm disease
  2. Acute hookworm disease
  3. Chronic hookworm disease
  4. Secondary hookworm disease
70
Q

Peracute hookworm disease

A
  • transmammary infection
  • puppy health deteriorates 2weeks post infection (pale mm, dark, liquid feces, treatment often doesnt work)
  • treat bitches with fenbendazole day 40 of gestation to day 14 of lactation
71
Q

Acute hookworm disease

A

Sudden exposure of older pups

72
Q

Chronic hookworm disease

A

Without clinical signs will find eggs in feces, and reduced RBC count or PCV

73
Q

Secondary hookworm disease

A

Found in older dogs

  • anemic, malnourished, emaciated
  • if not responsive to treatment: supportive therapy
74
Q

How is ancylostoma diagnosed?

A

Fecal FLOATATION

75
Q

Treatment for ancylostoma

A
  • there is no resistance with these worms. You just have to treat adults and L4s (infective stage of larva) which is different from other species
    Adults
    A. Caninum: fenbendazole
    A. Braziliense: pyrantel
    U. Stenocephala: pyrantel, fenbendazole
    A. Tubaeformae: ivermectin, milbemycin, moxidectin, pyrantel

L4s (in intestine)
Moxidectin

76
Q

Ancylostoma control

A

Difficult bc of hypobiosis

  • keep kennels dry and clean
  • pick up feces daily!!!
77
Q

Zoonosis of ancylostoma

A

Cutaneous larval migrans (CLM)

  • ancylostoma braziliense
  • causes “sand worms,” “plumber’s itch,” or “creeping eruption”
  • L3s penetrate skin

Rarely enter SI and mature to adults

78
Q

Trichuris Vulpis, Trichuris campanula, Trichuris serrata

  • common name
  • where they are found and in what species
  • geographic distribution
A

WHIPWORMS

  • T. Vulpis = found in the SI of dogs
  • T. Campanula, T. Serrata = found in the SI of cats
  • found worldwide
79
Q

Trichura spp.

Adult and egg characteristics

A
  • adults are “whip-like” with a thick posterior end and an anterior end that weaves in and out of mucosa
  • eggs are bi-polar, fairly large and golden brown in color
80
Q

Lifecycle of Trichuris

what is the Infective stage?

A
  1. Females produce nonembryonated eggs that are passed in feces
  2. Eggs embryonate in soil and can be viable for years
  3. Embryonated eggs are ingested - L2s
  4. Larvae enter the wall of the small and large intestines where they develop to an L4
  5. Larvae return to the lumen and migrate to the cecum where they mature to adults
  • L2 is the infective stage
81
Q

Clinical signs and pathogenicity of Trichuris

A

Clinical signs:

  • most infections are asymptomatic
  • adults: blood feeders - disease depends on age of host, numbers of worms present but if you see signs they will be:

Anemia, bloody mucoid diarrhea, weight loss, dehydration and death

82
Q

Diagnosis of Trichuris spp.

A
  • fecal exam - high specific gravity; may need to do a few fecals in a row
  • long prepatent period may show clinical signs prior to eggs in feces
  • eggs shed intermittently
83
Q

Treatment of Trichuris spp.

A
  • Drontal plus (febantel, pyrantel, praziquantel) single dose
  • fenbendazole
  • treat once a month for 3 months

Heartworm preventatives also approved for whipworms: interceptor, sentinel, advantage multi, trifexis

Control = feces removal! There is no intermediate host so the way you control whipworms is by picking up feces!

84
Q
Strongyloides Stercoralis
Strongyloides tumefaciens
- common name
- where it's found and in what species
- describe the 2 forms of worms
A

= THREADWORMS

  • S stercoralis found in the SI of dogs, primates and humans
  • S. tumefaciens found in the SI of cats
  • there are two forms - a free living normal male and female worm and a parasitic stage which is all parthanogenic females in which she will produce her offspring on her own.
85
Q

S. Stercoralis and tumefaciens

  • adult characteristics: what is unique?
  • egg characteristics
A

Adults

  • pathogenic females are long, thread-like and entwined in mucosa
  • free-living males and females are small, thick, have a rhabditiform esophagus
  • something unique about the free-living males and females is its rhabditiform esophagus which contains a corpus, isthmus and bulb

Egg characteristics
- ellipsoidal, thick shelled, embryonated

86
Q

Life cycle of s. Stercoralis and s. Tumefaciens

A

Life cycle is dependent on environmental conditions.
1. Embryonated eggs are passed in feces and develop into an L1. In case of s. Stercoralis L1s are directly passed in feces.

  1. If conditions are good, they will enter a heterogonic cycle where free living males and females mate. Eggs hatch and develop into an L3. If conditions are bad, they enter a homogonic cycle where 3N females survive and larvae develop to an L3.
  2. Infective 3N larvae (L3) infect vertebrate host - they penetrate skin or are ingested (ingested via milk or colostrum).
  3. They then migrate to lungs, trachea, descend to esophagus and intestine.
  4. Mature from L4 to L5 to adult parthenogenic females (3N)
87
Q

The infective stage of the s. Stercoralis and tumefaciens

A

The 3N Larvae

88
Q

Clinical signs and pathogenicity of strongyloides spp. (Aka s. Stercoralis and tumefaciens)

  • what is the most common clinical sign?
A
  • usually asmptomatic
  • if young animal or large number of worms will see erosion of mucosa, diarrhea, weight loss and inappetence
  • the most common clinical sign is diarreha and it smells horrible!

Can also be autoinfectious: meaning they can just stay in their host, they dont need to be passed into the environment in order to become an adult. Will see this with immunocompromised animals. Then they will develop pneumonia. This is the worst case scenario with this parasite.

89
Q

Diagnosis and treatment of strongyloides spp.

A
  • fecal exam: look for eggs of S. Tumefaciens and larve for both s. Stercoralis and s. Tumefaciens
  • diagnostic feature is the larva have a fork on the tail that looks like a “Y”
  • treat with ivermectin and fenbendazole.
90
Q

Ancylostoma caninum

  • common name
  • where its found and in what species
A

= HOOKWORMS

- found in the SI of dogs

91
Q

Ancylostoma caninum

Adult and egg characteristics

A

Adults

  • have two pairs of teeth or 3 pairs of teeth
  • medium sized nematodes and may be red in color
  • male has copulatory bursa on posterior end - looks like fingers

Eggs
- wil larvate

92
Q

Differences bteween ancylostoma tubaeformae and Ancylostoma braziliense

A

A. Tubaeformae

  • SI of cats
  • 3 pairs of teeth

A. Braziliense

  • SI of dogs and cats
  • 2 pair of teeth
93
Q

Unicaria stenocephala

  • what type of worm is it? (Big group)
  • where is it found and in what species?
  • identifying characteristics?
  • geographic distribution?
A
  • HOOKWORM (ancylostoma)
  • found in SI of dogs
  • they have large buccal cavity with cutting plates
  • found in N. America
94
Q

What is the difference between an ancylostoma caninum and an ancylostoma braziliense?

A

A. Caninum has 3 pairs of teeth.

A. Braziliense has 2 pairs of teeth

95
Q

Lifecycle of a. Caninum and infective stage

A
  1. Adults in SI are attahced to mucsa. Non-larvated eggs leave DH via feces.
  2. Eggs embryonate in environment - they like moisty sandy soil
  3. In 24hrs, L1 develops in the egg and hatches.
  4. L1 molts to an L2 which then matures to an L3 and remains ensheathed. This is the infective stage of the worm.
  5. Then infects the DH
96
Q

Name the 5 ways the a. Caninum can infect its DH:

A
  1. Oral - ingestion of L3
  2. Skin penetration by L3
  3. Prenatal/transplacental infeciton
  4. Lactogenic infection
  5. Ingestion of paratenic host (just like toxocara)
97
Q

Describe DH infection of a. Caninum via oral infection

A
  • ingestion of L3 larvae
  • rare; not found in nature
  • no larval migration; adults mature in SI
98
Q

Describe DH infection of a. Caninum via skin penetration in dogs

A
  • L3s penetrate skin via paw pads or oral mucus membranes
  • undergo extensive migration: reach systemic circulation, carried to heart or lungs, pass into alveoli, swallowed, mature to adults in SI
99
Q

Describe DH infection of a. Caninum in dogs > 3 months old

A
  • L3s penetrate skin
  • undergo extensive migration: reach systemic criculation and follow a “somatic route” where they become dormant (hypobiotic) and encyst in muscle and remain there until pregnant if female.
100
Q

Describe DH infection of a. Caninum via transplacental transmission, lactogenic transmission and paratenic host transmission

A

Transplacental

  • rare
  • L3s enter bloodstream, pass to placenta and enter fetus

Lactogenic

  • hypobiotic larvae migrate to mammary glands
  • L3s recovered from milk up to 20d after whelping
  • adults mature in SI; no migration

Paratenic hosts

  • ingest host that harbors encysted hypobiotic L3s (mice and rats)
  • adults migrate in SI; no migration
101
Q

Identify hookworm lifecycle differences in ancylostoma tubaeformae and unicaria stenocephala

A

In a. Tubaeformae, they are only acquired after birth via environmental contamination

In unicaria stenocephala, oral infection is most successful

102
Q

Clinical signs of ancylostoma spp.

A
  • diarrhea with blood (mucus-y, black or tarry)
  • poor appetite
  • poor growth/hair coat
  • weak
  • pale mucus membranes
  • hemorrhagic pneumonitis
  • moist eczema (skin penetration)
103
Q

Ancylostoma pathogenciticy

Which ones are most pathogenic?

A
  • anemia: attachment sites continue to bleed, puppies are the hardest hit
  • A. Caninum, A. Tubaeformae are most pathogenic - they are voracious bloodsuckers
104
Q

What are the 4 clinical forms of disease from hookworms (ancylostoma)?

A
  1. Peracute hookworm disease
  2. Acute hookworm disease
  3. Chronic hookworm disease
  4. Secondary hookworm disease
105
Q

Peracute hookworm disease

A
  • transmammary infection
  • puppy health deteriorates 2weeks post infection (pale mm, dark, liquid feces, treatment often doesnt work)
  • treat bitches with fenbendazole day 40 of gestation to day 14 of lactation
106
Q

Acute hookworm disease

A

Sudden exposure of older pups

107
Q

Chronic hookworm disease

A

Without clinical signs will find eggs in feces, and reduced RBC count or PCV

108
Q

Secondary hookworm disease

A

Found in older dogs

  • anemic, malnourished, emaciated
  • if not responsive to treatment: supportive therapy
109
Q

How is ancylostoma diagnosed?

A

Fecal FLOATATION

110
Q

Treatment for ancylostoma

A
  • there is no resistance with these worms. You just have to treat adults and L4s (infective stage of larva) which is different from other species
    Adults
    A. Caninum: fenbendazole
    A. Braziliense: pyrantel
    U. Stenocephala: pyrantel, fenbendazole
    A. Tubaeformae: ivermectin, milbemycin, moxidectin, pyrantel

L4s (in intestine)
Moxidectin

111
Q

Ancylostoma control

A

Difficult bc of hypobiosis

  • keep kennels dry and clean
  • pick up feces daily!!!
112
Q

Zoonosis of ancylostoma

A

Cutaneous larval migrans (CLM)

  • ancylostoma braziliense
  • causes “sand worms,” “plumber’s itch,” or “creeping eruption”
  • L3s penetrate skin

Rarely enter SI and mature to adults

113
Q

Trichuris Vulpis, Trichuris campanula, Trichuris serrata

  • common name
  • where they are found and in what species
  • geographic distribution
A

WHIPWORMS

  • T. Vulpis = found in the SI of dogs
  • T. Campanula, T. Serrata = found in the SI of cats
  • found worldwide
114
Q

Trichura spp.

Adult and egg characteristics

A
  • adults are “whip-like” with a thick posterior end and an anterior end that weaves in and out of mucosa
  • eggs are bi-polar, fairly large and golden brown in color
115
Q

Lifecycle of Trichuris

what is the Infective stage?

A
  1. Females produce nonembryonated eggs that are passed in feces
  2. Eggs embryonate in soil and can be viable for years
  3. Embryonated eggs are ingested - L2s
  4. Larvae enter the wall of the small and large intestines where they develop to an L4
  5. Larvae return to the lumen and migrate to the cecum where they mature to adults
  • L2 is the infective stage
116
Q

Clinical signs and pathogenicity of Trichuris

A

Clinical signs:

  • most infections are asymptomatic
  • adults: blood feeders - disease depends on age of host, numbers of worms present but if you see signs they will be:

Anemia, bloody mucoid diarrhea, weight loss, dehydration and death

117
Q

Diagnosis of Trichuris spp.

A
  • fecal exam - high specific gravity; may need to do a few fecals in a row
  • long prepatent period may show clinical signs prior to eggs in feces
  • eggs shed intermittently
118
Q

Treatment of Trichuris spp.

A
  • Drontal plus (febantel, pyrantel, praziquantel) single dose
  • fenbendazole
  • treat once a month for 3 months

Heartworm preventatives also approved for whipworms: interceptor, sentinel, advantage multi, trifexis

Control = feces removal! There is no intermediate host so the way you control whipworms is by picking up feces!