Superfamily Ascaroidea Flashcards

(33 cards)

1
Q

Two families within the superfamily Ascaroidea

A
  1. Ascarididae (ascarids)
    - -Terrestrial mammals, reptiles, and birds
  2. Anisakidae (anisakids)
    - -Marine mammals and fish-eating birds (larval stage is present in birds)
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2
Q

Important Ascarids

A
  • Ascaris suum (pig) - 15-40 cm
  • Parascaris equorum (horse) - 15-50 cm
  • Toxocara canis (dog) - 10-18 cm
  • Toxocara cati (cat) - 3-10 cm
  • Toxascaris leonina (dog and cat) - 7-10 cm
  • Baylisascaris procyonis (raccoon and dog) - 10-24 cm
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3
Q

Adult Ascarid morphology

A
  • Large, thick bodied
  • Females are larger than males
  • Have three well-developed lips around the stoma
  • Cervical alae (present in T. leonina and Toxocara spp.)
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4
Q

Ascarid life-cycle

A
  • Adult ascarids present in the small intestine
  • Lays eggs, found in fresh feces (non-infective)
  • After 2-3 weeks, eggs containing larvae are found in the soil (infective) - appears to be coiled inside the egg
  • Ingestion (fecal-oral or paratenic host)
  • Transmission to the definitive host
  • Migration in the definitive host (hepato-pulmonary-tracheal migration)
  • Adult ascarids present in the small intestine
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5
Q

Life-cycle and transmission types

A

Direct: Ascaris suum and Parascaris equorum
–Ingestion of larvated eggs from contaminated environment
Direct/Indirect: Toxocara, Toxascaris, and Baylisascaris
–Paratenic host (T. canis and T. cati)
–Prenatal or transplacental (T. canis)
–Transmammary (T. canis and T. cati)

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6
Q

Development in the environment

A
  • Ascarids are prolific egg producers –> shed millions of eggs per day
  • Eggs are extremely resistant
  • -Last for years in the soil
  • –Single most important factor in epidemiology!
  • Eggs are very sticky
  • -Adhere to surfaces and objects (need to clean with chlorine or bleach, not just soap)
  • Development is temperature dependent
  • -Optimal temp is 25-30 degrees Celsius
  • -Takes ~2-4 weeks to become infective (embryonated) in the environment (exception: T. leonina, 3-5 days)
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7
Q

Direct life-cycle

A
  • Ascaris suum and Parascaris equorum
  • Eggs are shed in the feces –> develop infective larva within the egg –> ingested –> larvae hatch –> penetrate the intestine –> migrate through the liver, lungs (L4), trachea, then intestine (adult)
  • Prepatent period:
  • –Ascaris suum = 60-62 days
  • –Parascaris equorum = 72-94 days
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8
Q

Clinical disease: Ascaris suum and Parascaris equorum

A

Common to both:
-Infective egg - polluted soil or stuck to mammary skin
-Hepatic migration - mechanical damage, eosinophilic inflammation, scarring (possible)
-Migration in the lung - verminous pneumonitis
-Immature adults return to the intestine - no significant clinical disease
-Small intestine - catarrhal enteritis, interference with nutrient absorption and growth (stunting growth), economic losses, GI obstruction, aberrant migration, GI perforation
Ascaris suum only:
–ZOONOTIC (will migrate and develop in humans)
—Often seen in children who are around swine in many parts of the world (occasional reports in US)
–Swine lung: petechial hemorrhage (respiratory distress, rapid and shallow, audible expiration (thumps))
–Liver: milk spots (fibrotic areas - migration of the larvae)

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9
Q

Toxascaris leonina general info

A
  • Host = dogs, cats, foxes, wolves, and big cats
  • Not zoonotic
  • Clinical disease is rarely observed
  • Prevalent in geographical regions with cooler climates
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10
Q

Toxascaris leonina life-cycle

A
  • Adult in small intestine
  • Eggs containing one single cell are shed in the feces
  • Takes 3-5 days to become egg containing infective larva in the soil
  • From there, can go down two different routes
    1. Eggs ingested by definitive host (dog or cat) and travel via mucosal migration
  • -Prepatent period = 2-2.5 months
  • -Adult in small intestine
    2. Eggs are ingested by a paratenic host (rodent) and travel via lymphatics or contiguity of tissues
  • -Larvae are arrested in the tissues
  • -Dog or cat eats the paratenic host
  • -Adult in small intestine
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11
Q

Toxocara canis adult morphology

A
  • Host = dogs and wild canids
  • Robust adults (10-15 cm long)
  • Cervical alae present on anterior end
  • Digitiform appendage on male worm
  • Spicules found on male worm
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12
Q

T. canis routes of transmission

A
  • Ingestion of infective egg
  • Transplacental
  • -MOST important route of transmission
  • -Ensures that most puppies (90%) are infected at birth
  • Transmammary
  • -Can be passed at larval stage
  • Paratenic host
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13
Q

Toxocara canis life-cycle

A
  • Adult in small intestine
  • Eggs containing one cell shed in feces
  • After four weeks, the eggs contain infective larvae, present in the soil
  • From there, can go down two different routes
    1. Eggs ingested by the dog
  • -From there, can go down two different routes
  • –1. Tracheal migration in puppies < 3 months of age (prepatent period is 4-5 weeks)
  • —Adult in small intestine
  • –2. Somatic migration in puppies > 3 months of age (prepatent period is 4-5 weeks)
  • —Infective larvae is arrested in the tissues of the bitch
  • —Larvae are reactivated during pregnancy
  • —From there, can go down two different routes
  • —-1. Larvae enter the pups in utero during the third trimester
  • —–Larvae in lungs of pups
  • —–Pups born, larvae mature, patent at 3 weeks post partum
  • —–Adult in small intestine
  • —-2. Larvae shed in the milk, if mother infected during lactation, ingested by the pups
  • —–Adult in small intestine
    2. Eggs ingested by the paratenic host
  • -Somatic migration (liver –> lung –> tissue)
  • -Infective larvae arrested in tissues of paratenic host
  • -Dog eats paratenic host
  • -Adult in small intestine
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14
Q

T. canis general info

A
  • Complex life-cycle
  • Clinical disease may be absent in adult dogs
  • Most patent infections occur in puppies < 6 months of age
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15
Q

T. canis clinical disease

A
  • Pot-bellied appearance
  • Unthriftiness
  • Rough hair coat
  • Poor appetite
  • Abdominal discomfort with vocalization
  • Hepatic migration damage, verminous pneumonitis, kidney scarring, catarrhal enteritis, obstruction of gut, perforation of gut, interference with absorption, diarrhea, vomiting, aberrant migration of worms
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16
Q

Toxocara cati general info

A
  • Found in cats
  • Arrow-headed worm
  • Similar clinical disease as T. canis
17
Q

T. cati life-cycle

A
  • Adult in small intestine
  • Eggs containing one cell found in feces
  • Eggs containing infective larvae found in soil after four weeks
  • From there, can go down two different routes
  • -1. Eggs ingested by cat
  • –From there, can go down two different routes
  • —1. Tracheal migration (prepatent period = 2 months)
  • —-Adult in small intestine
  • —2. Somatic migration
  • —-Infective larvae arrested in tissues of queen
  • —-Larvae shed in milk, if mother infected during lactation, ingested by kittens
  • —-Mucosal migration
  • —-Adult in small intestine
  • -2. Eggs ingested by paratenic host
  • –Infective larvae arrested in tissues of paratenic host
  • –Cat eats paratenic host
  • –Mucosal migration
  • –Adult in small intestine
18
Q

Differences of transmission between T. cati and T. canis

A

T. cati
-No transplacental transmission
-Transmammary transmission does occur
–Does not occur in chronically infected queens
–Might occur if acute infection present during late-pregnancy
-Tracheal or somatic migration occurs
–But host age related differential migration does not
–Prepatent period is ~8 weeks
-Paratenic host ingestion occurs
–Prepatent period is ~3 weeks
T. canis
-Transplacental transmission does occur
-Transmammary transmission does occur
-Tracheal or somatic migration does occur
-Host age related differential migration is present
-Paratenic host ingestion does occur

19
Q

Comparison of T. cati, T. canis, and T. leonina

A

Cervical alae

  • T. canis and T. leonina have thinner alae
  • T. cati has a much thicker alae
20
Q

Ascarid infection characteristics

A
  • Acute to chronic clinical disease
  • Always worse in young animals
  • Varies with intensity of infection and frequency of reinfection
  • Pathology is related to location of adults and migration paths of larvae
  • Larval migration causes:
  • -Mechanical damage and hemorrhages
  • -Edema and marked eosinophilic inflammation
  • Immunopathological responses may also occur
21
Q

Diagnosis of ascarid infections

A
  • Clinical signs (adult animals rarely show clinical signs)
  • Necropsy lesions
  • Adult recovery at necropsy (or surgery)
  • Eggs in feces
  • Adult and immature worm recovery from vomitus or feces (often in T. canis and T. cati infections)
  • Ultrasound
  • Endoscopy
22
Q

How to ID eggs

A
  • Size
  • Shape
  • Color
  • Internal structures
  • Surface features
23
Q

Baylisascaris procyonis

A
  • Found in raccoons and dogs (definitive hosts)
  • Adult worms are present in the small intestine
  • Eggs are shed in the feces
  • Dogs can also be accidental hosts
24
Q

Accidental host

A
  • Presence of migrating larvae in the body tissues of the host
  • This host is not involved in the completion of the life cycle
25
B. procyonis life-cycle
- Transmission is similar to other carnivores - Ingestion of embryonated eggs - Ingestion of paratenic host harboring larvae
26
B. procyonis: factors increasing risk of exposure
- Distribution and adaptability of raccoons - -Extremely common - -Well adapted to co-exist with humans - Encouraged feeding - frequent raccoon visits and establishing latrines - Raccoons as pets
27
Ascarid public health considerations
- A. suum will migrate and develop in humans - Members of Toxocara and Baylisascaris - Larva migrans (larva migration pattern) - -Visceral, ocular, and neural (Ascarids do not do cutaneous migration) - -Prolonged migration and persistence of helminth larvae in organs and tissues of humans and animals - -Extensive tissue damage and inflammation
28
Serological assays for diagnosis
- Antibody detection assays - Differentiate larva migrans caused by Toxocara spp. and Baylisascaris spp. - Testing centers: - -CDC and National reference Center for Parasitology
29
Control and prevention
- Reduce environmental contamination - -Fecal clean up - -Remove/replace contaminated soil - -Heat - Limit contact with contaminated areas - Rodent control - Strategic or routine deworming (cats and dogs)
30
Treatment
T. canis, T. cati, and T. leonina - Fenbendazole, Febantel, milbemycin oxime, moxidectin, and pyrantel pamoate - Piperazine - For cats: - -Also Selamectin, Eprinomectin, and Emodepside - For puppies: - -Initial deworming at 2-4-6-8 weeks, then monthly preventatives - For kittens: - -Do not need to be treated until 8 weeks old - --Various combination of products, primarily heartworm preventatives are approved as they contain the above drugs - For B. procyonis infections: - -No approved drugs - For A. suum infections: - -Hygromycin B, Piperazine, Dichlorvos, Fenbendazole, Levamisole, Ivermectin, doramectin, and pyrantel tartrate - For P. equorum infections: - -Piperazine, Fenbendazole, Oxibendazole, Ivermectin, Moxidectin, and Pyrantel pamoate - -Resistance to macrocyclic lactones is widespread
31
Pyrantel
Preferred for treating nursing animals and young pups
32
Piperazine
Lower efficacy than other drugs for cats and dogs
33
Pyrantel tartrate
- Feed additive | - Preventative that kills the infective larvae immediately after it hatches