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Parasitology > Ascarids (Ca & Fe) > Flashcards

Ascarids (Ca & Fe) Flashcards

1
Q

What are ascarids?

A
  • NEMATODES
  • family ascarididae (roundworms)
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2
Q

What are the ascarids we care about?

A
  1. Toxascaris leonina (Ca & Fe)
  2. Toxocara canis (Ca)
  3. Toxocara cati (Fe)
  4. Baylisascaris spp. (Ca)
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3
Q

Where are ascarids found?

A

stomach & small intestines

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4
Q

Defining features of adult Toxascaris leonina?

A
  • two long & narrow lateral cervical alae @ the anterior end
  • males have no finger-like projection at the posterior end (unlike Toxocara canis)
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5
Q

Defining features of Toxascaris leonina eggs?

A
  • sub-spherical (“squash ball” appearance) w/ thick smooth shell
  • each egg contains 1 or 2 cells when passed
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6
Q

Hosts of Toxascaris leonina?

A
  • Ca & Fe
  • other canids & felids (as definitive hosts)
  • other mammals & birds (as paratenic hosts where the parasite remains as larvae in tissues & does not complete its development to adults in the GI system)
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7
Q

What is the geographic distribution of Toxascaris leonina?

A
  • around the world
  • in 3% of shelter Ca in national study, somewhat higher in Western Canada
  • Not detected in shelter Fe in national study & @ low prevalence in owned & free roaming/rural cats in other studies in Western Canada
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8
Q

What is the life cycle of Toxascaris leonina?

A
  • adult nematodes live in the intestine of the canid or felid definitive host & produce eggs shed in feces
  • larvae dev w/in eggshell to infective 3rd stage (L3) @ temp dep rate (generally 1-4 wks)
  • infective third stage larvae w/in the eggs are ingested by Ca or Fe
  • then larvae is released to undergo mucosal migration (GI tract lumen to mucosa to lumen) w/in GI system.
  • 8-10 week prepatent period
  • neither pre-natal nor trans-mammary transmission, nor somatic larvae
  • life cycle may also involve, but does not require, sm mammal paratenic hosts, in which 3rd stage larvae are hatched from ingested eggs follow somatic migration (GI tract to portal vessels to liver to heart to lungs to heart to somatic tissues)
  • 3rd larvae in tissues of paratenic host are infective for the Ca or Fe definitive hosts
  • following ingestion by a Ca or Fe, these larvae too undergo a mucosal migration (8-10 wk PPP)
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9
Q

What is the epidemiology of Toxascaris leonina?

A
  • mjr route of transmission among Ca is probably through infective eggs & for Fe through infected paratenic hosts
  • eggs are v resistant to adverse enviro conditions & can survive & remain infective for months or perhaps years
  • eggs are not immediately infective, but require @ least a wk in enviro to become infective for DHs & paratenic hosts
  • eggs can be inactivated by strong phenol, cresol, or bleach solns, high temps (> 45 C), & desiccation
  • eggs are more freeze tolerant than those of Toxocara spp. & freezing @ -20 C will not reliably inactivate them
  • eggs are not inactivated by most common disinfectants, nor by fixation in formalin or ethanol
  • frequent occurrence in Ca in N. Canada suggests that parasite is well adapted to relatively cool & harsh enviro
  • has been detected in Arctic fox well above the Arctic circle
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10
Q

What is the pathology & clinical signs of Toxascaris leonina?

A
  • larval & adult have effects in GI tract similar to those of Toxocara canis & are generally mild unless lrg # of parasites are present in young animals or in those that are otherwise compromised
  • in Ca & Fe, it does not migrate beyond GI mucosa
  • clinical signs seen in juveniles are often asymptomatic, pot belly, poor growth, staring coat, diarrhea, respiratory signs, seizures, & death (v rare)
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11
Q

How is Toxascaris leonina diagnosed?

A
  • usually vague clinical signs associated w/ it aren’t helpful
  • adult parasites may be found in feces or vomit
  • eggs may be detected on routine fecal float (relatively sensitive for ascarid eggs)
  • newer coproAg & coproPCR methods are increasingly avail & useful in detection of ascarid infections (including PPP)
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12
Q

Is Toxascaris leonina zoonotic?

A

no

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13
Q

Defining features of adult Toxocara canis?

A
  • two long & narrow lateral cervical alae
  • 3 “lips” @ anterior end
  • males have short finger-like projection @ posterior end
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14
Q

Defining features of eggs of Toxocara canis?

A
  • sub-spherical (“golf ball” appearance) w/ thick, rough shell
  • each egg contains 1 or 2 cells when freshly passed
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15
Q

What is the host range & geographic distribution of Toxocara canis?

A
  • occurs in Ca & other canids (as DH) & wide range of mammals & Av (as paratenic hosts), throughout the world
  • in canada, it is most common helminth parasite of Ca
  • prevalence in healthy, owned, adult pets is much lower
  • human infection w/ larval T. canis (visceral, ocular, & occult larva migrans) is significant health prob in some areas of world, esp. in children
  • @ northern latitudes, it is replaced by Toxascaris leonina
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16
Q

What is the life cycle of Toxocara canis?

A
  • Adults are located in sm intestine of Ca
  • eggs leave host in feces
  • infective L3 larva devs in each egg after 3-4 wks in ideal enviro conditions
  • this dev rate is temp dep
  • following ingestion of infective L3 w/in eggs, in pups < 3 months old larvae migrate via vasculature through liver to lungs, where they break out from branches of pulmonary artery into airways, are coughed up, swallowed, & mature to adults in GI system (hepatotracheal migration - PPP 4-5 wks)
  • in older dogs (> ~ 6m), initially larvae follow similar migration route, but once in lungs do not enter airways but leave lungs in pulmonary veins & are distributed in bloodstream to variety of tissues (somatic migration)
  • btwn 3 & 6 months of age, there is gradual transition from primarily tracheal to primarily somatic migration
  • if female Ca becomes pregnant, larvae in tissues are mobilized @ start of 3rd trimester, enter vasculature, cross placenta, & enter livers of fetal pups (pre-natal infection)
  • when pups are born, larvae undergo hepatotracheal migration & mature to adults in intestine
  • eggs can be present in feces of pre-natally infected pups by 2-3 wks after birth
  • less commonly than prenatal infections, larvae infecting female in late pregnancy/ early lactation can enter mammary glands of female & be transmitted to suckling pups in milk during first 4 or 5 wks of lactation (trans-mammary infection)
  • nursing females may occasionally ingest eggs containing L3, L4, L5, or adult nematodes passed in feces or vomit of pups
  • these, as well as any larvae that were activated from somatic tissues of female during pregnancy & entered her intestine, can produce usually transient patent infection in female
  • larvated, infective eggs may also be ingested by paratenic host, in which larvae are released following somatic migration
  • if paratenic host is eaten by Ca, larvae are released, undergo mucosal migration, & establish adult infection in Ca’s GI system (PPP 4 wks)
  • paratenic hosts include wide range of verts, including sm mammals, birds, livestock, & people
  • these life cycle patterns mean that it is generally more prevalent & infections are more intense in young pups than in older pups or adult animals
  • however, older animals can dev patent infections, esp. if immunocompromised or malnourished
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17
Q

What is the epidemiology of Toxocara canis?

A
  • mjr route of transmission to pups is prenatally from mothers (vs transmammary) & for older Ca, through consumption of infective eggs in enviro (vs consumption of L3 in paratenic hosts)
  • female Ca w/ somatic larvae can infect multiple litters
  • eggs are v resistant to adverse enviro conditions & can survive & remain infective for months or perhaps even yrs, esp. in cool, damp conditions
  • eggs are not immediately infective, but require several wks in enviro to become infective for Ca, people, & other hosts
  • eggs can be inactivated by strong phenol, cresol, or bleach solutions, high temps, desiccation, & freezing @ -20 C or below for wks to m
  • eggs are not inactivated by most common disinfectants, nor by fixation in formalin or ethanol
  • eggs (of unknown viability) can be found in hair coat of Ca, but significance of these in parasite transmission is unknown
18
Q

What is the pathology & clinical signs of Toxocara canis?

A
  • in young puppies, esp. those infected prenatally, migrating larvae in lungs may be associated w/ resp signs
  • in untreated pups, adult parasites in GI system can be associated w/ sub-optimal growth & dev, poor body condition (“pot-belly”), staring coat, & diarrhea, as well as possibly “seizures” & death (rare)
  • pathogenesis of these clinical signs is not fully understood
  • in older Ca, neither adult parasites nor migrating larvae are commonly associated w/ clinical abnormalities, although multifocal retinitis (ocular larval migrans) associated w/ larvae has been reported
19
Q

How is Toxocara canis diagnosed?

A
  • fecal float, CoproAg, coproPCR
  • large adult worms in vomit or stool
20
Q

What is the public health significance of Toxocara canis?

A
  • can be associated w/ ocular, visceral, & occult larva migrans in people (1st particularly in young children)
  • human infection usually follows ingestion of infective eggs, & clinical syndrome that devs depends on primary location of migrating larvae that hatch from these eggs
  • rarely, human infections are associated w/ ingestion of tissues from animals & Av containing larval stages of parasite (other paratenic hosts)
  • infection in people appears to be much more common than clinical disease
  • all 3 syndromes are v rare in Canada
  • human infections can be prevented by regular removal of Ca feces (as infective larvae take @ least 2 wks to dev), good hand hygiene following handling of Ca & Ca feces, washing all produce & cooking meat prior to consumption, & keeping Ca out of play areas used by children
21
Q

What are the defining features of adult Toxocara cati?

A
  • 2 broad, arrowhead-shaped lateral cervical alae @ anterior end, & 3 “lips”
  • males have short finger-like projection @ posterior end
22
Q

What are the defining features of the eggs of Toxocara cati?

A
  • sub-spherical (“golf ball” appearance) w/ thick, rough shell
  • each egg contains 1 or 2 cells when freshly passed
  • eggs are slightly smaller than those of Toxocara canis, although definitive differentiation often relies on molecular methods
23
Q

What is the host range & geographic distribution of Toxocara cati?

A
  • occurs in domestic Fe & other felids (DH)
  • other mammals & birds (paratenic hosts)
  • around the world, including in Canada
  • in paratenic hosts, parasite remains as larvae in tissues & does not complete its dev to adults in GI system
  • in Canada, it is most common helminth parasite of Fe
  • prevalence in healthy, owned, adult cats is much lower
24
Q

What is the life cycle of Toxocara cati?

A
  • life cycle is believed to be similar to that of Toxocara canis in Ca (w/ a few exceptions)
  • Adults are located in sm intestine of Fe
  • eggs leave host in feces
  • infective L3 devs in each egg after 2-4 wks in ideal enviro conditions
  • dev rate is temp dep
  • after ingestion of infective L3 w/in egg, larvae undergo hepatotracheal migration & dev into adults in intestine of younger cats (PPP of 8 wks)
  • in lactating female cats, larvae that have dev’d from eggs ingested during late gestation reach mammary gland following somatic migration (GI tract to portal vessels to liver to heart to lungs to heart to mammary gland)
  • can be present in milk throughout lactation
  • transmammary transmission of larvae acquired by mother in late pregnancy/early lactation is primary rout of infection for young kittens (who can have patent infections by 6 wks of age)
  • prenatal infection w/ somatic larvae does not occur
  • b/c Fe feed on sm prey animals & usually bury their feces, infection is more commonly acquired by older kittens & adult Fe from paratenic hosts (vs from ingesting L3 in eggs from enviro)
  • these larvae undergo simple mucosal migration & PPP is 6 wks
25
Q

What is the epidemiology of Toxocara cati?

A
  • mjr route of transmission among kittens is ingestion of L3 in milk from mothers & in older Fe, through ingestion of L3 in tissues of paratenic hosts
  • like Toxocara canis in pups, it has a higher prevalence & intensity in kittens than in older Fe
  • parasite transmission through infective eggs in enviro is facilitated by eggs that are v resistant to adverse enviro conditions & can survive & remain infective for months or perhaps yrs (esp. in cool, damp conditions)
  • eggs are not immediately infective, but require several wks in enviro to become infective for Fe & paratenic hosts
  • eggs can be inactivated by strong phenol, cresol, or bleach solns, high temps, desiccation, & freezing @ -20 C or below for wks to m (eggs may be more freeze tolerant than those of Toxocara canis)
  • eggs are not inactivated by most common disinfectants, nor by fixation in formalin or ethanol
  • use of litter boxes & frequent burying of feces by Fe probably helps to reduce transmission
26
Q

What is the pathology & clinical signs of Toxocara cati?

A
  • in young kittens, esp those infected from milk, migrating larvae in lungs may be associated w/ resp signs
  • in untreated kittens, adult parasites in GI system can be associated w/ suboptimal growth & dev, poor coats, poor body condition (“pot-belly”), & diarrhea, as well as possible “seizures” & death (rare)
  • pathogenesis of these clinical signs is not fully understood
  • in older Fe, neither adult parasites nor migrating larvae are commonly associated w/ clinical abnormalities
27
Q

How is Toxocara cati diagnosed?

A
  • fecal float, coproAg, coproPCR
  • lrg adult worms in vomit or stool
28
Q

What is the public health significance of Toxocara cati?

A
  • v rarely, has been associated w/ visceral & possibly ocular larval migrans in people
  • as w/ Toxocara canis, human infection from ingestion of infective eggs from enviro, or possibly from ingestion of L3 in a paratenic host (including domestic livestock)
  • probably more common in people than is any clinical disease associated w/ parasite
29
Q

What is the host range and geographic distribution of Baylisascaris procyonis?

A
  • natural DH is raccoon
  • parasite is present wherever raccoons are established in NA
  • in Canada, raccoons occur in S. halves of prairie provinces & Ontario, in Maritime provinces, in S. BC, & in Quebec adjacent to US border
  • has been found in surveys of raccoons in BC, MB, Ont, QB, NS, & PEI
  • Ca can, rarely, support patent infections of adults
  • wide range of mammals & Av, including Ca & people can serve as paratenic hosts
29
Q

What are the defining features of Balisascaris procyonis eggs?

A
  • ellipsoidal, w/ thick, rough, granular shell
  • closely resemble eggs of Toxocara canis, which are sub-spherical but larger & have a pitted shell similar to a golf ball
30
Q

What is the life cycle of Baylisascaris procyonis?

A
  • PPP is ~ 2 m, eggs take 2 wks to dev into L3 larvae in enviro
  • raccoon passes eggs in feces
  • in eggs, L1 -> L2 -> L3 -> back into raccoon via ingestion
  • OR into Canine DH (L3 -> hatches from eggs -> mucosal migration -> adults -> eggs in feces)
  • OR into mammal/ avian (including dogs) paratenic host (L3 -> hatches from eggs -> somatic (sometimes neural) migration) -> (sometimes consumed by Ca))
  • OR into human paratenic host (L3 -> hatch from eggs -> neural larva migrans)
31
Q

Prevalence of Baylisascaris procyonis?

A
  • v rare in Ca
  • highly variable infection rate in raccoons
32
Q

What are the 3 paths Baylisascaris can take in Ca?

A
  1. Paratenic host
    - v bad for this dog
    - larva migrans
    - dead end host
    - Dx: clinical signs, histo, serology
    - tx: nonspecific
  2. DH
    - intestinal infection
    - not bad for this dog
    - source of eggs in enviro
    - dx: single celled eggs in fresh feces
    - tx: as for other GI nematodes
  3. transport host
    - spurious infection
    - not bad for this Ca
    - spread of eggs in enviro
    - dx: larvated eggs in fresh feces
    - tx: none needed
33
Q

How should we control GI nematodes in Ca & Fe according to the CPEP guidelines?

A
  • administer anthelmintic treatment (macrocyclic lactones, pyrantel, benzimidazoles, emodepside, nitroscanate) @ 2, 4, 6, & 8 wks of age, followed by monthly treatments to age of 6 months (CAN START A BIT LATER FOR KITTENS)
  • can synchronize w/ vx (3x @ 2 wk intervals)
  • treat nursing females @ 2 wks post partum (may be patent due to ingestion of stages shed by pups, or reactivation of somatic larvae)
  • treat pregnant females off label
  • conduct fecal exams 2-4x during 1st yr of life & 1-2x per yr in adults
  • adults: treat only high risk pets, pets in high risk households, & those w/ positive fecal tests
34
Q

Which animals are considered high risk?

A
  1. high risk animals (young (< 6m); HIGHLY EXPOSED: DOG PARKS, OUTDOOR ACCESS, SCAVENGERS, HUNTERS, RAW FOOD DIETS, COPROPHAGIC; highly susceptible (immunocompromised, pregnant, nursing)
  2. animals in high risk households or occupations (YOPI (young, old, pregnant, immunocompromised), service animals)
  3. clinically ill animals

TEST HIGH RISK ANIMALS @ LEAST 2x/yr
TREAT HIGH RISK ANIMALS @ LEAST 3-4x/yr

35
Q

What are animal management methods of parasite prevention?

A
  • regular disposal of feces (before become infective)
  • compliance w/ pooper-scooper laws
  • feed pets cooked, canned, or dry pet food
  • prevent predatory & scavenging behaviour
  • spay females
36
Q

What are public health measures for parasite prevention?

A
  • hand washing
  • covering sandboxes
  • wearing gloves when gardening
  • wash or cook veggies for human consumption
  • cook meat thoroughly
37
Q

What is mucosal migration?

A

larvae will start in intestines -> move into mucosal lining of intestines to moult -> & repeat process to become adults

38
Q

what is the hepatotracheal migration?

A

starts from GI tract -> liver -> R heart -> lungs -> they will then be coughed up & swallowed returning to GI tract

39
Q

What is somatic migration?

A

same as hepatotracheal until lungs -> then larvae migrate around body instead of developing -> often they will end up in muscle, but can end up in other organs like eyes or brain

Parasitology (13 decks)

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