Dog and Cat GI Nematodes- Toxocara spp. Flashcards
Nematodes of small animals
Superfamily Ascaridoidea Genus Toxocara
Species of Toxocara and their hosts
T. canis- host=dog/fox
T. cati- host=cat
(T. vitulorum)- host=cattle
Toxascaris leonina- host=dog/cat
T. canis- routes of infection
Direct life cycle with 4 possible routes of infection
- oral (direct)- L3 enclosed within the egg
- transplacental- most important route, very effective
- transmammary- back-up route to transplacental
- paratenic host- more important in t. cati d/t mouse/rodent as paretenic host
Outcome of T. canis infection
Outcome depends on the age of the animal.
if animal is younger than 3 months, adult worms develop in SI
If animal is older than 3-6 months, larvae tend to arrest in the tissues
T. canis infection in animals less than 3 months of age
Results in a patent infection- produces eggs.
Adults in the SI release eggs. Egg matures in environment and egg containing the L3 is ingested. L3 hatches in the SI and migrates via hepatotracheal migration (this extendsPPP and is also when we might see clinical signs in young animal). L3 goes to SI via trachea- in lungs, coughed and swallowed. L3 moults to L4 and L4 moults to adult in the small intestine. Adult in the SI releases eggs. Eggs are present as a source of infection in the environment for a very long time.
T. canis infection in older bitches- i.e. giving rise to transplacental infection
Bitch ingests L3, L3 hatches in the SI and L3 migrates into the tissue. In the tissues, it arrests and goes into a hypobiotic state. 3 weeks pre-partum, L3 re-acticates likely due to decreased immunity in the pregnant bitch, also some hormal influence. In the pup, the L3 migrates to the fetal lung. At birth, L3 goes to SI via trachea, L3-L4-adult in the SI.
PPP of T. canis
16 days to 21 days. Should be treating for worms at ~2 weeks of age.
T. canis: transplacental transmission
L3 reactivated 3 weeks pre-partum
Migrates to fetal lung. L3 travels to SI via trachea. Ensures 100% infection. Arrested larvae in tissues can’t be diagnosed.
T. canis: mammary transmission
L3 in the milk for up to 5 weeks
no migratory phase via this route of infection i.e. L3s go straight to the SI (not to the lungs)
T. canis- ALD and ALD+pregnancy
Arrested L3 is hypobiotic- resistant to commonly used anthelmintics. Survive fo the life of the bitch. Arrested L3 can re-activate (when immunocompromised).
ALD is a means of avoiding host IR in older animals.
In pregnant animals, when immunity is lower, L3s can become reactivated
Paratenic hosts of toxocara
L3 arrest in tissues of bird/rodent. No migration following infection of the dog.
Bird/rodent ingests eggs–> L3 arrest in tissues–> no development in paratenic host.
PPP = 3 weeks
paratenic hosts more important in T. cati
Important features of T. canis epidemiology
100% of pups infected via transplacental route.
Transmammary transmission for ~5 weeks
highest level of infection in pups less than 6 months old
GI infection in pup is temporary. Most worms expelled by 6-8 months old
Arrested L3 is very reisstant- 12-20% of adult dogs can be producing eggs in feces.
T. canis egg
Females produce 1000s of eggs/day
Unemvryonated egg is not infective, ~4 weeks to reach infectivity
eggs and are sticky and resistant- can stick to fingers or dogs’ coat etc.
Survive for ~14 months in 2% formalin
Ball of cells need to larvate and moult from L1–> L3- temperature dependent process
egg is the reservoir of infection in the environment
T. canis persistence in dog population
persists due to the variety of different routes of transmission. tissue migration gives rise to the transplacental and trans-mammary routes. Paratenic hosts can spread infection. resistance of eggs in environment.
Clinical signs of T. canis
- migratory phase: coughing, increased resp. rate, pneumonia in v. heavy infections
- enteral phase: pot-bellied pups, failure to thrive
T. canis in man- visceral larva migrans
Visceral larva migrans- liver, lungs, spleen. Migration of L3 through viscera. to see any symptoms, need to have ingested a LOT of eggs. More common in children. Clinical signs: few swollen LNs, sometimes asthma and infection just dies out naturally.
T. canis in man- ocular larva migrans
L3 encysts in eye- only takes a single worm.
Diagnosis of T. canis in humans
Antibody detected against T. canis larval ES antigens. This shows you’ve been exposured to this infection. Arrested L3 maintainted for months in vitro. Excrete large quantities of ES antigen.
Antigen is concentration and used in ELISA to detect antibodies.
Control of T. canis
Education, regular de-worming, safe disposal of dog feces, limit access of dogs to play areas, reduce stray dog numbers
Treatment of T. canis
Principle is to prevent environmental contamination. Minimum PPP is 16 days. Start treatment before parasite lays eggs, continue to remove milk- acquired infection; treat bitch at sam time.
Give high dose fenbendazole, 3 weeks pre-partum and 2 days post-partum— kills majority of reactivated L3. does NOT kill arrested larva because they’re hypobiotic. Only a proporition of worms can be reactivated during one pregnancy, therefore need to deworm during subsequent pregnancies.
T. cati routes of infection
No transplacental infection
Oral: hepatotracheal migration
Transmammary is the most important for kittens. No migration- less pathogenic in kittens than T. canis in puppies
Paratenic host
PPP ~ 8 weeks
Egg similar to t. canis
Often found with toxascaris leonina. Can tell apart based on arrowhead appearance of adult worm.
Toxascaris leonina
Affects cats and dogs
Direct tranmission or paratenic host transmission
NO transmammary and transplacental
Egg contains L3, paratenic hos carries L3
No migratory phase
Egg sheel is SMOOTH, not pitted like T. canis
PPP ~11 weeks.
Toxocara vitulorum
Life cycle similar to T. cati, found in exotic cattle and buffalo
Transmmary route is more important- L3 in milk for up to 1 month
No tissue migration in calf
Likely not zoonotic
PPP ~3-4 weeks
Eggs have a pitted but thinner shell than T. canis or T. cati
Ascarid general characteristics
typically large white worms (chunky and thick) with a direct life cycle. L3 in egg is infective (L3 develops inside the egg). Typically
