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_____________:Host in which sexual stages of a parasite develop
definitive host
___________: Host in which a parasite passes through part of its life cycle, associated with further development or differentiation with or without asexual reproduction
intermediate host
___________:Host which harbors parasite stages, usually infectious ones, which do not develop further nor multiply
paratenic host
___________:Atypical host in which a parasite can settle, develop and persist, but which does not play an epidemiological role
accidental host
__________:Act of establishment of a pathogen in a host, associated with host reactions and usually with proliferation of the pathogen
infection
____________:Time period between infection of a host by a parasite and first release of products of reproduction (e.g., eggs,…) in feces, urine, skin, body fluids,…
prepatency
___________:Time period after prepatency, during which parasite stages are detectable in feces, urine, body fluids,…
patency
__________:Time between infection and manifestation of disease symptoms/clinical signs
incubation time
__________:Temporarily interrupted (arrested) development of juvenile stages (3rd, 4th, 5th stage) of parasitic nematodes in infected hosts
hypobiosis
___________: Number of infected or diseased individuals at a defined point or period of time, related to a population and the number of individuals examined (expressed in %)
prevalence
____________:Capability of a host to provide suitable living conditions for a certain parasite species
susceptibility
___________:Genetically determined, innate antigen-independent defense mechanism of hosts against infections
resistance
_________________: Different degree of specialisation of a parasite to live within a specific host; host specificity of different parasite stages of the same parasite species can vary
host specificity
___________:Capacity of a parasite species to cause disease (yes or no); within a species the degree of pathogenicity may vary
pathogenicity
__________________: The relative ability of a pathogen to cause disease, corresponding to degree of pathogenicity
virulence
_________________: Parasite which can make use of favorable opportunities to infect and harm a host
opportunistic parasite
____________:Infectious disease, the agent of which are transmissible under natural conditions between vertebrate animals and humans
zoonosis
____________:Organisms which are native in a habitat or country (endemic)
autochtonous
___________: A parasite that infects only one host species in its life cycle (direct life cycle)
monoxeny
___________: Involvement of different types of hosts in the life cycle of a parasite (indirect life cycle)
heteroxeny
_________________: Parts of the parasite population, which are not treated to have a next generation of non- resistant parasites. This dilutes the population of resistant parasites and reduces anthelmintic resistance development.
parasite refugia
Are infection and disease the same thing?
No.
parasitic infection can lead to clinical disease but not all animals that are infected with parasites show signs of disease.
True or False: clinical signs of parasitic diseases are often non-specific.
True
True or false: Nematodes are parasites of animals and plants and cannot be free-living (ex: in soil).
False: they are parasites of animals and plants but can also be free-living in certain species.
Describe the morphology of nematodes.
elongated, spindle or thread-like bodies that are unsegmented and bilaterally symmetrical. They range from millimeters to meters in size.
Describe the general development of most nematodes.
Nematode reproduction is sexual. Eggs contain undifferentiated embryo cells called the morula which will embryonate into a first stage larvae (L1) and hatch out of the egg. The larvae develops through stages until they are a pre-adult (L5) and then become an adult of either male or female sex.
True or False: Female nematodes can be oviparous, ovoviviparous, or viviparous (depends on species)
True
The development of nematodes to the next stage occurs through _________________.
moulting (shedding of the cuticle)
Nematode life cycles can be _______(monoxenic, without intermediate host) or _______ (heteroxenic, with intermediate host(s)) and can contain
paratenic hosts.
direct
indirect
What are five infection routes for nematodes in the definitive hosts?
oral uptake of eggs containing larvae
oral uptake of third stage larvae (form environment, lactogenic, intermediate host or paratenic host)
cutaneous invasion of larvae
injection of larvae through blood sucking arthropods
prenatal/transplacental
Describe the general direct life cycle of nematodes.
eggs or L1 are excreted into the environment. They develop into the infectious L3 which is taken up by the definitive host. L3 develops into L5 to pre-dult stahe then to female and male adult stages.
describe the general indirect life cycle of nematodes.
Nonembryonic of L1 eggs/larvae are excreted. They develop into L2 to L3 in an intermediate host. Excreted L3 infectious larvae are taken up by the definitive host, develop into L4 to L5 pre adults and then finally into male and female adults.
What is toxocara canis commonly known as?
dog roundworm
What are the hosts and localizations of toxocara canis?
dogs and wild canids localized in the small intestine (very important in puppies)
Describe the morphology of toxocara canis?
several inches long yellow-white to pale pink worms with a mouth divided into 3 lips and also has cervical alae.
Describe the general life cycle of toxocara canis?
Direct life cycle where millions of eggs are passed with the feces. Infective third stage larvae (L3) develop inside the eggs in 2-4 weeks. Paratenic hosts like rodents and rabbits, birds and earthworms are possible.
NOTE: ingestions of eggs before L3 does not lead to infection
What are five infection routes for toxocara canis?
ingestion of eggs containing L3
prenatal/transplacental infection (most important route)
infection of the bitch (pre and post partum)
infection after ingestion of paratenic host
transmammary/lactogenic infection
What are the two routes toxocara canis can take if ingestion of eggs containing L3 occurs? What is most common for puppies? Adults?
Tracheal migration: larvae penetrate gut, migrate to liver then lugs via bloodstream. Coughed up and swallowed. In the small intestine the larvae mature into adults (prepatency 32-60 days. Most common migration route in puppies.
Somatic migration: larvae penetrate gut and enter blood circulation where they are transported to the lungs, migrate through lungs, re-enter blood circulation and carried to various organs where they encyst into hypobiotic stages (most common route in adult dogs)
Describe the prenatal/transplacental infection pathway for toxocara canis? How long is the prepatency period?
In the mothers, hypobiotic larvae are reactivated around day 42 of gestation. Larvae migrate from mother via placenta to liver of fetus. After birth, tracheal migration occurs.
Prepatency in prenatally infected puppies is 21 days
What are the two ways that infection of the bitch (pre and post partum) can develop into adult toxocara canis?
a) b) During gestation hypobiotic stages reactivate and undergo tracheal migration
b)Ingestion of L4 and preadult stages (excreted by puppies) while grooming and cleaning puppies → develop to adults in mother
How does infection of toxocara canis work after ingestion of paratenic hosts?
• Paratenic host ingests eggs containing L3 → somatic migration, encystation in tissue
• After ingestion of paratenic hosts L3 migrate into dog’s intestinal mucosa and re-enter the intestinal lumen to mature (mucosal migration)
When does transmammary/lactogenic infection of toxocara canis occur?
Lactogenic transmission of larvae (somatic migration to mammary glands) is only possible after forst infection of the bitch during the last 2-3 weeks of pregnancy or after first infection during the beginning of lactation.
What is the general prepatent period in toxocara canis?
2-4 weeks depending on the infection route.
Describe the occurence and epidemiology of toxocara canis?
worldwide with a very high prevalence in adult dogs and foxes. Eggs are extremely resistant in the environment. Can carry hypobiotic stages for years and reactivate each litter.
What is the most important transmission route for toxocara canis?
from the infected bitch to her puppies
How does toxocara canis cause issues?
migrating larvae cause damage in the organs
toxic metabolic products released by intestinal stages damage the intestine and can have systemic effects
rarely: intestinal obstruction/perforation
What are the clinical signs of toxocara canis in adults? Puppies?
Adults: usually subclinical
Puppies: chronic ill-thrift syndrome (pot-belly with intermittent diarrhea or constipation and vomiting), poor weight gain, shaggy, lethargy, anemia, emaciation, nasal discharge (during migration to lungs), swollen joints. Rare cases can be life threatening and cause still births or neonatal deaths.
How can toxocara canis be diagnosed?
egg detection from fecal flotation
passed adult specimens in vomit or feces
post-mortem necropsy
history and clinical signs in prepatent period
What do the eggs of toxocara canis look like?
ellipsoidal to round, brown, thick shell wall with a single dark cell (when fresh— older may have morula). Surface resembles a golfball with a pitted shell wall surface
Describe the preventative control program for toxocara canis.
treat puppies and dam every other week starting two weeks after birth until 2 weeks after weaning
treat puppies monthly form 12 weeks to 6 months of age and do periodic fecal exams 2-4 times in first year of life
in adults, fecal exams 4x year and treat if needed.
treat pregnant dogs 2 weeks before birth to prevent prenatal and lactogenic transmission
What are three reasons preventative measures for toxocara canis are so important?
1.We want healthy animals: kill parasites and cure animals of disease
2. Prevent infection of other animals or spread of the parasite
3. Prevent human infections
Describe the zoonotic importance of toxocara canis.
Toxocara canis is the causative agent of ‘larva migrans interna’ and ‘larva migrans visceralis’ in humans. Humans may get infected through ingestion of eggs shed in the environment (main route) or through ingestion of raw or under-cooked meat or raw vegetables. In humans, larvae will undergo somatic migration and migrate to various organs. Exposure to a high number of infective eggs causes flu-like symptoms, but usually resolves without treatment. The long term consequences of larval migration in the central nervous system are still unknown. Exposure to a low number of eggs often leads to infection of the eye (ocular larva migrans). Larvae migrate beneath the retina and cause damage to the eye. One to 2 million people get infected each year in the USA. Children are the population at greatest risk of infection but infection in adults can also occur.