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146 Cards in this Set
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In humans, Toxocara canis cannot reproduce, and larval migrans can cause blindness and other problems. Humans in this case are an example of what kind of host? |
Aberrant host |
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What is the difference between definitive, intermediate, and paratenic hosts? |
definitive= sexual stages of parasite intermediate= some development, but parasite does not reach sexual maturity paratenic = transport. no development occurs |
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Parasites can be monoxenous or heteroxenous. What's the difference? |
monoxenous = no intermediate host. fleas, some ticks, lice, trichomonads, giardia, coccidia heteroxenous= requires intermediate host to compete life cycle |
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If man is the definitive host, what type of host are the other animals indicated? |
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What is the difference between an aberrant host and a dead-end host? |
Aberrant hosts did not co-evolve with the parasite and typically show clinical disease due to host's strong inflammatory response. They are "accidental". Dead-end hosts typically don't cause as much pathology in the host, but the worm isn't able to complete it's lifecycle because of other factors (ex: man is dead-end host for Trichinella because human has to be eaten for worm to continue lifecycle) |
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What is "A state of resistance to infection which is established after an acute infection has become chronic and which lasts while the organism is present" What's an example of this? |
Premunition Trichostrongyles |
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You deworm a herd of sheep and then a week later notice that previously healthy sheep have developed clinical presentation consistent with an acute parasitic infection. What happened? |
Sheep had premunition, and when you dewormed them they lost their state of resistance and became susceptible to acute infection again. |
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What does it mean if a species is dioceious? |
They have two separate sexes (M and F). They are not hermaphroditic |
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If you are looking at adult worms under the microscope, which sex will you look at for species identification? Why? |
Males have a caudal copulatory bursa which is easier to identify and use for species differentiation. |
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The _______ is an external protective covering of nematodes that has to ________ several times as the animal grows (between each larval stage) |
The _cuticle_ is an external protective covering of nematodes that has to _molt_ several times as the animal grows. |
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Pathogenicity of adult nematodes is often related to this aspect of nematode morphology. |
Buccal cavity/mouth size. Larger mouth size typically indicates that the worm feeds on mucosa, which is more damaging to the host (anemia). Bonus point: What is the term for nematodes that feed on mucosa? |
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What larval stage is typically the infective stage for vertebrates? |
L3 |
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Adult nematodes can shed several kinds of eggs. What are the 3 types? What's the difference? |
Unembryonated: no development has occured yet Embryonating: partial development Embryonated: fully developed larvae, still within egg (ready to hatch) |
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Oxyuris equi common name? host? where do adults live? what stage are eggs when shed? prepatency? |
pinworms host= horses adults live in lower intestine eggs are unembryonated, but embryonate very quickly (4-5 days) prepatency= around 5 months |
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Describe the lifecycle of oxyuris species |
unembryonated eggs in environment develop into L3s within the egg. L3 in egg is ingested, hatches in duodenum, develops in SI, then adult moves to LI where it reproduces. females migrate to perianal region to lay eggs |
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What is the infective stage of oxyuris species? |
the egg is eaten from the environment and then hatches in the duodenum |
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Oxyuris equi pathogenesis? |
adults may cause inflammation and damage to mucosa in small intestine. adults crawl to perianal region to deposit eggs, which causes itching, rectal irritation, and tail rubbing. |
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Oxyuris equi treatment? |
Ivermectin or pyrantel Resistance to ivermectin is being reported! |
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Why do we especially want to avoid parasite infections in research animals (besides for the health of the animal)? |
non-protocol induced variation in research experiments= nematode infections can have unforeseen effects on research. |
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Within the order Rhabditida, what is the important genus to veterinary medicine? |
Strongyloides (don't confuse these with 'true' strongyles!) |
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Many Rhabditids are facultative parasites. What does this mean? |
They do not have to live within a host. They are "opportunistic" parasites. Rhabditids are free-living soil-dwelling nematodes that feed on bacteria |
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Most Rhabditid species have a narrow host range. What does this mean? |
They are fairly host-specific. Example: Strongyloides westeri will only infect horses, won't be able to infect other species. |
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Strongyloides can develop into two different kinds of L3 larvae. What is the morphological difference? |
Filariform larvae: have a larger buccal cavity and are capable of directly penetrating the skin to infect the host. Rhabdiform larvae: have a rhabdiform esophagus and feed on bacteria in the soil. free-living and non-pathogenic |
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How is the lifecycle of Strongyloides stercoralis different from other Strongyloides? What is the host species? |
Infects dogs can only go through one free-living life cycle, then has to infect a host. can directly penetrate into GI tract (skips tracheal migration) autoinfection |
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Draw Strongyloides life cycle |
Make sure you included: adult forms egs L1, L2, and L3 free-living and parasitic forms autoinfection |
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How do infective L3 filariform larvae infect the host? |
penetrate skin enter bloodstream migrate to lungs, break into alveoli, coughed up and swallowed (tracheal migration) colonize gut |
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How is the lifecycle of Strongyloides westeri different from the normal Strongyloides lifecycle? |
Strongyloides westeri infections in adults DO NOT result in adults shedding eggs or larvae. Larvae undergo transmammary migration into foals. Only foals shed eggs |
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Strongyloides stercoralis in dogs can burrow into the skin and migrate straight to the gut. What step are they skipping that other stronyloides have to go through? |
Tracheal migration |
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Strongyloides stercoralis is capable of autoinfection. What does this mean? |
eggs hatch and molt twice in intestine (instead of being shed as L1 larvae, develop into filariform larvae within intestine) L3 filariform larvae in large intestine penetrate intestinal mucosa or perianal skin, enter the bloodstream, and follow typical lifecycle. typically results in more clinical disease |
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Strongyloides species are capable of two different forms of reproduction. What are they and where do they occur? |
Sexual reproduction in free-living life-cycle Hermaphroditic females in parasitic life-cycle |
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Strongyloides species usually infect the host by burrowing through the skin. What is the other way they can be infective, and what is a common example of this? |
Strongyloides larvae can be directly ingested. Transmammary route is major route of infection for puppies in kennels as well as for horse foals (larvae travel in mother's milk) |
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There are three stages of pathology in Strongyloides infections. What are they? |
Invasive= dermal itching and secondary bacterial infections. Transient phase Pulmonary= coughing, pain, bloody mucus and larvae sometimes coughed up. Bronchiole pneumonia. Transient phase Intestinal= often asymptomatic. |
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How are Strongyloides infections diagnosed? Why are fresh stool samples particularly important? How are they treated? |
Identify embryonated eggs, rhabdiform or filariform larvae in stool. Very important to get fresh stool samples because larvae are often indistinguishable from free-living Rhabditis species Ivermectin is very effective |
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There are 3 important families within the order Strongylida. What are they? |
Trichostrongyloidea (hair worms) Strongyloidea (true strongyles) Ancylostomatidae (hookworms) |
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Trichostrongyles (hairworms) have 4 important genuses. What are they? |
Trichostrongylus Ostertagia/Teladosargia Nematodirus Haemonchus |
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many Trichostrongyles go into a dormant stage to escape stressful environmental conditions. What is this called? |
hypobiosis |
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What stage of Trichostronyle life-cycle goes into hypobiosis? Where do they live during this time? |
L3 goes into hypobiosis, L4 emerges within the wall of the abomasum |
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What is the trigger for Trichostrongyle larvae entering hypobiosis? For leaving? |
L3 larvae sense shortening days and colder temperatures, initiate hypobiosis. L3 develops into L4 and encysts within the wall of the abomasum. There is no specific trigger for exiting hypobiosis. Worms basically start a timer at the beginning and when it beeps they come out! |
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Draw the basic lifecycle for the Trichostrongyles |
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Do Trichostrongyles have a direct or indirect lifecycle? How many different types of host do they have? What stage is infective? Diagnostic? |
Direct lifecycle (no intermediate host) Only have a definitive host L3 is infective, unembryonated/embryonating eggs are diagnostic (laid as unembryonated, embryonate quickly) |
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what is the phenomenon known as 'spring rise' |
sudden rapid rise in fecal eggs per gram in the spring as larvae come out of hypobiosis, mature, and shed eggs |
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Describe the timing of Haemonchus life-cycle (how long in each stage) |
Egg to L3: 3-6 days prepatency (infection to adult): 2-3 weeks (short) larvae in pasture: can survive up to 6 months (long time) L4: can enter hypobiosis in winter |
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What is the pathogenicity of haemonchus? |
adult worm has small dorsal lancet in buccal cavity for blood-letting= causes anemia anemia leads to hypoproteinemia and edema (bottle jaw). May lead to lethargy, weight loss, and death |
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What is the common name for haemonchus? Why is it called that? |
Barber pole worm white gonads twisted around red blood-containing gut |
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Where do most Trichostrongyle adults live within the host? |
abomasum |
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What is the classical clinical presentation with Haemonchus? What species do we usually see this in? (hint: this is something evident from just looking at the animal) |
Bottle jaw (from edema) sheep and goats (some in cattle) |
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What is the most important strongyle of cattle? What is the common name for these worms? |
Ostertagia (genus) ostertagia (species) 'brown stomach worms' |
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What is the pathogenesis of Ostertagia in cattle? |
L3 larvae encyst in abomasal wall as they develop into L4 larvae. Cysts alter nutrient and ion absorption, leading to GI problems |
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What is the classic change in the GI tract seen with ostertagia? |
encysted larvae give the abomasum the appearance of 'Moroccan leather' |
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disease cause by Ostertagia is divided into two types. What are they? |
Type 1: naive calves and young cattle infected with L3 larvae in autumn and winter after weaning. pathogenesis from normal larval life cycle Type 2: hypobiotic larvae emerge, triggered by hormonal changes during pregnancy. pathogenesis from sudden emergence of all L4 larvae at once. typically in autumn/winter. |
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What genus within Trichostrongyloidea is characterized by its very small size (<7mm), lack of specialization around the mouth, and short massive spicules on posterior end? |
Trichostrongylus |
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What species are Trichostrongylus (the genus within Trichostrongyloidea) typically found in? |
sheep and cattle (less frequently in horses and pigs) |
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What genus is identified by it's huge egg? What is the most pathogenic species within this genus? |
Nematodirus (within the family trichostrongyloidea, order strongylida) N. battus is the species we see the most problems with. |
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Describe the life cycle of Nematodirus |
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Nematodirus has evolved an 'alternate hypobiosis'. What is this strategy? |
The development of the larvae (egg -> L1 -> L2 -> L3) takes place within the egg shell. This stage is slow (2mo) but protects the developing larvae from desiccation and cold. Hatching requires a prolonged period of chill L4 can also undergo traditional hypobiosis |
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Describe the pathologenesis of Nematodirus |
L3 is infective, and encysts in the abomasal wall, causing diarrhea followed rapidly by dehydration. adult larvae do not typically cause clinical signs |
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Why are trichostrongyles a disease of young animals? |
adults develop premunition |
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Resistance: clinically normal, with _____ number of worms Resiliance: clinically normal, with _____ number of worms |
Resistance: clinically normal, with _LOW_ number of worms Resiliance: clinically normal, with _HIGH_ number of worms |
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How are trichostronyle infections treated? |
benzimidazoles ('white wormers') imidazothiazoles mactrocyclic lactones (such as ivermectin) |
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What is the clinical definition of resistance? What is the technical definition of resistance? |
clinical: when normal therapueutic dose is no longer fully effective technical: when medication results in less than a 95% reduction in fecal egg count |
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Which occurs first: genotypic resistance or treatment resistance? |
genotypic resistance. This means that drug resistance starts developing long before it can be detected clinically |
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What causes resistance to anthelmintics? (list 5) |
1. frequent treatments (3X/yr) 2. treating and moving to clean pasture 3. under dosing 4. treating when few larvae are on pasture 5. treating all animals at the same time |
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what is the most important factor in preventing drug resistance selection in a population? |
Refugia |
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Typical distribution of parasites within a population follows what type of distribution? What does this mean? |
negative binomial Most animals have few parasites, a few animals have much heavier burdens (and are therefore responsible for most egg shedding) |
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How is the FAMACHA system used? What parasite is it particularly useful for? |
identify most anaemic animals to selectively treat (protect refugia). particularly useful for Haemonchus infections |
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Horse strongyles, or 'large strongyles' are part of what family and order? |
order Strongylida, family strongylidae, genus strongylus |
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Which large strongyle species has historically caused the most clinical disease? |
Strongylus vulgaris |
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Describe/draw the lifecycle of Strongylus vulgaris |
L3 infective stage eaten, get to small intestine. L3s penetrate intestinal mucosa and molt into L4s. L4s: extraintestinal migration to cranial mesenteric artery. Stay in artery until molt into L5s (immature adults). L5s migrate back to cecum and colon, encyst in mucosal wall. Rupture of nodules releases adults, which shed eggs in feces (egg -> L1 -> L2 -> L3 in environment) |
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Describe a timeline for Strongylus vulgaris infection |
very long prepatency period (5-7months) L3 ingested (day 0) L3 to L4 in intestinal mucosa= 7 days L4 penetrates endothelium, migrates to cranial mesenteric artery by day 21 (another 14 days) L4s spend 3-4 months in vasculature before molting to L5 L5s form nodules in the wall of the colon/cecum, then break out as adults. Adults mature in lumen of intestine for another 4 to 8 weeks |
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What lifestage(s) of Strongylus vulgaris are pathogenic? Describe how |
larvae (L3, L4 and L5): vascular damage, particularly to intestine, legs, and aorta. aneurysms, verminous arteritis, disruption of intestinal blood flow. adult: direct intestinal damage, anemia (adults are plug feeders) |
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How are large strongyle infections diagnosed and treated? |
diagnosed by ID of eggs and larvae in feces treat with ivermectin (very effective) |
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What type of Strongylida infection typically results in hepatitis and peritonitis? Name the specific species. |
Strongylus edentatus ingested L3s ---> gut wall to liver from liver migrate back to colon where they form nodules. mature in large intestine. prepatency period: very long, about 11 months |
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What is the most important internal parasite of horses? Why is this? |
small strongyles/cyathostomes ivermectin has made large strongyles less problematic |
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What is the genus name for the small strongyles (also known as redworms)? What is the difference between small and large strongyles? |
cyathostomes difference is the size of the buccal cavity. Large strongyles have well developed buccal capsules for feeding on mucosa. Small strongyles have much smaller mouths and do not attach to mucosa |
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What stage of cyathostome lifecycle causes the most damage to the host? |
the L4 larvae L3 larvae form nodules within the intestinal wall, where they go into hypobiosis during the winter. Then in the spring there is simultaneous emergence of L4 worms, which causes extensive damage to the intestinal wall. |
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Why are fecal egg counts not useful for the diagnosis of cyathostome infections for an individual? How can FEC still be useful for controlling cyathostome populations in a herd? |
Most clinical symptoms are caused by larvae, not egg-laying adults. Hypobiotic larvae can be over 90% of the total worm burden. Therefore an animal with a heavy burden of larvae may not have many adults. However, FEC can be useful to identify individuals shedding large numbers of eggs, to target treatment and prevent overall parasite load in a population |
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What clinical signs are seen with cyathostome infections? |
colic, weight loss, diarrhea, damage to colon mucosa, occasionally death |
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What is the developmental timeline for cyathostome larvae? How does this compare to large strongyles? |
cyathostome larvae can develop into adults in about 5 weeks. This is much faster than large strongyles (which take many months) |
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In general, are small strongyle eggs and larvae more susceptible in winter or summer. Why? How does this effect treatment strategies? |
Summer. Cold weather may slow development in the winter, but many eggs and larvae will survive. Desiccation in the summer is much more fatal, and fewer of these eggs will successfully reach L3 infective stage. Deworming during hot summer months is less critical because fewer eggs will survive to L3, but winter worming may be a good idea. |
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Fenbendazole (Panacur) is highly effective at killing encysted cyathostome L3 larvae, but it is not recommended excepts in cases of high egg burdens and clinical infections. Why? What should be used instead? |
Fenbendazole (Panacur) has resistance problems. Better to use ivermectin or moxidectin. These are less effective, but don't have resistance problems yet. |
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What is the scientific name for hookworms? |
ancylostomatoidea |
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Where in the body do hookworm adults live? |
small intestine |
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what is the characteristic morphology of hookworms? |
hooked dorsally anterior end has teeth or cutting plates well-developed bursa |
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What two genuses of hookworms infect dogs? |
Ancylostoma Uncinaria |
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Unicaria stenocephala has broad host specificity. What species does it infect? |
cats and dogs |
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Which hookworms of dogs can infect humans (zoonotic)? How do humans typically get infected? |
Ancylostoma caninum skin penetration from larvae on sandy beaches |
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Describe the lifecycle of Ancylostoma. What is the infective stage? prepatency? |
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What stage of hookworm development is most pathogenic to the host? How? |
adults large buccal cavity allows them to feed off of intestinal mucosa, leading to anemia |
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What are the 5 modes of transmission of A. caninum? |
skin oral transplacental transmammary paratenic hosts |
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Once Ancylostoma burrows through the host's skin, what path does it take? |
penetrate skin enter blood vessels travel to lungs -> trachea -> gut (tracheal migration) |
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Ancylostoma larvae can go into arrested development similar to hypobiosis. How is this process different from the hypobiosis seen in Trichostrongyles? How is it similar? |
Similar: L3 larvae encyst Different: stimulation to come out of arrested development for Ancylostoma is immune relaxation with pregnancy (larvae -> mammary glands). For Trichostrongyles there was not exit stimulus |
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In what species of nematode do you see larval "leaking" in adult dogs? |
Ancylostoma caninum larval leaking = persistent low level emergence of larvae in immune competent adults. |
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How is the cat hookworm Ancylostoma tubaeforme different from Ancylostoma caninus in terms of infection routes? |
No transmammary or transplacental Infection via paratenic hosts (mice) is more common |
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How do hookworms cause pathology? |
adult hookworms cause hemorrhage and severe anemia (also: weakness, poor growth, pale gums, black tarry stools, dull haircoat, emaciation, death). may see skin ulcers with heavy exposures |
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Which nematode infections show severe disease without the presence of large fecal egg counts? |
cyathostomes (small strongyles) in horses Ancylostoma caninis (hookworms) in dogs |
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How can you tell the difference betwen Ancylostoma caninis and Uncinaria stenocephala infections? |
look at eggs A. caninis eggs are slightly smaller (60 x 40mcm, vs. 75 X 45mcm for U. stenocephala) |
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A dog comes into your clinic in Portland with suspected hookworms. What species it is most likely to be? |
Uncinaria stenocephala Ancylostoma caninum is the most common canine hookworm in the country, but is predominately found in the SE |
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What problems do clinicians run into with treating hookworms? What should be used? |
many dewormers are only active in the gut, and are not effective against the arrested stage can use macrocylic lactones to get arrested stage |
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What kind of preventative care can be done in dogs to protect puppies from hookworms? |
pregnant bitches should be treated once during pregnancy and those with nursing litters at least twice |
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How is Uncinaria stenocephala morphologically different from Ancylostoma? How does this effect their pathogenesis? |
cutting plates instead of teeth infection is normally oral, not through skin penetration |
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The order Ascaridia is common known as what? |
roundworms |
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What are the four importent genuses within Ascaridia? |
Toxocara Taxascaris Parascaris Ascaris |
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How is the morphology of ascarids different from strongyles? |
much larger no teeth: have three lips at the anterior end no bursa on males |
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What is unique about ascarid eggs? How does this effect treatment? |
eggs have distinctive thick walls
practically indestructible (temp, dessication, chlorine, pH, UV, formalin, acids) sticky, tend to stick to surfaces (fur, hair) can last in the environment for years very hard to remove from environment |
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Describe general Ascarid lifecycle |
adults in SI eggs develop in soil (1 mo) eggs swallowed, hatch in SI tracheal migration, back to SI produce eggs in 40-65 days |
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What kind of pathogenesis is seen with Ascarid worms? What lifecycle stage causes the most problems to the host? |
larvae: migration larvae can get lost in other organs. Tracheal migration: damage lungs, hemorrhage, edema, clog air spaces, pneumonia, secondary infections adults: intestinal blockage, perforation, septicemia, malnutrition respiratory distress, pneumonia, poor growth, emaciation |
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What species of roundworms is seen in pigs? |
Ascaris suum |
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On necropsy, what classic pathology can be seen in pigs with Ascaris suum infections? |
milk spot lifer: chronic inflammatory changes associated with hypersensitivity reaction Lung lesions adults in intestine |
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How is Ascaris suum treated? |
warm soapy piggy bubble baths frequent treatment with ivermectin (also levamisole, fenbendazole, pyrantel tartarte) |
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What Ascaris species can infect humans? Which are zoonotic? |
Ascaris lumbricoides (human roundworm) Ascaris suum (from pigs, zoonotic) Toxocara canis (from dogs, zoonotic) Toxocara cati (from cats, zoonotic, but less commonly seen infecting people) |
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What ascaris species infects horses? What age is most susceptible? |
Parascaris equorum effects foals, older horses immune |
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What is the pathogenesis of Parascaris equorum? |
larvae: damage in lungs and liver adults: malnutrition, enlarged abdomen, dull coat, colic, impaction penetration of bowel: fatal peritonitis |
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Draw the lifecycle of Parascaris equorum |
eggs in feces larvae develop in eggs -> L2 eggs ingested, hatch in SI migrate to liver, molt to L3 tracheal migration -> SI adults |
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A farm deworms all its horses stabled together for Parascaris equorum at the same time. What happens to refugia? |
Eggs in the environment provide refugia because they last so long. |
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With horse ________ infections, it is recommended to remove all horse manure from the pasture. With horse _________ infections, it is recommended to spread the manure out over the pasture. Why? |
With Parascaris, pick up manure: eggs are indestructible. remove from environment With Strongyles, spread manure: larvae very sensitive to desiccation, will be killed easier. |
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Which ascarids infect dogs? cats? |
Toxacara cati Toxacara canis Toxascaris leonina (both, broad host specificity) |
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Draw the lifecycle of Toxacara canis |
adults in SI eggs in feces, embryonate in environment, ingested larvae in SI, tracheal migration, back to SI, produce eggs |
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How are T. canis infections different in puppies vs. adult females vs. adult males? |
puppies: infected transplacental or tranmammary, normal lifecycle adult females: infected by environmental eggs, paratenic host. larvae migrate out of intestine and encyst in tissue (arrested development), then come back out with pregnancy relaxation adult male: larvae encyst and are mostly "lost" |
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How are puppies infected with T. canis? |
transplacental larval migration into fetus, goes through tracheal migration and winds up in the lungs at birth, then completes migration to SI transmammary through milk puppies may also re-infect mom when she licks them. |
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How many host types does T. canis have? |
definitive host: dog paratenic host: rabbit/rodents aberrant host: humans |
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What happens to the T. canis lifecycle when it goes through a paratenic host? |
eggs ingested by paratenic host, hatch into L3 larvae start migration, encyst in tissues as L3 when paratenic host is eaten, larvae "reactivate". If the paratenic host is eaten by an adult dog, the larvae do not re-encyst, will continue to develop into adults |
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Which parasites form cutaneous larval migrans in humans? visceral larval migrans? |
cutaneous larval migrans: hookworms (A. caninum) visceral larval migrans: roundworms (T. canis) |
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T. canis infections can be lethal to entire litters of puppies. What is the pathogenesis? |
death due to rupture of intestines, develop secondary infections and septicemia |
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How common is T. canis in the United States? How can it be prevented? |
Very common (14% of people infected, up to 30% public parks positive for eggs) Treat with heartworm medicine (kills Toxocara larvae) |
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How is Toxascaris leonina different from Toxocara canis? How are they similar? |
Both Ascaris worms, both infect dogs T. leonina has broader host specifiicity similar lifecycle, but histiotrophic phage in gut wall, no extraintestinal migration (unlike T. canis) shorter prepatency (2 mo) less pathogenic not zoonotic |
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What worm is commonly found in vomitis? |
Toxocara cati |
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How does T. cati compare to T. canis? |
similar lifecycle infection via paratenic host more common transmammary and transplacental infection only occurs if queen was recently infected both zoonotic, but T. cati less common |
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What parasite is extremely common in raccoons, and extremely pathogenic in humans? |
Bayliscaris procyonis |
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In Bayliscaris procyonis infections, what kind of host are raccoons? dogs? humans? |
raccoons: normal definitive host dogs: aberrant host, but can support life cycle. Not clinical humans: accidental, dead end host. infections result in severe clinical signs |
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What kinds of symptoms are seen in humans with Baylisascaris procyonis infections? What stage of the pathogen causes these problems? |
neurological disease caused by larval migrans |
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What is the most important worm in each species: Swine Cattle Sheep Horses Dogs Cats |
Swine: Ascaris suum (roundworm) Cattle: Ostertagia ostertagia (trichostrongyle) Sheep: Haemonchus contortus and Nematodirus battus (both trichostrongyles) Horses: cyathostomes (small strongyles) Dogs: Ancylostoma caninum (hookworm) Cats: Toxacara cati (roundworm) |
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Which species is associated with the follow classic clinical presentation: Bottle jaw Moroccan leather Milk spot fever Cutaneous larval migran Visceral larval migran |
Bottle jaw: Haemonchus (trichostrongyle) Moroccan leather: Ostertagia ostertagia (trich) Milk spot liver: Ascaris suum (roundworm) Cutaneous LM: Ancylostoma caninum (K9 hook) Visceral LM: Toxacara canis (K9 round) and Baylisascaris pryocyonis |
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The egg is the infective stage for which worms? |
Oxyuris equi Roundworms (Ascarids) |
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Which worms are capable of infection by directly penetrating the skin? |
Strongyloides (westeri, stercoralis), Ancylostoma caninum (K9 hook), Ancylostoma tubaeforme (feline hook), Bunostomum phebotomum (cow hook) |
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Which worms are capable of entering arrested development or hypobiosis? |
Classical hypobiosis: all trichostrongyles cyathostomes (small strongyles) Ancylostoma caninum/tubaeforme (K9 and feline hooks) Roundworms |
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Which worms are capable of transmammary and transplacental transmission? |
Strongyloides (stercoralis and westeri) Ancylostoma caninum (K9 hook, no other hooks) Toxacara canis/cati (K9 and feline roundworms) |
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Which worms cause disease in foals, but do not tend to cause disease in adult horses? |
Strongyloides westeri Parascaris equorum (equine roundworm) |
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Both roundworms and hookworms have a species of worm that is capable of infecting both dogs and cats. What are these species? |
Roundworms: Toxascaris leonina Hookworms: Uncinaria stenocephala |
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Which worms are capable of tracheal migration? |
strongyloides roundworms (Ascarids) hookworms (Ancylostomatoidea) |
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Which worms do not undergo any extraintestinal migration (there's a tricky one here!) |
Trichostrongyles Oxyuris equi Toxascaris leonina Small strongyles (cyathostomes, go into hypobiosis in intestinal wall, but don't go to other organs) |
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In which worms may you see clinically severe disease in the absence of elevated fecal egg counts? |
Cyathostomes (small strongyles) Ancylostoma caninum (K9 hookworms) |
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What worms most likely to persist in the environment for a long time? |
Roundworms (ascarids, practically indestructible) Strongyloides (normal soil organism) |
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What worms can be transmitted by a paratenic host? |
Roundworms (of predators, T. canis, T. cati, Toxascaris leonina) and hookworms (of predators, A. caninum, A. tubaeformae, Uncinaria stenocephala) |
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Order these worms from shortest prepatent period to longest prepatency: Oxyuris equi Strongyloides Trichostrongyles Large Strongyles Hookworms Roundworms |
Strongyloides (1-3 weeks, but can be longer) Trichostrongyes (2-3 weeks) Hookworms (2-7 weeks) Roundworms (2-3 months) Oxyuris equi (5 months) Large Strongyles (6 to 11 months) |
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Which worms cause the most damage when they are in their adult stage of their lifecycle? |
Haemonchus (adult feeding causes anemia) Oxyuris equi (itching caused by females laying eggs) Hookworms (adults have those big teeth for chomping on mucosa) Roundworms (intestinal blockage) Large Strongyles may cause direct intestinal damage and anemia in adult stage. |
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Which worms cause the most damage when they are in the larval stage of their lifecycle? |
Small Strongyles (synchronus emergence of L4 larvae from hypobiosis) Large Strongyles (verminous arteritis during migration) Strongyloides (invasive stage and pulmonary stage) Osterstagia ostertagia (larvae cause Moroccan leather) Nematodirus (larvae feeding on gut wall) Roundworms (migrating larvae can get "lost" and wind up in abnormal organs. Tracheal migration can cause pneumonia) |
