Dog and Cat GI nematodes- Hookworms and Whipworms Flashcards
Hookworms
Superfamily strongyloidea
Genus: ancyclostoma
Hookworm- general characteristics
1-3 cm long (quite short)
tend to be more pathogenic than ascarids
Stout, short worms with a hooked head
Prediliction for SI
Direct, but complicated life cycle
L3 is infective
Cause severe anemia
Ancyclostoma species
A. Caninum- dog
A. braziliense- dog and cat
A. tubaeforme- cat
A. duodenale- humans
A. Caninum life cycle
Adult in SI–> eggs produced and passed in feces–> L1, L2–> L3 sheathed in L2 cuticle (can go from L1-L3 in 5 days if optimal conditions).
L3 can be ingested and go directly to SI or through the buccal mucosa to the lungs. Can also penetrate cutaneously.
If direct to SI, no migration to lung
If through buccal mucosa or percutaneous–> migration to lung.
In immune older animals, L3 from the lung will arrest in tissues. If not immune/older L3 can go to L4 in bronchi/trachea–> coughed and swallowed to SI–> adult in SI.
A. Caninum and ALD
Larva that migrate via the lungs can arrest as L3 in skeletal muscle.
Routes of infection in A. caninum
No transplacental infection
Transmamary infection is important- very important in pups. Worms are voracious blood feeders. Bitch can infect 3 consectuvie litters as re-activating L3 can produce a patent infection in the bitch.
Percutaneous route (skin of footpads or via buccal mucosa)
Oral route
Pathogenesis of A. caninum
Hookworm disease is a simple hemorrhage. Immature and adult worms feed with each female worm consuming ~40 microliters of blood per day. Worms change feeding sites up to 6 times daily. Vacated feeding site still leaks blood.
Hookworm head is buried in the mucosa and actively ingests blood and other tissues. Worms produce lytic factor, anti-coagulants and various proteases that degrade hemoglobin.
Clinical Signs of A. Caninum infection
Young animals: acute hemorrhagic anemia if acquired a large number of worms via transmammary infection
Older animals: chronic hemorrhagic anemia
Multiple infections: hypersensitivity to hookworms penetrating skin
Epidemiology of A. caninum
Minimum temperature of 15 degrees to go from L1-L3 (therefore more often seen in warmer climates)
Age and acquired immunity result in less severe and less common disease in older animals
2 sources of infection: transmammary and percutaenous/oral from environment
NB: parasites live well in grass, not on concrete.
Diagnosis of A. caninum
Clinical signs, history, fecal egg count (pathogenic in PPP because L4 and adults suck so much blood), typical strongyle egg (oval egg with ball of cells)
Control of A. caninum
Chemotherapy: benzimidazoles, ivermectin/moxidectin (evidence for pyrantel resistance)
High dose fenbendazole in pregnant bitch
Clean dry bedding, earth or grass runs suitable for survival of L3
Ancylostoma Excretory-Secretory (ES) products
Worms secrete anti-coagulants and proteases (break down Hb in host specific manner)
Vaccination against hookworms
Use antigens isolated from membrane of hookworm gut. Successful with hemonchus and ticks. Generates an AB response, ingest AB when blood feeding–> inhibits enzymes and hookworms can’t feed properly.
Hookworms feed on blood containing antibodies to the gut antigens. Antibodies bind to the surface of the gut and inhibit enzyme activity.
How does the vaccine work? AB binds to microvillar surface. Inhibitis digestion of blood, worms “starve” i.e. are less fecund, shorter and reduce anemia to the animal.
Zoonosis with A. caninum
Eosinophilic enteritis–> inflammation of intestines
nb: eosinophils often associated with helmintic infection
A. brasilense infection
affectes cats and dogs, much less pathogenic parasites (non-blood sucking), cause protein losing enteropathy
Causes cutaenous larva migrans in man, which dies out eventually (not v. pathogenic)
Uncinaria stenocephala (Northern hookworm)
Affects foxes and dogs
Found in colder climates
Infective L3 but only ORAL route of infection (no percutaenous, no transmammary)
Uncinaria stenocephala life cycle
Very simple:
Adult in SI–> produces eggs–> L1–>L2–> sheathed L3 ingested–> direct to SI–> L3-L4-adult
NB: temperature optimum is 20 degrees c
Egg–>L3 in 96 hours
Uncinaria stenocephala pathology
Not a voracious blood sucker, but rather causes protein-losing enteropathy.
Skin infection is abortive, i.e. L3 can penetrate skin, but the larvae die there.
Can reuslt in a hypersensitivity response upon re-exposure to the parasite.
Pedal dermatitis–> inflammatory response, particularly where worms have tried to penetrate
Diagnosis of uncinaria stenocephala
eggs in feces, similar to ancyclostoma, but slightly larger (70-80 microns cf. 60 microns)
Differential diagnosis requires larval cultures.
DDX of ancylostoma vs. uncinaria
Eggs look similar except uncinaria egg SLIGHTLY bigger
Adults can be distinguished based on head morphology
form follows function: ancylostoma has teeth (blood suckers) and uncinaria has cutting plates.
Trichuroidea
Trichuris species (whipworms)
Live in LARGE INTESTINE of animals, head often buries itself in mucosa.
Long thin end= head
Thicker end=tail
T. vulpis in dogs, T. suis in pigs, T. trichuria in man
Lifecycle of trichuris species
Adults in Large intestine–> eggs passed in feces. L1 is the infective form. L1 develops in egg (really resistant d/t thick eggshell)–> L1 ingested–> eggshell plugs digested and L1 is released. L1 penetrates the mucosal glands–> L2, L3, L4–> immature adults emerge.
PPP ~6-12 weeks
Trichuris vulpis pathology
usually asymptomatic, occasionally get diphtheritic enteritis–> inflammation of LI where top layer of epithelial cells slough off resulting in watery diarrhea (+/- blood)
Trichuris diagnosis
trichuris egg is very characteristic- egg with bipolar plugs (70-80 microns)
