Parasites (1/3)

taxonomy, host, morphology/diagnostics, life cycle, location in host, transmission dynamics, clinical signs

Giardia duodenalis

Taxonomy: flagellated protozoan

Geographic distribution: worldwide

Location in host: small intestine

Giardia duodenalis

direct life cycle: organism divides into two trophozoites within the cyst, excystation occurs in the small intestine. attachment of the trophozoites to epithelium and division by binary fission. Encystment of trophozoites occurs as organisms travels down GI tract, cysts are passed with or without trophozoites

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Prepatent period: 5-16 days

Giardia duodenalis

Morphology: Trophozoites within the small intestine and then cysts once passed into the environment

Giardia duodenalis

Diagnostics: wet mounts of a fresh sample is only way to observe trophozoites

* cysts are passed intermittently, hard to diagnose
* Modified double centrifugal floatation
* Immunofluorescent assays
* ELISAs
* can use PCR or wet mounts
* sometimes pressure can cause an organism to move to one side

Giardia duodenalis

Prevalence: zoonotic risk is not completely gone, increased among dogs that visit dog parks and is commonly spread through animal populated areas (kennels, shelters, etc)

Giardia duodenalis

Transmission Dynamics: occurs through ingestion of cysts acquired from fecal contaminated water, food or fomites; through self grooming

* does not spread between species
* human cases are primarily spread between humans

Giardia duodenalis

Clinical signs:

* asymptomatic in some cases
* chronic, pasty diarrhea, weight loss
* lethargy, flatulence
* failure to thrive, impacts on growth
* dry skin, poor haircoat

Giardia duodenalis

Site of infection: small intestine

Pathogenesis: attachment of trophozoites to enterocytes in small intestine, functional changes and blunting of intestinal villi, maldigestion/malabsorption and diarrhea

Giardia duodenalis

Treatment: no drugs are approved for treatment, metronizadole is used but efficacy is low, Fenbendazole is approved in europe, DrontalPlus is effective in treatment

* refractory treatment - failures may result from reinfection, inadequate drug levels, immunosuppresion, drug resistance

Prevention: avoid contaminated water, utilize disinfectants, proper feces removal

Cystoisospora spp.

C. felis, C. rivolta, C. canis, C. ohioensis-like

Cystoisospora spp.

Taxonomy: ampicomplexan - known as coccidia

Geographic location: worldwide

Location in host: small intestine

Cystoisospora spp.

Life cycle: 21 day cycle.

Ingestion by host, enters GI cells and undergoes first asexual phase called merogany and produces merozoites (2-3 rounds).

Second phase is called gametogany where male and female form come together forming an oocyst and destroy prior cells, making their way out of the host.

Undergoes sporulation outside of the host and becomes infectious outside the host

Cystoisospora spp.

Morphology: sporulated oocysts are usually used to identify the various species, shape of them helps to identify

Cystoisospora spp.

Prevalence: infections are more likely in young animals, 3-38% of dogs in north america infected

Cystoisospora spp.

Transmission dynamics: Canine coccidia are acquired by ingestion of sporulated oocysts from contaminated environments, HIGHLY HOST SPECIFIC (not zoonotic), development of sporulated oocyts has to occur within a temperature range of 20-40 degrees celsius

Cystoisospora spp.

Environmental factors: sporulated oocysts are very resistant to adverse environmental conditions and can survive as long as one year in moist, protected environments

Cystoisospora spp.

Clinical signs: diarrhea with weight loss, dehydration, could be with hemorrhage as well

severe signs include: anorexia, vomiting, depression, can be fatal

Cystoisospora spp.

Treatment: Sulfadimethoxine is only approved drug, ponazuril appears to be effective

Cystoisospora spp.

Prevention/control: daily removal of feces through steam and pressure washing, paint and seal kennel floors properly

* once infective, oocysts are very resistant to disinfectants and survive in environment for months

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Taxonomy: Nematoda (hookworms)

Geographic distribution: worldwide

* Ancylostoma spp - tropics/warm temp regions
* Uncinaria spp. - more northern latitudes

Location in host: small intestine

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Morphology: reddish gray in color, size and hook like posture

* males 12mm, females 15-20 mm
* bursate nematodes
* buccal cavity has three marginal teeth

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Diagnostics: eggs can be seen on fecal flotation, both species look the same, look like a package of grapes inside

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Direct life cycle: infection through skin penetration or ingestion with or without paratenic host (mouse).

Definitive host:

* Eggs develop L1-L3 in environment
* L3 penetrates skin/ingested
* Migration to lungs or maturation in GI tract
* L3 arrest, reactivate and move to mammary glands
* L3-L4 in SI crypts
* Larvae enter SI lumen and become adults

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Partenic host life cycle:

* Egg develop in environment L1-L3
* Somatic migration L3 dissminates in the body and arrests
* Cat eats mouse, larvae released
* Larvae enter SI crypts L3-L4
* Larvae enter SI lumen L4-adults

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Clinical signs:

* acute or chronic anemia (in younger dogs)
* mostly impacts puppies that get it via transmammary transmission, causes severe anemia
* always infected mother dog,
* can see ezema and ulceration at site of penetration
* diarrhea +/- blood and mucus
* +/- respiratory signs
* underweight, poor hair coat, anorexia, +/- pica
* edema of SQ tissues and messenteries in severe cases
* cachexia with chronic infections

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Pathogenesis: dormant L3 can resume development in GI tract of dogs and mothers with stress following treatment, reinfection can occur years later

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Control/Prevention:

* can still disease due to transmammary transmission
* environmental contamination most common with moist environments
* sun can help to kill the larvae

Ancylostoma spp (Ancylostoma caninum) and Uncinaria spp.

Treatment: reinfection can occur often if not followed with proper husbandry, always deworm puppies

Ancylostoma braziliense

Public health: cutaneous larval migrans through filaform larvae

* ground itch or creeping eruption
* can be caused by Strogyloides species as well
* L3 penetrate unbroken skin and wander in dermis
* larvae do not develop, skin lesions persist as a result
* can become dormant in the muscle

Toxocara canis, cati

Taxonomy: Nematoda

Geographic Distribution: worldwide (tropics/warm temperate regions)

Location in host: small intestine, can also have larvae in liver and lung tissue

Toxascaris spp.

Taxonomy: Nematoda

Geographic Distribution: worldwide (tropics/warm temperate regions)

Location in host: small intestine

Toxocara canis, cati

Morphology: adult worms large and white, have a simple mouth opening surrounded by three large lips

* eggs are round with pitted yellow-brown outer shell

Toxocara cati

Life cycle: In paratenic host, arrested development and then ingestion by definitive host

* undergoes L1-L3 when eggs are passed, prepatent period of 2-3 months
* can either migrate to hepatic/pulmonary system or mammary glands if pregnant, passes via transmammary transmission
* Migrates to small intestine
* goes from L4-adult in the lumen of the small intestine, live 1-2 years

Toxocara canis

Life cycle: can be ingested by paratenic host where it undergoes arrested development - gets further ingested by definitive host

* undergo L1-L3 in egg, can take months to develop, prepatent period of 2-3 months
* can be consumed by puppy
* hepatic/pulmonary migration
* undergoes L3-L4 in the stomach
* undergoes L4-adult in the small intestine, live 1-2 years
* Consumed by adult
* somatic migration
* in pregnant bitch, migration to mammary glands
* transplacental migration to fetal liver → lungs → stomach → small intestine
* Unembryonated eggs passed in feces

Toxascaris leonina

Route of infection: does not migrate in liver and lungs similar to toxocara, prenatal and transplacental does not occur for this species either

Toxocara, Toxascaris spp.

Route of infection: peroral

Toxascaris spp.

Life cycle: paratenic host gets ingested by definitive host

* eggs undergo L1-L3
* ingested by host, no migration in tissues
* L3 molts to L4
* L4- adult in the lumen of the small intestine

Toxocara spp.

Transmission dynamics: eggs are very resistant to heat, cold, chemicals, desication and will live for years in environment

* small mammals are important paratenic hosts
* zoonotic disease (VISCERAL LARVAL MIGRANS)

Toxocara spp.

Clinical signs: mild to moderate infections

* adults in intestine cause potbelly, failure to thrive, diarrhea, entire worms may be passed in feces or vomited

Heavy infection

* pulmonary damage, focal hemorrhages in lungs
* increased respiratory rate
* fatality associated with pulmonary migration

Toxocara and Toxascaris spp.

Treatment: routine deworm beginning at 2 weeks of age until 4-8 weeks of age, placed on monthly product against ascarids

* new infections should be continuing monthly intestinal parasite control

Toxocara spp.

Public health: Visceral larval migrans

* juvenile nematodes gain entry to tissue, migration causes pathology
* can cause granulomas in the retina
* Diagnosis is done through ELISA, tissue biopsy of infected areas
* need to treat household pets and proper disposal of pet feces

Toxascaris leonina

Pathogenesis: no migration as seen with many other ascarids

* egg with 2nd stage larvae or paratenic host with L3 are ineffective
* pre-patent period is typically 10-11 weeks

Toxascaris leonina

Treatment: causes potbelly, diarrhea but not super pathogenic

* treat with benzimidazoles, piperazine and pyrantel

Trichuris spp. (Trichuris vulpis - K9, T. suis - swine, T. trichiura - humans)

Taxonomy: nematoda (whipworms)

Geographic distribution: worldwide

Location in host: large intestine

Trichuris spp.

Morphology: Adults are 4-6 cm

* eggs are lemon shaped with bipolar plugs, appear yellow to brown in feces and are passed unembryonated

Trichuris spp.

Life cycle: unembryonated eggs passed in feces

* ineffective L1 larvae develop within egg 1-2 months in environment, eggs require shade and appropriate temp/moisture
* digestion of eggs releases larvae
* L1 penetrates glands of cecal mucosa
* four molts occur in the glands, emerge as adults on the surface of mucosa with anterior ends embedded
* adult worms live in large intestine and live several years
* prepatent period 6-12 weeks

Trichuris spp.

Clinical signs: severe infections primarily in young animals

* most infections are light and asymptomatic
* diarrha, may be bloody and contain mucus
* dehydration, anima
* weight loss, growth impairement

Trichuris spp.

Pathogenesis: adult worms are more pathogenic than larvae

* worms feed on cell contents and blood, cause trauma to the intestinal epithelium and submucosa
* inflammation of cecal mucosa
* catarrhal enteritis with necrosis and hemorrhage

Tritrichomonas foetus

Host: cattle, other ruminants

Pathogenesis: disease and reproductive effects in herds

* chronic diarrhea or large bowel diarrhea

Whipworm

Dipylidium caninum

Taxonomy: Cestoda (tapeworm)

Geographic distribution: worldwide

Location in host: small intestine

Dipylidium caninum

Morphology: 25-30 eggs/packet, proglottids with bilateral pores that are cucumber seed-shaped. has two sets of reproductive organs and genital pore on each side

* armed rostellum and 4 suckers when adults

Dipylidium caninum

Diagnostics: fecal floatation or squash prep

Dipylidium caninum

Indirect life cycle: flea intermediate host or a louse

* gravid proglottids shed into environment by definitive host
* arthopod contains a cysticercoid
* when ingested, cysticercoid is liberated and attaches to distal half of intestine
* oncospheres hatch from eggs and penetrate intestinal wall of larvae, develop in body cavity into cysticercoid
* adult flea develops and harbors cysticercoid, getting ingested by definitive host

Dipylidium caninum

Prevalence: variable and depends on flea ingestion

Dipylidium caninum

Tranmission dynamics: pre-patent period is 2-3 weeks, proglottids persist in environment under certain conditions

Dipylidium caninum

Clinical signs: asymptomatic for the most part

Dipylidium caninum

Treatment/Prevention: Praziquantel and epsiprantel, heartworm preventatives and flea control

Dipylidium caninum

Public health: zoonotic!! spreads to humans through ingested fleas from cats or dogs

Taenia spp.

Taxonomy: Cestoda (tapeworms)

Geographic distribution: ubiquitous

Location in host: small intestine

Taenia spp.

Morphology: eggs contain embryo with six hooks, eggs are indistinguishable from Echinococcus, might have proglottids

Taenia spp.

Indirect life cycle: proglottids containing eggs are shed into the environment

* vertebrate intermediate host consumes tapeworm eggs, larval cysts develop
* larval (metacestode) cysts ingested by definitive host while scavenging
* cysticercus (small, bladder like)
* coenurus (large, bladder like)
* strobilocercus (developed form of cysticercus)

Taenia spp.

Clinical signs: rarely pathogenic, occurs within the small intestine

Taenia spp.

Treatment/prevention: want to break behavior of animal that is going out and eating things, prevent predation of small mammals. Treated with praziquantel or epsiprantel

Taenia spp.

Public health: zoonotic risk rare

* T. solium and T. saginata are zoonotic with undercooked pork
* Cysticercosis is where organs harbor cyticerci of T. solium, can be present in every organism

Sarcocystis spp.

Taxonomy: Protozoan (ampicomplexan), ectointestinal coccidia

Geographic distribution: worldwide

Location in host: small intestine

Sarcocystis spp.

Morphology: in definitive host oocysts sporulate and wall breaks down during passage in intestine, causes sporocysts to pass in feces

* sarcocysts seen in muscle tissue, long spindle shaped and can be seen grossly
* contains the slowly dividing form of parasite

Sarcocystis spp.

Lift cycle: heteroxenous life cycle where there is a herbivore intermediate host (reptiles, rodents, birds, hooved animals, chickens) that harbor tissue cysts

* carnivorous definitive host
* Sporocysts are ingested
* sporozoites are released into blood stream and undergo schizogony
* schizonts rupture, releasing merozoites that penetrate muscle cells and develop into cysts with bradyzoites

can be zoonotic if contaminated food ingested by humans

Spirocerca lupi

Taxonomy: Nematoda

Geographic distribution: tropical and subtropical regions

Location in host: digestive - esophagus, stomach

Spirocerca lupi

Morphology: adults are 3-8 cm and spirally coiled

* eggs have thick shells are larvated when passed in feces
* look like paper clips on fecal flotation, eggs may not be seen in fecal with adult infections where granulomas have no openings to the lumen of esophagus
* L3 are liberated upon ingestion, penetrate stomach wall and enter circulation, 3 months later they migrate to esophagus and induce granuloma formation in which they develop into adults

Spirocerca lupi

Indirect life cycle: dogs, fox, wild canids are definitive hosts with potentially cats, wild felids. beetles are intermediate hosts and rodents, birds, insectivores and repitles are paratenic hosts

Spirocerca lupi

Clinical signs: migrating larvae

* hemorrhage, scarring and fibrotic nodules in internal wall of aorta
* esophageal granulomas may be 4 cm
* dysphagia, vomiting, regional inflammation
* development of esophageal osteosarcoma in some cases
* spondylosis of thoracic vertebrae
* sometimes dogs have no signs with aortic lesions and esophageal granulomas

Spirocerca lupi

Treatment/prevention: treatment is rarely practical

Physaloptera spp.

Taxonomy: nematoda (“stomach worm”)

Geographic distribution: China, Africa, North and South america

Location in host: stomach

Physaloptera spp.

Morphology: adults are stout and resemble ascarids, eggs are larvated with a thick, clear shell

Physaloptera spp.

Indirect life cycle: Definitive hots are cats/wild felids, occasionally dogs. Intermediate hosts are beetles, cockroaches and crickets

Physaloptera spp.

Transmission dynamics/Prevalence: variable based on region and prevalence depends on intensity of intermediate hosts, most common in outdoor cats

Physaloptera spp.

Pathogenesis: adults have small teeth that leave small ulcers when attached to mucosa, bleed when parasites move to new sites

Physaloptera spp.

Clinical signs: catarrhal gastritis and emesis +/- blood in feces, may see inflammation in stomach with mucus, vomitng and anorexia in heavy infections

Strongyloides stercoralis

Taxonomy: nematode

Geographic distribution: worldwide

Location in host: small intestine

Strongyloides stercoralis

Diagnostics: Baermann to test for larvae and they leave the sample when surrounded by warm water. Can also diagnose with serodiagnosis by ELISA for antigens

Strongyloides stercoralis

Morphology: free living and parasitic phases of life cycle

* L1 is passed in feces (rhabditiform larvae)
* L3 are filaform larvae and are infectious, do not develop further until in definitive host
* homogonic and heterogonic cycles are dependent on ambient temperature, developmental switch occurs during L1 with whether or not they will remain in host or molt to become free living females

Strongyloides stercoralis

Direct life cycle: (autoinfection, kept in check by immune system)

* Rhabditiform larvae in large intestine become filariform larvae and penetrate intesinal mucosa, migrate randomly to other organs
* filariform larvae (L3) become adults and the adult female worm deposits eggs in intestinal mucosa, migrating to lumen after hatching
* they are excreted through feces (L1)

Indirect life cycle:

* rhabditiform larvae go into the environment and develop into free living adult female worms (L4)
* eggs are produced and fertilized with males and females
* rhabditiform larvae hatch from embryonated eggs, develop into infective filariform larvae that get ingested

Strongyloides stercoralis

Transmission dynamics: usually infected through contracting juveniles in contaminated soil or water

* transmammary infection can occur in dogs, may occur in people
* predominantly a tropical disease
* prevalent in conditions of poor sanitation

Strongyloides stercoralis

Pathogenesis: infection is often inapparent

* effects can be invasive, pulmonary or intestinal
* penetration of the skin
* damage to the lung tissue → pulmonary eosinophilic lung infiltrates
* worms may migrate randomly to the intestinal mucosa, can deposit eggs and repeatedly burrow/exit the epithelial layer
* destruction of tissues by adults and larval forms can result in sloughing of GI mucosa

Strongyloides stercoralis

Clinical signs: if skin is penetrated, can cause hemorrhage, swelling, pruritus, inflammation if bacteria further introduced

if pulmonary system: wheezing, burning sensation, non-productive cough

* lung phase may be mistaken for asthma

if GI system

* fibrosis in chronic cases
* septicemia
* intestinal ulceration

can be asymptomatic at first then develop later on to chronic case

Strongyloides stercoralis

Public health: can contribute to cutaneous larval migrans in humans

Dioctophyma renale

Taxonomy: nematoda (“kidney worm”), bursate

geographic distribution: various geographic regions

Location in host: urogenital system (kidney)

Dioctophyma renale

Morphology: very large nematode, blood red in color with blunt ends

* eggs are lemon shaped and are found in the urine, adults can be recovered in surgery

Dioctophyma renale

Indirect life cycle: unembryonated eggs are shed in the urine

* eggs embryonate in the water
* eggs ingested by intermediate host (earthworms)
* can be ingested by definitive host or ingested by paratenic hosts (fish/frogs)
* ingested by definitive host (canids and mustelids), become adults and infectious in definitive host

Dioctophyma renale

Transmission dynamics: eggs require 2 weeks to 3 months to embryonate, temperature dependent

Dioctophyma renale

Clinical signs: loss of kidney function, can penetrate renal capsule and wander around cavity

Dirofilaria immitis

Taxonomy: nematoda (“heartworm”)

Geographic distribution: worldwide

Location in host: pulmonary arteries

Dirofilaria immitis

Morphology: microfilariae negative can occur due to single sex adult infections (male)

* microfilariae must be differentiated from those of Acanthocheilonema reconditum and other spp., look at the difference in length

Dirofilaria immitis

Diagnostics: test annually

* Ag based tests and Knott’s tests, not helpful when adult female worms are not present
* ELISAs, ICT tests, detection of microfilariae, rads, echocardiogram
* need to repeat positive tests using different platform just in case

Dirofilaria immitis

Indirect life cycle: Microfilariae which reside in the blood are ingested by female mosquitoes

* molt to L2 and then L3 in two weeks, infective L3s are present in mosquito mouth parts
* L3s migrate through bite wound into host, molting to L4 in subcutaneous tissues
* L4 migrates for several weeks, molts 2 months after infection to adult phase
* young adults enter circulation, moving to right side of heart and pulmonary arteries 70 days post infection
* Wolbachia sp. bacteria are harbored, symbiosis of both

Dirofilaria immitis

Prevalance: more common in humid and hot areas where mosquito season is high

* heartworm in cats is mostly male worms

Dirofilaria immitis

Clinical signs: cardiac output reduced, pulmonary hypertension

* cough, dyspnea, weight loss, ascites, jugular venous distension, exercise intolerance, arrhythmias

in cats

* respiratory insufficiency
* chronic cough
* vomiting
* exercise intolerance

Dirofilaria immitis

Pathogenesis: pulmonary endothelial damage

* dead and dying heartworms induce thrombosis, granulomas, local inflammation, pulmonary vessels may become thickened and tortuous

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Dirofilaria immitis

Treatment/Prevention: annual testing of all dogs for antigen and microfilariae

* treat infected dogs with adulticides and microfilaricides as soon as possible
* use heartworm preventative all year round

Hepatozoon americanum

Taxonomy: protozoa (apicomplexan)

Geographic distribution: worldwide

Location in host: skeletal muscle, circulation