GI Parasites Flashcards
1
Q
describe parasitic mechanisms of disease
A
- trauma:
-direct destruction of host cells or tissues: cystiospora, haemonchus, small strongyles
-indirect destruction of host cells or tissues: giardia, tritrichomonas
-organ occlusion: parascaris
- nutrient robbing: tapeworms
- excretion of toxins or other pathogens: nanophyetus
- interactions with host immune/inflammatory responses: dirofilaria immitus, fleas
2
Q
describe giardia
A
- coccidian protozoan
- the more fluid the stool, the more trophozoites (active, motile stage), the more solid the stool, the more custs
3
Q
describe the life cycle of giardia
A
primary host:
1. many species
2. colonize SI on mucosal surface
tranmission: fecal-oral
1. ingest cysts via feces or contaminated water, food, fomites, self-grooming
2. NOT trophozoites: will not survive the stomach
stages:
1. trophozoite: active, noninfective
2. cysts: dormant, infective
reproduction: binary fission of trophozoites
4
Q
describe pathogenesis of giardia
A
- indirect destruction:
-trophozoite attaches to surface of SI, damages epithelial cells and enterocytes, decreasing GI permeability and blunting intestinal villi and microvilli, resulting in reduced surface area so
-maldigestion, malabsorption, hypersecretion: DIARRHEA
5
Q
describe clinical disease of giardia
A
- persistent diarrhea: mucoid, pale, soft, loose, fatty (blood is uncommon), typical of small bowel diarrhea
-can be acute, intermittent, or chronic - +/- vomiting, anorexia, dehydratio
- some animals are subclinical shedders
- malabsorption syndrome:
-signs of poor nutrition: lethargy, weight loss, etc.
6
Q
describe diagnosis of giardia
A
- direct microscopic fecal analysis
-loose stool: motile trophozoites on fresh wet mounts - fecal float centrifugation:
-solid stool: cysts stage (don’t confuse with yeast)
-use fecal float centrifugation with ZINC SULFATE solution
-recommended for routine creening - antigen (cysts) detection kits, ELIDA
-rapid in house, high specificity
-NOT rec for routine screening - PCR:
-increased Se and Sp
-not rec for routine screening unless owner concerned (immunosuppressed)
7
Q
describe treatment for giardia
A
- fenbendazole FIRST
-or metronidazole but do NOT start with metro - probiotics and fiber/psyllium
- treatment duration depends on drug but rage 3-8days
- follow up with strict environmental decontamination, bathing the animal, etc. bc can reinfect themselves!!
- treat only symptomatic dogs and cats to decrease development of resistance to antiprotozoals
- some animals will persistently shed cysts despite treatment and resolution of clinical signs
8
Q
describe control of giarfia
A
- strict prevention of fecal contamination
- outdoor environment: pick up and dispose of feces
- indoor env: clean (soap and water), disinfect, dry out cysts
- bathe contaminated fur
- cysts can survive for months
9
Q
describe zoonotic implications of giardia
A
- contains some molecular assemblages that are host specific so zoonosis is rare but
- concern for immunocompromised people:
-humans: assemblages A and B
-canines: C and D
-felines: assemblage F
10
Q
describe cytsoisospora
A
- oocysts:
-species specific size and shape, unsporulated when passes - sporulated oocysts contains 2 sporocysts with 4 sporozoites each
- 8 sporozoites total
11
Q
describe the life cycle of cystoisospora
A
- definitive host: asexual and sexual replication occurs
-unsporulated oocysts pass in feces - sporulate in 2-3 days
-ingestion by paratenic host, encyst in tissue, forming a cystozoite (does not directly cause dz in paratenic host) - direct host ingests paratenic host
12
Q
describe pathogensis of cystoisospora
A
- direct destruction of enterocytes (SI):
-destruction of epi lining (rare hemorrhagic ulcers)
-villous atrophy
-malabsorption
-increased permeability, loss of fluids, +/- blood
-immune response causes hyper-secretion
13
Q
describe clinical disease of cystoisospora
A
- mild to moderate diarrhea
-loose, mucoid, sometimes watery
-sometimes bloody (rare) - most often reported in nursing or recently weaned pets
- large infective dose of sporulated oocysts = worse clinical disease
14
Q
describe diagnosis of cystoisospora
A
- animal age and history:
-young, immunocompromised, stress - fecal float centrifugation:
-look for unsporulated oocysts in fresh sample
-sporulated oocysts in older sample
-diarrhea may occur prior to oocysts excretion (prepatent period)
-may need to differentiate between eimeria (coprophagy) vs cystoisospora - PCR
15
Q
describe treatment of cystoisospora
A
- anticoccidials:
-sulfa drugs: static (albon, bactrovet, tribrissen); unclear efficacy against acute disease
-ponazuril (cidal): marquis, ponalrestat; may be more effective
- supportive therapy for symptoms
- once infected, have immunity against that species
16
Q
describe control of cystoisospora
A
- sanitation:
-sporulated oocysts are resistant, can survive (up to a year) in moist protected environments
-susceptible to freezing or extremely high temperatures and ammonia solution - prevent access to paratenic hosts
-mainly rodents - good nutrition is important
- keep stress low
17
Q
describe canine cystoisospora
A
- puppy diarrhea!
-copious, watery, may persist for weeks (small bowel diarrhea) - cystoisospora canis:
-large, oval oocyst
-low pathogenicity in adult dogs - C. ohioensis complex:
-small-medium sized spherical oocyst
- +/- diarrhea
18
Q
describe feline cystoisospora
A
- kitten diarrhea! small bowel diarrhea
- cystoisospora felis: large, oval oocyst
+/- pathogenic for kittens - C. rivolta: small-medium spherical oocyst
-small bowel diarrhea in newborn kittens
19
Q
list the 4 most common hookworms
A
- ancyclostoma caninum: dogs
- ancyclostoma tubaeforme: cats
- uncinaria stenocephala: dogs and cats
- ancyclostoma braziliense: dogs and cats
20
Q
describe the life cycle of ancyclostoma caninum
A
- adult worms live in small intestine of dogs
- eggs passed in feces, develop, hatch
- L1 and L2 in the environment develop to infective L3
- transmision:
-skin penetration of L3
-ingestion of L3
-ingestion of infected paratenic host
-transmammary transmission: female to puppies
21
Q
describe diagnostics and treatment nof ancyclostoma caninum
A
diagnostics:
1. clin signs: pale MM and anemia, ill thrift, failure to gain weight, poor hair coat, dehydration, dark tarry feces (melena) +/- diarrhea
- dx tests:
-fecal float centrifugation
-fecal antigen tests: detect PPP infections
-PCR tests: detect PPP infections and MDR strains - regular testing to check program efficacy
-adult dogs at least 2x/year
-puppies at least 4x in 1st year of life
treatment:
1. puppies: at 2-3wks of age with a drug that controls hookworms and ascarids, repeat every 2 weeks until 2 months when put on HW prevention program
- dams: deworm close to whelping to minimize transmammary transmission to puppies
-fenbendazole daily starting at 40th day of gestation until 2 weeks post whelping
-selamectin during periparturient period and at whelping - multidrug resistance = common issue
22
Q
describe control and zoonosis of ancyclostoma caninum
A
control:
1. monthly HW prophylactic that is also effective against GI nematodes
- sanitation:
-prompt removal of feces will minimize contamination of environment
-keeping habitat dry allows for rapid dessication of larvae - prevent predation to avoid infection via paratenic hosts
zoonosis:
1. cutaneous larval migrations
-intensely pruritic serpentine lesions of skin
-caused by skin penetration of infective L3 in contaminated habitats (parks, beaches, etc.)
- eosinophilic gastroenteritis (very rare)
23
Q
describe the life cycle of ancyclostoma tubaeforme
A
- adult worms live in small intestine of cats
- eggs passed in feces, hatch
- L1 and L2 in environment develop to infective L3 stage
- transmission:
-skin penetration of L3s
-ingestion of L3s
-ingestion of infected paratenic host
-NO transmammary transmission
24
Q
describe diagnostics and treatment of ancyclostoma tubaeforme
A
diagnostics:
1. clinical signs: pale MM and anemia, ill thrift
2. dx:
-fecal float centrifugation
-fecal antigen tests
-PCR tests
3. regular testing to check program efficacy
-adults at least 2x/yr
-kittens at least 4x/1st year of life
treatment:
1. kittens at 2-3 weeks of age with drug that control hookworms and ascarids, repeat every 2 weeks until can be put on HW prevention
control:
1. monthly HW prophylactic also effective against GI nematodes
2. sanitation: like for dog one
3. prevent predation to avoid infection via paratenic
zoonosis: cutaneous larval migrans like dog one
25
describe uncinaria stenocephala
1. has cutting plates (not fangs)
2. less common hookworm of dogs, cats, and foxes
3. found in northern cooler regions
4. relatively non-pathogenic
5. transmission: only via ingestion of L3
26
describe ascarids in general
1. large adult worms live in small intestine
-non-bursate
-mouth surrounded by 3 fleshy lips
2. host specific adult stage
-toxocara canis in dogs, cati in cats
-baylisascaris procyonis in raccoons
-parascaris equorum in horses
-ascaris suum in pigs
-ascaris lumbricoides in humans
3. larval stage can infect other hosts, including humans
4. eggs:
-distinct appearance: thick-walled, many have textured outer coat
-highly resistance: can persist in soil for years
-female worms extremely fecund: approx 200,000 eggs/day; ascarids flood environment with eggs to ensure infection of next host
27
describe toxocara canis
1. SI ascarid in dogs
2. thick, white, large (10-15cm) adult worms
3. anterior end: moderate cervical alae
4. life cycle:
-adult worms in SI
-take approx 4 weeks to infective eggs
-routes of infection:
--ingest infective eggs: followed by tracheal migration in puppies, somatic migration in mature dogs
--transuterine to pups (MAJOR)
--transmammary to pups (minor)
--paratenic hosts to adult dogs
-prepatent period: 3 weeks transuterine, 5 weeks egg ingestion
5. zoonotic: visceral larval migrans
28
describe toxocara cati
1. SI ascarid of cats
2. thick, white, large (4-12 cm) adult worms
3. anterior end: prominent cervical alae
4. life cycle:
-adult worms in small intestine, take approx 4 weeks to develop infective eggs
-routes of infection
--ingest infective egg: followed by tracheal migration in kittens, somatic migration in mature cats
--NO transuterine!! transmammary to kittens possible but still minor
--paratenic hosts to adult cats
-prepatent period: 8 weeks via egg ingestion
5. zoonotic: visceral larvae migrans
29
describe pathology of toxocara canis and toxocara cati
1. nutrient robbing (ingest host food)
2. enteritis:
-inflam of intestine
-hypersensitivity: ascarids and their excretions are hyperallergenic
3. verminous pneumonia (rare): due to tracheal migration of larvae through lungs causing traumatic damage with hemorrhage and inflammation
4. intestinal obstruction/intussusception (rare)
-due to very large burden of adult worms
30
describe clinical signs of toxocara canis and toxocara cati
1. often subclinical, esp in adults
2. mainly disease of young puppies/kittens
-lack of growth, loss of condition
-ill-thrift, dull coat
-abdominal pain, pot-bellied
- +/- fetid, mucoid diarrhea
-contributor to fading puppy/kitten syndrome: feline less severe due to lack of transuterine transmission
31
describe diagnostics of toxocara canis and toxocara cati
1. discovery diagnostics: to confirm a suspect infection
-observation of clinical signs
-fecal float with centrifugation
-fecal antigen tests
-adult worms in vomit or feces
2. fecal monitoring (CAPC)
-confirm efficacy of deworming program (during routine health checks)
-fecal float with centrifugation and fecal antigen tests
-puppies and kittens: 4x/1st year
-older dogs and cats: 2x/year
3. fecal egg reduction test (FERT):
-to verify reduction/elimination of an infection
-to confirm efficacy of specific dewormer vs resistant worm population: check fecal 7-14d after tx
32
describe treatment of toxocara canis and toxocara cati
treat an active infection:
1. to eliminate: many dewormers effective against adults, few against migrating or arrested larvae
2. plan:
-2 treatments: 1st to elim standing adult pop, 2nd to elim recently matured adult worms
-fecal check 7-14d after 2nd tx to confirm efficacy, warn owner about dead worms in poop
prophylactic deworming:
1. deworm female dog to decrease transuterine transmission: fenbendazole starting at 40th day of gestation until 2 weeks post whelping
OR selamectin effectively kills larvae that have migrated to puppies when mother is treated at or near parturition
2. deworm newborn kittens/puppies
-start at 2-3 wks old, repeat every 2 weeks until 2 months old and can start monthly HW and intestinal worm prophy: liquid pyrantel is more palatable/preferred for nursing babies
-deworm dams at same time as deworming nursing puppies/kittent to ensure no transmammary transmission
33
describe control and zoonosis of toxocara canis and toxocara cati
1. environmental:
-good sanitation practices: prompt feces disposal (before rains/dung beetles disperse feces and worm eggs)
-clean surfaces, dispose of feces
-wash hands thoroughly after handling (ZOONOTIC)
2. routine fecal checks
-confirm efficacy of dewormer
-check for gaps in control program
-check for gaps in owner compliance
3. routine dewormer control:
-use monthly (HW) preventative that also has efficacy intestinal worms
-eliminate worms prior to maturity/production of eggs that contaminate environment
ZOONOSIS:
1. migration of larvae in tissues of aberrant host (humans)
2. ingestion of infective egg: beware sandboxes and gardens
3. ocular larvae migrans: in children, larvae may settle in retina and cause granulomatous reaction
4. 14% of people have antibodies to toxocara sp.
34
describe trichuris/whipworms in general
1. in cecum and LI
2. worms: anterior thin, posterior thick
-anterior end embedded in epithelial cels of gut
3. egg: bipolar plugs, smooth shell
-very hardy, can survive many years
-resistant to dessication, high temps and UV light
-very difficult to control
4. species:
-trichuris ovis: sheep and goats, asymptomatic
-trichuris discolor: cattle, asymptomatic
-trichuris vulpis: canid, pathogenic
-trichuris suis: swine, pathogenic
35
describe life cycle of trichruis vulpis
1. transmission: fecal-oral; ingestion of infective egg ONLY
2. in host:
-eggs hatch in SI
-larvae penetrate mucosa of SI and develop in 8-10 days
-juvenile worms return to lumen of gut and migrate down to cecum and colon: juvenile worms resistant to most dewormers
-adults in cecum and colon mature and produce ova: adults susceptible to most dewormers
36
describe pathology, clinical signs, and diagnosis of trichuris vulpis
pathology and clinical signs:
1. animals older than neonate
2. lesions of cecum and large intestine: inflammation, hemorrhagic foci, pathology by immature and mature adults
3. number of worms:
-few worms: asymptomatic in most cases
-many worms: hemorrhagic cecum and colon (intermittent diarrhea with mucus and blood)
-severe infections: hella bloody diarrhea, dehydration, death (rare)
diagnosis:
1. fecal float with centrifugation
-eggs are heavy, slow to float with passive floatation
-false negatives: prepatent infection (but showing clin signs), intermittent shedders, poor technique to find heavy eggs
2. commercial fecal antigen tests: good for dx poor egg shedders and prepatent infections
3. diagnostic clues: dogs on dirt lots, yards, unsanitary kennels, intermittent bloody diarrhea
37
describe treatment and prophylactic control of trichuris vulpis
basic treatment:
1. remove from contaminated area
2. deworm every month for 3 months: juvenile and immature adults resistant for 1st two months
3. recheck fecal
prophylactic control:
-utilize a monthly HW preventative that is also effective against whipworms, esp if owner cannot remove dog from contam area
