exam 2 Flashcards
giardia spp distribution and clinical
-high prevalence in cattle, mostly dairy
-worldwide distribution, mainy young.
-clinical disease uncommon, maybe diarrhea.
-reduce feed intake.
-not all species are zoonotic, many different strains
giardia diagnosis and management
-daily fecal sample-3 days.
-zinc sulphate flotation or PCR snap test.
-management: fenbendazole, address contaminated water/ environment. with filtration or ozonation NOT cholrination.
Tritrichomonas foetus
(flagellates) cattle and cat strains
-NO FREE LIVING OR CYST STAGE - direct transmission only.
* T. blagburni in cats – intestinal, chronic diarrhea, flatulence, tenesmus and fecal incontinence
* T. foetus in cattle – venereal, pyometra, embryonic death, late-term abortions
Tritrichomonas foetus
(flagellates) tranmission and path
-live in genital mucosa
-sexually transmitted
-bulls (asymptomatic carriers and primary source, infected for life)
-infected cows: abortion, pymetra, and decreases preg rates. re-infection is possible. can cycle again and have pregnancy, some will remain carriers.
Tritrichomonas foetus
Diagnosis in Cattle
-decreased preg rates, increasaed in open cows in newly infected herds.
-cows: parasite or DNA on cervial mucous, uterine fluids from aborting cows.
-abortus: stomach fluid
-bulls: (most reliable herd level) use preputial scrapings 3x a week sampling.
-culture or pcr.
-DO NOT FREEZE OR CHILL
Control in cattle
Tritrichomonas foetus
-no effective treatment or vaccine
-cows: do not breed for 3 months, cull carriers
-quarentine herd
-test bulls and cull.
-only use young bulls on pasture or tested bulls.
-CFIA notifiable
-suspected or confirmed case notify chief provincial veterinarian
apicoplexa phylym cattle and sheep
-intracellular parasites
-ubiquitous, host specific
-intestinal direct lifecycle
-* Eimeria spp- coccidiosis
* Cattle and sheep have own species, variable pathogenicity
* Cryptosporidium
Tissue cyst forming, indirect life cycle
* Sarcocystis
* Neospora (cattle)
* Toxoplasma (sheep)
Coccidia (emeria)
- Obligate intracellular
parasites - Parasitize gut epithelium
- Worldwide distribution / High prevalence
- Complex life cycle
- Infective stage – sporulated oocyst
◦ Highly resistant to cleaning agents and harsh environmental conditions
eimeria Coccidiosis – relevance and risk factors
- High cost to livestock industry
- Clinical disease most often with intensive production systems
◦ Sub-clinical disease impacts production - Risk factors
- Stocking density
- Poor hygiene
- Stress
- History of coccidiosis
life cycle emeria coccidosis
-direct
-PPP 2-3 weeks
-merogony and gametogony in enterocytes
-unporulated oocysts shed in feces
-sporulation in environment
-sporulated oocyts with 8 sporoziotes and 4 sporocyts ingested.
Bovine coccidiosis disease
-Multiple species are described in cattle, but they have different disease potential
-13 species in cattle and bison (host specific)
-indoors most common in young calves 2-12 months age.
-acute or chronic diarrhea
-source of infection: high # oocysts can be present without clinical signs. or may show signs without oocysts.
bovine coccidiosis clinical
-diarrhea, anorexia, abdominal pain.
-at necropsy: thickened intestinal mucosa, hemorrhage, mucosal sloughing
Impact of bovine coccidiosis in dairy calves 3 types
-acute: young animals, infected from dams, triggered by stress, high morbidity.
-chronic: chronic diarrhea, reduced growth rates, puberty.
-nervous: muscle tremors, hyperesthesia, nystamus with high mortality.
diagnosis of bovine coccidiosis
-clinical signs
-counting oocysts in feces
* Species identification based on features of sporulated
oocysts
* Flotation technique
-hard to do.
coccidiosis prevention at farm
- Impossible to achieve an “Eimeria- free” environment
- Aim: to minimize the build-up of sporulated oocysts in the environment and allow
the gradual acquisition of immunity to reduce disease risk.
-oocysts can survive long periods.
-good hygine, avoid overcrowding. clean water and feed bunks. disinfect holding areas between groups. bleach.
coccidiosis prevention management / treatment
-monitor: fecal samples, oocyt counts for risk assesment.
-preventative or theraputic chemotherapy: in feed, water. treat all exposed calves. Sulfonamides / Ionophores.
-toltraxuril (coccidiocidal)
Cryptosporidium
- Worldwide distribution
- Intracellular, but
- Infects the microvilli brush border
*Oocysts are IMMEDIATLY INFECTIVE and
very resistant to environmental
conditions (sporogony happens inside the host) - Infections can be subclinical or cause diarrhea of varying severity
- Zoonotic potential
-c. parvum: young calves
-c. andersoni: post weaned/ adults.
Cryptosporidiosis affected and how
-Usually affects young animals
-Acquired through ingestion of contaminated feed, water and by grooming
-Auto infection is possible, can be serious in immunocompromised individuals
-Important cause of neonatal diarrhea
◦ Almost 100% prevalence, millions of oocysts/gram of feces
-Low infectious dose (1 oocyst)
Cryptosporidiosis – clinical signs
-malabsorptive diarrhea, yellow. self limiting. epithelial cell damage affects nutrient uptake.
-depression, anorexia. abdominal pain.
-C. andersoni: gastroenteritis, production losses (reduced milk production), present in
about 10% of adult cattle abomasal glands
Cryptosporidium – diagnosis and control
-detection of oocysts in feces
-multiple samples over 2-3d.
-centrifugal flotation (sugar solution), fecal smears, IMMUNOFLORENSCENT STAINING is used in lab.
-treatment: sanitation (resistant to chlorine), supportive care.
sarcocystis life cycle
-Sporulated sporocyst from
DH host feces
(containing sporozoites) go into IH.
-IMMEDIANTLY INFECTIVE
-in IH Sarcocyst with bradyzoites forms tissue cyst,.
-DH eats tissues of IH.
-asexual merogony repro in IH.
-sexual gametogony in DH
Clinical syndromes of sarcosysts
-Acute (Dalmeny disease, S. cruzi = bovicanis)
* Caused by merogony in vascular endothelium
* Fever, emaciation, anemia, abortion, rarely CNS signs (sheep too)
* High morbidity and mortality
-Chronic (eosinophilic myositis)
* Post-mortem diagnosis, incidental finding
* Greenish focal stripes in skeletal muscles
* Breakdown of sarcocysts inducing immune response
diagnosis of sarcocytis / control
Diagnosis
* Post-mortem (incidental finding)
* Abortus: Histology and IHC, PCR
Control:
* Prevent dog from eating abortuses, dead
stock or raw meat
* Keep feed away from wild and domestic canids and felids
* No treatment
Neospora caninum life cycle
-the most important cause of bovine abortion in Canadian cattle
-indirect
-canid DH has meronogy and gametogony in intestines.
-shed unsporulated oocysts which sporulate in environment.
-cattle eat sporulated oocysts. merogony in IH.
-causes tissue cycts and abortion. DH eats.
-both DH, IH can have transplacental transmission
Outcomes of Neospora infection in pregnant cattle
Early pregnancy: fetal death and resorption
Mid pregnancy:
* Abortion (typical)
* Infected, neurological calf
* Underweight, unable to stand, flexed or hyper-extended limbs, lack of coordination, decreased
reflexes and sensory perception
Late pregnancy:
* Infected, but clinically normal – may infect their own offspring
* Uninfected calf (rare)
Infected cows may have problems with subsequent pregnancies
neospora causing abortions in cattle can have problems in sebsequent pregnancys by
Endemic abortion (endogenous) – recrudescence of chronic infection
Epidemic abortion (exogenous) – acute infection following ingestion of sporulated
oocysts – abortion storms
Diagnosis and Control
Neospora in cattle
diagnosis: clinincal and epidemiology. ELISA. tissues from abortuses
control: prevent DH from eating abortuses, raw meat, dead cattle. do not breed seropositive cattle.
Toxoplasma gondii clinical
Relevant in sheep and goats
Abortion storms in naïve animals
Outcome depends on time of infection:
* Early: fetal death and resorption
* Mid: abortion or stillborn
* Late: weak or normal lambs
Tissue cysts common in sheep, goats, pigs
Less common in cattle, horses and poultry
toxoplasma gondii life cycle
-indirect or direct
-DH cats
-IH get tachyziotes tissue cysts containing bradyziotes.
-shed in cat feces
-sporulate in environment
-enter IH become cysts (humans, cattle, cats) can have prenatal infection and abortion.
-DH eats tissue cycts with bradyziotes.
Diagnosis of Toxoplasma
ndirect methods
* Serology, IgG (chronic) and IgM (acute)
Direct methods
* Gross pathology: macroscopic necrosis in cotyledons
* Histology, PCR
Control of Toxoplasma gondii
- Regional variation in seroprevalence in sheep (20-100%)
- Prevent access of cats to sheep feed
- Vaccines have been developed
- To prevent zoonotic transmission:
- After handling aborted or stillborn fetuses, thorough hand washing
- Cook lamb and mutton to 70ºC or freeze at -20ºC for at least 3 days
Dictyocaulus viviparus a non GI nematode lifecycle
-cattle lungworm
-direct lifecycle
-L3 ingested, transmucosal migration to lungs. shed as adults, L1-L3 translation in WET environment 5 days.
-PPP 3-4 weeks
Dictyocaulus viviparous clinical / control
-Rare, but important cause of pneumonia in pastured cattle
* Can be subclinical
* Coughing, dyspnea, sawhorse stance
* Morbidity and mortality can be high
– Vaccine (irradiated L3) used in Europe, given to calves before first turn-out
– Anthelmintics (especially ML): given at midpoint of first grazing season
-baermann on fresh samples!! no eggs, L1
Protostrongylids, Muellerius, Protostrongylus
-small lungworms of sheep/ goats
* Adult parasites live in lung parenchyma
and/or small airways
* Indirect life cycle with gastropod IHs L1 shed, then snail IH, L3 ingested by sheep.
* Notable lung lesions but rarely clinical
Stephanofilaria stilesi dig. clinical. treatment
-dermal nematode in cattle
-skin lesions alopecia, scaling
-in western CAD
- Diagnosis: clinical symptoms, microfilaria in skin biopsy
* Treatment:
– ML kill the microfilaria and resolve skin lesions within 2-3 weeks
– Adults resist treatment and survive for years
LIFE CYCLE: Stephanofilaria stilesi
-PPP 6-8 weeks
-L1 in dermis, fly eats translation in IH hornly L1-L3 then fly bites DH
-L3 devleop to adults in hair follicle
-development in IH 3 weeks
Life cycle of Setaria sp.
-L1 microfilarie in blood of cattle
-L1-L3 in IH hornfly or mosquito which takes blood meal.
-develop 12-16 days
-go back to DH as L3
-adults live in peritoneal cavity.
-little to no clinical significance
LIFE CYCLE
Moniezia spp. and
Thysanosoma spp.
-cestodes
-more pathogenic in sheep (lambs diarrhea, and weight loss)
-eggs shed feces
-free living mite with cytercercoids IH. develop in IH 1-4 months.
-oral ingestion of mite.
-adults in DH.
Taenia ovis (ovine cysticercosis)
-eggs in feces ingested by sheep
-sheep develop tissue cyst cystercerci
-eaten by canines which shed eggs.
Dx:
* No clinical signs associated with adult stages in dogs or cysticerci in sheep
Control:
* No treatment for sheep
* Treat dogs with praziquantel AT LEAST twice per year
* Prevent dogs from eating infected sheep carcasses
Taenia saginatta (bovine cysticercosis)
- Most common in beef-eating countries other than Canada
– Eastern Europe, Russia, eastern Africa and Latin America - Rare cause of carcass condemnation in feedlot cattle in Canada
- Predator-prey indirect life cycles:
– Human definitive hosts (DH)
– Cattle intermediate hosts (IH) - Eggs immediately infective and resistant (18 mos)
LIFE CYCLE:
Taenia saginata (bovine cysticercosis)
-adults in humans, shed gravid segments and eggs
-eaten by cattle
-Cysticerci in cardiac and
skeletal muscle of cattle. 12 week incubation period.
-human eats infected meat with cystercerci.
Control and treatment of Taenia saginatta
Definitive hosts
– Treatment of carrier people with cestocides
– Goal: halt environmental contamination with immediately infective eggs
– Prevent access to IH (raw or undercooked meat in endemic regions)
– Cook meat to the safe internal temperature (160◦F|71◦C)
* Intermediate hosts (cattle)
– No treatment available or suitable
– Meat inspection
– Prevent livestock access to human feces
-CFIA
Bovine cysticercosis in Canada CFIA
Reportable disease under Health of Animals Act: meat inspectors, vets, and
labs must immediately report even suspicion of disease to CFIA district vet
-quarentine premises and source farms
-license remaining animals to slaughter have enhanced inspection froze for 10 days.
-lift quarentine after certain number of animals are negative.
Fasciola hepatica
-liver fluke
The most important trematode of livestock
– Rare in western Canada
* Grey-brown leaf shaped fluke primarily in bile
ducts
* Can infect many species – cattle, sheep, goats,
deer, horses, pigs
* Infection occurs only where there is suitable
aquatic snail habitat
* Zoonotic
LIFE CYCLE:
Fasciola hepatica
-eggs shed from cattle or sheep
-eggs-> miracidium-> IN snail where they undergo asexual repro.
-in snail go from sporocytys to redia.
-cecaraie after snail and metacercaria on vegatation ingested by DH.
-10-12 week PPP
Pathology –
F. hepatica
- Often asymptomatic
- Acute/subacute fasciolosis (in sheep)
- Migrating juvenile flukes in liver tissue (prepatent)
- Anemia, hypoalbuminaemia, sudden death
- Submandibular edema (bottle jaw), ascites, eggs present
- Chronic fasciolosis (in cattle)
- Adult flukes in bile ducts
- Generally sub-clinical
- Reduced growth and fertility, progressive loss of condition
- Post-mortem: chronic cholangitis, calcified bile ducts
- In all livestock, migrating flukes can trigger Clostridial disease
F. hepatica diagnostics
-too dense to float
-Coproantigen, antibodies in bulk tank milk
Bloodwork: +/- anemia
LIFE CYCLE:
Fascioloides
magna
-liver fluke
DH caribo, eggs shed
-eggs-> micarcidium which penetrates snail foot IH. undergoes asexual repro. to redia.
-6-8 weeks develop outside host
-after snail metacercaria on vegitation ingested by sheep, cattle (Dead end hosts) or cervideds (DH)
-can be fatal for sheep
Fascioloides magna
-liver fluke
* Relatively common in cervids in western Canada:
– Deer, elk, caribou are normal definitive hosts (shed eggs)
* Livestock and other ungulates are dead end hosts
-Chronic or asymptomatic in cattle
– Flukes walled off in liver parenchyma
– no eggs shed, no clinical signs, unless flukes activate clostridial
spores in liver (bacillary hemoglobinuria, aka redwater disease)
Control of flukes in cattle & sheep
- Rarely necessary in western Canada in cattle
- In problem herds (herd level diagnosis), prevention:
- Avoid known contaminated pastures
- Avoid liquid manure as fertilizer from infected herds near water.
-treatment of flukes in cattle and sheep
Control of F. hepatica in problem herds involves:
* Treatment of all exposed ruminants on farm
* Closantel (Flukiver) or triclabendazole in fall (resistance observed to latter in
Europe) to kill juvenile flukes - SHEEP
* Albendazole in early winter to kill adult flukes – DAIRY
* Vaccination for Clostridial diseases (at least every 6 months)
Dicrocoelium dendriticum
-zombie ant fluke
* Small fluke which lives in bile ducts
* Incidental finding in cattle, sheep, deer, rabbits, gophers, people
* Introduced into B.C. and Cypress Hills in Canada
* TERRESTRIAL cycle – ant as second IH
LIFE CYCLE:
Dicrocoelium dendriticum
-eggs shed from DH cattle
-ingested by snail and miracirdium released first snail IH
-caercarie in snail slime eaten by ant, develop 2 months. second IH with metacecarie which is ingested by DH cattle.
-TERRESTRIAL, not aquatic, life cycle
-PPP 8 weeks
parasitic nematodes in ruminants
-causes parasitic gasteroenteritis (PGE)
-sub clinical disease causes major production losses (decreased feed intake, loss of protein)
-diagnosis relies on quantitative fecal egg counts
-Anthelmintic resistance is currently one of the MAIN CHALLENGES for parasite control
Trichostrongyles
-most important nematodes in grazing ruminants
– Direct life cycle, infective L3, PPP ~21d, eggs look very similar
– Commonly occur as mixed infection
-control with broad spectrum anthelmintics
GI nematodes of the abomasum in cattle
-Ostertagia ostertagi*
-Haemonchus placei
GI nematodes of the SI in cattle
Cooperia spp.*
Nematodirus spp
Basic Trichostrongyle Life Cycle
-worms mature in dig tract and lay eggs.
-eggs shed in feces
-L1-L3 in environment
-L3 ingested and immature worms go into mucosa.
Ostertagia ostertagi
-abomasum
* Most important parasitic nematode species in cattle in Canada and Northern US
* L4 may enter arrested development (hypobiosis) to survive harsh weather conditions
-morocco leather abomasum apperance. thick mucosa, red.
-causes ostertagiosis
gastric gland infections
-no acid production from parietal cells.
-pepsinogen cannot be activated to pepsin so no protein digestion, hypoprotenemia, malabsorptive diarrhea, bacterial overgrowth, increase abomasal pH.
OSTERTAGIOSIS – 2 syndromes
-TYPE 1 summer (july to october): crazing calves, gradual onset, larvae on pasture, large number of adult worms so high FEC, bright green diarrhea watery, weight loss, anorexia.
-TYPE 2 winter (march to may): larvae in dorment stage, yealrings can be off pasture, sudden onset. inhibited larvae emerge at once so low FEC. * Hypoalbuminemia, submandibular edema
* Low morbidity, high mortality
-diarrhea
Haemonchus placei
-bovine abomasum
-barber pole warm, BLOOD SUCKER
-L4 may enter hypobiosis, not common in CAD more south
-white on worm
Haemonchus placei clinical signs cattle
- Hyperacute - Sudden death due to haemorrhagic anemia
- Acute - Anemia, bottle-jaw, ascites, dark feces, anorexia
- Chronic - Weight loss, weakness, anorexia
- FEC can be low (PPP), or very high (Thousands of EPG
-NOT DIARRHEA sucks blood.
-hard to treat many resistance.
-diagnose with L3, PCR.
Cooperia spp
Common and sometimes dominant GIN in cattle
* Adults ~1cm long
* Contributes to PGE as part of mixed infection
* C. oncophora: mild pathogen, temperate areas, very common in Canada. C. punctana more in north USA.
-parasitic stage develop on surface of SI mucosa
-inappetance
Nematodirus helvetianus
-Development to L3 inside the egg
* Eggs overwinter on pasture, hatch with temperature rises in spring
* Shedding rare in animals > 6 months of age (immunity)
* Pasture contamination predominantly from calves
* Acute diarrhea in young calves in pasture
Bunostomum spp
-bovine SI
* Hookworm (Ancylostomatidae): Blood feeders
* Ingestion of L3 or SKIN PENETRATION by L3
* Rare in Canada
Strongyloides papillosus
- Only adult females are parasitic
- Warm and wet regions of the World
- Not seen in Western Canada
- Unlike most GIN, transmit well off pasture
- Larvated eggs, relatively small
- Ingestion of L3 or SKIN PENETRATION
-bovine SI
LIFE CYCLE
Strongyloides papillosus
heterogenic cycle: where they survive in environment
homogenic cycle: where they survive in host.
Oesophagostomum spp
-bovine LI
* Nodular bowel worm
* Life cycle similar to trichostrongyles, except pre-adult larvae create nodules in
large intestinal mucosa
* Limited pathogenicity
Trichuris spp.
-bovine LI
Whipworm
* Host-specificity, T. globulosa (cattle)
* Direct life cycle, larvated eggs infectious, PPP4-6 weeks
* Transmits well off pasture (thick wall)
* Very mild pathogen
* Commonly seen during fecal egg counts in Canadian cattle –
incidental finding
Basic Epidemiology of GIN in Cattle
Infection thru ingestion of infective stages from PASTURE
– Build up of large amounts of L3 on pasture
* Possible sources of springtime pasture contamination
– Overwintered eggs or larvae (esp. Nematodirus) on pasture
– Reactivation of hypobiotic larvae
* Peak pasture contamination: 2nd half of grazing season
* Outcome of infection largely depends on immune status
-rise in june/july
DIAGNOSIS of GIN IN RUMINANTS
-history
-clinical signs
-fecal egg counts FEC. Trichostrongylid eggs are usually undistinguishable
Not usually a very sensitive measure of parasite burden in cattle
-coproculture + morphology
Management of GI Nematodes of Cattle
-management: quarentine, good husbandry, pasture management
-anthelmintics: long acting rumen boluses Macrocylic lactones (ivermectin)
-strategic treatments: cows in spring to reduce pasture contamination then graze young animals later
-targeted selective treatment
GI Nematodes of Sheep
-young animals, pasture transmission
* Clinical disease is more common and widespread (worse in goats)
* Anthelmintic resistance a huge global problem
-anemia, bottlejaw, diarrhea, reduced production.
3 main GI nematodes in sheep
*
Haemonchus contortus: anaemia, death in some cases
*
Trichostrongylus colubriformis, Teladorsagia circumcincta: chronic
diarrhea, production loss
*
Nematodirus battus: problem in lambs
life cycle of sheep GI nematodes
eggs on feces, hatch, L1-L3 in egg develop, grass as L3 eaten by DH. goes to L4 in stomach to adults then shed eggs.
epidemiology in sheep
-ewes have peri parturient rise L4 reactive where they are about to lamb have a drop in immunity and the nematodes reproduce and multiply. the hypobiotic L3 reactivate. rise in eggs shed. increase in spring.
-leads to increase in pasture eggs FEC end of spring and summer
-lambs turned out in pasture in fall and have increase in lamb FEC
