Exam2 Flashcards

1
Q

Gastrointestinal Nematodes of Horses

A
**Strongyles
Large 
-3 species
Small -Several different genera 
-Many different species 
**Ascarids 
-Parascaris equorum 
**Pinworms 
-Oxyuris equi
**Spiruid worms of incidental interest
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2
Q

Large stongyles and small strongyles

A

a. k.a: Cyathostomes Small strongyles
- Adults in large intestine or colon
- Direct life cycle
- Infective stage: L3 larvae in pasture environment
- Primary target for control by equine owners
- ~40 species

Large strongyles Morphology

-Medium size worms
-Males (14-35 mm) with capulatory bursa
-Femalres (20-47 mm)
-Dimorphic
*Prominent buccal capsule
-Adults in large intestine
Life Cycle
-Eggs passed in feces ~14 days and develop into L3 larvae
-Larvae migrate externally
-Arrive In the large intestine and reproduce (6, 8, or 12 mts)
-Long PPP or ERP following treatment

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3
Q

Large Strongyles
Strongylus Vulgaris 6 mts
Strongylus equinis 8 mts
Strongylus edentatus 12 mts

A

Strongylus vulgaris **most important disease causing

  • Larvae migrate in walls of small arteries and anterior mesenteric artery
  • arrive in cecum/colon mature and reproduce
  • PPP = 6 mts

Strongylus equinis

  • Larvae migrate in peritoneal cavity and liver
  • Arrive cecum/colon
  • PPP 8 mts

Strongylus edentatus

  • Larvae migrate in peritoneal cavity and liver
  • arrive in cecum/colon
  • PPP 12 mts

Disease in older foals occurs in the PPP
-pathology associated with larvae migration through arteries **cranial mesenteric artery
-Host inflammatory response
-Aneruysm and infraction
-Colic by interruption of blood supply
-Diarrhea when adult worms reach large intestine
-Adult worms suck blood
**Fecal exams can be negative
Dx: clinical signs, age, and risk factors
-Associated with older animals w high FEC
-No consistent worming program

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4
Q

Small Strongyles

Large Strongyles

A
  • Cylicocyclus (10-25 mm)
  • Cyathostomum (5-12 mm)

Sexually dimorphic

  • Males capulatory bursa
  • **Anterior end w/ prominent “corona radiata”

Life cycle

  • eggs passed in feces 2 wks = L3 infective satage
  • Larvae penetrates and encyst in intestinal wall
  • Late L3 becomes reproducing adult
  • Eggs in feces 9 wks post infection without hypobiosis
  • 9 wks PPP

Clinical Disease
-Foals diarrhea, disease occurs before worms sexually mature
-Mass encysted parasites wall of LI
-Damage from emergence out of colonic wall
Dx: clinical signs, age, and risk factors
-Associated with older animals w high FEC
-No consistent worming program
**Red worms (L4) passed in feces
-Possible detection of eggs by fecal flotation
-ERP 28 days for some species, 6-12 wks for others

Large Strongyles

  • ERP 6,8,12 mts
  • Hatch and later identify larvae
  • FEC useful to monitor drug effectiveness, pasture contamination, identification of wormy animals can’t not be used to predict worm burden
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5
Q

Deworming products

A

3 families

  1. Bensimidazoles (B-tubulin synthesis)
  2. Imidazothiazole (nicotinic agonists)/ Tetrahydropyrimidines
  3. Macrocyclic Lactones (gated glutamate chloride channels.
  • Large strongyles: no resistance
  • Small strongyles: responsive to macrolcylic lactones with shorter ERPs.

Pharmacologic Control

-Interval dosing: most common, deworm all horses at fixed intervals. suppressive deworming to minimize contamination. Shorter than ERPs (2 mts or 8 wks)
-Strategic dosing: Active grazing period deworming, at greater risk. Lifecycle while hypobiosis. Fewer treatments, less intensity
-Continuous daily treatment: Pyrantel tartrate (Strongid C). Kills L3 before it can invade mucosal tissue. Believed to have fostered resistance
-Selective treatment: only horses above FEC threshold.
Allows REFUGIA: the portion of the parasite population not subject to drug selection pressure.

Practice Control

  • Not target adults: small strongyles still mass emerge, large strongyles still larvae invasion
  • Interval treatment: Pyrantel, Benzimidazoles (FBZ, TBZ, etc). Low levels of persistent in tissues allow for rapid reinfection.
  • Maturing sexually active worms result in bad things for pasture

Survival of parasite populations

  • Adult worms are short lived 35-55 days
  • Seasonally hostile conditions reduce population
  • Summer in TN Cyathostome hypobiosis, in Fall/Spring favorable for pasture

**Minimum treatment of “selective deworming” high FEC animals to reduce pasture contamination and preserves genetic diversity

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6
Q

Nematodes of Horses
Ascarids
Pinworms
Draschia/Habronema

A

Parascaris equorum

  • Large stout worm Males 15-28 cm, Females up to 50 cm
  • Dimorphic
  • Anterior opening w/ 3 lips
  • Adults parasites in small intestine
  • Direct life cycle
  • Infective larvated eggs
  • Tracheal migration
  • *primarily parasites of Foals
  • PPP ~ 12 wks
  • Round eggs ~90um (look like ascarids canis eggs)

Clinical signs:

  • Diarrhea, enteritis, respiratory issues and nasal discharge
  • dull hair coat and poor growth
  • Extreme infections can be fatal
  • Large worm burden, worm grows faster than Foals’ intestinal tract
  • Impaction colic, intestinal perforation and rupture (4 worms trying to get out through the same hole)

Tx and control:

  • Clean mare’s udders, provide clean nursing environment
  • Graze low FECs animals
  • **Effective therapy @ 2,4,6,7 months
  • Pyratel pamoate (early)
  • Fenbendazole (early)
  • Macrocyclic lactone (widespread)
  • Potential of colic if all and too many killed at once
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7
Q

OXyuris equi

Equine Pinworm

A

Medium size worms

  • dimorphic males (9-12 mm) Females (40-150 mm)
  • Adult worms: long tail with acute distal end, Muscular bulb (esophagus)
  • Adults parasitic in colon, small, and large intestines.

Direct life cycle

  • Embryonated eggs infective
  • Larvae hatches and penetrates the colon wall develop and return to lumen to reproduce
  • Females deposit cement eggs in perianal folds
  • PPP ~5 mts
  • Eggs flake off and adhere to everything
  • Infective eggs after 4-5 days in the environment developing

Clinical significance

  • Intense anal prutitis and itching
  • Behavioral issues

Tx and control

  • Adult worms susceptible to treatment
  • Pyrantel
  • Ivermectin paste
  • L4 larva stages were >99% susceptible to drugs
  • No evidence of drug resistance
  • **Attention to hygiene
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8
Q

Strongyloides westeri

Equine Threadworm

A

-Small worms
-Adults in small intestine
**only females are parasitic
-morphology and life cycle similar to canine species
**Homogonic life cycle
**Hetrogonic
-Infection in foals
Lactogenic
-PPP= ~7 days
-L3 infective
-Percutaneous
-Eggs: 50x35 um

Clinical significance

-Primarily infection of foals
Eggs disappear from feces by 24 wks of age
Arrested in tissue for life
-Diarrhea, dehydration, poor growth
-Treatment to remove adults from small intestine
-Supportive care

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9
Q

Draschia and Habronema

Equine Stomach Worms

A
  • Adults live in the stomach of horses
  • Small worms usually dimorphic
  • *Obligate indirect life cycle
  • Transmission of infective worm larvae via FLY
  • FLY intermediate host
  • Larvae in cutaneous wounds
  • Eggs passed in feces, ingested by maggots
  • *Trans-stadial transmission
  • Horses accidentally ingest fly
  • PPP ~5mts
  • Eggs 45x12 occasionally seen

Clinical significance

Disease process associated with deposited larvae by fly

  • Cutaneous Harbronemiasis a.k.a ‘summer sore’, ‘swamp cancer’
  • Granulomatous lesion persistent through the fly season
  • Worldwide distribution
  • Tx single dose macrocyclic lactone is usually effective
  • Fly control important
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10
Q

Ecology, epidemiology and disease risk horses

A

-Horse feral, nomadic, little contact with the same infective pasture before domestication
Principles of parasite control

  1. Pasture contamination: best 1-2 horse/Acre
  2. Pasture infectivity: Low FEC horses allow to graze
  3. Differential risk of infection/disease: young animals associated with high FEC
    - Parascarids equorum
  4. Pasture hygiene and management
  5. No pharmacologic solutions for poor pasture management : “smart deworming”

Resistance

  • Drug treatment increases the frequency of naturally occurring ‘resistance’ genes in the parasite population
  • Parasites that are treatment resistant reproduce differently without competition from other worms
  • management factors: exclusive use of a single drug, resistant worms reproduce continually through ERP
  • Frequent use of drug: denies susceptible worms an opportunity to reproduce
  • *Benzimidazoles, Panacur, Safeguard: widespread resistance in small strongyles, none in large and early indication in Parascaris
  • *Mycrocyclic lactones, Ivermectin, Moxidectin: widespread resistance Parascarids, none large, some in small strongyles

Differential selection by drug used:

  • Pyrantel, adults only, no effect on encysted eggs (best refugia)
  • Ivermectin, Late L3 and Adults
  • Moxidectin, Early and Late L3 and adults (poor refugia)

Selective treatment

  • Maximizes refugia
  • Mitigate negative selection pressure of treatments
  • Facilitates heterogenous mix of susceptible and resistant parasite types

Parasite targets:

  • Age based susceptibility
  • Adults >3 yrs old acquired immunity
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11
Q

Parasite control for 1st year, @nd year, 3rd year

A

Deworm @ 8 weeks: FBZ targets Parascaris, Pyrantel when worm burden is low

Deworm @ 16 weeks: Pyrantel to target Prascaris, IVM for Cyathostomes

Deworm @ 24 weeks: Macrocyclic lactone to target small strongyles

Deworm @ 32-24 weeks: Macrocyclic lactone to target small strongyles

Deworm @ 52 weeks

2nd year

Consider animals with high FEC
Tx: @ 10-12 weeks intervals,
-Fall, winter, spring
-Season with highest pasture transmission 
-Largest possible REFUGIA

3rd year

  • Tx at least once annually for large strongyles and Tapeworms. Macrocyclic lactones and Prazinquantel
  • Identify and treat high FEC shedders by selective deworming. **No more than x3 @ 12 wks intervals.
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12
Q

Trichostrogylid Nematode Parasite of Cattle, sheep, goats, and camelids

A
  • Small gut-dwelling nematodes
  • No extensive tissue migration
  • Arrested development (hypobiosis) as an important adaptation to survival and maintenance of parasite populations
  • Primary target of producers initiated control programs

Arrested development

  • remains juvenile for several months in gut tissue
  • arrested larvae waits for favorable reproductive conditions, avoids adverse environmental conditions. Seed the pasture each season

Life Cycle

  • Adults in gut and reproduce
  • Infective larvae develops in environment
  • PPP ~21 days

Dx:

  • periodic assessment of herd health
  • High FEC
  • Eggs 70-90 x 40-45 um. Thin shell and morulated. Look like hookworm eggs
  • fecal flotation
  • McMasters Quantitative FEC
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13
Q

Ostertagia spp.

Brown stomach worm

A
  • Adults in abomasum
  • small dimorphic. males w/ copulatory bursa. SPICULES
  • Direct life cycle
  • Arrested development in gastric pits
  • Type 1 and 2 disease
  • *most economically important parasite in cattle
  • Controlled with Smart deworming: as little as possible

Type 1 disease

  • Usually young animals (1st season on pasture)
  • Favorable environmental conditions, October/March
  • Larvae begins hypobiosis April/Sep
  • Larvae lives 30-52 days
  • Damage when larvae matures, leaves the glands and reproduces
  • Profuse water diarrhea
  • Bottle jaw
  • Loss of appetite, loss of BCS
  • Positive response to timely treatment

Type 2 disease

  • Occurs months after infection
  • Older animals (2nd season on pasture)
  • Larvae enters the gastric glands and remain dormant
  • Leave the glands ‘en masse’ during summer-fall months
  • Catastrophic or protracted
  • Associated with stress (calving)
  • Clinical signs similar to type 1 but more severe
  • Fecal floatation likely negative
  • Brown watery diarrhea
  • Rumen pH approaches neutral
  • *Poor response to treatment
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14
Q

Other trichostrongylid parasites of cattle

A
  • Trichostrongylus sp.
  • less pathogenic
  • Young and stressed animals at greater risk
  • Cooperia sp.
  • Typically associated with calves
  • Losses subclinical production
  • Emerging drug resistance
  • Macrocyclic lactones
  • Pour on ML for fly control = resistance
  • Nematodirus spp.
  • Seasonal Spring hatching concentrates infective worms
  • Disease typically associated with calves in late spring
  • Large egg ~200 um x 90 um
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15
Q

Anthelmintic control of parasite in herd animals

A

Strategic deworming: removal of parasite from the host, targeting biological infective stages. Removal of adult parasites, less worm burden

Selective deworming: selected FEC high hosts. Allows refugia, heterogenicity. Host selection based on risk mapping. Ex: young vs. old, high FEC vs. low

**Treat young animals, high infective shedders, reduce adult worm burden, target inhibited larvae seasonally, reduce overall or selected portion of parasite population

Disease Mapping Ostertagia sp.

Type 1.

  • Target young cattle
  • Goal is to reduce pasture contamination and hazardous infection
  • March/April

Type 2

  • Older heifers
  • Mass emergence of arrested larvae
  • Fecal exams likely negative
  • Sep/Oct
  • Stockers and new addition must be treated

SMART Deworming

  • Seasonal variation, life cycle, biology, disease risks
  • Few as possible treatmens
  • Time before ERPs
  • Benzimidazole, Imidazothiazole, Tetrahydropyrimidine drugs: provide ~21 EPR protection. Use for Cooperia if drug resistance is an issue
  • IVM, MOC remove adults, inhibited larvae, protection from reinfection 21 PPP + 21 ERP = 42 days
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16
Q

Haemonchus contortus ‘Barber Pole Worm”

Gastrointestinal Nematode Sheep and Goat

A
  • *The most pernicious parasite affecting sheep and goats
  • Bottle jaw anemia
  • Multi-drug resistance is widespread.
  • NAVLE: treat the whole herd in the fall
  • Adult worms in abomasum
  • Medium size worms, dimorphic
  • Adult worms single tooth in small buccal capsule
  • Blood filled gut spirally encircling white ovaries
  • Most economically significant in small ruminants

Direct life cycle

  • prolific egg producers 1000’s per day eggs
  • PPP = ~21 days
  • Larvae in pasture are sensitive to environmental conditions. Don’t like dry cold
  • Arrested development likely over winter
  • Summer best larvae development

Clinical signs of Haemonchosis
-Anemia PVC <15%
-Pale mucous membranes
-Hypoproteinemia
Submandibular edema (bottle jaw)
**God never intended for goats to live in a humid subtropical environment
-No immunity
-Degree of acquire immunity to regulate parasite numbers
-Goats: relative absence of acquired immunity

17
Q

Other Trichostrongylid parasites of Sheep and Goats

A
  • Teladorsagia circumcincta spp. a.k.a Ostertagia
  • Less pathogenic than in cattle
  • Disease associated with emergence of large number of worms
  • Trichostrongylus sp.
  • Less pathogenic
  • Disease associated with large numbers (10-100k) in nutritionally stressed animals
  • Nematodirus sp.
  • Less pathogenic
  • 10k worms considered significant
  • Spring concentration of larvae
  • Lambs and kids sick during late spring
18
Q

Basic principles of parasite control

A
  • ~5 sheep per acre
  • Reduce pasture contamination
  • Appreciate risk of disease (age susceptibility)
  • Use effective antihelmintics and know resistance status of drugs at the herd-level
  • FECs
  • Mixed cross species pastures, equids and ruminants do not share parasites
  • FECR was 68% at all dosages (IVM, Doramectin)

Fecal egg count reduction test

  • treat animals with preferred deworming drug
  • Follow up with FEC (7-10 days later)
  • Pre Tx EPG-Post Tx EPG/Pre Tx EPG x 100
  • Drugs with FECRs <90% effective should be discontinued
  • widespread drug resistance ~75-80%
  • *Use FAMACHA in combination w/ FEC as basis for selective deworming (High FEC shedders)
  • Prevent re-infection
  • Identify genetically resistant animals for breeding
  • Should not be used alone to make Tx decisions on individual animals
19
Q

FAMACHA scoring

Selective Deworming

A

3 cut off point. Use for practical basis to prescribe anthelmintic treatment at risk animals

Selective Deworming

  • just removing 50% of worms can result in clinical improvement most of the time
  • Let a few worms live is best
  • Treat high FEC shedders, which are responsible for 80% of pasture contamination
  • Reduces pasture contamination w/ less out of pocket cost for Tx of entire herd/flock
  • Allows animal to develop and maintain natural immunity
  • Highest FEC in TN late October
  • Use FEC to identify resistant livestock
  • Worm resistance is 1/4 inheritable and may be used for breeding stock
20
Q

Gastrointestinal Nematode

Parasites of Swine

A
  • Ascaris suum
  • Tricuris suis
  • Oesophagostomum dentatum
  • Stephanurus dentatus
  • Trichinella spiralis
  • Low in commercial operations
  • More common in organic “range-fed” production
21
Q

Ascarids suum

Swine round worm

A
  • Living in small intestines
  • Large
  • Dimorphic
  • Oral opening with three prominent lips
  • Worldwide distribution

Direct life cycle

  • 200k eggs/day
  • Infective larvated/embryonated egg ~28days in environment
  • Eggs resistant to freeze, up to 7 years
  • Paratenic host mouse
  • Tracheal migration
  • PPP = 8wks
  • Eggs 62x45um
  • Thick, albuminous coat

Clinical significance

  • Stunted growth and poor feed efficiency
  • Inflammation and hypoproteinemia from worm presence in gut
  • Impaction in severe cases
  • Pneumonia, respiratory distress
  • Liver contamination with granuloma from larvae migration “milk spots”
  • Sows infected while gestation on pasture MICE paratenic host ingestion
  • Piglets infected by sticky eggs on sows hair
  • Prevention by treatment, removal of paratenic host
  • FBZ effective in removal of adults and immature stages. NO WITHDRAWL Time
  • Pyrantel daily to prevent migration, 24 hrs WITHDRAWL time
  • Hygiene: wash sow prior to farrowing

Zoonotic significance

  • Case reports of larval migrants: eosinophilic pneumonia, hepatic lesions, test specificity questionable.
  • Use of untreated swine feces for manure fertilizer risk of contamination/infection to humans
22
Q

Trichuris suis

Swine Whipworm

A
  • Medium size worm
  • Live in cecum and large intestine
  • Sexually dimorphic
  • Stout body with whip-like esophagus

Direct Life cycle

  • Infective eggs larvated/embryonated develops in ~21 days in environment
  • Larvated eggs infective, persist in the environment for up to 7 years
  • Eggs resistant to freeze
  • Larvae may develop underneath epithelium
  • PPP = 7-9 wks
  • Eggs: bipolar lugs, 55x25um, golden brown, uninfective when passed in feces

Clinical significance

  • Stunted growth and poor feed efficiency in piglets
  • Ages 8-14 wks most affected
  • Anemia, diarrhea, dehydration, Dysorexia (abnormal appetite), weight loss.
  • Inflammatory response, Colitis, Mucosal necrosis and edema, Focal hemorrhage.

Zoonotic significance

  • Human trichuris morphologically indistinguishable from trichuris suis.
  • No evidence that transmissibility of parasite results in human disease
  • Recent induced infections to treat human autoimmune disorders
  • “hygiene hypothesis” and Chron’s disease
  • Down regulation of inflammatory and immune mechanisms influential in the disorder
23
Q

Oesophagostomum dentatum

Swine Nodular Worm

A
  • Sexually dimorphic males 8-10 mm, females 11-14 mm
  • Typical strongyle morphology
  • *Buccal capsule w/ leaf crown

Direct life cycle

  • Adults live in large intestine
  • Larvated eggs after 6-7 days in environment
  • L3 infective stage
  • Eggs need optimal temperature/humidity. Larvae subject to desiccation and extreme temperature
  • PPP = 6-7 wks
  • Larvae penetrates intestinal wall, develop and return to lumen as sub mature (L4 stage)
  • Become adults and reproduce

Clinical significance

  • Stunted growth and poor feed efficiency in piglets
  • *Nodule formation in gut and associated inflammation
  • Enteritis, Dysorexia, Blood-stained feces
  • Growers/finishers put on contaminated pastures at significant risk
  • Economic losses from condemned sausage casings

Dx:

  • Fecal flotation
  • Eggs 60-80 um x 35-40 um
  • Thin shelled morulated

Zoonotic significance

  • Not known to be zoonotic
  • African primates occasionally infected w/ own species of Oesophagostomum
24
Q

Stephanurus dentatus

Swine Kidney Worm

A
  • Strongyle-type worms living around the kidney
  • Dimorphic, males 20-30 mm, females 30-45 mm
  • Typical strongyle morphology
  • Well defined buccal capsule
  • Cosmopolitan distribution: worldwide

Direct life cycle

  • Adults live in ureters
  • Eggs passed in urine
  • Infective larvated eggs 4 days development in environment
  • Eggs need optimal temperature, subject to desiccation and extreme temperatures
  • L3 infective stage: larvae skin penetration, ingestion, ingestion of earthworm
  • Behaves like large strongyles
  • Larvae penetrates stomach wall and enters the hepatic blood supply
  • Extensive destruction resulting from migrations (3- 9 mts)
  • PPP = 9-16 mts

Clinical significance
-Pathology due to larvae migration
-Liver capsule, Peritoneal Cavity, Peri renal tissues
-Liver cirrhosis
-Typically a herd-wide health issue w/ overall ‘lack of growth’
-Dysorexia, poor growth, poor feed efficiency
-Condemnation at slaughter of liver, kidney, other choice cuts
Prevention:
-Attention to hygiene, avoid infection source
-Gilts only breed (keep 1 season only)

Dx:

  • Eggs 90-120 um x 43-70 um
  • Thin-shelled morulated
  • Uninfective passed in urine
  • Urine sample, mature in ureters

Zoonotic significance
-Not known
-Ocassionally found in situ with commercial meat
“indicative of poor butchering technique”

25
Q

Strongyloides ransomi

Swine Threadworm

A
  • Small worms
  • Adults in small intestine
  • *Only females parsitic

Homogonic and Heterogonic life cycle

  • Infection of neonatal piglets by hypobiotic larvae
  • Lactogenic route
  • PPP = 7 days of life!

High pathogenicity in suckling pigs
-Diarrhea, anemia, emaciation

Other routes of infection

  • *Ingestion of L3
  • *Percutaneous

Eggs: thin-shelled larvated, 50x35 um fecal flotation

26
Q

Trichinella sp.

Trichina worm

A
  • Salvatic life cycle
  • Rodents reservoir host
  • Encysted larva in meat
  • Zoonotic
  • ingestion of undercooked infected meat
  • Human dead end host
  • Larva in mucosa release circulation.
  • *Bear meat consumption risk of infection

Tx and prevention

  • Anthelmintic choices: IVM
  • Safeguard
  • No evidence of drug resistance
  • Attention to hygiene
  • Eggs must develop to infective stage
  • Larvae from strongylate species do not survive indoors
  • Segregate by age groups “All in All out”
27
Q

Gastrointestinal Parasites of Poultry

A

**Heterakis gallinarium vector for Histomonas meleagridis to turkey

  • Ascaridia galli
  • Heterakis gallinarium
  • Syngamus trachea
  • Spiruid nematodes

Impact of parasitism in poultry production large a factor of natural organic range-free operations

28
Q

Ascaridia galli

Poultry Roundworm

A
  • Stout worms with three lips
  • Dimorphic
  • Adults live in the small intestine

Direct life cycle

  • Ingestion of larvated eggs
  • Develop in intestine
  • No tracheal/somatic migration
  • Pathology from penetration and inflammation in duodenal mucosa: impaction in severe infections
  • *young birds most susceptible to disease
  • Age acquired immunity >3mts of age

Clinical signs
-Weak birds, emaciated, decreased egg production

29
Q

Heterakis gallinarum

Poultry Cecal worm

A
  • Adults live in the cecum
  • Stout worms with two lips
  • Dimorphic

Direct life cycle

  • Earthworm as paratenic host
  • *Vectors of “Blackhead” (enterohepatitis) in turkey: Histomonas meleagridis protozoan parasite remains viable/protected in eggs
  • Pathology marked by thickening of cecal mucosa
  • Contrast with H.isolonche (in game brids): nodular lesions, typhlitis, caseous lesions, diarrhea, wasting and death

Dx:

  • Eggs in fecal flotation, similar morphology for Ascaridia & Heterakis.
  • Heterakis 65-80 x 35-45 um
  • Ascariadia 73-92 x 45-57 um
  • *Not immediately infective
  • *Must undergo development to infective stage in the environment
  • *Similar biological features in common with all Ascarid-type nematodes
30
Q

Capillaria spp.

A
  • Adults live in the intestine, esophagus, or crop of bird
  • Stout body with elongated whip-like esophagus

Direct, facultative and indirect life cycles

  • Earthworm as paratenic host, perhaps intermediate host
  • Pathology based on the site of infection
  • Emaciation, hemorrhagic diarrhea, Dysorexia, death
  • Hyperplasia of crop and esophagus
  • Important in deep litter poultry houses, range yards, where hyper-contamination occurs
31
Q

Syngamus trachea

Gape Worm

A
  • Strongylate parasites
  • Living in the trachea of birds
  • Medium size worms
  • Bright red coloration
  • Permanently in copula

Direct and Facultative indirect live cycle

  • Eggs coughed up, discharged from host
  • Larvae susceptible to adverse environmental conditions
  • Earthworm important paratenic host
  • Ingested larvae undergoes tracheal migration
  • *Reproduction in bronchi and trachea

Clinical signs

  • Ecchymoses, edema, lobar pheumonia
  • ‘Gape” behavior
  • Open mouth, dyspnea and asphyxia from accumulated mucus in mouth
  • Emaciation and death
32
Q

Spiruid Nematodes

A

-Adults live in the gizzard, proventriculus, esophagus, etc.

Obligate indirect life cycle
-Orthoptera (crickets) Coleoptera (beatles) intermediate host

Clinical signs

  • Pathology and etiology associated with site of infection
  • Emaciation, hemorrhagic diarrhea w/ intestinal species
  • mild infections unremarkable
  • Disease susceptibility in younger birds

Tx:

  • Prevention based on avoidance of hyper-contaminated environments
  • Segregate by age group “All in All out”
  • Wide selection of anthelmintic drugs: withdrawal times