Exam2 Flashcards
Gastrointestinal Nematodes of Horses
**Strongyles Large -3 species Small -Several different genera -Many different species **Ascarids -Parascaris equorum **Pinworms -Oxyuris equi **Spiruid worms of incidental interest
Large stongyles and small strongyles
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
Large Strongyles
Strongylus Vulgaris 6 mts
Strongylus equinis 8 mts
Strongylus edentatus 12 mts
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
Small Strongyles
Large Strongyles
- 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
Deworming products
3 families
- Bensimidazoles (B-tubulin synthesis)
- Imidazothiazole (nicotinic agonists)/ Tetrahydropyrimidines
- 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
Nematodes of Horses
Ascarids
Pinworms
Draschia/Habronema
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
OXyuris equi
Equine Pinworm
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
Strongyloides westeri
Equine Threadworm
-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
Draschia and Habronema
Equine Stomach Worms
- 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
Ecology, epidemiology and disease risk horses
-Horse feral, nomadic, little contact with the same infective pasture before domestication
Principles of parasite control
- Pasture contamination: best 1-2 horse/Acre
- Pasture infectivity: Low FEC horses allow to graze
- Differential risk of infection/disease: young animals associated with high FEC
- Parascarids equorum - Pasture hygiene and management
- 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
Parasite control for 1st year, @nd year, 3rd year
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.
Trichostrogylid Nematode Parasite of Cattle, sheep, goats, and camelids
- 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
Ostertagia spp.
Brown stomach worm
- 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
Other trichostrongylid parasites of cattle
- 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
Anthelmintic control of parasite in herd animals
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
Haemonchus contortus ‘Barber Pole Worm”
Gastrointestinal Nematode Sheep and Goat
- *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
Other Trichostrongylid parasites of Sheep and Goats
- 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
Basic principles of parasite control
- ~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
FAMACHA scoring
Selective Deworming
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
Gastrointestinal Nematode
Parasites of Swine
- Ascaris suum
- Tricuris suis
- Oesophagostomum dentatum
- Stephanurus dentatus
- Trichinella spiralis
- Low in commercial operations
- More common in organic “range-fed” production
Ascarids suum
Swine round worm
- 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
Trichuris suis
Swine Whipworm
- 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
Oesophagostomum dentatum
Swine Nodular Worm
- 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
Stephanurus dentatus
Swine Kidney Worm
- 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”
Strongyloides ransomi
Swine Threadworm
- 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
Trichinella sp.
Trichina worm
- 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”
Gastrointestinal Parasites of Poultry
**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
Ascaridia galli
Poultry Roundworm
- 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
Heterakis gallinarum
Poultry Cecal worm
- 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
Capillaria spp.
- 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
Syngamus trachea
Gape Worm
- 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
Spiruid Nematodes
-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
