broiler syndromes and internal parasites
TRANSCRIPT
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Broiler Syndromes & Internal Parasites
Rafael Monleon, DVM, MSpVM, ACPVRegional Technical Services Veterinarian (ASIA)
Aviagen School – June 08th 2012Huntsville, AL (USA)
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Topics• Spiking Mortality Syndrome (SMS)• Inflammatory Process / Cellulites• Ascites• Monleon-India Metabolic Syndrome (MIMS)• Green Muscle / Oregon Disease• Runting / Stunting Syndrome (RSS)• Gangrenous Dermatitis• Internal Parasites
– Not Coccidia
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Syndromes• What is a syndrome?
– Disease of unknown or poorly understood cause– Usually multifactorial– Often difficult to fix
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Spiking Mortality Syndrome (SMS)• Broiler disease characterized by
– Head and body tremors– Blindness– +/- spike in mortality– Litter eating– Low Blood Sugar (Hypoglycemia)– Incoordination
• Seen in all breeds and breed crosses, particularly in the fastest growing breeds and with males
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SMS - Clinical Signs• Age of onset
– Usually 7 – 20 days of age– May be as late as 35 days of age
• Clinical signs– Prostration– Blood glucose <150 mg/dl– Affected birds usually 40 – 100 mg /d (seen 18mg!!)– Blindness
• Post mortem lesions– Litter in gizzard– Rickets– Signs of being “off feed”
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SMS – Diagnosis
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SMS – Clinical Signs
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SMS – Post Mortem
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SMS – Post Mortem
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SMS - Secondary Problems• Leg Health Issues
– Rickets– Hock join infections– Tibial Dyschondroplasia (TD)– Osteomyelitis (FHN)
• Poor body weights and uniformity• Airsacculitis
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SMS - Secondary Problems
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SMS - Etiology
• Most commonly related to:– Rapid growth rate– Inadequate feed availability / accessibility– Stressful environment
• Management– Poor ventilation– Poor temperature control (cold brooding)– Lighting (24 hours light)
• Recent Vaccination– Small eggs / Small chicks– Viral Infection ?? – Arenavirus
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SMS - Possible Contributors
• High Level of animal by-products in starter feed
• Poor quality soy bean meal (SBM)• Mycotoxins• Repeat Farms• Light/Dark Cycle – related to melatonin
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SMS - Treatments
• Immediately place flock on 6 continuous hours of darkness
• Check for feed availability problems– Migration away from trigger pan– Inadequate feeder space
• Vitamin supplementation (Vitamin D)• Sugar administration in drinking lines
– 0.5kg / 4l stock solution• Ensure lines cleaned prior administration
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Prevention of SMS – Aviagen Lighting Program
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Prevention of SMS – Lighting Program
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Prevention of SMS – Alternative Lighting Program
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SMS - Prevention• Do not let chicks run out of feed, especially
during ages of increase likelihood for SMS• Proper cleaning and disinfection between flocks• Proper lighting program• Minimize stress• Coccidiosis control
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• Necrotic Dermatitis ; “Inflammatory Process”• Commonly Associated to E. coli y S. aureus
• TRIGGER > Skin Scratches > SQ Inflammatory Lesion
• Downgrades and Condemnations Processing• Incidence is ↑ if scratches are recent (<7d)
• Gangrenous Dermatitis / Colisepticemia
IP / Cellulitis
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IP – Environment
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IP – Environment
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IP – Lesions
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• Density
• Feed Space / Water Space
• Feeding Programs
• Slow-feathering breeds
• Nutritional
• Lighting Programs
• Other Management Factors
• Mechanical Failures
• Farmer
IP / Cellulitis - Factors
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Ascites• Ascites can be triggered by many factors
– Ascites = Fluid in abdominal cavity• Liver, Kidney, Lungs, Others
• Hypoxia (lack of oxygen)– Broiler chicken high demand for oxygen necessary to
fuel metabolic processes– Metabolic needs under various conditions forces the
heart to pump more blood through the lungs – Extreme stress on the right ventricle of heart
• Normally the right ventricle is relatively small, but in the case of ascites, this ventricle becomes greatly dilated
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Ascites - Pathogenesis
INCREASED CARDIAC OUTPUT
Hepatic Congestion Transudation
Ascites
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Ascites
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Ascites - Genetic Selection
• Oxymeter• Stress test: grow under harsh condition• Electrocardiogram• High altitude growing
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Minimizing Ascites
• Slow down early growth rate– Lighting programs– Nutrition - heat-feeding
• Temperature control– No cold brooding temps (YES, Tropical Countries!)
• Good ventilation• Grow males at lower altitude• Caution with salt levels in diet• Limit respiratory disease
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Monleon-India Metabolic Syndrome • New Presentation• Leading cause of mortality in South Asia• Males / Heavy birds more affected• Uniformity problems from day 8-10 and
onwards• After 19-28 days Respiratory Noise• >28 – High Mortality• T: Rapid growth, heat, feed availability
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MMS• 8-10 days
– Early Heart Abnormalities – Friction Marks– Decreased Uniformity
• 17-19 days– Moderate Panting at fair EC– Mild respiratory noise – Moderate Hydropericardium and RVH
• 26-28d > Onwards– Severe Panting - Severe respiratory noise at fair EC– Severe Hydropericardium and RVH, Congested liver, Ascites
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IN PICTURES
Mortality Records Late MortalityCRD???
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CLINICAL SIGNS
Birds Panting Continuously – even when temperature was below 29C (Fair EC)
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CLINICAL SIGNS
CRD???????
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POST-MORTEM EXAMINATION
12d Friction Marks21/28d
Hydropericardium
21/28d Right Ventricular
Hypertrophy
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PM – Open
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PM – Open
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PM – Open
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PM – Open
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POST-MORTEM EXAMINATION
21/28dAscites
Liver Congestion Hydropericardium
21/28d Ascites
Liver CongestionRight Ventricular
Hypertrophy
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1. TRIGGER (i.e. HEAT) 2. INCREASED METABOLIC RATE 3. INCREASED OXYGEN DEMAND
4. INCREASED CARDIAC OUTPUT 5. PULMONARY HYPERTENSION
6. RIGHT VENTRICULAR HYPERTROPHY 7. RIGHT VENTRICULAR VALVE INSUFFICIENCY
8. RIGHT VENTRICULAR FAILURE 9. OEDEMA - ASCITES
10.DEAD
AT SOME POINT DURING 4/5 THERE IS AN INCREASE IN PERICARDIAL FLUIDTHAT CONTINUES TO THE POINT OF MAKING DIFFICULT THE NORMAL
BREATHING OF THE BIRDS – THEREFORE THE PANTING AND RESP SOUND.
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… PLUSFORCED PANTING
RESPIRATORY ALKALOSISINCREASE IN BLOOD pH
DEPLETION OF K (POTASSIUM) + OTHER ELECT.DECREASE AMMOUNT OF IONIZED Ca
(increased pH binds Ca to proteins)
DEAD
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MIMS - Control• How do we fix this?• MANAGEMENT
– FEED RESTRICTION• Feed Restriction from 7d and onwards seems THE BEST
– LIGHT• Follow Aviagen Program
– OTHERS
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MIMS - Control
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MIMS - Control
A A
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MIMS - Control
A A
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Green Muscle Disease
• Oregon Disease / Deep Pectoral Myopathy
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Green Muscle Disease
• First seen in heavy turkeys• Now common in heavy broilers
– Generally >2.5kg• Necrosis of deep pectoral breast muscle
– Lack of blood supply (ischemia)• No infectious• No public health significance• Affects appearance of meat
– Consumer complaints
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Pathogenesis
• Deep pectoral muscle has a tough, inelastic outer sheath
• The outer of major muscle is surrounded by loose connective tissue that moves easily over the muscle surface as the muscle profile changes
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Pathogenesis
• Wing flapping increases the blood supply to the deep pectoral muscle
• As muscular work continues and the muscle grows / expands the sheath around it restricts movement expansions
• Increase intra-muscular pressure restricts blood supply to the muscle eventually leading to ischemic necrosis
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Green Muscle Disease
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Category 1
• Acute inflammatory lesions as red, hemorrhagic muscle and hemorrhages on fibrous sheath.
• Serous fluid in the area so appears wet.
• Likely associated with a handling event such as catching and will be present for about 48 hrs.
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Category 2• Inner filet well defined
sometimes circumscribed by hemorrhagic ring
• Pale pink to plum colored
• Changes consistent with early coagulative necrosis of muscle,tissue texture becomes fibrous
• This stage continues until about 6-7 days after initial event
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Category 3
• Greening of the damaged tissue
• Often only the middle part of the fillet is involved
• Lesion/area becomes “putty” like consistancy
• Green/necrotic area will persist for many months
• Symmetry of breast lost in some older birds
• Generally > 7d
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Green Muscle Disease
• Reported incidence highly variable• > 50% lesions reported as category 2 type and
occur a week before slaughter• Of the remainder the rest appear as
– Category 1 type : Catching and Hauling– category 3 type : Thinning and Weighing
• Killed injections into deep pectoral muscle in breeders
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Green Muscle Disease - Prevention
• Reduce density• Adequate feed/water space• Lighting programs
– Dimmers? – Intensity too high in house
• Prevent over excitation of birds • IBV
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Green Muscle Disease - Prevention
• Handling and catching practices– During the day? Too much activity?
• Live haul/Unloading/Hanging conditions– Too much light
• Proper levels of Vitamins E, C, and Selenium
• Are there also scratches in broilers?
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Spot the difference!
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Runting Stunting Syndrome
• Synonyms – RSS– Malabsorption Syndrome– Many Others
• Differentiate RSS from 1-2% “bottom end” birds in an average broiler flock
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RSS - Clinical Signs
• Usually starts at 4-8 days – Affected chicks 20-40g lighter than normal flock
• Huddling behavior • Ruffled feathers / down• Coprophagia (feces/litter eating) • Mucoid diarrhea/ pasted vents
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RSS - Clinical Signs
• Two weeks of age– Retained down feathers head and neck– “Yellow heads”– Broken displaced primary feathers – “Helicopter birds” – Pale shanks – Feed passage??
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RSS – Gross Lesions
• Often no lesions except intestinal• Intestines
– Thin / Pale– Often contain watery or mucoid material– Cecas often distended (foamy, watery)
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RSS – Gross Lesions
• Secondary lesions– Rickets – Atrophied bursa, thymus– Gizzard erosions – Proventriculitis
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RSS
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RSS
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RSS
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RSS
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Pale Shanks
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Ricketts
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RSS
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RSS
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RSS
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Litter in Gizzard
Mucous droppings
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RSS
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RSS – Breeder Influence
• Often young breeder flocks involved– 35 weeks of age or less– Increased focus on brooding
• Often more problems in high performing flocks
• Progeny from flocks Salmonella enteriditis positive more prone to RSS
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RSS – Breeder Influence
• Chick Rectal Temperatures-Hatcher• >104.5F(40.5C can cause long term
damage to intestinal cells• Poor growth rates and FCR
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RSS – Management and Health Factors• Biosecurity• Adequate down time between flocks > 14
days• Excellent clean-out/disinfection helps
– 10% formalin very good– Suggests viral/bacterial component
• Multiage facilities worse • Younger age on farm usually more
affected
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RSS – Management and Health Factors• Brooding Temperatures
– Critical on broilers from young breeder flocks– Chick behavior best indicator
• Feed and Water Availability and Access– Don’t remove all supplemental water and
feeders on one day– Usually remove over 3days
• Brooding area – Don’t leave in too small an area too long
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… not really good for brooding areas
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… not really good for brooding areas
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… not really good for brooding areas
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… better for brooding
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RSS
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RSS
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RSS
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RSS - Possible Etiology• It is most likely that a virus is involved in
this syndrome• Many virus isolated from clinical case
– Reovirus – Astrovirus – Rotavirus – Adenovirus– Others?
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RSS – Virus Etiology• Hard to re-create the disease with the
viruses– Need the interaction of other environmental,
disease, management or nutritional factors• If a virus is involved is it vertically shed?• If a virus is identified, killed vaccines to
parents could be helpful in certain situations to give progeny early protection– i.e.Reovirus
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Gangrenous Dermatitis• Multifactorial condition with a complex
interaction of bacteria and predisposing factors
• >30 through 45d• Problem has re-emerged after
disappearing for many years– “Clean House Syndrome”
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Gangrenous Dermatitis• Etiology
– Clostridium septicum – Clostridium perfringens – Staphylococcus aureus
• Contributing factors – Immunosuppression – Scratches – Intestinal health
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Gangrenous Dermatitis – Clinical Signs• Usually seen after
28 days of age• Fever, depression,
mortality (5-25%), little condemnations
• Abdomen, hip, leg and wing
• Edema, fluid and gas
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Barnes, NCSU
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Clostridium
PasteurellaStaph
Coliforms
Immunosuppression + infections with opportunistic
bacteria =GANGRENOUS DERMATITIS
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GD – Immunosuppression• Immunization and serology against CAV
– Pullets 100% antibody positive before onset of production
• Maternal immunity vs. IBDV– including variant strains
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GD – Intestinal Health• Growing evidence that intestine is source
of infection in many cases• Cocci and intestinal bacteria population
shifts are possible factors– Clostridium > N.E.
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GD – Prevention• No cold brooding • Reduce bacterial load in the environment
– Down time (<14 days increases risk) – Cleaning and disinfection (repeat farms) – Floor treatments: sulfur, salt, muratic acid– Litter pH (acidifiers)
• Light control to reduce skin scratches
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GD – Treatment• If mortality <0.1% /day
– Vitamin E– Water Acidifiers
• And/or selenium• And/or copper
sulfate
• If mortality >0.1% /day
– Penicilin– Lincomycin– Erythromycin– Oxytetracycline– Tylosin tartrate
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Internal Parasites
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Common Internal Parasites of Chickens
• Worms – Round worms - Ascaridia sp. – Cecal worms - Heterakis gallinarum – Hair worms - Capillaria obsignata– Tape worms - Raillietina cesticillus + others
• Histomoniasis (“Blackhead”)• Others
– Leukocytozoonosis
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Intestinal Worms• Commonly diagnosed during necropsy• Severe intestinal worm infestations can
cause diarrhea, poor absorption of nutrients, and enteritis
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Intestinal Worms – Clinical Signs• Clinical signs commonly seen include:
– rough feathering – retarded growth – pasty vents– pale birds
• Worms can be carriers of infectious diseases, including Blackhead (Histomonas meleagridis)
• Early preventative programs are necessary for control of intestinal worms
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Intestinal Worms – Prevention• Cleaning out houses every flock minimizes
exposure to intestinal worms– ↓ worm eggs for the next flock – ↓ darkling beetles associated as carriers for worm
transmission• Although clean-out programs are ideal,
occasionally outbreaks will occur
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Intestinal Worms – Ascaridia • Ascaridia galli most common in chickens• Mature worms - A. galli size
– Males - 1 1/2-2 1/2 in. long– Females - 2-4 in. long – Size affected by crowding
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Ascaridia – Life Cycle
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Ascaridia – Transmission & Clinical Signs
• Transmission– Ingestion of sporulated eggs from contaminated
environment• Clinical signs usually seen only in backyard
flocks – Depression, loss of weight, diarrhea
Retarded growth• Lowered egg production in heavy infection (can
occur in caged layers exposed to contaminated flies)
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Ascaridia – Treatment• Worming
– Piperazine: NOT very effective• Fast resistance develops • Only paralyze adult worms – Juvenile not affected
– Levamisole hydrochloride – Albendazole – Oxfendazole – Fenbendazole– Ivermectin
• Management:cleanout,treatdirtfloors(salt),fly control (they can carry eggs mechanically)
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Intestinal Parasites - Cecal Worms• Heterakis gallinarum• Primary importance - transmitting Blackhead
(Histomoniasis) in turkeys and chickens• Mature worms - 3/8 to 3/4 inch long
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Cecal Worms – Heterakis gallinarum
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Cecal Worms – Life Cycle• DIRECT - similar to ascarids. About 65 days to
complete. (Not seen in broilers)• Eggs infective up to 230 weeks on the ground• May be transmitted by earthworms• H. gallinarum eggs pick up Histomonads
(Protozoa) in gut of infected birds
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Cecal Worms – Treatment• Worming
– Levamisole hydrochloride – Albendazole – Oxfendazole – Fenbendazole – Ivermectin
• Management: clean out, treat dirt floors (salt)
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Cecal Worms – Prevention of Blackhead
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Hair Worms – Capillaria• Rarely a problem in broilers• Can cause severe problems specifically in
pullets/cockerels:– Unthriftiness, poor uniformity and BW, poor
feathering, decreased EP.• Severe emaciation, diarrhea, hemorrhagic
enteritis, anemia• ½ - ¾ in.long - hair-like • Life cycle – direct & indirect (e.g. earthworms• Eggs infective up to 102 weeks
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Hair Worms – Capillaria
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Hair Worms – Capillaria Screening
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Hair Worms – Capillaria Eggs
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Capillaria - Treatment• Worming
– Levamisole hydrochloride – Albendazole – Oxfendazole – Fenbendazole – Ivermectin
• Drugs often take a higher dose than for Ascarids (e.g. levamisole need 2 X for treatment of Caps vs. Roundworms)
• Hygromycin best for prevention and not treatment• Treat multiple times if stay on same litter
– Best treat before move to breeder house
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Tape Worms• Seven species affect chickens• All require intermediate hosts (e.g. insects)• Raillietina cesticillus most commonly found - darkling
beetle - intermediate host
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Tape Worms
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Tape Worms - Treatment• Worming
– Albendazole• Treat the intermediate host population
– insect control
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Histomoniasis – Blackhead
• Multifaceted disease process affecting chickens and turkeys
• More common in turkeys due to their increased susceptibility
• Recently, clinical cases associated with management practices have been identified in pullets and cockerels
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Blackhead – Infectious Agents Involved
Four components:
1. Primary agent - Protozoal organism • Histomonas meleagridis
2. Cecal worm - Heterakis gallinarum3. Exposure to live coccidias
4. Secondary bacterial infections
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• Other possible vectors– darkling beetles– flies– crickets
• Extended survival of the protozoa is accomplished through the survivability of the cecal worm ova (built-up litter)
Other Factors
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• Range from mild and/or unnoticable to severe with high mortality
• May resemble cecal coccidiosis– i.e. bloody cecal discharge– cecal cores
• Can affect uniformity and future reproductive performance of the flock
• Often in chickens associated with coccidiosis.
Blackhead – Clinical Symptoms
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Characteristic liver lesions
- usually a circular, depressed area of necrosis
- up to 1 cm in diameter
- circumscribed by a raised ring
- in heavy infections, may be small and numerous
Blackhead - Necropsy Lesions
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Cecal cores- cecal walls may
be thickened- serous and/or
hemorrhagic exudate may be present in the cecal lumen
- caceous or cheesy cores, with ulceration of cecal wall in advanced cases
Blackhead - Necropsy Lesions
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• Control of cecal worm• Hygromycin (Hygromix-B, Elanco)• Extra-label use of dewormers
– Levamisol– Ivermectin
• Piperazine is not effective against the cecal worm• Often there is a misconception about the potential risk
of this parasite!
Prevention and Control
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• Proper litter management - will help to decrease bacterial load and reduce cecal worm ova– Moisture control – Litter treatments– House cleaning and disinfection
• Insecticides may help to reduce insect populations
Prevention and Control
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Prevention and Control
• Problem is effective treatments for “Blackhead” have been removed from some markets– Old drugs to treat : Nitroimidazoles,
Nitrofurans and Phenylarsonic Acid Derivates
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• Nitarsone (Histostat - Alpharma)– Mainly prevention
• Hygromycin-B (Hygromix - Elanco) – Prevention – Some effect on outbreaks
Prevention and Control
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3-nitro and feed boost
• Very useful to help the flocks recover from infections
• May be used in flocks as young as 4 wks
• Less efficacious in flocks >12 wks
Prevention and Control
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Leukocytozoonosis
• Chicken Malaria• Protozoan organism which infects blood
cells and tissues.• Mostly seen in very hot or tropical areas in
which mosquitoes or biting flies are common.
• Young birds more affected.• Mortalities can be very high with no
treatment or prevention.
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Leukocytozoonosis
• Transmission - Through insect only– Insect remains infective for 18 days– Infected poultry are the vectors
• Signs– Acute outbreaks - anemia, fever, weakness, loss of
appetite, dullness, lameness, decreased egg production, death
– Fatalities begin a week after exposure
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Leukocytozoonosis
• Lesions– Anemia, enlarged liver and spleen,
hemorrhages muscle, respiratory distress.• Diagnosis
– Blood smear to look for organism– Associated signs with known prevalence of
disease in the area.
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Leukocytozoonosis• Treatment:
– Sulfa Drugs - Best is Daimeton sodium [contains 98% Sodium sulfamonomethoxine], which usually comes in 100 gm packs.Give 40 gm Daimeton/400 gallons for 3-5 days[watch out sulfa drugs in hot weather].
• Prevention: – 55 ppm of Daimeton sodium in the feed to laying birds
2 weeks per month during insect season [for example during the rainy season]
– Control insects, usually less of a problem where closed housing is practiced.