broiler syndromes and internal parasites

Broiler Syndromes & Internal Parasites

Rafael Monleon, DVM, MSpVM, ACPVRegional Technical Services Veterinarian (ASIA)

Aviagen School – June 08th 2012Huntsville, AL (USA)

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

Syndromes• What is a syndrome?

– Disease of unknown or poorly understood cause– Usually multifactorial– Often difficult to fix

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

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”

SMS – Diagnosis

SMS – Clinical Signs

SMS – Post Mortem

SMS - Secondary Problems• Leg Health Issues

– Rickets– Hock join infections– Tibial Dyschondroplasia (TD)– Osteomyelitis (FHN)

• Poor body weights and uniformity• Airsacculitis

SMS - Secondary Problems

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

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

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

Prevention of SMS – Aviagen Lighting Program

Prevention of SMS – Lighting Program

Prevention of SMS – Alternative Lighting Program

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

• 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

IP – Environment

IP – Lesions

• Density

• Feed Space / Water Space

• Feeding Programs

• Slow-feathering breeds

• Nutritional

• Lighting Programs

• Other Management Factors

• Mechanical Failures

• Farmer

IP / Cellulitis - Factors

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

Ascites - Pathogenesis

INCREASED CARDIAC OUTPUT

Hepatic Congestion Transudation

Ascites

Ascites

Ascites - Genetic Selection

• Oxymeter• Stress test: grow under harsh condition• Electrocardiogram• High altitude growing

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

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

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

IN PICTURES

Mortality Records Late MortalityCRD???

CLINICAL SIGNS

Birds Panting Continuously – even when temperature was below 29C (Fair EC)

CLINICAL SIGNS

CRD???????

POST-MORTEM EXAMINATION

12d Friction Marks21/28d

Hydropericardium

21/28d Right Ventricular

Hypertrophy

PM – Open

POST-MORTEM EXAMINATION

21/28dAscites

Liver Congestion Hydropericardium

21/28d Ascites

Liver CongestionRight Ventricular

Hypertrophy

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.

… 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

MIMS - Control• How do we fix this?• MANAGEMENT

– FEED RESTRICTION• Feed Restriction from 7d and onwards seems THE BEST

– LIGHT• Follow Aviagen Program

– OTHERS

MIMS - Control

MIMS - Control

A A

Green Muscle Disease

• Oregon Disease / Deep Pectoral Myopathy


• 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

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

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

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.

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

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


• 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

Green Muscle Disease - Prevention

• Reduce density• Adequate feed/water space• Lighting programs

– Dimmers? – Intensity too high in house

• Prevent over excitation of birds • IBV

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?

Spot the difference!

Runting Stunting Syndrome

• Synonyms – RSS– Malabsorption Syndrome– Many Others

• Differentiate RSS from 1-2% “bottom end” birds in an average broiler flock

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

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??

RSS – Gross Lesions

• Often no lesions except intestinal• Intestines

– Thin / Pale– Often contain watery or mucoid material– Cecas often distended (foamy, watery)

RSS – Gross Lesions

• Secondary lesions– Rickets – Atrophied bursa, thymus– Gizzard erosions – Proventriculitis

Pale Shanks

Ricketts

Litter in Gizzard

Mucous droppings

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

RSS – Breeder Influence

• Chick Rectal Temperatures-Hatcher• >104.5F(40.5C can cause long term

damage to intestinal cells• Poor growth rates and FCR

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

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

… not really good for brooding areas

… better for brooding

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?

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

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”

Gangrenous Dermatitis• Etiology

– Clostridium septicum – Clostridium perfringens – Staphylococcus aureus

• Contributing factors – Immunosuppression – Scratches – Intestinal health

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

Barnes, NCSU

Clostridium

PasteurellaStaph

Coliforms

Immunosuppression + infections with opportunistic

bacteria =GANGRENOUS DERMATITIS

GD – Immunosuppression• Immunization and serology against CAV

– Pullets 100% antibody positive before onset of production

• Maternal immunity vs. IBDV– including variant strains

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.

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

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

Internal Parasites

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

Intestinal Worms• Commonly diagnosed during necropsy• Severe intestinal worm infestations can

cause diarrhea, poor absorption of nutrients, and enteritis

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

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

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

Ascaridia – Life Cycle

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)

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)

Intestinal Parasites - Cecal Worms• Heterakis gallinarum• Primary importance - transmitting Blackhead

(Histomoniasis) in turkeys and chickens• Mature worms - 3/8 to 3/4 inch long

Cecal Worms – Heterakis gallinarum

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

Cecal Worms – Treatment• Worming

– Levamisole hydrochloride – Albendazole – Oxfendazole – Fenbendazole – Ivermectin

• Management: clean out, treat dirt floors (salt)

Cecal Worms – Prevention of Blackhead

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

Hair Worms – Capillaria

Hair Worms – Capillaria Screening

Hair Worms – Capillaria Eggs

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

Tape Worms• Seven species affect chickens• All require intermediate hosts (e.g. insects)• Raillietina cesticillus most commonly found - darkling

beetle - intermediate host

Tape Worms

Tape Worms - Treatment• Worming

– Albendazole• Treat the intermediate host population

– insect control

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

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

• 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

• 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

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

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

• 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

• 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



• Problem is effective treatments for “Blackhead” have been removed from some markets– Old drugs to treat : Nitroimidazoles,

Nitrofurans and Phenylarsonic Acid Derivates

• Nitarsone (Histostat - Alpharma)– Mainly prevention

• Hygromycin-B (Hygromix - Elanco) – Prevention – Some effect on outbreaks


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


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.

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

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.

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.

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broiler syndromes and internal parasites

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