Bordetellosis is an upper respiratory disease, primarily seen in young turkeys, caused by infection with
Bordetella avium. This subject has recently been reviewed (Skeels and Arp, 1997). The disease is characterized in young turkeys by sneezing, oculonasal discharge, mouth breathing, tracheal collapse, and stunted growth. The disease is most commonly referred to as turkey coryza because its clinical appearance is somewhat similar to the clinical signs of infectious coryza in chickens.
Bordetella avium infects and causes disease in turkeys, chickens, and Japanese quail. The disease in chickens is mild in comparison to the disease in turkeys and B. avium may play only a secondary role in respiratory
disease in young chickens. In young turkeys, the disease is very contagious and acute signs of upper respiratory disease spread rapidly through a flock. Morbidity may reach 100% but the mortality rate is typically 5% or less.
Feed intake and body weight gain are negatively impacted, which contributes to the overall poor performance
of a B. avium-infected young turkey flock. The signs of the respiratory disease typically abate in 2 to 4
wk. Vaccination of turkeys to prevent bordetellosis has had only limited success. Inactivated B. avium whole cell bacterins have been used to immunize turkey breeder hens for the purpose of producing high levels of
maternal antibodies in the progeny. Although it appears that maternal antibodies delay the onset of infection in
the progeny, they do not successfully prevent infection nor eliminate the signs of the disease. A temperaturesensitive live vaccine has also been extensively used to immunize young poults. The use of the vaccine has generally been less than successful. It may be that poults are incapable of responding adequately to B. avium antigens at a very young age. Antibiotic treatment of flocks suffering with bordetellosis has provided minimal clinical improvement.
Porcine Reproductive & Respiratory Syndrome (PRRS)
PRRS is caused by a virus which was first isolated and classified as an arterivirus as recently as 1991. The disease syndrome had been first recognised in the USA in the mid 1980's and was called "mystery swine disease". It has also been called blue ear disease. The name porcine arterivirus has been proposed recently.
The virus of PRRS has a particular affinity for the macrophages particularly those found in the lung. Macrophages are part of the body defences. Those present in the lung are called alveolar macrophages. They ingest and remove invading bacteria and viruses but not in the case of the PRRS virus. Instead, the virus multiplies inside them producing more virus and kills the macrophages. Once it has entered a herd it tends to remain present and active indefinitely.
Up to 40% of the macrophages are destroyed which removes a major part of the bodies defence mechanism and allows bacteria and other viruses to proliferate and do damage.
A common example of this is the noticeable increase in severity of enzootic pneumonia in grower/finisher units when they become infected with PRRS virus.
It may take up to a year for all breeding stock, particularly in large herds, to become infected for the first time and although the virus appears to spread rapidly in a herd it may be some 4 -5 months before at least 90% of the sows have become sero-positive. Some sows remain naive. Furthermore, it is not uncommon for sow herds 1-2 years after infection to contain less than 20% of serological positive animals. This does not however necessarily mean they are not still immune nor does it mean that they have stopped passing on immunity to their offspring. Adult animals shed virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.
The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRS for the first time one will show no recognisable disease, the second would show mild disease and the third moderate to severe disease. The reasons for this are not clearly understood. However the higher the health status of the herd, the less severe are the disease effects. It may be that the virus is mutating as it multiplies, throwing up some strains that are highly virulent and some that are not.
PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.
The virus of PRRS has a particular affinity for the macrophages particularly those found in the lung. Macrophages are part of the body defences. Those present in the lung are called alveolar macrophages. They ingest and remove invading bacteria and viruses but not in the case of the PRRS virus. Instead, the virus multiplies inside them producing more virus and kills the macrophages. Once it has entered a herd it tends to remain present and active indefinitely.
Up to 40% of the macrophages are destroyed which removes a major part of the bodies defence mechanism and allows bacteria and other viruses to proliferate and do damage.
A common example of this is the noticeable increase in severity of enzootic pneumonia in grower/finisher units when they become infected with PRRS virus.
It may take up to a year for all breeding stock, particularly in large herds, to become infected for the first time and although the virus appears to spread rapidly in a herd it may be some 4 -5 months before at least 90% of the sows have become sero-positive. Some sows remain naive. Furthermore, it is not uncommon for sow herds 1-2 years after infection to contain less than 20% of serological positive animals. This does not however necessarily mean they are not still immune nor does it mean that they have stopped passing on immunity to their offspring. Adult animals shed virus for much shorter periods of time (14 days) compared to growing pigs which can excrete for 1-2 months.
The clinical picture can vary tremendously from one herd to another. As a guide, for every three herds that are exposed to PRRS for the first time one will show no recognisable disease, the second would show mild disease and the third moderate to severe disease. The reasons for this are not clearly understood. However the higher the health status of the herd, the less severe are the disease effects. It may be that the virus is mutating as it multiplies, throwing up some strains that are highly virulent and some that are not.
PRRS infects all types of herd including high or ordinary health status and both indoor and outdoor units, irrespective of size.
Dysenterie
De ziekte dysenterie Dysenterie, ook wel bekend als ‘Vibrio’, is een infectie in de dikke darm die diarree veroorzaakt.
Verschijnselen Dysenterie komt vooral voor bij vleesvarkens en opfokvarkens, maar ook bij gespeende biggen en zeugen kan de ziekte zich voordoen. Kenmerkend is een betonkleurige diarree, meestal gemengd met slijm (glimmend) en soms met bloed (stolsels, donkere slierten). Meestal is dit enkele weken na opleg te zien. Het duurt namelijk enkele weken voordat de ziekteverschijnselen na het moment van infectie merkbaar worden. Vaak treden verschijnselen pas op na een voerverandering of verhoging van het rantsoen.
Oorzaak Dysenterie, ook wel bekend als ‘Vibrio’, wordt veroorzaakt door de kiem Brachyspira hyodysenteriae. Binnen de familie van de Brachyspira worden meerdere soorten onderscheiden, zoals B. innocens, B. murdochii, B. intermedia en B. pilosicoli. Alleen B. hyodysenteriae en B. pilosicoli zijn de pathogene (ziekteverwekkende) kiemen binnen deze familie.
Besmettingsroute Brachyspira wordt in grote aantallen uitgescheiden met de mest en daarom is mest het belangrijkste materiaal waarmee deze infectie verspreid wordt. Varkens, mensen, huisdieren, ongedierte en vliegen kunnen Brachyspira verspreiden. Dieren die worden aangevoerd kunnen ook met Brachyspira besmet zijn en zijn daarmee een belangrijke bron van besmetting voor bedrijven.
Schade Dysenterie zorgt voor schade in de vorm van een verminderde groei. Vaak ontwikkelen zich ‘slijters’. Een enkele keer treedt door een uitbraak sterfte op, soms zelfs bij zeugen.
Diagnose dysenterie
Vanoudsher wordt voor de diagnostiek van Brachyspira gebruik gemaakt van een immuun fluorescentie test (IFT). Een ongunstig testresultaat in de IFT toont alleen aan dat een lid van de familie Brachyspira in de mest aanwezig was. Deze IFT maakt echter geen onderscheid tussen de verschillende Brachyspira-soorten. Een ongunstige uitslag kan dus net zo goed veroorzaakt worden door een niet ziekmakende Brachyspira. Een behandeling instellen op basis van een ongunstige IFT kan dus onterecht zijn. Het is daarom beter de gebruik te maken van zogenaamde PCR testen. Met deze testen zijn B. hyodysenteriae en B. pilosicoli van elkaar en van de andere soorten te onderscheiden, zodat een juiste diagnose mogelijk is. Het onderscheid tussen B. hyodysenteriae en B. pilosicoli is belangrijk omdat B. pilosicoli een mildere ontsteking van de dikke darm veroorzaakt en dus ook een milder ziekteverloop, maar wel met afwijkende mest.
Risicofactoren dysenterie Mest is de belangrijkste verspreidingsbron van Brachyspira. Via varkens, mensen, huisdieren, ongedierte en vliegen kan Brachyspira worden verspreid. Ook de aanvoer van dieren op het bedrijf is een belangrijke bron van besmetting.
Aanpak van dysenterie Therapie Ter bestrijding van dysenterie zijn verschillende antibiotica beschikbaar. Overleg hierover met uw dierenarts. De basis is een zogenaamde curatieve behandeling van één tot twee weken van alle aanwezige varkens in een afdeling of soms zelfs van het hele bedrijf, gevolgd door een nabehandeling van enkele weken met een lagere dosering. De curatieve behandeling wordt via het drinkwater of met injecties (zieke dieren) uitgevoerd.
Preventie De belangrijkste maatregelen zijn het verbeteren van hygiëne: niet dezelfde laarzen gebruiken voor besmette en niet-besmette afdelingen, vliegenbestrijding, professionele muizenbestrijding en strikt all-in/all-out hanteren. De
voeding speelt eveneens een rol. Streef naar geleidelijke voerovergangen, makkelijk verteerbare eiwitbestanddelen in het voer en voldoende ruwe celstof.
De belangrijkste preventieve maatregelen zijn:
• all-in/all-out hanteren
• lege afdelingen zorgvuldig reinigen, ontsmetten en laten drogen
• per afdeling vleesvarkens van één herkomst opleggen
• zorgen voor geleidelijke voerovergangen
• zorgen voor lichtverteerbaar voer, liefst met voldoende ruwe celstof
• goede vliegenbestrijding hanteren
• goede ongediertebestrijding hanteren
• zorgen voor goede erfverharding (erf en gangen opruimen en schoonhouden)
• zorgvuldig gebruik maken van een toevoegstal voor de aanvoer van gelten en beren
Verschijnselen Dysenterie komt vooral voor bij vleesvarkens en opfokvarkens, maar ook bij gespeende biggen en zeugen kan de ziekte zich voordoen. Kenmerkend is een betonkleurige diarree, meestal gemengd met slijm (glimmend) en soms met bloed (stolsels, donkere slierten). Meestal is dit enkele weken na opleg te zien. Het duurt namelijk enkele weken voordat de ziekteverschijnselen na het moment van infectie merkbaar worden. Vaak treden verschijnselen pas op na een voerverandering of verhoging van het rantsoen.
Oorzaak Dysenterie, ook wel bekend als ‘Vibrio’, wordt veroorzaakt door de kiem Brachyspira hyodysenteriae. Binnen de familie van de Brachyspira worden meerdere soorten onderscheiden, zoals B. innocens, B. murdochii, B. intermedia en B. pilosicoli. Alleen B. hyodysenteriae en B. pilosicoli zijn de pathogene (ziekteverwekkende) kiemen binnen deze familie.
Besmettingsroute Brachyspira wordt in grote aantallen uitgescheiden met de mest en daarom is mest het belangrijkste materiaal waarmee deze infectie verspreid wordt. Varkens, mensen, huisdieren, ongedierte en vliegen kunnen Brachyspira verspreiden. Dieren die worden aangevoerd kunnen ook met Brachyspira besmet zijn en zijn daarmee een belangrijke bron van besmetting voor bedrijven.
Schade Dysenterie zorgt voor schade in de vorm van een verminderde groei. Vaak ontwikkelen zich ‘slijters’. Een enkele keer treedt door een uitbraak sterfte op, soms zelfs bij zeugen.
Diagnose dysenterie
Vanoudsher wordt voor de diagnostiek van Brachyspira gebruik gemaakt van een immuun fluorescentie test (IFT). Een ongunstig testresultaat in de IFT toont alleen aan dat een lid van de familie Brachyspira in de mest aanwezig was. Deze IFT maakt echter geen onderscheid tussen de verschillende Brachyspira-soorten. Een ongunstige uitslag kan dus net zo goed veroorzaakt worden door een niet ziekmakende Brachyspira. Een behandeling instellen op basis van een ongunstige IFT kan dus onterecht zijn. Het is daarom beter de gebruik te maken van zogenaamde PCR testen. Met deze testen zijn B. hyodysenteriae en B. pilosicoli van elkaar en van de andere soorten te onderscheiden, zodat een juiste diagnose mogelijk is. Het onderscheid tussen B. hyodysenteriae en B. pilosicoli is belangrijk omdat B. pilosicoli een mildere ontsteking van de dikke darm veroorzaakt en dus ook een milder ziekteverloop, maar wel met afwijkende mest.
Risicofactoren dysenterie Mest is de belangrijkste verspreidingsbron van Brachyspira. Via varkens, mensen, huisdieren, ongedierte en vliegen kan Brachyspira worden verspreid. Ook de aanvoer van dieren op het bedrijf is een belangrijke bron van besmetting.
Aanpak van dysenterie Therapie Ter bestrijding van dysenterie zijn verschillende antibiotica beschikbaar. Overleg hierover met uw dierenarts. De basis is een zogenaamde curatieve behandeling van één tot twee weken van alle aanwezige varkens in een afdeling of soms zelfs van het hele bedrijf, gevolgd door een nabehandeling van enkele weken met een lagere dosering. De curatieve behandeling wordt via het drinkwater of met injecties (zieke dieren) uitgevoerd.
Preventie De belangrijkste maatregelen zijn het verbeteren van hygiëne: niet dezelfde laarzen gebruiken voor besmette en niet-besmette afdelingen, vliegenbestrijding, professionele muizenbestrijding en strikt all-in/all-out hanteren. De
voeding speelt eveneens een rol. Streef naar geleidelijke voerovergangen, makkelijk verteerbare eiwitbestanddelen in het voer en voldoende ruwe celstof.
De belangrijkste preventieve maatregelen zijn:
• all-in/all-out hanteren
• lege afdelingen zorgvuldig reinigen, ontsmetten en laten drogen
• per afdeling vleesvarkens van één herkomst opleggen
• zorgen voor geleidelijke voerovergangen
• zorgen voor lichtverteerbaar voer, liefst met voldoende ruwe celstof
• goede vliegenbestrijding hanteren
• goede ongediertebestrijding hanteren
• zorgen voor goede erfverharding (erf en gangen opruimen en schoonhouden)
• zorgvuldig gebruik maken van een toevoegstal voor de aanvoer van gelten en beren
Pullorum Disease and Fowl Typhoid
Salmonella Pullorum or Pullorum Disease (PD) and Salmonella Gallinarum or Fowl Typhoid (FT) are caused by sub-species of Salmonella, pullorum and gallinarum respectively. Both are economically important diseases of chickens but may infect other birds as well.
PD and FT have been mostly eradicated in the United States, Canada, Japan, Western Europe and Australia. PD and FT are both reportable diseases. If you suspect your flock has either of these diseases, contact your state veterinarian for more information.
Chickens and turkeys are the natural hosts for FT and PD, but naturally occurring outbreaks occur in other birds, both wild and domestic. As a naturally occurring disease, Salmonellosis caused by S. pullorum has also been reported in humans.
Transmission
PD and FT are spread by:
bird-to-bird contact
hen to egg to chick (recovered hens will pass on the disease to roughly 1/3 of her eggs)
chick to chick
cannibalism of infected carcasses
wound contamination
fecal contamination of feed, water and litter
Wild birds, mammals and flies are capable of spreading these diseases, proper biosecurity measures will prevent the spread of infective material from house to house and from farm to farm.
Signs
When hatched from infected eggs, chicks and poults will begin to sicken and die soon after hatching. Birds are weak, with poor appetite and stunted growth. They will make shrill chirping and peeping sounds while attempting to eliminate chalky white droppings from their vents. In some cases signs won’t appear for 5 to 10 days after hatching, but then will increase for 7 -10 days, with most deaths occurring by the second to third week of life.
••••••
Pullorum disease in semi-mature and mature flocks may cause diarrhea, depression, dehydration and low feed intake. Survivors have reduced growth rates, and are under-developed and poorly feathered. Infected flocks have a high rate of carriers at maturity. Infected growing and mature fowl may exhibit little or no signs of disease, especially with pullorum disease.
Signs of an acute outbreak of FT include a sudden drop in feed intake, droopy and depressed birds, ruffled feathers, reduced fertility, and reduced hatch rate, all depending on the severity of infection. Death can occur in as few as 5 days, with 5-10 days being most common. Death may occur with no previous signs.
Morbidity and Mortality
The number of birds infected (morbidity) and the number of birds that die (mortality) varies by age, strain of bird, management, nutritional status, route and dose of exposure, and other disease stresses in the flock. PD in chicks can have up to 100 percent mortality, with the highest losses in the second week of life. FT has a 10 percent to 90 percent infection rate, with morbidity higher than mortality. Some chicks affected with FT recover on their own.
Diagnosis
Diagnosis is made by clinical signs, flock history, post-mortem lesions and mortality. Definitive diagnosis requires isolation and identification of the virus by qualified laboratory personnel. Home blood test kits are available for use; to eliminate carriers, the flock must have 2 negative blood tests at least 21 days apart.
National Poultry Improvement Plan (NPIP)
The NPIP is a cooperative program begun in the 1930s by federal/state governments and industry to coordinate efforts to eliminate PD from poultry flocks and hatcheries. Since then, the NPIP has adapted to changes in the poultry industry.
Years of dedicated effort have led to the eradication of PD from commercial poultry flocks. Outbreaks still occur, reinforcing the need for continued diligence and surveillance. Many states require either a negative Pullorum test within the past 90 days or participation in the NPIP for poultry to legally enter the state or be exhibited at fairs and other public exhibitions. To participate in the NPIP, contact the office of your state veterinarian.
Prevention
To prevent the introduction of PD and FT to your flock:
Obtain birds and hatching eggs from certified-pullorum-free flocks.
Don’t mix certified flocks with birds of unknown status.
Clean and sanitize an area before introducing new chicks.
Keep feed in clean, sanitary conditions to eliminate contamination.
Practice sound biosecurity to prevent introduction of disease.
Treatment
Treatment of Salmonella Pullorum and Salmonella Gallinarum is neither feasible nor desirable. Eradication
is the preferred method of control, as recovered birds have a tendency to become carriers.
PD and FT have been mostly eradicated in the United States, Canada, Japan, Western Europe and Australia. PD and FT are both reportable diseases. If you suspect your flock has either of these diseases, contact your state veterinarian for more information.
Chickens and turkeys are the natural hosts for FT and PD, but naturally occurring outbreaks occur in other birds, both wild and domestic. As a naturally occurring disease, Salmonellosis caused by S. pullorum has also been reported in humans.
Transmission
PD and FT are spread by:
bird-to-bird contact
hen to egg to chick (recovered hens will pass on the disease to roughly 1/3 of her eggs)
chick to chick
cannibalism of infected carcasses
wound contamination
fecal contamination of feed, water and litter
Wild birds, mammals and flies are capable of spreading these diseases, proper biosecurity measures will prevent the spread of infective material from house to house and from farm to farm.
Signs
When hatched from infected eggs, chicks and poults will begin to sicken and die soon after hatching. Birds are weak, with poor appetite and stunted growth. They will make shrill chirping and peeping sounds while attempting to eliminate chalky white droppings from their vents. In some cases signs won’t appear for 5 to 10 days after hatching, but then will increase for 7 -10 days, with most deaths occurring by the second to third week of life.
••••••
Pullorum disease in semi-mature and mature flocks may cause diarrhea, depression, dehydration and low feed intake. Survivors have reduced growth rates, and are under-developed and poorly feathered. Infected flocks have a high rate of carriers at maturity. Infected growing and mature fowl may exhibit little or no signs of disease, especially with pullorum disease.
Signs of an acute outbreak of FT include a sudden drop in feed intake, droopy and depressed birds, ruffled feathers, reduced fertility, and reduced hatch rate, all depending on the severity of infection. Death can occur in as few as 5 days, with 5-10 days being most common. Death may occur with no previous signs.
Morbidity and Mortality
The number of birds infected (morbidity) and the number of birds that die (mortality) varies by age, strain of bird, management, nutritional status, route and dose of exposure, and other disease stresses in the flock. PD in chicks can have up to 100 percent mortality, with the highest losses in the second week of life. FT has a 10 percent to 90 percent infection rate, with morbidity higher than mortality. Some chicks affected with FT recover on their own.
Diagnosis
Diagnosis is made by clinical signs, flock history, post-mortem lesions and mortality. Definitive diagnosis requires isolation and identification of the virus by qualified laboratory personnel. Home blood test kits are available for use; to eliminate carriers, the flock must have 2 negative blood tests at least 21 days apart.
National Poultry Improvement Plan (NPIP)
The NPIP is a cooperative program begun in the 1930s by federal/state governments and industry to coordinate efforts to eliminate PD from poultry flocks and hatcheries. Since then, the NPIP has adapted to changes in the poultry industry.
Years of dedicated effort have led to the eradication of PD from commercial poultry flocks. Outbreaks still occur, reinforcing the need for continued diligence and surveillance. Many states require either a negative Pullorum test within the past 90 days or participation in the NPIP for poultry to legally enter the state or be exhibited at fairs and other public exhibitions. To participate in the NPIP, contact the office of your state veterinarian.
Prevention
To prevent the introduction of PD and FT to your flock:
Obtain birds and hatching eggs from certified-pullorum-free flocks.
Don’t mix certified flocks with birds of unknown status.
Clean and sanitize an area before introducing new chicks.
Keep feed in clean, sanitary conditions to eliminate contamination.
Practice sound biosecurity to prevent introduction of disease.
Treatment
Treatment of Salmonella Pullorum and Salmonella Gallinarum is neither feasible nor desirable. Eradication
is the preferred method of control, as recovered birds have a tendency to become carriers.
Marek’s Disease
Marek’s Disease is a viral tumor-causing disease of chickens. Marek’s is distributed worldwide and is so common that if you have birds, they have been exposed to Marek’s, regardless of whether they show symptoms or not. There are 4 different forms of Marek’s:
Marek’s Disease is caused by 6 different herpes viruses that primarily affect young birds. The virus concentrates in feather follicles and is shed in dander. Marek’s disease-causing virus particles can survive for months in chicken-house dust and litter.
Transmission
Marek’s is highly contagious and spreads by bird-to-bird contact, by contact with infected dust and dander, and by darkling beetles and mealworms that live in the chicken house, although the virus has no affect on the beetles or mealworms.
Other organisms common to chicken houses such as free-living mites, mosquitoes and coccidia do not transmit the disease. Chickens are most commonly exposed to Marek’s by contact with residual dust and dander in previously infected houses, by aerosol (air) contamination from a nearby house, or by virus particles carried by personnel and equipment. The virus doesn’t survive the incubation process well and is not spread by hatching eggs. Immune transfer from the hen to the chick provides some protection to the chick for the first few days of life.
Signs
The signs and symptoms of Marek’s Disease vary depending on the form of disease present.
Cutaneous form: Enlarged reddened feather follicles and white bumps on the skin that form
brown crusty scabs.
Neural form: Characterized by one, all, or none of the following symptoms -
• Progressive paralysis, usually of the leg or wing, a typical leg-paralysis victim will
have one leg extended forward and one leg extended back. A swelling of the sciatic
nerve is the cause.
• Weight loss
• Labored breathing
• Diarrhea
• Starvation and death due to an inability to reach feed and water and to trampling by penmates.
• Cutaneous (skin form)
• Neural (nerve form)
• Ocular (eye form)
• Visceral (internal-organ form)
Ocular form:
• Gray eye color
• Misshapen iris
• Weight loss
• Blindness
• Death
Visceral Form: Tumors on internal organs including heart, ovary, liver and lung.
Morbidity and mortality
Morbidity (number affected) in unvaccinated flocks can reach 60 percent. Vaccinated flocks fare better with less than 5 percent affected. Mortality is high in affected birds reaching nearly 100 percent over a 10-week period. Pullets are more likely to be affected than cockerels.
Diagnosis
Diagnosis is derived from the flock history, symptoms and necropsy findings.
Prevention
• Breed for resistance.
• Good sanitation and ventilation.
• Brood chicks separately from adults until 5 months of age.
• Keep turkeys with chickens (this may help the chickens with Marek’s, but can lead to black
head disease in the turkeys).
• Vaccinate all chicks at 1 day old; keep chicks from exposure until immunity has developed, about 7 days.
Treatment
None. Cull affected birds. Some birds develop temporary paralysis that disappears after 1-2 days. They appear to return to normal, but frequently die from internal tumors a short time later.
Marek’s Disease is caused by 6 different herpes viruses that primarily affect young birds. The virus concentrates in feather follicles and is shed in dander. Marek’s disease-causing virus particles can survive for months in chicken-house dust and litter.
Transmission
Marek’s is highly contagious and spreads by bird-to-bird contact, by contact with infected dust and dander, and by darkling beetles and mealworms that live in the chicken house, although the virus has no affect on the beetles or mealworms.
Other organisms common to chicken houses such as free-living mites, mosquitoes and coccidia do not transmit the disease. Chickens are most commonly exposed to Marek’s by contact with residual dust and dander in previously infected houses, by aerosol (air) contamination from a nearby house, or by virus particles carried by personnel and equipment. The virus doesn’t survive the incubation process well and is not spread by hatching eggs. Immune transfer from the hen to the chick provides some protection to the chick for the first few days of life.
Signs
The signs and symptoms of Marek’s Disease vary depending on the form of disease present.
Cutaneous form: Enlarged reddened feather follicles and white bumps on the skin that form
brown crusty scabs.
Neural form: Characterized by one, all, or none of the following symptoms -
• Progressive paralysis, usually of the leg or wing, a typical leg-paralysis victim will
have one leg extended forward and one leg extended back. A swelling of the sciatic
nerve is the cause.
• Weight loss
• Labored breathing
• Diarrhea
• Starvation and death due to an inability to reach feed and water and to trampling by penmates.
• Cutaneous (skin form)
• Neural (nerve form)
• Ocular (eye form)
• Visceral (internal-organ form)
Ocular form:
• Gray eye color
• Misshapen iris
• Weight loss
• Blindness
• Death
Visceral Form: Tumors on internal organs including heart, ovary, liver and lung.
Morbidity and mortality
Morbidity (number affected) in unvaccinated flocks can reach 60 percent. Vaccinated flocks fare better with less than 5 percent affected. Mortality is high in affected birds reaching nearly 100 percent over a 10-week period. Pullets are more likely to be affected than cockerels.
Diagnosis
Diagnosis is derived from the flock history, symptoms and necropsy findings.
Prevention
• Breed for resistance.
• Good sanitation and ventilation.
• Brood chicks separately from adults until 5 months of age.
• Keep turkeys with chickens (this may help the chickens with Marek’s, but can lead to black
head disease in the turkeys).
• Vaccinate all chicks at 1 day old; keep chicks from exposure until immunity has developed, about 7 days.
Treatment
None. Cull affected birds. Some birds develop temporary paralysis that disappears after 1-2 days. They appear to return to normal, but frequently die from internal tumors a short time later.
Newcastle Disease
Newcastle disease occurs in two basic forms, the common form, or Newcastle Disease, and Exotic Newcastle Disease. Exotic Newcastle Disease is rare and is a federally reportable disease. If fifty percent or more of your flock dies suddenly, contact your state veterinarian, who will provide information on how and where to get a definitive diagnosis of the disease affecting your flock.
Newcastle Disease is more common, causes fewer, less severe symptoms and is less economically important. This fact sheet will focus on Newcastle Disease. For more information on Exotic Newcastle Disease visit http://www.aphis.usda.gov/animal_health/birdbiosecurity/END/ for a complete description of the disease and the measures in place to prevent widespread disease.
Transmission
Newcastle Disease virus is present in high concentrations in the bodily secretions of infected birds. The virus is spread by air, contact with body secretions, and by contaminated water and feed.
Signs
Young, growing birds exhibit respiratory signs such as wheezing, gasping, coughing and chirping. Nervous symptoms may follow in 10 to 14 days, resulting in leg, wing and/or neck paralysis. If nervous symptoms are present, high death losses may result from an inability to reach food and water and from trampling by pen mates.
Adult birds show only slight respiratory signs including nasal discharge, and cloudy eye. Additionally, there may be a slight decrease of egg production. Eggs may be misshapen and have rough shells.
Morbidity and Mortality
A large number of the flock may be affected, but death losses will be low unless nervous symptoms develop. Adult birds may show few if any signs and recover without intervention. Recovered birds can remain carriers for up to one month.
Diagnosis
Diagnosis is made from the symptoms, respiratory and nervous, in young birds, and by positive identification of the virus through laboratory tests.
Prevention
If Newcastle Disease is prevalent in your area, vaccinate at 1 day of age, (vaccine may be delayed to 7-10 days of age) and re-vaccinate every 4 months. Vaccinate adult birds when you first vaccinate the young. Other prevention measures include adherence to bio-security and breeding for resistance.
Treatment
Once signs appear, provide supportive therapy, and keep the flock warm and well-fed. Protect birds exhibiting nervous symptoms from being trampled. Watch for secondary, opportunistic bacterial infection.
Newcastle Disease is more common, causes fewer, less severe symptoms and is less economically important. This fact sheet will focus on Newcastle Disease. For more information on Exotic Newcastle Disease visit http://www.aphis.usda.gov/animal_health/birdbiosecurity/END/ for a complete description of the disease and the measures in place to prevent widespread disease.
Transmission
Newcastle Disease virus is present in high concentrations in the bodily secretions of infected birds. The virus is spread by air, contact with body secretions, and by contaminated water and feed.
Signs
Young, growing birds exhibit respiratory signs such as wheezing, gasping, coughing and chirping. Nervous symptoms may follow in 10 to 14 days, resulting in leg, wing and/or neck paralysis. If nervous symptoms are present, high death losses may result from an inability to reach food and water and from trampling by pen mates.
Adult birds show only slight respiratory signs including nasal discharge, and cloudy eye. Additionally, there may be a slight decrease of egg production. Eggs may be misshapen and have rough shells.
Morbidity and Mortality
A large number of the flock may be affected, but death losses will be low unless nervous symptoms develop. Adult birds may show few if any signs and recover without intervention. Recovered birds can remain carriers for up to one month.
Diagnosis
Diagnosis is made from the symptoms, respiratory and nervous, in young birds, and by positive identification of the virus through laboratory tests.
Prevention
If Newcastle Disease is prevalent in your area, vaccinate at 1 day of age, (vaccine may be delayed to 7-10 days of age) and re-vaccinate every 4 months. Vaccinate adult birds when you first vaccinate the young. Other prevention measures include adherence to bio-security and breeding for resistance.
Treatment
Once signs appear, provide supportive therapy, and keep the flock warm and well-fed. Protect birds exhibiting nervous symptoms from being trampled. Watch for secondary, opportunistic bacterial infection.
Cannibalism
“Henpecked” seems innocent enough, unless you’re on the receiving end!
Feather-pecking is a natural expression of dominance in poultry flocks. The severity of the damage associated with feather-pecking can be influenced by management factors and the breed of hens. Pecking behavior leads to feather damage, feather loss, reduced ability to regulate body temperature and reduced egg production in affected birds.
In some cases, feather-pecking leads to bleeding at the feather site. Bleeding attracts more pecking, not only by the dominant hen but by all members of the flock. Severe injury, resulting in culling or death may result. If left in the coop a severely injured or dead bird will be cannibalized by the flock.
Vent-picking is usually a problem when birds begin to lay, either for the first time or returning to egg production after molting. Vent-picking occurs immediately after an egg is laid while the mucus membrane is exposed. It’s more prevalent in overcrowded floor systems with birds laying eggs on the floor.
There may be a genetic component to feather-pecking, since the light breeds are more prone to the behavior than the heavier breeds. Feather-pecking can also be a learned behavior; once one bird starts the practice in your coop, the others quickly learn to join in. Once feather- pecking and cannibalism have occurred in your flock, it is a difficult habit to break. While there is no agreement on the exact causes of feather pecking and cannibalism, there are things you can do to limit or prevent pecking in your flock.
Provide adequate floor space for the age, number and size of the birds.
Provide adequate space at food and water, provide free-choice feed and water at all times. A little too much is better than not enough.
Provide enough nesting sites. Nest boxes should be 12″ x 12″ x 12″, fairly private and dark inside. You should provide 1 nest box for every 5 hens in the flock. Again, too many is better than not enough.
Moderate the light intensity. High light intensity and continuous lighting cause stress that can lead to pecking.
Provide proper nutrition. Feather-pecking may have a nutritional component. Feed a diet balanced for the age and stage of production of your flock.
Remove injured and dead birds from the flock. Injured and dead birds, regardless of the cause, may be pecked and cannibalized by the flock. This may not only cause the spread of disease in your flock, but may also promote pecking and cannibalism.
Feather-pecking is a natural expression of dominance in poultry flocks. The severity of the damage associated with feather-pecking can be influenced by management factors and the breed of hens. Pecking behavior leads to feather damage, feather loss, reduced ability to regulate body temperature and reduced egg production in affected birds.
In some cases, feather-pecking leads to bleeding at the feather site. Bleeding attracts more pecking, not only by the dominant hen but by all members of the flock. Severe injury, resulting in culling or death may result. If left in the coop a severely injured or dead bird will be cannibalized by the flock.
Vent-picking is usually a problem when birds begin to lay, either for the first time or returning to egg production after molting. Vent-picking occurs immediately after an egg is laid while the mucus membrane is exposed. It’s more prevalent in overcrowded floor systems with birds laying eggs on the floor.
There may be a genetic component to feather-pecking, since the light breeds are more prone to the behavior than the heavier breeds. Feather-pecking can also be a learned behavior; once one bird starts the practice in your coop, the others quickly learn to join in. Once feather- pecking and cannibalism have occurred in your flock, it is a difficult habit to break. While there is no agreement on the exact causes of feather pecking and cannibalism, there are things you can do to limit or prevent pecking in your flock.
Provide adequate floor space for the age, number and size of the birds.
Provide adequate space at food and water, provide free-choice feed and water at all times. A little too much is better than not enough.
Provide enough nesting sites. Nest boxes should be 12″ x 12″ x 12″, fairly private and dark inside. You should provide 1 nest box for every 5 hens in the flock. Again, too many is better than not enough.
Moderate the light intensity. High light intensity and continuous lighting cause stress that can lead to pecking.
Provide proper nutrition. Feather-pecking may have a nutritional component. Feed a diet balanced for the age and stage of production of your flock.
Remove injured and dead birds from the flock. Injured and dead birds, regardless of the cause, may be pecked and cannibalized by the flock. This may not only cause the spread of disease in your flock, but may also promote pecking and cannibalism.
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