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DSC000111

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gross image

  • congestion: trachea
  • edema: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Acute multifocal petechia

Clinical Description

In chickens infected with highly pathogenic avian influenza, lesions distributed throughout the upper respiratory tract are common. Tracheal findings can range from normal to severe. In this image of the tracheal mucosa, there is severe edema, congestion, and hemorrhage.

Pathologic Description

The trachea has been opened to reveal the mucosal surface. The mucosa is stippled with numerous, small, red, punctate hemorrhages.

3.4.08.DSC00285.JPG

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gross image

  • congestion: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Tracheal mucosa: Mild congestion

Clinical Description

This image was taken 2 days post experimental inoculation with highly pathogenic avian influenza. The range of tracheal lesions observed may vary greatly from mucous accumulation to severe hemorrhagic tracheitis. Here, mild congestion of the tracheal mucosa can be observed.

Pathologic Description

The trachea has been opened to reveal the mucosal surface. The blood vessels are prominent and congested.

3.4.08.2DSC00045.JPG

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gross image

  • congestion: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Diffuse hemorrhage and congestion

Clinical Description

This image was taken 2 days post experimental inoculation with highly pathogenic avian influenza. In HPAI, hemorrhagic tracheitis may be severe enough to be visible on the outer surface of the trachea.

Pathologic Description

The blood vessels on the adventitial surface of the trachea are congested and prominent. They are evident running parallel to the tracheal rings. The trachea is diffusely red and irregular red to purple foci can be seen throughout the tracheal wall.

3.5.08.aDSC_0095.JPG

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gross image

  • catarrhal lesions: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Severe acute cattarhal tracheitis with hemorrhage

Clinical Description

This image was taken 3 days post experimental inoculation with highly pathogenic avian influenza. In HPAI, the upper respiratory tract may have catarrhal lesions including fibrinous, serofibrinous, mucopurulent (seen here), or fibrinopurulent exudates.

Pathologic Description

The mucosa of the trachea is dark red and there are numerous coalescing dark red areas throughout the wall. The tracheal lumen is filled with increased amounts of mucus.

3.5.08.aDSC_0135.JPG

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gross image

  • congestion: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Severe acute diffuse mucosal hemorrhage

Clinical Description

This image was taken 3 days post experimental inoculation with highly pathogenic avian influenza. There is severe diffuse hemorrhagic tracheitis.

Pathologic Description

The trachea has been opened to reveal the dark red color to the mucosa.

3.5.08.bDSC_0151.JPG

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gross image

  • atrophy: thymus gland
  • congestion: trachea
  • hemorrhages: trachea
  • thymus gland
  • Trachea

thymus gland, trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Acute diffuse mucosal hemorrhage. Thymus: Moderate atrophy.

Clinical Description

This image was taken 3 days post experimental inoculation with highly pathogenic avian influenza. There is severe diffuse hemorrhagic tracheitis which can be seen from the outer surface of the trachea. The thymus, adjacent to the trachea, also shows moderate atrophy in this 16 week old chicken.

Pathologic Description

This image shows a dissection of the neck. The trachea runs horizontally along the bottom of the picture. Immediately above the trachea is a thymic lobule. The trachea is closed, however the extensive reddening of the mucosa can be seen through the wall. Additionally, given the age of the chicken (16 weeks), the amount of thymic tissue is decreased.

3.6.08.bDSC_0208.JPG

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  • edema: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Severe tracheitis with hemorrhage

Clinical Description

This image was taken 4 days post experimental inoculation with highly pathogenic avian influenza. As seen here, hemorrhagic laryngotracheitis can become quite severe.

Pathologic Description

This is a closed segment of trachea with larynx (right side of image). The dark red mucosa can be seen through the adventitia of the trachea and the dark color of the proximal trachea suggests the presence of luminal exudate.

3.6.08.bDSC_0211.JPG

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gross image

  • catarrhal lesions: trachea
  • congestion: trachea
  • edema: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Severe acute catarrhal tracheitis with hemorrhage

Clinical Description

This image was taken 4 days post experimental inoculation with highly pathogenic avian influenza. Mucus accumulation is variable and, when pronounced, can lead to respiratory distress.

Pathologic Description

The mucosal surface of the trachea is bright red with several ill defined darker foci. The lumen of the trachea contains increased amounts of mucus.

3.6.08.bDSC_0225.JPG

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gross image

  • catarrhal lesions: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Mild cattarhal tracheitis with petechia

Clinical Description

This image was taken 4 days post experimental inoculation with highly pathogenic avian influenza virus. There is mucopurulent catarrhal exudate in the lumen of the trachea.

Pathologic Description

The mucosal surface of the trachea is stippled by numerous pinpoint red foci and the lumen contains increased amounts of mucus.

ND-019A.jpg

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  • congestion: trachea
  • hemorrhages: trachea
  • Trachea

trachea

Newcastle Disease

chicken (Gallus gallus)

Clinical Description

Highly virulent Newcastle disease virus results in hemorrhagic lesions in the trachea. The tracheal lesions normally do not include free blood in the lumen.

ND-051A.jpg

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  • congestion: trachea
  • hemorrhages: trachea
  • Trachea

oropharynx, trachea

Newcastle Disease

chicken (Gallus gallus)

Clinical Description

In viscerotropic velogenic NDV, congestion and hemorrhages may be observed in the pharynx and proximal trachea, as seen here. These hemorrhages in the tracheal wall are typically not associated with free-blood in the lumen.

DSC00018

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  • hemorrhages: trachea
  • Trachea

trachea

Newcastle Disease

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Mild multifocal petechia

Clinical Description

Velogenic viscerotropic Newcastle disease. This image is from an acute outbreak, where many birds were suddenly found dead. On post-mortem exam, no severe lesions were found due to the rapid onset of the infection. Only mild hemorrhagic lesions in the mucosa of the trachea were observed (as seen here). In flocks unvaccinated for NDV, massive deaths within the flock may occur quickly, without any prior signs of illness and few post-mortem lesions.

Pathologic Description

Pinpoint red foci are scattered along the mucosal surfaces. These foci are particularly dense in areas running parallel to the cartilaginous rings.

DSC00043

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  • hemorrhages: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Moderate acute multifocal hemorrhage

Clinical Description

There are multiple strains of laryngotracheitis virus, producing a range of mild to severe tissue lesions. On post-mortem examination, the trachea and larynx are the most common areas to find gross lesions. Here the trachea has been opened revealing diffuse inflammation and hemorrhages. These are common gross lesions associated with the more severe epizootic form of the viral infection.

Pathologic Description

The mucosal surface of the trachea shows numerous small, sometimes coalescing, bright red foci (petechiae).

tracheitis2

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  • hemorrhages: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Mild to moderate acute hemorrhage

Clinical Description

This image depicts the varying degree to which laryngotracheitis can produce lesions in the trachea and larynx of chickens. In laryngotracheitis, tracheal lesions can range from mild mucus accumulation in the lumen to varying degrees of inflammation, necrosis, and hemorrhage associated with epithelial damage.

Pathologic Description

This image shows the trachea of three birds infected with laryngotracheitis. The trachea at the bottom of the image is least affected, while the one at the top of the image is most affected. The mucosal surface of each organ is stippled by varying degrees of bright red hemorrhage.

POX-050A.jpg

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  • diptheritic membranes: trachea

trachea

Avian Pox

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Diffuse necrosuppurative tracheitis with locally extensive diptheretic membrane.

Clinical Description

This image shows a typical diphtheritic lesion caused by avian pox. The fibrino-necrotic proliferative lesions form on mucous membranes. These lesions may develop in the oral cavity, tongue, esophagus, or upper trachea. If the lesions are located in the lower respiratory tract (e.g. the syrinx), they can compromise breathing, resulting in dyspnea.

Pathologic Description

The trachea has been partially opened to reveal the mucosal surface which is diffusely red. Within the lumen there is a focal accumulation of wet, pale tan, mucoid material along with a partially occlusive plug composed of dry, friable, yellow tan material.

POX-052A.jpg

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  • diptheritic membranes: trachea

trachea

Avian Pox

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Diffuse tracheitis with locally extensive diptheritic membrane.

Clinical Description

This image shows typical diphtheritic lesions on the trachea, caused by avian pox. The fibrino-necrotic proliferative lesions form on mucous membranes. In the early stages, these plaques begin as as small white opaque nodules that frequently enlarge into larger yellow diptheritic membranes. These lesions may develop in the oral cavity, tongue, esophagus, or upper trachea. If the lesions are located in the lower respiratory tract (e.g. the syrinx), they can compromise breathing, resulting in dyspnea.

Pathologic Description

The trachea has been opened to reveal the mucosal surface. The proximal trachea is covered by a large coagulum of pale yellow, friable material that is adherent to the underlying mucosa. The remaining tracheal mucosa is red, glistening and undulating.

POX-053A.jpg

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  • diptheritic membranes: trachea

larynx, trachea

Avian Pox

chicken (Gallus gallus)

Morphologic Diagnosis

Trachea: Locally extensive fibrinonecrotic tracheitis with multifocal petechia.

Clinical Description

Diphtheritic (wet) form of avian pox. On post-mortem examination, if these diptheritic membranes are removed, bleeding erosions are sometimes found beneath these membranes.

Pathologic Description

The trachea has been opened to reveal the mucosal surface. Within the cranial portion of the esophagus (right side of picture) there is a large aggregate of dry, pale tan, friable material. The material overlies a bright red and wet section of mucosa. Small pinpoint red foci are scattered along more distal portions of the tracheal mucosa.

IBV-004A.jpg

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  • congestion: trachea
  • hemorrhages: trachea

trachea

Infectious Bronchitis

chicken (Gallus gallus)

Clinical Description

In infectious bronchitis virus infection, tracheal lesions may be quite severe and include congestion and hemorrhages, as seen here in the proximal trachea and oropharynx of 2 infected chickens.

IBV-034A.jpg

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gross image

  • caseous exudate: syrinx

bronchi, syrinx, trachea

Infectious Bronchitis

chicken (Gallus gallus)

Clinical Description

Here, mild to moderate inflammation of the trachea and bronchi can be seen. There is also an accumulation of white caseous exudate in the syrinx and primary bronchi.

tracheitis

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  • congestion: trachea
  • hemorrhages: trachea

trachea

Infectious Bronchitis

Unknown

Clinical Description

On post-mortem examination, infectious bronchitis virus is typically associated with tracheal lesions. Here, the proximal trachea shows edema and congestion. In more advanced cases, the trachea may have accumulations of serous, catarrhal, or caseous exudate.

DSC00010

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gross image

  • catarrhal exudate: trachea

trachea

Infectious Bronchitis

chicken (Gallus gallus)

Clinical Description

There is mild catarrhal exudate in the lumen of this trachea.

LT-005A.jpg

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gross image

  • diptheritic membranes: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

Diphtheritic changes along the entire length of trachea caused by laryngotracheitis infection.

LT-010A.jpg

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gross image

  • diptheritic membranes: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

Diphtheritic changes with hemorrhages in the trachea caused by laryngotracheitis infection.

LT-008A.jpg

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gross image

  • diptheritic membranes: trachea
  • hemorrhages: larynx
  • hemorrhages: trachea

larynx, trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

Diphtheritic changes in the trachea and focal areas of hemorrhages in the tracheal wall and larynx caused by laryngotracheitis infection.

LT-006A.jpg

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gross image

  • hemorrhagic exudate: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

This photo shows hemorrhagic exudate in the tracheal lumen caused by laryngotracheitis infection. In laryngotracheitis infections, exudate may range from mild mucus accumulations to diptheritic or hemorrhagic casts.

LT-007A.jpg

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gross image

  • hemorrhagic exudate: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

Hemorrhages in the trachea related to laryngotracheitis infection. This gross image shows bloody exudate in the tracheal lumen.

LT-049A.jpg

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gross image

  • caseous exudate: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

This image shows plugs of caseous exudate occluding the upper trachea of a chicken infected with laryngotracheitis. In cases such as this, birds will show signs of dysnea including open-mouth breathing and gasping.

LT-009A.jpg

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gross image

  • hemorrhages: larynx

larynx, trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

Mucopurulent exudate in the tracheal lumen and mild hemorrhages in the larynx caused by laryngotracheitis infection.

LT-050A.jpg

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gross image

  • caseous exudate: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

This photo shows a cross section of the trachea taken from a chicken infected with laryngotracheitis virus. The lumen of the trachea is completely occluded with exudate. A normal tracheal lumen is shown on the right for comparison.

LT-048A.jpg

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gross image

  • hemorrhages: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

In severe epizootic forms of laryngotracheitis, severe tracheal hemorrhage and necrosis, such as this, can be found.

LT-033A.jpg

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gross image

  • diptheritic membranes: trachea

trachea

Infectious Laryngotracheitis

chicken (Gallus gallus)

Clinical Description

Severe diphtheritic changes in the trachea due to laryngotracheitis infection. These lesions are one of the most common lesions observed with this viral infection.

MYCOPLASMOSIS-019A.jpg

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gross image

  • caseous exudate: bronchi
  • caseous exudate: trachea

bronchi, trachea

Mycoplasma gallisepticum

chicken (Gallus gallus)

Clinical Description

In Mycoplasma gallisepticum infections, mucoid to caseous exudate may be seen in nasal passages, sinuses, trachea, and bronchi. This image shows plugs of exudate in the lumen of the trachea and bronchi.

MYCOPLASMOSIS-016A.jpg

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gross image

  • mucoid exudate: trachea

trachea

Mycoplasma gallisepticum

chicken (Gallus gallus)

Clinical Description

On post-mortem exam, chickens and turkeys infected with Mycoplasma gallisepticum may have lesions distributed throughout their upper and lower respiratory tract. This image shows mild tracheitis with a small amount of mucoid exudate in the tracheal lumen.

MYCOPLASMOSIS-015A.jpg

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gross image

  • catarrhal exudate: trachea
  • congestion: trachea

trachea

Mycoplasma gallisepticum

chicken (Gallus gallus)

Clinical Description

In this bird, infected with Mycoplasma gallisepticum, there is marked inflammation and congestion of the trachea and catarrhal exudate can been seen in the tracheal lumen.

DSC00032

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gross image

  • congestion: trachea
  • mucoid exudate: trachea

trachea

Mycoplasma gallisepticum

chicken (Gallus gallus)

Clinical Description

Very mild tracheitis is present in the first stages of the Mycoplasma infection.

21_trachea_cartilage

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normal

trachea

Normal Reference

chicken (Gallus gallus)

Clinical Description

The trachea is a thin tube completely encircled by cartilagenous rings. The trachea should be uniform in color, ranging from pale pink to tan or white and the external surface should be smooth. Upper respiratory disease may produce tracheal lesions that are sometimes visible on the outer surface. Look for discoloration, nodules, or irregularities in the tracheal cartilages.

Trachea3

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normal

trachea

Normal Reference

chicken (Gallus gallus)

Clinical Description

The trachea should be uniform in color, ranging from pale pink to tan or white and the external surface should be smooth. Upper respiratory disease may produce tracheal lesions that are sometimes visible on the outer surface. Look for discoloration, nodules, or irregularities in the tracheal cartilages.

palate2

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normal

trachea

Normal Reference

chicken (Gallus gallus)

Clinical Description

The trachea is a thin tube completely encircled by small cartilagenous rings. The trachea should be uniform in color, ranging from pale tan to white and the external surface should be smooth. Look for discoloration, nodules, or irregularities in the tracheal cartilages.

Syrinx1

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normal

syrinx, trachea

Normal Reference

chicken (Gallus gallus)

Clinical Description

At the terminal end of the trachea lies the syrinx, a flattened area at the junction of the trachea and the primary bronchi. The syrinx is responsible for generating vocal sounds.

Trachea4

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normal

trachea

Normal Reference

chicken (Gallus gallus)

Clinical Description

View of the inside lumen of the trachea.

Avian Influenza

Avian Influenza

Avian Influenza

Etiology

Avian Influenza (AI) [also known as Fowl Plague] is a viral infection affecting wild and domestic birds. These influenza viruses occur naturally in the intestinal tract of many species of wild birds with no disease outcome. However, pathogenic forms of the Avian Influenza virus can result in a highly contagious respiratory infection. Many species of birds are susceptible to AI including chickens, turkeys, guinea fowl, and other domestic birds, as well as a some wild avian species. AI viruses are classified into two general types based on their pathogenicity for chickens: Low Pathogenic (LP) and Highly Pathogenic (HP) types.

AI is caused by viruses that are members of the family Orthomyxoviridae, and the genus Influenzavirus, Type A. Influenza viruses Type B and C are pathogenic for humans but not for birds. Virus classification is based on antigenic differences in the nucleoprotein (NP) and matrix proteins (M1). Further subtyping of the AI virus is made based on the presence of 2 glycoproteins on the surface of the virus, hemagglutinin (HA) and neuraminidase (NA). Each AI virus has 1 of 16 different HA subtype glycoproteins and 1 of 9 different NA subtype glycoproteins (e.g. H5N1).

The HA and NA protein subtypes confer differences in viral pathogenicity. In LP strains, the HA protein can be cleaved by proteases present only in the respiratory and digestive tracts. In HP strains, proteases in most cells of the body can cleave the protein, resulting in a much wider tissue tropism than mildly pathogenic strains.

The HA protein is the major antigen that elicits antibodies which protect against clinical signs and death. Such antibodies are HA subtype specific. The antigenicity of influenza viruses may change gradually by point mutation (antigenic drift) or drastically by genetic reassortment (antigenic shift). Immunological pressure on HA and NA is thought to drive antigenic drift.

AI subtype classification requires viral isolation and characterization. Further subtyping is based on the antigenicity of the two surface glycoproteins, HA and NA. Classification cannot be made through clinical observations alone because the severity of the infection depends not only on the subtype of the virus but also the host species, the age of the bird, the host's immune status, and the presence of any secondary infections or environmental stress.

Due to the significant economic and public health implications of an AI outbreak, the World Organization for Animal Health (OIE) requires notification of any bird that is diagnosed with low pathogenic notifiable AI (LPNAI) or highly pathogenic notifiable AI (HPNAI). For the purposes of international trade the OIE defines notifiable avian influenza (NAI) as an infection of poultry caused by any influenza A virus of the H5 or H7 subtypes or by any AI virus with an intravenous pathogenicity index (IVPI) greater than 1.2 or, as an alternative, if the virus produces at least 75% mortality after inoculation.

HPNAI viruses have an IVPI greater than 1.2 in 6-week-old chickens or, as an alternative, cause at least 75% mortality in 4 to 8-week-old chickens infected intravenously. H5 and H7 virus isolates that do not have an IVPI of 1.2 or greater, nor produce 75% mortality under experimental conditions, but have an amino acid sequence at the cleavage site of the hemagglutinin that is similar to that observed for other HPNAI isolates, should be considered as HPNAI. LPNAI are all influenza A viruses of H5 and H7 subtype that do not display features of HPNAI viruses.

To date, all highly pathogenic strains of AI have been of the H5 or H7 subtypes. Although most H5 and H7 subtypes are in fact low pathogenic strains, since AI is unstable, there is a potential for LPNAI to mutate into HPNAI. Therefore all H5 and H7 subtypes require reporting to the OIE in order to facilitate global virus control measures. Within the United States, these pathotypes are considered exotic diseases and, in addition to being reported to the OIE, they should also be reported to the State and Federal veterinary authorities.

Host range

The AI viruses have been shown to naturally infect a wide variety of wild and domestic birds. The viruses have been isolated from more than 90 avian species however, in free-living birds most natural infections do not produce recognizable disease. The practice of housing birds in captivity and the development of commercial poultry systems have altered the normal epidemiology of the virus, resulting in clinically significant disease within domestic poultry.

In chickens, AI is capable of producing significant disease and economic losses. Ducks and other waterfowl are susceptible to the Asian HPAI H5N1 currently circulating in Asia, but have innate resistance to most other strains of Avian Influenza. Migratory waterfowl can act as carriers and transport viruses between geographic areas, helping to spread AI viruses to other susceptible animals.
In general, mammals are poorly susceptible to AI. However, several infections of highly pathogenic notifiable Avian Influenza (HPNAI) viruses have been reported since 1997 in humans, pigs and other mammals. Most of these cases have been linked to close contact with infected poultry. Although chicken-to-human infections have been rare, the virus is highly unstable and can alter pathotypes by passage in various animal species. The recombination of avian and human influenza viruses in pigs may be a potential source for sporadic pandemics of human influenza.

Epidemiology

AI viruses are distributed worldwide and identified frequently from clinically normal migratory waterfowl, imported birds, and species in live-bird markets. Data shows migratory waterfowl are the reservoir for AI viruses. Migratory birds introduce LPNAI viruses into poultry and, once introduced, the virus adapts to poultry and spreads from flock-to-flock, mostly by human activity. Most outbreaks of HPNAI in poultry arise from mutations in a LPNAI strain.

AI is excreted from the nares, mouth, and cloaca of infected birds. Spread occurs rapidly among birds housed on the floor but is slower in caged birds. Spread is primarily through contaminated feces and aerosol from the respiratory tract. The ingestion of contaminated feed and drinking water is another common source of transmission. The virus may also be transmitted indirectly by fomites such as contaminated equipment, personnel, clothing, foot wear, artificial insemination, and other human activity.

The incubation for AI is usually 1-7 days and depends on the strain, the dose, the species, and the age of the bird. The typical incubation period for an individual bird is approximately 3 days. It may take up to 14 days for an entire flock to become ill.
The morbidity of LPNAI is variable and the mortality is usually low, unless secondary infections are present or the birds are housed under poor management conditions. The morbidity and mortality of HPNAI may be near 100% within 2-12 days after the onset of the first signs of illness.

Clinical Signs

The severity of clinical signs depends on factors such as age, sex, species, concurrent infections, environment, as well as the pathogenicity of the virus.

Low pathogenic AI in wild birds usually produces no clinical signs. In domestic poultry, clinical signs reflect abnormalities in the respiratory, digestive, urinary, and reproductive organs. Generalized signs include depression, decreased activity, huddling, ruffled feathers, decreased feed and water consumption and occasionally greenish diarrhea. Respiratory manifestations include mild to severe coughing, sneezing, rales, rattles, excessive lacrimation, matted eyelids, and nasal discharge. Increased broodiness and a 5-30% decrease in egg production are observed in laying hens and breeders. Turkeys, infected with swine flu, may experience a much larger drop in egg production. Eggs may be thin-shelled and misshapen, but production will usually return to near-normal levels following recovery. Some viral strains may be associated with egg yolk peritonitis.

Some strains of highly pathogenic AI replicate poorly in wild birds and domestic ducks, producing few clinical signs. Ducks, quail, and turkeys may have mild sinusitis. Recent HPAI Asian H5N1 strains have produced more severe clinical signs in ducks and some wild birds.

In chickens, highly pathogenic AI produces clinical signs that reflect widespread viral replication and damage to multiple body systems. The disease may be fulminate, with some birds found dead without exhibiting any clinical signs. Birds that survive 3-7 days post infection may exhibit depression, ruffled feathers, decreased feed and water consumption, and a precipitous drop or total cessation of egg production. Diarrhea is often present. Early in the course of the disease, the feces may be bright green and watery. As the disease progresses, the droppings may become totally white. Birds may show cyanosis and edema of the skin, particularly of the combs, wattles, and periocular areas. Occasionally, edema and ecchymoses of the shanks and feet may also be observed. In some cases neurologic disease develops. Nervous deficits can include head and neck tremor, inability to stand, torticollis, loss of perching reflex and opisthotonus. Respiratory signs are less prominent in HPNAI than with LPNAI but may include coughing, sneezing (with blood tinged discharge), and rales. Most birds will die within 1-2 days following the onset of illness but some birds may survive for as long as a week. Recovery is uncommon.

Post-mortem Lesions

Lesions are variable in distribution and severity, depending greatly on host species, pathogenicity, and secondary infections.
Domestic ducks with LPNAI may have sinusitis, conjunctivitis, and other mild respiratory lesions. In chickens, lesions are more pronounced and are distributed throughout the upper respiratory tract and include catarrhal, fibrinous, serofibrinous, mucopurulent, or fibrinopurulent exudates. The tracheal mucosa may be edematous with congestion and hemorrhages. The infraorbital sinuses may be swollen and mucoid to mucopurulent nasal discharge may be present. Catarrhal to fibrinous inflammation may be observed in the coelomic cavity. The ovaries may be hemorrhagic with ova involution and degeneration. Eggs may be misshapen and fragile. The coelomic cavity may contain ovules or be filled with egg yolk, from ruptured ova, resulting in egg yolk peritonitis. This peritonitis may cause air sacculitis and diffuse coelomic cavity inflammation in birds that survive for 7-10 days post infection. Catarrhal to fibrinous enteritis may also be observed in the ceca and in the intestines.

Birds infected with HPNAI that die peracutely may not show any gross lesions. In chickens infected with the acute to subacute form, significant gross lesions are usually observed. At gross necropsy, one of the most frequent external findings is edema, manifested by swelling of the head (combs, wattles and periocular regions), upper neck, and feet. This edema may be accompanied by petechial and ecchymotic hemorrhages. Additionally, areas of nonfeathered skin such as the wattles and combs, are commonly cyanotic and have dark areas, caused by ecchymotic hemorrhages and necrotic foci. Internally, generalized hemorrhages and edema can be found in the muscles, especially the pectoral muscles, as well as the tissues of the hocks and feet. With most strains of HPNAI, pinpoint petechial hemorrhages are frequently observed along the abdominal fat, pericardium, serosal surfaces and peritoneum. Visceral organs may also be marked by hemorrhages. The glands of the proventriculus may have hemorrhagic lesions, particularly at the junction with the ventriculus (gizzard). The lining of the ventriculus may peel easily, frequently revealing underlying hemorrhages, erosions, and ulcers. The intestinal mucosa may have hemorrhagic areas, especially in the lymphoid tissue of the cecal tonsils and Peyer's patches in the small intestine.

In laying birds, the ovary may be hemorrhagic or degenerated with darkened areas of necrosis. In birds that survive, the peritoneal cavity is frequently filled with yolk from ruptured ova, causing severe airsacculitis and inflammation. The eggs are frequently soft and fragile due to decreased calcium deposition.

The trachea may appear normal, with the exception of excessive mucous accumulation, or it may be severely affected, with extensive hemorrhagic tracheitis. The lungs may be deep red in color, due to congestion and hemorrhage, and may exude edematous fluid when cut. The bursa of Fabricius and thymus are usually atrophic. The kidneys may be swollen, severely congested, and may by plugged with white urate deposits in the tubules. Necrotic foci may be present in the pancreas, spleen, heart, and occasionally the liver and kidneys.

Differential Diagnosis

AI should be differentiated from other respiratory diseases such as: Newcastle disease, infectious bronchitis, infectious laryngotracheitis, avian pneumovirus, and infectious coryza, among others. Other diseases that cause sudden death and septicemias, such as fowl cholera, should also be considered. Particular attention should be given to differentiating AI from mycoplasmosis, chlamydiosis and fowl cholera in young turkeys.

Diagnosis

In cases where HPAI is suspected, it is important to submit clinical samples to a recognized laboratory capable of carrying out AI diagnosis. Currently, there are a number of laboratories in the United States and around the world that have the capabilities to perform molecular testing, such as reverse transcriptase-polymerase chain reaction (RT-PCR) or a simplified faster real time reverse transcriptase polymerase chain reaction (rRT-PCR), to detect the presence of AI from clinical samples. The validated testing procedures performed at these laboratories are very sensitive, accurate, and rapid.

Cases involving respiratory signs and drop in egg production should be investigated for LPNAI. A presumptive diagnosis can be made in the field if compatible clinical signs and gross lesions are accompanied by a positive influenza type A test result, via commercial antigen capture immunoassay. However, because this test does not distinguish between LPAI and LPNAI, and may produce false-positive results, additional laboratory testing will be needed.

HPNAI should be suspected in any flock experiencing peracute death, high mortality, severe depression, inappetence, and a drastic decline in egg production. The presence of compatible gross lesions and the detection of Type A influenza antigen in oropharyngeal or tracheal swabs, supports a field diagnosis of HPNAI. However, these findings should be followed by more specific tests to identify and characterize the virus's antigenic and pathogenic type.

For HPNAI or LPNAI testing, collect and submit tracheal or cloacal swab samples as well as tissue samples taken from several internal organs such as the trachea, lung, spleen, cecal tonsils, or brain. Specimens should be collected from several birds, as it is not unusual for many specimens to fail to yield virus. If large numbers of birds are dead, you can submit up to 5 swab samples in one tube but do not mix swabs taken from different sites.

Blood for serum testing should be collected from several birds using standard serum tubes. If the specimens can be delivered to a laboratory within 24 hours, they should be placed on cold packs for shipping. If delivery will take longer, quick freeze the specimens in dry ice or liquid nitrogen, but do not allow the samples to thaw during transit. Freezing and storage at standard freezer temperature (-20 degrees C) is not recommended.

In the laboratory, virus isolation is usually performed by inoculation of embryonated chicken eggs with organ homogenizates or with tracheal or cloacal swabs. The AI virus is detected if the allantoic fluid of inoculated eggs hemagglutinates chicken red blood cells. The virus can be sub-typed using specific sera against all known HA and NA proteins. Specific hemagglutination inhibition is the basis of the serologic test for influenza antibodies. The ELISA (enzyme-linked immunosorbent assay) and AGID (agar gel immunodiffusion) tests can be used for determining the presence of antibody in the sera.

Any suspected case of Notifiable Avian Influenza (NAI) in the United States should be immediately reported to the State Veterinarian for the State where the case is suspected. A current list of animal health officials (State Veterinarians) contact information is available at http://www.usaha.org/members.shtml#agency . For suspected cases of NAI in other countries, notification should be given to the Chief Veterinary Officer (or OIE Country Delegate) of the country or territory where the case is suspected. A current list of Chief Veterinary Officers is available at http://www.oie.int/eng/OIE/PM/en_PM.htm?e1d1 .

Given the changes in the zoonotic potential recently seen with the emergence of human infections with the HPAI Asian H5N1 strain, it is recommended to treat any future HPAI as a potentially zoonotic disease. Seek the advice of the Public Health authorities in dealing with any outbreak action. A current list of Public Health authorities in the US is available at: www.astho.org or at http://www.statepublichealth.org/. Information on Public Health authorities outside the US is available at: http://www.who.int/countries/en/

Prevention and Control

The recommended strategy for controlling NAI is eradication. This requires 5 components including: 1) inclusion and exclusion biosecurity practices, 2) increasing host resistance through vaccination, 3) diagnostics and surveillance, 4) elimination of infected animals from the flock, and 5) educating personnel in AI control strategies.
1) Implementing biosecurity practices includes controlling human traffic, quarantining birds before introduction, proper cleaning and disinfection of facilities, keeping healthy birds away from contact with sick birds and wild birds, and incubating eggs only from clean flocks. Strict quarantine measures not only reduce the possibility of introducing Avian Influenza to a farm but also to a region or country.
2) Inactivated vaccines have been shown to be effective but are fairly expensive. Recombinant fowl poxvirus, carrying an inserted H5 gene, have shown similar efficacy in chickens. However, no vaccine will provide absolute prevention against infections or control environmental contamination. Other major drawbacks to current vaccines for controlling NAI include the labor associated with administering vaccine injections to individual birds and the need to match the vaccine to the field hemagglutination subtype in order to confer protection.
3) Diagnostics and surveillance play a critical role in controlling NAI. In the field, appropriate diagnostic samples should be collected and submitted to an accredited laboratory, capable of carrying out AI diagnosis. If NAI is suspected, field samples are inoculated into embryonated eggs, and after incubation for several days, allantoic fluid from inoculated eggs are tested for hemagglutinating activity. Upon detection of any hemaglutinating virus, a presumptive diagnosis of NAI is made and an immediate quarantine of the farms under testing should be made. This quarantine is designed to limit the movement of birds, equipment, and personnel to prevent potential viral dissemination. Agents that show hemagglutinating activity are then further identified in the laboratory by a number of techniques including the newer rapid rRT-PCR .
4) If NAI infection is confirmed by laboratory testing, all birds within the flock should be culled, utilizing humane euthanasia techniques, and disposed of properly. This depopulation effort requires the use of proper personal protective equipment (PPE) in accordance with national or international standards.
5) Finally, it is important to have personnel trained in animal disease control measures before a potential outbreak event. The success of disease control activities requires advanced preparation and familiarity with proper biosecurity and emergency management protocols
Due to the significant economic and public health implications of an AI outbreak, all cases of LPNAI and HPNAI must be reported to the State and federal veterinary authorities in order to facilitate global virus control measures.

Selected References

  1. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  2. Swayne, D.E. 2008. Avian Influenza. In Foreign Animal Diseases, 7th ed. United States Animal Health Association. C. Brown and A. Torres (ed.).. Boca Publications Group, Inc. Boca Raton, FL. (http://www.usaha.org/pubs/fad.pdf)
  3. Swayne, D.E. and D.A. Halvorson. 2008. Influenza. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  4. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Dennis Senne
Alfonso Torres
Alejandro Banda
Benjamin Lucio-Martinez
Jose Bruzual
Jaime Ruiz
John Coakley

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Newcastle Disease

Newcastle Disease

Newcastle Disease

Etiology

Newcastle disease (ND) is an acute viral infection of great economic significance to the poultry industry worldwide. The disease is caused by the Newcastle disease virus, also called avian paramyxovirus-1 (APMV-1), that is an RNA, negative sense, single stranded, non-segmented, enveloped virus which belongs to the family Paramyxoviridae and the genus Avulavirus.

Although there is only one serotype, there are a number of different strains of Newcastle disease virus. Within a given host such as the chicken, variations in Newcastle virus strains are associated with a wide range of clinical signs. Much of this variation is the result of differences in 2 surface glycoproteins, hemagglutinin-neurominidase (HN) and fusion (F), which play an important role in the binding and fusion of the virus to host cells, initiating infection. Furthermore, the key to viral immunity involves a response to these glycoproteins.

Historically, strains of NDV have been grouped into five pathotypes or forms, based on the clinical signs seen in infected chickens. These have been defined as:

  1. Viscerotropic velogenic: a highly pathogenic form in which hemorrhagic intestinal lesions are frequently seen
  2. Neurotropic velogenic: a form that presents with high mortality, usually following respiratory and nervous signs
  3. Mesogenic: a form that presents with respiratory signs, occasional nervous signs, but low mortality
  4. Lentogenic or respiratory: a form that presents with mild or subclinical respiratory infection
  5. Asymptomatic enteric: a form that usually consists of a subclinical enteric infection."

Currently, ND virus strains are classified according to the World Organization for Animal Health (OIE) system. This classification system serves as the basis for determining whether an outbreak of ND should be reported to the OIE and other local veterinary authorities to facilitate global disease control measures.
The OIE definition for a reportable outbreak of ND is as follows:

Newcastle disease is defined as an infection of birds caused by a virus of avian paramyxovirus serotype 1 (APMV-1) that meets one of the following criteria for virulence:

a) The virus has an intracerebral pathogenicity index (ICPI) in day-old chicks (Gallus gallus) of 0.7 or greater.

or

b) Multiple basic amino acids have been demonstrated in the virus (either directly or by deduction) at the C-terminus of the F2 protein and phenylalanine at residue 117, which is the N-terminus of the F1 protein. The term

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Mycoplasma gallisepticum

Mycoplasma gallisepticum

Mycoplasma gallisepticum infection

Etiology

Mycoplasma gallisepticum (MG) infection is typically associated with slowly progressive chronic respiratory disease in chickens and infectious sinusitis in turkeys. MG is a eubacteria, a small self-replicating prokaryote lacking a cell wall. MG is the most pathogenic and economically significant of the mycoplasma pathogens known to affect poultry. Numerous strains of MG exist and there is wide variability in the relative virulence of these strains. Synergism between MG and other infectious agents, such as Newcastle disease and infectious bronchitis, is common.

Host range

Mycoplasma gallisepticum is primarily a respiratory disease affecting chickens and turkeys in commercial production; however ducks, geese, pheasants, peafowl, quail, and some wild avian species are also susceptible to the infection. MG has recently been implicated in natural outbreaks of conjunctivitis in free-ranging house finches (Carpodacus mexicanus) in the Eastern United States. In finches, the infection causes conjunctivitis and periorbital swelling. Avian mycoplasma infections appear to be limited to avian species and pose no threat to humans.

Epidemiology

Mycoplasma gallisepticum is spread primarily via horizontal transmission, through both direct contact with infected birds and indirect contact with contaminated equipment, environment, and personnel. MG can survive outside the host (e.g. in feces, feathers, and litter) for several days. Aerosol spread also occurs. The infection enters a susceptible bird through the upper respiratory tract and/or conjunctiva. Exposure of susceptible birds to clinically or subclinically infected birds can play a significant role in the spread of this disease within a flock. Vertical transmission can also occur in eggs laid by hens that are in the acute phase of the disease, and at a lower level during chronic infections. The disease tends to be most severe in younger birds and outbreaks frequently occur in winter.

MG is distributed worldwide. In the United States, most breeder flocks are free from MG; however, infections in growing turkeys and broilers continue to occur. MG infection is endemic in many large multiple-age commercial egg production complexes. The infection may enter a commercial poultry flock via a number of routes including exposure to carrier birds in backyard flocks, exposure to free-ranging wild species, and poor biosecurity practices.

Clinical Signs

MG has a long and variable incubation period, typically ranging from 6-21 days. The clinical signs are highly variable and depend on the host species, age, virulence of the strain, the presence of concurrent infections, as well as any environmental or physiological stress (e.g onset of egg production).

In chickens, the disease may produce no clinical signs or it may produce nasal discharge, coughing, and rales. Conjunctivitis, periorbital edema, and eyelid edema may also occur. Other more general signs may include inappetence, weight loss, and a drop in egg production. The highest morbidity and mortality usually occurs in the presence of concurrent infections and environmental stress.

In turkeys, MG is sometimes associated with more severe clinical signs than typically observed in chickens. Signs may begin with nasal discharge and a foamy ocular discharge, followed by swelling of the infraorbital sinuses. Swelling may become so severe that the birds can no longer open their eyes. As the disease progresses, coughing, rales, and dyspnea may occur. Generalized depression, inappetence, weight loss, and drop in egg production often occur. In 12-16 week old commercial turkeys, torticollis and opisthotonus has been documented.

Although morbidity due to MG is high, mortality is generally low, except in cases complicated with concurrent infections or environmental stress. However, broilers and market turkeys may suffer high condemnation due to airsacculitis and, in layer flocks, the overall production rate may be compromised.

Post-mortem Lesions

On post-mortem examination, lesions may be found throughout the upper and lower respiratory tract. Catarrhal exudate may be present in the nasal passages, infraorbital sinuses, trachea, and bronchi. Caseous exudate may be seen in the air sacs. Other findings may include fibrinous or fibrinopurulent perihepatitis and pericarditis, conjunctivitis, corneal opacities, and periocular edema. Sinusitis is most frequently observed in turkeys but may be present in chickens and other avian species as well.

Differential Diagnosis

It is necessary to differentiate MG from other respiratory diseases of poultry. Pulmonary and air sac lesions may be confused with colibacillosis.

In turkeys, sinusitis can also be caused by avian influenza, Mycoplasma synoviae, aspergillosis, pasteurellosis, chlamydiosis, cryptosporidiosis, Newcastle disease, and turkey rhinotracheitis. Fowl cholera (Pasteurella multocida) is a frequent complication in turkeys and may be accompanied by fibrinous pneumonia.

In chickens, MG must be differentiated from respiratory diseases including Newcastle disease, infectious coryza (Avibacterium paragallinarum), infectious bronchitis, avian influenza, chlamydiosis, Fowl Cholera (Pasteurella multocida) or respiratory cryptosporidiosis.

Diagnosis

Isolation and identification of the MG organism is the gold standard for diagnosis. It is commonly performed by culturing swabs collected from tracheal, sinus, or air sac exudates, or from choanal swabs or tissue samples collected from the turbinates or lungs. In the acute stages of infection, collect and submit samples from 10-20 live birds. In chronic infections, collect samples from 30-100 birds in order to improve the chances of recovering the organism. Mycoplasma broth should be inoculated directly from the bird (via a swab of exudate or tissue sample) and incubated immediately. If the sample must be shipped, store the sample on cold pack for less than 24 hours and use an overnight carrier. In the laboratory, growing cultures are plated out on mycoplasma agar. Suspect colonies may be identified by immunofluorescence tests. Isolation and identification of Mycoplasmas requires specialized media and reagents that are often not commercially available. Detection of MG DNA by polymerase chain reaction (PCR) is becoming a common diagnostic test. A commercial PCR test for MG is available and PCR is performed if it is urgent to determine the flock status.

Serologic testing is used for flock monitoring programs and to aid in diagnosis when infection is suspected. Serology tests of sera for antibodies against MG may include serum plate agglutination (sometimes used for rapid initial screening), enzyme-linked immunosorbent assay (ELISA), and hemagglutination-inhibition (HI). Because of the rapid turn around time, serum plate agglutination is often the standard initial screening test. However, because sera from birds with M. synoviae may cross-react, MG is confirmed with the HI or ELISA test.

Prevention and Control

The best way to prevent Mycoplasma gallisepticum infections is to start with clean stock, maintain good biosecurity, and if possible, practice all-in all-out management. The use of antimicrobial therapy may be used to reduce morbidity and mortality, losses at processing, or egg transmission. Mycoplasma gallisepticum live vaccines are highly effective to control the infection. Bacterins and a recombinant fowlpox-MG vaccine are also available.

Selected references

  1. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  2. Glisson, J.R. 1998. Bacterial respiratory disease of poultry. Poult Sci Aug;77(8):1139-42. Review.
  3. Kleven, S.H. 2008. Mycoplasmosis. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
  4. Lancaster, J.E. and J. Fabricant. 1988. The history of Avian medicine in the United States. IX Events in the History of Avian Mycoplasmosis 1905-70. Avian Dis 32:607-623.
  5. Levisohn, S. and S.H. Kleven. 2000. Avian Mycoplasmosis (Mycoplasma gallisepticum). Rev Sci Tech Aug;19(2):425-42. Review.
  6. Ley, D.H. 2008. Mycoplasma gallisepticum Infection. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  7. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing this material:

Naola Ferguson-Noel
Jaime Ruiz
Jose Bruzual

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Avian Pox

Avian Pox

Avian Pox

Etiology

Fowl pox is a slow-spreading viral infection of birds. The virus belongs to the genus Avipoxvirus, and is in the family Poxviridae. Clinically, fowl pox occurs in two forms. In the cutaneous or dry form, discrete nodular proliferative skin lesions occur in the nonfeathered parts of the body. In the diphtheritic or wet form, fibrino-necrotic and proliferative (canker) lesions form on the mucous membranes of the mouth, pharynx, esophagus, and trachea. Fowl pox is an economically important disease of commercial poultry because it is associated with a drop in egg production and may cause mortality.

Host Range

Many species of birds are susceptible to avian pox including domestic poultry (chickens and turkeys), pet birds, and more than 60 species of free-living birds, representing 20 families. Avian pox occurs in all age groups of birds. Avian pox does not represent a risk to human heath, however some mammalian species may be susceptible to the virus. In the distant past, the disease was mistakenly thought to be related to small pox or chicken pox in humans.

Epidemiology

The avian pox virus is usually transmitted mechanically to pen-mates through skin abrasions. Humans can also inadvertently spread the virus through contact with infected poultry (via ocular infection) during vaccination regimens. Mosquitoes, other flying insects, and parasites can serve as mechanical vectors. In contaminated environments, the dried virus can also become aerosolized and gain entry into birds' mucous membranes and respiratory tracts.

The incubation time varies by species but is typically 4-10 days in chickens and turkeys. Morbidity in chickens and turkeys varies from a few birds to an entire flock, depending on virulence and control measures. The course of the disease may last approximately 2-8 weeks, during which time birds can lose weight and egg production may be retarded. Although mortality is typically low, it may be as high as 50% with virulent strains or if secondary infections complicate the disease.

Avian pox is distributed worldwide. Wild birds are a reservoir for this virus.

Clinical Signs

Clinical signs are somewhat variable depending on the host species, virulence of the virus strain, distribution of lesions, and other complicating factors. The disease onset is often gradual in poultry and usually goes undetected until skin lesions are obvious. Only a few birds develop lesions at one time. In chickens and turkeys, signs may vary with two overlapping forms of the disease:

Cutaneous (dry pox): Common form in most outbreaks. The dry form begins with a pimple or scab on nonfeathered areas of the skin such as the comb, wattles, eyelids, feet, and legs. Eventually, the infection may spread to other feathered areas of the body (especially in turkeys). Infected birds often have difficulty eating and reduced feed intake and weight loss is common. Other signs may include drop in egg production, facial swelling, blindness (caused by ocular and periocular involvement) and loss of vigor. Mortality is usually low in uncomplicated cases, unless secondary infections become a problem.

Diphtheritic (wet pox): The wet-mucous form produces diphtheritic, yellow canker lesions on oral mucous membranes, tongue, esophagus, or trachea. Lesions in the upper digestive and respiratory tract may result in inappetence and dyspnea, respectively. Other mild to severe respiratory signs may also occur. Lesions in the eye and nasal cavity lead to oculonasal discharges. Mortality often results from suffocation or starvation.

Avian pox is generally associated with a more chronic condition in turkeys than in chickens. Canary pox causes systemic infection with high mortality.

Post-mortem Lesions

Cutaneous (dry pox): this form is characterized by a local epithelial hyperplasia involving the epidermis and feather follicles. The nodules begin as small white foci, which rapidly increase in size and turn yellow. Within 5-6 days, papules develop and progress into vesicles. These vesicles may coalesce and turn grey to dark brown, with a rough wart-like texture. Within two weeks, the pox lesions develop inflammation and hemorrhage around their base. Over time, the lesions turn into scabs which eventually slough, often revealing a smooth scar.

Diphtheritic (wet pox): this form is characterized by the development of white opaque nodules on the mucous membranes of the digestive and respiratory tracts, such as the oral cavity, tongue, larynx, esophagus, trachea, and sinuses. These nodules enlarge and coalesce into yellow diptheritic membranes. On post-mortem examination, if these diptheritic membranes are removed, bleeding erosions will be found beneath the membranes. In some cases, birds may have a localized pox infection, with small nodules found on internal organs.

Birds may have a combination of both cutaneous pox lesions (typically involving the comb, wattles, and eye region) as well as diptheritic lesions in the digestive and respiratory tracts.

Differential Diagnosis

For the cutaneous form, bacterial dermatitis should be ruled out. Cutaneous lesions, caused by pantothenic acid or biotin deficiency in young chicks, or by T-2 toxin could be mistaken for pox lesions.

For the diptheritic form, when respiratory signs are present, rule outs must include diseases such as avian influenza and infectious bronchitis. The diphtheritic lesions may resemble signs of infectious laryngotracheitis. Histologic examination of poxvirus lesions will reveal epithelial hyperplasia with intracytoplasmic inclusion bodies; whereas, laryngotracheitis, caused by a herpesvirus, produces intranuclear inclusions. In doves and pigeons, diphtheritic pox lesions may be mistaken for lesions caused by Trichomonas gallinae, which is diagnosed by microscopic examination of smears or by culture.

Diagnosis

A presumptive diagnosis can be made in the field based on characteristic skin lesions. The diagnosis should be confirmed by laboratory testing. Collect and submit cutaneous and diptheritic tissue lesions to the laboratory. Diagnosis is confirmed by the presence of cytoplasmic inclusions found on microscopic examination of affected tissue sections, stained with H & E (haematoxylin and eosin) stain. Inclusions are also detected by fluorescent antibody and immunoperoxidase methods. Viral particles, with typical poxvirus morphology, can be detected by electron microscopy. The virus can be isolated in the chorioallantoic membrane (CAM) of chicken embryos, susceptible birds, or avian cell cultures. Field viruses can be detected in the laboratory by polymerase chain reaction (PCR) and can be compared by restriction endonuclease digestion.

Prevention and Control

In the United States, pox has been a common problem for commercial poultry. The large DNA virus is highly resistant and can survive in dried scabs in the environment for months to years, infecting replacement birds.

Fowl pox and pigeon pox live virus vaccines are commonly used for immunization of chickens. Administration in laying birds is performed around four weeks of age, following by a boost one or two weeks before the onset of egg production. Broilers are only vaccinated at an early age in areas in which the disease is endemic. On average, immunity develops around two weeks post-vaccination.

Vaccination is commonly applied by the wing-web method and induces a mild form of the disease. The evidence of a "take" should be verified in the wing web seven to ten days after vaccination. A "take" is a swelling of the skin or a scab at the site where the vaccine was applied and is evidence of successful vaccination.

No treatment exists for birds infected with avian pox viruses.

Selected References

  1. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  2. Tripathy, D.N. and W.M. Reed. 2008. Pox. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
  3. Tripathy, D.N. and W.M. Reed. 2008. Pox. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  4. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Richard Chin
Jaime Ruiz

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Infectious Bronchitis

Infectious Bronchitis

Infectious Bronchitis

Etiology

Infectious bronchitis (IB) is a highly contagious respiratory disease capable of producing a range of clinical signs in chickens. The disease can vary from asymptomatic to involvement of the respiratory, renal, and reproductive organs. The disease is caused by the infectious bronchitis virus (IBV), a single stranded, RNA, positive sense, enveloped virus and a member of the family Coronaviridae, genus Coronavirus. There are many strains of IBV with considerable variation in the virulence.

Host Range

The chicken is the only species known to be naturally susceptible to IBV. Susceptibility to the virus varies by breed and age. Young chicks develop the most severe respiratory forms of the infection, whereas older birds are most susceptible to reproductive lesions and drops in egg production. Although all ages of chickens are susceptible, as birds mature, they become more resistant to these effects. Environmental factors and the presence of concurrent infections often play a significant role in the severity of clinical signs. IBV does not appear to pose a threat to human health.

Epidemiology

The IB virus is shed in the nasal excretions and feces of infected birds. The virus is highly infectious and typically spreads quickly from bird to bird, via direct and indirect contact with contaminated feed, water, equipment, and other infected birds. In some birds, internal organs become persistently infected, resulting in intermittent shedding of the virus. These carriers increase the possibility of flock-to-flock spread of the virus via unknowingly contaminated personnel.

The incubation time for the IBV varies from 18-36 hours. Morbidity is 100%, however mortality varies greatly depending on the virulence of the strain, host age, immune status, and the presence of physiologic stress and concurrent infections. Mortality is usually less than 5%, however secondary infections with Eschericia coli and Mycoplasma can significantly increase the mortality rate.

The IB virus is distributed worldwide, with different serotypes found in different regions of the world. Despite vaccination efforts, outbreaks of IB occur frequently because vaccines against one serotype do not cross-protect against a different serotype.

Clinical Signs

The clinical signs of the infection vary and depend on the age of the bird, host immune status, and virulence of the virus. In chicks, depression, ruffled feathers, and huddling near heat sources are common early signs. Within 24 hours, respiratory signs are typically observed and may include coughing, sneezing, nasal discharge, tracheal rales, and gasping. Ocular discharge (epiphora) may be present and the sinuses may become swollen. Feed intake may drop and subsequent weight loss may be observed. Chicks, less than 2-weeks of age may suffer damage to the oviduct, resulting in permanent impairment to their egg-laying capacity. Some highly virulent strains have also been associated with facial edema and airsacculitis.

In birds older than 6 weeks of age, the signs are similar but often less severe. In adults, respiratory signs may be so subtle as to be observable only at night when the birds are normally quiet. In layers, egg production may drop by up to 50% (depending on virus strain and period of lay) and eggs are often misshapen, soft-shelled, and contain watery albumen. Birds that recover from the infection may never return to pre-infection egg laying levels.

Some strains of IBV are nephropathogenic. Birds generally recover from early respiratory signs only to later develop diarrhea, sometimes with fatal secondary urolithiasis.

Post-mortem Lesions

The trachea, nasal passages, and sinuses may be edematous and typically have serous, catarrhal, or caseous exudate present on post-mortem examination. A caseous plug may occlude the trachea or bronchi in dead chicks. The lungs may show evidence of pneumonia. The air sac membranes may be cloudy and caseous yellow exudate may be present. The kidneys may be swollen and pale, due to interstitial nephritis and necrosis, and white urates may be present in increased amounts in the distended tubules and ureters. The oviduct may be occluded and hypoglandular. Egg yolk peritonitis may be found within the coelomic cavity, secondary to ruptured follicles.

Differential Diagnosis

The clinical signs of IB may resemble other acute respiratory diseases in chickens, such as Newcastle disease, laryngotracheitis, avian influenza and infectious coryza. Laboratory testing is necessary to differentiate these infections. In IB, allantoic fluid from inoculated embryos does not hemagglutinate erythrocytes. For Newcastle disease virus, and avian influenza virus, allantoic fluid from inoculated embryos will be positive for hemagglutination.

Diagnosis

Clinical history, gross lesions, seroconversion and molecular tests for antigen and viral nucleic acid detection are commonly used to diagnose infectious bronchitis.

Diagnostic samples should be collected as soon as clinical signs are observed. Tracheal swabs should be collected from 5-10 birds per affected flock. Additionally, paired serum samples should be collected. Fresh tissue samples should be taken from the lung, kidney, oviduct, and cecal tonsils using aseptic technique. Swabs and tissue samples should be frozen and all samples shipped to the laboratory.

In the laboratory, swab tube broth or tissue homogenates are used to inoculate 9 to 11 day old embryonated eggs. After several days, chorioallantoic fluid is harvested and should produce a negative hemagglutination reaction with chicken red blood cells. Curling, stunting and death of embryos can be seen in IBV positive embryos. Confirmation of IBV, and its serotypes, can be performed by various antibody detection methods including: virus neutralization (VN), immunoflourescent antibody assay (IFA), antigen-capture enzyme-linked immunosorbent assay (AC-ELISA), and monoclonal antibodies. However, only the VN test and some monoclonal antibodies can distinguish between different serotypes. Reverse transcriptase-polymerase chain reaction (RT-PCR), followed by restriction fragment length polymorphism (RFLP), and/or sequencing of the S1 gene are commonly used to identify IBV types. The immunoflourescent antibody assay (IFA) or electron microscopy can be used on tracheal samples for rapid diagnosis but those tests do not distinguish between different IBV types.

Seroconversion, and specifically a rise in IBV antibody titer indicating IBV infection, is determined by ELISA, VN test, modified hemagglutination inhibition (HI), immunofluorescence, and immunodiffusion tests.

Prevention and Control

Prevention and control in the field is difficult using common sanitary and biosecurity measures because IBV is highly infectious. Good cleaning and disinfection practices, during the downtime period, may help to prevent recurrent infections in problem farms. Farm complexes with multiple ages, such as the ones that have table egg layers, are a common source of infection. In these types of flocks, it is very common to see drops in egg production due to chronic disease.

Infectious bronchitis is extremely difficult to control because different serotypes of the virus do not cross-protect. Attenuated live and inactivated vaccines are used for infectious bronchitis immunization. Attenuated live vaccines delivered in the drinking water or by spray, are commonly used in broilers and for the initial vaccination of laying birds. Inactivated oil-emulsion vaccines are used in breeders and layers before the beginning of the production cycle. The administration is performed either by intramuscular or subcutaneous injection. These types of vaccines reduce the incidence of viral replication in the respiratory tract and may limit the spread and transmission to other susceptible birds. Broilers are commonly vaccinated with a live vaccine in the hatchery, followed by a second vaccination of the same or different serotype between 10 and 18 days of age.

No specific treatment exists for infectious bronchitis. The use of antibacterials against secondary opportunistic bacterial infections in the first stages of the disease may reduce the incidence of severe multifactorial respiratory disease, associated with poor conversion performance and increased mortality.

Selected References

  1. Cavanagh, D. and J. Gelb. 2008. Infectious bronchitis. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  2. Cavanagh, D. 2007. Coronavirus avian infectious bronchitis virus. Vet Res Mar-Apr;38(2):281-97.2007. Review.
  3. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  4. Fabricant, J. 1998. The early story of infectious bronchitis. Avian Diseases 42:648-650.
  5. Gelb, J. and M.W. Jackwood. 2008. Infectious bronchitis. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
  6. Ignjatovi?, J. and S. Sapats. 2000. Avian infectious bronchitis virus. Rev Sci Tech Aug;19(2):493-508. Review.
  7. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Mark Jackwood
Jaime Ruiz
Jose Bruzual

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Infectious Laryngotracheitis

Infectious Laryngotracheitis

Infectious Laryngotracheitis

Etiology

Infectious Laryngotracheitis (ILT) is a highly contagious upper respiratory infection caused by the infectious laryngotracheitis virus (ILTV). The virus belongs to the Herpesviridae family and is in the subfamily Alphaherpesvirinae. Mild to severe enzootics of the disease have been observed.

Host Range

Infectious Laryngotracheitis is primarily an infection of chickens. Rarely, pheasant and peafowl may be affected. Wild avian species appear to be resistant to the disease. Chickens of all ages are susceptible; however birds older than 4 weeks of age have increased susceptibility to infection. There is no known public health risk to humans associated with ILTV.

Epidemiology

ILT is transmitted primarily through direct contact between susceptible birds and clinically recovered carriers. Mechanical transmission can also occur through contaminated equipment and litter. The virus enters the host through the upper respiratory tract and eyes and targets the epithelial cells of the respiratory tract as well as other mucous membranes.

ILT has a worldwide distribution. In countries with intensive poultry production, the disease is mainly controlled through vaccination. In these areas, when the disease does occur, it is usually the milder enzootic form. In developing countries, the virus typically exists as an endemic infection.

Clinical Signs

The incubation of ILT virus is approximately 6-12 days. The clinical presentation varies according to the pathotype of the virus as well as environmental and host factors. In the mild enzootic form, infection is characterized by general unthriftiness, 5-15% drop in egg production, as well as ocular and respiratory signs. The clinical signs may include conjunctivitis (including epihora /watery discharge or hemorrhage), nasal discharge, and swelling of the infraorbital sinuses. The virus primarily affects the cells of the tracheal mucosa and conjuntiva, but occasionally the lungs and air sacs are also affected.

Most chickens recover within 10-14 days, if the infection is not complicated by immunosuppression or a secondary bacterial or mycoplasma infection. The morbidity of the mild forms is typically about 5% and the mortality is very low. However, the economic losses due to reduced egg production are increasingly important in many poultry producing areas in the United States and around the world.

In severe epizootic forms, clinical signs may include coughing, rales, dyspnea, gasping, nasal discharge, and hemorrhagic mucoid expectorations. The morbidity of these forms of ILT is 90-100% and the mortality is typically 10-20%.

Post-mortem Lesions

In mild enzootic forms, gross lesions may be limited to the epithelium of the conjunctiva and infraorbital sinuses. Lesions may include congestion and edema.

In severe epizootic forms, gross lesions may extend throughout the upper and lower respiratory tract and include the ocular conjunctiva. Lesions are most consistently observed in the trachea and larynx. These may range from mild mucus accumulations to varying degrees of inflammation, diptheritic mucoid or hemorrhagic casts, and necrosis. In severe cases, hemorrhage may be found in the trachea, nasal, and oral cavities.

Differential Diagnosis

Respiratory disease associated with ILT must be distinguished from other respiratory pathogens of poultry producing similar clinical signs and gross lesions. These include the diphtheritic form of avian pox virus and infections caused by Newcastle disease virus, avian influenza virus, infectious bronchitis virus, fowl adenovirus, and Aspergillus spp.

Diagnosis

In severe acute infections, with high mortality and expectoration of blood, a tentative field diagnosis of ILT can be made. A definitive diagnosis will require laboratory testing. Keep in mind that silent and subclinical forms of ILT have been identified through laboratory testing. In the laboratory, confirmatory testing may include virus isolation, microscopic detection of intranuclear inclusion bodies in respiratory and conjunctival epithelial cells, and the detection of ILT viral antigens in tracheal tissues or respiratory mucus. Demonstration of viral antigen in clinical samples can be performed through the use of fluorescent antibody, immunoperoxidase, electron microscopy, DNA hybridization, antigen capture enzyme-linked immunosorbent assay (ELISA) and by Polymerase Chain Reaction (PCR) tests. PCR assays for the detection of viral nucleic acid, has been widely utilized as a confirmatory fast assay. Also, serologic tests like agar gel immunodiffusion test (AGID), serum neutralization, and ELISA could be used in conjunction with other laboratory tests.

Prevention and Control

Attenuated live vaccines available to control ILT are either tissue culture or chicken embryo origin viruses. Despite the fact that most ILT vaccines are often administered by coarse spray and by drinking water, they are labeled for eye drop application. Broilers are only vaccinated in the phase of an outbreak and it is recommended not to vaccinate broilers before 2 weeks of age or after 3 weeks of age. Layer and breeder replacements are vaccinated by eye drop application one or two times during the growing period, using either a tissue culture or embryo-adapted vaccine. Inactivated vaccines are only available at the experimental level because of the high-cost of preparation and delivery.

Selected References

  1. Barhoom, S.A., A. Forgacs, and F. Solyom. 1986. Development of an inactivated vaccine against laryngotracheitis (ILT)-serological and protection studies. Avian Pathol 15:213-221.
  2. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  3. Cove, M.S. 1996. The early history of infectious laryngotracheitis. Avian Diseases 40:494-500.
  4. Guy, J.S. and M. Garcia. 2008. Laryngotracheitis. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  5. Roberston, G.M., and J.R. Egerton. 1981. Replication of infectious laryngotracheitis virus in chickens following vaccination. Aust. Vet. J. 57:119-123.
  6. Tripathy, D.N. and M. Garcia. 2008. Infectious laryngotracheitis. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
  7. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Maricarmen Garcia
Jaime Ruiz
Jose Bruzual

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