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  • congestion: ovary
  • hemorrhages: ovary
  • involution: ovary
  • ovary

follicle, ovary

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Ovary: Moderate multifocal follicular and intrafollicular hemorrhage and congestion. Ovary: Follicular atresia.

Clinical Description

This image was taken 2 days post experimental inoculation with highly pathogenic avian influenza. The follicles on this ovary are congested and some areas have hemorrhages. Some follicles are undergoing involution and degeneration and the ovary is inactive. These findings typically correlate with a precipitous drop in egg production among infected breeders and layers. There is also some yellow proteinaceous material on the periphery of the ovary that is consistent with an unrelated chronic egg yolk peritonitis.

Pathologic Description

The blood vessels over the ova are prominent and congested and, in some follicles, there are large, poorly demarcated red foci. The intrafollicular tissue is dark red. There are no mature ova on the ovary. Some of the follicles are becoming paler and slightly flaccid (atresia). Depending on the timing of the lay cycle, the lack of mature follicles and increased atresia can indicate disease.

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  • congestion: ovary
  • follicular atresia: ovary
  • hemorrhages: ovary
  • ovary

follicle, ovary

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Ovary: Acute congestion and hemorrhage with follicular atresia

Clinical Description

This image was taken 2 days post experimental inoculation with highly pathogenic avian influenza. In HPAI, ovaries such as this one, may become hemorrhagic with ova involution and degeneration.

Pathologic Description

This ovary contains follicles in numerous stages of development. The follicular vessels are congested and in some areas the follicles and intrafollicular spaces are dark red. Several of the large follicles are flaccid and some are collapsed (atresia).

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  • enlargement: spleen
  • spleen

ovary, spleen

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Ovarian follicles: Atresia and multifocal hemorrhage. Spleen: Mild splenomegaly.

Clinical Description

This image was taken 3 days post experimental inoculation with highly pathogenic avian influenza. The hemorrhagic and atresic follicles on this ovary are typical of HPAI. An enlarged, firm spleen is occasionally observed.

Pathologic Description

Several of the ovarian follicles are shrunken and flaccid. One of the follicles is dark green and some contain red areas. The spleen is slightly enlarged with an enhanced reticular pattern.

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  • follicular atresia: ovary
  • hemorrhages: ovary
  • ovary

follicle, ovary

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Ovarian follicles: Atresia and multifocal hemorrhage

Clinical Description

This image was taken 3 days post experimental inoculation with highly pathogenic avian influenza. The dark green follicle in the center of the image is undergoing atresia.

Pathologic Description

Several of the ovarian follicles are shrunken and flaccid. One of the follicles is dark green and some contain red areas.

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gross image

  • congestion: ovary
  • hemorrhages: ovary
  • ovary

follicle, ovary

Newcastle Disease

chicken (Gallus gallus)

Morphologic Diagnosis

Ovarian follicles: Severe acute hemorrhage and congestion

Clinical Description

Velogenic viscerotropic Newcastle disease. The ovaries in this infected bird show marked hemorrhages. The egg production in such birds often drops dramatically. Even in birds that survive the acute infection, the reproductive system may be permanently damaged and egg production may not return to normal.

Pathologic Description

The surfaces of these well developed ovarian follicles are covered by extensive dark red areas and prominent blood vessels.

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  • congestion: ovary
  • follicular atresia: ovary
  • hemorrhages: ovary
  • ovary

follicle, ovary

Newcastle Disease

chicken (Gallus gallus)

Morphologic Diagnosis

Ovarian follicles: Atresia with hemorrhage and congestion

Clinical Description

In chickens infected with velogenic viscerotropic Newcastle disease, ovaries frequently have gross lesions. These may include hemorrhage and necrosis (causing discoloration) and follicles may be flaccid and degenerative.

Pathologic Description

This ovary contains several large follicles that have become flaccid and shrunken. The blood vessels over many follicles are prominent and the ventral-most follicle is dark red.

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  • congestion: ovary
  • hemorrhages: ovary
  • ovary

follicle, ovary

Newcastle Disease

chicken (Gallus gallus)

Morphologic Diagnosis

Ovarian follicles: Marked acute hemorrhage and congestion

Clinical Description

Velogenic viscerotropic Newcastle disease. Hemorrhagic follicles on the ovaries are commonly found in infected birds and are accompanied by a drop in egg production.

Pathologic Description

The ovarian follicles are covered by prominent blood vessels and areas of red discoloration.

DSC00066

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gross image

  • congestion: ovary
  • hemorrhages: ovary
  • ovary

ovary

Newcastle Disease

chicken (Gallus gallus)

Morphologic Diagnosis

Ovarian follicles: Marked acute hemorrhage and congestion

Clinical Description

Velogenic viscerotropic Newcastle disease. Hemorrhagic follicles on the ovaries are commonly found in infected birds and are accompanied by a drop in egg production.

Pathologic Description

The ovarian follicles are covered by prominent blood vessels and areas of red discoloration. The oviduct is present on the right size of the image. The large size of this structure indicates that the bird was in an active phase of egg production.

IBV-035A.jpg

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gross image

  • follicular atresia: ovary
  • involution: ovary

follicle, ovary

Infectious Bronchitis

chicken (Gallus gallus)

Clinical Description

On post-mortem examination, the reproductive tract may be affected. The ovarian follicles may be undergoing involution and may appear flaccid, as seen here. These lesions are non-specific for infectious bronchitis, as many other acute diseases can be associated with this finding.

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  • nodules: ovary

ovary

Marek's Disease

Unknown

Clinical Description

Marek's disease tumors in the ovary.

MD-064A.jpg

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  • nodules: ovary

ovary

Marek's Disease

chicken (Gallus gallus)

Clinical Description

Marek's disease tumors in the ovary.

MD-069A.jpg

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  • nodules: ovary

kidney, ovary

Marek's Disease

chicken (Gallus gallus)

Clinical Description

In Marek's disease, as the nodules on organs enlarge, as shown on this kidney and ovary, the normal architecture of the organ is destroyed and sometimes areas of tissue necrosis can occur.

PAST-028A.jpg

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  • congestion: ovary
  • ovary

follicle, ovary

Fowl Cholera

chicken (Gallus gallus)

Clinical Description

In fowl cholera, lesions of the ovary may include hyperemia and flaccid mature follicles. The ovary of this hen with acute fowl cholera shows a severe hyperemia of the follicular membranes.

ovariesjaime

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  • congestion: ovary
  • ovary

follicle, ovary, oviduct

Fowl Cholera

chicken (Gallus gallus)

Clinical Description

Hyperemia (vascular congestion) of the follicles associated with acute fowl cholera infection. This image also shows that there is an egg in the oviduct (on the right), indicating that the bird was in lay. Birds in peak egg production are under greater physiologic stress and may die from this infection.

PAST-029A.jpg

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  • congestion: ovary
  • follicular atresia: ovary
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  • involution: ovary
  • ovary

follicle, ovary

Fowl Cholera

chicken (Gallus gallus)

Clinical Description

Acute fowl cholera showing necrotic, misshapen, and discolored ovarian follicles.

37_ovary

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normal

ovary

Normal Reference

chicken (Gallus gallus)

Clinical Description

This image shows the normal ovary of a sexually immature female, approximately 10 weeks of age. Here, the ovary is small and inactive.

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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Fowl Cholera

Fowl Cholera

Fowl Cholera (Pasteurella multocida)

Etiology

Fowl cholera (FC) is a highly contagious disease of domestic and wild birds. The disease is caused by Pasteurella multocida, a gram-negative, non-spore-forming, rod shaped bacteria. There are 16 somatic serotypes of Pasteurella multocida, of which 1, 3, and 3x4 are the most common. The pathogenicity of Pasteurella multocida strains is quite variable and the degree of expression of clinical signs varies by host species as well as variations within the host's immune system.

Host Range

Outbreaks of FC occur most frequently in turkeys, chickens, ducks, and geese. The disease is particularly severe in turkeys. Other bird species raised in captivity, as well as wild avian species, may also develop clinical disease. Some domestic mammals are also susceptible.

Epidemiology

FC is spread via horizontal transmission through contact with infected birds, contaminated equipment, personnel, etc. Pasteurella multocida can enter through mucous membranes, including oral, nasal, and conjunctival, as well as through cutaneous wounds. Chronically infected carriers play a major role in the spread of this disease and infected birds can remain carriers for life. The prevalence of Pasteurella multocida among wild birds, rodents, and other domesticated and non-domesticated species is likely responsible for the introduction of the infection into most domesticated poultry flocks.

FC is widely distributed, with periodic enzootic outbreaks occurring in most countries throughout the world. The disease usually manifests as a septicemia, sometimes with high morbidity and high mortality. However, a more chronic and asymptomatic form of the disease can also occur. Young adults are most susceptible to FC infection and physiologic stresses, such as egg lay cycles and seasonal changes, influence susceptibility. FC is more prevalent in the cooler seasons of the year.

Clinical Signs

Signs vary depending on the course of the disease. In the acute form of FC, infected birds may develop fever, ruffled feathers, anorexia, increased respiratory rate, and cyanosis. Cyanosis is often easiest to appreciate on the non-feathered skin of the comb and wattles. Mucoid discharge from the mouth and diarrhea may also occur. Diarrhea often begins as watery and whitish in color, progressing to a greenish color with mucus. In the acute form, signs may be absent and birds may be found dead in their nests. Birds that survive the acute septicemia may later die of dehydration and emaciation. Some birds may survive but remain chronically infected.

In the chronic form of FC, birds that survive acute infection or birds exposed to a low virulence strain, generally exhibit localized infections. The wattles, sinuses, foot pads, sternal bursa, and leg and wing joints may become swollen. Exudative pharyngeal and conjunctival lesions may be present. Sometimes tracheal rales and dyspnea may occur secondary to respiratory tract infections. Infected birds may also exhibit torticollis from middle ear infections and meningeal involvement. The chronic form of FC may last 3 to 4 weeks and may sometimes persist for years.

Post-mortem Lesions

In the acute form of FC, lesions associated with vascular disturbances are common. The veins of the abdominal viscera, especially the duodenum, may be markedly hyperemic. Petechiael and ecchymotic hemorrhages are frequently found throughout the viscera, most commonly the lungs, intestines, heart, and abdominal fat. Excessive fluid may be found in the pericardium and coelomic cavity. In infections with virulent strains of Pasteurella multocida, there may be liver enlargement and coagulative necrosis. Other findings may include pneumonia, especially in turkeys, and excessive mucous along the digestive tract. Lesions of the ovaries may include flaccid follicles, hyperemia, and egg-yolk peritonitis from ruptured ova.

In the chronic form of FC, localized infections may be found throughout the body including the hock joints, foot pads, oviduct, and coelomic cavity. Suppurative lesions are frequently found in the respiratory tract and pneumatic bones. Pneumonia is especially common in turkeys. Caseous exudate and fibrin may also infiltrate the calvarial bones, middle ear, meninges, and air spaces.

Differential Diagnosis

Fowl cholera must be differentiated from erysipelas, acute colibacillosis, Avibacterium gallinarum and complicated Mycoplasma gallisepticum in turkeys and other birds that may have both diseases. Erysipelas is caused by a gram-positive rod. Cholera can be differentiated from other septicemic diseases by isolation of P. multocida. Related organisms that cause cholera-like diseases in poultry include P. gallinarum, P. haemolytica, and P. anatipestifer.

Diagnosis

Culture samples can be taken from the liver, lungs, spleen, wattles or affected joints at necropsy. Additionally, impression smears of the liver and heart blood can also be obtained. Gram-stained impression smears may reveal bipolar, gram-negative rods suggestive of P. multocida. Use of Wright's stain or methylene blue readily demonstrates the bipolar morphology of P. multocida. Rabbits, hamsters, or mice can be inoculated for pure culture. P. multocida grows readily on blood agar but does not grow on MacConkey agar. Isolates should be tested for antibiotic sensitivity and resistance.

Prevention and Control

The elimination of reservoirs of Pasteurella multocida (such as rats, mice, cats, raccoons, skunks, etc.) in contact with domesticated and commercial poultry is one of the most effective management procedures to control the disease.

Both live and inactivated Pasteurella multocida vaccines are available for use in chickens. Three live products are available in the United States; the Clemson University CU low virulent strain; M-9, a mutant of CU of very low virulence; and PM-1, a mutant of CU intermediate in virulence between CU and M-9. Inactivated bacterins are primarily trivalent whole cell products containing the most common serotypes. Autogenous vaccines are also commonly used. A combination of inactivated and live vaccines can reduce the incidence of fowl cholera in susceptible broiler breeder flocks. Since FC is primarily a disease of older birds, broilers are not commonly vaccinated.

Selected References

  1. Brogden, K.A., K.R. Rhoades, and K.L. Heddleston. 1978. A new serotype of Pasteurella multocida associated with fowl cholera. Avian Dis 22:185-90.
  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. Glisson. J.R., C.L. Hofacre, and J.P. Christensen. 2008. Pasteurellosis and other respiratory bacterial infections. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  4. Glisson, JR. 1998. Bacterial respiratory disease of poultry. Poult Sci Aug;77(8):1139-42. Review.
  5. Harper, M., J.D. Boyce and B. Adler. 2006. Pasteurella multocida pathogenesis: 125 years after Pasteur. FEMS Microbiol Lett. Dec;265(1):1-10. Review.
  6. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Charles Hofacre
Jaime Ruiz
Jose Bruzual

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Marek's Disease

Marek's Disease

Marek's Disease

Etiology

Marek's disease (MD) is a transmissible neoplastic disease, primarily affecting chickens. The disease is caused by a cell-associated herpesvirus, containing double-stranded DNA. There are three serotypes of MDV but oncogenicity is only associated with serotype 1 MDVs. Within this serotype however, there are many strains of MDV, whose pathogenicity varies widely. Subsequently, clinical signs in infected chickens vary from asymptomatic infection to neurologic disease, skin disease, and ocular lesions.

Host Range

Marek's disease is primarily a disease of commercial chickens, but it can also affect turkeys. MD often occurs in 2-5 month-old (sexually immature) chickens but can also occur after the onset of egg production. This form of the disease is referred to as

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  • Avian Encephalomyelitis
  • Erythroblastosis
  • Genetic Grey Eye
  • Histomoniasis
  • Lymphoid leukosis
  • Myeloblastosis
  • Myelocytomatosis
  • Newcastle Disease
  • Ovarian Carcinoma
  • Reticuloendotheliosis
  • Riboflavin Deficiency
  • Tuberculosis

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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