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Pathology of the Immune System in the Diagnosis of Immunosuppression in Poultry

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Diagnosis

Conteúdo disponível em: English

Modern poultry lines are characterised by high performance and specialisation. Advances in genetics, feeding, management, diagnosis, environment and breeding have significantly improved production parameters.

While today’s birds are more efficient and productive, they are also less hardy than in the past, making them more susceptible to disease.

Due to the multifactorial aetiology for immunosuppression, diagnosis is not always straightforward, requiring a clinical history, necropsies and complementary laboratory tests if necessary.

In the following, the most relevant aspects of immunosuppression-oriented pathology of the immune system are discussed.

The avian immune system consists of primary and secondary lymphoid organs.

The interpretation of lesions in lymphoid organs requires taking into account the age of the birds and vaccination schedule, as primary lymphoid organs atrophy when birds reach sexual maturity and most routine vaccines cause changes in the lymphoid organs.

Bursa of Fabricius

It is present only in birds, located in the dorsal part of the cloaca, connected to the intestine by a duct.

Inside the bursa of Fabricius there are major and minor folia, these folia are lined by a columnar epithelium and contain the lymphoid follicles supported by a matrix of connective tissue.

Figure 1. Bursa of Fabricius in 4-week-old birds (Photo: Courtesy of María Teresa Casaubon Hugenin).

The bursa of Fabricius, in the absence of infectious agents or immunosuppressants, should be present until 12 to 14 weeks of age, at which time it begins to involute, so that by 20 weeks only traces remain.

In 1-day-old chicks, clusters of heterophils are frequently found in the subepithelial tissue; these are foci of extramedullary granulopoiesis and are common in various tissues of the chick.

THYMUS

The thymus in birds is located along the neck and is composed of 6 to 7 lobes running parallel to the jugular veins and the vagus nerve.

In the absence of infectious or immunosuppressive agents, the thymus should remain until 15 to 17 weeks, after which time it begins to involute so that by 30 weeks only vestiges remain.

BONE MARROW

Only non-pneumatic bones such as the femur and tibiotarsus have bone marrow, it is considered a primary and secondary lymphoid organ as bone marrow is the source of:

SPLEEN

The spleen is attached to the gizzard and proventriculus by its visceral side. It is a secondary lymphoid organ, made up of a capsule of connective tissue and trabeculae on which it is supported:

The spleen in young chicks is a centre of granulopoiesis and in older birds a centre of antigen presentation.

LYMPHOID ORGAN ATROPHY

In addition to the age-related involution of birds, there are many factors that cause lymphoid atrophy.

Birds are subjected during the production process to stress factors such as:

Which trigger the secretion of glucocorticoids which cause apoptosis in lymphoid cells.

APOPTOSIS PROCESS

The process of apoptosis is normal in birds during negative selection processes of clones that are not useful. A histological slice of lymphoid organs shows apoptosis, which is described in texts as ‘starry sky’.

On the other hand, mycotoxins are considered to be immunosuppressive agents that cause atrophy of lymphoid organs, the mechanism of atrophy following two pathways:

If decreased lymphoid organ size is observed, mycotoxins should be considered in the differential diagnosis.

In the case of the thymus, atrophy due to abundant apoptosis occurs in cases of infection with infectious anaemia virus. This vertically transmitted virus targets T lymphocytes and bone marrow germ cells.

Birds under 5 weeks of age show severe atrophy of the thymus cortex, decreasing considerably the size of the thymus, sometimes at necropsy the thymus may go unnoticed.

Figure 2. Severe thymus atrophy in 8-week-old bird (Arrow).

NECROSIS AND INFLAMMATION

In addition to apoptosis, necrosis also leads to atrophy of lymphoid organs, but in this case the inflammatory process may transiently increase the size of the organ.

These changes are not exclusive to IBF, as other agents such as Marek’s disease virus (MDV), Reovirus and Newcastle disease virus (NDV) can also cause necrosis and inflammation.

A particular case is IBF virus infection by variant strains, as they do not cause necrosis and inflammation and the bursa of Fabricius only atrophies, these viruses cause lymphoid cell death by apoptosis.

Regeneration depends on the absence of secondary infections, if there is a bacterial complication or cryptosporidium infestation the bursa of Fabricius has a fibrinous to fibrinocaseous exudate that may fill the bursa.

LYMPHOPROLIFERATIVE DISEASES

In birds, Marek’s disease (MD) and Lymphoid Leukosis (LL) viruses cause lymphoid cell neoplasms (lymphomas) occurring in various organs.

Figure 3. Marek’s disease lymphoma in the heart and lung of a 12-week-old bird.

Marek’s disease

Marek’s disease has 5 presentations depending on the site of T-cell infiltration. With the exception of the cutaneous presentation, all other presentations are nonproductive transforming, that is, complete virions are not produced and the infected cell becomes neoplastic.

Clinical manifestations depend on the organ infiltrated, thus birds present:

The above depends on the organ infiltrate in the visceral presentation. In this case the organs present firm, white nodules in most cases. Muscular presentation is the rarest.

Lymphoid Leukosis

Within the differential diagnosis with LL, it should be considered that LL is only visceral, so it is important:

Lymphoid leukosis presents intrafollicular infiltration (within the lymphoid follicles) in the bursa of Fabricius and the tumour is frequent. While in cases of MD the infiltration is interfollicular (outside the follicle, occupying the connective tissue between the epithelium and follicles) and on the other hand the presence of nodules is less frequent.

In recent years, molecular tests have provided valuable data in the diagnosis and epidemiology of immunosuppressive viral diseases, however, it should not be lost sight of the fact that a positive PCR test result does not always have diagnostic value.

For example: in the case of common infectious anaemia virus in six to seven week old broilers or 10 week old replacement pullets. At this age, virus infection does not cause immunosuppression, so the presence of virus genetic material in the sample alone is not necessarily the origin of the observed picture and other possibilities must be ruled out.

FINAL CONSIDERATIONS

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