infectious bursal disease in poultry

Introduction

Infectious bursal disease, also known as Gumboro disease, has caused great economic losses in the poultry industry in different parts of the world due to mortality and immunosuppression. It is a contagious acute viral disease of young birds. The disease may be clinical with variable mortality, and subclinical without mortality. The clinical form of the disease occurs in birds from the third week of age and subclinical disease occurs when birds are less than 3 weeks old. The incubation period of the disease is very short and clinical signs are observed between 2 to 3 days after exposure. Immunosuppression is the main consequence of the infectious bursal disease (Santos et al., 2009). Injuries to the birds' immune system are more severe and difficult to reverse if they become infected before the third week, developing immunosuppression symptoms. In this case, the birds show increased susceptibility to infectious agents, so they may develop more diseases, in addition to not adequately responding to vaccines. If infection occurs after the third week of age, the birds tend to develop immunosuppression clinical signs that may not be as severe, with a tendency to recovery. This paper describes an outbreak of Gumboro in hens with eight weeks of age, four days after vaccination with the low-passage bursal disease virus.

Materials & Methods

The materials for this work were obtained from a batch of 10,000 commercial layer pullets of 8 weeks of age, with a history of increased mortality, decreased feed intake by 50%, diarrhea, tremors, apathy and prostration. Clinical signs began to be observed 4 days after vaccination against infectious bursal disease with low-passage attenuated virus.

Five birds with the above-mentioned clinical signs were sent to the Avian Health Study Unit of the Department of Veterinary Medicine, Federal University of Viçosa, which were sacrificed by cervical dislocation, followed by a gross examination; bursa samples were then taken for histological tests. For that purpose, samples were fixed in a neutral 10% formalin saline solution, buffered to pH 7.2 by following the routine histological techniques for paraffin embedding. The histological sections obtained were stained with hematoxylin eosin (HE) according to Luna (1968) and examined by light microscopy.

Results & Discussion

The birds showed clinical signs of depression, anorexia, tremors, watery diarrhea, dehydration, prostration (Figure 1) and ultimately death. The necropsy found hemorrhages in the subcutaneous tissue, and especially in the muscles of the leg and thigh regions (Figure 2). The hemorrhagic lesions were in the glandular portion of the proventriculus. The spleen was found enlarged and intestines showed a thick mucosa and excess mucus. The bursa, that is the target organ of the virus, was found enlarged and had a jelly-like material on the serosal surface (Figure 3). The kidneys were congested, enlarged and with urates. The clinical signs and lesions mentioned were compatible with Gumboro in the clinical or acute form, characterized by symptoms of septicemia, which may be caused by toxic substances released by macrophages during infection by the infectious bursal disease virus (Van Der Berg, 2000).

Microscopically, the bursal lesions were characterized by edema, hemorrhage, necrosis of follicular cells and presence of large numbers of polymorphonuclear type inflammatory cells (Figure 4). These bursal lesions could be the result of the formation of immune complexes (Skeeles et al., 1979), because they resemble an Arthus reaction. This reaction is a type of immune injury induced by antigen-antibody complexes and complement (Tizard, 1998). These immune complexes stimulate tissue macrophages to secrete tumor necrosis factor, interleukins, platelet-activating factor, nitric oxide and free radicals. Immune complexes cause vascular lesions (Tizard, 1998), which justifies the presence of hemorrhage found in clinical disease. In addition, tissues damaged during the virus replication release vasoactive molecules that increase vascular permeability, including venules and capillaries resulting in local edema (Van Der Berg, 2000). It should be noted that viral infection stimulates macrophages to release interferon and other cytokines, which alter the response measured by cells of increasing the number of suppressor cells and reducing competition from helper T cells, which may be the cause of bird death (Tizard, 1998). We emphasize that the vaccine virus retains the original features of the field virus, being capable of causing infectious bursal disease by easily reversing to its pathogenicity (Santos et al., 2009). In addition, the susceptibility of the lineage of birds affected by the infection (Enterradossi & Saif, 2008) may have contributed to the exacerbation of the aggressiveness of the viral agent.

Figure 1. Birds with clinical signs of prostration, depression and dehydration

Occurrence of infectious bursal disease after vaccination with a low-passage attenuated virus - Image 1

Figure 2. Muscles of the leg and thigh with hemorrhages

Occurrence of infectious bursal disease after vaccination with a low-passage attenuated virus - Image 2

Figure 3. Enlarged bursa and jelly-like material on the serosal surface Enlarged congested kidneys and presence of urates

Occurrence of infectious bursal disease after vaccination with a low-passage attenuated virus - Image 3

Figure 4. Histological section of the bursa with necrosis of follicular cells, empty spaces, cellular debris, lymphocyte pyknosis, edema, congestion, hemorrhage and infiltration of heterophils in the interfollicular septa. Hematoxylin-eosin staining and 200x image

Occurrence of infectious bursal disease after vaccination with a low-passage attenuated virus - Image 4

Conclusions

The clinical or acute infectious bursal disease, as evidenced by this study, is characterized by septicemia. Macroscopic and microscopic aspects observed may be due to toxic products released by macrophages, which is related to an Arthus reaction.

References

Luna LG. 1968. Manual of histoloc staining methods of the Armed Forces Institute of Pathology. MacGraw-Hill. New York.

Enterradossi N & Saif YM. 2008. Infectious bursal disease. pp. 185-208. In Diseases of poultry, Saif YM, Fadly AM, Glisson JR, McDougald LR., Nolan LK, Swayne DE. ed. Ames: Blackwell publishing. Iowa USA.

Santos BM, Moreira MAS, Dias CCA. 2009. Manual de doenças avícolas. Editora UFV. Viçosa.

Skeeles JK, Lukert EV, De Buysescher OJ. 1979. Infectious bursal disease vírus infections. I.Complement and vírus-neutralizing antibody response following infection of susceptible-chickens. Avian Dis. 23:95-106.

Tizard IR. 1998. Imunologia veterinária. Ed. Roca. São Paulo Brasil.

Van Der Berg TP. 2000. An acute infetious bursal disease in poultry: a review. Avian. Pathol. 29:175-194.