The histopathological examination of livers from Balady chicken subjected to Pasteurella multocida infection showed degenerative changes of the hepatocytes, congestion of blood vessels with hemolytic RBCs in the lumen and focal heterophilc infiltration (Mohamed, 2009). Degenerative changes of the hepatocyte were associated with congestion of blood vessels, focal heterophilic infiltration and coagulative necrosis.
There was also a petechial hemorrhage in cardiac muscle, necrotic parenchymatous hepatitis, together with congestion and hemorrhages in the intestinal mucosa (Mohamed et al., 2012). Shilpa et al. (2006) pointed out that the histopathological signs of FC were hemorrhage, congestion and lymphoid cell infiltration in liver, heart and spleen. Panna et al. (2015) observed lymphocytic infiltration in the central vein in livers of chicken infected with P. multocida.
After inoculation of chicken with P. multocida the pathological examination showed marked septicemic lesions consisting of white necrotic foci and hemorrhages in heart, liver and spleen (Zahoor and Siddique, 2006 and Panna et al., 2015). The same investigators demonstrated a huge lymphocytic infiltration in central vein of liver with inflammatory cells in the pericardium of heart, and lymphocytic infiltration was also noticed in the red areas of spleen in chicken treated with Pasteurella multocida.
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In chicken embryo, Pasteurella multocida infection was induced in embryonated chicken eggs by chorio-allantoic membrane inoculation (Ballal et al., 1998). The bacteria were demonstrated by transmission electron microscopy, either extracellularly or multiplying intracellularly in hepatocytes, heart tissue, and in the hyperplastic layer of the chorio-allantoic membrane. Such infection led to damage in the cellular organelles, and severe tissue changes.
In a study carried out in Nigeria to declare the clinicopathological features occurring in commercial chicken infested with Pasteurella Multocida, Yakubu et al. (2015) recorded gross and histopathological alterations in organs of fowls. The gross lesions represented by petechial and ecchymotic haemmorhages on the heart and breast muscles, congestion of the liver and lungs. The histopathological lesions observed were mononuclear cellular infiltration and pulmonary congestion. The congested liver, spleen, lungs as well as petechial and ecchymotic haemorrhages that were observed at postmortem in the experimentally challenged chickens, also confirmed the findings of Visut et al. (2010).
On histopathological examination, avian pasteurellosis was associated with multifocal areas of coagulative necrosis and haemorrhages (Cynthia, 2005; Anitha and Mammen, 2013). Petechial haemorrhages with pinpoint necrotic spots throughout the parenchyma of severely congested livers of birds were demonstrated due to pasteurellosis caused by Pasteurella mutocida (Shilpa et al., 2015).
Pathology of Pasteurella in chicken lung:
Pasteurella multocida is an important Gram-negative bacillus pathogen involved in respiratory infections due to the development of respiratory diseases in several animal species. Among the mechanisms of virulence, the formation of biofilms is an important factor for bacterial survival in hostile environments (de Emery et al., 2017). Therefore, the authors evaluated the biofilm formation capacity of Pasteurella multocida strains isolated from cases of fowl cholera and swine lungs and its relationship with pathogenicity. Their results concluded that low virulence strains may suggest a higher biofilm formation capacity. A biofilm is a structured community of bacterial cells enclosed in a self-produced polymeric extracellular matrix that is attached to a biotic or abiotic surface (Dolan& Costerton, 2002; Hall-Stoodley& Stoodley, 2009).
In the poultry industry, many investigators attributed the great economic losses to mortalities associated with respiratory diseases (Mensah & Brain, 1982; Ficken et al., 1986; Maina, 2002). These mortalities were attributed to the relatively small numbers of the free (surface) avian respiratory macrophages (Toth &Siegel, 1986; Evans, 1996; Klika et al., 1996; Spira, 1996). Toth et al. (1988) pointed out that the paucity of the free macrophages in the avian respiratory system suggests a deficiency in the defense system of the respiratory tract of poultry against bacteria, mycoplasma, fungi, and viruses. Furthermore, the polymorphonuclear leucocytes of birds are reported to have certain enzymatic deficiencies in their oxidative metabolism (Penniall & Spitznagel, 1975; Bellavite et al., 1977; Toth et al., 1987).
In the normal steady-state respiratory tract of poultry there is a very limited number of resident macrophages (Toth et al., 1988). Therefore, poultry must rely heavily on active migration of phagocytic cells to the lungs and air sacs in defending against respiratory pathogens.
Pulmonary macrophages are considered to be primarily responsible for clearance of organisms from bronchioles and alveoli (Ross 2006). Therefore, it assumed that an alteration in the ability of pulmonary macrophages to phagocytose or kill bacteria is part of the pathogenesis (Muller and Kohler 1997; Purdy et al. 2003).
Klika et al. (1996) found that no free macrophages can be observed (at either the light or electron microscopic level) in the most peripheral parts of the lung, i.e. the atria, infundibula and air capillaries. Results of Lorz and Lopez (1997) confirmed that the avian respiratory macrophages are always located in the subepithelial connective tissue and they have never been observed on the luminal face of atrial or parabronchial epithelia. Other investigators demonstrated free avian respiratory macrophages on the surface of the luminal cells (Fletcher, 1980; Richard & Thurston, 1983). Others have been successfully examined, harvested and counted from the respiratory surfaces of birds (Ficken et al., 1986; Toth & Siegel, 1986; Toth et al., 1987; Maina & Cowley, 1998). Moreover, Klika et al. (1996) documented that the interstitial macrophage cells situated beneath the epithelium at the atrial and infundibular levels do not migrate from the subepithelial tissue compartment to the airway surfaces. The high susceptibility of birds to respiratory diseases and pathological afflictions is based largely on the scarcity of the free avian respiratory macrophages (Ficken et al. 1986; Toth & Siegel, 1986; Klika et al., 1996). They clear the air capillaries and the blood–gas barrier of the lung of any obstruction to gas exchange by passive diffusion (Nganpiep and Maina, 2002).
The little number of the free avian respiratory macrophages reflects the presence of a weak front-line defence on the surface of the avian respiratory system. These low numbers of macrophages may exhibit exceptionally efficient phagocytotic activity to protect the lung adequately. Moreover, Toth et al. (1988) observed signifcant increases in the free avian respiratory macrophages of the polymorphonuclear leucocyte type by three orders of magnitude within 24 h after intratracheal administration of a live, apathogenic Pasteurella multocida vaccine to chickens. These investigators found that intratracheal inoculation of live, apathogenic Pasteurella multocida evoked a dramatic increase in the free avian respiratory macrophages.
Reese et al. (2006) pointed out that the lung is a major target organ for numerous viral and bacterial diseases of poultry. These authors considered that the most prominent in the avian lung is the bronchus-associated lymphoid tissue which is located at the junctions between the primary bronchus and the caudal secondary bronchi.
Several important poultry pathogens enter the host through the lung surface and subsequently disseminate to their target organs in the body (Glisson, 1998). Therefore, animal health significantly depends on the successful control of pathogen invasion and pathogen replication at the bronchus-associated mucosal surface and in the lung tissue. The histopathological findings recorded by Yakubu et al. (2015) indicated a moderate to severe lymphocytic, heterophilic and macrophagic cellular infiltration in lungs of chickens infected with P. multocida. Anitha and Mammen in 2013 observed congestion of lungs in pasteurellosis together with haemorrhages and pneumonic changes. Likewise, lungs of domestic and wild birds suffering pasteurellosis in Turkey were congested exhibiting oedema and pneumonia (Shilpa et al., 2015).
