Caseous material is found in the tracheas of poultry in cases of viral infection.

Why can’t we get rid of these cheeses?

Dr. Milad Ibrahim Oraibi

31/8/2026

 

Initially, when the virus enters the poultry house and is inhaled through the nose, it attacks ciliated epithelial cells, leading to their death and damage. This results in the infiltration of many heterophile cells into the trachea due to severe inflammation. These cells lack the enzyme myeloperoxidase, which breaks down proteins as neutrophils do in mammals. Consequently, the dead cells do not decompose into mucus but rather clump together into a thick, coagulated tissue. Fibrin, along with other inflammatory fluids rich in fibrinogens from damaged blood vessels, transforms into a network of fibrin fibers composed of dead cells, heterophiles, and any secondary viruses and bacteria present in the tracheal lumen. This material then gradually dries and hardens within the trachea due to the inhaled and exhaled air. Then it turns into a yellow substance with a gelatinous consistency, and then into a strong, curd-like substance that resembles cheese in appearance.

The important thing in the process is that the heterophile cells in poultry lack strong enzymes for breakdown such as (MPO and Elastase). These enzymes lead to the breakdown of dead cells and their breakdown with damaged tissues into a final product called (liquid pus), as in mammals. The absence of this mechanism will lead to the retention of dead cells with heterophile cells, which, if they turn into a liquid form, will adhere strongly to each other, which will be the caseous mass (liquefactive necrosis failure).

There is an important point: when the virus enters the epithelial cells and the endothelial cells, a strong immune response will occur, and pro-inflammatory cytokines will be secreted, namely IL, IB, IL6, and TNF-a. Because of this process, vascular permeability will increase, and this in turn will allow large quantities of proteins and high molecular weight plasma to pass through, the most important of which is fibrinogen.

When fibrinogen comes into contact with factors such as tissue factor released from dead and damaged epithelial cells, coagulation, clotting, or hardening will occur, and fibrin will be converted into insoluble fibrin meshwork, which will trap the damaged and destroyed cells inside.

Then this network turns into (coagulation and caseous necrosis) where there is a lack of blood supply to the damaged and destroyed area caused by the blockage of microscopic capillaries by (microthrombosis) and eventually (coagulative necrosis) will occur.

After the rapid passage of air through inhalation and exhalation, and due to accelerated breathing (hyperventilating) resulting from a lack of oxygen in the body, drying of the formed materials will occur and form (fibrinonecrotic mass), then it gradually turns from a soft mucous consistency to a solid, cohesive consistency resembling cheese called (caseous plug) and takes the shape of a tracheal cast.
The cause of chicken death is:
1- Mechanics due to respiratory tract obstruction
2- Lack of oxygen and the heart’s inability to work
3- Blood poisoning caused by gas retention and bacterial contamination

 

 

 

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