Factors involving the host

1. General health of host. For example, starvation, hemorrhagic shock, chronic debilitating diseases like diabetes mellitus, alcoholism, etc. render the host more susceptible to infections.

2. Immune state of host. Immunodeficiency helps in spread of infections rapidly, e.g. in AIDS.

3. Leukopenia. Patients with low WBC count with neutropenia or agranulocytosis develop spreading infection.

4. Site or type of tissue involved. For example, the lung has loose texture as compared to bone and thus both tissues react differently to acute inflammation.

5. Local host factors. For instance, ischemia, presence of foreign bodies and chemicals cause necrosis and are thus harmful.

Type of exudation. The appearance of escaped plasma determines the morphological type of inflammation. These are:

1. Serous, when the fluid exudate resembles serum or is watery, e.g. pleural effusion in tuberculosis, blister formation in burns.

2. Fibrinous, when the fibrin content of the fluid exudate is high, e.g. in pneumococcal and rheumatic

pericarditis. Two types may be croupous and diphtheroid fibrinous inflammation.

3. Purulent or suppurative exudate is formation of creamy pus as seen in infection with pyogenic bacteria, e.g. abscess, acute appendicitis, phlegmon.

4. Hemorrhagic, when there is vascular damage, e.g. acute hemorrhagic pneumonia in influenza.

5. Catarrhal, when the surface inflammation of epithelium produces increased secretion of mucus, e.g. common cold.

Cellular proliferation. Variable cellular proliferation is seen in different types of inflammations.

1. There is no significant cellular proliferation in acute bacterial infections except in typhoid fever in which there is intestinal lymphoid hyperplasia.

2. Viral infections have the ability to stimulate cellular proliferation, e.g. epidermal cell proliferation in herpes simplex, chickenpox and smallpox.

3. In glomerulonephritis, there is proliferation of glomerular capsular epithelial cells resulting in formation of «crescents».

4. In chronic inflammation, cellular proliferation of macrophages, fibroblasts and endothelial cells occurs.

Necrosis. The extent and type of necrosis in inflammation is variable. In gas gangrene, there is extensive necrosis with discolored and foul smelling tissues. In acute appendicitis, there is necrosis as a result of vascular obstruction. In chronic inflammation such as tuberculosis, there is characteristic caseous necrosis.