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Infection is the major cause of morbidity and mortality in burn patients who are hospitalized. There is an estimation that 75% of the mortality associated with burn injuries is related to sepsis in developing countries. Burn injury leads to a state of immune system dysfunction that predisposes patients to infection which is aided by the loss of the natural skin barrier. There is interplay of pro and anti-inflammatory signals that result in dysregulation off the innate and adaptive immune responses. After a burn injury there is a massive release of humoral factors, including cytokines, prostaglandins, vasoactive prostanoids and leukotrienes. The neutrophils have a decreased chemotaxis and bactericidal activity. There is less phagocytic activity and lymphokine production by macrophages. Natural killer cells activity are diminished. It is due to presence of high amount of dead cells. As foreign bodies and dead cell are abundant in burnt areas the macrophages reach there and pus will develop as an end result. The reason for this is due to secondary immunodeficiency. With the decrease in immune system, burns provide a suitable site for bacterial multiplication and are rich sources of infection because the dead cells provide nutrients to extremophiles.

Bacteriological Profile of Burn Patients and Antimicrobial Susceptibility Pattern of their Wound Isolates at Nepal Cleft and Burn Center