Candida Albican

Introduction

Despite major advances in burn care and management, infections remain a leading cause of mortality, morbidity, and cost in burn patients . While the broad acceptance of topical antibiotics, early excision and grafting, and patient isolation practices have resulted in a significant decline in bacterial wound infections, the incidence of fungal wound infections remains unchanged. Since the most severely burned patients suffer from major suppression of the host immune system, patients with large areas of third degree burns are at the highest risk for fungal infections that are difficult to prevent or eradicate . The problem of fungal infections has become even more urgent today due to the increasing emergence of antifungal resistant pathogen. Candida albicansis the most common fungal pathogen responsible for fungal infection in burn patients and is now the fourth most common organism found in blood cultures in intensive care unit patients .

Although it has been known for the last 100 years that ultraviolet (UV) light (particularly UVC with a wavelength range of 240-280 nm) is highly germicidal , its use to treat wound or other localized infections remains at an early stage of development. There is a widely held perception that UV fight is so damaging to skin and other normal human tissue that any positive benefits of killing microorganisms with UV would be outweighed by known dangers of UV in causing carcinogenesis and other UV photodamage. However, most of the studies on the damaging effects of UV on skin have been carried out with UVB light (290-340 nm) and UVA (340-400 nm) because these wavelength ranges are contained in sunlight and humans have been exposed to UVB and UVA throughout human history . By contrast there is no natural source of UVC and there has therefore been little impetus to study it . It should be noted that mammalian cells have efficient DNA repair systems and since the use of UVC for infections is likely to involve a single treatment or a limited number of treatments, it is possible that any UVC-induced damage to host tissue may be readily repaired. Most carcinogenesis studies of UV have used a large number of chronic exposures over weeks and months and moreover, the extremely limited penetration of UVC through the stratum corneum provides another layer of protection.

Discussion

The mechanism of UVC inactivation of organisms is to damage the genetic material in the cell . The UVC-induced damage to the DNA and RNA of an organism often results from the dimerization of adjacent pyrimidine molecules in DNA chains. In particular, thymine (which is found only in DNA) produces cyclobutane dimers. When these molecules are dimerized, it becomes very difficult for the nucleic acids to replicate and if replication does occur it often produces a defect that prevents the organism from being viable. There have been two clinical reports from one group to demonstrate UVC treatment of wound infections . It was shown that UVC irradiation had the ability to reduce bacterial burden and improve wound status in patients with chronic ...