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For many years, fungal infections were classified as either superficial "nuisance diseases," such as athletes foot or vulvovaginal candidiasis, or as relatively rare infections confined primarily to endemic areas of the country.(1) Advances in medical technology, including organ and bone marrow transplantation, cytotoxic chemotherapy, the widespread use of indwelling intravenous catheters, and the increased use of potent, broad spectrum antimicrobial agents have all contributed to the dramatic increase in the incidence of fungal infections worldwide. Fungal infections have emerged as a major cause of death among cancer patients and transplant recipients.(2)
Candida sp. is a unicellular yeast that has an oval shape and produces a pasty or mucoid looking colony on agar media that resembles staphylococci. Candida albicans is a normal commensal of the skin, female genital tract, and the entire GI tract of humans. Therefore, merely its presence in a clinical specimen does not necessarily indicate the presence of invasive disease.
Candidiasis may cause mucotaneous infections including oral, esophageal, and vulvovaginal infections, or it may cause systemic infection including endocarditis, peritonitis, arthritis, and infection of the CNS. Of the more than 150 species of Candida known, approximately eight are considered to be pathogenic in humans. These are C. albicans, C. tropicalis, C. parapsilosis, C. krusei, C. stellatoidea, C. guilliermondi, C. lusitaniae, and C. glabrata.(3)
Up to this point, the term systemic candidiasis has been used to describe infections that invade beyond the membranes of the skin or mucosa. Some clinicians have proposed that the name hematogenous candidiasis be used to describe the clinical occasions where hematogenous seeding to deep organs such as the eye, brain, heart, and kidney occur. Also, specific anatomic reference should be made as to the site of infection, thus an infection of the peritoneum would be Candida peritonitis. This would eliminate the term systemic candidiasis.
The role of intact integument is crucial in the prevention of mucotaneous or hematogenous candidiasis. Once candida invades the dermis or enters the bloodstream, polymorphonuclear leukocytes (PMNs) play a major role in the defense of the patient, since PMNs are capable of damaging pseudohyphae and can phagocytize and kill blastoconidia.(4) In addition to PMNs, neutrophils, lymphocytes, monocytes, macrophages, complement, and eosinophils play a role in the prevention of infection.
Clearly, the immunocompromised patient is at greatest risk of infection.(5, 6) C. albicans adheres to the oral mucosa and GI tract to cause colonization, and the GI tract is often the portal of entry for many forms of disseminated infection. Factors that affect adherence are very important in pathogenesis. Mucotaneous infections are divided into oropharyngeal candidiasis (thrush), esophageal candidiasis, GI candidiasis, and vaginal candidiasis. Also considered in this category, are patients who have a syndrome known as chronic mucotaneous candidiasis. These patients are plagued by chronic or recurrent infections of the skin, nails, and mucous membranes, by C. albicans. Most of these patients exhibit abnormalities in cell-mediated immunity. Generally, infections respond well to conventional antifungal therapy, however, relapses are common when therapy is stopped. Candida is generally acquired via the GI tract, although organisms may enter the bloodstream via indwelling IV catheters or urinary catheters.(7)
- Risk factors for disseminated disease include prior therapy with antibiotics, recent surgery, indwelling IV or urinary catheters, extensive burns, concomitant bacterial infections, and administration of total pare
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