Effects of Amphetamine on Development of Oral Candidiasis in Rats

Abstract

Experiments were conducted to evaluate the effects of amphetamine (0.4 mg/kg of body weight/day) on the development of oral candidiasis in Sprague-Dawley rats. Animals were submitted to surgical hyposalivation in order to facilitate the establishment and persistence of Candida albicans infection. Treatment with drugs (placebo or amphetamine) was initiated 7 days before C. albicans inoculation and lasted until the end of the experiments, day 15 postinoculation. Establishment of C. albicansinfection was evaluated by swabbing the inoculated oral cavity with a sterile cotton applicator on days 2 and 15 after inoculation, followed by plating on YEPD (yeast extract-peptone-dextrose) agar. Tissue injury was determined by the quantification of the number and type (normal or abnormal) of papillae on the dorsal tongue per microscopic field. A semiquantitative scale was devised to assess the degree of colonization of the epithelium by fungal hyphae. Our results show that amphetamine exacerbates C. albicans infection of the tongues of rats. Significant increases in Candida counts, the percentage of the tongue’s surface covered with clinical lesions, the percentage of abnormal papillae, and the colonization of the epithelium by fungal hyphae were found in amphetamine-treated rats compared to those found in the rats injected with a placebo. The last two parameters increased in rats treated with the placebo compared to the parameters of the untreated control rats.

Methylenedioxymethamphetamine (‘Ecstasy’)‐induced immunosuppression: a cause for concern?

“…Over the last two decades, investigators have documented the ability of a number of drugs of abuse such as cocaine, opioids, cannabinoids and amphetamines to impair many aspects of immune function, either directly or via neuroimmune pathways (Nunez‐Iglesias et al ., 1996; Klein et al ., 1998; Mellon and Bayer, 1998b; Pellegrino and Bayer, 1998a; Yu et al ., 2002; Friedman et al ., 2003; In et al ., 2005). Moreover, numerous pre‐clinical reports indicate that a range of drugs of abuse result in diminished host resistance to infections (Nunez et al ., 1993; Baldwin et al ., 1998; Cabral and Dove Pettit, 1998; Donahoe and Vlahov, 1998; Freire‐Garabal et al ., 1998; 1999; Gavrilin et al ., 2002; Cabral and Marciano‐Cabral, 2004). Indeed, some investigators have implicated drug abuse as a co‐factor in susceptibility to infection with HIV or other viruses (Nunez et al ., 1993; Baldwin et al ., 1998; Donahoe and Vlahov, 1998; Gavrilin et al ., 2002).…”

Antifungal activity of human salivary mucin‐derived peptide, MUC7 12‐mer, in a murine model of oral candidiasis

“…Oral candidiasis, as a result of infection by the opportunistic fungus, Candida albicans , is a major cause of oral and esophageal infection in immunocompromised individuals (1,2), including up to 90% of AIDS affected patients (3). Despite excellent pharmacokinetic characteristics and low toxicity of known efficacious antifungal agents like fluconazole, treatment failures are still encountered because of the emergence of antifungal‐resistant C. albicans (3–5).…”

Biological assessment of ozone therapy on experimental oral candidiasis in immunosuppressed rats

“…This procedure was repeated for 3 consecutive days. Establishment of C. albicans infection was evaluated by swabbing the inoculated oral cavity with sterile cotton applicator 6 days after inoculation, followed by plating on yeast extract- peptone- dextrose agar [4] .…”

“…The epidemiological surveys indicate that Candida organisms are considered as commensals in the oral cavities of approximately 40% of healthy subjects [1] and that Candida albicans specifically is carried as a commensal organism in the mouths of approximately one-third of the population [2] . The opportunistic fungus C. albicans is a major cause of oral and esophageal infections in immunocompromised patients [3] , [4] and affects up to 90% of patients with human immunodeficiency virus infection or AIDS [5] . This opportunistic human pathogen preferentially causes invasive and disseminated infections in patients with defective phagocytic defenses and serious mucocutaneous infection in patients with deficiencies in T-cell function.…”