Epidemiological Trends and Clinicomycological Profile of Chronic Dermatophytosis: A Descriptive Study From South India.

BACKGROUND: Chronic dermatophytosis refers to persistent or recurrent episodes of dermatophytosis lasting for more than 1 year despite adequate treatment with topical and systemic antifungal agents. The rise in the number of these cases is alarming over the past 5 to 6 years, and a thorough knowledge about the reasons for chronicity of dermatophytosis may go a long way in the treatment and prevention of this infection. AIMS AND OBJECTIVES: The aim of this study was to investigate the epidemiology, various clinical types, and factors associated with chronicity in patients with chronic dermatophytosis, and to isolate the etiological agents and study the clinicomycological correlation. MATERIALS AND METHODS: Detailed history and clinical details of all patients with chronic dermatophytosis who presented to our tertiary care center over a span of 1 year were recorded. Skin scrapings from these patients were subjected to potassium hydroxide mount and culture in modified Sabouraud's dextrose agar medium. RESULTS: Sixty-four patients were enrolled in this study with a mean age of 44.5 years. The mean duration of infection was 3.14 years. Tinea corporis was the most common clinical type seen in 46 (71.9%) patients, affecting commonly the waist area in females and the back in males. Bronchial asthma was the most frequent systemic association affecting 20 (31.3%) patients followed by diabetes mellitus, which was present in 13 (20.3%) patients. About 34% patients had a history of long-term steroid use. Among the 28 isolates, Trichophyton mentagrophytes was the most frequent species isolated (46.4%), followed by Trichophyton rubrum (39.3%). Trichophyton tonsurans and Trichophyton verrucosum were isolated from two patients each. CONCLUSION: Extensive area of involvement, atopy, diabetes, and long-term use of systemic corticosteroids were associated with chronicity. Unlike in the yesteryears, T. mentagrophytes has emerged as the most common etiological agent of chronic dermatophytosis.

Elusive Toxin in Cleistanthus collinus Causing Vasoconstriction and Myocardial Depression: Detailed NMR Analyses and Biological Studies of Cleistanthoside A.

Cleistanthus collinus leaf extracts are consumed for suicidal purposes in southern India. The boiled decoction is known to be more toxic than the fresh leaf juice. Although several compounds have been isolated and their toxicity tested, controversy remains as to which compounds are responsible for the high level of toxicity of C. collinus. We report herein that cleistanthoside A is the major toxin in the boiled aqueous extract of fresh leaves and causes death in rats in small doses. The toxicity of the boiled extract prepared in the manner described can be attributed entirely to cleistanthoside A. Cleistanthin A could also be isolated from the boiled extract, albeit in trace amounts. As hypotension not responding to vasoconstrictors is the cause of death in patients who have consumed the boiled extract, effects of cleistanthoside A on the determinants of blood pressure, namely, force of cardiac contraction and vascular resistance, were tested in isolated organ experiments. Cleistanthoside A has a direct vasoconstrictor effect; however, it inhibits ventricular contractility. Therefore, the notion that the shock in C. collinus poisoning is of vascular origin must be considered carefully, and the possibility of cardiogenic shock must be studied. We present the crystal structure of cleistanthin A and show the potency of fast NMR methods (NOAH4-BSCN-NUS) in the full spectral assignment of cleistanthoside A as a real-world sample of a natural product. We also compare the results of the NOAH4-BSCN-NUS NMR experiments with conventional NMR methods.

Correction: Phenylephrine induces relaxation of longitudinal strips from small arteries of goat legs.

[This corrects the article DOI: 10.1371/journal.pone.0227316.].

Phenylephrine induces relaxation of longitudinal strips from small arteries of goat legs.

Alpha adrenergic stimulation is known to produce vasoconstriction. We have earlier shown that, in spiral strips of small arteries Phenylephrine (PE) caused vasorelaxation under high nitric oxide (NO) environment. However, on further experimentation it was realized that the PE-induced vasorelaxant response occurred only with longitudinal strips of small arteries even under normal NO environment while circular strips showed contraction with PE even under high NO environment. Such PE-induced vasorelaxation of longitudinal strips was blocked by Phentolamine, an alpha-adrenergic receptor blocker. On delineation of specific receptor subtype, PE-induced relaxation was found to be mediated through alpha 1D receptor. However, this phenomenon is specific to small artery, as longitudinal smooth muscle of aorta showed only contractile response to adrenergic stimulation. There is no prior report of longitudinal smooth muscle in small artery up to our knowledge. The results of this study and histological examination of vessel sections suggest the presence of longitudinal smooth muscle in small artery and their relaxant response to alpha adrenergic stimulation is a novel phenomenon.

Phenylephrine Decreases Vascular Tension in Goat Arteries in Specific Circumstances.

Phenylephrine (PE) causes vasoconstriction through alpha adrenergic receptors. PE-induced vasodilatation has also been reported earlier in pre-constricted vessels. Here we demonstrate in spiral strips of goat arteries that addition of PE can decrease tone even from base-line levels (i.e. not pre-constricted) and show that this process requires nitric oxide (NO) and alpha adrenergic stimulation, but is cGMP-independent. Under control conditions, PE caused vasoconstriction, but under conditions where NO levels are higher, as with L-Arginine or sodium nitroprusside, PE decreased vessel tension. L-Arginine/PE combination was not able to decrease tension when alpha adrenoceptors were blocked with Phentolamine or endothelial nitric oxide synthase (eNOS) was blocked with Nω-Nitro-L-arginine (L-NNA). Propranolol, a beta blocker, was unable to prevent the reduction in tension by the L-Arginine/PE combination. Adrenaline and noradrenaline (and not isoproterenol) also reduced vessel tension in the presence of L-Arginine. Even when NO levels were not enhanced, relieving NO from having to stimulate the enzyme soluble guanylyl cyclase (sGC) (either by using sGC blockers, namely ODQ or methylene blue, or by enhancing cGMP levels (with sildenafil) which by negative feedback probably inhibits sGC) led to PE-induced reduction of vascular tension. PMA-phorbol myristate acetate-an agonist which stimulates Protein Kinase C was able to prevent the ability of PE to reduce vascular tension in a high NO environment. Our conclusion is that PE reduces vascular tension through alpha adrenoceptors if there is excess NO availability to activate a putative pathway. Though the reduction of vessel tone by PE is dependent on NO, it is independent of cGMP. Prior treatment with PMA or PE itself can prevent further PE-induced reduction of tension in a high NO environment. The results here suggest, counter-intuitively, that alpha blockers may be of help in the treatment of septic shock where nitric oxide levels are high.