Guest guest Posted March 4, 2008 Report Share Posted March 4, 2008 Fungal Infections (See also Ch. 158.) Etiology Fungal infections of the urinary tract primarily affect the bladder and kidneys. Candida sp, the most common cause, are normal commensals of humans and are frequently recovered from the oral cavity, GI tract, vagina, and damaged skin. However, all invasive fungi (eg, Cryptococcus neoformans, Aspergillus sp, Mucoraceae sp, histoplasmosis, blastomycosis, coccidioidomycosis) may infect the kidneys as part of systemic or disseminated mycotic infection. Lower UTI with Candida is mainly due to local urinary catheters. In general, most Foley catheter-related fungal infection follows bacteriuria and antibiotic therapy, although Candida and bacterial infections frequently occur simultaneously. Renal candidiasis is usually spread hematogenously and commonly originates from the GI tract. Ascending infection from nephrostomy tubes, other permanent indwelling devices, and stents also occurs. At high risk are patients who are immunocompromised because of neoplasm, AIDS, chemotherapy, or immunosuppressive drugs. A major nosocomial source of candidemia in such patients is an indwelling intravascular catheter. Renal transplantation increases the risk because of the combination of indwelling catheters, stents, antibiotics, anastomotic leaks, obstruction, and immunosuppressive therapy. Symptoms and Signs Most patients with candiduria are asymptomatic but have easily identifiable predisposing factors. Whether Candida can cause symptomatic urethritis (mild urethral itching, dysuria, watery discharge) is controversial. A fungal cause for these symptoms in men should be considered only when all other causes of nongonococcal urethritis have been excluded. Candidal urethritis is rare in women, and symptoms of dysuria usually result from the urine coming into contact with inflamed periurethral tissue. C. albicans prostatitis is infrequent in diabetic patients, usually following instrumentation. Cystitis due to Candida may result in frequency, urgency, dysuria, and suprapubic pain. Hematuria is common, and, in poorly controlled diabetic patients, pneumaturia and emphysematous cystitis have been described. One or more fungus balls or bezoars may be found in the bladder lumen from local or upper tract formation and occasionally cause urethral obstruction. Most patients with hematogenous renal candidiasis lack symptoms referable to the kidney except for antibiotic-resistant fever, candiduria, and unexplained deteriorating renal function. Ascending infection commonly produces fungus ball elements in the ureter and renal pelvis. These masses frequently are associated with hematuria and cause urinary obstruction. Occasionally, papillary necrosis occurs, and intrarenal and perinephric abscesses may form. Clinical manifestations of dissemination to other sites (CNS, skin, eye, liver, spleen) may be present. Diagnosis Unexplained candiduria should prompt evaluation for urinary tract structural abnormalities. Patients with verified candiduria can present clinically with asymptomatic candiduria, urethritis and prostatitis, cystitis (with or without bezoar formation or gas formation), primary renal candidiasis, and hematogenously disseminated candidiasis. Unlike in bacterial UTI, the level at which candiduria reflects true Candida UTI and not merely colonization of a catheter or contamination of a urine specimen is unknown. Cystitis is usually diagnosed in high-risk patients in the presence of bladder inflammation or irritation and candiduria. Passage of fungus-derived material is sometimes observed. Cystoscopy and ultrasonography of the kidney and bladder may help detect bezoar formation and obstruction. The presence of fever and candiduria and occasionally the presence of papillary necrosis and passage of fungal balls suggest the diagnosis of ascending renal candidiasis. Although renal function frequently declines, severe renal failure rarely occurs in the absence of postrenal obstruction. Imaging of the urinary tract may help evaluate the degree of involvement. Blood cultures for Candida are frequently negative. Treatment Candiduria may respond to flucytosine 50 to 150 mg/kg/day po q 6 hr for 1 to 2 wk but often is resistant. Of the newer antifungal azole derivatives, fluconazole appears best for fungal UTI because of high oral bioavailability, once-per-day dosing, and excellent penetration into urine and CSF. Flucytosine or fluconazole 200 mg/day po should be prescribed for asymptomatic candiduria. Symptomatic cystitis in the noncatheterized patient can be treated with flucytosine or fluconazole for 1 to 4 wk. Excellent results have also been obtained with a single dose of amphotericin B 0.3 mg/kg IV. In the presence of permanent indwelling catheters, flucytosine and fluconazole may reduce but rarely eradicate the funguria; bladder irrigation may be successful. In patients with renal candidiasis, amphotericin B and high-dose fluconazole (>= 400 mg/day) are equally effective in the primary treatment of invasive infection with C. albicans and C. tropicalis. Even when amphotericin B is used initially, oral fluconazole should be substituted early in the course of treatment. However, some less common candidal species are not susceptible to fluconazole. Dermatophyte Infections (Ringworm) Infections caused by dermatophytes--fungi that invade only dead tissues of the skin or its appendages (stratum corneum, nails, hair). Trichophyton, Epidermophyton, and Microsporum are most commonly involved, but clinical differentiation of dermatophytes is difficult. Transmission is usually from person to person or animal to person. Fomites are not usually responsible. Some dermatophytes produce only mild or no inflammation or immune reaction; in such cases, the organism may persist indefinitely, causing intermittent remissions and exacerbations of a gradually extending lesion with a scaling, slightly raised border. In other cases, infection may be acute, typically causing a sudden vesicular and bullous disease of the feet or an inflamed boggy lesion of the scalp (kerion) that results from a strong immune reaction to the fungus; such infection is usually followed by remission or cure. Diagnosis Diagnosis is made clinically according to site of infection and confirmed by direct microscopic examination of scales dissolved in a solution of potassium hydroxide or by culture, demonstrating the pathogenic fungus in scrapings of lesions (see also Special Diagnostic Methods in Ch. 109). Treatment Most skin infections respond very well to topical antifungal preparations, such as the imidazoles (miconazole, clotrimazole, econazole, ketoconazole), ciclopirox, naftifine, or terbinafine. Resistant cases or those with widespread involvement require systemic therapy. Newer systemic drugs include itraconazole and fluconazole, oral triazoles, and terbinafine, a second-generation allylamine. These drugs appear to be safer and more effective than ketoconazole (see also General Therapeutic Principles in Ch. 158), a broad-spectrum oral imidazole derivative that is effective for dermatophyte infections, although occasional liver toxicity (severe or even fatal) limits its use. Itraconazole interacts with many commonly prescribed drugs. Terbinafine delays gastric emptying, and GI side effects occur in 3 to 5% of patients. Disturbances of taste occur less frequently, and hematologic and hepatic side effects are rare. However, liver function should be evaluated at baseline and periodically thereafter. The new antifungals are more effective than griseofulvin in all dermatophytoses, except possibly tinea capitis. Until recently, griseofulvin was the most widely used systemic antifungal drug, but its use as first-line treatment of cutaneous fungal infections is decreasing with the availability of newer drugs. The adult dosage is microsize griseofulvin 250 mg po bid to qid, best given with a high-fat meal. Ultramicrosize griseofulvin is better absorbed and should be given in a single or divided total dose of 250 to 330 mg po for tinea corporis, capitis, or cruris and 500 to 660 mg po for tinea pedis. Headache is the most common side effect, and the drug occasionally causes GI distress, photosensitivity, rashes, or leukopenia. Angioedema has been reported. Vertigo and, rarely, exacerbation of lupus erythematosus or transient hearing reduction may occur. Topical imidazoles used with oral griseofulvin increase the cure rate. TINEA CORPORIS (Ringworm of the Body) Trichophyton sp is usually the cause. The characteristic pink-to-red papulosquamous annular plaques have raised borders, expand peripherally, and tend to clear centrally. Differential diagnosis includes pityriasis rosea, drug eruptions, nummular dermatitis, erythema multiforme, tinea versicolor, erythrasma, psoriasis, and secondary syphilis. A variant form appears as nummular scaling patches studded with small papules or pustules. For mild-to-moderate lesions, an imidazole, ciclopirox, naftifine, or terbinafine in cream, lotion, or gel form should be rubbed in twice daily for at least 7 to 10 days after lesions disappear. Inflammatory types of tinea corporis usually respond readily to specific topical antifungal medications. Extensive and resistant lesions occur in patients infected with Trichophyton rubrum and in persons with debilitating systemic diseases. For extensive or resistant tinea corporis, the most effective therapy is oral itraconazole or terbinafine (see above). TINEA PEDIS (Ringworm of the Feet; Athlete's Foot) Tinea pedis is common. Trichophyton mentagrophytes infections typically begin in the 3rd and 4th interdigital spaces and later involve the plantar surface of the arch. Toe web lesions often are macerated and have scaling borders; they may be vesicular. Acute flare-ups, with many vesicles and bullae, are common during warm weather. Infected toenails become thickened and distorted. T. rubrum produces scaling and thickening of the soles, often extending just beyond the plantar surface in a " moccasin " distribution. Itching, pain, inflammation, or vesiculation may be slight or severe. Tinea pedis may be complicated by secondary bacterial infection, cellulitis, or lymphangitis, which may recur. Tinea pedis may be confused with maceration (from hyperhidrosis and occlusive footgear), contact dermatitis (from sensitivity to various materials in shoes, particularly adhesive cement), eczema, or psoriasis. Itraconazole and terbinafine are the most effective treatments for mycologically proven tinea pedis but may have little immediate effect on an acute inflammatory infection, which is a cell-mediated immune reaction. Either drug may be used to treat chronic infections and prevent acute exacerbations. Interdigital infections can be successfully treated with topical agents. Systemic treatment for infected nails (onychomycosis) may require therapy for many months and is especially difficult if the toenails are involved. Because of the keratophilic characteristics of these newer drugs, itraconazole 200 mg/day for 1 mo or pulse therapy with 200 mg bid 1 wk/mo for 1 to 2 mo often cures uncomplicated tinea pedis. Concomitant topical antifungal use may reduce recurrences. Good foot hygiene is essential. Interdigital spaces must be dried after bathing, macerated skin gently debrided, and a bland, drying antifungal powder (eg, miconazole) applied. Light permeable footwear is recommended, especially during warm weather; many patients even benefit from going barefoot. During acute vesicular flare-ups, bullae may be drained at the margin, but the keratinous blister roof should not be removed. Drying agents include tap water or dilute Burow's solution (twice-daily soaks). Cure with topical treatment is difficult, but control may be obtained with long-term therapy. Recurrence is common after therapy is discontinued. TINEA UNGUIUM (Ringworm of the Nails) This form of onychomycosis is usually caused by Trichophyton sp. Infections of the fingernails are less common than those of the toenails. The nails thicken and become lusterless, and debris accumulates under the free edge. The nail plate becomes thickened and separated, and the nail may be destroyed. Differentiating a Trichophyton infection from psoriasis is particularly important because drug therapy for tinea unguium is specific, and long-term treatment is required. When griseofulvin is used to treat onychomycosis, long-term cure is achieved in < 20% of cases. Therefore, systemic treatment with oral itraconazole or oral terbinafine is probably the treatment of choice. Itraconazole 200 mg po bid 1 wk/mo for 4 mo or terbinafine 250 mg/day achieves a high cure rate for fingernail and toenail infections. For onychomycosis of fingernails, the duration of terbinafine treatment is 6 wk, and for toenails, 12 wk. It is not necessary to treat until all abnormal nail is gone because these drugs remain bound to the nail plate and continue to be effective after oral administration has ceased. Topical treatments for nail infections are rarely effective, except for the superficial white type, in which infection occurs on the nail surface only. TINEA CAPITIS (Ringworm of the Scalp) Tinea capitis mainly affects children. It is contagious and may become epidemic. Trichophyton tonsurans is the common cause in the USA; other Trichophyton sp (eg, Trichophyton violaceum) are common causes elsewhere. T. tonsurans infection of the scalp is often subtle in onset. Inflammation is often low-grade and persistent; the lesions are not annular or sharply marginated, so the disorder resembles seborrheic dermatitis. Characteristic black dots on the scalp result from broken hairs. Inflammatory infections can occur. Trichophyton sp may persist in adults. Microsporum audouinii and M. canis, once predominant, are less common causes of tinea capitis in the USA. M. audouinii lesions are small, scaly, semi-bald grayish patches with broken, lusterless hairs. Infection may be limited to a small area or extend and coalesce until the entire scalp is involved; sometimes ringed patches extend beyond the scalp margin. M. canis and M. gypseum usually cause an inflammatory reaction, with shedding of the infected hairs. A raised, inflamed, boggy granuloma (kerion) may also occur and may be mistaken for an abscess or a pyoderma; it is followed shortly by healing. Trichophyton, an endothrix, produces chains of arthrospores that can be seen microscopically within the hair; the hairs do not fluoresce under Wood's light. Diagnosis of a Microsporum infection is facilitated by examining the scalp under Wood's light; infected hairs may fluoresce a light, bright green. Microsporum is also an ectothrix, producing spores to form a sheath around the hair. The sheath can be seen on microscopy. Culture of the fungus is also important in establishing the diagnosis. Children with Trichophyton infection should be given microsize griseofulvin suspension 10 to 20 mg/kg/day or ultramicrosize griseofulvin 5 to 10 mg/kg/day with meals or milk for at least 4 wk or until all signs of infection are gone. Until tinea capitis is cured, an imidazole or ciclopirox cream should be applied to the scalp to prevent spread, especially to other children, and selenium sulfide 2.5% shampoo should be used daily. TINEA CRURIS (Jock Itch) Tinea cruris, more common in males, may be caused by various dermatophytic organisms. Typically, a ringed lesion extends from the crural fold over the adjacent upper inner thigh. Both sides may be affected. Scratch dermatitis and lichenification often occur. Lesions may be complicated by maceration, miliaria, secondary bacterial or candidal infection, and reactions to treatment. Recurrence is common because fungi may repeatedly infect susceptible persons. Flare-ups occur more often during summer. Tight clothing or obesity tends to favor growth of the organisms. The infection may be confused with contact dermatitis, psoriasis, erythrasma, or candidiasis. In dermatophyte infections, scrotal involvement is usually absent or slight; however, the scrotum is often inflamed in candidal intertrigo or lichen simplex chronicus. Topical therapy with a cream or lotion, as in tinea corporis, is often effective. In some cases, itraconazole 200 mg/day or terbinafine 250 mg/day po for 3 to 6 wk may be needed. TINEA BARBAE (Ringworm of the Beard; Barber's Itch) Mycotic infection of the beard area is rare. Infections in this area are more commonly bacterial (see Folliculitis in Ch. 112) but may be fungal, especially in agricultural workers. The causative agent is established microbiologically. Oral terbinafine is the best treatment. If the lesions are severely inflamed, a short course of prednisone should be added (to lessen symptoms and perhaps reduce the chance for scarring), starting with 40 mg/day po (for adults) and tapering the dose over 2 wk. DERMATOPHYTIDS OR ID ERUPTIONS These fungus-free skin lesions are of variable morphology and occur elsewhere on the body during an acute vesicular or inflammatory dermatophyte infection; they are thought to result from hypersensitivity to a fungus. Although sometimes caused by a dermatophyte infection or id reaction, vesicular dermatitis of the hands is most commonly something else (see Chronic Dermatitis of Hands and Feet in Ch. 111). Treatment of an id reaction consists of diagnosis and treatment of the underlying dermatophyte infection. A topical corticosteroid cream or lotion and an oral antihistamine (eg, hydroxyzine hydrochloride 25 mg qid) may provide some relief. Yeast Infections CANDIDIASIS (Moniliasis) Infections of skin (usually of moist, occluded, intertriginous areas), skin appendages, or mucous membranes caused by yeasts of the genus Candida. (See also Genital Candidiasis in Ch. 164.) Candidiasis is usually limited to the skin and mucous membranes; uncommonly, the infection may be systemic and cause life-threatening visceral lesions. Systemic candidiasis (candidosis) is discussed in Ch. 158. Pathogenesis and Etiology Candida albicans is a ubiquitous, usually saprophytic, yeast that can become pathogenic if a favorable environment or the host's weakened defenses allow the organisms to proliferate. The interrelation of these factors and the mechanisms that increase susceptibility to infection are discussed in Ch. 151. Specifically, intertriginous and mucocutaneous areas where heat and maceration provide a fertile environment are most susceptible. Systemic antibacterial, corticosteroid, and immunosuppressive therapy; pregnancy; obesity; diabetes mellitus and other endocrinopathies; debilitating diseases; blood dyscrasias; and immunologic defects increase susceptibility to candidiasis. Symptoms and Signs Intertriginous infections, the most common type, appear as well- demarcated, erythematous, sometimes itchy, exudative patches of varying size and shape. The lesions are usually rimmed with small red-based papules and pustules and occur in the axillae, inframammary areas, umbilicus, groin, and gluteal folds (eg, diaper rash); between the toes; and on the finger webs. Perianal candidiasis produces white macerated pruritus ani. Candidal paronychia begins around the nail as a painful red swelling that later develops pus. It may result from improperly performed manicures and is common in kitchen workers and others whose hands are continually in water. Subungual infections are characterized by distal separation of one or several fingernails (onycholysis) with white or yellow discoloration of the subungual area. Defects in cell-mediated immune responses (which, in children, are sometimes genetic) may lead to chronic mucocutaneous candidiasis (candidal granuloma--see also Specific Immunodeficiencies in Ch. 147), which is characterized by red, pustular, crusted, and thickened plaques resembling psoriasis, especially on the nose and forehead and invariably associated with chronic oral moniliasis. In immunodeficient patients, other more typical candidal lesions or systemic candidiasis may also occur. Diagnosis Candida can be shown by finding yeast and pseudohyphae in gram- stained specimens or in potassium hydroxide mounts of scrapings from a lesion. Because Candida is a commensal of humans, isolation of the organism in culture from the skin, mouth, vagina, urine, sputum, or stool should be interpreted cautiously. To confirm the diagnosis, a characteristic clinical lesion, exclusion of other causes, and, at times, histologic evidence of tissue invasion are needed. Treatment Topical nystatin, the imidazoles, and ciclopirox are usually effective; these agents will suppress both dermatophyte and candidal skin infections. Treatment must be chosen according to the site of infection and administered three or four times daily. When anti- inflammatory and antipruritic actions are desired, equal amounts of antifungal cream and a low-strength corticosteroid (eg, hydrocortisone) cream can be mixed, or each may be applied separately. The drug is not absorbed and therefore cannot be given orally to treat candidiasis of skin. Typically, itraconazole 200 mg/day po for 2 to 6 wk is required. For candidal diaper rash, the skin should be kept dry by changing diapers frequently and by generously applying nystatin powder or an imidazole cream twice daily; in severe cases, rubber pants and disposable diapers with plastic coverings should be avoided. Treatment of paronychial infections is discussed in Ch. 112. Oral itraconazole is effective for many forms of acute and chronic mucocutaneous candidiasis (including vaginal). TINEA VERSICOLOR An infection characterized by multiple, usually asymptomatic, scaly patches varying from white to brown and caused by Pityrosporum orbiculare (formerly Malassezia furfur). Symptoms and Signs Tinea versicolor is common in young adults. Tan, brown, or white, very slightly scaling lesions that tend to coalesce occur most frequently on the chest, neck, and abdomen and occasionally on the face. The scaling may not be apparent unless the lesion is scratched. The patient may notice the condition only in the summer because the lesions do not tan; instead they appear as variously sized hypopigmented sun spots. Itching is rare and usually occurs only when the patient is overheated. Diagnosis The condition is diagnosed from the clinical appearance and by finding groups of yeasts and short plump hyphae on microscopic examination of scrapings from the lesions. The extent of involvement can be determined by the golden fluorescence or pigment changes under Wood's light. Diagnosis does not require culture of the organism, which is difficult without special media. Treatment Numerous topical therapies effectively clear tinea versicolor, including selenium sulfide, the imidazoles, zinc pyrithione, and sulfur-salicylic acid combinations. Undiluted selenium sulfide 2.5% in shampoo form (Caution: Keep out of reach of children) is applied to all involved areas, including the scalp but avoiding the scrotum, for 3 or 4 days at bedtime and washed off in the morning. If irritation occurs, selenium sulfide should be washed off after 20 to 60 min, or treatment should be stopped for a few days. If irritation is severe, either 2% zinc pyrithione or 2% micropulverized sulfur and 2% salicylic acid in a shampoo base may be applied at bedtime for 2 wk, or the topical imidazoles (see Dermatophyte Infections, above) may be applied bid for 2 wk. Short-term oral itraconazole (200 mg/day for 7 days) is effective and well tolerated. Oral ketoconazole is also effective, but long- term systemic treatment for this usually trivial disease rarely seems warranted because of potential toxicity. However, in some studies, one 200-mg tablet/day for 1 to 5 days effectively eliminated tinea versicolor for several months. Lesions may not repigment until the fungus is clear and the patient is exposed to sun. Eventual recurrence is almost universal because the causative organism is a normal skin inhabitant. The scalp may be the reservoir. Quote Link to comment Share on other sites More sharing options...
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