Skin Disease in HIV

HIV-infected patients carry a heavy burden of cutaneous illness. As many as 90% have at least one skin disease; most have several [1, 2]. Mucocutaneous diseases in HIV patients are a significant source of morbidity. They can cause chronic itching or pain, lead to secondary superinfection, or reflect the presence of a life-threatening malignancy or invasive infection.

Importantly, skin disease is also a clinical marker of immunosuppression. Many conditions are seen preferentially in those with low CD4 counts, while a high number of skin diseases correlate with low CD4 and worse prognosis [3, 4]. Skin conditions in HIV-infected patients may occur as a manifestation of HIV itself, an opportunistic infection, a neoplastic process, a primary dermatologic condition, a drug reaction, or as part of the immune reconstitution inflammatory syndrome. Appropriate recognition and treatment of these conditions is vital to the care of patients with HIV.

Primary HIV

Acute retroviral syndrome (ARS) or primary HIV infection may be the presenting sign in 40–90% of patients. It is often asymptomatic and non-specific. ARS consists of a mononucleosis-like illness with fever, lymphadenopathy, pharyngitis, and neurologic symptoms. The skin rash may be recognized in about half of symptomatic patients and typically is a non-specific maculopapular exanthem [5, 6]. Oral and genital ulcers may also occur, as may infiltrated plaques on the chest and back [7, 8]. There should be a high index of suspicion for HIV infection in patients presenting with these symptoms [9]. Patients with primary HIV infection may be highly infectious because of the presence of a high viral burden in blood and genital secretions [10]. Confirmation of ARS can be made by finding positive plasma HIV RNA and negative HIV antibody [11]. Treatment with ART early in this phase may decrease the severity of the disease, alter the initial viral set point, and reduce the rate of viral replication. However, therapy may cause drug toxicities and potential resistance if it fails [8]. Studies to determine the optimal time to start therapy are ongoing.

Pigmentation

HIV infection is associated with pigment disorders, both hyperpigmentation and hypopigmentation. Hyperpigmentation has been reported in HIV-infected persons with background pigment. Advanced HIV infection and immunosuppression has also been associated with more diffuse hyperpigmentation. In a Chinese HIV-infected population in Malaysia, hyperpigmentation was the most common skin disorder, representing 36% of the whole group studied, while 47% of an Indian population in a separate study were affected [4, 12]. Pigmentation is most commonly seen in sun-exposed areas but becomes more diffuse over the body. Photodistributed hyperpigmentation has been noted with CD4 counts < 100 cells/mm³ and may be the presenting sign of HIV infection [13]. Gray coloration of the nails and pigmented oral mucosa may be other markers of more advanced stages of immunosuppression with CD4 counts < 200 cells/mm³ [14, 15]. Cutaneous hyperpigmentation has also been linked with eczematous features, in both the acute and chronic forms [16].

Several reasons for hyperpigmentation have been postulated [17]. Medications used for the treatment and prophylaxis of AIDS-related conditions can cause photosensitivity [18]. These drugs include trimethoprim-sulfamethoxazole, azithromycin, dapsone, ketoconazole, and anti-tuberculosis drugs. Antiretroviral medications like indinavir, saquinavir, and efavirenz have been associated with photosensitivity [19]. Zidovudine (AZT) may result in the hyperpigmentation of the nails, oral mucosa, and skin and appears to be related to increased melanogenesis and not to drug deposition or photosensitivity [20]. Concomitant diseases in HIV-infected individuals, such as Porphyria cutanea tarda, which causes photosensitivity, and Mycobacteria avium intracellulare, which can affect the adrenal glands and cause adrenal suppression, can eventuate in hyperpigmentation [21]. Sunscreen (SPF15 or higher) and avoidance of sun exposure can improve symptoms.

Pigmented oral lesions are not uncommon, particularly in India and Africa [22]. Similar oral lesions are noted in Caucasians with HIV infection who have not been on any medications.

Hypopigmentation in HIV infection in the form of vitiligo has been reported. Vitiligo has been considered to be an autoimmune disorder like alopecia areata, possibly reflecting concomitant B-cell dysfunction in HIV infection, though the mechanism is poorly understood. Both the onset and resolution of vitiligo have been reported in persons with increasing CD4 cell counts on antiretroviral therapy (ART) [23, 24].

Itching

Itching is a common complaint among HIV-infected patients. Pruritus without a rash is less common than originally thought and can be associated with concomitant systemic diseases like hepatitis C, chronic renal failure, lymphomas, and methamphetamine use. When a pruritic dermatitis is noted, a careful history and physical examination usually reveals a primary dermatologic condition for which standard treatment for the underlying condition can proceed. Included in this heterogeneous group of diseases are xerosis, eczema, seborrheic dermatitis, psoriasis, Staphylococcal aureus folliculitis, eosinophilic folliculitis, prurigo nodularis, pruritic papular eruption (PPE) of HIV, arthropod assaults, scabies, and drug rashes. Biopsy and cultures of lesions can be helpful in distinguishing these conditions [16].

As early as 1983, reports from sub-Saharan Africa, Haiti, Brazil, and Thailand described an eruption of intensely pruritic papules and nodules that begins on the extensor surfaces of the extremities and subsequently involves the trunk and face [25–28]. Called the pruritic papular eruption of HIV, these lesions have not been reported in Europe or America but are exceedingly common in the tropics, affecting 11–46% of HIV-infected patients in those regions. When present, PPE is highly predictive of HIV infection and in fact is often the presenting sign [29, 30]. A marker of more advanced immunosuppression, it may improve dramatically with effective ART [31]. Biopsy findings include a mild to moderate dermal perivascular and periadnexal infiltrate. Early lesions biopsied in Uganda have revealed histology consistent with arthropod bites [32]. It has been hypothesized that this condition represents an altered and hyperactive immune response to arthropod bites [33, 34]. Cytokine profiles of individuals with PPE show lower levels of interleukin-2 and γ-interferon, arguing for a dysregulated immune system [35]. In addition to immune reconstitution, potent topical steroids, antihistamines, and ultraviolet light may bring symptomatic relief [36–39]. Eosinophilic folliculitis (EF) has been reported in Southeast Asia, Africa, India, Europe, and North America [16, 22, 40, 41]. This disease presents with pruritic urticarial papules and nodules on the scalp, neck, face, upper chest, and back and is therefore differentiated clinically from PPE. It is usually associated with a nadir CD4 count < 100 cells/mm³ and a current CD4 count < 200 cells/mm³. This condition can also be seen in individuals starting ART as part of an immune reconstitution syndrome [42]. Clinicians should be aware of this possibility and should not confuse the eruption with a medication reaction or stop therapy. The pathogenesis of EF remains elusive [43]; however, it presumably involves an enhanced Th2 response with elevated interleukin-4, interleukin-5, and chemokine recruitment of eosinophils [44]. Histologically, there is a predominant perifollicular infiltrate of eosinophils [38, 45]. Biopsy of lesions can differentiate this condition from other pruritic disorders. Treatment [46] options include waiting out the immune reconstitution period (the first 12 weeks of ART), potent topical steroids and antihistamines, itraconazole, UVB therapy, and isotretinoin [47].

Prurigo nodularis has been reported globally and is characterized by pruritic dome-shaped nodules initially presenting on the photoexposed areas of the extremities and eventually involving the trunk [16]. These nodules are bilateral and symmetric and appear in persons with background pigment, usually with CD4 counts < 100 cells/mm³. The incessant rubbing and scratching of these lesions can lead to lichenification of the skin as well as pigment change, both hyper- and hypopigmentation. A search for an underlying, treatable condition like scabies or eczema is warranted [48, 49]. Immune reconstitution and reduction of viremia with ART are helpful. Regimens that include raltegravir may be particularly useful in refractory cases [50]. Potent topical steroids and antihistamines are of benefit. Ultraviolet light and thalidomide have been somewhat helpful when other therapies have failed [51].

Scabies is noted globally and usually presents with pruritic papules with accentuation in the intertriginous areas, genitalia, and fingerwebs [48, 49]. With advancing immunosuppression, the infestation may become more widespread and refractory to treatment [52]. Crusted scabies may also occur with advanced HIV and presents with thick crusts that are non-pruritic and teeming with mites [53]. Outbreaks of scabies in institutional settings like orphanages, hospitals, and hospices are particularly challenging [54]. Topical treatment of scabies is with benzyl benzoate 10%, sulfiram 2% (in Europe), or permethrin 5% cream (available in the USA and UK). Gamma-benzene hexachloride (lindane) is contraindicated in HIV, as it has been associated with the development of peripheral neuropathies. Oral ivermectin can also be used for treatment of scabies in an institution or for crusted scabies. Treatment of contacts and proper cleaning of garments and linens is essential in treatment and infection control, particularly in institutional settings [55, 56]. The risk of secondary staphylococcal and streptococcal infection of scabietic lesions is high in tropical environments, so antibacterial therapy should also be used when necessary [57–59].

Staphylococcal aureus Skin Infections

Staphylococcus aureus is the most common cutaneous bacterial infection in patients with HIV disease [60]. Community-acquired infections of subcutaneous and deep tissues are common throughout the world [61]. In the Caribbean Islands and Africa, bacterial infection in HIV represent up to 40% of all skin diseases as either primary infection or secondary superinfection of eczema or scabies [62].

Rates of S. aureus carriage are high, and persistent colonization among HIV-infected patients is common. These factors increase the risk of soft tissue infections [63–65]. Staphylococcus aureus in the skin can manifest in many ways, including bullous impetigo, ecthyma, folliculitis, abscesses, and furuncles. Occasionally, infected follicles coalesce to form violaceous plaques that may be studded with pustules. Rarely, abscesses of the muscle (pyomyositis) as well as deep tissue involvement in the form of necrotizing fasciitis may occur.

Over the past decade, HIV-infected patients have shown a high and growing rate of soft tissue infection with methicillin-resistant S. aureus (MRSA). In Cook County, Illinois, the incidence of MRSA infection among HIV-infected patients was six times higher than among HIV-uninfected patients, while between 2000–2003 and 2004–2007, the incidence of MRSA among HIV patients increased 3.6-fold [66]. Risk factors for the development of MRSA in HIV include low CD4 counts, recent hospitalization or antibiotic exposure, high-risk sexual practices, intravenous drug use, and environmental exposures [67, 68]. Some studies suggest the widespread use of trimethoprim-sulfamethoxazole prophylaxis may increase rates of S. aureus resistance to that medication [69]; however, this does not always appear to be the case [70].

Knowing the organism and its sensitivities is imperative where at all possible. Otherwise, local resistance patterns should guide empiric therapy. Increasing resistance to β-lactam drugs and fluoroquinolones has been reported. Erythromycin, clindamycin, sulfamethoxazole, gentamicin, and intravenous vancomycin are still used. Tetracycline drugs are being used with more frequency [71]. Linezolid is an expensive alternative and should be reserved for cases in which there is documented resistance to the above-mentioned antibiotics [72]. Incision and drainage of abscesses is critical. Hibiclens and Betadine washes may have a role but can often dry out the skin, leading to eczematous eruptions prone to secondary bacterial infections. Mupirocin ointment reduces carriage rates in HIV but does not decrease infection rates and there is concern for emerging mupirocin resistance [73, 74]. Rifampin can be used in combination with other antibiotics to reduce carriage rates of S. aureus. It acts synergistically with other antibiotics but cannot be used with many of the antiretroviral medications, particularly the protease inhibitors, because of drug–drug interactions [75]. In Mali, an algorithm for treatment of skin diseases was developed. Patients were first evaluated for signs of pyoderma by looking for presence of yellow crusts, pus, sores, or blisters. Depending on the degree of pyoderma, patients were treated with topical antiseptics or oral antibiotics and returned for a follow-up visit. Abscesses were incised and drained and not treated with antibiotics. The use of this algorithm correctly identified pyodermas and secondarily infected eczemas 96–98% of the time and decreased the use of steroids and antifungals [48].

Bacillary Angiomatosis

Bacillary angiomatosis (BA), a treatable opportunistic infection, can present with vascular, easily friable papules or subcutaneous nodules in patients with advanced HIV disease. The agents causing this infection have been classified as Bartonella, and at least 15 species have been identified worldwide in association with various vectors [22, 76]. Cutaneous manifestations of BA in the HIV-infected population are primarily caused by two species, Bartonella henselae and Bartonella quintana [77, 78]. Epidemiologically, B. henselae has been associated with cat and flea exposure. B. quintana has been associated with low income, homelessness, and exposure to lice [79]. BA has been reported in North and South America, Europe, India, and Africa [76, 80–84]. Studies from multiple regions have shown that the seroprevalence among HIV-infected patients is high [85–87]. In countries where Kaposi’s sarcoma (KS) is prevalent, BA may be under-recognized, as it can mimic the vascular lesions typically associated with KS. Diagnostic accuracy is important because the response of BA to prompt antibiotic therapy can be excellent, whereas the prognosis of untreated, disseminated BA or KS is more guarded. Lesions of BA may also be confused with pyogenic granuloma and lymphoma [88].

Bacillary angiomatosis initially was considered a disorder of the skin, but systemic involvement is common. Visceral disease may present as osseous lesions, hepatic and splenic tumors, lymph node disease, pulmonary lesions, brain lesions, bone marrow, and widespread fatal systemic involvement. Bacillary angiomatosis can present with unexplained fever, bacteremia, or endocarditis in HIV-infected patients [89]. Lesions should be biopsied and examined with hematoxylin and eosin staining and Warthin–Starry silver staining, which reveals the organisms. Culture, indirect fluorescent antibody testing, and polymerase chain reaction can be performed on lesions and serum. Immunohistochemical staining for anti-HHV8 can be used to differentiate KS from BA [90].

Treatment with erythromycin or doxycycline for at least 3 months is recommended even though cutaneous lesions resolve in 3–4 weeks. Relapses can occur if treatment is not continued appropriately. Severely ill patients should be treated with i.v. doxycycline with either gentamicin or rifampin for at least 4 months.

Cancrum Oris

Noma, or cancrum oris, is an infectious disease that starts as necrotizing ulcerative gingivitis, progresses with tumefaction, and destroys adjacent structures around and deep to the area [91]. It occurs in countries where there is extreme poverty, malnutrition, and HIV, particularly in sub-Saharan Africa [92]. It tends to occur in children and young adults (2–16) [93]. Local debridement and antibiotics are established treatments, but in the absence of timely therapy, mortality is high [94].

Syphilis

Worldwide, there has been a dramatic increase in the reported number of cases of syphilis in recent years [95–99]. The majority of cases in large urban settings have been in men, particularly men having sex with men [100, 101]. In Europe and the USA, the overall proportion of syphilis patients co-infected with HIV is 50% [102]. Over 70% of these co-infected patients were already aware of their HIV infection at the time that they were diagnosed with syphilis [98, 103–106]. Methamphetamine use has been implicated in the rising incidence of syphilis in the USA and Europe, particularly with cases of re-infection of syphilis [107, 108]. Among women with syphilis and HIV, sex work, limited or no use of condoms, and alcohol and drug use were found to be risk factors [95, 98]. Screening of syphilis, even in asymptomatic HIV-infected patients, is recommended [109, 110].

Primary and secondary cutaneous presentations of syphilis are similar in HIV- and non-HIV-infected individuals [111]. Lesions include chancres, sometimes with rapid evolution to secondary stages, papulosquamous lesions on the trunk and palmar/plantar regions, patchy alopecia, and osteochondritis of the sternal region [112–114]. Uveitis with or without rash is another common manifestation [115]. Oral lesions are also common [22]. Tertiary cutaneous lesions are characterized by verrucous or hyperkeratotic nodules. Lues maligna has been reported in HIV infection [116]. Skin biopsies or dark field microscopy of cutaneous lesions demonstrates spirochetes and establishes the diagnosis [110]. Negative serologic tests may not be adequate for ruling out secondary syphilis, as HIV infection may delay development of serologic evidence of Treponema pallidum. However, for the majority of patients, serologic testing is adequate [117].

Central nervous system (CNS) involvement may manifest early in HIV, and relapse in the CNS may be more common even after standard treatment. Clinicians should carefully follow HIV-infected patients who have been treated with standard therapies for early syphilis. If CNS signs or symptoms develop, clinicians should perform appropriate evaluation for early CNS relapse, including lumbar puncture and VDRL of the cerebrospinal fluid [118]. Lumbar puncture of patients with CD4 < 350 cells/mm³ and/or rapid plasma reagin (RPR) titer ≥ 1:32 without regard to stage may improve the ability to diagnosis neurosyphilis [119] in asymptomatic patients.

The CDC recommends treating primary and secondary syphilis with 2.4 million units of benzathine penicillin given intramuscularly at a single session. Some specialists recommend benzathine penicillin 2.4 million units intramuscularly, once per week for 2 or 3 weeks. In late latent disease, three doses of benzathine penicillin are recommended 1 week apart. For penicillin-allergic patients, doxycycline and tetracycline are recommended. Erythromycin is not recommended because treatment failures have been noted with azithromycin [120]. Since the relapse rate of neurosyphilis is approximately 17% in patients treated with standard regimens, HIV-infected patients should be evaluated clinically and serologically for treatment failure at 3, 6, 9, 12, and 24 months after therapy. Although of unproven benefit, some specialists recommend a CSF examination 6 months after therapy [117].

Serologic clearance of syphilis appears largely unaffected by HIV status in the “highly active” ART era (91.8% in HIV-infected versus 98.3% in HIV-uninfected, p = 0.14) [121]. HIV-infected patients who meet the criteria for treatment failure should be managed in the same manner as HIV-uninfected patients (i.e. a CSF examination and re-treatment). CSF examination and re-treatment also should be strongly considered for patients whose nontreponemal test titers do not decrease fourfold within 6–12 months of therapy. Most specialists would re-treat patients with benzathine penicillin G administered as three doses of 2.4 million units i.m. each at weekly intervals, if CSF examinations are normal [117].

Patients with neurosyphilis should be treated with crystalline penicillin G, 2.4 million units i.v. every 4 hours for at least 10 days [117].

Cutaneous Tuberculosis

Cutaneous and intraoral tuberculosis (TB), like pulmonary TB, appear to be more common among HIV-infected patients [122] than in the general population. Lesions have been described most frequently in India, Brazil, Thailand, and Africa [22, 123–127]. Many such cases have been associated with pulmonary disease, but this need not be the case [123]. In several instances, unsuspected pulmonary disease was discovered on chest X-ray and sputum samples after the diagnosis of cutaneous disease was made. This is particularly true of TB in the oral cavity [124]. Lesions present most often as scrofuloderma [125] or the infiltrated plaques of lupus vulgaris. Single or multiple lesions, nodules, or papillomas are also seen such that cutaneous TB can mimic fungal or bacterial infections, KS, neoplastic processes, and herpetic infections and should be considered in the differential diagnosis of those diseases [126]. Disseminated military TB may also mimic the papular pruritic eruption of HIV and should be considered if the eruption fails to improve with antiretrovirals alone. Biopsy and tissue culture confirm the diagnosis [123, 127]. An id reaction in the form of papulonecrotic id has also been described in a patient with immune reconstitution [128, 129].

Mycobacterium avium-intracellulare (MAI) infrequently presents with skin manifestations, although it has been reported to form single or multiple nodules and cervical lymphadenitis in persons whose CD4 counts are < 200 cells/mm³ [130]. A search for systemic disease should be undertaken with blood cultures and bone marrow aspirates for culture [131]. MAI is seen more frequently in the developed world and has been infrequently reported in Trinidad, Kenya, and other places [132].

Leprosy

Studies have indicated that HIV infection does not affect the clinical presentation or incidence of leprosy [133]. However, immunosuppression due to HIV infection may cause a relapse of leprosy in persons already treated [134]. Several reports document inflammatory and vasculo-ulcerative reactions of leprosy within 2–6 months after starting ART [135–137]. This is thought to be part of the immune reconstitution syndrome and has been documented particularly in patients whose CD4 counts were < 100 cells/mm³ when initiating ART. Occasionally, anti-inflammatory medications such as prednisone and thalidomide have been used in addition to leprosy and HIV medications with varying success. While leprosy may worsen during the first few weeks of ART when there is immune reconstitution, lesions improve with appropriate multidrug therapy for leprosy [138].

Nocardiosis

Nocardiosis is a localized infection or disseminated infection caused by an aerobic actinomyces that is geographically distributed worldwide. It has been reported in HIV-infected patients in the USA, Africa, and Thailand [139, 140]. There are fewer reports of Nocardia and HIV infection from Europe, although there have been recent reports from Spain and France. Nocardia predominantly affects the pulmonary system. Skin is the second most common site of infection and presents as cutaneous or subcutaneous abscesses [141]. Intravenous drug use has been identified as a risk factor in HIV-infected patients. Most HIV-infected patients with Nocardia have CD4 cell counts < 200 cells/mm³, with the majority having a known diagnosis of AIDS at the time of infection [142]. Diagnosis can be made by using a modified acid fast stain on tissue or by culturing tissue, fluid, or blood [142]. The treatment of choice is trimethoprim-sulfamethoxazole, though dual therapy is often used [143]. Sensitivities to cultured material can be done. In a study from Thailand, patients who were resistant to trimethoprim-sulfamethoxazole succumbed to death [139]. Imipenem, amikacin, minocycline, amoxicillin-clavulanic acid, and third-generation cephalosporins have been proposed with unclear outcomes. Where possible, debridement of skin lesions is indicated as adjunctive therapy to antibiotics. Previous studies have reported that most patients respond to therapy in an average of 4 months. Cessation of therapy can be followed by recurrence and progression of disease despite reinitiation of therapy. Some authors have suggested that lifelong therapy should be instituted in the treatment of nocardiosis in HIV co-infected patients, particularly those who have evidence of advanced HIV disease. It is unclear what role ART has in this group of patients.

Leishmania

Leishmania—cutaneous, mucocutaneous, and visceral—has been reported in HIV co-infected persons [144, 145]. This is a protozoan disease transmitted by the sandfly and occurs in HIV-infected patients who live in or have traveled to endemic areas. In Spain and southwest Europe, there is a high prevalence of visceral leishmaniasis (kala-azar) among HIV-infected patients [146, 147]. The absence of an effective TH1 immune response, as seen in HIV infection, increases the risk of progression from asymptomatic disease to visceral leishmaniasis. It may also lead to poor treatment response and frequent relapses [148]. Conversely, leishmania induces more robust HIV replication [149]. Co-infected patients with cutaneous leishmaniasis can present with a few spontaneously healing lesions, diffuse non-healing lesions, mucocutaneous lesions, or localized or diffuse hyperpigmentation. Diagnosis is made by biopsy demonstrating amastigotes in the tissue [145]. Bone marrow can be biopsied in cases of suspected visceral involvement [144]. However, it should be noted that in persons with visceral leishmaniasis, any skin lesion (not only those of leishmania) can harbor amastigotes due to generalized involvement of macrophages [150]. Culture of tissue is standard so that the species of leishmania can be identified and correct therapy can proceed, particularly for Leishmania braziliensis and L. panamensis, so that the risk of mucocutaneous disease can be reduced [145]. Local therapy can be used for localized lesions and includes cryotherapy and paromycin ointment. Proven therapies include antimonials, pentamidine, amphotericin B, interferon with antimony, and miltefosine [151]. All HIV-infected patients should be carefully monitored after treatment to ensure that treatment was successful and that relapses do not occur.

Superficial Fungal (Dermatophyte) Infections

Superficial mycoses are particularly prevalent in developing countries and account for up to 50% of dermatologic disease in HIV-infected patients [152]. It is not clear whether the prevalence among HIV patients is increased compared to the general population, but cutaneous involvement may be more widespread, severe, or atypical [153, 154].

Tinea of the Skin, Hair, and Nails

Clinically, tinea corporis is characterized by well-demarcated, annular, erythematous, scaling plaques with central clearing. The hands, feet, lower trunk, groin, and buttocks are commonly involved. Onychomycosis is characterized by opacification and thickening of the nails. It is quite common among HIV-infected patients despite the use of ART [155]. Tinea can spread to hair-bearing areas, especially on the face and lower legs, presenting like plaques of folliculitis known as Majocchi’s granuloma. Direct examination of skin scrapings and culture for identification of species is helpful. The most common causal organism is Trichophyton rubrum [156].

Tinea of the palms, soles, and other localized areas of the body can be treated with topical imidazoles or terbinafine. If extensive areas are involved, oral antifungals may be a more effective alternative that can be used for shorter periods of time [157]. For tinea involving hair follicles, oral antifungals are required for approximately one month. For nail infections, oral antifungals are required but should be used selectively for patients in whom potential benefits outweigh risks. Relapse rates for onychomycosis are high, while transaminitis and drug–drug interactions through the cytochrome P450 system can complicate treatment. Oral terbinafine can be taken daily for 3 months at a dose of 250 mg. Itraconazole can be taken 7 days per month for 3 months at a dose of 400 mg. Griseofulvin requires a 12- to 18-month course; the success rate is lower, but it is the least hepatotoxic. The efficacy and relapse rates of onychomycosis in the HIV-infected population bear further study.

Deep (Systemic) Fungal Infections

Invasive or systemic fungal infections reported in HIV include cryptococcosis, histoplasmosis, sporotrichosis, aspergillosis, coccidiomycosis, actinomycosis, phaeohyphomycosis, and chromoblastomycosis.

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