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Fever and rash in immunocompromised patients without HIV infection

Fever and rash in immunocompromised patients without HIV infection
Literature review current through: Jan 2024.
This topic last updated: May 25, 2022.

INTRODUCTION — At least 20 percent of immunocompromised hosts will develop skin lesions, frequently accompanied by fever [1-3]. Immunocompromising diseases can cause multiple defects in host defenses, which, in turn, lead to heightened susceptibility to various types of infections. Knowledge of these immune defects and the specific associated infections can assist the clinician in the initial evaluation and management of the immunocompromised patient with skin lesions. These lesions sometimes reflect disseminated infection; evaluation of the skin may provide the most rapid diagnosis and thus may be lifesaving.

Some of the common infectious agents and dermatologic manifestations observed in selected immunodeficient states will be reviewed here. Fever and rash in immunocompetent patients and human immunodeficiency virus (HIV)-infected individuals are discussed separately. (See "Fever and rash in the immunocompetent patient" and "Fever and rash in patients with HIV".)

TYPES OF IMMUNOCOMPROMISE — Underlying diseases that affect various host defenses may predispose the patient to different types of infections. This section provides a brief overview of the different categories of immunocompromise and the types of pathogens that are most likely to affect patients in each category. It is not intended to provide comprehensive details on the immunology of each condition or an exhaustive list of infections that each type of host might experience. Following this overview of immunocompromising conditions, pathogens that most frequently cause fever and rash in immunocompromised hosts will be discussed.

Neutropenia or neutrophil dysfunction — Patients with prolonged or profound neutropenia or neutrophil dysfunction are at increased risk for developing infections with a variety of organisms, including gram-positive, gram-negative, and anaerobic bacteria, as well as fungi.

The most common cause of neutropenia is the administration of chemotherapeutic agents to patients with cancer. However, a number of other conditions also lead to neutrophil depletion or dysfunction, including acute myeloproliferative disorders, myelodysplastic syndromes, aplastic anemia, congenital or cyclic neutropenia, overwhelming sepsis, Felty syndrome, chronic granulomatous disease, or receipt of certain other drugs including azathioprine, vancomycin, sulfonamides, mycophenolate mofetil, ganciclovir, and tumor necrosis factor (TNF)-alpha inhibitors.

Infections may be difficult to appreciate because induration and erythema may not be present secondary to blunting of the host inflammatory response, although characteristic skin manifestations such as ecthyma gangrenosum may occur. (See "Overview of neutropenic fever syndromes" and "Diagnostic approach to the adult cancer patient with neutropenic fever", section on 'Skin and mucous membranes'.)

Humoral immune dysfunction — Patients with humoral immune dysfunction, particularly primary immunoglobulin and complement deficiencies, are at risk for certain bacterial, viral, and parasitic infections, particularly infections with encapsulated bacteria such as Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Other frequent pathogens include Salmonella spp, Mycoplasma spp, Giardia spp, rotavirus, and enteroviruses [4].

This group of disorders includes hypogammaglobulinemia states, which can be congenital or due to conditions such as multiple myeloma, Waldenström macroglobulinemia, common variable immune deficiency, nephrotic syndrome, non-Hodgkin lymphoma, and chronic lymphocytic leukemia, as well as antibody-depleting therapies such as plasmapheresis and administration of anti-B cell monoclonal antibody therapy [5]. (See "Primary humoral immunodeficiencies: An overview" and "Risk of infections in patients with chronic lymphocytic leukemia".)

Splenic dysfunction — Patients without a spleen or with hypofunction of the spleen are at increased risk for infection due to defects in antibody production, decreased ability to remove bacteria from the blood, and decreased production of important opsonin-associated proteins like tuftsin [6]. Conditions associated with functional hyposplenia include systemic lupus erythematosus (SLE), rheumatoid arthritis, graft-versus-host disease, amyloidosis, celiac disease, ulcerative colitis, sickle cell anemia, hereditary spherocytosis, and hemoglobin SC disease [7].

Asplenic and hyposplenic patients are particularly susceptible to infections with encapsulated bacteria (S. pneumoniae, N. meningitidis, H. influenzae) and may develop overwhelming sepsis with these organisms as well as Capnocytophaga spp (associated with dog or cat bites), Enterobacteriaceae, group A and B streptococci, and others. These patients are also at increased risk for severe babesiosis. (See "Clinical features, evaluation, and management of fever in patients with impaired splenic function".)

Cell-mediated immune dysfunction — Patients with cell-mediated immune (CMI) dysfunction are at increased risk of infection with a myriad of intracellular bacteria and mycobacteria, viruses, fungi, and parasites.

Conditions other than HIV that are associated with CMI dysfunction include DiGeorge syndrome, Hodgkin lymphoma, lymphocytic leukemia, receipt of total lymphoid irradiation, pregnancy, development of anti-interferon-gamma autoantibodies, defects in the interferon-gamma pathway, and receipt of drugs such as glucocorticoids, tacrolimus, methotrexate, thymoglobulin, and cyclosporine (such as after organ transplantation or hematopoietic cell transplantation).

Fever and rash in HIV-infected individuals are discussed separately. (See "Fever and rash in patients with HIV".)

Tumor necrosis factor-alpha inhibitors — TNF-alpha inhibitors including etanercept, adalimumab, infliximab, certolizumab pegol, and golimumab are being used with increased frequency in the treatment of patients with inflammatory disorders such as inflammatory bowel disease, rheumatoid arthritis, psoriasis, and seronegative spondyloarthropathies. These agents interfere with cell-mediated host defenses against intracellular pathogens, and adverse effects include serious bacterial, mycobacterial, fungal, viral, and parasitic infections [8-10].

Pathogens that have been reported to cause fever and rash in patients taking TNF-alpha inhibitors include Nocardia spp [11,12], Mycobacterium tuberculosis and nontuberculous mycobacteria [13-16], Cryptococcus spp [17,18], endemic fungi such as Histoplasma and Coccidioides spp [19-21], and Leishmania spp [22-24]. Invasive fungal infections secondary to Candida and Aspergillus have also been reported [25]. The data are conflicting as to whether the risk for herpes zoster is greater with TNF-alpha inhibitors when compared with other nonbiologic disease-modifying antirheumatic drugs. Hepatitis B virus infections can reactivate during treatment with these agents. (See "Risk of mycobacterial infection associated with biologic agents and JAK inhibitors" and "Tumor necrosis factor-alpha inhibitors: Bacterial, viral, and fungal infections" and "Cutaneous leishmaniasis: Clinical manifestations and diagnosis", section on 'CL in immunocompromised hosts'.)

Cirrhosis — Patients with cirrhosis can have immune deficits that include impaired phagocytosis and chemotaxis, decreased complement levels, and poor opsonization. Cirrhotic patients are particularly vulnerable to skin and soft tissue infections due to Vibrio vulnificus and Vibrio parahaemolyticus after consumption of raw shellfish or exposure to bodies of water containing the organisms (see "Vibrio vulnificus infection"). Other gram-negative organisms to consider in cirrhosis-associated necrotizing skin and soft tissue infections include Aeromonas species and Klebsiella species [26].

Diabetes mellitus — Defects in immune function in diabetics include depressed neutrophil and T cell function [27,28]. Skin and soft tissue infections, especially of the feet, are common infectious complications of diabetes and may be exacerbated by peripheral vascular disease and neuropathy. These include ulcers, abscesses (including carbuncles and furuncles), cellulitis, and necrotizing infections. Superficial necrotizing infections involve epifascial soft tissue or superficial fascia; the microbiology may be monomicrobial or polymicrobial and includes anaerobes, aerobic staphylococci and streptococci, and/or aerobic gram-negative bacilli. (See "Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities".)

Diabetes mellitus is also a risk factor for polymicrobial necrotizing fasciitis of the perineum (Fournier gangrene), which typically results from breaches in the urethral or gastrointestinal mucosa [29]. Deep necrotizing infections can also involve the deep muscle compartments and include clostridial and nonclostridial myonecrosis and necrotizing fasciitis. (See "Clostridial myonecrosis" and "Necrotizing soft tissue infections".)

Diabetic ketoacidosis is an important risk factor for the development of rhino-orbital-cerebral mucormycosis (picture 1 and picture 2) [30]. Cutaneous mucormycosis, most commonly following trauma to the skin and involving the extremities, can also occur in diabetics (and in those with organ transplantation, leukemia, and neutropenia) [31]. (See "Mucormycosis (zygomycosis)".)

Systemic lupus erythematosus — SLE can result in defects in complement, neutrophil, immunoglobulin, T cell, and splenic/reticuloendothelial function, and therapy for SLE (including glucocorticoids, cyclophosphamide, mycophenolate mofetil, rituximab, cyclosporine, and azathioprine) also produces immunosuppression [32,33]. Skin infections have been reported in as many as 34 percent of patients with SLE [34-36]. These infections include cellulitis, abscesses, ulcers, and necrotizing fasciitis [35,37-39].

Etiologic agents of skin infection include Staphylococcus aureus, group A Streptococcus, varicella-zoster virus, and herpes simplex virus; Escherichia coli, Candida spp, Cryptococcus spp, agents of mucormycosis, and mycobacterial species are less commonly reported. Patients with SLE also appear to be at increased risk for skin and soft tissue infections caused by S. pneumoniae [40]. (See "Clinical manifestations and diagnosis of systemic lupus erythematosus in adults", section on 'Clinical manifestations'.)

INFECTIOUS CAUSES — The following section reviews different types of pathogens and their cutaneous manifestations as well as the types of immunocompromised hosts in which they are most likely to occur. It is important to note, however, that infection with these pathogens is not limited to the groups mentioned below.

Bacterial infections

Staphylococci — Staphylococcus species, especially S. aureus, is commonly implicated as a cause of skin and soft tissue infections, presenting as cellulitis, a macular or maculopapular rash, a localized painful erythematous rash, or, less commonly, as subcutaneous abscesses or ecthyma gangrenosum-like lesions [41]. Patients with diabetes mellitus are also at increased risk for S. aureus infections manifesting as furuncles, carbuncles, and abscesses. (See "Clinical manifestations of Staphylococcus aureus infection in adults", section on 'Skin and soft tissue infection' and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Streptococci — Several streptococcal species cause skin and soft tissue infections in immunocompromised patients:

Bacteremia due to viridans group streptococci has increased in frequency in neutropenic patients and generally arises when chemotherapy damages the normal barrier of the oral mucosa [42-45]. Cutaneous manifestations include erythema, maculopapular rash(es), erythema multiforme, petechiae, and purpura; desquamation of palms and/or soles may also be observed [46,47].

Streptococcus pyogenes (group A Streptococcus) should be considered as a potential cause of skin and soft tissue infection in both immunocompetent and immunocompromised patients. Presentations range from superficial infections including cellulitis and erysipelas to deep invasive infections including necrotizing fasciitis with toxic shock syndrome.

Risk factors for invasive pneumococcal infections include alcohol abuse, HIV infection, splenectomy, connective tissue disease including systemic lupus erythematosus, glucocorticoid use, diabetes mellitus, and injection drug use [48]. In patients with splenic dysfunction, Streptococcus pneumoniae can cause cellulitis, pyomyositis, subcutaneous abscess, peripheral gangrene, and livedo reticularis/acrocyanosis. In patients with disseminated intravascular coagulation and overwhelming postsplenectomy sepsis caused by S. pneumoniae, petechial and purpuric lesions may progress to hemorrhagic bullae and peripheral gangrene known as purpura fulminans (picture 3 and picture 4). Pneumococcal cellulitis and necrotizing fasciitis have been described in patients with systemic lupus erythematosus, nephrotic syndrome, cirrhosis, diabetes mellitus, and hematologic disorders such as multiple myeloma [38,40,49].

In nonpregnant adults, risk factors for invasive disease with Streptococcus agalactiae (group B Streptococcus) include diabetes mellitus, liver disease, renal disease, and cancer, among others. Skin and soft tissue infections caused by group B Streptococcus are commonly associated with invasive disease and include cellulitis, erysipelas, infected foot ulcers, infected pressure ulcers, and necrotizing fasciitis with toxic shock-like syndrome [50,51].

Clostridium species — Bloodstream infections with Clostridium septicum, Clostridium perfringens, and Clostridium tertium can be seen in neutropenic patients with gastrointestinal, genitourinary, and hematologic malignancies. C. septicum infection in particular is associated with gastrointestinal tumors. Associated skin and soft tissue infections include abscesses, spreading cellulitis, and myonecrosis with possible associated ecchymoses and bullae formation (ie, gas gangrene). The last two entities are often associated with a rapidly progressive and fatal outcome [52,53]. Both C. septicum and C. perfringens can cause massive, rapidly progressive toxin-mediated hemolysis that is associated with mortality rates >70 percent [54,55]. Gram stain of aspirated fluid and histopathology of infected tissue will frequently reveal characteristic gram-positive "boxcar-like" rods with a dearth of polymorphonuclear leukocytes (picture 5 and picture 6). (See "Clostridial myonecrosis".)

Pseudomonas aeruginosa — Pseudomonas aeruginosa is a feared nosocomial pathogen in immunocompromised hosts and is especially common in neutropenic patients with cancer, although the incidence of bacteremia due to this pathogen has decreased in recent years in this group, concomitant with a rise in gram-positive organisms [56,57].

Cutaneous manifestations of pseudomonal bacteremia have been reported to occur in up to almost one-third of cases, particularly in neutropenic patients; lesions include abscesses, folliculitis, cellulitis, necrotizing fasciitis, vesicles, maculopapular or subcutaneous nodules, plaques, bullae, pustules, petechiae, and ecthyma gangrenosum [46,58-62]. (See "Pseudomonas aeruginosa skin and soft tissue infections".)

Initially erythematous, painless, and macular, ecthyma gangrenosum lesions evolve into areas of induration that develop into pustules and/or bullae (picture 7). Ultimately, these lesions become ulcerative with a necrotic center and hemorrhagic border (picture 8). Ecthyma lesions typically progress rapidly (within 12 to 18 hours).

Classically, ecthyma gangrenosum lesions are found in the axilla, perineum, or trunk. Once thought to be pathognomonic of P. aeruginosa bacteremia, ecthyma gangrenosum-like lesions can also be caused by gram-positive organisms such as S. pyogenes and S. aureus, other gram-negative organisms (eg, Stenotrophomonas maltophilia, Aeromonas hydrophila, Enterobacteriaceae), fungi (eg, Fusarium, Mucor, Candida, and Aspergillus spp), and herpes simplex virus (HSV) [60,63-68]. (See "Pseudomonas aeruginosa bacteremia and endocarditis", section on 'Clinical features' and "Mucormycosis (zygomycosis)", section on 'Cutaneous mucormycosis' and "Clinical manifestations and diagnosis of Fusarium infection", section on 'Cutaneous lesions' and "Clinical manifestations and diagnosis of candidemia and invasive candidiasis in adults", section on 'Clinical manifestations'.)

Of note, ecthyma gangrenosum lesions due to P. aeruginosa can develop in immunocompromised hosts in the absence of bacteremia [69,70].

Stenotrophomonas maltophilia — S. maltophilia has become a more common gram-negative nosocomial pathogen in neutropenic patients, particularly in patients with underlying hematologic malignancies. Mucocutaneous and soft tissue infections caused by this organism include primary cellulitis (often associated with catheter use), metastatic cellulitis with associated tender and firm nodules, multiple subcutaneous lesions, ecthyma gangrenosum, purpura, necrosis, and ulcers of the oral cavity [71-76]. (See "Stenotrophomonas maltophilia".)

Aeromonas hydrophila — A. hydrophila can cause extraintestinal infection including bacteremia and skin and soft tissue infections in neutropenic hosts. Although these infections may result from fresh- or saltwater exposure, nosocomial acquisition is more common. Cutaneous lesions include cellulitis (picture 9), which may be extensive, purpura, ulcers, ecchymoses, necrosis, and ecthyma gangrenosum [46]. (See "Aeromonas infections".)

Vibrio vulnificus/Vibrio parahaemolyticus — As mentioned above, patients with cirrhosis are susceptible to infections with V. vulnificus and V. parahaemolyticus, particularly after eating raw shellfish, especially oysters, or after exposure to contaminated seawater or flood waters [77-80]. Infections can present as overwhelming sepsis, frequently with associated skin lesions.

Skin lesions are usually found on the extremities, beginning as a cellulitis before developing into hemorrhagic vesicular or bullous lesions (picture 10) and ulcers; necrotizing fasciitis with associated septic shock can occur (picture 11 and picture 12) [81,82]. Similar necrotizing cutaneous lesions can be caused by Aeromonas spp and Escherichia coli [83,84]. (See "Vibrio vulnificus infection".)

Nocardiosis — Skin lesions associated with Nocardia spp in immunocompromised hosts are usually due to disseminated disease originating in the lungs; skin involvement occurs in approximately 10 to 40 percent of cases [85-90]. Often located on the extremities and trunk, these lesions are typically subcutaneous abscesses, panniculitis/cellulitis, pustules, or nodules with or without ulcerations (picture 13) [85]. Biopsy of the lesion reveals gram-positive or partially acid-fast organisms that are described as beaded, branching, and filamentous. (See "Nocardia infections: Epidemiology, clinical manifestations, and diagnosis", section on 'Skin' and "Nocardia infections: Clinical microbiology and pathogenesis", section on 'Microbiology'.)

Mycobacteria — A variety of mycobacteria can cause skin infections in immunocompromised hosts [91]. Detection of mycobacterial species from infected lesions is important for establishing the diagnosis.

Mycobacterium tuberculosis — The skin as a site of extrapulmonary tuberculosis is uncommon. The manifestations of cutaneous tuberculosis depend upon the route of infection in addition to the immune status of the host [92,93]. Although most primary tuberculosis is acquired through inhalation, exogenously acquired disease typically results from direct percutaneous inoculation. The tuberculosis chancre that results from primary inoculation of M. tuberculosis initially presents as a painless papulonodular lesion that later ulcerates. Painless localized lymphadenopathy is characteristic. Initially tuberculin skin test (TST) negative, TST positivity develops later in the disease. Tuberculosis verrucosa cutis is also a result of direct inoculation but differs from the tuberculous chancre because the host is an immunocompetent individual previously infected with tuberculosis. These patients are TST positive early in the course of disease. Initially papular, skin lesions later become verrucous plaques, and localized lymphadenopathy is typically absent.

During acute disease, skin lesions due to exogenously acquired M. tuberculosis are often described as red-brown papules, vesicles, nodules, macules, or purpura. Cutaneous manifestations of reactivated tuberculous disease include subcutaneous abscesses (picture 14), papules, and nodules (picture 15) [94]. Lupus vulgaris describes skin manifestations (plaque, hypertrophic, papulonodular, and ulcerative types) associated with hematogenous, lymphatic, or contiguous spread of M. tuberculosis (picture 16). Scrofuloderma describes a nodule that ulcerates over a contiguous focus of tuberculous disease (picture 17). The characteristic site of this cutaneous manifestation is the neck, reflecting involvement of the underlying cervical lymph nodes. (See "Cutaneous manifestations of tuberculosis".)

It is important to note that immunocompromised hosts, particularly those with depressed cell-mediated immunity, may not mount a response to the TST or the interferon-gamma release assay (IGRA), so a negative TST or IGRA should not dissuade clinicians from attempting to establish a diagnosis of tuberculosis. (See "Cutaneous manifestations of tuberculosis", section on 'Diagnostic approach' and "Cutaneous manifestations of tuberculosis", section on 'Specific tests'.)

Nontuberculous mycobacteria — Nontuberculous mycobacteria also cause skin infections. Skin lesions in the immunocompromised host often develop in the absence of traumatic injury (in contrast with immunocompetent patients).

Mycobacterium marinum is found in fresh and salt water, including fish tanks. Skin lesions include either a localized papule or nodule at the site of inoculation (with or without lymphangitis) or, when disseminated, multiple potentially ulcerated skin nodules (picture 18), which can develop a sporotrichoid-like pattern [95-97].

Mycobacterium kansasii usually causes seromas or cellulitis, although subcutaneous nodules, sporotrichoid papules, abscesses, and necrotic papulopustules have also been reported [98].

Mycobacterium haemophilum infections, primarily seen in immunocompromised patients, often involve the skin and underlying soft tissues of the extremities, including extensor surfaces of elbows and legs, likely because the organism grows best at cooler temperatures [99,100]. One review of 23 patients with M. haemophilum infections seen at one institution over 11 years revealed only skin lesions at initial presentation in over 50 percent of these patients [101]. Multiple tender, erythematous/violaceous nodules or papules are initially present before progressing to cutaneous ulcerations [99,102].

Skin infections due to rapidly growing mycobacteria (Mycobacterium fortuitum, Mycobacterium chelonae, and Mycobacterium abscessus) include cellulitis, subcutaneous nodules or abscesses (which may break down and drain) (picture 19), sporotrichoid lesions, and venous catheter-related infections [103,104]. Sternal wound infections with rapidly growing mycobacteria have been described [105].

Disseminated Mycobacterium avium complex infections can be seen in immunocompromised patients who are not infected with HIV. In a small series of these patients, 16 percent developed nodular skin lesions [106]. Erythematous papules, lupus-vulgaris-like lesions, and panniculitis have also been reported [107]. (See "Rapidly growing mycobacterial infections: Mycobacteria abscessus, chelonae, and fortuitum".)

Fungal infections — Important causes of fungal infection are broadly divided into the categories of yeasts (including Candida spp, Trichosporon spp, and Cryptococcus spp), molds (including Aspergillus spp, Fusarium spp, the agents of mucormycosis, dematiaceous fungi, and dermatophytes), and dimorphic fungi (including the endemic mycoses due to Histoplasma capsulatum, Coccidioides spp, Blastomyces dermatitidis, Paracoccidioides spp, and Talaromyces [formerly Penicillium] marneffei). Patients with neutropenia due to cancer chemotherapy are particularly susceptible to invasive fungal infections, especially those with neutropenia of greater than seven days' duration and with profound neutropenia (neutrophil count <100 cells/uL) [108]. Candida spp and Aspergillus spp account for most invasive fungal infections during neutropenia. Invasive fungal infections also occur in other types of immunocompromised hosts, including solid organ transplant recipients, hematopoietic cell transplant recipients (especially those with graft-versus-host disease), diabetics with uncontrolled hyperglycemia, patients with defects in cell-mediated immunity, patients receiving a tumor necrosis factor-alpha inhibitor (particularly associated with reactivation of endemic mycoses), and patients receiving glucocorticoids.

Candida species — Candida spp are commensal organisms of the skin, oropharynx, and gastrointestinal tract. Infections due to Candida spp that involve the skin range from superficial to invasive depending upon underlying host illnesses and comorbidities. Superficial candidal infections of the skin include intertrigo, folliculitis, and balanitis. Oral mucosal candidiasis (thrush) is common in neutropenic patients and in those with altered cellular immune function, including solid organ transplant recipients, and may progress to esophageal candidiasis. Chronic mucocutaneous candidiasis is a heterogeneous group of syndromes with common features including chronic noninvasive Candida infections of the skin, nails, and mucous membranes and associated autoimmune manifestations (most commonly endocrinopathies); it is caused by genetic faults in the immune system. (See "Overview of Candida infections", section on 'Balanitis' and "Balanitis in adults" and "Esophageal candidiasis in adults" and "Chronic mucocutaneous candidiasis" and "Intertrigo" and "Infectious folliculitis", section on 'Fungal folliculitis'.)

Disseminated candidiasis is most commonly seen in neutropenic patients. C. albicans, C. glabrata, C. tropicalis, C. krusei, C. parapsilosis, C. lusitaniae, and C. kefyr are clinically important Candida species in neutropenic patients [109], particularly those who are not receiving azole antifungal prophylaxis or who have severe oral or gastrointestinal mucositis. Skin lesions accompany invasive candidiasis in approximately 15 percent of patients, dependent on the underlying disease (severity of neutropenia) and infecting species, with C. tropicalis, C. krusei, and C. albicans causing skin lesions most frequently [95,110]. Discrete and erythematous macronodular (picture 20), pustular (picture 21), macular, plaque-like, cellulitic, or papular lesions that may develop associated hemorrhage or necrosis are often described (picture 22) [111]; ecthyma gangrenosum-like lesions and subcutaneous abscesses have also been reported [63,110]. Lesions typically involve the trunk and extremities; they may be scattered and few or numerous. Larger areas of skin involvement have also been observed overlying a muscle abscess (picture 23). Histopathology from infected tissue reveals characteristic yeast and pseudohyphae. Blood cultures may not be positive for Candida spp in these situations, so diagnosis by skin biopsy is often important. (See "Overview of Candida infections".)

Trichosporon species — Disseminated Trichosporon spp infections resemble invasive candidiasis and have associated skin manifestations in almost one-third of cases [112,113]. These lesions are typically erythematous, nontender, and maculopapular, papulonodular, purpuric, or papulopustular with or without ulceration or central necrosis; they are often found on trunk, extremities, or face [108,114]. Microscopic examination of infected tissue demonstrates hyphae and pseudohyphae, rectangular arthroconidia, and blastoconidia. (See "Infections due to Trichosporon species and Blastoschizomyces capitatus (Saprochaete capitata)".)

Cryptococcus species — Disseminated Cryptococcus infections involve the skin in approximately 10 to 20 percent of cases of Cryptococcus neoformans infection [115], and skin involvement appears to be more common in solid organ transplant recipients than in other immunocompromised hosts with defects in cell-mediated immunity. Skin involvement can also occur in patients with Cryptococcus gattii infections. Although the majority of skin lesions result from disseminated infection, primary cryptococcal skin infections by direct inoculation have also been reported [116].

The most common cutaneous findings of cryptococcal infections include crusted granulomas, often resembling molluscum contagiosum lesions (picture 24), papules, pustules, nodules, necrotic ulcers, subcutaneous swellings, abscesses, cellulitis, panniculitis, violaceous dermal plaques, ecchymoses, palpable purpura, and pyoderma gangrenosum, often involving the lower extremities (picture 25) [115,117-121]. Histopathologic examination of infected tissue for characteristic encapsulated yeast forms and isolation of the organism in culture are used for diagnosis. Cellulitis due to Cryptococcus spp may mimic bacterial cellulitis and may consequently go undiagnosed initially. An episode of cellulitis in a solid organ transplant recipient that does not respond to antibacterial therapy should be investigated for possible cryptococcosis. Necrotizing soft tissue infections, including necrotizing fasciitis and myositis, have been described in solid organ transplant recipients [122]. (See "Cryptococcus neoformans infection outside the central nervous system", section on 'Clinical manifestations' and "Cryptococcus gattii infection: Clinical features and diagnosis", section on 'Other features'.)

Aspergillus species — Cutaneous disease due to Aspergillus spp may be secondary to disseminated infection that begins after inhalation into the respiratory tract. Lesions may be nodular or initially papulopustular (often erythematous and tender) before ulcerating and developing central necrosis [123]; cellulitic, bullous, and zosteriform lesions have also been described [124,125]. Primary cutaneous infections can occur at intravenous catheter sites or underneath adhesive dressings and contaminated intravenous arm boards [126-128]. Tender, erythematous indurated plaques or bullae at the wound site often progress to a necrotic ulcer with eschar formation [129,130]. The differential diagnosis includes lesions due to Fusarium, the agents of mucormycosis, Aeromonas, and P. aeruginosa. Skin biopsies reveal septate hyphae that branch at acute angles. (See "Epidemiology and clinical manifestations of invasive aspergillosis".)

Agents of mucormycosis — Members of the Mucoraceae family (eg, Mucor, Rhizopus, and Apophysomyces spp) may cause cutaneous or rhino-orbital-cerebral disease in immunocompromised hosts (picture 1 and picture 2) [131]. Inoculation through traumatized skin or beneath nonsterile occlusive adhesive dressings can result in primary cutaneous infections that initially manifest as papulonodular lesions with erythema and induration [132]. The lesions may progress to necrosis with the formation of a black eschar and surrounding erythema (ecthyma gangrenosum-like) [133]. These lesions may be a source for hematogenous dissemination of disease.

Lesions associated with disseminated disease (usually from a primary infection in the lungs) can appear nodular, pustular, vesicular, or papular and are subcutaneous in location. Like the primary cutaneous lesions, lesions associated with disseminated infection can also ulcerate and develop an eschar. A skin biopsy reveals broad right-angle branching aseptate hyphae. (See "Mucormycosis (zygomycosis)".)

Erythematous skin lesions with or without necrosis can also be seen overlying affected areas of patients with rhino-orbital-cerebral mucormycosis.

Fusarium species — While superficial Fusarium infections commonly occur (in the form of onychomycosis or keratitis), disseminated infection is seen primarily in neutropenic patients, patients with hematologic malignancies, and/or hematopoietic cell transplant recipients with graft-versus-host disease [134]. In a review of 232 immunocompromised patients with cutaneous Fusarium infections, 88 percent of skin lesions reflected disseminated disease [135]. Elsewhere, cutaneous involvement is reported in approximately 70 percent of disseminated Fusarium infections [136,137].

Metastatic skin lesions include pustules, papules (picture 26), erythematous or necrotic macules or plaques, erythematous subcutaneous nodules, ulcers (picture 27), target lesions (picture 28), ecthyma gangrenosum-like lesions (picture 29), or, rarely, bullae (picture 30). Fusarium lesions are often tender, in contrast with those caused by Aspergillus.

Progressive soft tissue infection can also be seen by contiguous spread from a preexisting area of onychomycosis; Fusarium infection should therefore be considered in neutropenic patients presenting with toe (or, less commonly, finger) paronychia or cellulitis with associated onychomycosis (picture 31 and picture 32).

Like aspergillosis, infected tissue reveals septate hyaline hyphae that branch at acute angles. Filamentous organisms that can undergo asexual reproduction in vivo, such as Fusarium species and Scedosporium species (including Pseudoallescheria boydii), typically have higher fungal burdens and potential for positive blood cultures and frequent skin lesions in multiple stages of development [138,139]. In one study, blood cultures grew Fusarium in 41 percent of patients [140]. (See "Mycology, pathogenesis, and epidemiology of Fusarium infection" and "Clinical manifestations and diagnosis of Fusarium infection".)

Phaeohyphomycosis — Phaeohyphomycosis refers to infection caused by dematiaceous (pigmented) molds. Most infections due to these fungi are noninvasive and superficial. However, invasive complications of Alternaria and Exophiala species-associated infections involving the skin and subcutaneous tissues have been described in immunocompromised hosts [141,142]. Most commonly located on the upper and lower extremities, lesions can be multiple or solitary and include abscesses, plaques, papules, pustules, cellulitis, ulcers, and nodules [143].

Endemic fungi — Systemic fungal infections can be caused by soil-colonizing fungi that are prevalent in certain areas of the United States and Canada, including B. dermatitidis (south-central, north central, Manitoba and Northwest Ontario, and along the St. Lawrence Seaway), Coccidioides species (southwest), and H. capsulatum (Ohio and Mississippi River valleys, southern Ontario, St. Lawrence River valley, and focal areas on the East Coast). Skin lesions, seen in 40 to 80 percent of patients with extrapulmonary disease, are usually due to disseminated infection [144].

B. dermatitidis-associated skin lesions are most commonly ulcerative, pustular, or verrucous; other manifestations include plaques and subcutaneous nodules (picture 33 and picture 34) [145-147]. Biopsies of these lesions reveal broad-based budding yeast.

Disseminated Coccidioides infections can result in verrucous or granulomatous papules, nodules, or plaques; cold subcutaneous abscesses, ulcers, and pustules may also develop [148-151]. Microscopic examination of biopsies from skin lesions demonstrates characteristic spherules.

In patients with histoplasmosis, oropharyngeal lesions are more common than skin lesions (picture 35). Oral lesions are also common in patients with paracoccidioidomycosis and are seen less commonly in those with blastomycosis. (See "Pathogenesis and clinical manifestations of disseminated histoplasmosis", section on 'Skin involvement' and "Clinical manifestations and diagnosis of blastomycosis", section on 'Other sites' and "Clinical manifestations and diagnosis of chronic paracoccidioidomycosis", section on 'Mucosa'.)

The skin lesions of disseminated histoplasmosis may take a wide variety of forms including hyperpigmented painless macules, papules (picture 36), nodules with or without ulceration, pustules, plaques, purpuric lesions, and vasculitic lesions [152-155]. Necrotizing vasculitis mimicking pyoderma gangrenosum and granulomatous panniculitis mimicking erythema nodosum have been described [156,157]. The histopathology of infected skin includes granulomatous inflammation and small budding yeast forms within macrophages. Primary cutaneous histoplasmosis has also been reported [158], although it is much less common than disseminated histoplasmosis with cutaneous manifestations.

Paracoccidioidomycosis occurs in parts of Central and South America and may be associated with skin lesions, including ulcers, papules, and verrucous lesions (picture 37 and picture 38) [159,160]. In acute/subacute (juvenile) paracoccidioidomycosis, superficial lymph node involvement is most common in the cervical, axillary, and inguinal regions, and draining fistulae may develop (picture 39).

T. marneffei is endemic in Southeast Asia, southern China, Taiwan, Hong Kong, and northeastern India and can cause disseminated disease including skin involvement in patients with impaired cell-mediated immunity [161]. The classic skin lesion is a papule that then takes on an umbilicated appearance resembling molluscum contagiosum. Of note, one retrospective cohort study showed that patients with non-HIV-associated T. marneffei infection were less likely than HIV-infected patients to have umbilicated papules but more likely to have acute febrile neutrophilic dermatosis (ie, Sweet syndrome) [162]. (See "Epidemiology and clinical manifestations of Talaromyces (Penicillium) marneffei infection", section on 'Signs and symptoms'.)

Emergomyces (previously Emmonsia) species are more recently reported endemic fungi from Asia, Africa, North America, and Europe that can cause disseminated disease primarily in patients with impaired cell-mediated immunity [163,164]. Disseminated disease frequently manifests cutaneously as pustules, papules, subcutaneous nodules, plaques, and ulcers [165,166].

Viruses

Herpes simplex virus and varicella-zoster virus — Patients with cell-mediated immune dysfunction are at increased risk for reactivation of HSV and varicella-zoster virus (VZV) infections [41], which may be either localized or disseminated. Mucous membrane involvement in the form of oropharyngeal ulcerations is a common manifestation of HSV reactivation. Skin lesions due to HSV in immunocompromised hosts are more likely to be chronic, nonhealing, and extensive; extracutaneous dissemination can occur. Painful vesicular lesions may become ulcerative, hemorrhagic, and necrotic and, in the case of VZV, develop in multiple dermatomes (picture 40 and picture 41 and picture 42). In hematopoietic cell transplant recipients, in particular, VZV lesions may be nonvesicular and atypical in appearance (macules, papules, plaques), leading to delays in diagnosis. VZV without rash can also occur, with characteristic hyperesthesia, paresthesias, or neuropathic pain in a dermatomal distribution without visible lesions. Differentiation of HSV and VZV based upon culture, nucleic acid amplification testing, or direct fluorescent antibody staining is helpful in dictating the antiviral therapy dosing as VZV infection requires higher doses than HSV. (See "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection" and "Epidemiology, clinical manifestations, and diagnosis of herpes zoster".)

Hepatitis B virus — Hepatitis B virus (HBV) reactivation can occur in solid organ transplant recipients, hematopoietic cell transplant recipients, and patients receiving glucocorticoids or other immunosuppressive therapies such as tumor necrosis factor-alpha inhibitors. Extrahepatic complications of chronic hepatitis B infection include polyarteritis nodosa (PAN) and mixed cryoglobulinemia. Cutaneous manifestations of PAN include palpable purpura, erythematous nodules, ulcers, and livedo reticularis [167]. Mixed cryoglobulinemia can be associated with palpable purpura and ulcers [168]. (See "Tumor necrosis factor-alpha inhibitors: Bacterial, viral, and fungal infections", section on 'Hepatitis B' and "Hepatitis B virus: Clinical manifestations and natural history", section on 'Extrahepatic manifestations'.)

Other viruses — Other viruses that can cause skin manifestations in immunocompromised hosts include cytomegalovirus (ulcerations, nodules, maculopapular rash, vesicles), molluscum contagiosum (umbilicated papules/vesicles), human papillomavirus (verrucous lesions), Epstein-Barr virus (in the form of posttransplant lymphoproliferative disease), hepatitis C virus (leukocytoclastic vasculitis/essential mixed cryoglobulinemia, porphyria cutanea tarda, lichen planus, necrolytic acral erythema), and human herpes virus (HHV-) 8 (in the form of Kaposi sarcoma). (See "Molluscum contagiosum" and "Epidemiology, clinical manifestations, and diagnosis of post-transplant lymphoproliferative disorders" and "Classic Kaposi sarcoma: Clinical features, staging, diagnosis, and treatment".)

Viruses that can cause acute fever and rash in any host, including immunocompromised hosts, include HHV-6 and HHV-7 (roseola), measles, rubella, parvovirus, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; coronavirus disease 2019 [COVID-19]). Additional viruses that can cause fever and rash in any host and that are associated with specific geographic regions include dengue, chikungunya, Zika virus, Ebola virus, and other causes of hemorrhagic fever. (See "Clinical manifestations, diagnosis, and treatment of human herpesvirus 6 infection in adults" and "Human herpesvirus 6 infection in hematopoietic cell transplant recipients" and "Measles: Clinical manifestations, diagnosis, treatment, and prevention" and "Clinical manifestations and diagnosis of parvovirus B19 infection" and "Dengue virus infection: Clinical manifestations and diagnosis" and "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis" and "Clinical manifestations and diagnosis of Ebola virus disease" and "Diseases potentially acquired by travel to Central Africa", section on 'Other viral hemorrhagic fevers' and "Zika virus infection: An overview".)

It is important to obtain a travel history from patients presenting with fever and rash. (See "Approach to illness associated with travel to East Asia" and "Approach to illness associated with travel to Southeast Asia" and "Approach to illness associated with travel to Latin America and the Caribbean" and "Approach to illness associated with travel to South Asia" and "Approach to illness associated with travel to West Africa" and "Diseases potentially acquired by travel to Southern Africa" and "Diseases potentially acquired by travel to East Africa" and "Diseases potentially acquired by travel to Central Africa" and "Diseases potentially acquired by travel to North Africa".)

Human papillomavirus infections are common in transplant recipients, leading to increased risk for skin, cervical, and anal cancers. Many long-term survivors after solid organ transplantation often have many verruciform lesions and must undergo careful surveillance for skin cancer development. However, these infections are slowly progressive and are not generally seen as a cause of fever and rash. (See "Human papillomavirus infections: Epidemiology and disease associations".)

NONINFECTIOUS CAUSES — Important noninfectious causes of fever and rash in immunocompromised hosts include the following:

Drug eruptions – Diffuse maculopapular drug rashes are particularly common in patients with protracted neutropenia who require long-term antibiotic therapy for neutropenic fever. These are often attributed to chemotherapy (especially cytarabine), beta-lactam antibiotics, vancomycin, and other agents, although it is often difficult to identify a cause in the setting of multiple concomitant therapies. (See "Drug eruptions".)

Skin lesions accompanied by fever (often relatively high fever) are also features of severe drug reactions, specifically drug reaction with eosinophilia and systemic symptoms (DRESS), Stevens Johnson syndrome, and toxic epidermal necrolysis. These rare reactions typically develop one to three weeks after the initiation of the culprit agent. (See "Drug reaction with eosinophilia and systemic symptoms (DRESS)" and "Stevens-Johnson syndrome and toxic epidermal necrolysis: Pathogenesis, clinical manifestations, and diagnosis".)

Graft-versus-host disease. (See "Clinical manifestations, diagnosis, and grading of acute graft-versus-host disease", section on 'Skin'.)

Sweet syndrome. (See "Sweet syndrome (acute febrile neutrophilic dermatosis): Pathogenesis, clinical manifestations, and diagnosis".)

Vasculitis. (See "Evaluation of adults with cutaneous lesions of vasculitis" and "Overview of cutaneous small vessel vasculitis".)

Leukemia cutis. (See "Clinical manifestations, pathologic features, and diagnosis of acute myeloid leukemia", section on 'Skin'.)

Cutaneous lymphoma. (See "Approach to the patient with a diagnosis of atypical lymphocytic infiltrate of the skin" and "Primary cutaneous large B cell lymphoma, leg type" and "Primary cutaneous follicle center lymphoma" and "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides" and "Primary cutaneous marginal zone lymphoma".)

Pyoderma gangrenosum. (See "Pyoderma gangrenosum: Pathogenesis, clinical features, and diagnosis".)

Engraftment syndrome following hematopoietic cell transplantation – Skin rash, fever, and sometimes organ dysfunction and a capillary leak syndrome can be seen in engraftment syndrome after autologous stem cell transplantation or, less commonly, after allogeneic hematopoietic cell transplantation. (See "Pulmonary complications after autologous hematopoietic cell transplantation", section on 'Engraftment syndrome and PERDS' and "Pulmonary complications after allogeneic hematopoietic cell transplantation: Causes", section on 'Engraftment syndrome'.)

SUMMARY

Types of immunocompromise − Immunocompromising diseases can cause multiple defects in host defenses, which, in turn, lead to heightened susceptibility to various types of infections. Knowledge of these immune defects and the specific associated infections can assist the clinician in the initial evaluation and management of the immunocompromised patient with skin lesions. These lesions sometimes reflect disseminated infection; evaluation of the skin may provide the most rapid diagnosis and thus may be lifesaving. (See 'Introduction' above and 'Types of immunocompromise' above.)

Bacterial infections

Pseudomonas aeruginosa is a feared nosocomial pathogen in immunocompromised hosts, particularly in those who are neutropenic. Cutaneous manifestations of pseudomonal bacteremia reportedly occur in almost one-third of cases; lesions in immunocompromised hosts include abscesses, folliculitis, cellulitis, vesicles, maculopapular or subcutaneous nodules, plaques, bullae, pustules, petechiae, and ecthyma gangrenosum. (See 'Pseudomonas aeruginosa' above.)

Other bacterial species that can cause rash and fever in neutropenic patients include Stenotrophomonas maltophilia, Aeromonas hydrophila, Streptococcus viridans, and clostridial species as well as Nocardia spp and mycobacteria. (See 'Bacterial infections' above.)

Fungal infections

Important causes of fungal infection are broadly divided into the categories of yeasts (including Candida spp, Cryptococcus spp, Trichosporon spp), molds (including Aspergillus spp, Fusarium spp, the agents of mucormycosis, dematiaceous fungi, and dermatophytes), and dimorphic fungi (including the endemic mycoses due to Histoplasma capsulatum, Coccidioides spp, Blastomyces dermatitidis, Paracoccidioides spp, and Talaromyces marneffei). (See 'Fungal infections' above.)

Patients with neutropenia due to cancer chemotherapy are particularly susceptible to invasive fungal infections, especially those with neutropenia of greater than seven days' duration and with profound neutropenia (neutrophil count <100 cells/uL). Candida spp and Aspergillus spp account for most invasive fungal infections during neutropenia. (See 'Candida species' above and 'Aspergillus species' above.)

Viral infections

Common viral causes of fever and rash include herpes simplex virus and varicella-zoster virus. (See 'Herpes simplex virus and varicella-zoster virus' above.)

Other viruses that can cause skin manifestations in immunocompromised hosts include hepatitis B virus, cytomegalovirus (ulcerations, nodules, maculopapular rash, vesicles), molluscum contagiosum (umbilicated papules/vesicles), human papillomavirus (verrucous lesions), Epstein-Barr virus (in the form of posttransplant lymphoproliferative disease), and human herpesvirus (HHV-) 8 (in the form of Kaposi sarcoma). (See 'Hepatitis B virus' above and 'Other viruses' above.)

Viruses that can cause acute fever and rash in any host, including immunocompromised hosts, include HHV-6 and HHV-7 (roseola), measles, rubella, and parvovirus. (See 'Other viruses' above.)

Additional viruses that can cause fever and rash in any host and that are associated with specific geographic regions include dengue, chikungunya, Zika virus, Ebola virus, and other causes of hemorrhagic fever. (See 'Other viruses' above.)

Noninfectious causes − Important noninfectious causes of fever and rash in immunocompromised hosts include drug eruptions, graft-versus-host disease, Sweet syndrome, vasculitis, leukemia cutis, cutaneous lymphoma, pyoderma gangrenosum, and engraftment syndrome following hematopoietic cell transplantation. (See 'Noninfectious causes' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Kieren A Marr, MD, who contributed to an earlier version of this topic review.

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Topic 1409 Version 29.0

References

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