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W1979894908 abstract "After completing this article, readers should be able to: The term “dimorphic fungus” refers to a fungus that assumes one of two different physical forms, as dictated by environmental influences such as temperature and humidity. In the environment, and when grown in culture at ambient temperatures, these mold forms (also known as “saprobic,” “saprophytic,” and “mycelial” forms) consist of long hyphae, which are difficult to distinguish macroscopically from other molds. The saprophytic forms have microscopic aerosolizable elements, which not only lead to wide environmental distribution but also are infectious on inhalation. Following infection in humans, or when grown in culture at 37.0°C, the organisms appear as individual round “yeast” forms. These fungal elements are not contagious but will grow into either the yeast or mold form, depending on the incubation temperature.Histoplasmosis, coccidioidomycosis, blastomycosis, sporotrichosis, penicilliosis, and paracoccidioidomycosis all are infections caused by dimorphic fungi (Table). Histoplasmosis and coccidioidomycosis are relatively well known in North America; blastomycosis and sporotrichosis cause sporadic infections in North America and throughout the rest of the world. Prior to the human immunodeficiency virus (HIV) epidemic, only 29 cases of infection due to Penicillium marneffei were reported in the medical literature. Penicilliosis is now a relatively common acquired immune deficiency syndrome (AIDS)-related opportunistic infection in Southeast Asia. Paracoccidioides immitis causes cutaneous and osteoarticular infections, primarily in South America. Most pediatric clinicians in North America are unlikely to encounter penicilliosis or paracoccidioidomycosis, although a familiarity with histoplasmosis, coccidioidomycosis, blastomycosis, and sporotrichosis is important because of the geographic distribution of the pathogens and the outdoor activities of many pediatric patients.Although the epidemiologic and clinical features of each species are unique, some characteristics are shared among the dimorphic fungi. Because the mold forms contain infectious particles, the laboratory must be notified if such infections are suspected. The gold standard for diagnosis is culture, but serologic or antigen detection methods may be available. Selective fungal media can be incubated for many weeks without significant bacterial overgrowth. A dimorphic fungus may be suspected based on the microscopic appearance of the saprophytic phase and is confirmed by the microscopic appearance of the typical yeast forms when grown at higher temperatures. Because the sensitivity of fungal culture varies, a presumptive diagnosis often can be made based on cytopathologic examination of affected tissue. The presence of noncaseating granulomas suggests, among other disorders, the presence of a fungal infection. Although yeast forms may be seen with standard staining, fungal stains, such as Gomori-methenamine silver, can highlight the organisms in tissue dramatically.Cell-mediated immunity is vital to control fungal infections, as demonstrated by the increased risk of dissemination in people living with HIV/AIDS, patients receiving chemotherapy for malignancies, or recipients of tumor necrosis factor-neutralizing monoclonal antibodies. Pregnancy is associated with depressed cell-mediated immunity and, therefore, presents a higher risk of severe infection. The duration of treatment often is dictated by the status of the patient's immunity.The treatment of the dimorphic fungi has many parallels. Amphotericin-based compounds remain the treatment of choice for severe infections and for pregnant women, in whom azole therapy is contraindicated due to teratogenicity. Several formulations of amphotericin are available for children. Amphotericin B-deoxycholate (AB-D) has been used for decades and is associated with higher rates of renal toxicity and adverse infusion-related events than the newer formulations. AB-D, however, is the drug of choice for fungal infections of the urinary tract. Amphotericin B lipid complex (AB-LC), amphotericin B liposomal, and amphotericin B colloidal dispersion are used widely in place of AB-D, primarily due to intolerance of AB-D or the risk of renal toxicity. Few pharmacokinetic data exist to suggest the superiority of one lipid formulation over another, although AB-LC most often is used for central nervous system (CNS) infection due to a small body of literature supporting superior CNS penetration. AB-D generally is administered intravenously at a dose of 0.6 to 1.0 mg/kg per day daily, and the lipid formulation doses are 3 to 5 mg/kg per day or higher.Generally, the dimorphic fungi are susceptible to itraconazole and variably susceptible to fluconazole. Recent data suggest that voriconazole, as well as the most recent addition to the azole family, posaconazole, are highly active against dimorphic fungi. Oral route of administration, tolerability, and excellent tissue penetration are favorable aspects of azole therapy, particularly for mild-to-moderate infections. Combination antifungal therapy occasionally is used for severe fungal infections, although no definitive data exist to confirm the superiority of such regimens.First described in Argentina in 1892 by Dr Alejandro Posadas, coccidioidomycosis now is recognized as a significant health problem for those who live in or travel to endemic regions. The Coccidioides genus is subdivided into two distinct strains, referred to as C immitis and C posadassi, although a distinction between the two is clinically irrelevant.The saprophytic phase of Coccidioides is found in the soil of regions that have hot and dry summers, few winter freezes, and low annual rainfall. Single-cell spores known as arthroconidia are aerosolized by wind or soil disruption. Once inhaled, or rarely percutaneously implanted, arthroconidia enter the parasitic phase, where they enlarge to a spherule and produce hundreds of endospores (Fig. 1). The spherule ruptures, releasing endospores into nearby tissue. Each endospore is capable of producing another spherule.Coccidioides are endemic to the southwestern United States, particularly southern Arizona, and central California (Fig. 2) as well as parts of Mexico and Central and South America. The risk of exposure is increased by severe wind and dust storms, earthquakes, construction, and wildfires. The incidence of coccidioidomycosis varies by geographic location. In highly endemic areas, the incidence of infection may be as high as 91 cases per 100,000 population, although this figure probably is an underestimation of total infections, given the high rate of asymptomatic or mildly symptomatic illnesses.Person-to-person transmission of coccidioidomycosis does not occur, and infected individuals do not require isolation. Coccidioides, however, may grow on fomites, such as bandages or under plaster casts. Perinatal transmission of coccidioidomycosis occurs rarely.Sixty percent of infected individuals are asymptomatic. The remaining 40% of individuals present with symptoms ranging from a self-limited flulike illness to a life-threatening disseminated infection. Risk factors for severe disease include young and old age, immunosuppression, pregnancy, and Filipino or African descent.Clinically apparent infections typically present as a process known as “valley fever.” Cough, fever, and chest pain occur 1 to 3 weeks after inhalation of arthroconidia. Systemic symptoms commonly include headache, sore throat, arthralgias, and fatigue. In most cases, valley fever is a self-limited illness lasting 2 to 3 weeks, although fatigue can last for several months. Radiographic abnormalities include a unilateral infiltrate, hilar adenopathy, or pleural effusion. Approximately 5% of individuals who contract valley fever have pulmonary sequelae, including pulmonary nodules, cavities, or chronic fibrocavitary pneumonia, although these complications are uncommon in children. A diffuse reticulonodular pneumonia may develop in immunocompromised individuals or in otherwise healthy individuals exposed to a large inoculum.Night sweats, fever, and cough are present in most of the 1% of infected individuals who develop disseminated disease. Involvement of the skin, lymph nodes, osteoarticular structures, or meninges is evidence of dissemination. Although papules, plaques, and pustules imply dissemination, erythema nodosum or erythema multiforme represent the host response to infection. Radionuclide bone scans generally are performed in cases of disseminated coccidioidomycosis (particularly in young children) to identify occult osteoarticular foci, which often require surgical drainage.CNS infection is the most serious manifestation of disseminated coccidioidomycosis and is almost universally fatal, if untreated. The classic history of coccidioidal meningitis is a gradual onset of headache, vomiting, lethargy, fever, and altered mental status occurring weeks to months after a febrile respiratory illness. Lumbar puncture should be performed on all individuals showing signs of meningeal irritation and should be considered for all those who have disseminated disease. Lymphocytic pleocytosis, elevated protein concentrations, and low glucose values are classic cerebrospinal fluid (CSF) findings. Hydrocephalus occurs in 30% to 50% of cases of coccidioidal meningitis and generally requires CSF shunting. Abscess, hemorrhage, and infarction are other complications of CNS involvement. Intracranial involvement has been described in infants as young as 4 months of age.Serology is the method used most commonly to diagnose coccidioidomycosis. Although false-positive results occur rarely, antibodies disappear within months of a resolved infection, making any positive test result significant. A negative test result must be interpreted with caution because serologic results are insensitive during the initial weeks of infection and can remain negative indefinitely in immunocompromised hosts. Immunoglobulin M (IgM) antibodies generally are present within 3 weeks of the onset of symptoms. The complement fixation (CF) IgG is considered the most reliable method for serologic detection and can be “trended” to measure the success of therapy. CF is a complex test and should be ordered from laboratories experienced in the procedure. Although some laboratory variation may occur, disseminated disease generally is considered to be present with titers in the range of 1:16 or greater. The “coccidioidin” skin testing is not useful clinically. Although growth of Coccidioides from any site is diagnostic, the sensitivity of culture is low.The decision to treat coccidioidomycosis is based on risk factors for severe disease, the severity of pulmonary infection, and the presence or absence of dissemination. Guidelines are available at the Infectious Diseases Society of America (IDSA) web site (http://www.idsociety.org). For mild pulmonary illnesses that generally self-resolve, no strong data support treatment. Some experts recommend treating all cases of pulmonary coccidioidomycosis, particularly those patients at high risk of dissemination.Azoles have replaced amphotericin-based compounds as the first line of treatment of coccidioidomycosis. In most cases of meningitis, fluconazole is the treatment of choice due to its excellent CNS penetration. Amphotericin-based regimens are preferred for immunocompromised and critically ill hosts as well as for those who have diffuse pulmonary disease and rapidly progressive infections.The duration of therapy for pulmonary coccidioidomycosis ranges from 3 to 6 months. In disseminated infections, a minimum of 1 year of therapy is recommended. Lifetime suppressive therapy may be required to prevent relapses in immunocompromised patients and is standard for patients who have meningitis. Rising or unchanging CF titers while the patient is receiving therapy indicate treatment failure, most often due to noncompliance, or an occult focus that might require surgical drainage.Histoplasmosis, first described in Panama in 1905, is caused by Histoplasma capsulatum variety capsulatum and Histoplasma capsulatum variety duboisii. The most common cause of endemic mycosis in the United States and throughout the world is H capsulatum var capsulatum. H capsulatum var duboisii exists only in Africa. As the name “capsulatum” implies, the saprophytic form of the organism has round macroconidia that appear to be encapsulated, although this is not a true capsule. The infectious particles are aerosolizable elements called microconidia (Fig. 3). Histoplasma grow well in warm, moist environments. Certain soil compositions, including high nitrogen content, high carbon content, and lower pH, have been shown to enhance growth of the organism. Caves and buildings containing bird and bat guano classically have been associated with the presence of H capsulatum. Although birds are not infected by the fungus, bats and other mammals can be infected. As with coccidioidomycosis, infection occurs following inhalation of microconidia. A specific exposure usually cannot be identified, but certain activities, such as spelunking, increase the risk of inhalation of microconidia. Construction that causes soil agitation has been associated with large outbreaks. Human-to-human transmission does not occur.In North America, H capsulatum var capsulatum is distributed throughout the central United States, particularly in the Mississippi and Ohio river valleys. Exposure studies that tested for cutaneous sensitivity to H capsulatum antigen (akin to a purified protein derivative test for tuberculosis) demonstrated low endemicity in the southern and southwestern United States (Fig. 4).Ninety-five percent of infected individuals are asymptomatic. Approximately 60% to 90% of those who are symptomatic manifest acute pulmonary symptoms, which are nearly impossible to distinguish from bacterial and viral lower respiratory tract infections. Although symptoms often last only a few days, the prolonged duration and greater severity of fever, malaise, and fatigue that can accompany and follow the pulmonary symptoms may lead to a suspicion of histoplasmosis. High-risk exposures, clusters of acute lower respiratory tract infections, or prolonged respiratory symptoms also can lead clinicians to test for acute histoplasmosis. Other pulmonary or parapneumonic manifestations of H capsulatum include chronic cavitary disease, mediastinal lymphadenopathy or granulomas, pleural effusions, and broncholithiasis.Bloodborne dissemination is common during acute histoplasmosis, but host immunity generally controls the infection. Dissemination can lead to infection of virtually any organ, which is highlighted by reports of cutaneous lesions, osteoarticular infections, endocarditis, interstitial nephritis, parotitis, and Histoplasma meningitis or cerebritis. Gastrointestinal involvement mimicking Crohn disease has been described. Immune dysfunction causing an inability to control the organism during dissemination leads to a syndrome termed “progressive disseminated histoplasmosis” (PDH). PDH generally manifests with undifferentiated fever, weight loss, organomegaly, and hematologic abnormalities. Although children most often are diagnosed with uncomplicated acute pulmonary histoplasmosis, PDH is well described in infants and immunocompromised children. A single case of congenital infection with H capsulatum var capsulatum has been reported.Infections with H capsulatum can be associated with postinfectious sequelae, such as pericarditis, mediastinal fibrosis, and articular inflammation, which are presumed to be immune-mediated. Pericarditis may be present in as many as 10% of children who have histoplasmosis and can be severe enough to cause pericardial tamponade.The organism may take up to 6 weeks to identify, but isolation of H capsulatum from sputum or any normally sterile site is considered definitive proof of infection. The sensitivity of culture varies based on the site of infection and host risk factors. Although sputum culture may be positive in only 10% of cases of acute pulmonary histoplasmosis, the sensitivity rises to 60% among those who have cavitary histoplasmosis and 90% in bronchoalveolar lavage specimens from AIDS patients who have pulmonary histoplasmosis. Histopathology is a valuable diagnostic tool for histoplasmosis, often demonstrating noncaseating granulomas. The parasitic yeast form can be found wherever invasion occurs (Fig. 5). In disseminated disease, it occasionally is visible on routine blood smears, such as those performed for a complete blood count (Fig. 6).One of the methods used most commonly to diagnose histoplasmosis is the Histoplasma urine antigen test. With a sensitivity of 95% in disseminated infections, detection of antigenuria can be a valuable diagnostic tool, although the urine antigen test is positive in only 10% to 40% of patients who have acute pulmonary disease. Serologic tests to detect antibodies directed against H capsulatum are available commercially, but cross-reactivity with other dimorphic fungi, false-positive and -negative results, and testing in areas of high endemicity all must be considered when interpreting the results. Although 10% of people living in an endemic area have positive CF test results, high titers are associated with more severe disease and, in combination with immunodiffusion, can be a valuable tool in discerning active versus previous infection. Skin testing, used for research and epidemiologic studies, is neither available nor clinically useful because positive reactions may represent prior infection, and negative results in acute and disseminated disease are common.The IDSA has published guidelines for the treatment of histoplasmosis (www.idsociety.org). Acute pulmonary histoplasmosis in immunocompetent individuals generally does not require treatment, although treatment may be considered for severe or prolonged disease. The route of medication delivery and the drug of choice vary by severity of infection. In general, itraconazole is the preferred oral antifungal; amphotericin-based regimens are recommended for more serious infections such as disseminated histoplasmosis and for infections during pregnancy, in which itraconazole is contraindicated. Long-term treatment or even lifelong suppression may be considered for persons who have immunocompromising conditions.Nonsteroidal anti-inflammatory and, occasionally, corticosteroid medications are administered for postinfectious complications such as mediastinal fibrosis and pericarditis. Itraconazole may be considered for treating postinfectious complications, although the benefit of antifungal therapy in such circumstances has been questioned.In 1904, B.R. Schenck first described the dimorphic fungus, which later became his namesake. Sporothrix schenckii has a worldwide distribution, although most cases have been reported from South America and, to a lesser extent, North America. Many clinicians recall this organism as the causative agent of “rose-gardener disease,” an apt description because of its association with infection at sites of trauma contaminated with soil. S schenckii has been described as a cause of occupational outbreaks, including outbreaks due to contaminated timber and sphagnum moss. Several recent reports highlight the high prevalence in South America, particularly in children. In one series of 238 cases of cutaneous sporotrichosis in Peru, 60% of the patients were younger than 15 years of age. Contact with cats that have cutaneous disease caused by sporotrichosis is a well-described risk factor for infection in humans. Scratches from other digging animals, such as armadillos, also have been associated with disease in humans. Inhalation of conidia leading to primary pulmonary disease rarely occurs.The most common manifestation of sporotrichosis is a subacute or chronic skin ulcer, particularly on the face or extremities. Cutaneous lesions often are associated with lymphangitis and regional lymphadenopathy (Fig. 7). Disseminated disease, osteoarticular infections, pulmonary infections, and meningeal infections have been reported. As with the other dimorphic fungi, more severe disease is associated with deficits of cell-mediated immunity. Although pathogens such as Staphylococcus aureus and Streptococcus pyogenes tend to cause more rapidly progressive skin and soft-tissue infections, it is difficult to differentiate S schenckii from other indolent infections, such as those caused by Nocardia, Leishmania, and nontuberculous mycobacteria.No serologic tests are available clinically to aid in the diagnosis of sporotrichosis. Material from cutaneous lesions may be aspirated or scraped and sent for fungal culture. Growth of the mold occurs between 1 and 4 weeks. Pathologic examination of biopsy specimens can reveal granulomatous inflammation in the presence of the cigar-shaped yeast. The diagnosis of visceral and CNS infections often is delayed due to the reliance on culture or histopathology.All cutaneous lesions should be treated because spontaneous resolution is rare. The mainstay of therapy for adults and children is oral itraconazole. Terbinafine can be used as an alternative to itraconazole, although fluconazole generally is not recommended due to an overall poor efficacy compared with other antifungal agents. Saturated solution of potassium iodide (SSKI) has been used for more than a century and is effective, although adverse effects such as gustatory changes, gastrointestinal intolerance, and rashes may lead to cessation of therapy. Treatment of cutaneous disease is continued for 2 to 4 weeks after resolution of the lesion. Although uncomplicated pulmonary or osteoarticular infections can be treated initially with itraconazole, serious invasive infections such as meningeal, disseminated, or extensive osteoarticular disease are treated initially with amphotericin B, followed by oral itraconazole for maintenance therapy. Lifelong suppression may be required if the patient is immunocompromised.Treatment of pregnant women presents a unique challenge because the azole class is teratogenic and SSKI is toxic to the fetal thyroid. If treatment during pregnancy is deemed necessary, amphotericin B generally is used. Local hyperthermia (daily exposure of the lesion to temperatures from 42.0° to 43.0°C for many weeks) has been reported to be effective for treating cutaneous lesions and may be an option for pregnant women or other patients in whom oral treatment is contraindicated or not tolerated.Children who have cutaneous lesions may be given itraconazole. One drop of SSK1 three times daily with an escalation up to 1 drop/kg (maximum 40 to 50 drops) three times daily is an alternative, but gastrointestinal adverse effects limit the usefulness of this regimen in children.Blastomycosis, occasionally referred to as “Gilchrist disease” after its discovery by Dr Thomas Casper Gilchrist in 1894, is an unusual infection in children. Like H capsulatum, B dermatitidis generally is transmitted via inhalation of conidia and is endemic to the Ohio and Mississippi river valleys, with cases occurring from Canada to the southern United States. Sporadic cases also have been reported from India, Africa, and the Middle East. The mycelial phase of B dermatitidis grows in warm moist soil with high organic content, although such growth is short-lived because the organism rarely is identified in the environment in conjunction with an outbreak. Blastomycosis in nonhuman mammals has been described. Blastomycosis in a pet, particularly a dog, raises the possibility of a common exposure in the owner.Pulmonary infection is the most common manifestation of blastomycosis, with as many as 50% of infections being asymptomatic. With nonspecific findings such as fever, cough, malaise, and pulmonary infiltrates, patients initially may be diagnosed with community-acquired pneumonia. The frequency of spontaneous resolution of acute pulmonary blastomycosis is unknown, and many patients eventually seek care for a combination of chronic pulmonary and systemic symptoms, which may mimic tuberculosis. In addition, radiographs reveal a mass in up to one third of patients, often leading to a presumptive diagnosis of malignancy. Occasionally, diffuse pulmonary infiltrates with acute respiratory distress syndrome occur and are associated with a poor prognosis.Extrapulmonary disease occurs in at least 50% of patients who seek care, often seen concomitantly with pulmonary symptoms. As the name B dermatitidis implies, the skin commonly is affected. Lesions are verrucous or ulcerative and originate from disseminated disease, although accidental inoculation in the laboratory has been reported to cause primary cutaneous blastomycosis. Osteoarticular disease (especially vertebral), genitourinary disease (especially prostate), and CNS disease all have been described. Children infrequently are diagnosed with blastomycosis, but it is unknown if this situation signifies fewer infections or a higher rate of undiagnosed infections than adult counterparts. Congenital blastomycosis in infants of acutely infected women is exceedingly rare.Serologic diagnosis of blastomycosis is problematic because of antigenic cross-reactivity with other fungi as well as the lack of sensitivity of current assays. Sputum may be submitted for microscopy in patients who have pulmonary symptoms. Identification of the organism in culture or by microscopic examination of tissue specimens is the most common method for diagnosis. Although the mycelial form is nonspecific, the single broad-based bud and highly refractile cell wall of the yeast make microscopic diagnosis of B dermatitidis relatively easy.Acute pulmonary infections may resolve without treatment, but the high rates of extrapulmonary disease following a primary pulmonary infection lead many experts to recommend treatment for all cases of blastomycosis. All patients who have persistent or progressive pulmonary disease, all who have extrapulmonary disease, and all immunocompromised patients should be treated. Amphotericin-based therapy is preferred for severe and life-threatening infections as well as for infections occurring during pregnancy. Treatments for children are not well established, although children whose disease is severe should be treated with an amphotericin-based compound. Oral itraconazole may be considered for treating mild infections in children and adults." @default.
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W1979894908 title "North American Dimorphic Fungal Infections in Children" @default.
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