Infectious Diseases: Mycotic

Fungal infections have assumed an increasingly important role as use of broad-spectrum antimicrobial agents has increased and the number of immunodeficient patients has risen. Some pathogens (eg, Crypto-coccus, Candida, Fusarium) virtually never cause serious disease in normal hosts. Other endemic fungi (eg, Histoplasma, Coccidioides, Paracoccidioides) commonly cause disease in normal hosts but tend to be more aggressive in immunocompromised ones.

The major fungal diseases are discussed in this chapter.


Essentials of Diagnosis

General Considerations

Candida albicans can be cultured from the mouth, vagina, and feces of most people. Oral and cutaneous lesions are discussed in other chapters. The risk factors for invasive candidiasis include cellular immunodefi-ciency, prolonged neutropenia, diabetes mellitus, broad-spectrum antibiotic therapy, the presence of intravascular catheters (especially when providing total parenteral nutrition), and intravenous drug use. When no other underlying cause is found, persistent oral candidiasis should arouse a suspicion of HIV infection; over the course of their disease, AIDS patients will almost without exception have candidiasis as a complication.

Clinical Findings & Treatment

Esophageal involvement is the most frequent type of invasive mucosal disease. Individuals present with substernal odynophagia, gastroesophageal reflux, or nausea without substernal pain. Examination reveals oral candidiasis only 50% of the time. Diagnosis is best confirmed by endoscopy with biopsy and culture, since radiographically the condition may be difficult to distinguish from other infectious esophagitis. Therapy depends upon the severity of disease. If patients are able to swallow and take adequate amounts of fluid orally, ketoconazole, 200-100 mg/d, will usually suffice. In the individual who is more ill, a 10- to 14-day course of amphotericin B at a dose of 0.2 mg/kg/d usually results in resolution.

Candida funguria usually resolves with discon-tinuance of antibiotics or removal of bladder catheters; rarely, bladder irrigation with 5 mg/d of amphotericin B is necessary, since renal clearance of the imidazoles is generally low.

Candidal fungemia may represent a benign, self-limited process or may be a sign of serious disseminated disease. If fungemia resolves with removal of intravascular catheters, there are often no further complications, though some would recommend a short course of intravenous amphotericin B to a total dose of 200-500 mg. If fungemia is documented repeatedly or if Candida is isolated from other sites, that is generally accepted as evidence of disseminated disease even if no other clinical stigmas are present. Important clinical findings in disseminated candidiasis are fluffy white retinal infiltrates and raised, erythematous skin lesions that may be painful. However, these are insensitive findings seen in less than 50% of cases. Other organ system involvement in disseminated disease may include the brain, meninges, and myocardium. Amphotericin B to a total dose of 1 g is the agent of choice. Flucytosine is added if central nervous system involvement occurs. Culture of skin lesions has a good diagnostic yield if fungemia is not documented, as is the case about 50% of the time. Unfortunately, serologic tests for Candida have not proved helpful in differentiating transient fungemia from disseminated disease.

Candidal endocarditis rarely is a complication of transient fungemia. It usually results from direct inoculation at the time of open heart surgery or repeated inoculation with intravenous drug use. Splenomegaly and petechiae are common, and there is a predilection for large-vessel embolization. Nonalbicans species such as Candida parapsilosis and Candida tropicalis may be important etiologic agents. As in other forms of fungal endocarditis, blood cultures have a poor yield of as low as 20%. The diagnosis is established definitively by culturing Candida from emboli or from large vegetations at the time of valve replacement. Valve destruction (usually aortic or mitral) is common, and surgical therapy is necessary in addition to a prolonged course of amphotericin therapy, usually to a total dose of 1-1.5 g intravenously.

A newly recognized form of disseminated disease is hepatosplenic candidiasis. This results from aggressive chemotherapy and prolonged neutropenia in patients with underlying hematologic cancers. Patients typically present with fever and variable abdominal pain weeks after chemotherapy, when neutrophil counts have recovered. Blood cultures are generally negative. Liver function tests reveal an alkaline phosphatase elevation that may be marked. CT scanning of the abdomen shows hepatosplenomegaly, most of-ten with multiple low-density defects in the liver. Diagnosis is established by liver biopsy and culture. Amphotericin B is given to a total dose of 1 g intravenously.

In all forms of invasive candidiasis, an important element of therapy is reversal of the underlying predis-posing factor when possible.


Essentials of Diagnosis

General Considerations

Histoplasmosis is caused by Histoplasma capsulatum, a mold that has been isolated from soil in endemic areas (central and eastern USA, eastern Canada, Mexico, Central America, South America, Africa, and southeast Asia). Infection presumably takes place by inhalation of spores. These convert into small budding cells that are engulfed by phagocytic cells in the lungs. The organism proliferates and may be carried hematogenously to other organs.

Clinical Findings

A. Symptoms and Signs: Most cases of histoplasmosis are asymptomatic or mild and so are unrecognized. Past infection is recognized by the development of a positive histoplasmin skin test and occasionally by pulmonary and splenic calcification. Symptomatic infections may present mild influenza-like characteristics, often lasting 1-4 days. Signs and symptoms of pulmonary involvement are usually absent even in patients who subsequently show areas of calcification on chest x-ray. Moderately severe infections are frequently diagnosed as atypical pneumonia. These patients have fever, cough, and mild chest pain lasting 5-15 days. Physical examination is usually negative. Radiographic findings are variable and nonspecific.

Severe infections occur in several forms: (1) Acute histoplasmosis frequently occurs in epidemics. It is a severe disease manifested by marked prostration, fever, and relatively few pulmonary complaints even when x-rays show pneumonia. The illness may last from 1 week to 6 months but is almost never fatal. (2) Acute progressive histoplasmosis is usually fatal within 6 weeks or less. Symptoms usually consist of fever, dyspnea, cough, loss of weight, and prostration. Diarrhea is usually present in children. Ulcers of the mucous membranes of the oropharynx may be present. The liver and spleen are nearly always enlarged, and all the organs of the body are involved. (3) Chronic progressive histoplasmosis is usually seen in older patients with chronic obstructive lung disease and immunocompromised patients. The lungs show chronic progressive changes, often with cavities. Clinically, chronic histoplasmosis appears to be primarily confined to the lungs, though any organ may be involved in the terminal stage. (4) In contrast, disseminated disease in the profoundly immunocompromised host usually represents reactivation of prior infectious foci. This form is commonly seen in patients with underlying HIV infection and is characterized by fever and multiple organ system failure. Chest x-rays may show a miliary pattern.

B. Laboratory Findings: In the moderately to severely ill patient, the sedimentation rate is elevated. Leukopenia may be present, with normal differential count or neutropenia. Most patients with progressive disease show anemia of chronic disease. In pulmonary disease, sputum culture is rarely positive; in contrast, blood or bone marrow cultures from immunocom-promised patients with acute disseminated disease are positive over 50% of the time. Conversely, the sensitivity of screening immunodiffusion or complement fixation serologic tests is better than 95% in pulmonary disease but only 70% in disseminated histoplasmosis in immunocompromised patients. Since skin test reactivity may persist for years following infection, it is generally not useful for establishing the diagnosis.


Self-limited pulmonary disease requires no specific therapy. Resection is rarely necessary. Amphotericin B in a low total dose (150-500 mg) has given excellent results in severe acute pulmonary disease. For disseminated disease, 2-3 g of amphotericin B is given. Relapses are rare, though a subset of patients with relapsing disease has recently been described. For immunocompromised patients, maintenance ketoconazole is given after initial intravenous amphotericin B therapy. Ketoconazole, 400-600 mg orally daily for several months, is an alternative for progressive pulmonary disease.


Essentials of Diagnosis

General Considerations

Coccidioidomycosis should be considered in the diagnosis of any obscure illness in a patient who has lived in or visited an endemic area.

Infection results from the inhalation of arthroconidia of Coccidioides immitis, a mold that grows in soil in certain arid regions of the southwestern USA, in Mexico, and in Central and South America.

About 60% of infections are subclinical and unrecognized other than by the subsequent development of a positive coccidioidin skin test. In the remaining cases, symptoms may be of severity warranting medical attention. Fewer than 1% show dissemination, but among these patients the mortality rate is high.

Clinical Findings

A. Symptoms and Signs: Symptoms of primary coccidioidomycosis occur in about 40% of infections. These vary from mild to severe and prostrating and resemble those due to viral, bacterial, or other mycotic infections. The onset (after an incubation period of 10-30 days) is usually that of a respiratory tract illness with fever and occasionally chills. Pleuritic pain is common. Nasopharyngitis may be followed by bronchitis accompanied by a dry or slightly productive cough. Weakness and anorexia may become marked, leading to prostration. A morbilliform rash may appear 1-2 days after the onset of symptoms.

Arthralgia accompanied by periarticular swellings, often of the knees and ankles, is common. Erythema nodosum may appear 2-20 days after onset of symptoms. Erythema multiforme may appear on the upper extremities, head, or thorax. Breath sounds may be-come bronchial in nature. Persistent pulmonary lesions, varying from cavities and abscesses to parenchymal nodular densities or bronchiectasis, occur in about 5% of diagnosed cases.

About 0.1% of white and 1% of nonwhite patients are unable to localize or control infection caused by C immitis. Symptoms in progressive coccidioidomycosis depend upon the site of dissemination. Any organ may be involved. Pulmonary findings usually become more pronounced, with mediastinal and hilar lymph node enlargement, cough, and increased sputum production. Pulmonary abscesses may rupture into the pleural space, producing an empyema. Extension to bones and skin may take place, and pericardial and myocardial extension is not unusual. Dissemination may be associated with fungemia, characterized clinically by a diffuse miliary pattern on chest x-ray and by early death.

Lesions in the bones are often in the bony prominences and the ends of long bones. Meningitis occurs in 30-50% of cases of dissemination. Subcutaneous abscesses and verrucous skin lesions are especially common in fulminating cases. Lymphadenitis may occur and may progress to suppuration. Mediastinal and retroperitoneal abscesses are not uncommon.

B. Laboratory Findings: In primary coccidioidomycosis, there may be moderate leukocytosis and eosinophilia and an elevated sedimentation rate. A persisting elevated or increasing sedimentation rate is a sign of progressive disease. The coccidioidin skin test becomes positive early after infection and may remain positive for years. Serologic testing is useful for both diagnosis and prognosis. The immuno-diffusion test (CIE) is useful for screening, but the complement fixation test is needed for confirmation and quantitation. An initial eosinophilia of 15% or higher together with a persistent rising complement fixation tier ( 1:8) may indicate desseminated disease. Demonstrable antibodies in spinal fluid are pathognomonic for coccidioidal meningitis. Spinal fluid findings include increased cell count with lymphocytosis and reduced glucose. Sporangia filled with endospores may be found in clinical specimens. These should be cultured only by trained technicians using strict safety precautions because of the danger of laboratory infection. Blood cultures in appropriate media are positive in about 30% of cases of acutely disseminated disease. Spinal fluid culture is positive in ap-proximately 30% of meningitis cases.

C. Imaging: Radiographic findings vary, but patchy, nodular pulmonary infiltrates and thin-walled cavities are most common. Hilar lymphadenopathy may be visible. There may be pleural effusions and lesions in bone.


Pulmonary infiltrations persisting for 6 or more weeks should be suspected of possible progression, especially with increase in area, enlargement of mediastinal and hilar nodes, cavity enlargement, and hemoptysis. Progressive disease is more likely to appear in blacks, Filipinos, and Mexicans. Immunodeficient patients, including those with HIV infection, and pregnant women of any race are also more vulnerable to dissemination.


General symptomatic therapy is given as needed for disease limited to the chest with no evidence of progression. For progressive pulmonary or extrapulmonary disease, amphotericin B intravenously has proved effective in some patients. Therapy should be continued to a total dose of 2.5-3 g. For meningitis, systemic maintenance amphotericin B may be required for the lifetime of the individual as guided by symptoms and spinal fluid complement fixation titers. Intrathecal amphotericin B, 1-5 mg monthly, may be needed if systemic therapy fails. Oral ketoconazole, 200-800 mg daily 1-2 hours be-fore breakfast, is an alternative for disease limited to the chest; however, therapy must be continued for 6 months or longer in order to prevent relapse.

Thoracic surgery is occasionally indicated for giant, infected, or ruptured cavities. Surgical drainage is also useful for subcutaneous abscesses. Amphotericin B is advisable following extensive surgical manipulation of infected tissue.


The prognosis in the case of limited disease is good, but persistent pulmonary cavities may cause complications. Nodules, cavities, and fibrotic residuals may rarely progress after long periods of stability or regression. Disseminated and meningeal forms still have significant long-term mortality rates.


Essentials of Diagnosis

General Considerations

Cryptococcosis is caused by Cryptococcus neoformans, an encapsulated budding yeast that has been found worldwide in soil and on dried pigeon dung.

Infections are acquired by inhalation. In the lung, the infection may remain localized, heal, or disseminate. Immunocompetent hosts rarely develop clinically apparent cryptococcal pneumonia. Progressive lung disease and dissemination most often occur in the setting of cellular immunodeficiency, including underlying hematologic cancer, long-term corticosteroid therapy, or HIV infection.

Clinical Findings

A. Symptoms and Signs: Disseminated disease may involve any organ, but central nervous system disease usually predominates. Headache is usually the first symptom of meningitis. Confusion and cranial nerve abnormalities may be seen as the disease progresses. Nuchal rigidity and meningeal signs are seen about 50% of the time but are uncommon in HIV-infected patients with this complication. Intracerebral mass lesions (cryptococcomas) are rarely seen. Obstructive hydrocephalus may complicate the course.

B. Laboratory Findings: Mild anemia, leukocytosis, and increased sedimentation rate are found. Spinal fluid findings include increased pressure, variable pleocytosis, budding encapsulated fungus cells, increased protein, and decreased glucose. Cryptococcal antigen in cerebrospinal fluid and culture establish the diagnosis 90% of the time. As many as 50% of AIDS patients may have no pleocytosis. These patients have a high incidence of extrameningeal disease, so that fungal blood culture and serum cryptococcal antigen tests are diagnostically helpful.


A combination of amphotericin B (0.3 mg/kg/d administered as for coccidioidomycosis) and flucytosine, 150 mg/kg/d orally or intravenously divided into 4 equal doses and given every 6 hours, is as effective as higher doses of amphotericin B alone and may cause less toxicity. On the other hand, flucytosine may not be tolerated, particularly in AIDS patients, because of diarrhea and leukopenia. Oral ketoconazole is effective for nonmeningeal cryptococcosis. Newer imidazoles such as fluconazole may eventually prove more useful. Intrathecal amphotericin B may be necessary if sterilization of fluid has not occurred after several weeks of therapy and clinical deterioration has taken place. Ventricular shunting may be important if hydrocephalus is a complication.


Factors that indicate a poor prognosis include lymphoid cancer, lack of spinal fluid pleocytosis, high initial antigen titer, and presence of extraneural disease. These factors may not be predictive in AIDS-related cryptococcal meningitis.


Aspergillus fumigatus is the usual cause of aspergillosis, though many species may cause a wide spectrum of disease. Burn eschar and detritus in the external ear canal are often colonized by these fungi. Clinical illness results either from an aberrant immunologic response or tissue invasion.

Allergic bronchopulmonary aspergillosis leads to severe asthma and transient pulmonary infiltrates. This diagnosis should be considered when eosinophilia, high levels of IgE, and Aspergillus precipitins are present in the blood. Corticosteroids-rather than antifungal antibiotics-are the mainstay of therapy.

Important invasive manifestations may be seen in immunocompetent adults. These include chronic sinusitis and colonization of preexisting pulmonary cavities. Sinus disease may require long courses of antibiotics as well as surgical debridement. Aspergillomas of the lung may be found by incidental radiographic studies but may also present with significant hemoptysis. Intracavitary instillation of amphotericin B and bronchoscopic removal have been tried, but the most effective therapy for symptomatic aspergilloma remains surgical resection.

Life-threatening invasive disease most commonly occurs in profoundly immunodeficient patients, particularly those with prolonged severe neutropenia. AIDS patients do not have an increased incidence of invasive aspergillosis. Pulmonary disease is most common, with patchy infiltration leading to a severe necrotizing pneumonia. There is often distal infarction as the organism grows into blood vessels. Late in the course, there may be hematogenous dissemination to the central nervous system, skin, and other organs. Early diagnosis and reversal of any correctable immunosuppression are essential. Blood cultures have very low yield, and serologic tests are of little use. Isolation of Aspergillus from pulmonary secretions does not necessarily imply invasive disease. Therefore, the mainstay of diagnosis is demonstration of Aspergillus in tissue. Histologically, one sees branched septate hyphae. Biopsy specimens will not invariably grow the organism.

When severe invasive aspergillosis is considered clinically or microbiologically, rapid institution of high doses of amphotericin B may be life-saving. After a test dose, the total daily dose is increased to 0.8-1 mg/kg/d intravenously as tolerated for the first several weeks of therapy. Thereafter, more traditional doses of 0.6 mg/kg/d are continued until a total dose of at least 2 g has been reached. The addition of flucytosine is of unclear benefit. Itraconazole has activity against Aspergillus but has not been proved to be effective in severely ill patients. The mortality rate of pulmonary or disseminated disease in the immunocompromised patient still approaches 50%.


The term "mucormycosis" (zygomycosis, phycomycosis) is applied to opportunistic infections caused by members of the genera Rhizopus, Mucor, Absidia, and Cunninghamella. Predisposing conditions include diabetic acidosis and treatment with steroids or cytotoxic drugs. These appear in tissues as broad, branching nonseptate hyphae. Biopsy is almost always required for diagnosis. Invasive disease of the sinuses, orbits, and, rarely, the lungs may be noted. The diagnosis should be considered in acidotic diabetic patients with black necrotic lesions of the nose or sinuses or with new cranial nerve abnormalities. High-dosage amphotericin B therapy initiated early, control of diabetes or other underlying conditions; and extensive surgical removal of necrotic, nonperfused tissue are essential. The prognosis is poor, with a 30-50% mortality rate.


Blastomyces dermatitidis causes this chronic sys-temic fungus infection. The disease occurs more often in men and in a geographically delimited area of the central and eastern USA and Canada. A few cases have been found in Mexico and Africa.

Pulmonary infection may be asymptomatic. When dissemination takes place, lesions are most frequently seen on the skin, in bones, and in the urogenital system.

Cough, moderate fever, dyspnea, and chest pain are evident in symptomatic patients. These may re-solve or progress, with bloody and purulent sputum production, pleurisy, fever, chills, loss of weight, and prostration. Radiologic studies usually reveal in-filtrates and enlarged mediastinal nodes. Raised, ver-rucous cutaneous lesions that have an abrupt downward sloping border are usually present in disseminated blastomycosis. The border extends slowly, leaving a central atrophic scar. These lesions persist untreated for long periods, mimicking skin cancer. Bones-often the ribs and vertebrae-are frequently involved. Lesions appear to be both destructive and proliferative on radiography. Epididymitis, prostatitis, and other involvement of the male urogenital system may occur. Central nervous system involvement is uncommon.

Laboratory findings usually include leukocytosis, anemia, and elevated sedimentation rate. The organ-ism is found in clinical specimens as a thick-walled cell 5-20 wm in diameter that may have a single bud. It grows readily on culture. Serologic tests are not well standardized.

Amphotericin B in a total dose of 1.5-2 g intravenously is the best drug for treatment of severe or progressive disease. Ketoconazole is an effective alternative in immunocompetent patients with nonmeningeal disease. Large abscesses or bronchopleural fistulas rarely require drainage.

Careful followup for early evidence of relapse should be made for several years so that therapy may be resumed or another drug instituted. Patients with limited cutaneous lesions have the best prognosis.


(South American Blastomycosis)

Paracoccidioides brasiliensis infections have been found only in patients who have resided in South or Central America or Mexico. Long asymptomatic periods enable patients to travel far from the endemic areas. Ulceration of the naso- and oropharynx is usually the first symptom. Papules ulcerate and enlarge both peripherally and deeper into the subcutaneous tissue. Extensive coalescent ulcerations may eventually result in destruction of the epiglottis, vocal cords, and uvula. Extension to the lips and face may occur. Eating and drinking are extremely painful. Skin lesions may occur, usually on the face. Variable in appearance, they may have a necrotic central crater with a hard hyperkeratotic border. Lymph node enlargement may follow mucocutaneous lesions, eventually ulcerating and forming draining sinuses. Lymph node enlargement may be the presenting symptom, with subsequent suppuration and rupture through the skin. In some patients, hepatosplenomegaly is noted. Cough, sometimes with sputum, indicates pulmonary involvement, but the signs and symptoms are often mild, even though radiographic findings indicate severe parenchymatous changes in the lungs. The extensive ulceration of the upper gastrointestinal tract may prevent sufficient intake and result in cachexia.

Laboratory findings are nonspecific. Serologic studies may be helpful. A high titer usually indicates progressive disease; a descending titer is a favorable sign. The fungus is found in clinical specimens as a spherical cell that may have many buds arising from it.

Oral ketoconazole, 200-400 mg daily 1-2 hours before breakfast, generally results in a clinical response within 1 month and effective control after 6 months. The rare relapse responds to resumed ketoconazole therapy. Newer imidazoles, such as itraconazole, appear promising.


Sporotrichosis is a chronic fungal infection caused by Sporothrix schenckii. It is worldwide in distribution; most patients have had contact with soil, plants, or decaying wood. Infection takes place when the organism is inoculated into the skin-usually on the hand, arm, or foot.

The most common form of sporotrichosis begins with a hard, nontender subcutaneous nodule. This later becomes adherent to the overlying skin and ulcerates. Within a few days to weeks, similar nodules usually develop along the lymphatics draining this area, and these may ulcerate. The lymphatic vessels become indurated and are easily palpable. Blood-borne dissemination is rare, and the general health of the patient is not affected.

Disseminated sporotrichosis is rare in the immunocompetent host but may present with lung, bone, joint, and central nervous system involvement in com-promised patients.

Cultures are needed to establish diagnosis. Serologic tests may be useful for diagnosis of disseminated disease.

Potassium iodide taken orally in increasing dosage is the treatment of choice for cutaneous disease. Give as the saturated solution, 5 drops 3 times a day after meals, increasing by 1 drop per dose until 40 drops 3 times a day are being given. Continue until signs of the active disease have disappeared. The dosage is then decreased by 1 drop per dose until 5 drops are being given, and then is discontinued. Care must be taken to reduce the dosage if signs of iodism appear or thyroid disease is present. Amphotericin B intravenously, 1.5-2 g, has been effective in systemic infection. Surgery is usually contra-indicated except for simple aspiration of secondary nodules.

The prognosis is good for all forms of sporotrichosis except the disseminated type.


Chromoblastomycosis is a chronic, principally tropical cutaneous infection caused by several species of closely related black molds (Fonsecaea sp and Phialophora sp).

Lesions are slowly progressive and occur most frequently on a lower extremity. The lesion begins as a papule or ulcer. Over months to years, papules enlarge to become vegetating, papillomatous, verrucous elevated nodules. Satellite lesions may appear along the lymphatics. There may be secondary bacterial infection. Elephantiasis may result.

The fungus is seen as brown, thick-walled, spherical, sometimes septate cells in pus. The type of reproduction found in culture determines the species.

Oral flucytosine, 150 mg/kg/d, thiabendazole, 25 mg/kg/d, itraconazole, 200 mg/d, ketoconazole and intralesional amphotericin B have proved effective.

Mycotic Keratitis

Candida albicans, Fusarium, orAspergillus is most often responsible for mycotic keratitis. Trauma to the cornea followed by corticosteroid and antibiotic therapy is often a predisposing factor. Prompt withdrawal of corticosteroids, removal of the infected necrotic tissue, other surgical procedures, and application of natamycin or ketoconazole are useful in man-agement. Amphothericin B and flucytosine are used for fungal endophthalmitis. Natamycin does not penetrate corneal epithelium adequately for treatment of deep fungal keratitis or intraocular infections.

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