Nonbacterial Infectious Pneumonia

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Chapter 26 Nonbacterial Infectious Pneumonia

William Graham Carlos, III , Chadi A. Hage

Nonbacterial causes of infectious pneumonia are important diagnostic considerations in the evaluation of patients who are immunocompromised, who have recognized structural lung disease, or who do not respond to appropriate antibiotic therapy for presumed bacterial pneumonia. A detailed clinical history can assist the astute clinician in making the diagnosis of a nonbacterial cause of infectious pneumonia in these circumstances. Important information to gather includes travel history, geographic location, occupational history, and recreational activities. This chapter presents an overview of common fungal and parasitic causes of pneumonia, including clinical presentation, diagnostic considerations, and treatment options.

Fungal Pneumonias

Aspergillosis

Aspergillus organisms are ubiquitous saprophytic fungi. They grow well in soil and decaying vegetation. These fungi also have been found in hospitals, ventilation and water systems, and dust associated with construction activity. Disease manifestations depend on the immune status and lung structure of the host. Clinical manifestations include allergic disease, airway colonization, aspergilloma formation, tracheobronchial disease, chronic necrotizing pneumonia, and invasive disseminating disease. Allergic disease generally is seen in immunocompetent patients and may encompass airway hyperreactivity, allergic bronchopulmonary aspergillosis (ABPA), and hypersensitivity pneumonitis. Airway colonization occurs in patients with impaired mucociliary clearance or distorted lung structure such as in bronchiectasis. Aspergillomas, or “fungus balls,” thrive in cavitary lung lesions such as those associated with tuberculosis. Tracheobronchial aspergillosis and chronic necrotizing pneumonia (locally invasive aspergillosis) are manifestations found in patients with acquired immunodeficiency syndrome (AIDS), recipients of transplanted organs (especially lungs), and patients with obstructive lung disease who use inhaled or systemic steroids. Finally, invasive or disseminated aspergillosis develops in the context of profound and protracted granulocytopenia (Figure 26-1).

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Figure 26-1 Examples of pulmonary fungal pathogens. A, Aspergillus fumigatus hyphae in BAL fluid from a neutropenic patient with invasive aspergillosis (Gomori methenamine silver nitrate [GMS] stain). B, Histoplasma capsulatum seen inside phagocytes on a peripheral blood smear from a patient with AIDS complicated by disseminated histoplasmosis (Giemsa stain). C, Large, broad-based budding Blastomyces dermatitidis yeasts in BAL fluid from a patient with pulmonary blastomycosis (Giemsa stain). D, Coccidioides immitis spherule containing numerous small spores in a lung biopsy specimen from a patient with acute pulmonary coccidioidomycosis. E, Cluster of narrow based-budding, small Cryptococcus neoformans yeasts, extracellularly located, in BAL fluid from a patient with AIDS complicated by disseminated cryptococcosis (GMS stain). F, Extracellularly located Pneumocystis jiroveci cysts (GMS stain) in BAL fluid from a patient with AIDS who presented with respiratory failure. AIDS, acquired immunodeficiency syndrome; BAL, bronchoalveolar lavage.

Fungal culture and histopathologic examination constitute the “gold standard” for the diagnosis of aspergillosis. The diagnosis has been simplified by the advent of the galactomannan detection assay, which confers a high degree of sensitivity and specificity. The treatment of aspergillosis is tailored to the disease manifestation. Allergic manifestations are managed with routine asthma care that includes avoidance of allergen exposures and maintenance bronchodilators. Steroids are reserved for severe cases. ABPA mandates treatment with corticosteroids initially and may require the addition of itraconazole. Aspergillomas can be followed clinically and generally remain dormant but can manifest with massive hemoptysis necessitating embolization or surgical resection. Voriconazole is the preferred agent for treatment of invasive aspergillosis. Liposomal amphotericin B, posaconazole, and echinocandins are reserved for salvage therapy.

Histoplasmosis

Histoplasmosis is the most prevalent endemic mycosis in North America. Histoplasma capsulatum is a dimorphic fungus existing as a mold in nature. It forms spores that become aerosolized, facilitating inhalation. After inhalation, H. capsulatum grows as yeast forms in the host.

The clinical manifestations of histoplasmosis are variable and depend on the intensity of exposure along with the immune status and underlying lung architecture of the host. The Mississippi and Ohio River valleys are highly endemic. Histoplasmosis also is endemic to parts of Central America, South America, Africa, and Asia. Moist soil is an ideal habitat for Histoplasma, especially when supplemented with bird or bat guano. Activities that can lead to infection include spelunking (caving), excavation, demolition, and cleaning of chicken coops or old buildings. After inhalation, the spores are converted into yeasts, which are phagocytosed by macrophages. The organism is able to survive and proliferate inside macrophages, allowing it to disseminate. Within 2 weeks, however, a protective cellular immune response usually develops, which contains the fungus by forming granulomas (often seen as calcified granulomas on chest radiographs). Most otherwise healthy persons infected with a low inoculum remain asymptomatic (i.e., the infection is subclinical) or are minimally symptomatic. Patients with impaired immunity that fails to contain the infection can develop progressive disseminated histoplasmosis, with involvement of the bone marrow, liver, spleen, adrenal glands, gastrointestinal tract, and central nervous system (CNS). This manifestation typically is seen in persons with AIDS or patients taking immunosuppressive medications such as prednisone, methotrexate, and anti-TNF-α agents. Common clinical manifestations of disseminated disease include fever, weight loss, hepatosplenomegaly, pancytopenia, meningitis, focal brain lesions, ulcerations of the oral mucosa, gastrointestinal ulcerations, and adrenal insufficiency. Disseminated histoplasmosis carries a high mortality rate unless promptly diagnosed and appropriately treated (Table 26-1).

Table 26-1 Types of Fungal Pneumonia

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Patients who inhale larger inocula of Histoplasma conidia during outbreaks or in an enclosed space may develop severe pulmonary disease with a flulike illness that can lead to respiratory failure. When the infection occurs in the context of structural lung disease (bullous emphysema), it may not be effectively contained, and patients can develop chronic cavitary histoplasmosis with upper lobe infiltrates, cavitations, and pleural thickening. Other late manifestations of histoplasmosis include fibrosing mediastinitis (a late complication associated with high morbidity), calcification of mediastinal nodes, and broncholithiasis.

Identification of H. capsulatum is accomplished using a combination of tests. Fungal culture remains the “gold standard.” However, H. capsulatum may require up to 4 weeks to be grown in culture, limiting its utility in severe cases. Rapid diagnostic testing using antigen detection in serum or urine samples is useful in patients with moderate to severe disease. Antigen detection in bronchoalveolar lavage (BAL) fluid may help make the diagnosis of pulmonary histoplasmosis. Rapid diagnosis also can be achieved through cytopathologic examination, albeit with lower sensitivity than that attained with culture or antigen detection. Histoplasma serologic testing (immunodiffusion and complement fixation) is particularly useful in chronic (cavitary) and subacute disease, because detectable levels of antibody appear after 4 weeks of infection.

Treatment for histoplasmosis is reserved for patients with chronic pulmonary, disseminated, or acute moderate to severe disease. Liposomal amphotericin B followed by itraconazole is the preferred regimen for severe cases. Mild to moderate disease can be treated with itraconazole exclusively. Corticosteroids also may be useful in cases of severe, life-threatening acute pulmonary histoplasmosis. The duration of treatment for acute pulmonary histoplasmosis is 6 to 12 weeks, whereas that for disseminated and chronic pulmonary histoplasmosis is 12 to 18 months.

Fibrosing mediastinitis and broncholithiasis represent chronic reactions to past infection and do not respond to antifungal therapy. Treatment consists of endoscopic or surgical removal of partially or completely eroded broncholiths. Placement of endovascular stents may be required in advanced fibrosing mediastinitis causing obstruction of major mediastinal vessels. Obstruction of central airways or the esophagus also can occur and may necessitate balloon dilatation or stenting.

Blastomycosis

Blastomyces dermatitidis is a dimorphic fungus that causes pulmonary and systemic disease. Most cases of blastomycosis have been reported in North America, where it occurs predominantly in the Midwestern states and Canadian provinces surrounding the Great Lakes. In the United States, the endemic region overlaps significantly with that of H. capsulatum along the Mississippi and Ohio River valleys. Cases have been reported from Africa and India as well. When outbreaks occur, they usually are associated with outdoor recreational activities or work around waterways. As with histoplasmosis, the mechanism of infection involves inhalation of the spores, which are then converted to the yeast form in the lung; however, polymorphonuclear cells are abundant in blastomycosis lesions, mimicking pyogenic infections.

Blastomycosis can manifest clinically in a variety of ways. The most common presentation is pulmonary disease, followed by involvement of the skin, bone, joints, and CNS. Acute pulmonary blastomycosis resembles community-acquired pneumonia and often is mistakenly treated for bacterial pneumonia before the correct diagnosis is made. Signs and symptoms include fever, chills, productive cough, and chest pain. Radiographic findings include consolidation, cavities, nodules, and miliary patterns. Mediastinal adenopathy and pleural effusions are uncommon. Acute blastomycosis can progress to acute respiratory distress syndrome (ARDS), even in immunocompetent patients. Risk factors for severe infection include diabetes and diffuse pulmonary involvement. Chronic pulmonary blastomycosis mimics lung cancer or tuberculosis and can be insidious in onset and progression and minimally symptomatic. Skin lesions often are mistaken for squamous cell carcinoma or pyoderma gangrenosum.

Definitive diagnosis requires growth of Blastomyces from sputum, BAL fluid, or biopsy material. Rapid identification is made by visualization of the characteristic broad-based budding yeast in clinical specimens. Typically, blastomycosis is diagnosed when a presumed community-acquired bacterial pneumonia fails to respond to antimicrobial therapy or if a mass suspicious for malignancy is detected. When the clinical presentation includes cutaneous manifestations, the diagnosis can be secured by skin biopsy. Blastomyces antigen can be found in the urine, serum, or BAL fluid, providing a reliable means for establishing a rapid diagnosis, especially in severe cases. The current antigen assays do not differentiate histoplasmosis from blastomycosis, as a consequence of cross-reactivity. Histopathologic and cytopathologic analysis can be helpful in differentiating histoplasmosis from blastomycosis and should be routinely ordered with invasive testing procedures.

In view of the cross-reactivity of the antigen assay, it is fortunate that the treatment for severe life-threatening blastomycosis is similar to that for histoplasmosis. Intravenous administration of amphotericin is the treatment of choice, and corticosteroids may be added in cases of ARDS. Non–life-threatening cases can be managed with itraconazole. In patients who are intolerant of itraconazole or who have CNS involvement, fluconazole can be used. Almost all patients with blastomycosis should be treated (Figure 26-2), although patients with self-limited disease may not require treatment.

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Figure 26-2 A, Acute pulmonary blastomycosis in a 51-year-old woman. The chest film shows a left upper lobe infiltrate. B, Acute pulmonary coccidioidomycosis in an otherwise healthy man. Chest computed tomography (CT) scan shows area of consolidation in the right upper and middle lobes. C, Progressive disseminated histoplasmosis in a 35-year-old patient with AIDS. The chest film shows bilateral reticulonodular interstitial infiltrates. AIDS, acquired immunodeficiency syndrome.

Coccidioidomycosis

Coccidioidomycosis, also known as “valley fever,” is caused by the dimorphic soil-dwelling fungus Coccidioides. It is endemic in the southwestern United States and northern Mexico. Recent surges in case numbers have been recently reported in Arizona, where 60% of the cases occur. The mechanism of infectivity is similar to that for histoplasmosis and blastomycosis, involving inhalation of spores, leading to neutrophilic inflammatory responses. Case clusters have occurred in patients 2 weeks after they were exposed to dust in endemic areas while excavating or rock hunting, or during a windstorm.

Most patients who become infected with Coccidioides are asymptomatic or have a self-limited illness. Patients who become symptomatic usually experience a flulike illness with symptoms including fever, chills, arthralgia, myalgia, and headaches. In addition, cough, pleuritic chest pain, dyspnea, and rarely hemoptysis may occur. Cutaneous manifestations often are reported with acute pulmonary coccidioidomycosis and may include maculopapular rash, erythema nodosum, and erythema multiforme. Chest radiographs initially show one or more areas of consolidation, with hilar or mediastinal lymphadenopathy. Fibrocavitary lesions can result from progressive disease. Areas of pneumonitis may heal by the formation of a coinlike lesion called a coccidioidoma that can persist for life.

Primary progressive coccidioidomycosis with diffuse pneumonia occurs in settings of intense environmental exposure or immunosuppression and often is associated with fungemia and respiratory compromise. Several months after the infection manifests, disseminated coccidioidomycosis may develop, with involvement of skin, bones, joints, genitourinary system, and the meninges. Risk factors for extrapulmonary dissemination include African American or Filipino ancestry, pregnancy during the second or third trimester, and depressed cellular immunity.

The gold standard for the diagnosis of coccidioidomycosis is culture or direct visualization of the fungus in tissue or respiratory secretions. Serologic testing plays an important role in establishing the diagnosis of coccidioidomycosis, in view of its speed and simplicity. Serologic studies are more likely to be positive in patients with disseminated disease and chronic disease. In contrast with Histoplasma and Blastomyces, Coccidioides grows within 3 to 7 days of culture.

The treatment of coccidioidomycosis is similar to that of histoplasmosis and blastomycosis and relies on triazoles (itraconazole or fluconazole) for diffuse pulmonary or nonmeningeal disseminated disease. Amphotericin B generally is reserved for immunocompromised patients with severe or disseminated disease unresponsive to triazoles as well as for pregnant women. For uncomplicated primary pneumonia in a normal host close observation often is all that is needed.

Paracoccidioidomycosis

Paracoccidioidomycosis, formerly named “South American blastomycosis,” is caused by a fungus endemic to South and Central America, Paracoccidioides brasiliensis. Paracoccidioidomycosis is highly endemic in Brazil, Colombia, Venezuela, and Ecuador, with reported infectivity rates as high as 50% to 75% in some areas. Like the other thermal dimorphic fungi, P. brasiliensis is inhaled and undergoes transformation in the alveoli. Most cases are subclinical, and only a minor proportion of hosts will develop signs or symptoms weeks after inhalation. Reactivation of disease can occur years after inoculation, and the condition may disseminate hematogenously to the adrenal glands, gastrointestinal tract, and other viscera.

Pulmonary disease frequently is seen in chronic paracoccidioidomycosis. Chest imaging typically reveals pulmonary opacities that can cavitate, in a pattern involving both medial pulmonary fields and resembling a “butterfly wing.” The diagnosis of paracoccidioidomycosis can be reliably made by histopathologic examination of clinical specimens revealing characteristic yeast cells with multiple buds. Definitive diagnosis relies on culture of the organism. Serologic testing can suggest the diagnosis and monitor the response to treatment. In severe or disseminated cases of paracoccidioidomycosis, amphotericin B is recommended. Itraconazole is the drug of choice for milder disease.

Cryptococcosis

Cryptococcus neoformans is a yeast with a thick capsule. Two species of Cryptococcus are recognized to cause disease in humans: Cryptococcus gattii and Cryptococcus neoformans. C. neoformans has emerged as a leading cause of CNS infection in patients with AIDS. Recent outbreaks of C. gattii infection causing pulmonary disease in immunocompetent persons have been reported from the northwestern United States and neighboring Vancouver Island in Canada. The two species of Cryptococcus have geographic and clinical differences. Whereas C. gattii typically is associated with flowering eucalyptus trees, C. neoformans can be found around bird guano throughout the world. Overall, cryptococcosis is a rare infection and usually is asymptomatic and self-limited in immunocompetent patients. In those who have impaired cell-mediated immunity, it may cause lung infection and meningitis. Cryptococcosis is emerging as the third leading fungal infection behind candidiasis and aspergillosis in recipients of organ transplants.

The CNS is the most common site of disease activation. Symptoms of cryptococcal pneumonia include fever, malaise, cough, and chest pain. The chest radiograph may show large, nonspecific nodules or infiltrates, sometimes associated with lymphadenopathy. Pulmonary infections have a tendency toward spontaneous resolution and frequently are asymptomatic. Hematogenous spread to the brain can lead to lesions in gray matter and basal ganglia. CNS disease can manifest as meningoencephalitis with papilledema and high cerebrospinal fluid opening pressure. A patient with AIDS presenting with fever and headache should prompt consideration of a diagnosis of cryptococcal meningitis. Lumbar puncture with an increased opening pressure and India ink smear of centrifuged cerebrospinal fluid is useful in this scenario. In patients who do not have AIDS, levels of cerebrospinal fluid glucose are low, and protein levels are high and can correlate with a lymphocytic pleocytosis. Cryptococcal capsular antigen usually is detected in cerebrospinal fluid or serum by latex agglutination testing, with sensitivity and specificity approaching 90%.

Treatment of cryptococcosis is tailored to the site of involvement and severity. Severe pulmonary disease and CNS involvement require amphotericin B with flucytosine. Mild to moderate disease can be effectively treated with fluconazole.

Pneumocystis

Pneumocystis jiroveci is a fungus known to cause pneumonia in patients that are immunocompromised. It is a ubiquitous organism. Commonly found in patients with human immunodeficiency virus (HIV) infection or AIDS, infection is rare in normal hosts. Infection with Pneumocystis should be considered in any immunocompromised patient presenting with bilateral infiltrates on chest radiographs. Computed tomography (CT) generally reveals ground glass shadowing in affected areas, and sparing of the pleural surfaces has been noted frequently. The diagnosis of pneumocystosis is readily made through demonstration of the organism using fungal stains. Diagnostic specimens typically are obtained by BAL. Rarely, dissemination can occur, causing renal disease, cutaneous popular skin lesions, choroiditis, and intestinal plaques.

The treatment of pneumocystosis depends on the severity of hypoxemia once the organism has been identified. Patients with a PaO2 less than 70 mm Hg on room air require treatment with steroids in addition to intravenous trimethoprim-sulfamethoxazole or pentamidine. Mild cases can be treated with trimethoprim-sulfamethoxazole, dapsone, pentamidine, atovaquone, or clindamycin plus primaquine. Various prevention regimens are available for patients who are severely immunosuppressed (e.g., persons with AIDS whose CD4+ counts are less than 200 cells/µL, patients on long-term immunosuppressants). They include trimethoprim-sulfamethoxazole, dapsone, and aerosolized pentamidine.

Parasitic Pneumonias

Amebiasis

Entamoeba histolytica is endemic in tropical developing countries, particularly Mexico, India, and nations of Central and South America, tropical Asia, and Africa. The disease is acquired predominantly after ingestion of contaminated food or water. After intestinal infection, trophozoites can invade intestinal vasculature and reach the liver through the portal venous system. From the liver, the infection may disseminate to the lungs or brain. Liver abscess is the hallmark of invasive disease. Peripheral liver abscesses can erode through the diaphragm, causing pleuropulmonary disease.

Symptomatic amebiasis is predominantly an intestinal infection causing diarrhea and abdominal cramps to dysentery or even intestinal perforation because of mucosal ulcerations. Pleuropulmonary signs and symptoms include cough, dyspnea, and pleuritic pain (usually right-sided) associated with fever and chills, diaphoresis, and weight loss. The chest radiograph may show elevation of the right hemidiaphragm, pleural effusion, atelectasis, lung consolidation (which usually affects the right lower lobe), or lung abscess. Hepatobronchial fistulas have been reported in patients who have pleuropulmonary complications of amebiasis; this finding is associated with the production of copious volumes of chocolate-colored sputum. Pericardial involvement also may be observed in such patients. The diagnosis can be readily established by demonstrating amebic cysts or trophozoites in the stool, pleural fluid, or bronchial secretions. Serologic tests are highly sensitive and specific in invasive disease. Metronidazole is the agent of choice for treatment of invasive amebiasis.

Malarial Lung

Severe falciparum malaria often is complicated by noncardiogenic pulmonary edema, which can develop despite effective antimalarial therapy. This syndrome of malarial lung carries a high mortality rate. Pulmonary involvement is a manifestation of the cytokine storm that follows heavy infection and destruction of red cells. It often leads to ARDS, with capillary congestion, pulmonary edema, and alveolar hemorrhage. Bilateral pulmonary infiltrates and pleural effusions are seen on chest radiographs. It is commonly associated with cerebral disease and high levels of parasitemia. The diagnosis of malaria is established after demonstration of asexual forms of the parasite inside erythrocytes on peripheral blood smears stained with Giemsa or Wright stain. Besides quinine-based antimalarial therapy, exchange transfusion and supportive care with supplemental oxygen and mechanical ventilation are required for severe cases.

Pulmonary Ascariasis

Ascaris lumbricoides is the largest intestinal nematode parasite of humans. Ascaris is widely distributed in tropical and subtropical areas. Most infected persons are asymptomatic. After egg ingestion, larvae hatch in the jejunum, invade the mucosa, and migrate to the lungs, causing a pneumonitis 1 to 2 weeks after ingestion. The presentation is that of eosinophilic pneumonitis (Löffler-like syndrome), with cough, occasional hemoptysis, wheezing, dyspnea, and high-grade fever. The illness usually is self-limited. Abdominal symptoms and cutaneous reactions also may be present. The chest radiograph can show unilateral or bilateral patchy, migratory, peribronchial infiltrates. The diagnosis is easily established by demonstrating characteristic Ascaris eggs in stool. During the transpulmonary migratory phase (eosinophilic pneumonitis), larvae can be found in sputum or gastric aspirates before the eggs appear in the stool. Antihelmintic treatment usually is not required for pulmonary ascariasis, because it usually is self-limited. Symptomatic treatment with bronchodilators and oxygen therapy and potentially corticosteroids is appropriate.

Strongyloidiasis

Strongyloides typically is found in tropical climates and is especially common in Southeast Asia, sub-Saharan Africa, and Brazil. The southeastern United States has endemic regions as well. Strongyloides stercoralis is unique among helminths in that it is capable of replicating in the human host. This feature allows the worm to autoinfect the host, where it may persist for decades. Infection begins when the filariform larvae in contaminated soil penetrate the exposed skin of the host. The larvae migrate through the lymphatic and venous circulation and eventually settle in the capillaries and alveoli of the lungs. Eventually the larvae ascend the tracheobronchial tree to the larynx, are swallowed, and mature into adult egg-laying females. Eggs hatch in the mucosa and pass with feces into the soil. Eggs can transform within the intestine into filariform larvae, which can penetrate the bowel wall and reenter the circulation. These larvae can carry bacteria as they penetrate through the gastrointestinal tract, causing polymicrobial bacteremia, septicemia, or hyperinfection in immunosuppressed patients.

Strongyloidiasis may have a variety of clinical manifestations. Although uncomplicated disease may remain subclinical for years, some patients will develop mild pulmonary disease in the form of cough and bronchospasm, whereas others will progress to ARDS. Recurrent urticaria and larva currens, or “running larva,” can cause raised skin lesions. Nonspecific abdominal pain and colitis can develop, as can bowel obstructions. Eosinophilia is common during parasitemia. Radiographic abnormalities can range from a diffuse pneumonitis to chronic migratory pulmonary opacities. Immunosuppressed persons (e.g., patients with AIDS, glucocorticoid users) are susceptible to hyperinfection, with ensuing gram-negative sepsis, pneumonia, or meningitis. In patients with massive infection, pulmonary involvement can be extensive, leading to respiratory failure and pulmonary hemorrhage. Pleural effusions, pulmonary cavitations, and abscesses also have been documented, usually in cases associated with higher burdens of organisms.

The diagnosis of strongyloidiasis can be readily established by demonstrating rhabditiform larvae in stool as well as in sputum, BAL fluid, or biopsy specimens in disseminated disease. Serologic testing may help establish the diagnosis in chronic cases. Even in asymptomatic patients, a diagnosis of strongyloidiasis warrants treatment, in view of the potential for autoinfection and the fatal hyperinfection syndrome. Ivermectin is the preferred therapeutic agent, given daily for 1 or 2 days or up to 7 days in cases of disseminated disease.

Visceral Larva Migrans (Toxocariasis)

Visceral larva migrans is caused by Toxocara spp. These nematodes are parasitic for nonhuman hosts but do not mature in humans. Consequently, most infections in humans remain subclinical. However, the larvae occasionally may travel through host tissues, where they can elicit profound eosinophilic inflammation, resulting in the syndrome of visceral larva migrans. All feline and canine species can carry Toxocara. Nursing mothers can pass larvae to suckling puppies, and pregnant bitches can infect their pups transplacentally. In puppies, the larvae can develop into adult worms, which produce eggs released in their feces. Humans (usually preschool children) acquire toxocariasis by ingesting soil contaminated by pup feces.

Although most infections are subclinical, the infection can progress as the larvae invade the liver, lungs, CNS, and other sites. In such cases, the ensuing intense eosinophilic granulomatous response may be associated with fever, malaise, cough, wheezing, and rashes. Radiographic manifestations consist of migratory infiltrates. Rarely, death results from severe neurologic, pulmonary, or cardiac involvement.

The diagnosis of toxocariasis is made by serologic testing or histologic examination of infected tissues. Stool examination is not helpful, because the larvae do not develop into egg-producing adults in humans. Although most infections with Toxocara are self-limited, requiring no treatment, steroids may be warranted for cases associated with severe inflammation. The anthelmintic albendazole given for 5 days appears to be effective in eradicating the organism.

Tropical Pulmonary Eosinophilia

Tropical pulmonary eosinophilia develops after infection with lymphatic filarial species (Wuchereria bancrofti or Brugia malayi) that are found in tropical and subtropical areas. The infection is transmitted by mosquitos. Circulating filariae are cleared from the bloodstream by the lungs, releasing antigens that cause a pulmonary hypersensitivity reaction.

Clinical manifestations include paroxysmal cough and wheezing (usually nocturnal), weight loss, fever, adenopathy, and peripheral eosinophilia and elevated serum immunoglobulin E (IgE) levels. Chest radiographs may show bilateral interstitial infiltrates and vascular congestion. The diagnosis is based on clinical findings. The clinician must rule out similar entities such as asthma, Löffler syndrome, ABPA, Churg-Strauss syndrome, chronic eosinophilic pneumonia, and the idiopathic hypereosinophilic syndrome. Daily administration of diethylcarbamazine for 2 to 3 weeks is the standard therapy. Signs and symptoms usually resolve within 5 to 7 days after the initiation of therapy. Corticosteroids and antihistamines may also be used to control symptoms.

Paragonimiasis

Paragonimus species such as Paragonimus westermani are hermaphroditic flukes that are endemic in Southeast Asia, South America, and South Africa. They are rarely found in North America and Europe. They infect humans who ingest undercooked crabs or crayfish that contain the encysted parasite. In many endemic regions, these crustaceans are consumed raw or pickled. The organisms penetrate the gut wall and travel to the lung by way of the peritoneal cavity, diaphragm, and pleural space. Mature flukes can be found in bronchioles surrounded by cysts. Parasite eggs are expectorated with sputum or swallowed and expelled with feces. The life cycle is then completed in snails or freshwater crustaceans.

Although some infections remain subclinical, the illness occurs during the first weeks of infection when the parasite is migrating from the intestine to the lung. Signs and symptoms include abdominal pain, diarrhea, hypersensitivity reactions (urticaria, eosinophilia, and fever), chest pain, cough, and hemoptysis. In most cases, however, no clinical manifestations emerge until the adult parasite begins to produce eggs in the lung, causing local inflammation with formation of cavities and cysts. Pulmonary signs and symptoms may include cough productive of rusty-brown sputum or frank hemoptysis. Sometimes the disease is mistaken for tuberculosis or lung cancer. Areas of fibrosis or pleural thickening are common. Pleural effusions are uncommon, but when they occur are characterized by high eosinophil counts in the pleural fluid. Of note, although eosinophilia is common in paragonimiasis, its absence does not rule out this disease.

The diagnosis is based on demonstrating eggs in bronchial secretions, pleural fluid, or feces. A number of serologic tests also are available. The preferred treatment is with praziquantel.

Schistosomiasis

Pulmonary schistosomiasis develops when Schistosoma eggs are trapped in the pulmonary circulation, causing either pulmonary hypertension or formation of lung nodules. Skin is the portal of entry. The immature parasites migrate in the bloodstream and mature in venous plexuses. Eggs are then released and deposited in organs, where they cause a granulomatous reaction. Pulmonary hypertension is the most frequent and significant pulmonary manifestation of infection with Schistosoma mansoni or Schistosoma japonicum. The diagnosis is established by visualizing the characteristic eggs in organ biopsy specimens. Serologic tests also are available. Praziquantel is the preferred agent for treatment of schistosomiasis.

Echinococcosis

Echinococcosis is caused by the larval stage of Echinococcus granulosus or E. multilocularis, both of which may produce cystic lesions in any organ, mainly the liver and lungs. The infection is acquired through the ingestion of eggs. The parasite is transported in the bloodstream to the end organs. Pulmonary symptoms most often are related to compression of adjacent structures. Occasionally cysts may rupture into the airways or pleural space, causing an allergic reaction or superinfection. Chest CT typically shows sharply demarcated cysts with calcified borders and numerous smaller daughter cysts. The diagnosis is based on clinical and epidemiologic data. Serologic test findings are supportive, and aspiration of the cyst should be avoided, to limit the possibility of dissemination and associated hypersensitivity reactions. Surgical resection with complete removal of the cysts is the treatment of choice. Surgery should be done by experienced operators. Postoperative albendazole prophylaxis is recommended.

Suggested Readings

Carmona EM, Limper AH. Update on the diagnosis and treatment of Pneumocystis pneumonia. Ther Adv Respir Dis. 2011;5:41–59.

Chapman SW, Dismukes WE, Proia LA, et al. Clinical practice guidelines for the management of blastomycosis: 2008 update by the Infectious Diseases Society of America. Clin Infect Dis. 2008;46:1801–1812.

Dutkiewicz R, Hage CA. Aspergillus infections in the critically ill. Proc Am Thorac Soc. 2010;7:204–209.

Galgiani JN, Ampel NM, Blair JE, et al. Infectious Diseases Society of America: Coccidioidomycosis. Clin Infect Dis. 2005;41:1217–1223.

Hage CA, Wheat LJ, Loyd J, et al. Pulmonary histoplasmosis. Semin Respir Crit Care Med. 2008;29:151–165.

Kuzucu A. Parasitic diseases of the respiratory tract. Curr Opin Pulm Med. 2006;12:212–221.

Taylor WR, White NJ. Malaria and the lung. Clin Chest Med. 2002;23:457–468.

Wheat LJ, Freifeld AG, Kleiman MB, et al. Infectious Diseases Society of America: Clinical practice guidelines for the management of patients with histoplasmosis: 2007 update by the Infectious Diseases Society of America. Clin Infect Dis. 2007;45:807–825.

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