DOI: 10.1148/rg.251045043
RadioGraphics 2005;25:135-155
© RSNA, 2005
Thoracic Manifestations of Tropical Parasitic Infections: A Pictorial Review1
Santiago Martínez, MD2,
C. Santiago Restrepo, MD,
Jorge A. Carrillo, MD,
Sonia L. Betancourt, MD,
Tomás Franquet, MD,
Claudia Varón, MD,
Paulina Ojeda, MD and
Ana Giménez, MD
1 From the Department of Radiology, Hospital de San José, Fundación Universitaria de Ciencias de la Salud, Bogotá, Colombia (S.M.); the Department of Radiology, Louisiana State University Health Sciences Center, New Orleans, La (C.S.R.); the Departments of Radiology (J.A.C.) and Pathology (P.O.), Hospital Santa Clara, Bogotá, Colombia; the Department of Radiology, Hospital de la Samaritana, Bogotá, Colombia (S.L.B.); the Department of Radiology, Hospital de Sant Pau, Barcelona, Spain (T.F., A.G.); and the Department of Radiology, Fundación Cardioinfantil, Bogotá, Colombia (C.V.). Recipient of a Certificate of Merit award for an education exhibit at the 2003 RSNA Scientific Assembly. Received March 16, 2004; revision requested April 20 and received June 23; accepted June 23. All authors have no financial relationships to disclose. Address correspondence to S.M. (e-mail: smart4@lsuhsc.edu).
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Abstract
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Parasitic infections are distributed worldwide and affect hundreds of millions of individuals—primarily those living in endemic areas or in regions with a high rate of immigration from endemic areas—causing significant morbidity and mortality. A broad spectrum of parasitic infections (eg, amebiasis, malaria, trypanosomiasis, ascariasis, strongyloidiasis, dirofilariasis, cystic echinococcosis, schistosomiasis, paragonimiasis) frequently affect the lungs, mediastinum, and thoracic wall, manifesting with abnormal imaging findings that often make diagnosis challenging. Although most of these infections result in nonspecific abnormalities, familiarity with their imaging features as well as their epidemiologic, clinical, and physiopathologic characteristics may be helpful to the radiologist in formulating an adequate differential diagnosis.
© RSNA, 2005
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LEARNING OBJECTIVES FOR TEST 5
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After reading this article and taking the test, the reader will be able to:
- Identify the most common tropical parasitic diseases that affect the thorax.
- Describe these diseases in terms of their clinical manifestations and geographic distribution.
- Discuss the correlation between the clinical, radiologic, and pathologic features of these diseases.
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Introduction
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Parasites are organisms that obtain nourishment and shelter from other organisms. In this association, the parasite derives all the benefits, whereas the host may either be unaffected or suffer harmful consequences, with the development of a parasitic disease. The parasites responsible for these diseases are called obligate if they can live only in association with a host and facultative if they can live either in a host or independently. Furthermore, the parasites vary widely in size and complexity, from relatively simple unicellular protozoans (eg, amebae) to more complex multicellular organisms (eg, worms, flukes).
Parasitic diseases are distributed worldwide, with a higher prevalence in developing countries, especially in areas with inadequate sanitation. Some of these diseases are restricted to tropical and subtropical regions. Parasitic diseases represent one of the most common types of human infection throughout the world and are still the cause of much human morbidity and mortality. Epidemics of parasitic diseases (eg, malaria) have devastated large populations and pose a serious barrier to progress in many developing countries. Profound economic and social changes over the past decades are stimulating rural-to-urban migration in most endemic areas; consequently, parasitic diseases that are more common in rural areas are no longer entirely absent in the urban population. In industrialized countries, risk groups for parasitic diseases includes travelers, recent immigrants, institutionalized populations, and patients with acquired immunodeficiency syndrome (AIDS).
In this article, we review the radiographic and computed tomographic (CT) characteristics of several common and rare tropical parasitic infections with thoracic involvement, including infections from protozoa (amebiasis, malaria, trypanosomiasis), nematodes (ascariasis, strongyloidiasis, dirofilariasis), cestodes (cystic echinococcosis), and trematodes (schistosomiasis, paragonimiasis). We also discuss and illustrate the corresponding clinical and histopathologic findings.
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Protozoa
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Amebiasis
Amebiasis is a protozoan infection caused by Entamoeba histolytica and is the third most common cause of mortality among parasitic infections after malaria and schistosomiasis. Approximately 1% of the world’s population is thought to be infected, with 40,000–110,000 related deaths reported annually. Although distributed worldwide, amebiasis is most frequently seen among the lower socioeconomic classes in tropical and subtropical climates (1). The infection is acquired by ingestion of cysts that become trophozoites in the colon and may invade the bowel wall (Fig 1) (1–7).
After liver abscesses, pleuropulmonary involvement is the most common manifestation of extraintestinal amebiasis (8,9). The most common proposed route of infection is direct extension from a liver abscess to the thorax (tertiary route), which occurs in 6%–40% of patients with hepatic compromise. Hematogenous spread (secondary route) and, less frequently, aspiration (primary route) have also been reported (8). Pericardial compromise is present in less than 2% of all thoracic complications related to amebic hepatic abscesses and is more common when the left hepatic lobe is affected. Pain, cardiac tamponade, and sepsis are the most common clinical findings (9–11).
Thoracic amebiasis with pleural manifestations is suspected in patients from endemic areas with or without an obvious liver abscess. Stool examination is of limited value because (a) cysts or trophozoites are seen in only 15%–33% of patients with extraintestinal amebiasis (8), and (b) many pleuropulmonary manifestations may be unrelated to E histolytica, even if parasites are present in the feces. There is also a high prevalence of positive-stool asymptomatic carriers. The classic "anchovy sauce" content can be obtained from an amebic hepatic abscess or from expectorate that has traveled through a hepatobronchial fistula. The isolation of ameba in these samples is variable, with a broad range of values reported in the literature. Cultures can be obtained only in feces, since the protozoan does not grow in pus. Serologic analysis is helpful for the diagnosis of invasive disease in nonendemic populations (7,8).
Pleural effusion is a common finding in the setting of an amebic abscess. Such effusion can be either sterile, as in inflammatory pleural reactions, or an empyema if the hepatic abscess ruptures and traverses the diaphragm. Classically, elevation of the right hemidiaphragm precedes the visualization of pleural or pulmonary lesions. Airspace consolidation (Fig 2) and cavitation (Fig 3) are frequently seen. A hepatobronchial or bronchobiliary fistula can form if the abscess drains through a bronchus. Consolidations that are not continuous with the diaphragm have been described, since other routes of infection do exist. Invasion of the inferior vena cava occurs infrequently and may result in pulmonary thromboembolism. Pericarditis and pericardial effusion can result from an acute inflammatory reaction or abscess drainage to the pericardium from the liver (Fig 4) (8–11).
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Figure 2a. Right-sided amebic pleural empyema and pneumonia in a 43-year-old man with an abscess of the right hepatic lobe. (a) Initial chest radiograph shows pleural effusion and right-sided basal consolidation. (b) Chest CT scan helps confirm pleural involvement and right-sided basal alveolar infiltrates. Trophozoites of E histolytica were obtained at bronchoalveolar lavage.
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Figure 2b. Right-sided amebic pleural empyema and pneumonia in a 43-year-old man with an abscess of the right hepatic lobe. (a) Initial chest radiograph shows pleural effusion and right-sided basal consolidation. (b) Chest CT scan helps confirm pleural involvement and right-sided basal alveolar infiltrates. Trophozoites of E histolytica were obtained at bronchoalveolar lavage.
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Figure 3a. Right-sided amebic pneumonia in a 35-year-old man with a hepatic abscess. (a) Chest radiograph shows elevation of the right hemidiaphragm and right-sided basal consolidation with cavitation. (b) Photograph of the gross specimen demonstrates an irregular cavitary lesion (arrows). Anchovy sauce content and trophozoites of E histolytica (not shown) were found on the lesion wall.
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Figure 3b. Right-sided amebic pneumonia in a 35-year-old man with a hepatic abscess. (a) Chest radiograph shows elevation of the right hemidiaphragm and right-sided basal consolidation with cavitation. (b) Photograph of the gross specimen demonstrates an irregular cavitary lesion (arrows). Anchovy sauce content and trophozoites of E histolytica (not shown) were found on the lesion wall.
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Figure 4a. Amebic pericardial tamponade in a 27-year-old man with an abscess of the left hepatic lobe. The patient presented with pulsus paradoxus, fever, and chills. (a) Chest radiograph shows enlargement of the cardiac silhouette. (b) Chest CT scan shows extensive pericardial effusion that resulted from rupture of a left hepatic lobe abscess (not shown) into the pericardial space.
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Figure 4b. Amebic pericardial tamponade in a 27-year-old man with an abscess of the left hepatic lobe. The patient presented with pulsus paradoxus, fever, and chills. (a) Chest radiograph shows enlargement of the cardiac silhouette. (b) Chest CT scan shows extensive pericardial effusion that resulted from rupture of a left hepatic lobe abscess (not shown) into the pericardial space.
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Malaria
Various Plasmodium species—P falciparum, P vivax, P ovale, and P malariae—are responsible for human malaria. The parasite is transmitted by the Anopheles mosquito. Merozoites develop from schizonts within erythrocytes and are released by hemolysis at different time intervals depending on the species (Fig 5). These time intervals correlate with the periodicity of the episodic fever (tertian or quartan) (1–6,12). Malignant tertian fever (P falciparum) manifests with irregular fever spikes, whereas benign tertian fever (P vivax, P ovale) and quartan fever (P malariae) manifest with fever spikes every 48 and 72 hours, respectively (2). Between 400 and 490 million people are infected, and about 2.2–2.5 million deaths result annually worldwide in endemic areas such as South America, Africa, and southern Asia (Fig 6) (1,2).
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Figure 6. Drawing illustrates the geographic distribution of malaria (red dots). The infection is distributed widely in many tropical and subtropical climates. P vivax is the most prevalent worldwide type of malaria. P ovale is especially prevalent in tropical west Africa. Infection with P falciparum has the highest mortality rate.
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Fever with chills, sweating, anemia, leucopenia, and splenomegaly are the most common clinical findings. The diagnosis is usually made by identifying trophozoites or other parasitic forms within the erythrocytes in a thin blood smear or parasites in a thick smear. Serologic and nucleic acid amplification tests are also available (1,3–5,12).
Adult respiratory distress syndrome (ARDS) is the primary manifestation of malaria in the lung and was included in 1990 by the World Health Organization as a criterion for the definition of both severe and complicated malaria. Although the pathophysiologic features of ARDS are still unclear, changes result from vascular injury related to red blood cell sequestration and destruction, the release of parasite and erythrocyte material into the circulation, and the host response to these events. Severe P falciparum infection is the type most commonly associated with ARDS (Fig 7), but cases caused by P vivax and P ovale have also been reported. Radiographic and CT findings are consistent with noncardiogenic pulmonary edema. Pleural effusion, diffuse interstitial edema, and lobar consolidation may also be seen (12–21). Occasionally, bronchiolitis obliterans organizing pneumonia has been reported (22). Eosinophilic pneumonia with bilateral patchy consolidation has also been described in association with the use of pyrimethamine (23).
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Figure 7. ARDS in a 31-year-old man with P falciparum malaria. Chest radiograph demonstrates patchy bilateral areas of increased opacity. P falciparum trophozoites were found in a thick blood smear.
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Trypanosomiasis
Trypanosomiasis is caused by Trypanosoma cruzi, which is acquired through the bite of an insect from the Reduviidae family (genera Triatoma, Rhodnius, and Panstrongylus). Trypomastigotes are inoculated into the human body through the rubbing of reduviid bug feces over a bite or some other skin defect. They multiply within the macrophages, which ultimately rupture, releasing amastigotes that invade diverse organs via the bloodstream, including the heart and the gastrointestinal tract (esophagus and colon) (Fig 8) (1–6). Chagas disease, a form of trypanosomiasis, is endemic to areas of Central and South America, where nearly 24 million people are infected and 60,000 deaths result each year (Fig 9). Chagas disease has also been described in the south-western United States among immigrants from endemic areas (1,24,25).
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Figure 9. Drawing illustrates the geographic distribution of Chagas disease (American trypanosomiasis) (red dots). The disease is endemic to Central and South America. In North America, although the reservoir host (from the Reduviidae family) and the parasite can be found, most cases are related to immigration from endemic areas.
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Acute manifestations of trypanosomiasis are uncommon and include a febrile illness with facial or unilateral palpebral edema ("Romaña sign") and acute myocarditis. Direct visualization of trypomastigotes in a blood smear and xenodiagnosis are the mainstays of diagnosis. Late cardiac manifestations include chronic myocarditis with focal and diffuse loss of myocytes, fibrosis, and focal atrophy, as well as involvement of the conduction system with a bundle branch block, which can progress to a complete atrioventricular block. Late gastrointestinal compromise is related to damage to neurons of the myenteric plexus, with development of achalasia and megacolon (2,24–28). Bronchopathy has rarely been described when denervation of the bronchial walls occurs. Although the pathogenesis of bronchopathy is not well understood, this disease entity seems to have a small clinical impact. Serologic tests are preferred for the diagnosis of chronic forms.
Radiologic findings reflect the aforementioned clinical features. Acute myocarditis can cause acute heart failure (Fig 10). Severe cardiomegaly with or without signs of chronic heart failure (septal lines, pulmonary edema, pleural effusion) is frequently seen in dilated cardiomyopathy (Fig 11) (24–28). Achalasia and megacolon are usually confirmed with barium studies when appropriate clinical data suggest these diagnoses (Fig 12) (2,26). Bronchiectasis and tracheomegaly are rarely seen (29).
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Figure 10a. Acute Chagas disease in a 17-year-old boy with acute myocarditis. (a) Chest radiograph shows cardiogenic pulmonary edema, which resolved after 72 hours. Two days later, the patient had a sudden episode of arrhythmia and died. (b) Low-power photomicrograph (original magnification, x10; hematoxylin-eosin stain) demonstrates extensive acute myocarditis. Amastigotes of T cruzi were found within a myofiber.
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Figure 10b. Acute Chagas disease in a 17-year-old boy with acute myocarditis. (a) Chest radiograph shows cardiogenic pulmonary edema, which resolved after 72 hours. Two days later, the patient had a sudden episode of arrhythmia and died. (b) Low-power photomicrograph (original magnification, x10; hematoxylin-eosin stain) demonstrates extensive acute myocarditis. Amastigotes of T cruzi were found within a myofiber.
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Figure 11a. Chronic Chagas disease in a 39-year-old man with chronic dilated cardiomyopathy. (a) Chest radiograph shows global cardiomegaly with pulmonary congestion. (b) Photograph of the gross specimen demonstrates dilatation of the cardiac chambers with thickening of the ventricular myocardium. Scale is in centimeters. (c) Low-power photomicrograph (original magnification, x10; Giemsa stain) shows T cruzi amastigotes within a myofiber (arrow).
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Figure 11b. Chronic Chagas disease in a 39-year-old man with chronic dilated cardiomyopathy. (a) Chest radiograph shows global cardiomegaly with pulmonary congestion. (b) Photograph of the gross specimen demonstrates dilatation of the cardiac chambers with thickening of the ventricular myocardium. Scale is in centimeters. (c) Low-power photomicrograph (original magnification, x10; Giemsa stain) shows T cruzi amastigotes within a myofiber (arrow).
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Figure 11c. Chronic Chagas disease in a 39-year-old man with chronic dilated cardiomyopathy. (a) Chest radiograph shows global cardiomegaly with pulmonary congestion. (b) Photograph of the gross specimen demonstrates dilatation of the cardiac chambers with thickening of the ventricular myocardium. Scale is in centimeters. (c) Low-power photomicrograph (original magnification, x10; Giemsa stain) shows T cruzi amastigotes within a myofiber (arrow).
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Figure 12. Chagasic achalasia in a 13-year-old girl with Chagas disease. Barium esophagogram shows diffuse and severe dilatation of the esophagus. Histologic analysis demonstrated T cruzi amastigotes within the esophageal wall.
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Nematodes
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Ascariasis
The nematode Ascaris lumbricoides is acquired by ingesting food or fluids contaminated with feces (Fig 13). The resulting infection is distributed worldwide and is one of the most common parasitic infections, affecting 1.3 billion people and causing about 1,550 deaths per year (1). Parasites migrate from the small intestine to the pulmonary circulation, where they mature and produce destruction of capillaries and alveolar walls with subsequent edema, hemorrhage, and epithelial cell desquamation, causing chemotaxis of neutrophils and eosinophils (1–6).
The diagnosis is suspected in the appropriate clinical setting (fever, cough, expectoration, and eosinophilia, among other findings) and is confirmed by identifying larvae in the sputum. In patients from nonendemic areas who present with the clinical features described earlier, the diagnosis is suggested when eggs are present in the stool (2,30).
Chest radiography and CT demonstrate migratory, patchy alveolar infiltrates that characteristically clear within 10 days (Fig 14). Lobar consolidation and alveolar hemorrhage have also been described (2,7,30).
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Figure 14a. Ascariasis in a 35-year-old man with migratory infiltrates. (a) Chest radiograph shows areas of ground-glass increased opacity in the right lower and middle lobes. (b) High-resolution CT scan shows areas of ground-glass attenuation that correspond to the findings in a. The resolution of radiologic findings 1 week later demonstrated the transient nature of the disease. Larvae and eggs of A lumbricoides were found at bronchoalveolar lavage and in a fecal smear, respectively, during the acute stage.
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Figure 14b. Ascariasis in a 35-year-old man with migratory infiltrates. (a) Chest radiograph shows areas of ground-glass increased opacity in the right lower and middle lobes. (b) High-resolution CT scan shows areas of ground-glass attenuation that correspond to the findings in a. The resolution of radiologic findings 1 week later demonstrated the transient nature of the disease. Larvae and eggs of A lumbricoides were found at bronchoalveolar lavage and in a fecal smear, respectively, during the acute stage.
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Strongyloidiasis
Humans are the primary host of Strongyloides stercoralis, a microscopic nematode with infective larvae that invade the lungs and small intestine through the skin from the soil (Fig 15) (1–7). A chronic pathway of continuous autoinfection can lead to a massive and life-threatening parasitic infestation (hyperinfection syndrome), especially in AIDS patients and in patients who are receiving ongoing glucocorticoid therapy, in whom mortality may exceed 70% (31). The parasite is found in all tropical and subtropical regions. The highest infection rates in the United States are in the Southeast and Puerto Rico. Around 35 million people are infected worldwide (1).
Diagnosis is suggested clinically in patients who (a) have traveled to or live in an endemic area, (b) present with peripheral blood eosinophilia associated with pneumonia, bronchospasm, or bronchitis, and (c) exhibit abdominal pain or diarrhea. Severe compromise with systemic inflammatory response syndrome in immunocompromised patients should raise suspicion for hyperinfection syndrome, in which eosinophilia may be absent. Definitive diagnosis is made by identifying larvae in the sputum (2,7,31).
Physiopathologic events in S stercoralis involving the lung are similar to those seen in ascariasis and correspond with the imaging findings: ill-defined, patchy, migratory airspace consolidation (Fig 16) that typically resolves in 1–2 weeks. Hyperinfection syndrome can manifest with extensive pneumonia, alveolar hemorrhage, and ARDS. Although rare, a miliary pattern has also been described (Fig 17). Pleural effusion and secondary superimposed bacterial infection with cavitation and abscess formation are not uncommon findings (31–37).
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Figure 16a. Strongyloidiasis in an 18-year-old man with hemoptysis. (a) Chest radiograph demonstrates extensive bilateral patchy areas of consolidation. (b) High-resolution CT scan more clearly delineates the areas of consolidation. Bronchoalveolar lavage revealed larvae of S stercoralis.
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Figure 16b. Strongyloidiasis in an 18-year-old man with hemoptysis. (a) Chest radiograph demonstrates extensive bilateral patchy areas of consolidation. (b) High-resolution CT scan more clearly delineates the areas of consolidation. Bronchoalveolar lavage revealed larvae of S stercoralis.
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Figure 17a. Hyperinfection syndrome and strongyloidiasis in a 63-year-old man with hemoptysis and chronic renal failure who was being treated with corticosteroids. (a) Chest radiograph shows nodular and reticular infiltrates. (b) High-resolution CT scan of the lungs demonstrates areas of ground-glass attenuation and micronodules that display a miliary pattern. (c) Photomicrograph (original magnification, x40; Giemsa stain) obtained after bronchoalveolar lavage shows a larva of S stercoralis (arrow) surrounded by erythrocytes.
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Figure 17b. Hyperinfection syndrome and strongyloidiasis in a 63-year-old man with hemoptysis and chronic renal failure who was being treated with corticosteroids. (a) Chest radiograph shows nodular and reticular infiltrates. (b) High-resolution CT scan of the lungs demonstrates areas of ground-glass attenuation and micronodules that display a miliary pattern. (c) Photomicrograph (original magnification, x40; Giemsa stain) obtained after bronchoalveolar lavage shows a larva of S stercoralis (arrow) surrounded by erythrocytes.
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Figure 17c. Hyperinfection syndrome and strongyloidiasis in a 63-year-old man with hemoptysis and chronic renal failure who was being treated with corticosteroids. (a) Chest radiograph shows nodular and reticular infiltrates. (b) High-resolution CT scan of the lungs demonstrates areas of ground-glass attenuation and micronodules that display a miliary pattern. (c) Photomicrograph (original magnification, x40; Giemsa stain) obtained after bronchoalveolar lavage shows a larva of S stercoralis (arrow) surrounded by erythrocytes.
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Dirofilariasis
Although not common in humans, dirofilariasis is occurring with increasing frequency as the canine population grows. It is caused by Dirofilaria immitis, a filarial nematode that is transmitted by mosquitoes from dogs to humans (Fig 18). An immature adult worm unable to mature in the accidental human host can reach a peripheral vein and travel in the bloodstream until it lodges in a pulmonary vein (1,2). The disease has been reported predominantly in the temperate climates of the East Coast and South in the United States, but sporadic cases have been found worldwide (38).
Once the parasite lodges in a pulmonary vein, an infarction can originate. Frequently, there are no symptoms, although cough, pain, and hemoptysis have been described on rare occasions. A solitary pulmonary nodule 3 cm or less in diameter is the most common radiologic finding (Fig 19) (38–40). Serologic tests are available but are not very helpful. Definitive diagnosis is usually made at histopathologic analysis of the excised nodule and, sporadically, with aspiration of the nodule and demonstration of fragments of the parasite (7,38).
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Figure 19a. Dirofilariasis in an asymptomatic 14-year-old girl with a solitary pulmonary nodule. (a) Chest radiograph shows a soft-tissue-opacity nodule in the right upper lung. (b) Photomicrograph (original magnification, x40; Masson stain) obtained after surgical resection shows an infarcted peripheral vessel surrounded by necrotic lung tissue. Some remnants of the parasites are present in the lumen (arrows).
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Figure 19b. Dirofilariasis in an asymptomatic 14-year-old girl with a solitary pulmonary nodule. (a) Chest radiograph shows a soft-tissue-opacity nodule in the right upper lung. (b) Photomicrograph (original magnification, x40; Masson stain) obtained after surgical resection shows an infarcted peripheral vessel surrounded by necrotic lung tissue. Some remnants of the parasites are present in the lumen (arrows).
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Cestodes
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Echinococcus granulosus, E multilocularis, and E vogeli can cause cystic echinococcosis in humans. Infection is acquired by ingesting food or fluids contaminated with egg-containing feces. In the intestine, the released oncospheres (larvae) invade the bowel wall and migrate primarily to the liver through the portal system (Fig 20). E granulosus is the most common causative parasite and may be seen in the Mediterranean region, Eastern Europe, Africa, South America, the Middle East, Australia, and New Zealand (1–7). E multilocularis can be found in the Arctic (eg, Alaska, Canada, the entire tundra region) and in some regions of Asia (Russia, China, Japan) and northern Europe (central and eastern France, Switzerland, Austria, Germany) (41,42). E vogeli is most frequently seen in the tropical regions of South America (2,43,44). An estimated 65 million people in endemic areas are infected (Fig 21) (1).
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Figure 21. Drawing illustrates the geographic distribution of hydatid disease from E granulosus (red dots), E multilocularis (black dots), and E vogeli (green dots). E granulosus is the most common of the Echinococcus species.
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Unilocular Cystic Echinococcosis
E granulosus is responsible for unilocular cystic echinococcosis. Thoracic involvement may occur via a transdiaphragmatic route (0.6%–16% of cases of hepatic disease) or by means of hematogenous spread (41). The former results from the migration of the parasite from the liver to the pleural cavity. Pulmonary parenchymal involvement and chronic bronchial fistula can also be found. Hematogenous dissemination directly to the lung can occur, the lung being the second most common site of involvement (after the liver) in adults (10%–30% of cases) and the most common site in children (41,45).
Infection remains asymptomatic for months to years. When affecting the lung, it may manifest with cough, hemoptysis, bilioptysis, pneumothorax, pleuritis, lung abscess, parasitic pulmonary embolism, anaphylaxis secondary to cyst rupture, or cyst superinfection (41,45). At histologic analysis, cysts consist of three layers: (a) the pericyst, composed of fibroblasts, giant cells, and eosinophils, which form a rigid layer; (b) an acellular middle laminated membrane with nutrient functions; and (c) a thin, translucent inner germinal layer, which contain various scolices and generates daughter cysts (46). Indirect hemagglutination and enzyme-linked immunosorbent assay (ELISA) tests in association with abdominal ultrasonography can be used as screening tools in high-risk populations. Definitive diagnosis is made at histopathologic analysis. The differential diagnosis includes metastasis, Wegener granulomatosis, and other granulomatous diseases.
The most relevant radiographic and CT feature is the presence of cystic lesions, which can be solitary (60% of cases) or multiple, can be unilateral or bilateral (20%–50%), are predominantly found in the lower lobes (60%), and have a diameter between 1 and 20 cm (Fig 22). The coexistence of liver and lung disease is present in only 6% of patients (45). Uncomplicated cysts may be seen as round or oval masses that have well-defined borders, enhance after contrast material injection, and have a low-opacity or hypoattenuating content relative to the capsule. The "meniscus sign," or "crescent sign," which is characterized by the presence of air between the pericyst and the laminated membrane, appears as growth continues and the cysts erode adjacent bronchioles (Fig 23). Some authors consider this phenomenon to be a sign of impending rupture. Cystic rupture may result in different radiologic signs. The "cumbo sign," or "onion peel sign," is defined as the presence of the meniscus sign and an air-fluid level within the endocyst. The "water lily sign" represents an endocyst floating in a partially fluid-filled cyst, whereas an endocyst floating in a completely fluid-filled cyst is said to have a "mass within the cavity" appearance. Rupture can be associated with consolidation adjacent to the cyst. Radiographic and CT findings in transdiaphragmatic dissemination include pleural effusion, hemidiaphragm elevation, pulmonary consolidation, laminar basal atelectasis, pleural cysts, and, rarely, empyema (47–50). Other less common thoracic manifestations of the disease include invasion of the mediastinum, pericardium, chest wall (51–54), cardiovascular system, or inferior vena cava, the latter being associated on occasion with recurrent pulmonary embolism (55).
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Figure 22. Pulmonary hydatid disease from E granulosus in a 43-year-old man. Chest radiograph shows a large cyst in the right lower lung. (Courtesy of Ricardo Videla, MD, Hospital Italiano, Rosario, Argentina.)
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Figure 23a. Pulmonary hydatid disease from E granulosus in a 32-year-old woman. (a) CT scan of the lung shows a hypoattenuating crescent sign (meniscus sign) (arrows). (b) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) obtained after surgical resection demonstrates the inner germinal layer, to which several daughter protoscolices of E granulosus are attached.
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Figure 23b. Pulmonary hydatid disease from E granulosus in a 32-year-old woman. (a) CT scan of the lung shows a hypoattenuating crescent sign (meniscus sign) (arrows). (b) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) obtained after surgical resection demonstrates the inner germinal layer, to which several daughter protoscolices of E granulosus are attached.
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Alveolar Echinococcosis and Polycystic Echinococcosis
Alveolar echinococcosis and polycystic echinococcosis are caused by E multilocularis and E vogeli, respectively. They have a similar clinicopathologic course and are acquired through the same mechanism, similar to that described for E granulosus. The parasite grows from the metacestode (larva) in the liver and, in so doing, resembles a neoplasm. Lung involvement, which is less frequent than in unilocular cystic echinococcosis, results from metastatic dissemination or direct extension (2,41–43,56).
Infection becomes symptomatic after 5–15 years secondary to local compression or dysfunction of the affected organ, usually the liver. Nonspecific signs and symptoms such as fatigue, weight loss, cough, and hemoptysis can be present. A mass of fibrous tissue containing several scattered cavities of widely varying diameters with necrotic areas is frequently seen, as are calcifications. Definitive diagnosis can be made with immunohistochemical and histologic analysis. Serologic tests are also available and are important for early detection of asymptomatic cases (41).
CT and magnetic resonance imaging are the imaging modalities of choice for better defining the location and extent of pulmonary disease, which invariably coexists with liver infection. Metastatic lung disease (Fig 24) and chest wall compromise (Fig 25) are commonly seen. Calcifications may develop as the disease progresses (33%–100% of cases) (41–43). Secondary lung compromise by direct extension may mimic a lung cancer. A rare form of right atrial metastasis can cause recurrent episodes of pulmonary embolism (41).
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Figure 24a. Polycystic echinococcosis of the lung from E vogeli in a 25-year-old man. (a) Chest radiograph demonstrates multiple peripheral round areas of soft-tissue opacity. (b) CT scan shows a clearly defined capsule with a relatively hypoattenuating center, a finding that reflects the cystic nature of the lesions. E vogeli was identified at pathologic analysis as the etiologic agent.
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Figure 24b. Polycystic echinococcosis of the lung from E vogeli in a 25-year-old man. (a) Chest radiograph demonstrates multiple peripheral round areas of soft-tissue opacity. (b) CT scan shows a clearly defined capsule with a relatively hypoattenuating center, a finding that reflects the cystic nature of the lesions. E vogeli was identified at pathologic analysis as the etiologic agent.
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Figure 25a. Polycystic echinococcosis of the chest wall from E vogeli in a 13-year-old boy. (a) Chest CT scan shows cystic thickening of the pleura with chest wall involvement. (b) Photograph of the surgically resected gross specimen demonstrates osseous expansion secondary to rib invasion (scale is in centimeters). Histologic analysis revealed E vogeli. (Case courtesy of Humberto Varón, MD, Fundación Cardioinfantil, Bogotá, Colombia, and Susana Onatra, MD, Hospital de la Misericordia, Bogotá, Colombia.)
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Figure 25b. Polycystic echinococcosis of the chest wall from E vogeli in a 13-year-old boy. (a) Chest CT scan shows cystic thickening of the pleura with chest wall involvement. (b) Photograph of the surgically resected gross specimen demonstrates osseous expansion secondary to rib invasion (scale is in centimeters). Histologic analysis revealed E vogeli. (Case courtesy of Humberto Varón, MD, Fundación Cardioinfantil, Bogotá, Colombia, and Susana Onatra, MD, Hospital de la Misericordia, Bogotá, Colombia.)
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Trematodes
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Schistosomiasis
There are three important Schistosoma species: S hematobium, S mansoni, and S japonicum. Although all three species can cause pulmonary disease, S mansoni and S japonicum are the ones most frequently observed. S mansoni is endemic to Africa, Saudi Arabia, Madagascar, Brazil, Surinam, Venezuela, and Puerto Rico, whereas S japonicum is more frequently seen in east Asia. Infection is acquired through exposure of the skin to water contaminated with cercariae excreted by snails, which have the ability to penetrate the skin or the intestinal wall, then migrate to the lung and afterward to the liver, where the parasite continues its life cycle (Fig 26) (2,44). Schistosomiasis is the second most common cause of mortality among parasitic infections after malaria, affecting 150–200 million people and causing 500,000 deaths each year (Fig 27) (1).
Pulmonary compromise is divided into early and late forms. Early pulmonary schistosomiasis (3–8 weeks after parasitic penetration) results from immunologic (type 3) reaction, in which eosinophils are sequestered in the lungs. Common clinical findings include shortness of breath, wheezing, and dry cough. The diagnosis is suggested in patients who live in or have traveled to endemic areas and who present with eosinophilia. Patients may have both clinical and radiologic manifestations after the onset of treatment. In Katayama fever, pulmonary symptoms coincide with febrile illness, and this condition is thought to be an immunologic reaction to the parasite eggs. Associated symptoms include urticaria, arthralgia, hepatosplenomegaly, hepatitis, eosinophilia, and pulmonary disease. Small nodular lesions with ill-defined borders (Fig 28) or, less commonly, a reticulonodular pattern or bilateral diffuse areas of ground-glass increased opacity or hyperattenuation may be seen at radiography and CT. Asymptomatic cases that manifest with abnormal radiologic findings may also be seen, but their real prevalence is unknown. Sensitivity is low for the examination of stool and urine for eggs in this stage of infection, although rectal biopsy may help improve the diagnosis. ELISA is a better initial step, but positive results must be confirmed with enzyme-linked immunoelectrotransfer blot. Because serologic tests remain positive for years even after treatment, they are not helpful for the diagnosis of reinfection or for determining the success of treatment (44,57).
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Figure 28. Early pulmonary schistosomiasis in a 28-year-old man who had traveled to Mali. Initially, the patient had fever and urticaria, after which he experienced dry cough, predominantly at night. Chest CT scan shows multiple nodular lesions with ill-defined borders in the lower lobes. Histologic analysis revealed S mansoni. (Courtesy of E. Schwartz, MD, Center for Geographical Medicine and Tropical Diseases, and J. Rozenman, MD, Department of Radiology, Sheba Medical Center, Tel Hashomer, Israel.)
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Chronic pulmonary disease results from granulomatous (type 4) reaction to eggs deposited in the pulmonary vasculature, which leads to intimal fibrosis, pulmonary hypertension, and cor pulmonale. It is often preceded by liver involvement by portal hypertension, which allows the eggs to shunt from the portal system into the pulmonary vasculature. The clinical picture includes dyspnea, chest pain, fatigue, palpitations, cough, and, lately, right-sided heart failure. Radiographic and CT findings are also consistent with these clinical findings and include cardiomegaly and pulmonary arterial enlargement. Diagnosis is made by identifying eggs in stool or urine samples or at rectal biopsy. Serologic tests are not very helpful because they cannot help differentiate a former infection from current disease (44,57–60).
Paragonimiasis
Human paragonimiasis is caused by the trematode Paragonimus westermani or other Paragonimus species through the ingestion of raw or partially cooked freshwater crabs or crayfish infected with the metacercaria (Fig 29). The main endemic areas are east Asia, Southeast Asia, Latin America (primarily Peru), and Africa (primarily Nigeria) (Fig 30) (1–7). Many cases have been reported in the United States among Indo-Chinese and Latin American immigrants (61–63). It is believed that 195 million people are at risk, and 20.7 million are infected in endemic areas (1).
The lung is the target organ, although cutaneous and cerebral paragonimiasis have also been described. Patients present with fever, chest pain, and respiratory symptoms such as chronic cough and hemoptysis. Diagnosis is confirmed by detecting parasite eggs in the sputum, pleural fluid, or feces; in addition, larvae can often be found at bronchial brushing. Intradermal and serologic tests are also available. Tuberculosis is the main alternative in the differential diagnosis (61).
Radiologic findings correlate well with the stage of the disease. The penetration of juvenile worms through the diaphragm into the pleural cavity can cause pleural effusion or pneumothorax. Once the parasites get to the lung, patchy airspace consolidation can occur, a phenomenon that reflects the presence of an exudative or hemorrhagic pneumonia (Fig 31) which can cavitate (Fig 32). Contrast material–enhanced CT performed during this stage may show hypoattenuating fluid-filled cysts surrounded by hyperattenuating consolidation in the adjacent lung. Linear areas of increased opacity or hyperattenuation indicate peripheral atelectasis or worm migration. Worm cysts, whose diameters range from 0.5 to 1.5 cm, are better visualized after the consolidation resolves and manifest as either solitary or multiple nodules (Fig 33) or gas-filled cysts depending on their content and their communication with the airway. Chest radiographic and CT findings include a ring shadow usually less than 3 mm thick and a crescent-shaped area of increased opacity or hyperattenuation within the cyst that represents worms attached to the wall. Complications of cysts include pleural effusion, empyema, and pneumothorax (61–67).
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Abstract
LEARNING OBJECTIVES FOR TEST...
