Parasitic Infections


Pathogenic parasites that involve the lungs include multicellular helminths as well as unicellular protozoa. Although parasitic infections have classically been associated with tropical and subtropical regions, some are prevalent worldwide. Moreover, travel and immigration have resulted in globalization of formerly geographically restricted infectious diseases, and some of these affect the lungs.

Certain parasitic infections commonly present with pulmonary manifestations, while for others, pulmonary in­­volvement is an unusual complication. With the exception of Paragonimus, the lung fluke, few parasites specifically target the lungs, although many helminths migrate through the lungs en route to the gastrointestinal tract. Some parasites that infect the lungs more commonly infect other sites such as the gastrointestinal tract ( Entamoeba , Echinococcus ); while others involve the lungs as part of a generalized systemic infection ( Toxoplasma, Plasmodium ) ( Table 39-1 ).

Table 39-1

Characteristics of the Most Common Parasites Causing Pulmonary Pathology

Parasite Distribution Pulmonary Manifestation Diagnosis Treatment
Ascariasis: Ascaris lumbricoides Worldwide, but widely in tropics Loeffler syndrome, usually 9 to 12 days after exposure to eggs
Substernal discomfort
Crackles and wheezing
Transient opacities
Examination of sputum
Eosinophilia during larval migration
Stool ova and parasites: usually positive after pulmonary symptoms resolved
Dirofilariasis (dog heartworm): Dirofilaria immitis and D. repens Worldwide (associated with dogs) Pulmonary nodule Usually requires biopsy to rule out other causes None (benign, so no treatment necessary)
Hookworm: Ancylostoma duodenale and A. caninum ; Necator americanus, N. brasiliense Worldwide especially tropics Loeffler syndrome
Transient opacities
Eosinophilia during larval migration Albendazole
Strongyloidiasis (also a hookworm, but unique due to autoinfection cycles): Strongyloides stercoralis (and sometimes other Strongyloides species) Worldwide but particularly in tropic or subtropical regions Loeffler syndrome
Chronic cough
Pneumonia or sepsis in hyperinfection
Sputum examination
Eosinophilia during larval migration
Stool ova and parasites
Serology (cannot discriminate acute vs. past)
Ivermectin (may need longer doses for immunocompromised hosts); due to risk of hyperinfection, consider treating all seropositives
Trichinosis (also a hookworm but encysts): Trichinella spiralis Worldwide zoonosis Respiratory distress
Radiographic appearance variable
Serology Albendazole
Tropical pulmonary eosinophilia (lymphatic filariasis): Wucheria bancrofti and Brugia malayi Tropics, particularly South Asia Tropical eosinophilic pneumonia with interstitial sopacities
Chronic cough
Serology, Bronchoalveolar lavage
Doxycycline (treats symbiont)
Visceral larval migrans (nonhuman ascarid): Toxocara canis and T. cati Worldwide Interstitial opacities with eosinophilic pneumonia Serology
Eosinophils in blood and sputum
May not be needed
Albendazole (or ivermectin) in severe cases
Hydatid cyst: Echinococcus granulosus and E. multilocularis Worldwide (especially in sheep-rearing locales) Pulmonary cyst; second most common site after liver; hemoptysis Serology, Eosinophilia rare Surgical, albendazole
Paragonimiasis (Lung flukes): Paragonimus westermani, P. africanus, P. caliensis, P. kellicotti (US) Southeast Asia, Central and South America, Africa; US Pulmonary parenchymal invasion (larvae mature in lung) with cavitary lesions
Eggs in sputum or stool
Schistosomiasis: Schistosoma mansoni, S. haematobium, S. japonicum, S. intercalatum Asia, South America, Africa Hematogenous seeding with heavy infection
Pulmonary hypertension
Stool ova and parasites
Amebiasis: Entameba histolytica Worldwide; mostly tropical Abscess
Lungs 2nd most common extraintestinal site after liver
Percutaneous aspiration
Malaria: Plasmodium species ( falciparum, vivax, ovale, malariae, knowlesi) Africa, Asia, Central and South America Interstitial opacities
Acute respiratory distress syndrome
Blood smear
Rapid diagnostic test
Antimalarial treatment; specifics depend on species and geographic distribution of drug resistance
Toxoplasmosis: Toxoplasma gondii Worldwide; most common in immunocompromised, especially HIV-infected with CD4 < 100 Interstitial pneumonia usually associated with disseminated disease Smear of bronchoalveolar lavage
Serology (cannot discriminate acute from past)
Rarer Protozoan Pulmonary Parasite Syndromes
Free-living ameba: Acanthamoeba castellani or A. polyphagia , Balamuthia mandrillaris, Naegleria fowleri Worldwide Rare, usually immunocompromised; more frequently seen as central nervous system disease Smear/tissue section No highly effective treatment. Treatment varies according to species involved in the infection.
Babesiosis: Babesia microti, Babesia divergens US, Europe Interstitial opacities: acute respiratory disease syndrome Blood smear, PCR, serology Quinine/clindamycin
Cryptosporidiosis: Cryptosporidium parvum and C. hominus Worldwide Primarily gastrointestinal; respiratory syndrome and transmission proposed Smear of bronchoalveolar lavage or sputum
Stool ova and parasites
No highly effective treatment (nitazoxanide approved for children with diarrhea)
Leishmaniasis: Leishmania donovani Africa, Central and South America Interstitial pneumonia usually associated with disseminated disease Smear or histopathology of tissue
PCR, serology
Pentavalent antimonials
Amphotericin B
Microsporidiosis (related to fungi): Many species Worldwide; especially in immunocompromised Interstitial pneumonia
Chromotrope 2A stains of sputum, smears, or tissue Albendazole
American trypanosomiasis: Trypanosoma cruzi Central and South America Interstitial pneumonia usually associated with disseminated disease Serology, Blood smear, PCR Nifurtimox

Serologic testing can be performed by enzyme-linked immunosorbent assay (ELISA), immunofluorescence, or Western blot. In general ELISA is most common in that there are standardized cut-off points and less operator variability.

Antigen tests can be performed by Western blot or ELISA designed to detect the antigen of choice.

PCR, polymerase chain reaction.

Increasing use of immunosuppressive therapy, organ transplantation, and human immunodeficiency virus (HIV)/ acquired immunodeficiency syndrome (AIDS), have led to expansion of populations vulnerable to selected parasitic diseases. Moreover, climate change and ecologic perturbations have affected the transmission and geographic range of human parasites. These factors necessitate greater familiarity of all physicians with infections that were previously seen only by specialists in tropical medicine. Clinical presentations of parasitic infections may be nonspecific and pulmonary specialists must be aware of potential pulmonary presentations.

This chapter reviews the pulmonary complications of parasitic infections that exhibit four major patterns: (1) parasites that primarily involve the lungs; (2) parasites that involve the lungs as a transient event in their life cycles; (3) parasites that involve the lungs less often than they involve other organs such as those of the gastrointestinal tract; (4) those that involve the lungs during widespread, systemic infections.

Some topics in this chapter also are discussed in the chapters on pulmonary complications of HIV ( Chapter 90 ) and on eosinophilic lung diseases ( Chapter 68 ).

Evaluation of a Patient with Possible Parasitic Infection of the Lung

Because specific parasitic infections differ in their geographic distribution, clinicians must consider the diseases that are prevalent in the areas where a patient has traveled or resided. A detailed travel history with information on food and liquids consumed, swimming or wading, insect bites, and medications taken are especially useful in formulating a differential diagnosis. The interval between the time of travel or emigration and the onset of symptoms may provide clues: enteric protozoa or helminthic infections typically present more than 2 weeks after exposure and some parasites such as Strongyloides, Plasmodium vivax or ovale, and Entamoeba histolytica can present years after exposure.

Some parasites have complex life cycles with numerous hosts and many are vector borne, while others are acquired by exposures to contaminated soil or water. Many emerging parasitic infections are zoonoses, in which the disease is spread from nonhuman animals to humans. In developing a differential diagnosis for respiratory complaints that may have a parasitic etiology, knowledge of the geographic distribution of various parasites, of potential vectors, and of potential sources of environmental contamination is essential.

Laboratory tests that may be helpful in initial evaluations include a complete blood count with differential, liver function tests, and a basic metabolic panel; in some contexts, examination of the sputum and/or stool samples is essential. Peripheral eosinophilia suggests a potential parasitic cause of pulmonary disease but most protozoan infections are not associated with eosinophilia, and a lack of eosinophilia does not exclude parasitic infection. Diagnosis of intestinal parasites is most often dependent upon microscopic examinations that require adequate specimens and experienced laboratory personnel. Depending on the parasite suspected, stool antigen tests ( E. histolytica) , microscopic examination of blood smears (malaria and Babesia ), or collection of respiratory samples including sputum or bronchoalveolar lavage (BAL), or serologic tests ( Strongyloides enzyme-linked immunosorbent assay [ELISA]) may be warranted. Specialized laboratories are able to perform polymerase chain reaction (PCR) tests or other nucleic acid–based tests for specific parasites but these are often not routinely available. Rapid antigen tests for the diagnosis of malaria are approved and are becoming increasing available. In some cases, specialized testing is available at the Centers for Disease Control and Prevention (CDC); the CDC website provides useful resources for diagnostic testing ( ), and the CDC provides access for certain medications that are not routinely available in the United States.


Helminths, or worms, cause the most common parasitic infections worldwide. They are classified into two major phyla: (1) nematodes, or round worms, include the major intestinal worms, and the filarial worms that cause lymphatic filariasis and onchocerciasis; (2) platyhelminths or flat worms include flukes (or trematodes), such as Schistosoma, and tapeworms (or cestodes). Helminths mainly infect rural and impoverished people, and chronic infection in children may be associated with growth stunting and long-term effects on health and cognitive function. With the exception of Strongyloides, helminths do not have internal autoinfection cycles in the host, and disease is generally proportional to worm burden, as assessed by the number of eggs per gram of feces.

Helminths are a common cause of eosinophilic pneumonia, although the differential diagnosis of eosinophilic pneumonia includes other infectious and noninfectious syndromes. (See also Chapter 68 .) Helminth infections classically present with Loeffler syndrome, characterized by transient interstitial pulmonary opacities and eosinophilia that result when larval forms of helminths migrate through the lungs. These helminth infections are often accompanied by peripheral eosinophilia, bronchospasm, and elevated immunoglobulin (Ig) E levels. Larvae migrate through the lungs, up the respiratory tree and then are swallowed, thereby reaching the gastrointestinal tract. Because the larvae have not yet matured into egg-bearing adults, stool ova and parasite examinations may not be helpful during acute infection. Depending on the burden of infection, helminth infestation and the accompanying eosinophilic pneumonia may result in an asthma-like syndrome, or in pulmonary damage due to release of cytotoxic cationic proteins from eosinophil granules.


The parasitic nematodes (round worms) of humans that cause ascariasis, hookworm disease, trichinosis, and strongyloidiasis have a lower respiratory phase as part of their life cycles. In each, larvae migrate through the lungs in transit to the gastrointestinal tract. In most cases, this migratory phase is asymptomatic, but cough, substernal discomfort and wheezing may be accompanied by transient radiographic opacities and eosinophilia (Loeffler syndrome).


Ascariasis caused by the nematode Ascaris lumbricoides is the most common human helminth infection and is estimated to infect almost 1 billion people. Although it has a worldwide distribution, ascariasis is most common in tropical and semitropical regions. Although highly prevalent, ascariasis is associated with chronic disability rather than death. An estimated 4 million people in the United States are infected, primarily children in rural areas of the southern United States. Humans are the only known host of A. lumbricoides , although the pig species A. suum is similar biochemically and morphologically. Females produce eggs that are shed in stool. The eggs mature in moist environments; humans are infected by swallowing ova that contaminate water, food, or soil. In regions where there are high worm burdens, infection can also be acquired by inhalation of ova. The eggs bear rhabditiform larvae that hatch in the intestine. The resulting larvae are released, burrow through the intestinal wall, and enter the hepatic circulation via capillaries and lymphatics. They then migrate via the right side of the heart into the lungs. The worms migrate up the bronchial tree, are swallowed, and make their way to the duodenum, where they mature into adults after several months. Once the worms reach the intestines, children may have nausea, vomiting, abdominal pain, and anorexia, reflecting high worm burdens that can lead to obstruction or chronic malnutrition. Adult worms can live in the human intestine for several years.

Clinical Features.

Infected individuals, usually children, are typically asymptomatic. The most common symptoms are nonspecific abdominal complaints. However, some may experience malaise and fever with or without respiratory symptoms such as cough, chest pain, dyspnea, bronchospasm, and hemoptysis. Pulmonary symptoms develop 9 to 12 days after ingestion of eggs and can persist 2 to 3 weeks. This stage of the infection may be associated with leukocytosis and eosinophilia. Acute eosinophilic pneumonia resulting in respiratory distress and requiring intubation has been reported but is rare. In some regions of the world, pneumonitis is seasonal, due to climate conditions that favor transmission of ascariasis.


Chest imaging during the initial stage of infection may reveal transient unilateral or bilateral opacities ( eFig. 39-1 ). The diagnosis is difficult to confirm during the acute stage, because ova do not appear in the stool until 2 to 3 months after infection. Peripheral eosinophilia may be detected, and larvae, eosinophils, or Charcot-Leyden crystals may be found in sputum or gastric contents.


The treatment of choice for ascariasis is albendazole, although mebendazole and ivermectin are also efficacious against adult worms. Although the pulmonary phase is self-limiting, the persistent gastrointestinal phase warrants treatment to relieve symptoms and reduce transmission.

Hookworm Disease

Hookworm disease is caused by Ancylostoma duodenale, Ancylostoma ceylanicum, or Necator americanus . These helminths infect at least a half billion people worldwide, primarily in tropical and subtropical regions. They reside in the small intestine where they attach to the mucosa and feed on blood and host tissue, causing iron deficiency anemia as the major cause of morbidity. Unlike other helminths, hookworm prevalence increases with age, and there is no protective immunity.

Clinical Features.

Hookworm ova are passed in the stools of an infected person, which then hatch into rhabditiform larvae that molt and become filariform larvae. Filariform larvae in the soil penetrate the skin of a human host; this can be associated with a pruritic rash. The larvae enter the lymphatics or venules and ultimately reach the pulmonary circulation. Some persons experience cough, bronchospasm, and transient pulmonary opacities with or without fever. Bronchitis and/or pneumonia may develop when the larvae break through capillaries and enter the alveolar spaces. Peripheral and pulmonary eosinophilia are common during this stage of infection.

Once the worms reach the intestine, an individual may have nonspecific gastrointestinal symptoms including nausea and abdominal pain. Iron deficiency anemia is the most important consequence of hookworm infection and can lead to cognitive problems. Malnutrition and hypoproteinemia can also complicate hookworm infection.

Diagnosis and Treatment.

Stool examination reveals hookworm ova 2 to 3 months after pulmonary symptoms, but in cases of light infection, concentration of stool may be necessary to detect the ova. Diagnosis during the pulmonary phase is difficult and relies upon isolation of larvae from respiratory secretions, BAL fluid, or gastric secretions. The treatment of choice is albendazole (single dose) or mebendazole (twice daily for 3 days). These drugs kill the adult worms but are not effective against the pulmonary larval stages. Patients should be screened for ova in stools 1 month after treatment and, if ova are still present, retreatment is indicated to eliminate adults that developed after the initial treatment.


Although there are more than 50 species of Strongyloides, Strongyloides stercoralis is the most common in humans. This helminth has a worldwide distribution and is endemic in Latin America, south Asia, sub-Saharan Africa, the United States (especially the southern states and Appalachia), Europe, and Australia. Up to 100 million people are estimated to be infected, although some experts believe that the worldwide prevalence of Strongyloides infection may be much higher. Due to lack of awareness amongst clinicians and its prevalence in people in resource poor settings, Strongyloides infection is often undiagnosed or diagnosed late.

Strongyloides has a complex life cycle consisting of free-living and parasitic forms. Humans are the primary reservoir and acquire infection from soil or vegetation contaminated with human feces. Similar to hookworm infection, strongyloidiasis is initiated by penetration of the skin by infective filariform larvae, frequently through the soles of the feet. After penetration of the infective larvae through the skin or gut mucosa, they are carried via the circulation to the lungs and penetrate into alveoli and then ascend the tracheobronchial tree. The larvae are swallowed and reside in the small intestine where they ultimately develop into adult worms. Ova are released and hatch into rhabditiform larvae, which are passed in feces. These larvae transform into filariform larvae. The larvae can also molt and transform into free-living adults in soil, where they may transform into infective filariform larvae. Some rhabditiform larvae may molt into filariform larvae while still in the small bowel and then invade the mucosa of the bowel or the perianal area. Filariform larvae that form internally can cause autoinfection in which they migrate through the circulation to the lungs, thereby recapitulating the early migratory phase. Infection can also take place through the mucosa of the lower gastrointestinal tract or the perianal area from larva that have transformed into infective filariform larvae in the gut.

Infection with Strongyloides results in a variety of clinical syndromes ranging from a mild disease to the hyperinfection syndrome seen in immunocompromised hosts. Cell-mediated immunity that develops after primary infection limits the extent of autoinfection, so larvae and adult worms largely remain confined to the intestine, where they can survive for decades in immunocompetent individuals. With immune suppression, especially caused by steroids, and other immunodeficient states, especially infection with human T-lymphotropic virus-1 (HTLV-1), autoinfection can become pronounced and lead to hyperinfection.

Clinical Features.

The clinical manifestations of strongyloidiasis depend on the intensity of infection and immunologic status of the individual. Acute infection is rarely symptomatic but pneumonitis can develop during the larval migration phase. More than 50% of patients with chronic infections are asymptomatic. Up to 75% of symptomatic patients have peripheral eosinophilia and elevated serum IgE levels; strongyloidiasis should be in the differential diagnosis of any person who presents with persistent eosinophilia.

Patients can present with abdominal pain, diarrhea, and weight loss. Dermatologic symptoms include pruritus, urticaria, and skin eruptions including larva currens, which is manifest as linear streaks that can be seen on the trunk, thighs, and buttocks due to migrating larvae ( Fig. 39-1 ). The common pulmonary manifestations in immunocompetent individuals are transient pulmonary opacities with productive cough, dyspnea, and bronchospasm. Chest radiographs range from normal to bilateral nonspecific opacities. Strongyloidiasis may cause asthma, and improvement may follow eradication of the infection. Reactive arthritis, nephrotic syndrome, chronic malabsorption, duodenal obstruction, and hepatic lesions have also been associated with chronic strongyloidiasis. Patients from highly endemic areas who have asthma or chronic obstructive pulmonary disease with eosinophilia should always be screened for Strongyloides infection before instituting steroid therapy to avoid hyperinfection.

Figure 39-1


A, Larva currens in a patient with chronic strongyloidiasis. B, Filariform larva in a pulmonary biopsy specimen ( arrow ). C, Filariform ( arrow ) and rhabditiform ( arrowheads ) larval stages of Strongyloides stercoralis in the stool from a patient with hyperinfection syndrome. These were also found in the sputum.

( A and B, from Herman Zaiman’s “A Pictorial Presentation of Parasites” with permission of the American Society of Tropical Medicine and Hygiene.)

The Strongyloides hyperinfection syndrome develops due to accelerated autoinfection. Hyperinfection is usually observed in the setting of immunosuppression, especially when caused by high-dose corticosteroids although other immunosuppressive drugs and radiation therapy have also been implicated. Infection with human T-lymphotropic virus-1 markedly predisposes to hyperinfection; this is thought to be secondary to deficiency of T-helper 2 cells that normally contribute to control of helminths. In addition, immunosuppression associated with lymphoma, leukemia, malnutrition, organ transplantation, and HIV/AIDS predispose to Strongyloides hyperinfection (see eFig. 90-30 ), although some studies indicate the risk is not increased by HIV.

Strongyloides hyperinfection is characterized by prominent gastrointestinal symptoms, including abdominal pain, nausea, vomiting, diarrhea, and ileus. The lung is also an important target in patients with Strongyloides hyperinfection. As filariform larvae migrate through the lungs, they cause pneumonitis with cough, hemoptysis, and respiratory failure. As the larvae leave the lumen of the gastrointestinal tract and invade the intestinal mucosa, they may carry bacteria from the gastrointestinal tract, resulting in polymicrobial bacteremia, bacterial pneumonia, acute respiratory distress syndrome, and gram-negative bacillary meningitis. Strongyloides hyperinfection has also been reported to mimic accelerated idiopathic pulmonary fibrosis. Mortality of disseminated strongyloidiasis can be as high as 90%.


In Strongyloides hyperinfection, larvae, ova, and adult worms may be observed in sputum, urine, BAL fluid, and other body fluids (see Fig. 39-1 , see eFig. 90-30C ). Diagnosis of Strongyloides infection may be difficult if the parasite load is low, because the most common diagnostic test is based on detection of Strongyloides ova in stool samples (see Fig. 39-1 ). Recently developed serology assays use ELISA or immunofluorescence to detect serum antibodies to Strongyloides . While ELISA is more sensitive than detecting ova in stool, the specificity of this test is suboptimal in regions where other nematodes such as filariae are endemic, because cross-reactive antibodies are common. Eosinophilia is common during hyperinfection; lack of eosinophilia is often associated with a poor prognosis.


Ivermectin is the treatment of choice and eliminates the worm in more than 90% of subjects; ivermectin is significantly more effective than albendazole. Although ivermectin is usually prescribed as a 2-day course, treatment is usually extended and individualized for the hyperinfection syndrome, to ensure eradication. Human T-lymphotropic virus-1 coinfection is associated with a higher rate of treatment failure, and some patients may require additional therapy to prevent recurrence. Combination treatment with ivermectin and albendazole has also been proposed in severe cases or in chronic infections with human T-lymphotropic virus-1 coinfection when ivermectin alone has failed. In hyperinfection cases where oral treatment cannot be absorbed or tolerated, the veterinary preparation of ivermectin has been administered subcutaneously. There is no reliable test to monitor for cure but many individuals have reversion or decline of IgG serologies with successful treatment. All patients with S. stercoralis infection should be treated, because of the risk of autoinfection and dissemination.

Some experts recommend that patients from highly endemic areas have a screening serology for strongyloidiasis before (or at the time of) starting steroids or organ transplantation and, if seropositive, treatment is indicated to prevent the hyperinfection syndrome.

Tropical Pulmonary Eosinophilia

Tropical pulmonary eosinophilia (TPE) is a distinct clinical syndrome in patients from tropical areas endemic for lymphatic filariasis such as Wuchereria bancrofti or Brugia malayi . Most cases have been described in India, Pakistan, Sri Lanka, Southeast Asia, parts of the African continent, and South America, especially Brazil and Guyana. TPE is now recognized in nonendemic areas, predominantly in immigrants; TPE is thought not to be a significant risk during a brief visit to an endemic area.

Filariae have five morphologic stages; humans are infected with third stage larvae transmitted by mosquitoes. Infective larvae molt twice and develop into adults that survive in a human host for up to 20 years. The first stage larvae, or microfilariae, are released into the circulation by female adult worms. Wucheria and Brugia microfilariae circulate in the blood in a temporal pattern that coincides with the feeding habits of their mosquito vectors.

Clinical Features.

TPE is seen predominantly (80%) in males, usually in middle age. The major clinical features of TPE include nocturnal paroxysmal cough and bronchospasm, low-grade fever, weight loss, and lymphadenopathy; some patients also have hepatosplenomegaly. Leukocytosis, marked peripheral eosinophilia, and elevated serum IgE levels are common, and sputum or BAL specimens often contain eosinophils. Pulmonary function tests reveal both restrictive and obstructive defects. Although TPE is caused by filaria, patients with TPE do not have detectable microfilaremia. The pathogenesis of TPE is poorly understood but is believed to represent a response to microfilariae that are trapped in the lungs.


The diagnosis of TPE is based on the combination of clinical, radiologic, epidemiologic, and laboratory data, without the need for lung biopsy. Patients have nocturnal dyspnea with eosinophilia, elevated serum IgE, and a positive serologic test (ELISA) for antibodies to filarial antigens. Because the specificity of filarial serology tests is compromised by cross-reactivity with other helminths, other data are important for an accurate diagnosis. Chest radiographs usually reveal increased bilateral bronchovascular markings and reticulonodular opacities or diffuse miliary lesions, or opacities in the middle and lower lung fields ( Fig. 39-2 , eFig. 39-2 ). Cavitation, bronchiectasis, and pleural effusion have been reported but are uncommon; chest radiographs may also be normal. When pathological specimens have been obtained, eosinophilic infiltration of the interstitial and perivascular areas, eosinophilic abscess formation and eosinophilic granulomas can be observed, and worm fragments are occasionally found. Electron microscopic examination of the lung has demonstrated degranulation of the eosinophils, implying that tissue destruction may be mediated by cytotoxic granule proteins released by these cells. Fibrosis may be present if the course of the disease is prolonged.

Figure 39-2

Tropical pulmonary eosinophilia.

A, Chest radiograph of a patient from Sri Lanka with confirmed tropical pulmonary eosinophilia shows subpleural right lung consolidation, subpleural left midlung opacity, and bilateral perihilar interstitial thickening. B, Chest radiograph of the same patient after treatment with diethylcarbamazine. Note the improved parenchyma.


All patients should be treated because TPE can progress to chronic restrictive lung disease. Administration of diethylcarbamazine, an antifilarial drug, results in improvement in the signs and symptoms of TPE, with reduced eosinophilia and serum IgE levels. Some experts have suggested ivermectin therapy either alone or in combination with diethylcarbamazine, although ivermectin has little effect on adult filariae and some patients require retreatment, regardless of the regimen. Recent studies have shown that doxycycline, which eliminates the bacterial ( Wolbachia ) endosymbiont of W. bancrofti , is efficacious in treatment of both adults and microfilaria of filariasis. An endosymbiont is an organism that lives within another with mutual benefit; Wolbachia is thought to play an important role in the disease caused by Wuchereria and to its survival. It is proving a valuable target for many of the filarial diseases, especially because it can be targeted with doxycycline, which is better tolerated than diethylcarbamazine. Steroid therapy should be administered with caution because TPE and pulmonary strongyloidiasis have similar presentations and steroids may enhance the morbidity and mortality of strongyloidiasis.

Visceral Larva Migrans

Visceral larva migrans (VLM) is a clinical syndrome caused by infection of humans by the dog ascarid Toxocara canis or the cat ascarid Toxocara cati in temperate and tropical climates. Children acquire infection by ingesting embryonated eggs in contaminated soil or sandbox contents; a history of pica is common in infected children. Although VLM usually afflicts children, adults have also been described with VLM. A VLM-like syndrome has also been reported as a result of infection with A. suum , the parasite of pigs, and Baylisascaris procyonis , the raccoon ascarid.

Because the hatched larvae cannot mature into adults in humans (which are dead-end hosts), the larvae migrate throughout the visceral organs of humans causing an acute eosinophilic syndrome.

Clinical Features.

Toxocara infection affects diverse organ systems. Pulmonary manifestations are present in 80% of cases and include cough, shortness of breath, and wheezing, resembling asthma. Although symptoms are usually mild, severe respiratory symptoms have been reported. These manifestations are a result of damage to the lung by the larvae and by immune responses to them. Other manifestations may include urticaria, lymphadenopathy, hepatosplenomegaly, and seizures. Involvement of the central nervous system, eye, and myocardium have been reported but are not common.

Diagnosis and Treatment.

The radiographic appearance in VLM is variable and includes bilateral or segmental and patchy opacities, which can be migratory; subpleural opacities may be detected by computed tomography (CT). Laboratory evaluation may reveal leukocytosis, marked eosinophilia, elevated anti-A or anti-B isohemagglutinin titers, and abnormal liver function tests; IgE levels are frequently elevated. The diagnosis is made by ELISA and immunoblot testing. Because larvae do not mature to adults in humans, there are no ova in the stool.

Because VLM is a self-limited syndrome, antiparasitic drugs may not be required. However, if the symptoms are moderate or severe, albendazole is the drug of choice; diethylcarbamazine is an alternative therapy. In severe cases, adjunctive steroids may accelerate symptom resolution. Preventive measures include control of soil contamination, curbing pica, and regular deworming of dogs and cats.

Other Ascarids

Infection with Baylisascaris procyonis , an ascarid of raccoons, results in a systemic disease characterized by eosinophilia. Pulmonary involvement has been reported in this infection, although the major clinical manifestations are neurologic and ocular. There is no proven therapy, although albendazole may be beneficial.


Dirofilaria immitis , the dog heart worm, is an important cause of morbidity and mortality in dogs. It is transmitted by mosquitoes, but humans are dead-end hosts. In the United States, most cases have been described in the Southeast. The worms migrate via the venous circulation and right heart where they reach the pulmonary arteries. In humans, the filariae are vascular parasites in the pulmonary artery, inducing vasculitis and formation of a pulmonary nodule upon death of the parasite ( Fig. 39-3 ). Chest radiographs usually reveal a well-defined homogeneous spherical or oval coin lesion with smooth edges. The majority of cases are asymptomatic, although some individuals may have cough and pneumonitis. Eosinophilia is absent. Because there is no reliable noninvasive test for Dirofilaria infection, nearly all cases require biopsy to establish the diagnosis. Surgery is both diagnostic and curative.

Figure 39-3

Dirofilarial infection in the lung.

Chest radiograph showing a solitary nodule ( arrows ) in the lung from a patient with confirmed Dirofilaria immitis.

(From McCall GW, Genchi C, Kramer LH, et al: Heartworm disease in animals and humans. Adv Parasitol 66:193–285, 2008.)


Trichinosis is caused by the parasites of the genus Trichinella, especially T. spiralis ; these are the only nematodes that occupy an intracellular location and that are acquired by ingestion of contaminated meat. Humans usually acquire the infection by ingesting cysts containing the coiled larvae in raw or partially cooked pork, pork products, or game. The larvae that emerge from the ingested cysts invade the small intestine.

Clinical Features.

The enteral stage may be either asymptomatic or may be accompanied by signs and symptoms of gastroenteritis. During the ensuing parenteral stage, newborn larvae enter the bloodstream and circulate to various organs. However, they only encyst in peripheral skeletal muscle, forming the “nurse cell,” consisting of an infected myocyte fed by vessels formed by neoangiogenesis. Most symptoms are due to inflammation associated with the invasion of larvae through the intestine and with influx of eosinophils and mast cells in the region of nurse cells. During the acute stage of infection, common symptoms include malaise, abdominal pain, fever, nausea, vomiting, myalgias, and muscle weakness with facial and generalized edema. Respiratory tract involvement is uncommon but, in severe cases, there may be dyspnea and transient pulmonary opacities. Dyspnea may result from larval invasion of the diaphragm and the accessory muscles of respiration ; however, lung inflammation may also play a role.

Diagnosis and Treatment.

Trichinosis is usually diagnosed based on clinical presentation, epidemiology, eosinophilia, and a positive ELISA. Muscle biopsy is definitive but is not recommended because of low sensitivity. Treatment is with albendazole; corticosteroids may be added in severe cases, especially those with pneumonitis, myocarditis, or meningoencephalitis. It is unclear whether treatment alters the course of infection, particularly because it does not appear to affect worms after they have already encysted. Trichinosis is prevented by consuming meats that are fully cooked to a temperature of 140°F.


Gnathostomiasis is caused by helminths of the genus Gnathostoma and is endemic in South Asia and Southeast Asia, China, and Latin America, especially in cultures in which uncooked fish is consumed. Gnathostoma spinigerum is the most common agent of human gnathostomiasis. Humans are accidental hosts; cats and dogs are the definitive hosts. G. spinigerum has a complex life cycle involving two intermediate hosts. Humans usually become infected with third-stage larvae by ingesting raw or inadequately cooked freshwater fish or other intermediate hosts such as snakes, frogs, and chickens. However, alternative routes of infection have also been suggested such as ingestion of water containing infected copepods and penetration of the skin of food handlers by third-stage larvae from infected meat. The infective larvae released in the gut migrate to the liver and abdominal cavity and return to the stomach, where they are embedded in the wall, resembling a tumor with an aperture communicating with the lumen to release eggs. The mechanical damage of migrating larvae has been cited as the primary cause of symptoms. Migration of larvae through tissues results in characteristic hemorrhagic tracts, surrounded by eosinophilic infiltration. When the lungs are involved, patients present with cough, pleuritic chest pain, hemoptysis, lobar consolidation, lobar collapse, pleural effusion, pneumothorax, or hydrothorax. Subcutaneous swellings, unexplained eosinophilic pleural effusion, and peripheral eosinophilia are considered a clinical triad and should prompt consideration of gnathostomiasis.

Diagnosis and Treatment.

Diagnosis of gnathostomiasis is based on the presence of eosinophilia, migratory inflammation, and history of exposure risk. The diagnosis can be confirmed by identification of the worm in tissue or by serology. The treatment of choice is albendazole or ivermectin.



The lung flukes of the genus Paragonimus encompass several species important in human disease. Paragonimus westermani is found in humans and animals in Asia, Africa, and South America. However, greater than 90% of the cases are seen in Asia; P. westermani is rarely contracted in the United States. Most cases of paragonimiasis acquired in the United States are due to Paragonimus kellicotti after ingestion of crayfish. The parasite has a complex life cycle involving freshwater snails, crustaceans, and mammals.

Humans become infected by ingesting raw, partially cooked, or pickled crab or crayfish containing metacercaria, which excyst in the duodenum and penetrate the intestinal wall to enter the peritoneal cavity. Larval forms penetrate the diaphragm and enter the pleural cavity and lung parenchyma where they mature to adult worms. Pairs of adult worms live in cystic cavities near bronchial passages ( Fig. 39-4 ) and produce eggs. Cystic cavities eventually rupture into a bronchiole, allowing eggs to be expectorated or swallowed and passed in feces.

Figure 39-4

Paragonimus westermani.

A, Chest radiograph of a patient who presented with hemoptysis shows minimal perihilar left and right infrahilar linear and reticular opacities. B, Granuloma surrounding ova. C, Cross section of a pair of adults in the lung. D, Ovum in the sputum.

(From Herman Zaiman’s “A Pictorial Presentation of Parasites” with permission of the American Society of Tropical Medicine and Hygiene.)

Clinical Features.

A minority of infected individuals have a symptomatic stage of acute infection approximately 2 weeks after exposure, marked by abdominal pain, diarrhea, fever, chest pain, cough, urticaria, peripheral eosinophilia, and elevated levels of IgE. In contrast, most infections have an insidious onset with clinical manifestations 5 to 10 years following exposure. Symptoms of later stage infections include cough productive of thick, rusty-colored or bloody sputum with Charcot–Leyden crystals, with or without pleuritic chest pain. There may be frank hemoptysis resembling that in tuberculosis. Fever and eosinophilia can be absent in chronic infections; a common finding is an abnormal chest radiograph in an asymptomatic patient (see Fig. 39-4 ).


Chest radiographs may reveal a variety of lesions including focal involvement or consolidation. Cavitary lesions appear as the flukes mature and may measure up to 4 cm in diameter; small cysts and calcified or noncalcified nodules ( eFig. 39-3 ) may be present. Pleural effusion, pneumothorax, and pleural thickening may develop in a minority of patients. The pleural fluid characteristically contains leukocytes, many eosinophils, elevated concentrations of protein and lactate dehydrogenase, and low concentrations of glucose. Histopathologic examination of the lung reveals adult worms within fibrous cysts communicating with bronchi or bronchioles; granulomas may contain eggs at the center (see Fig. 39-4 ). Pneumonia, bronchiectasis, and vasculitis may be present. Acute and chronic pathologic changes may coexist within the same pulmonary lesions.

When the diagnosis of paragonimiasis is suspected, it can be confirmed by finding morphologically characteristic eggs in sputum, stool, gastric aspirates, or tissue (see Fig. 39-4 ). Bloody sputum is the most likely to yield positive results. ELISA and immunoblot assays that detect antibodies to Paragonimus antigens are offered by the CDC in Atlanta, Georgia.


Praziquantel is the drug of choice. Untreated pulmonary paragonimiasis may resolve within 5 to 10 years (the life span of the adult worms) but chronic infection may be accompanied by extensive fibrosis. Paragonimiasis can be prevented by cooking crabs and crayfish fully before ingesting.


Schistosomiasis is one of the most important parasitic infections of humankind. It is found in tropical and subtropical areas of the world including South America, Africa, the Middle East, and East Asia, including the Philippines. The World Health Organization estimates that more than 200 million people are infected worldwide. Five species of schistosomes cause human disease: Schistosoma hematobium, S. mansoni, S. japonicum, S. mekongi, and S. intercalatum . Infection is acquired when cercariae penetrate the skin during interaction with fresh water while bathing, wading, or doing laundry. After penetrating the skin, the cercariae lose their tails and quickly transform into juvenile forms (schistosomula) that migrate to the lung and liver. These transform into adults that mate and then travel to their tissue destination. S. hematobium are found in the venous plexus of the urinary bladder while S. mansoni and S. japonicum reside in mesenteric veins . Female worms lay eggs that are excreted either in the urine ( S. hematobium ) or feces ( S. mansoni , S. japonicum ). Adult schistosomes may live and produce eggs for as long as 30 years.

Clinical Features.

A skin reaction (erythematous raised 1- to 3-cm lesions) may develop within hours (and as late as 1 week) after cercarial penetration in those infected for the first time. In some previously unexposed persons, acute schistosomiasis, known as Katayama fever, develops after heavy exposure to S. japonicum or S. mansoni . Symptoms usually develop between 4 and 8 weeks after exposure, which coincides with maturation of adults and the beginning of egg laying. Acute schistosomiasis is characterized by urticaria, fever, chills, cough, wheezing, headaches, lymphadenopathy, hepatosplenomegaly, peripheral eosinophilia, and elevated serum IgE levels. This acute phase usually resolves within several weeks but can lead to death in rare instances.

The major pathologic findings in schistosomiasis in any organ are granulomas surrounding eggs ( Fig. 39-5 ). Chronic pulmonary schistosomiasis may be the result of deposition of eggs in pulmonary vessels followed by granuloma formation and obstruction of blood flow. However, vasospasm and inflammation also contribute to the pulmonary findings. Chronic pulmonary hyper­tension develops in approximately 5% of patients with hepatosplenic schistosomiasis, usually after many years of untreated infection.

Jul 21, 2019 | Posted by in CARDIOLOGY | Comments Off on Parasitic Infections

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