Parasites of the Air Passages - 2014

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journal.publications.chestnet.org CHEST / 145 / 4 / APRIL 2014 883

CHEST

Helminthic and protozoal infestations cause signif-icant morbidity and mortality worldwide. A decline

in parasitic infestations has been observed in the pastdecade as a result of improved socioeconomic condi-tions and better hygiene practices. However, the rapidurbanization of cities around the world, global warm-ing, international traveling, and increasing numbersof immunocompromised individuals have increased

the vulnerability of the world population to parasiticdiseases.1 The diagnosis of parasitic diseases of therespiratory system is challenging because the clinicalmanifestations and radiologic findings are nonspecific.Thus, a high index of suspicion and detailed interro-gation regarding travel history are critical. Most para-sitic infestations of the respiratory system either involvethe airways or require bronchoscopy for diagnosis. Hel-minthes can affect the airways during both the larvaland the mature adult phases of their life cycle. Thelarvae can cause airway inflammation (paragonimiasis),

whereas migration of the mature adult worms maycause mechanical obstruction of the airways (ascariasis).This article provides a comprehensive review of bothhelminthic and protozoal infestations, including clin-ical, radiographic, bronchoscopic, and pathologic man-ifestations, that may be helpful to pulmonologists inmanaging this important entity (Table 1).

Nematodes

Nematodes, also known as roundworms, have a sym-metrical, tube-like body with an anterior mouth and alongitudinal digestive tract.

Ascariasis

Ascaris lumbricoides is one of the most commonparasitic infestations, affecting. 1 billion of the world’spopulation and causing . 1,000 deaths annually.1 Alumbricoides is transmitted via the feco-oral route. An

Ascaris larva migrates to the lungs through either thelymphatics or the venules of the portal system. Larvalascariasis causes Löffler’s syndrome, a concomitanceof wheezing, pulmonary infiltrations, and eosinophilia.2 It can cause alveolar inflammation, necrosis, and hem-orrhage. Diagnosis of an ascariasis infestation during itslarval phase is difficult. The sputum may show numer-ous eosinophils; stool examination, however, remainsnegative for eggs during the larval stage.3 The diagno-sis requires a high degree of suspicion. Occasionally,

Parasitic infestations affect millions of the world’s population. Global immigration and climatechange have led to changes in the natural distribution of parasitic diseases far removed fromendemic areas. A broad spectrum of helminthic and protozoal parasitic diseases frequently affectsthe respiratory system. The wide varieties of clinical and radiographic presentations of parasiticdiseases make the diagnosis of this entity challenging. Pulmonologists need to become familiar

with the epidemiology, clinical presentation, pathophysiologic characteristics, and bronchoscopicfindings to provide proper management in a timely fashion. This review provides a comprehen-sive view of both helminthic and protozoal parasitic diseases that affect the respiratory system,especially the airways. CHEST 2014; 145(4):883–895

Abbreviations: BALF5

BAL fluid; DEC5

diethylcarbamazine; ELISA5

enzyme-linked immunosorbent assay;PAH5pulmonary artery hypertension; TPE5 tropical pulmonary eosinophilia

Parasites of the Air Passages

Danai Khemasuwan , MD , MBA ; Carol F. Farver , MD ; and Atul C. Mehta , MD , FCCP

Manuscript received September 1, 2013; revision accepted

December 16, 2013. Affiliations: From Pulmonary, Allergy and Critical Care Medicine(Drs Khemasuwan and Mehta), Respiratory Institute, and theDepartment of Anatomical Pathology (Dr Farver), Cleveland ClinicFoundation, Cleveland OH.Correspondence to: Atul C. Mehta, MD, FCCP, Pulmonary,Allergy and Critical Care Medicine, Respiratory Institute, ClevelandClinic Foundation, 9500 Euclid Ave, A-90, Cleveland, OH 44195;e-mail: [email protected]© 2014 American College of Chest Physicians. Reproductionof this article is prohibited without written permission from theAmerican College of Chest Physicians. See online for more details.DOI: 10.1378/chest.13-2072


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884 Special Features

the diagnosis can be confirmed by identifying larvaein the sputum. Solitary pulmonary nodules can alsodevelop if the larva dies causing granulomatous inflam-mation.4 Adult ascaris has been reported to cause airways obstruction in a child, producing a complete lobarcollapse.5 Mebendazole and albendazole are the mosteffective agents against ascariasis.

Ancylostomiasis (Hookworm Disease)The most common hookworms are Ancylostoma duo-

denale and Necator americanus . The latter is foundin parts of the southern United States. Hookworm larvae enter human hosts via the skin, producing itchingand local infection. The larvae are also infective viathe oral route.6 Hookworm infestations involve larvalmigration through the lungs via the bloodstream, result-ing in a hypersensitivity reaction. Patients usually pre-sent with transient eosinophilic pneumonia (Löffler’ssyndrome).6 If the patient ingests a large number of larvae, he/she may develop a condition known as “Wakana

disease,” characterized by nausea, vomiting, dyspnea,and eosinophilia. This clinical picture represents a severehypersensitivity-like reaction to A duodenale .6 Larvalmigration may also cause alveolar hemorrhage.7 Sim-ilar to ascariasis, the diagnosis of a hookworm infesta-tion during the larvae phase could be difficult to make.CT scanning of the chest may reveal transient, migra-tory, patchy alveolar infiltrates.8 Sputum examinationmay reveal occult blood, eosinophils and, rarely, migrat-ing larvae (Fig 1A).9 Bronchoscopic examination mayreveal airway erythema and high eosinophil counts inBAL fluid (BALF).10 Patients can become profoundlyanemic and malnourished. These manifestations may

provide clinical clues to support the diagnosis. The anti-parasitic agents for hookworm are mebendazole andalbendazole.

Strongyloidiasis

Strongyloides stercoralis is a common roundwormthat is endemic throughout the tropics but is found worldwide in all climates. Infective filariform larvaecan penetrate the skin and infect human hosts. The larvae migrate through the soft tissues and enter the lungs via the bloodstream. A majority of roundworms migrateup the bronchial tree to the pharynx and are swallowed,

entering the GI tract.11

The larvae can reenter the cir-culatory system, returning to the lungs and causingautoinfection.11 The life cycle of Strongyloides can becompleted entirely within one host. The term “hyper-infection syndrome” describes the presentation of sep-sis from enteric flora, mostly in immunocompromisedpatients.12 The hallmarks of hyperinfection are an exac-erbation of GI and pulmonary symptoms and the detec-tion of more larvae in the stool and sputum.13 Commonpulmonary symptoms include wheezing, hoarseness,

dyspnea, and hemoptysis. A chest radiograph usuallydemonstrates focal or bilateral interstitial infiltrates.Pleural effusions are present in 40% of patients, andlung abscess is found in 15%.14 Diffuse alveolar hem-orrhage is usually found in patients with disseminatedstrongyloidiasis. ARDS may result as a reaction to thedeath of the organisms. Migration of a massive numberof larvae through the intestinal wall can result in sep-

sis, because larvae may convey gram-negative bacteriainto the bloodstream.13

The diagnosis can be confirmed by the presence oflarvae in the stool, duodenal aspirate, sputum, pleuralfluid, or BALF or lung biopsy specimens (Figs 1B, 1C).15 The sensitivity of a stool examination for ova and larvaeis 92% when performed on three consecutive samples.16 An enzyme-linked immunosorbent assay (ELISA) mea-sures IgG responses to the Strongyloides antigen. How-ever, false-negative results can occur during acuteinfection because it takes 4 to 6 weeks to mount theimmune response.17 The ELISA is sensitive but non-specific because of cross-reactivity with filarial infes-

tations.15 Oral ivermectin remains the treatment ofchoice for uncomplicated Strongyloides infestation.13,18

Syngamosis

Nematoda of the genus Mammomonogamus affectthe respiratory tract of domestic mammals. Occasion-ally, however, humans can become infested via therespiratory tract. Most cases of human syngamosis arereported from tropical areas, including South America,the Caribbean, and Southeast Asia.19 Two hypotheseshave been proposed regarding its life cycle. One is thathumans become infested via the ingestion of food or

water contaminated with larvae or embryonated eggs.The larvae complete the life cycle in the pulmonarysystem, and the adult worms migrate to the central airways as the preferred site of infection.20 An alternativehypothesis is that patients are infected by the adult worms present in contaminated food or water. Thismode of transmission is supported by its short incuba-tion period (6-11 days).21 The diagnosis requires flex-ible bronchoscopy unless the worms are expelledthrough vigorous coughing (Fig 1D). The removal ofparasites through bronchoscopy is sufficient to improvesymptoms. To date, no studies have supported theeffectiveness of antihelminthic therapy.21,22

Dirofilariasis

Dirofilaria immitis is the filarial nematode that pri-marily infects dogs. Humans are considered accidentalhosts because D immitis is unable to mature to an adultform. D immitis is transmitted to humans by mosqui-toes harboring infective third-stage larvae. The larvatravels to the right ventricle and develops into an imma-ture adult worm. It is then swept into the pulmonary


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Table 1 —Parasitic Infection of Respiratory System

Parasite Infective Form Endemic Area Mode of Transmission Pulmonary Presentation

NematodesAscariasis ( Ascaris lumbricoides ) Eggs and larva Asia, Africa, and

South America

Ingestion Eosinophilic

pneumonia, cough, wheezing, dyspnea

Hookworm ( Ancyclostomaduodenale ) ( Necatoramericanus )

Larva Tropical andsubtropical areas

Skin penetration Eosinophilicpneumonia, cough,

wheezing, dyspnea,alveolar hemorrhage

Strongyloidiasis(Strongyloides stercoralis )

Fi lariform larvae Tropical andsubtropical areas

Skin penetration Eosinophilicpneumonia, cough,

wheezing, dyspnea,hyperinfectionsyndrome

Syngamosis (Mammomonogamuslaryngeus )

Eggs or adult worms

Asia, Africa, andSouth America

Ingestion Foreign body-likelesion in bronchus,nocturnal cough

Dirofilariasis (Dirofilaria immitis ) Larva Tropical andsubtropical areas Mosquito-borneinfection Cough, chest pain,fever, dyspnea, mildeosinophilia, andlung nodules

Tropical pulmonaryeosinophilia (Brugia malayi )(Wuchereria bancrofti )

Larva Tropical andsubtropical areas(South andSoutheast Asia)

Mosquito-borne infection Eosinophilicpneumonia, cough,

wheezing, dyspnea,restrictive pattern onspirometry, decreaseddiffusion lung capacity

Visceral larva migrans(Toxocara canis )(Toxocara catis )

Larva Worldwide Ingestion Eosinophilic pneumonia,episodic wheezing

Trichinella infection(Trichinella spiralis )

Larva Worldwide Ingestion Cough, pulmonaryinfiltrates, dyspneadue to respiratorymuscles involvement

TrematodesSchistosomiasis

(Schistosoma species)Cercarial larvae East Asia,

South America,Sub-Saharan Africa

Skin penetration Pulmonaryhypertension andKatayama fever


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arteries. The worm dies as a result of the inflammatoryresponse and evokes granuloma formation.23 A majorityof patients with pulmonary dirofilariasis are asymptom-atic. However, some patients (about 5%) may developcough, hemoptysis, chest pain, fever, dyspnea, and mildeosinophilia.24 A peripheral or a pleural-based solitarypulmonary nodule is a typical presentation. The nod-ule may show increased fluorodeoxyglucose avidity on

a PET scan25,26 and is often confused with malignancy.Calcification occurs within only 10% of these nodules.CT scanning may show a branch of the pulmonary arteryentering the nodule.27 Serology has poor specificitybecause of cross-reactivity with other helminths. Thediagnosis is established by identifying the worm in theexcised lung tissue (Fig 1E). Needle biopsy and brush-ings are usually nondiagnostic because of the smallsample size. The condition does not require any spe-cific treatment because it is a self-limiting condition.24

Tropical Pulmonary Eosinophilia

Tropical pulmonary eosinophilia (TPE) is a syndromeof immunologic reaction to microfilaria of the lymphatic-dwelling organisms Brugia malayi and Wuchereria bancrofti. It is a mosquito-borne infestation. The larvae reside in the lymphatics and develop into matureadult worms. The microfilariae are released into thecirculation and may be trapped in the pulmonary cir-culation.28 Trapped microfilariae demonstrate a strongimmunogenicity and trigger antimicrofilarial antibod-ies, resulting in asthma-like symptoms. The hallmarkof TPE is a high absolute eosinophil count (5,000-80,000/mm3) .29 The radiologic features include retic-ulonodular opacities, predominantly in the middle and

the lower lung zones; miliary mottling; and predomi-nant hila with increased vascular markings at the bases.30 Chest CT scanning may demonstrate bronchiectasis,air trapping, calcification, and mediastinal lymphade-nopathy.31 Pulmonary functions indicate a restrictivedefect with mild airways obstruction.29 BALF may con-tain numerous eosinophils. Occasionally, microfilariacan be identified on brushings or needle biopsy spec-imens.32 The chronic phase of TPE may lead to pro-gressive and irreversible pulmonary fibrosis.28

The standard treatment of TPE is diethylcarbama-zine (DEC). Patients usually show improvement within3 weeks. However, a mild form of interstitial lung dis-

ease with diffusion impairment may remain.33

Toxocariasis

Toxocara canis and cati are roundworms that affectthe dog and cat, respectively. These roundworms arecommon parasites that cause visceral larva migransand eosinophilic lung disease in humans. Toxocariasisis transmitted to humans via ingestion of food that iscontaminated with parasite eggs. The larvae can migrate P a

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T a b l e 1 — C o n t i n u e d


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Figure 1. A, Hookworm larva in the sputum sample (wet smear, original magnification3 88). Morphologically, hookworm larvae have longbuccal cavities, whereas Strongyloides larvae have short buccal cavities. (Reprinted with permission from Beigel et al.9 ) B, Bloody aliquotfrom BAL sample and Strongyloides larvae from BAL (hematoxylin and eosin [H&E], original magnification3 200). Note: short buccalcavity distinguishes Strongyloides from the hookworm (inset) (H&E, original magnification3 400). C, Strongyloides larvae (arrow) presentin alveolar space in lung with diffuse alveolar damage (H&E, original magnification3 400). D, Bronchoscopic findings in anterior basalsegment of right lower lobe. The syngamosis male is smaller and attached to the copulatory bursa of the female body (arrow). The parasitecan be seen in bronchoscopy because they reside in the bronchial mucosa. (Reprinted with permission from Kim et al.19 ) E, Cross-sectionsof coiled Dirofilaria worms within involved artery causing surrounding infarction of lung tissue. Note the smooth cuticle at the externallayer (Movat stain, original magnification3 200). F, Schistosomal ova in the lung biopsy specimen. The arrow points to ova within thegranulomatous reaction (H&E, original magnification3 100).


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Figure 2. A, Bronchoscopic findings showed mucosal nodularity on the right upper lobe (RUL). (Reprinted with permission from Jeon et al.51 )

B, Microscopic examination of bronchial tissue obtained from the RUL bronchus showing thickening of the basement membrane andchronic inflammation with eosinophilic infiltration (H&E, original magnification3 200). (Reprinted with permission from Jeon et al.51 )Inset: Paragonimus kellicotti egg in a BAL sample. The arrow points to the operculum ridges of the egg (Papanicolaou, original magnifica-tion3 400). (Image courtesy by Gary Procop, MD.) C, Granulomas in the pleura in a patient with paragonimiasis. The arrow points toa light brown egg within the granuloma (H&E, original magnification3 100). (Image courtesy by Gary Procop, MD.) D, Protruded hydatidcyst from left lower lobe bronchus. (Image courtesy by Farid Rashidi, MD.) E, Echinococcus cyst fragments in lung biopsy specimen. Thearrows highlight the collapsed chitinous layer of a death hydatid cyst (H&E, original magnification3 44). F, Echinococcus cyst fragmentsin lung biopsy specimen. The fragmented ecchinococus cyst with collapsed chitinous layer resides within the granulomatous reaction(H&E, original magnification3 200). See Figure 1 legend for expansion of other abbreviation.


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tive larva). After the cercarias have penetrated the skin,they migrate to the lung and the liver. There are sev-eral case reports of a high incidence of acute schistoso-miasis (Katayama fever) among travelers with a historyof swimming in Lake Malawi and rafting in sub-SaharanAfrica.41

In acute schistosomiasis, patients present with dys-pnea, wheezing, dry cough, abdominal pain, hepatos-

plenomegaly, myalgia, and eosinophilia.42 Patientsexperience shortness of breath because of an immuno-logic reaction to antigens released by the worms. Thelevel of circulating immune complexes correlates withthe symptoms and with the intensity of infection.

In chronic schistosomiasis, embolization of the eggsin the portal system causes periportal fibrosis and por-tal hypertension. Pulmonary involvement can occuras a result of the systemic migration of parasitic eggsfrom the portal system. The eggs trigger an inflamma-tory response that leads to pulmonary arterial hyper-tension (PAH) and subsequent development of corpulmonale in 2% to 6% of patients.43 Apoptosis of the

endothelial cells in the pulmonary vasculature playsa role in the pathogenesis of schistosomal-associatedcor pulmonale.44

Chest radiographs and CT scanning may show a dif-fuse reticulonodular pattern or ground-glass opacities.45 In the acute phase, BALF may reveal eosinophilia inthe absence of parasites. The diagnosis is confirmed bymicroscopic examination of stool and urine or by rec-tal biopsy. However, the sensitivity of these tests is lowfor an early infection. ELISA can be used as a screen-ing test and is confirmed by enzyme-linked immune-electrotransfer blot. These tests become positive within2 weeks after the infestation. Schistosomal ova canbe found in the lung biopsy specimen (Fig 1F).

Acute schistosomiasis is treated with praziquantel.The treatment is repeated within several weeks becauseit has no antihelminthic effect on the juvenile stagesof the parasites.46 Acute pneumonitis, which is believedto be related to lung embolization by adult worms inthe pelvic veins, can be observed 2 weeks after thetreatment.47 Patients with schistosomal-associated PAHcan be treated with PAH-specific therapy along withantiparasitic medications.47

Paragonimiasis

Paragonimus species, including westernmani, causeparagonimiasis that usually involves the lungs. Themode of transmission is ingestion of the metacercaria(infective larvae) from undercooked crustaceans. Under-cooked meat of crab-eating mammals (wild boars, rats)can infect humans as an indirect route of transmission.48 The larvae penetrate the intestinal wall and migratethrough the diaphragm and the pleura into the bron-chioles.49 The eggs are produced by the mature adult

throughout the host’s body, including the lungs.34 Thepathology of visceral larva migrans is a hypersensi-tivity response to the migrating larvae. Visceral larvamigrans can present with fever, cough, wheezing, sei-zures, and anemia. Leukocytosis and severe eosino-philia are demonstrated in a peripheral smear. A chestradiograph reveals pulmonary infiltrates with hilar andmediastinal lymphadenopathy. Bilateral pleural effu-

sion can occur.35 Noncavitating pulmonary noduleshave also been reported.36 The diagnosis of toxocariasisis established by an ELISA for the larval antigens.37

The treatment of choice is DEC; however, it mayexacerbate the inflammatory reaction because of theresulting death of the larvae. It is advisable to combineDEC with corticosteroids.34

Trichinella Infection

Trichinella spiralis is the most common Trichinella species that infects humans. Trichinella is a food-borne disease from undercooked pork containing larval

trichinellae. In addition to the pork meat, meat from wild animals such as bear may contain T spiralis .38 Thelarvae migrate and reside in the GI tract until theydevelop into an adult form. Fertilized female wormsrelease first-stage larvae into the bloodstream and thelymphatics.39 Pulmonary involvement, although uncom-mon, produces shortness of breath and pulmonary infil-trates. Dyspnea is caused by parasitic invasion of thediaphragm and the accessory respiratory muscles.39 The diagnosis is confirmed by muscle biopsy, whichmay demonstrate T spiralis larvae. An ELISA usinganti-Trichinella IgG antibodies can confirm the diag-nosis in humans.40 A 2-week course of mebendazole,

along with analgesics and corticosteroids, is the rec-ommended treatment.39

Trematodes

Trematodes (flatworms) have a flat body with a suckernear the mouth that is used for attachment to the host.Most flatworms are hermaphrodites, except Schisto- soma species , which have separate sexes.

Schistosomiasis

Five schistosomes species cause disease in humans:Haematobium , Mansoni , Japonicum , Intercalatum ,and Mekongi .7 After malaria, schistosomiasis is the mostcommon cause of mortality among parasitic infections,annually affecting 200 million individuals worldwide.1 Schistosoma haematobium resides in the urinary blad-der, whereas Schistosoma mansoni and Schistosoma japonicum reside in the mesenteric beds.34 Humansbecome infested through the skin from contact withfresh water containing Schistosomal cercaria (infec-


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include cough, fever, dyspnea, and chest pain. Thecyst may rupture into a bronchus and cause hemop-tysis and/or expectoration of cystic fluid containingparasitic components (hydatoptysis), which is con-sidered a pathognomonic finding of cystic rupture.55 The patients may present with hydropneumothoraxor empyema. Occasionally, a ruptured cyst can causean anaphylactic-like reaction and pneumonia.8 Cystic

hydatidosis is diagnosed by chest radiography, whichdemonstrates a well-defined, homogenous, fluid-filled,round opacity. Ruptured cysts may have characteristicfeatures, including air crescent, pneumocyst, floatingmembrane (“water lily sign”) (Fig 3), or completelyempty cavity images.56 A “meniscus” or “crescent” signor Cumbo’s sign (onion peel) have also been described.Thoracic ultrasonography may be useful to confirmthe cystic structure, demonstrating the characteristicdouble-contour (pericyst and parasitic membraneendocyst) of intact cysts. However, daughter cysts arealso observed occasionally in pulmonary hydatidosis.56 Bronchoscopic examination reveals sac-like cysts in

the airway (Fig 2D). A surgical lung biopsy may revealechinococcus cyst fragments (Figs 2E, 2F).

Bronchoscopic extraction of the hydatid cyst is pos-sible; however, because of the risk of cyst rupture, itshould be considered on a case-by-case basis. Serologictests are more sensitive in patients with liver involve-ment (80%-94%) than in those with lung hydatidosis(65%).34 Hydatid cyst rupture can increase the sensi-tivity of serologic tests to . 90%.55

Cystic hydatidosis is the only infestation that needssurgical treatment. Complete resection of the cystis the cornerstone of the management of pulmonaryhydatidosis: to remove the intact cyst, preserve as much viable lung tissue as possible, and treat the associated

worms, which are expelled in the sputum or swallowedand passed with the stool. Typically acute symptomsinclude fever, chest pain, and chronic cough with hemop-tysis.50 Pleural effusion and pneumothorax may be thefirst manifestation during the migration of the juvenile worms through the pleura. A chest radiograph dem-onstrates patchy infiltrates, nodular opacities, pleuraleffusion, and fluid-filled cysts with ring shadows.34 Chest

CT scans may reveal a band-like opacity abutting the visceral pleura (worm migration tracks), bronchial wallthickening, and centrilobular nodules. Bronchoscopicexamination may reveal airway narrowing from mucosaledema (Fig 2A).51 A lung biopsy specimen may showchronic eosinophilic inflammation (Fig 2B). The diag-nosis is confirmed by the presence of eggs or larvae inthe sputum sample or BALF (Fig 2C). The pleural fluid, when present, is an acidic exudate with eosinophilia,mostly sterile, without the presence of any organisms.52 Eosinophilia and elevated serum IgE levels are alsoobserved in more than 80% of infected patients.34 Sero-logic tests with ELISA and a direct fluorescent anti-

body are highly sensitive and specific for establishingthe diagnosis.53 Praziquantel and triclabendazole arethe treatments of choice, with a cure rate of 90% and98.5%, respectively.34

Cestodes

Cestodes are a subclass of tapeworms; parasites inthis group have no digestive system. These parasiteslive in the digestive tract of mammals. The body is com-posed of multiple, successive segments (proglottids).Tapeworms are exclusively hermaphrodites with both

male and female reproductive systems in their body.

Echinococcosis

Echinococcus granulosus and multilocularis are theparasite species that cause hydatid disease in humans.E granulosus is endemic in sheep-herding areas of theMediterranean, Eastern Europe, the Middle East, andAustralia. An estimated 65 million individuals in theseareas are infected.1 Humans become accidental hostseither by direct contact with the primary hosts (usuallydogs) or by the ingestion of food contaminated withfeces, containing parasite eggs.34 The larvae reach the

lymphatics of the intestines and the bloodstream andthen migrate to the liver, the main habitat in humanhosts.

Two different presentations of echinococcosis arenoted: (1) cystic hydatidosis and (2) alveolar echinococ-cosis. An ecchinococcal infection becomes symptom-atic after 5 to 15 years, secondary to local compressionor dysfunction of the affected organ. Pulmonary cystsexpand at a rate of 1 to 5 cm/y, and calcification is lesscommon.54 Pulmonary symptoms from the intact cyst

Figure 3. Water lily sign. CT scan obtained at level of right middlelobe shows ruptured hydatid cyst. After rupture and discharge ofcyst fluid into pleural cavity, endocyst collapses, sediments, and floatsin remaining fluid at bottom of original cyst. (Image courtesy byFarid Rashidi, MD.)


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Figure 4. A, Bronchoscopy revealed pinkish mulberry-like rhinosporidiosis mass in the right main stem bronchus. (Reprint with permissionfrom Singh et al.64 ) B, Microscopic examination of the resected specimen shows bronchial subepithelium with sporangia of Rhinosporodium;filled with small round endospores (H&E, original magnification3 100). (Reprint with permission from Singh et al.64 ) C, Amebic lungabscess from lung biopsy specimen. The arrows point to trophozoites of Entamoeba histolytica (H&E, original magnification3 200).D, Transbronchial needle biopsy specimen of a mediastinal lymph node shows histiocytes containing abundant Leishmania amastigotes(arrows) (H&E, original magnification3 1,000). Inset shows a close-up view of an amastigote. Its ovoid shape, eccentric nucleus, and kineto-plast are discerned (same magnification as image). (Reprint with permission from Kotsifas et al. 68 ) E, Lung infected with Toxoplasmosis

gondii (arrow) with diffuse alveolar damage (H&E, original magnification3 100). Inset shows bradyzoites of T gondii present in cytoplasmof alveolar macrophage (H&E, original magnification3 1,000). See Figure 1 legend for expansion of abbreviation.


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parenchymal and bronchial disease. The lung paren-chyma around a hydatid cyst is often affected by thelesion and may exhibit chronic congestion, hemorrhage,and interstitial pneumonia, which often resolve afterthe surgery.57 Spillage of hydatid fluid must be avoidedto prevent secondary hydatidosis. Medical therapy mayhave a role in poor surgical candidates and in intraop-erative spillage of fluid from a hydatid cyst. Antihel-

minthic agents, such as mebendazole or albendazole,have shown only 25% to 34% cure rates.58 The draw-back of antihelminthic therapy is that it weakens thecyst wall and increases the risk of rupture. In addi-tion, if the parasite dies because of the drug, the cystmembrane may remain within the cavity and lead tosecondary complications, including infections.59 Per-cutaneous treatment by puncture-aspiration-injection-reaspiration has rarely been used in pulmonary cystsbecause of the risk of anaphylactic shock, pneumo-thorax, pleural spillage, and bronchopleural fistulae.60

Pulmonary alveolar echinococcosis is a rare butsevere and potentially fatal form of echinococcosis but

it is restricted to the Northern Hemisphere. The liveris the first target for the parasite, with a long, silentincubation period. Pulmonary involvement resultsfrom either dissemination or the direct extension ofthe hepatic echinococcosis with intrathoracic rupturethrough the diaphragm into the bronchial tree, pleuralcavity, or mediastinum. Chest radiograph or CT scan-ning may aid in the diagnosis. ELISAs and indirecthemagglutination assay are available and offer earlydetection in endemic areas. Radical resection oflocalized lesions is the only curative treatment yet, israrely possible in invasive and disseminated disease.Mebendazole and albendazole can be used, but therequired treatment duration need is a minimum of2 years after the radical surgery.61

Mesomycetozoea

Mesomycetozoea is a group of organisms at theborder of the animal-fungal kingdom.62 They appearin host tissues as sphere-shaped spores.

Rhinosporidiosis

Rhinosporidiosis is a chronic granulomatous infec-

tious disease caused by Rhinosporidium seeberi . Thiscondition has a high prevalence in South Asia, especiallySri Lanka.63 Patients usually present with recurrentpolypoidal, friable, hemorrhagic, lesions. The com-mon sites of involvement are the nose and nasopharynx.However, lesions can involve the tracheobronchialtree, leading to partial or complete airway obstruc-tion (Figs 4A, 4B).64 CT imaging is the preferredstudy because it defines the extent of disease. Thera-peutic bronchoscopy plays a major role in bronchialrhinosporidiosis.

Dapsone is the only medication to arrest the matu-ration of the sporangia, but the lesions may recur aftermonths or years.65 Follow-up bronchoscopy is recom-mended to monitor signs of recurrence.

Protozoal Parasites

Protozoa parasites are single-celled organisms thatare mostly intracellular in humans (Table 2). Pulmonaryamebiasis is caused by Entamoeba histolytica tropho-zoites invading the intestinal mucosa and entering thebloodstream, effecting systemic infection. Pleuropul-monary amebiasis occurs mainly by local extension fromthe amoebic liver abscess. Patients usually present withfever, right-upper-quadrant abdominal pain, and cough.Sterile pleural effusion, lung abscess, hepatobronchial

Table 2 —Protozoal Infection of Respiratory System

Protozoal Parasites Endemic AreaMode of

Transmission Presentation Bronchoscopic Evaluation Treatment

Pulmonaryamebiasis

Worldwide Ingestion Fever, right upperquadrant abdominalpain, lung abscess,hepatobronchialfistula

Surgical lung biopsyspecimen showsEntamoeba histolytica trophozoites

Metronidazole

Pulmonaryleishmaniasis

Asia, Africa,Central andSouth America

Sand fly-borneinfection

Pneumonitis, pleuraleffusion, mediastinallymphadenopathy

Transbronchial needle biopsyspecimen of a mediastinallymph node showinghistiocytes containing

Leishmania donovani organisms

Pentavalent antimonialsand liposomalamphotericin B

Pulmonarytoxoplasmosis

Worldwide Ingestion Generalizedlymphadenopathy,interstitial pneumonia,diffuse alveolardamage

Histologic examination oflung biopsy specimen canidentify Toxoplasma gondii tachyzoites in necrotic area

Pyrimethamine andsulfadiazine


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Conclusions

Although helminthic and protozoal parasitic infes-tations are dominant mainly in tropical and subtropicalareas, global warming, immigration, and an increasinguse of immunosupressives have changed their distri-bution. To manage these challenging clinical scenarios,pulmonologists must understand the epidemiology,life cycles, and clinical presentation of these infesta-

tions, as well as the bronchoscopic and laboratory find-ings and treatment options.

Acknowledgments

Financial/nonfinancial disclosures: The authors have reportedto CHEST that no potential conflicts of interest exist with anycompanies/organizations whose products or services may be dis-cussed in this article.Other contributions: We thank Gary Procop, MD, and FaridRashidi, MD, for contribution of figures.


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