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Parasites of the Air Passages

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 CHEST Special Features

Parasites of the Air Passages

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

Parasitic infestations affect millions of the world’s population. Global immigration and climate
change have led to changes in the natural distribution of parasitic diseases far removed from
endemic areas. A broad spectrum of helminthic and protozoal parasitic diseases frequently affects
the respiratory system. The wide varieties of clinical and radiographic presentations of parasitic
diseases make the diagnosis of this entity challenging. Pulmonologists need to become familiar
with the epidemiology, clinical presentation, pathophysiologic characteristics, and bronchoscopic
findings 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: BALF 5 BAL fluid; DEC 5 diethylcarbamazine; ELISA 5 enzyme-linked immunosorbent assay;
PAH 5 pulmonary artery hypertension; TPE 5 tropical pulmonary eosinophilia

Helminthic and protozoal infestations cause signif-

icant morbidity and mortality worldwide. A decline
in parasitic infestations has been observed in the past
decade as a result of improved socioeconomic condi-
tions and better hygiene practices. However, the rapid
urbanization of cities around the world, global warm-
ing, international traveling, and increasing numbers
of immunocompromised individuals have increased
the vulnerability of the world population to parasitic
diseases.1 The diagnosis of parasitic diseases of the
respiratory system is challenging because the clinical
manifestations 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 involve
the airways or require bronchoscopy for diagnosis. Hel-
minthes can affect the airways during both the larval
and the mature adult phases of their life cycle. The
larvae can cause airway inflammation (paragonimiasis),
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 the
Department of Anatomical Pathology (Dr Farver), Cleveland Clinic
Foundation, Cleveland OH.
Correspondence to: Atul C. Mehta, MD, FCCP, Pulmonary,
Allergy and Critical Care Medicine, Respiratory Institute, Cleveland
Clinic Foundation, 9500 Euclid Ave, A-90, Cleveland, OH 44195;
e-mail: Mehtaa1@ccf.org
© 2014 American College of Chest Physicians. Reproduction
of this article is prohibited without written permission from the
American College of Chest Physicians. See online for more details.
DOI: 10.1378/chest.13-2072
whereas migration of the mature adult worms may
cause mechanical obstruction of the airways (ascariasis).
This article provides a comprehensive review of both
helminthic and protozoal infestations, including clin-
ical, radiographic, bronchoscopic, and pathologic man-
ifestations, that may be helpful to pulmonologists in
managing this important entity (Table 1).
Nematodes
Nematodes, also known as roundworms, have a sym-
metrical, tube-like body with an anterior mouth and a
longitudinal digestive tract.
Ascariasis
Ascaris lumbricoides is one of the most common
parasitic infestations, affecting . 1 billion of the world’s
population and causing . 1,000 deaths annually.1 A
lumbricoides is transmitted via the feco-oral route. An
Ascaris larva migrates to the lungs through either the
lymphatics or the venules of the portal system. Larval
ascariasis causes Löffler’s syndrome, a concomitance
of wheezing, pulmonary infiltrations, and eosinophilia.2
It can cause alveolar inflammation, necrosis, and hem-
orrhage. Diagnosis of an ascariasis infestation during its
larval phase is difficult. The sputum may show numer-
ous eosinophils; stool examination, however, remains
negative for eggs during the larval stage.3 The diagno-
sis requires a high degree of suspicion. Occasionally,

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 the diagnosis can be confirmed by identifying larvae
in the sputum. Solitary pulmonary nodules can also
develop if the larva dies causing granulomatous inflam-
mation.4 Adult ascaris has been reported to cause air-
ways obstruction in a child, producing a complete lobar
collapse.5 Mebendazole and albendazole are the most
effective agents against ascariasis.
Ancylostomiasis (Hookworm Disease)
The most common hookworms are Ancylostoma duo-
denale and Necator americanus. The latter is found
in parts of the southern United States. Hookworm lar-
vae enter human hosts via the skin, producing itching
and local infection. The larvae are also infective via
the oral route.6 Hookworm infestations involve larval
migration through the lungs via the bloodstream, result-
ing in a hypersensitivity reaction. Patients usually pre-
sent with transient eosinophilic pneumonia (Löffler’s
syndrome).6 If the patient ingests a large number of lar-
vae, he/she may develop a condition known as “Wakana
disease,” characterized by nausea, vomiting, dyspnea,
and eosinophilia. This clinical picture represents a severe
hypersensitivity-like reaction to A duodenale.6 Larval
migration 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 examination
may reveal occult blood, eosinophils and, rarely, migrat-
ing larvae (Fig 1A).9 Bronchoscopic examination may
reveal airway erythema and high eosinophil counts in
BAL fluid (BALF).10 Patients can become profoundly
anemic and malnourished. These manifestations may
provide clinical clues to support the diagnosis. The anti-
parasitic agents for hookworm are mebendazole and
albendazole.
Strongyloidiasis
Strongyloides stercoralis is a common roundworm
that is endemic throughout the tropics but is found
worldwide in all climates. Infective filariform larvae
can penetrate the skin and infect human hosts. The lar-
vae migrate through the soft tissues and enter the lungs
via the bloodstream. A majority of roundworms migrate
up 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 causing
autoinfection.11 The life cycle of Strongyloides can be
completed entirely within one host. The term “hyper-
infection syndrome” describes the presentation of sep-
sis from enteric flora, mostly in immunocompromised
patients.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 Common
pulmonary symptoms include wheezing, hoarseness,
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dyspnea, and hemoptysis. A chest radiograph usually
demonstrates focal or bilateral interstitial infiltrates.
Pleural effusions are present in 40% of patients, and
lung abscess is found in 15%.14 Diffuse alveolar hem-
orrhage is usually found in patients with disseminated
strongyloidiasis. ARDS may result as a reaction to the
death of the organisms. Migration of a massive number
of larvae through the intestinal wall can result in sep-
sis, because larvae may convey gram-negative bacteria
into the bloodstream.13
The diagnosis can be confirmed by the presence of
larvae in the stool, duodenal aspirate, sputum, pleural
fluid, or BALF or lung biopsy specimens (Figs 1B, 1C).15
The sensitivity of a stool examination for ova and larvae
is 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 acute
infection because it takes 4 to 6 weeks to mount the
immune response.17 The ELISA is sensitive but non-
specific because of cross-reactivity with filarial infes-
tations.15 Oral ivermectin remains the treatment of
choice for uncomplicated Strongyloides infestation.13,18
Syngamosis
Nematoda of the genus Mammomonogamus affect
the respiratory tract of domestic mammals. Occasion-
ally, however, humans can become infested via the
respiratory tract. Most cases of human syngamosis are
reported from tropical areas, including South America,
the Caribbean, and Southeast Asia.19 Two hypotheses
have been proposed regarding its life cycle. One is that
humans become infested via the ingestion of food or
water contaminated with larvae or embryonated eggs.
The larvae complete the life cycle in the pulmonary
system, and the adult worms migrate to the central air-
ways as the preferred site of infection.20 An alternative
hypothesis is that patients are infected by the adult
worms present in contaminated food or water. This
mode of transmission is supported by its short incuba-
tion period (6-11 days).21 The diagnosis requires flex-
ible bronchoscopy unless the worms are expelled
through vigorous coughing (Fig 1D). The removal of
parasites through bronchoscopy is sufficient to improve
symptoms. To date, no studies have supported the
effectiveness of antihelminthic therapy.21,22
Dirofilariasis
Dirofilaria immitis is the filarial nematode that pri-
marily infects dogs. Humans are considered accidental
hosts because D immitis is unable to mature to an adult
form. D immitis is transmitted to humans by mosqui-
toes harboring infective third-stage larvae. The larva
travels to the right ventricle and develops into an imma-
ture adult worm. It is then swept into the pulmonary
Special Features
 Table 1—Parasitic Infection of Respiratory System

Bronchoscopic
Parasite Infective Form Endemic Area Mode of Transmission Pulmonary Presentation Evaluation Treatment
Nematodes
Ascariasis (Ascaris lumbricoides) Eggs and larva Asia, Africa, and Ingestion Eosinophilic Presence of parasite Mebendazole and
South America pneumonia, cough, in the airways albendazole
wheezing, dyspnea

journal.publications.chestnet.org
Hookworm (Ancyclostoma Larva Tropical and Skin penetration Eosinophilic Presence of hookworm Mebendazole and
duodenale) (Necator subtropical areas pneumonia, cough, in sputum, a albendazole
americanus) wheezing, dyspnea, marked eosinophil
alveolar hemorrhage predominance
from BAL
Strongyloidiasis Filariform larvae Tropical and Skin penetration Eosinophilic Bloody BAL and Ivermectin and
(Strongyloides stercoralis) subtropical areas pneumonia, cough, presence of parasite albendazole
wheezing, dyspnea, from BAL under
hyperinfection microscopic
syndrome examination
Syngamosis (Mammomonogamus Eggs or adult Asia, Africa, and Ingestion Foreign body-like Presence of parasite Removal through
laryngeus) worms South America lesion in bronchus, in the airways bronchoscopy
nocturnal cough
Dirofilariasis (Dirofilaria immitis) Larva Tropical and Mosquito-borne Cough, chest pain, Surgical lung biopsy None (self-limited)
subtropical areas infection fever, dyspnea, mild
eosinophilia, and
lung nodules
Tropical pulmonary Larva Tropical and Mosquito-borne infection Eosinophilic BAL shows Diethylcarbamazine
eosinophilia (Brugia malayi) subtropical areas pneumonia, cough, eosinophils more
(Wuchereria bancrofti) (South and wheezing, dyspnea, than 50% of
Southeast Asia) restrictive pattern on the total cells
spirometry, decreased

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diffusion lung capacity
Visceral larva migrans Larva Worldwide Ingestion Eosinophilic pneumonia, N/A Diethylcarbamazine
(Toxocara canis) episodic wheezing
(Toxocara catis)
Trichinella infection Larva Worldwide Ingestion Cough, pulmonary N/A Mebendazole
(Trichinella spiralis) infiltrates, dyspnea
due to respiratory
muscles involvement
Trematodes
Schistosomiasis Cercarial larvae East Asia, Skin penetration Pulmonary An eosinophil Praziquantel
(Schistosoma species) South America, hypertension and predominance from
Sub-Saharan Africa Katayama fever BAL in the absences
of parasites

CHEST / 145 / 4 / APRIL 2014

(Continued)

885
 arteries. The worm dies as a result of the inflammatory

Surgical removal of

by mebendazole
and albendazole
triclabendazole

cysts, followed
Praziquantel and
response and evokes granuloma formation.23 A majority

bronchoscopy
Treatment

and dapsone
of patients with pulmonary dirofilariasis are asymptom-

Therapeutic
atic. However, some patients (about 5%) may develop
cough, hemoptysis, chest pain, fever, dyspnea, and mild
eosinophilia.24 A peripheral or a pleural-based solitary
pulmonary nodule is a typical presentation. The nod-
Bronchial stenosis due

ule may show increased fluorodeoxyglucose avidity on

examination reveals
sac-like cyst in the

mass in the airway

to mucosal edema
Bronchoscopic

revealed pinkish
a PET scan25,26 and is often confused with malignancy.

rhinosporidiosis
Evaluation

mulberry-like
Calcification occurs within only 10% of these nodules.
and mucosal

Bronchoscopic

Bronchoscopy
nodularity

CT scanning may show a branch of the pulmonary artery

airway entering the nodule.27 Serology has poor specificity
because of cross-reactivity with other helminths. The
diagnosis is established by identifying the worm in the
excised lung tissue (Fig 1E). Needle biopsy and brush-
Pulmonary Presentation

lesion, expectoration

ings are usually nondiagnostic because of the small

and hypersensitivity
hemoptysis, pleural
hemoptysis, chest

sample size. The condition does not require any spe-

pain, and pleural

nasal congestion
Chest pain, cough,

of cyst contents,

polyps, epitasis,
nasopharyngeal
Strawberry-like,

cific treatment because it is a self-limiting condition.24

Fever, cough,

reaction
effusion

Tropical Pulmonary Eosinophilia

Tropical pulmonary eosinophilia (TPE) is a syndrome
of immunologic reaction to microfilaria of the lymphatic-
dwelling organisms Brugia malayi and Wuchereria
Mode of Transmission

infested crustaceans

bancrofti. It is a mosquito-borne infestation. The lar-

Table 1—Continued

vae reside in the lymphatics and develop into mature

contaminated

adult worms. The microfilariae are released into the

Ingestion of

Ingestion of

circulation and may be trapped in the pulmonary cir-

Ingestion

water

culation.28 Trapped microfilariae demonstrate a strong

immunogenicity and trigger antimicrofilarial antibod-
ies, resulting in asthma-like symptoms. The hallmark
of TPE is a high absolute eosinophil count (5,000-
(especially Middle East)

80,000/mm3).29 The radiologic features include retic-

ulonodular opacities, predominantly in the middle and
Endemic Area

South America,

the lower lung zones; miliary mottling; and predomi-

Southeast Asia,

nant hila with increased vascular markings at the bases.30

Worldwide

South Asia

Chest CT scanning may demonstrate bronchiectasis,

Africa

air trapping, calcification, and mediastinal lymphade-

nopathy.31 Pulmonary functions indicate a restrictive
defect with mild airways obstruction.29 BALF may con-
(infective larvae)

tain numerous eosinophils. Occasionally, microfilaria

Infective Form

can be identified on brushings or needle biopsy spec-

Metacercaria

imens.32 The chronic phase of TPE may lead to pro-

gressive and irreversible pulmonary fibrosis.28
Spores
Eggs

The standard treatment of TPE is diethylcarbama-

zine (DEC). Patients usually show improvement within
3 weeks. However, a mild form of interstitial lung dis-
ease with diffusion impairment may remain.33
Paragonimiasis (Paragonimus

(Echinococcus granulosus)

(Rhinosporidium seeberi)

Toxocariasis
Toxocara canis and cati are roundworms that affect
N/A 5 not available.
Rhinosporidiosis
Hydatid disease

Mesomycetozoea

the dog and cat, respectively. These roundworms are

common parasites that cause visceral larva migrans
species)

and eosinophilic lung disease in humans. Toxocariasis

Cestodes
Parasite

is transmitted to humans via ingestion of food that is

contaminated with parasite eggs. The larvae can migrate

886 Special Features

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 Figure 1. A, Hookworm larva in the sputum sample (wet smear, original magnification 3 88). Morphologically, hookworm larvae have long
buccal cavities, whereas Strongyloides larvae have short buccal cavities. (Reprinted with permission from Beigel et al.9) B, Bloody aliquot
from BAL sample and Strongyloides larvae from BAL (hematoxylin and eosin [H&E], original magnification 3 200). Note: short buccal
cavity distinguishes Strongyloides from the hookworm (inset) (H&E, original magnification 3 400). C, Strongyloides larvae (arrow) present
in alveolar space in lung with diffuse alveolar damage (H&E, original magnification 3 400). D, Bronchoscopic findings in anterior basal
segment of right lower lobe. The syngamosis male is smaller and attached to the copulatory bursa of the female body (arrow). The parasite
can be seen in bronchoscopy because they reside in the bronchial mucosa. (Reprinted with permission from Kim et al.19) E, Cross-sections
of coiled Dirofilaria worms within involved artery causing surrounding infarction of lung tissue. Note the smooth cuticle at the external
layer (Movat stain, original magnification 3 200). F, Schistosomal ova in the lung biopsy specimen. The arrow points to ova within the
granulomatous reaction (H&E, original magnification 3 100).

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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 and
chronic inflammation with eosinophilic infiltration (H&E, original magnification 3 200). (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-
tion 3 400). (Image courtesy by Gary Procop, MD.) C, Granulomas in the pleura in a patient with paragonimiasis. The arrow points to
a light brown egg within the granuloma (H&E, original magnification 3 100). (Image courtesy by Gary Procop, MD.) D, Protruded hydatid
cyst from left lower lobe bronchus. (Image courtesy by Farid Rashidi, MD.) E, Echinococcus cyst fragments in lung biopsy specimen. The
arrows highlight the collapsed chitinous layer of a death hydatid cyst (H&E, original magnification 3 44). F, Echinococcus cyst fragments
in lung biopsy specimen. The fragmented ecchinococus cyst with collapsed chitinous layer resides within the granulomatous reaction
(H&E, original magnification 3 200). See Figure 1 legend for expansion of other abbreviation.

888 Special Features

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 throughout the host’s body, including the lungs.34 The
pathology of visceral larva migrans is a hypersensi-
tivity response to the migrating larvae. Visceral larva
migrans can present with fever, cough, wheezing, sei-
zures, and anemia. Leukocytosis and severe eosino-
philia are demonstrated in a peripheral smear. A chest
radiograph reveals pulmonary infiltrates with hilar and
mediastinal lymphadenopathy. Bilateral pleural effu-
sion can occur.35 Noncavitating pulmonary nodules
have also been reported.36 The diagnosis of toxocariasis
is established by an ELISA for the larval antigens.37
The treatment of choice is DEC; however, it may
exacerbate the inflammatory reaction because of the
resulting death of the larvae. It is advisable to combine
DEC 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 The
larvae migrate and reside in the GI tract until they
develop into an adult form. Fertilized female worms
release first-stage larvae into the bloodstream and the
lymphatics.39 Pulmonary involvement, although uncom-
mon, produces shortness of breath and pulmonary infil-
trates. Dyspnea is caused by parasitic invasion of the
diaphragm and the accessory respiratory muscles.39
The diagnosis is confirmed by muscle biopsy, which
may demonstrate T spiralis larvae. An ELISA using
anti-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 sucker
near 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 most
common 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 Humans
become infested through the skin from contact with
fresh water containing Schistosomal cercaria (infec-
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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 history
of swimming in Lake Malawi and rafting in sub-Saharan
Africa.41
In acute schistosomiasis, patients present with dys-
pnea, wheezing, dry cough, abdominal pain, hepatos-
plenomegaly, myalgia, and eosinophilia.42 Patients
experience shortness of breath because of an immuno-
logic reaction to antigens released by the worms. The
level of circulating immune complexes correlates with
the symptoms and with the intensity of infection.
In chronic schistosomiasis, embolization of the eggs
in the portal system causes periportal fibrosis and por-
tal hypertension. Pulmonary involvement can occur
as a result of the systemic migration of parasitic eggs
from the portal system. The eggs trigger an inflamma-
tory response that leads to pulmonary arterial hyper-
tension (PAH) and subsequent development of cor
pulmonale in 2% to 6% of patients.43 Apoptosis of the
endothelial cells in the pulmonary vasculature plays
a role in the pathogenesis of schistosomal-associated
cor 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 in
the absence of parasites. The diagnosis is confirmed by
microscopic examination of stool and urine or by rec-
tal biopsy. However, the sensitivity of these tests is low
for 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 within
2 weeks after the infestation. Schistosomal ova can
be found in the lung biopsy specimen (Fig 1F).
Acute schistosomiasis is treated with praziquantel.
The treatment is repeated within several weeks because
it has no antihelminthic effect on the juvenile stages
of the parasites.46 Acute pneumonitis, which is believed
to be related to lung embolization by adult worms in
the pelvic veins, can be observed 2 weeks after the
treatment.47 Patients with schistosomal-associated PAH
can be treated with PAH-specific therapy along with
antiparasitic medications.47
Paragonimiasis
Paragonimus species, including westernmani, cause
paragonimiasis that usually involves the lungs. The
mode 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 migrate
through the diaphragm and the pleura into the bron-
chioles.49 The eggs are produced by the mature adult
CHEST / 145 / 4 / APRIL 2014 889
 worms, which are expelled in the sputum or swallowed
and passed with the stool. Typically acute symptoms
include fever, chest pain, and chronic cough with hemop-
tysis.50 Pleural effusion and pneumothorax may be the
first manifestation during the migration of the juvenile
worms through the pleura. A chest radiograph dem-
onstrates patchy infiltrates, nodular opacities, pleural
effusion, 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 wall
thickening, and centrilobular nodules. Bronchoscopic
examination may reveal airway narrowing from mucosal
edema (Fig 2A).51 A lung biopsy specimen may show
chronic eosinophilic inflammation (Fig 2B). The diag-
nosis is confirmed by the presence of eggs or larvae in
the 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 also
observed 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 establishing
the diagnosis.53 Praziquantel and triclabendazole are
the treatments of choice, with a cure rate of 90% and
98.5%, respectively.34
Cestodes
Cestodes are a subclass of tapeworms; parasites in
this group have no digestive system. These parasites
live 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 the
parasite species that cause hydatid disease in humans.
E granulosus is endemic in sheep-herding areas of the
Mediterranean, Eastern Europe, the Middle East, and
Australia. An estimated 65 million individuals in these
areas are infected.1 Humans become accidental hosts
either by direct contact with the primary hosts (usually
dogs) or by the ingestion of food contaminated with
feces, containing parasite eggs.34 The larvae reach the
lymphatics of the intestines and the bloodstream and
then migrate to the liver, the main habitat in human
hosts.
Two different presentations of echinococcosis are
noted: (1) cystic hydatidosis and (2) alveolar echinococ-
cosis. An ecchinococcal infection becomes symptom-
atic after 5 to 15 years, secondary to local compression
or dysfunction of the affected organ. Pulmonary cysts
expand at a rate of 1 to 5 cm/y, and calcification is less
common.54 Pulmonary symptoms from the intact cyst
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include cough, fever, dyspnea, and chest pain. The
cyst may rupture into a bronchus and cause hemop-
tysis and/or expectoration of cystic fluid containing
parasitic components (hydatoptysis), which is con-
sidered a pathognomonic finding of cystic rupture.55
The patients may present with hydropneumothorax
or empyema. Occasionally, a ruptured cyst can cause
an anaphylactic-like reaction and pneumonia.8 Cystic
hydatidosis is diagnosed by chest radiography, which
demonstrates a well-defined, homogenous, fluid-filled,
round opacity. Ruptured cysts may have characteristic
features, including air crescent, pneumocyst, floating
membrane (“water lily sign”) (Fig 3), or completely
empty cavity images.56 A “meniscus” or “crescent” sign
or Cumbo’s sign (onion peel) have also been described.
Thoracic ultrasonography may be useful to confirm
the cystic structure, demonstrating the characteristic
double-contour (pericyst and parasitic membrane
endocyst) of intact cysts. However, daughter cysts are
also observed occasionally in pulmonary hydatidosis.56
Bronchoscopic examination reveals sac-like cysts in
the airway (Fig 2D). A surgical lung biopsy may reveal
echinococcus cyst fragments (Figs 2E, 2F).
Bronchoscopic extraction of the hydatid cyst is pos-
sible; however, because of the risk of cyst rupture, it
should be considered on a case-by-case basis. Serologic
tests 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 needs
surgical treatment. Complete resection of the cyst
is the cornerstone of the management of pulmonary
hydatidosis: to remove the intact cyst, preserve as much
viable lung tissue as possible, and treat the associated
Figure 3. Water lily sign. CT scan obtained at level of right middle
lobe shows ruptured hydatid cyst. After rupture and discharge of
cyst fluid into pleural cavity, endocyst collapses, sediments, and floats
in remaining fluid at bottom of original cyst. (Image courtesy by
Farid Rashidi, MD.)
Special Features
 Figure 4. A, Bronchoscopy revealed pinkish mulberry-like rhinosporidiosis mass in the right main stem bronchus. (Reprint with permission
from 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 magnification 3 100). (Reprint with permission from Singh et al.64) C, Amebic lung
abscess from lung biopsy specimen. The arrows point to trophozoites of Entamoeba histolytica (H&E, original magnification 3 200).
D, Transbronchial needle biopsy specimen of a mediastinal lymph node shows histiocytes containing abundant Leishmania amastigotes
(arrows) (H&E, original magnification 3 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 magnification 3 100). Inset shows bradyzoites of T gondii present in cytoplasm
of alveolar macrophage (H&E, original magnification 3 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 the
lesion and may exhibit chronic congestion, hemorrhage,
and interstitial pneumonia, which often resolve after
the surgery.57 Spillage of hydatid fluid must be avoided
to prevent secondary hydatidosis. Medical therapy may
have 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 the
cyst wall and increases the risk of rupture. In addi-
tion, if the parasite dies because of the drug, the cyst
membrane may remain within the cavity and lead to
secondary complications, including infections.59 Per-
cutaneous treatment by puncture-aspiration-injection-
reaspiration has rarely been used in pulmonary cysts
because of the risk of anaphylactic shock, pneumo-
thorax, pleural spillage, and bronchopleural fistulae.60
Pulmonary alveolar echinococcosis is a rare but
severe and potentially fatal form of echinococcosis but
it is restricted to the Northern Hemisphere. The liver
is the first target for the parasite, with a long, silent
incubation period. Pulmonary involvement results
from either dissemination or the direct extension of
the hepatic echinococcosis with intrathoracic rupture
through the diaphragm into the bronchial tree, pleural
cavity, or mediastinum. Chest radiograph or CT scan-
ning may aid in the diagnosis. ELISAs and indirect
hemagglutination assay are available and offer early
detection in endemic areas. Radical resection of
localized lesions is the only curative treatment yet, is
rarely possible in invasive and disseminated disease.
Mebendazole and albendazole can be used, but the
required treatment duration need is a minimum of
2 years after the radical surgery.61
Mesomycetozoea
Mesomycetozoea is a group of organisms at the
border of the animal-fungal kingdom.62 They appear
in host tissues as sphere-shaped spores.
Rhinosporidiosis
Rhinosporidiosis is a chronic granulomatous infec-
tious disease caused by Rhinosporidium seeberi. This
condition has a high prevalence in South Asia, especially
Sri Lanka.63 Patients usually present with recurrent
polypoidal, friable, hemorrhagic, lesions. The com-
mon sites of involvement are the nose and nasopharynx.
However, lesions can involve the tracheobronchial
tree, leading to partial or complete airway obstruc-
tion (Figs 4A, 4B).64 CT imaging is the preferred
study because it defines the extent of disease. Thera-
peutic bronchoscopy plays a major role in bronchial
rhinosporidiosis.
Dapsone is the only medication to arrest the matu-
ration of the sporangia, but the lesions may recur after
months or years.65 Follow-up bronchoscopy is recom-
mended to monitor signs of recurrence.
Protozoal Parasites
Protozoa parasites are single-celled organisms that
are mostly intracellular in humans (Table 2). Pulmonary
amebiasis is caused by Entamoeba histolytica tropho-
zoites invading the intestinal mucosa and entering the
bloodstream, effecting systemic infection. Pleuropul-
monary amebiasis occurs mainly by local extension from
the amoebic liver abscess. Patients usually present with
fever, right-upper-quadrant abdominal pain, and cough.
Sterile pleural effusion, lung abscess, hepatobronchial

Table 2—Protozoal Infection of Respiratory System

Mode of
Protozoal Parasites Endemic Area Transmission Presentation Bronchoscopic Evaluation Treatment
Pulmonary Worldwide Ingestion Fever, right upper Surgical lung biopsy Metronidazole
amebiasis quadrant abdominal specimen shows
pain, lung abscess, Entamoeba histolytica
hepatobronchial trophozoites
fistula
Pulmonary Asia, Africa, Sand fly-borne Pneumonitis, pleural Transbronchial needle biopsy Pentavalent antimonials
leishmaniasis Central and infection effusion, mediastinal specimen of a mediastinal and liposomal
South America lymphadenopathy lymph node showing amphotericin B
histiocytes containing
Leishmania donovani
organisms
Pulmonary Worldwide Ingestion Generalized Histologic examination of Pyrimethamine and
toxoplasmosis lymphadenopathy, lung biopsy specimen can sulfadiazine
interstitial pneumonia, identify Toxoplasma gondii
diffuse alveolar tachyzoites in necrotic area
damage

892 Special Features

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 fistula, empyema, and pyopneumothorax have also
been reported.1 Live trophozoites of E histolytica
can be demonstrated in sputum, pleural pus, or lung
biopsy specimens (Fig 4C). The presence of amoeba
in the stool does not indicate an active E histolytica
infection because two other nonpathologic Entamoeba
species are found in humans.66 Metronidazole is the
treatment of choice for invasive amoebiasis.
Leishmania causes visceral leishmaniasis, which has
been reported in patients who have undergone lung
transplants.67 Pulmonary manifestations include pneu-
monitis, pleural effusion, and mediastinal lymphade-
nopathy.34 Leishmania organisms can also be found in
the alveoli (Fig 4D)68 and the BALF.69 The diagnosis
of leishmaniasis is confirmed by the presence of the
parasites in bone marrow aspirates or by polymerase
chain reaction identification in tissue biopsy specimens.
Treatments of choice include pentavalent antimonials
and liposomal amphotericin B. Miltefosine can be used
as an oral agent against visceral leishmaniasis.70
Toxoplasmosis is caused by the protozoan, Toxo-
plasma gondii. Cats are the primary hosts of T gondii.71
Humans become infected by consuming contaminated
undercooked food. Pulmonary toxoplasmosis has been
reported with increasing frequency in HIV-infected
patients. Pulmonary manifestations include interstitial
pneumonia, diffuse alveolar damage, or necrotizing
pneumonia.72 Histologic examination of lung biopsy
specimens can identify T gondii tachyzoites in necrotic
areas in both intracellular and extracellular forms
(Fig 4E).73 The diagnosis of toxoplasmosis is based on
the detection of the protozoa in bodily tissues. Diag-
nostic real-time polymerase chain reaction-based assays
of BALF have been reported for HIV-positive patients.
Toxoplasmosis can be treated with a combination of
pyrimethamine and sulfadiazine for 3 to 4 weeks.74
Conclusions
Although helminthic and protozoal parasitic infes-
tations are dominant mainly in tropical and subtropical
areas, global warming, immigration, and an increasing
use 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 reported
to CHEST that no potential conflicts of interest exist with any
companies/organizations whose products or services may be dis-
cussed in this article.
Other contributions: We thank Gary Procop, MD, and Farid
Rashidi, MD, for contribution of figures.
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