Parasitic lung infections
Vannan Kandi Vijayan
Vallabhbhai Patel Chest Institute, University of Delhi,
Delhi, India
Correspondence to Dr Vannan Kandi Vijayan, MD,
PhD, DSc, FAMS, Director, Vallabhbhai Patel Chest
Institute, University of Delhi, Delhi 110007, India
Tel: +91 11 27667027; fax: +91 11 27667420;
e-mail: vijayanvk@hotmail.com
Current Opinion in Pulmonary Medicine 2009,
15:274–282
Introduction
Parasitic lung infections are an important group of infec-
tious diseases of the lung that are frequently neglected,
leading to a delay in accurate diagnosis and prompt
treatment. Though many parasitic infections have a
benign course, a large number of parasitic infections will
cause considerable morbidity and mortality [1]. There
is a renewed interest in parasitic lung infections due to
globalization and travel across the continents [2]. In
addition, global climate change and population explosion
can change the natural ecosystem, leading to an increase
in the transmission of parasites to human beings. The
emergence of HIV infection/AIDS, the frequent use of
immunosuppressive drugs in many diseases, and the
increasing numbers of organ transplantations have also
resulted in resurgence of parasitic lung infections [3].
This review deals with the recent developments in the
field of parasitic lung infections. The important pulmon-
ary diseases that can occur due to parasitic infections are
listed in Table 1.
1070-5287 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Purpose of review
Global climate change and population explosion leading to changes in natural
ecosystem and travel across the continents have resulted in an increase in the
transmission of parasites to human beings. This review focuses on recent
advancements in parasitic lung infections.
Recent findings
Invasive parasitic diseases including lung infections are increasingly being reported in
patients with immunodeficiency syndromes. A recombinant kinesin-related antigen of
Leishmania donovani has been validated with ELISA using urine samples for the
diagnosis of visceral leishmaniasis. Pyruvate kinase deficiency has been shown to
provide protection against Plasmodium falciparum infection. Intravenous artesunate is
an alternative drug for the treatment of severe malaria. The best way to protect from
malaria is the use of long-lasting insecticide-treated bednets. Biennial treatment with
praziquantel has been found to be cost-effective treatment for control of infection with
Schistosoma haematobium. Pulmonary paragonimiasis can be diagnosed by fine
needle aspiration biopsy of pulmonary nodules. Strongyloides stercoralis hyperinfection
can mimic accelerated idiopathic pulmonary fibrosis. Migratory nodular shadows with
halos are important chest computed tomographic findings in human toxocariasis.
Summary
Patients with immunodeficiency syndromes (HIV infection, organ transplantation and
immunosuppressive drugs, including corticosteroids) should be evaluated for early
detection of parasitic lung infections.
Keywords
babesiosis, malaria, paragonimiasis, parasitic pneumonias, strongyloidiasis, tropical
pulmonary eosinophilia
Curr Opin Pulm Med 15:274–282
ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
1070-5287
Entamoeba histolytica infection
Amoebiasis is one of the most common infections in
the world. It has been estimated that approximately
50 million cases of invasive Entamoeba histolytica disease
occur worldwide each year, with up to 100 000 deaths
[2]. Ingestion of mature E. histolytica cysts in fecally
contaminated food, water or hands causes infection.
Trophozoites are released in the small intestine by
encystations induced by stomach acids and then migrate
to the large intestine. Trophozoites multiply in the
intestine by binary fission and produce cysts that are
passed in formed feces. Cysts can survive in the external
environment for weeks to months because of the protec-
tive chitinous cell walls. Trophozoites that are passed in
diarrheal stools are destroyed once outside the body.
Trophozoites can remain in the intestinal lumen of
individuals who are asymptomatic carriers and pass cysts
in their stool. In some individuals, the trophozoites
invade the intestinal mucosa causing intestinal disease.
In others, the trophozoites pass through the bloodstream
DOI:10.1097/MCP.0b013e328326f3f8
 Parasitic lung infections Vijayan 275

Table 1 Pulmonary diseases caused by parasitic infections
Diseases
I. Protozoa
1. Pulmonary amoebiasis
2. Pulmonary leishmaniasis
3. Pulmonary malaria
4. Pulmonary babesiosis
5. Pulmonary toxoplasmosis
II. Helminths
a) Cestodes
1. Pulmonary hydatid disease
b) Trematodes
1. Pulmonary schistosomiasis
2. Pulmonary paragonimiasis
c) Nematodes
1. Pulmonary ascariasis
2. Pulmonary ancylostomiasis
3. Pulmonary strongyloidiasis
4. Tropical pulmonary eosinophilia
(filarial infection)
5. Pulmonary dirofilariasis
6. Visceral larva migrans
7. Pulmonary trichinellosis
Parasites
Entamoeba histolytica
Leishmania donovani
Plasmodium vivax
Plasmodium falciparum
Plasmodium malariae
Plasmodium ovale
Babesia microti
Babesia divergens
Toxoplasma gondii
Echinococcus granulosus
Echinococcus multilocularis
Schistosoma haematobium
Schistosoma mansoni
Schistosoma japonicum
Paragonimus westermani
Ascaris lumbricoides
Ancylostoma duodenale
Necator americanus
Strongyloides stercoralis
Wuchereria bancrofti
Brugia malayi
Dirofilaria immitis
Dirofilaria repens
Toxocara canis
Toxocara catis
Trichinella spiralis
dazole to reduce toxicity of metronidazole [8]. Tinidazole
has been found to be more effective and fewer side-
effects than metronidazole in the treatment of amoebiasis
[9].
Leishmania donovani infection
Leishmania donovani, transmitted by various species of
Phlebotomus, the sand fly, causes visceral leishmaniasis
[10]. Pulmonary manifestations in leishmaniasis include
pneumonitis, pleural effusion and mediastinal adenopa-
thy, especially in patients coinfected with HIV. Visceral
leishmaniasis has also been reported in lung transplant
patients [11]. Development of a simple and rapid test for
the detection of PCR-amplified Leishmania has been
described [12], and it has been observed that PCR
alone provides a marker for infection rather than a marker
for disease [13]. A recombinant kinesin-related protein
(rKRP42) antigen of L. donovani has been validated
with ELISA using urine samples and has been found
to be useful in the diagnosis of visceral leishmaniasis,
especially in epidemiological studies [14]. The drugs
for the treatment of leishmaniasis include pentavalent
antimonials, amphotericin B, especially the liposome
formulations, and pentamidine. Miltefosine is the first
orally administered drug against leishmaniasis [15].

to reach extra-intestinal sites such as liver, brain and
lungs, resulting in pathological lesions. Pulmonary amoe-
biasis occurs primarily due to extension of the amebic
liver abscess [4]. Invasive amoebiasis is an emerging
parasitic disease in HIV-infected patients [5]. The main
manifestations of pleuro-pulmonary amoebiasis are fever,
right upper quadrant abdominal pain, chest pain and
cough. Hemoptysis and expectoration of ‘anchovy
sauce-like’ pus indicate amoebiasis [6]. The diagnostic
findings in pleuro-pulmonary amoebiasis are elevated
hemidiaphragm, tender hepatomegaly, pleural effusion
and basal pulmonary involvement. Active trophozoites of
E. histolytica can be demonstrated in sputum or pleural
pus. Microscopic examination of stool samples may reveal
cysts or trophozoites of amoebae. The presence of
amoeba in the stool does not signify that the disease is
due to E. histolytica, as other two nonpathogenic species
found in humans (E. dispar and E. moshkovskii) are
indistinguishable morphologically. Other diagnostic tests
include culture of E. histolytica and serological tests
(indirect hemagglutination test, ELISA and indirect
fluorescent antibody test). Metronidazole is the treat-
ment of choice. Drug resistance in amoebiasis can result
from indiscriminate use of metronidazole [7]. Lactoferrin
and lactoferricins have been found to kill E. histolytica,
and it has been suggested that lactoferrin and lactoferri-
cin can be coadministered with a low dose of metroni-
Malarial infection
The malarial parasites that infect humans are Plasmodium
vivax, P. falciparum, P. malariae and P. ovale and are
transmitted primarily by the bite of an infected female
Anopheles mosquito. Falciparum malaria is the most deadly
type of malaria infection. Pyruvate kinase deficiency
has been shown to provide protection against infection
and replication of P. falciparum in human erythrocytes,
and it has been suggested that mutant pyruvate kinase
alleles may confer a protective advantage against malaria in
humans [16]. The pulmonary manifestations range
from cough to severe and rapidly fatal noncardiogenic
pulmonary edema and acute respiratory distress syndrome
(ARDS). It has also been reported that ARDS can occur in
vivax malaria [17]. A coagulation–inflammation cycle
that may contribute to organ dysfunction in falciparum
malaria has recently been described [18].
Light microscopy of stained thick and thin blood smears
is the gold standard for the diagnosis of malaria.
Thin smears allow identification of malaria species.
Radiological findings in severe falciparum malaria
include lobar consolidation, diffuse interstitial edema,
pulmonary edema and pleural effusion. PCR detection
of P. falciparum in human urine and saliva samples has
been described [19]. Intravenous artesunate has been
found to be useful for the treatment of severe malaria
in adults and children [20]. A systematic review has

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 276 Infectious diseases

found that parenteral artemisinin derivatives have similar
safety profiles as parenteral quinidine in the treatment of
severe malaria in children [21]. Patients with respiratory
failure require mechanical ventilation [22,23]. Travelers to
malarial endemic regions, in which there is chloroquine-
resistant malaria, are advised to have primary prophylaxis
with atovaquone–proguanil, mefloquine or doxycycline
[24]. The best way to prevent malaria is found to be
the use of long-lasting insecticide-treated bednets
[25].
Babesial infection
Babesiosis is caused by hemoprotozoan parasites, Babesia
microti and B. divergens [26,27]. Humans get the infec-
tion by the bite of an infected tick, Ixodes scapularis, and
can also be infected from a contaminated blood transfu-
sion [28]. The parasites attack the red blood cells and
can be misdiagnosed as Plasmodium. The symptoms are
fever, drenching sweats, tiredness and loss of appetite,
myalgia and headache. ARDS, occurring a few days after
initiation of medical therapy, is the important pulmonary
manifestation [29]. Splenic infarction and spontaneous
splenic rupture have also been reported in babesiosis
[30,31]. Immunocompromised individuals with babe-
siosis are at increased risk of developing persistent and
relapsing babesiosis [32]. Specific diagnosis is made
by examination of a Giemsa-stained thin blood smear.
Treatment is with a combination of clindamycin (600 mg
every 6 h) and quinine (650 mg every 8 h) or atovaquone
(750 mg every 12 h) and azithromycin (500–600 mg on
first day and 250–600 mg on subsequent days) for
7–10 days [33].
Toxoplasma infection
Toxoplasmosis is caused by the protozoan parasite,
Toxoplasma gondii. Cats are the primary carriers of the
organism [34]. Humans get the infection by eating para-
sitic cyst-contaminated raw or undercooked meat, veg-
etables or milk products. Plasmacytoid dentritic cells, a
prominent subset of dentritic cells, have been found to be
expanded in initial stages of T. gondii infection to present
parasite antigen, leading to the production of cytokines
and controlling infection [35]. The symptoms of tox-
oplasmosis are flu-like syndrome, enlarged lymph nodes
or myalgia. Pulmonary toxoplasmosis has been reported
with increasing frequency in patients with HIV infection.
Toxoplasma pneumonia can manifest as interstitial pneu-
monia/diffuse alveolar damage or necrotizing pneumonia
[36]. Diagnosis of toxoplasmosis is based on the detection
of the protozoa in body tissues. A real-time PCR-based
assay in bronchoalveolar lavage (BAL) fluid has been
reported in HIV-positive patients [37,38]. Toxoplasmo-
sis can be treated with a combination of pyrimethamine
and sulfadiazine. T. gondii protease inhibitor-1 (TgPI-1)
antigen has been suggested as a good candidate for
development of vaccine against toxoplasmosis, as it has
been found to elicit a strong specific immune response
against both acute and chronic T. gondii infection [39].
Echinococcus infection
The parasite species that cause hydatid disease in
humans are Echinococcus granulosus and E. multilocularis.
Pulmonary alveolar echinococcosis caused by E. multi-
locularis is due to hematogenous dissemination from
hepatic lesions, and E. granulosus causes cystic lesions
[40]. Pulmonary symptoms include cough, fever, dyspnea
and chest pain. Signs and symptoms can occur due to
compression of adjacent tissue by the cysts. Rupture of
the cysts into a bronchus may result in hemoptysis and
expectoration of cystic fluid containing parasite mem-
brane and can cause anaphylactic shock, respiratory dis-
tress, asthma-like symptoms, persistent pneumonia and
sepsis [41,42]. Rupture into the pleural space results in
pneumothorax, pleural effusion and empyema. Bronch-
iolitis obliterans organizing pneumonia, as an unusual
manifestation of hydatid disease, has been reported [43].
Chest radiographs show solitary or multiple round opa-
cities mimicking lung tumors (Figs 1 and 2). Metabolic
activity in human alveolar ecchinococcosis can be
assessed by [18F]fluorodeoxyglucose (FDG)-PET, and
lack of metabolic activity indicates suppressed parasite
activity and not parasite death [44]. Treatment of
hydatid cyst is primarily surgical. Parenchyma-preserving
surgery (cystotomy alone or cystotomy and capitonnage)
is the preferred treatment [45]. Radical surgery including
pneumonectomy, lobectomy and segmentectomy should
be avoided. Pharmacotherapy with albendazole or
mebendazole has also been found to be useful, especially
Figure 1 Chest radiograph of a patient with ruptured hydatid
cyst

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Figure 2 Chest CT scan of the same patient with hydatid cyst
CT, computed tomography.
in recurrent and multiple cysts. The efficacy of treatment
can be improved by combining albendazole with prazi-
quantel [46]. The treatment of alveolar echinococcosis
is radical surgical resection of the entire parasitic lesion.
Pharmacotherapy with mebendazole, albendazole or
praziquantel is given continuously for many years in
inoperable cases [47].
Schistosoma infection
The schistosomes that cause human disease are Schisto-
soma haematobium, S. mansoni and S. japonicum. The
schistosome eggs are passed in urine (S. haematobium)
or in feces (S. mansoni and S. japonicum) by the infected
humans. The final habitat of S. haematobium is urinary
bladder vesicle beds and of S. mansoni and S. japonicum is
the mesenteric beds. The eggs released in fresh water are
then ingested by snails (intermediate host), in which
the eggs hatch and develop into cercariae. The infective
cercariae are excreted into the water, and these cercariae
penetrate human skin or are ingested to penetrate the
gut. Pulmonary schistosomiasis can manifest clinically as
an acute form and a chronic form. The acute form, also
known as Katayama syndrome, presents with fever, chills,
weight loss, diarrhea, abdominal pain, myalgia, urticaria,
shortness of breath, wheezing and dry cough and is seen
in nonimmune patients [48]. Diffuse pulmonary infil-
trates are seen radiologically in Katayama syndrome, and
almost all patients have eosinophilia [49]. Pulmonary
nodules and pleural effusions have been reported in
the acute phase of infection with S. mansoni [50]. Patients
with chronic schistosomiasis present with features
of pulmonary hypertension and cor pulmonale [51].
Diagnosis of chronic schistosomiasis is based on the
demonstration of eggs in stool or urine by direct micro-
scopy or rectal/bladder biopsy. Acute schistosomiasis
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Parasitic lung infections Vijayan 277
can be treated with praziquantel 40 mg/kg for 3 days
(for S. mansoni or S. haematobium) and 60 mg/kg for 6 days
(for S. japonicum) with and without steroids [3,49].
Praziquantel can be repeated several weeks later to
eradicate the adult flukes. Artemisinin has been found
to be useful in the early stage after exposure, as the
drug has been found to act on juvenile forms of the
schistosomes and may reduce the risk of the Katayama
syndrome [52]. Chronic schistosomiasis can also be
treated with praziquantel with the same dosage.
Biennial treatment with praziquantel in school-age
children in sub-Saharan Africa has resulted in signifi-
cant and sustained reduction in S. haematobium infection,
suggesting that this can be a cost-effective treatment
strategy for control programmes in resource-limited
countries [53].
Paragonimus infection
Ninety percent of the cases occur in Asia, where nearly
20 million people are infected [54]. Paragonimiasis
is caused by infection with Paragonimus species and
manifests as subacute or chronic inflammation of the
lung. The main species that cause paragonimiasis in
humans is P. westermani. Adult worms live in the lungs,
and the eggs are voided in the sputum or feces. The
unembryonated eggs of P. westermani are excreted in
the sputum, or they can be swallowed and passed with
stool. The eggs become embryonated in the external
environment, and miracidia are produced. The miracidia
penetrate the soft tissues of the first intermediate host, a
snail and go through several developmental stages inside
the snail forming free-swimming cercariae. Many cercariae
then emerge from the snail and invade the second inter-
mediate host, a crustacean such as a crab or crayfish.
Cercariae encyst and produce metacercariae that are
the infective stage for the mammalian host. The humans
get infection, when raw or undercooked crabs or crayfishes
infected with infective metacercariae are ingested.
The metacercariae excyst in the duodenum, penetrate
through the intestinal wall into the peritoneal cavity,
then through the abdominal wall and diaphragm into the
lungs. In the lungs, they become encapsulated and develop
into adults.
Pulmonary paragonimiasis manifests as fever, chest pain,
chronic cough and hemoptysis [3]. Chest radiographs
may show infiltrative, nodular and cavitating shadows.
Pleural effusion or pneumothorax is an important finding
in paragonimiasis. Eggs can be demonstrated in sputum
samples, BAL fluid or lung biopsy specimens. Fine
needle aspiration biopsy of pulmonary nodule has been
found to be useful in the diagnosis of pulmonary para-
gonimiasis [55]. Peripheral blood eosinophilia and
elevated serum IgE levels are seen in more than 80%
of patients with paragonimiasis [1]. A recombinant
 278 Infectious diseases
protein of P. westermani egg antigen, assessed by ELISA
using sera from patients infected with P. westermani, has
been found to be highly sensitive and specific for the
diagnosis of Paragonimus infection [56]. Paragonimiasis
can be treated with praziquantel (75 mg/kg per day for
3 days), bithionol (30–40 mg/kg in 10 days on alternate
days), niclofolan (2 mg/kg as a single dose) or triclaben-
dazole (20 mg/kg in two equal doses) [57].
Ascaris infection
Ascaris lumbricoides is the most common intestinal hel-
minthic infection [1]. Pulmonary migration of larvae is
usually asymptomatic. Symptomatic pulmonary disease
may range from mild cough to a Loffler’s syndrome [3].
The respiratory symptoms include chest pain, cough with
mucoid sputum, hemoptysis, shortness of breath and
wheezing. Leucocytosis, particularly eosinophilia, is an
important laboratory finding. Chest radiographs demon-
strate unilateral or bilateral, transient, migratory, nonseg-
mental opacities of various sizes. Larvae can sometimes
be demonstrated in respiratory or gastric secretions. Pul-
monary disease due to ascariasis usually does not require
any treatment, as it is a self-limiting disease. Treatment is
with mebendazole given in a dose of 100 mg twice a day
for 3 days. Ivermectin has also been found to be useful
[58].
Ancylostoma infection
Hookworm disease in humans results from infections due
to Ancylostoma duodenale and Necator americanus. Bronchi-
tis and bronchopneumonia can occur when the larvae
break through the pulmonary capillaries to enter the
alveolar spaces. Pulmonary larval migration can elicit
peripheral blood and pulmonary eosinophilia. During
pulmonary larval migration, patients may present with
fever, cough, wheezing and transient pulmonary infil-
trates in chest radiographs [3]. A direct microscopic
examination of stool demonstrates the presence of
characteristic hookworm eggs. Concentration method
may be used when the infection is light. Both mebenda-
zole and albendazole are useful in the treatment of
hookworm. Mebendazole is given as 100 mg twice daily
for 3 days, and albendazole is given as a single dose of
400 mg [1].
Strongyloides infection
Strongyloides stercoralis is seen worldwide, but common in
South America, South-East Asia, sub-Saharan Africa and
the Appalachian region of the United States [1]. The
cell-mediated immunity that develops following primary
infection prevents reinfection. As a result, the larvae and
adult worms remain confined to the intestine, and
the tissue invasion is prevented in immunocompetent
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
individuals. When there is immunosuppression as seen in
patients with immunosuppressive therapy (especially
corticosteroids) and other immune-deficient states
(malnutrition, lymphoma and leukemia and more), auto-
infection is exaggerated and leads to hyperinfection [59].
During migration of filariform larvae through the lungs,
bronchopneumonia and hemorrhages in the alveoli can
occur. These areas are infiltrated with eosinophils. This is
associated with elevated IgE and eosinophilia in the
blood. As the larvae penetrate the intestinal mucosa,
Gram-negative bacteria from the gut are carried by the
larvae on their cuticle. As a result of invasion of bacteria
along with larvae, diffuse and patchy bronchopneumonia
and pulmonary abscess can occur. Pulmonary signs and
symptoms include cough, shortness of breath, wheezing
and hemoptysis [3]. In patients at high risk for strongyloi-
diasis, ARDS and septicemia due to intestinal transmural
migration of bacteria can occur as a result of pulmonary
hyperinfection or disseminated strongyloidiasis [60]. S.
stercoralis hyperinfection can mimic accelerated idiopathic
pulmonary fibrosis [61]. In immunocompetent patients
with strongyloidiasis, the parasite load is usually low, and
the larval output is irregular. As a result, the diagnosis of
strongyloidiasis by examination of a single stool specimen
using conventional techniques usually fails to detect larvae
in up to 70% of cases [1]. The diagnostic yield can be
increased by examination of several stool specimens on
consecutive days. In disseminated disease, larvae and adult
parasites can be seen in sputum, urine, BAL fluid and other
body fluids.
Ivermectin, thiabendazole or albendazole can be used
for treatment of strongyloidiasis in immunocompetent
individuals without complications. Ivermectin is given
in a dosage of 200 mg/kg orally for 1 or 2 days. Thia-
bendazole is given orally as 25 mg/kg twice a day for
2 days. Albendazole 400 mg twice a day for 5 days has
been found to be useful in the treatment of strongy-
loidiasis. In immuno-compromised individuals with dis-
seminated strongyloidiasis, the dose of thiabendazole
has to be doubled, and the duration of treatment may
be several weeks. Corticosteroids should not be pre-
scribed to prevent life-threatening hyperinfection syn-
drome [59].
Filarial infection
Immunologic hyperresponsiveness to human filarial para-
sites, Wuchereria bancrofti and Brugia malayi results in an
occult form of filariasis known as tropical pulmonary
eosinophilia (TPE) [62,63]. TPE is prevalent in filarial
endemic regions of the world, especially South-East Asia
[1]. TPE should be considered in the differential diag-
nosis if a patient traveling from a filarial endemic region
presents with ‘asthma-like’ symptoms [64]. TPE patients
usually present with paroxysmal cough, breathlessness,

Figure 3 Chest radiograph showing bilateral diffuse mottling in
a patient with tropical pulmonary eosinophilia
Adapted from [3,62].
wheeze and chest pain. The symptoms occur predomi-
nantly at night, but can persist during the day. The
sputum often shows clumps of eosinophils and rarely
Charcot–Leyden crystals. Leucocytosis with an absolute
increase in eosinophils in the peripheral blood is the
hallmark of TPE. Absolute eosinophil counts are usually
more than 3000 cells/ml and may range from 5000 to
80 000 cells/ml [65]. The chest radiological features of
TPE include reticulonodular shadows predominantly
seen in the mid and lower zones and miliary mottling
of 1–3 mm in diameter often indistinguishable from
miliary tuberculosis (Fig. 3). Lung function tests reveal
mainly a restrictive ventilation defect, with superim-
posed airways obstruction [1,63]. The treatment is with
oral diethylcarbamazine citrate (DEC) given in a dosage
of 6 mg/kg per day for 3 weeks [63]. A chronic mild
interstitial lung disease has been found to persist in
TPE despite treatment [63,66].
Dirofilarial infection
Pulmonary dirofilariasis is a zoonotic infection caused
by filarial nematodes, Dirofilaria immitis and D. repens.
Clinical symptoms are chest pain, cough, fever, hemop-
tysis and dyspnea. Computed tomography (CT) scan may
show a well defined nodule with smooth margin con-
nected to an arterial branch [67]. A definitive histopatho-
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Parasitic lung infections Vijayan 279
logical diagnosis of pulmonary dirofilariasis can be made
in tissue specimens obtained by wedge biopsy, video-
assisted thoracoscopy or rarely by fine needle biopsy [68].
There is no specific treatment for human dirofilariasis.
Toxocara infection
The common parasites that cause visceral larva migrans
and eosinophilic lung disease in humans are a dog ascarid
(Toxocara canis) and less commonly a cat ascarid (T. catis).
Visceral larva migrans is characterized by leucocytosis
and eosinophilia [3]. The main symptoms are fever,
cough, wheezing, seizures, anemia and fatigue. Pulmon-
ary manifestations are reported in 80% of cases, and
patients may present with severe asthma. There will
be intense blood eosinophilia. Chest radiograph may
reveal focal patchy infiltrates. In some cases, severe
eosinophilic pneumonia may lead to respiratory distress.
Other clinical features include generalized lymph
node enlargement, hepatomegaly and splenomegaly.
Migratory nodular shadows with halos on chest CT have
been described in toxocariasis [69]. Treatment with
antihelminthic drugs may exacerbate the inflammatory
reactions in the tissues due to the killing of larvae. It is,
therefore, advised to combine antihelminthic treatment
with corticosteroids. DEC can be given in a dose of
6 mg/kg per day for 21 days. Mebendazole is prescribed
in a dose of 20–25 mg/kg per day for 21 days.
Trichinella infection
Five species of Trichinella (T. spiralis, T. nativa, T. nelsoni,
T. britovi and T. pseudospiralis) can infect humans. The
most important species that infect humans is T. spiralis.
Humans get infection from raw and partially cooked
pork, after eating infected pig’s muscle containing larval
trichinellae. Pulmonary involvement, though uncom-
mon, includes shortness of breath, dyspnea and pulmon-
ary infiltrates. Dyspnea results from parasite invasion of
the diaphragm and the accessory muscles of respiration
[70]. A definitive diagnosis can be made by muscle biopsy
(usually deltoid muscle) that may demonstrate larvae of
T. spiralis. An ELISA using excretory/secretory antigens
to detect anti-Trichinella IgG antibodies in human sera
has been validated for the diagnosis of human trichinel-
losis [71]. Symptomatic treatment includes analgesics
and corticosteroids. Specific treatment is with mebenda-
zole 200–400 mg three times a day for 3 days, followed by
400–500 mg three times a day for 10 days. Trichinellosis
can be prevented by consuming properly cooked
pork.
Rare pulmonary protozoal infections
Free-living Acanthamoeba species can cause syste-
mic disease with pulmonary manifestations of nodular
 280 Infectious diseases

Table 2 Rare pulmonary protozoal infections in immunocom-

promised individuals References and recommended reading
Papers of particular interest, published within the annual period of review, have
Diseases Parasites been highlighted as:
 of special interest
1. Pulmonary acanthamoebiasis Acanthamoeba castellanii  of outstanding interest
Acanthamoeba polyphaga Additional references related to this topic can also be found in the Current
2. Pulmonary balamuthiasis Balamuthia mandrillaris World Literature section in this issue (p. 289).
3. Pulmonary naegleriasis Naegleria fowleri
4. Pulmonary trichomoniasis Trichomonas vaginalis 1 Vijayan VK. Tropical parasitic lung diseases. Indian J Chest Dis Allied Sci
Trichomonas tenax  2008; 50:49–66.
A comprehensive review study incorporating the pathogenesis, clinical features,
Trichomonas hominis
diagnosis and management of tropical parasitic lung diseases.
5. Pulmonary lophomoniasis Lophomonas blattarum
6. Pulmonary trypanosomiasis Trypanosoma cruzi 2 Roy S, Herwaldt B. Prevention of specific infectious diseases: amebiasis. In:
Trypanosoma brucei gambiense  Arguin PM, Kozarsky PE, Reed C, editors. CDC Health Information for
International Travel 2008. Atlanta: Centres for Disease and Control; 2008.
Trypanososma brucei
http://wwwn.cdc.gov/travel/yellowBook.aspx. [Accessed 18 October 2008]
rhodesiense A concise book from Centres for Disease Control and Prevention, Atlanta, USA,
7. Pulmonary cryptosporidiosis Cryptosporidium parvum with essential instructions on prevention, recognition and management of travel-
Cryptosporidium hominis related health problems including parasitic infections.
Cryptosporidium meleagridis 3 Vijayan VK. How to diagnose and manage common parasitic pneumonias.
8. Pulmonary cyclosporidiasis Cyclospora cayetanensis Curr Opin Pulm Med 2007; 13:218–224.
9. Pulmonary encephalitozoonosis Encephalitozoon cuniculi
Encephalitozoon hellem 4 Ackers JP, Mirelman D. Progress in research on Entamoeba histolytica
pathogenesis. Curr Opin Microbiol 2006; 9:367–373.
Encephalitozoon intestinalis
10. Pulmonary entercytozoonosis Enterocytozoon bieneusi 5 Hsu MS, Hsieh SM, Chen MY, et al. Association between amebic liver
11. Pulmonary balantidiasis Balantidium coli  abscess and human immunodeficiency virus infection in Taiwanese subjects.
BMC Infect Dis 2008; 8:48; doi: 10.1 186/1471-2334-8-48.
This study describes the clinical features and treatment outcomes in amebic liver
abscess patients infected with HIV and suggests that invasive amebiasis is an
emerging infection in patients with HIV infection.
infiltrates, pneumonitis and respiratory failure in immu-
6 Shamsuzzaman SM, Hashiguchi Y. Thoracic amoebiasis. Clin Chest Med
nocompromised patients [72]. Cryptosporidium parvum 2002; 23:479–492.
infection has been reported to produce interstitial pul- 7 Bansal D, Malla N, Mahajan RC. Drug resistance in amoebiasis. Indian J Med
monary infiltrates and focal areas of consolidation in Res 2006; 123:115–118.
AIDS patients [73]. Recurrent aspiration, secondary 8 Leon-Sicairos N, Reyes-Lopez M, Ordaz-Pichardo C, de la Garza M. Micro-
bicidal action of lactoferrin and lactoferricin and their synergistic effect with
to mega esophagus, can lead to pneumonitis, lung abscess metronidazole in Entamoeba histolytica. Biochem Cell Biol 2006; 84:327–
and bronchiectasis in Trypanosoma cruzi infection (Cha- 336.
ga’s disease). Cardiogenic pulmonary edema and pul- 9 Muneizel S, Halasah N, Yassin M. Nitroimidazoles in the treatment of intestinal
 amoebiasis. Middle East J Fam Med 2008; 6:6–8.
monary hypertension, secondary to cardiac failure and In this randomized clinical trial, the efficacy and tolerability of tinidazole is
dilatory cardiomyopathy, have also been reported in compared with metronidazole.
Chaga’s disease. East-African trypanosomiasis due to T. 10 Piscopo TV, Mallia AC. Leishmaniasis. Postgrad Med J 2006; 82:649–657.

brucei rhodesiense has been reported to cause noncardio-
genic pulmonary edema and ARDS in acute stage. Other
rare pulmonary protozoal infections that have been
reported in immunocompromised individuals are listed
in Table 2 [74].
Conclusion
Though parasitic lung infections are prevalent mainly in
the tropical and subtropical regions, these infections are
now increasingly being reported in many parts of the
world due to globalization and climate change. In
addition, the increasing numbers of organ transplan-
tations and the frequent use of immunosuppressive drugs
have also resulted in resurgence of parasitic lung infec-
tions. Pulmonary involvement is frequently seen in many
protozoal and helminthic infections, especially during
the larval migration of the parasites through the lungs.
The pulmonary infection due to parasites may range
from asymptomatic disease to severe life-threatening
conditions. The availability of new molecular diagnostic
methods and antiparasitic drugs enable us to detect
parasitic lung infections early and to treat them success-
fully.
11 Morales P, Torres JJ, Salavert M, et al. Visceral leishmaniasis in lung trans-
plantation. Transplant Proc 2003; 35:2001–2003.
12 Deborggraeve S, Laurent T, Espinosa D, et al. A simplified and standardized
 polymerase chain reaction format for the diagnosis of leishmaniasis. J Infect
Dis 2008; 198:1565–1572.
A simple and rapid test for the detection of PCR-amplified Leishmania DNA has
been described in this article.
13 Deborggraeve S, Boelaert M, Rijal S, et al. Diagnostic accuracy of a
 new Leishmania PCR for clinical visceral leishmaniasis in Nepal and its
role in diagnosis of disease. Trop Med Int Health 2008; 13:1378–
1383.
This study has evaluated the utility of a newly developed PCR in the diagnosis of
visceral leishmaniasis in endemic regions and indicates that this PCR test alone
provides a marker for infection rather than a marker for disease.
14 Islam MZ, Itoh M, Takagi H, et al. Enzyme-linked immunosorbent assay to
 detect urinary antibody against recombinant rKRP42 antigen made from
Leishmania donovani for the diagnosis of visceral leishmaniasis. Am J Trop
Med Hyg 2008; 79:599–604.
This study has evaluated a recombinant kinesin-related protein of L. donovani by
ELISA using urine samples and has found that this test is useful for the diagnosis of
visceral leishmaniasis.
15 Croft SL, Engel J. Miltefosine: discovery of the antileishmanial activity of
phospholipid derivatives. Trans R Soc Trop Med Hyg 2006; 100 (Suppl 1):
54–58.
16 Ayi K, Min-Oo G, Serghides L, et al. Pyruvate kinase deficiency and malaria.
 N Engl J Med 2008; 358:1805–1810.
This study shows that pyruvate kinase deficiency provides protection against
infection and replication of P. falciparum in human erythrocytes.
17 Tan LK, Yacoub S, Scott S, et al. Acute lung injury and other serious
 complications of Plasmodium vivax malaria. Lancet Infect Dis 2008; 8:449–
454.
This study highlights that P. vivax malaria, though classified as benign in nature,
can cause life-threatening complications.

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

18 Francischetti IM. Does activation of the blood coagulation cascade have a role
 in malaria pathogenesis. Trends Parasitol 2008; 24:258–263.
Activation of blood coagulation cascade has been proposed to contribute to organ
dysfunction in P. falciparum malaria.
19 Mharakurwa S, Simoloka C, Thuma PE, et al. PCR detection of Plasmodium
falciparum in human urine and saliva samples. Malar J 2006; 5:103; doi:
10.1186/1475-2875-5-103.
20 Rosenthal PJ. Artesunate for the treatment of severe falciparum malaria.
 N Engl J Med 2008; 358:1829–1836.
This study reviews the evidence showing the superiority of intravenous artesunate
in the treatment of severe falciparum malaria.
21 Praygod G, De Fray A, Eisenhut M. Artemisin derivatives versus quinine in
 treating severe malaria in children: a systematic review. Malar J 2008; 7:210.
This systematic review of 12 randomized studies in children has shown that
there was no statistically significant difference between two treatment groups
(parenteral artemisinin versus parenteral quinine) in parasite clearance time, fever
clearance time, incidence of neurological sequelae and 28th day cure rate.
22 WHO. Guidelines for the treatment of malaria. Geneva: World Health
Organisation; 2006. pp. 1–266.
23 Talwar A, Fein AM, Ahluwalia G. Pulmonary and critical care aspects of severe
malaria. In: Sharma OP, editor. Lung biology in health and disease: tropical lung
diseases, 2nd ed. New York: Taylor & Francis Group; 2006. pp. 255–279.
24 Freedman DO. Clinical practice: malaria prevention in short-term travelers.
 N Engl J Med 2008; 359:603–612.
This review focuses on the management of the risk of malaria in short-term travelers
to regions where malaria is endemic.
25 Hassan Sel-D, Malik EM, Okoued SI, Eltayeb EM. Retention and efficacy of
 long-lasting insecticide-treated nets distributed in eastern Sudan: a two-step
community-based study. Malar J 2008; 7:85; doi: 10.1186/1475-2875-7-85.
Long-lasting insecticide-treated nets have been found to be efficacious for malaria
control in a study from Sudan.
26 Vannier E, Gewurz BE, Krause PJ. Human babesiosis. Infect Dis Clin North Am
 2008; 22:469–488.
This review article describes the epidemiology, clinical features, diagnosis and
treatment of human babesiosis.
27 Genchi C. Human babesiosis: an emerging zoonosis. Parassitologia 2007;
49 (Suppl 1):29–31.
28 Cirino CM, Leitman SF, Williams E, et al. Transfusion-associated babesiosis
 with an atypical time course after nonmyeloablative transplantation for sickle
cell disease. Ann Intern Med 2008; 148:794–795.
This case report highlights that babesiosis can be transmitted by blood transfusion.
29 Boustani MR, Lepore TJ, Gelfand JA, Lazarus DS. Acute respiratory failure in
patients treated for babesiosis. Am J Respir Crit Care Med 1994; 149:1689–
1691.
30 Florescu D, Sordillo PP, Glyptis A, et al. Splenic infarction in human babe-
 siosis: two cases and discussion. Clin Infect Dis 2008; 46:e8–e11.
This is a report of two cases with splenic infarction in patients with babesiosis.
31 Kuwayama DP, Briones RJ. Spontaneous splenic rupture caused by Babesia
 microti infection. Clin Infect Dis 2008; 46:e92–e95.
This case report is the first one to describe that babesiosis can be associated with
spontaneous splenic rupture.
32 Krause PJ, Gewurz BE, Hill D, et al. Persistent and relapsing babesiosis in
 immunocompromised patients. Clin Infect Dis 2008; 46:370–376.
This study describes that the immunocompromised individuals are at increased
risk of persistent relapsing illness requiring prolonged (6 weeks) antibabesial
treatment for a cure.
33 Raju M, Salazar JC, Leopold H, Krause PJ. Atovaquone and azithromycin
treatment for babesiosis in an infant. Pediatr Infect Dis 2007; 26:181–183.
34 Dodds EM. Toxoplasmosis. Curr Opin Ophthalmol 2006; 17:557–561.
35 Pepper M, Dzierszinski F, Wilson E, et al. Plasmacytoid dendritic cells are
 activated by Toxoplasma gondii to present antigen and produce cytokines.
J Immunol 2008; 180:6229–6236.
The role of plasmacytoid dendritic cells in the initial stages of T. gondii infection is
described in this article.
36 Nash G, Kerschmann RL, Herndier B, Dubey JP. The pathological manifesta-
tions of pulmonary toxoplasmosis in the acquired immunodeficiency syndrome.
Hum Pathol 1994; 25:652–658.
37 Petersen E, Edvinsson B, Lundgren B, et al. Diagnosis of pulmonary infection
with Toxoplasma gondii in immunocompromised HIV-positive patients by real-
time PCR. Eur J Clin Microbiol Infect Dis 2006; 25:401–404.
38 Contini C. Clinical and diagnostic management of toxoplasmosis in the
 immunocompromised patient. Parassitologia 2008; 50:45–50.
This study highlights the clinical features, diagnostic procedures, especially the
role of real time PCR, and management strategies in toxoplasmosis.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Parasitic lung infections Vijayan 281
39 Cuppari AF, Sanchez V, Ledesma B, et al. Toxoplasma gondii protease
 inhibitor-1 (TgPI-1) is a novel vaccine candidate against toxoplasmosis.
Vaccine 2008; 26:5040–5045.
This study demonstrates that TgPI-1 elicits strong specific immune response,
making it a good candidate in a vaccine against toxoplasmosis.
40 Gottstein B, Reichen J. Hydatid lung disease (echinococcosis/hydatidosis).
Clin Chest Med 2002; 23:397–408.
41 Kuzucu A. Parasitic diseases of the respiratory tract. Curr Opin Pulm Med
2006; 12:212–221.
42 Fanne RA, Khamaisi M, Mevorach D, et al. Spontaneous rupture of lung
echinococcal cyst causing anaphylactic shock and respiratory distress syn-
drome. Thorax 2006; 61:550.
43 Kilic D, Findikcioglu A, Kocer E, Hatipoglu A. Unusual manifestation of
 bronchiolitis obliterans organizing pneumonia. Acta Chir Belg 2008;
108:468–470.
A case of bronchiolitis obliterans organizing pneumonia, probably secondary to
suppuration of a hydatid cyst has been described in this case report.
44 Reuter S, Grüner B, Buck AK, et al. Long-term follow-up of metabolic activity in
 human alveolar echinococcosis using FDG-PET. Nuklearmedizin 2008;
47:147–152.
This is the first study that has evaluated the metabolic activity on a long-term basis
to assess the utility of FDG-PET for the evaluation of disease progression and
response to treatment in alveolar echinococcosis.
45 Kavukcu S, Kilic D, Tokat AO, et al. Parenchyma-preserving surgery in the
management of pulmonary hydatid cysts. J Invest Surg 2006; 19:61–68.
46 Haralabidis S, Diakou A, Frydas S, et al. Long-term evaluation of patients with
 hydatidosis treated with albendazole and praziquantel. Int J Immunopathol
Pharmacol 2008; 21:429–435.
This is a retrospective study that compared two treatment groups (a combined
chemotherapy of albendazole and praziquantel with surgical removal of cysts and
the chemotherapy alone group without surgery). The difference between the two
kinds of treatment was found to be not significant. However, after additional
chemotherapy with albendazole for 3–6 months, all patients were cured at
8.5 years of follow-up.
47 Gottstein B, Reichen J. Hydatid lung disease. In: Sharma OP, editor. Lung
biology in health and disease: tropical lung disease, 2nd ed. New York: Taylor
& Francis Group; 2006. pp. 327–350.
48 Doherty JF, Moody AH, Wright SG. Katayama fever: an acute manifestation of
schistosomiasis. Br Med J 1996; 313:1071–1072.
49 Ross AG, Vickers D, Olds GR, et al. Katayama syndrome. Lancet Infect Dis
2007; 7:218–224.
50 Lambertucci JR, Silva LC, de Queiroz LC. Pulmonary nodules and pleural
effusion in the acute phase of schistosomiasis mansoni. Rev Soc Bras Med
Trop 2007; 40:374–375.
51 Lapa MS, Ferreira EV, Jardim C, et al. Clinical characteristics of pulmonary
hypertension patients in two reference centres in the city of Sao Paulo. Rev
Assoc Med Bras 2006; 52:139–143.
52 Utzinger J, Xiao SH, Tanner M, Keiser J. Artemisinins for schistosomiasis and
beyond. Curr Opin Investig Drugs 2007; 8:105–116.
53 Touré S, Zhang Y, Bosqué-Oliva E, et al. Two-year impact of single
 praziquantel treatment on infection in the national control programme
on schistosomiasis in Burkina Faso. Bull World Health Organ 2008; 86:
780–787.
In this longitudinal survey, it has been demonstrated that biennial treatment with
praziquantel in the National Control Programme in Burkina Faso has resulted in
significant and sustained reduction in S. haematobium infection.
54 Strobel M, Veasna D, Saykham M, et al. Pleuro-pulmonary paragonimiasis.
Med Mal Infect 2005; 35:476–481.
55 Zarrin-Khameh N, Citron DR, Stager CE, Laucirica R. Pulmonary paragoni-
 miasis diagnosed by fine-needle aspiration biopsy. J Clin Microbiol 2008;
46:2137–2140.
A case of paragonimiasis diagnosed by fine needle aspiration biopsy of a
pulmonary nodule is described in this case report.
56 Lee JS, Lee J, Kim SH, Yong TS. Molecular cloning and characterization of a
major egg antigen in Paragonimus westermani and its use in ELISA for
the immunodiagnosis of paragonimiasis. Parasitol Res 2007; 100:677–
681.
57 Keiser J, Engels D, Buscher G, Utzinger J. Triclabendazole for the treatment of
fascioliasis and paragonimiasis. Expert Opin Investig Drugs 2005; 14:1513–
1526.
58 Belizaro VY, Amarillo ME, de Leon WU, et al. A comparison of the efficacy of
single dose of albendazole, ivermectin and diethylcarbamazine alone or in
combination against Ascaris and Trichuris spp. Bull World Health Organ
2003; 81:35–42.
 282 Infectious diseases
59 Gorman SR, Craven DE. Images in clinical medicine. Strongyloides stercoralis
 hyperinfection. N Engl J Med 2008; 359:e12.
This case highlights the fact that when an individual with subclinical S. stercoralis
infection receives corticosteroid therapy, a severe, life-threatening hyperinfection
syndrome can occur.
60 Ghoshal UC, Ghoshal U, Jain M, et al. Strongyloides stercoralis infestation
associated with septicemia due to intestinal transmural migration of bacteria.
J Gastroenterol Hepatol 2002; 17:1331–1333.
61 Janssen R, Vlaminckx BJM, Seldenrijk CA, et al. Strongyloides stercoralis
 hyperinfection mimicking accelerated form of idiopathic pulmonary fibrosis.
Lancet Infect Dis 2008; 8:456.
A patient diagnosed as idiopathic pulmonary fibrosis after surgical biopsy was
treated with methyl prednisolone and developed S. stercoralis hyperinfection
syndrome. This case report highlights the importance of screening for S. stercor-
alis in patients from endemic regions before starting corticosteroids and immuno-
suppressive drugs.
62 Vijayan VK. Immunopathogenesis and treatment of eosinophilic lung diseases in
the tropics. In: Sharma OP, editor. Tropical lung disease (lung biology in health
and disease). New York: Taylor & Francis Group; 2006; 211. pp. 195–239.
63 Vijayan VK. Tropical pulmonary eosinophilia. Curr Opin Pulm Med 2007;
13:428–433.
64 Jiva TM, Israel RH, Poe RH. Tropical pulmonary eosinophilia masquerading as
acute bronchial asthma. Respiration 1996; 63:55–58.
65 Cooray JH, Ismail MM. Re-examination of the diagnostic criteria of tropical
pulmonary eosinophilia. Respir Med 1999; 93:655–659.
66 Rom WN, Vijayan VK, Cornelius MJ, et al. Persistent lower respiratory tract
inflammation associated with interstitial lung disease in patients with tropical
pulmonary eosinophilia following treatment with diethylcarbamazine. Am Rev
Respir Dis 1990; 142:1088–1092.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
67 Oshiro Y, Murayama S, Sunagawa U, et al. Pulmonary dirofilariasis: computed
tomographic findings and correlation with pathologic features. J Comput
Assist Tomogr 2004; 28:796–800.
68 Miyoshi T, Tsubouchi H, Iwasaki A, et al. Human pulmonary dirofilariasis: a
case report and review of the recent Japanese literature. Respirology 2006;
11:343–347.
69 Hisamatsu Y, Ishii H, Kai N, et al. Case of toxocariasis showing migratory
 nodular shadows with halos. Nihon Kokyuki Gakkai Zasshi 2008; 46:420–
424.
This case report describes that migratory nodular shadows with halos are
important chest CT findings in human toxocariasis.
70 Bruschi F, Murrell K. Trichinellosis. In: Guerrant R, Walker DH, Weller PF,
editors. Tropical infectious diseases: principles, pathogens and practice
[volume 2]. Philadelphia: Churchill Livingstone; 1999. pp. 917–925.
71 Gomez-Morales MA, Ludovisis A, Amati M, et al. Validation of an ELISA for the
 diagnosis of human trichinellosis. Clin Vaccine Immunol 2008; 15:1723–
1729.
This study has validated the ELISA using excretory/secretory antigens to detect
anti-Trichinella IgG antibodies for the diagnosis of human trichinellosis.
72 Duarte AG, Sattar F, Granwehr B, et al. Disseminated acanthamebiasis after
lung transplantation. J Heart Lung Transplant 2006; 25:237–240.
73 Corti M, Villafane MF, Muzzio E, et al. Pulmonary cryptosporidiasis in AIDS
 patients. Rev Argent Microbiol 2008; 40:106–108.
This study describes the epidemiological, clinical, radiological and microbiological
findings in AIDS patients with pulmonary cryptosporidiosis.
74 Martinez-Giron R, Esteban JG, Ribas A, Doganci L. Protozoa in respiratory
 pathology: a review. Eur Respir J 2008; 32:1354–1370.
This review article describes the new emerging respiratory protozoal infections,
especially in individuals with suppressed immunity.