Review

Parasitic infections of the lung: a guide for the

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respiratory physician
H Kunst,1 D Mack,2 O M Kon,3 A K Banerjee,4 P Chiodini,2,5 A Grant5
1
Department of Respiratory ABSTRACT Dogs are the definitive host for E granulosus and
Medicine, Birmingham Parasitic infections of the lung occur worldwide among harbour the adult worms in their gut. The eggs
Heartlands Hospital, shed in dog faeces remain viable for many weeks
Birmingham, UK both immunocompetent and immunocompromised
2
Department of Clinical patients and may affect the respiratory system in and are able to contaminate food sources of inter-
Parasitology, Hospital for a variety of ways. This review provides an update on the mediate hosts such as sheep, cattle and horses.
Tropical Diseases, London, UK presenting symptoms, signs, investigation and When humans become accidental intermediate
3
Department of Respiratory management of diseases affecting the lung caused by hosts after eating food contaminated with eggs, the
Medicine, St Mary’s Hospital,
Imperial College Healthcare NHS protozoa, nematodes and trematodes. The clinical ingested eggs hatch, releasing larvae which migrate
Trust, London, UK presentations and radiographic findings of several of from the gastrointestinal tract to the circulation.
4
Department of Radiology, these diseases may mimic tuberculosis and malignancy. The eggs travel to the liver or lungs and slowly
Birmingham Heartlands It is important to consider parasitic infections in the develop into hydatid cysts over a period of several
Hospital, Birmingham, UK months or years. Occasionally, lung cysts form
5
Department of Clinical differential diagnosis of such lung diseases. If identified
Research, London School of early, most parasitic diseases that affect the lung are after transdiaphragmatic spread of parasites
Hygiene and Tropical Medicine curable with medical or surgical treatments. following the rupture of liver cysts.
and Hospital for Tropical
Diseases, London, UK Presentation
Primary infection is asymptomatic and patients
Correspondence to INTRODUCTION may remain asymptomatic for years, during which
Heinke Kunst, Department of With increasing travel and migration, rates of time lung lesions may be discovered incidentally on
Respiratory Medicine,
Birmingham Heartlands
parasitic lung and pleural diseases are increasing in a chest x-ray. In Europe the average patient is in
Hospital, Bordesley Green East, the immunocompetent population in developed their 30s at diagnosis.1 Cysts may cause symptoms
Birmingham B9 5SS, UK; countries as well as among immunocompromised by compression of adjacent structures, and lung
[email protected] patients. Respiratory physicians should consider cysts may present with chest pain, cough,
parasitic diseases in the differential diagnosis of haemoptysis or pneumothorax. Symptoms may
Received 29 November 2009
Accepted 28 May 2010 lung conditions such as tuberculosis and malig- also occur if antigenic material is released from the
Published Online First nancy, with which parasitic lung diseases may be cyst, causing a hypersensitivity reaction with fever,
29 September 2010 confused. wheeze and urticaria and, rarely, anaphylaxis. Cysts
This review describes the presentation, investi- may become secondarily infected causing empyema
gation and management of common parasitic or lung abscess formation.
infections affecting the lung caused by protozoa,
nematodes and trematodes. The diseases have been Imaging features
grouped according to their manner of presentation: Cysts can be seen as single or multiple well-defined
(1) those presenting with focal lesions and (2) those homogenous lesions surrounded by otherwise
which characteristically present with diffuse lung normal lung parenchyma on a plain chest x-ray.
disease. Focal lung lesions have been divided into The lower lobes, posterior lung segments and the
cystic lung lesions, coin lesions and consolidation/ right lung are affected most frequently.2 The cyst
pleural effusion. Diffuse lung disease has been wall often calcifies over time. A CT scan of the
divided into transient pulmonary infiltrates and chest may reveal further diagnostic features
alveolar/interstitial lung changes. Diseases that including collapse of the laminated membrane from
may present in a variety of ways are fully described the surrounding host tissue, the presence of
only the first time they are mentioned. daughter cysts and the presence of cyst rupture.3
Air between the host tissue and laminated
CONDITIONS PRESENTING WITH FOCAL LUNG membrane of ruptured cysts may produce crescent-
LESIONS shaped lucencies. A pleural effusion or a hydro-
Cystic lung lesions pneumothorax may develop following the rupture
Hydatidosis of a pulmonary cyst into the pleural space.
Distribution and life cycle Collapsed laminated membrane may float in the
Hydatid disease is caused by larvae of Echinococcus cyst cavity, producing the ‘water lily’ sign (figures 1
tapeworm species, the definite hosts of which are and 2).3 4
members of the Canidae family (dogs and foxes). Laboratory diagnosis
Most cases are caused by Echinococcus granulosus Peripheral blood eosinophilia may be found in no
which has a worldwide distribution including more than 50% of cases. A substantial rise in
South America, countries surrounding the Medi- eosinophil count is often associated with a leakage
terranean, the Middle East, some sub-Saharan of antigenic material from the cyst. Serological tests
African countries, Russia and China. Although to support the initial diagnosis are available at
most cysts form in the liver, 20e30% form in the reference laboratories but are less sensitive for the
lung. diagnosis of lung disease than for hepatic disease.1

528 Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217

 Review

Coin lesions

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Dirofilariasis
Distribution and life cycle
Pulmonary dirofilariasis is caused by the dog heartworm Diro-
filaria immitis and has been reported from Japan, Australia, the
USA and Italy (D repens). Adult worms live in the right ventricle
of the definitive canine hosts and produce circulating microfilaria
which can be transmitted by a variety of mosquito species to
humans. In humans the worms pass through the right ventricle
but fail to mature and are swept away to peripheral pulmonary
arteries.
Presentation
Most patients are asymptomatic, although symptoms including
chest pain, cough, haemoptysis, wheezing, fever, chills and
malaise have been reported.12
Figure 1 Chest x-ray showing a hydatid cyst in the left lower lobe with Imaging features
a collapsed hydatid cyst exhibiting the ‘lily pad’ sign lying above it. The most common presentation is with a coin lesion on chest
radiography. These are usually 1e3 cm in diameter and sharply
Postoperatively, serological tests may be used to monitor the defined. In established lesions a central necrotic area is
immunological response to treatment.5 surrounded by a granulomatous reaction and fibrous wall.13
While percutaneous aspiration of liver cysts under ultrasound Dead worms may calcify. Positron emission tomographic scan-
guidance can support the diagnosis by demonstrating the pres- ning may show an increased uptake of fluorodeoxyglucose
ence of protoscolices or hooklets, this is not generally recom- around necrotic nodules, a feature also seen in other infectious
mended because of the risk of leakage resulting in an lung nodules.14
anaphylactic reaction. Laboratory diagnosis
Eosinophilia may be present in a small number of patients.
Management
6 There are no reliable serological tests available commercially.
In a small number of cases hydatid cysts resolve spontaneously.
Most cases are diagnosed by identifying the worm in biopsy
In the majority of cases the treatment of choice is surgical
specimens after thoracatomy for a pulmonary nodule thought to
excision of cysts with a view to preserve as much lung paren-
be a malignancy.15
chyma as possible.7 Albendazole should be avoided preopera-
tively as it may soften the cyst wall and increase the chance of Management
rupture. It may be given as adjunctive therapy once the cyst has Chemotherapy is ineffective. The only treatment is surgical
been removed.8 When surgery is contraindicated or not feasible excision if indicated.
in patients with multiorgan involvement, medical treatment
with albendazole with or without praziquantel is recom- Consolidation/pleural effusion
mended.9 Expert advice should be sought regarding chemother- Paragonimiasis
apeutic regimens before and after surgery and for cases where Distribution and life cycle
surgery is not to be carried out. While aspiration followed by Pulmonary paragonimiasis is most frequently seen in south east
injection of a scolicidal agent and re-aspiration (PAIR) has been Asia but also occurs in central Africa and South America. It is
used as a therapeutic tool when surgery is contraindicated,10 the caused by lung flukes of the genus Paragonimus. Paragonimus
World Health Organization states that PAIR is contraindicated westermani is responsible for most cases. The adult worms are
for lung cysts11 and the authors endorse that view. found in pulmonary cysts, usually in pairs. Adult worms
produce eggs which are secreted in sputum or faeces. Humans
are usually infected by eating the second intermediate host,
fresh water crab or crayfish, if raw or lightly cooked. After
ingestion the larvae penetrate the intestinal wall and migrate to
the lung parenchyma. They mature in a fibrous host-derived
capsule, usually in the upper zones of the lung.
Presentation
Presenting symptoms include pleuritic chest pain, haemoptysis,
chronic cough and fever. If pulmonary cysts erode into adjacent
bronchi, patients may suffer life-threatening haemoptysis.16
Imaging features
Radiographic features of paragonimiasis include patchy air space
consolidation, cystic changes and ring shadows. Pleural effusions
and pneumothoraces may occur. On the CT scan round low-
attenuation cystic lesions filled with fluid or gas may be seen
within an area of consolidation. Peripheral linear opacities seen
on chest x-rays are suggestive of worm migration tracks on
Figure 2 CT scan of the thorax showing a ruptured hydatid cyst in the corresponding CT scans. Intracystic worms may be detected on
left upper lobe of the lung. a CT scan of the thorax.17 18 Patients with pulmonary

Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217 529

 Review

paragonimiasis who present with parenchymal lesions on a CT formation which carries a mortality of 15e35%.25 Infiltration of

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scan of the thorax may have bronchial stenosis on broncho- the lung parenchyma may result in pneumonia or lung abscess
scopy.19 Paragonimiasis is often misdiagnosed as tuberculosis or formation. Furthermore, a hepatobronchial fistula leading to
malignant disease and should be considered in the differential expectoration of ‘anchovy sauce-like’ purulent sputum can
diagnosis of these conditions in those who have lived in endemic develop. Rarely, a bronchobiliary fistula may occur causing bile
countries.20e22 expectoration.
Laboratory diagnosis Radiographic features
Peripheral blood eosinophilia is mainly seen during larval Common radiological features include right pleural effusion and
migration through the lung and total serum IgE may be raised. basal lung disease. Right lower lobe consolidation may develop,
The eosinophil counts are usually elevated in pleural and bron- which may progress to abscess formation (figure 3).
choalveolar lavage fluids. The identification of the characteristic
Laboratory investigations
operculated eggs in faeces, sputum or bronchoalveolar lavage
Eosinophilia is not a feature of amoebic infections. If symptoms
fluid confirms the diagnosis. Specific serological testing is not
of dysentery are present, freshly passed stools should be exam-
performed in the UK but samples may be referred to overseas
ined for amoebic trophozoites. Trophozoites are seldom found in
laboratories for specific IgG and IgM antibody testing when
sputum, pleural fluid or abscess aspirates. Antibodies directed
paragonimiasis is suspected.20 23
against the parasite may be detected by a variety of methods.
Management Antibody tests start to become positive after approximately
Medical treatment is usually with praziquantel. Some patients 1 week and have a sensitivity of 95% for the diagnosis of
may require surgery for persistent pneumothorax, pleural effusion amoebic liver abscess but are only positive in approximately 75%
or empyema.24 of cases of intestinal infection. The E histolytica adhesin may be
detected in faecal specimens by ELISA. This test is also helpful in
Amoebiasis differentiating between E histolytica and E dispar in asymptom-
Distribution and life cycle atic patients who pass amoebic cysts.
Amoebiasis is caused by Entamoeba histolytica, a protozoan found
Management
worldwide. E histolytica is the causative agent of invasive
Medical treatment consists of a course of tinidazole or metro-
amoebiasis but is morphologically indistinguishable from
nidazole to kill trophozoites in tissue, followed by diloxanide
a related but non-pathogenic species, E dispar. E histolytica is
furoate or paromomycin to eliminate cysts from the intestinal
endemic in regions with poor sanitation and poor socioeconomic
lumen.28 29 Surgical treatment of pulmonary amoebiasis may be
conditions. The motile trophozoite forms of the parasite live in
required when there is direct pulmonary involvement or spread
the lumen of the large intestine where they multiply and
to pleura.
differentiate into the cyst forms. Cysts are passed in the faeces
and are highly resistant to environmental conditions, facilitating
faecal-oral transmission. Ingested cysts are transformed into CONDITIONS PRESENTING WITH DIFFUSE LUNG DISEASE
trophozoites. Transient pulmonary infiltrates
Ascariasis
Presentation Distribution and life cycle
In most infections the organism does not invade the gut mucosa. Ascariasis is caused by Ascaris lumbricoides, the round worm. It is
In a subset of cases the E histolytica trophozoites bind to intes- common worldwide in areas with poor sanitation where there is
tinal epithelial cells via a lectin expressed on the parasite surface. faecal contamination of soil or food. Transmission of the disease
This leads to lysis of the epithelial cells and invasive amoebiasis is faecal-oral. After eggs are ingested they hatch and larvae
resulting in colitis. Blood-borne spread of the parasite may lead migrate via the portal circulation to the liver then via the heart
to the formation of an amoebic liver abscess which may present to reach the lungs 2 weeks after ingestion. Larvae then ascend to
several months after the initial infection when diarrhoea may be the trachea, are swallowed and eventually develop into adults in
absent. the small intestine, producing eggs 10e12 weeks after ingestion.
Amoebic liver abscess may cause irritation of the diaphragm
and the patient may present with cough. A serous pleural
effusion may occur in conjunction with an amoebic liver abscess
and does not indicate extension of the disease.25 Amoebic liver
abscess may also present with chest pain due to hepatic
enlargement and inflammation. Elevation of the hemidiaphragm
can cause segmental atelectasis of the lung and lead to secondary
bacterial pneumonia.26
Amoebic pleuropulmonary disease is the most common
complication of amoebic liver abscess, occurring in 15% of
patients with amoebic liver disease and in 1% of patients with
amoebic dysentery.27 It most commonly occurs by direct
extension from a superior right lobe hepatic abscess through the
diaphragm into the right lower lobe of the lung, presenting with
cough, pleuritic pain and dyspnoea.25 Pleuropulmonary amoe-
biasis may also occur following haematogenous spread of
organisms to the lungs or lymphatic spread from the liver to the
diaphragm. Intrathoracic complications include rupture of an Figure 3 Chest x-ray showing right basal consolidation and pleural
amoebic liver abscess into the pleural cavity with empyema effusion secondary to amoebic liver abscess.

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 Review

Presentation Toxocariasis

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During the second week of infection, as the larvae invade the Distribution and life cycle
lung tissue, a small proportion of patients become symptomatic. Human toxocariasis is usually caused by the dog round worm
Loeffler’s syndrome is caused by larval migration into the alveoli Toxocara canis which commonly infects juvenile dogs and has
which triggers an allergic response leading to respiratory a worldwide distribution. Humans, who are incidental hosts, are
symptoms including cough, wheeze, dyspnoea, chest pain, fever usually infected by the ingestion of eggs. The disease primarily
and haemoptysis. The illness usually resolves spontaneously affects children, who acquire the infection through contact with
after several weeks. soil contaminated with embryonated eggs. Fresh animal faeces
are not infectious as the eggs require 2e3 weeks to embryonate
Imaging features
in the soil. Ingested eggs hatch in the stomach. Larvae penetrate
During pulmonary migration, transient nodular or diffuse
the mucosa of the gut and enter the mesenteric vessels from
pulmonary infiltrates on the chest x-ray support the diagnosis of
where they migrate to the lungs and other organs.
Loeffler’s syndrome. Chronic eosinophilic pneumonia has been
associated with ascariasis of the lung.30 Spontaneous pneumo- Presentation
thoraces have been described infrequently.31 Most infections occur in children and most are asymptomatic.
Patients may present with immunologically-mediated symp-
Laboratory diagnosis toms including cough, dyspnoea and wheeze which may present
During larval migration a leucocytosis and peripheral blood as asthma or bronchitis. Presenting signs may include hepato-
eosinophilia are often present and total serum IgE may be megaly, splenomegaly and ocular lesions.
elevated. Eosinophils and larvae may be found in sputum. The
diagnosis is confirmed by finding characteristic Ascaris eggs in Radiographic features
the stool on microscopy, although these may not be passed until Radiological features may include transient localised changes or
after resolution of the pulmonary symptoms. Serological tests widespread patchy areas of consolidation.13
are not routinely available.
Laboratory diagnosis
Management Toxocara larvae do not develop into adults in the human host, so
A single dose of albendazole is the treatment of choice. Meben- eggs are not passed in human faeces. Visceral larva migrans is
dazole, piperazine and pyrantel pamoate are alternatives.28 characterised by persistent peripheral eosinophilia and leuco-
cytosis. A high degree of eosinophilia in the differential cell
Hookworm infections count of bronchoalveolar lavage fluid may support the diag-
Distribution and life cycle nosis.32 33 Serological tests are available at reference laboratories.
Ancylostomiasis is common in tropical and subtropical coun- Although positive Toxocara serology supports a diagnosis of
tries, caused by two species of hookworm (Ancylostoma duodenale visceral larva migrans, titres may remain elevated for years and
and Necator americanus). A duodenale is also found in the Middle other causes of illness should be considered.34 Children
East and southern Europe; N americanus is found sporadically in suspected of ingesting infective Toxocara eggs may be investi-
the southeastern USA. Hookworm eggs are passed in faeces and gated with full blood count and Toxocara serology tests at
develop in soil into filariform larvae able to penetrate the skin of baseline and at 3 months. In practice this is seldom required as,
the human host. Poor sanitation and the absence of footwear in many cases where dog faeces have been ingested, it is possible
favour transmission. The larvae penetrate blood vessels and to establish that the sample is relatively fresh and thus not likely
undergo heartelung migration before breaking out into the to contain embryonated eggs. Tissue biopsy is not required for
alveoli and ascending to the pharynx from where they are the diagnosis of visceral larva migrans.
swallowed. The hookworms subsequently mature into adults in Management
the small intestine. Eggs first appear in the stool 5 weeks after Ocular disease is treated under the supervision of an ophthal-
skin invasion. mologist with local or systemic steroids. Anthelminthics are not
usually given. Visceral larva migrans is treated with albendazole.
Presentation Corticosteroids may be required in more severe cases.28
Pulmonary manifestations are usually mild. During larval
migration in the lung the hookworm may cause symptoms and
signs consistent with Loeffler’s syndrome including dry cough, Alveolar/interstitial changes
wheeze, dyspnoea and fever. Schistosomiasis
Distribution and life cycle
Imaging features Schistosomiasis is endemic throughout the tropics and it is
The radiographic changes are consistent with Loeffler’s estimated that more than 200 million people worldwide are
syndrome and an eosinophilic pneumonia with transient infected.35 There are three main species of schistosomes: Schis-
non-segmental areas of consolidation.13 tosoma mansoni, Schistosoma haematobium and Schistosoma japo-
nicum. The adult trematode worms are found in the vesical
Laboratory diagnosis
plexus (S haematobium) or in the mesenteric veins (S mansoni and
Peripheral blood eosinophilia is found during larval migration
S japonicum). Their eggs are excreted in urine or faeces respec-
and commonly persists during gastrointestinal infection.
tively. Humans are infected by cercariae during contact with
Although their appearance may be delayed, finding eggs in the
fresh water. The organisms enter the circulation and pass
stool supports the diagnosis. Serological tests are not useful in
through the heart, lungs and then the liver to reach the target
view of many cross-reactions with other helminthic infections.27
venous plexus. There the worms mature and mate, releasing
Management eggs 4e6 weeks after skin penetration. The initial release of eggs
Recommended treatment consists of a single dose of albenda- may give rise to acute schistosomiasis which occurs predomi-
zole. Mebendazole and pyrantel pamoate are alternatives.28 nantly in non-immune hosts. Eggs that are not passed into the

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 Review

bladder or intestinal lumen are the main cause of chronic disease,

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causing granulomatous reactions and fibrosis. In severe long-
standing S mansoni and S japonicum infections, the development
of hepatosplenomegaly and portal hypertension may lead to
diversion of eggs to the lung vasculature. This results in oblit-
erative arteritis which may cause pulmonary hypertension.
Presentation
In non-endemic countries, returned non-immune travellers may
present with acute schistosomiasis while migrants from endemic
countries may present with chronic disease. Acute schistosomiasis
(Katayama fever) may present with fever, cough, dyspnoea, rash
and arthralgias.36 The precise pathogenesis of Katayama fever is
unknown, but it is thought to be due to an immune complex
phenomenon initiated by eggs laid by maturing schistosomes.
Typically, symptoms occur 4e6 weeks after infection. In acute
schistosomiasis, serological tests are often negative and eggs are not
detectable, requiring the diagnosis to be made on clinical and Figure 5 CT scan of the thorax showing the halo sign in pulmonary
epidemiological grounds. In heavy infections, the migratory phase schistosomiasis.
through the lungs may produce a pneumonitis resembling that
produced during hookworm migration. A Loeffler-like syndrome Laboratory investigation
may occur during the treatment of heavy infections. Acute symp- Peripheral blood eosinophilia is present in more than 65% of
toms are usually self-limiting. In the chronic stage the commonest patients.43 Eggs of the Schistosoma species may be found in
symptoms are dyspnoea, reduced exercise tolerance and chest pain. faeces, urine and sputum or bronchoalveolar lavage 6 weeks after
Clinical signs of severe hypoxaemia such as digital clubbing may be infection. Eggs of S haematobium are most likely to be found in
seen. Since schistosomiasis is an important cause of pulmonary late morning urine samples.44 Terminal urine specimens maxi-
hypertension, it should always be considered as a differential mise sensitivity.45 IgG antibodies to Schistosoma egg antigen are
diagnosis in patients from endemic countries.37 The chronic form of detectable 6e12 weeks following infection and can be measured
schistosomiasis may also cause pulmonary arteriovenous fistulas.38 by ELISA. Such assays have sensitivities of >90% for the diag-
Radiological features nosis of schistosomiasis.46 These tests may remain positive for
Nodular ill-defined lesions or reticulonodular changes may be several years and are not helpful for monitoring response to
seen on the chest x-ray in acute pulmonary schistosomiasis treatment. Serological testing in asymptomatic travellers should
(figure 4).39 Although radiological findings are usually transitory be delayed for a period of 3 months following exposure to fresh
in acute infection, chest x-rays may show features resembling water to allow time for seroconversion. Schistosomal serology
granulomatous disease or tuberculosis.40 41 In chronic lung may be negative, especially in Katayama fever, but if positive it
disease, interstitial or granulomatous changes are caused by the provides helpful diagnostic information.43 47
widespread deposition of eggs in the pulmonary vasculature. A Management
CT scan of the thorax may show nodular changes and ground The treatment of choice for schistosomiasis is praziquantel.28 48
glass opacification (figure 5).42 In acute schistosomiasis (Katayama fever) praziquantel is
administered under steroid cover. A second course of prazi-
quantel may need to be given 3e6 months later to eradicate any
schistosomes that may have survived the first course of treat-
ment.47 Treatment is less beneficial in advanced chronic disease.

Strongyloidiasis
Distribution and life cycle
Strongyloidiasis is caused by the nematode Strongyloides stercor-
alis and is prevalent in tropical and subtropical countries.
Filariform larvae penetrate the skin, enter blood vessels and
undergo heart and lung migration. They migrate into alveoli
and subsequently ascend to the trachea. Larvae are swallowed
and develop in the small intestine into adult worms which
produce eggs. These are deposited in the intestinal mucosa
where they hatch into rhabditiform larvae which are excreted in
faeces. Occasionally, rhabditiform larvae mature to the filariform
stage while still in the bowel lumen. These filariform larvae may
penetrate the bowel wall or the perianal skin to initiate a new
cycle (autoinfection). Thus, in the absence of treatment, an
individual may harbour Strongyloides for several decades.
Presentation
Figure 4 Chest x-ray showing widespread pulmonary nodules in Clinically the infection is often asymptomatic, but mild symp-
pulmonary schistosomiasis. Reproduced with permission from Waldman toms may occur in the initial stages of lung migration. In the
et al.42 immunocompromised patient (including those on steroid

532 Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217

 Table 1 Overview of parasitic lung diseases
Condition Presentation Imaging features Geographical distribution Incubation period Investigations Treatment
Focal disease
Cystic lesions
Hydatidosis Symptoms due to mass Single or multiple lung cysts Wide distribution: Months to decades after Hydatid serology positive in Surgery
effect Pleural effusion Mediterranean borders, exposure 50-60% Albendazole with or without
Chest pain, cough, Pneumothorax East and Central Asia, Blood eosinophilia praziquantel
haemoptysis Hydro-pneumothorax sub-Saharan Africa, Russia, uncommon unless cyst Aspiration
Hypersensitivity reaction China, South America leaking
Secondary abscess Aspiration and microscopy
formation
Coin lesions
Dirofilariasis Chest pain, cough, Coin lesion with or without Pulmonary dirofilariasis May be years after exposure Blood eosinophilia Surgical excision
haemoptysis, wheezing calcification reported from USA, Japan, uncommon
Fever, malaise Australia, South America Biopsy usually diagnostic
Consolidation/pleural effusion
Paragonimiasis Pleuritic chest pain, cough, Pulmonary infiltrates Asia, West Africa, Central 1e27 months Eggs in stool or sputum Praziquantel

Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217

fever, haemoptysis Consolidation or cystic and South America Eosinophilia in peripheral
lesions blood, pleural fluid or
Pleural effusion bronchoalveolar lavage
Pneumothorax Serology
Amoebiasis Right upper quadrant or Pleural effusion, atelectasis, Widely distributed Weeks to years after Serology (may be negative, Tinidazole (or metronidazole)
shoulder tip pain Empyema exposure especially in early disease) followed by diloxanide
Cough and bile expectoration Amoebic lung abscess Does not cause eosinophilia; furorate or paromomycin
Secondary pneumonia usually does cause
Hepatobronchial fistula neutrophilia
Diffuse disease
Transient pulmonary
infiltrates
Ascariasis Cough, wheeze, dyspnoea, Transient pulmonary Worldwide in areas where 1e2 weeks from infection Larvae in pulmonary, gastric Albendazole, mebendazole,
chest pain, fever infiltrates sanitation is poor (faecal-oral to onset of pulmonary secretions piperazine, or pyrantel
Loeffler’s syndrome Bacterial pneumonia, transmission) symptoms Eggs in stool in established pamoate
Haemoptysis eosinophilic pneumonia infection with adult worms,
Pneumothorax may be absent in larval
migratory phase
Blood eosinophilia during
larval migration
Hookworm infection Cough, wheeze, dyspnoea, Transient pulmonary Widely distributed: (infection Pulmonary manifestations Blood eosinophilia during Albendazole, mebendazole or
chest pain, fever infiltrates usually by contact of bare start within 10 days of migration, which may persist pyrantel pamoate
Loeffler’s syndrome Eosinophilic pneumonia feet with faecally exposure, can continue for Eggs in stool in established
contaminated soil) more than one month infection with adult worms
Eggs may be absent in larval
migratory phase
Toxocariasis Cough, dyspnoea, wheeze, Pulmonary infiltrates Worldwide distribution (adult Several weeks Peripheral blood eosinophilia Albendazole for visceral
asthma or bronchitis Secondary bacterial worms live in gut of cats and common disease
Hepatomegaly, pneumonia dogs) Eosinophilia in
splenomegaly, ocular lesions bronchoalveolar lavage
Toxocara serology
Alveolar/ interstitial changes

Continued
Review

533
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 Review

therapy), a hyperinfection syndrome can result in severe

Ivermectin, albendazole less

Diethylcarbamazine with or

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disseminated infection which may cause Gram-negative sepsis
and death. Respiratory symptoms may be non-specific and,

without albendazole
apart from gastrointestinal complaints, symptoms of asthma
might be the only feature. In patients with new onset bronchial
Praziquantel
Treatment

asthma or worsening of asthmatic episodes concurrent with

effective
immunosuppression, S stercoralis infection should be considered,
especially in patients from endemic countries.49 50 In immuno-
suppressed patients with hyperinfection, symptoms and signs
consistent with adult respiratory distress syndrome may be

No microfilariae in peripheral
sputum in chronic infection;
Blood eosinophilia common
Larvae in stool or duodenal
sputum, or bronchoalveolar

seen.51 52 In disseminated disease, extensive intra-alveolar

aspirate but not usually in
haematobium) after about

positive after 6-12 weeks

Chronic disease: eggs in

In hyperinfection also in
sputum, body fluids on
Acute disease: eggs in

haemorrhage has been reported and should be considered as

Strongyloides serology
Schistosomal serology

microscopy or culture

Filarial serology (IgG)

eosinophilia common
Acute disease: blood

lavage after 6 weeks

stool and/or urine (S

a cause of acute deterioration.53

Blood eosinophilia
Investigations

Radiological findings
In Strongyloides hyperinfection, pulmonary infiltrates are the most
6 weeks

frequent feature seen on chest radiography. Radiographic changes

blood
may include miliary nodules, reticular opacities and airspace
opacities ranging from multifocal to lobar distribution. These are
thought to be due to secondary infection, haemorrhage, inflam-
infection; hyperinfection may
Acute disease: 5e7 weeks

Pulmonary symptoms may

matory pneumonitis and bacterial abscess formation.13 52 If

occur up to decades after

Up to years after leaving

Chronic disease: years

occur days after acute

widespread air space shadowing is seen on chest radiography,

Incubation period

adult respiratory distress syndrome should be strongly suspected.

after exposure.

Rare manifestations of pulmonary strongyloidiasis include gran-

endemic area

ulomatous changes leading to pulmonary fibrosis.54

infection

Laboratory investigations
Blood eosinophilia is seen in more than 75% of patients with
chronic infection but may be absent in the hyperinfection
syndrome in immunocompromised patients.55 A definitive diag-
Geographical distribution

Asia, sub-Saharan Africa,

nosis is made by demonstration of rhabditiform larvae in stool,

Africa, South America,
south east Asia, China

Worldwide distribution
where sanitation poor

sputum or duodenal aspirates. Filariform larvae may also be seen.

Larvae may be identified on direct microscopy but specialised
South America

culture techniques are more likely to yield positive results.

Antibody assays have sensitivities of approximately 90%;
however, cross-reactions occur with other helminth infections
and antibody levels may be low in immunocompromised
patients.
granulomatous lung disease,

pulmonary infiltrates, miliary

Management
In hyperinfection syndrome:

nodules, airspace opacities

ARDS in severe disease,
pulmonary hypertension,
Acute disease: transient

Treatment with ivermectin is usually effective. In cases of

reticulonodular changes

Bilateral reticulonodular
pulmonary AV fistulae

rarely granulomatous

hyperinfection, repeated treatments are required and expert

Imaging features

lymphadenopathy

parasitological advice should be sought.28 56e58

Chronic disease:

Mediastinal
shadowing

Tropical pulmonary eosinophilia

changes

Presentation
Tropical pulmonary eosinophilia (TPE) typically results from
a hypersensitivity reaction to the lymphatic filarial parasites
Wuchereria bancrofti and Brugia malayi found in endemic regions
asthma, ARDS, intra-alveolar
fever with cough, dyspnoea,

In hyperinfection syndrome:

Fever, malaise, weight loss

Chronic disease: dyspnoea,

Cough, dyspnoea, wheeze

of south east Asia, India, China and Africa. The most common
Acute disease: Katayama

pulmonary hypertension

clinical manifestation of filariasis is elephantiasis resulting from

rash, and arthralgias
Loeffler’s syndrome,

filarial obstruction of lymphatic vessels. The syndrome of TPE is

thought to be an immunological response to microfilariae rather
Presentation

haemorrhage
pneumonitis

than acute infection. Clinically, TPE typically has slow onset

over several months, with respiratory symptoms including
cough, dyspnoea and wheeze which may be worse at night.
Systemic features including fever, malaise and weight loss may
occur. By contrast, Loeffler’s syndrome is caused by larval
migration of nematodes such as Strongyloides, Ascaris or hook-
Table 1 Continued

worm which results in wheeze, cough and dyspnoea of acute

eosinophilia (filariasis)

onset and rarely lasts more than a few weeks.

Tropical pulmonary
Schistosomiasis

Strongyloidiasis

Radiological findings
Bilateral fine nodular or reticulonodular shadowing have been
Condition

described on plain chest radiography.59 However, it has been

suggested that a CT scan of the thorax might be more sensitive

534 Thorax 2011;66:528e536. doi:10.1136/thx.2009.132217

 Review

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Provenance and peer review Not commissioned; externally peer reviewed.
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