This document discusses various helminthic infections that can affect the lungs. It describes the life cycles and pathogenesis of roundworms (Ascaris lumbricoides, hookworms, Strongyloides stercoralis), tapeworms (Echinococcus granulosus), filarial worms (Wuchereria bancrofti, Brugia malayi, Dirofilaria immitis), and flukes (Paragonimus spp.) that can infect the lungs. It details the clinical presentations of lung infections like Loeffler's syndrome, tropical pulmonary eosinophilia, and others. Treatment options for these infections involving antihelminthic drugs are also outlined.

1. Helminthic Infections of Lungs
Nanditha Ramsingh

2. • The helminths that parasitize humans include
1. Nematodes (roundworms)
2. Platyhelminthes (flatworms)
- cestodes (tapeworms)
- trematodes (schistosomes and other flukes).
• Ectoparasites (e.g., the Annelida, such as
leeches, ragworms, or earthworms)-
uncommonly associated with lung disease

4. Diseases due to Nematodes
(Roundworms)

5. Human infections :
• Ascariasis - Ascaris lumbricoides
• Hookworms - Ancylostoma duodenale and
Necator americanus,
• Strogyloidiosis - S. stercoralis are among the
most prevalent helminthiases worldwide.

6. ASCARISIS – LIFE CYCLE

7. HOOKWORM – LIFE CYCLE

8. • Most prominent pulmonary pathologic changes-
ascariasis / hyperinfection syndrome of strongyloidiasis.
• Pulmonary symptoms from Ascaris - 1 to 3 weeks after
primary infection.
• Portions of larvae - seen in the pulmonary parenchyma,
surrounded by a patchy infiltrate of neutrophils and
eosinophils.
• The alveoli contain a serous exudate and the production
of bronchial mucus is increased. Later, migrating larvae
are destroyed within aggregates of eosinophils.
• The intensity of the reaction depends on the number of
parasite larvae and previous sensitization.
• Endemic areas- pulmonary reactions more frequent.

9. Immunocompetent Host
• Pulmonary disease caused by hookworms or S.
stercoralis - minimal (worm burden is low)
• Majority of the rhabditiform - passed in the
stool - outside - transform into the infective
filariform larvae.
• Few infective filariform larvae - develop in the
gut - penetrate the intestinal mucosa – restart
developmental cycle(autoinfection).

10. Immunosuppressed
• Change to infective filariform larvae more frequently occurs
within the gut lumen – sharp increase in worm burden.
• The infective filariform larvae penetrate the intestinal mucosa
resulting in massive invasion of almost every organ, lungs.
• Life threatening infection with S. Stercoralis – premature
development of filariform larvae – invade gut wall or perianal
skin - carry intestinal bacteria into peritoneum and bloodstream.
• Tissue migration of the worms – most body organs,lung.
• Some - bronchopneumonia and lung abscesses develop.
• Fatal cases – intra-alveolar hemorrhages and inflammation.

12. Loeffler’s Syndrome
• The major clinical manifestations caused by
infection of the lungs with the larval forms of
intestinal nematodes.
• Typically - patients with Ascaris pneumonia
• Rarely - Hookworm pneumonia

13. Features
• Persistent, irritating, nonproductive cough,
• Substernal pain,
• Hemoptysis
• Dyspnea
• Eosinophilia - most consistent laboratory finding.
• Radiographic signs –patchy or miliary infiltrate.

14. • The onset of the Loeffler-like syndrome - (intestinal
nematodes) - 1 to 3 weeks after infection
• Coincides - larval migration from pulmonary circulation
to alveoli
• Typical pulmonary symptoms - 10 -15 days later
• Some – marked respiratory failure.
• In locations with cyclic transmission of ascariasis –
pneumonitis occurs seasonally.
• Mild symptoms - persons with hookworm infection /
immunocompetent pts with strongyloidiasis.

15. • Most clinically significant pulmonary syndrome -
caused by - Hyperinfection with S. stercoralis
• Immunosuppressed - lymphomas and leukemias,
organ transplantation.
• May develop - 75 years after initial exposure

16. Features
• Asthma
• Pulmonary opacities - cavitation, consolidation,diffuse
patchy infiltrates.
• Widespread dissemination of nematode - gram-negative
meningitis and sepsis
• Eosinophilia - often absent in hyperinfection syndrome,
(defective cell-mediated immunity /use of corticosteroids)
• Hyperinfection syndrome - often fatal
• Mortality - 87% of people with disseminated infections

17. Management
• Stool Mx - negative at this point (adults have
not yet reached the small intestine and begun
producing eggs).
• Later stage – Mx - characteristic eggs of
hookworms / Ascaris / larvae of S. stercoralis.
• Specific antihelminthic Tx - ineffective during
pulmonary stage
• Cures infection - once parasites reach maturity
in small intestine.

19. Treatment
• Albendazole, 400 mg orally once / Mebendazole, 100
mg /day for 2 to 3 days (or 500 mg orally once) – DOC
– ascariasis and hookworms
• Ivermectin, 200 μg/kg per day for 2 days (longer for
hyperinfection syndrome) – strongyloidiasis.
• This treatment may be repeated at 2 weeks (the
duration of one autoinfection cycle) - to ensure
eradication is complete.
• Albendazole, 400 mg orally daily for 2 days - used as
an alternative, but it is less effective.

20. Strongyloides - Management
• Suspected hyperinfection syndrome :
1. Early diagnosis
2. Modification of immunosuppressive therapy
3. Prompt anti-Strongyloides chemotherapy
4. Adjunctive antibacterial therapies
• Diagnosed only shortly before death or at autopsy.
• Examination of stools, duodenal aspirates, sputum and
bronchial washings – parasite larvae
• Treatment - continued daily for at least 2 weeks after last +
stool Mx (= duration of one autoinfective cycle).
• Empirical Ivermectin - Serologically positive individuals for
Strongyloides – treated before immunosuppression (organ
transplantation / cancer chemotherapy)

22. Pulmonary Filariasis
• Wuchereria bancrofti and Brugia malayi
• Acute or chronic lung disease- tropical
pulmonary eosinophilia.
• H/o residence in filaria-endemic areas
• C/c nocturnal paroxysmal cough
• Marked eosinophilia
• Positive serology
• Therapeutic response to diethylcarbamazine
citrate (DEC).

24. Pathogenesis
• Show evidence of humoral hyperreactivity (seen as
increased serum levels of total IgE and antifilarial
IgG and IgE)
• Histopathologically – Earliest lesions – histiocytic
infiltrates in the interstitium and alveolar spaces.
• Cell infiltrate - predominantly - eosinophils,
lymphocytes, histiocytes
• Without therapy - end-stage disease - fibrosing
alveolitis and honeycombing occurs.

25. Features
• Young males – predominantly affected
• Episodes of dry night cough, low-grade fever, general fatigue.
• Clinically – mistaken for asthma
• Chest - coarse crackles + rhonchi
• PFT - restrictive pattern with superimposed obstruction in
which VLC, TLC and RV are all decreased.
• Rx - reticulonodular opacities and increased BV markings.
• Sera and BAL fluid - high IgE levels and specific ABs to filariae.
• Eosinophill counts in peripheral blood - > 3000/mm3.

26. Treatment
• DEC – DOC for TPE (6 mg per kg daily for 21 days)
• Doxycycline, 100 mg orally twice daily for 4 to 6
weeks (works by killing the symbiotic Wolbachia
bacteria necessary for nutrition and fertility)
• Recurrences of TPE - 20% of individuals – 2nd course
of antihelminthic Tx : (WHO : DEC : 6–12 mg/ kg
orally daily for 21–30 days).
• Unfortunately, symptoms – may persist after therapy
(lung damage incurred prior to treatment)

27. Dirofilaria immitis
• Dirofilaria immitis (dog heartworm) – another
filarial parasite
• Transmitted to humans by mosquito bite -
intermediate vector
• Infection - discovered as a pulmonary nodule on
CXR (worm lodged in the pulmonary arteries)
• Often mistaken as cancer.
• Cough, chest pain, hemoptysis, and eosinophilia.
• Definitive diagnosis – Mx of excised lesions

29. Toxocariasis (Visceral Larva Migrans)
• Human infection with animal parasites.
• Humans - accidental hosts
• Toxocara canis and T. Cati
• Most commonly - in children.
• Invading larvae migrate in human tissues, but
cannot mature to adult worms.

31. Pathology
• Tissue injury - results from : the invasion of
different organs by the parasite larvae
- from encapsulation and death of
some organisms (by immediate & delayed-
hypersensitivity responses of host)
• MC affected organ - liver

32. Clinical Features
• Children - 1 and 5 years.
• Common - history of pica
• Older individuals - associated with h/o raw meat intake.
• 2 main presenting features - chest and abdomen.
• Pulmonary complaints - cough and wheezing
• Pulmonary infiltrates in > 1/3 symptomatic children.
• Hepatomegaly, rarely splenomegaly
• Peripheral eosinophilia – marked, persist for years.
• The concentrations of both total and specific
immunoglobulins - increased in the serum

33. Management
• Diagnosis - clinical presentation and serologic
evidence of anti-Toxocara antibodies.
• Chest imaging- transient, migratory infiltrates.
• D/s - benign self-limited - efficacy of antihelminthics
doubtful, no specific therapy recommended.
• Severe symptoms - Albendazole
• Corticosteroids - limit the inflammatory response -
extensive disease of the lungs or CNS.

34. DISEASES DUE TO CESTODES
(SEGMENTED WORMS)

35. ECHINOCOCCOSIS
• Infection with larval stage of tapeworm E.
granulosus -most important helminthic
pulmonary diseases.
• 2 unique life cycles for E. granulosus.
• Pastoral life cycle - definitive host –dog
• ntermediate hosts - pigs, sheep, and cattle.
• Sylvatic life cycle - definitive hosts - wolves, foxes,
or coyotes, intermediate hosts -moose, deer, elk,
and caribou.
• Pastoral life cycle –MCC of infection, more severe

37. Pathology
• Hydatid cysts –MC - lungs (children)
• Slowly enlarging, SOL - well tolerated.
• Cysts in the lungs are usually discovered early in
the course of the disease (CXRs – very common)
• Pulmonary cysts are solitary - 60%
• 50% to 80% - only one lobe.
• Initially - The cyst is surrounded by a
granulomatous reaction on the part of the host;
later - the inflammatory reaction is succeeded by
fibrosis - leading to a calcified solid mass.

38. • Spontaneous rupture of a viable hydatid cyst can
occur through a bronchus - expectoration of
scoleces in sputum
• Rupture into mediastinum/pleural cavity -secondary
implantations and new daughter cysts.
• Fluid content of a hydatid cyst - immunogenic,
leakage of the cyst -anaphylactic response
• Eosinophilia – reported to accompany Hydatid cyst

39. Clinical Features
• Hydatid cysts - usually asymptomatic
• 1/5th of the clinically diagnosed cysts - lungs
• Most patients - children
• Adults - cysts confined to the liver.
• Cough; dyspnea or chest pain.
• Chest Rx - the lesions vary in diameter from 1 to 20 cm;
• Cyst is surrounded by an area of pneumonitis or
atelectasis. Fluid level may be seen – “water lily sign”
• Serology, CT and MRI –improving the characterization
of the lesions.

40. Management
• Combination of epidemiologic, clinical, and laboratory
findings (imaging or serology).
• Surgery – TOC - hydatid disease (lungs)
• Depending on size and location of cysts
- enucleation of the intact cyst
- Cystotomy
- Removal of the cyst after aspiration may be chosen.
• Large cyst - drain may be left for some time in residual
pericystic area.
• Extensive procedures (lobectomy and segmental
resection) - usually not necessary

41. • The use of the “PAIR procedure,” including
Percutaneous Aspiration Injection of cysticidal agent
(hypertonic saline, absolute alcohol, or other agents),
and Re-aspiration using radiographic guidance.
• Current WHO recommendation - PAIR should not be
used for pulmonary cysts.
• If PAIR is chosen – it is coupled with albendazole,
beginning 4 hours before, and continuing for 28 days
after drainage
• (400 mg orally BD for patients >60 kg, and 15 mg/kg
divided into two doses for patients <60 kg).

43. Schistosomiasis
• Southeast Asia, the Middle East, Africa, the
Caribbean, and South America.
• Schistosoma haematobium, S. mansoni, S.
japonicum, S. mekongi, and S. intercalatum.
• The schistosomes are blood flukes.
• Human infection is initiated by penetration of
intact skin by the free-living cercariae that are
shed by specific freshwater snails

45. • S. haematobium worms parasitize the vesical
venous plexus - connects directly with IVC – eggs
seed to the lungs
• By contrast, adult worms of other species -
mesenteric veins- doesn’t allow parasite ova to
travel directly through PV to hepatic and systemic
circulations.
• Eggs typically reach lungs - late stages of infection
• Pulmonary symptoms may still occur early –
result of immune-complex deposition.

46. • Pulmonary circulation - schistosome eggs usually
gather in small arterioles - form delayed-
hypersensitivity granulomas, (eosinophils,
lymphocytes, macrophages neovascul, fibrosis)
• Curtailment of pulmonary vasculature and
decreased distensibility by perivascular fibrosis –
PHTN and cor pulmonale.
• PFT - predominantly restrictive pattern of disease
and is accompanied by a decrease in DC

47. • Migration of schistosomula through lungs - provoke
cough and bronchospasm
• Fever and dyspnea,
• Chest Rx - small nodules with or without ground-
glass halos may be seen in a hematogenous
parenchymal distribution.
• Clinical features and Rx findings in schistosomal PHT
and cor pulmonale - not distinctive

48. Management
• Diagnosis - finding the parasite eggs in urine or stools
• Most severe pulmonary disease - occurs years after infection,
finding parasite ova in urine or stool - difficult.
• Demonstrating the characteristic pathologic changes, finding
ova directly in the tissue, or positive serology - confirm the
diagnosis.
• Active schistosome infections - Praziquantel, which kills adult
worms, stops further destruction of tissue by ova deposition.
• Dose of 20 mg/kg BD for 1 day (2 total doses) for S. mansoni
and S. haematobium infection
• TID (3 total doses) - S. japonicum infection.
• Reversal of pathologic lesions in lungs after antischistosomal
chemotherapy – not documented.

49. Paragonimus
• Lung fluke - Southeast Asia, Africa, and South and
Central America.
• Contamination of water sources with feces or
sputum of infected individuals.
• Water contamination - infection of intermediate
snail and crustacean hosts.
• Human infection - acquired from food sources.
• Classically described in individuals consuming raw or
pickled crustacea (freshwater crayfish and crabs) –
harboring infective parasite stage (metacercariae)
• Consumption of raw, wild boar.

51. Pathology
• The primary site of infection in humans is the lungs, brain 25%
• 3 stages of parasite development occur within the lungs—
primary infection, encystation, and death.
• Initial invasion of the lungs - maturing adult worms, parasite
tunnels in the pulmonary parenchyma (periphery)
• Encystation- the parasites are enclosed within cystic lesions that
may communicate with each other or with a nearby bronchus.
• Death - leads to collapse of the cyst, disintegration of the
parasite, and fibrosis or calcification.
• The surrounding pulmonary tissue - atelectasis, bronchiectasis,
or compensatory emphysema, some- secondary infection and
lung abscess develop in the cystic lesions.

52. • IP between infection and the development of
maturing adults in the lungs is 2 to 20 days.
• Light worm infection - usually asymptomatic.
• Moderate to heavy worm loads - complaints of
cough, respiratory discomfort (early morning),
rusty, blood-tinged sputum containing - parasite
eggs, necrotic material, Charcot–Leyden crystals.
• Frank hemoptysis - mild to severe
• Individuals - mistaken for having TB or malignancy.
• Eosinophilia - only clue that the cause is parasitic,
- found in 80% to 90% of affected individuals.

53. • The chest Rx is normal in 10% to 20% of infected persons
• Rx- infiltrates, cavitation, fibrosis, PE, pulmonary thickening.
• Findings - unilateral or bilateral.
• Radiographic changes over time corresponds to 3 stages:
1) On arrival to the lungs, maturing worms are associated with
the development of radiographic opacities;
2) succeeded by nodules - correspond to the parasite cysts;
3) eventually, fibrosis or calcification ensues.
• The characteristic ring shadow - with a crescent corona -
seen in some infected persons.

54. • Diagnosis - detection of the characteristic eggs in sputum or
stools of infected persons.
• Serologic testing is helpful in egg-negative cases.
• DOC - Praziquantel.
• Orally -25 mg/kg three TID for 2 days
• Or Bithionol 30 to 50 mg/kg orally on A/Ds for 5 doses.
• Therapy usually leads to :
1. Cessation of egg passage in sputum and stools
2. Clearing of the chest Rx in 2/3 of treated patients
3. Decrease in serum IgG antibodies directed against parasite.

56. Thank You