Lung parasitic infections

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