Parasitic disease of lung definition etiology pathogenesis clinical features diagnostic and treatment with drug dosage from fishman and Murray only
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Here is the full, detailed answer based exclusively on Fishman's Pulmonary Diseases and Disorders (Chapters 135 & 136) and Murray & Nadel's Textbook of Respiratory Medicine (Chapter 58).
Parasitic Diseases of the Lung
DEFINITION
Parasitic pneumonias are rare infections requiring endemic exposures in which the organism's life cycle includes the lungs. Pulmonary involvement occurs via two broad mechanisms:
- Transit through the lung during larval migration (producing Loeffler-like syndrome, eosinophilic pneumonia)
- Direct pulmonary invasion or encystation producing cysts, nodules, abscesses, or consolidation
Parasitic infections of the thorax are generally quite rare. Other infectious and noninfectious processes can mimic their presentation, and the clinician must be aware of these pathogens, especially in endemic regions. Diagnostics can be challenging and may necessitate invasive procedures.
- Fishman's, Chapter 135-136; Murray & Nadel's, Chapter 58
CLASSIFICATION OF PARASITES CAUSING PULMONARY DISEASE
| Category | Organisms |
|---|---|
| Protozoa | Entamoeba histolytica (amebiasis), Toxoplasma gondii, Cryptosporidium spp. |
| Helminths - Nematodes | Ascaris lumbricoides, Strongyloides stercoralis, Wuchereria bancrofti / Brugia malayi (filariasis), Toxocara canis/cati, Dirofilaria immitis |
| Helminths - Cestodes | Echinococcus granulosus (cystic hydatid), E. multilocularis (alveolar hydatid) |
| Helminths - Trematodes | Paragonimus westermani (lung fluke), Schistosoma spp. |
PROTOZOA
1. AMEBIASIS (Entamoeba histolytica)
Etiology
E. histolytica is a protozoan found worldwide. It is endemic in areas with poor sanitation - Mexico, Central and South America, Africa, and the Indian subcontinent. Seroprevalence reaches 5-50% in impoverished populations. Transmission: fecal-oral via contaminated food/water, or oral-anal contact. It infects 500 million people and causes 40,000-100,000 deaths yearly. A morphologically identical but nonpathogenic species, Entamoeba dispar, is 10x more prevalent and must be distinguished by antigenic, genetic, or immunologic methods.
- Fishman's, Ch. 135
Pathogenesis
E. histolytica has a simple life cycle: infectious cysts survive weeks-months in the environment. After ingestion, cysts excyst in the small intestine, each forming 8 daughter trophozoites. Trophozoites adhere to and invade the intestinal mucosa. In 4-10% of infected individuals, trophozoites invade the intestinal mucosa to cause intestinal disease; in others they enter the bloodstream and establish infection in the liver, brain, or lungs. Pleuropulmonary amebiasis occurs by:
- Sympathetic effusion from an intact, unruptured amebic liver abscess irritating the diaphragm
- Direct extension through the diaphragm (transdiaphragmatic rupture) causing empyema
- Hematogenous spread with parenchymal abscess, consolidation, or hepatobronchial fistula
Pleuropulmonary complications complicate amebic liver abscess in 7-20% of cases; the chest radiograph is abnormal in nearly 50% of cases.
- Murray & Nadel's, Ch. 58; Fishman's, Ch. 135
Clinical Features
- Intestinal: abdominal pain, tenesmus, bloody/mucoid/watery diarrhea, fever (in <50%)
- Extraintestinal: The typical patient is an adult male who acquired infection in an endemic area, presenting with fever and right upper quadrant pain without intestinal symptoms (amebic hepatic abscess is ~10x more common in men)
- Pulmonary: right lower lobe most commonly involved; elevated right hemidiaphragm, right pleural effusion, right lobe atelectasis, pulmonary consolidation with abscess formation, hepatobronchial fistula
- Transdiaphragmatic rupture: abrupt exacerbation of right upper quadrant pain, tearing sensation, then progressive respiratory distress, sepsis, occasionally shock. Massive pleural effusion with opacification of entire hemithorax and mediastinal shift
- Characteristic "anchovy paste" or "chocolate sauce" pleural fluid on thoracentesis
Diagnosis
- Gel diffusion, indirect hemagglutination (IHA), or enzyme-linked immunosorbent assay (ELISA) tests are positive in >98% of patients with extraintestinal invasive amebiasis
- Stool microscopy for cysts/trophozoites (note: does not distinguish E. histolytica from E. dispar); antigen detection or PCR preferred
- CT scan to identify liver abscess and diaphragmatic involvement
Treatment (Drug Dosage)
- Metronidazole 750 mg three times daily for 7-10 days (drug of choice for invasive/extraintestinal disease)
- Followed by a luminal agent: paromomycin 500 mg three times daily for 7 days, or iodoquinol
- For transdiaphragmatic rupture: urgent tube thoracostomy + same antiamebic drugs; bacterial co-infection occurs in ~1/3 of cases, requiring appropriate antibiotics
- Patients with sympathetic effusions: antiamebic drugs alone (drainage usually not required)
- Fishman's, Ch. 135; Murray & Nadel's, Ch. 58
2. TOXOPLASMA (Toxoplasma gondii)
Clinical Features and Treatment
Acute infection in the immunocompetent host is generally asymptomatic, with cervical lymphadenopathy as the hallmark. May be confused with EBV or CMV mononucleosis. Fever, malaise, sore throat, hepatosplenomegaly, and atypical lymphocytosis are seen. Rarely, acute disease may present with severe dissemination marked by pneumonitis, hepatitis, encephalitis, polymyositis, or myocarditis. Pneumonitis is more common and severe in immunocompromised patients.
Treatment: Pyrimethamine + sulfadiazine + leucovorin for severe/immunocompromised cases.
- Fishman's, Ch. 25
HELMINTHS - NEMATODES
3. ASCARIASIS (Ascaris lumbricoides)
Etiology
A. lumbricoides is the most common intestinal helminth worldwide. Infection occurs through ingestion of embryonated eggs in contaminated soil or food.
Pathogenesis
After ingestion, larvae hatch in the small intestine, penetrate the intestinal wall, enter the portal circulation, and travel to the liver, right heart, and then the lungs (Loeffler stage). In the lungs, larvae break into the alveoli, migrate up the airway, are swallowed, and mature into adult worms in the intestine. Pulmonary symptoms arise during larval migration.
Clinical Features - Loeffler Syndrome
- Transient pulmonary infiltrates with peripheral eosinophilia
- Cough, dyspnea, wheezing, hemoptysis, chest pain
- CT shows patchy bilateral nodular areas of ground-glass opacity
- Symptoms are self-limited (days to weeks) and coincide with larval lung transit
- Note: stool microscopy for ova should be ordered 4-8 weeks after onset of pulmonary symptoms (larvae do not appear in stool until adult worms mature)
Diagnosis
- Peripheral eosinophilia is the hallmark during Loeffler stage
- Stool O&P microscopy (positive 4-8 weeks after pulmonary phase begins)
- Chest imaging: bilateral patchy ground-glass opacities, nodules
Treatment
| Drug | Dose |
|---|---|
| Albendazole (preferred) | 400 mg orally as a single dose |
| Mebendazole (alternate) | 500 mg orally single dose, or 100 mg twice daily for 3 days |
Note: Anthelmintic treatment is only effective against adult worms in the intestinal phase.
- Fishman's, Ch. 136 (Table 136-1)
4. STRONGYLOIDIASIS (Strongyloides stercoralis)
Etiology
S. stercoralis is unique in its ability to autoinfect the host, allowing the infection to persist for decades and to produce overwhelming hyperinfection and dissemination in immunocompromised patients (corticosteroids, HTLV-1, hematological malignancy).
Pathogenesis
Filariform larvae penetrate the skin, travel to the lung, ascend the airways, are swallowed, and mature in the intestine. In hyperinfection syndrome, massive larval load transports intestinal bacteria into the bloodstream, causing post-obstructive pneumonitis and polymicrobial systemic sepsis and meningitis.
Clinical Features
- Uncomplicated: cough, eosinophilia, larva currens (migratory urticarial skin rash)
- Hyperinfection: respiratory failure, polymicrobial bacteremia/meningitis, massive eosinophilia; carries high mortality
Diagnosis
- Stool O&P (multiple samples needed); Strongyloides ELISA (high sensitivity); duodenal aspiration
- Sputum or BAL may show filariform larvae in hyperinfection
Treatment
| Drug | Dose | Notes |
|---|---|---|
| Ivermectin (preferred) | 200 µg/kg orally, single dose | Uncomplicated infection |
| Ivermectin ± albendazole | Oral or parenteral; duration extended | Hyperinfection/disseminated disease |
Ivermectin is only effective against the intestinal stages.
- Fishman's, Ch. 136 (Table 136-1)
5. TROPICAL PULMONARY EOSINOPHILIA - FILARIASIS (Wuchereria bancrofti, Brugia malayi)
Etiology
Caused by lymphatic filariae transmitted by mosquitoes. Endemic in South and Southeast Asia, Africa, South America.
Pathogenesis
Microfilariae trapped in the pulmonary vasculature trigger an intense eosinophilic inflammatory response in the lung parenchyma.
Clinical Features
- Paroxysmal nocturnal cough, dyspnea, wheezing
- Extreme peripheral eosinophilia (>3000/µL)
- Bilateral perihilar nodules or diffuse reticulonodular opacities on CXR
- Elevated IgE
- Responds dramatically to diethylcarbamazine
Diagnosis
- High IgE, high eosinophilia, positive Wuchereria serology
- Microfilariae rarely found in blood (nocturnal periodicity)
- CXR/CT: bilateral perihilar nodules, interstitial infiltrates
Treatment
| Drug | Dose |
|---|---|
| Diethylcarbamazine (DEC) | 6 mg/kg divided in 3 daily doses for 21 days |
Corticosteroids used as adjunctive therapy, though clinical trials lack definition of dose/duration.
- Fishman's, Ch. 136 (Table 136-1)
6. TOXOCARIASIS (Toxocara canis/T. cati)
Etiology
Worldwide distribution; US seroprevalence ~5%. Humans are accidental hosts; infection by ingestion of infective eggs from contaminated soil, fruits/vegetables, or undercooked meat. The larval life cycle normally occurs in dogs and cats.
Pathogenesis
After ingestion, larvae penetrate the intestinal mucosa, enter venous circulation, and migrate to virtually any organ. Damage arises from migrating larvae, eosinophilic infiltrates, and eosinophilic granulomas.
Clinical Features
Two syndromes:
- Visceral Larva Migrans (VLM): children <5 years; fever, anorexia, chronic nonproductive cough, dyspnea, wheezing, hepatomegaly, splenomegaly, seizures, eosinophilia, hypergammaglobulinemia. CXR: bilateral peribronchial/parenchymal infiltrates. CT: multifocal pulmonary nodules with surrounding ground-glass opacities.
- Ocular Larva Migrans (OLM): children 5-10 years; unilateral decrease in visual acuity, strabismus, uveitis, scleritis, endophthalmitis.
Diagnosis
- ELISA (recombinant antigens): sensitivity ~78%, specificity ~92%; cannot distinguish T. canis from T. cati
- Definitive diagnosis: larvae in affected tissue (rarely performed)
- OLM: ophthalmologic exam (ELISA sensitivity lower in OLM)
Treatment
| Condition | Drug | Dose |
|---|---|---|
| Mild VLM | Supportive | Self-limited course, no anthelmintic needed |
| Moderate-severe VLM | Albendazole | 400 mg orally twice daily for 5 days |
| OLM | Albendazole + corticosteroids | 400 mg orally twice daily for 14 days |
Some experts add corticosteroids to VLM treatment to mitigate immune response to dying larvae.
- Fishman's, Ch. 136
HELMINTHS - CESTODES
7. ECHINOCOCCOSIS (E. granulosus - Cystic Hydatid Disease)
Etiology
Caused by larvae of the dog tapeworm E. granulosus (cystic echinococcosis/hydatid disease). Endemic in pastoral communities of South America, Australia, Eastern Europe, North Africa, Middle East, Central Asia, and Western China. The infection cycle:
- Definitive host: dogs/canids ingest hydatid cysts in viscera of intermediate hosts (sheep, pigs, cattle)
- Adult tapeworm matures in canine intestine and sheds embryonated eggs in feces
- Humans accidentally infected by ingesting eggs in contaminated food/water or from dog handling
- Embryo oncospheres are released in the stomach, penetrate the intestine, and spread via bloodstream to liver or lungs
The lungs are the second most common location (20%) after the liver (80%).
- Fishman's, Ch. 136
Pathogenesis
The cyst has three layers:
- Outer pericyst: host-derived, composed of compressed lung and granulomatous inflammation that progresses to fibrosis
- Middle laminated layer: acellular, defines the parasite wall
- Inner endocyst/germinal layer: deposits hydatid sand and daughter cysts into the enlarging cyst
The cyst grows slowly over years to decades. Lung disease is more common in children (lungs accommodate faster growth). Eventually the cyst may degenerate and calcify, or acutely rupture into the bronchial tree, pleural space, or pericardium - with risk of anaphylaxis.
Clinical Features
- Long asymptomatic period (years to decades) while cyst enlarges
- Cough, hemoptysis, chest pain from mass effect
- Rupture into bronchus: sudden expectoration of cyst contents including daughter cysts and salty fluid ("grape skin" membrane), followed by secondary infection
- Rupture into pleural space: anaphylactic shock, bilateral seeding (secondary echinococcosis)
- CXR/CT: well-defined homogeneous spherical mass, often with a characteristic "water lily" sign (floating membranes after cyst rupture), "crescent sign" (air between pericyst and laminated layer)
Diagnosis
- Serology: ELISA, indirect hemagglutination (IHA), immunoblot for Echinococcus antigens
- CT/MRI chest: cyst morphology, daughter cysts, calcification
- Serology positive in only ~80% of pulmonary CE (liver CE higher)
- Caution: percutaneous aspiration carries risk of anaphylaxis - must be done under albendazole cover
Treatment
| Modality | Details |
|---|---|
| Surgery (mainstay) | Cystectomy/pericystectomy; recommended for most pulmonary hydatid cysts |
| Albendazole (adjunct) | 400 mg orally twice daily for 3-6 months; recommended for small cysts, inoperable patients, or as pre/post-operative cover to prevent secondary seeding |
| PAIR (Puncture-Aspiration-Injection-Re-aspiration) | Used mainly for liver cysts; less standard for pulmonary |
For alveolar echinococcosis (E. multilocularis): radical resection followed by long-term albendazole. If inoperable, life-long albendazole.
- Fishman's, Ch. 136 (Table 136-1); Murray & Nadel's, Ch. 58
HELMINTHS - TREMATODES
8. PARAGONIMIASIS (Paragonimus westermani)
Etiology
Caused by lung flukes (trematodes) from the genus Paragonimus (>15 species). Infection acquired by consumption of raw, undercooked, or pickled freshwater crabs or crayfish infected with metacercariae. Causes >20 million infections globally; highest prevalence in Southeast Asia (P. westermani). Other species in Africa and South/Central America. Autochthonous North American cases by P. kellicotti associated with freshwater crayfish.
Pathogenesis
After ingestion, metacercariae excyst in the intestine, penetrate the intestinal wall, migrate through the peritoneal cavity and diaphragm into the pleural space and lungs. In the lungs, they mature into reddish-brown hermaphroditic adult worms in cystic cavities, producing golden-brown operculated eggs (~100 × 55 µm) that are coughed up in sputum or swallowed and shed in feces.
Three disease stages:
- Primary infection and migration: inflammation, hemorrhage, tissue necrosis as flukes tunnel from the periphery toward bronchioles; surrounding neutrophilic and eosinophilic inflammation with Charcot-Leyden crystals
- Encystation: worms encyst forming clusters of encapsulated cysts that communicate with each other or bronchi (forming fistula), allowing eggs into the airways
- Death/degeneration: cysts involute, leaving fibrotic nodules or calcifications
Clinical Features
- Chest pain, chronic cough, hemoptysis (can mimic tuberculosis)
- Pleuritic pain during migration phase
- Peripheral eosinophilia
- Pleural effusion is common
- CXR: patchy bilateral linear opacities and interstitial thickening with small nodules; ring shadows (cysts communicating with bronchi); bilateral infiltrates
- Ectopic paragonimiasis: larvae may migrate to the brain (seizures, headache) or abdomen
Diagnosis
- Sputum/stool microscopy: demonstration of operculated eggs (sensitivity limited)
- ELISA serology: sensitive and specific for P. westermani
- BAL, pleural fluid for eggs
- CT: ring-shaped or nodular lesions, cysts, linear tracts
- Lung biopsy: operculated eggs in tissue
Treatment
| Drug | Dose | Notes |
|---|---|---|
| Praziquantel (preferred) | 75 mg/kg/day divided in 3 doses for 2-3 days | Drug of choice |
| Triclabendazole (alternate) | 10 mg/kg once or twice | Effective alternative |
- Fishman's, Ch. 136; Murray & Nadel's, Ch. 58
9. SCHISTOSOMIASIS (Schistosoma spp.)
Pathogenesis & Clinical Features
Pulmonary disease arises from:
- Larval lung transit: during acute infection (Katayama fever/acute schistosomiasis) - fever, urticaria, cough, eosinophilia
- Egg deposition in pulmonary vasculature: chronic phase - pulmonary arterial hypertension from granulomatous inflammation around trapped eggs
Treatment
| Species | Drug | Dose |
|---|---|---|
| S. haematobium, S. mansoni, S. intercalatum | Praziquantel | 40 mg/kg for one day (1-2 divided doses) |
| S. japonicum, S. mekongi | Praziquantel | 60 mg/kg for one day (2 divided doses) |
- Check urine/stool for viable eggs ≥6 weeks post-treatment; retreat if positive
- In acute schistosomiasis syndrome: corticosteroids are primary treatment; praziquantel given only after symptoms fully resolve, usually 4-6 weeks later
- Anthelmintic therapy can reverse pulmonary nodules from deposited eggs, but cannot reverse irreversible late-stage lung pathology
- Fishman's, Ch. 136
GENERAL DIAGNOSTIC APPROACH (Fishman's Figure 136-1)
Workup for suspected pulmonary helminthic disease:
- CBC (eosinophilia is a key clue), CMP
- CT chest (for cysts, nodules, infiltrates)
- Stool O&P microscopy (order 4-8 weeks after pulmonary symptom onset for Ascaris/hookworms)
- Serology (ELISA for specific organisms)
- Sputum/BAL (for eggs, larvae)
- Bronchoscopy/lung biopsy if needed
SUMMARY TREATMENT TABLE (Fishman's Table 136-1)
| Parasite | Preferred Drug | Dose | Alternate |
|---|---|---|---|
| Ascaris lumbricoides | Albendazole | 400 mg orally single dose | Mebendazole 500 mg single dose or 100 mg BID × 3 days |
| Ancylostoma duodenale | Albendazole | 400 mg orally single dose | Mebendazole as above |
| Strongyloides stercoralis | Ivermectin | 200 µg/kg orally, single dose (uncomplicated); extended with albendazole for hyperinfection | - |
| W. bancrofti / B. malayi | Diethylcarbamazine | 6 mg/kg ÷ 3 daily doses × 21 days | - |
| Toxocara canis/cati (VLM) | Albendazole | 400 mg BID × 5 days | - |
| Toxocara canis/cati (OLM) | Albendazole + corticosteroids | 400 mg BID × 14 days | - |
| E. granulosus (hydatid) | Surgery (mainstay); Albendazole (adjunct) | 400 mg BID × 3-6 months | - |
| Paragonimus westermani | Praziquantel | 75 mg/kg/day ÷ 3 doses × 2-3 days | Triclabendazole 10 mg/kg × 1-2 doses |
| Schistosoma mansoni/haematobium | Praziquantel | 40 mg/kg/day × 1 day | - |
| S. japonicum/mekongi | Praziquantel | 60 mg/kg/day × 1 day (2 divided doses) | - |
| Entamoeba histolytica | Metronidazole | 750 mg TID × 7-10 days + luminal agent | - |
Sources:
- Fishman's Pulmonary Diseases and Disorders, 2-Volume Set (ISBN 9781260473940) - Chapters 25, 135, 136
- Murray & Nadel's Textbook of Respiratory Medicine, 2-Volume (ISBN 9780323655873) - Chapters 58 and 109
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