A 27-Year-Old With a Non-Resolving Cavitary Lung Lesion

Lokesh Venkateshaiah, MD

Fellow

Division of Pulmonary, Critical Care and Sleep Medicine

Case Western Reserve University

Cleveland, Ohio

J. Daryl Thornton, MD MPH

Assistant Professor

Division of Pulmonary, Critical Care and Sleep Medicine

Case Western Reserve University

Cleveland, Ohio

A 27-year-old man presented to the pulmonary clinic for evaluation of a non-resolving lung cavity. Four months earlier, he had been diagnosed with pulmonary tuberculosis and was started on four-drug antituberculous directly observed therapy. A PPD placed at that time measured 22 mm of induration.

During the pulmonary clinic visit, the patient stated that over the last year and a half he had a cough occasionally productive of minimal blood-streaked sputum. He had denied other symptoms including nocturnal diaphoresis, anorexia, weight loss, or fevers.

The patient’s past medical history was remarkable for an abnormal chest radiogram that was noted one and a half years ago and one episode of malaria.

Other than his recent antituberculous therapy he took no regular medications.

He smoked one-half pack daily for the past 12 years. He occasionally snorted cocaine but did not use alcohol or other recreational drugs. He emigrated from Malaysia to the United States 8 months ago. He was originally from Burma but was a refugee in Malaysia. It was in Malaysia that he was noted to have an abnormal chest radiogram. He underwent additional investigations while there but was not given a diagnosis nor treatment.

The patient appeared comfortable and was in no acute distress. Vital signs were unremarkable. The cardiac exam demonstrated regular rate and rhythm, a normal S1 and S2, and no murmur, gallop or rub. Breath sounds were equal bilaterally and absent of adventitious sounds. The abdomen was soft and without organomegaly. The patient’s extremities were without clubbing or edema. There was a scar on the left upper arm from a prior BCG injection. No other skin lesions were noted.

White blood cell count was 10,000 per mm3 with 66% Neutrophils, 14% Lymphocytes and 12% eosinophils

Hematocrit 49%

Platelet count was 309,000 per mm3

Urea nitrogen was 12 mg /dl, and serum creatinine was 0.7 mg/dl

Liver function tests were within normal limits

Stools and sputum for ova and parasites were negative

Sputum for AFB times five was negative

Fig 1: Chest computed tomography 4 months prior to current presentation

Fig 2: Chest computed tomography at presentation (4 months following initiation of antituberculous therapy)

Cysts for Paragonimus were identified on BAL and transbronchial biopsy.

Paragonimiasis is caused by lung flukes of the genus Paragonimus. There are 43 species of Paragonimus, 12 of which infect humans. Paragonimus westermani is the most prevalent, especially in eastern and Southeast Asia. Infection with these organisms occurs worldwide but predominantly in several parts of Central and South America, West Africa, and Asia (1). In the United States, the disease is diagnosed most commonly in immigrants from endemic countries (2). Endogenous infections do occur and usually are caused by Paragonimus kellicot mainly in the midwestern and eastern United States (3-6).

Pulmonary tuberculosis is less likely given several negative sputum AFB stains and cultures. Alveolar lavage by bronchoscopy elso exhibited negative AFB stain and culture. In addition, the cavitation worsened on computed tomography despite receiving multidrug direct observed therapy. Acute bronchitis is not a common cause of pulmonary cavitation.

Pulmonary manifestations of chronic schistosomiasis are generally found in patients with a heavy infectious burden and significant clinical symptoms. Schistozome eggs may embolize from the liver to the pulmonary circulation where they may lead to granulomatous endarteritis, pulmonary hypertension, and cor pulmonale.

Paragonimus has a complex life cycle (5, 7-8) and involves freshwater snails, crustaceans, and mammals (see figure). Unembryonated Paragonimus eggs can be passed via sputum or stool. There they become embryonated and infect their first intermediate host, a snail. Inside the snail, they undergo several developmental changes from sporocysts to cercariae. The cercariae then infect the second intermediate host, crustacians (crabs or crayfish). When humans (or other mammals) ingest infected raw or undercooked crustaceans or use contaminated utensils, the larvae excyst in the duodenum, penetrate the intestinal wall, and enter the peritoneal cavity where they develop into immature flukes. These migrate through the diaphragm and pleura into the lungs. There, worm pairs encyst together near bronchial passages and mature into adult worms that lay eggs 5 to 6 weeks after infection. When the cysts rupture into a bronchiole, the eggs are expectorated or swallowed and shed with the feces.

Clinical Manifestations:

Most clinical infections are asymptomatic and even the symptomatic patients frequently look well despite a prolonged course. Symptoms develop depending on the severity of the infection and which organs are involved. The respiratory system is most commonly involved, but extrapulmonary involvment may subsequently occur, particularly with certain species, such as Paragonimus skrjabini. Virtually every organ system may become involved.

In contrast to Tuberculosis, paragonimiasis is only rarely accompanied by rales or other adventitious sounds. The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia both peripheral and also in the BAL samples (7). The acute stage corresponds to the period of invasion and migration of the lung flukes and consists of abdominal pain, diarrhea and urticaria, followed roughly 1 to 2 weeks later by fever, pleuritic chest pain, cough and/or dyspnea (9). During the chronic phase, pulmonary manifestations are frequently mild and include cough, expectoration of discolored sputum, hemoptysis, and chest radiographic abnormalities (7, 9). The radiographic abnormalities (10-13) include pleural effusions, focal fibrotic pleural thickening, sub-pleural or subfissural nodules, parenchymal mass lesions, migratory infiltrates, cavitary lesions, ring shadow lesions and rarely air-fluid levels (14-15). The most common symptomatic extrapulmonary site is the central nervous system. Flukes in the brain can lead acutely to headache, dizziness, and visual disturbances. Chronic infection can manifest as seizures, paralysis, or mental retardation (16).

The American Thoracic Society improves global health by advancing research, patient care, and public health in pulmonary disease, critical illness, and sleep disorders. Founded in 1905 to combat TB, the ATS has grown to tackle asthma, COPD, lung cancer, sepsis, acute respiratory distress, and sleep apnea, among other diseases.

AMERICAN THORACIC SOCIETY
25 Broadway
New York, NY 10004
United States of America

Phone: +1 (212) 315-8600
Fax: +1 (212) 315-6498
Email: atsinfo@thoracic.org

	A.	Pulmonary tuberculosis Incorrect!
	B.	Acute Bronchitis Incorrect!
	C.	Paragonimiasis Correct!
	D.	Schistosomiasis Incorrect!

	A.	Inhalation Incorrect!
	B.	Ingestion Correct!
	C.	Innoculation Incorrect!
	D.	Inconclusive Incorrect!

	A.	Peptobismol Incorrect!
	B.	Cipro Incorrect!
	C.	Praziquantel Correct!
	D.	Albendazole Incorrect!

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