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Parasitic infections of the respiratory tract (diagnosis and management). K LahiriDept of Pediatrics, Seth GS Medical College, Parel, Bombay, Maharashtra.
Correspondence Address: Source of Support: None, Conflict of Interest: None PMID: 0008051645 Keywords: Biopsy, Case Report, Child, Child, Preschool, Diagnosis, Differential, Diagnostic Imaging, Female, Human, Lung, pathology,Lung Diseases, Parasitic, diagnosis,pathology,therapy,Male, Pulmonary Eosinophilia, etiology,pathology,therapy,
The lung is involved in 2 forms of human hydatidosis caused by the cystic larval stage of the tapeworm, Echinococcus. Cystic hydatid disease is caused by Echinococcus granulosis and alveolar hydatid disease by Echinococcus multi-locularis[1]. 1. Diagnosis: Awareness of the disease is most important. Cystic hydatid disease is diagnosed on the basis of the following criteria: a) history of residence in an endemic area, b) history of contact with an infected dog is obtained in 29-48% of cases, c) clinical observation and d) radiographic evidence. Physical examination is rarely definitive. On rare occasions, a fluid thrill can be heard over a large cyst. Demonstration of scolices and hooklets of the parasite in vomitus, urine and sputum is pathognomonic. Needle aspiration is dangerous as leakage may induce anaphylactic shock. An increased specific serum lgE may be observed but eosonophilia is more often unreliable. Serological tests give false negative results in 10-30% cases. The Casoni's test involves injection of hydatid fluid in the dermis which produces an erythematous papule in 50-80% of patients in less than 60 minutes. It can be very useful if this test is strongly positive; at times a false negative test is due to an infected cyst. Casoni's test remains positive for life. Serum antibody testing by complement fixation is positive in 52-60% cases and in 72% with live cysts. It reverts to normal after successful removal of a cyst within 1-2 yrs or after death of a cyst. If both Casoni's test and complement fixation are positive, it can detect 84% cases. But because of low sensitivity and specificity, most centres have discontinued their use. Other serological tests such as indirect haemaggi uti nation, immunotluorescence antibodies and Elisa have 50% sensitivity for lung cysts. But at present, no single test can effectively rule out the disease. The main tool is a radiographic study, which is 98-100% accurate. But an inflammatory reaction masks both closed and ruptured cysts. On radiography, an unruptured cyst is seen as a, round or oval homogenous lesion with a sharply defined smooth border surrounded by normal lung or atelectasis. It may be unilateral or bilateral, single or multiple and located either at the hilum, centre or periphery and of varying sizes. As the cyst grows, it erodes into the adjacent structures and the surrounding vessel producing bronchial leaks into the Cyst[2]. As a result, different classic forms emerge. Meniscus sign or crescent sign is seen above the homogenous cyst on deep inspiration when air penetrates between adventitia and ectocyst[3]. As air dissection continues, the parasite's membrane is torn and some fluid flows out and there is a formation of air fluid level within the cyst (Double air layer appearance or Cumbo sign)[2]. The cyst wall may get detached from the adventitia, crumbles, collapses and floats on the cyst fluid (waterlily sign or Camelotte sign). These are most often single unilocular cysts. Inferior lobes are generally affected. In children, ratio of unruptured to ruptured cyst is 3:1. Calcification is rare. USG helps distinguish cystic lesions from solid tumours. Pathognomonic sign is multiple daughter cysts within a cyst, separation of laminated membrane from the wall of the cyst and sonographically collapsed Cyst[4]. CT Scan may aid the diagnosis by determining the location, extent of involvement and demonstration of internal anatomy of the cysts[5]. Angiography can demonstrate a halo effect around the cyst and determine the number and location of cysts. Histopathology depends on the size, time after rupture and allergic reactivity of the host. Unruptured cysts shows strong allergic eosinophilic reaction in the surrounding lung tissue. Cysts ruptured less than 10 days before show reversible inflammatory infiltrates of lymphoeytes or giant cell granulomata around parasitic components. Cysts ruptured more than 10 days ago show severe fibrosis leading to scarring. The following are two of our published case reports illustrating the diagnostic value of the above-mentioned investigations. Case 1: A five-year-old girl presented with fever. There was no history of cough, haemoptysis, allergic manifestation or dog exposure. MT was strongly positive, Casoni's test was negative. X-ray chest revealed a homogenous density in the right lower zone. There was no radiological improvement after 6 weeks of antituberculous therapy. Again USG and bronchogram did not provide any clues. Diagnosis of hydatid cyst was confirmed after surgical exploration and on histopathology[7]. Case 2: An eight year old boy presented with fever, cough, haemoptysis and chest pain off and on for two years. There was no history of allergic manifestation or dog exposure. X-ray chest revealed bilateral homogenous densities. USG and CT Scan did not provide any clues. MT and Casoni's test were negative. Diagnosis of hydatid cyst was confirmed after surgical exploration and on histopathology[7]. 2. Management. Surgical management: It is important to perform surgery immediately after diagnosis because of the weak adventitial reaction and possibility of bronchial communication which may lead to rupture with intrapulmonary dissemination. Success depends on the size and location of cyst and skill of the surgery. Spontaneous cure is possible after coughing but infection and toxaemia from residual cysts may follow. The aim of surgery is total eradication with evacuation of the cyst to prevent rupture and consequent dissemination during operation and obliteration of the residual cavity. The posterolateral approach is favoured. Surgical techniques are puncture and aspiration of the cyst in situ, excision of entire cyst by enucleation, wedge resection, segmentectomy, lobectomy, pneumonectomy, resection may be done with severe inflammation, large and multiple cysts that have destroyed lung parenchyma[8]. Rupture and spillage may occur and may lead to dissemination and anaphylaxis and may prove fatal. To prevent recurrence, the cavity is injected with scolicidal agents such as formalin, hypertonic saline, absolute alcohol. Silver nitrate has been used to freeze the cyst wall. Complications occur with formalin and saline, hence hydrogen peroxide has been used with good results. The residual cavity is either obliterated by sutures or left open to communicate with pleural space. Common surgical complications include atelectasis, hydropneumothorax, infection, pleural reaction, hemothorax, abscess, emphysema, septicaemia pneumothorax, bronchobiliary fistula, biliary pleura; fistula, bronchiectasis, anaphylactic shock and death. Peri-operative mortality is 3-10% and mortality rate is 0.5%. Medical management: When surgery is impractical, mebendazole in a dose of 30-50 mgm/kg/day for 1-6. months is recommended. Mebendazole interferes with glycogen uptake by the cestodes but is poorly absorbed and therefore has low blood level concentration, hence 50-100 mgm for 3 months has been recommended? The peak therapeutic level is 80 ?g/ml. Repeated courses are necessary. Subjective improvement'is seen in 75%. However, no controlled studies have been done. CBC, LFT and renal function monitoring is essential weekly for the first month and bi-weekly thereafter. Albendazole, a new benzimidazole derivative has shown to be more effective in a preliminary study because of high blood and tissue levels. For patients with age ? 10 yrs, 28 days course separated by 14 days drug free period has been recommended[10]. Prevetion and follow-up: This disease is preventable. Preventive measures include the use of veterinary taenicides for dogs, proper disposal of carcasses and extracts of animal and proper handling of food and drink to prevent contamination from dog. Follow-up abdominal USG should be done annually for 5 years and chest x-ray to be repeated after 2 or 3 years and at 5 years.
1. Diagnosis: Tropical eosinophilia is suspected in individuals staying in an area endemic for human filariasis and having prolonged and severe eosinophilia. Presence of anti-filarial antibody can be detected in the serum by complement fixation, haemagglutination and Elisa test. lgE is in the range of 1000-5000 lu/ml. Eosinophilia is prominent. Diagnosis is confirmed by rnicro-filaria seen in lymph nodes, pulmonary nodules surrounded by necrotic tissue and eosinophils and from favourable response to treatment[11],[12],[13]. 2. Treatment: Treatment for microfilarial infection is best done with diethylcarbamazine (Hetrazan) 5 mg/kg/day for 7-10 days. Steroids can be used in severely ill patients.
In many instances of pulmonary infiltrates with eosinophilia, no etioiogic agent can be determined. Careful history, laboratory findings and radiology can clinch the diagnosis. Nova and Ottesan (1978)[12] devised a new classification based on etiology. The etiological factors include parasites, fungus, drugs, vasculitis or idiopathic. Parasites include migratory phase of Ascaris, Toxocara, Microfilaria, Ankylostoma and Trichuris[11],[14],[15],[16]. Infection with Ascaris lumbricoide was known to be present in some of the Loeffler's cases. This syndrome is characterised by mild symptoms, moderate eosinophilia (10-20%) accompanied with fleeting density on chest x-ray. 1. Diagnosis. Stool should be examined for ova and parasites of ascaris, toxocara, hook worm and strongyloid infection at the time of initial evaluation and at an interval of 2-4 weeks. Eosinophil count is upto 50% with an absolute count 3000 cells/mm[3]. IgE level exceeds 10,000 iu/ml. Elisa shows the presence of toxocara antibodies and is sensitive because it differentiates toxocara from ascaris. 2. Management. PIE is a self limiting disease. In toxocara infection, thiabendazole 25-30 mgm/kg/day in divided doses for 7-10 days is given. A repeated course after 4 weeks is to be given. Steroids are indicated when symptoms are rare[14].
This term is applied to a clinical syndrome consisting of eosinophilia, hepatomegaly and pneumonitis that results from prolonged migration through human viscera by nematode larvae. The most common cause is a dog ascarid: Toxocara'canis and cat ascarid: T. catis. 1. Diagnosis. Diagnosis is based on history of pica, dirt eating and exposure to dogs in addition to clinical findings and chronic sustained eosinophilia, hepatomegaly and hypergammaglobulinemia. Accurate diagnosis is made by biopsy of a lesion and finding of typical nematode larvae in eosinophilic granuloma. The major antigen of T. canis is present in the embryonated egg and hatched larvae, which can be detected using Elisa. It is specific for toxocara and appears in high titres. 2. Management. No satisfactory treatment is recognised at present. Diethycarbamazine or mebendazole have not been useful. Adrenocorticoids have been life saving for patients highly sensitive to larval nematode especially those with severe pneumonitis. Otherwise treatment is primarily symptomatic and supportive with stress on correction of anaemia. It is important to prevent children from eating dirt contaminated with eggs. Antibiotics should be given to dogs and stool examined[14].
Schistosomial infection of humans represent one of the major endemic helminthiasis. Three species represent the most common and clinically significant infections: Schistosoma haematobium, S. mansoni and S. japonicurn. 1. Diagnosis: Early phase of the disease is usually not associated with pulmonary disease but chronic infection may cause the development of cor pulmonale. Diagnosis may be achieved by finding egg in urine or stools or finding ova in tissues several years after infection. 2. Management: Active schistosomial infections are treated with praziquantel as a single oral dose of 40 mgm/kg for S. japonicurn. It kills the adult worms and stops further destruction of tissue by ova deposition[17].
Symptomatic paragonimiasis is characterised by cough and bloody sputum that may lead to bronchiectasis or abscesses, Patients with mild infection are asymptomatic but those with severe ones may complain of cough, rusty sputum containing eggs, necrotic material and Charcot Leyden crystals[17]. Chest radiography is normal in 10-20% of children. Others may show infiltrate, cavitation, fibrosis and thickening. Diagnosis is made by detection of eggs in sputum or stools. The drug of choice is praziquantel 75 mgm/kg/day for 2 days[18].
Entarnoeba histoMica. The overall incidence of amoebic involvement of the lung and pleura as a complication is low. As the hepatic abscess enlarges upward, adhesions are formed between the surface of the liver and the diaphragm. The amoebic infection burrows into the pleural space or the lung causing empyema, pneumonitis, abscess or hepatobronchial fistula[19]. An acute rupture into the pleural space may evoke excruciating. pain in the right shoulder and back with fever, dyspnoea and even circulatory collapse. A hepatobronchial fistula is associated with anchovy paste Sputum[20]. 1. Diagnosis: In amoebic pneumonitis and abscess, wet mounts from sputum show trophozites. In the lung, trophozites are the hallmark of invasive amoebiasis. Serologic tests have proved positive in 90% of the cases. Most sensitive tests are indirect haemagglutination, ELISA, indirect immunofluorescence and counterimmunoelectophoresis. Latex agglutination test is used for quick and easy screening[19],[20]. 2. Management: Combined treatment is instituted using metronidazole 20 mgm/kg, three times daily for 10-15 days along with chloroquine base 10 mgm/kg for 2 days, then 5 mgm/kg for 14 days. Rupture of livar abscess into the pleural cavity requires surgical drainage[20]. Pneurnocystis carinii. A pneumonia caused by a protozoan, prompts a search for a defect in host immunity and coexistence of other infections either pulmonary or extrapulmonary. Pulmonary Pneurnocystis carinii may be associated with infection of the lung by aspergillus or cytomegalovirus, of the intestine by cryptosporidium or of the CNS by toxoplasma. 1. Diagnosis: Since early diagnosis enhances the prospects of successful therapy, the handling of tissue and sputum specimens for detecting the organism should be done as quickly as possible. Touch smear or impression smear are made by pressing the cut surface of the fresh lung against labeled sterile slides for routine histopathological or special examination[19]. The infant with the disease fails to thrive and has decreased albumin levels. Early signs include fever, diarrhoea, poor feeding and coryza. The respiratory manifestations then progress to nasal flaring, retractions, and cyanosis. Early radiological appearance shows fine bilateral, perihilar diffuse infiltrates which progress to an interstitial alveolar butterfly pattern. Identification of P. carinii requires the demonstration of the organisms in lung washings, secretions, impressions or histologic sections[21]. Invasive procedures: 1. Tracheal aspirate. The yield is low and the hazards in experienced hands is high. In intubated patients, respiratory secretions should be smeared on slides. 2. Fiberoptic bronchoscopy. This is one of the chosen procedures because the reported yield is upto 95 percent. Bronchial lavage, brushing, lung biopsies are the diagnostic procedures wherein 50 ml of physiological saline is used for alveolar washings. Trophozoites predominate in bronchial washing. 3. Percutaneous needle aspiration. This procedure has shown high success rates but with a high incidence of pneumothorax. 4. Lung biopsy. This is one of the most unequivocal avenue for diagnosis. Biopsies and aspirates should be utilised for fungal, bacterial, mycobacterial or viral cultures and to make slides for rapid staining with toluidine blue, Gomori Giemsa or Wright stains. Early diagnosis is frequently made and therapy initiated on such smears especially in AIDS[19]. 2. Management: Two agents are used for treating P. carinii:- pentamidine and co-trimoxazole. Pentamidine isethionate is given 4 mgm/kg per day, im/iv for 14 days. Pentamidine achieves therapeutic levels in the lungs over 5-7 days. Trials of inhalation route for pentamidine therapy for prophylaxis is ongoing. Pentamidine has been largely supplanted by cotrimoxazole for the therapy of pneumocystis infection in the non- AIDS patient, but it continues to be used in infection refractory to cotrimoxazole or patients allergic to trimethoprim or sulfonamides. Trimethoprim 20 mgm/kg/day or sulfamethoxazole 100 mgm/kg/day is given oral or IV in four doses for 14 days. Prophylaxis therapy is 5 mgm/kg/day orally for an indefinite period. Supportive therapy is largely to improve hydration, nutrition, and arterial oxygenation. AIDS patients failing to respond to antibiotics may need a short course of high dose corticosteroids to reduce inflammation and improve oxygenation till the infection abates[19],[21]. Toxoplasma gondii. Pulmonary disease due to Toxoplasma gondii is seen in neonates, children and immunocompromised hosts. The congenital form occurs in infants as a complication of an acute maternal infection. Pneumonitis due to T. gondii in immunocompromised hosts present with dyspnoea minimal sputum production and few clinical and radiologic findings. It evokes diffuse disease in the lung viz. interstitial infiltrates, bronchopneumonia and pulmonary infection[19]. 1. Diagnosis: Diagnosis of T. gondii infection is usually difficult and proof depends on demonstration of invasive organisms in tissue and/or serologic testing. The trophozoites have been found in BAL and lung biopsy. But cysts are known to survive in tissue for years and hence active infection is based on demonstrating trophozoites in body fluids, tissue or serology[22]. 2. Management: Drug therapy instituted is a synergistic combination of pyrimethamine 50 mgm oral loading followed by 25 mgm by mouth daily for 3-6 weeks. To combat bone marrow suppression folinic acid 5 mgm daily is administered. In addition, sulfadiazine 2 g loading followed by 75 mgm/kg/day in divided doses is given for 3-6 weeks[19]. Cryptosporidium, This organism reaches the lung either by aspiration of gastrointestinal organisms or airborne transmission. These patients present with dyspnoea, cough and heavy frothy sputum. There may be scattered rales and chest radiography shows mild, diffuse increase in bronchial markings. 1. Diagnosis: depends on the identification of oocysts in the stools and sputum of patients. In the sputum, it is either identified by a modified acid fast kin youn stain or Giemsa stain using a light green counterstain. They appear as refractile bodies without internal sutures[22]. Using serologic tests, positive antibody titres (>1:20) take upto 2 weeks to develop and reach thei~ peak 8-10 weeks after the start of infection. The positive titres may persist for more than a year after infection[22]. 2. Management: Treatment i s largely symptomatic. In immunocompetent children, the disease is self limited[19].
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