nematode infestations of the lungs

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clinical aspects of parasitic nematode infestations of the lung and their management


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By Dr. Mahmoud M. Alsalahy Assist prof of Chest Medicine Banha University, Egypt PARASITIC LUNG DISEASES : NEMATODES

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NEMATODES Intestinal Ascaris Ankylostoma Strongyloides Tissue-Dwelling Nematodes: Lymphatic filariasis Dirofilariasis Trichinosis Viceral larva migrans

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Ascriasis Ankylostomiasis Strongyloidiasis Incidence Infection Lung pass Pathologically Clinically Radiology Diagnosis Treatment Prevention 1.3 billions Fecal oral 9-12 days after infection, lasts 2-3 wks After maturation penetrate alveoli, creep up airways 1.2 billions Skin to blood 2 wks to 3 months according degree of infestations Same as ascaris 50-100 millions Skin to blood Few days to 3 wks Same as ascaris Interstitial eosinophilic pneumonitis with granuloma around larvae ( Lofler´s pneumonia ) Alveolar hemorrhage, Bronchitis Cough, dyspnea, wheezing, skin rashes, during migration in the lung Adult ascaris worm may cause upper airway obstruction and can inter a lung cavity NAD, consolidation, nodular shadows , interstitial infiltrates Eggs in stool, larvae in sputum or BAL, Eosinophilia, serology Mebendazol , Albendazol/ 3 days Ivermectin daily/ wk Sanitation, protective shoes, control infection

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Larvae in sputum Larvae in lung tissue

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TISSUE DWELLER NEMATODES FILARIASIS: 8 species, infect 150 millions worldwide in tropics Wuchereria bancrofti & Brugia malayi inhabit lymphatic vessels and cause elephantiasis In males, scrotum and groin are mainly affected while in females, axillae, breasts and arms W. Bancrofti & B. malayi are responsible for tropical pulmonary eosinophilia Infection is by mosquitoes bites (Anopheles, Culex , Aedes ) containing microfilaria

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Pathology and pathogenesis: After injection of infective filarial larvae by mosquitoes into patient blood, they pass through the lung Larvae induce cell mediated and humoral immune response with complement activation 1 st attacked by eosinophils, followed by aggregation of histocytes and lymphocytes with granuloma formation Larvae that reach lymphatic vessels mature into adult worms while those in blood are killed and removed Intense eosinophilic granulomatous infiltrations of the interstitium that can pass to alveoli associated with marked blood eosinophilia Later granulomas are replaced by fibrosis

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Clinical picture (TPE): Any age but common in 3 rd & 4 th decades Occurs in 0.1-0.4% of patients with lymphatic disease Systemic serum sickness like syndrome with cough, dyspnea and wheezing The disease commonly mistaken for asthma Pulmonary functions are obstructive in early cases and restrictive in late cases and diffusion may be affected Evidence of lymphangitis or lymphedema Chronic cases may cause cor pulmonale

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Diagnosis: Pulmonary symptoms + lymphedema TPE needs : 1. Clinically: History of PND, Rapid response to antifilarial drugs 2. Radiologically: Pulmonary opacities on radiology 3. Lab: Eosinophilia > 3000 /µL, High IgE levels, High antifilarial Abs Microfilaria detected by: Night Bl. Smear, 10 pm-6 am Filarial Abs. by ELISA Immunochromatographic card test BAL: eosinophilic alveolitis (>50% eosinophils) Radiology: non specific, most common is micronodular (miliary) pattern, consolidation, cavitation, may be pleural effusion D.D: other eosinophilias and eosinophilic granulomas

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Treatment: Diethylcarbamazine (DEC): 6mg/kg/day/12 days If DEC in this dose is not effective: double the dose and prolong the duration DEC is very effective, so failure must point to other diagnosis Doxycycline for 6 wks is an effective addition to DEC Prevention: Mass treatment for filariasis Control mosquitoes Prophylactic DEC for travellers to endemic areas

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DIROFILARIASIS: Caused by dirofilaria immitis The definitive host is carnivores esp. dogs, man is an incidental Called dog heart worm because it lives in dogs heart Most common in USA , Japan , Brazil , Italy Transmission is like human filariasis In dogs , microfilariae circulate and settle in the heart to mature while in humans cant mature and die then embolized to the lung and induce granuloma formation

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Pathology: An eosinophilic granuloma 1-3 cm with surrounding eosinophilic pneumonitis Lesions are most commonly sub pleural Microscopically, remnants of larvae can be seen inside the granulomas Clinically: Commonly in patients >50 yrs Usually asymptomatic May be cough, dyspnea, wheezing with minimal hemoptysis Common presentation is a sub pleural nodule in x-ray mostly on Rt. side with the dilemma of SPN diagnosis Eosinophilia occurs only in 10% of patients Treatment: No treatment needed, excision is to exclude malignancy

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TRICHINOSIS: Caused by Trichinella spiralis The only known intracellular nematode The definitive host is humans Most common in Europe and USA The adult lives in sub mucosa of small intestine Intermediate host : pigs, horse, boar, bear Larvae live in muscle cells of intermediate hosts Transmission is by eating poorly cooked meat of intermediate hosts

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within 5-7 days

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Pathology: An eosinophilic granulomas in skeletal muscles with muscle edema Diaphragm and other respiratory muscles are affected and can lead to RF Heart and CNS can also be involved and results in death Lung is rarely involved with eosinophilic pneumonia Clinically: Any age Generalized muscle pain and swelling Heart failure, arrhythmias, RF, hoarsness Diagnosis: Serology: detection of nematode antigen Lab: high LDH, CK, IgE Muscle biopsy is definitive Treatment: Albendazol: 400-800mg/day/7-14 days

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VISCERAL LARVA MIGRANS: Caused by larvae of canine nematodes toxocara canis and cati Definitive host is canines, man infected incidentally Life cycle is similar to ascaris and ankylostoma but cant complete life cycle in human Larvae can live for months or years in the lung Infection is more in children especially in presence of dogs and cats More in conditions with poor hygiene as infection is through contaminated hands, food or water

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P athogenesis: Very similar to intestinal nematodes (ascaris & ankylostoma) Larvae pass through the lung and other tissues mainly liver and brain inducing eosinophilic granulomatous reaction T. canis larvae induce intense airway inflammation Granulomas are replaced by fibrosis later on A mixed obstructive and restrictive ventilatory defect occurs Protective immunity is slow, so re-infection occurs with more lung damage

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Clinically: Any age but more in children Asthma like picture with chronic cough more at night Eosinophilic pneumonitis with consolidation Cavitation may occur with hemoptysis Diagnosis: Need high clinical suspicion in any child with unexplained fever and cough Radiology: lung nodules, consolidation +/- cavitation Serology: detection of nematode antigen Lab: high IgE, IgG, IgM + eosinophilia Muscle biopsy is definitive Treatment: Albendazol: 400mg/BID/5 days 10 mg/kg/day/5days for children

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ECHINOCOCCOSIS: Caused by Echinococcus granulosus (dog tapeworm) and multilocularis (fox tapeworm) Cause hydatid disease (cystic & alveolar) The definitive host is canines esp. dogs & foxes Intermediate host: sheep, goats, kangaroo and other herbivores Worldwide distribution but most common in Mediterranean, south and central America, Russia, China & sub-Saharan Africa E. multilocularis is endemic in northern hemisphere E. granulosus is more common but E. multilocularis is more pathogenic CESTODES

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Pathogenesis and pathology: Cysts enlarge very slowly: 1cm/ yr in liver and 5cm/ yr in lung May take decades before symptomatizing Cyst has 3 layers: Pericyst: fibrous layer by the host tissue Exocyst : carbohydrate rich, parasite derived, laminated layer Endocyst : germinal layer, produce protoscolices, cyst fluid Symptoms develop due to complications: ▪ Compression ▪ Rupture ▪ Infection In E. multilocularis, pericyst is poor → tumor like behavior Liver affected in 60%, lung in 20-30%, 10% other sites In lungs: More on right (65% vs. 35%) More in lower lobes (65% vs. 35%) Solitary cyst in 80% Associated liver disease in 10-40%

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Clinically: Latent period of 5-15 yr , so common after age of 20 Asymptomatic for decades Pulmonary symptoms in 70-90% : cough, fever, chest pain, sometimes hemoptysis Bilioptysis and pneumothorax and pleuritis are rare Cyst rupture (30%): expectoration of watery fluid with salty and peppery taste, may be parts of the cyst Anaphylaxis with respiratory failure may occure with rupture Rarely a cyst ruptures in pleura, pericardium or mediastinum Infected cyst (30%): picture of lung abscess Vascular: Pulmonary embolism if rupture in hepatic veins or PA Aortic pseudo aneurysm

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Diagnosis: Suspected if relation to dogs was positive in a clinically and radiologically compatible picture X-ray: A homogenous round or oval shadow Air crescent sign if pericyst ruptures Water Lilly sign if endocyst ruptures A cavity with air fluid level Pleural effusion Cyst wall may calcify CT: changes in X-ray are better seen in CT MRI: Cyst and daughter cysts are well seen on T1 while capsule is well seen on T2 Bronchoscopy is not recommended unless malignancy is possible Immunodiagnosis: Serodiagnosis: is 96% sensitive and specific Echinococcin test: intra dermal injection of echinococcus protein s NB. Aspiration of cysts must be avoided if hydatid disease is suspected

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Treatment: Surgical removal is the best for resectable cysts Peri -operative albendazol in 10-15 mg/kg/day in 2 doses at least 4 days before resection and continued for at least 1 month after surgery For E. multilocularis a safety margin must be resected with cysts Addition of praziquantel 25mg/kg/day for 1 month before surgery is more effective Non surgical candidates are treated by Albendazol for prolonged time and for life in E. multilocularis Medical treatment offers cure in 50% Puncture, Aspiration, Injection, re-aspiration ( PAIR ): hepatic cysts Prevention: Dog deworming Dog vaccination Sanitation

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