TROPICAL - TROPICAL MEDICINE FOR THE PULMONOLOGIST(MALARIA,HYDATID DISEASE,AMOEBIASIS,LEPTOSPIROSIS DR.AMIT RAODEO MALARIA 1 INTRODUCTION Malaria

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Unformatted text preview: TROPICAL MEDICINE FOR THE PULMONOLOGIST(MALARIA,HYDATID DISEASE,AMOEBIASIS,LEPTOSPIROSIS) DR.AMIT RAODEO MALARIA 1 INTRODUCTION Malaria remains a major public health problem in endemic Malaria areas. Responsible for 1.5 to 2.7 million deaths each year worldwide. Responsible Tropical African countries are estimated to contribute >90% of Tropical the total malaria incidence and great majority of malarial deaths. Respiratory tract involvement ranging from upper respiratory Respiratory symptoms to ARDS is seen in 3-10% cases. 3Incidence of pulmonary edema was around 1per 1000 cases in Incidence a large study from vietnam. vietnam. SEVERE MALARIA Definition:Presence of P.falciparum asexual parasitaemia and no other obvious cause of their symptoms,the presence of one or more of the following clinical/laboratory features is classified as severe malaria malaria CLINICAL: CLINICAL: a) b) c) d) e) f) g) g) h) i) Prostration Impaired consciousness Respiratory distress(acidotic breathing) Multiple convulsions Circulatory collapse Pulmonary edema Abnormal bleeding Jaundice Hemoglobinuria a) b) c) d) e) f) LAB: LAB: Severe anaemia Hypoglycemia Acidosis Renal impairment Hyperlactataemia hyperparasitaemia 2 COMPARISON BETWEEN LEPTOSPIROSIS,MALARIA AND DENGUE Clinical difference Leptospirosis Malaria dengue Splenomegaly + ++ + or - Subconjunctival hemorrhage Classically present Can be present Rare Can be present Myalgia Classically present Usually present Can be present Hemoptysis Common Uncommon Uncommon Encephalopathy Uncommon Common Uncommon Abdominal pain Common Uncommon Uncommon Arthralgia Less common Uncommon common COMPARISON BETWEEN LEPTOSPIROSIS,MALARIA AND DENGUE Lab difference Leptospirosis Malaria Dengue Hemoglobin Normal unless bleeding Anemia Elevated/normal unless bleeding TLC Leucocytosis Usually normal,leucocytosis can be present Increased TLC bad prognostic sign Normal/leucopenia Potassium levels Hypokalemia common common Hyperkalemia poor prognostic Hyperkalemia(IV hemolysis/ ARF) hemolysis/ /hypokalemia Normal/raised/reduced DIC Uncommon Common Common P.S Left shift Malarial parasite Atypical lymphocyte Hypoglycemia Uncommon Common Uncommon Pulmonary involvement Pulmonary hemorrhage ARDS Pnuemonia Diffuse nodular shadows Cardiogenic pulmonary edema ARDS Fluid overload Pulmonary sequestration due to parasite Less common ALI/ARDS ABG Normal anion gap,acidosis more common High anion gap metabolic acidosis(lactic) acidosis(lactic) Lactic acidosis less common Ascites / bilateral pleural effusion Absent Absent Present Myocarditis Common Less common Less common 3 HOW COMMON IS MALARIA AS CAUSE OF ARDS? PATHOGENESIS OF ALI/ARDS IN MALARIA 4 PATHOGENESIS OF ARDS AND PULMONARY EDEMA IN MALARIA DIFFERENTIAL DIAGNOSIS OF HYPOXEMIA IN MALARIA 1) 2) 3) 4) 5) ARDS Fluid overload Aspiration pneumonia Gram negative bacteremia Sequestration of parasitised RBCs in pulmonary vasculature 5 BACTERIAL SUPERINFECTION IN MALARIA Both community acquired as well as nosocomial infections Both are common. Mechanism: Mechanism: 1)Transient immunosuppression. 1)Transient immunosuppression. 2)Impaired splanchnic perfusion-translocation of gut 2)Impaired perfusionbacteria. Most common infection is aspiration pneumonia. Most Recommendation:-Empirical antibiotics in severely ill Recommendation:patients without delay. COMMUNITY ACQUIRED BACTERIAL INFECTIONS IN SEVERE MALARIA PARAMETER SEVERE MALARIA(n=93) MALARIA(n=93) LESS SEVERE MALARIA Number of episodes 13(14%) 6(6%) Number of patients 13(14%) 6(6%) Site of infection 17 6 Pneumonia 6 1 Bacteremia 5 1 Urinary tract infection 3 1 Miscellaneous 3 3 6 LAB DIAGNOSIS OF MALARIA METHOD ADVANTAGE 1) Thick blood film • DISADVANTAGE Sensitive(0.001% parasitemia) parasitemia) •Species specific. •Inexpensive. Requires experience. Underestimates true count. • • Rapid Species specific. •Provides prognostic information in severe malaria. •Insensitive (>0.05% parasitemia). parasitemia). •Uneven distribution of P.vivax. P.vivax. Rapid Sensitivity similar to or slightly less than thick film (>0.001% parasitemia). parasitemia). Detects only P.falci. P.falci. Remains +ve after weeks of +ve infection. •Does not give quantitative analysis. 4) Plasmodium LDH dipstick or card test Rapid Sensitivity similar to PFHRP2dipstick. •Less sensitive diagnosis for P.vivax,malarie and ovale. ovale. •Slightly more difficult than PFHRP2. •Miss low levels of parasitemia with other malarias. •Does not provide quantitative analysis. 5)Membrane concentration methods with acridine orange staining •Sensitivity similar or superior to that of thick films (~ 0.001% parasitemia). parasitemia). •Ideal for processing large no. of samples rapidly. Does not specify or quantitate. quantitate. Requires fluorescence microscopy. 2)Thin blood film • • 3)PFHRP2 dipstick or card test • • • • • • • • PROGNOSTIC MARKERS IN MALARIA PARAMETER SURVIVORS (n=83) NONSURVIVORS (n=10) P VALUE Unrousable coma,n(%) coma,n(%) 25(30) 9(90) <0.001 Severe anaemia,n(%) 7(8) anaemia,n(%) 1(10) 1 Renal failure,n(%) failure,n(%) 40(48) 7(70) 0.3 Pulmonary edema,n(%) edema,n(%) 5(6) 5(50) <0.001 Hypoglycemia,n(%) Hypoglycemia,n(%) 3(4) 0 1 Shock,n(%) Shock,n(%) 12(15) 8(80) <0.001 Bleeding/DIC,n(%) Bleeding/DIC,n(%) 19(23) 3(30) 0.7 Seizures,n(%) Seizures,n(%) 2(2) 0 1 Acidosis,n(%) Acidosis,n(%) 11(13) 8(80) <0.001 Coma and acidosis,n(%) acidosis,n(%) 2(2) 8(80) <0.001 Coma and shock,n(%) shock,n(%) 3(4) 8(80) <0.001 Parasitemia of more than 5%,n(%) 32/79(41) 7/9(78) 0.07 7 TREATMENT OF SEVERE FALCIPARUM MALARIA Trial No. of patients (SEAQUAMAT) (SEAQUAMAT) 1461 Wellcome Trust Clinical Research 560 Unit Faculty of Tropical Medicine, Mahidol University 131 Faculty of Tropical Faculty Medicine, Mahidol University 102 Drugs Results Reference Artes(730) Vs. Quin(731) 34.7% absolute mortality Lancet 2005; 366: 717–25 717– Artem(284) Vs. Quin(276) Faster Parasite clearance N Engl J Med. 1996 Jul 11;335(2):76-83. 11;335(2):76- Faster Parasite clearance, mortality Clin Infect Dis. 2003 Clin Jul 1;37(1):7-16 1;37(1):7- Faster Parasite clearance, mortality Trans R Soc Trop Med Hyg. 1995 NovHyg. Nov- Artes Vs. Quin Artem(50) Vs. Quin(52) Dec;89(6):668-71. Dec;89(6):668- CURRENT RECOMMENDATION Artimisinin derivatives like artisunate , artimether are drug of Artimisinin choice for severe malaria. Artisunate has the advantage of being water soluble and can be Artisunate given I.V. 8 CURRENT RECOMMENDATION FOR EXCHANGE BLOOD TRANSFUSION Currently there are no randomized control trials to show any Currently benefits of exchange blood transfusion over conventional therapy. Procedure is hazardous and availability of blood is a limiting Procedure factor. Currently WHO does not recommend exchange blood Currently transfusion in the management of severe malaria. OTHER ADJUVANT THERAPY Corticosteroids Corticosteroids No survival benefit No GI bleed GI Anticonvulsants Anticonvulsants Phenobarb Phenobarb Others Others Adrenaline Adrenaline Heparin Heparin Prostacyclin Prostacyclin Pentoxyfylline - No established role Pentoxyfylline Cyclosporin A Cyclosporin Iron chelators Iron Anti TNF Anti 9 ROLE OF aPC IN MALARIA/LEPTOSPIROSIS Report Clinical scenario Inference Reference Drotrecogin alfa (activated) in severe falciparum malaria severe falciparum malaria parasitaemia levels of 40% MODS aPC for 96 hrs f/b gradual improvement Anaesthesia, 2006, Anaesthesia, 61, pages 899–902 899– Case series of 10 patients with tropical infections Includes 4 cases of falciparum and I leptospirosis 1 out 4 died Intensive care Med (2006) 32:1281– 32:1281– 1282 LEPTOSPIROSIS 10 INTRODUCTION Zoonotic disease. Zoonotic Transmitted by contact with infected urine and rarely Transmitted blood of infected rodent. Penetration recurs through intact mucous membrane Penetration or abraded skin. PATHOGENESIS Septicemic phase – vascular injury Septicemic Immune phase – immune complex deposition Immune 11 PATHOGENESIS OF LUNG INJURY In contrast to liver and kidney, isolation of leptospires is In uncommon from lung tissue. Antigenic debris is also less common in lungs. Antigenic Widespread but subtle inflammatory process. Widespread Presence of antibody along the septal wall in infected guinea Presence pigs may suggest an autoimmune response similar to Goodpastures disease (Abs to type IV collagen).But renal tissue did not reveal glomerulonephritis characteristic of Goodpasture disease. The exact mechanism is largely unknown. The CLASSICAL FEATURES OF LEPTOSPIROSIS CLASSICAL Biphasic illness -1)Septicemic phase Biphasic 2)Brief afebrile period 3)Immune phase (liver and kidney) Diagnosis in early phase is commonly missed. Diagnosis Hence Faine proposed a clinical scoring system which has Hence good sensitivity (81.8%) and specicity(72.9%). Usually helpful in excluding diagnosis because of high Usually negative predictive value. J Postgraduate Med.2005 Sept.51(3),169 Post 12 LUNG INVOLVEMENT Ist publication of lung involvement in leptospirosis is Ist attributable to Moeschlin in 1943. Varies between 20%-70% in all cases in various studies. Varies 20%Pulmonary examination ranges from normal to extensive Pulmonary alveolar hemorrhage and respiratory failure. Patients with severe alveolar hemorrhage can die within 24 Patients hrs. BAL examination in patients with leptospirosis by D u couedic BAL and colleagues found that alveolar hemmorrhage was present in all patients with sign /symptom of respiratory involvement and 7/10 patients in asymptomatic patients. Med Trop.1992,25:21-30 Trop.1992,25:21- 13 LUNG INVOLVEMENT (CONTD) There is absence of significant inflammation in areas of There hemorrhage. Usually associated with hepato-renal involvement but can Usually hepatooccur in the absence of these. J.Infect.Disease.1998;178;1457-63 J.Infect.Disease.1998;178;1457- LAB DIAGNOSIS OF LEPTOSPIROSIS TEST ADVANTAGE DISADVANTAGE DGM Convenient Lacks sensitivity and specificity. Immunofluoroscent staining Can be done on blood, urine or rarely CSF. 10,000 leptospira/ml for leptospira/ml visualization is necessary. Immunoperoxidase staining Can be done on blood, urine or rarely CSF. 10,000 leptospira/ml for leptospira/ml visualization is necessary. A)MICROSCOPY 14 LAB DIAGNOSIS OF LEPTOSPIROSIS TEST ADVANTAGE DISADVANTAGE B) SEROLOGY MAT Complex Gold standard Requires maintaining strains Highly sensitive Detects group specific Abs. for preparation of Ag. IgM ELISA Most widely used ( sensitivity 100% and specificity 93%) IgG ELISA High rate of false positive. Indirect Fluorescent Rapidity Antibody test Microscopic slide agglutination High sensitivity and specificity CIEP LAB DIAGNOSIS OF LEPTOSPIROSIS LAB TEST ADVANTAGE DISADVANTAGE C) Culture Gives confirmed diagnosis Low sensitivity Cumbersome Requires atleast 1 month before can be declared negative D) Molecular diagnosis 1)Dot blotting 2)In situ hybridization 3)PCR Useful for DNA detection in serum and urine. Useful when other tests fail to establish diagnosis. Used for post mortem diagnosis. Inability to identify serovar. serovar. Cost and availability. 15 PROGNOSTIC MARKERS Multivariate analysis revealed three variables associated Multivariate with mortality VARIABLE ODDS RATIO P VALUE Hemodynamic disturbance 6 (CI 0.9-38.5) 0.9- 0.005 Serum 10.6 (0.9-123.9) (0.9creatinine>265.2um creatinine>265.2um ol/l 0.02 Serum potassium>4 19.9 (1.2-342) (1.2- 0.009 TREATMENT OF LEPTOSPIROSIS Ceftriaxone was found effective in severe Ceftriaxone leptospirosis in a study by Raptis et al . 23 patients were given ceftriaxone out of which 21 23 survived.No significant ADR noted. Int J Antimicrobial Agent 2006 Sept,28(3);259-61 Sept,28(3);259- 16 TREATMENT OF LEPTOSPIROSIS A prospective,open label, randomized trial in prospective,open Thialand was conducted in 2000-2001,where they compared ceftriaxone(1 gm/day for 7 days) with sodium penicillin G (1.5 MU 6 hrly for 7 days). Both were found equally effective with median Both duration of fever was 3 days and equal number of deaths (5) were found in each group. ROLE OF STEROIDS IN LEPTOSPIROSIS 17 AMOEBIASIS INTRODUCTION Protozoan infection caused by Entamoeba histolytica. Protozoan histolytica. Third most common cause of death from parasitic diseases Third after malaria and schistosomiasis worldwide. Extraintestinal manifestations are the most comon cause of Extraintestinal death. 18 EXTRAINTESTINAL SITES INVOLVED 1) 2) 3) 4) 5) Amoebic liver abscess-most common. abscessPleuro-pulmonary – second most common. PleuroPericardial. Brain. Genitourinary tract. RISK FACTORS FOR AMOEBIASIS 5) Lower socio-economic class Poor hygiene Lack of safe drinking water Male homosexuals Travellers 6) Prisoners 1) 2) 3) 4) 19 RISK FACTORS FOR PULMONARY AMOEBIASIS 1) 2) 2) 3) Malnutrition Alcoholism ASD with left to right shunt MODES OF PULMONARY INVOLVEMENT Primary - Very rare Primary - Inhalation of dust containing cysts. - Aspiration of cysts or triphozoites of amoeba. Secondary- Infrequent. Secondary- Hematogenous spread from colon. Tertiary - Most common. Extension of amoebic liver abscess Tertiary 20 ROUTES OF INVOLVEMENT Routes of involvement 1) Abcess extending from liver 2) Bronchohepatic 3) Empyema extending from liver 4) Hematogenous spread without liver involvement 5) Hematogenous lung abcess and independent liver abcess Percent 37.2 19.6 17.6 14.3 10.4 TYPES OF LUNG INVOLVEMENT Types of lung involvement 1) Heptobronchial fistula 2) Pleural effusion and empyema 3) Lung abscess 4) Consolidation Percent 47 19 14 10 21 CLINICAL FEATURES Fever of weeks duration and right upper abdominal and right Fever pleuritic type of chest pain. Dramatic presentation of severe pain,respiratory distress and Dramatic shock. Hepatomegaly in 50% cases. Hepatomegaly Hemoptysis is common followed by expectoration of Hemoptysis ancchovy sauce like pus. Bile in sputum is important clue toward hepatic origin. Bile DIAGNOSIS When to suspect amoebiasisWhen amoebiasis1)Elevated hemidiaphragm. hemidiaphragm. 2)Hepatomegaly. 3)Pleural effusion. 4)Basal pulmonary involvement in patient from endemic area >3 years age. 22 DIAGNOSIS 1) 2) 3) 4) 5) Lateral radiograph: Lateral Upward hump like prominance which can be anterior, middle or posterior.Anterior hump is more common. Consolidation which may have cavitation. cavitation. Pleural effusion. Hydropneumothorax-bronchopleural fistula. HydropneumothoraxCavity with air fluid level in case of bronchial communication. DIAGNOSIS DIAGNOSIS Stool examionation :Limited value. Limited Only positive in 15-33% cases of extraintestinal amoebiasis. Only 15amoebiasis. Pathogenic and nonpathogenic amoeba can be differentiated Pathogenic by zymodeme analysis,ELISA,RFLP. analysis,ELISA,RFLP. Sputum examination ::Usually sterile and paucicellular unless superinfected. Usually superinfected. 23 ROLE OF ULTRASONOGRAPHY Monitoring response to therapy. Monitoring To detect small pleural effusion. To To look for subpulmonic collection. To To differentiate from bacterial empyemas – loculations and To septations are rare in amoebic empyemas. empyemas. WHAT IS ROLE OF CT SCAN? Can detect intrapleural fluid anywhere in the thorax example Can beneath scapula or within fissure which is usually missed by USG. Guide interventional procedure. Guide To differentiate empyema with bronchopleural fistula from To lung abscess. 24 IMMUNOLOGICAL TESTS IN AMOEBIASIS A)ConventionalA)Conventional1)IHA 2)ELISA for IgG and IgM , IgM is more specific 3) IFAT B)NewerB)Newer1) Gal or GalNAC inhibitable - Potential role in extraintestinal adherence lectin IgM amoebiasis. amoebiasis. 2) Gal-GalNAC Ag by ELISA- >90% sensitivity before Gal ELISA treatment. 3) E.histolytica Ag detection kit- useful for sputum and pleural kitfluid. 4) DNA by PCR- most sensitive method of detection of pleuropulmonary PCRamoebiasis. amoebiasis. DIFFERENTIAL DIAGNOSIS OF AMOEBIASIS Lung carcinoma Lung Pulmonary tuberculosis Pulmonary Lung abscess Lung Sarcoidosis Sarcoidosis Hydatidosis Hydatidosis Presence of palpable liver can be mistaken as secondary. Presence Anterior basal segment of right lower lobe involvement is Anterior characteristic of amoebic origin. 25 TREATMENT OF AMOEBIASIS Oral or parentral metronidazole 800 mg (35-50 mg/kg/day) Oral (35three times daily for 5-10 days is the treatment of choice. 5Chloroquin and emetine are other alternatives but should be Chloroquin avoided because of potential cardiovascular side effects. PULMONARY HYDATID 26 INTRODUCTION Hydatidosis is one of the most geographically Hydatidosis widespread zoonoses in the world. Four species of Echinococcus are recognised. Four EPIDEMIOLOGY OF HYDATID DISEASE Species Geographical Definitive Intermediate Transmission distribution Host Host E.granulos Mediterrean region,eastern us Dogs Sheeps Feco-oral route Feco- Rodents Ingestion Europe,Africa,South america middle east,China,Australia, New Zealand E.multiloc Arctic,Asia,Wester Foxes, ularis n central europe Wolves E.Vogeli South America --- --- E.oligarthia South America --- --- 27 LUNG INVOVLEMENT IN HYDATID Through transdiaphragmatic thoracic involvement- most Through involvementcommon. Hematogenous dissemination. Hematogenous Lymphatic dissemination. Lymphatic LUNG INVOLVEMENT IN HYDATID Sometimes lesions develop in area of lung remote from Sometimes diaphragmdiaphragm1)Hematogenous spread. 2)Transbronchial spread. 3)Rupture of liver abscess into inferior vena cava and thromboembolic disease which may progress to pulmonary hypertension and cor pulmonale. pulmonale. 28 PLEURO-PULMONARY MANIFESTATIONS OF HYDATID HYDATID CYST RUPTURE PLEURAL SPACE BRONCHUS ASYMPTOMATIC PRESSURE EFFECT COUGH DYSPNOEA PNUEMOTHORAX PERSISTENT PNUEMONIA PLEURAL EFFUSION RECURRENT HEMOPTYSIS EMPYEMA CHEST PAIN VOMIT LIKE CYSTIC FLUID ALLERGIC OR ANAPHYLACTIC REACTION DIAGNOSIS OF HYDATID DISEASE 1) Specific serum antibodies. 2) Chest X-ray – XSolitary lesions- 60% cases. Solitary lesionsMultiple –unilateral/bilateral lesions in 25-50%. Multiple 25Ruptured cyst-Consolidation surrounding area. Ruptured cystIt communicates with bronchus-air fluid level. bronchusMiniscus sign or crescent sign. Miniscus Cumbo’s sign (onion peel sign). Cumbo’ Water lily sign. Water Mass within a cavity. Mass Newer signs Rim sign. Rim Inverse crescent sign. Inverse 29 TREATMENT OF PULMONARY HYDATID Surgery is the mainstay of the therapy – as complete Surgery elimination of parasite can only lead to cure. The principle is to preserve as much lung tissue as possible. The Akin et al observed that radical resection is too aggressive and Akin often not necessary. Paraenchyma around a hydatid cyst is often affected by lesion Paraenchyma and may show chronic congestion,hemorrhage,bronchopneumonia or interstitial pneumonia. These changes often resolve after surgery, hence parenchymal These resection is rarely indicated. TREATMENT OF PULMONARY HYDATID (CONTD) Conservative surgery are preferred. 1)Enucleation. 2)Pericystectomy. 3)Simple cystectomy. cystectomy. 4)Cystectomy with cappitonage. cappitonage. Spillage of daughter cyst is to be avoided. Spillage Recurrence can occur but fresh infection is also reported in Recurrence person living in endemic area. Bilateral pulmonary hydatid :One stage/two stage surgery. One Larger cyst/ruptured cyst area treated first. Larger 30 RECENT ADVANCES N THE TREATMENT OF PULMONARY HYDATID Thoracophrenotomy is less invasive & preferred method of Thoracophrenotomy surgery in cases of combined lung & liver hydatid Br.J.surg.2005;92(6);729-33 Br.J.surg.2005;92(6);729- Recent reports have described VATS in pulmonary hydatid. Recent CAN J SURG.2004;47,380-381 SURG.2004;47,380- TREATMENT OF PULMONARY HYDATID (CONTD) Medical therapy:Medical Advocated by few authors. Advocated Mebendazole/Albendazole. Mebendazole/Albendazole. 68-70% of patients with pulmonary hydatid show some degree 68of response. 25-34% cure rates have been documented. 25Considering high risk of complications, hydatidosis patients Considering should be followed closely. PARASITOL.INT.2005;54;135-138 PARASITOL.INT.2005;54;135- 31 DRAWBACKS OF MEDICAL THERAPY Poor compliance and ADR due to long course of treatment. Poor Poor follow up – most patients are from rural areas. Poor Poor cure rates. Poor High risk of complications. High CONSENSUS Lung hydatids produce more complications than liver,hence all Lung patients of pulmonary hydatid irrespective of size or presence/absence of complications are to be surgically treated. Medical therapy should be used to prevent recurrence. Medical Recommended regimen – mebendazole 1 month preoperative Recommended & 3 interrupted courses postoperatively 32 TROPICAL PULMONARY EOSINOPHILIA (FILARIASIS IN LUNG) INTRODUCTION One of the many syndromes with pulmonary infiltrates and One peripheral blood eosinophilia. eosinophilia. Originally described in India in 1940. Originally ILD thought to be due to immunological hyperresponsiveness ILD to human lymphatic dwelling filarial parasites-W.bancrofti and parasitesB.malayi. B.malayi. 33 DIAGNOSTIC CRITERIA FOR TPE Cough worse at night. Cough count >3300/cube mm. count Clinical Residence in filarial endemic areas. Clinical Eosinophil and hematological response to DEC. Eosinophil Filarial antibody test has little value. RESP. MED. 1999;93;655-659 1999;93;655- PATHOGENESIS Out of 90 million people infected worldwide,<1% Out manifest symptoms of TPE. Exact reason is not known. Exact Intense inflammation of lung parenchyma to trapped Intense microfilaria which are released into circulation by adult worms residing in lymphatic system. Microfilaria are always absent in peripheral blood Microfilaria smear. Sometimes detected in lung biopsy specimens. Sometimes 34 PATHOGENESIS (CONTD…) BAL of affected individuals reveal that polyclonal IgE and BAL filarial specific IgM,IgG and IgE accumulate in the lung. Eosinophilic alveolitis. Eosinophilic alveolitis. Profound dysregulation in otherwise tightly regulated IgE Ab Profound response. Limited evidence to suggest underlying genetic basis. Limited Usually complete resolution after therapy with DEC but in Usually some cases some degree of irreversible interstitial fibrosis occurs. Pathogenesis in some aspects analogues to atopic asthma Pathogenesis - obstructive ventilatory picture. - partial reversibility with beta2 agonists. - high levels of serum IgE. IgE. 35 ...
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This note was uploaded on 12/03/2011 for the course MEDICINE 350 taught by Professor Dr.aslam during the Winter '07 term at Medical College.

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