Tuberculosis is a classic example of “host parasite” relationship. The host response in tuberculosis is the result of quantitative and qualitative interactions to various constituents of the wall of the bacillus which acting as foreign substance mobilize the immune response of the host. The net result is due to the interplay of cell-mediated immunity and delayed hypersensitivity.1

Tubercle bacilli, when they infect man are rapidly phagocytosed by Polymorph-neutrophils cells, in which they rapidly multiply and then kill them. Next, the battle is taken up by macrophages, which are derived from bone marrow and constitute the reticuloendothelial system. In lungs they are concentrated as alveolar macrophages, which play an important role in defense against tubercle bacilli. Macrophages are the body’s mechanism for expressing Tuberculo-Immunity. But how, it is a mystery. Later on it was established that lymphocytes from immune animals were the “Affecter Cells”. It is proved that immunity to tuberculosis was lymphokine mediated. Lymphokines are produced by lymphocytes. The lymphocytes modulate the functions of macrophages, T cells are the “Affecter Cells” of cell-mediated immunity.2 They regulate all types of response by either activity as helper or suppressor cells. Tuberculosis is still common in India and tuberculosis pleural effusion is one of the most common forms of extra pulmonary tuberculosis. The diagnoses of tuberculosis pleural effusion can be established directly by Demonstrating tubercle bacilli in pleural effusion, fluid or pleural biopsy specimen or Antibody or antigen detection in either sputum or pleural fluid, pleural fluid polymerase chain reaction (PCR) for mycobacterium tuberculosis

Indirect evidence with granuloma in pleura or increased level of pleural fluid adenosine deaminase. A couple of antigens secreted by M tuberculosis have been purified, which are present both in inactive and active tuberculosis e.g. 17 Kda to 80 Kda were recognized by the IgG antibodies present in the plasma of active and inactive TB patients. These antigens3,4 are responsible for increasing humoralresponse (IgM, IgG, IgA) which usually peaks after the Tcell medicated immune response has declined. This antibody response shows promising results for the diagnoses of pulmonary and extra pulmonary tuberculosis. However, recent reports have revealed a discrepancy in different study populations.

The aim of this study is to confirm the comparative diagnostic value of serum and pleural fluid effusion, antibody test (IgG, IgA) and ADA test in patients presenting with pleural effusion.

Fifty patients who underwent diagnostic evaluation for pleural effusion between March 1999 and March 2002 at Mumbadevi Homoeopathic Hospital Pathology Laboratory along with 50 non-Tuberculous Pleural effusion (Lymphocytic) patients who were enrolled in this study. The patients were aged 13 years or more and were diagnosed as having pleural effusion by clinical symptoms, physical examination and radiographic evidence. Patients with clinical suspicion of human deficiency virus co-infection were tested after counselling.

Pleural tap was performed under local anaesthesia and aseptic precaution.

About 50 ml of fluid was collected

5 ml for cell count and differential count

The diagnostic criteria were MT +ve, Pleural fluid TB IgG, IgA +ve or -ve.

25 ml for protein and sugar and adenine deaminase

5 ml for antibody estimation TB IgG, IgA, by ELISA technique.

Simultaneously serum sample were also collected for ADA and TB IgG, TB IgA were estimated by ELISA (enzyme linked immuno-sorbant Assay). Using Andaelisa mycobacterium karactac kit Deaminase by deaminase kit by Giust’s method.

Pleural fluid sugar, proteins by GODPOD and Biurete from Ranbaxy Ltd. and Biolab Ltd. Mantoux test (intradermal test) by using PPD from Span Diagnostic 10 Tu.

Lymphocyte count increased in pleural fluid, Protein increased; sugar decreased in pleural fluid and haemorrhage in pleural fluids were determined. Any one or two positive parameters were considered for diagnosis.

Tuberculosis is entirely regulated by cell mediated immune response (CMI) of the host. When bacillary antigens are present at low levels the CMI response causes macrophages to accumulate, get activated and then destroy the bacilli. When the bacillary antigen are present at high levels the CMI response causes necrosis of tissue.5-6

Immune response against myc. Tuberculosis involves both macrophages and lymphocytes, dead organism, are broken down relatively within the granuloma, releasing large quantities of glyco-lipid and polysaccharides, antigen into the draining lymphnodes leads to predominately humoral immune response.

But viable mycobacterium release small quantities of glycoproteins, antigen which induces a delayed hyper sensitivity and cell mediated immune response.

When more and more tubercle bacilli are killed by the immune host, good amount of glycolipid and polysaccharide antigens are released from the cell wall of Mycobacterium Tuberculosis. These antigens are responsible for increasing humoral response (IgM IgA) which peak after the T cell mediated immune response has declined.7,8

TBIgA has a potent inflammatory potential. Immune complexes with IgA activate complement and can trigger inflammation in different organs. During an infection (Asymptomatic or overt), the production of IgA antibodies occur usually after the initial surge of IgM antibodies. The presence of IgA antibodies occur usually after the initial surge of IgM antibodies. The presence of IgA antibodies in the serum, sputum other biological fluids of tuberculosis patients indicates that the immunological response of these patients has been partially or totally misdirected, on rare occasions, it is the only specific antibody that can be detected. Its search is thus warranted when an immune anergy has depressed the synthesis of IgM and IgG antibodies.9-12

In tuberculosis patients suffering from extrapulmonary infections. The presence of IgA antibodies detected in body fluids at a 1:20 dilution (pleural fluid, pericardial etc.) is a sure sign of a mycobacterial infection and its detection in these fluids is, in difficult cases a precious diagnostic clue that complements the seric detection of TBIgM antibodies.13,14

TBIgG antibodies appear when an infection becomes established. This indicates a good immunological response of the patients to the infection.

TBIgM plus TBIgG measurements are analyzed together to detect reactivation cases in chronic infection.

TBIgM plus TBIgG measurements are analyzed together to detect reactivation cases in chronic infection.

TBIgG antibodies are routinely analysed in chronic infection and during therapy. They give an evaluation of the activity of the disease. A successful therapy, is often accompanied by an increase in IgG titres, followed of course by a decrease at the end of the therapy.15-16 Persistence of low levels of antibodies after therapy is supposed to indicate the presence of non-evacuated antigenic pouches. TBIgA antibodies are applied in difficult cases presenting an anergy i.e. lack of tuberculin reactivity and no synthesis of IgG antibodies TBIgA antibodies strengthen the diagnosis in cases of suspected meningitis, pleuritis and pericarditis renal tuberculosis and AIDS syndrome.16

In the present study pleural fluid TBIgG and TBIgA antibodies and ADA values were significantly higher than in serum.

Higher Titres of TBIgG were supposed to be due to active disease which can be clearly distinguish from control. TBIgG (Anti 60 to IgG) were supposed to be more specific than total IgG levels. Many workers have reported lower IgG titres in primary tuberculosis than in past primary tuberculosis. This might be the reason of low positivity in 0-14 yrs of age group patients as chances of primary TB aremore in younger patient11-12 Patel et al have been also reported low of sero positivity in childhood tuberculosis.5-8

ADA levels in non-tubercular lymph pleural effusion seldom exceeds the diagnostic cut off for TB effusion.17-19 ADA levels cannot be predicted from total or differentiated Leucocyte count. ADA is stable in effusion fluid and it is measurement in reproducible in pleural fluid ADA were significantly higher in TB as compared with control group. Pleural fluid ADA were higher than serum ADA in TB as compared with control group.20-23

Pleural fluid ADA was found to have a sensitivity of 96% and specificity of 96%. The mean values of pleural fluid ADA in tuberculosis group were higher positive, which was significantly higher than control group. Because of low sensitivity of microscopic examination of pleural fluid for tubercular bacilli. Pleural fluid ADA may be investigation of choice in diagnosis of tuberculous pleuritis and pleural biopsy in selected cases.24-26

From the study it is concluded that it is possible to avoid pleural biopsy and do pleural fluid ADA, TBIgA TBIgG to ascertain the diagnosis of Tubercular Pleuritis.