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HIV & TB

HIV & TB. ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara , Nepal. Mature in B.marrow to become “B LYMPHOCYTE” react with free antigen directly. stem cells Lymphocytes. plasma cells. Thymus. T cells. recognise the antigen with the help of macrophages.

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HIV & TB

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  1. HIV & TB ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal

  2. Mature in B.marrow to become “B LYMPHOCYTE” react with free antigen directly stem cellsLymphocytes plasma cells Thymus T cells recognise the antigenwith the help of macrophages Cytotoxic T cells Helper T cells (CD4 surface protein) activated lymphocytes enter the tissue and meet antigen again results in multiplication and secretion of cytokines or immunoglobins in order to destroy the antigen Th1 cells - involved in cell mediated immunity. Produce interferon gamma, interleukin 2 & TNF beta. Th2 cells: play a role in humoral responses responsible for Atopy and allergy

  3. Immune response in T.B. Infection It manages to evoke both immunity & hypersensitivity in the body • Immunity – Good for body –not good for bacteria It localizes the bacteria and clears the infection efficiently with out causing much tissue destruction • Hypersensitivity – good for bacteria – not good for body • Infection can not be localized • Plenty of tissue destruction with on going caseation & necrosis

  4. HIV & TB

  5. Introduction • Tuberculosis and HIV - closely linked since the emergence of AIDS. HIV infection has contributed to a significant increase in the worldwide incidence of tuberculosis • Over 4 million persons worldwide have been infected with HIV and tuberculosis • Most common cause of death in AIDS patients

  6. Have instantly clicked together & linked since the emergence of AIDS • Love at first sight • No generation gap

  7. HIV & TB both affect each other T.B. HIV

  8. Effect of HIV on TB HIV T.B.

  9. HIV increases the incidence of TB

  10. Now answer these 2 questions: • What % of world population get Mycobacterium infection at some point in their life (without developing active disease) ? • Of them how many of develop active disease ?

  11. HIV increases the T.B. infection • It is estimated that 1/3rd population of the world are infected by the Mycobacterium tuberculosis • Out of them only 10% have life time chances of developing tuberculosis • This scenario is changing with the advent of HIV infection

  12. Tuberculosis normally develop through:- • progression of recently acquired infection -primary disease • reactivation of latent infection • exogenous reinfection

  13. Concomitant HIV infection increases the possibility of development of T.B. in all the above categories • People co-infected with both HIV and latent TB have an up to 800% greater risk of developing active tuberculosis disease and becoming infectious compared to people not infected with HIV

  14. Gohn focus

  15. Now answer these questions: • What is the main lesion in post primary T.B. • Is there hilar lymphadenopathy • Which lobes are predominently affected • What is the likelihood of pleural effusion

  16. Clinical features of HIV-associated post primary pulmonary tuberculosis (in adults) are frequently atypical, particularly in the late stage of HIV infection • Non-cavitary disease • Lower lobe infiltrates • Hilar lymphadenopathy • Pleural effusion -Lack of hypersensitivity Lack of immunity

  17. Immunity Hypersensitivity

  18. Tuberculosis can be a relatively early manifestation of HIV-1 infection • Risk of developing tuberculosis, and of disseminated infection, increases as the CD4 T-cell count decreases

  19. Immune system is unable to contain the infection resulting in: • An increased frequency of extrapulmonary tuberculosis • Positive mycobacterial blood cultures • Atypical chest radiographic findings

  20. Patients with extrapulmonary tuberculosis may present with signs and symptoms specific to the involved site, such as • lymphadenopathy • headache • meningismus • pyuria • abscess formation • back pain • abdominal pain

  21. Increased incidence of MDR TB in HIV • Acquired resistance (Organisms are sensitive at the beginning) in MDR TB is associated with co-infection due to HIV & tuberculosis • In MDRTB outbreaks approximately 90% of the cases were HIV seropositive

  22. Spread of TB poses a serious threat to the world health scenario Multi Drug Resistant

  23. Summary Effect of HIV on TB: • Increases the incidence of TB by converting the latent infection into active one • Changes the clinical features of the post primary tuberculosis • non-cavitary disease • lower lobe infiltrates • hilar lymphadenopathy • pleural effusion • More extrapulmonary involvement • Increased incidence of MDR TB in HIV

  24. T.B. HIV

  25. T.B. – opportunistic infection in HIV/AIDS • Relatively early manifestation of HIV-1 infection median CD4 T-cell count was >300 cells/mm3 • Risk of developing tuberculosis & of disseminated infection, increases as the CD4 T-cell count decreases What is normal CD4 cell count ? 600 -1200/ml

  26. AIDS generally occurs when • CD4 count is below 200/mL • or a CD4 lymphocyte percentage below 14% • Characterized by the appearance of opportunistic infections, eg.: • Tuberculosis • Pneumocystis carinii pneumonia • Toxoplasmosis • Meningitis and other brain infections • Fungal infections • Malignancies: lymphoma, cervical Ca., Kaposi's sarcoma

  27. Tuberculosis acts to accelerate the clinical course of HIV infection • 5- to 160-fold increase in viral replication during the acute phase of untreated tuberculosis leads to increased HIV viral load

  28. Clinical Presentation of Tuberculosiswith HIV

  29. Diagnostic difficulties initially because the early symptom - fever, weight loss, and malaise in both TB & HIV are same • Earlier in the course of HIV disease TB is more likely to present as classical reactivation-type disease • Patients with advanced immuno suppression are more likely to present with findings consistent with primary tuberculosis

  30. bilateral hilar lymphadenopathy with diffuse interstitial and airspace opacities. CD4 count<200

  31. Extensive right paratracheal lymphadenopathy

  32. Treatment of HIV-Related Tuberculosis

  33. Good, early clinical response to therapy as long as the regimen contains INH and a Rifampicin • Sputum culture conversion & treatment failure rates were similar to those in patients without HIV infection

  34. Treatment of HIV & TB together poses many problems

  35. Requires close monitoring because • Development of resistance • Frequent drug toxicities • Possible drug-drug interactions • Paradoxical reactions

  36. Rifamycins: • Rifampicin or Rifampin • Rifabutin • Rifapentine – long acting so only once a week dose required

  37. Patients treated with a once-weekly Isoniazid /Rifapentine continuation-phase regimen Relapse with rifamycin monoresistant T.B. In HIV-seropositive tuberculosis • HIV-seropositive people with tuberculosis should not be treated with a once-weekly isoniazid/rifapentine regimen

  38. Adverse drug reactions • Most commonly seen with Rifampicin • Rifampicin should be avoided/replaced • Rash - Thiacetazone should not be used in the treatment of HIV-related tuberculosis because of skin reactions • Paresthesia – B6 should be given with INH • Incidence of drug induced hepatitis is many times more in HIV+ TB patients - Frequent monitoring of liver function tests are required

  39. Drug-Drug Interactions

  40. Certain antituberculosis drugs may interact adversely with medications commonly used by HIV-infected individuals • Rifamycin derivatives • Rifampicin(most potent inducer) • Rifabutin • Rifapentine(less potent) induce the hepatic cytochrome P450 enzyme system

  41. Results in increased metabolism & reduced serum levels of certain drugs which includes • protease inhibitors (PIs) • nonnucleoside reverse transcriptase inhibitors (NNRTIs) Used for the treatment of AIDS

  42. This results in subtherapeutic levels and the potential development of viral resistance to these important agents • Rifabutin can be substituted for Rifampicin in the treatment regimen

  43. PIs and NNRTIs affect the metabolism of rifabutin, resulting in altered serum levels and the possibility of drug toxicity, adjustments in rifabutin dosage are often necessary • Patients can take the standard rifampin-based treatment regimen if not taking PIs or NNRTIs

  44. Paradoxical Reactions

  45. Temporary exacerbation of symptoms, signs, or radiographic manifestations of tuberculosis seen after beginning ATT • Occur in HIV-infected patients with active tuberculosis • Develop after simultaneous administration of both antiretroviral & ATT

  46. Due to increase in the cellular immunity caused by ART • Diagnosis of a paradoxical reaction should be made after a thorough evaluation to exclude other etiologies, such as tuberculosis treatment failure

  47. Initiation of Antiretroviral Therapy in coinfected Patient No standard regimens! . Lot of confusion & uncertainity prevails at present

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