TB Flashcards
TB Susceptible treatment
2HRZE4HR
TB Shorter treatment
Consider in milder disease - no cavitation and smear <2+ BUT stratifying treatment is difficult in a high burden setting
TB Natural history
Most infection does not lead to disease, infection is a dynamic continuum not a binary state, self-cure is probably common but we cannot test for it, active pulmonary TB is a chronic cavitatory pneumonia. TB further impoverishes the poor
TB Key clinical features of PTB
Cough, fever, weight loss, night sweats are cardinal features
TB Diagnostic approach PTB
Sputum is key sample, microscopy widely used and detects the most infectious cases but misses half. Auramine improves performance over ZN. Xpert MTB/RIF detects MTB DNA. Sputum culture is usedd less and less, mainly if concerned about drug resistance. CXR useful and automated (CAD) reading of digital imaging increases access
TB Therapeutic principles
Multidrug therapy for 6m remains standard (2HRZE4HR), shorter 4m regimens endorsed but not implemented, TRUNCATE-TB shows we can go shorter if we can find the right regimen
TB Access
TB diagnostic and treatment services are free of charge in the public sector
TB Vaccines
TB vaccine enthusiasts believe no attempt at TB control will work without a new, effective vaccine, BCG is most widely used but efficacy is limited, objective of vaccine design (and thus study population in vaccine trials) vary, particular focus on prevention of infection (POI) and prevention of disease (POD) in those already infected, major hurdle is correlate of protection - there is no Ab level or other biomarker identified that can predict a vaccine will work, so large and long trials are needed. Therapeutic vaccines aim to improve outcome of treatment of active disease (add to standard treatment) tough as standard treatment already works well
TB LTBI Diagnosis
TST and IGRA are tests of immunoreactivity (not viable latent infection). Indeterminate IGRA means no assessment of TB risk can be made - the test is not valid, the PPV ~5% (fewer than 5% with positive result will go on to develop active TB disease)
TB LTBI Treatment
6H or 3HP (weekly) or 1HP (daily) - (P=rifapentine)
TB Epidemiology
Global TB report tracks national and global data on TB diagnosis, treatment, prevention, screening, financing, social determinants and research - also tracks progress against END-TB targets - progress has been glacial, and short on intermediate milestones, 70% TB burden in 8 countries
TB WHO 2030 END-TB Targets
90% reduction in TB patients, 95% reduction in TB deaths, reduce costs that increase poverty
TB HIV and Diabetes
Predispose to active TB, relative importance of each varies in different parts of the world, HIV is major driver in sub-Saharan Africa but not in Sth America
TB 8 top countries
India 27%, Indonesia 10%, China 7%, Phillippines 7%, Pakistan 6%, Nigeria 5%, Bangladesh 4%, DRC 3%
TB Diabetes
Risk of TB is 3x higher in diabetes than non-diabetes in same population, holds true in both low and high TB burden settings. T2DM is rapidly increasing and accounts for vast majority of this effect, risk in T1DM is probably higher but much less common. People diagnosed with TB should be tested for DM as the TB might be the first manifestation of DM (as for HIV). Screening people with DM for TB is low yield and not cost effective. TB in people with DM is not substantially different to TB in people without DM, treatment is the same
TB Natural history
Some clear infection, most control infection and develop latent TB, of those with LTBI 10% will go on to develop active TB in their lifetime (90% don’t), some develop active TB (develops over weekls to months)
TB HIV coinfection
Different natural history, phenotype and diagnosis, HIV increases probability of early progression, and probability of TB reactivation to 10% per year
TB Paediatric TB
Different natural history, phenotype and diagnosis, larger number go on to active disease
TB TB control
Stop transmission, treat adults with pulmonary TB who are the infectious source