ALTHOUGH CURABLE, TB frequently leaves the individual with chronic physical and psycho-social impairment, but these consequences have been largely neglected. The 1st International Post-Tuberculosis Symposium (Stellenbosch, South Africa) was held to discuss priorities and gaps in addressing this issue. A barrier to progress has been the varied terminology and nomenclature, so the Delphi process was used to achieve consensus on definitions. Lack of sufficient evidence hampered definitive recommendations in most domains, including prevention and treatment of post-TB lung disease (PTLD), but the discussions clarified the research needed. A consensus was reached on a toolkit for future PTLD measurement and on PTLD patterns to be considered. The importance of extra-pulmonary consequences and progressive impairment throughout the life-course was identified, including TB recurrence and increased mortality. Patient advocates emphasised the need to address the psychological and social impacts post TB and called for clinical guidance. More generally, there is an urgent need for increased awareness and research into post-TB complications.

Tuberculous effusion is a common disease entity with a spectrum of presentations from a largely benign effusion, which resolves completely, to a complicated effusion with loculations, pleural thickening and even frank empyema, all of which may have a lasting effect on lung function. The pathogenesis is a combination of true pleural infection and an effusive hypersensitivity reaction, compartmentalized within the pleural space. Diagnostic thoracentesis with thorough pleural fluid analysis including biomarkers such as adenosine deaminase and gamma interferon achieves high accuracy in the correct clinical context. Definitive diagnosis may require invasive procedures to demonstrate histological evidence of caseating granulomas or microbiological evidence of the organism on smear or culture. Drug resistance is an emerging problem that requires vigilance and extra effort to acquire a complete drug sensitivity profile for each tuberculous effusion treated. Nucleic acid amplification tests such as Xpert MTB/RIF can be invaluable in this instance; however, the yield is low in pleural fluid. Treatment consists of standard anti‐tuberculous therapy or a guideline‐based individualized regimen in the case of drug resistance. There is low‐quality evidence that suggests possible benefit from corticosteroids; however, they are not currently recommended due to concomitant increased risk of adverse effects. Small studies report some short‐ and long‐term benefit from interventions such as therapeutic thoracentesis, intrapleural fibrinolytics and surgery but many questions remain to be answered.

Tuberculosis (TB) is the leading infectious cause of death worldwide, and the commonest cause of death in people living with HIV. Globally, pleural TB remains one of the most frequent causes of pleural exudates, particularly in TB-endemic areas and in the HIV positive population. Most TB pleural effusions are exudates with high adenosine deaminase (ADA), lymphocyte-rich, straw-coloured and free flowing, with a low yield on mycobacterial culture. TB pleurisy can also present as loculated neutrophil-predominant effusions which mimic parapneumonic effusions. Rarely, they can present as frank TB empyema, containing an abundance of mycobacteria. Up to 80% of patients have parenchymal involvement on chest imaging. The diagnosis is simple if M. tuberculosis is detected in sputum, pleural fluid or biopsy specimens, and the recent advent of liquid medium culture techniques has increased the microbiological yield dramatically. Where the prevalence of TB is high the presence of a lymphocyte-predominant exudate with a high ADA has a positive predictive value of 98%. In low prevalence areas, the absence of an elevated ADA and lymphocyte predominance makes TB very unlikely, and pleural biopsy should be performed to confirm the diagnosis. Pleural biopsy for liquid culture and susceptibility testing must also be considered where the prevalence of drug resistant TB is high. Treatment regimens are identical to those administered for pulmonary TB. Initial pleural drainage may have a role in symptom relief and in hastening the resolution of the effusion. Surgical intervention may be required in loculated effusions and empyemas.

OBJECTIVETo investigate infection-related mortality in individuals with type 1 and type 2 diabetes. RESEARCH DESIGN AND METHODSA total of 1,108,982 individuals with diabetes who were registered with the Australian Diabetes register between 2000 and 2010 were linked to the National Death Index. Mortality outcomes were defined as infection-related A-B death (ICD codes A99-B99), pneumonia (J12-J189), septicemia (A40 and A41), and osteomyelitis (M86). RESULTSDuring a median follow-up of 6.7 years, there were 2,891, 2,158, 1,248, and 147 deaths from infection-related A-B causes, pneumonia, septicemia, or osteomyelitis, respectively. Crude mortality rates from infections A-B were 0.147 and 0.431 per 1,000 person-years in type 1 and type 2 diabetes, respectively. Standardized mortality ratios (SMRs) were higher in type 1 and type 2 diabetes for all outcomes after adjustment for age and sex. For infection-related A-B mortality, SMRs were 4.42 (95% CI 3.68-5.34) and 1.47 (1.42-1.53) for type 1 and type 2 diabetes (P < 0.001), respectively. For pneumonia in type 1 diabetes, SMRs were approximately 5 and 6 in males and females, respectively, while the excess risk was ∼20% for type 2 (both sexes). For septicemia, SMRs were approximately 10 and 2 for type 1 and type 2 diabetes, respectively, and similar by sex. For osteomyelitis in type 1 diabetes, SMRs were 16 and 58 in males and females, respectively, and ∼3 for type 2 diabetes (both sexes). CONCLUSIONSAlthough death owing to infection is rare, we confirm that patients with diabetes have an increased mortality from a range of infections, compared with the general population, and that the increased risk appears to be greater for type 1 than type 2 diabetes.Individuals with type 1 and type 2 diabetes are widely considered to be more prone to infections than those without diabetes (1). Evidence to support this hypothesis can be traced back as far as 1915 when Lichty noted a range of acute infections in patients with diabetes who subsequently died (2). Several decades later, two wellcited studies showed that bacteremia and bacteriuria are more common in adult women with diabetes versus those without (1,3). The factors thought to explain the excess risk of infections in these women were microvascular complications such as