Concomitant pleural and disseminated tuberculosis in AIDS: immune response or HIV infection compartmentalization?

Although, pleural (PT) and disseminated tuberculosis (DT) have been considered as extreme endpoints of the Th1-Th2 immunological spectrum of the Mycobacterium tuberculosis infection, these conditions can occur together. The presence of PT and DT could be explained by (1) PT as primary condition, with progression of HIV infection possibly leading to dissemination of bacilli located in the pleura; (2) preexisting PT, with reinfection at lower LTCD4+ count explaining the DT form; (3) simultaneous acute PT and DT, considering immune compartmentalization phenomena in pleura. There are several important aspects of the immune response and its compartmentalization in co-infected patients with tuberculosis and HIV. PT and DT should not be always considered as extremes of the immunological response against M. tuberculosis, both diseases together may be explained after the understanding of compartmentalization of immune response. Associations between these entities are not so rare, while they remain incompletely explained. This brief review discusses several points of this contradictory association.     

Superior mesenteric artery syndrome and disseminated tuberculosis: “Double troubleˮ

Superior Mesenteric Artery (SMA) Syndrome is a rare condition characterized by compression of the third part of the duodenum between the aorta and superior mesenteric artery due to decreased angle between these two vessels due to loss of intervening pad of fat. Tuberculosis is one of the causes, and its association with it is rare. However, SMA syndrome with significant gastrointestinal symptoms in TB poses a greater challenge in management, particularly in dissemination. Strong clinical suspicion, timely diagnosis and appropriate antituberculosis therapy are the keys to successful management.     

Metabolic syndrome: Why the controversy?

As originally conceived, the metabolic syndrome defined a clustering of cardiovascular disease risk factors with insulin resistance as the common, underlying pathophysiologic determinant. The definition of the syndrome has evolved since then, with several groups proposing somewhat differing definitions. Partly, this has been motivated by efforts to make the syndrome a clinically useful entity. However, recent articles have called the clinical use of the metabolic syndrome into question. In this review, some of these concerns and counterarguments for the continued use of the metabolic syndrome are reviewed.     

Lyme disease: why the controversy?

Some Australians have become convinced of the existence of locally acquired Lyme disease (LD). The history of LD, since its recognition in the early 1970s, is reviewed as a model for investigative approaches to unknown syndromes. Australian Management Guidelines for LD include the requirement for diagnostic testing by National Association of Testing Authorities‐accredited laboratories using Therapeutic Goods Administration‐licensed tests, which result in the efficient diagnosis of LD in overseas travellers. Despite this, patients who have not left Australia pay many thousands of dollars for non‐specialist consultations and testing at overseas laboratories. Unproven long‐term therapy with multiple antibiotics has resulted in serious complications, including allergies, line sepsis, pancreatitis and pseudomembranous colitis. Studies have shown that LD vectors are not found in Australia, and Lyme Borrelia has not been found in Australian vectors, animals or patients with autochthonous illnesses. I propose that (i) A non‐controversial name for the chronic syndrome should be adopted, ‘Australian Multisystem Disorder’. (ii) Research funding should enable the development of a consensus case definition and studies of the epidemiology of this syndrome with laboratory investigations to identify an aetiology and surrogate markers of disease. Prospective, randomised treatment studies could then be undertaken using ethical protocols.     

Inside or outside the phagosome? The controversy of the intracellular localization of Mycobacterium tuberculosis

The localization of Mycobacterium tuberculosis (Mtb) inside the macrophage has been a matter of debate in recent years. Upon inhalation, the bacterium is taken up into macrophage phagosomes, which are manipulated by the bacterium. Subsequent translocation of the bacilli into the cytosol has been observed by several groups, while others fail to observe this phenomenon. Here, we review the available literature in favour of and against this idea, and scrutinize the existing data on how human macrophages control Mtb infection, relating this to the robustness of the host cell. We conclude that both phagosomal maturation inhibition and escape from the phagosome are part of the greater infection strategy of Mtb. The balance between the host cell and the infecting bacterium is an important factor in determining the outcome of infection as well as whether phagosomal escape occurs and can be captured.