Tuberculosis etiology

The most common nonmalignant etiology of SVCS is catheter-related thrombosis primarily owing to the increasing use of central access devices. Other causes include benign teratoma, tuberculosis, silicosis, and sarcoidosis. 

Therapy depends on etiology. In individuals who are suspected of having tuberculosis, diagnosis should make use of a purified protein derivative skin test, chest radiograph, and sputum cultures if necessary. These individuals should be referred for comanagement to their primary physician or to an infectious disease specialist. Though antituberculin agents are systemically administered, the ocular lesions are appropriately treated with topical steroids. In most instances, patients respond to 1% prednisolone acetate every 3 to 4 hours for the first day, subsequently tapered rapidly on the basis of the clinical response. 

Current predictions suggest that the twin epidemics of obesity and diabetes worldwide will result in an increase in CVD rates, which have sharply declined over the past 30 years, after the introduction of effective lipid-lowering and antihypertensive therapies. The World Health Organization (WHO) reported that in 2002, deaths from CVD outnumbered deaths from the major communicable diseases (AIDS, tuberculosis, and malaria) by 3 to 1 (2). By 2015, an estimated 20 million people will die annually from CVD. Therefore, with the advent of the new millennium, there is a sense of urgency to address the burden of chronic cardiometabolic diseases worldwide. The information on the prevalence and etiology of cardiometabolic diseases, which is cited in this section was obtained from the WHO and Centers for Disease Control (CDC) websites (2-6). 

Hydroxykynurenine excretion in pathological states was also first reported by Japanese workers (573), who identified it as the substance causing the diazo reaction and the Weiss urochromogen reaction in urines from cases of severe tuberculosis. This was confirmed in the author s laboratory (178), where it was also shown that the excretion is unrelated to tuberculosis as such. Hydroxykynurenine excretion occurs in a large proportion of patients with fevers of varying etiology and is in all probability due to the increased rate of breakdown of body proteins in fever. Presumably the protein breakdown induces an adaptive increase in tryptophan peroxidase-oxidase, and the capacity of the available kynureninase, which comes later in the metabolic chain and is not an adaptive enzyme (480), is exceeded. 

Indications Latter stages of warm diseases, yin fluids consumed and damaged, evils hidden in the yin division. Advanced stages of various infectious diseases, pulmonary tuberculosis, chronic nephritis, kidney tuberculosis, fevers of unknown etiology, typhoid fever convalescence, and post-surgical fevers... 

Mycohaaerium tuberculosis, the etiological agent of tuberculosis (TB), is able to persist inside the host for long periods of time without clinical symptoms, a condition that may exist through the host s life. It is estimated that more than one-third of the world s population is infected with tubercle bacilli and 5-10% of these individuals will develop TB at some point in their lifetime with a death toll of approximately 1.7 million people in 2007. ... 

Definition. The definition of CB is based on the clinical symptoms of chronic productive cough for at least three months of the year for two successive years. Other etiologies for these symptoms must be excluded before the diagnosis can be accepted ( ).. Among the diseases with which CB can be confused are tuberculosis. 

Pathophysiology. The etiology of CB is not known. One suspects that there is an individual susceptibility which may predispose to the development of CB which is likely dependent on inherited and acquired host defense capability. A classification of host defense factors would include cellular, immune, non-immune humoral and mucociliary functions (7), Acquired host defense problems may be related to the patient s concomitant disease(s) such as CBA, tuberculosis, sickle cell disease, etc. 

Muthu DC. Pulmonary Tuberculosis Its Etiology and Treatment—Record of Twenty-Two Years Observation and Work in Open-Air Sanatoria. London BaiUiere, Tindall and Cox, 1922. 

Familial associations in sarcoidosis. A report to the Research Committee of the British Thoracic and Tuberculosis Association. Tubercle 1973 54(2) 87-98. Rybicki BA, lannuzzi MC, Frederick MM, et al. Familial aggregation of sarcoidosis. A case-control etiologic study of sarcoidosis (ACCESS). Am J Respir Crit Care Med 2001 164(11) 2085-2091. 

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