Tuberculosis how does it obtain energy

Like all living things, M. Right now, scientists do not know much about how this microbe eats. Most bacteria like to consume ammonium as their main nitrogen source, but they may also use select amino acids as a nitrogen source. Now, Agapova et al.

In the experiments, the bacteria were fed different nitrogen sources. Then, they tracked how well the bacteria grew. The experiments showed that M.

It is a small bacillus that can withstand most disinfectants and often remains in its dormant state. To survive, it needs oxygen: it is thus called an aerobic bacterium.

Mycobacterium tuberculosis grows slowly: it reproduces itself every 24 to 48 hours. This is extremely slow for bacteria. There are other bacteria that reproduce every 20 minutes. The bacillus has a rod-shaped body and is approximately 0. It cannot be seen with the naked eye; one needs a microscope to detect it.

Inside the bacillus are so-called organelles, small micro-units that ensure that the bacillus can create the energy it needs to survive. In its anatomy, mycobacterium tuberculosis resembles a lot of other bacteria, but it has unique features that make it difficult to diagnose and treat. Its cell wall is extraordinarily thick and complex. It is these mycolic acids that are also responsible for a particular characteristic of all mycobacteria, which is used to identify Mycobacterium tuberculosis in diagnostic tests.

It has been suggested that leptin mediates anorexia in chronic inflammatory states In this report, we present leptin, body composition, and energy metabolism data from a prospective observational study of patients with pulmonary tuberculosis. The primary hypothesis was that, after control for fat mass, leptin would be higher in patients during active tuberculosis than after their recovery.

Furthermore, we hypothesized that higher leptin concentrations would correlate with increased proinflammatory cytokine activity, increased resting energy expenditure REE , and reduced food intake. In this prospective longitudinal study, measures of energy metabolism, body composition, and immune response were assessed at 3 time points: within 3 d of the initiation of antimycobacterial treatment, after 1 mo of treatment, and after 6 mo of treatment.

Diagnosis was based on standard microbiologic or clinical criteria, ie, acid-fast bacilli in sputum microscopy, Mycobacterium tuberculosis in sputum culture, or a combination of typical signs on chest X-ray, typical clinical symptoms, and clinical response to empirical antimycobacterial treatment. Patients were excluded if HIV co-infection was documented but were allowed to enter the study if the HIV status was still unknown.

Further exclusion criteria were severe renal, hepatic, or cardiac insufficiency; diabetes mellitus; or intake of corticosteroids at baseline. Patients with a final primary diagnosis other than tuberculosis and those later diagnosed with HIV co-infection were excluded from the data analysis.

Repeated freeze-thaw cycles were avoided. All measurements were done in triplicate. Gas calibration was performed before each measurement. To prevent cross-infection in patients with active pulmonary tuberculosis, the tube connecting the canopy to the calorimeter was replaced with a single-use disposable polyethylene tube attached to an airway filter Ultipor BB50TE; Pall Corp, Newquay, United Kingdom.

Validation of this method is described in a separate report REE was compared between patients and controls and with values predicted by the Harris-Benedict equation Food energy intake was assessed by h recall protocols and a food-frequency questionnaire covering the previous wk. The higher estimate of energy intake from these 2 methods was used for further analysis. Professional interpreters were available during the assessment for any subjects who were not fluent in English.

Body weight was measured on a calibrated scale to the nearest 0. The weight of such clothing, calculated from the average of 10 measurements of each standard clothing item, was subtracted. Height was measured on a calibrated wall-mounted scale to the nearest 0.

The local research ethics committee approved the study, and the rules of the Helsinki Declaration revision of were followed.

The ratio between reported energy intake and measured REE was used as a variable of energy balance. Changes between time points ie, baseline, 1 mo, and 6 mo were tested by repeated-measures analysis of variance with sex, time, and sex-by-time interaction as independent variables. The correlation between fat mass and leptin was tested by analysis of variance, with controls for time and sex.

Two methods were used to test whether associations between leptin and values of proinflammatory cytokine response or energy metabolism were partly independent from fat mass and energy balance.

For continuous variables, this testing was done by partial correlation, calculated separately for each time point. For categorial variables time points, sex, prior weight loss , this testing was done by calculating the residuals for leptin, ie, the difference between measured and predicted log 10 leptin , from linear regression against percentage body fat and energy balance. Residuals were then compared between time points or between subgroups at each time point by paired or unpaired t test.

Significance testing was adjusted for multiple comparisons with the use of the Bonferroni method. Statistics were calculated with SPSS software, version Between June and November , patients with a clinical diagnosis of pulmonary tuberculosis were screened for eligibility. Diagnosis was confirmed in 80 of them, but 24 had concomitant diseases that excluded them from the study 5 diabetes, 11 HIV co-infection, and 8 other. Sixteen patients did not give informed consent.

One patient died of a cause unrelated to tuberculosis, and 7 patients withdrew for personal reasons. The age of the subjects was The racial or ethnic background was South Asian, white, African, and Hispanic in 18, 9, 4, and 1 patients, respectively. All patients but one were considered to have made a satisfactory clinical response to anti-tuberculous chemotherapy at the end of 6 mo, and none were found to have multi-drug—resistant mycobacteria.

One patient developed new pulmonary infiltrates in the 4th mo of antimycobacterial treatment but recovered during an extended 9-mo course of treatment. The body mass index at baseline was A weight history could be obtained in 28 patients, 26 Clinical recovery was accompanied by increases in weight and body fat, both in absolute values and in percentage of body weight Table 1.

These changes tended to be more pronounced in men than in women, although this sex difference was not statistically significant Table 1. Longitudinal gain over 6 mo amounted to 9. This weight gain represented recovery of most of the weight previously lost: patients reached Body composition and leptin concentrations during treatment of tuberculosis, by group 1. As expected, absolute REE was higher in men than in women 5. However, neither changes in REE during treatment nor REE results normalized for age, sex, height, and weight Harris-Benedict prediction; 14 or for fat-free mass differed significantly between men and women.

Therefore, all further data are presented for the sexes combined Table 2. Because measured REE was also significantly lower than predicted in 11 healthy controls Likewise, REE did not change between time points when expressed per kilogram of fat-free mass Table 2. Cytokines and energy metabolism during treatment of tuberculosis 1.

There were no significant differences between men and women for the above variables in this model. By contrast, energy intake increased significantly during treatment Table 2. Plasma IL-6, sTNFR1, and C-reactive protein were above the reference range at baseline, and they decreased by 1 mo and 6 mo, without a difference between the sexes Table 2.

Fasting plasma leptin concentrations increased between baseline and 1 mo and 6 mo Table 1. The median increase in leptin in individual patients amounted to Women had higher leptin concentrations than did men Table 1. Correlation between leptin concentration and percentage fat mass. Regression lines did not differ significantly between time points.

Patients with such a degree of wasting had lower baseline leptin concentrations than did patients with lesser degrees of weight loss 6. No further significant correlations between these variables were found at 1 mo data not shown. Log leptin was not significantly correlated to any of the cytokines. Neither REE nor reported food intake was correlated with leptin in this study. Residual leptin at 1 mo was 1.

Pearson's bivariate top right triangular area and partial bottom left triangular area correlation coefficients r between leptin, proinflammatory cytokines, and energy balance at baseline 1.

Pearson's bivariate top right triangular area and partial bottom left triangular area correlation coefficients r between leptin, proinflammatory cytokines, and energy balance at 6 mo 1. This study provides no support for the concept that leptin is the missing link between immune defense and wasting in pulmonary tuberculosis. No additional influence of disease activity or inflammatory cytokines was found. In theory, leptin would have been an intriguing candidate for this role.

Leptin is both a recipient of and a stimulus for immunologic signals. In animal models, its production increases in response to bacterial lipopolysaccharide 10 , 11 and turpentine 9. Its molecular structure is similar to that of the IL-6 cytokine family Furthermore, it has a trophic effect on components of the immune system.

The immunosuppression induced by starvation in mice is abolished if leptin is substituted 19 , including stimulation of a Th1 pattern of proinflammatory cytokine production Evidence for such a role for leptin in humans is equivocal. Ex vivo stimulation of human peripheral blood mononuclear cells with leptin results in a Th1 pattern of cytokine release Increased leptin concentrations were found in patients with sepsis 22 — It is not known to what extent such findings are explained by hyperglycemia and hyperinsulinemia, which are common findings in such patients and a major stimulus for leptin production Leptin concentration increases during acute surgical stress but returns to normal within 24 h 26 — Similar findings were reported in patients with cancer-related cachexia Finally, people with genetic leptin deficiency have largely normal immune function Taken together, these data suggest that the leptin system reacts to acute metabolic stress but does not to contribute to chronic wasting in humans.

Leptin has been suggested as a component of a Th1 pattern of cytokines, the same pattern that is required for protective immunity against M. Stimulation of leptin production during active tuberculosis may therefore contribute to wasting, in concert with other proinflammatory cytokines. Indeed, one study found higher leptin concentrations in patients with active pulmonary tuberculosis than in healthy controls, and leptin increased further during treatment However, both effects were significant only in 8 female patients, and not in 22 male patients.

Body fat mass was estimated from BMI rather than being directly measured in that study Such estimates are of very limited validity