Tuberculosis

Author(s):  
Richard E. Chaisson ◽  
Jean B. Nachega

Tuberculosis is caused by organisms of the Mycobacterium tuberculosis complex, including M. tuberculosis (the most important), M. bovis, and M. africanum. It has been present since antiquity and is the second leading infectious cause of death after HIV infection. An estimated 2 billion people worldwide carry latent infection, when ...

2020 ◽  
pp. 1126-1149
Author(s):  
Richard E. Chaisson ◽  
Jean B. Nachega

Tuberculosis is caused by organisms of the Mycobacterium tuberculosis complex, including M. tuberculosis (the most important), M. bovis, and M. africanum. It has been present since antiquity and is the leading infectious cause of death ahead of HIV infection. An estimated 2 billion people worldwide carry latent infection, when M. tuberculosis persists within cells and granulomas, with the potential to reactivate to cause disease decades later. Tubercle bacilli are transmitted between people by aerosols generated when an infectious person coughs. Proximity to an infectious person determines the risk of infection. Host immunity and factors affecting it—most importantly HIV infection but also diabetes, cigarette smoking, and alcohol and drug abuse—determine the risk of active disease following infection.


PEDIATRICS ◽  
1996 ◽  
Vol 98 (6) ◽  
pp. 1007-1019 ◽  
Author(s):  
Bernard Guyer ◽  
Donna M. Strobino ◽  
Stephanie J. Ventura ◽  
Marian MacDorman ◽  
Joyce A. Martin

Recent trends in the vital statistics of the United States continued in 1995, including decreases in the number of births, the birth rate, the age-adjusted death rate, and the infant mortality rate; life expectancy at birth increased to a level equal to the record high of 75.8 years in 1992. Marriages and divorces both decreased. An estimated 3 900 089 infants were born during 1995, a decline of 1% from 1994. The preliminary birth rate for 1995 was 14.8 live births per 1000 total population, a 3% decline, and the lowest recorded in nearly two decades. The fertility rate, which relates births to women in the childbearing ages, declined to 65.6 live births per 1000 women 15 to 44 years old, the lowest rate since 1986. According to preliminary data for 1995, fertility rates declined for all racial groups with the gap narrowing between black and white rates. The fertility rate for black women declined 7% to a historic low level (71.7); the preliminary rate for white women (64.5) dropped just 1%. Fertility rates continue to be highest for Hispanic, especially Mexican-American, women. Preliminary data for 1995 suggest a 2% decline in the rate for Hispanic women to 103.7. The birth rate for teenagers has now decreased for four consecutive years, from a high of 62.1 per 1000 women 15 to 19 years old in 1991 to 56.9 in 1995, an overall decline of 8%. The rate of childbearing by unmarried mothers dropped 4% from 1994 to 1995, from 46.9 births per 1000 unmarried women 15 to 44 years old to 44.9, the first decline in the rate in nearly two decades. The proportion of all births occurring to unmarried women dropped as well in 1995, to 32.0% from 32.6% in 1994. Smoking during pregnancy dropped steadily from 1989 (19.5%) to 1994 (14.6%), a decline of about 25%. Prenatal care utilization continued to improve in 1995 with 81.2% of all mothers receiving care in the first trimester compared with 78.9% in 1993. Preliminary data for 1995 suggests continued improvement to 81.2%. The percent of infants delivered by cesarean delivery declined slightly to 20.8% in 1995. The percent of low birth weight (LBW) infants continued to climb in 1994 rising to 7.3%, from 7.2% in 1993. The proportion of LBW improved slightly among black infants, declining from 13.3% to 13.2% between 1993 and 1994. Preliminary figures for 1995 suggest continued decline in LBW for black infants (13.0%). The multiple birth ratio rose to 25.7 per 1000 births for 1994, an increase of 2% over 1993 and 33% since 1980. Age-adjusted death rates in 1995 were lower for heart disease, malignant neoplasms, accidents, and homicide. Although the total number of human immunodeficiency virus (HIV) infection deaths increased slightly from 42 114 in 1994 to an estimated 42 506 in 1995, the age-adjusted death rate for HIV infection did not increase, which may indicate a leveling off of the steep upward trend in mortality from HIV infection since 1987. Nearly 15 000 children between the ages of 1-14 years died in the United States (US) in 1995. The death rate for children 1 to 4 years old in 1995 was 40.4 per 100 000 population aged 1 to 4 years, 6% lower than the rate of 42.9 in 1994. The 1995 death rate for 5-to 14-year-olds was 22.1,2% lower than the rate of 22.5 in 1994. Since 1979, death rates have declined by 37% for children 1 to 4 years old, and by 30% for children 5 to 14 years old. For children 1 to 4 years old, the leading cause of death was injuries, which accounted for an estimated 2277 deaths in 1995, 36% of all deaths in this age group. Injuries were the leading cause of death for 5-to 14-year-olds as well, accounting for an even higher percentage (41%) of all deaths. In 1995, the preliminary infant mortality rate was 7.5 per 1000 live births, 6% lower than 1994, and the lowest ever recorded in the US. The decline occurred for neonatal as well as postneonatal mortality rates, and among white and black infants alike. Sudden infant death syndrome (SIDS) rates have dropped precipitously since 1992, when the American Academy of Pediatrics issued recommendations that infants be placed on their backs or sides to sleep to reduce the risk of SIDS. SIDS dropped to the third leading cause of infant death in 1994, after being the second leading cause of death since 1980. Infant mortality rates (IMRs) have also declined rapidly for respiratory distress syndrome since 1989, concurrent with the widespread availability of new treatments for this condition.


2019 ◽  
Vol 2019 (2) ◽  
Author(s):  
Edgar Stroppa Lamas ◽  
Ricardo Jose Rogoni Bononi ◽  
Mario Vinicius Angelete Alvarez Bernardes ◽  
Junior Luiz Pasin ◽  
Hector Aurelio Davial Soriano ◽  
...  

Medicina ◽  
2020 ◽  
Vol 56 (4) ◽  
pp. 202 ◽  
Author(s):  
Carmen Adella Sirbu ◽  
Elena Dantes ◽  
Cristina Florentina Plesa ◽  
Any Docu Axelerad ◽  
Minerva Claudia Ghinescu

In this paper, we reported on four cases of severe pulmonary active tuberculosis in patients with multiple sclerosis (MS) undergoing interferon beta-1b (IFNβ-1b) therapy. Disease-modifying therapies (DMTs) in MS may increase the risk of developing active tuberculosis (TB) due to their impact on cellular immunity. Screening for latent infection with Mycobacterium tuberculosis (LTBI) should be performed, not only for the newer DMTs (alemtuzumab, ocrelizumab) but also for IFNβ-1b, alongside better supervision of these patients.


2020 ◽  
Vol 202 (7) ◽  
Author(s):  
Prabhat Ranjan Singh ◽  
Anil Kumar Vijjamarri ◽  
Dibyendu Sarkar

ABSTRACT Mycobacterium tuberculosis retains the ability to establish an asymptomatic latent infection. A fundamental question in mycobacterial physiology is to understand the mechanisms involved in hypoxic stress, a critical player in persistence. Here, we show that the virulence regulator PhoP responds to hypoxia, the dormancy signal, and effectively integrates hypoxia with nitrogen metabolism. We also provide evidence to demonstrate that both under nitrogen limiting conditions and during hypoxia, phoP locus controls key genes involved in nitrogen metabolism. Consistently, under hypoxia a ΔphoP strain shows growth attenuation even with surplus nitrogen, the alternate electron acceptor, and complementation of the mutant restores bacterial growth. Together, our observations provide new biological insights into the role of PhoP in integrating nitrogen metabolism with hypoxia by the assistance of the hypoxia regulator DosR. The results have significant implications on the mechanism of intracellular survival and growth of the tubercle bacilli under a hypoxic environment within the phagosome. IMPORTANCE M. tuberculosis retains the unique ability to establish an asymptomatic latent infection. To understand the mechanisms involved in hypoxic stress which play a critical role in persistence, we show that the virulence regulator PhoP is linked to hypoxia, the dormancy signal. In keeping with this, phoP was shown to play a major role in M. tuberculosis growth under hypoxia even in the presence of surplus nitrogen, the alternate electron acceptor. Our results showing regulation of hypoxia-responsive genes provide new biological insights into role of the virulence regulator in metabolic switching by sensing hypoxia and integrating nitrogen metabolism with hypoxia by the assistance of the hypoxia regulator DosR.


2016 ◽  
Vol 283 (1831) ◽  
pp. 20160499 ◽  
Author(s):  
Rebecca H. Chisholm ◽  
Mark M. Tanaka

Mycobacterium tuberculosis has an unusual natural history in that the vast majority of its human hosts enter a latent state that is both non-infectious and devoid of any symptoms of disease. From the pathogen perspective, it seems counterproductive to relinquish reproductive opportunities to achieve a détente with the host immune response. However, a small fraction of latent infections reactivate to the disease state. Thus, latency has been argued to provide a safe harbour for future infections which optimizes the persistence of M. tuberculosis in human populations. Yet, if a pathogen begins interactions with humans as an active disease without latency, how could it begin to evolve latency properties without incurring an immediate reproductive disadvantage? We address this question with a mathematical model. Results suggest that the emergence of tuberculosis latency may have been enabled by a mechanism akin to cryptic genetic variation in that detrimental latency properties were hidden from natural selection until their expression became evolutionarily favoured.


2010 ◽  
Vol 207 (13) ◽  
pp. 2869-2881 ◽  
Author(s):  
Christof Geldmacher ◽  
Njabulo Ngwenyama ◽  
Alexandra Schuetz ◽  
Constantinos Petrovas ◽  
Klaus Reither ◽  
...  

HIV-1 infection results in the progressive loss of CD4 T cells. In this study, we address how different pathogen-specific CD4 T cells are affected by HIV infection and the cellular parameters involved. We found striking differences in the depletion rates between CD4 T cells to two common opportunistic pathogens, cytomegalovirus (CMV) and Mycobacterium tuberculosis (MTB). CMV-specific CD4 T cells persisted after HIV infection, whereas MTB-specific CD4 T cells were depleted rapidly. CMV-specific CD4 T cells expressed a mature phenotype and produced very little IL-2, but large amounts of MIP-1β. In contrast, MTB-specific CD4 T cells were less mature, and most produced IL-2 but not MIP-1β. Staphylococcal enterotoxin B–stimulated IL-2–producing cells were more susceptible to HIV infection in vitro than MIP-1β–producing cells. Moreover, IL-2 production was associated with expression of CD25, and neutralization of IL-2 completely abrogated productive HIV infection in vitro. HIV DNA was found to be most abundant in IL-2–producing cells, and least abundant in MIP-1β–producing MTB-specific CD4 T cells from HIV-infected subjects with active tuberculosis. These data support the hypothesis that differences in function affect the susceptibility of pathogen-specific CD4 T cells to HIV infection and depletion in vivo, providing a potential mechanism to explain the rapid loss of MTB-specific CD4 T cells after HIV infection.


Author(s):  
Richard M. Selik ◽  
Robert N. Anderson ◽  
Matthew T. McKenna ◽  
Harry M. Rosenberg

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