Tuberculosis (TB), caused by the human pathogens Mycobacterium tuberculosis (Mtb) and Mycobacterium africanum, has plagued humanity for millennia and remains the deadliest infectious disease in the modern world. Mycobacterium tuberculosis and M. africanum can be subdivided phylogenetically into seven lineages exhibiting a low but significant degree of genomic diversity and preferential geographic distributions. Human genetic variability impacts all stages of TB pathogenesis ranging from susceptibility to infection with Mtb, progression of infection to disease, and the development of distinct clinical subtypes. The genetic study of severe childhood TB identified strong inborn single-gene errors revealing crucial pathways of vulnerability to TB. However, the identification of major TB-susceptibility genes on the population level has remained elusive. In particular, the replication of findings from candidate and genome-wide association studies across distinct human populations has proven difficult, thus hampering the characterization of reliable host molecular markers of susceptibility. Among the possible confounding factors of genetic association studies is Mtb genomic variability, which generally was not taken into account by human genetic studies. In support of this possibility, Mtb lineage was found to be a contributing factor to clinical presentation of TB and epidemiological spread of Mtb in exposed populations. The confluence of pathogen and human host genetic variability to TB pathogenesis led to the consideration of a possible coadaptation of Mtb strains and their human hosts, which should reveal itself in significant interaction effects between Mtb strain and TB-susceptibility/resistance alleles. Here, we present some of the most consistent findings of genetic susceptibility factors in human TB and review studies that point to genome-to-genome interaction between humans and Mtb lineages. The limited results available so far suggest that analyses considering joint human–Mtb genomic variability may provide improved power for the discovery of pathogenic drivers of the ongoing TB epidemic.

Tuberculosis (TB) is one of the most contagious diseases that cause many deaths. TB disease is caused by Mycobacterium tuberculosis bacteria that commonly affect the lungs and other organs such as lymph nodes, intestines, kidneys, womb, bones and brain. World Health Organization (WHO) stated that in 2015 there are 60% of TB cases found in developing countries including India, Indonesia, China, Nigeria, Pakistan and South Africa. By 2015 the TB death rate is 1.4 million. One way to reduce the spread of TB disease is vaccination and treatment. The treatment given is in the form of several types of drugs that should be taken by infected individuals within a certain period of time. Therefore, it is necessary to do a scientifically acceptable analysis of the spread of TB disease. Mathematical model for analyzing the spread of TB disease have been widely developed. One is SEIR type. In this model the population is divided into four groups, namely S for susceptible individuals, E for exposed individuals, I for infected individuals, R for recovered individuals. This article discusses the model of SEIR type TB disease with vaccination and treatment.

Mycobacterium tuberculosis is a major health burden worldwide. The disease may present as an individual case, community outbreak, or more rarely as a nosocomial outbreak. Even in countries with a low prevalence such as the UK, tuberculosis (TB) presents a risk to healthcare workers (HCWs). To report an outbreak which manifested 12 months after a patient with pulmonary tuberculosis was admitted to Queen Elizabeth Hospital Birmingham. We present the epidemiological and outbreak investigations; the role of whole genome sequencing (WGS) in identifying the outbreak and control measures to prevent further outbreaks. Subsequent to a diagnosis of open TB in a patient, transmission was confirmed in one HCW who had active TB; HCWs with latent TB infection (LTBI) were also identified among seven HCW contacts of the index patient. Of note, all the LBTI patients had other risk factors for TB. Routine use of WGS identified the outbreak link between the index patient and the HCW with active TB disease, and informed our investigations. Exposure most likely occurred during an aerosol-generating procedure (AGP) which was done in accordance with national guidance at that time without using respiratory protection. Enhanced control measures were implemented following the outbreak.

Graphical abstract Mycobacterium bovis is a slow-growing (16–20 h generation time), Gram-positive and acid-fast bacterium member of the Mycobacterium tuberculosis complex pathogen group (MTBC). They are characterized by a complex, protective cell wall containing mycolic acids. The MTBCs are the causative agents of tuberculosis (TB). Following initial infection, subsequent pathological changes, and the progress of infection depend on the interplay between host defence mechanisms and mycobacterial virulence factors and the balance between the immunologic protective responses and the damaging inflammatory processes. Progression of the disease is characterized by the formation of typical caseous tuberculous granuloma (inflammatory mononuclear cell aggregates) because of the host's immune response to infection. The transmission and epidemiology of Mycobacterium bovis are complex and vary depending on the situation and ecosystem. In the UK, the spread of BTB in the UK cattle herd can occur by transmitting the disease from cattle to cattle and between badgers but also between badgers and cattle. The disease is thought to be primarily a respiratory disease with spread between individuals through mechanisms such as coughing or transfer of bacteria in respiratory secretions. It is also thought that environmental contamination may also lead to some transmission. The protective cell wall of the organism is believed to allow the organism to survive outside an animal host, which can then transfer to new hosts following subsequent environmental exposure. In some situations, ingestion of pathogens in food can lead to infection. The relative contribution of these routes and precise transmission mechanisms needs to be better understood.

Mycobacterium tuberculosis (MTB) causes active TB infections that result in pulmonary tuberculosis (PTB), relapse even after treatment, and latent TB. Tuberculosis is a bacterium airborne pulmonary infectious disease. Extra pulmonary tuberculosis (EPTB) results from an illness which is too severe with Mycobacterium tuberculosis entering into the circulatory system. A really bad situation with further multi-drug TB. In the nation, pulmonary TB is spreading as well as reemerging. Recent findings of an increase in cases in the area pose a mortality burden and infection spread risk. The group of bacteria genetically organisms known as the Mycobacterium tuberculosis complex (MTBC) are accountable for human as well as animal tuberculosis. Among the primary reasons of mortality or morbidity worldwide continues to remain this sickness even now. The mycobacteria infiltrate the host via breathing that is phagocytated by macrophage as they reach the respiratory tract. It may cause the bacteria responsible to be quickly destroyed or cause an aggressive TB disease. Precisely a result of its human immunological reaction, multiple distinct virulence indicators have emerged among MTBC subgroups. The purpose of this research is to discuss the bacterial genes or enzymes that are to be crucial to determining the pathogenicity of MTBC strains through in vivo infections paradigm. As a way to eradicate various illnesses as well as get closer to a future without infections such as tuber emerging medicines or therapies must take into account the virulence aspects of MTBC.

Tuberculosis (TB) is a disease caused by bacteria that are spread through the air from person to person. If not treated properly, TB disease can be fatal. People infected with TB bacteria who are not sick may still need treatment to prevent TB disease from developing in the future. Tuberculosis (TB) is currently one of the greatest problems in public health. Mycobacterium tuberculosis infects about one third of the world's population, of whom more than 80% are living in developing countries. The incidence and prevalence of TB are very different in various parts of Iran and also throughout the world. Learn to recognize the symptoms of TB disease and find out if you are at risk.

Co-infection with Mycobacterium tuberculosis is the leading cause of death in individuals infected with HIV-1. It has long been known that HIV-1 infection alters the course of M. tuberculosis infection and substantially increases the risk of active tuberculosis (TB). It has also become clear that TB increases levels of HIV-1 replication, propagation and genetic diversity. Therefore, co-infection provides reciprocal advantages to both pathogens. In this Review, we describe the epidemiological associations between the two pathogens, selected interactions of each pathogen with the host and our current understanding of how they affect the pathogenesis of TB and HIV-1/AIDS in individuals with co-infections. We evaluate the mechanisms and consequences of HIV-1 depletion of T cells on immune responses to M. tuberculosis. We also discuss the effect of HIV-1 infection on the control of M. tuberculosis by macrophages through phagocytosis, autophagy and cell death, and we propose models by which dysregulated inflammatory responses drive the pathogenesis of TB and HIV-1/AIDS.

Tuberculosis is a bacterial disease caused by Mycobacterium tuberculosis (TB). The risk for TB infection greatly increases with HIV infection; TB disease occurs in 7-10% of patients with HIV infection each year, increasing the potential for transmission of drug-resistant Mycobacterium tuberculosis strains. In this paper a deterministic model is presented and studied for the transmission of TB-HIV/AIDS co-infection. Optimal control theory is then applied to investigate optimal strategies for controlling the spread of the disease using treatment of infected individuals with TB as the system control variables. Various combination strategies were examined so as to investigate the impact of the controls on the spread of the disease. And incremental cost-effectiveness ratio (ICER) was used to investigate the cost effectiveness of all the control strategies. Our results show that the implementation of the combination strategy involving the prevention of treatment failure in drug-sensitive TB infectious individuals and the treatment of individuals with drug-resistant TB is the most cost-effective control strategy. Similar results were obtained with different objective functionals involving the minimization of the number of individuals with drug-sensitive TB-only and drug-resistant TB-only with the efforts involved in applying the control.

Introduction: Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis. The leading cause of death worldwide is responsible for 1.5 million deaths each year. The cause of tuberculosis infection is the tubercle bacillus discovered by Robert Koch in 1882. The organism causing it is Mycobacterium tuberculosis.The spread of new cases is divided in several regions including Southeast Asia and Africa, which are the regions that have the biggest contribution to the prevalence of tuberculosis. So it takes pillars and components of TB control that cover all lines. Method: This study aims to discuss the potential of herbal plants spread in Indonesia as herbal medicines that have the potential to treat tuberculosis infection. This study uses a literature study method which prepares the same as other research, but the sources and methods of data collection are by taking data from the library, reading, taking notes, and processing research materials. Result: One of the components that are currently being developed in TB infection intervention methods is the development of herbal medicines for tuberculosis control. The herbal medicines used come from garlic (Allium sativum), Centellaasiatica, beluntas leaves, Hibiscus rosasinensis L., Boechmeria virgate (Forst) Guill, tobacco leaves, Morindacitrifolia L., Javanese wood bark, Spondiaspinnata (Lf)Kurz. Conclusion: The herbal medicinal ingredients contain major chemicals such as alicin, ajoene, asiaticoside, asiatic acid, madecassic acid, and madecassoside, alkaloids, flavonoids, tannins, saponins, phenolic, and triterpenoids which have the ability to have a bactericidal effect to kill the Mycobacterium tuberculosis bacteria.

Tuberculosis (TB) is a heterogeneous disease manifesting in a subset of individuals infected with aerosolized Mycobacterium tuberculosis (Mtb). Unlike human TB, murine infection results in uniformly high lung bacterial burdens and poorly organized granulomas. To develop a TB model that more closely resembles human disease, we infected mice with an ultra-low dose (ULD) of between 1-3 founding bacteria, reflecting a physiologic inoculum. ULD-infected mice exhibited highly heterogeneous bacterial burdens, well-circumscribed granulomas that shared features with human granulomas, and prolonged Mtb containment with unilateral pulmonary infection in some mice. We identified blood RNA signatures in mice infected with an ULD or a conventional Mtb dose (50-100 CFU) that correlated with lung bacterial burdens and predicted Mtb infection outcomes across species, including risk of progression to active TB in humans. Overall, these findings highlight the potential of the murine TB model and show that ULD infection recapitulates key features of human TB.