Introduction

Mycobacterium tuberculosis is a significant human pathogen. This bacterium primarily causes pulmonary disease but can spread to involve any organ and manifest as acute, chronic, or latent infection.[1] Tuberculosis is a global disease, but the disease burden disproportionately impacts low-income countries and vulnerable populations, including those who are homeless or unsheltered, incarcerated, or who use intravenous drugs.[2] The financial burden of tubercular illness and treatment can consume livelihoods among these populations.[3]

In high-income countries with a low prevalence of tuberculosis, public health interventions focus on detecting and treating patients with latent tuberculosis (TB) infection.[4] Latent TB infection may reactivate to cause active and infectious TB disease that can spread throughout the population. Identification and characterization of individuals with latent TB infection and at risk of reactivation is imperative for public health but requires balancing the benefits of therapy with potential harms. 

For a comprehensive discussion of the epidemiology, etiology, pathophysiology, histopathology, evaluation, and management of tuberculosis, please see StatPearls' companion topic, "Tuberculosis."

Etiology

The bacterium Mycobacterium tuberculosis is the causative agent of TB disease. The genus Mycobacterium contains many nontuberculous mycobacteria (NTM), but all mycobacteria are bacilli with a cell envelope containing high levels of mycolic acids.[5] The unique cell envelope of mycobacteria is impervious to Gram stain; visualization with light microscopy requires acid-fast stains such as the auramine-rhodamine or Ziehl-Neelsen stains.[6][7] 

Mycobacteria are aerobic and slow-growing; several weeks of culture may be required to achieve a positive result.[8] The identification of M tuberculosis isolated from culture is typically based on morphologic and biochemical characteristics. Rapid diagnostic techniques such as nucleic acid amplification testing may be performed for the identification of M tuberculosis and can target gene sequences known to confer drug resistance.[7]

Epidemiology

Approximately one-third of the global population is infected with M tuberculosis. Despite being a treatable and curable condition, TB kills approximately 1.5 million people annually worldwide.[9] However, the burden of infection disproportionately falls on low-income countries. High rates of infection, defined as greater than 300 per 100,000 population per year, are seen in India and countries in sub-Saharan Africa. Tuberculosis rates in Eastern Europe are as high as 154 per 100,000 population per year.[2]

Countries with a low incidence of TB infection, such as the United States, are defined by an incidence of TB of less than 100 per 100,000 population per year.[9] A majority of cases in the United States occur in people who were born overseas.

The incidence of TB is higher in males than females; in one study, the pulmonary TB rate in males was 31.8 cases per 100,000 person-years compared to 20.1 cases per 100,000 person-years in females.[10] Approximately 12% of newly diagnosed global TB occurs in people coinfected with HIV; the interpretation of interferon-gamma diagnostic results can be affected by the degree of HIV-induced immunosuppression.[11][12][13] 

Following inhalational exposure to the bacterium, approximately 5% to 15% of infected individuals will develop active TB during their lifetime. While latency may last for decades following infection, most patients who progress to active TB disease do so within the first 2 years following exposure.[14][15]

Pathophysiology

Inhalation of the M tuberculosis bacterium is met by varying immune responses between hosts. The immune response in some patients, particularly those who are immunocompetent, is characterized by the elimination of the bacterium by alveolar macrophages. In other patients, the innate immune system in the lungs produces a granulomatous reaction to contain the bacterium called a tubercle.[16]

A spectrum of containment from latent tuberculosis infection to active tuberculosis disease correlates with the bacteria escaping from the tubercle according to host-pathogen interactions.[17][16] A bacteremic phase may occur, particularly in those with HIV, and mycobacteria may hematogenously spread to any organ.[18] The definition of latent TB infection is evidence of immunological response to M tuberculosis without evidence of clinical disease.[19]

In the absence of treatment, the risk of reactivation of latent tuberculosis infection is 5% to 15% across the lifetime of the infected patient.[20] However, this risk varies depending on the coincident pathogen, host, and environmental factors. Bacterial pathogenic factors include the varied virulence of different clades of M tuberculosis that co-evolve with human host populations and differences in progression to active disease between species within the M tuberculosis complex.[14]

Host factors that increase the risk of progression to active TB disease include immunosuppression and advancing age. The age-related decline in the immune response, mutations in Toll-like receptors, T-cell depletion, and changes in the expression of cytokines such as interferon-gamma and tumor necrosis factor.[9] Patients utilizing biological therapies for rheumatological diseases may also be at increased risk of reactivation from latent TB, as these treatments affect key cytokine responses in cellular immunity.[21] Other conditions that decrease the immune response and are risk factors for progression to active TB include HIV infection, diabetes, smoking, malignancy, corticosteroid use, and solid organ or hematological transplant.[21]

Bacterial factors include the varied virulence of different clades of M tuberculosis that co-evolve with human host populations and differences in progression to active disease between species within the M tuberculosis complex.[14]

History and Physical

Patients with latent TB infection are asymptomatic.[19] Therefore, obtaining a medical history is dual-purposed: identifying patients with indications for testing for latent TB infection and excluding active tuberculosis disease.

Indications for latent TB infection testing include patients at high risk of reactivation in low-incidence countries, patients at high risk of a new TB infection, or patients at moderate-to-high risk of reactivation in a high-incidence area.[22] A thorough exploration of risk factors for reactivation is required; these risk factors include a personal history of hematological or solid organ transplantation, dialysis, silicosis, anti-tumor necrosis factor treatment, and HIV coinfection.[21] Additionally, individuals of all ages who are in contact with patients with active TB infection are at a significantly increased risk of developing a new TB infection.

Symptoms that may indicate active TB disease include a cough for more than 2 weeks, shortness of breath, hemoptysis, chest pain, fevers, night sweats, and weight loss.[22] People at high risk for exposure to cases of pulmonary TB include prisoners, healthcare workers, homeless persons, illicit drug users, those with silicosis, and people who have emigrated from high TB incidence to low-incidence countries.[4][23][24] 

The physical examination should focus on identifying features of active TB disease, including pulmonary and extrapulmonary signs. Weight loss, sputum jars of hemoptysis, fevers, and diaphoresis may be indicative of active TB disease. Extrapulmonary signs include lymph node enlargement, skin changes such as erythema nodosum or panniculitis, pallor indicative of anemia, meningeal, peritoneal, and osteoarticular signs.[22] Features that may predispose risk for reactivation seen on examination include intravascular catheters or arteriovenous fistulas for dialysis, signs of organ transplantation and treatment, and steroid-related changes.

Evaluation

No single test can accurately distinguish between active and latent TB disease. The diagnosis of latent TB infection relies on evidence of cellular immune response to M tuberculosis and the reasonable exclusion of active TB disease.

Immune-Based Testing

Immune-based tests include the tuberculin skin test (TST) and the interferon-gamma release assay (IGRA). TST and IGRA are frequently utilized in high-income, low-incidence countries where the Bacille Calmette–Guérin (BCG) vaccine is less often used for population-based management of TB.[25] The TST and IGRA should lack the sensitivity and specificity to detect active TB and should not be used to diagnose active TB; mycobacterial culture and molecular methods are used for this purpose.[26]

The TST involves intradermal administration of a small volume of tuberculin antigens (tuberculoprotein preparation, or PPD) to allow for T-cell–mediated recognition and induration formation secondary to TB-sensitised T cells.[27] Developing skin test conversion following active M tuberculosis infection may take up to 12 weeks.[28] Approximately 50% of individuals with past exposure to M tuberculosis do not react when challenged with a TST; this may represent a failure of T_H1-driven cellular immunity or that infection with the mycobacterium did not occur.[29] If cellular immunity is intact and the patient has previously been exposed to the antigens, a delayed-type hypersensitivity reaction will result in induration and erythema.[30] Patients return 2 to 5 days following PPD administration for measurement of skin induration by a skilled clinician.

The TST is not specific for M tuberculosis. Falsely positive results may occur in patients exposed to environmental NTM, vaccinated with the BCG vaccine, or with past exposure to M tuberculosis but have cleared the infection. Incorrect TST technique or interpretation may also contribute to a false-negative result. NTM that are cross-reactive with the TST include Mycobacterium avium-intracellulare, Mycobacterium simiae, Mycobacterium scrofulaceum, and Mycobacterium kansasii. M kansasii and M avium-intracellulare complex can cause clinically significant pulmonary infections, particularly in patients with underlying structural lung disease.[31][32] However, globally, NTM is a less important cause of false-positive TST results, except in areas of higher NTM but low M tuberculosis prevalence.[33] False-negative results may occur in patients who have impaired cellular immunity. [34] 

The IGRA is a blood test that measures in vitro cellular responses to M tuberculosis-specific antigens not found in the BCG vaccine or most NTM.[34][35] Three tubes of blood are required to perform an IGRA: a negative control, a positive control with phytohemagglutinin, and a tube specific for M tuberculosis antigens.[27] The blood is incubated for up to 24 hours and separated into plasma; results are released as positive, negative, or indeterminate. Unlike the TST, IGRA tests will not react to prior BCG vaccinations or NTM.[36]

IGRA has a higher specificity than TST for M tuberculosis exposure but is more expensive and resource-intensive in many countries.[37] However, emerging evidence in high-income countries shows that IGRAs can be cost-effective for detecting latent TB infection in high-risk populations.[37][38] A false-negative IGRA can occur in patients with central nervous TB infection or an impaired immune response, including older patients or those with an innate or acquired interferon-gamma deficiency.[39][40] False positive IGRA results may occur secondary to specimen contamination with live TB organisms.[41] An indeterminate result may be secondary to reduced immune responses to the mitogen control, as in immunosuppression, or secondary to elevated interferon-gamma in the negative controls, such as the presence of heterophile antibodies, incorrect antigens, or autoimmune conditions such as systemic lupus erythematosus and rheumatoid arthritis.[22][42]

There is limited utility to using TST or IGRA when monitoring the response to TB treatment. Though there may be a decline in IGRA-positive rates after TB treatment, many cases remain positive despite latent TB therapy.[43][44] Similarly, TST measures the hypersensitivity of T-cell responses to tuberculin rather than as a treatment response or immunity measure.[30]

Chest Radiography and Sputum Samples

A chest radiograph may be adequate to exclude active tuberculosis in patients without symptoms of TB disease. However, patients with clinical or radiological abnormalities should be further investigated for TB disease or other conditions. Other conditions that may mimic TB include silicosis, malignancy, sarcoidosis, autoimmune causes such as rheumatoid arthritis and vasculitis, and infections including NTM, Nocardia, Cryptococcus, Histoplasma, and Aspergillus.[45][46][47][48][49]

Another test for active TB is the evaluation of 3 early morning sputum samples for acid-fast staining, mycobacterial culture, and nucleic acid amplification testing.[22] Identifying M tuberculosis on a sputum sample is diagnostic for active TB infection; such a patient can infect others and requires isolation. This situation also requires public health notification for contact tracing to limit community transmission of TB.[50] Patients with isolated extrapulmonary manifestations of TB are noninfectious.[51]

Treatment / Management

Mycobacteria such as M tuberculosis are intrinsically resistant to most commonly used antibiotics.[52] The treatment regimen for latent TB infection typically comprises 1 or 2 drugs active against mycobacteria.[53] In comparison, the standard treatment regimen for sensitive pulmonary TB disease is much more complex: rifampicin, isoniazid, pyrazinamide, and ethambutol for 2 months, and if testing confirms susceptibility to rifampicin and isoniazid, continuation of those 2 drugs for an additional 4 months with cessation of the pyrazinamide and ethambutol.[53][54] Susceptibility testing cannot be used to guide treatment for latent TB as M tuberculosis cannot be cultured.[55]

Individuals in close contact with patients with multidrug-resistant TB (MDR-TB) are more likely to have latent TB, and close contacts with active TB are more likely to have MDR-TB themselves.[56][57] Despite this, the evidence to inform best practices regarding managing close contacts of MDR-TB is limited.[56] Given the lack of evidence of better treatment outcomes in treating latent TB based on MDR-TB close contact susceptibilities, the selection of latent TB management in these cases has been guided by expert opinion and the discretion of the treating clinician on the individual risk of acquiring MDR-TB.[58][59]

The goal of latent TB infection treatment is to prevent progression to active disease. Given that most patients will not reactivate during their lifetime if untreated, the risk of this progression must be balanced against the risk of toxicity from treatment, particularly hepatotoxicity with isoniazid-based therapy.[60][61] To assist clinicians in evaluating this risk-benefit equation, several clinical calculators have been developed to estimate the likelihood that the patient has true-positive testing for latent TB, their risk of reactivation, and their risk of serious hepatotoxicity from the treatment of latent TB.[62][63]

The 3 most commonly utilized regimens for the treatment of latent tuberculosis are rifampicin monotherapy daily for 3 to 4 months, rifampicin or rifapentine plus isoniazid for 3 to 4 months, or isoniazid monotherapy daily for 6 to 9 months.[53] Choosing among these regimens is influenced by cost, efficacy, likelihood of adherence, and adverse effects, including hepatotoxicity.

Isoniazid is an antimycobacterial antibiotic that inhibits the synthesis of the mycolic acids essential for the cell envelope of mycobacteria.[64] Isoniazid is cheaper than rifamycin but carries a higher risk of adverse effects. The rifamycins are a class of antibiotics that inhibit bacterial DNA-dependent RNA-polymerase and are active against a broad range of bacteria, including mycobacteria.[65] The rifamycins most useful for treating latent TB are rifampicin and rifapentine; rifapentine has a longer half-life and can be dosed weekly.[66]

The protective efficacy of established regimens for latent TB ranges from 60% to 90% for up to 19 years.[67] In persons with HIV infection in areas with a high incidence of tuberculosis, the optimal duration of therapy for latent TB infection is not well established due to the risks of repeated or ongoing exposure and host immune status changes.[68][69]

Differential Diagnosis

Diagnosing latent TB infection can be challenging. No single test is adequate for diagnosis, and assessing for the condition requires careful clinical and radiological evaluation and interpretation of immunological tests. Patients with latent TB infection are asymptomatic by definition and detected solely through screening. The most pertinent differential diagnoses are active or previously treated TB disease and other NTM infections that predispose to falsely positive immune-based tests.[34]

Active Tuberculosis Disease

• The minimum requirement for the exclusion of active TB disease is the patient is asymptomatic of TB disease with a normal chest radiograph.[70] If there is uncertainty, obtaining three early morning sputum samples for acid-fast staining, mycobacterial culture, and nucleic acid amplification testing must be considered. Signs or symptoms of extrapulmonary TB disease may require imaging, biopsy, and lumbar puncture.

Resolved Tuberculosis Infection

• Asymptomatic patients with immunological evidence of prior exposure to M tuberculosis characterized by a positive TST or IGRA may have had a previously treated or cleared TB infection. Obtaining a careful timeframe of prior exposures and treatment history is critical. The decision to treat latent TB infection is often a patient-specific risk-benefit analysis; clinical calculators may assist the clinician.[62][63]

Bacille Calmette–Guérin (BCG) Vaccination

• The TST is not specific for M tuberculosis, and false-positive results may occur in those vaccinated with BCG as derived from M bovis.[34]

Nontuberculous Mycobacterial Infection

• The TST is not specific for M tuberculosis, and false-positive results may occur for those exposed to environmental NTM, such as M avium-intracellulare complex, M simiae, M scrofulaceum, and M kansasii.[31][32]

Pertinent Studies and Ongoing Trials

One of the most significant challenges in the treatment of latent TB infection is the difficulty in achieving an accurate diagnosis. The current diagnostic tests for M tuberculosis rely on cellular immune responses to prior exposure to antigens produced by the bacteria. These tests, particularly the TST, can be positive in patients who have cleared the infection and those with active pulmonary disease.[71] Next-generation diagnostics under development include immunodiagnostic biomarkers that seek to improve the capacity to differentiate latent TB infection.[32]

Toxicity and Adverse Effect Management

The most concerning adverse effect of latent TB treatment is drug-induced hepatitis, which may require hospitalization for acute liver injury but is rarely fatal.[72][73] Drug-induced hepatotoxicity is most commonly seen with regimens containing isoniazid but can also occur with rifamycins.[74] Risk factors for developing serious hepatotoxicity include higher pretreatment baseline transaminase levels, active liver disease, hypoalbuminemia, increased age, antiretroviral therapy, HIV infection, pretreatment hepatitis B surface antigen seropositivity, alcohol use disorder, coadministration of hepatotoxic medications, and pregnancy.[72][73][75][76][77][78][79] Hepatoxicity rates are higher for Indian patients compared to other populations; the etiology of this is unknown.[80] Children of all ethnicities have a higher incidence of hepatotoxicity compared to adults. Patients with risk factors for drug-induced hepatitis should have their liver function assessed before commencing antibiotic therapy and monthly until therapy is complete.[81] Patients should be educated about the symptoms associated with hepatitis and instructed to seek early evaluation should symptoms occur. 

Peripheral neuropathy can be induced by isoniazid due to vitamin B6 deficiency.[82] Pyridoxine administration is not routinely recommended for all patients. Still, it should be prescribed to reduce the risk of neuropathy in patients with risk factors such as pregnancy, HIV infection, diabetes, malnutrition, alcohol misuse, chronic kidney disease, or advanced age.[83][84] Rifamycin-related adverse effects include the orange-red discoloration of bodily fluids, hypersensitivity reactions, drug-drug interactions, renal impairment, hemolytic anemia, and thrombocytopenic purpura.[85][86][73] Drug-drug interactions are common with rifamycins; a comprehensive medication history should be obtained before initiating rifamycin therapy. The anticoagulants warfarin, apixaban, and rivaroxaban present a relative contraindication to rifamycin therapy due to interactions in the cytochrome p450 enzyme pathway.[87]

Prognosis

Treating latent TB infection kills the mycobacteria before the development of active TB disease. The protective efficacy of established regimens for treating latent TB infection ranges from 60% to 90%.[88][89] Without treatment, 5 % to 15% of patients with latent TB infection will reactivate during their lifetime.[20] While there are known host, pathogen, and environmental factors that will put some individuals at higher risk, it is impossible to perfectly predict which patients will go on to have TB disease.[9][21] This equates to 90% of patients treated for latent TB infection are exposed to the adverse effects of treatment without benefit; careful assessment of patients is required before commencing therapy for latent TB infection.

Complications

Minimizing the risk of harm from the treatment of latent TB infection is imperative and is best accomplished through monitoring liver function in patients at increased risk of hepatotoxicity during regular clinic or case management visits.[81] The concerns regarding the risk of increasing drug resistance by treating latent TB infection have not been validated by comprehensive, systematic meta-analyses. [81][90] However, drug resistance surveillance systems should be in place to monitor for this potential outcome.[91]

Deterrence and Patient Education

Medication adherence is one of the significant variables in successfully treating latent TB infection. There has been a clinical shift to shorter and less complex treatment regimens to increase medication adherence.[92] Peer support, case management, and educational interventions also improve medication adherence.[93] Educating patients about the nature of TB infection and the importance of treatment promotes patient engagement and medication adherence. Patients must be counseled regarding the potential adverse effects of treatment, including the risk of hepatotoxicity and when to seek additional care.

Enhancing Healthcare Team Outcomes

In high-income, low-tuberculosis prevalence regions like the United States, where population-wide screening data for preventing active TB is lacking, public health interventions prioritize testing high-risk individuals and those prone to TB progression or new infections.[94][95] TB-oriented clinics and public health services are pivotal in screening close contacts of active TB cases. Yet, services led by rheumatologists, primary care practitioners, sexual health services, and clinicians aid vulnerable populations in identifying high-risk patients and referring them for further assessment and treatment.[96][97][98][99]

Interprofessional collaboration involving pharmacists, nurses, and social workers significantly enhances patient safety and treatment outcomes. Pharmacists contribute expertise in treatment regimens for latent TB, managing risks like hepatotoxicity and drug interactions with rifamycin-containing therapies. TB-trained nurses or cultural health workers also aid in case management, optimizing medication adherence, and monitoring treatment-related adverse effects to ensure patient well-being. This integrated approach across healthcare disciplines is crucial in effectively managing latent TB in low-prevalence areas.

Screening for and treating latent TB infection in high-income, low-incidence countries demands a coordinated and interprofessional approach involving physicians, advanced practice practitioners, nurses, pharmacists, and other health professionals. A comprehensive knowledge of and competence in TB screening methods, including interpreting TST and IGRA results, is required. Effective interprofessional communication, particularly surrounding social determinants and barriers to treatment, supports holistic patient care and improves outcomes. In high-income, low-incidence countries, the challenge lies in maintaining vigilance despite lower prevalence rates. Effective teamwork, continuous education, standardized protocols, and a patient-centered approach bolstered by ethical considerations are pivotal in achieving successful screening, treatment, and improved outcomes for patients with latent TB infection.

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References

1.

Nissapatorn V, Kuppusamy I, Anuar AK, Quek KF, Latt HM. Tuberculosis: clinical manifestations and outcomes. Southeast Asian J Trop Med Public Health. 2003;34 Suppl 2:147-52. [PubMed: 19238668]

2.

Munteanu I, Cioran N, van Hest R, Abubakar I, Story A, Chiotan D, de Vries G, Mahler B. Tuberculosis Surveillance in Romania Among Vulnerable Risk Groups Between 2015 and 2017. Ther Clin Risk Manag. 2022;18:439-446. [PMC free article: PMC9035834] [PubMed: 35478731]

3.

Tanimura T, Jaramillo E, Weil D, Raviglione M, Lönnroth K. Financial burden for tuberculosis patients in low- and middle-income countries: a systematic review. Eur Respir J. 2014 Jun;43(6):1763-75. [PMC free article: PMC4040181] [PubMed: 24525439]

4.

Getahun H, Matteelli A, Abubakar I, Aziz MA, Baddeley A, Barreira D, Den Boon S, Borroto Gutierrez SM, Bruchfeld J, Burhan E, Cavalcante S, Cedillos R, Chaisson R, Chee CB, Chesire L, Corbett E, Dara M, Denholm J, de Vries G, Falzon D, Ford N, Gale-Rowe M, Gilpin C, Girardi E, Go UY, Govindasamy D, D Grant A, Grzemska M, Harris R, Horsburgh CR, Ismayilov A, Jaramillo E, Kik S, Kranzer K, Lienhardt C, LoBue P, Lönnroth K, Marks G, Menzies D, Migliori GB, Mosca D, Mukadi YD, Mwinga A, Nelson L, Nishikiori N, Oordt-Speets A, Rangaka MX, Reis A, Rotz L, Sandgren A, Sañé Schepisi M, Schünemann HJ, Sharma SK, Sotgiu G, Stagg HR, Sterling TR, Tayeb T, Uplekar M, van der Werf MJ, Vandevelde W, van Kessel F, van't Hoog A, Varma JK, Vezhnina N, Voniatis C, Vonk Noordegraaf-Schouten M, Weil D, Weyer K, Wilkinson RJ, Yoshiyama T, Zellweger JP, Raviglione M. Management of latent Mycobacterium tuberculosis infection: WHO guidelines for low tuberculosis burden countries. Eur Respir J. 2015 Dec;46(6):1563-76. [PMC free article: PMC4664608] [PubMed: 26405286]

5.

PaweŁczyk J, Kremer L. The Molecular Genetics of Mycolic Acid Biosynthesis. Microbiol Spectr. 2014 Aug;2(4):MGM2-0003-2013. [PubMed: 26104214]

6.

Gizaw N, Abera A, Sisay S, Desta K, Kreibich S, Gerwing-Adima L, Gebre-Selassie S. The yield of Auramine O staining using led microscopy with bleach treated sputum samples for detection of pulmonary tuberculosis at St. Peter tuberculosis specialized hospital, Addis Ababa, Ethiopia. J Clin Tuberc Other Mycobact Dis. 2020 Feb;18:100140. [PMC free article: PMC6939099] [PubMed: 31909226]

7.

Kumar M, Kumar G, Kumar R, Muni S, Choubey S, Kumar S, Kumari N. A Comparative Analysis of Microscopy, Culture, and the Xpert Mycobacterium tuberculosis/Rifampicin Assay in Diagnosing Pulmonary Tuberculosis in Human Immunodeficiency-Positive Individuals. Cureus. 2023 Aug;15(8):e42962. [PMC free article: PMC10475316] [PubMed: 37667708]

8.

Vongthilath-Moeung R, Poncet A, Renzi G, Schrenzel J, Janssens JP. Time to Detection of Growth for Mycobacterium tuberculosis in a Low Incidence Area. Front Cell Infect Microbiol. 2021;11:704169. [PMC free article: PMC8418320] [PubMed: 34490143]

9.

Chen Y, Liu J, Zhang Q, Wang Q, Chai L, Chen H, Li D, Qiu Y, Wang Y, Shen N, Wang J, Xie X, Li S, Li M. Epidemiological features and temporal trends of HIV-negative tuberculosis burden from 1990 to 2019: a retrospective analysis based on the Global Burden of Disease Study 2019. BMJ Open. 2023 Sep 28;13(9):e074134. [PMC free article: PMC10546119] [PubMed: 37770275]

10.

Jiménez-Corona ME, García-García L, DeRiemer K, Ferreyra-Reyes L, Bobadilla-del-Valle M, Cano-Arellano B, Canizales-Quintero S, Martínez-Gamboa A, Small PM, Sifuentes-Osornio J, Ponce-de-León A. Gender differentials of pulmonary tuberculosis transmission and reactivation in an endemic area. Thorax. 2006 Apr;61(4):348-53. [PMC free article: PMC2104608] [PubMed: 16449260]

11.

Gao J, Zheng P, Fu H. Prevalence of TB/HIV co-infection in countries except China: a systematic review and meta-analysis. PLoS One. 2013;8(5):e64915. [PMC free article: PMC3669088] [PubMed: 23741419]

12.

Trinh QM, Nguyen HL, Nguyen VN, Nguyen TV, Sintchenko V, Marais BJ. Tuberculosis and HIV co-infection-focus on the Asia-Pacific region. Int J Infect Dis. 2015 Mar;32:170-8. [PubMed: 25809776]

13.

Aabye MG, Ravn P, PrayGod G, Jeremiah K, Mugomela A, Jepsen M, Faurholt D, Range N, Friis H, Changalucha J, Andersen AB. The impact of HIV infection and CD4 cell count on the performance of an interferon gamma release assay in patients with pulmonary tuberculosis. PLoS One. 2009;4(1):e4220. [PMC free article: PMC2626632] [PubMed: 19156218]

14.

Lin PL, Flynn JL. Understanding latent tuberculosis: a moving target. J Immunol. 2010 Jul 01;185(1):15-22. [PMC free article: PMC3311959] [PubMed: 20562268]

15.

Behr MA, Edelstein PH, Ramakrishnan L. Revisiting the timetable of tuberculosis. BMJ. 2018 Aug 23;362:k2738. [PMC free article: PMC6105930] [PubMed: 30139910]

16.

Huang L, Nazarova EV, Russell DG. Mycobacterium tuberculosis: Bacterial Fitness within the Host Macrophage. Microbiol Spectr. 2019 Mar;7(2) [PMC free article: PMC6459685] [PubMed: 30848232]

17.

Ehrt S, Schnappinger D, Rhee KY. Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis. Nat Rev Microbiol. 2018 Aug;16(8):496-507. [PMC free article: PMC6045436] [PubMed: 29691481]

18.

Pavlinac PB, Lokken EM, Walson JL, Richardson BA, Crump JA, John-Stewart GC. Mycobacterium tuberculosis bacteremia in adults and children: a systematic review and meta-analysis. Int J Tuberc Lung Dis. 2016 Jul;20(7):895-902. [PMC free article: PMC5827940] [PubMed: 27287641]

19.

Kiazyk S, Ball TB. Latent tuberculosis infection: An overview. Can Commun Dis Rep. 2017 Mar 02;43(3-4):62-66. [PMC free article: PMC5764738] [PubMed: 29770066]

20.

Comstock GW, Livesay VT, Woolpert SF. The prognosis of a positive tuberculin reaction in childhood and adolescence. Am J Epidemiol. 1974 Feb;99(2):131-8. [PubMed: 4810628]

21.

Ai JW, Ruan QL, Liu QH, Zhang WH. Updates on the risk factors for latent tuberculosis reactivation and their managements. Emerg Microbes Infect. 2016 Feb 03;5(2):e10. [PMC free article: PMC4777925] [PubMed: 26839146]

22.

Loddenkemper R, Lipman M, Zumla A. Clinical Aspects of Adult Tuberculosis. Cold Spring Harb Perspect Med. 2015 Feb 06;6(1):a017848. [PMC free article: PMC4691808] [PubMed: 25659379]

23.

Narasimhan P, Wood J, Macintyre CR, Mathai D. Risk factors for tuberculosis. Pulm Med. 2013;2013:828939. [PMC free article: PMC3583136] [PubMed: 23476764]

24.

Iossifova Y, Bailey R, Wood J, Kreiss K. Concurrent silicosis and pulmonary mycosis at death. Emerg Infect Dis. 2010 Feb;16(2):318-20. [PMC free article: PMC2958007] [PubMed: 20113570]

25.

Hermansen T, Lillebaek T, Hansen AB, Andersen PH, Ravn P. QuantiFERON–TB Gold In-Tube test performance in Denmark. Tuberculosis (Edinb). 2014 Dec;94(6):616-21. [PubMed: 25448289]

26.

Menzies D, Pai M, Comstock G. Meta-analysis: new tests for the diagnosis of latent tuberculosis infection: areas of uncertainty and recommendations for research. Ann Intern Med. 2007 Mar 06;146(5):340-54. [PubMed: 17339619]

27.

Pollock L, Basu Roy R, Kampmann B. How to use: interferon γ release assays for tuberculosis. Arch Dis Child Educ Pract Ed. 2013 Jun;98(3):99-105. [PubMed: 23580543]

28.

Huebner RE, Schein MF, Bass JB. The tuberculin skin test. Clin Infect Dis. 1993 Dec;17(6):968-75. [PubMed: 8110954]

29.

Morrison J, Pai M, Hopewell PC. Tuberculosis and latent tuberculosis infection in close contacts of people with pulmonary tuberculosis in low-income and middle-income countries: a systematic review and meta-analysis. Lancet Infect Dis. 2008 Jun;8(6):359-68. [PubMed: 18450516]

30.

Nayak S, Acharjya B. Mantoux test and its interpretation. Indian Dermatol Online J. 2012 Jan;3(1):2-6. [PMC free article: PMC3481914] [PubMed: 23130251]

31.

Haimi-Cohen Y, Zeharia A, Mimouni M, Soukhman M, Amir J. Skin indurations in response to tuberculin testing in patients with nontuberculous mycobacterial lymphadenitis. Clin Infect Dis. 2001 Nov 15;33(10):1786-8. [PubMed: 11595991]

32.

Lindeboom JA, Kuijper EJ, Prins JM, Bruijnesteijn van Coppenraet ES, Lindeboom R. Tuberculin skin testing is useful in the screening for nontuberculous mycobacterial cervicofacial lymphadenitis in children. Clin Infect Dis. 2006 Dec 15;43(12):1547-51. [PubMed: 17109286]

33.

Farhat M, Greenaway C, Pai M, Menzies D. False-positive tuberculin skin tests: what is the absolute effect of BCG and non-tuberculous mycobacteria? Int J Tuberc Lung Dis. 2006 Nov;10(11):1192-204. [PubMed: 17131776]

34.

Pai M, Behr M. Latent Mycobacterium tuberculosis Infection and Interferon-Gamma Release Assays. Microbiol Spectr. 2016 Oct;4(5) [PubMed: 27763261]

35.

Yang C, Luo X, Fan L, Sha W, Xiao H, Cui H. Performance of Interferon-Gamma Release Assays in the Diagnosis of Nontuberculous Mycobacterial Diseases-A Retrospective Survey From 2011 to 2019. Front Cell Infect Microbiol. 2020;10:571230. [PMC free article: PMC7930076] [PubMed: 33680977]

36.

Augustynowicz-Kopeć E, Siemion-Szcześniak I, Zabost A, Wyrostkiewicz D, Filipczak D, Oniszh K, Gawryluk D, Radzikowska E, Korzybski D, Szturmowicz M. Interferon Gamma Release Assays in Patients with Respiratory Isolates of Non-Tuberculous Mycobacteria - a Preliminary Study. Pol J Microbiol. 2019;68(1):15-19. [PMC free article: PMC7256814] [PubMed: 31050249]

37.

Nienhaus A, Schablon A, Costa JT, Diel R. Systematic review of cost and cost-effectiveness of different TB-screening strategies. BMC Health Serv Res. 2011 Sep 30;11:247. [PMC free article: PMC3196701] [PubMed: 21961888]

38.

Mahon J, Beale S, Holmes H, Arber M, Nikolayevskyy V, Alagna R, Manissero D, Dowdy D, Migliori GB, Sotgiu G, Duarte R. A systematic review of cost-utility analyses of screening methods in latent tuberculosis infection in high-risk populations. BMC Pulm Med. 2022 Oct 05;22(1):375. [PMC free article: PMC9533619] [PubMed: 36199061]

39.

Nguyen DT, Teeter LD, Graves J, Graviss EA. Characteristics Associated with Negative Interferon-γ Release Assay Results in Culture-Confirmed Tuberculosis Patients, Texas, USA, 2013-2015. Emerg Infect Dis. 2018 Mar;24(3):534-540. [PMC free article: PMC5823348] [PubMed: 29460756]

40.

Yamasue M, Komiya K, Usagawa Y, Umeki K, Nureki SI, Ando M, Hiramatsu K, Nagai H, Kadota JI. Factors associated with false negative interferon-γ release assay results in patients with tuberculosis: A systematic review with meta-analysis. Sci Rep. 2020 Jan 31;10(1):1607. [PMC free article: PMC6994686] [PubMed: 32005930]

41.

Slater M, Parsonnet J, Banaei N. Investigation of false-positive results given by the QuantiFERON-TB Gold In-Tube assay. J Clin Microbiol. 2012 Sep;50(9):3105-7. [PMC free article: PMC3421800] [PubMed: 22785197]

42.

Powell RD, Whitworth WC, Bernardo J, Moonan PK, Mazurek GH. Unusual interferon gamma measurements with QuantiFERON-TB Gold and QuantiFERON-TB Gold In-Tube tests. PLoS One. 2011;6(6):e20061. [PMC free article: PMC3110578] [PubMed: 21687702]

43.

Chee CB, KhinMar KW, Gan SH, Barkham TM, Koh CK, Shen L, Wang YT. Tuberculosis treatment effect on T-cell interferon-gamma responses to Mycobacterium tuberculosis-specific antigens. Eur Respir J. 2010 Aug;36(2):355-61. [PubMed: 19926734]

44.

Dyrhol-Riise AM, Gran G, Wentzel-Larsen T, Blomberg B, Haanshuus CG, Mørkve O. Diagnosis and follow-up of treatment of latent tuberculosis; the utility of the QuantiFERON-TB Gold In-tube assay in outpatients from a tuberculosis low-endemic country. BMC Infect Dis. 2010 Mar 08;10:57. [PMC free article: PMC2842274] [PubMed: 20210999]

45.

Wong B, Tan E, McLean-Tooke A. Pulmonary granulomas in a patient with positive ANCA and history of tuberculosis: case report. BMC Pulm Med. 2020 Aug 14;20(1):219. [PMC free article: PMC7427886] [PubMed: 32795275]

46.

Gupta D, Agarwal R, Aggarwal AN, Jindal SK. Sarcoidosis and tuberculosis: the same disease with different manifestations or similar manifestations of different disorders. Curr Opin Pulm Med. 2012 Sep;18(5):506-16. [PubMed: 22759770]

47.

Banner AS. Tuberculosis. Clinical aspects and diagnosis. Arch Intern Med. 1979 Dec;139(12):1387-90. [PubMed: 92919]

48.

Saavedra FT, Sierra LL, Zuluaica AM, Botero EC. Diagnosing Caplan syndrome in a patient with silicosis and rheumatoid arthritis: imaging shows miliary pattern and cavity lung lesions. Lancet. 2023 Jun 24;401(10394):2148. [PubMed: 37355292]

49.

Nakatudde I, Kasirye P, Kiguli S, Musoke P. It is not always Tuberculosis! A case of pulmonary cryptococcosis in an immunocompetent child in Uganda. Afr Health Sci. 2021 Sep;21(3):990-994. [PMC free article: PMC8843282] [PubMed: 35222559]

50.

Kasaie P, Andrews JR, Kelton WD, Dowdy DW. Timing of tuberculosis transmission and the impact of household contact tracing. An agent-based simulation model. Am J Respir Crit Care Med. 2014 Apr 01;189(7):845-52. [PubMed: 24559425]

51.

Chaw L, Mat Salleh L, Abdul Hamid R, Thu K. Epidemiology of extrapulmonary tuberculosis in Brunei Darussalam: a retrospective cohort study. BMJ Open. 2023 Aug 23;13(8):e073266. [PMC free article: PMC10450043] [PubMed: 37612110]

52.

Gygli SM, Borrell S, Trauner A, Gagneux S. Antimicrobial resistance in Mycobacterium tuberculosis: mechanistic and evolutionary perspectives. FEMS Microbiol Rev. 2017 May 01;41(3):354-373. [PubMed: 28369307]

53.

Huaman MA, Sterling TR. Treatment of Latent Tuberculosis Infection-An Update. Clin Chest Med. 2019 Dec;40(4):839-848. [PMC free article: PMC7043866] [PubMed: 31731988]

54.

Nahid P, Dorman SE, Alipanah N, Barry PM, Brozek JL, Cattamanchi A, Chaisson LH, Chaisson RE, Daley CL, Grzemska M, Higashi JM, Ho CS, Hopewell PC, Keshavjee SA, Lienhardt C, Menzies R, Merrifield C, Narita M, O'Brien R, Peloquin CA, Raftery A, Saukkonen J, Schaaf HS, Sotgiu G, Starke JR, Migliori GB, Vernon A. Executive Summary: Official American Thoracic Society/Centers for Disease Control and Prevention/Infectious Diseases Society of America Clinical Practice Guidelines: Treatment of Drug-Susceptible Tuberculosis. Clin Infect Dis. 2016 Oct 01;63(7):853-67. [PMC free article: PMC6366011] [PubMed: 27621353]

55.

Heyckendorf J, Gillespie SH, Ruhwald M. Culture-free proof of Mycobacterium tuberculosis - a new assay for viable bacteria. EBioMedicine. 2020 Dec;62:103117. [PMC free article: PMC7658474] [PubMed: 33181467]

56.

Chang V, Ling RH, Velen K, Fox GJ. Latent tuberculosis infection among contacts of patients with multidrug-resistant tuberculosis in New South Wales, Australia. ERJ Open Res. 2021 Jul;7(3) [PMC free article: PMC8450450] [PubMed: 34549043]

57.

Kritski AL, Marques MJ, Rabahi MF, Vieira MA, Werneck-Barroso E, Carvalho CE, Andrade Gde N, Bravo-de-Souza R, Andrade LM, Gontijo PP, Riley LW. Transmission of tuberculosis to close contacts of patients with multidrug-resistant tuberculosis. Am J Respir Crit Care Med. 1996 Jan;153(1):331-5. [PubMed: 8542139]

58.

van der Werf MJ, Sandgren A, Manissero D. Management of contacts of multidrug-resistant tuberculosis patients in the European Union and European Economic Area. Int J Tuberc Lung Dis. 2012;16(3):426. [PubMed: 22640458]

59.

Fox GJ, Schaaf HS, Mandalakas A, Chiappini E, Zumla A, Marais BJ. Preventing the spread of multidrug-resistant tuberculosis and protecting contacts of infectious cases. Clin Microbiol Infect. 2017 Mar;23(3):147-153. [PubMed: 27592087]

60.

Nolan CM, Goldberg SV, Buskin SE. Hepatotoxicity associated with isoniazid preventive therapy: a 7-year survey from a public health tuberculosis clinic. JAMA. 1999 Mar 17;281(11):1014-8. [PubMed: 10086436]

61.

Ngongondo M, Miyahara S, Hughes MD, Sun X, Bisson GP, Gupta A, Kumwenda J, Lavenberg JA, Torres TS, Nyirenda M, Kidonge KK, Hosseinipour MC., AIDS Clinical Trials Group A5274 (REMEMBER) Study Team. Hepatotoxicity During Isoniazid Preventive Therapy and Antiretroviral Therapy in People Living With HIV With Severe Immunosuppression: A Secondary Analysis of a Multi-Country Open-Label Randomized Controlled Clinical Trial. J Acquir Immune Defic Syndr. 2018 May 01;78(1):54-61. [PMC free article: PMC5889344] [PubMed: 29406428]

62.

Puyat JH, Shulha HP, Balshaw R, Campbell JR, Law S, Menzies R, Johnston JC. How Well Does TSTin3D Predict Risk of Active Tuberculosis in the Canadian Immigrant Population? An External Validation Study. Clin Infect Dis. 2021 Nov 02;73(9):e3486-e3495. [PMC free article: PMC8631069] [PubMed: 32556316]

63.

Scolarici M, Dekitani K, Chen L, Sokol-Anderson M, Hoft DF, Chatterjee S. A scoring strategy for progression risk and rates of treatment completion in subjects with latent tuberculosis. PLoS One. 2018;13(11):e0207582. [PMC free article: PMC6237398] [PubMed: 30440033]

64.

Timmins GS, Deretic V. Mechanisms of action of isoniazid. Mol Microbiol. 2006 Dec;62(5):1220-7. [PubMed: 17074073]

65.

Wehrli W. Rifampin: mechanisms of action and resistance. Rev Infect Dis. 1983 Jul-Aug;5 Suppl 3:S407-11. [PubMed: 6356275]

66.

Zheng C, Hu X, Zhao L, Hu M, Gao F. Clinical and pharmacological hallmarks of rifapentine's use in diabetes patients with active and latent tuberculosis: do we know enough? Drug Des Devel Ther. 2017;11:2957-2968. [PMC free article: PMC5644564] [PubMed: 29066867]

67.

Lobue P, Menzies D. Treatment of latent tuberculosis infection: An update. Respirology. 2010 May;15(4):603-22. [PubMed: 20409026]

68.

Zenner D, Beer N, Harris RJ, Lipman MC, Stagg HR, van der Werf MJ. Treatment of Latent Tuberculosis Infection: An Updated Network Meta-analysis. Ann Intern Med. 2017 Aug 15;167(4):248-255. [PubMed: 28761946]

69.

Person AK, Sterling TR. Treatment of latent tuberculosis infection in HIV: shorter or longer? Curr HIV/AIDS Rep. 2012 Sep;9(3):259-66. [PMC free article: PMC3410968] [PubMed: 22581360]

70.

Sia IG, Wieland ML. Current concepts in the management of tuberculosis. Mayo Clin Proc. 2011 Apr;86(4):348-61. [PMC free article: PMC3068897] [PubMed: 21454737]

71.

Zellweger JP, Sotgiu G, Corradi M, Durando P. The diagnosis of latent tuberculosis infection (LTBI): currently available tests, future developments, and perspectives to eliminate tuberculosis (TB). Med Lav. 2020 Jun 26;111(3):170-183. [PMC free article: PMC7809945] [PubMed: 32624559]

72.

Aouam K, Chaabane A, Loussaïef C, Ben Romdhane F, Boughattas NA, Chakroun M. [Adverse effects of antitubercular drugs: epidemiology, mechanisms, and patient management]. Med Mal Infect. 2007 May;37(5):253-61. [PubMed: 17336011]

73.

Campbell JR, Trajman A, Cook VJ, Johnston JC, Adjobimey M, Ruslami R, Eisenbeis L, Fregonese F, Valiquette C, Benedetti A, Menzies D. Adverse events in adults with latent tuberculosis infection receiving daily rifampicin or isoniazid: post-hoc safety analysis of two randomised controlled trials. Lancet Infect Dis. 2020 Mar;20(3):318-329. [PubMed: 31866327]

74.

Fountain FF, Tolley EA, Jacobs AR, Self TH. Rifampin hepatotoxicity associated with treatment of latent tuberculosis infection. Am J Med Sci. 2009 May;337(5):317-20. [PubMed: 19295414]

75.

Schaberg T, Rebhan K, Lode H. Risk factors for side-effects of isoniazid, rifampin and pyrazinamide in patients hospitalized for pulmonary tuberculosis. Eur Respir J. 1996 Oct;9(10):2026-30. [PubMed: 8902462]

76.

Franks AL, Binkin NJ, Snider DE, Rokaw WM, Becker S. Isoniazid hepatitis among pregnant and postpartum Hispanic patients. Public Health Rep. 1989 Mar-Apr;104(2):151-5. [PMC free article: PMC1580026] [PubMed: 2495549]

77.

Yimer G, Gry M, Amogne W, Makonnen E, Habtewold A, Petros Z, Aderaye G, Schuppe-Koistinen I, Lindquist L, Aklillu E. Evaluation of patterns of liver toxicity in patients on antiretroviral and anti-tuberculosis drugs: a prospective four arm observational study in ethiopian patients. PLoS One. 2014;9(4):e94271. [PMC free article: PMC3979833] [PubMed: 24714066]

78.

Sharma SK, Balamurugan A, Saha PK, Pandey RM, Mehra NK. Evaluation of clinical and immunogenetic risk factors for the development of hepatotoxicity during antituberculosis treatment. Am J Respir Crit Care Med. 2002 Oct 01;166(7):916-9. [PubMed: 12359646]

79.

Anand AC, Seth AK, Paul M, Puri P. Risk Factors of Hepatotoxicity During Anti-tuberculosis Treatment. Med J Armed Forces India. 2006 Jan;62(1):45-9. [PMC free article: PMC4923276] [PubMed: 27407844]

80.

Steele MA, Burk RF, DesPrez RM. Toxic hepatitis with isoniazid and rifampin. A meta-analysis. Chest. 1991 Feb;99(2):465-71. [PubMed: 1824929]

81.

Zhao H, Wang Y, Zhang T, Wang Q, Xie W. Drug-Induced Liver Injury from Anti-Tuberculosis Treatment: A Retrospective Cohort Study. Med Sci Monit. 2020 Mar 07;26:e920350. [PMC free article: PMC7077058] [PubMed: 32145061]

82.

Aita JF, Calame TR. Peripheral neuropathy secondary to isoniazid-induced pyridoxine deficiency. Md State Med J. 1972 Oct;21(10):68-70. [PubMed: 4353461]

83.

Snider DE. Pyridoxine supplementation during isoniazid therapy. Tubercle. 1980 Dec;61(4):191-6. [PubMed: 6269259]

84.

ZILBER LA, BAJDAKOVA ZL, GARDASJAN AN, KONOVALOV NV, BUNINA TL, BARABADZE EM. THE PREVENTION AND TREATMENT OF ISONIAZID TOXICITY IN THE THERAPY OF PULMONARY TUBERCULOSIS. 2. AN ASSESSMENT OF THE PROPHYLACTIC EFFECT OF PYRIDOXINE IN LOW DOSAGE. Bull World Health Organ. 1963;29(4):457-81. [PMC free article: PMC2554998] [PubMed: 14099673]

85.

Martínez E, Collazos J, Mayo J. Hypersensitivity reactions to rifampin. Pathogenetic mechanisms, clinical manifestations, management strategies, and review of the anaphylactic-like reactions. Medicine (Baltimore). 1999 Nov;78(6):361-9. [PubMed: 10575418]

86.

Girling DJ, Hitze KL. Adverse reactions to rifampicin. Bull World Health Organ. 1979;57(1):45-9. [PMC free article: PMC2395744] [PubMed: 311712]

87.

MacDougall C, Canonica T, Keh C, P Phan BA, Louie J. Systematic review of drug-drug interactions between rifamycins and anticoagulant and antiplatelet agents and considerations for management. Pharmacotherapy. 2022 Apr;42(4):343-361. [PubMed: 35152432]

88.

Kim HW, Kim JS. Treatment of Latent Tuberculosis Infection and Its Clinical Efficacy. Tuberc Respir Dis (Seoul). 2018 Jan;81(1):6-12. [PMC free article: PMC5771748] [PubMed: 29332319]

89.

Comstock GW. How much isoniazid is needed for prevention of tuberculosis among immunocompetent adults? Int J Tuberc Lung Dis. 1999 Oct;3(10):847-50. [PubMed: 10524579]

90.

den Boon S, Matteelli A, Getahun H. Rifampicin resistance after treatment for latent tuberculous infection: a systematic review and meta-analysis. Int J Tuberc Lung Dis. 2016 Aug;20(8):1065-71. [PMC free article: PMC5642842] [PubMed: 27393541]

91.

Balcells ME, Thomas SL, Godfrey-Faussett P, Grant AD. Isoniazid preventive therapy and risk for resistant tuberculosis. Emerg Infect Dis. 2006 May;12(5):744-51. [PMC free article: PMC3374455] [PubMed: 16704830]

92.

Sterling TR, Njie G, Zenner D, Cohn DL, Reves R, Ahmed A, Menzies D, Horsburgh CR, Crane CM, Burgos M, LoBue P, Winston CA, Belknap R. Guidelines for the Treatment of Latent Tuberculosis Infection: Recommendations from the National Tuberculosis Controllers Association and CDC, 2020. MMWR Recomm Rep. 2020 Feb 14;69(1):1-11. [PMC free article: PMC7041302] [PubMed: 32053584]

93.

Hirsch-Moverman Y, Colson PW, Bethel J, Franks J, El-Sadr WM. Can a peer-based intervention impact adherence to the treatment of latent tuberculous infection? Int J Tuberc Lung Dis. 2013 Sep;17(9):1178-85. [PMC free article: PMC4477799] [PubMed: 23928167]

94.

Kahwati LC, Feltner C, Halpern M, Woodell CL, Boland E, Amick HR, Weber RP, Jonas DE. Primary Care Screening and Treatment for Latent Tuberculosis Infection in Adults: Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA. 2016 Sep 06;316(9):970-83. [PubMed: 27599332]

95.

US Preventive Services Task Force. Mangione CM, Barry MJ, Nicholson WK, Cabana M, Chelmow D, Coker TR, Davis EM, Donahue KE, Jaén CR, Li L, Ogedegbe G, Rao G, Ruiz JM, Stevermer J, Underwood SM, Wong JB. Screening for Latent Tuberculosis Infection in Adults: US Preventive Services Task Force Recommendation Statement. JAMA. 2023 May 02;329(17):1487-1494. [PubMed: 37129649]

96.

Kunin M, Timlin M, Lemoh C, Sheffield DA, Russo A, Hazara S, McBride J. Improving screening and management of latent tuberculosis infection: development and evaluation of latent tuberculosis infection primary care model. BMC Infect Dis. 2022 Jan 12;22(1):49. [PMC free article: PMC8756639] [PubMed: 35022023]

97.

Kerani RP, Shapiro AE, Strick LB. A Pilot TB Screening Model in a U.S. Prison Population Using Tuberculin Skin Test and Interferon Gamma Release Assay Based on Country of Origin. J Correct Health Care. 2021 Dec;27(4):259-264. [PMC free article: PMC8917832] [PubMed: 34652245]

98.

Rendleman NJ. Mandated tuberculosis screening in a community of homeless people. Am J Prev Med. 1999 Aug;17(2):108-13. [PubMed: 10490052]

99.

Mehta B, Zapantis E, Petryna O, Efthimiou P. Screening Optimization of Latent Tuberculosis Infection in Rheumatoid Arthritis Patients. Arthritis. 2015;2015:569620. [PMC free article: PMC4532802] [PubMed: 26294972]

Disclosure: Cody Price declares no relevant financial relationships with ineligible companies.

Disclosure: Andrew Nguyen declares no relevant financial relationships with ineligible companies.