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Introduction

In contrast with the current world situation, Australia is fortunate in having a low but relatively constant pattern of tuberculosis (TB). This is due predominantly to the reactivation of latent infection in people who were previously infected in their countries of birth or during their childhood in Australia when community TB rates were much higher. The incidence of TB in Australia averages around 1000 new cases per year (in Victoria, 250-320 per year). Approximately 85 per cent of TB notifications occur in people born overseas, with 50 per cent of these cases occurring in the first five years of residence in Australia. There is evidence of only a low level of person-to-person transmission within Australia, mainly in specified risk groups, as shown by DNA fingerprinting studies, that only occasionally demonstrate similar patterns in cases that may be associated. Active TB, therefore, is primarily a disease of human stress due to overcrowding, poverty, poor living conditions, malnutrition, associated illnesses such as HIV co-infection and/or AIDS, malignancies, diabetes, migration, relocation and/or family disruption.

Mycobacterium tuberculosis and the other members of the M. tuberculosis complex - M. bovis, M. africanum and M. microti - are parasites of the pulmonary macrophage. Once infected droplet nuclei are inhaled and deposited on the bronchial mucosa, the organisms are ingested by macrophages and transported into the pulmonary lymphatic system. In the majority of people exposed to infected droplet nuclei, their pulmonary macrophages do not destroy the organisms by phagolysis; rather the organisms are able to inhibit the phagocytic process, and thus replicate within the macrophages whilst being transported to regional lymph nodes or the pleura. This replication occurs before the development of effective cell-mediated immune responses, which normally take between six and 12 weeks (demonstrated by tuberculin skin test conversion). In highly susceptible persons however, extensive lymphatic and haematogenous spread can occur in this period, resulting in widespread seeding of TB, particularly in children and those who are immunosuppressed for whatever reason. This seeding occurs through the lungs, brain, lymph nodes and other organs such as the bones and kidneys. Miliary TB, tuberculous meningitis and TB septicaemia are life-threatening consequences and still represent major causes of death from TB around the world. Over the past couple of centuries, when previously unexposed indigenous populations were exposed to TB infection, high mortality rates from TB disease would follow. Mortality would be due to a septicaemic illness of only a few weeks duration, with the illness rapidly progressing in a manner similar to that of typhoid fever.

In most exposed people, however, the pulmonary macrophages remain contained at the site of infection and in the local regional lymph nodes. As a result, a primary granulomatous lesion (Gohn’s focus) develops, including a local area of pneumonitis and swelling of regional lymph nodes, healing by resolution, scarring, and the eventual deposit of calcium within the scar tissues. Residual infected macrophages can be identified within this scar tissue, containing bacilli that have gone into a state of ‘dormancy’ or latency and that are maintained in this state by the individual’s normal cell-mediated immunity. This state of latency can last for many decades, often until the death of the host (unless some event impairs the cell-mediated defence mechanisms). This ability of M. tuberculosis to change its metabolic state to dormancy over many decades accounts for the persistence of the organism within the macrophage environment, and for the potential for reactivation at any time, resulting in possible transmission to other individuals.

When cell-mediated defence mechanisms are impaired, the bacilli may become metabolically active again, replicate and move outside the macrophage into the surrounding tissues. This is known as 'reactivation', which is the usual pattern of disease development in most cases of active TB in our community. In general terms, only 5-10 per cent of all those who have been infected with TB develop active disease, with the greatest period of risk being in the first two years after infection.

Contents

Foreword
Acknowledgments

1. Introduction
   
   
2. Tuberculin Testing
   • Introduction
   • The Mantoux Text
   • Who Needs a Tuberculin Skin Test?
   • QuantiFERON-TB Assay
   • Information for Service Providers
     
     
3. Laboratory Diagnostic Services for TB and Other Mycobacterial Diseases
   • Introduction
   • Level of Laboratory Service - Mycobateriology
   • Quality Assurance
   • Standards
   • Recent Technological Developments
     
     
4. Treatment of TB
   • Treatment of Active TB Disease
   • Treatment Regimens
   • General Principles
   • Non-Tuberculosis or Opportunistic Mycobacterial Infections
     
     
5. Directly Observed Therapy
   • Introduction
   • Directly Observed Therapy (Short Course) in TB Control
   • Supervision of Treatment in Victoria
     
     
6. Hospital Care of TB
   • Introduction
   • Identification of Patients with Confirmed or Suspected Active TB
   • Guidelines for the Management of Hospitalised Patients with Confirmed or Suspected Active TB
   • Cessation of TB Isolation
   • Management of Patients with Confirmed or Suspected Active TB in Ambulatory Care Settings and Emergency Departments
     
     
7. Preventing TB Infection and Disease among Health Care Workers
   • Introduction
   • Occupational Health and Safety Legislation-Duty of Care of Employers and Employees
   • Strategies for Health Care Institutions
     
     
8. Preventing TB in Institutions
   • Introduction
   • Administrative Controls
   • HIV in the Prison Population
     
     
9. BCG Vaccination
   • Introduction
   • Indications for BCG Vaccination
   • Contraindications to BCG Vaccination
   • Adverse Reactions and Complications
   • Availability of Vaccine
   • Conclusion
     
     
10. Treatment of Latent TB Infection (Preventative Therapy)
    
    
11. HIV Infection and TB
    • Importance
    • Interactions Between HIV and TB
    • Clinical Manifestations
    • Diagnosis
    • Prevention
    • Treatment
    • Monitoring
    • Outcome
      
      
12. TB in Children and Adolescents
    • Introduction
    • Risk of Disease Following Primary Infection
    • Infectivity
    • Diagnosis
    • Treatment of Latent TB Infection
    • Treatment
      
      
13. TB and Pregnancy
    • Effect of Pregnancy on TB
    • Effect of Pregnancy on Latent TB
    • Effect of TB on Pregnancy
    • Anti-Tuberculosis Drugs in Pregnancy
    • Breast Feeding and Anti-Tuberculosis Drugs
    • Management of the Newborn after Delivery
    • Screening for TB During Pregnancy
    • Treatment of Latent TB Infection During Pregnancy
      
      
14. Airlines
    • Introduction
    • Risk of Transmission of TB
    • Recommendations
    • What To Do if a Patient Informs You That They Intend to Travel
    • Contact Tracing
      
      
15. Migrant Screening for TB
    • Introduction
    • Management of TBUs
      
      
16. Contact Tracing
    • Introduction
    • Role of the TB Program, Department of Human Services
    • Management of Contacts
    • BCG Vaccination
    • Special Categories

Appendix A: Abbreviations
Appendix B: Comment on Draft Guidelines

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Management, prevention and control of tuberculosis: Guidelines for health care providers 2002-2005 (400k pdf)