Introduction
Tuberculosis (TB), also known as consumption, wasting disease and the
white plague, has impacted many people over the centuries. In 1865,
French surgeon, Jean-Antoine Villemin proved that the disease was
contagious. In the early 1800s, it was thought that TB was hereditary.
In 1882, German scientist Robert Koch discovered the tubercle bacillus
that causes the disease. Prior to Koch’s discovery, the disease was a
slow death sentence without a cure. Sanatoriums were a means of
isolating the person and the disease from the general population.
A breakthrough came in 1943. American scientist Selman Warksman
discovered a drug that could kill TB bacteria. Between 1943 and 1952,
two more drugs were found. After these discoveries, many people with TB
were cured, and the death rate for TB in the United States dropped
dramatically.
Before the discovery of these antibiotics for TB, there was no cure.
Mortality of those with pulmonary tuberculosis was approximately 50
percent. The introduction of anti-tuberculosis drugs in the 1950s and
the development of the various drug regimens meant that by the 1980s,
there was a 98 percent chance of cure. However, treatment must be
continued for as long as six months to ensure cure.
Tuberculosis is a treatable disease if it is diagnosed early, but
nearly two-thirds of the people in the world with active TB are not
receiving treatment. In developing countries, patients are not always
able to afford the medications or they discontinue treatment early. This
leads to an increase in drug-resistant strains. The incidence of
single-drug resistance and multi-drug resistant TB strains is a concern
because these forms of TB are more difficult and expensive to treat.
Tuberculosis is the second most common infectious disease in the
world and the leading cause of death among women and persons with AIDS.
In the second half of the 19th century, a new movement for the
treatment of tuberculosis came into existence, the sanatoria. These were
something of a cross between a hotel and a hospital where tuberculosis
patients would spend months or even years. Treatment was a combination
of sunlight, diet and gentle exercise. It is doubtful whether the
sanatoria improved survival of the patients but may have reduced
tuberculosis in the community by removing infectious patients, thereby
reducing transmission.
By the end of the 1930s, surgeons were providing some means of
treatment for tuberculosis by various surgical procedures, attempting to
obliterate the cavities that formed in the lung of seriously ill
tuberculosis patients by collapsing part of the lung itself. These
techniques varied from introducing air into the pleural cavity (the
artificial pneumothorax) to removing some of the upper ribs
(thoracoplasty). Surgery usually took place in the sanatoria. The
surgical methods of treatment remained in vogue for the next thirty
years until it was realized that drug treatment alone provided effective
cure.
By the end of the 1950s, the introduction of drug therapy for
tuberculosis was considerably reducing the need for sanatoria beds in
most developed countries. It was also realized that drug treatment,
which could be given at home, might be able to eliminate the need for
hospitalization for all but the sickest tuberculosis patients.
By the mid-1970s, most sanatoriums in the United States had closed.
In the next two decades, people began to hope that TB could be
eliminated from the United States like polio and smallpox.
Tb is spread from person to person through the air. When a person
with pulmonary TB coughs, sneezes, speaks or sings, droplet nuclei
containing mycobacterium tuberculosis or the tubercle bacillus are
expelled into the air. Depending on the environment, these tiny
particles (1-5 microns in diameter) can remain suspended in the air for
several hours. The TB infection begins when the tubercle bacilli
multiply in the small air sacs of the lungs. A small number enter the
bloodstream and spread throughout the body, but the body’s immune
system usually keeps the bacilli under control.
In latent tuberculosis, the body’s immune system has walled off the
bacteria into tiny capsules called tubercles. Although the TB-causing
bacteria are in your body, you cannot spread the infection to others.
However, you are at risk of developing active TB if your immune system
becomes weakened. If another person inhales air containing droplet
nuclei, transmission may occur. The probability that TB will be
transmitted depends on four factors:
1. The infectiousness of the person with TB (the number of organisms
expelled into the air)
2. The environment in which exposure occurred
3. The duration of the exposure
4. The virulence of the organism
The best way to stop transmission is to isolate patients with
infectious TB immediately and start effective TB therapy. Infectiousness
declines rapidly after adequate therapy is started, as long as the
patient strictly adheres to the prescribed regimen.
When droplet nuclei are inhaled, most of the larger particles become
lodged in the upper respiratory tract, where infection is unlikely to
develop. However smaller droplet nuclei containing the tubercle bacilli
may reach the alveoli, where the infection begins.
The tubercle bacilli that reached the alveoli are ingested by
alveolar macrophages; and the majority of these bacilli are destroyed or
inhibited. A small number multiply intracellularly and are released when
the macrophages die. These bacilli can spread through the lymphatic
channels to regional lymph and then through the bloodstream to more
distant tissues and organs, including areas in which TB disease is most
likely to develop: the apices of the lung, the kidneys, the brain and
bone. Extracellular bacilli attract macrophages from the bloodstream.
The immune system kills most of the bacilli, leading to the formation of
a granuloma. At this point, the person has TB infection, which can be
detected using the tuberculin skin test. It may take two to 10 weeks for
the infected person to develop a positive reaction to the tuberculin
skin test. Immune responses soon develop to kill the bacilli. Within two
to 10 weeks after infection, the immune system is usually able to halt
the multiplication of the tubercle bacilli, preventing further spread.
Infection usually requires repeated exposure to TB bacteria. TB
spreads more rapidly in cramped, enclosed and poorly ventilated spaces
where the chance of repeated exposure is greater.
Tuberculosis is the No. 1 killer among infectious diseases in the
world. The disease kills more people worldwide than AIDS, malaria and
tropical diseases combined, according to the World Health Organization.
Can tuberculosis be prevented by vaccination?
Many individuals who grew up in Canada or other countries outside of
the U.S. have received the Bacille Calmette-Guerin (BCG) vaccine -- an
attenuated strain of mycobacterium. It is generally
accepted that Bacille Calmette-Guerin provides a certain degree of
protection (particularly in young children) against serious forms of
tuberculosis such as miliary tuberculosis and tuberculous meningitis.
BCG is the most widely used TB vaccination; however, the use of this
vaccine makes the diagnosis of latent TB difficult to differentiate an
induration induced by BCG vaccine or from one caused by miliary TB.
Vaccination in childhood has little impact on controlling the spread of
tuberculosis microorganisms in the community because the type of
tuberculosis prevented by it is usually not the infectious form
(smear-positive pulmonary tuberculosis), as this form is infrequent in
childhood.
BCG vaccine is usually given at birth. The vaccine is injected
intradermally on the upper portion of the left arm, at a dose of 0.05 ml
for those up to one year and a dose of 0.1 ml for those more than one
year of age. There is no scientific justification for revaccination with
BCG, and this practice is a waste of resources.
Signs and symptoms of the active disease may include
- Persistent cough of greater than three weeks
- Low-grade fever
- Fatigue
- Loss of appetite and weight
- Night sweats
- Pain with breathing or coughing, and pain in the spine or in the
large joints
- Hemoptysis.
Once infection is established, clinical tuberculosis (TB) may develop
within months or may not occur for years or even decades. In developed
countries, human TB occurs almost exclusively from inhalation of
dispersed droplet nuclei from a person with pulmonary tuberculosis whose
sputum smear is positive. Mycobacterium tuberculosis may float in the
air for several hours, thus increasing the chance of spread. Spread can
occur in mycobacteriology laboratories and autopsy rooms, in part
because the hydrophilic nature of the organism facilitates
aerosolization. Fomites appear to play no role in the spread of disease.
Case rates vary from country, age, race, sex, and socioeconomic status.
TB is still prevalent persons older than 70 years, in whom the disease
occurs in both sexes and all races. TB is twice as prevalent in blacks
as in whites in all age groups. Although specific immunologic defense
against TB occurs only after infection, considerable innate defense may
occur against its initial invasion. Consequently, many healthcare
personnel can work closely with TB patients for years without a
conversion of a skin test.
The following factors increase the risk of contracting tuberculosis:
Lowered immunity: when the immune system is
healthy, a type of white blood cell called a macrophage engulfs the
tuberculosis bacteria and walls it off from the rest of the body.
Weakening of the immune system leaves the body the most vulnerable to
all infections, including tuberculosis. Poor antibody protection allows
the tuberculosis bacteria to spread to other parts of your body.
Poverty, homelessness and drug use: People in such
situations are often in poor health and are more susceptible to
tuberculosis. Conditions that are crowded and poorly ventilated also
help to spread the disease.
Crowded living conditions: People who live in
nursing homes, dormitories or poverty like conditions may experience
greater exposure to the tuberculosis bacteria.
Age: Weakening of the immune system accompanies
aging.
Malnutrition: Poor nutritional status weakens
immunity.
Healthcare work: Regular contact with people who
are ill increase the chances of exposure to the tuberculosis bacteria.
International travel: As people migrate and travel
widely, they may expose others or be exposed to the tuberculosis
bacteria.
Medical Evaluation
A complete medical evaluation for TB includes: medical history,
physical examination, Mantoux tuberculin skin test, chest X-ray,
bacteriologic and/or histological examinations. It is important to ask
persons suspected of having TB about their history of exposure,
infection, or disease.
Screening & Diagnosis
Tests to determine exposure to the tuberculosis bacteria or active
tuberculosis disease include skin test, chest X-ray and culture tests.
The tuberculin skin test, purified protein derivative (PPD), is
performed with an extract of protein from killed tuberculosis germ that
is injected into the skin. If a person has been infected with
tuberculosis, a lump will form at the site of the injection. This is
called a positive skin test. This generally means that TB germs have
infected the body. It does not usually mean the person has the active
disease. People with positive skin tests but without active disease
cannot transmit the infection to others.
A negative reaction to the skin test does not exclude the diagnosis
of TB, especially with patients with severe TB illness or infection with
human immunodeficiency virus (HIV). Also, some persons may not react to
the tuberculin skin test if they are tested too soon after being exposed
to TB. In general it takes two to 10 weeks after infection to develop an
immune response to tuberculin. Persons who have recently been around
someone with TB and who have a negative reaction to the tuberculin skin
test should be retested 10 to 12 weeks after the last time they were
exposed to infectious TB. Children younger than 6 months of age may not
react to the tuberculin skin test because their immune systems are not
fully developed.
Part II of this course will cover tests for screening and
diagnosis, the treatment of TB, practical management, plans of action,
and controls (administrative, engineering, etc.), as well as personal
protective equipment.
Bibliography
American National Standards Institute. American National Standards
for Respiratory Protection. New York: American National Standards
Institute, 1992.
American Thoracic Society/CDC. Diagnositic standards and
classification of tuberculosis. Am Rev of Respir Dis 1990; 142:725-35.
American Thoracic Society/CDC. Treatment of Tuberculosis in the
United States. Am Rev Respir Dis 1992; 1624-35.
CDC. The use of preventative therapy for tuberculosis infection in
the United States: recommendations of the Advisory Committee for
Elimination of Tuberculosis. MMWR. 1990; 39:9-12.
CDC. National action plan to combat multi-drug resistant
tuberculosis. Atlanta: US Department of Health and Human Services,
Public Health Service, CDC, 1992.
CDC. Guidelines for preventing the transmission of tuberculosis in
health-care settings with specific focus on HIV-related issues. MMWR
1990; 39.
CDC. Guidelines for prevention of TB transmission in hospitals.
Atlanta: US Department of Health and Human Services, Public Health
Service, CDC, 1982; DHHS publication no. (CDC) 82-8371.
Crawford JT, Eisenach KD, Bates JH. Diagnosis of Tuberculosis:
Present & Future. Semin Respir Infection 1989; 4:171-81.
Dueli RC, Madden RN. Droplet nuclei produced during dental
treatment of tubercular patients. Oral Surg 1970; 30:711-6.
Howard TP, Solomon DA. Reading the Tuberculin Skin Test: who, when,
and how? Arch Intern Med 1988; 148:2457-9.
Hueber RE, Schein MF, Bass JB Jr. The tuberculin skin test.
Clinical Infect Dis 1993; 17:968-75.
Iseman MD, Madsen LA. Drug –resistant tuberculosis. Clin Chest
Med 1989; 341-5310:
Klien NC, Duncanson FP, Lenox TH III, et al. Use of mycobacterial
smears in the diagnosis of pulmonary tuberculosis in AIDS/ARC
patients. Chest 1989; 95: 1190-2.
Riley RL. Airborne Infection. Am J Med 1974; 466-75.
Riley RL, O’Grady F. Airborne infection: transmission and
control. New York: McMillan, 1961
Sabiston, D. Textbook of Surgery. 1991. Saunders. Chapter IX; p;
1729-1737.
Snider DE Jr. The tuberculosis skin test. Am Rev Respir Dis 1982;
125:108-18.
Williams WW. Guidelines for infection control in hospital
personnel. Infection Control 1983;4 9 (supplement): 326-49.
