2 B.

TUBERCULOSIS (See Exemple)

Mr M 12 year old, admitted to dr soetomo hospital his chief complain is severe
cough(hardly at night)since two year ago very severe cough. she had been taken medicine from
public hospital,but she hasn't recovered from illness ,and she still suffering and hardly to normal
breathing .he has allergic with seafood and cool weather .respratory rate 30x/min breathing
bronchovesicular ,ronchi + on left right lobus of lung O2 adm mucus secretion yelow viscous
KEY WORD

Mr M 12 year old
Complain is severe cough(hardly at night)since two year ago very severe cough
He has allergic with seafood and cool weather
Respiratory rate 30x/min breathing bronchovesicular ,ronchi + on left right lobus
of lung O2 adm mucus secretion yelow viscous

PROBLEMS

Mr M suffered from tuberculosis because of the experienced symptoms similar to

symptoms of tuberculosis disease

TUBERCULOSIS

Defenition of Tubercolosis
Tuberculosis (TB) is a chronic, progressive infection with a period of latency

following initial infection. It occurs most commonly in the lungs. Pulmonary symptoms include
productive cough, chest pain, and dyspnea. Diagnosis is most often by sputum culture and smear.
Treatment is with multiple antimicrobial drugs.

Etiology Tubercolosis

TB properly refers only to disease caused by Mycobacterium tuberculosis. Similar disease

occasionally results from the closely related mycobacteria, M. bovis, M. africanum, and M.
microti.
TB results almost exclusively from inhalation of airborne particles (droplet nuclei)
containing M. tuberculosis. They disperse primarily through coughing, singing, and other forced
respiratory maneuvers by people who have active pulmonary TB and whose sputum contains a
significant number of organisms (typically enough to render the smear positive). People with
pulmonary cavitary lesions are especially infectious. Droplet nuclei containing tubercle bacilli
may remain suspended in room air currents for several hours, increasing the chance of spread.
However, once these droplets land on a surface, it is difficult to resuspend the organisms (eg, by
sweeping the floor, shaking out bed linens) as respirable particles. Although such actions can
resuspend dust particles containing tubercle bacilli, these particles are far too large to reach the
alveolar surfaces necessary to initiate infection. Fomites (eg, contaminated surfaces, food, and
personal respirators) do not appear to facilitate spread.
Although there is wide variability, patients with pulmonary TB infect about 7 close contacts,
on average, but most of those infected do not develop active disease. Transmission is enhanced
by frequent or prolonged exposure to a patient who is dispersing large numbers of tubercle bacilli
in overcrowded, enclosed, poorly ventilated spaces; thus, people living in poverty or in
institutions are at particular risk. Health care practitioners who have close contact with active
cases have increased risk. However, once effective treatment begins, cough rapidly decreases,
organisms are inactivated, and within weeks, TB is no longer contagious.

Much less commonly, spread results from aerosolization of organisms after irrigation of
infected wounds, in mycobacteriology laboratories, or in autopsy rooms. TB of the tonsils,
lymph nodes, abdominal organs, bones, and joints was once commonly caused by ingestion of
milk or milk products (eg, cheese) contaminated with M. bovis, but this transmission route has
been largely eradicated in developed countries by slaughter of cows that test positive on a
tuberculin skin test and by pasteurization of milk. Tuberculosis due to M. bovis still occurs in
developing countries and in immigrants from developing countries where bovine tuberculosis is
endemic (eg, some Latin American countries).

Risk Factors Tuberculosis

HIV infection is the greatest single medical risk factor because cell-mediated immunity,
which is impaired by HIV, is essential for defense against TB; other immunosuppressive illnesses
(eg, diabetes) or therapies (eg, tumor necrosis factor [TNF] inhibitors, corticosteroids) increase
risk but less than HIV.
Age has traditionally been considered an independent risk factor because the elderly have
more years of potential exposure and are more likely to have impaired immunity. However, in
the US, the difference in the age-specific case rate is no longer as large, probably because the
incidence of infectious cases (and hence lifetime risk of significant exposure) has declined.

Pathophysiology

Tubercle bacilli initially cause a primary infection, which only rarely causes acute illness.
Most (about 95%) primary infections are asymptomatic and followed by a latent (dormant)
phase. However, a variable percentage of latent infections subsequently reactivate with
symptoms and signs of disease. Infection is usually not transmissible in the primary stage and is
never contagious in the latent stage.
Primary infection: Infection requires inhalation of particles small enough to traverse the
upper respiratory defenses and deposit deep in the lung, usually in the subpleural airspaces of the
lower lung. Large droplets tend to lodge in the more proximal airways and typically do not result
in infection. Infection usually begins from a single initial focus.

To initiate infection, tubercle bacilli must be ingested by alveolar macrophages. Tubercle

bacilli that are not killed by the macrophages actually replicate inside them, ultimately killing the
host macrophage (with the help of CD8 lymphocytes); inflammatory cells are attracted to the
area, causing a focal pneumonitis that evolves into the characteristic tubercles seen
histologically. In the early weeks of infection, some infected macrophages migrate to regional
lymph nodes (eg, hilar, mediastinal), where they access the bloodstream. Organisms may then
spread hematogenously to any part of the body, particularly the apical-posterior portion of the
lungs, epiphyses of the long bones, kidneys, vertebral bodies, and meninges.
In 95% of cases, after about 3 wk of uninhibited growth, the immune system suppresses
bacillary replication before symptoms or signs develop. Foci of infection in the lung or other
sites resolve into epithelioid cell granulomas, which may have caseous and necrotic centers.
Tubercle bacilli can survive in this material for years; the balance between the host's resistance
and microbial virulence determines whether the infection ultimately resolves without treatment,
remains dormant, or becomes active. Infectious foci may leave fibronodular scars in the apices of
one or both lungs (Simon foci), calcified scars from the primary infection (Ghon foci), or
calcified hilar lymph nodes. The tuberculin skin test (see Mycobacteria: Skin testing) and the
newer interferon- release assay become positive.
Less often, the primary focus immediately progresses, causing acute illness with pneumonia
(sometimes cavitary), pleural effusion, and marked mediastinal or hilar lymph node enlargement
(which, in children, may compress bronchi). Small pleural effusions are predominantly
lymphocytic, typically contain few organisms, and clear within a few weeks. This sequence may
be more common among young children and recently infected or reinfected immunosuppressed
patients. Extrapulmonary TB at any site can sometimes manifest without evidence of lung
involvement. TB lymphadenopathy is the most common extrapulmonary presentation; however,
meningitis is the most feared because of its high mortality in the very young and very old.
Active disease: In about 10% of immunocompetent patients, latent infection develops into
active disease, although the percentage varies significantly by age and other risk factors. In 50 to
80% of those who develop active disease, TB reactivates within the first 2 yr, but it can occur
decades later. Any organ initially seeded may become a site of reactivation, but reactivation

occurs most often in the lung apices, presumably because of favorable local conditions such as
high O2 tension. Ghon foci and affected hilar lymph nodes are much less likely to be sites of
reactivation.
Conditions that facilitate activation include impaired immunity (particularly HIV infection),
certain immunosuppressants (eg, corticosteroids, infliximab ,other TNF inhibitors), gastrectomy,
jejunoileal bypass surgery, silicosis, renal insufficiency, stress, diabetes, head or neck cancer,
significant weight loss, adolescence, and advanced age (particularly > 70 yr).
TB damages tissues through delayed-type hypersensitivity (DTHsee Allergic and Other
Hypersensitivity Disorders: Type IV), typically producing granulomatous necrosis with a caseous
histologic appearance. Lung lesions are characteristically but not invariably cavitary, especially
in immunosuppressed patients with impaired DTH. Pleural effusion is less common than in
progressive primary TB but may result from direct extension or hematogenous spread. Rupture
of a large tuberculous lesion into the pleural space may cause empyema with or without
bronchopleural fistula and sometimes causes pneumothorax. In the prechemotherapy era, TB
empyema sometimes complicated medically induced pneumothorax therapy and was usually
rapidly fatal, as was sudden massive hemoptysis due to erosion of a pulmonary artery by an
enlarging cavity.
The course varies greatly, depending on the virulence of the organism and the state of host
defenses. The course may be rapid among blacks, American Indians, and other populations who
have not had as many centuries of selective pressure to develop innate or natural immunity as
descendents of the European and American TB epidemics have had. The course is often more
indolent in the latter populations.
Acute respiratory distress syndrome (ARDS), which appears to be due to hypersensitivity to
TB antigens, develops rarely after diffuse hematogenous spread or rupture of a large cavity with
spillage into the lungs

Symptoms and Signs

In active pulmonary TB, even moderate or severe disease, patients may have no symptoms,
except not feeling well, anorexia, fatigue, and weight loss, which develop gradually over
several weeks, or they may have more specific symptoms. Cough is most common. At first, it
may be minimally productive of yellow or green sputum, usually on rising, but cough may
become more productive as the disease progresses. Hemoptysis occurs only with cavitary TB
(sometimes due to fungal growth in a cavity). Low-grade fever is common but not invariable.
Drenching night sweats are a classic symptom but are neither common in nor specific for TB.
Dyspnea may result from lung parenchymal damage, spontaneous pneumothorax, or pleural TB
with effusion.
With HIV coinfection, the clinical presentation is often atypical because DTH is impaired;
patients are more likely to have symptoms of extrapulmonary or disseminated disease.
Diagnosis

Chest x-ray
Tuberculin skin test
Acid-fast stain and culture
When available, DNA-based testing

Pulmonary TB is often suspected based on chest x-rays taken while evaluating respiratory
symptoms (cough > 3 wk, hemoptysis, chest pain, dyspnea), an unexplained illness, FUO, or a
positive tuberculin skin test (see Mycobacteria: Skin testing).
Initial tests are chest x-ray, sputum examination, and tuberculin skin testing. If the chest xray is highly characteristic (upper lobe lung cavitation) in patients with TB risk factors, sputum
examination is still required, but skin testing is often not done.

Chest x-ray
In adults, a multinodular infiltrate above or behind the clavicle (the most characteristic

location, most visible in an apical-lordotic view or with CT) suggests reactivation of TB. Middle
and lower lung infiltrates are nonspecific but should prompt suspicion of primary TB in patients
(usually young) whose symptoms or exposure history suggests recent infection, particularly if

there is pleural effusion. Calcified hilar nodes may be present; they may result from primary TB
infection but also may result from histoplasmosis in areas where histoplasmosis is endemic (eg,
the Ohio River Valley).

Sputum examination
Sputum is tested for the presence of acid-fast bacilli (AFB). Tubercle bacilli are

nominally gram-positive but take up Gram stain inconsistently; samples are best prepared with
Ziehl-Neelsen or Kinyoun stains for conventional light microscopy or fluorochrome stains for
fluorescent microscopy.
Drug susceptibility tests (DSTs) should be done on initial isolates from all patients to identify an
effective anti-TB regimen. These tests should be repeated if patients continue to produce culturepositive sputum after 3 mo of treatment or if cultures become positive after a period of negative
cultures. Results of DSTs may take up to 8 wk if conventional bacteriologic methods are used.
However, several new molecular DSTs can detect drug resistance in a sputum sample within
hours.

Tests of other specimens

Transbronchial biopsies can be done on infiltrative lesions, and samples are submitted for
culture, histologic evaluation, and molecular testing. Gastric washings, which are culturepositive in a minority of samples, are no longer commonly used except in small children, who
usually cannot produce a good sputum specimen. Ideally, biopsied samples of other tissue should
be cultured fresh, but NAAT can be used for fixed tissues (eg, for biopsied lymph node if
histologic examination unexpectedly detects granulomatous changes). The latter use of NAAT
has not been approved but can be extremely useful, although positive and negative predictive
values have not been established.

Skin testing

Multiple-puncture devices (tine test) are no longer recommended. The tuberculin skin test
(TST; Mantoux or PPDpurified protein derivative) is usually done, although it is a test of

infection, latent or active, and is not diagnostic of active disease. The standard dose in the US of
5 tuberculin units (TU) of PPD in 0.1 mL of solution is injected on the volar forearm. It is critical
to give the injection intradermally, not subcutaneously. A well-demarcated bleb or wheal should
result immediately. The diameter of induration (not erythema) transverse to the long axis of the
arm is measured 48 to 72 h after injection. Recommended cutoff points for a positive reaction
depend on the clinical setting:

Treatment of Tuberculosis

Most patients with uncomplicated TB and all patients with complicating illnesses (eg, AIDS,
hepatitis, diabetes), adverse drug reactions, or drug resistance should be referred to a TB
specialist. (See also the Joint Statement from the American Thoracic Society, Centers for Disease
Control and Prevention, and the Infectious Diseases Society of America: Treatment of
Tuberculosis.) However, most TB can be fully treated at home with instructions on how to avoid
spreading disease; these measures include
1. Staying at home
2. Avoiding visitors (previously exposed family members may stay)
3. Covering coughs with a tissue or hand
Surgical face masks for TB patients are stigmatizing and are generally not recommended for
cooperative patients. For drug-susceptible TB that is being treated effectively, precautions must
be continued for at least 2 wk in or outside the hospital. For patients with MDR-TB and XDRTB, response to treatment may be slower, and the consequences of transmission greater; thus,
precautions are continued longer, until there is clear evidence of treatment response.

Hospitalization

The main indications for hospitalization are

1. Serious concomitant illness

2. Need for diagnostic procedures

3. Social issues (eg, homelessness)
4. Need for respiratory isolation, as for people living in congregate settings where
previously unexposed people would be regularly encountered
Initially, all hospitalized patients should be in respiratory isolation, ideally in a negativepressure room with 6 to 12 air changes/h. Anyone entering the room should wear a respirator
(not a surgical mask) that has been appropriately fitted and that meets National Institute for
Occupational Safety and Health certification (N-95 or greater). Because risk of exposing other
hospitalized patients is high, release from respiratory isolation usually requires 3 negative
sputum smears over 2 days, including at least one early-morning negative specimen.

Public health considerations: To improve treatment adherence, ensure cure, and limit
transmission and the development of drug-resistant strains, public health programs
closely monitor treatment, even if patients are being treated by a private physician. In
most states, TB care (including skin testing, chest x-rays, and drugs) is available free
through public health clinics to reduce barriers to treatment.

Increasingly, optimal patient case management includes supervision by public health

personnel of the ingestion of every dose of drug, a strategy known as directly observed therapy
(DOT). DOT increases the likelihood that the full treatment course will be completed from 61%
to 86% (91% with enhanced DOT, in which incentives and enablers such as transportation
vouchers, child care, outreach workers, and meals are provided). DOT is particularly important
1. For children and adolescents
2. For patients with HIV infection, psychiatric illness, or substance abuse
3. After treatment failure, relapse, or development of drug resistance
In some programs, selective self-administered treatment (SAT) is an option for patients who
are committed to treatment; ideally, fixed-dose combination drug preparations are used to avoid

the possibility of monotherapy, which can lead to drug resistance. Mechanical drug monitors
have been advocated to improve adherence with SAT.
Public health departments usually visit homes to evaluate potential barriers to treatment (eg,
extreme poverty, unstable housing, child care problems, alcoholism, mental illness) and to check
for other active cases and close contacts. Close contacts are people who share the same breathing
space for prolonged periods, typically household residents, but often include people at work,
school, and places of recreation. The precise duration and degree of contact that constitutes risk
vary because TB patients vary greatly in infectiousness. For patients who are highly infectious as
evidenced by multiple family members with disease or positive skin tests, even relatively casual
contacts (eg, passengers on the bus they ride) should be referred for skin testing and evaluation
for latent infection (see Mycobacteria: Screening); patients who do not infect any household
contacts are less likely to infect casual contacts.