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Tuberculosis
Etiology
• Mycobacterium
tuberculosis
• Aerobic
• Slow-Growing(24-36 hr.
Doubling time)
• Complex cell wall
• Acid fast
• Resistant to drying
EPIDEMIOLOGY
• Susceptibility to infection with M. tuberclosis
disease depends on exposure and person's immune
system
• Without treatment, tuberculosis disease develops
in 5% to 10% of immunologically normal adults with
tuberculosis infection at some time during their
lives
• An estimated 8 million new cases of tuberculosis
occur each year among adults, and 3 million deaths
are attributedto the disease annually.
• In developing countries, 1.3 million new cases of
the disease occur in children younger than 15 years
of age, and 450,000 children die
each year of tuberculosis
• Most children with tubercolusis infection and
disease acquire M. tuberculosis from an adult with
tuberculosis.
• Transmission:person to person
• Children with primary pulmonary tuberculosis
disease rarely, if ever, infect other children or
adults.
• Most initially infectious patients become
noninfectious within 2 weeks of starting effective
treatment, and many become noninfectious within
several days.
CLINICAL MANIFESTATIONS
• Tuberculosis infection (latent tuberculosis)
• Tuberculosis disease(tuberculosis)
Primary pulmonary tuberculosis
• in older infants and children is usually an
asymptomatic infection
• positive TST with minimal abnormalities on the
chest radiograph, such as an infiltrate with hilar
lymphadenopathy or Ghon complex
• Malaise, low-grade fever, erythema nodosum,or
symptoms resulting from lymph node enlargement
may occur after the development of delayed
hypersensitivity,
Progressive primary disease
• is characterized by a primary pneumonia that
develops shortly after initial infection
• Progression of the primary complex to pulmonary
disease or disseminated miliary disease or
progression of CNS granulomas to meningitis
occurs most commonly in the first year of life
Tuberculous pleural effusion
• accompany primary infection, generally represents
the immune response to the organisms
• Pleurocentesis reveals lymphocytes and an
increased protein level
• pleural biopsy may be necessary
Reactivation pulmonary tuberculosis
• Common in adolescents and typical in adults with
tuberculosis
• usually is confined to apical segments of upper
lobes or superior segments of lower lobes.
• There is usually little lymphadenopathy and no
extrathoracic infection as a result of established
hypersensitivity
• This is a manifestation of a secondary expansion of
infection at a site seeded years previously during
primary infection
• Advanced disease is associated with cavitation and
endobronchial spread of bacilli.
• Symptoms include fever, night sweats, malaise, and
weight loss.
• A productive cough and hemoptysis often herald
cavitation and bronchial erosion.
Lymphadenopathy
• is common in primary pulmonary disease
• The most common extrathoracic sites of
lymphadenitis are the cervical, supraclavicular, and
submandibular areas (scrofula)
• Enlargement may cause compression of adjacent
structures.
Miliary
tuberculosis
• widespread hematogenous dissemination with
infection of multiple organs
• characterized by fever, general malaise,weight
loss, lymphadenopathy, night sweats, and
hepatosplenomegaly
• Diffuse bilateral pneumonitis is common, and
meningitis may be present
• The chest radiograph reveals bilateral miliary
infiltrates, showing overwhelming infection
• The TST may be nonreactive as a result of
anergy
• Liver or bone marrow biopsy is useful for the
dagnosis.
Tuberculous meningitis
• most commonly occurs in children younger than 5
years old and often within 6 months of primary
infection.
• Tubercle bacilli that seed the meninges during the
primary infection replicate,triggering an
inflammatory response.
• This condition may have an insidious onset, initially
characterized by low-grade fever, headache, and
subtle personality change.
• Progression of the infection results in basilar
meningitis with impingement of the cranial nerves
and is manifested by meningeal irritation and
eventually increased intracranial pressure,
deterioration of mental status, and coma.
• CT scans show hydrocephalus, edema,
periventricular lucencies, and infarctions
• CSF analysis reveals increased cell number (50 to
500/mm3 leukocytes), which early in the course of
disease may be either lymphocytes or
polymorphonuclear leukocytes
• Glucose is low, and protein is significantly elevated
• Acid-fast bacilli are not detected frequently in the
CSF by either routine or fluorescent staining
procedures.
• Although culture is the gold standard for dagnosis,
PCR for M. tuberculosis is useful to make this
diagnosis.
• Treatment regimens for tuberculous meningitis
generally include four antituberculous drugs and
corticosteroids.
Skeletal tuberculosis
• from either hematogenous seeding or direct
extension from a caseous lymph node.
• Radiographs reveal cortical destruction; biopsy and
culture are essential for proper diagnosis
• Tuberculosis of the spine, Pott disease, is the most
common skeletal site, followed by the hip and the
fingers and toes (dactylitis).
Other forms
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•
•
•
Abdominal tuberculosis
Tuberculous peritonitis
Urogenital tuberculosis
Tuberculous pericarditis
LABORATORY AND IMAGING STUDIES
• Tuberculin Skin Test
• Only persons at high risk should be offered a
Mantoux test
• Culture
Induration ≤5 mm
•Children in dose contact with known or suspected
contagious cases of tuberculosis disease
•Children suspected to have tuberculosis disease
Findings on chest radiograph consistent with
active or previously active tuberculosis
Clinical evidence of tuberculosis disease*
•Children receiving immunosuppressive therapy or
immunosuppressive conditions, including HIV
infection
•Induration≤ l O mm
•Children at increased risk of disseminated disease
Children <4 years old
Children with other medical conditions, including
Hodgkin disease, lymphoma, diabetes mellitus, ihronl
renal failure, or malnutrition
•Children with increased exposure to tuberculosis disease
Children born, or whose parents were born, in high
prevalence regions of the world
Children frequently exposed to adults who are Hiv
infected, homeless, users of illicit drugs, residents of
nursing homes, incarcerated or institutionalized, or
migrant farm workers
• Children who travel to high-prevalence region of the
world
Induration ≤15 mm
Children ≤4 years old without any risk
factors
Diagnostic Imaging
• The initial parenchymal inflammation that
follows deposition of infected droplet nuclei in
the alveoli of the lung usually is not visible
radiographically.
• A localized, nonspecific infiltrate with an
overlying pleural reaction may be seen,
however. This lesion usually resolves within 1
to 2 weeks.
• All lobar segments of the lung are at equal risk
of being the focus of the initial infection.
• In 25% of cases, two or more lobes of the
lungs are involved, although disease usually
occurs at only one site.
• Spread of infection to regional lymph nodes
occurs early.
• The hallmark of childhood pulmonary
tuberculosis is the relatively large size and
importance of the hilar lymphadenitis
compared with the less significant size of the
initial parenchymal focus, together historically
referred to as the Ghon complex (with or
without calcification of the lymph nodes).
Diagnostic Imaging
• Hilar lymphadenopathy
• Partial bronchial obstruction(air trapping,
hyperinflation, and lobar emphysema)
• lobar pneumonia without impressive hilar
lymphadenopathy.
• thin-walled primary tuberculous cavity
tuberculous spine
• usually show collapse and destruction of the
vertebral body with narrowing of the involved
disc spaces.
• Radiographic findings in bone and joint
tuberculosis range from mild joint effusions
and small lytic lesions to massive destruction
of the bone.
DIFFERENTIAL DIAGNOSIS
• in early disease the symptoms and signs may
be nonspecific.
• In pulmonary disease, tuberculosis may
appear similar to pneumonia, malignancy, and
any systemic disease in which generalized
lymphadenopathy occurs.
• The diagnosis of tuberculosis should be
suspected if the TST is positive or if there is
history of tuberculosis in a contact.
• The differential diagnosis of tuberculous
lymphadenopathy includes infections caused
by:
• atypical mycobacteria,
• catscratch disease,
• fungal infection,
• viral or bacterial disease,
• toxoplasmosis,
• sarcoidosis,
• drug reactions,
• and malignancy.
TREATMENT
• For patients with large populations of bacilli, such as
adults with cavities or extensive infiltrates, at least
two antituberculous drugs must be given
• For patients with tuberculosis infection but no
disease, the bacterial population is small, and a
single drug, such as isoniazid, can be given
• Isoniazid and rifampin are bactericidal Along with
pyrazinamide
• Ethambutol, ethionamide, streptomycin,
and cycloserine are bacteriostatic
• A 9-month regimen of isoniazid and refampin cures
more than 98% of cases of drug-susceptible pulmonary
• The addition of pyrazinamide and another drug
(ethambutol or an aminoglycoside at the beginning of
the regimen reduces the duration of necessary
treatment to 6 months.
• Meningitis, bone/joint:2 mo of isoniazid,
rifampin,pyrazinamide, and an aminoglycoside or
ethionamide,once a day, followed by 7-10 mo of
isoniazid and rifampin, once a day or twice a week
(9-12 mo total)
• Pulmonary and extrapulmonary(except meningitis
and bone joint) :2 mo of isoniazid, rifampin, and
pyrazinamide daily, followed by 4 mo of isoniazid
and rifampin twice weekly under DOT
COMPLICATIONS
• Tuberculosis of the spine may result in
angulation or gibbus formation that requires
surgical correction after the infection is cured
• With extrapulmonary tuberculosis, the major
problem is often delayed recognition of the
cause of disease and delayed