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Who Discovered Tuberculosis? • In 1882, Robert Koch discovered TB and soon he found out that it was caused by a microorganism Mycobacterium tuberculosis. After discovering that this disease was infectious, he started to consider treatments. Many treatments were tried but none were discovered until the year of 1943 were the activity of streptomycin was discovered.
Microbiology: The agent of human tuberculosis is M. tubercle. The tubercle bacilli is aerobic, non-motile,non-spore-forming, high in lipid content, and acid and alcohol-fast , weakly gram-positive curved rods. A hallmark of all mycobacteria is acid fastness: the capacity to form stable mycolate complexes with arylmethane dyes. The term acid-fast bacilli is practically synonymous with mycobacteria. Mycobacteria grow slowly. Isolation from clinical specimens on solid synthetic media usually takes 3 to 6 weeks, and drug-susceptibility testing requires an additional 4 weeks.
Pathogenesis: • Transmission of M. tuberculosis is from person to person, usually by respiratory droplets that become airborne when the ill individual coughs, sneezes, laughs, sighs, or breathes. • Infected droplets dry and become droplet nuclei, which may remain suspended in the air for hours, long after the infectious person has left the environment. • To become infected with TB germs, a person usually needs to share air space with someone sick with TB disease (e.g., live, work, or play together) • The amount of time, the environment, and how sick the person is all contribute to whether or not you get infected • Only particles less than 10 μm in diameter can reach the alveoli and establish infection. • Incubation period range from several days to several wks.
How Are TB Germs NOT Spread? • Through quick, casual contact, like passing someone on the street • By sharing utensils or food • By sharing cigarettes or drinking containers • By shaking hands • Using public telephones
Children with primary pulmonary tuberculosis disease rarely, if ever, infect other children or adults ,because: • 1.)Tubercle bacilli are relatively sparse in the endobronchial secretions of children with primary pulmonary tuberculosis • 2.)a significant cough is usually lacking. • 3.)When young children do cough, they rarely produce sputum, and they lack the tussive force necessary to project and suspend infectious particles of the correct size.
Who Gets Tuberculosis? Anyone can get tuberculosis. Some people are at higher risks than others. The people who have more of a chance getting TB are: • People who share same breathing space • Poor people/homeless people • Prisoners • Alcoholics or Drug users • People with medical conditions (cancer, diabetes)
TERMS: • Tuberculosis infection (latent tuberculosis)describes the asymptomatic stage of infection with M. tuberculosis in which The tuberculin skin test (TST) is positive, but the chest radiograph is normal, and there are no signs or symptoms of illness. • Tuberculosis diseaseoccurs when there are clinical signs and symptoms or abnormal chest radiographs or extrapulmonary tuberculosis becomes apparent. • The term tuberculosis usually refers to the disease.
1.Primary pulmonary tuberculosis • Occurs in older infants and children ,it is usually an asymptomatic infection . clinical features: Malaise, low-grade fever, tachypnea , dyspnea, erythemanodosum, or symptoms resulting from lymph node enlargement. Partial bronchial obstruction caused by external compression from the enlarging nodes can cause air trapping, hyperinflation, and lobar emphysema. • There is no night sweating, no haemoptysis • When should we suspect pulmonary TB? • 1. HISTORY of contact with TB patient • 2. chronic respiratory symptoms. • 3. respiratory features not responding to antibiotics.
2.Progressive primary disease : • If the infection is progressively destructive, liquefaction of the lung parenchyma leads to formation of a thin-walled primary tuberculous cavity . • it is characterized by a primary pneumonia that develops shortly after initial infection. • Progression of the primary complex to pleura,pericardium,or disseminated miliary disease or progression of CNS granulomas to meningitis occurs most commonly in the first year of life.
3.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. • Symptoms include fever, night sweats, malaise, and weight loss,productive cough and hemoptysis.
PowerPoint Template Miliary Tuberculosis
Miliary tuberculosis • . Miliary tuberculosis refers to widespread hematogenous dissemination with infection of multiple organs. The lesions are of roughly the same size as that of a millet seed, from which the name miliary is derived. • The term miliary TB is now used to denote all forms of progressive, widely disseminated hematogenous tuberculosis, even if the classical pathologic or radiologic findings are absent. • Miliary tuberculosis is characterized by fever, general malaise, weight loss, lymphadenopathy, night sweats, and hepatosplenomegaly. Choroid tubercle in the eye may occur also (pathognomonic). • The chest radiograph reveals bilateral miliary infiltrates. • The TST may be negative in 50%. • Liver or bone marrow biopsy is useful for the diagnosis.
Milliary Tuberculosis acute milliary tuberculosis
Tuberculousmeningitismost 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 (3stages): • Stage 1 (1-2 wks): non specific features flu like illness • Stages 2(1-2 wks): signs of meningitis. • Stages 3 (1-2wks): signs of CNS complications (decerebrate, decorticate,coma…). • CT scans show hydrocephalus, edema, periventricularlucencies, and infarctions. • CSF analysis reveals increased cell number ,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 diagnosis, PCR for M. tuberculosis is useful to make this diagnosis. • Note:highly suspected TB meningitis if : • No response to antibiotics • Rapid CNS complication • History of contact with TB. • Mass in the brain after meningitis (tuberculoma). • Any meningitis in endemic area with Tb.
Other forms of tuberculosis include abdominal tuberculosisthat occurs from swallowing infected material. • Tuberculous peritonitisis associated with abdominal tuberculosis and presents as fever, anorexia, ascites, and abdominal pain. • Urogenital tuberculosisis a late reactivation complication and is rare in children. Symptomatic illness presents as dysuria, frequency, urgency, hematuria, and "sterile" pyuria.
LABORATORY AND IMAGING STUDIES • Tuberculin Skin Test (TST): MANTOUX TEST: The most important diagnostic tool for tuberculosis is the TST. The TST response to tuberculin antigene is a manifestation of a T cell-mediated delayed hypersensitivity. It is usually positive 2 to 6 weeks after onst of infection (occasionally 3 months) and at the time of symptomatic illness. The Mantoux test, an intradermal injection of 5 TU (tuberculin units) purified tuberculous antigen (purified protein derivative standard [PPD-S]) from mycobacterium bovis usually on the volar surface of the forearm, is the standard for screening high-risk populations and for diagnosis in all ill patients or contacts. The result should be read after 2-3 days (size of induration not size of redness).
.Definitions of Positive Tuberculin Skin Test Results in Infants, Children, and Adolescents • Induration ≥5 mm • Children in close contact with known or suspected contagious cases of tuberculosis disease • Findings on chest radiograph consistent with active or previously active tuberculosis • Clinical evidence of tuberculosis disease† • Children receiving immunosuppressive therapy‡ or with immunosuppressive conditions, including HIV infection • Induration ≥10 mm • Children with other medical conditions, including Hodgkin disease, lymphoma, diabetes mellitus, chronic renal failure, or malnutrition • 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, • Children who travel to high-prevalence regions of the world • Induration ≥15 mm Children ≥4 years old without any risk factors.
False-negative responses may occur early in the illness, with use of inactivated antigen (as a result of poor storage practice or inadequate administration), or as a result of immunosuppression (secondary to underlying illness, AIDS, malnutrition, or overwhelming tuberculosis, measles, rubela, chicken pox, hepatitis). • False positive responses may occur in: • 1.) BCG USE (within 5year of injection). • 2.) atypical mycobacterium infection.
OTHER TESTS: • GASTRIC LAVAGE FOR AFB: • 3 consecutive days at early morning • PCR (nuclic acid amplification): • Rapid result (within 1-2 hours) on blood or pleural or csf or peritonial fluid. • Culture (lownstein-jensen media)
Chest x-ray • THE hallmark of the pulmonary TB IN infant and children is large size hilaror paratreachial LN compared with less significant initial parenchymalfocus(Ghon focus). • All lobar segments of the lung are at equal risk of being the focus of the initial infection • The primery focus is too small to produce abnormal sign on physical examination but it is visible on Cxay as fluffy,opacity with adiameter of1-2 cm. • The mediastinallymphnodeson the affected side may be enlarged together with primery focus form (GHON COMPLEX). • There is no cavity
CHEST X- Ray • In older children and adulcentprimery illness present as an upper lobe infilteration& cavitation without calcifiction.
1st line drugs: Rifampicin,INH, Ethambutol, streptomycin,pyrazinamide • 2nd line drugs: Amikacin, capreomycin, ethaionamide, ciprofloxacin,……….. Steroid: used in following: Tb meningitis (2wks),Tb pericarditis, Tb peritonitis,miliary Tb.
Latent tuberculosis infection (positive TST result, no disease): 9 mo of isoniazid, once a day, If daily therapy is not possible, DOT twice a week can be used for 9 mo. if Isoniazid-resistant ,6 mo of rifampin, once a day. 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. If possible drug resistance is a concern, another drug (ethambutol or an aminoglycoside) is added to the initial 3-drug therapy until drug susceptibilities are determined. 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).
Noncompliance, or nonadherence, is a major problem in tuberculosis control because of the long-term nature of treatment and the sometimes difficult social circumstances of the patients. As treatment regimens become shorter, adherence assumes an even greater importance. Improvement in compliance occurs with directly observed therapy (DOT), which means that the healthcare worker is physically present when the medications are administered.
Note: Most initially infectious patients become noninfectious within 2 weeks of starting effective treatment, and many become noninfectious within several days.
PREVENTION The most effective intervention for TB control are those that improve living condition like housing condition ,nutrition and social deprivation . • BCG • Chemoprophylaxis: When child contact with active Tb we should put him/her on( INH )FOR 3 months and then do TST ,if positive continue INH for further 6 months, if negative stop it.
