This document provides an outline and overview of tuberculosis (TB). It discusses the epidemiology and pathogenesis of TB, as well as the clinical presentation of different forms of the disease including pulmonary TB, extrapulmonary TB, and TB's co-infection with HIV. The diagnosis, treatment, prevention and follow up of TB are also outlined. Key points include that over 5.7 million new TB cases were reported in 2013, mostly in developing countries, and 1.49 million deaths were estimated to be from TB. M. tuberculosis transmission typically occurs via inhalation of aerosolized droplets from infectious pulmonary TB cases.

1. Oct. 10,2017
Dep’t of Internal Medicine
Melaku Yitbarek(M.D.)

2. OUTLINE:
 Epidemiology
 Pathogenesis
 Clinical pictures
 TB-HIV Co-infection
 Diagnosis
 Treatment ,Prevention& Follow up

3.  More than 5.7 million new cases of TB (all
forms, both pulmonary And
extrapulmonary)Were reported to WHO in
2013; 95% of cases were reported from
developing countries.
 It is further estimated that 1.49 million (range,
1.32–1.67 million) deaths from TB, including
0.36 million among people living with HIV
infection

4.  M. tuberculosis is most commonly transmitted from a
person with infectious pulmonary TB by droplet
nuclei, which are aerosolized by coughing, sneezing, or
speaking
 Important determinants of likelihood of transmission:
 The probabilityof contact with a person who has an
infectious form of TB,
 the intimacy and duration of that contact
 The degree of infectiousness of the case
 and the shared environment in which the contact takes place.

5.  TB patients whose sputum contains AFB visible by
microscopy (sputum smear–positive cases) are the
most likely to transmit the infection.
 The most infectious patients have cavitary pulmonary
disease
 Patients with sputum smear–negative/culture-positive
TB are less infectious,
 Crowding in poorly ventilated rooms is one of the
most important factors in the transmission of tubercle
bacilli because it increases the intensity of contact with
a case

6.  Unlike the risk of acquiring infection with M.
tuberculosis, the risk of developing disease
after being infected depends largely on
endogenous factors,
 such as the individual’s innate immunologic and non
immunologic defenses
 and the level at which the individual’s cell-mediated
immunity(CMI) is functioning.

7.  Clinical illness directly following infection is classified as
primary TB and is common among children in the first few
years of life and among immunocompromised persons.
 Although primary TB may be severe and disseminated, it
generally is not associated with high-level transmissibility.
 When infection is acquired later in life, the chance is greater
that the mature immune system will contain it at least
temporarily.
 Bacilli, however, may persist for years before reactivating to
produce secondary (or postprimary) TB,which, because of
frequent cavitation, is more often infectious than is primary
disease.

8.  Overall, it is estimated that up to 10% of
infected persons will eventually develop active
TB in their lifetime
 The risk is much higher among HIV-infected
persons.
 Reinfection of a previously infected individual,
which is common in areas with high rates of TB
transmission,may also favor the development
of disease

10.  untreated TB is often fatal
 About one-third of patients died within 1 year after diagnosis, and more
than 50% died within 5 years.
 The 5-year mortality rate among sputum smear–positive cases was 65%.
 Of the survivors at 5 years, ~60% had undergone spontaneous remission,
while the remainder were still excreting tubercle bacilli.
 With effective, timely, and proper chemotherapy, patients have a very
high chance of being cured
 However, improper use of anti-TB drugs, while reducing mortality rates,
may also result in large numbers of chronic infectious cases, often with
drug-resistant bacilli

11.  Mycobacteria:belongto
the family Mycobacteriaceae and orderActinomycetales
 M. tuberculosiscomplex, which comprises eight distinct subgroups, the
most common and important agent of human disease is M.tuberculosis
 M .tuberculosis complex includes
 M.bovis,
 M.caprea,
 M.africanum,
 M.microti,
 M.pennipeddi,
 M.canneti

12.  M. tuberculosis is a rod-shaped, non-spore-
forming, thin aerobic Bacterium measuring 0.5µm
by 3µm
 Mycobacteria, including M. tuberculosis, are often
neutral on Gram’s staining
 However, once stained, the bacilli cannot be
decolorized by acid alcohol;
 this characteristic justifies their classification as
acid-fast bacilli

14. 5.plasma membrane
6.lipoarabinomannan (LAM
7.phosphatidylinositol
mannoside
8.cell wall skeleton

16.  The interaction of M. tuberculosis with the
human host begins when droplet nuclei
containing viable microorganisms propelled
into the air by infectious patients are inhaled by
a close bystander
 Although the majority of inhaled bacilli are
trapped in the upper airways and expelled by
ciliated mucosal cells, a fraction (usually <10%)
reach the alveoli
 There, alveolar macrophages that have not yet
been activated phagocytose the bacilli

19.  In the initial stage of host–bacterium
interaction, prior to the onset of an acquired
CMI response, M. tuberculosis disseminates
widely through the lymph vessels, spreading
to other sites in the lungs and other organs, and
undergoes a period of extensive growth within
naïve unactivated macrophages
 additional naïve macrophages are recruited to
the early granuloma

20.  Ultimately,the chemo-attractants and bacterial
products released during the repeated rounds of
cell lysis and infection of newly arriving
macrophages enable dendritice cells to access
bacilli
 these cells migrate to the draining lymph nodes
and present mycobacterial antigens to T
lymphocytes
 At this point,the development of CMI and humoral
immunity begins.
 These initial stages of infection are usually
asymptomatic

21.  About 2–4 weeks after infection, two host
responses to M. tuberculosis develop:
 a macrophage-activating CMI response
 T cell–mediated phenomenon resulting in the activation of
macrophages that are capable of killing and digesting
tubercle bacilli
 and a tissue-damaging response
 the result of delayed type hypersensitivity (DTH) reaction
various to bacillary antigens;
 it destroys unactivated macrophages that contain
multiplying bacilli but also causes caseous necrosis of the
involved tissues

22.  Although both of these responses can inhibit
mycobacterial growth, it is the balance between the
two that determines the forms of TB that will
develop subsequently
 With the development of specific immunityand the
accumulation of large numbers of activated
macrophages at the site of the primary lesion,
granulomatous lesions (tubercles) are formed
 These lesions consist of accumulations of
lymphocytes and activated macrophages that
evolve toward epithelioid and giant cell
morphologies

23.  TB is classified as pulmonary, extrapulmonary,
or both.
 Dependingon several factors linked to
different populations and bacterial strains,
 extrapulmonary TB may occur in 10–40% of
patients.
 Furthermore, upto two-thirds of HIV-infected
patients with TB may have both pulmonary
and extrapulmonary TB or extrapulmonary TB
alone.

24. Pulmonary TB:
 Pulmonary TB is conventionally categorized as
primary or postprimary(adult-type, secondary)
 a large percentage of cases of adult pulmonary
TB result from recent infection (either primary
infection or reinfection) and not from
reactivation

25. Primary Pulmonary TB:
 Primary pulmonary TB occurs soon after the initial infection
with tubercle bacilli
 It may be asymptomatic or may present with fever and
occasionally pleuritic chest pain.
 In areas of high TB transmission, this form of disease is
often seen in children
 In the majority of cases, the lesion heals spontaneously and
becomes evident only as a small calcified nodule
 TheGhon focus, with or without overlying pleural reaction,
thickening, and regional lymphadenopathy, is referred to as
the Ghon complex.

26. Primary Pulmonary TB:
 In young children with immature CMI and in persons with
impaired immunity (e.g., those with malnutrition or HIV
infection),primary pulmonary TB may progress rapidly to clinical
illness
 Pleural effusion, which is found in up to two-thirds of cases,
results from the penetration of bacilli into the pleural space from
an adjacent subpleural focus.
 In severe cases, the primary site rapidly enlarges, its central
portion undergoes necrosis, and cavitation develops (progressive
primary TB)
 TB in young children is almost invariably accompanied by hilar or
paratracheal lymphadenopathy due to the spread of bacilli from
the lung parenchyma through lymphatic vessels

28. Primary Pulmonary TB:
 Enlarged lymph nodes may compress bronchi, causing
total obstruction with distal collapse partial
obstruction with large-airway wheezing or a ball-valve
effect with segmental/lobar hyperinflation.
 Occult hematogenous dissemination commonly
follows primary infection
 However, in the absence of a sufficient acquired
immune response, which usually contains the
infection,disseminated or miliary disease may result

31. Postprimary (Adult-Type) Disease :
 also referred to as reactivation or secondary TB,
 It is usually localized to the apical and
posterior segments of the upper lobes, where
the substantially higher mean oxygen tension
(compared with that in the lower zones) favors
mycobacterial growth
 The extent of lung parenchymal involvement
varies greatly, from small infiltrates to
extensive cavitary disease

32. Postprimary (Adult-Type) Disease:
 Early in the course of disease, symptoms and signs are often non
specific and insidious, consisting mainly of diurnal fever and
nightsweats due to defervescence, weight loss, anorexia, general
malaise,and weakness.
 However, in up to 90% of cases, cough eventually develops—often
initially nonproductive and limited to the morning and
subsequently accompanied by the production of purulent
sputum,sometimes with blood streaking
 Hemoptysis develops in 20–30% of cases, and massive hemoptysis
may ensue as a consequence of the erosion of a blood vessel in the
wall of a cavity.
 Pleuritic chest pain,dyspnea

33. Post primary (Adult-Type) Disease:
P/E:
 Many patients have no abnormalities detectable by
chest examination
 whereas others have detectable rales in the
involved areas during inspiration, especially after
coughing.
 Occasionally, rhonchi due to partial bronchial
obstruction
 and classic amphoric breath sounds in areas with
large cavities maybe heard

34. Post primary (Adult-Type) Disease:
P/E:
 Systemic features include fever (often low-grade and intermittent)
in up to 80% of cases and wasting
 absence of fever,however,notexclude TB.
 In some cases, pallor and finger clubbing develop
 The most common hematologic findings are mild
anemia,leukocytosis, and thrombocytosis with a slightly elevated
erythrocyte sedimentation rate and/or C-reactive protein level
 None of these findings is consistent or sufficiently accurate for
diagnostic purposes.

35.  In order of frequency, the extrapulmonary sites
most commonly involved in TB are the lymph
nodes, pleura, genitourinary tract, bones and
joints, meninges, peritoneum, and pericardium
 However, virtually all organ systems may be
affected
 As a result of hematogenous dissemination in
HIV-infected individuals,extrapulmonaryTB is
seen more commonly today than in the past in
settings of high HIV prevalence.

36. Lymph Node TB (Tuberculous Lymphadenitis):
 The most common presentation of extrapulmonary
TB in both HIV- sero-negative and HIV-infected
patients (35% of cases worldwide and more than
40%ofcases in the United States in recent series)
 lymph node disease is particularly frequent among
HIV-infected patients and among children
 Lymph node TB presents as painless swelling of
the lymph nodes, most commonly at posterior
cervical and Supraclavicular sites (a condition
historically referred to as scrofula)

37.  Lymph nodes are usually discrete in early disease but
develop into a matted non tender mass over time and
may result in a fistulous tract draining caseous material
 Associated pulmonary disease is present in fewer than
50% of cases, and systemic symptoms are uncommon
except in HIV infected patients
 The diagnosis is established by fine-needle aspiration
biopsy (with a yield of up to 80%) or surgical excision
biopsy.
 cultures are positive in 70–80% of cases

38. Pleural TB:
 Involvement of the pleura accounts for ~20% of
extrapulmonary cases in the United States and
elsewhere
 Isolated pleural effusion usually reflects recent
primary infection, and the collection of fluid in the
pleural space represents a hypersensitivity response to
mycobacterial antigens
 Depending on the extent of reactivity, the effusion may
be small, remain unnoticed, and resolve spontaneously
or may be sufficiently large to cause symptoms such as
fever, pleuritic chest pain,and dyspnea

39. Pleural TB:
 Physical findings are those of pleural effusion: dullness to percussion and
absence of breath sounds
 A chest radiograph reveals the effusion and, in up to one-third of
cases,also shows parenchymal lesion.
 Thoracentesis is required to ascertain the nature of the effusion and to
differentiate it from manifestations of other etiologies
 The fluid is straw colored and at times hemorrhagic;
 It is an exudate with a protein concentration >50% of that in serum
 Neutrophils may predominate in the early stage, but lymphocyte
predominance is the typical finding later

40. TB of the upper Airways:
 Nearly always a complication of advanced
cavitary pulmonary TB
 TB of the upper airways may involve the
larynx, pharynx, and epiglottis
 Symptoms include hoarseness, dysphonia, and
dysphagia in addition to chronic productive
cough
 Acid-fast smear of the sputum is often positive,
but biopsy maybe necessary in some cases to
establish the diagnosis

41. Genitourinary TB :
 accounts for ~10–15% of all extrapulmonary cases
 Local symptoms predominate, and up to 75% of patients have chest radiographic
abnormalities suggesting previous or concomitant pulmonary disease.
 Urinary frequency, dysuria, nocturia, hematuria, and flank or abdominal pain are
common presentations
 Urinalysis gives abnormal results in 90% of cases, revealing pyuria and hematuria
 The documentation of culture-negative pyuria in acidic urine should raise the
suspicion of TB
 Culture of three morning urine specimens yields a definitive diagnosis in nearly
90% of cases

42. Genitourinary TB:
 Genital TB diagnosed more commonly in female
than in male patients
 In female patients, it affects the fallopian tubes and
the endometrium and may cause infertility, pelvic
pain, and menstrual abnormalities.
 In male patients, genital TB preferentially affects
the epididymis, producing a slightly tender mass
that may drain externally through a fistulous tract;
orchitis and prostatitis may also develop

43. Skeletal TB:
 In the United States, TB of the bones and joints is responsible for ~10% of
extrapulmonary cases
 In bone and joint disease,pathogenesis is related to reactivation of hematogenous
foci or to spread from adjacent paravertebral lymph nodes.
 Weight-bearing joints (the spine in 40% of cases, the hips in 13%, and the knees in
10%) are most commonly affected
 Spinal TB (Pott’s disease or tuberculous spondylitis; often involves two or more
adjacent vertebral bodies
 With advanced disease, collapse of vertebral bodies results in kyphosis
(gibbus)
 A catastrophic complication of Pott’s disease is paraplegia, which is usually due to
an abscess or a lesion compressing the spinal cord.

44. Tuberculous Meningitis and Tuberculoma :
 TB of the central nervous system accounts for~5%of
extrapulmonary cases in the United States
 It is seen most often in young children but also develops in
adults, especially those infected with HIV.
 Tuberculous meningitis results from the hematogenous
spread of primary or postprimary pulmonary TB or from
the rupture of a subependymal tubercle into the
subarachnoid space
 The disease often presents subtly as headache and slight
mental changes after a prodrome of weeks of low-grade
fever, malaise, anorexia, and irritability.

45. Tuberculous Meningitis and Tuberculoma :
 If not recognized, tuberculous meningitis may evolve acutely with severe
headache, confusion, lethargy, altered sensorium, and neck rigidity
 Typically, the disease evolves over 1–2 weeks, a course longer than that of
bacterial meningitis
 Lumbar puncture is the cornerstone of diagnosis. In general, examination
of cerebrospinal fluid (CSF) reveals a high leukocyte count
(upto1000/µL), usually with a predominance of lymphocytes but
sometimes with a predominance of neutrophils in the early stage
 Culture of CSF is diagnostic in up to 80% of cases and remains the gold
standard
 If unrecognized, tuberculous meningitis is uniformly fatal

46. Tuberculous Meningitis and Tuberculoma :
 Tuberculoma, an uncommon manifestation of
central nervous systemTB, presents as one or more
space-occupying lesions
 and usually causes seizures and focal signs.
 CT or MRI reveals contrast-enhanced Ring lesions,
 but biopsy is necessary to establish the diagnosis.

47. Gastrointestinal TB:
 Gastrointestinal TB is uncommon, making up 3.5% of
extrapulmonary cases in the United States.
 Various pathogenetic mechanisms areinvolved:swallowing of
sputum with direct seeding,hematogenous spread, or (largely in
developing areas) ingestion of milk from cows affected by bovine
TB.
 Although any portion of the gastrointestinal tract may be affected,
the terminal ileum and the cecum are the sites most commonly
involved
 Abdominal pain (at times similar to that associated with
appendicitis) and swelling,obstruction, hematochezia, and a
palpable mass in the abdomen are common findings at
presentation.

48. Gastrointestinal TB:
 Fever, weight loss, anorexia, and night sweats are also common.
 Tuberculous peritonitis follows either the direct spread of tubercle
bacilli from ruptured lymph nodes and intraabdominal organs
(e.g.,genital TB in women) or hematogenous seeding
 Nonspecific abdominal pain, fever, and ascites should raise the
suspicion tuberculous peritonitis
 In tuberculous peritonitis, paracentesis reveals an exudative fluid
with a high protein content and leukocytosis that is usually
lymphocytic (although neutrophils occasionally predominate)
 peritoneal biopsy (with a specimen best obtained by laparoscopy)
is often needed to establish the diagnosis

49. Pericardial TB (Tuberculous Pericarditis):
 pericardial TB has often been a disease of the elderly in
countriesWith low TB prevalence
 However,it also develops frequently in HIV-infected
patients.
 The onset may be subacute, although an acute
presentation, with dyspnea, fever, dull retrosternal
pain, and a pericardial friction rub, is possible
 An effusion eventually develops in many cases;
cardiovascular symptoms and signs of cardiac
tamponade may ultimately appear

50. Miliary or Disseminated TB:
 Miliary TB is due to hematogenous spread of tubercle bacilli.
 Although in children it is often the consequence of primary
infection, in adults it may be due to either recent infection or
reactivation of old disseminated foci
 Clinical manifestations are nonspecific and protean, depending
on the predominant site of involvement.
 fever, night sweats, anorexia, weakness, and weight loss are
presenting symptoms in the majority of cases
 Physical findings include hepatomegaly,splenomegaly, and
lymphadenopathy

51.  A high index of suspicion is required for the diagnosis
of miliary TB.
 Frequently, chest radiography reveals a miliary
reticulonodular pattern ,although no radiographic
abnormality may be evident early in the course and
among HIV-infected patients
 Sputum-smear microscopy is negative in most cases
 If it goes unrecognized,miliary TB is lethal; with proper
early treatment, however, it is amenable to cure

52.  TB is one of the most common diseases among
HIV-infected persons worldwide and a major
Cause of death in this population
 more specifically, it is responsible for an
estimated 24% of all HIV-related mortality
 A new TB infection acquired by an HIV-
infected individual may evolve to active
disease in a matter of weeks rather than
months or years
 TB can appear at any stage of HIV infection,
and its presentation varies with the stage.

53.  When CMI is only partially compromised, pulmonary
TB presents in a typical manner with upper-lobe
infiltrates and cavitations and without significant
lymphadenopathy or pleural effusion
 In late stages of HIV infection, when the CD4+ Tcell
count is <200/µL, a primary TB–like pattern, with
diffuse interstitial and subtle infiltrates, little or no
cavitations, pleural effusion, and intrathoracicl
ymphadenopathy, is more common
 Overall, sputum smears are less frequently positive
among TB patients with HIV infection than among
those without; thus, the diagnosis of TB may be
difficult
 Extrapulmonary TB is common among HIV-infected
patients

54.  The diagnosis of TB in HIV-infected patients may be
complicated not only by the increased frequency of sputum-
smear negativity (up to 40% in culture proven pulmonary
cases) but also by atypical radiographic findings, a lackof
classic granuloma formation in the late stages
 The Xpert MTB/RIF assay (see “Nucleic Acid Amplification
Technology,” below) is the preferred initial diagnostic
option, and therapy should be started on the basis of a
positive result because treatment delays may be fatal
 A negative Xpert MTB/RIF result does not exclude a
diagnosis of TB, and culture remains the gold standard

55. Immune reconstitution inflammatory syndrome (IRIS):
 Exacerbations in systemic (lymphadenopathy) or respiratory symptoms,
signs, and laboratory or radiographic manifestations of TB
 have been associated with the administration of ART and occur in ~10%
of HIV-infected TB patients
 Usually developing 1–3 months after initiation of ART, IRIS is more
common among patients with advanced immuno suppression and
extrapulmonary TB
 The earlier ART is started and the lower the baseline CD4+ T cell count,
the greater the risk of IRIS
 Death due to IRIS is relatively infrequent and occurs mainly among
patients who have a high preexisting mortality risk

56.  The key to the diagnosis of TB remains a high index of
suspicion
 Sputum Direct light Smear Microscopy
 mainstay of diagnostic methods to test for the presence of acid
fast bacilli(AFB).
 Light emitting diode (LED) microscopy
 a newly introduced diagnostic tool to complement the
conventional microscopy
 It is recommended for centers with high case load as it saves
time and improves sensitivity.
 Sputum culture and medicine susceptibility test
 a highly sensitive diagnostic method
 Culture remains the gold standard in mycobacterial detection

57. Line Probe Assay
 a new test to identify the presence of specific
mutations on the genes of TB bacilli which are
responsible for Isoniazid and Rifampicin resistance
 It is a rapid and accura te test to identify cases
with MDR-TB.
Gene Xpert MTB/RIF
 a new, rapid and fully automated DNA/molecular
diagnostic test to detect TB and Rifampicin
medicine resistance simultaneously
 It is indicated for the diagnosis of TB in high MDR-
TB and TB/HIV settings.

58.  Fine needle aspiration
 from accessible mass like peripheral enlarged lymph
nodes and histopathological examination.
 Tissue biopsy
 from any body tissues such as serous membranes,
skin, endometrium, bronchial, pleural, gastric or liver
tissue for histophatological examination
 Chest x-ray
 Other investigation: HIV test, ESR, CSF
analysis

59. Objectives
 Cure the TB patient and restore quality of life and
productivity
 Prevent death from active TB or its late effects
 Prevent TB relapse
 Prevent the development and transmission of
medicine resistance
 Decrease transmission.

60. Non pharmacologic
 Counselling
 Good nutrition
 Adequate rest
 Admission for severely ill patients

61. Pharmacologic:
 Treatment of TB is with a combination of 4 or more
anti-TB medicines the treatment is standardized by
putting patients into different treatment groups based
on smear status and previous history of treatment for
TB
 standardized treatment means that all patients in a
defined group receive the same treatment regimen
 TB treatment strategy is referred to as DOT indicating
that treatment is given under direct observation of a
health worker or treatment supporter daily throughout
the course of treatment

62. Treatment with 1st line anti-TB Medicines:
 TB Patients with strains susceptible to first line anti-TB medicines are
treated with standardized first line treatment regimen for 6 or 8 months,
depending on the history of previous TB treatment
 The first line anti-TB medicines available for TB treatment in Ethiopia are:
 Rifampicin(R)
 Ethambutol (E)
 Isoniazid (H)
 Pyrazinamide (Z) and
 Streptomycin (S)

63. 1.TB treatment regimen with first line anti-TB medicines
 Treatment regimen for new patients: newly diagnosed smear
positive, smear negative and extrapulmonary TB patients who
have never had treatment for TB,or have taken anti-TB medicines
for less than 1 month
 This regimen consists of 8 weeks (2 months) treatment with
Rifampicin, Isoniazid, Pyrazinamide and Ethambutol during the
intensive phase, followed by four months with Rifampicin and
Isoniazid in the continuation phase (2RHZE/4RH).
 Other Previously treated Smear Negative PTB and EPTB cases
(Case definition ‘Other’) who were previously cured or treatment
completed will be treated with New TB patient regimen

64. 1.Treatment regimen for previously treated patients
(Re-treatment Regimen)
 Patients who have previously received 1 month or
more of anti-TB medicines.
 This regimen consists of an eight week (2 month)
treatment with Streptomycin, Rifampicin,
Isoniazid, Pyrazinamide and Ethambutol followed
by a four week (1 month) treatment with
Rifampicin, Isoniazid, Pyrazinamide and
Ethambutol during the intensive phase, followed
by five months on Rifampicin, Isoniazid and
Ethambutol: 2SRHZE/1RHZE/5(RH)E

65. Common drug Side effects:
 Isoniazide: hepatitis, peripheral neuropathy
 Rifampicine:GI reaction, hepatitis
 Pyrazinamide: hepatitis,arthralgia
 Streptomycine: hypersensitivity, vestibular/ fetal
auditory damage
 Ethambutol: optic neuritis

66. Precautions during treatment with 1St line anti-TB
medicines
 Treatment of patients with renal failure
 Consult expert. If not possible to consult then avoid
Streptomycin & Ethambutol; therefore the recommended
regimen is 2RHZ/4RH.
 Treatment of patients with (previously known)
liver disorder (e.g. hepatitis, cirrhosis)
 Most anti-TB medicines can cause liver damage.
 Do not give Pyrazinamide because this is the most
hepatotoxic anti-TB medicine.
 Isoniazid & Rifampicin plus one or two non-hepatotoxic
medicines, such as Streptomycin and Ethambutol, can be
used for a total treatment duration of eight months.

67. Pericardial tuberculosis:
 For patients with pericardial tuberculosis, the
same regimen (as pulmonary) of antiTB
treatment is recommended (need expert
opinion in diagnosis and treatment
 Corticosteroids are recommended as adjunctive
therapy for 11 weeks during the first period of
anti-tuberculosis therapy.

68. Pleural tuberculosis
 Tuberculous empyema, a chronic, active
infection of the pleural space containing a large
number of tubercle bacilli, usually occurs when
a cavity ruptures into the pleural space.
 Treatment consists of drainage (often requiring
a surgical procedure) and anti-TB medicines.

69. Tuberculous meningitis :
 Patients presenting with more severe brain
impairment such as drowsiness neurological
signs, or coma have a greater risk of
neurological sequelae and higher mortality.
 Chemotherapy should be initiated with RHZS
in an initial phase for 2 months and RH
should be continued for 7 to 10 months in the
continuation phase
 Adjunctive corticosteroid therapy is
recommended for all patients

70. Treatment during pregnancy and breast-feeding:
 Avoid Streptomycin because of the risk of toxic
effects on the fetus.
 Chemotherapy should not be discontinued
during breast-feeding.
 When a breast-feeding mother has PTB, the
infant should, regardless of prior vaccination
with BCG, be given chemo-prophylaxis and
then be vaccinated with BCG if not previously
vaccinated.

71. Treatment of patients also infected with HIV
 HIV infection and Active TB disease should be
started on HAART irrespective of CD4 cell
count
 Patients infected with HIV usually respond
equally well to TB treatment as those without
HIV infection, with a few exceptions:
 They should always be treated with short course
chemotherapy.
 Initiation of ART in the course of treatment for
tuberculosis should follow the WHO guidelines

72. Treatment monitoring :
 Health worker or a community TB treatment supporter must observe and ensure each
patient swallows every single dose of the medicines; this is called directly observed
treatment or DOT.
 During treatment follow-up, monitoring of patient’s progress involves: clinical
assessment of signs and symptoms, weight measurement and follow-up AFB sputum
examination.
 Follow-up sputum examination is done for all new smear positive TB cases at the 2nd,
5th and 6th month
 If smear result is positive at 2nd sputum smear examination is done at the 3rd month,
and if it is still positive, the sample must be sent for DST.
 If smear result is positive at 5th month or later, it is declared that treatment has failed
and patient will be started on re treatment regimen and sputum is examined for DST.
 If smear is negative at 5month of follow-up, patient is declared cured

73.  Follow-up sputum examination is done for all
previously treated smear positive TB cases at 3rd, 5th
and 8th month
 If smear result is positive at the 3rd month, sample must
be sent for DST.
 If smear result is positive at the 5th month or later, it
is declared that treatment has failed and patient must
be started on 2nd line treatment regimen pending the
DST result.
 If smear is negative at 5th and 8th month of follow-up,
patient is declared cured.

74. Medicine resistant TB:
 TB is considered medicine-resistant (DR) when the
TB causative agent (mycobacterium tuberculosis)
is not killed by one or more of the available anti-TB
medicines.
 Mono-resistance: Rresistance to one anti-
tuberculosis medicine.
 Poly-resistance: Resistance to more than one anti-
tuberculosis medicine, other than Isoniazid and
Rifampicin.
 Multimedicine-resistance (MDR)-TB: Resistance
to at least isoniazid and rifampicin.

75.  Extensive medicine-resistance (XDR-TB):
Resistance to any of the fluoroquinolones, and
at least one of the three injectable Second Line
Medicines (capreomycin, kanamycin and
Amikacin), in addition to resistance to INH and
rifampicin
 Total medicine-resistance (TDR-TB):
resistance to all anti TB medicines.
 The clinical features of medicine susceptible
and medicine resistant TB are the same.

76. References:
 Harrison’s Principles of Internal Medicine19th,Edition.
 Standard Treatment Guideline,2014
 Uptodate 21.6

77. Thank You…