2. ObjectivesObjectives
• Introduction
• Estimated burden of tuberculosis in India
• Defination
• Epidemiology
• Pathophysiology
• Immunology
• Clinical Presentations
• Complication and sequelae .


3. INTRODUCTIONINTRODUCTION
 Tuberculosis is a chronic infectious disease caused byTuberculosis is a chronic infectious disease caused by
Mycobacterium tuberculosisMycobacterium tuberculosis characterized by vaguecharacterized by vague
constitutional symptoms and a protracted course ofconstitutional symptoms and a protracted course of
illness with remissions and exacerbations.illness with remissions and exacerbations.
 Tuberculosis is the reaction of tissues of the humanTuberculosis is the reaction of tissues of the human
host to the presence and multiplication ofhost to the presence and multiplication of MycobacteriumMycobacterium
tuberculosistuberculosis..
 The clinical states arising from TB infection are theThe clinical states arising from TB infection are the
outcome between the capacity of the host to containoutcome between the capacity of the host to contain
and eliminate the organism versus the capacity of theand eliminate the organism versus the capacity of the
organism to multiply and proliferate.organism to multiply and proliferate.

4. Tuberculosis is a chronic granulomatousTuberculosis is a chronic granulomatous
inflammatory reaction of the tissues to the presenceinflammatory reaction of the tissues to the presence
of causative agent Mycobacterium tuberculosis,beingof causative agent Mycobacterium tuberculosis,being
characterized by a local aggregation of large numbercharacterized by a local aggregation of large number
of macrophages,some of which undergo strikingof macrophages,some of which undergo striking
structural & functional alterations in the form of theirstructural & functional alterations in the form of their
transformation to epithelioid cells,foreign body gianttransformation to epithelioid cells,foreign body giant
cells & Langhancells & Langhan’s giant cells i.e. formation of’s giant cells i.e. formation of
TUBERCLE.TUBERCLE.

5. MAGNITUDEMAGNITUDE
 1/31/3rdrd
of the worldof the world’s population is or has been’s population is or has been
infected with tubercle bacilli.infected with tubercle bacilli.
 India accounts for one third of the word TBIndia accounts for one third of the word TB
burdenburden
Prevalence of the disease in IndiaPrevalence of the disease in India::
 15-25 per 1000 population15-25 per 1000 population
 15 million infected, 25% sputum positive15 million infected, 25% sputum positive
 3 to 4 million infected are children3 to 4 million infected are children

6. World TB incidence. Cases per 100,000; Red => 300, orange = 200–300, yellow = 100–
200, green = 50–100, blue =< 50 and grey = n/a. Data from WHO, 2006World TB
incidence. Cases per 100,000; Red => 300, orange = 200–300, yellow = 100–200, green
= 50–100, blue =< 50 and grey = n/a. Data from WHO, 2013

7. EPIDEMIOLOGYEPIDEMIOLOGY
 Agent : Mycobacterium tuberculosis, M. bovisAgent : Mycobacterium tuberculosis, M. bovis
 Reservoir : Infected patientReservoir : Infected patient
 Mode of infection : Droplet infection, dust, ingestion,Mode of infection : Droplet infection, dust, ingestion,
skin, mucous membrane, skinskin, mucous membrane, skin
 Host FactorsHost Factors
 Age : all ages affected, congenital is rareAge : all ages affected, congenital is rare
 Sex : Girls > boys at PubertySex : Girls > boys at Puberty
 Malnutrition : more succeptibleMalnutrition : more succeptible
 Intercurrent infections : eg measles, whooping coughIntercurrent infections : eg measles, whooping cough
 Environment : overcrowding, inadequate ventillation,Environment : overcrowding, inadequate ventillation,
damp, insanitary and unhygenic conditionsdamp, insanitary and unhygenic conditions

8. ETIOLOGY

9. CLASSIFICATION OF MYCOBACTERIA
Typical Mycobacteria
•M tuberculosis
•M bovis
•M bovis BCG
•M africanum
Atypical Mycobacteria
•Photochromogens: M. Kansasii, M. marinum , M
simiae
•Scotochromogens: M scrofulaceum, M gordonae
•Non Photochromogens : M avium , M
paratuberculosis,
Rapid Growers: M Fortuitum, M chelonae
Non-Cultivable Mycobacteria
•M leprae
Saprophytic Mycobacteria
•M butyricum
•M pheli
•M smegmatis

10. MORPHOLOGY OF MYCOBACTERIUM
TUBERCULOSIS
• Straight or slightly curved rod.
• 3 µm X 0.3 µm.
• Occurring slightly in pairs or small clumps.
• The size depends on condition of growth and long
filamentous club shaped and branching forms may
sometimes be seen.
• Tubercle bacilli are weakly gram positive
• Are ‘ACID – FAST’ & ‘ALCOHOL FAST’
• Acid fastness has been ascribed to the presence of
mycolic acid in the bacillus, which resist
decolourization by 20% sulphuric acid & absolute
alcohol for 10 minutes.

11. Mycobacterium tuberculosis: Ziehl-Neelsen stain

12. Lipid Rich Cell Wall Of Mycobacterium
tuberculosis

13. Pathogenesis of Pediatric TB
• The primary complex of tuberculosis includes the local infection of
the portal of entry and the regional lymph nodes that drain the area,
the lung is the portal of entry in > 98%of cases .
• The tubercule bacilli multiply within the alveoli and the alveolar ducts
initially. Most of the bacilli are killed, but some survive within the
inactivated macrophages which carry them through the lymphatic to
the regional lymph nodes.
• When the primary infection is in the lung the hilar lymph nodes
usually are involved although the upper lobe of the focus may drain
in to the paratracheal nodes.

14. • Cell mediated immunity develops 2- 12 weeks after the initial
infection , along with tissue hypersensitivity. After bacilli
enters the macrophages, lymphocytes that recognizes the
mycobacterial antigens proliferate and secrete lymphokines
and other mediators that attract other lymphocytes and
macrophages.
Certain lymphokines activate macrophages causing
them to develop high concentration of lytic enzymes
that enhances their mycobactericidal capacity.
• Development of specific cellular immunity prevents
progression of initial infection in most individual .

15. • The parenchymal portion of the primary complex often heals
completely by calcification , after undergoing caseous necrosis and
encapsulation. Ocassionally this portions enlarges resulting in focal
pnumonitis and plueritis.
• If caseation is intense , the centre liquifies and empties in to the
associated bronchus leaving a residual cavity.
• During the development of primary complex (Ghon Complex ) which
is the combination of parenchymal pulmonary lesion and
corresponding lymph node site , tubercle bacilli are carried to the most
tissue of the body through blood and lymphatic vessels.
• Partial obstruction of the bronchus caused by external compression
may cause hyperinflation in distal lung segment. Complete obstruction
results in Atelectasis

17. The histopathological hallmark of tuberculosis is Granuloma , which is a
latin term from grain / granulum . Granuloma is a focal collection of
inflammatory cells in which mononuclear cells predominate. Macrophages
predominate in the centre attempting to phagocytose the mycobacteria.
Activated macrophages form epitheloid cells characterized by pale
eosinophillic cytoplasm. This is called Epitheloid cell granuloma. Caseation
necrosis is seen in the centre of the granuloma. There are two types of
granuloma :
 Soft granuloma : These are poorly circumscribed granulomas ,
characterized by loose collection of neutrophils , lymphocytes, macrophages
and epitheloid histiocytes with minimal fibroblastic proliferation . These
lesion are more likely to contain AFB

18.  Hard granuloma : These are well circumscribed granulomas with
epitheloid histiocytes and lymphocytes with numerous langhans giant
cells . More marked fibroblastic proliferation and few AFB is the
characteristics .
Soft caseating granuloma Hard non caseating granuloma

23. Pregnancy & Newborn
Pulmonary and particularly extrapulmonary tuberculosis
other than lymphadenitis in pregnancy is associated with
increased risk for prematurity , intrauterine growth retardation ,
low birth weight , and perinatal mortality.
Congenital tuberculosis is rare because the most common result
of female genital tract tuberculosis is infertility.
Congenital transmission is possible from a lesion in the placenta
through the umbilical vein or aspiration of amniotic fluid or
hematogenous spread .

24. In hematogenous spread the tubercle bacilli first reach the
fetal liver , where the primary focus with periportal lymph
node involvement may occur.
Organism pass through the liver in to the main fetal
circulation and infect the other organs. The bacilli in the
lung usually remain dormant until birth , when the
pulmonary oxygenation and circulation increases
significantly.
Congenital tuberculosis may also be caused by aspiration or
ingestion of infected amniotic fluid.

25. The micro-organism usually enters the body by inhalation through
the lungs where infection is presented by a primary lesion.
The infectious case (smear positive) of tuberculosis expels micro-
organisms into air in tiny droplets 0.5 to 5 µm in diameter when
coughing, sneezing or laughing.
These small droplets dry rapidly, become droplet nuclei carrying the
micro-organism and may remain suspended in air for several hours .
These droplet nuclei containing micro-organisms may be inhaled by
another person who enters the room.
After inhalation, the big particles usually expelled by the secretions
and cilia of the upper respiratory system while the smaller particles
are settled in the lung, multiplying and causing a primary lesion
from which infection may spread to other parts of the body
through blood and lymphatic system

26. Inhalation of mycobacteria does not mean occurrence of
tuberculosis, as the amount of bacilli inhaled may be not sufficient
to be manifested by illness and this case is called "tuberculosis
infection". Only 10% of those infected individuals may progress to a
manifest disease.
The infectiousness of a person with TB disease is directly related to the number of
tubercle bacilli that he or she expels into the air. Persons who expel many tubercle
bacilli are more infectious than patients who expel few or no bacilli.

27. Portal of entry for tuberculosisPortal of entry for tuberculosis
 Inhalation of Tubercle bacilli in >95% (M.TB)Inhalation of Tubercle bacilli in >95% (M.TB)
 Ingestion of milk containing Bovine TubercleIngestion of milk containing Bovine Tubercle
bacilli (M. bovis)bacilli (M. bovis)
 Contamination of superficial skin or mucousContamination of superficial skin or mucous
membrane lesion with tubercle bacillimembrane lesion with tubercle bacilli
 Congenital infection occurs when mother hasCongenital infection occurs when mother has
lymphohematogenous spread during pregnancylymphohematogenous spread during pregnancy
OROR tuberculous endometritistuberculous endometritis

28. Latent Tuberculosis Infection (LTBI)
Persons with LTBI have M. tuberculosis in their bodies, but do not have TB disease
and cannot spread the infection to other people. A person with LTBI is not regarded
as a case of TB. The process of LTBI begins when extracellular bacilli are ingested by
macrophages and presented to other white blood cells. This triggers the immune
response in which white blood cells kill or encapsulate most of the bacilli, leading to
the formation of a granuloma. At this point, LTBI has been established.
LTBI may be detected by using the tuberculin skin test (TST) or an interferon-gamma
release assay (IGRA) .It can take 2 to 8 weeks after the initial TB infection for the
body’s immune system to be able to react to tuberculin and for the infection to be
detected by the TST or IGRA. Within weeks after infection, the immune system is
usually able to halt the multiplication of the tubercle bacilli, preventing further

29. In some people, the tubercle bacilli overcome the immune system and multiply,
resulting in progression from LTBI to TB disease . Persons who have TB disease
are usually infectious and may spread the bacteria to other people. The
progression from LTBI to TB disease may occur at any time, from soon to many
years later. Body fluid or tissue from the disease site should be collected for AFB
smear and culture. Positive culture for M. tuberculosis confirms the diagnosis of
TB disease.
Persons who have TB disease may spread the bacteria to other people.

30. Latent TB Infection (LTBI)Latent TB Infection (LTBI) TB Disease (in the lungs)TB Disease (in the lungs)
Inactive, contained tubercle bacilli
in the body
Active, multiplying tubercle bacilli
in the body
TST or blood test results usually
positive
TST or blood test results usually
positive
Chest x-ray usually normal Chest x-ray usually abnormal
Sputum smears and cultures
negative
Sputum smears and cultures may
be positive
No symptoms Symptoms such as cough, fever,
weight loss
Not infectious Often infectious before treatment
Not a case of TB A case of TB
LTBI vs. TB Disease

31. • Children exposed to open case of tuberculosis.
• children with viral infections like measles, mumps,
pertussis , varicella.
• Infants and children < 4yrs of age
• Children co infected with HIV.
• Childrens with skiin test conversion in the past 1-2 yrs.
• Childrens who are immunocompromised especially in
cases of malignancy and solid organ transplantation ,
immunosuppressive medical treatments including anti-
tumour necrosis factor, diabetes mellitus, chronic renal
failure, silicosis, and malnutrition.
• Homeless childrens.

32. Primary tuberculous infectionPrimary tuberculous infection
Primary Focus (GhonPrimary Focus (Ghon’s focus)’s focus)
 at the site of first implantationat the site of first implantation
 usually single and Subpleuralusually single and Subpleural
 in most, - heals and disappears, orin most, - heals and disappears, or
 it heals by calcification.it heals by calcification.
Primary Complex:Primary Complex:
 primary focus + Hilar lymphnodes + drainingprimary focus + Hilar lymphnodes + draining
lymphaticslymphatics
 complications arise more commonly from regionalcomplications arise more commonly from regional
adenitis than from the primary focusadenitis than from the primary focus

33. Pulmonary lesions in tuberculosisPulmonary lesions in tuberculosis
- the primary complex- the primary complex

34. Primary infectionPrimary infection
Children vs. AdultsChildren vs. Adults
 In adults,In adults,
- regional lymphadenitis less marked- regional lymphadenitis less marked
- bronchial erosion less frequent- bronchial erosion less frequent
- less risk of dissemination- less risk of dissemination
 Thus, adult primary infection tends to beThus, adult primary infection tends to be
more local and pulmonary.more local and pulmonary.

35. Progressive primary tuberculosisProgressive primary tuberculosis
 Progression of TB depends on the age of theProgression of TB depends on the age of the
child, number of tubercle bacilli, and hostchild, number of tubercle bacilli, and host
resistance.resistance.
 Apparently healed focus or nodes may containApparently healed focus or nodes may contain
viable organisms for many years.viable organisms for many years.
 During 1During 1stst
4-8 weeks, organisms are disseminated4-8 weeks, organisms are disseminated
in the blood stream.in the blood stream.

36. Progressive pulmonary diseaseProgressive pulmonary disease
 Progressive primary infectionProgressive primary infection: Progression of: Progression of
recently acquired pulmonary primary infection.recently acquired pulmonary primary infection.
 Endogenous exacerbationEndogenous exacerbation: reactivity of: reactivity of
organisms and breakdown of primary lesionsorganisms and breakdown of primary lesions
acquired > 5 years previously.acquired > 5 years previously.
 Exogenous exacerbationExogenous exacerbation: Re-infection by newly: Re-infection by newly
acquired bacilli in persons with healed primaryacquired bacilli in persons with healed primary
lesions.lesions.

37. Primary complex TB

38. Progressive primary pulmonary -TB

39. Pleural TB
Miliary TB

40. Complications of regional nodesComplications of regional nodes
1. Incomplete (ball-valve) bronchial obstruction,
emphysema of middle & lower lobes
2. Complete bronchial obstruction, collapse of
right lower lobe
3. Erosion of node into bronchus & segmental
consolidation
4. Rupture of node into pericardium: tuberculous
pericardial effusion

41. Sequelae of bronchial complicationsSequelae of bronchial complications
1. Stricture of bronchus at site of erosion
2. Cylindrical bronchiectasis in area of old collapse
3. Wedge shadow: contracture & fibrosis of
segmental lesion
4. Linear scar of fibrosis following segmental
lesion

42. 42
Sites of TB Disease (2)Sites of TB Disease (2)
Location Frequency
Pulmonary
TB
Lungs Most TB cases are
pulmonary
Extrapulm
onary TB
Places other than lungs such
as:
• Lymph nodes
• Pleura
• Brain
• Kidneys
• Bones and joints
Found more often in:
• HIV-infected or
other
immunosuppressed
persons
• Young children
Miliary TB Carried to all parts of body,
through bloodstream
Rare

43. Symptoms of childhoodSymptoms of childhood
tuberculosistuberculosis
1.1. PulmonaryPulmonary : dry cough , low grade fever,: dry cough , low grade fever,
predominantly evening rise of temperature, weight loss,predominantly evening rise of temperature, weight loss,
loss of appetite. Rarely hemoptysis can occur .loss of appetite. Rarely hemoptysis can occur .
2.2. Lymph nodeLymph node : fever , lymphadenopathy (mediastinal: fever , lymphadenopathy (mediastinal
lymph node) , cold abcess, cough and fever .lymph node) , cold abcess, cough and fever .
3.3. PlueraPluera : cough (non productive ) , pl ueritic chest: cough (non productive ) , pl ueritic chest
pain .pain .
4.4. GenitourinaryGenitourinary : dysuria , nocturia, increased frequency,: dysuria , nocturia, increased frequency,
tenderness / swelling of testis / epididymis . Presence oftenderness / swelling of testis / epididymis . Presence of
sterile pyuria should always lead to search forsterile pyuria should always lead to search for
tuberculosis.tuberculosis.

44. 5. Skeletal TB (POTTS SPINE ) : fever , backache is
commonly seen. Paresis or plegia depending upon duration of
development is a cause of concern. Joint pain / cold abcess
formation is also commonly seen.
6. CNS TB : fever , malaise , anorexia , iritability , later on as the
diesease preogress neurological symptoms develop like
progressive headache, lethargy , impaired cognition , memory
disturbance, confusion and then stupor – coma with or with out
neurological deficit. Features of meningitis may be present.
8. Abdominal : peritonotis followed by ileo-caecal , ano rectal and
mesentric lymph nodes infection. In peritoneal tuberculosis TB
fever , ascitis , pain , anorexia , / weight loss are common.

45. 8. Pericardial : fever , dyspnoea , tachycardia , neck vein distension
edema , hepatomegaly , paradoxical pulse , pericardial rub.
9.Disseminated and miliary Koch’s : This is a haematogenous spread
and amongst one of the serious manifestations of tuberculosis .
patients are cachetic and present with fever , weight loss and multi
organ symptoms . Bone marrow involvement now a days frequently
seen.

47. Miliary tuberculosisMiliary tuberculosis
 most common within 1most common within 1stst
3 to 6 months after3 to 6 months after
infectioninfection
 due to heavy hematogenous spread of tubercledue to heavy hematogenous spread of tubercle
bacillibacilli
 Onset: Insidious, withOnset: Insidious, with
Fever and weight lossFever and weight loss
Palpable liver and/or spleenPalpable liver and/or spleen
Tachypnoea with normal chest findingsTachypnoea with normal chest findings

48. Miliary tuberculosisMiliary tuberculosis
 Hematogenous dissemination leads to progressiveHematogenous dissemination leads to progressive
development of small lesions throughout the body,development of small lesions throughout the body,
with tubercles in thewith tubercles in the
 lung, spleen, liver,lung, spleen, liver,
 bone marrow, heart, pancreasbone marrow, heart, pancreas
 brain, choroid, skinbrain, choroid, skin
 Radiologic diagnosisRadiologic diagnosis::
 ““Snow stormSnow storm”” appearanceappearance
(Multiple small lung nodules 1mm size and above in(Multiple small lung nodules 1mm size and above in
both lung fields).both lung fields).

49. Miliary TBMiliary TB

50. Cutaneous TuberculosisCutaneous Tuberculosis
1.1. Associated with primary complexAssociated with primary complex
(Direct inoculation into Traumatized Area)(Direct inoculation into Traumatized Area)
 - Painless nodule, leading to non healing ulcer with regional- Painless nodule, leading to non healing ulcer with regional
lymphadenitislymphadenitis
 - Scrofuloderma over ruptured caseous lymph node- Scrofuloderma over ruptured caseous lymph node
2.2. Associated with Hematogenous disseminationAssociated with Hematogenous dissemination
 - Papulonecrotic tuberculids- Papulonecrotic tuberculids
papules with soft centers on trunk, thighs and facepapules with soft centers on trunk, thighs and face
 - Tuberculosis verrucosa cutis- Tuberculosis verrucosa cutis
Large tuberculids on arms and legsLarge tuberculids on arms and legs
3.3. Associated with hypersensitivity to tuberculinAssociated with hypersensitivity to tuberculin
 - Erythema nodosum- Erythema nodosum
painful indurated nodules on shins, elbows, forearms thatpainful indurated nodules on shins, elbows, forearms that
subside in 2-3 weekssubside in 2-3 weeks

51. TB verrucosa cutisTB verrucosa cutis

52. Erythema nodosumErythema nodosum

53. Tuberculosis of superficialTuberculosis of superficial
lymph nodes (scrofula)lymph nodes (scrofula)
 Tonsillar / submandibularTonsillar / submandibular
(Spread from paratracheal nodes)(Spread from paratracheal nodes)
 SupraclavicularSupraclavicular
(From primary lesion in upper lobe)(From primary lesion in upper lobe)
 Axillary / epitrochlearAxillary / epitrochlear
(From skin lesion on hand)(From skin lesion on hand)
 InguinalInguinal
(From ulcer on sole of foot)(From ulcer on sole of foot)

54. Scrofula, most common, infection of the
superficial lymph nodes, tonsillar and
submandibular. Early firm non tender discrete,
enlarge slowly or rapid enlargement with
fever, tenderness, fluctuance. Rupture and
sinus if untreated.

55. • The nodes usually enlarge gradually in the early stage of the lymph node
disease the lymph nodes are discrete , firm , matted , nontender , often
fixed to the under lying skin . It is usually unilateral , but bilateral
involvement may also occur because of the cross over drainage pattern
of the lymphatics.
• Systemic signs and symptoms other than low grade fever are usually
absent . The tuberculin skin test is usually reactive. But the chest
radiograph is also normal in 70% of cases .
• Lymph node TB may require surgical removal , due to the rupture of
the capsule of lymph node resulting in the formation of the draining
sinus tract. The tuberculosis lymph adenitis can usually by fine needle
aspiration of the node . It responds to ATT .
Although the lymph nodes do not return to the normal size for months
or even years.

56. Differential diagnosis for TB lymphadenitis are :
• Non Tuberculous Mycobacteria (NTM)
• Cat scratch disease ( BARTONELLA HENSELAE)
• Tularemia
• Brucellosis
• Toxoplasmosis
• Tumor
• Branchial cyst
• Cystic hygroma
• Pyogenic infection.

57. Ocular TuberculosisOcular Tuberculosis
 Primary tuberculous conjunctivitisPrimary tuberculous conjunctivitis (after trauma)(after trauma)
Yellowish – gray nodules on palpebral conjunctivaYellowish – gray nodules on palpebral conjunctiva
with preauricular adenopathywith preauricular adenopathy
 Phlyctenular conjunctivitisPhlyctenular conjunctivitis (Hypersensitivity)(Hypersensitivity)
Nodules on limbus recurring in crops for weeksNodules on limbus recurring in crops for weeks
 Tubercles of choroidTubercles of choroid (with miliary TB)(with miliary TB)

58. Choroidal tuberclesChoroidal tubercles

59. GI and Abdominal TBGI and Abdominal TB
 Hematogenous spread from lungs or swallowingHematogenous spread from lungs or swallowing
of infected sputum.of infected sputum.
 Painless ulcer in gingivolabial sulcus withPainless ulcer in gingivolabial sulcus with
submental or submandibular adenopathysubmental or submandibular adenopathy
 Ulcer on tonsilUlcer on tonsil
 Esophageal diverticulum secondary to rupture ofEsophageal diverticulum secondary to rupture of
mediastinal nodes into lumenmediastinal nodes into lumen

60.  Tuberculous toxemiaTuberculous toxemia
 Present with colicky abdominal pain, vomiting andPresent with colicky abdominal pain, vomiting and
constipation.constipation.
 Abdomen feels doughy.Abdomen feels doughy.
 Rolled up omentum and enlarged lymph nodes mayRolled up omentum and enlarged lymph nodes may
appear as irregular nodular masses with ascitesappear as irregular nodular masses with ascites
 Tuberculous enteritisTuberculous enteritis
Ulcers, mesenteric adenitis, peritonitisUlcers, mesenteric adenitis, peritonitis
Adhesions, subacute intestinal obstruction,Adhesions, subacute intestinal obstruction,
HepatosplenomegalyHepatosplenomegaly

61. • Tuberculous peritonitis: which occurs in young men and
adolescence rare in children arises from the subclinical or
haematogenous dissemination .
Localised peritonitis is caused by direct extension from
abdominal lymphnode ,intestinal focus/ genitourinay
tuberculosis.
• Abdominal pain / tenderness , ascites , anorexia ,
low grade fever are the typical manifestations.
The tuberculin test is usually reactive.

62. GI TBGI TB

63. Renal tuberculosisRenal tuberculosis
 Tubercles in glomeruli lead to shedding ofTubercles in glomeruli lead to shedding of
tubercle bacilli into tubulestubercle bacilli into tubules
 Caseous mass / Cavity between cortex andCaseous mass / Cavity between cortex and
pyramidspyramids
 TB of bladder (Tuberculous cystitis)TB of bladder (Tuberculous cystitis)
 SymptomsSymptoms: dysuria, hematuria,: dysuria, hematuria,
pyuria with TB bacillipyuria with TB bacilli

64. Caseous renal tuberculosisCaseous renal tuberculosis

65. Skeletal tuberculosisSkeletal tuberculosis
 Bones involved in order of frequencyBones involved in order of frequency::
Vertebrae > knee > hip > elbowVertebrae > knee > hip > elbow
Upper extremities and non-weight-bearing bonesUpper extremities and non-weight-bearing bones
(skull, clavicle) rarely involved(skull, clavicle) rarely involved
 Tuberculous spondylitisTuberculous spondylitis most commonlymost commonly
Thoracic / Lumbar / Both (Decreasing frequency)Thoracic / Lumbar / Both (Decreasing frequency)
 X-ray findingsX-ray findings::
Narrowing of disc space, Collapse of vertebralNarrowing of disc space, Collapse of vertebral
bodybody
Extensive destruction with kyphosis (Pott disease)Extensive destruction with kyphosis (Pott disease)
 ComplicationsComplications:Para vertebral abscess (Pott abscess):Para vertebral abscess (Pott abscess)
Psoas Abscess. Paraplegia, Quadriplegia (cervical)Psoas Abscess. Paraplegia, Quadriplegia (cervical)

66. HistoryHistory
 Presentation depends on the following:Presentation depends on the following:
 Stage of diseaseStage of disease
 SiteSite
 Presence of complications such as neurologic deficits, abscesses,Presence of complications such as neurologic deficits, abscesses,
or sinus tractsor sinus tracts
 The reported average duration of symptoms at the time ofThe reported average duration of symptoms at the time of
diagnosis is 3-4 months.diagnosis is 3-4 months.
 Back pain is the earliest and most common symptom.Back pain is the earliest and most common symptom.
 Patients have usually had back pain for weeks prior toPatients have usually had back pain for weeks prior to
presentation.presentation.
 Pain can be spinal or radicular.Pain can be spinal or radicular.
 Constitutional symptoms include fever and weight loss.Constitutional symptoms include fever and weight loss.

67.  Neurologic abnormalities occur in 50% of cases and canNeurologic abnormalities occur in 50% of cases and can
include spinal cord compression with paraplegia, paresis,include spinal cord compression with paraplegia, paresis,
impaired sensation, nerve root pain, or cauda equinaimpaired sensation, nerve root pain, or cauda equina
syndrome.syndrome.
 Cervical spine tuberculosis is a less common presentation isCervical spine tuberculosis is a less common presentation is
characterized by pain and stiffness.characterized by pain and stiffness.
Patients with lower cervical spine disease can presentPatients with lower cervical spine disease can present
with dysphagia or stridor.with dysphagia or stridor.
Symptoms can also include torticollis, hoarseness, andSymptoms can also include torticollis, hoarseness, and
neurologic deficits.neurologic deficits.
 The clinical presentation of spinal tuberculosis in patientsThe clinical presentation of spinal tuberculosis in patients
infected with the human immunodeficiency virus (HIV) isinfected with the human immunodeficiency virus (HIV) is
similar to that of patients who are HIV negative; however,similar to that of patients who are HIV negative; however,
the relative proportion of individuals who are HIV positivethe relative proportion of individuals who are HIV positive
seems to be higher.seems to be higher.

68. Osseous Clinical manifestationsOsseous Clinical manifestations
 TB osteitisTB osteitis
 Synovitis/epiphysitis, destructive arthritis, fusionSynovitis/epiphysitis, destructive arthritis, fusion
in deformed positionsin deformed positions
 Abscesses may track through tissues (psoas)Abscesses may track through tissues (psoas)
 TB arthritis (PonchetTB arthritis (Ponchet’s Disease)’s Disease)
 1-5% children if TB untreated1-5% children if TB untreated
 Knee/hip/elbow/dacylitisKnee/hip/elbow/dacylitis
 Thick, inflammatory synovium, invades articularThick, inflammatory synovium, invades articular
surface, with erosion and fibrosis jointsurface, with erosion and fibrosis joint

69. PottPott’s Disease’s Disease

70. TB osteitisTB osteitis

71. Genital tuberculosisGenital tuberculosis
 Uncommon before pubertyUncommon before puberty
 Usually due to lympho-hematogenous spreadUsually due to lympho-hematogenous spread
 Occasionally by direct extension fromOccasionally by direct extension from
adjacent lesion of bone, gut, or urinary tractadjacent lesion of bone, gut, or urinary tract

72. Genital tuberculosisGenital tuberculosis
 SalpingitisSalpingitis
 EndometritisEndometritis
 OophoritisOophoritis
 CervicitisCervicitis
 Infertility is commonest sequelInfertility is commonest sequel
 in malesin males::
 Primary tuberculosis of penis after circumcisionPrimary tuberculosis of penis after circumcision
with inguinal adenopathywith inguinal adenopathy
 Epididymitis / Epididymo – orchitis in earlyEpididymitis / Epididymo – orchitis in early
childhoodchildhood

73. CNS ManifestationsCNS Manifestations
 Rich focus, vessels infiltrated by exudateRich focus, vessels infiltrated by exudate
 Inflamation/infarctionInflamation/infarction
 Brain stem: CN III,VI,VII dysfunctionBrain stem: CN III,VI,VII dysfunction
 Basilar cisterns obstructed: hydrocephalusBasilar cisterns obstructed: hydrocephalus
 TB meningitisTB meningitis
 Children < 4 yrs age, most common in 3-6 month of primary infectionChildren < 4 yrs age, most common in 3-6 month of primary infection
 Gradual onset, rapid in infants HydrocephalusGradual onset, rapid in infants Hydrocephalus
 Tuberculomas (20-37%)Tuberculomas (20-37%)
 Mortality (<10% w/ Rx) Morbidity high (MR, Sz, hemiparesis)Mortality (<10% w/ Rx) Morbidity high (MR, Sz, hemiparesis)
 TST – in 40%, CXR nl 50%TST – in 40%, CXR nl 50%
 CSF: cell # 10-100, glucose low, protein highCSF: cell # 10-100, glucose low, protein high
 TuberculomaTuberculoma
 Most common in < 10yrs ageMost common in < 10yrs age
 Infratentorial: headaches, Seizures, increased ICPInfratentorial: headaches, Seizures, increased ICP

74. Tuberculous meningitisTuberculous meningitis
TB meningitis seen in 1/300 Primary infectionsTB meningitis seen in 1/300 Primary infections
Pathophysiology:Pathophysiology:
Rupture of a subcortical caseous focus (RichRupture of a subcortical caseous focus (Rich’s) into the’s) into the
subarachnoid space.subarachnoid space.
Inflammatory exudates form about base of brain and alongInflammatory exudates form about base of brain and along
cerebral vessels as they pass over hemispheres.cerebral vessels as they pass over hemispheres.
Raised intracranial pressure due to increased secretion ofRaised intracranial pressure due to increased secretion of
CSFCSF
Adhesions along base and roof of 4Adhesions along base and roof of 4thth
ventricles lead toventricles lead to
obstruction to CSF flow and hydrocephalus,obstruction to CSF flow and hydrocephalus,
involvement of cranial nerves III VI VII and optic chiasma.involvement of cranial nerves III VI VII and optic chiasma.
Cerebral endarteritis narrows lumen, reduces blood flow,Cerebral endarteritis narrows lumen, reduces blood flow,
leads to cerebral thrombosis and infarction.leads to cerebral thrombosis and infarction.

75. CN palsy 3, 6, 7CN palsy 3, 6, 7

76. Stages of TB meningitisStages of TB meningitis
Stage I Irritability, anorexia, headache, drowsiness,Stage I Irritability, anorexia, headache, drowsiness,
vomiting, fever, malaise.vomiting, fever, malaise.
Stage II : Focal neurological signs, cranial nerve palsiesStage II : Focal neurological signs, cranial nerve palsies
Seizures, squint, lethargy, positive Kernig andSeizures, squint, lethargy, positive Kernig and
Brudzinki sign.Brudzinki sign.
Stage III : Loss of consciousness, hemiplegia, Coma,Stage III : Loss of consciousness, hemiplegia, Coma,
Papilloedema, Decerebrate rigidity and eventuallyPapilloedema, Decerebrate rigidity and eventually
death.death.

77. Complications of TB meningitisComplications of TB meningitis
HydrocephalusHydrocephalus
Subdural effusionSubdural effusion
Late: Hemiplegia / ParaplegiaLate: Hemiplegia / Paraplegia
Intellectual impairmentIntellectual impairment
BlindnessBlindness
DeafnessDeafness
Intracranial calcifications leading toIntracranial calcifications leading to
hypothalamic and pituitary dysfunctionhypothalamic and pituitary dysfunction
- Growth failure- Growth failure
- Diabetes insipidus- Diabetes insipidus
- Failure of development of secondary sexual- Failure of development of secondary sexual
characteristicscharacteristics

78. Diagnosis of TB meningitisDiagnosis of TB meningitis
 Signs of meningeal irritationSigns of meningeal irritation
 X-ray chestX-ray chest
 CT scan – basal exudates, inflammatory granulomas etcCT scan – basal exudates, inflammatory granulomas etc
 Tuberculin testingTuberculin testing
 Retinoscopy for choroidal tuberclesRetinoscopy for choroidal tubercles
 Lumbar punctureLumbar puncture
Elevated CSF pressure(30 – 40cm h2o)Elevated CSF pressure(30 – 40cm h2o)
Cobweb Coagulum/ pellicle on standingCobweb Coagulum/ pellicle on standing
100 – 500 WBCs / cu.mm100 – 500 WBCs / cu.mm
protein are elevated (400 – 5000 mg/dl)protein are elevated (400 – 5000 mg/dl)
secondarily to hydrocephalus and spinal block.secondarily to hydrocephalus and spinal block.
Low / Normal sugar< 40mg/dlLow / Normal sugar< 40mg/dl
AFB smear & cultureAFB smear & culture

79. Prognosis in TB meningitisPrognosis in TB meningitis
100% mortality in 3-4 weeks without treatment100% mortality in 3-4 weeks without treatment
100% survival with treatment started in Stage I100% survival with treatment started in Stage I
75% survival with treatment started in Stage II75% survival with treatment started in Stage II
Stage III – variable survival, all will have sequelaeStage III – variable survival, all will have sequelae

80. Tuberculoma : A tumour like mass arising from the
aggregation of caseous tubercles clinically presenting as a
brain tumour.
•Lesions are most often singular but may be
multiple.Tuberculoma in children are located infratentorial
located at the base of the brain near Cerebellum.
•Clinical presentation is similar to neurocysticercosis.
• Tuberculoma rings are usually large . On CT or MRI of the
brain the lesion often has a thick irregular wall , ring
enhancing lesion and associated with severe perilesional
edema.

81. Treatment -Antituberculous therapy is recommended for 1
year as for tubercular meningitis along with
corticosteroides for initial 6-8 weeks. Corticosteriods are
given initially to reduce the edema.

82. TuberculomasTuberculomas

83. ReferencesReferences
 NelsonNelson’’s textbook of paediatricss textbook of paediatrics
 Pediatric tuberculosis , by Vimlesh sethPediatric tuberculosis , by Vimlesh seth
 IAP TextbookIAP Textbook
 Essentials of tuberculosis in children by kabra skEssentials of tuberculosis in children by kabra sk
 InternetInternet