Dr. Gireesh presented on TB lymphadenitis and CNS tuberculosis. TB lymphadenitis is the most common form of extra-pulmonary TB in children from endemic areas, usually developing within the first year of primary infection. It presents as enlarged, non-tender lymph nodes. Diagnosis is made through fine needle aspiration or biopsy. Treatment involves antitubercular medications for 6-9 months. CNS tuberculosis can manifest as tuberculous meningitis, tuberculomas, or Pott's disease of the spine. Tuberculous meningitis commonly presents with fever, vomiting, and altered sensorium. Diagnosis is challenging and treatment involves prolonged antitubercular therapy along with cort

1. Presenter - Dr. Gireesh
Moderator – Dr. Suba

3. TB Lymphadenitis

4. Most common form of EPTB in children from TB
endemic areas.
ETIOLOGICAL AGENTS :-
1. Mycobacterium tuberculosis in endemic
areas.
2. Mycobacterium bovis in areas where control
of bovine tuberculosis is poor.
3. BCG vaccination in severely immune
compromised children.

5. PATHOGENESIS :-
 Develops within first 6-12 months of primary
infection.
 TB lymphadenitis represents glandular component of
Primary complex (Ghon’s complex).
 Lymph nodes involved reflect most likely site of
Ghon’s focus.
Submandibular group – lung and intrathoracic nodes
Supraclavicular – Apex of lung
Cervical nodes – Tonsils, oropharynx, head and neck
Axillary or Inguinal – Local skin lesion at some distal
point

6. INITIAL TUBERCLE FORMATION
LYMPHOID HYPERPLASIA
CASEATION AND NECROSIS
MATTING DUE TO PERIADENITIS
LIQUEFACTION OF CASEOUS MATERIAL
COLD ABSCESS
(Soft fluctuant node with violaceous discolouration of overlying skin)
SPONTANEOUS DRAINAGE AND SINUS FORMATION
HEALING WITH SCARRING AND/OR CALCIFICATION

8. CLINICAL FINDINGS :-
 History
 LN
Characteristics
1. Location
2. Size &
Character
 Duration
Contact with an adult index case with PTB
Cervical, rarely inguinal or axillary ( If axillary
nodes ipsilteral to site of BCG vaccination,
consider BCG adenitis)
Visible, > 2*2 cm
Non-tender and / or matted, usually solid but
may be fluctuant (may also be secondarily
infected)
Persistent for > 1 month
Despite excluding / treating potential local
causes

9.  Reactive
tuberculin skin
test (TST)
 Chest Radiograph
10 mm or more in all children (94% cases)
5 mm or more in HIV infected children
Suggestive of TB (<50% cases)
•Equal frequency in all age groups bur rare in infancy.
•Secondary infection leads to red, warm and painful nodes.

10. DIAGNOSIS :-
 FINE NEEDLE ASPIRATION provides excellent
bacteriological yield and is a minimal invasive
procedure, especially when a 22G needle is used.
Culture from a discharging sinus if sinus is
present.
Excision biopsy particularly in cases of NTM
disease where therapeutic response to
chemotherapy is suboptimal.

11. Treatment :-
• ATT – 2HRZ + 4HR
• Surgery is advised for exceptionally tense
fluctuant nodes or in presence of severe
discomfort.
• Full excision has to be done (no incision and
drainage).

12. • M. bovis is inherently resistant to
pyrazinamide and M. bovis BCG show
intermediate resistance to INH.
• So, ordinary ATT is not effective in M.bovis
and M.bovis BCG adenitis. INH to be given
atleast 10-15 mg/kg and fourth drug is
required in place of PZA.
• Surgical intervention is advised if there is no
spontaneous resolution or severe discomfort.

13. CNS TUBERCULOSIS

14. CLASSIFICATION OF CNS TUBERCULOSIS
Intracranial TB
• Tubercular Meningitis
• Space Occupying Lesions
(SOL)
1. Tuberculomas
2. Tubercular abscess
• Tubercular encephalopathy
• Tubercular vasculopathy
Spinal TB
• Pott’s spine & paraplegia
• Tubercular arachnoiditis
• Non-osseous spinal
tuberculoma
• Spinal meningitis

15. Pathogenesis :-
• TB meningitis (TBM) is the commonest type of CNS
TB in children in INDIA.
•Two-step model proposed by Arnold Rich and McCordock
1. Within 2-4 weeks after infection with MTB, through blood
circulation, bacilli spread to extrapulmonary sites and produce
small granulomas in meninges and brain parenchyma called as
“RICH FOCUS”.
2. MTB contained within these lesions are released into
subarachnoid space which might happen months or years after
initial bacteremia. Decreased immunity may result in rupture of
Rich foci.

16. • Miliary TB is directly involved in pathogenesis
of TBM. Bacilli enter CNS by crossing blood
brain barrier because extracellular MTB can
traverse through endothelial cells.
• Microglia produce variety of chemokines like
TNF-alpha and IFN-gamma. Elevated levels of
CSF and serum of these chemokines have
positive correlation with severity of TBM.
• HIV coinfection with TBM attenuate
inflammatory changes which leads to very low
level of CSF IFN-gamma concentration.

17. Pathology :-
• Characteristic pathological features are
1. Meningeal inflammation
2. Dense basal exudates
3. Vasculitis
4. Hydrocephalus
5. Other paernchymal changes are infarction, diffuse edema
and tuberculoma.
• Exudates result in blocking of
1. Middle meningeal arteries, Circle of Willis, Basilar vessels
2. Brainstem
3. Cranial nerves
4. CSF absorption

18. Clinical Features :-
• 75-85 % cases are below the age of 5 years.
• Uncommon before 6 months and rare before 3
months of age.
• Peak incidence in 3-5 years of age group.
• Boys > Girls
• Onset – Subacute or Chronic (>3 weeks to
develop)

19. STAGE I
• Non-specific symptoms
• May be triggered by any condition which
lowers resistance
• Occasionally triggered by head injury
• Spans 2 to 3 weeks
• Few or no signs of meningeal irritation

20. • Low grade fever, anorexia, sleep disturbances,
apathy, irritability, altered behavior, headache and
vomiting.
• In infants and children < 3 years of age,
presentation may be acute and simulate pyogenic
meningitis.
• In older children with subacute onset, there are
behavioral changes, movement disorders and are
sometimes referred to psychiatrist.

21. STAGE II
• Signs of meningeal irritation along with
symptoms of raised intracranial pressure.
• May present with convulsions and cranial
nerve defects, hemiplegia, extrapyramidal
signs.
• Becomes semi comatose and can be aroused
with painful stimulus.

22. STAGE III
• Progressive neurological deficits with dilated
pupils.
• Signs of brain stem compression with well
marked neck retraction, opisthotonic posturing,
decorticate followed by decerebrate spasms.
• Reappearance of neonatal reflexes even after 1
year of age.
• Irregular breathing, hemiplegia, deep coma,
deterioration of vital signs, death.

23. • Fever
• Convulsions
• Vomiting
• Altered sensorium
• Hemiplegia
• Cranial nerve palsies
• Hydrocephalus
• Vasculitis
• 80-90%
• 50-60%
• 40-45%
• 20-45%
• 20%
• 25%
• 70%
• 41%
 Most common CN involved is 6th CN

24. Complications :-
• Acute gastric ulcers may result from
hypothalamic lesions.
• Autonomic dysfunctions like perspiration,
abdominal pain and hyperperistalsis.
• Communicating hydrocephalus is more
common than obstructive hydrocephalus.

25. • Vasculitis can lead to infarction. In TBM, basal
ganglionic infarcts are the commonest
because of involvement of perforating vessels.
• Ocular– Papillitis>optic atrophy>papilledema.
Choroidal tubercles are rarely seen but are
pathognomonic of CNS TB.
• Spinal tuberculous arachnoiditis is a rare
complication. Thoracic > lumbar > cervical.

26. Diagnosis :-
• Global encephalopathy with focal deficit is the
hallmark of TBM.
• CSF staining and culture are rarely positive.
• CSF analysis if inconclusive should be repeated
after 48-72 hours after antibiotic therapy. If it
shows no change in clinical status and CSF
results, it may favor diagnosis of TBM.

27. Modified Ahuja Criteria

28. Cob-Web appearance in CSF

29. Treatment :-
• Antitubercular Treatment :-
2HRZE + 10HRE
• Corticosteroids :-
Steroids like dexamethasone have immune
modulating effect in CNS.
Steroids reduce spinal block, decrease CSF
protein and pleocytosis besides depressing
tuberculin hypersensitivity.

30. • Oral prednisolone 2 mg/kg/day for 3 weeks
and then tapered over next 3 weeks (or)
• Dexamethasone 0.4 mg/kg/day followed by
oral prednisolone
• Total duration of steroids is 6-8 weeks.

31. Use of steroids in TB :-
1. TB Meningitis.
2. TB percardial effusion.
3. Miliary TB.
4. Addison’s disease.

32. • Antiepileptic Drugs (AED) :-
Indications for starting longterm AED -
1. Seizures occuring later than first week
2. Associated with tuberculoma or infarct
3. Recurrent GTCS and tonic seizures
4. Focal seizures

33. • Phenobarbitone should not be used as AED as it
has cerebral depressant effect and induces hepatic
microsomal enzymes which lead to acetylation of
INH causing increased hepatotoxicity.
 Mannitol is used to cerebral edema – 5 ml/kg
stat followed by 2 ml/kg 6th hourly for 8 doses.
Repeated administration leads to rebound
phenomenon (Fluid and electrolyte imbalance
with a secondary increase in ICT)

34. Paradoxical Response to ATT :-
• Transient worsening of disease, at a pre-
existing site, or development of new
tuberculous lesions (new granulomas or
abscesses or hydrocephalus) in a patient who
initially improved on ATT.
• Occurs mostly within first 2 weeks after
starting ATT, sometimes even upto 1 year.
• More common in HIV positive (30%) than in
immunocompetent (10%).

35. Surgical Management of Hydrocephalus :-
 Ventriculo-peritoneal shunting.
 Endoscopic 3rd ventriculostomy (ETV).
• Indications :-
1. Noncommunicating hydrocephalus.
2. Communicating hydrocephalus not
responding to medical treatment.
3. Grade II and III hydrocephalus.

36. Grade Sensorium Neurological
Deficit
I Normal -
II Normal Present
III Altered +/- Dense
deficit
IV Deeply
comatose
+/-
Decorticate/D
ecrebrate
posturing
Palur Staging for TBM with Hydrocephalus :-

37. Prognosis :-
• Mortality and disability depend on stage of
presentation.
• Other factors are age, BCG vaccination, CN
palsies, hydrocephalus, High CSF lactate, CSF
leucopenia, low CSF glucose, drug resistance.

38. TUBERCULOMA

39. • Tuberculoma is a manifestation TB which occurs
in solid organs.
• Begins in an area of TB cerebritis as a cluster of
microgranulomas, which coalesce into a mature
noncaseating granuloma.
• Incidence is more in developing countries

40. Pathogenesis :-
• Conglomerate mass of tissue made up of small
tubercles which consist of a central core of
epithelioid cells surrounde by lymphocytes.
• Center becomes necrotic forming caseous
debris and periphery tends to encapsulate
with fibrous tissue.
• Liquefaction of center result in formation of
Tubercular abscess in extreme cases.

41. • Intracranial tuberculomas are mostly
infratentorial in patients aged < 20 years.
•Supratentorial lesions predominate in adults.
•Gross – Hard, nodular, comparatively avascular
and easy to shell out.
•Edema is so extensive and out of proportion to
size of tuberculoma.
•There may be a connection with meninges and
resemble meningioma.

43. Clinical Features :-
• Depend on size and site of leson as well as
presence of concurrent meningitis.
• Usually present with seizures without associated
meningeal signs or evidence of TB elsewhere in
the body.
• Various cerebellar or brainstem syndromes
depending on location
• Infratentorial tuberculoma may present with
raised ICT.

44. Diagnosis :-
• Evidence of extracranial TB and a close family
contact point to diagnosis in pediatric age.
• Differential diagnosis to be considered are
neurocysticercosis, brain abscess, fungal
infection and malignancy.
• Ring enhancing lesions on imaging.

49. Treatment :-
• ATT – 2HRZE + 10HRE
• Symptomatic management of raised ICT and
seizures.
• Steroids for cerebral edema.
• Paradoxical response to ATT may cause
increase in size or new lesions.

50. • Radiological response to ATT starts in 6-8 weeks.
• Usually resolve over 3-6 months of ATT.
• Surgical decompression or excision may be
required in large masses.
• Calcification rarely occurs.

51. TUBERCULOSIS OF SPINE
(POTT’S SPINE)

52. • Spine is the most common bone involved in TB
(50% of osteoarticular TB).
• Secondary to a primary focus elsewhere in the
body.
• Hematogenou spread either through arteries or
through Batson’s plexus of veins.
• Lymphatic spread may occur from mesenteric
lymph nodes through cisterna chyli.

53. • Thoracolumbar > lower thoracic > upper lumbar.
• Due to excessive mobility in these regions.
• More severe in children < 10 years of age.
• Sites of involvement (in decreasing frequency)-
1. Metaphyseal – Most
common type.
Leads to diminution of
intervertebral disc space.
Because intercostal artery
supplies two adjacent
vertebrae.

54. 2. Central – leads to wedge shaped vertebra.

55. 3. Anterior – Under anterior longitudinal ligament.
4. Appendiceal such as lamina, spinous process
5. Posterior – Extremely rare

56. Clinical Features :-
• Pain is the predominant symptom
• Constitutional symptoms like fever, cough, loss of
appetite, weight loss.
• Back pain more at night time localised over
affected area of spine.
• Girdle pains along intercostal nerves.
• Tenderness at local site and paraspinal muscle
spasms.

57. • Cold Abscess :-
Pus comes out of vertebra and present on
radiography as ‘prevertebral’ or ‘paravertebral
abscess’ or clinically as ‘cold abscess’.

58. • Pus from cold abscess spreads along fascial sheaths
and neurovascular bundles.
ORIGIN COLD ABSCESS
1. Cervical spine i. Retropharyngeal
abscess
ii. Posterior or anterior
triangle
iii. Mediastinum
2. Thoracic spine i. Paravertebral
abscess
ii. Anterior chest wall

59. ORIGIN COLD ABSCESS
3. Lumbar spine i. Psoas abscess
ii. Lumbar triangle
iii. Medial side of upper
thigh
4. Lumbosacral junction i. Pelvic abscess
ii. Gluteal abscess

60. • Pott’s Paraplegia –
Due to compression of spinal cord.
Incomplete or complete with bladder and bowel
involvement.
C-spine lesion may lead to quadriplegia (upper limbs
are involved before lower limbs).
Unsteady gait is the earliest symptom.
Clonus is the earliest sign.

61. Tuli’s Clinical Staging :-
STAGE FEATURES
I Ankle clonus, exaggerated DTRs.
II Motor deficit present.
Sensory examination normal.
III Paraplegia in extension.
Sensory loss <50%
IV Paraplegia in flexion.
Sensory loss >50%
Sphincter disturbances.

62. Causes of paralysis in TB spine :-
1. Pressure on cord due to abscess, granulation
tissue or edema.
2. Mechanical pressure on cord by sequestra,
pus and granulation tissue.
3. Angular deformity of spine with subluxation.
4. Thrombosis of anterior spinal artery.
5. Tuberculoma or diffuse extradural granuloma
of cord.

63. Deformity :-
• Collapse of vertebra leads to kyphus/gibbus deformity.
• Collapse in children is more marked because of large
amount of cartilage.
• When metaphyseal region gets destroyed and
posterior elements continue to grow (differential
growth), deformity keeps increasing even after disease
becomes quiescent.
• Deformity itself leads to paraplegia and
cardiopulmonary complications.
• TB of any joint causes fibrous ankylosis except TB spine
(bony ankylosis).

64. Investigations :-
1. Plain X-ray -

65. • Spine at risk radiologic signs

66. • Spinal instability score >2/4 is associated with
high chances of progression of kyphosis and
paraplegia in future.
• These signs are useful clinically because they
occur early in course and preventive surgery for
progressive collapse can be advocated.
2. IOC - MRI
3. Gold standard – CT guided biopsy

67. Treatment :-
• Good rest and nutrition.
• ATT – 2HRZE + 10 HR
• Abscess or paraplegia may increase in some
cases despite adequate ATT and may require
surgical intervention.

68. Indications for Surgery (Middle path regimen) :-
i. Neurological deficit not improving with
adequate chemotherapy (3-4 weeks).
ii. Neurological deficit developing during ATT.
iii. Neurological deficit worsening during ATT.
iv. Recurrence of neurological complication.
v. Difficulty in deglutition / respiration with
cervical abscess.
vi. Advanced acute neurological deficit with
flaccid / flexor spasms and bladder
involvement.

69. Surgical Procedures :-
• Costotransversectomy
• Anterolateral decompression
• Hongkong Operation (Radical anterior
decompression) – for TB cervical spine.

70. ABDOMINAL TUBERCULOSIS

71. Abdomial TB is defined as TB infection of abdomen
including GIT, peritoneum, omentum, mesentery,
lymph nodes and other solid organs like liver,
spleen and pancreas.
Causative organisms – M. tubeculosis
M. bovis
M. intracellulare, M. avium can cause disease in
immunocompromised hosts.

72. Pathogenesis :-
• Ingestion of tubercle bacilli along with sputum
in cases of pulmonary TB.
• Ingestion of infected milk or milk products.
• Most common site of involvement is ileocecal
region followed by small bowels and colon.

73. Predisposing factors for Intestinal TB :-
• Rich in lymphoid tissue : Peyer’s patches and
lymph nodes.
• AFB affinity for lymphoid tissue.
• Number of bacilli ingested.
• Virulence of bacilli.
• Nutritional and immunological status.
• Alkaline pH in small and large intestine.
• Stasis in ileocecal area (Ileal break).

75. Types of Abdominal TB in Children :-
SITE TYPES
1. Intestine •Ulcerative
•Hypertrophic
•Ulcerohypertrophic
•Stricture formation
•Fistula
•Miliary (granular)
2. Peritoneum •Peritonitis – Ascitic
(Generalised or localised)
•Dry plastic type –
Adhesions, Fibroplastic
•Miliary (Yellow white)

76. SITE TYPES
3. Omentum •Rolled up
•Miliary
4. Lymph nodes •Tabes mesenterica
•Retroperitoneal
•Peripancreatic
•Porta hepatis
5. Others •Hepatobiliary, Spleen,
Pancreas.

77. Ulcerative Type :-
• Induration and edema of diseased segment
with ulcers (solitary or multiple).
• Girdle ulcers.
• Skip lesions
• Depth – submucosa to muscularis propria or
even upto serosa.

78. • Napkin ring strictures (Healing).
•Adhesions between bowel loops prevent free
perforation but promote fistula formation.
•Mesenteric nodes may caseate to form
mesenteric abscess.
•More often found in malnourished children.
•Present with chronic diarrhea and malabsorption.

80. Stricturous / Hypertrophic Type :-
• In young well nourished patients. Low volume
infection by less virulent organisms in a relatively
healthy host.
• Commonest site – Caecum.
• Extensive inflammation and fibrosis causing
adhesion of bowel, mesentery and lymphnodes
into a mass.
• Caseation is common in mesenteric LN.

81. • Presents with features of subacute intestinal
obstructionin form of constipation, obstipation,
vomiting, diarrhea, abdominal distension and
colicky abdominal pain
• Gurgling, feeling of ball of wind moving in
abdomen.
• May also present as enterocutaneous or
enteroenteric fistula (Single or multiple).
• Mimics Crohn’s disease in many ways.

82. Peritoneal TB :-
• Female predominance.
• High risk in HIV patients, cirrhosis, diabetes,
malignancy, continuous ambulatory peritoneal
dialysis.
• Abdominal distension and ascites or as soft
cystic lump due to loculated ascites.
• Constitutional symptoms like fever and night
sweats.

83. • Diffuse abdominal tenderness, doughy abdomen,
hepatomegaly and ascites on examination.
•Mesenteric LN may present as vague abdominal
pain.
 Esophagus, stomach and duodenum are rarely
involved.
Colorectal – Weight loss, anemia and lower GI
bleed. Diffuse or segmental. Simulate Crohn’s and
ulcerative colitis.

84. Diagnosis of ATB is based on any of the following
positive criteria in presence of strong clinical
suspicion –
i. Demonstartion of AFB in lesion or ascitic fluid.
ii. Growth of MTB on culture of tissue or ascitic
fluid.
iii. Histological evidence of caseating granuloma.
iv. Operative evidence of ATB.
v. Good theraupeutic response to chemotherapy.

85. • Caseation is a histological marker for ATB and
helps in differentiating it from Crohn’s disease.
• Working diagnosis is mainly based on history,
clinical findings and histology.

86. Demonstration of AFB :-
1. FNAC from intra-abdominal mass (LN or
rolled up omentum or hypertrophied lesion
of intestine).
2. AFB in the biopsy tissue obtained by
endoscopy.
3. Ascitic fluid.

87. Various ways to obtain biopsy are-
• Upper GI Endoscopy
• Lower GI Endoscopy
• Peritoneal biopsy
• Laporoscopy / Peritoneoscopy
• Laporotomy
• Liver biopsy
• Splenic aspirate by FNA

88.  Mantouxt test is positive in only 33-58 % of
cases.
 X-ray Chest – Abnormal in 50-75% cases.
Positive family history in 37-66% cases.
 Plain Xray abdomen shows mottled calcification
in mesenteric LN or calcified granulomas in
retroperitoneal LN and liver. Multiple air fluid
levels and relative paucity of gas in colon.

89. Barium Meal Follow-through :-
• Accelerated intestinal transit.
• Hypersegmentation of barium column
(chicken intestine).

90. •Thickened folds.
•Luminal stenosis with smooth but stiff contours
(hour glass stenosis).
•Multiple strictures with segmental dilatation.
•Enteroclysis (small bowel enema) delineates single
or multiple strictures in jejunum and ileum clearly.

92. Barium Enema :-
• Fleischner or Inverted umbrella sign –
thickening of lips of ileocecal valve and / or
wide gaping of valve with narrowing terminal
ileum.

93. • Conical caecum – Caecum is shrunken in size and
pulled out of iliac fossa due to contraction and fibrosis
of mesocolon.

97.  Stierlin and string sign are also seen in Crohn’s
disease.
Enteroclysis followed by barium enema is the
best protocol for evaluation of intestinal TB.

98. Percutaneous Fistulogram :-

99. • Advanced disease –
1. Napkin ring stenosis and obstruction
2. Retraction and shortening
3. Pouch formation
4. Amputation of caecum (May be seen in amebiasis).

100. Napkin Ring Stenosis

101. Abdominal USG :-
In early ATB, characteristic USG features are
• Mesenteric thickness of 15 mm or more (also
seen in portal HTN and lymphomas).
• Increased mesenteric echogenicity.
• Mesenteric lymphadenopathy.

103. • Intra-abdominal fluid – free or loculated, clear or
complex with debris & septae.
• ‘Club sandwich’ or ‘Sliced bread Sign’ - Local
exudation from inflamed bowel forms interloop
ascites leading to localised fluid between radially
oriented bowel loops.
• Matted fixed bowel loops, omental inflammation
and thickened bowel walls.

104. Club-Sandwich Sign

105.  CT abdomen demonstrates lymphadenopathy,
organ lesions, conglomerate masses and omental
cakes.

106. Ascitic Fluid Analysis :-
• Straw coloured or clear.
• Exudative (Proteins > 3 g/dl).
• Cells > 1000/cumm (mostly lymphocytes).
• Ascitic/blood glucose ratio < 0.96.
• Serum Ascitic Albumin Gradient(SAAG)
< 1.1 g/dl.
• Adenosine deaminase (ADA) is a useful
screening test (> 33 IU/L ).

111. Complications :-
• Intestinal obstruction – most common
complication.
• Fistulae – single or multiple. Most common
are enteroenteric, enterocutaneous, perineal.
• Perforation – more in terminal ileum.
• Intestinal hemorrhage (mild).

112. • Enteroliths – radiolucent center with dense
rim is characteristic radiographic feature. May
also be radio-opaque.
• Abdominal cocoon (Sclerosing encapsulating
peritonitis) –encasement of small bowel by a
fibrocollagenic cocoon like sac that causes
obstruction.

116. Treatment :-
• ATT – 2HRZE + 7HR
• ATT can be continued upto 12 months if there
isnodal involvement.
• If M.bovis is isolated, pyrazinamide can be
stopped because of its innate resistance.
• Hepatic enzymes are monitored periodically
till the completion of therapy.

117. • Role of surgery is mostly diagnostic in case of
peritoneal and nodal TB.
•Ileocecal TB – Right hemicolectomy with 5 cm
margin.
•Stricturoplasty or resection if multiple strictures
are present.
•Surgery is done for fistulas if they persist after 3-4
months of ATT.

118. CUTANEOUS TB

119. A. Exogenous TB :-
1. TB Chancre – Flask shaped undermined
ulcers.
2. TB Verrucosa Cutis – Cauliflower like masses
on skin.
3. Lupus vulgaris –
Healing with central scarring, progressive
lesions, buttocks, Apple jelly nodules
(Diascopy), Biopsy – Non-caseating
tuberculoid granuloma.

121. B. Endogenous TB :-
1. Scrofuloderma – Nonhealing sinus above an
internal focus of TB like lymphnode.
2. Peri-orificial – Ulcers around mouth and
anus.

123. C. Tuberculids :-
1. Micropapular tuberculid (Lichen
scrofulosorum)
2. Papulonecrotic tuberculid
3. Nodular tuberculid (Bazin’s disease /
Erythema induratum) – Red tender nodules
on calf which ulcerate.

125. Pericardial TB

126. • Pericardial effusion (serofibrinous /
hemorrhagic).
• Constrictive pericarditis.
• Xray chest, ECG, Ultrasound.
• Pericadiocentesis – exudative fluid with
lymphocytosis, raised ADA levels.
• AFB smear and culture
• Biopsy if required
• Standard ATT
• Steroids

127. TB in Eye and Conjunctiva
• Primary infection of conjunctiva leads to
preauricular LN enlargement.
• Choroid tubercles – establishes diagnosis if
there is no radiological evidence.
• Panophthalmitis
• ATT

129. TB in ENT
• MC site of TB in nose – Anterior end of inferior
turbinate.
• TB Ear – Multiple perforations in tympanic
membrane, painless.
• Painful condition – TB Larynx
• MC site in larynx – Posterior commissure
• MC symptom – Weakness of voice
• MC sign – Loss of adduction of vocal cords
• Earliest sign – Hyperemia of posterior
commissure
• Mouse bitten appearance of vocal cord
• Pseudoedema of epiglottis (Turban epiglottis)

130. BCG Vaccine

131. • Prepared by Albert Calmette and Camille
Guerin.
• Mycobacterium bovis – Danish1331 strain.
• Lyophilised freeze dried vaccine.
• Stabiliser – Sodium glutamate.
• Diluent – Normal saline (Distilled water causes
local reaction).

132. • Usually given as birth vaccine along with OPV
and Hepatitis-B vaccines.
• Catchup period – 5 years of age.
• Vaccine can be repeated one time within 5
years of age if there is no information about
vaccination and no scar.

133. • After reconstitution, use within 3 hours. If used
after 3 hours, leads to Toxic shock syndrome due
to contamination.
• Dose – 0.1 ml intradermal left deltoid. Produces a
wheal of 8 mm diameter. Subcutaneous injection
leads to ugly, retracted scar. No rubbing or hot
fomentation at the injection site.
• Induration – 3-4 weeks
Papule – 6 weeks
Ulcer - 8 weeks
Scar - 10-12 weeks (No need to repeat vaccine
if scar is not formed).

134. • Can be given at other site if there is eczema or
other dermatological disease.
• Breast feeding can be continued after BCG.
• Sub-zero (-20 C) – 2 years
Middle compartment of refrigerator(2-4 C) – 6
months
Peripheries (2-8 C) – 1 week
• Transported in thermos flasks with ice to
outreach immunisation clinics. Ambered coloured
bottles wrapped in black paper/cloth.

135. • Protective efficacy – 0% against pulmonary TB,
0-80% against TBM and miliary TB, 20-40%
against leprosy (cross-protection).
• Complications –
1. Prolonged severe ulceration.
2. BCG lymphadenitis – Symptomatic treatment
3. BCG osteomyelitis - ATT
4. Disseminated BCG infection - ATT

136. Contraindications :-
• Congenital immunodeficiency
• HIV disease
• Leukemia, lymphoma or other malignancies
• On steroids, immunosuppressant drugs,
alkylating agents, antimetabolites or radiation.
• Avoid for a period of 4-6 weeks following a
viral infection, for a period of atleast 3 months
in those who have received immunoglobulins.

137. • In case of baby born to a HIV positive mother,
wait for 9-10 months and test for HIV. Give
vaccine if negative. Avoid vaccine if positive
even if child is stable.