1. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis and affects mostly the lungs. It is both preventable and curable. 2. The most common age group affected is 15-45 years old. Factors that increase the burden of TB include HIV, poor socioeconomic status, poor nutrition, and limited access to healthcare. 3. TB treatment aims to cure patients, prevent transmission and death, and prevent drug resistance. Treatment follows principles of using multiple drug combinations under direct observation to ensure adherence and prevent resistance.

1. TUBERCULOSIS
 PRESENTER
MARY MUTINDA
FACILITATOR
Dr.Ngugi
VENUE MLKH CME ROOM
Date. 25/11/2022

2. Definition
 Tuberculosis(TB)is a chronic airborne illness caused by mycobacterium tuberculum
.
Mycobacterium tuberculum is an acid-alcohol fast rod shaped bacillus
 Mostly affect lungs but can affect other parts of the body.
 TB is both preventable and curable.

3. Cause:
• Mycobacterium tuberculosis also called the “tubercle bacillus”
Mode of transmission:
• Coughing, sneezing, laughing and even talking
Natural history of TB:
 Most people who get infected do not develop disease
 The TB germs are contained by the immune system, and remain dormant for the rest of a person’s li
fe without causing any problem.

4.  Routes of infection
Inhalation
Ingestion
Inoculation
EPIDEMIOLOGY
 The commonest affected age group is from 15-45 years with males>females. Contributing fac
tors to increasing burden;
 HIV epidemic
 Poor socio-economic status leading to overcrowded slums
 Poor nutrition
 Limited access to health services

5. classification
Tb case definition.
 a) A presumptive TB case: one who presents with symptoms or signs suggestive of TB
 b)Bacteriologically confirmed TB case: one from whom a biological specimen is positive by smear microsco
py, culture or WHO-approved rapid diagnostics (WRD) such as GeneXpert MTB/RIF.
 c) A clinically diagnosed TB case; A clinically diagnosed TB case is one who does not fulfill the criteria for
bacteriological confirmation but has been diagnosed with active TB by a clinician or other medical practition
er who has decided to give the patient a full course of TB treatment. This definition includes cases diagnosed
on the basis of X-ray abnormalities or suggestive histology and extra-pulmonary cases without laboratory co
nfirmation
Classification based on anatomical site
Pulmonary tuberculosis (PTB)
Any bacteriologically confirmed or clinically diagnosed case of TB involving the lung parenchyma or the trache
obronchial tree. This exclude pleural effusion
Extra-pulmonary TB
Any bacteriologically confirmed or clinically diagnosed case of TB involving organs other than the lung parench
yma, e.g. pleura, lymph nodes, abdomen, genitourinary tract, skin, joints and bones, meninges.
NB. Any organ can be affected apart from the nails and the hair.

6. Primary TB
 Mostly affects lungs and GIT
 You can get TB by breathing in air droplets from a cough or sneeze of an infected pe
rson. The resulting lung infection is called primary TB. Most people recover from pr
imary TB infection without further evidence of the disease. The infection may stay i
nactive (dormant) for years.
 Primary tuberculosis often causes middle and lower lung field opacities associated w
ith mediastinal adenopathy
 A peripheral lesion forms (Ghon focus), & its draining nodes are infected (Ghon co
mplex). There is early distant spread of the bacilli, then an immune response suspen
ds further multiplication at all sites

7. Pathogenesis
 The lung is the portal of entry in over 98% of cases
 The primary complex includes local infection at the p
ortal of entry and the regional lymph nodes
 Multiplication occurs initially within the alveoli and al
veolar ducts

8. Pathogenesis
 Primary infection
Often self-limiting
May result in complications such as
 Pleural effusion
 Enlarged mediastinal nodes leading to obstruction
 Cavitation
 Enlarged focus (coin shadow)
 Pericardial effusion
 Collapse and bronchiectasis

9. Pathogenesis
 Bacilli carried by non-activated macrophages to re
gional lymph nodes
 Haematogenous spread to most tissues in the body
 Time from infection to clinical disease depends on:
Infecting dose
Host immune responses
Age (infants and children < 3yrs)
Confection with HIV
Other immune compromising diseases (malnutrition,
measles, malignancies)
Immunosuppressive medications

10. Signs/symptoms
 Cough
 Sputum ± AAFBs
 Fever
 Night Sweats
 Weight loss
 Erythema nodosum - tender red nodules, predomi
nantly in the pretibial region but occasionally involvi
ng the arms or other areas.
 Anorexia
 General malaise

11.  GastroIntestinal –
 Typically affects the ileocaecal junction & associated
lymph nodes following consumption of raw milk/me
at containing M. Bovis

12. Pulmonary TB(PTB)
This is the commonest form of TB
SIGNS AND SYMPTOMS
• Cough (of any duration)
• Hotness of body/ body temperature > 37.50 C
• Drenching night sweats
• Unintended weight loss/ BMI less than 18.5
• Chest pain

13.  DIAGNOSIS OF PULMONARY TB
Gene expert
The Genexpert diagnoses TB by detecting the presence of TB bacteria. The test is a molecular TB t
est which detects the DNA in TB bacteria. It uses a sputum sample and can give a result in less
than 2 hours.
The Genexpert can also detect the genetic mutations associated with resistance to the drug Rifa
mpicin.
Smear microscopy(fluorescent and light microscopy)
Also known as AFB SMEAR
AFB smear. In this test, your sample is "smeared" on a glass slide and looked at under a microsco
pe. It can provide results in 1–2 days. These results can show a possible or likely infection, but
can't provide a definite diagnosis.

14. AFB CULTURE
In this test, your sample is taken to a lab and put in a special environment to encourag
e the growth of bacteria. An AFB culture can positively confirm a diagnosis of TB or oth
er infection. But it takes 6–8 weeks to grow enough bacteria to detect an infection.
CHEST XRAY
Possible radiological findings in Primary TB
•Lymphadenopathy,
•consolidation,
•pleural effusion
•Milliary nodules

15. Possible radiological findings in Post primary TB
•Consolidation and/or focal infiltration mainly involving the apical or posterior segments of the up
per lobes and superior segments of the lower lobes
•cavitation,
•nodules
•fibrosis

16.  Urine TB LAM
Tests based on the detection of mycobacterial lipoarabino
mannan (LAM) antigen in urine have emerged as potenti
al point-of-care tests for TB.
N/B
A negative TB lam and smear microscopy does not rule out
PTB.
Quantiferon Tbgold test.its an allternative to tuberculin sk
in test. It's a blood test that aids in detection of mycobact
erium tuberculosis

17. Extrapulmonary TB
1.TB adenitis
Slow & painless fluctuant enlargement of lymph nodes
especially the cervical, followed by matting & eventual
ly discharge of pus. Generalised lymph node enlargem
ent is common in HIV.
Usually unilateral, most common site is the cervical ar
ea.
Fistula and sinus formation
Diagnosis
Node aspirate
Node biopsy for both histology and culture

18. Tuberculous Adenitis
Auxiliary TB adenitis Cervical TB adenitis wi
th sinuses

19. 2.Pleural effusion (exudative)
Difficulty in breathing
Pain on the affected side of the chest
Slight cough
Stony dullness to percussion
Mediastinal deviation depending on the size of effusio
n.
Reduced breath sound

20.  Tuberculous Pleural Effusion

21. 3.Miliary TB
Occurs following haematogenous dissemination of
multiple tiny foci throughout the body
CXR shows characteristic reticulonodular shadowin
g with miliary lesions <3mm.
 Enlarged liver and spleen are common
 Choroid tubercles on fundoscopic examination
 Constrictive pericarditis is an uncommon complication

22. Miliary TB

23. 4. Tb meningitis
Formation of caseous lesion in the cerebral cortex or
meninges
Bacilli discharged into the sub-arachnoid space. Ex
udates infiltrate the blood vessels causing inflamma
tion and obstruction and subsequent infarction
Base of the brain most commonly affected
Frequent involvement of cranial nerves II, VI, VII
Exudate may result in a communicating hydroceph
alus

24. Tuberculous meningitis
Clinical stages:
 Prodromal phase - mild headache, fever, malaise
 2. Meningitic phase - headache, vomiting, confusion,
meningismus
 3. Paralytic phase - stupor, coma, seizures, hemiparesi
s

25. Ct of TB meningitis
The diagnosis of tuberculosis meningitis is made by:
• Examination of cerebrospinal fluid (CSF) obtained following a lumbar puncture:
•High cell count- lymphocytes
•High protein
•Low sugars
. WBC 100-500cells/mm3
Glucose 20-40mg/dL
Protein >400mg/dL
AFB positive in 30%
Culture in 70% if 10mls of CSF
• CT Scan of the brain with contrast which shows basal meningitis, tuberculomas and development of hydroce
phalus.
Chest x-ray is normal in 50% of the cases

26. 5.Genitourinary TB
 originates in the cortex of the kidney.
 It progresses slowly; it may take 15-20 years to destroy a kidney in a patient who has good res
istance to the infection.
 There is no renal pain and little or no clinical disturbance of any type until the lesion has invo
lved the calyces or the pelvis, at which time pus and organisms may be discharged into the uri
ne..
 It is only at this stage that symptoms (of cystitis) are manifested.
 The infection then proceeds to the pelvic mucosa and the ureter, particularly its upper and ves
ical ends.
 This may lead to stricture and back pressure (hydronephrosis).
 Parenchymal destruction may occur, causing spread into the medulla and associated papillary
necrosis or cavitation
 Diagnosis—urine for AAFBs, Renal ultrasound
 Treatment—Anti TBs, Nephrectomy if one kidney severely damaged

27. 6.TB of the Adrenals
 The adrenals may become infected with tuberculosis o
rganisms via the bloodstream, causing adrenal masses.
TB may also cause calcification and adrenal insufficien
cy (Addison's disease).

28. 7.TB BONES
TB can affect any bones or joints, primarily the large bones/ joints e.g hip and
spine
The spine is affected in many instances with a characteristic ‘gibbus’ deformity
of the spine.
 When primary TB occurs in children while the epiphyses are open and the b
lood supply to bone ends is rich, bacilli often disseminate to the vertebrae an
d ends of the long bones.
 Infection may spread into the articular capsule, causing a monarticular art
hritis.
 Weight-bearing joints are commonly involved, but bones of the wrist, hand,
and elbow also may be involved, especially after injury.


29.  Clinical presenation
Localised pain
Swelling
Discharge of pus
Muscle weakness/paralysis
Joint stiffness

30. 8.Skin TB
• Lupus vulgaris:
Persistent and progressive form of cutaneous TB. It occurs as small sharply defined reddish-brow
n lesions with a gelatinous consistency (called apple jelly nodules). Untreated, lesions persist f
or years, leading to disfigurement
Scrofuloderma: Skin lesions result from direct extension of underlying TB infection of lymph node
s, bone or joints. Often associated with TB of the lungs. Firm, painless lesions that eventually
ulcerate with a granular base. May heal even without treatment but this takes years and leave
s unsightly scars
The diagnosis is usually made or confirmed by a skin biopsy.
Typical tubercles are caseating epithelioid granulomas that contain acid-fast bacilli.
These are detected by tissue staining, culture and polymerase chain reaction (PCR)

31. 9.TB pericarditis
• Shortness of breath (the most common symptom).
• Chest pain.
• Cough.
• Leg swelling.
• Fever.
• Usually has a high pulse rate (tachycardia).
• May have a low blood pressure, impalpable apex beat, quiet heart sounds and sign
s of heart failure like a large liver, ascites and leg edema
Chest x-ray shows a large globular heart
Echocardiography often required to confirm diagnosis
A pericardial tap for diagnostic purpose is rarely required but may be life saving if ther
e are signs of cardiac compression (tamponade).

32. TB pericarditis
Pericardial fluid accumulation leading
to globular
shape of the heart

33. 10.TB peritonitis
Tuberculous Peritonitis and Ascites usually presents with
• abdominal pain and swelling
• disturbance of bowel motion i.e., constipation or diarrhea fever.
Ultrasonography may show matted loops of bowel with free fluid
.
Peritoneal biopsy rarely done: many of these end up with a surgic
al biopsies during laparotomy

34. 10.TB SPINE
Incidence
 50-60% of Extrapulmonary TB
 Regions;
Children - T6-T11
Adults - T8-L2
Elderly - L3-L4

35.  Clinical presentation
 Pain - 85%
 Paraplegia approx. 50%
 Deformity is a late sign; Gibbus; Kyphosis/Scoliosis
 Angulated kyphosis without scoliosis (Gibbus)
Anterior erosion of vertebral bodies
Large joint disease

36.  Pathophysiology
Infection in the visceral organs or lungs is spread through retro
grade spread of infection through valveless veins of the thoraci
c spinal cord (Veins of Burton).
Basic lesions include;
Vertebral osteomyelitis
Facet joint arthritis
 Sites of Infection
Anterior vertebral body
Para-discal regions
Central body
Articular posterior intervertebral joints

37.  Investigation– vertebral xrays
Narrow disc space - 2° to articular cartilage destruction
Local osteoporosis
Vertebral body collapse (konstantina effect) - 2° to ant
erior infection of the paradiscal vertebrae leading to co
llapse of disc → Kyphosis
Paraspinal mass

38. Aims of TB Treatment
The overall goals of TB therapy include:
Cure patients and therefore prevent suffering.
Prevent transmission of the infection.
Prevent death.
 Prevent long-term complications or sequelae of TB.
Prevent relapse of the disease. 6) Prevent the development of d
rug resistant TB.

39. Principles of TB treatment
The principles of TB treatment include the following:
 Never use single drugs - this increases the likelihood of selection of naturally
occurring resistant mutants to M. tuberculosis
 Always use drugs in combinations - using Fixed Dose Combinations (FDCs)
to avoid selection of naturally occurring resistant mutants to M. tuberculosis
 Drug dosage is based on weight - to achieve therapeutic drug levels in the bo
dy and prevent medication side effects
Drug intake should be directly observed for all patients - to ensure adherence,
prevent emergence of drug resistance, assess for medication side effects and to
follow clinical response closely
Ensure the entire treatment is taken as recommended.

40. Treatment
Purpose of anti tbs
Bactericidal - the ability to kill the rapidly dividing, metabolically active bacilli found in the wall
s of cavities and in the sputum of patients with microscopy smear positive pulmonary tuberculosis
. Drugs with high early bactericidal activity such as Isoniazid will make the patient non-infectious
as early as possible.
Sterilization - the ability to kill the persisting, dormant or intermittently active bacilli, responsibl
e for relapses. Drugs with rapid sterilization ability such as Rifampicin and Pyrazinamide will lead
to the shortening of treatment.
Phases of treatment
Intensive phase lasts for 2 months and consists of four drug
s RHZE
Continuation phase lasts for 4 to 10 months and consists of 2
drugs RH

41. Ist line ant-TBS RHZE( rifampicin, isoniazid , pyrazinamide and ethambutol )
 all forms of TB except TB meningitis and osteoarticular
TB—2RHZE/4RH
 TB meningitis and osteoarticular TB
2RHZE/10 RH
Note. A sputum positive patient is considered ineffective after at least 2 weeks after initiation of tr
eatment
all patients receiving ati TBS should receive pyridoxine once daily based on their weight to redu
ce risk of peripheral neuropathy associated with isoniazid
weight Pyridoxine dosage
1-13.9kg 12.5mg
14-25kg 25mg
>25kg 50mg

42. FDC (FIXED
DRUG C0M
BINATION)d
osages
formulation 30-39kg 40-54kg 55-69kg 0ver 70kg
RHZE(150m
g,75mg,400
mg,275mg)
Intensive ph
ase
2 3 4 5
RH(150mg,7
5mg)
Continuatio
n phase
2 3 4 5

43. Steroid therapy
Corticosteroids have been proven in clinical trials to improve the morbidity and mortal
ity outcomes in patients with the following conditions:
 TB meningitis
TB pericarditis
TB Immune Reconstitution Inflammatory Syndrome in PLHIV
For TB meningitis, dexamethasone in the dose of 0.4 mg/kg/day is recommended in a
dults (>14 years) in conjugation with antitubercular drugs.
The dose should be reduced over 6–8 weeks.
In other conditions, Prednisolone is the preferred corticosteroid used.

44. dosage for prednisolone
dosage Week 1-4 Week 5-6 Week 7
<30kg 1-2mg/kg(max 60mg) 0.5-1mg/kg 0.25-0.5mg
/kg
>30kg 1mg/kg(max 60mg ) 0.5mg/kg 0.25mg/kg

45. Side effects of anti TBs
 Isoniazid
 Has a 20-60% CNS penetration
 Peripheral neuropathy - treat with pyridoxine 50mg/d or Vit B co
mplex
 * Isoniazid promotes the excretion of pyridoxine
 Hepatitis - jaundice
 Agranulocytosis
 GIT disturbance - take drug with light meal or before going to be
d
 Pellagra - Isoniazid therapy has also been associated with niacin
deficiency, presumably because of induced pyridoxine deficiency
, which decreases the conversion of tryptophan to niacin.

46.  Rifampicin
Hepatitis - jaundice (Withdraw if LFTs >*3)
Red urine & tears
Flu-like syndrome (fever, chills, malaise & headache)
Pruritus ± flushing ± rash involving the face & scalp oft
en with redness & watering of the eyes
Abdominal pain & nausea
Pyrazinamide causes acute hepatotoxicity

47.  Ethambutol
Blurred vision & red-green colour blindness; optic neu
ritis
 Streptomycin
Numbness around the mouth & tingling
Tinitus - risk increases with dosage & age; may lead to
CN-VIII damage → Deafness ± ataxia - reduce dose by 1
/4gm

48. Drug resistance TB
 Monoresistance Resistance to one first-line anti-TB medicine only.
Rx ISONIAZID mono resistance 6 RZE/Lfx (with pyridoxine) 6 months
 Poly-drug resistance (PDR) Resistance to more than one first-line anti-TB medicine (other th
an both Isoniazid and Rifampicin)
Rx 9 RZE/Lfx (with pyridoxine) 9 Months
 Multi-drug resistance (MDR) Resistance to at least both Isoniazid and Rifampicin
Rx Intensive phase: 6 months Bdq/Cfz/Lfx/Cs/Lzd
Continuation phase: 12 months Cfz/Lfx/Cs .treatment duration is 18 months
 Extensive drug resistance (XDR) Resistance to any Fluoroquinolone and at least one of three
second-line injectable drugs (Capreomycin, Kanamycin and Amikacin), in addition to multidru
g resistance.
Rx Individualized regimen 18-24 months
Bdq –bedaquilline
Cfx –clofozamine
Lfx –levofloxacin
Cs –cycloserine
Lzd -linezolid

49. Complications of PTB
 Massive Hemoptysis Usually seen in cavitary disease and sources include the pulm
onary artery, bronchial arteries, intercostal arteries, and other vessels supplying the l
ung. Tuberculous vascular lesions include pulmonary) .consider life-threatening if th
ere is approximately 150mls of blood in 24 hours
 Lung Abscess Necrosis of the pulmonary parenchyma caused by microbial infection
. Seen in extensive lung damage after tuberculosis.
 Lung Fibrosis Replacement of normal lung parenchyma with collagenous tissue res
ults in changes in the lung, such as thickening and stiffening of the lung walls follow
ing long term injury of the lungs.
 Spontaneous pneumothorax this is the presence of air in pleural cavity, results fro
m rupture of TB cavity adjacent to the pleural space-
expansion of the lung with underwater seal drainage tube is therapeutic
 Bronchiectasis Chronic lung disease often secondary to an infectious process that re
sults in the abnormal and permanent distortion of one or more of the conducting bro
nchi or airways.
 Chronic pulmonary aspergillosis
Result of colonization of tuberculous cavities or bronchiectatic lesions with the fungus
Aspergilus.

50. References
TB Guidelines 2021 final.
Essential Tuberculosis