SlideShare a Scribd company logo
TUBERCULOSIS
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT:
hermyc@live.com
 A 46 years old male pt who was admitted from home
with history of coughing blood on two different
occasions in the past two weeks associated with fever,
profuse nocturnal sweating, loss of appetite,
significance weight loss of 8 kg in less than a month and
easy fatiguability. POSITIVE hx of IV drug use.
 On Physical examination, He was Ill looking, cachexic,
febrile T- 39.6, PR- 110 Bpm, RS- 20 bpm, BP- 130/76,
SPO2- 98%
 RR; Unilateral right side crepitation, more on the upper
lobes
 Initial chest x-ray; infiltration on the right upper lobe
with a sign of Cavitation.
 Provisional diagnosis.?? Ddx??
 Other investigation that we can order?
 Mostly likely organism?
 Pathogenesis/Immunology of the disease?
 Is the patient high risk or low risk patient?
 Most likely co- infection?
 Initial treatment?
 Prevention and prophylaxis measures
Tuberculosis
Presenter : SAIMON MAGANGA
ILLUMINATA KAFUMU
Supervisor: Prof. STEPHEN MSHANA
Presentation outline
 Introduction
 Structural differences between Tb and other bacteria
 Transmission
 Pathogenesis / Immunology
 Clinical presentation of different forms of Tb.
 Diagnostic tools/methods and challenges
 Treatment and resistance challenges
 MDR/XDR
 MDR Treatment
 Tb vaccination
 Prevention and Prophylaxis
 Discussion
INTRODUCTION
 Tuberculosis. Describes as a chronic infectious
disease with broad range of clinical illness caused
by Mycobacterium tuberculosis complex.
 In humans the commonest cause is Mycobacterium
tuberculosis.
 other mycobacterium spp such as;
• Mycobacterium bovis,
• Mycobacterium avium complex (MAC),
• Mycobacterium canetti and
• Mycobacterium Africanum may rarely cause TB,
Introduction
 Tuberculosis is primarily the disease of the lungs
however it can affect other organs e.g. meninges,
lymph nodes, brain, kidney, GIT, bones and joints etc
 Humans are the only known
reservoir for Mycobacterium
tuberculosis
epidemiology
 Over 30% of people in the world are
infected with TB
 Majority of TB patients (80%) are in
22 high burden countries
 Tanzania has an incidence of (253/100,000) is ranked 14th
out of 30 (Source: WHO report 2020)
TB Prevalence in Tanzania
 In year 2018, a total of 75,845 cases of all forms were
notified, which is an increase of 6,205 cases or 9%
compared to the year 2017. New and relapse TB cases
notified were 74,692 among them, 48% were
bacteriological confirmed TB cases, 79% were pulmonary
TB cases (NTLP 2018)
CELL WALL STRUCTURE
Microbiology of TB
 Mycobacterium tuberculosis was discovered by Robert
Koch in 1882.
 They are Obligate aerobic, non spore forming acid fast
bacilli
 Called acid fast bacillus because the resist
decolourisation with acid or alcohol after being stained
by carbofuschin dye.
 They have cell wall made of mycolic acid which
contributes to pathogenicity also have waxy layer which
help to survive in adverse conditions
Microbiology cont
 M. Tuberculosis can be differentiated
from other mycobacteria:-
Grow slowly and lack pigment
Produce niacin
Reduce nitrates
Produce heat sensitive catalase (
inactivated by heating to 68C at pH of
7.0)
Other mycobacteria produce large
amount of heat stable catalase
Transmission
 Transmission is from human with active disease through
aerosal droplets.
 Transmission occurs significantly while coughing,
sneezing, singing, talking or spiting
At this time, they expel infectious aerosol droplets 0.5 to 5
µm in diameter.
 Avoid prolonged, frequent and intense contact with
active Tb patients especially for immunocompromised
non Tb infected people.
Pathogenesis
 About 90% of those infected with M.tuberculosis have
asymptomatic, latent TB infection.
 With only a 10% lifetime chance that a latent infection
will progress to TB disease.
 TB infection begins when the mycobacteria reach the
pulmonary alveoli, where they invade and replicate
within the endosomes of alveolar macrophages.
Pathogenesis cont
 In the few weeks (4-6wks) the body has
almost no immune defense against
infection with M. tuberculosis.
 Bacterial multiplication proceeds for
weeks both in the initial focus and
lymphohematogenous metastatic foci
until the development of
hypersensitivity and cellular immunity
 Lymphocytes, mostly CD4+ cells bearing
the alpha form of the T cell receptor
are capable of recognizing mycobacteria
that have been processed and presented
by macrophage
Mycobacteria Evasion
mechanism
Pathogenesis cont
 When lymphocytes encounter antigen in
association with MHC class II molecule on
the macrophage surface it is activated
and proliferates producing a clone of
reactive lymphocytes
 T cells produce many lymphokines which
attract, retain and activate macrophage
at the site of antigen
 Activated macrophage accumulate high
concentrations of lytic enzymes and
reactive metabolites that
mycobactericidal
Pathogenesis cont
 Alveolar macrophage secrete a number
of cytokines
 Interleukin I contribute to fever
 IL -6 contributes to hyperglobulinemia
 Tumor necrotic factor alpha (TNF-
alpha)contributes :
• Killing of mycobacteria
• Formation of granulomas
• Systemic symptoms such as fever and
weight loss
Pathogenesis cont
 Qualitative and quantitative defect of CD4+ T
cells explain inability of HIV +ve pt to contain
mycobacteria proliferation
 When the population of activated
lymphocytes reach a certain size, cutaneous
delayed reactivity to tuberculin becomes
manifest
 The pathological features of tuberculosis are
the result of the degree of hypersensitivity
and the local concentration of antigen
Pathogenesis cont
 Necrosis in tuberculosis tend to be
incomplete resulting in solid or semisolid
acellular and amorphous material known
as caseous necrosis
 The chemical environment and low
oxygen tension inhibit microbial
multiplication
 The primary site of infection in the lungs
is called the Ghon focus, and is generally
located in either the upper part of the
lower lobe, or the lower part of the upper
lobe.(commonly at the subpleural)
Granuloma
Granuloma
Caseous NECROSIS
Pathogenesis cont
 Macrophages, T lymphocytes, B lymphocytes and
fibroblasts are among the cells that aggregate to form a
granuloma, with lymphocytes surrounding the infected
macrophages.
Pathogenesis cont
 The granuloma functions not only to prevent
dissemination of the mycobacteria, but also
provides a local environment for communication
of cells of the immune system.
 Within the granuloma, T lymphocytes secrete
cytokines such as interferon gamma, which
activates macrophages to destroy the bacteria
with which they are infected.
 Cytotoxic T cells can also directly kill infected
cells, by secreting perforin and granulysin.
 Mycobacteria are not always eliminated within the
granuloma, but can become dormant, resulting in
a latent infection.
Pathogenesis cont
 Another feature of the granulomas of human
tuberculosis is the development of cell death,
also called necrosis, in the center of
tubercles
 To the naked eye this has the texture of soft
white cheese and was termed caseous
necrosis.
 If TB bacteria gain entry to the bloodstream
from an area of damaged tissue they spread
through the body and set up many foci of
infection, all appearing as tiny white
tubercles in the tissues.
Pathogenesis cont
 This severe form of TB disease is most common in
infants and the immunocompromised pts, elderly and is
called miliary tuberculosis.
 Patients with this disseminated TB have a fatality rate
of approximately 20%, even with intensive treatment.
 Tissue destruction and necrosis are balanced by healing
and fibrosis.
 Affected tissue is replaced by scarring and cavities
filled with cheese-like white necrotic material.
 During active disease, some of these cavities are joined
to the air passages bronchi and this material can be
coughed up.
Natural history
 After 5 years 50% of pulmonary disease will die of the
disease.
 25% will be self cured(health)
 Another 25% will be ill with chronic infectious disease
Types of tuberculosis
I. Pulmonary tuberculosis
II. Extra- Pulmonary tuberculosis
 Pulmonary tuberculosis
Clinical features
 Typical symptoms of pulmonary TB include a
productive cough, fever, and weight loss.
Occasionally, patients may present with
hemoptysis or chest pain.
 Other systemic symptoms include anorexia,
fatigue, or night sweats.
Extrapulmonary tuberculosis
Tuberculous meningitis
 Patients may present with a
headache that is either intermittent
or persistent for 2-3 weeks.
 Subtle mental status changes may
progress to coma over a period of
days to weeks.
 Fever may be low-grade or absent.
Extrapulmonary cont
Skeletal TB
 The most common site of involvement is the
spine (Pott disease).
 Symptoms include back pain or stiffness.
 Lower extremity paralysis occurs in as many as
half the patients with undiagnosed Pott’s
disease.
 Tuberculous arthritis usually involves only 1
joint.
 Although any joint may be involved, the hip or
the knee is affected most commonly, followed
by the ankle, elbow, wrist, and shoulder.
 Pain may precede radiographic changes by
weeks to months.
Extrapulmonary cont
Tuberculous lymphadenitis
 The most common site is in the
neck along the sternocleidomastoid
muscle.
 It usually is unilateral, with little or
no pain.
 Advanced disease may suppurate
and form a draining sinus.
Gastrointestinal TB
 Any site along the gastrointestinal tract may become infected.
 Symptoms are referable to the site infected, including the following:
 Non healing ulcers of the mouth or anus
 Difficulty swallowing with esophageal
disease
 Abdominal pain mimicking peptic ulcer
disease with stomach or duodenal infection
 Malabsorption with infection of the small
intestine
 Pain, diarrhea, or hematochezia with
infection of the colon.
Genital urinary TB
 Reported symptoms include flank pain,
dysuria, or frequency.
 In men, genital TB may manifest as
epididymitis or a scrotal mass.
 In women, genital TB may mimic pelvic
inflammatory disease.
 TB causes approximately 10% of sterility
in women worldwide and approximately
1% in industrialized countries.
Cutaneous TB
 Direct inoculation may result in an
ulcer or wartlike lesion.
 Contiguous spread from an infected
lymph node typically results in a
draining sinus.
 Hematogenous spread may result in
a reddish brown plaque on the face
or extremities (lupus vulgaris) or
tender nodules or abscesses.
Other forms of
extrapulmonary TB
 TB of the pleura
 TB peritonitis
 TB pericarditis
Diagnosis of TB
 The diagnosis of TB starts with proper history and physical examination.
 Laboratory examinations
 AFB microscopy for sputum and aspirates
 Culture - sputum, aspirates for EPT
 Histological examination - Biopsy tissue
 Gene Xpert (NAA test, RIF/MTB, LPA)
 Interferon Gamma Release Assay
 Radiological test, although alone NOT reliable
 Chest X ray or CT scan
 For patients unable to produce any sputum
(eg, children), early morning gastric aspirate
may produce a good specimen.
Sputum smear
 It is the gold standard investigation for PTB
 Standard 2: All patients (adults,
adolescents, and children who are
capable of producing sputum)
suspected of having pulmonary TB
should have at least two, and
preferably three, sputum specimens
obtained for microscopic examination.
When possible, at least one early
morning specimen should be obtained.
Sputum smear cont
 Direct smears of unconcentrated sputum are common
worldwide
 They are fast simple and cheap
 Ziehl Neelsen stain with Carbofuschin dye is more
common
Ziehl-Neelsen Stain
Chest X ray
 People with chest X ray suggestive of PTB should submit their sputum for
microscopy
Culture
 Available culture methods use either solid or liquid media
 A sample of sputum or tissue require initial liquefication
and decontamination
 Mostly used is N-acetyl –L-cysteine as a mucolytic in 1% NaCl
 This kills other organisms, M.tb are protected by their fatty
acid rich cell wall
 The sample is then neutralized, centrifuged and the
sediment is inoculated in the media
 Uncontaminated fluid or normally sterile tissues should not
be contaminated as some loss mycobacterial viability
Culture cont
 Solid culture media are of two general types:
 Agar bases e.g Middlebrook 7H11
 Egg based e.g Lowenstein Jensen
 The BACTEC radiometric system for culturing
mycobacteria
 It is a liquid system which uses radioactive
palmitate as a sole carbon source
 Inclusion of p-nitro-alpha-acetylamino- -
hydroxypropiophenone in the incubation media
inhibit the growth of M.Tb complex (including M.
bovis and M. africunum
 But does not inhibit mycobacteria other than
tuberculosis
 Pleural, cerebrospinal, peritoneal, and pericardial fluids
should be analyzed for protein and glucose (compared
with simultaneous blood glucose).
 Cell and differential counts should be obtained.
 A high protein (> 50% of the serum protein
concentration), lymphocytosis, and a low glucose are
usually found in tuberculous infections, but neither
their presence nor their absence is diagnostic.
 For pleural tuberculosis the diagnostic yield can be
increased by obtaining pleural tissue for histologic study
and culture by needle biopsy at the time of diagnostic
thoracentesis.
 Peritoneal biopsies are best obtained via laparoscopy.
Mantoux tuberculine skin test
 Used for screening especially for children
 Can also be used for high risk individuals
 A purified protein derivative is injected intradermal in
the forearm (0.1ml)
 The induration is read after 48 to 72 hrs
 Induration > 10mm in children less than 4 yrs a/c risk of
disemminated disease
 Induration >15mm in children more than 4 yrs is also
significant
False positive TST
 Prior infections/exposures to non tuberculous
mycobacterium
 Recent BCG vaccination
TB AND HIV
 TB is the third highest cause of
morbidity and mortality in Tanzania
after HIV/AIDS and malaria
 Immune compromised people are
very prone to develop TB, including
PLHIV
 TB is the leading cause of death for
PLHIV
 HIV frequently co-exists with TB
TB AND HIV
 14 million people are co-infected world wide
 9% of TB cases are attributable to HIV world wide
 Infection after exposure10-20% vs
5,10%
 Progressive primary disease after
infection 30% vs 5 -10%
 Reactivation of latent infection 5-
10% annual vs 5-10% lifetime
TB in HIV Infection
 In pre HIV era 80-85% of TB infection presented as PTB.
 Up to 15% as EPTB
 5% mixture of PTB and EPTB
 While in HIV era 60-70% PTB,while EPTB 50-60%
 PTB presentation depends on HIV progression
 In low CD4 PTB presents with high fever,dyspnoea and
wt loss
 In low CD4 sputum smear often –ve,no typical chest x
ray findings of PTB(cavitation or infiltates in lung apex)
Treatment of tuberculosis
 It is important with the aim of curing the patient and
preventing the spread of the disease to the community.
 Case definition in TB treatment
 New case: a patient who has never had treatment for
TB before or has been on treatment for not more than 4
weeks
 Relapse: a patient declared cured or treatment
completed who reports back to health services and is
found to be AFB positive
 Failure: a patient who, while on treatment, is AFB
positive at 5-months or later during the course of
treatment
Case definition cont
 Return after default: a patient who returns to
treatment bacteriological positive, after having
interrupted treatment for 2-months or more and who
had been on RX for more than 4 weeks
 Transfer-in: a registered TB patient on Rx received
from another region
 Other: any TB patient who does not fit in one of the
above definitions
TB treatment regimen
 There are two TB treatment phases: initial phase
(intensive) and continuation phase
 During initial phase:
 There is rapid killing of the TB bacilli
 Initial phase takes 2months with 4 drugs
 Patients mostly become non-infectious after about 2
weeks
 During continuation phase:
 Drugs kill the persisters
 Prevent relapse after completion of treatment
 Continuous phase takes 2 drugs for 4 or 6 months
Treatment regimen cont
 1st line drugs-
isoniazid,rifampicin,rifapentine,rifabutin,ethambutol
and pyrazinamide
 2nd line drugs –
cycloserine,ethionamide,levofloxacine,moxifloxacin,gat
ifloxacine,P aminosalicylic
acid,streptomycin,amikacin/kanamycin,capreomycin
1/13/202
3
TB IN CHILDREN, DR MERCY 61
Reasons for combination
therapy
 the biological different populations of
the bacteria needs specific metabolic
acting drugs.
 combination therapy reduces resistance.
In each population there are spontaneous
mutations of resistant bacteria which
would be selected under inadequate
therapy.
 combination therapy reduces the toxicity
of the different substances.
Side effects of first line ant
tuberculosis drugs
 Isoniazid:-mild LFT elevation or hepatitis-
peripheral neuritis-hypersensitivity
 Rifampin:-orange colored secretions-
hepatitis or thrombocytopenia-OCP may
be ineffective
 Pyrazinamide-hepatotoxicity-
hyperuricemia
 Ethambutol-optic neuritis (usually
reversible)-decreased red-green color
discrimination-GI tract disturbances-
hypersensitivity
Treatment of extrapulmonary
TB
 Most of extrapulmonary TB can be treated for 6
months,except TB of bone and joints can be treated for
6 to 9 months,Tb meningitis for 9 to 12 months.
Drug Resistant TB
This is a form of TB in which first-line anti-TB drugs have little or
no effect against M. tuberculosis. The diagnosis is confirmed
through molecular tests and culture and DST of M.
tuberculosis strains.
Four different categories of drug resistance have been identified:
• Mono resistant TB: Resistance to any single first-line anti-TB
drug.
• MDR TB: Resistance to at least both isoniazid and rifampicin.
• XDR TB: This is multidrug resistance, with additional resistance
to any fluoroquinolones (ofloxacin, levofloxacin, moxifloxacin)
and at least one of the three injectable drugs (amikacin,
kanamycin, capreomycin).
TB drug resistance
 Multidrug resistance(MDR-TB)-resistance to at least
Isoniazid and Rifampicin.
 It is a man made phenomenon due to inadequate
treatment regimen or poor adherence to treatment
 It common to people with HIV and Tb coinfection
 It causes pts to use 2nd line drugs with longer treatment
duration,more toxicity and expensive
Former MDR TB REGIMENS TANZANIA
Group Drugs
Group A – Fluoroquinolones Levofloxacin (Lfx), Moxifloxacin (Mfx),
Group B – Injectable agents Kanamycin (Km), Amikacin (Am) ; Capreomycin (Cm)
Group C – Other core second-line
agents
Ethionamide (Eto), Protionamide (Pto), Cycloserine (Cs), Linezolid (Lzd),
Clofazimine (Cfz)
Group D - Add-on agents
(not part of the core MDR-
TB regimen)
D1 Pyrazinamide (Z), Ethambutol (E),
High-dose isoniazid (Hh)
D2 Bedaquiline (Bdq), Delamanid (Dlm)
D3 p-aminosalicylic acid (PAS)
Amoxicillin-clavulanate (Amx-Cl)
Grouping of anti-TB agents used to treat DR-TB
Former MDR TB REGIMENS TANZANIA (phasing out)
Standardised short regimen
4-6 Km, Mfx, Pto, Cfz, E, Z, H(h)
5 Mfx Cfz E Z
Individualized Long MDR TB Regimen;
MDR TB
8 Km/Cm, Cs, Lfx, Eto, Z,
12 Cs, Eto, Z, Lfx
Individualized Long MDR TB Regimen;
XDR TB
12Cm Lfx, Bdq, Dlm6 , Lzd, Cfz, PAS.
12 Lfx, Lzd, Cfz, PAS
❑DR-TB is generally treatable, however,
extensive treatment - 9 months up to
24 months
❑Using eligibility criteria patients can be
started on;
• Standardized shorter regimen (9-11
months)
• Individuslized Long regimen (20
months) - MDR-TB patients
• Individualised Long regimen (24
months) - XDR-TB patients
SECOND LINE ANTI TB MEDICINES STOCKS
Currently existing stock of recommended second line drugs and MOS
Group A SOH MOS Group B SOH MOS Group C SOH MOS
Lfx 500mg 65,800 7 Cfz 100mg 50,000 4 E 400mg 100,800 8
Bdq 100mg 22,550 12 Cs 250mg 0 - Dlm 50mg 2,016
Lzd 600mg 23,050 12 Z 500mg 443,520 11
PASER 1,2600 7
ETO 250mg 28,400 2
PTO 184,400 5
Proposed regimens - Tanzania
1. Long regimen adults (routine)
 6 Lfx - Bdq - Lzd - Cfz – Cs / 12 Lfx - Cfz - Cs
 Substitute; E, Eto, PAS, Z, Dlm
2. Short regimen adults (Operational Research);
 6 Bdq – Lzd – Lfx – Cfz – Cs – Z / 3-5 Lfx – Cfz – Cs – Z
 6 Bdq – Dlm– Lfx – Cfz – Cs – Z / 3-5 Lfx – Cfz – Cs – Z
3. Short Regimen children (routine)
 6 Lfx – Bdq – Lzd – Cs / 3 Lfx – Lzd – Cs
 Substitute; PAS, Dlm, E, Eto, Z, Mfx
 BQD not used for children <6yrs, Delanamid <3yrs
 Treatment prolonged (12-15 mths)in selected cases ; meningitis, TB bone, Spine
1/13/202
3
TB IN CHILDREN, DR MERCY 71
Extensive drug resistance TB
 It is MDR plus resistance to floroquinolones and one of
the 3 second line
injectables.kanamycin,amikacin,capreomycin
 South Africa has reported the number of XDR-TB
 It is common in HIV pts
 98% dies with an avarage of 25 days since admission
1/13/202
3
TB IN CHILDREN, DR MERCY 73
Anti-TB resistance
 Primary drug-resistance: “New Cases”
Drug resistance in a patient who has never
been treated for tuberculosis or received
less than one month of therapy
 Secondary (acquired) drug-resistance:
“Previously Treated Cases”
Drug resistance in a patient who has
received at least one month of anti-TB
therapy
Prophylaxis and vaccination
 All infant born to smear +ve mother are
given INH 5mg/kg for six months.
 Isoniazid Preventive Therapy (IPT)
 Can be given to people with HIV who have a high TB risk and
have been screened to exclude active TB
 Adults: 300 mg daily for 6 to 9 months
vaccination
 Many countries use Bacillus Calmette-Guérin (BCG)
vaccine as part of their TB control programs, especially
for infants.
 The protective efficacy of BCG for preventing serious
forms of TB (e.g. meningitis) in children is greater than
80%
references
 Principles and practice of infectious diseaes 4th ed by
Mandell L et al.
 Medical microbiology 19th ed by Jawetz et al.
 Harrison’s Principles of Internal medicine 16th ed by
Kasper et al.
 National guideline for management of HIV and TB latest
edition.

More Related Content

Similar to Tuberculosis.pptx

TUBERCULOSIS (TB)1.pptx
TUBERCULOSIS (TB)1.pptxTUBERCULOSIS (TB)1.pptx
TUBERCULOSIS (TB)1.pptx
AugustusCaesar7
 
Mycobacterium .pptx
Mycobacterium .pptxMycobacterium .pptx
Mycobacterium .pptx
KensonPKanesious1
 
Pathophysiology tubercuslosis
Pathophysiology tubercuslosisPathophysiology tubercuslosis
Pathophysiology tubercuslosis
Nem kumar Jain
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
Ngk Sharma
 
Mycobacterium tuberculosis by Sikander ali Sumalani
Mycobacterium tuberculosis by Sikander ali SumalaniMycobacterium tuberculosis by Sikander ali Sumalani
Mycobacterium tuberculosis by Sikander ali Sumalani
sikandarsikandar3
 
Tetanus, Tuberculosis, H1N1
Tetanus, Tuberculosis, H1N1 Tetanus, Tuberculosis, H1N1
Tetanus, Tuberculosis, H1N1
HARINATHA REDDY ASWARTHA
 
tuberculosis .pptx
tuberculosis .pptxtuberculosis .pptx
tuberculosis .pptx
SaketKumar946153
 
tuberculosis (2).pptx
tuberculosis (2).pptxtuberculosis (2).pptx
tuberculosis (2).pptx
SaketKumar946153
 
Tuberculosis.pptx
Tuberculosis.pptxTuberculosis.pptx
Tuberculosis.pptx
Fuad952583
 
Tuberculosis in pediatrics
Tuberculosis in pediatricsTuberculosis in pediatrics
Tuberculosis in pediatrics
El Verlain
 
Infectious Diseases.pptx
Infectious Diseases.pptxInfectious Diseases.pptx
Infectious Diseases.pptx
Sunil Kardani
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
Tripthi Saliyan
 
TUBERCULOSIS IN CHILDREN (1).pptx
TUBERCULOSIS IN CHILDREN (1).pptxTUBERCULOSIS IN CHILDREN (1).pptx
TUBERCULOSIS IN CHILDREN (1).pptx
MishiSoza
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
D Venkatesh Kumar
 
Pulmonary Tuberculosis.pptx
Pulmonary Tuberculosis.pptxPulmonary Tuberculosis.pptx
Pulmonary Tuberculosis.pptx
AnushkaShrestha14
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
Dr Shahnawaz Shah
 
TUBERCULOSIS pharmacology notes types cure
TUBERCULOSIS pharmacology notes types cureTUBERCULOSIS pharmacology notes types cure
TUBERCULOSIS pharmacology notes types cure
Affrin Shaik
 
TUBERCULOSIS
TUBERCULOSISTUBERCULOSIS
TUBERCULOSIS
samthamby79
 
Lec 3 tuberculosis 3
Lec 3 tuberculosis 3Lec 3 tuberculosis 3
Lec 3 tuberculosis 3
DOCTOR WHO
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
Dr. Ravi Prakash
 

Similar to Tuberculosis.pptx (20)

TUBERCULOSIS (TB)1.pptx
TUBERCULOSIS (TB)1.pptxTUBERCULOSIS (TB)1.pptx
TUBERCULOSIS (TB)1.pptx
 
Mycobacterium .pptx
Mycobacterium .pptxMycobacterium .pptx
Mycobacterium .pptx
 
Pathophysiology tubercuslosis
Pathophysiology tubercuslosisPathophysiology tubercuslosis
Pathophysiology tubercuslosis
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
 
Mycobacterium tuberculosis by Sikander ali Sumalani
Mycobacterium tuberculosis by Sikander ali SumalaniMycobacterium tuberculosis by Sikander ali Sumalani
Mycobacterium tuberculosis by Sikander ali Sumalani
 
Tetanus, Tuberculosis, H1N1
Tetanus, Tuberculosis, H1N1 Tetanus, Tuberculosis, H1N1
Tetanus, Tuberculosis, H1N1
 
tuberculosis .pptx
tuberculosis .pptxtuberculosis .pptx
tuberculosis .pptx
 
tuberculosis (2).pptx
tuberculosis (2).pptxtuberculosis (2).pptx
tuberculosis (2).pptx
 
Tuberculosis.pptx
Tuberculosis.pptxTuberculosis.pptx
Tuberculosis.pptx
 
Tuberculosis in pediatrics
Tuberculosis in pediatricsTuberculosis in pediatrics
Tuberculosis in pediatrics
 
Infectious Diseases.pptx
Infectious Diseases.pptxInfectious Diseases.pptx
Infectious Diseases.pptx
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
 
TUBERCULOSIS IN CHILDREN (1).pptx
TUBERCULOSIS IN CHILDREN (1).pptxTUBERCULOSIS IN CHILDREN (1).pptx
TUBERCULOSIS IN CHILDREN (1).pptx
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
 
Pulmonary Tuberculosis.pptx
Pulmonary Tuberculosis.pptxPulmonary Tuberculosis.pptx
Pulmonary Tuberculosis.pptx
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
 
TUBERCULOSIS pharmacology notes types cure
TUBERCULOSIS pharmacology notes types cureTUBERCULOSIS pharmacology notes types cure
TUBERCULOSIS pharmacology notes types cure
 
TUBERCULOSIS
TUBERCULOSISTUBERCULOSIS
TUBERCULOSIS
 
Lec 3 tuberculosis 3
Lec 3 tuberculosis 3Lec 3 tuberculosis 3
Lec 3 tuberculosis 3
 
Tuberculosis
TuberculosisTuberculosis
Tuberculosis
 

More from Mkindi Mkindi

Electrolyte and fluid balance in elderly.pptx
Electrolyte and fluid balance in elderly.pptxElectrolyte and fluid balance in elderly.pptx
Electrolyte and fluid balance in elderly.pptx
Mkindi Mkindi
 
Approach to disease in elderly.pptx elderly
Approach to disease in elderly.pptx elderlyApproach to disease in elderly.pptx elderly
Approach to disease in elderly.pptx elderly
Mkindi Mkindi
 
Approach to disease in elderly.pptx bwire bwire
Approach to disease in elderly.pptx bwire bwireApproach to disease in elderly.pptx bwire bwire
Approach to disease in elderly.pptx bwire bwire
Mkindi Mkindi
 
01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas
01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas
01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas
Mkindi Mkindi
 
Arterial thrombi in details#MkindiArterial thrombi#Mkindi Arterial thrombi#M...
Arterial thrombi in details#MkindiArterial thrombi#Mkindi  Arterial thrombi#M...Arterial thrombi in details#MkindiArterial thrombi#Mkindi  Arterial thrombi#M...
Arterial thrombi in details#MkindiArterial thrombi#Mkindi Arterial thrombi#M...
Mkindi Mkindi
 
02-Investigations kidney Urinalysis.pptx
02-Investigations kidney Urinalysis.pptx02-Investigations kidney Urinalysis.pptx
02-Investigations kidney Urinalysis.pptx
Mkindi Mkindi
 
SELECTIVE TOXICITY.ppt
SELECTIVE TOXICITY.pptSELECTIVE TOXICITY.ppt
SELECTIVE TOXICITY.ppt
Mkindi Mkindi
 
Case Control Studies.pptx
Case Control Studies.pptxCase Control Studies.pptx
Case Control Studies.pptx
Mkindi Mkindi
 
02-Gouty arthritis.pptx
02-Gouty arthritis.pptx02-Gouty arthritis.pptx
02-Gouty arthritis.pptx
Mkindi Mkindi
 
malabsorptionsyndromes-3.pptx
malabsorptionsyndromes-3.pptxmalabsorptionsyndromes-3.pptx
malabsorptionsyndromes-3.pptx
Mkindi Mkindi
 
Hepatitis remade K H.pptx
Hepatitis remade K H.pptxHepatitis remade K H.pptx
Hepatitis remade K H.pptx
Mkindi Mkindi
 
3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....
3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....
3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....
Mkindi Mkindi
 
UGIB - ppt 2023.pptx
UGIB - ppt 2023.pptxUGIB - ppt 2023.pptx
UGIB - ppt 2023.pptx
Mkindi Mkindi
 
HEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptx
HEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptxHEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptx
HEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptx
Mkindi Mkindi
 
TOXOPLASMOSISI.ppt
TOXOPLASMOSISI.pptTOXOPLASMOSISI.ppt
TOXOPLASMOSISI.ppt
Mkindi Mkindi
 
CNS EXAMINATION Lecture notes AMO.pptx
CNS EXAMINATION Lecture notes AMO.pptxCNS EXAMINATION Lecture notes AMO.pptx
CNS EXAMINATION Lecture notes AMO.pptx
Mkindi Mkindi
 
DISORDER OF LIPIDS METABOLISM PART 1.pptx
DISORDER OF LIPIDS METABOLISM PART 1.pptxDISORDER OF LIPIDS METABOLISM PART 1.pptx
DISORDER OF LIPIDS METABOLISM PART 1.pptx
Mkindi Mkindi
 
ADULT MALNUTRITION.pptx
ADULT MALNUTRITION.pptxADULT MALNUTRITION.pptx
ADULT MALNUTRITION.pptx
Mkindi Mkindi
 
CML. kamk.pptx
CML. kamk.pptxCML. kamk.pptx
CML. kamk.pptx
Mkindi Mkindi
 
61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt
61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt
61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt
Mkindi Mkindi
 

More from Mkindi Mkindi (20)

Electrolyte and fluid balance in elderly.pptx
Electrolyte and fluid balance in elderly.pptxElectrolyte and fluid balance in elderly.pptx
Electrolyte and fluid balance in elderly.pptx
 
Approach to disease in elderly.pptx elderly
Approach to disease in elderly.pptx elderlyApproach to disease in elderly.pptx elderly
Approach to disease in elderly.pptx elderly
 
Approach to disease in elderly.pptx bwire bwire
Approach to disease in elderly.pptx bwire bwireApproach to disease in elderly.pptx bwire bwire
Approach to disease in elderly.pptx bwire bwire
 
01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas
01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas
01-INVESTIGATIONS IN KDInvesting ckd bugando cuhas
 
Arterial thrombi in details#MkindiArterial thrombi#Mkindi Arterial thrombi#M...
Arterial thrombi in details#MkindiArterial thrombi#Mkindi  Arterial thrombi#M...Arterial thrombi in details#MkindiArterial thrombi#Mkindi  Arterial thrombi#M...
Arterial thrombi in details#MkindiArterial thrombi#Mkindi Arterial thrombi#M...
 
02-Investigations kidney Urinalysis.pptx
02-Investigations kidney Urinalysis.pptx02-Investigations kidney Urinalysis.pptx
02-Investigations kidney Urinalysis.pptx
 
SELECTIVE TOXICITY.ppt
SELECTIVE TOXICITY.pptSELECTIVE TOXICITY.ppt
SELECTIVE TOXICITY.ppt
 
Case Control Studies.pptx
Case Control Studies.pptxCase Control Studies.pptx
Case Control Studies.pptx
 
02-Gouty arthritis.pptx
02-Gouty arthritis.pptx02-Gouty arthritis.pptx
02-Gouty arthritis.pptx
 
malabsorptionsyndromes-3.pptx
malabsorptionsyndromes-3.pptxmalabsorptionsyndromes-3.pptx
malabsorptionsyndromes-3.pptx
 
Hepatitis remade K H.pptx
Hepatitis remade K H.pptxHepatitis remade K H.pptx
Hepatitis remade K H.pptx
 
3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....
3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....
3. Ananthakrishnan - Management of Severe UC and Pouch-Related Complications....
 
UGIB - ppt 2023.pptx
UGIB - ppt 2023.pptxUGIB - ppt 2023.pptx
UGIB - ppt 2023.pptx
 
HEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptx
HEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptxHEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptx
HEPATOCELLULAR AND GALL BLADDER CARCINOMA.pptx
 
TOXOPLASMOSISI.ppt
TOXOPLASMOSISI.pptTOXOPLASMOSISI.ppt
TOXOPLASMOSISI.ppt
 
CNS EXAMINATION Lecture notes AMO.pptx
CNS EXAMINATION Lecture notes AMO.pptxCNS EXAMINATION Lecture notes AMO.pptx
CNS EXAMINATION Lecture notes AMO.pptx
 
DISORDER OF LIPIDS METABOLISM PART 1.pptx
DISORDER OF LIPIDS METABOLISM PART 1.pptxDISORDER OF LIPIDS METABOLISM PART 1.pptx
DISORDER OF LIPIDS METABOLISM PART 1.pptx
 
ADULT MALNUTRITION.pptx
ADULT MALNUTRITION.pptxADULT MALNUTRITION.pptx
ADULT MALNUTRITION.pptx
 
CML. kamk.pptx
CML. kamk.pptxCML. kamk.pptx
CML. kamk.pptx
 
61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt
61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt
61.Cerebral blood flow, the cerebrospinal fluid and brain me.ppt
 

Recently uploaded

clinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdfclinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdf
Priyankaranawat4
 
ANATOMY AND BIOMECHANICS OF HIP JOINT.pdf
ANATOMY AND BIOMECHANICS OF HIP JOINT.pdfANATOMY AND BIOMECHANICS OF HIP JOINT.pdf
ANATOMY AND BIOMECHANICS OF HIP JOINT.pdf
Priyankaranawat4
 
Your Skill Boost Masterclass: Strategies for Effective Upskilling
Your Skill Boost Masterclass: Strategies for Effective UpskillingYour Skill Boost Masterclass: Strategies for Effective Upskilling
Your Skill Boost Masterclass: Strategies for Effective Upskilling
Excellence Foundation for South Sudan
 
CACJapan - GROUP Presentation 1- Wk 4.pdf
CACJapan - GROUP Presentation 1- Wk 4.pdfCACJapan - GROUP Presentation 1- Wk 4.pdf
CACJapan - GROUP Presentation 1- Wk 4.pdf
camakaiclarkmusic
 
Executive Directors Chat Leveraging AI for Diversity, Equity, and Inclusion
Executive Directors Chat  Leveraging AI for Diversity, Equity, and InclusionExecutive Directors Chat  Leveraging AI for Diversity, Equity, and Inclusion
Executive Directors Chat Leveraging AI for Diversity, Equity, and Inclusion
TechSoup
 
Liberal Approach to the Study of Indian Politics.pdf
Liberal Approach to the Study of Indian Politics.pdfLiberal Approach to the Study of Indian Politics.pdf
Liberal Approach to the Study of Indian Politics.pdf
WaniBasim
 
Lapbook sobre os Regimes Totalitários.pdf
Lapbook sobre os Regimes Totalitários.pdfLapbook sobre os Regimes Totalitários.pdf
Lapbook sobre os Regimes Totalitários.pdf
Jean Carlos Nunes Paixão
 
MARY JANE WILSON, A “BOA MÃE” .
MARY JANE WILSON, A “BOA MÃE”           .MARY JANE WILSON, A “BOA MÃE”           .
MARY JANE WILSON, A “BOA MÃE” .
Colégio Santa Teresinha
 
The basics of sentences session 5pptx.pptx
The basics of sentences session 5pptx.pptxThe basics of sentences session 5pptx.pptx
The basics of sentences session 5pptx.pptx
heathfieldcps1
 
S1-Introduction-Biopesticides in ICM.pptx
S1-Introduction-Biopesticides in ICM.pptxS1-Introduction-Biopesticides in ICM.pptx
S1-Introduction-Biopesticides in ICM.pptx
tarandeep35
 
PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.
Dr. Shivangi Singh Parihar
 
Types of Herbal Cosmetics its standardization.
Types of Herbal Cosmetics its standardization.Types of Herbal Cosmetics its standardization.
Types of Herbal Cosmetics its standardization.
Ashokrao Mane college of Pharmacy Peth-Vadgaon
 
Main Java[All of the Base Concepts}.docx
Main Java[All of the Base Concepts}.docxMain Java[All of the Base Concepts}.docx
Main Java[All of the Base Concepts}.docx
adhitya5119
 
Hindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdfHindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdf
Dr. Mulla Adam Ali
 
DRUGS AND ITS classification slide share
DRUGS AND ITS classification slide shareDRUGS AND ITS classification slide share
DRUGS AND ITS classification slide share
taiba qazi
 
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptxC1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
mulvey2
 
PIMS Job Advertisement 2024.pdf Islamabad
PIMS Job Advertisement 2024.pdf IslamabadPIMS Job Advertisement 2024.pdf Islamabad
PIMS Job Advertisement 2024.pdf Islamabad
AyyanKhan40
 
Digital Artefact 1 - Tiny Home Environmental Design
Digital Artefact 1 - Tiny Home Environmental DesignDigital Artefact 1 - Tiny Home Environmental Design
Digital Artefact 1 - Tiny Home Environmental Design
amberjdewit93
 
How to Manage Your Lost Opportunities in Odoo 17 CRM
How to Manage Your Lost Opportunities in Odoo 17 CRMHow to Manage Your Lost Opportunities in Odoo 17 CRM
How to Manage Your Lost Opportunities in Odoo 17 CRM
Celine George
 
Advanced Java[Extra Concepts, Not Difficult].docx
Advanced Java[Extra Concepts, Not Difficult].docxAdvanced Java[Extra Concepts, Not Difficult].docx
Advanced Java[Extra Concepts, Not Difficult].docx
adhitya5119
 

Recently uploaded (20)

clinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdfclinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdf
 
ANATOMY AND BIOMECHANICS OF HIP JOINT.pdf
ANATOMY AND BIOMECHANICS OF HIP JOINT.pdfANATOMY AND BIOMECHANICS OF HIP JOINT.pdf
ANATOMY AND BIOMECHANICS OF HIP JOINT.pdf
 
Your Skill Boost Masterclass: Strategies for Effective Upskilling
Your Skill Boost Masterclass: Strategies for Effective UpskillingYour Skill Boost Masterclass: Strategies for Effective Upskilling
Your Skill Boost Masterclass: Strategies for Effective Upskilling
 
CACJapan - GROUP Presentation 1- Wk 4.pdf
CACJapan - GROUP Presentation 1- Wk 4.pdfCACJapan - GROUP Presentation 1- Wk 4.pdf
CACJapan - GROUP Presentation 1- Wk 4.pdf
 
Executive Directors Chat Leveraging AI for Diversity, Equity, and Inclusion
Executive Directors Chat  Leveraging AI for Diversity, Equity, and InclusionExecutive Directors Chat  Leveraging AI for Diversity, Equity, and Inclusion
Executive Directors Chat Leveraging AI for Diversity, Equity, and Inclusion
 
Liberal Approach to the Study of Indian Politics.pdf
Liberal Approach to the Study of Indian Politics.pdfLiberal Approach to the Study of Indian Politics.pdf
Liberal Approach to the Study of Indian Politics.pdf
 
Lapbook sobre os Regimes Totalitários.pdf
Lapbook sobre os Regimes Totalitários.pdfLapbook sobre os Regimes Totalitários.pdf
Lapbook sobre os Regimes Totalitários.pdf
 
MARY JANE WILSON, A “BOA MÃE” .
MARY JANE WILSON, A “BOA MÃE”           .MARY JANE WILSON, A “BOA MÃE”           .
MARY JANE WILSON, A “BOA MÃE” .
 
The basics of sentences session 5pptx.pptx
The basics of sentences session 5pptx.pptxThe basics of sentences session 5pptx.pptx
The basics of sentences session 5pptx.pptx
 
S1-Introduction-Biopesticides in ICM.pptx
S1-Introduction-Biopesticides in ICM.pptxS1-Introduction-Biopesticides in ICM.pptx
S1-Introduction-Biopesticides in ICM.pptx
 
PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.
 
Types of Herbal Cosmetics its standardization.
Types of Herbal Cosmetics its standardization.Types of Herbal Cosmetics its standardization.
Types of Herbal Cosmetics its standardization.
 
Main Java[All of the Base Concepts}.docx
Main Java[All of the Base Concepts}.docxMain Java[All of the Base Concepts}.docx
Main Java[All of the Base Concepts}.docx
 
Hindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdfHindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdf
 
DRUGS AND ITS classification slide share
DRUGS AND ITS classification slide shareDRUGS AND ITS classification slide share
DRUGS AND ITS classification slide share
 
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptxC1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
 
PIMS Job Advertisement 2024.pdf Islamabad
PIMS Job Advertisement 2024.pdf IslamabadPIMS Job Advertisement 2024.pdf Islamabad
PIMS Job Advertisement 2024.pdf Islamabad
 
Digital Artefact 1 - Tiny Home Environmental Design
Digital Artefact 1 - Tiny Home Environmental DesignDigital Artefact 1 - Tiny Home Environmental Design
Digital Artefact 1 - Tiny Home Environmental Design
 
How to Manage Your Lost Opportunities in Odoo 17 CRM
How to Manage Your Lost Opportunities in Odoo 17 CRMHow to Manage Your Lost Opportunities in Odoo 17 CRM
How to Manage Your Lost Opportunities in Odoo 17 CRM
 
Advanced Java[Extra Concepts, Not Difficult].docx
Advanced Java[Extra Concepts, Not Difficult].docxAdvanced Java[Extra Concepts, Not Difficult].docx
Advanced Java[Extra Concepts, Not Difficult].docx
 

Tuberculosis.pptx

  • 2.  A 46 years old male pt who was admitted from home with history of coughing blood on two different occasions in the past two weeks associated with fever, profuse nocturnal sweating, loss of appetite, significance weight loss of 8 kg in less than a month and easy fatiguability. POSITIVE hx of IV drug use.  On Physical examination, He was Ill looking, cachexic, febrile T- 39.6, PR- 110 Bpm, RS- 20 bpm, BP- 130/76, SPO2- 98%  RR; Unilateral right side crepitation, more on the upper lobes  Initial chest x-ray; infiltration on the right upper lobe with a sign of Cavitation.
  • 3.
  • 4.  Provisional diagnosis.?? Ddx??  Other investigation that we can order?  Mostly likely organism?  Pathogenesis/Immunology of the disease?  Is the patient high risk or low risk patient?  Most likely co- infection?  Initial treatment?  Prevention and prophylaxis measures
  • 5. Tuberculosis Presenter : SAIMON MAGANGA ILLUMINATA KAFUMU Supervisor: Prof. STEPHEN MSHANA
  • 6. Presentation outline  Introduction  Structural differences between Tb and other bacteria  Transmission  Pathogenesis / Immunology  Clinical presentation of different forms of Tb.  Diagnostic tools/methods and challenges  Treatment and resistance challenges  MDR/XDR  MDR Treatment  Tb vaccination  Prevention and Prophylaxis  Discussion
  • 7. INTRODUCTION  Tuberculosis. Describes as a chronic infectious disease with broad range of clinical illness caused by Mycobacterium tuberculosis complex.  In humans the commonest cause is Mycobacterium tuberculosis.  other mycobacterium spp such as; • Mycobacterium bovis, • Mycobacterium avium complex (MAC), • Mycobacterium canetti and • Mycobacterium Africanum may rarely cause TB,
  • 8. Introduction  Tuberculosis is primarily the disease of the lungs however it can affect other organs e.g. meninges, lymph nodes, brain, kidney, GIT, bones and joints etc  Humans are the only known reservoir for Mycobacterium tuberculosis
  • 9. epidemiology  Over 30% of people in the world are infected with TB  Majority of TB patients (80%) are in 22 high burden countries  Tanzania has an incidence of (253/100,000) is ranked 14th out of 30 (Source: WHO report 2020)
  • 10. TB Prevalence in Tanzania  In year 2018, a total of 75,845 cases of all forms were notified, which is an increase of 6,205 cases or 9% compared to the year 2017. New and relapse TB cases notified were 74,692 among them, 48% were bacteriological confirmed TB cases, 79% were pulmonary TB cases (NTLP 2018)
  • 11.
  • 13.
  • 14. Microbiology of TB  Mycobacterium tuberculosis was discovered by Robert Koch in 1882.  They are Obligate aerobic, non spore forming acid fast bacilli  Called acid fast bacillus because the resist decolourisation with acid or alcohol after being stained by carbofuschin dye.  They have cell wall made of mycolic acid which contributes to pathogenicity also have waxy layer which help to survive in adverse conditions
  • 15. Microbiology cont  M. Tuberculosis can be differentiated from other mycobacteria:- Grow slowly and lack pigment Produce niacin Reduce nitrates Produce heat sensitive catalase ( inactivated by heating to 68C at pH of 7.0) Other mycobacteria produce large amount of heat stable catalase
  • 16. Transmission  Transmission is from human with active disease through aerosal droplets.  Transmission occurs significantly while coughing, sneezing, singing, talking or spiting At this time, they expel infectious aerosol droplets 0.5 to 5 µm in diameter.  Avoid prolonged, frequent and intense contact with active Tb patients especially for immunocompromised non Tb infected people.
  • 17. Pathogenesis  About 90% of those infected with M.tuberculosis have asymptomatic, latent TB infection.  With only a 10% lifetime chance that a latent infection will progress to TB disease.  TB infection begins when the mycobacteria reach the pulmonary alveoli, where they invade and replicate within the endosomes of alveolar macrophages.
  • 18. Pathogenesis cont  In the few weeks (4-6wks) the body has almost no immune defense against infection with M. tuberculosis.  Bacterial multiplication proceeds for weeks both in the initial focus and lymphohematogenous metastatic foci until the development of hypersensitivity and cellular immunity  Lymphocytes, mostly CD4+ cells bearing the alpha form of the T cell receptor are capable of recognizing mycobacteria that have been processed and presented by macrophage
  • 19.
  • 21. Pathogenesis cont  When lymphocytes encounter antigen in association with MHC class II molecule on the macrophage surface it is activated and proliferates producing a clone of reactive lymphocytes  T cells produce many lymphokines which attract, retain and activate macrophage at the site of antigen  Activated macrophage accumulate high concentrations of lytic enzymes and reactive metabolites that mycobactericidal
  • 22. Pathogenesis cont  Alveolar macrophage secrete a number of cytokines  Interleukin I contribute to fever  IL -6 contributes to hyperglobulinemia  Tumor necrotic factor alpha (TNF- alpha)contributes : • Killing of mycobacteria • Formation of granulomas • Systemic symptoms such as fever and weight loss
  • 23. Pathogenesis cont  Qualitative and quantitative defect of CD4+ T cells explain inability of HIV +ve pt to contain mycobacteria proliferation  When the population of activated lymphocytes reach a certain size, cutaneous delayed reactivity to tuberculin becomes manifest  The pathological features of tuberculosis are the result of the degree of hypersensitivity and the local concentration of antigen
  • 24. Pathogenesis cont  Necrosis in tuberculosis tend to be incomplete resulting in solid or semisolid acellular and amorphous material known as caseous necrosis  The chemical environment and low oxygen tension inhibit microbial multiplication  The primary site of infection in the lungs is called the Ghon focus, and is generally located in either the upper part of the lower lobe, or the lower part of the upper lobe.(commonly at the subpleural)
  • 28.
  • 29. Pathogenesis cont  Macrophages, T lymphocytes, B lymphocytes and fibroblasts are among the cells that aggregate to form a granuloma, with lymphocytes surrounding the infected macrophages.
  • 30. Pathogenesis cont  The granuloma functions not only to prevent dissemination of the mycobacteria, but also provides a local environment for communication of cells of the immune system.  Within the granuloma, T lymphocytes secrete cytokines such as interferon gamma, which activates macrophages to destroy the bacteria with which they are infected.  Cytotoxic T cells can also directly kill infected cells, by secreting perforin and granulysin.  Mycobacteria are not always eliminated within the granuloma, but can become dormant, resulting in a latent infection.
  • 31. Pathogenesis cont  Another feature of the granulomas of human tuberculosis is the development of cell death, also called necrosis, in the center of tubercles  To the naked eye this has the texture of soft white cheese and was termed caseous necrosis.  If TB bacteria gain entry to the bloodstream from an area of damaged tissue they spread through the body and set up many foci of infection, all appearing as tiny white tubercles in the tissues.
  • 32.
  • 33. Pathogenesis cont  This severe form of TB disease is most common in infants and the immunocompromised pts, elderly and is called miliary tuberculosis.  Patients with this disseminated TB have a fatality rate of approximately 20%, even with intensive treatment.  Tissue destruction and necrosis are balanced by healing and fibrosis.  Affected tissue is replaced by scarring and cavities filled with cheese-like white necrotic material.  During active disease, some of these cavities are joined to the air passages bronchi and this material can be coughed up.
  • 34. Natural history  After 5 years 50% of pulmonary disease will die of the disease.  25% will be self cured(health)  Another 25% will be ill with chronic infectious disease
  • 35. Types of tuberculosis I. Pulmonary tuberculosis II. Extra- Pulmonary tuberculosis  Pulmonary tuberculosis Clinical features  Typical symptoms of pulmonary TB include a productive cough, fever, and weight loss. Occasionally, patients may present with hemoptysis or chest pain.  Other systemic symptoms include anorexia, fatigue, or night sweats.
  • 36. Extrapulmonary tuberculosis Tuberculous meningitis  Patients may present with a headache that is either intermittent or persistent for 2-3 weeks.  Subtle mental status changes may progress to coma over a period of days to weeks.  Fever may be low-grade or absent.
  • 37. Extrapulmonary cont Skeletal TB  The most common site of involvement is the spine (Pott disease).  Symptoms include back pain or stiffness.  Lower extremity paralysis occurs in as many as half the patients with undiagnosed Pott’s disease.  Tuberculous arthritis usually involves only 1 joint.  Although any joint may be involved, the hip or the knee is affected most commonly, followed by the ankle, elbow, wrist, and shoulder.  Pain may precede radiographic changes by weeks to months.
  • 38. Extrapulmonary cont Tuberculous lymphadenitis  The most common site is in the neck along the sternocleidomastoid muscle.  It usually is unilateral, with little or no pain.  Advanced disease may suppurate and form a draining sinus.
  • 39. Gastrointestinal TB  Any site along the gastrointestinal tract may become infected.  Symptoms are referable to the site infected, including the following:  Non healing ulcers of the mouth or anus  Difficulty swallowing with esophageal disease  Abdominal pain mimicking peptic ulcer disease with stomach or duodenal infection  Malabsorption with infection of the small intestine  Pain, diarrhea, or hematochezia with infection of the colon.
  • 40. Genital urinary TB  Reported symptoms include flank pain, dysuria, or frequency.  In men, genital TB may manifest as epididymitis or a scrotal mass.  In women, genital TB may mimic pelvic inflammatory disease.  TB causes approximately 10% of sterility in women worldwide and approximately 1% in industrialized countries.
  • 41. Cutaneous TB  Direct inoculation may result in an ulcer or wartlike lesion.  Contiguous spread from an infected lymph node typically results in a draining sinus.  Hematogenous spread may result in a reddish brown plaque on the face or extremities (lupus vulgaris) or tender nodules or abscesses.
  • 42. Other forms of extrapulmonary TB  TB of the pleura  TB peritonitis  TB pericarditis
  • 43. Diagnosis of TB  The diagnosis of TB starts with proper history and physical examination.  Laboratory examinations  AFB microscopy for sputum and aspirates  Culture - sputum, aspirates for EPT  Histological examination - Biopsy tissue  Gene Xpert (NAA test, RIF/MTB, LPA)  Interferon Gamma Release Assay  Radiological test, although alone NOT reliable  Chest X ray or CT scan  For patients unable to produce any sputum (eg, children), early morning gastric aspirate may produce a good specimen.
  • 44. Sputum smear  It is the gold standard investigation for PTB  Standard 2: All patients (adults, adolescents, and children who are capable of producing sputum) suspected of having pulmonary TB should have at least two, and preferably three, sputum specimens obtained for microscopic examination. When possible, at least one early morning specimen should be obtained.
  • 45. Sputum smear cont  Direct smears of unconcentrated sputum are common worldwide  They are fast simple and cheap  Ziehl Neelsen stain with Carbofuschin dye is more common
  • 47. Chest X ray  People with chest X ray suggestive of PTB should submit their sputum for microscopy
  • 48. Culture  Available culture methods use either solid or liquid media  A sample of sputum or tissue require initial liquefication and decontamination  Mostly used is N-acetyl –L-cysteine as a mucolytic in 1% NaCl  This kills other organisms, M.tb are protected by their fatty acid rich cell wall  The sample is then neutralized, centrifuged and the sediment is inoculated in the media  Uncontaminated fluid or normally sterile tissues should not be contaminated as some loss mycobacterial viability
  • 49. Culture cont  Solid culture media are of two general types:  Agar bases e.g Middlebrook 7H11  Egg based e.g Lowenstein Jensen  The BACTEC radiometric system for culturing mycobacteria  It is a liquid system which uses radioactive palmitate as a sole carbon source  Inclusion of p-nitro-alpha-acetylamino- - hydroxypropiophenone in the incubation media inhibit the growth of M.Tb complex (including M. bovis and M. africunum  But does not inhibit mycobacteria other than tuberculosis
  • 50.  Pleural, cerebrospinal, peritoneal, and pericardial fluids should be analyzed for protein and glucose (compared with simultaneous blood glucose).  Cell and differential counts should be obtained.  A high protein (> 50% of the serum protein concentration), lymphocytosis, and a low glucose are usually found in tuberculous infections, but neither their presence nor their absence is diagnostic.  For pleural tuberculosis the diagnostic yield can be increased by obtaining pleural tissue for histologic study and culture by needle biopsy at the time of diagnostic thoracentesis.  Peritoneal biopsies are best obtained via laparoscopy.
  • 51. Mantoux tuberculine skin test  Used for screening especially for children  Can also be used for high risk individuals  A purified protein derivative is injected intradermal in the forearm (0.1ml)  The induration is read after 48 to 72 hrs  Induration > 10mm in children less than 4 yrs a/c risk of disemminated disease  Induration >15mm in children more than 4 yrs is also significant
  • 52. False positive TST  Prior infections/exposures to non tuberculous mycobacterium  Recent BCG vaccination
  • 53. TB AND HIV  TB is the third highest cause of morbidity and mortality in Tanzania after HIV/AIDS and malaria  Immune compromised people are very prone to develop TB, including PLHIV  TB is the leading cause of death for PLHIV  HIV frequently co-exists with TB
  • 54. TB AND HIV  14 million people are co-infected world wide  9% of TB cases are attributable to HIV world wide  Infection after exposure10-20% vs 5,10%  Progressive primary disease after infection 30% vs 5 -10%  Reactivation of latent infection 5- 10% annual vs 5-10% lifetime
  • 55. TB in HIV Infection  In pre HIV era 80-85% of TB infection presented as PTB.  Up to 15% as EPTB  5% mixture of PTB and EPTB  While in HIV era 60-70% PTB,while EPTB 50-60%  PTB presentation depends on HIV progression  In low CD4 PTB presents with high fever,dyspnoea and wt loss  In low CD4 sputum smear often –ve,no typical chest x ray findings of PTB(cavitation or infiltates in lung apex)
  • 56.
  • 57. Treatment of tuberculosis  It is important with the aim of curing the patient and preventing the spread of the disease to the community.  Case definition in TB treatment  New case: a patient who has never had treatment for TB before or has been on treatment for not more than 4 weeks  Relapse: a patient declared cured or treatment completed who reports back to health services and is found to be AFB positive  Failure: a patient who, while on treatment, is AFB positive at 5-months or later during the course of treatment
  • 58. Case definition cont  Return after default: a patient who returns to treatment bacteriological positive, after having interrupted treatment for 2-months or more and who had been on RX for more than 4 weeks  Transfer-in: a registered TB patient on Rx received from another region  Other: any TB patient who does not fit in one of the above definitions
  • 59. TB treatment regimen  There are two TB treatment phases: initial phase (intensive) and continuation phase  During initial phase:  There is rapid killing of the TB bacilli  Initial phase takes 2months with 4 drugs  Patients mostly become non-infectious after about 2 weeks  During continuation phase:  Drugs kill the persisters  Prevent relapse after completion of treatment  Continuous phase takes 2 drugs for 4 or 6 months
  • 60. Treatment regimen cont  1st line drugs- isoniazid,rifampicin,rifapentine,rifabutin,ethambutol and pyrazinamide  2nd line drugs – cycloserine,ethionamide,levofloxacine,moxifloxacin,gat ifloxacine,P aminosalicylic acid,streptomycin,amikacin/kanamycin,capreomycin
  • 62. Reasons for combination therapy  the biological different populations of the bacteria needs specific metabolic acting drugs.  combination therapy reduces resistance. In each population there are spontaneous mutations of resistant bacteria which would be selected under inadequate therapy.  combination therapy reduces the toxicity of the different substances.
  • 63. Side effects of first line ant tuberculosis drugs  Isoniazid:-mild LFT elevation or hepatitis- peripheral neuritis-hypersensitivity  Rifampin:-orange colored secretions- hepatitis or thrombocytopenia-OCP may be ineffective  Pyrazinamide-hepatotoxicity- hyperuricemia  Ethambutol-optic neuritis (usually reversible)-decreased red-green color discrimination-GI tract disturbances- hypersensitivity
  • 64. Treatment of extrapulmonary TB  Most of extrapulmonary TB can be treated for 6 months,except TB of bone and joints can be treated for 6 to 9 months,Tb meningitis for 9 to 12 months.
  • 65. Drug Resistant TB This is a form of TB in which first-line anti-TB drugs have little or no effect against M. tuberculosis. The diagnosis is confirmed through molecular tests and culture and DST of M. tuberculosis strains. Four different categories of drug resistance have been identified: • Mono resistant TB: Resistance to any single first-line anti-TB drug. • MDR TB: Resistance to at least both isoniazid and rifampicin. • XDR TB: This is multidrug resistance, with additional resistance to any fluoroquinolones (ofloxacin, levofloxacin, moxifloxacin) and at least one of the three injectable drugs (amikacin, kanamycin, capreomycin).
  • 66. TB drug resistance  Multidrug resistance(MDR-TB)-resistance to at least Isoniazid and Rifampicin.  It is a man made phenomenon due to inadequate treatment regimen or poor adherence to treatment  It common to people with HIV and Tb coinfection  It causes pts to use 2nd line drugs with longer treatment duration,more toxicity and expensive
  • 67. Former MDR TB REGIMENS TANZANIA Group Drugs Group A – Fluoroquinolones Levofloxacin (Lfx), Moxifloxacin (Mfx), Group B – Injectable agents Kanamycin (Km), Amikacin (Am) ; Capreomycin (Cm) Group C – Other core second-line agents Ethionamide (Eto), Protionamide (Pto), Cycloserine (Cs), Linezolid (Lzd), Clofazimine (Cfz) Group D - Add-on agents (not part of the core MDR- TB regimen) D1 Pyrazinamide (Z), Ethambutol (E), High-dose isoniazid (Hh) D2 Bedaquiline (Bdq), Delamanid (Dlm) D3 p-aminosalicylic acid (PAS) Amoxicillin-clavulanate (Amx-Cl) Grouping of anti-TB agents used to treat DR-TB
  • 68. Former MDR TB REGIMENS TANZANIA (phasing out) Standardised short regimen 4-6 Km, Mfx, Pto, Cfz, E, Z, H(h) 5 Mfx Cfz E Z Individualized Long MDR TB Regimen; MDR TB 8 Km/Cm, Cs, Lfx, Eto, Z, 12 Cs, Eto, Z, Lfx Individualized Long MDR TB Regimen; XDR TB 12Cm Lfx, Bdq, Dlm6 , Lzd, Cfz, PAS. 12 Lfx, Lzd, Cfz, PAS ❑DR-TB is generally treatable, however, extensive treatment - 9 months up to 24 months ❑Using eligibility criteria patients can be started on; • Standardized shorter regimen (9-11 months) • Individuslized Long regimen (20 months) - MDR-TB patients • Individualised Long regimen (24 months) - XDR-TB patients
  • 69. SECOND LINE ANTI TB MEDICINES STOCKS Currently existing stock of recommended second line drugs and MOS Group A SOH MOS Group B SOH MOS Group C SOH MOS Lfx 500mg 65,800 7 Cfz 100mg 50,000 4 E 400mg 100,800 8 Bdq 100mg 22,550 12 Cs 250mg 0 - Dlm 50mg 2,016 Lzd 600mg 23,050 12 Z 500mg 443,520 11 PASER 1,2600 7 ETO 250mg 28,400 2 PTO 184,400 5
  • 70. Proposed regimens - Tanzania 1. Long regimen adults (routine)  6 Lfx - Bdq - Lzd - Cfz – Cs / 12 Lfx - Cfz - Cs  Substitute; E, Eto, PAS, Z, Dlm 2. Short regimen adults (Operational Research);  6 Bdq – Lzd – Lfx – Cfz – Cs – Z / 3-5 Lfx – Cfz – Cs – Z  6 Bdq – Dlm– Lfx – Cfz – Cs – Z / 3-5 Lfx – Cfz – Cs – Z 3. Short Regimen children (routine)  6 Lfx – Bdq – Lzd – Cs / 3 Lfx – Lzd – Cs  Substitute; PAS, Dlm, E, Eto, Z, Mfx  BQD not used for children <6yrs, Delanamid <3yrs  Treatment prolonged (12-15 mths)in selected cases ; meningitis, TB bone, Spine
  • 72. Extensive drug resistance TB  It is MDR plus resistance to floroquinolones and one of the 3 second line injectables.kanamycin,amikacin,capreomycin  South Africa has reported the number of XDR-TB  It is common in HIV pts  98% dies with an avarage of 25 days since admission
  • 74. Anti-TB resistance  Primary drug-resistance: “New Cases” Drug resistance in a patient who has never been treated for tuberculosis or received less than one month of therapy  Secondary (acquired) drug-resistance: “Previously Treated Cases” Drug resistance in a patient who has received at least one month of anti-TB therapy
  • 75. Prophylaxis and vaccination  All infant born to smear +ve mother are given INH 5mg/kg for six months.  Isoniazid Preventive Therapy (IPT)  Can be given to people with HIV who have a high TB risk and have been screened to exclude active TB  Adults: 300 mg daily for 6 to 9 months
  • 76. vaccination  Many countries use Bacillus Calmette-Guérin (BCG) vaccine as part of their TB control programs, especially for infants.  The protective efficacy of BCG for preventing serious forms of TB (e.g. meningitis) in children is greater than 80%
  • 77. references  Principles and practice of infectious diseaes 4th ed by Mandell L et al.  Medical microbiology 19th ed by Jawetz et al.  Harrison’s Principles of Internal medicine 16th ed by Kasper et al.  National guideline for management of HIV and TB latest edition.