AIR BORN DISEASE

Disease that transmitted by

inhalation

10/24/2023 1
 Outline

 Objective
 Introduction to Airborne Disease
 Cause
 Clinical Presentation
 Management
 Prevention & Control

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 Objective

At the end of this session, students will be able to:

 Define airborne Disease

 Identify cause

 List clinical presentation

 Manage patients with airborne diseases

 Design and implement prevention & control methods

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 1 MENIGITIS
Definitions
 An inflammation of membrane surrounding the brain
and spinal cord
 It can be caused by Bacteria, Viral, fungal other
organisms
 It further classified in to:
Aseptic Meningitis
Septic Meningitis
Tuberculosis Meningitis

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 Bacterial meningitis (Meningococcal)
Definitions: An acute or sub acute purulent infection of the
meninges.
It associated with CNS inflammatory reaction that may result in
unconsciousness, seizures, IICP and stroke.

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Cause

 Monocytogenes streptococcal aglactiae, group

B streptococcus, escherichia coli, and listerine
are major causes in infant
 Neisseria meningitides -meningococcal
meningitis
 Streptococcus pneumonae common in adult
 Haemophilus influenzae, streptococcus
pneumoniae pneumococcus are common
children and young adult
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 Bacterial meningitis cont’d
Epidemiology
 While the largest epidemics of meningococcal disease affect
mainly sub-Saharan African countries with meningitis belt,
epidemic meningitis becomes WW problem.
 African meningitis belt extends from Ethiopia in East to
Senegal in the west.
 The onset is generally in middle of dry season (Dec-Feb)
 N. Meningitides has 13 sero types
 Serotype (A, B, C, Y and W-135) are responsible for more than
90% of cases WW.
 Serotype A predominantly involved during Epidemics (1981, 1989,
2000)
 Type C also involved less extend

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 Bacterial Meningitis…
Mode of transmission:
 Directly by respiratory droplet from nose and throats
of infected person.
I/P: 2-10days
PC: As long as bacteria present in discharge
Susceptibility and Resistance
 Susceptibility is low and decrease with age
 Group specific immunity is unknown.

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 Bacterial meningitis cont’d
Pathogenesis 0f bacterial meningitis
 The infectious agent colonizes or establishes as localized infection of
the skin, nasopharynx, respiratory tract, gastrointestinal tract, or
genitourinary tract.
 Most meningial pathogens are transmitted through the respiratory
route,
 Once inside the CNS, the infectious agents likely survive.
 The presence and replication of infectious agents remain
uncontrolled and result in meningial inflammation
 Release of chemical reaction in Meninges and underlying cortex
result in thrombosis & decreased b/d flow to brain.
 Alteration in intracranial physiology
 Increased permeability of BBB
 cerebral oedema
10/24/2023
IICP 9
 Bacterial Meningitis cont’d
C/M
 Symptoms are result from infection & IICP
 Signs of cerebral Dysfunction
 Confusion
 Irritability
 Delirium
 Coma
 Usually accompanied by fever and photophobia
 Head ache: initial symptom
 Signs of meningial irritation (only approximately 50% of
patients with bacterial meningitis).

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 Bacterial Meningitis C/M Cont’d
Positive Kerning sign
 In a supine patient, flex the hip to 90° while the knee
is flexed at 90°.
 An attempt to further extension of the knee produces
pain in the hamstrings and resistance to further
extension.
Or
 When the pt lying with the thigh flexed on the
abdomen, the leg cannot completely extended

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 Bacterial
Bacterial meningitis cont’d
Meningitis C/M cont’d
 Positive Brudzinski sign
 Passively flex the neck while the patient is in a supine
position with extremities extended.
 This maneuver produces flexion of the hips in
patients with meningial irritation
 Or
 when the pt neck is flexed, flexion of leg & knee
occur
or
 Passive flexion of leg cause similar movement of the
other
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 Bacterial meningitis C/M cont’d

Nuchal Rigidity:
 Resistance to passive flexion of the neck is also a sign.
 Exacerbation of existing headache by repeated
horizontal movement of the head, at a rate of 2-3 times
per second, may also suggest meningial irritation.

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Clinical signs of Meningitis

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 Bacterial
Bacterial meningitis cont’d
Meningitis C/M cont’d
 Photophobia
 Seizure occur in approximately 30% of patients
 Sign of IICP;
 change in vital sign ,Bradycardia, Headache ,Vomiting,
decreased level of consciousness, Cranial nerve palsies,
Coma
 Rash
 Fulminating infection
 Occur in 10% (sudden onset, rapid course)
 Sign of septicaemia
 High fever, extensive purpuric lesion,
 Sock –death.
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 Bacterial Meningitis cont’d

Diagnosis

 Clinical and Epidemiological ground

 CSF analysis

 CSF gram staining

 CSF sensitivity test

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 Bacterial meningitis MX cont’d
MX
Un identified bacteria (Empirical) or clinical Treatment )
Benzyl Penicillin(crystalline penicillin)
C.A.F 500mg
Known Ethnology
 N.Meningitidis and S. pneumonae
Benzyl penicillin
 H. influenzae
¨ Chloramphenicole
¨ Alternatively
– Ampicillin ,Gentamycin, Ceftriaxone

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Recommended Empiric Antibiotics According to Predisposing Factors for
Patients with Suspected Bacterial Meningitis

Predisposing Feature Antibiotic(s)

Age 0-4 weeks Ampicillin plus cefotaxime or an amino glycoside

Age 1-3 months Ampicillin plus cefotaxime plus vancomycin

Age 3 months to 50 years Ceftriaxone or cefotaxime plus vancomycin

Ampicillin plus ceftriaxone or cefotaxime plus
Older than 50 years
vancomycin

Impaired cellular immunity Ampicillin plus ceftazidime plus vancomycin

Neurosurgery, head trauma,

Vancomycin plus ceftazidime
or CSF shunt

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 Specific Antibiotics and Duration of Therapy for Patients with Acute Bacterial Meningitis

Bacteria Antibiotic(s) Duration

S.Pneumoniae Penicillin G 10-14

Ceftriaxone or cefotaxime
Ceftriaxone or cefotaxime plus vancomycin or
Rifampin
H. Influenzae Ampicillin 7
Ceftriaxone or cefotaxime
N. Meningitides Penicillin G or Ampicillin 7
L .Monocytogenes Ampicillin or penicillin G plus an aminoglycoside 14-21

S. Agalactiae Penicillin G plus an aminoglycoside, if warranted 14-21

Enterobacteriaceae Ceftriaxone or cefotaxime plus an aminoglycoside 21

P. Aeruginosa Ceftazidime plus an aminoglycoside 21

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 Bacterial Meningitis MX cont’d

Surgical Care
– In certain cases of increased ICP, repeated lumbar puncture
or the insertion of a ventricular drain may be necessary to
relieve the effects of increased ICP.
Consultations: Consultation with an infectious diseases specialist
Diet: No strict dietary restriction is necessary.

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 Bacterial Meningitis cont’d

Prevention and control

 Meningitis is weekly reportable diseases
 Educate personal hygiene
 Prevent over crowding
 Vaccination particularly in time of epidemic
 Chemoprophylaxis
 Rrefampicin .20 mg/kg/d for 4 days
 Sulphonamide can also be used.
 Report to authority
 Treatment of cases
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 Bacterial Meningitis cont’d

Complications
 Hearing impairment
 Obstructive hydrocephalus
 Brain parenchymal damage:
This is the most important feared complication of
bacterial meningitis.
 It could lead to sensory and motor deficits,
cerebral palsy, learning disability

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 Tuberculosis

Definitions
A Chronic infectious disease important as major
cause of death and illness in many parts of the
world.
Aetiology
 M. Tuberculosis (most common cause)
 M. Bovis (caw) avium (birds & man)
 M. Africanum.
 M. kansasii.
 M. interacellularis.
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 Characteristics of mycobacterium

 Mycobacterium is slender, road, shaped, acid fast

aerobic organism with complex cell wall

 It also known as Tubercle or acid fast (AFB) Bacilli.

 Remain in tissue and dormant for many years.

 Withstand weak disinfectants and survive in a dry

state for weeks, but can only grow in a host

organism
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 History of TBC
 TB is as old as the human species.

 Fragments from the spinal column of Egyptian mummies dating

from 2400 BC show definite pathological signs of tubercular decay.

 The name “tuberculosis” has been used from the middle of the last

century.

 Tuberculosis, also called phthisis or consumption, and nicknamed

“white plague”, first appeared in Greek literature.

 At around 460 BC Hippocrates described it as the most

widespread disease of its time

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 2. TUBERCULOSIS (Mycobacterium TBC)
Epidemiology

 TB caused great public concern (19th and early 20th

centuries ) as the endemic disease of the poor.
 Following the development of effective treatment,
in the 1950s the general view, especially in
industrialised countries, the disease no longer
posed a public health threat .

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 TB Epidemiology cont’d

 In industrialised countries the steady drop of TB incidence

began in the mid-1980s and then stagnated or even
began to increase.
 In order to intensify efforts to limit its spread, in 1993, TB
was declared a “global emergency
 TB ranks seventh as a global cause of death, but may
likely to remain a major killer through 2020, if not more
focused attention is given
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 TB Epidemiology cont’d

 Affects all sex and ages

 Age b/n 15-45 seriously are affected.

 About one third of the world’s population is infected

by mycobacterium tuberculosis.
 M. Tuberculosis kills more people than any other
single infectious agent

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 TB Epidemiology cont’d

 Deaths from TB comprise 25% of all avoidable

deaths in developing countries.
 95% of TB cases and 98% of TB deaths are in
developing countries.
 Rate of sero-posetivily for HIV in TB cases reach
60-70% in Africa and 40% of TB pt test positive
for HIV in Ethiopia
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 TB Epidemiology cont’d

 In Ethiopia TBC is the leading cause of morbidity,

the fourth cause of hospital admission and 2nd
cause of hospital death.
 Ethiopia is one the 22 HBCs.

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 TB Epidemiology cont’d

According to the WHO global TB report 2011, in

Ethiopia there were an estimated
220,000 (261 per 100,000) incident
330,000 (394 per 100,000) prevalent
29,000 (35 per 100,000) deaths

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 TB Epidemiology cont’d

According to health and health related indicators of the FMoH,

tuberculosis is
 The second cause of death in Ethiopia

 a total of 159,017 TB cases were notified in Ethiopia

 Among these 151,866 (95.5%) were new cases of TB, all

forms

The proportion of new smear-positive, smear negative and EPTB

among all new cases is 32.7%, 34.9%, and 32.5% respectively

Retreatment cases represent about 2.9% of all TB cases notified

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 Reason for increasing Burden of TB globally

 Poverty and the widening gap between rich and poor in various
Populations,
 changing demography (increasing world population and
changing age structure);
 Neglect of disease (inadequate case detection ,Diagnosis &
Treatment (cure)
 Collapse of health infrastructure
 economic crisis
 Impact of HIV pandemic
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Reservoir: Human, cattle, bird (avium)
M. T
 Air born infection
 Spread by minute particle called droplet nuclei.
 Ingestion of unpasteurized milk

P.C.: As far as the bacilli present in sputum

IP : 12 weeks

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 Risk of TB infection

 Depends on the extent of an individual’s exposure to

droplet nuclei and on susceptibility to infection
 Two factors determine an individual’s risk of exposure:

1. The concentration of droplet nuclei in contaminated air

2. The length of time spent breathing that air
high with close, prolonged, indoor exposure to a person
with sputum smear-positive pulmonary TB.

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 Groups at High Risk for TB exposures
 Prolonged close indoor contact of person with in facetious
TB
 Foreign born persons from where TB is uncommon
 Migrant workers or homeless persons
 Under five children
 Immunocompromised persons
 Any person with pre existing medical conditions such as
diabetes
 Malnutrition
 Age
 Presence of HIV infection

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 Natural history of TBC
 In 90-95% persons infected individuals M. Tuberculosis,
suppressed (silent focus) causing ‘latent M. Tuberculosis
infection
 5-10% of such infected persons (primary infection) develop
active disease
 If untreated, within 5 years
• Death in at least half of the patients
• 20 to 25% could have natural healing
• 25 to 30% could remain chronically ill, thus continuing to
spread the disease in the community

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 Pathophysiology of pulmonary TBC
 Susceptible individuals inhales mycobacterium bacilli
 The bacilli initiate granulomatous inflammatory
response
 the hyper sensitivity response evoked is responsible for
tissue distraction
 2-10 weeks after exposure accumulation of exudates in
alveoli Causing bronchopneumonia, pneumonitis
(primary infection).

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 Pathophysiology of pulmonary TBC

 Formation of new tissue mass of granulomas which are

clumps of live and dead bacilli surrounded by
macrophages forming protective wall.
 Fibrous tissue (its internal portion is called Ghon
tubercle which undergo necrosis and forms a yellowish
cheesy mass called caseous necrosis,
 Healing of the lesion occur as collagenous scar tissue
formation and encapsulated lesion
 Lesions calcified and seen under x-ray film
 Secondary TB occur from reactivation of previously
healed primary lesion in impaired body defence
mechanisms

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Outcome of primary infection
No clinical disease
 Positive Tuberculin skin test
 90% cases
Hypersensitivity
Pulmonary and pleural Cxn
Pleural effusion
Tuberculosis pneumonia
Disseminated Disease
Lymphadenopaty
Meningitis
Pericardits
Miliary Disease
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 Active VS latent TB
Characteristics
Active TB latent TB
M. tuberculosis in the Yes Yes
body
Tuberculin skin test reactio Positive Positive
Symptoms Yes No
Chest x-ray Abnormal if Normal
pulmonary
Sputum smears and *Positive/negative Negative
culture
Infectiousness Pulmonary TB is Not
infectious
A case of TB
10/24/2023 Yes No 41
 Post primary /Secondary TB)

 TB occur after latent periods of months or years of

primary infection
 It may occur either by reactivation or re-infection
 It can involve
 Pulmonary
 Extra pulmonary

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 Pulmonary TBC
 Most common and potentially most contagious type of
active TB.
 Small areas in the lung infected with the bacilli gradually
merge to form a bigger lesion filled with infected material.
 Usually Upper lobe infiltrate, progressive pneumonia and
tuberculosis empyema
 This material can become liquid, which is then coughed
out, leaving a cavity in the lung

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 Pulmonary TBC cont’d
 The process continues causing extensive damage to the
lung tissue and its blood vessels, generating more
infectious material and inflammation
 In the early stages , someone with pulmonary TB may
well not be infectious and have few easily definable
symptoms.
 As the disease progresses and causes more damage,
they will become infectious and experience worsening
symptoms.
 The challenge is to identify people in the early stages to
prevent transmission

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 Extra pulmonary TBC
 TB can affect any organ in the body including:
 Lymph nodes (most commonly Cervical lymph glands )
 Bone (particularly the spine)
 Kyphosis
 Lordosis: out ward curvature of Lumbar Spine
 Scoliosis (lateral curvature of Spine
 Pleural cavity (causing pleural effusion)
 Kidney and genitourinary tract
 Intestines and peritoneum
 Pericardium
 CNS (meningitis, cerebral tuberculoma)
 Skin
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 Sign and symptoms of tuberculosis
General pulmonary TBC Extra-pulmonary

Fever(Low grade) Asymptomatic when Localised pain/swelling

Night sweats lesion confined to apex (depending on site of
unexplained initially Dry cough then disease)
Weight loss productive cough Matted, drainage of pus and
Fatigue Chest pain slow pain less enlarged
Loss of appetite Shortness of breath lymph node
Later blood traces are Swelling of bone
coughed up in the Asciets
sputum (haemoptysis) Neck stiffness
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 Diagnostic Methods Of Tuberculosis –

1. History and S/S of tuberculosis

2. The Bacteriologic Examination
1. Sputum Smear Examination for AFB:
2. Sputum culture
3. Light Emitting Diode (LED) Fluorescence Microscopy
4. Line Probe Assay (LPA
5. GeneXpert MTB/RIF
3. Radiology (Chest x-ray),
4. Histopathology , Histo-pathological exam by FNA
5. ESR

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 TB Related Concepts/Definitions

TB cases findings
 TB case finding means identifying TB suspect within a health
facility and community as early as possible.
 Any person who has coughed for 2 weeks or more is a “TB
suspect” for pulmonary tuberculosis and should have a
sputum examination

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 A Definite/proven case of tuberculosis

 A patient with two sputum smears (one for HIV positive

patients) or culture positive for MTBC or a patient with

MTBC complex identified from a clinical specimen, either
by culture or by a newer method such as molecular line
probe assay or one in which a health worker has diagnosed
TB and has decided to treat the patient with a full course
of TB treatment.

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 Classification of TB Cases

1. Anatomical site of disease;

2. Bacteriological results (including drug
resistance)
3. History of previous treatment;
4. HIV status of the patient

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 Based on anatomical site

1. Pulmonary tuberculosis (PTBC)

2. Extra-pulmonary (EP TBC):

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 Pulmonary Tuberculosis (PTBC)
 Lesion in the lung

 Refers to a case of TB involving the lung parenchyma. E.g.

Miliary tuberculosis
 Include a patient with both pulmonary and extra pulmonary TB

 It further classified as

 Sputum Smear-positive Pulmonary TB (PTB+): Any patient

with both sputum smear positive pulmonary TB (PTB+) and
Extra-pulmonary TB (EPTB) should be classified as PTB+
 Sputum Smear-negative Pulmonary (PTB-):

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 Extra-pulmonary (EP TBC):

 Refers to a case of TB involving organs other than the

lungs, e.g. pleura, lymph nodes, abdomen, genitourinary

tract, skin, joints and bones, meninges

 TB in organs other than the lungs, proven by one culture-

positive specimen from an extra-pulmonary site or histo-

pathological evidence from a biopsy, Or TB based on strong

clinical evidence consistent with active EPTB and the decision

by a physician to treat with a full course of anti-TB therapy.

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 Based on bacteriological results

Smear positive PTB+

Patient with at least two initial sputum smear examinations
positive for AFB by direct microscopy, Or patient with one
initial smear examination positive for AFB by direct
microscopy and culture positive, Or patient with one initial
smear examination positive for AFB by direct microscope
and radiographic abnormalities consistent with active TB as
determined by a clinician.

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 Smear negative PTB-
1. A patient having symptoms suggestive of TB with at least 3
initial smear examinations negative for AFB by direct
microscopy and

 No response to a course of broad-spectrum

antibiotics again three negative smear examinations

by direct microscopy, Radiological abnormalities
consistent with pulmonary tuberculosis

 Decision by a clinician to treat with a full course of

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 Based History of previous treatment
New patients
 Have never had treatment for TB, or have taken anti-TB drugs for less than 1
month.
 May have positive or negative bacteriology and may have disease at any
anatomical site.
Previously treated patients
 Have received 1 month or more of anti-TB drugs in the past
 May have positive or negative bacteriology and may have disease at any
anatomical site.
 They are further classified by the outcome of their most recent course of
treatment.
1. Relapse (R)
2. Treatment after Failure (F)
3. Return after default (D)
4. Transfer in (T)
5. Other (O):
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Relapse (R):
 A patient declared cured or treatment completed of any form
of TB in the past, but who reports back to the health facility
and is now found to be AFB smear-positive or culture positive.
Treatment after Failure (F):
 A patient who, while on treatment, is smear-positive at the
end of the fifth month or later, after commencing.
 Also includes a patient who was initially sputum smear-
negative but who becomes smear-positive during treatment
Return after default (D)
 A patient previously recorded as defaulted from treatment
and returns to the health facility with smear-positive sputum
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Transfer in (T)

 A patient who is transferred in to continue treatment in a given

treatment unit after starting treatment in another treatment unit.

 The patient must have taken anti-TB treatment for at least one month

or 4 weeks in the transferring health facility.

 The receiving treatment unit should register such patients as

“transfer in” or “T” in the unit TB registers

Other (O):

 A patient who does not fit in any of the above mentioned categories

(e.g., a PTB smear negative who returns after treatment interruption)

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 Based on HIV status
Smear-positive PTB:
 One sputum smear examination positive for Acid-fast bacilli(AFB) and
 Laboratory confirmation of HIV infection, or
 Strong clinical evidence of HIV infection
Smear Negative PTB:
 At least three sputum specimens negative for AFB, and
 Radiologic abnormalities consistent with active tuberculosis, and
 Laboratory confirmation of HIV infection, or
 Strong clinical evidence of HIV infection, and
 Decision by a clinician to treat with full course of Anti-TB chemotherapy, or
 A patient with AFB smear-negative sputum which is culture-positive for MTB.
Extra pulmonary TB
 One specimen from an extra pulmonary site culture for MTB or smear Positive
for AFB, or Histological or strong clinical evidence consistent with active extra
pulmonary TB.
 Laboratory confirmation of HIV infection, or Strong clinical evidence of HIV
infection, and Decision by a clinician to treat with full course of Anti-TB
chemotherapy.
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 Treatment outcome of TB patients

 Cured

 Treatment completed

 Treatment failure

 Died

 Defaulter

 Transfer out

 Treatment success
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Cured:
• A patient whose sputum smear or culture was positive at
the beginning of the treatment but who was smear- or
culture-negative in the last month of treatment and on at
least one previous occasion
Treatment completed:
• A patient who completed treatment but who does not
have a negative sputum smear or culture result in the last
month of treatment and on at least one previous occasion

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Treatment failure:
A patient whose sputum smear or culture is positive at 5 months or
later during treatment. or Patients found to harbour a multidrug-
resistant (MDR) strain at any point of time during the treatment,
whether they are smear-negative or -positive.
Died: A patient who dies for any reason during the course of TB
treatment
Defaulter: A patient who has been on treatment for at least four
weeks and whose treatment was interrupted for eight or more
consecutive weeks
Transfer out: A patient who has been transferred to another
recording and reporting unit and whose treatment outcome is
unknown.
Treatment
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success: A sum of cured and completed treatment 62
 TB Treatment

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 Objective of TB treatments

1. Cure the patient

2. Prevent death from active TB or its late effects
3. Prevent relapse
4. Prevent the development of drug resistance
5. Decrease TB transmission rate

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 Anti TB Treatment

The anti TB medication should be

1. An appropriate combination of drugs
2. Prescribed in the correct dosage
3. Taken regularly by the patient and
4. For a sufficient period of time

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 TBC-Treatment
The essential anti-TB drugs
Bactericidal ability:
 Isoniazid & Rifampicin are the most powerful bactericidal drugs,
active against all populations of TB bacilli
 Pyrazinamide and streptomycin are also bactericidal against certain
populations of TB bacilli.
 Pyrazinamide is active in an acid environment against TB bacilli inside
macrophages.
 Streptomycin is active against rapidly multiplying extra cellular Bacilli.
Sterilizing ability
 Ethambutol and Thiocetazone are bacteriostatic drugs used in
association with more powerful bactericidal drugs to prevent the
emergence of resistant bacilli
10/24/2023 resistance: INH and Refampicin
Prevent 66
 Drugs used for Treatment of TBC are
1. Streptomycin (S) bactericidal (15mg/kg/IM/daily (12-18)
IM injection
2. Refampin (R) bactericidal 10mg/Kg (8-12)450-600mg
po/daily
3. Ethambutole (E) bacteriostatic 15mg/Kg (15-20) 400 mg
PO daily BID
4. Thiacetazone (T) bacteriostatic 2.5 mg/Kg150mg PO daily
not applicable
5. Isonazid (INH) (H) bactericidal 5 mg/Kg (4-6) 300mg PO
daily
6. Parazinanide (Z) bactericidal 25mg/Kg(20-30) 400mg PO
TID

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 Drugs available in fixed dose combination
(FDC)

1. Rifampicin, Isoniazid, Pyrazinamide and

Ethambutol (RHZE) 150/75/400/275 mg;

2. Rifampicin, Isoniazid and Pyrazinamide (RHZ

150/75/400 mg);

3. Rifampicin and Isoniazid (RH 150/75 mg);

4. Ethambutol and Isoniazid (EH 400/150mg)

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The drugs available as single (loose) drug:

1. Ethambutol 400 mg
2. Isoniazid 100 mg and 300 mg
3. Streptomycin sulphate vials 1 g

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 Phases of TB treatment

1. Intensive (initial) phase

2. Continuation phase

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 Intensive (initial) phase
 Consists of treatment with combination of four drugs for the
first 8 weeks for new cases

 Combination of five drugs for the first eight weeks followed

by four drugs for the next four weeks for re-treatment cases

 Renders the patient non-infectious by rapidly reducing the

load of bacilli in the sputum, usually within 2-3 weeks
except in case of drug resistance

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 Continuation Phase

 Immediately follows the intensive phase

 Iis important to ensure cure or completion of treatment
 is necessary in order to avoid relapse after completion of
treatment
 Requires treatment with a combination of two drugs, to be
taken for 4 months for new cases and treatment with a
combination of three drugs for re-treatment cases for
5months.

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 BASICS OF DRUG RESISTANT TUBERCULOSIS

• TB is considered drug-resistant (DR) when

mycobacterium tuberculosis) is not killed by anti-TB
drugs and can be confirmed by a laboratory test
called drug susceptibility test (DST)

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 Forms of DR-TB

1. Mono-resistant TB:
2. Poly-resistant TB:
3. Multi-drug resistant TB:
4. Extensive–drug resistant TB:

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Mono-resistant TB: Resistant to one first-line anti-TB drug.
I.e HRZES
Poly-resistant TB: Resistance to more than one first line
anti-TB drugs, but not to both Isoniazed and refampicin
• Example: HE-resistant, ES-resistant etc

Multi-drug resistant TB: Resistant to at least both HR

Extensive–drug resistant TB:
• Resistance to at least HR, and to any fluoroquinolone,
and to at least one of the three following injectable
drugs used in anti-TB treatment: capreomycin,
kanamycin and amikacin
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 Potential Causes of Resistance
Health-care Drug related factors: Patient- related factors:
provider/program inadequate supply inadequate drug intake
related factors or quality
 Inappropriate  Poor quality  Poor
guidelines  Unavailability of adherence/default
 Non-compliance with certain drugs  Lack of or inadequate
guidelines due to stock- patient information
 Absence of guidelines outs of delivery  If Treatment not given
 Poor training disruptions for free
 Poor supervision  Poor storage  Lack of transportation
 No monitoring of conditions money or support
treatment  Wrong doses or  Drug adverse
 Poorly organized or combinations effects/interaction,
funded TB control manufacture  Social barriers
program related)  Mal-absorption
 Inadequate regimens  Substance/alcohol
 Lack of DST dependence
Poor access to health
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 Risk Factors For MDR-TB

 Previous exposure to Anti-TB treatment

 Exposure to a known MDR-TB case

 History of using poor or unknown quality TB drugs

 Treatment in poorly-performing control program

 Co-morbid conditions associated with mal-absorption

 HIV/AIDS

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 MDR-TB suspects

 Treatment Failure of previously treated cases

 Symptomatic close contacts of confirmed MDR-TB cases
 Symptomatic individuals from known high risk groups
 Previously treated cases
 Failure
 New cases ( smear +ve & -ve) who remain smear positive at the
end of third month
 Other retreatment cases: more than 8 weeks…
 defaulted patients coming with smear negative TB, EPTB, or
previously treated patients with unknown treatment outcome
 SS+ve interrupters who took treatment for more than 8 weeks…

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 General principle of treating MDR-TB

 Include at least five drugs

 Include any first line to which the strain is susceptible

 Include an injectable for prolonged period ( minimum

of six month)
 Include a quinolone

 Consider drug resistance data

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MDR-TB treatment is complicated
 It require 18-24 month treatment of chemotherapy

 Patient remain infectious for longer

 Patient requires direct observation while taking medication and

have complex psychological, social and economic needs

 Second line anti-TB drugs regimens may cause serious side

effects, which required high level of medical management

 The drugs are very expensive and in short supply

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 Nursing interventions in TB Mx

 Patient education
 Monitor side effect
 Drug adherence(education)
 Balanced diet

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 TBC- Prevention& control

TB prevention and control is the role of every body

 Chemotherapy for cases using DOTS
 Chemoprophylaxis /INH for 6 month)
 Vaccination of under one children by BCG
 Public health education
 Promptly identify potentially infectious cases (triage),
separate them, control the spread of pathogens (cough
etiquette) and minimize time in health care facilities.
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 Assignment

Leprosy

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