Tuberculosis and Suppurative

Lung diseases
Dr TSM
31.1.2022
Tuberculosis
 Outlines

 Epidemiology
 Pathology and pathogenesis
 Factors increasing the risk of TB
 Clinical features
 Investigations and Diagnosis
 Management
 latent TB
 Drug-resistant TB
 Prognosis
 Epidemiology
 Tuberculosis (TB) is one of the most prevalent infections of human beings
and contributes considerably to illness and death around the world

 It is caused by infection with Mycobacterium tuberculosis (MTB), which is

part of a complex of organisms including M. bovis (reservoir cattle) and M.
africanum (reservoir humans)

 An estimated 9.6 million new cases were recorded in 2014, with the
majority presenting in the world’s poorest nations, which struggle to cover
the costs associated with management and control programmes

 In the same year, 1.5 million men, women and children died of TB, and TB
continues to rank alongside HIV as a leading cause of death
 Pathology and pathogenesis
 M. bovis infection arises mainly drinking non-sterilised milk from infected
cows
 M. tuberculosis is spread by the inhalation of aerosolised droplet nuclei
from other infected patients
 Once inhaled, the organisms lodge in the alveoli and initiate the
recruitment of macrophages and lymphocytes
 Macrophages undergo transformation into epithelioid and Langhans cells,
which aggregate with the lymphocytes to form the classical tuberculous
granuloma
 Numerous granulomas aggregate to form a primary lesion or ‘Ghon focus’
(a pale yellow, caseous nodule, usually a few millimetres to 1–2 cm in
diameter), which is characteristically situated in the periphery of the lung.
 Spread of organisms to the hilar lymph nodes is followed by a similar
pathological reaction, and the combination of the primary lesion and
regional lymph nodes is referred to as the ‘primary complex of Ranke’.
• Reparative processes encase the primary complex in a fibrous capsule,
limiting the spread of bacilli.
• If no further complications ensue, this lesion eventually calcifies and is
clearly seen on a chest X-ray.
• Lymphatic or haematogenous spread may occur before immunity is
established, however, seeding secondary foci in other organs, including
lymph nodes, serous membranes,meninges, bones, liver, kidneys and lungs,
which may lie dormant for years
• The only clue that infection has occurred may be the appearance of a cell-
mediated, delayed-type hypersensitivity reaction to tuberculin,
demonstrated by tuberculin skin testing or an interferon gamma release
assay (IGRA): so-called latent TB
• If these reparative processes fail, primary progressive disease ensues .
• The estimated lifetime risk of developing disease after primary infection is
10%, with roughly half of this risk occurring in the first 2 years after
infection.
Factors increasing the risk of TB
Natural history of untreated primary
TB
 Clinical features
Pulmonary disease
Primary Pulmonary TB
• Primary TB refers to the infection of a previously uninfected (tuberculin-
negative) individual.
• A few patients develop a self limiting febrile illness but clinical disease
occurs only if there is a hypersensitivity reaction or progressive infection
• Progressive primary disease may appear during the course of the initial
illness or after a latent period of weeks or months.
Miliary TB
• Blood-borne dissemination gives rise to miliary TB
• is characterised by 2–3 weeks of fever, night sweats, anorexia,
weight loss and a dry cough.
• Hepatosplenomegaly may develop and the presence of a headache
may indicate coexistent tuberculous meningitis.
• Auscultation of the chest is frequently normal but in more advanced
disease widespread crackles are evident
• Fundoscopy may show choroidal tubercles.
• The classical appearances on chest X-ray are of fine 1–2 mm lesions
(‘millet seed’) distributed throughout the lung fields
• Anaemia and leucopenia reflect bone marrow involvement.
• ‘Cryptic’ miliary TB is an unusual presentation sometimes seen in
old age
Cryptic TB
 Post-primary pulmonary TB
Exogenous (‘new’ infection) or endogenous (reactivation of a dormant
primary lesion) infection
• The onset is usually insidious, systemic symptoms include fever, night
sweats, malaise and loss of appetite and weight, and are accompanied by
progressive pulmonary symptoms
• Radiological changes include ill-defined opacification in one or both of the
upper lobes, and as progression occurs, consolidation, collapse and
cavitation develop to varying degrees .
• It is often difficult to distinguish active from quiescent disease on
radiological criteria alone but the presence of a miliary pattern or cavitation
favours active disease.
• In extensive disease, collapse may be marked and results in significant
displacement of the trachea and mediastinum
• Occasionally, a caseous lymph node may drain into an adjoining bronchus,
leading to tuberculous pneumonia.
 Clinical features: Extrapulmonary
disease
Lymphadenitis
• Cervical and mediastinal glands are affected most frequently, followed by
axillary and inguinal
• The nodes are usually painless and initially mobile but become matted
together with time.
• When caseation and liquefaction occur, the swelling becomes fluctuant and
may discharge through the skin with the formation of a ‘collar-stud’ abscess
and sinus formation.
Pericardial disease
• Pericardial effusion and constrictive pericarditis.
• Pulsus paradoxus, a raised JVP, hepatomegaly, prominent ascites and
peripheral oedema are common to both types.
• Pericardial effusion is frequently blood-stained.
• The addition of glucocorticoids to antituberculosis treatment has been
shown to help both forms of pericardial disease.
Gastrointestinal tuberculosis
• Can affect any part of the bowel
• Ileocaecal disease accounts for approximately half of abdominal TB cases.
• Fever, night sweats, anorexia and weight loss are usually prominent and a
right iliac fossa mass may be palpable.
• Up to 30% of cases present with an acute abdomen.
• Tuberculous peritonitis is characterised by abdominal distension, pain and
constitutional symptoms.

Central nervous system disease

• Meningeal disease -the most important form of central nervous system TB.
• Unrecognised and untreated, it is rapidly fatal.
• Even when appropriate treatment is prescribed, mortality rates of 30% have
been reported, while survivors may be left with neurological sequelae.
Bone and joint disease
• The spine is the most common site for bony TB (Pott’s disease), typically
involves the lower thoracic and lumbar spine.
• Paravertebral and psoas abscess formation in the inguinal region.
• TB can affect any joint but most frequently involves the hip or knee.

Genitourinary disease
• are rare with renal tract TB
• Haematuria, frequency and dysuria are often present, with sterile pyuria found on
urine microscopy and culture.
• In women, infertility from endometritis, or pelvic pain and swelling from
salpingitis or a tubo-ovarian abscess occurs occasionally.
• In men, genitourinary TB may present as epididymitis or prostatitis.
CXR
 Classification of Anti TB drugs
First line drugs Second line drugs
 Isoniazid  Ethionamide
 Rifampicin  Kanamycin
 Pyrazinamide  Capreomycin
 Ethambutol  Amikacin
 Streptomycin  Para-aminosalicylic acid
 Fluoroquinolone
 Management
Chemotherapy
Treatment is based on the principle of
• Initial intensive phase - to reduce the bacterial population rapidly,
followed by
• Continuation phase - to destroy any remaining bacteria
• Standard treatment involves 6 months’ treatment with isoniazid and
rifampicin, supplemented in the first 2 months with pyrazinamide and
ethambutol
• Six months of therapy is appropriate for all patients with new-onset
pulmonary TB and most cases of extrapulmonary TB.
• 12 months of therapy is recommended for meningeal TB, including
involvement of the spinal cord in cases of spinal TB
• Pyridoxine should be prescribed in pregnant women and malnourished
patients to reduce the risk of peripheral neuropathy with isoniazid.
• patients can be assumed to be non-infectious after 2 weeks of appropriate
therapy.
• Glucocorticoids reduce inflammation and limit tissue damage; they are
currently recommended when treating pericardial or meningeal disease.
• Surgery should be considered in cases complicated by massive
haemoptysis, loculated empyema,constrictive pericarditis, lymph node
suppuration, and spinal disease with cord compression, but usually only
after a full course of antituberculosis treatment.
• The effectiveness of therapy for pulmonary TB is assessed by further
sputum smear at 2 months and at 5 months.
• Treatment failure is defined as a positive sputum smear or culture at 5
months or any patient with a multidrug-resistant strain, regardless of
whether they are smear-positive or negative.
• Extrapulmonary TB must be assessed clinically or radiographically, as
appropriate.
 Control and prevention
• TB is preventable, particularly so in those with latent TB.
• latent TB is an important component of this goal.
Detection of latent TB
• The majority of individuals exposed to MTB harbour the bacteria,which
remain dormant.
• They do not develop any signs of active disease and are non-infectious.
• They are however, at risk of developing active TB disease and becoming
infectious.
• The lifetime risk of TB disease for a person with documented latent TB
infection is estimated at 5–15%, with the majority of cases occurring within
the first 5 years after initial infection.
• Latent TB may be identified by the presence of immune responses to M.
tuberculosis antigens.
• Contact tracing is a legal requirement in many countries
• Cases are commonly identified using the tuberculin skin test or an IGRA .
• Chemoprophylaxis should be considered for HIV-infected close contacts
of a patient with smear-positive disease.
• A course of rifampicin and isoniazid for 3 months or isoniazid for 6 months
is effective.
• False-positive Tuberculin skin testing - BCG vaccination and in non-
tuberculous mycobacteria
• Falsely negative - immunosuppression or overwhelming TB infection.
• IGRAs detect the release of interferon-gamma (IFN-γ) from
• sensitised T cells in response to antigens
• IGRAs are more specific than skin testing
 TB and HIV/AIDS

 It is recommended that all patients with TB should be tested for HIV

infection.
 Mortality is high and TB is a leading cause of death in HIV patients.
 Drug-resistant TB
• Drug-resistant TB is defined by the presence of resistance to any first-line
agent.
• Multidrug-resistant tuberculosis (MDR-TB) is defined by resistance to at
least rifampicin and isoniazid, with or without other drug resistance.
• Extensively drug-resistant tuberculosis (XDR-TB) is defined as resistance
to at least rifampicin and isoniazid, in addition to any quinolone and at least
one injectable second-line agent.
• An estimated 9.7% of people with MDR-TB have XDR-TB. The
prevalence of MDR-TB is rising
• It is more common in individuals with a prior history of TB, particularly if
treatment has been inadequate, and those with HIV infection.
• Diagnosis is challenging,especially in resource-poor settings, and
although cure may be possible, it requires prolonged treatment with less
effective,more toxic and more expensive therapies.
• The mortality rate from MDR-TB is high and that from XDR-TB higher
still
 Vaccines

• BCG (the Calmette–Guérin bacillus), a live attenuated vaccine derived

from M. bovis, is the most established TB vaccine.
• It is administered by intradermal injection and is highly immunogenic.
• BCG appears to be effective in preventing disseminated disease,including
tuberculous meningitis, in children, but its efficacy in adults is inconsistent
and new vaccines are urgently needed.
• Current vaccination policies vary worldwide according to incidence and
health-care resources, but usually target children and other high-risk
individuals.
• BCG is very safe, with the occasional complication of local abscess
formation.
• It should not be administered to those who are immunocompromised (e.g.
by HIV) or pregnant.
 Prognosis

• Following successful completion of chemotherapy, cure should be

anticipated in the majority of patients.
• There is a small (< 5%) and unavoidable risk of relapse.
• Most relapses occur within 5months and usually have the same drug
susceptibility.
• In the absence of treatment, a patient with smear-positive TB will remain
infectious for an average of 2 years; in 1 year, 25% of untreated cases will
die.
• HIV-positive patients have higher mortality rates and a modestly increased
risk of relapse.
Factors contributing to the emergence of
drug-resistant tuberculosis

 Drug shortages
 Poor-quality drugs
 Lack of appropriate supervision
 Transmission of drug-resistant strains
 Prior antituberculosis treatment
 Treatment failure (smear-positive at 5 months)
Suppurative Lung diseases
 Suppurative Lung diseases
• Disorders associated with pus formation within the
lungs and named according to site

Bronchi –Bronchiectasis
Lung parenchyma—Lung abscess
Pleural space– Empyema
 Bronchiectasis
• Irreversible dilatation of bronchi and bronchioles
 Investigations

• Sputum culture may reveal Pseudomonas aeruginosa and

Staphylococcus aureus, fungi such as Aspergillus and various
mycobacteria.
• Chest X-ray - thickened airway walls, cystic bronchiectatic spaces
and associated areas of pneumonic consolidation or collapse may be
visible.
• CT is much more sensitive and shows thickened, dilated airways
• Spirometry-obstructive pattern
• Bronchoscopy-to localize site of haemoptysis or exclude obstruction
• Serum immunoglobulin
• Sweat test in cystic fibrosis
• Aspergillus precipitins or skin prick test
 Management

• Postural drainage should be performed twice daily

• Chest physiotherapy
• Antibiotics according to sensitivites
• Bronchodilators
• Corticosteriods
• Surgery
 Lung abscess
• A localized area of destruction of lung parenchyma in which
infection by pyogenic organism results in tissue necrosis and
suppuration and cavity formation

Etiology

• Primary abscess –arise from aspiration

• Secondary abscess –underlying pulmonary condition(post
obstructive),septic emboli,immunocompromised
condition,necrotizing pneumonia
 Clinical features
• Fever
• Cough with expectoration
• (copious and foul smelling)
• Chest pain
• Haemoptysis
• Dyspnoea
• Fatigue ,night sweat, anaemia
• Weight loss
• Clubbing
 Complications
• Massive haemoptysis
• Bronchiectasis
• Empyema
• Local spread to same or other lung
• Metastatic brain abscess
• Perinephric abscess
• Amyloidosis
 Investigations

• Sputum examination –Gram stain and Culture

• Blood culture,CBC
• CXR PA & Lateral view
• CT chest
• Bronchoscopy
• Upper GI endoscopy
 Management

Acute lung abscess

 Empirical antibiotics for 4 to 6 weeks

 Postural drainage
 Bronchoscopic aspiration and instillation of antibiotics
 Symptomatic treatment- analgesics for pain,expectorants
 Rest, good nutrition with high protein diet
Chronic lung abscess

 Continue medical treatment

 Surgical treatment (lobectomy or pneumonectomy) for serious
haemoptysis,failed medical therapy,suspected
neoplasm,congenital lung malformation
 Empyema
• A collection of pus in the pleural space, which may be as thin as serous
fluid or so thick that it is impossible to aspirate, even through a wide-bore
needle.
• Causes- secondary to infection in a neighbouring structure, usually the
lung, most commonly due to the bacterial pneumonias and tuberculosis.
• Other causes are infection of a haemothorax following trauma or surgery,
oesophageal rupture, and rupture of a subphrenic abscess through the
diaphragm.
• Over 40% of patients with community-acquired pneumonia develop an
associated pleural effusion (‘parapneumonic’ effusion) and about 15% of
these become secondarily infected.
• The condition is not adequately treated, pus may rupture into a bronchus,
causing a bronchopleural fistula and pyopneumothorax, or track
through the chest wall with the formation of a subcutaneous abscess or
sinus, so-called empyema necessitans.
 Clinical features
• Severe pleuritic chest pain
• persisting or recurrent pyrexia
• Dyspnoea
• Cough with big amount of sputum(bronchopleural fistula )
• Chronicity pallor,malaise,weakness ,fatigue,anorexia,weight
loss
• Clubbing
• Pleural rub
 Investigations

• Chest X-ray shows air –fluid level

• Ultrasound shows the position of the fluid, the extent of
pleural thickening and whether fluid is in a single
collection or multiloculated, containing fibrin and debris
• CT provides information on the pleura, underlying lung
parenchyma and patency of the major bronchi.
• Ultrasound or CT is used to identify the optimal site for
aspiration, which is best performed using a wide-bore
needle.
• If the fluid is thick and turbid pus, empyema is confirmed.
• Features suggesting empyema are a fluid glucose of less than
3.3 mmol/L (60 mg/dL), lactate dehydrogenase (LDH) of more
than 1000 IU/L, or a fluid pH of less than 7.0 (H+ > 100
nmol/L)
• The pus is frequently sterile on culture if antibiotics have
already been given.
• The distinction between tuberculous and non-tuberculous
disease can be difficult and may require pleural biopsy,
histology, culture and/or a NAAT.
 Management
 An empyema will heal only if infection is eradicated and the
empyema space is obliterated
 Appropriate antibiotic therapy for 2–4 weeks (e.g.
intravenous co-amoxiclav or cefuroxime with metronidazole)
 insertion of a wide-bore intercostal tube into the most
dependent part of the empyema space & pleurodesis
 Surgical ‘decortication’ of the lung
 Muscle flap closure of fistula
 Pleuropneumonectomy
Thank you