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Tuberculosis146
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MICRO-references
WHO Global TB Report 2014:
www.who.int/tb/publications/global_report/gtbr14_main_text.
pdf?ua=1
MICRO-case
A 34-year-old man of Indian origin presents to the GP with a productive
cough that has lasted for 3 weeks, along with chest pain. He has a low
grade fever and bronchial breathing on auscultation. The GP diagnoses a
chest infection and prescribes amoxicillin. The patient fails to respond to
amoxicillin after a week. He is subsequently changed to doxycycline and
then clarithromycin, with failure to respond to either.
The GP then decides to send off a sputum sample; he notes that the
sputum is rusty in colour and blood flecked. On further questioning it
emerges that the patient has lost 5 kg since the cough developed, but
he does not smoke. He also admits to being a frequent visitor to India on
business trips. He has never had a BCG vaccination. The GP sends him
for an urgent chest X-ray. The X-ray shows patchy consolidation, hilar
lymphadenopathy and a cavitating lesion in the apex of the right lung.
Adiagnosis of TB is made on radiological and clinical grounds.
The patient is referred to respiratory medicine. The diagnosis is
confirmed when acid-fast bacilli are identified in his sputum sample, and
3weeks later this is further confirmed by culture. He is started on rifampicin, isoniazid, ethambutol and pyrazinamide. He is advised to minimise
contact with others during the first 2 weeks of treatment and while symptomatic. The HPA is informed as the patient flew back from India while
symptomatic. Three weeks into treatment, the patient produces 3 negative sputum samples and is declared non-infectious. The patient finishes
his 6-month treatment course without incident.
Key Points
A high index of suspicion is needed in patients who may have TB.
•
Diagnosis should be considered in those from high-risk groups or
•
returning from abroad.
TB should be considered in a patient whose respiratory infection
•
does not respond to antibiotic therapy.
Therapy can be started on clinical and radiological evidence alone,
•
but it is always better to obtain adequate samples for culture first.
3 consecutive negative sputum samples are needed before the
•
patient is considered non-infectious if the patient was smear positive
prior to treatment.
TB requires the clinician to complete a notification form to the Health
•
Respiratory Medicine
Protection Agency in the UK and DoH.
9
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Bronchiectasis and
Cystic Fibrosis
9.1 DEVELOPMENT OF BRONCHIECTASIS
1. DEFINITION
A disease in which the airways of the lung are thick walled and permanently
•
dilated.
Bronchial walls are inflamed and irreversibly damaged, which results in
•
frequent infections.
2. EPIDEMIOLOGY
In the UK the incidence is approximately 1.3 per 100, 000 .
•
• Prevalence increases with age.
3. AETIOLOGY AND RISK FACTORS
Any insult that causes progressive irreversible bronchial damage can result
•
in bronchiectasis (See Table 9.1).
Table 9.1 Aetiology of bronchiectasis.
AETIOLOGY OF BRONCHIAL
DAMAGE CAUSES OF BRONCHIECTASIS
Bronchial obstruction • Foreign body
• Inspissated mucus
• Bronchial stenosis
• Tumour.
Post infectious • Prior childhood viral respiratory
infection, especially measles.
• Previous severe pneumonia or
mycobacterial infection, for example:
• Bordetella pertussis.
• TB.
• Staphylococcus aureus.
• Pseudomonas aeruginosa.
(Continued)
DOI: 10.1201/9781315113937-10
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Table 9.1 (continued) Aetiology of bronchiectasis.
AETIOLOGY OF BRONCHIAL
DAMAGE CAUSES OF BRONCHIECTASIS
• Klebsiella pneumoniae.
• Aspergillus infection.
• Swyer-James syndrome.
• Post infectious obliterative
bronchiolitis.
• Unilateral hyper-expanded lung.
• Reduced vascularity.
• Associated with bronchiectasis.
Immunodeficiency • HIV/AIDS.
• Immunoglobulin deficiency
(panhypogammaglobulinaemia or
selective deficiencies).
Genetic • Cystic fibrosis (CF).
• Primary ciliary dyskinesia (PCD).
• Kartagener’s syndrome (subgroup of
PCD with situs invertus).
• Alpha-1-antitrypsin deficiency
(consider if basal emphysema present).
Immunological over-response • Allergic bronchopulmonary
Others • Rheumatoid arthritis.
Cystic fibrosis is the most common cause in the developed world.
•
Worldwide HIV/AIDS and infectious causes (especially TB) are more
•
important.
Some groups have a greater risk of bronchiectasis, including:
•
• Women.
Respiratory Medicine
• e elderly.
• Smokers.
aspergillosis.
• Post lung transplant.
• Yellow nail syndrome.
• Idiopathic pulmonary fibrosis.
• Inflammatory bowel disease.
• Young’s syndrome: characterised by
azoospermia and sinusitis.
9.1 Development of Bronchiectasis
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• ose with serious childhood pulmonary infection.
• e immunodeficient.
• ose with inadequately treated pulmonary infection.
MICRO-print
Kartagener’s syndrome is a rare autosomal recessive congenital cause
of bronchiectasis. It is characterised by the triad:
Ciliary dyskinesia.
•
Dextrocardia.
•
Situs inversus (mirroring of major abdominal and thoracic viscera).
•
It is a cause of recurrent respiratory infections in childhood, which consequently lead to progressive bronchiectasis. The findings on physical
examination of the patient are pathognomonic.
4. PATHOPHYSIOLOGY
Permanent abnormal widening of the bronchi; this usually occurs due to the
•
repeated cycle shown in Figure 9.1.
149
Figure 9.1 Pathophysiology of development of bronchiectasis.
ere is progressive damage due to this process that leads to worsening air-
•
flow limitation.
Pathologically, four different phenotypes of bronchiectasis can be identified:
•
• Cylindrical
• Cystic or saccular
• Varicose
• Follicular.
Respiratory Medicine
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9.2 CLINICAL MANAGEMENT
1. CLINICAL FEATURES
Clinical features of bronchiectasis are summarised in Table 9.2.
•
Table 9.2 Clinical features of bronchiectasis.
SIGNS SYMPTOMS CHEST X-RAY FINDINGS
• Chest: • Productive cough: • ↑ Pulmonary markings
• Crackles lasting months to years (so-called tramline
• Rhonchi • Mucopurulent sputum markings)
• Scattered wheeze • Dyspnoea • Atelectasis
• Cyanosis • Haemoptysis • Honeycomb lung
• Clubbing • Malaise • Dilated bronchi
• Arthritis • Recurrent pneumonias • Clustered cysts
• Yellow nails (exacerbations) • May be normal
• Low-grade fever
• Pleuritic chest pain
• Wheeze
• ↑ Foul-smelling sputum
2. INVESTIGATIONS
FBC.
•
Serum immunoglobulins: G, A, M and E.
•
Serum IgE or skin prick test for Aspergillus fumigatus.
•
Sputum culture and sensitivity including AAFB culture (to look for Myco-
•
bacterium spp.).
Chest X-ray (usually insufficient alone to confirm diagnosis) (see Figure 9.1).
•
High-resolution chest CT is the gold standard for diagnosis (see Figure 9.2).
•
Sinus X-ray.
•
Sweat test (for diagnosis of CF, see section 9.3.6).
•
Serum alpha-1-antitrypsin in presence of emphysema.
•
Functional antibodies against Pneumococcus, Haemophilus influenza B and
•
tetanus.
Spirometry.
•
Respiratory Medicine
9.2 Clinical Management
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151
Figure 9.2 Chest CT of a patient with widespread bronchiectasis (CXR and HRCT of
bronchiectasis).
3. DIFFERENTIAL DIAGNOSIS
• COPD.
• Chronic sinusitis.
• Asthma.
• Pneumonia.
• Chronic bronchitis.
• TB.
• Gastro-oesophageal reflux disease (GORD).
Respiratory Medicine
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4. MANAGEMENT
e management for bronchiectasis differs slightly depending upon the
•
cause.
Management of non-CF bronchiectasis (see section 9.3.8. for management of
•
CF-bronchiectasis):
• Antibiotics:
– Sputum should be sent for bacterial and mycobacterial culture prior
to commencing therapy.
– For acute exacerbations, treatment is with a 10- to 14-day course of
one of the following:
◯
Amoxicillin
◯
Tetracycl ine
◯
A macrolide (e.g. erythromycin)
◯
Ciprofloxacin (for Pseudomonas).
– Long-term antibiotic therapy should be considered in patients with
>3 exacerbations a year. Nebulised colomycin or gentamicin can be
used in patients colonised with Pseudomonas, and for other patients a
regime of three times a week oral azithromycin is effective.
• Chest physiotherapy and pulmonary rehabilitation.
• Oral mucolytics (e.g. carbocysteine).
• Nebulised saline (either 09.%or 7% concentration) as a mucolytic.
• Short acting β2-agonist bronchodilators (e.g. salbutamol).
• Inhaled corticosteroids are not routinely used unless there is an associ-
ated indication (e.g. asthma/COPD).
• Prophylactic vaccination against influenza and pneumococcus.
Lifestyle interventions:
•
• Adequate nutrition with supplementation if necessary.
• Smoking cessation and avoidance of passive smoking.
Surgery can be considered in some cases:
•
• Lung resection in patients with localised disease unresponsive to medical
intervention.
• Bronchial artery embolism if massive haemoptysis occurs.
• Lung transplantation.
MICRO-references
The British Thoracic Society (BTS) have produced guidelines for the
management of non-CF bronchiectasis:
Respiratory Medicine
www.brit-thoracic.org.uk/document-library/guidelines/
bronchiectasis/bts-guideline-for-bronchiectasis-in-adults/
9.2 Clinical Management
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5. COMPLICATIONS
Repeated infections and progressive deterioration in lung function.
•
Empyema.
•
Lung abscess.
•
Respiratory failure.
•
Amyloidosis.
•
6. PROGNOSIS
Prognosis varies widely; most patients will have few symptoms and a normal
•
life expectancy.
• Previous to antibiotic therapy, the majority of patients would die within
5 years.
Improved survival is associated with:
•
• High body mass index (BMI).
• Up-to-date vaccinations.
Disease progression is associated with:
•
• Colonisation by P. aeruginosa.
• ↑ in number + severity of exacerbations.
• ↑ CRP.
Increased mortality is associated with:
•
• Hypoxaemia
• Hypercapnia
• ↑ dyspnoea
• Extensive radiological changes.
153
MICRO-case
A 62-year-old woman visits her GP with a cough productive of mucopurulent sputum. She is a non-smoker with no significant medical problems
in her history, and apart from appearing thin, she seems generally well.
However the doctor notes that she has been prescribed antibiotics
eight times in the last 18 months for bronchitis and has been repeatedly presenting complaining of tiredness. When questioned, the patient
admits to having had a persistent productive cough for over a year and
getting breathless at times. The GP refers her to a respiratory physician.
She does not report a history of heartburn, sinusitis or choking symptoms. She has no evidence of systemic inflammatory disease, no history
of TB or whooping cough and has no family history of lung disease.
Achest X-ray shows increased lung markings and some dilated airways.
An HRCT confirms the presence of dilated bronchi. Blood tests are
unremarkable. However when lung function tests are done they show
a decreased lung capacity and mild airflow obstruction
that improves with the use of bronchodilators. Repeated
Respiratory Medicine
continued…
Bronchiectasis and Cystic Fibrosis154
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continued…
nosis of bronchiectasis is made and the patient is started on bronchodilators, carbocysteine, chest physiotherapy and a 3-month course of
amoxicillin. Despite an improvement in symptoms, over the next year
exacerbations continue. Arotating cycle of month courses of amoxicillin
and doxycycline is recommended. This leads to a reduction in sputum
volume, purulence and exacerbation frequency.
Key Points
Although smokers are more likely to develop bronchiectasis, the
•
majority of people who develop it will be non-smokers.
Diagnosis can be delayed for months or years, with non-specific and
•
mild symptoms often misdiagnosed as bronchitis, asthma or recurrent
pneumonia.
Often a cause for the bronchiectasis cannot be identified.
•
Once diagnosed bronchiectasis requires a continuous health mainte-
•
nance programme, with intermittent aggressive treatment of respiratory infections.
sputum cultures grow Haemophilus influenzae. Adiag-
9.3 CYSTIC FIBROSIS
1. DEFINITION
Cystic fibrosis (CF) is an autosomal recessive multisystem disorder, character-
•
ised by frequent respiratory infections and pancreatic insufficiency.
2. EPIDEMIOLOGY
CF is the most common life limiting genetic condition amongst the Cau-
•
casian population.
1/ 2500 Caucasian newborns affected.
•
Carrier frequency is 1/25.
•
3. AETIOLOGY AND RISK FACTORS
CF is caused by a mutation in the Cystic Fibrosis Transmembrane Conduc-
•
tance Receptor (CFTR) gene found on chromosome 7.
Although there are ~1000 different mutations, the most common m utation –
•
delta-F508 – accounts for approximately 2/3 of cases of CF.
4. PATHOPHYSIOLOGY
CFTR is an ATP-responsive chloride channel.
•
Respiratory Medicine
Other functions include:
•
9.3 Cystic Fibrosis
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• Regulation of sodium transport across the respiratory epithelium.
• Acting as a cell surface glycoprotein.
• Immune defence.
Effects of a defective CFTR are described in Figure 9.3:
•
Figure 9.3 Pathophysiological basis of CF.
In the airway:
•
• e increased viscosity of the secretions impairs mucociliary clearance.
• Affected individuals suffer frequent respiratory infections.
• e cumulative effect of repeated respiratory infections results in pro-
gressive lung damage and loss of lung function.
In the gastrointestinal (GI) tract:
•
• Increased viscosity of pancreatic secretions leads to reduced secretion
from the pancreatic ducts into the small intestine.
– is causes pancreatic enzyme insufficiency and malabsorption.
• In the bile ducts, ion transfer is impaired resulting in more concen-
trated bile which can plug the ducts.
• Viscous secretions and water movement across the intestinal wall result
in intraluminal water deficiency resulting in:
– Constipation and bowel obstruction.
– Meconium ileus in the neonate.
Infertility:
•
• Infertility in males is caused by the failure of vas deferens development
as a direct result of the CFTR mutation.
Diabetes:
•
• Cystic fibrosis–related diabetes (CFRD) is caused by progressive pan-
creatic fibrosis and fatty infiltration, resulting in loss of beta islet cells.
155
Respiratory Medicine
5. CLINICAL FEATURES
CF may present at any age and the clinical features depend on the age at
•
which it presents.
In the neonate:
•
• Detection of increased immunoreactive trypsin in the Guthrie (heel-
prick) test.
• Meconium ileus.
• Neonatal jaundice.
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