8: Respiratory infections

CHAPTER 8
Respiratory infections


Abbreviations



AAFB
acid‐alcohol‐fast bacilli
ADA
adenosine deaminase
ALT
alanine transaminase
aMB
atypical mycobacterium
AST
aspartate aminotransferase
BAL
bronchoalveolar lavage
BCG
Bacille Calmette‐Guérin
BOOP
bronchiolitis obliterans organising pneumonia
BTS
British Thoracic Society
CAP
community acquired pneumonia
CF
cystic fibrosis
CFT
complement fixation test
CMV
cytomegalovirus
CNS
central nervous system
CO2
carbon dioxide
COPD
chronic obstructive pulmonary disease
CPAP
continuous positive airway pressure
CRPC
C‐reactive protein
CT
computed tomography
DOT
directly observed therapy
GCS
Glasgow Coma Scale
GP
General Practitioner
HAP
hospital acquired pneumonia
Hib
Haemophilus influenza B
HIV
human immunodeficiency virus
HRCT
high‐resolution computed tomography
ICU
intensive care unit
IGRA
interferon gamma release assay
INH
isoniazid
kPA
kilopascals
LFT
liver function test
LIP
lymphoid interstitial pneumonia
MAC
Mycobacterium avium complex
MAI
Mycobacterium avium intracellulare
MDRTB
multi‐drug resistant tuberculosis
MRSA
methicillin‐resistant Staphylococcus aureus
MTB
Mycobacterium tuberculosis
NICE
National Institute of Health and Care Excellence
NSIP
non‐specific interstitial pneumonia
PCR
polymerase chain reaction
PCT
pro‐calcitonin
PEG
percutaneous enterogastrostomy
PPD
purified protein derivative
PSI
pneumonia severity index
PYR
pyrazinamide
RIF
rifampicin
RSV
respiratory syncytial virus
SALT
speech and language therapy
SIADH
syndrome of inappropriate anti‐diuretic hormone
SOL
space‐occupying lesion
TB
tuberculosis
VAP
ventilator‐associated pneumonia
WHO
World Health Organisation

Introduction


The respiratory tract communicates with the environment, allowing micro‐organisms to directly enter the respiratory tract and lungs. Therefore, infections of the upper and lower respiratory tract are very common. The majority of these are self‐limiting and do not require any treatment. These infections are more prevalent in the very young, the elderly, and in those who do not have a competent immune system.


Respiratory tract infections


The diagnosis of a respiratory tract infection is made on clinical grounds. Viruses are a common cause of respiratory tract infections. Individuals with viral infections of the respiratory tract will develop a cough, a sore throat, headaches, nasal symptoms, fever, and myalgia. Investigations are rarely required except during epidemics, for example, an influenza epidemic, or when the patient’s symptoms are concerning. Most viral infections are self‐limiting and those affected will recover without any treatment within a few days. They should be advised to rest, ensure adequate hydration, and take analgesia as required. Many will take over‐the‐counter cough medications to ease their symptoms. Box 8.1 lists the viruses that cause respiratory infections.


The common cold, caused by Rhinovirus, affects most of the population at least once every year. It does not require any treatment but is responsible for many days off work. Most adults would have had asymptomatic cytomegalovirus (CMV) infection during childhood. Only individuals who are immunosuppressed, especially those with HIV and those who have had solid organ transplants, develop symptoms when infected with CMV. Respiratory syncytial virus (RSV) infection results in seasonal outbreaks of respiratory illness, usually in the winter months and can cause complications in those with chronic lung and heart disease. RSV is the commonest cause of lower respiratory tract infection in infants and can be severe in premature babies who present with wheezing and apnoea; there is a risk of sudden death. Many of these viruses can cause pneumonia which will be discussed later in this chapter.


Sinusitis can occur due to a viral or bacterial infection of the maxillary sinus or, less commonly, the frontal and paranasal sinuses. Symptoms of sinusitis include headaches, periorbital and per nasal pain, fever, cough productive of purulent sputum, purulent nasal discharge, and post nasal drip. A CT scan of the sinus will show opacification of the maxillary sinus and mucosal oedema. Treatment of sinusitis is with antibiotics, nasal decongestants, and hydration. Rarely, surgical drainage may be required if medical therapy has failed.


Epiglottitis is a severe and potentially life‐threatening infection of the epiglottis. It is common in young children and caused by haemophilus influenza type B (Hib) infection. Children will present with fever, sore throat, and cough, and the diagnosis must be made without delay. The treatment is with third generation cephalosporins, for example, cefotaxime. Epiglottitis can rapidly progress to respiratory distress and stridor caused by oedema of the epiglottis which can cause obstruction of the larynx. Children may require intubation and ventilation or an emergency tracheostomy. Children who are immunised with the Hib vaccine as protection against meningitis may also be protected against epiglottitis.


Laryngotracheobronchitis (croup) is most commonly caused by parainfluenza virus and is common in children in the winter months. It presents with a characteristic barking cough and fever, and can progress to respiratory distress and stridor. Treatment is with nebulised bronchodilators, nebulised steroids, and steam inhalation.


Acute bronchitis affects the lower respiratory tract and results in cough, breathlessness, pleuritic chest pain, and fever.


Pneumonia


Pneumonia is an infection of the lung parenchyma which can be viral or bacterial. Immunocompromised patients are also at risk of ‘opportunistic’ infections which do not normally affect healthy individuals. These opportunistic infections, which include fungal and protozoal infections, will be discussed in a later section. Aspiration of gastric content and lipoid material can also result in a chemical pneumonia.


Viral pneumonia


Common causes of a viral pneumonia include influenza, adenovirus, parainfluenza, respiratory syncytial virus (RSV) and human metapneumovirus. H1N1 and Avian influenza A (HSN1) occur in pandemics and result in significant morbidity and mortality, with patients often requiring admission to the intensive care unit (ICU).


Patients with a viral pneumonia present with symptoms of dry cough, breathlessness, fever, headache, and myalgia. Diagnosis is made on clinical history, examination, culture of appropriate respiratory samples (such as nasal secretions and bronchial lavage), and serological tests. Polymerase chain reaction (PCR)‐based diagnostic panels are available that can detect several respiratory viruses simultaneously. Viral cultures can take several days to process and are less sensitive than PCR analysis of respiratory secretions.


Patients with viral pneumonia can develop a secondary bacterial infection. This should be suspected if there is clinical deterioration, increase in the volume of sputum, which may be purulent, worsening breathlessness, and systemic symptoms. Blood tests will show an elevated white cell count with a neutrophilia, a rise in CRP and infiltrates or consolidation on the chest X‐ray (CXR). Secondary Staphylococcus aureus pneumonia can occur after an influenza infection.


Sputum samples are rarely recommended with a viral pneumonia as these can be difficult to analyse because many non‐pathogenic micro‐organisms colonise the respiratory tract. Therefore, any positive sputum culture result must be interpreted with the clinical presentation in mind. Certain organisms, such as coagulase‐negative Staphylococci and Candida species, are rarely pathogens.


Bacterial pneumonia


Bacterial pneumonia is a common cause of morbidity in the community and a common presentation to hospital. It is important to distinguish community acquired pneumonia (CAP) from hospital acquired pneumonia (HAP) as the latter is associated with a higher morbidity and mortality. Box 8.2 lists the common symptoms and signs of pneumonia.


Community acquired pneumonia (CAP)


Community acquired pneumonia (CAP) is a common acute lung infection that affects individuals living in the community. The annual incidence of CAP is 5–11/1000 of the adult population, with a higher incidence in children and the elderly. Every year between 0.5 and 1% of adults are diagnosed with a CAP. Risk factors include chronic lung disease, chronic renal disease, diabetes, abnormal immune system, and a preceding viral infection, such as influenza.


In a young and otherwise fit patient, CAP has a good prognosis and can be managed with oral antibiotics in the community. However, the morbidity and mortality can be high in the elderly and in the immunocompromised individual. Overall, 22–42% will require hospital admission and 1–10% will require admission to the ICU. Mortality ranges from 5% in the ambulatory setting to 35% in those admitted to ICU. Most pneumonia‐associated deaths occur in people over the age of 84 years.


Pathophysiology


Bacterial infection of the lung parenchyma results in an inflammatory response from the host, with an outpouring of neutrophils and exudate into the alveolar spaces, resulting in consolidation. This compromises the oxygen exchange because of the ventilation‐perfusion mismatch and results in type 1 respiratory failure. Inflammation of the pleura results in pleuritic chest pain and the development of a parapneumonic pleural effusion in a third of those with CAP. An empyema may develop in a certain percentage as discussed in Chapters 10 and 12. Table 8.1 lists the causes, typical clinical and radiological features, and the treatment of the common pneumonias.


Table 8.1 Causes of pneumonia.




































































































































































Type of organism Organism History Investigations Other features Treatment
Virus Influenza A or B Acute viral symptoms PCR: specificity >95% Can develop secondary bacterial infections Oseltamivir
Vaccination of young, old, and susceptible
Virus Parainfluenza Acute viral symptoms PCR Usually self‐limiting Aciclovir
Virus CMV Asymptomatic in immunocompetent PCR Severe in immunocompromised patients, especially after transplant Aciclovir
Ganciclovir
Virus Varicella Acute viral symptoms
Vesicular rash
Pneumonia can be severe
PCR
Serology
CXR shows multiple small nodules measuring 1–5 mm which coalesce
Mortality without treatment 10%
Aciclovir
Ganciclovir

Immunisation of young, old, and susceptible individuals
Virus Adenovirus Common cold, sore throat, bronchitis, pneumonia Usually none Usually mild. Symptomatic treatment Ribavirin if severe
Bacteria Streptococcus pneumonia Commonest pathogen (65%) Pneumococcal urinary antigen positive in 54%, sputum culture positive in 17% and blood culture positive in 16% Parapneumonic effusion in 30% Meningitis
Sinusitis
Otitis media
Sinusitis
Endocarditis
Osteomyelitis
Amoxicillin
Amoxicillin‐clavulanate
Ceftriaxone

Vaccination of old and susceptible
Bacteria Haemophilus influenza Common cause of lower respiratory tract infection and pneumonia. In children, HiB can cause bacteraemia, epiglottitis, and acute bacterial meningitis Bacterial culture on chocolate agar or latex particle agglutination from nasal or respiratory secretions Opportunistic pathogen in the immunocompromised and in those with COPD Cefotaxime
Ceftriaxone
Fluoroquinolones

Hib vaccine
Bacteria Legionella pneumophila Accounts for 2–9% of CAP Epidemics in areas with contaminated water source, such as hotels Legionella urinary antigen Jaundice
Abnormal liver function tests
Macrolide
Rifampicin
Bacteria Mycoplasma pneumophila Outbreaks occur in young adults. Cerebral symptoms Culture, PCR, and serology of nasopharyngeal samples Cold agglutinins
Ground‐glass changes on CXR
Macrolide
Fluoroquinolone
Tetracycline
Bacteria Gram negative (proteus, Escherichia coli) Usually gastroenteritis. Virulent strains can cause pneumonia and septic shock Blood cultures
Sputum
Can be severe in immunocompromised host Fluoroquinolone
Azithromycin
Rifaximin
Bacteria Staphylococcus aureus Can be severe with high mortality
Systemic infection causes shock secondary to sepsis
MRSA common cause of morbidity and mortality
Sputum
BAL
Blood cultures
Samples from lines, catheters
Swabs from cannula sites, PEG sites, skin
Cavitating lesion in lung
Lung abscess, parapneumonic effusion
Empyema
Osteomyelitis
Flucloxacillin
Clindamycin
Rifampin
Fusidic acid
Vancomycin for MRSA
Bacteria Klebsiella pneumonia Increased risk in alcoholics, malnourished individuals Respiratory secretions
BAL
Blood cultures
Cavitating lesion on CXR.
Lung abscess and empyema
Nosocomial infections
High mortality
Ampicillin
Piperacillin/Tazobactam
Ceftazidime
Meropenem
Ertapenem
Bacteria


Pseudomonas aeruginosa

Affects those with chronic lung disease (COPD, CF, bronchiectasis) Respiratory secretions
BAL
Blood cultures
Common cause of HAP and ventilator‐acquired pneumonia Often multi‐drug‐resistant Aminoglycosides
Quinolones
Cephalosporins
Carbapenems
Polymyxins
Bacteria Coxiella burnetti Flu‐like symptoms
Non‐productive cough
Pneumonia
Increase in antibody titre Usually mild but can progress rapidly to severe Tetracycline
Rifampin
Bacteria Chlamydia psittaci Transmitted by inhalation from poultry and farm animals
Flu‐like symptoms Rarely pneumonia
Complement fixation
PCR
Usually not severe Tetracycline
Macrolide
Bacteria Chlamydia pneumonia Laryngitis
Pharyngitis
Fever, cough, and headache.
Rarely severe pneumonia Myocarditis
Nasopharyngeal swabs to obtain samples, difficult diagnosis to make
Sputum
BAL
Usually asymptomatic or mild in immunocompetent Macrolide
Tetracycline
Fungus Pneumocystis jiroveci Occurs in immunocompromised: HIV positive with low CD4 count, solid organ transplant and haematological malignancies Sputum
BAL
Characteristic ground‐glass changes on CT Trimethoprim‐sulfamethoxazole (septrin)
Pentamidine
Atovaquone

Septrin prophylaxis
in the susceptible
Fungus Aspergillus fumigatus: invasive aspergillosis Occurs in immunocompromised individuals: HIV, chemotherapy, haematological malignancies.
SOB, cough, fever, haemoptysis
Blood cultures
BAL
Serological testing
Patchy shadowing on CXR and CT
High mortality
Itraconazole
Voriconazole
Amphotericin B (Ambisome)
Fungus Candida albicans Systemic infection (candidiasis) occurs in immunocompromised individuals, especially HIV
Mortality high
Sputum
BAL
Blood cultures
Oral, pharyngeal, and vaginal infections common Nystatin for oral infection
Fluconazole
Amphotericin B (Ambisome)
Fungus Histoplasmosis
capsulatum
Fever, joint pains, myalgia, dry cough, chest pain, SOB, and rash CXR shows ‘coin lesions’ and calcification of lymph nodes
Culture of blood and BAL
Rise in antibody titre
Inhalation of spores from bird and bat droppings
Endemic in North and Central USA Occurs in immunocompromised individuals
Itraconazole
Fluconazole
Amphotericin B (Ambisome)
Fungus Cryptococcus neoformans Cough, fever, SOB
Can cause meningitis in immunocompromised

Occurs in immunocompromised individuals, individuals with diabetics Amphotericin B
Flucytosine
Fungus Nocardia
asteroids
Found in soil Opportunistic infection Blood culture Systemic infection in immunocompromised with nocardiosis and endocarditis Trimethoprim‐sulfamethoxazole
Imipenem
Amikacin
Treatment for six months

As described in Box 8.2, CAP has a variety of presentations. Immunocompetent young adults present with a cough productive of green or rusty sputum, breathlessness, pleuritic chest pain, small volume haemoptysis, fever, rigors, night sweats, and myalgia. Patients with mycoplasma, chlamydia, and legionella pneumonias usually present with more systemic symptoms, for example, nausea, vomiting, diarrhoea, headaches, and myalgia. The elderly and the immunocompromised may not have these classic symptoms as they cannot mount an inflammatory response. They are more likely to present with anorexia, feeling generally unwell, with a new confusion, and a reduced mini‐mental test score.


Diagnosis of CAP


The diagnosis of pneumonia is made on the clinical symptoms and signs, and a chest X‐ray (CXR) confirming new parenchymal shadowing. Those presenting with symptoms suggestive of a CAP should have a comprehensive history, examination, and investigations to confirm the diagnosis of CAP and to determine the severity. Investigations should include blood tests, CXR, urinary pneumococcal and legionella antigens and sputum for microbiological analysis. A CURB‐65 score should be calculated in every patient presenting with a CAP; this guides management and has prognostic implications. Box 8.3 describes how the CURB‐65 score is calculated.


A full blood count will usually show an elevated white cell count, with a raised neutrophil count. Leukopenia, with a white cell count <4 × 109 l−1, is associated with a poorer outcome. Mycoplasma pneumonia can be associated with cold agglutinins and a haemolytic anaemia. An elevated eosinophil count should raise the possibility of an eosinophilic pneumonia and will warrant further investigations, such as a bronchoalveolar lavage (BAL), a lung biopsy, and a HRCT. Eosinophilic pneumonias are discussed in Chapter 7.


A raised urea signifies a worse prognosis. Hyponatraemia secondary to the syndrome of inappropriate anti‐diuretic hormone (SIADH) can be associated with CAP, particularly legionella pneumonia. The CRP is always elevated in bacterial CAP, with a sensitivity of 73% and a specificity of 65%, although there is usually a lag, so it may not be raised at the onset of symptoms. Serial CRP measurements can be useful in monitoring response to treatment. Pro‐calcitonin (PCT), a peptide precursor of calcitonin that is released by cells in response to bacterial toxins, can also be used to distinguish between bacterial and non‐bacterial causes of pneumonia. PCT levels may also correlate with the severity of pneumonia.


Abnormal liver function tests (LFT), particularly a raised alanine transaminase (ALT) level, can occur with legionella or mycoplasma pneumonia. Deranged LFTs can also occur after treatment with intravenous antibiotics, particularly macrolides.


Microbiological diagnosis of CAP


Patients with a low‐severity CAP do not routinely require sputum analysis. However, sputum should be sent in those presenting with moderate or severe CAP and when there is cavitation on the CXR. If the patient has a productive cough, then a deep cough sputum sample should be sent for Gram staining, culture, and sensitivity prior to starting antibiotics. There is huge variation in getting a positive sputum result, ranging from 10–80%. Some infections, such as Streptococcus aureus, are easily cultured, whereas Streptococcus pneumonia and Haemophilus influenzae are more difficult to culture, so false negative results can occur. Culture results are reported according to the amount of growth, with moderate or heavy growth indicating a true pathogen, whereas a light growth may indicate colonisation.


Bronchoscopy and bronchoalveolar lavage (BAL) samples are not routinely required, but should be considered in the immunocompromised patient, those who have an abnormal CXR suggestive of malignancy, and in those not improving on empirical antibiotic therapy. BAL samples should have Gram staining, Ziehl‐Neelsen staining for acid‐fast bacilli (AFB), silver staining for pneumocystis jerovici, and stains for fungi. Cultures can take several days to weeks.


Blood cultures should be taken in those presenting with fever and other symptoms of sepsis, even in the absence of fever. Blood cultures are positive in 12% of hospitalised patients, with two‐thirds growing Streptococcus pneumonia. Care should be taken when collecting blood for culture as there is a 10% rate of contamination with MRSA from the skin.


If Streptococcus pneumonia or legionella pneumophila infections are suspected, then urinary antigen testing is more sensitive and specific than blood cultures or sputum cultures, and gives a result more rapidly than cultures of sputum or blood. Urinary antigen testing has the advantage that the antigen will remain positive even after starting antibiotics, but as no pathogens are available, it is not possible to determine sensitivities. Therefore, it is recommended that sputum or BAL samples are also sent for microscopy, culture, and sensitivity.


Polymerase chain reaction (PCR) diagnostic kits are available to use on sputum samples which can give a result within a few hours for chlamydophila pneumoniae and mycoplasma pneumonia, although care must be taken to limit contamination from upper airway flora. If no sputum is available, then a throat swab for mycoplasma pneumonia PCR is recommended.


Complement fixation test (CFT), or paired serological test, can be used to diagnose legionella and mycoplasma infections, especially during outbreaks, and will show a fourfold rise in antibody titres. CFT is also recommended in any patient under 40 years presenting with pneumococcal pneumonia. The consultant microbiologist and public health consultant will usually be able to give advice about outbreaks and put in place public health safety measures, such as closure of infected hotels.


CMV serology can be requested if CMV pneumonia is suspected. Human immunodeficiency virus (HIV) test is recommended in any patient with an atypical presentation and an abnormal CXR.


Microbiological diagnosis is made in less than 40% of patients presenting with CAP. However, empiric antibiotic treatment results in outcomes as good as if the pathogen were detected, with only 1% treated in the community for CAP requiring hospitalisation because of treatment failure. The choice of initial antibiotic therapy is therefore made on the likelihood of the infecting organism.


Radiological diagnosis of CAP


The chest X‐ray (CXR) is an essential investigation in making the diagnosis of CAP. NICE and British Thoracic Society (BTS) guidelines recommend that a CXR should be done in a timely way so that antibiotics can be prescribed within 4 hours of the patient presenting to hospital. The CXR may appear normal very early on or show interstitial infiltrates which are better seen on HRCT (Figure 8.1). In established CAP, the CXR will show consolidation in one or more lobes or show patchy consolidation of bronchopneumonia (Figure 8.2, Figure 8.3). Radiographic changes do not correlate with the pathogen, although Streptococcus aureus pneumonia and Klebsiella pneumonia present with cavitating lesions, the differential diagnoses for which include Mycobacterium tuberculosis infection, lung cancer, and vasculitis.

Image described by caption.

Figure 8.1 CXR showing left upper zone infiltration suggestive of early infection.

Image described by caption.

Figure 8.2 CXR showing right lower lobe consolidation.

Image described by caption.

Figure 8.3 CXR showing right middle and right lower lobe consolidation.


The differential diagnosis of CAP includes an exacerbation of COPD, exacerbation of asthma, acute bronchitis, pulmonary oedema, pulmonary embolus, adenocarcinoma in situ, eosinophilic pneumonia, hypersensitivity pneumonia, cryptogenic organising pneumonia or diffuse parenchymal lung disease. If there is no clinical improvement with appropriate antibiotics, then further investigations will be required.


Management of CAP


Patients presenting to their General Practitioner (GP) with symptoms and signs of a CAP should have a CXR and blood tests, including CRP measurement, to guide management. Pulse oximetry may be helpful in determining whether a patient needs to be admitted to hospital.


NICE Guidelines recommend that a five‐day course of a single antibiotic should be given to those with a CRP of greater than 100 mg l−1 but with a CURB‐65 score of less than 2. The choice of antibiotic will depend on local antibiotic prescribing guidelines and any antibiotic allergy that the patient may have. NICE recommends amoxicillin or tetracycline, and a macrolide or tetracycline for those with penicillin allergy. If symptoms do not resolve within three days, then the duration of antibiotic therapy should be increased. For those with a CRP between 20 and 100 mg l−1, a delayed antibiotic prescription should be considered, and the patient should be instructed to take the antibiotic if symptoms worsen. Patients with a non‐severe CAP should expect clinical improvement within a week and complete resolution of symptoms by 6 weeks, although many report feeling fatigued for up to three months.


Radiological resolution usually takes up to six weeks after antibiotic treatment is completed. It is recommended that a CXR is done after 6 weeks to ensure complete resolution of changes.


Patients seen in hospital with a CURB‐65 score of 2 or less and with no other adverse prognostic features should be started on oral dual antibiotic therapy with amoxicillin and a macrolide for 7–10 days. Those who are allergic to penicillin should be given either a macrolide alone or a tetracycline. If there are no adverse features, they could be discharged home with follow‐up by the GP. The patient should be advised to rest, have adequate hydration, and seek medical help if their symptoms do not improve.


Patients with a diagnosis of CAP who have a CURB‐65 score > 2 and those who have adverse prognostic features should be hospitalised and receive intravenous antibiotics, intravenous fluids, oxygen, and thromboprophylaxis to prevent pulmonary emboli. Adverse features include fever, respiratory rate > 24 breaths per minute, tachycardia, systolic blood pressure < 90 mmHg, oxygen saturation < 90% on room air, and confusion.


The aim should be to maintain oxygen saturation in the range of 94–98%, ensuring that there is no evidence of CO2 retention. Empirical intravenous antibiotic therapy should be started without delay once appropriate samples have been sent for microbiological analysis. These patients should be given nutritional support, a mucolytic agent, and physiotherapy for sputum clearance. Patients with COPD and asthma may benefit from regular nebulised bronchodilators.


The choice of empiric antibiotic therapy for CAP is based on the likelihood of a specific pathogen, and the local antibiotic prescribing guidelines which are based on resistance patterns. Microbiological classification prior to treatment is not practical as the organism is not always identified and waiting for identification may result in treatment delay.


As Streptococcus pneumonia is the commonest cause of CAP, it is recommended that intravenous amoxicillin or benzylpenicillin, together with a macrolide, is given. This combination has been shown to decrease mortality and length of hospital stay. Patients who are allergic to penicillin should be commenced on a macrolide. Macrolides can cause prolongation of the QT interval and can interact with other drugs (discussed in Chapter 3). The prevalence of macrolide‐resistant Streptococcus pneumonia is on the increase. Fluoroquinolones, such a levofloxacin and moxifloxacin, are also active against Streptococcus pneumonia so could be used as monotherapy. However, these drugs can also cause prolongation of the QT interval and ventricular arrhythmias in the elderly. Vancomycin and Teicoplanin are reasonable options in those who have travelled abroad where penicillin and macrolide resistance are high.


The antibiotic regime should be reviewed after 48 hours. If the patient is improving clinically, the fever has settled, and the CRP is coming down, then the intravenous antibiotics should be changed to oral antibiotics. There is no trial evidence regarding the optimal duration of antibiotic therapy, but treatment for 5–10 days is usually given as this results in improvement while minimising the risk of antibiotic‐associated clostridium difficile infection.


Patients with a CURB‐65 score of 3 or 4 with evidence of sepsis may develop hypotension and severe hypoxaemia requiring inotropic support, intubation, and ventilation on ICU.


A parapneumonic effusion occurs in 30–50% of patients with a CAP and will usually resolve without any intervention (Figure 8.4). In some cases, the effusion can progress to an empyema, the diagnosis and management of which are discussed in Chapter 12. Certain organisms, such as Staphylococcus aureus and Klebsiella pneumonia, can predispose to the development of a lung abscess, which is discussed in Chapter 12.

Image described by caption.

Figure 8.4 CXR showing right lower lobe consolidation with cavitation and a parapneumonic effusion.


Prognosis with CAP


Predictors of mortality include the CURB‐65 score and the Pneumonia Severity Index (PSI) which is based on the patient’s gender, age, co‐morbidities (diabetes, cardiac failure, renal failure), results of clinical examination, blood test results, and CXR findings. Additional adverse features include hypoxaemia (SaO2 <92% or PaO2 <8 kPA), white cell count >20 × 10 9 l−1 or <4 × 10 9 l−1, multilobe involvement and positive blood culture. Leukopenia, thrombocytopenia, and a raised serum glucose concentration in a non‐diabetic patient, are also predictors of mortality.


A CT thorax should be considered when the CXR shows no improvement in the radiological changes, when there is a cavitating lesion, possible adenopathy, or clinical features of malignancy. These patients may also require a bronchoscopy to see if there is an obstructing lesion.


Mortality from CAP ranges from 5.1–13.6% (for all CURB‐65 scores) in the community, but increases to 36% in patients who require admission to ICU. Young patients with a CURB‐65 score of 0 have a good prognosis with a mortality of <1%. The majority will return to full health within a few weeks. The morbidity and mortality are greater in those over the age of 65 and those with co‐morbidities, such as diabetes and COPD. Patients with a CURB‐65 of 2 have a ninefold increase in risk of death. Those who survive complain of persistent fatigue, cough, and breathlessness. There is an increased risk of death in survivors over the next three years, with a one‐year mortality of 27%, as hypoxia and the acute inflammatory response due to CAP are associated with death due to acute cardiac events. Box 8.4 lists the mortality associated with CURB‐65 score.

Jun 4, 2019 | Posted by in RESPIRATORY | Comments Off on 8: Respiratory infections
Premium Wordpress Themes by UFO Themes