Bacterial community – acquired pneumonia

Bacterial community – acquired pneumonia

Pneumonia caught outside hospital, mostly by pneumococcus and its fellow pyogenic bacteria, with a lobe filling with pus, and how severity decides where it is treated.

Lobar pneumonia, from congestion to resolution

4 scenes, 0:37

A film in four scenes on a white page. A cluster of alveoli round a small airway, the respiratory bronchiole, which comes in from the upper left, is cut open towards the viewer, so the thin pink walls between the alveoli show in section, like a sponge cut through. First, small dark sage-green paired bacteria come down the airway and appear in the alveoli, the nearest first; the walls turn a deeper pink as their capillaries fill with blood, and the alveoli fill one after another with pale teal fluid, a few red cells and pale blue white cells in it and the bacteria free in it. Second, the alveoli turn red: their walls stay deep pink with blood, the fluid fills with more and more white cells, its red cells among them, thin green strands of fibrin cross each air space, and some bacteria disappear as the white cells take them up. Third, the red fades: the red cells go, the walls pale, and the alveoli crowd with pale blue white cells, larger ones appearing late, while the bacteria dwindle and the alveoli turn pale. Fourth, the fibrin strands melt away, the alveoli empty one by one, patch by patch, the large white cells go last, and the cluster is as it was, its air spaces open.

0:00 / 0:37

Congestion

Scenes

About this film

In lobar pneumonia, untreated, a whole lobe passes through four stages that shade into one another: congestion, red hepatisation, grey hepatisation and resolution. The alveoli fill with fluid, then with clotted exudate full of neutrophils, which makes the lobe solid like liver, red while its walls stay congested; then the congestion lessens and white cells crowd it; then the exudate liquefies and is cleared, and the lung recovers its normal structure. Antibiotics now cut the sequence short.

Simplified: not to scale: cells and bacteria drawn far larger than life, and far fewer; the cells, bacteria and fibrin drawn only on the cut face, as a section through lung shows them, with the capillaries in the walls shown only by the walls' colour; red cells, neutrophils and macrophages drawn as dots of their colours, and the pneumococci's capsules left out; one cluster of alveoli standing for the whole lobe, and the stages, which shade into one another and are patchy, drawn as one after the other; the red of red hepatisation drawn in the exudate as well as the walls, and the grey of grey hepatisation as a pale wash; days squeezed into seconds.

2 sources
  1. Kumar and Clark's Clinical Medicine, 10th edition. Elsevier, 2021. Chapter 28, Respiratory disease: community-acquired pneumonia (pp. 963–964).
  2. Corrin B, Nicholson AG. Pathology of the Lungs, 3rd edition. Churchill Livingstone, 2011. Chapter 5, Infectious diseases: lobar pneumonia.

At a glance

  1. Community-acquired pneumonia (CAP) is infection of the lung's air spaces, caught outside hospital or in the first 48 hours of an admission, in a person with normal immunity. Streptococcus pneumoniae is the commonest bacterial cause.
  2. Alveoli fill with fluid, neutrophils and fibrin, and the lung becomes solid (consolidation). In lobar pneumonia a whole lobe is affected; in bronchopneumonia the infection is patchy and centred on the airways.
  3. The picture is a fever, cough with purulent sputum, breathlessness and pleuritic chest pain, with dull percussion, bronchial breathing and crackles over the affected lobe. In the elderly the first sign may be confusion or a fall.
  4. The chest X-ray shows consolidation with air bronchograms. Severity is scored with CRB65 in the community and CURB65 in hospital, together with clinical judgement, and it decides the place of care.
  5. Give oxygen if needed and an antibiotic as soon as the diagnosis is made and within 4 hours of arrival in hospital, within an hour if the sepsis score is high risk. For adults, five days of antibiotic is enough unless the patient is still unstable.
  6. Most patients recover. Mortality is below 1 per cent when treated at home, about 6 to 14 per cent in patients admitted (18 per cent at 30 days in the first UK national audit), and over 30 per cent in those who reach intensive care.

Definition and overview

Pneumonia is inflammation of the substance of the lung, usually from infection. Community-acquired pneumonia (CAP) is pneumonia acquired outside hospital, or within 48 hours of admission, in a person with no marked immunosuppression. UK guidance includes pneumonia in nursing-home residents under this heading, while some textbooks set it with hospital-acquired disease.

The older division of CAP into typical and atypical pneumonia reflects two patterns of illness. The typical pattern, with a sudden fever and a lobe of the lung filled with pus, is that of the pyogenic bacteria described here. The atypical pattern is that of organisms such as Mycoplasma, Chlamydia and Legionella, and of viruses, which are covered in nonbacterial pneumonia.

Typical bacterial pneumoniaAtypical pneumonia
Onsetsudden, over a day or twogradual, with days of malaise and headache
Coughproductive, purulent or rusty sputumdry or scanty sputum
Chest signsfocal, with consolidationoften few, out of proportion to the film
Chest X-rayone lobe or segment consolidatedpatchy or bilateral shadowing
Blood counthigh neutrophil count, high CRPnormal or only slightly raised white cells
Usual organismspneumococcus, H. influenzae, S. aureus, KlebsiellaMycoplasma, Legionella, Chlamydia, viruses

Etiology and pathophysiology

Causes

Streptococcus pneumoniae, the pneumococcus, is the commonest cause overall. Even so, in 30 to 50 per cent of patients no organism is found, and in about one in five more than one is present; the share depends on how hard one looks, and in a large American study with PCR and serology (below), 62 per cent had none. The bacteria of typical CAP and the setting that suggests them are:

OrganismPicks out
Streptococcus pneumoniaeeveryone; the cause of most lobar pneumonia; the capsule is the virulence factor, and there are about 100 capsular types
Haemophilus influenzaesmokers and COPD, mostly the unencapsulated strains
Moraxella catarrhalisCOPD
Staphylococcus aureusafter influenza, intravenous drug use, nursing-home residents; necrotising pneumonia, abscesses and empyema
Klebsiella pneumoniaeheavy alcohol use, diabetes, old age; upper-lobe necrotising pneumonia
Streptococcus pyogenesuncommon; after influenza or in outbreaks; empyema
Anaerobesaspiration, poor dental hygiene, reduced consciousness
Pseudomonas aeruginosabronchiectasis, cystic fibrosis, advanced COPD

Modern tests with PCR find viruses in a large share of patients admitted with CAP. In a study of adults admitted to five hospitals in Chicago and Nashville, a pathogen was found in 38 per cent of the 2259 who had both bacterial and viral tests, and the commonest were human rhinovirus (9 per cent), influenza virus (6 per cent) and S. pneumoniae (5 per cent). Bacteria and viruses often act together: a viral infection damages the airway lining and is a classic prelude to pneumococcal and staphylococcal pneumonia.

Risk factors are age under 16 or over 65, chronic disease (HIV infection, diabetes, chronic kidney disease, malnutrition), chronic lung disease (COPD, bronchiectasis, cystic fibrosis), an obstructing lesion such as a cancer or an inhaled foreign body, smoking, heavy alcohol use, intravenous drug use, and immunosuppressant treatment.

How the infection reaches the lung and takes hold

Most pneumonia follows microaspiration of bacteria that live in the nose and throat; pneumococcus colonises the nasopharynx of many healthy people, especially children. Less often the organism is inhaled in droplets, spreads in the blood or arises from a neighbouring focus. The airways clear such inocula by cough, by the mucociliary escalator, and by alveolar macrophages with antibodies and complement. Pneumonia follows when the load is too heavy or the defence too weak: after a virus has stripped the cilia, in smokers and in COPD, in alcohol intoxication, impaired consciousness or swallowing, or in the very young and the very old.

In the alveolus the bacteria multiply, helped by the pneumococcal capsule, which resists phagocytosis until antibody coats it. The inflammatory response then floods the air space with fluid, neutrophils and fibrin. The classic account of untreated lobar pneumonia has four stages, which are mostly of historical interest, since antibiotics interrupt the sequence:

  1. 1

    Congestion

    Within the first 24 hours the capillaries are engorged and the alveoli hold fluid and bacteria.
  2. 2

    Red hepatisation

    The air spaces fill with red cells, neutrophils and fibrin. The lobe is firm, red and liver-like, and sputum may be rusty from broken-down red cells.
  3. 3

    Grey hepatisation

    The red cells break down and neutrophils and fibrin dominate. The lobe is grey and still solid.
  4. 4

    Resolution

    Macrophages clear the debris and the exudate is coughed up or absorbed, and the lung returns to normal, usually without scarring.

Bronchopneumonia is the other pattern: patchy foci centred on the bronchi and bronchioles, often in both lower lobes, and typical of older and debilitated patients and of Staph. aureus, H. influenzae and gram-negative bacteria.

Lobar pneumonia and bronchopneumonia
Two pairs of lungs seen from the front, side by side, each a pale pink pair of lungs with the trachea and the pale blue-grey bronchial tree branching inside them, the right lung, on the left of each picture, divided by two fissures into upper, middle and lower lobes, and the left lung by one fissure into upper and lower lobes. In the first pair, lobar pneumonia: the whole right upper lobe, from its edge to the fissure below it, is filled evenly with a solid rose-red consolidation speckled with white cells, the bronchi crossing it, while the other lobes are normal. In the second pair, bronchopneumonia: small rounded rose-red patches speckled with white are scattered through both lungs, more and larger towards the bases, with normal lung between them.

Point at a name or a part to light it.

Pneumonia can fill a whole lobe, or more than one, evenly: lobar pneumonia, classically pneumococcal. Or it can start in the bronchi and bronchioles and spread to the alveoli round them, in patches scattered through the lobules, larger and more numerous in the lower lobes: bronchopneumonia.

Simplified: the lungs seen from the front as a flat outline, so each lower lobe shows only where a front view sees it, below and outside its oblique fissure; lobar pneumonia drawn in the right upper lobe, where a front view shows a whole lobe, though the lower lobes are the ones most often affected, and more than one lobe can be; the bronchial tree drawn with far fewer branches than it has, and on top of the lungs; the patches of bronchopneumonia drawn larger and fewer than they are, scattered by chance rather than each at the end of a small airway.

2 sources
  1. Kumar and Clark's Clinical Medicine, 10th edition. Elsevier, 2021. Chapter 28, Respiratory disease: anatomy (pp. 930–931) and community-acquired pneumonia (p. 964).
  2. Corrin B, Nicholson AG. Pathology of the Lungs, 3rd edition. Churchill Livingstone, 2011. Chapter 5, Infectious diseases: lobar pneumonia and bronchopneumonia.

The consolidated lung is perfused but not ventilated, a shunt, so the blood leaves it unoxygenated. That is the cause of the hypoxaemia, and it does not respond well to oxygen alone. Inflammation of the overlying pleura gives the pleuritic pain and a rub, and the sepsis response gives the fever, tachycardia and, in severe cases, hypotension.

Clinical features

Typical pneumococcal pneumonia opens abruptly with fever and rigors, then a cough that becomes productive of purulent or rusty sputum, breathlessness, and a pleuritic chest pain that catches the breath on a deep inhalation. Haemoptysis is possible. Malaise and muscle aches are common, and a cold sore (herpes labialis) is a pointer to pneumococcus. Upper abdominal pain from lower-lobe pneumonia can be mistaken for an abdominal emergency. A swinging fever after some days is a sign of empyema.

On examination the patient is febrile and breathing fast (a respiratory rate of 30 or more marks a severe case), with a fast pulse, sometimes hypotension, and central cyanosis in severe disease. Over the consolidated lobe:

  • reduced chest expansion on that side;
  • a dull percussion note;
  • increased vocal fremitus and resonance;
  • bronchial breathing, with coarse crackles; and
  • a pleural rub early in the illness.

A parapneumonic effusion changes the dullness to a stony one with reduced breath sounds.

Complications include a parapneumonic effusion (in a third to a half of admitted patients in some series, fewer in others) and empyema, lung abscess, respiratory failure and acute respiratory distress syndrome, sepsis and septic shock, bacteraemia with spread to the meninges, the heart valves or the joints, pericarditis, hyponatraemia, acute kidney injury, atrial fibrillation and a myocardial infarction.

Diagnosis and management

Diagnosis

The diagnosis is clinical, supported by a chest X-ray that shows new consolidation: a dense shadow with air bronchograms (air-filled bronchi seen through the solid lung) that is confined to a lobe or segment. In hospital, the diagnosis, with the film, should be made within 4 hours of arrival. The X-ray can lag behind the illness by a day or two, so a negative film in a patient who looks to have pneumonia should be repeated. Lung ultrasound can help at the bedside, for example when heart failure or pleural fluid are the alternatives. Other conditions that mimic CAP are pulmonary embolism with infarction, heart failure, lung cancer, tuberculosis, organising pneumonia, eosinophilic pneumonia, vasculitis and pulmonary haemorrhage.

Severity is graded to decide where to treat. The CRB65 score (in the community) and the CURB65 score (in hospital, with urea) give one point each for confusion, a raised urea (above 7 mmol/L), a respiratory rate of 30 or more, a low blood pressure (systolic below 90 or diastolic 60 mmHg or lower) and age 65 or more.

ScoreRisk of deathPlace of care
CRB65 0low, below 1 per centat home, with safety-netting advice
CRB65 1intermediate, 1 to 10 per centat home with safety-netting, or hospital at home, a virtual ward, a same-day emergency care unit or an inpatient bed, by shared decision
CRB65 2intermediate, 1 to 10 per centrefer to hospital
CRB65 3 or 4high, above 10 per centrefer to hospital
CURB65 0 or 1low, below 3 per centcan go home, with primary care follow-up
CURB65 2intermediate, 3 to 15 per centvirtual ward, hospital at home, a same-day emergency care unit or an inpatient bed
CURB65 3 to 5high, above 15 per centinpatient care, with critical care if needed

The score is used together with clinical judgement: an unusually low oxygen saturation, a pleural complication, serious comorbidity or pregnancy can make a low score a poor guide. Other markers of severe disease include involvement of more than one lobe, a PaO2 below 8 kPa, a low albumin, a white cell count below 4 or above 20 ×10⁹/L, and positive blood cultures.

In hospital, beyond the film:

  • a baseline C-reactive protein (CRP), to consider;
  • a blood count, urea, creatinine and electrolytes, liver tests;
  • an arterial blood gas if the saturation is below 94 per cent;
  • an HIV test, since pneumonia is a common first presentation of HIV;
  • for moderate or high severity, sputum culture and blood cultures (UK guidance takes blood cultures when sepsis is suspected, many textbooks in all moderate or severe cases), a pneumococcal urinary antigen (to justify narrowing the antibiotic), and a legionella urinary antigen when there are risk factors;
  • no routine microbiological tests for low-severity disease; and
  • a pleural aspiration, under ultrasound, for any effusion large enough to sample, since a pH below 7.2 points to an infected effusion that needs drainage.

In pneumococcal pneumonia the white cells are usually high with a neutrophilia, and the CRP is often well above 100 mg/L.

Management

  • Oxygen to a saturation of 94 to 98 per cent, or 88 to 92 per cent if the patient is at risk of hypercapnia; high-flow nasal oxygen, CPAP or non-invasive ventilation when the target is not reached.
  • Fluids, intravenous if the patient is hypotensive or dry, and sepsis management if present.
  • Antibiotics as soon as the diagnosis is made and within 4 hours of arrival in hospital, and within an hour when the sepsis score is high risk, as for any high-risk pneumonia. Oral treatment is first choice. Amoxicillin covers pneumococcus; a macrolide or doxycycline is added or substituted when atypical organisms are suspected; and co-amoxiclav with clarithromycin is the usual UK choice for high-severity disease. Five days is enough for adults, unless the patient is still unstable. Choices, doses and the course are set out in the treatment of pneumonias.
  • A corticosteroid can be considered in addition for high-severity pneumonia in hospital (a CURB65 of 3 to 5 together with the clinician's judgement), for 4 to 7 days. Hydrocortisone is preferred: in a French trial of severe CAP in intensive care it reduced the 28-day mortality, though other trials did not show a clear benefit. A corticosteroid is best avoided in the same patient as a fluoroquinolone.
  • Analgesia for pleuritic pain, which lets the patient breathe deeply and cough, and chest physiotherapy only when sputum is retained.
  • Thromboprophylaxis with low-molecular-weight heparin for patients admitted for more than 12 hours, unless it is contraindicated.
  • Drain an empyema or a large effusion that is infected.

Review after 48 to 72 hours. A patient who has not improved needs the diagnosis reconsidered (a virus, an empyema or abscess, a resistant organism, an obstructing tumour, or another disease such as a pulmonary embolus), a sample of sputum if none has been sent, and a senior opinion. A raised CRP or procalcitonin on day 3 or 4 that has not fallen suggests treatment failure.

Discharge is not safe if in the previous 24 hours the patient has had two or more of a temperature above 37.5 °C, a respiratory rate of 24 or more, a pulse above 100, a systolic pressure of 90 or less, a saturation below 90 per cent on air, abnormal mental state, or an inability to eat without help.

Prevention: stop smoking. Influenza vaccination yearly for people at risk, and pneumococcal vaccination for older adults, the immunocompromised and people with chronic heart, lung, liver or kidney disease, with schedules that differ between countries. Children are given a conjugate vaccine as part of the routine schedule.

Epidemiology

CAP is among the commonest infections that bring adults to a doctor and into hospital, and it is a leading infectious cause of death in adults. In the United Kingdom 0.5 to 1 per cent of adults are affected every year, with 22 to 42 per cent of them admitted. Admission for CAP rises steeply with age: in the American study above the annual rate was 24.8 per 10 000 adults overall, 63 per 10 000 at 65 to 79 years and 164 per 10 000 at 80 or older.

The disease is commonest at the extremes of age and in winter, and in people with the risk factors listed above. Pneumococcal vaccination in childhood, which started in the 2000s, lowered the number of cases caused by the vaccine's serotypes in all ages, with the other serotypes taking some of their place.

Prognosis

Most previously healthy adults recover fully, and those treated at home do very well, with mortality under 1 per cent. Of UK patients admitted to hospital in earlier studies, 5.7 to 14 per cent died, and of the 1.2 to 10 per cent who reached intensive care, more than 30 per cent. The first national audit of unselected UK admissions (2009 to 2010) found that 18.3 per cent died within 30 days in hospital, with a mean age of 71. The figure depends on whom you count: in the American study, whose patients were younger (median age 57), 21 per cent of the 2320 adults with radiographic pneumonia needed intensive care and 2 per cent died. Mortality climbs with age, comorbidity and a higher CURB65 score (above 15 per cent in the high-risk group). Bacteraemia, multilobar disease, hypoxaemia, a low albumin and an empyema add to the risk.

Symptoms resolve slowly, and patients can be given a timetable: by one week the fever has gone; by four weeks the chest pain and sputum have substantially eased; by six weeks the cough and breathlessness have substantially eased; by three months most symptoms are gone, though tiredness may remain; and by six months most feel back to normal.

Pneumonia leaves a mark beyond the lung. In the weeks after, the risk of heart failure, arrhythmia and myocardial infarction is raised, and patients admitted with pneumonia have a higher death rate for years afterwards than people of the same age who were not. A film at six weeks is considered for smokers and those over 50, to exclude a tumour behind a persistent shadow.

Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.

1Which organism is the commonest bacterial cause of community-acquired pneumonia in adults?

2A man who drinks heavily has fever, a cough with thick, gelatinous, blood-stained sputum and an upper-lobe cavitating consolidation. Which organism fits best?

3Which findings go together in a lobe that is consolidated by pneumonia?

4A 72-year-old is newly confused, breathing at 26 breaths a minute, with a blood pressure of 110/70 mmHg. What is the CRB65 score, and where should they be treated?

5A 62-year-old smoker has recovered from a lobar pneumonia treated in hospital. What follow-up does the guideline advise?

Linked topicsThe concepts this topic shares, and the topics they tie it to.

See on the map

Pneumonia

Streptococcus pneumoniae is the commonest cause.

Bacterial cell wall

Amoxicillin treats most pneumococcal pneumonia.

Bacterial ribosome

A macrolide or doxycycline covers atypical bacteria such as Mycoplasma.