Chapter 23 Infections of the respiratory tract
The human respiratory tract is highly susceptible to infectious diseases, and morbidity of this region accounts for the majority of general practitioner consultations and almost a quarter of all absence from work due to illness in the western world. Most respiratory tract infections are mild, associated with cold, damp winter months when coughing and sneezing in enclosed spaces facilitate the spread of disease. Serious infections are seen in the very young and the very old, and in compromised patients, throughout the year.
Respiratory infections can be broadly classified into upper and lower respiratory tract infections, although both areas may be simultaneously affected by some agents, notably viruses. The throat, pharynx, middle ear and sinuses are involved in upper respiratory tract infections, while lower respiratory tract infections are confined to the trachea, bronchi and lungs.
In health, the nose and the throat are colonized by commensal bacterial species, while the lower respiratory tract (the lower bronchi and alveoli) contain only a few, if any, organisms. The nose is the habitat of a variety of streptococci and staphylococci, the most significant of which is Staphylococcus aureus, especially prevalent in the anterior nares. Other commensal flora of the upper respiratory tract include corynebacteria, Haemophilus spp. and neisseriae. In health, these endogenous (and other exogenous) organisms are unable to gain access to the tissues and cause disease because there is an effective array of defence mechanisms (Table 23.1).
IgA, immunoglobulin A.
Sore throat is a very common symptom that may or may not be accompanied by constitutional changes. A number of agents may cause a sore throat, but the majority (approximately two-thirds) of the infections are caused by viruses. The major bacterial pathogen involved is Streptococcus pyogenes (Lancefield group A). Sore throat is a frequent precursor of the common cold syndrome (see below).
Characteristic features are redness of the pharynx and tonsils, possible oedema of fauces and soft palate with exudate (acute follicular tonsillitis). Children 5–8 years old are most commonly affected. Spread of infection may cause a peritonsillar abscess (quinsy throat); further spread may cause sinus infection (sinusitis – commonly maxillary sinusitis) or middle-ear infection (otitis media). Scarlet fever, a childhood disease, is a complication of streptococcal upper respiratory tract infection and is accompanied by an erythematous rash and constitutional upset.
The condition is common, especially in winter, with the peak incidence in young schoolchildren with inadequate levels and range of antibodies. Transient streptococcal carriage for a few weeks is common after an acute episode. The rash in scarlet fever is due to the erythrogenic toxin produced by the aetiological agent (Streptococcus pyogenes).
Fever, pain, joint swelling and pancarditis (myocarditis, endocarditis and pericarditis) occur 2–5 weeks after streptococcal sore throat. Cardiac manifestations may lead to permanent heart damage. In developed countries, the incidence of rheumatic fever (and related heart disease) has declined markedly, possibly owing to changes in the virulence properties of the bacterium, improved affluence and social conditions, and effective antimicrobial therapy (e.g. penicillins). However, both rheumatic fever and consequent heart disease are still a major problem in the developing world.
The disease clears spontaneously but may lead to chronic valvular diseases of the heart such as stenosis or incompetence of the mitral or aortic valves in about 70% of patients. Affected individuals are highly susceptible to bacterial endocarditis later in life, when bacteraemias are created during dental or surgical procedures such as scaling. This complication can be prevented by prudent antibiotic prophylaxis prior to such procedures (see Chapter 24).
Diagnosis is mainly clinical; throat swabs are useful to confirm the presence of Streptococcus pyogenes. Swabs cultured on blood agar aerobically and anaerobically yield characteristic β-haemolytic colonies, which can subsequently be identified by Lancefield grouping.
Infection can be proved by serological analysis of paired clotted blood samples. Evidence for antibody to streptolysin O should be sought (streptolysin O is a haemolysin produced by Streptococcus pyogenes). Antibodies to other streptococcal products such as hyaluronidase and DNAase may also be demonstrated immediately after an infection.
Acute glomerulonephritis is another immunological complication that may follow streptococcal sore throat (and sometimes skin infection). The latent period between infection and symptoms is shorter than in rheumatic fever.
The condition presents 1–3 weeks after the sore throat; characteristically there is haematuria, albuminuria and oedema, which manifests as a puffed face, especially on waking, and as the day wears on, ankle oedema often develops. The disease spontaneously clears in the majority, but in some residual, kidney damage may progressively lead to renal failure.
Brief incubation period of 2–4 days and acute illness up to a week with a non-productive cough lasting up to 2–3 weeks. Average adult has up to two attacks per year. Symptoms: sneezing, nasal obstruction and discharge, sore throat accompanied possibly by headache, mild cough, malaise and a chilly sensation and fever. Secondary bacterial infection may lead to otitis media, sinusitis and bronchitis or pneumonia in children.
Virus enters the upper respiratory tract and multiplies in the surface epithelium of the nasal mucosa, leading to increased nasal secretion and oedema. Virus is essentially transmitted through close contact and through air in confined spaces; self-inoculation by hand contamination is considered a more important route than airborne transmission.
Antibodies develop in most after an acute episode but provide limited protection due to rapid decline in antibody levels and also due to multiple rhinovirus serotypes or other common cold viruses circulating during a single season.
After an incubation period of 2–5 days, a severe, acute inflammation of the upper respiratory tract, usually the throat, sets in. Severity of the disease is related to the infecting strain of the organism and the extent of the grey-white membrane that covers the fauces. The membrane is a product of a serocellular exudate. Nasal diphtheria is often milder than laryngeal diphtheria, which is serious because of the respiratory tract obstruction.
The disease is rare in developed countries because of the successful immunization programme with the diphtheria–tetanus–pertussis (DTP) vaccine. Outbreaks occur in non-immunized populations, especially in the developing world.
Vincent’s angina is caused by the fusospirochaetal complex (fusobacteria and oral spirochaetes). These are normal commensals of the mouth and may overgrow, mainly as a result of poor oral hygiene superimposed on nutritional deficiency, leukopenia or viral infections. The outcome may be necrotizing ulcerative gingivitis (Vincent’s stomatitis) if the infection is localized in the mouth (Chapter 33) or Vincent’s angina leading to massive tissue involvement in the tonsillar area. (Similar fusospirochaetal infections may occur in bite wounds, lung abscesses, bronchiectasis and leg ‘tropical’ ulcers.) The primary cause of these diseases is the anaerobic environment, due to local or systemic factors, which precipitate polymicrobial anaerobic growth.