23: Infections of the respiratory tract

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.

Normal flora

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).

Table 23.1 Natural antimicrobial defences of the respiratory tract

Mucociliary system

Nasal vibrissae
Action of cilia
Mucous glands and goblet cells

Bronchoconstriction
Cough reflex
Non-specific mucosal defences

Lactoferrin
Lysozyme
α-Antitrypsin

Alveolar macrophage system
Mucosal antibody (mainly secretory IgA)
Local cell-mediated immunity

IgA, immunoglobulin A.

Important pathogens of the respiratory tract

The major causative agents of bacterial and viral respiratory infections of both the upper and lower respiratory tract are illustrated in Figure 23.1.

image

Fig. 23.1 Major causative agents of respiratory tract infection. RSV, respiratory syncytial virus.

Infections of the upper respiratory tract

The following infections of the upper respiratory tract of clinical relevance to dentistry are noteworthy:

• the sore throat syndrome
• streptococcal sore throat
• rheumatic fever
• acute glomerulonephritis
• common cold syndrome
• diphtheria
• Vincent’s angina
• infectious mononucleosis (Chapter 21)
• candidiasis (Chapter 22).

Sore throat syndrome

Clinical features

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).

Streptococcal sore throat

Clinical features

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.

Pathogenesis and epidemiology

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).

Late sequelae of streptococcal infection

Immunologically mediated diseases can manifest in susceptible individuals as a late consequence of certain strains of Streptococcus pyogenes (group A) infection. These are rheumatic fever and acute glomerulonephritis.

Rheumatic fever

Clinical features

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).

Pathogenesis

A number of theories have been proposed for rheumatic carditis:

• rheumatic toxins: extracellular products of group A streptococci reacting with heart tissue
• autoimmunity: induced by the localization of extracellular streptococcal products and antibodies in tissues
• cross-reactivity: the group A streptococcus cell wall antigens and glycoproteins of human heart valves share the same antigenic determinants; thus, the antibodies produced against the bacterial cell wall may cross-react with the heart valve components, with resultant cardiac complications (Fig. 23.2).
image

Fig. 23.2 Pathogenesis and sequelae of rheumatic carditis (events leading to infective endocarditis are also illustrated).

Laboratory diagnosis

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.

Treatment

β-Haemolytic streptococci are universally sensitive to penicillin. Erythromycin is an alternative in cases of penicillin hypersensitivity. After eradication of Streptococcus pyogenes with penicillin, reinfection must be prevented by long-term prophylaxis.

Acute glomerulonephritis

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.

Clinical features

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.

Pathogenesis

Theories proposed include:

• nephrotoxins: production of toxic substances by nephritogenic streptococci, including streptolysin, cell wall extracts and uncharacterized diffusible substances released by the cells
• immunological cross-reactivity: between antigens of protoplasts of nephritogenic streptococci and soluble components of glomerular basement membrane
• immune complexes: thought to be formed by combinations of antistreptococcal antibody with either streptococcal antigens already circulating in the blood or deposited on the basement membranes.

Laboratory diagnosis

A clinical diagnosis is confirmed by past or present streptococcal infection.

Treatment

Penicillin is useful if the organism is still present at the infective focus.

Common cold syndrome

A number of viruses such as coronaviruses, adenoviruses and rhinoviruses cause the common cold, although rhinoviruses are by far the most common culprit.

Clinical features

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.

Pathogenesis

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.

Treatment

Only symptomatic treatment. Many attempts at vaccine preparation have failed, and antiviral drugs are equally ineffective. Nasal spray of interferon-α has shown some promise in preventing spread of rhinoviruses.

Diphtheria

Diphtheria is caused by Corynebacterium diphtheriae (three main biotypes: gravis, intermedius and mitis).

Clinical features

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.

Pathogenesis

Corynebacteria produce a powerful exotoxin that is cardiotoxic and neurotoxic. This toxin diffuses throughout the body, affecting the myocardium, adrenal glands and nerve endings.

Epidemiology

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.

Treatment

Antitoxin must be used in addition to penicillin or erythromycin.

Vincent’s angina

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.

Treatment

Penicillin or metronidazole combined with effective debridement, and removal of the underlying cause of tissue breakdown.

Infections of the paranasal sinuses and the middle ear

These can either be acute or chronic, and are often initiated as a secondary complication of a viral infection of the respiratory tract (e.g. a common cold). Some important examples are:

• acute infections:

image otitis media
image sinusitis

• chronic infections:

image chronic suppurative otitis media
image chronic sinusitis.

Acute infections

Otitis medi/>

Related posts:

  1. 16: Vibrios, campylobacters and Wolinella
  2. 18: Fusobacteria, Leptotrichia and spirochaetes
  3. 17: Bacteroides, Tannerella, Porphyromonas and Prevotella
  4. 32: Microbiology of dental caries
  5. 26: Infections of the gastrointestinal tract
  6. 4: Viruses and prions

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Jan 4, 2015 | Posted by in General Dentistry | Comments Off on 23: Infections of the respiratory tract

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