Lower respiratory tract infections

19 Lower respiratory tract infections


Diphtheria is caused by toxin-producing strains of Corynebacterium diphtheriae and can cause life-threatening respiratory obstruction

Diphtheria is now rare in resource-rich countries due to widespread immunization with toxoid (see Ch. 34), but it is still common in resource-poor countries. Non-toxigenic strains occur in the normal pharynx, but bacteria producing the extracellular toxin (exotoxin; see Ch. 2) must be present to cause disease. They can colonize the pharynx (especially the tonsillar regions), the larynx, the nose and occasionally the genital tract, and in the tropics or in indigent people with poor skin hygiene, the skin.

Adhesion is mediated by pili or fimbriae covalently attached to the bacterial cell wall. The bacteria multiply locally without invading deeper tissues or spreading through the body. The toxin destroys epithelial cells and polymorphs, and an ulcer forms, which is covered with a necrotic exudate forming a ‘false membrane’. This soon becomes dark and malodorous, and bleeding occurs on attempting to remove it. There is extensive inflammation and swelling (Fig. 19.1) and the cervical lymph nodes may be enlarged to give a ‘bull neck’ appearance.

Nasopharyngeal diphtheria is the most severe form of the disease. When the larynx is involved, it can result in life-threatening respiratory obstruction. Anterior nasal diphtheria is a mild form of the disease if it occurs on its own, because the toxin is less well absorbed from this site, and a nasal discharge may be the main symptom. The patient will, however, be highly infectious.

Diphtheria toxin can cause fatal heart failure and a polyneuritis

The toxin (Box 19.1 and Fig. 19.2) is absorbed into the lymphatics and blood, and has several effects:

Whooping cough

B. pertussis infection is associated with the production of a variety of toxic factors

Some of these toxic factors affect inflammatory processes, while others damage ciliary epithelium. They are:

B. pertussis infection is characterized by paroxysms of coughs followed by a ‘whoop’. After an incubation period of 7–10    days (range 5–21    days), B. pertussis infection is manifest first as a catarrhal illness with little to distinguish it from other upper respiratory tract infections. This is followed up to 1    week later by a dry non-productive cough, which becomes paroxysmal. A paroxysm is characterized by a series of short coughs producing copious mucus, followed by a ‘whoop’, which is a characteristic sound produced by an inspiratory gasp of air. Despite the severity of the cough, the symptoms are confined to the respiratory tract, and lobar or segmental collapse of the lungs can occur (Fig. 19.3).

Complications include central nervous system (CNS) anoxia, exhaustion and secondary pneumonia due to invasion of the damaged respiratory tract by other pathogens.

The early clinical picture is non-specific, and the true diagnosis may not be suspected until the paroxysmal phase. The organisms can be isolated on suitable media from throat swabs or on ‘cough plates’ (see Ch. 32), but they are fastidious and do not survive well outside the host’s environment.

Whooping cough can be prevented by active immunization

For many years, a whole cell vaccine comprising a killed suspension of B. pertussis cells was used, combined with purified diphtheria and tetanus toxoids and administered as ‘DPT’ or ‘triple’ vaccine. Although an effective vaccine, there were major concerns about side effects. These included fever, malaise and pain at the site of administration in up to 20% of infants; convulsions, thought to be associated with the vaccine in about 0.5% of vaccinees; and encephalopathy and permanent neurologic sequelae associated with vaccination, with an estimated rate of 1 in 100 000 vaccinations (<    0.001%).

Concern about side effects led to a marked fall in uptake of the vaccine and subsequently to a marked increase in the incidence of whooping cough (see Ch. 31).

Acellular pertussis vaccines became the dominant vaccine preparation as they provide the same or better protection against whooping cough and cause fewer side effects as they are highly purified with much reduced levels of endotoxin compared with whole cell vaccines. The acellular vaccines contain pertussis toxoid and other bacterial components, including the filamentous haemagglutinin and fimbriae, and are given in combination with other vaccines such as diphtheria, tetanus, polio and Haemophilus influenzae type B. In 2008, about 82% of all infants worldwide received three doses of pertussis vaccine. WHO estimated that global pertussis immunization prevented about 687 000 deaths that year and that about 16 million cases of pertussis occurred worldwide. Ninety-five per cent were in resource-poor countries and whooping cough led to about 195 000 childhood deaths.

Acute bronchitis

Acute bronchitis is an inflammatory condition of the tracheobronchial tree, usually due to infection

Causative agents include rhinoviruses and coronaviruses, which also infect the upper respiratory tract, and lower tract pathogens such as influenza viruses, adenoviruses and Mycoplasma pneumoniae. Secondary bacterial infection with Streptococcus pneumoniae and Haemophilus influenzae may also play a role in pathogenesis. The degree of damage to the respiratory epithelium varies with the infecting agent:

Respiratory syncytial virus infection


Pneumonia has long been known as ‘the old person’s friend’ as it is the most common cause of infection-related death in the USA and Europe. It is caused by a wide range of microorganisms giving rise to indistinguishable symptoms. The challenge lies not in the clinical diagnosis of pneumonia, except perhaps in children, in whom it may be more difficult to diagnose, but in the laboratory identification of the microbial cause.

The respiratory tract has a limited number of ways in which it can respond to infection

The host’s response can be defined by the pathologic and radiologic findings, but the terms can be confusing because they are applied differently in different situations. However, four descriptive terms are in common use (Fig. 19.6):

The outcomes common to all these conditions are respiratory distress resulting from the interference with air exchange in the lungs, and systemic effects as a result of infection in any part of the body.

A wide range of microorganisms can cause pneumonia

Age is an important determinant (Table 19.1):

Table 19.1 Causes of pneumonia related to age

Children Adults
Mainly viral (e.g. respiratory syncytial virus, parainfluenza) or bacterial secondary to viral respiratory infection (e.g. after measles) Bacterial causes more common than viral
Neonates may develop interstitial pneumonitis caused by Chlamydia trachomatis acquired from the mother at birth Aetiology varies with age, underlying disease, occupational and geographic risk factors

Pneumonia in children is more often viral in origin or bacterial secondary to a viral respiratory infection. In adults, bacterial pneumonia is more common.

Pneumonia acquired in hospital tends to be caused by a different spectrum of organisms, particularly Gram-negative bacteria. The causative agents of adult pneumonia are summarized in Figure 19.7. Although clinical and epidemiologic clues help to suggest the likely cause, microbiologic investigations are essential to confirm the diagnosis and ensure optimal antimicrobial therapy.

Viral pneumonias show a characteristic interstitial pneumonia on chest radiography more often than bacterial pneumonias (see Fig. 19.6C), and for the sake of clarity are described separately below. Infections with RSV have been described earlier in this chapter, and opportunist pathogens, such as Pneumocystis jirovecii, associated specifically with pneumonia in the immunocompromised, are described in Chapter 30.

Bacterial pneumonia

A variety of bacteria cause primary atypical pneumonia

When penicillin, an effective antibiotic treatment for pneumococcal infection, became widely available, a significant proportion of cases of pneumonia failed to respond to this treatment and were labelled ‘primary atypical pneumonia’. ‘Primary’ refers to pneumonia occurring as a new event, not secondary to influenza, for example, and ‘atypical’ to the fact that Strep. pneumoniae is not isolated from sputum from such patients, the symptoms are often general as well as respiratory, and the pneumonia fails to respond to penicillin or ampicillin. The causes of atypical pneumonia include Mycoplasma pneumoniae, Chlamydophila (formerly Chlamydia) pneumoniae and Chlamydophila (formerly Chlamydia) psittaci, Legionella pneumophila and Coxiella burnetii. The relative importance of these pathogens varies in different studies (Table 19.2). Infection with Chlamydophila pneumoniae is common. About 50% of adults have antibodies, and in the USA it causes up to 300 000 cases of pneumonia each year in adults. Mycoplasma pneumoniae and Chlamydophila pneumoniae appear to be solely human pathogens, whereas Chlamydophila psittaci and Coxiella burnetii are acquired from infected animals, and Legionella pneumophila is acquired from contaminated environmental sources (see Fig. 19.7).

Moraxella catarrhalis (previously Branhamella catarrhalis) is recognized increasingly as a cause of pneumonia, particularly in patients with carcinoma of the lung or other underlying lung disease. Other aetiologic agents of pneumonia associated with particular underlying diseases, occupations or exposure to animals and travel are summarized in Figure 19.7 and described in other chapters. It is important to note that a causative organism is not isolated in up to 35% of lower respiratory tract infections.

The usual laboratory procedures on sputum specimens from patients with pneumonia are Gram stain and culture

Examination of the Gram-stained sputum (see Ch. 32) can give a presumptive diagnosis within minutes if the film reveals a host response in the form of abundant polymorphs and the putative pathogen, e.g. Gram-positive diplococci characteristic of Streptococcus pneumoniae (Fig. 19.8). The presence of organisms in the absence of polymorphs is suggestive of contamination of the specimen rather than infection, but it is important to remember that immunocompromised patients may not be able to mount a polymorph leukocyte response. Also, remember that the causative agents of atypical pneumonia, with the exception of Legionella pneumophila (Fig. 19.9), will not be seen in Gram-stained smears.

Standard culture techniques will allow the growth of the bacterial pathogens such as Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae and Klebsiella pneumoniae and other non-fastidious Gram-negative rods. Special media or conditions are required for the causative agents of atypical pneumonia, including Legionella pneumophila (Fig. 19.9).

Rapid non-cultural techniques have been applied successfully to the diagnosis of pneumococcal pneumonia. Detection of pneumococcal antigen by agglutination of antibody-coated latex particles (see Ch. 32) can be used with both sputum and urine specimens, as antigen is excreted in the urine. Use of this technique means the result is available within 1    h of receipt of the specimen, but antibiotic susceptibility tests cannot be performed unless the organisms are isolated.

Jul 9, 2017 | Posted by in MICROBIOLOGY | Comments Off on Lower respiratory tract infections

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