BACTERIOLOGY
and additional surface proteins, all of which can add to the pathogenesis of Bordetella spp.16
Clinical symptoms
Pertussis disease, an infection of the lungs and respiratory tract usually presents over three phases.
Bordetella pertussis bacteria are small aerobic Gram-negative coccobacilli usually seen singularly or in pairs on Gram staining.
recorded mention of a pertussis-like disease appears to have originated within the late medieval period in Paris 1414 and in the early modern age in London, 1540.9
the disease in children: “Symptoms are severe, the lung is so irritated that, at every attempt to expel the cause of the distress, they can neither inhale or exhale. The sufferer seems to swell up and, as if about to strangle themself, holds their breath.”9
It was not until 1906 when Jules
Bordet and Octave Gengou from the Pasteur Institute in Brussels, isolated the Bordetella bacteria associated with the disease.9
They went on to describe the associated toxins and other virulence factors, which ultimately lead to the development of the whole-cell vaccine, developed in the 1930s by paediatrician Leila Denmark.11
In the UK routine
childhood vaccination for whooping cough using the whole-cell vaccine commenced in 1957 and resulted in a significant reduction in incidence of pertussis disease.12
was recorded in Paris 1578 by physician Guillaume de Baillou,10
The first known epidemic who described
to ciliated epithelial cells in the trachea and nasopharynx, where they replicate and colonise. Toxins are secreted which damage the epithelial lining resulting in loss of ciliated cells and inducement of the characteristic cough.14
The toxins
include pertussis, heat-liable, adenylate cyclase, lipopolysaccharide and tracheal cytotoxin which are associated with pathogenicity, with some enabling the bacteria to evade host immune response mechanisms. The pertussis toxin is considered a significant virulence factor for human disease, and is only produced by B. pertussis; however, both B. parapertussis and B. bronchiseptica possess genes for pertussis toxin without expressing them.15
This protein A less toxic acellular
vaccine was introduced in the 1980s and is widely used in many countries as part of global vaccination action plans.13
Pathogenicity There are numerous pathogenic mechanisms associated with pertussis infection and the bacteria produce various toxins to cause disease. The usual course of infection commences with bacteria entering the host’s respiratory tract via highly infectious airborne droplets. The bacteria adhere
exotoxin secreted by the bacteria consists of five different subunits, designated S1-S5, that formulate A and B subunits. The B subunit being associated cell adhesion and the A subunit for its range of virulence factors within the cell’s regulatory processes and intracellular communication.15 This family of bacteria has had a long time to evolve and is also capable of producing other virulence factors which include filamentous haemagglutinin, fimbriae, lipopolysaccharide, pertactin
The catarrhal phase, which lasts for one-to-two weeks, with usual upper respiratory tract symptoms mostly without fever. This is the most infectious stage and is often not diagnosed due to similar viral URT infections.14 The following paroxysmal phase lasts between one-to-six weeks but has been known to last longer. During this phase patients often have difficulty in expelling thick mucus, which can cause violent and uncontrolled coughing fits. These can produce characteristic short coughing bursts, usually at night followed by an inspiratory whoop, hence the term ‘whooping cough’. These coughing bouts are frequent and usually occur around 15 times in every 24 hours and are clinically diagnostic of pertussis disease. The coughing bouts commonly cause vomiting and cyanosis in children and sweating, facial flushing and (rarely) syncope in adults. Coughing usually increases in the first few weeks, remains for a further two-to-three weeks before gradually reducing. Fever is often absent and not all patients exhibit the characteristic whoop.17
The final convalescent phase lasts for a further two-to-three weeks where gradual improvement is seen; however, coughing fits may return with subsequent URT infections in the following months.17 Pertussis disease can rarely cause
severe complications including pneumonia, seizures and encephalopathy. Death following disease is mostly seen in infants under six months of age, and is usually seen in unvaccinated patients.17
Laboratory diagnosis Clinical diagnosis is often confirmed via bacterial culture within the laboratory, from pernasal swab, nasopharyngeal aspirate, or less commonly, nasal swab. This small aerobic Gram-negative coccobacillus is fastidious and usually requires specialist Bordet-Gengou or
In the UK routine childhood vaccination for whooping cough using the whole-cell vaccine commenced in 1957 and resulted in a significant reduction in incidence of pertussis disease
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