BORDETELLA PERTUSSIS: CHARACTERISTICS, MORPHOLOGY, PATHOLOGY - BIOLOGY - 2025

Bordetella pertussis is a Gram negative coccobacillary bacteria that causes the disease called whooping cough, whooping cough, or whooping cough. It was described for the first time by Bordet and Gengou in 1906. It is characterized by being a highly contagious respiratory tract pathology in all stages of the disease.

There is no passive immunity from mother to newborn, so babies are susceptible from birth. Fortunately, this disease is preventable with a vaccine and, as a result, the prevalence is low in developed countries.

Bordetella pertussis colonies on Bordetella pertussis Carbon / Gram Agar

However, in underdeveloped countries it is the main vaccine-preventable disease that causes more morbidity and mortality. Whooping cough is most common in children under 7 years of age, but deaths can occur in any unvaccinated or incompletely vaccinated age group.

Every year 48.5 million people are affected worldwide. There may be asymptomatic carriers but it is rare.

The name “whooping cough” comes from the respiratory howl that resembles that of a beast. This howl is heard in patients after suffering a grueling series of paroxysmal coughs. Paroxysmal means that the cough has a sudden onset and end.

characteristics

Bordetella pertussis has man as its only host. There is no known animal reservoir and it survives with difficulty in the environment.

They are obligate aerobic microorganisms, they thrive at 35-37ºC, they do not use carbohydrates and they are inactive to most biochemical tests. It is an immobile and very demanding bacteria from a nutritional point of view.

B. pertussis produces a siderophore called alkaline identical to that produced by Alcaligenes dentrificans, hence the genus Bordetella belongs to the Alcaligenaceae family.

Virulence factors

Pertussis toxin

It is a protein that has one enzymatic unit and five binding units.

It acts as a promoter of lymphocytosis, a pertussis, an activating factor of the islets of the pancreas and a sensitizing factor to histamine. Triggers hypoglycemia.

Filamentous hemagglutinin

It is a filamentous protein that comes from the fimbriae and mediates the adherence of B. pertussis to eukaryotic cells in vitro and to hair cells of the upper respiratory tract.

It also stimulates the release of cytokines and interferes with the T _H 1 immune response.

Pertactin

It is an immunogenic protein of the outer membrane that helps filamentous hemagglutinin to mediate the attachment of microorganisms to cells.

Tracheal cytotoxin

It has a necrotizing activity, it destroys the epithelial cells of the respiratory tract producing a decrease in ciliary movement.

It is believed to be responsible for the characteristic paroxysmal cough. It also affects the function of polymorphonuclear cells.

Lipopolysaccharide

It is endotoxic due to the content of lipid A, which is responsible for general manifestations such as fever during illness.

Agglutinogens O

It is a thermostable somatic antigen that is present in all species of the genus, and there are also thermolabile ones that help adherence.

Adenylate cyclase

It produces local sensitization to histamine and reduces T lymphocytes. With this, the bacteria evade the immune response and prevent phagocytosis.

Hemolysin

It is cytotoxic at the level of the cells of the respiratory system.

Taxonomy

Domain: Bacteria

Phylum: Proteobacteria

Class: Beta Proteobacteria

Order: Bulkholderiales

Family: Alcaligenaceae

Genus: Bordetella

Species: pertussis

Morphology

Bordetella pertussis occurs as a small Gram-negative coccobacillus mainly in primary cultures, but becomes pleomorphic in subcultures.

It measures around 0.3-0.5 μm wide and 1.0-1.5 μm long. It does not have flagella, therefore it is immobile. It also does not form spores and is encapsulated.

The colonies of B. pertussis in the special medium resemble a few drops of mercury, as they are small, shiny, smooth, with regular edges, convex and pearly in color.

Contagion

The pathology that Bordetella pertussis produces is highly contagious, it is transmitted through droplets of saliva that emerge from the mouth when we speak, laugh or cough, called Fludge droplets.

The disease strikes unimmunized people, that is, it is more common in unvaccinated children or with incomplete vaccination schedules.

It can also attack adults who were immunized in childhood and who may suffer a loss of immunological memory leading to the disease but modified, that is, less severe.

Pathogeny

The bacterium has a high tropism for the nasopharyngeal and tracheal ciliated respiratory epithelium, adhering to them through fimbrial hemagglutinin, pili, pertactin, and pertussis toxin binding subunits. Once fixed, they survive the host's innate defenses and multiply locally.

The bacteria immobilize the cilia and little by little the cells are destroyed and shed. This local damaging effect is produced by tracheal cytotoxin. In this way, the airways are devoid of the ciliary covering, which is a natural defense mechanism against foreign elements.

On the other hand, the combined action of pertussis toxin and adenylate cyclase act on the main cells of the immune system (neutrophils, lymphocytes and macrophages), paralyzing them and inducing their death.

At the bronchial level there is considerable inflammation with local exudates, however, B. pertussis does not invade deep tissues.

In the most severe cases, especially in infants, the bacteria spread to the lungs and cause necrotizing bronchiolitis, intraalveolar hemorrhage, and fibrinous edema. This can lead to respiratory failure and death.

Pathology

This pathology is divided into 3 periods or overlapping stages:

Prodromal or catarrhal period

It begins 5 to 10 days after acquiring the microorganism.

This stage is characterized by nonspecific symptoms similar to that of the common cold, such as sneezing, profuse, mucoid rhinorrhea, which persists for 1 to 2 weeks, red eyes, malaise, anorexia, cough, and mild fever.

In this period there is a large number of microorganisms in the upper respiratory tract, therefore during this stage the disease is highly contagious.

Culturing at this stage is ideal because there is a great chance that the microorganism will be isolated. However, due to the nonspecific symptoms, it is difficult to suspect Bordetella pertussis, therefore the sample is almost never taken at this stage.

The cough may appear at the end of this stage, becoming more persistent, frequent and severe as time passes.

Paroxysmal period

It presents approximately from day 7 to 14. This stage is characterized by the quintosus cough that ends with the prolonged audible inspiratory stridor at the end of the access.

There is wheezing as a result of inspiration through the swollen and stenosed glottis, caused by unsuccessful inspiratory effort during coughing.

Repeated bouts of coughing can cause cyanosis and vomiting. The attacks can be so severe that intermittent mechanical ventilation is often required.

The following complications may occur at this stage: secondary bacterial otitis media, high fever, seizures, inguinal hernia, and rectal prolapse associated with coughing spells.

Encephalopathy can also occur, explained by secondary anoxia and hypoglycemia produced by the paroxysmal cough crisis and by the effects of pertussis toxin, although it is also possible that it is due to intracerebral hemorrhage.

At this stage the number of microorganisms has decreased considerably.

Period of convalescence

It begins 4 weeks after the installation of the microorganism. At this stage, coughing spells decrease in frequency and severity and the bacteria are no longer present or very scarce.

Diagnosis

Whooping cough should be suspected in those patients with paroxysmal cough, inspiratory stridor and vomiting after coughing spells for more than two weeks.

The ideal sample for culture is the nasopharyngeal swab, taken in the catarrhal (ideal) stage or early in the paroxysmal stage.

The special culture medium for Bordetella pertussis is Bordet-Gengou (blood-glycerin-potato agar). It grows very slowly between 3 to 7 days of incubation, in a humid atmosphere.

Diagnostic confirmation of B. pertussis is performed by immunofluorescence with polyclonal or monoclonal antibodies. Also by agglutination with specific antisera of this bacterial strain.

Other diagnostic techniques that can be used are: the polymerase chain reaction (PCR), direct immunofluorescence (DIF) and serological methods such as the determination of antibodies by the ELISA method.

Treatment

Erythromycin or clarithromycin is used preferably, although clotrimoxazole or trimetropim-sulfamethoxazole is also useful, the latter being more used in babies.

Importantly, treatment is more about preventing secondary complications and infections than the actual effect of antibiotics on Bordetella pertussis bacteria.

This is because treatment is usually given in the late stage of the disease, where toxins from the bacteria have already wreaked havoc.

Prevention

Whooping cough or whooping cough is preventable by giving the vaccine.

There is the complete vaccine with killed bacilli, but it has side effects, and the acellular vaccine, which are safer purified preparations.

The pertussis vaccine is present in triple bacterial and pentavalent. It is advisable to administer the pentavalent vaccine from the second month of life.

The pentavalent vaccine, in addition to containing pertussis toxoid or dead Bordetella pertussis bacilli, contains tetanus toxoid, diphtheria toxoid, Hepatitis B virus surface antigen and Haemophilus influenzae capsular polysaccharide.

3 doses of 0.5 cc are recommended every 6 to 8 weeks, then a booster at 18 months with triple bacterial. Sometimes a second booster is necessary in the adult stage, since the immunity generated by the vaccine appears to be neither complete nor long-lasting.

In the event that you have a sick patient, it must be isolated and all objects contaminated with patient secretions must be decontaminated.

The patient should receive treatment to minimize contagion to family members and avoid complications. The earlier treatment is started the better it is to counteract the disease.

The patient's closest relatives should receive preventive treatment with antibiotics, whether they are vaccinated or not.

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