Bordetella pertussis

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Bordetella pertussis
Bordetella pertussis.jpg
Gram stain
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Bacteria
Phylum: Pseudomonadota
Class: Betaproteobacteria
Order: Burkholderiales
Family: Alcaligenaceae
Genus: Bordetella
Species:
B. pertussis
Binomial name
Bordetella pertussis
(Bergey et al. 1923) Moreno-López 1952

Bordetella pertussis is a Gram-negative, aerobic, pathogenic, encapsulated coccobacillus bacterium of the genus Bordetella , and the causative agent of pertussis or whooping cough. Its virulence factors include pertussis toxin, adenylate cyclase toxin, filamentous haemagglutinin, pertactin, fimbria, and tracheal cytotoxin.

Contents

The bacteria are spread by airborne droplets and the disease's incubation period is 7–10 days on average (range 6–20 days). [1] [2] Humans are the only known reservoir for B. pertussis. [3] The complete B. pertussis genome of 4,086,186 base pairs was published in 2003. [4] Compared to its closest relative B. bronchiseptica, the genome size is greatly reduced. This is mainly due to the adaptation to one host species (human) and the loss of capability of survival outside a host body. [5]

Like B. bronchiseptica , B. pertussis can express a flagellum-like structure, even though it has been historically categorized as a nonmotile bacterium. [6]

Taxonomy

The genus Bordetella contains nine species: B. pertussis,B. parapertussis, B. bronchiseptica, B. avium, B. hinzii, B. holmesii, B. trematum, B. ansorpii, and B. petrii. [5]

B. pertussis, B. parapertussis and B. bronchiseptica form a closely related phylogenetical group. B. parapertussis causes a disease similar to whooping cough in humans, and B. bronchiseptica infects a range of mammal hosts, including humans, and causes a spectrum of respiratory disorders. [5]

Evolution

The disease pertussis was first described by French physician Guillaume de Baillou after the epidemic of 1578. The disease may have been described earlier in a Korean medical textbook. [7] The causative agent of pertussis was identified and isolated by Jules Bordet and Octave Gengou in 1906. It is believed that the genus Bordetella may have evolved from ancestors that could survive in the soil according to 16S rRNA gene sequencing data. [8] 16S rRNA is a component of all bacteria that allows for the comparison of phyla within a sample. The expansion of human development into the agricultural field caused there to be an influx of human to soil contact. This increase not only created more advantageous environments for the ancestors of Bordetella not only to thrive in, but to spread to humans as well. Over time, Bordetella , like B. pertussis, has adapted to specifically infect humans and they are still able to multiply and thrive in soil conditions. [9]

It was initially determined that B. pertussis is a monomorphic pathogen in which majority of strains found had the same two types of alleles: ptxA1 or ptxA2. [10] Modern developments in genome sequencing have allowed B. pertussis to be studied more allowing for the discovery of the ptxP region. Through studying the gene, there has been evidence of mutations within the gene that show missing genomes present on the DNA strand. A study by Bart et al., revealed that 25% of the genes on the Tohama I reference strain of B. pertussis sequence were missing in comparison to the ancestral strains. These mutations were noted to be caused by an increase in intragenomic recombination with loss of DNA. Genes controlled by the BvgAS system have transformed B. pertussis into a much more contagious pathogen. [10] In particular, strains with the ptxP3 allele, that developed through mutations in the recent years, have an increased expression of toxins. Ultimately, this leads to higher acuteness of the disease when contracted.   [10] This has causes an upwards trend of most cases of B. pertussis being the ptxP3 strain, especially in developing countries. Since the 1990s, most cases in developed countries such as the United States have ptxP3 isolates rather than the ptxA1 causing it to become the more dominant strain. [9]

Growth requirements

Bordetella pertussis prefers aerobic conditions in pH range of 7.0-7.5, [11] optimal to thrive in the human body. The max pH level for their growth was at a pH level of 8.0. The minimum pH range for minimal growth was at pH 6.0-6.5. The bacteria are not able to reproduce at pH levels lower than 5.0.

In addition, Bordetella pertussis favors a temperature range of 35 °C to 37 °C. [12] It is a strict aerobe as mentioned previously and its nutritional requirements are meticulous in its requirement for nicotinamide supplement. It has been identified that growth of the bacteria is hindered in the presence of fatty acids, peroxide media, metal ions, and sulfides.

As a strict aerobe, the bacteria requires oxygen to grow and sustain. Such aerobes undergo cellular respiration to metabolize substances using oxygen. In such respiration, the terminal electron acceptor for the electron transport chain is oxygen. [13] The organism is oxidase positive, but urease, nitrate reductase, and citrate negative. [14]

Metabolism

B. pertussis presents unique challenges and opportunities for metabolic modeling, especially given its reemergence as a pathogen. Elevated glutamate levels were found to slow growth due to oxidative stress, revealing a complex relationship. This effect is compounded by observations suggesting that a small starting population could amplify oxidative stress through quorum sensing, a phenomenon deserving further investigation. [15]

When B. pertussis is in a balanced that medium of lactate and glutamate that does not accumulate ammonium, a partially faulty citric acid cycle in B. pertussis and its ability to synthesize and break down β-hydroxybutyrate is observed. Cultivating B. pertussis in this medium resulted in some production of polyhydroxybutyrate but no excretion of β-hydroxybutyrate, indicating a more efficient conversion of carbon into biomass compared to existing media formulations. [16]

In biofilm conditions, B. pertussis cells exhibited increased toxin levels alongside reduced expression of certain proteins, indicating a metabolic shift towards utilizing the full tricarboxylic acid (TCA) cycle over the glyoxylate shunt. [17] These changes correlated with heightened polyhydroxybutyrate accumulation and superoxide dismutase activity, potentially contributing to prolonged survival in biofilms. [17] The interplay between protein expression and metabolic responses highlights the intricate mechanisms influencing B. pertussis growth and adaptation. [18] Despite a less negative energy profile compared to host tissues like the human respiratory system, B. pertussis efficiently couples biosynthesis with catabolism, sustaining robust growth even after extended incubation periods. [18]

Host species

Humans are the only host species of B. pertussis. [19] Outbreaks of whooping cough have been observed among chimpanzees in a zoo, and among wild gorillas; in both cases it is considered likely that the infection was acquired as a result of close contact with humans. [20] Several zoos have a long-standing custom of vaccinating their primates against whooping cough. [21]

Research shows that some primate species are highly sensitive to B. pertussis, and developed a clinical whooping cough in high incidence when exposed to low inoculation doses. [22] [23] Whether the bacteria spread naturally in wild animal populations has not been confirmed satisfactorily by laboratory diagnosis. [24] In research settings, baboons have been used as a model of the infection although it is not known whether the pathology in baboons is the same as in humans. [25]

Pertussis

Pertussis is an infection of the respiratory system characterized by a "whooping" sound when the person breathes in. [26] B. pertussis infects its host by colonizing lung epithelial cells. The bacterium contains a surface protein, filamentous haemagglutinin adhesin, which binds to the sulfatides found on cilia of epithelial cells. Other adhesins are fimbriae and petractin. [27] Once anchored, the bacterium produces tracheal cytotoxin, which stops the cilia from beating. This prevents the cilia from clearing debris from the lungs, so the body responds by sending the host into a coughing fit. [28] B. pertussis has the ability to inhibit the function of the host's immune system. The toxin, known as pertussis toxin, inhibits G protein coupling that regulates an adenylate cyclase-mediated conversion of ATP to cyclic adenosine monophosphate. The result is that phagocytes convert too much adenosine triphosphate to cyclic adenosine monophosphate, causing disturbances in cellular signaling mechanisms, and preventing phagocytes from correctly responding to the infection. Pertussis toxin, formerly known as lymphocytosis-promoting factor, causes a decrease in the entry of lymphocytes into lymph nodes, which can lead to a condition known as lymphocytosis, with a complete lymphocyte count of over 4000/μl in adults or over 8000/μl in children. Beside targeting lymphocytes, it limits neutrophil migration to the lungs. It also decreases the function of tissue-resident macrophages, which are responsible for some bacterial clearance. [29]

The infection of B. pertussis occurs mostly in children under the age of one since this is when they are unimmunized, or children with faded immunity, normally around the ages 11 through 18. The signs and symptoms are similar to a common cold: runny nose, sneezing, mild cough, and low-grade fever. [30] The patient becomes most contagious during the catarrhal stage of infection, normally two weeks after the coughing begins. It may become airborne when the person coughs, sneezes, or laughs. The paroxysmal cough precedes a crowing inspiratory sound characteristic of pertussis. After a spell, the patient might make a "whooping" sound when breathing in, or may vomit. Transmission rates are expected to rise as the host experiences their most contagious stage when the total viable count of B. pertussis is at its highest. After the host coughs, the bacteria in their respiratory airways will be exposed into the air by way of aerosolized droplets, threatening nearby humans. [31]

A human host can exhibit a range of physical reactions as a result of the  B. pertussis pathogen, depending on how well their body is equipped to fight infection. [31] Adults have milder symptoms, such as prolonged coughing without the "whoop". Infants less than six months also may not have the typical whoop. A coughing spell may last a minute or more, producing cyanosis, apnea, and seizures.

Transmission and infection

B. pertussis is a highly contagious infection of the respiratory tract. [32] However, for B. pertussis to persist in a population the bacterium needs an uninterrupted chain of transmission as there are no animal reservoirs and the bacteria do not survive in the environment. B. pertussis primarily spreads through respiratory droplets, requiring direct contact between individuals due to its short survival time outside the body.

It was noted that between 1991 and 2008, there were 258 deaths for infants 8 months old and younger. [33]

Progression of disease

Pertussis manifests in three distinct stages. The dynamic progression of pertussis, characterized by its distinct phases from incubation to paroxysmal coughing, underscores the complexity of the disease's clinical manifestations and highlights the potential significance of toxin release in driving symptoms. [34]

Following exposure, an incubation period of 5–7 days ensues before symptoms appear. [34]

The catarrhal phase follows, characterized by cold-like symptoms lasting about a week, with a high isolation rate of the organism. This phase transitions into the paroxysmal phase, where the dry cough evolves into a severe, paroxysmal cough with mucous secretion and vomiting. [34]

The coughing fits, characterized by efforts to expel respiratory secretions, may result in a distinctive whooping sound. Recovery of the organism diminishes significantly during this phase. Although the organism is seldom detected in the blood, it is theorized that the clinical symptoms primarily stem from toxin release. The paroxysmal phase typically persists for a minimum of 2 weeks. [34]

Diagnosis

A nasopharyngeal swab or aspirate can be sent to the bacteriology laboratory for Gram stain (Gram-negative, coccobacilli, diplococci arrangement), with growth on Bordet–Gengou agar or buffered charcoal yeast extract agar with added cephalosporin to select for the organism, which shows mercury drop-like colonies. Endotracheal tube aspirates or bronchoalveolar lavage fluids are preferred for laboratory diagnostics due to their direct contact with the ciliated epithelial cells and higher isolation rates of the pathogen.

Laboratory diagnostic methods used to identify B. pertussis:

  1. Serology [35]
    1. Identification of specific agglutinating antibodies in the patient's blood serum with a high sensitivity and specificity rate.
    2. Able to detect the level of virulence and measure the immune response to the pathogen.
    3. Recommend those corresponding to the catarrhal phase of the illness. Not used in infants due to delay of positive results, often indicating the disease has progressed.
    4. Sparked the development of ELISA kits.
  2. Microbiological culture [35] [36]
    1. Known for high specificity, the ability to subtype the colonies presented and limited sensitivity. Ideal for antimicrobial resistant monitoring. Specificity results can be affected by age, immunization status, duration of symptoms, and even specimen handling.
    2. It is very difficult to cultivate separate pathogens and only high bacterial loads can lead to a positive culture. The ideal stage for isolation is the catarrhal stage or the beginning of the paroxysmal stage. Vaccinated persons also have a lower rate of isolation.
    3. Plates are incubated at 36 °C under high humidity for 7–10 days before obtaining results.
  3. Classical PCR assay [35]
    1. Being the test of choice, this procedure is known for its quick and high sensitivity, however; often inaccurate when identifying between Bordetella species.
    2. The primers used for PCR usually target the transposable elements IS481 and IS1001. [37]
    3. Recommend to be performed on infants and those corresponding to the catarrhal phase of the illness. It can detect the pathogens in atypical manifestations and vaccinated patients for longer periods, compared to the culture.
    4. Target genes within B. pertussis are IS481, IS1002, ptxS1, Ptx-Pr, and BP3385, however, B. bronchispeticaand B. holmesii contain similar gene expression, leaving it difficult to differentiate between the bacterium in the laboratory. The most effective technique to differentiate between the two bacteria is by human and animal isolates. Singleplex PCR identifies the target gene ptxS1.
  4. Direct Fluorescent Antibody Testing (DFA) [35]
    1. Inexpensive and direct results of Bordetella detection with poor sensitivity and specificity. This test stains the nasopharyngeal secretions with a fluorescent modified antibody that binds directly to the B. pertussis or B. parapertussis bacteria. If positive, the binding antibody would glow under the microscope. Because of the low specificity, it is common to receive false positives with polyclonal antibodies occurring.

Several diagnostic tests are available, particularly the enzyme-linked immunosorbent assay ELISA kits. These are designed to detect filamentous hemagglutinin (FHA) and/or anti-pertussis-toxin antibodies of IgG, IgA, or IgM. Some kits use a combination of antigens which leads to a higher sensitivity, but might also make the interpretation of the results harder since one cannot know which antibody has been detected. [38]

Misdiagnosis is common due to diagnostic techniques, misidentification between species in laboratories, and clinician error.  The misdiagnoses between Bordetella species further increase the likelihood of antibiotic resistance. These factors highlight the need for a procedure to target all species through specific and fast methods.

Treatment and prevention

Treatment

Whooping cough is treated by macrolides, for example erythromycin. The therapy is most effective when started during the incubation period or the catarrhal period. It is ideal for treatment should be within 1–2 weeks from onset of symptoms. When applied during the paroxysmal cough phase, the time of reconvalescence is not affected, only further transmission is reduced to 5–10 days after infection. [39] [40]

Prevention

Pertussis vaccine has been widely used since the second half of the 20th century. [41] [2] The first vaccines were whole-cell vaccines (wP), composed of chemically inactivated bacteria and given intramuscularly. When give, the inactive bacteria and antigens trigger the immune response and mimics natural infection.

Due to the frequent reports of reactions at the injection site, scientists started to replaced whole cell vaccines with acellular pertussis (aP) vaccines which have, recently, shown a decreased time of immunity and level of protection against colonization. [42] These acellular vaccines are also intramuscular and are composed of purified surface antigens, mainly fimbriae, filamentous hemagglutinin, pertactin and pertussis toxin. Both vaccines are still used today, with the aP vaccine predominantly used in developed countries.

The aP vaccine is also a part of the diphtheria, tetanus, and acellular pertussis (DTaP) immunization. [2] Those being administered these vaccines are recommended to receive boosters as they are only afford protection for about 4–12 years; while natural infection offers 7–20 years. [43] Cases in infants are common and often have serious impacts as they are more susceptible to Bordetella pertussis than adolescents and healthy adults. Therefore, to decrease likelihood of contracting and spreading this disease, parents are recommended to receive the preventative vaccine. [44]

With the resurgence of pertussis cases, there are concerns regarding the level of protection provided by the current vaccine. This vaccine does not offer protection against other species of Bordetella such as B. holmesii and B. bronchiseptica and further highlights the need for a revamped vaccine. Research is currently developing a novel vaccine such as the BPZE1, which is a live attenuated vaccine against B. pertussis and challenges the other pathogens in the 'Classical Bordetellae'. This new vaccine inactivates the gene encoding 3 major toxins with only a single intranasal dose. It is currently being studied for safety in immunocompromised patients and pregnant women. There are other promising vaccines that are under study and in trial periods for accuracy, efficacy, and safety. [43]

Related Research Articles

<span class="mw-page-title-main">Whooping cough</span> Human disease caused by the bacteria Bordetella pertussis

Whooping cough, also known as pertussis or the 100-day cough, is a highly contagious, vaccine-preventable bacterial disease. Initial symptoms are usually similar to those of the common cold with a runny nose, fever, and mild cough, but these are followed by two or three months of severe coughing fits. Following a fit of coughing, a high-pitched whoop sound or gasp may occur as the person breathes in. The violent coughing may last for 10 or more weeks, hence the phrase "100-day cough". The cough may be so hard that it causes vomiting, rib fractures, and fatigue. Children less than one year old may have little or no cough and instead have periods when they cannot breathe. The incubation period is usually seven to ten days. Disease may occur in those who have been vaccinated, but symptoms are typically milder.

<span class="mw-page-title-main">Acute bronchitis</span> Medical condition

Acute bronchitis, also known as a chest cold, is short-term bronchitis – inflammation of the bronchi of the lungs. The most common symptom is a cough. Other symptoms include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. The infection may last from a few to ten days. The cough may persist for several weeks afterward with the total duration of symptoms usually around three weeks. Some have symptoms for up to six weeks.

<span class="mw-page-title-main">Exotoxin</span> Toxin from bacteria that destroys or disrupts cells

An exotoxin is a toxin secreted by bacteria. An exotoxin can cause damage to the host by destroying cells or disrupting normal cellular metabolism. They are highly potent and can cause major damage to the host. Exotoxins may be secreted, or, similar to endotoxins, may be released during lysis of the cell. Gram negative pathogens may secrete outer membrane vesicles containing lipopolysaccharide endotoxin and some virulence proteins in the bounding membrane along with some other toxins as intra-vesicular contents, thus adding a previously unforeseen dimension to the well-known eukaryote process of membrane vesicle trafficking, which is quite active at the host–pathogen interface.

<i>Bordetella bronchiseptica</i> Species of bacterium

Bordetella bronchiseptica is a small, gram-negative, rod-shaped bacterium of the genus Bordetella. It can cause infectious bronchitis in dogs and other animals, but rarely infects humans. Closely related to B. pertussis—the obligate human pathogen that causes pertussis ; B. bronchiseptica can persist in the environment for extended periods.

<i>Bordetella</i> Genus of bacteria

Bordetella is a genus of small, Gram-negative, coccobacilli bacteria of the phylum Pseudomonadota. Bordetella species, with the exception of B. petrii, are obligate aerobes, as well as highly fastidious, or difficult to culture. All species can infect humans. The first three species to be described are sometimes referred to as the 'classical species'. Two of these are also motile.

<i>Corynebacterium diphtheriae</i> Species of prokaryote

Corynebacterium diphtheriae is a Gram-positive pathogenic bacterium that causes diphtheria. It is also known as the Klebs–Löffler bacillus because it was discovered in 1884 by German bacteriologists Edwin Klebs (1834–1912) and Friedrich Löffler (1852–1915). These bacteria are usually harmless, unless they are infected by a bacteriophage carrying a gene which gives rise to a toxin. This toxin causes the disease. Diphtheria is caused by the adhesion and infiltration of the bacteria into the mucosal layers of the body, primarily affecting the respiratory tract and causing the subsequent release of an exotoxin. The toxin has a localized effect on skin lesions, as well as a metastatic, proteolytic effects on other organ systems in severe infections. Originally a major cause of childhood mortality, diphtheria has been almost entirely eradicated due to the vigorous administration of the diphtheria vaccination in the 1910s.

<span class="mw-page-title-main">Kennel cough</span> Upper respiratory infection affecting dogs

Kennel cough is an upper respiratory infection affecting dogs. There are multiple causative agents, the most common being the bacterium Bordetella bronchiseptica, followed by canine parainfluenza virus, and to a lesser extent canine coronavirus. It is highly contagious; however, adult dogs may display immunity to reinfection even under constant exposure. Kennel cough is so named because the infection can spread quickly among dogs in the close quarters of a kennel or animal shelter.

<span class="mw-page-title-main">Pertussis toxin</span> Group of toxins

Pertussis toxin (PT) is a protein-based AB5-type exotoxin produced by the bacterium Bordetella pertussis, which causes whooping cough. PT is involved in the colonization of the respiratory tract and the establishment of infection. Research suggests PT may have a therapeutic role in treating a number of common human ailments, including hypertension, viral infection, and autoimmunity.

Adenylate cyclase toxin is a virulence factor produced by some members of the genus Bordetella. Together with the pertussis toxin it is the most important virulence factor of the causative agent of whooping cough, Bordetella pertussis. Bordetella bronchiseptica and Bordetella parapertussis, also able to cause pertussis-like symptoms, also produce adenylate cyclase toxin. It is a toxin secreted by the bacteria to influence the host immune system.

<i>Bordetella parapertussis</i> Species of bacterium

Bordetella parapertussis is a small Gram-negative bacterium of the genus Bordetella that is adapted to colonise the mammalian respiratory tract. Pertussis caused by B. parapertussis manifests with similar symptoms to B. pertussis-derived disease, but in general tends to be less severe. Immunity derived from B. pertussis does not protect against infection by B. parapertussis, however, because the O-antigen is found only on B. parapertussis. This antigen protects B. parapertussis against antibodies specific to B. pertussis, so the bacteria are free to colonize the host's lungs without being subject to attack by previous antibodies. These findings suggest B. parapertussis evolved in a host population that had already developed immunity to B. pertussis, where being able to evade B. pertussis immunity was an advantage.

The AB5 toxins are six-component protein complexes secreted by certain pathogenic bacteria known to cause human diseases such as cholera, dysentery, and hemolytic–uremic syndrome. One component is known as the A subunit, and the remaining five components are B subunits. All of these toxins share a similar structure and mechanism for entering targeted host cells. The B subunit is responsible for binding to receptors to open up a pathway for the A subunit to enter the cell. The A subunit is then able to use its catalytic machinery to take over the host cell's regular functions.

<span class="mw-page-title-main">Immunization during pregnancy</span>

Immunization during pregnancy is the administration of a vaccine to a pregnant individual. This may be done either to protect the individual from disease or to induce an antibody response, such that the antibodies cross the placenta and provide passive immunity to the infant after birth. In many countries, including the US, Canada, UK, Australia and New Zealand, vaccination against influenza, COVID-19 and whooping cough is routinely offered during pregnancy.

<span class="mw-page-title-main">Pathogenic bacteria</span> Disease-causing bacteria

Pathogenic bacteria are bacteria that can cause disease. This article focuses on the bacteria that are pathogenic to humans. Most species of bacteria are harmless and are often beneficial but others can cause infectious diseases. The number of these pathogenic species in humans is estimated to be fewer than a hundred. By contrast, several thousand species are part of the gut flora present in the digestive tract.

Bordet–Gengou agar is a type of agar plate optimized to isolate Bordetella, containing blood, potato extract, and glycerol, with an antibiotic such as cephalexin or penicillin and sometimes nicotinamide. The potato extract provided nitrogen and vitamins, and potato starch absorbed fatty acids present in nasal secretions or collection-swab cotton that inhibited growth; glycerol was a carbon source. Medical Microbiology, 4th edition, states that Regan-Lowe medium has replaced Bordet–Gengou medium as the medium of choice for routine Bordetella pertussis incubation.

<span class="mw-page-title-main">Pertussis vaccine</span> Vaccine protecting against whooping cough

Pertussis vaccine is a vaccine that protects against whooping cough (pertussis). There are two main types: whole-cell vaccines and acellular vaccines. The whole-cell vaccine is about 78% effective while the acellular vaccine is 71–85% effective. The effectiveness of the vaccines appears to decrease by between 2 and 10% per year after vaccination with a more rapid decrease with the acellular vaccines. The vaccine is only available in combination with tetanus and diphtheria vaccines. Pertussis vaccine is estimated to have saved over 500,000 lives in 2002.

Microbial toxins are toxins produced by micro-organisms, including bacteria, fungi, protozoa, dinoflagellates, and viruses. Many microbial toxins promote infection and disease by directly damaging host tissues and by disabling the immune system. Endotoxins most commonly refer to the lipopolysaccharide (LPS) or lipooligosaccharide (LOS) that are in the outer plasma membrane of Gram-negative bacteria. The botulinum toxin, which is primarily produced by Clostridium botulinum and less frequently by other Clostridium species, is the most toxic substance known in the world. However, microbial toxins also have important uses in medical science and research. Currently, new methods of detecting bacterial toxins are being developed to better isolate and understand these toxins. Potential applications of toxin research include combating microbial virulence, the development of novel anticancer drugs and other medicines, and the use of toxins as tools in neurobiology and cellular biology.

<span class="mw-page-title-main">Tracheal cytotoxin</span> Chemical compound

Tracheal cytotoxin (TCT) is a 921 dalton glycopeptide released by Bordetella pertussis, Vibrio fischeri, and Neisseria gonorrhoeae. It is a soluble piece of peptidoglycan (PGN) found in the cell wall of all gram-negative bacteria, but only some bacteria species release TCT due to inability to recycle this piece of anhydromuropeptide.

Bordetella avium is a gram negative, nonfermentative, strictly aerobic, motile bacterium from the genus Bordetella which has been isolated from patients with respiratory disease. B. avium has a global distribution, that mainly affects young domesticated turkeys. The disease in birds is called bordetellosis, and is largely associated with confined spaces and multi-aged flocks where management practices are sub optimal. In most infections, mortality is typically low but morbidity is very high.

Bordetella trematum is a species of Gram-negative bacteria identified in 1996 by comparison of 10 strains of B. trematum against other well characterized Bordetella and Alcaligenes species. The term trema refers to something pierced or penetrated, or to a gap. "Trematum" pertains to open things, and refers to the presence of bacteria in wounds and other exposed parts of the body. Strain LMG 13506T is the reference strain for this species.

Vaccine resistance is the evolutionary adaptation of pathogens to infect and spread through vaccinated individuals, analogous to antimicrobial resistance. It concerns both human and animal vaccines. Although the emergence of a number of vaccine resistant pathogens has been well documented, this phenomenon is nevertheless much more rare and less of a concern than antimicrobial resistance.

References

  1. ↑ Heymann DL, ed. (2008). Pertussis; in Control of Communicable Diseases Manual (19th ed.). Washington DC: American Public Health Association. p. 457. ISBN   978-0-87553-189-2.
  2. 1 2 3 Organisation mondiale de la santé, World Health Organization (1998). Relevé épidémiologique hebdomadaire (Online) = Weekly epidemiological record. Organisation mondiale de la sante. OCLC   301147153.
  3. ↑ Havers FP, Moro PL, Hariri S, Skoff T (2015). "Pertussis". In Atkinson W, Wolfe S, Hamborsky J (eds.). Epidemiology and Prevention of Vaccine-Preventable Diseases: The Pink Book (13th ed.). Centers for Disease Control and Prevention, Public Health Foundation.
  4. ↑ Parkhill J, Sebaihia M, Preston A, Murphy LD, Thomson N, Harris DE, et al. (September 2003). "Comparative analysis of the genome sequences of Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica". Nature Genetics. 35 (1): 32–40. doi: 10.1038/ng1227 . PMID   12910271.
  5. 1 2 3 Locht C (2007). Bordetella: molecular microbiology. Wymondham: Horizon Bioscience. ISBN   978-1-904933-31-1. OCLC   159579443.
  6. ↑ Hoffman CL, Gonyar LA, Zacca F, Sisti F, Fernandez J, Wong T, et al. (May 2019). "Bordetella pertussis Can Be Motile and Express Flagellum-Like Structures". mBio. 10 (3): e00787–19. doi:10.1128/mBio.00787-19. PMC   6520453 . PMID   31088927.
  7. ↑ "Origin and evolution of Bordetella pertussis". Sanger. 24 April 2014. Retrieved 2024-05-29.
  8. ↑ Hamidou Soumana I, Linz B, Harvill ET (2017). "Environmental Origin of the Genus Bordetella". Frontiers in Microbiology. 8: 28. doi: 10.3389/fmicb.2017.00028 . PMC   5258731 . PMID   28174558.
  9. 1 2 Belcher T, Preston A (November 2015). Carbonetti N (ed.). "Bordetella pertussis evolution in the (functional) genomics era". Pathogens and Disease. 73 (8): ftv064. doi:10.1093/femspd/ftv064. ISSN   2049-632X. PMC   4626590 . PMID   26297914.
  10. 1 2 3 Sealey KL, Belcher T, Preston A (2016-06-01). "Bordetella pertussis epidemiology and evolution in the light of pertussis resurgence". Infection, Genetics and Evolution. 40: 136–143. Bibcode:2016InfGE..40..136S. doi:10.1016/j.meegid.2016.02.032. ISSN   1567-1348. PMID   26932577.
  11. ↑ Remesh AT, Alagarasu K, Jadhav S, Prabhakar M, Viswanathan R (2024-02-28). "Pertussis Vaccines Scarcely Provide Protection against Bordetella parapertussis Infection in Children—A Systematic Review and Meta-Analysis". Vaccines. 12 (3): 253. doi: 10.3390/vaccines12030253 . ISSN   2076-393X. PMC   10974608 . PMID   38543887.
  12. ↑ Hulbert RR, Cotter PA (November 2009). "Laboratory Maintenance of Bordetella pertussis". Current Protocols in Microbiology. 15 (1): Unit 4B.1. doi:10.1002/9780471729259.mc04b01s15. ISSN   1934-8525. PMID   19885941.
  13. ↑ Borisov VB, Verkhovsky MI (2015). "Oxygen as Acceptor". EcoSal Plus. 6 (2). doi:10.1128/ecosalplus.ESP-0012-2015. ISSN   2324-6200. PMC   11575855 . PMID   26734697.
  14. ↑ Aryal S (2022-05-26). "Biochemical Test of Bordetella pertussis". microbenotes.com. Retrieved 2024-04-17.
  15. ↑ Vitelli M, Tamer IM, Pritzker M, Budman H (May 2023). "Modeling the effect of oxidative stress on Bordetella pertussis fermentations". Biotechnology Progress. 39 (3): e3335. doi: 10.1002/btpr.3335 . ISSN   8756-7938. PMID   36799126.
  16. ↑ Thalen M, van den IJssel J, Jiskoot W, Zomer B, Roholl P, de Gooijer C, et al. (October 1999). "Rational medium design for Bordetella pertussis: basic metabolism". Journal of Biotechnology. 75 (2–3): 147–159. doi:10.1016/s0168-1656(99)00155-8. ISSN   0168-1656. PMID   10553654.
  17. 1 2 Suyama H, Luu LD, Zhong L, Raftery MJ, Lan R (2023). "Integrating proteomic data with metabolic modeling provides insight into key pathways of Bordetella pertussis biofilms". Frontiers in Microbiology. 14. doi: 10.3389/fmicb.2023.1169870 . ISSN   1664-302X. PMC   10435875 . PMID   37601354.
  18. 1 2 Popović ME, Stevanović M, Pantović Pavlović M (April 2024). "Return of the forgotten nightmare: Bordetella pertussis uses a more negative Gibbs energy of metabolism to outcompete its host organism". Microbial Risk Analysis. 26: 100292. doi:10.1016/j.mran.2024.100292. ISSN   2352-3522.
  19. ↑ "15.3E: Whooping Cough". Biology LibreTexts. 2018-06-29. Retrieved 2024-03-29.
  20. ↑ Gustavsson OE, Röken BO, Serrander R (1990). "An epizootic of whooping cough among chimpanzees in a zoo". Folia Primatologica; International Journal of Primatology. 55 (1): 45–50. doi:10.1159/000156498. PMID   2394416.
  21. ↑ Loomis MR (1985). "Immunoprofylaxis in infant great apes". In Graham CE, Bowen JA (eds.). Clinical Management of Infant Great Apes. Monographs in Primatology. Vol. 5. New York: Liss. pp. 107–112.
  22. ↑ Gustavsson OE, Röken BO, Serrander R (1990-02-14). "An Epizootic of Whooping Cough among Chimpanzees in a Zoo". Folia Primatologica. 55 (1): 45–50. doi:10.1159/000156498. ISSN   0015-5713. PMID   2394416.
  23. ↑ Warfel JM, Merkel TJ (October 2014). "The baboon model of pertussis: effective use and lessons for pertussis vaccines". Expert Review of Vaccines. 13 (10): 1241–1252. doi:10.1586/14760584.2014.946016. ISSN   1476-0584. PMID   25182980.
  24. ↑ Ryan SJ, Walsh PD (2011). "Consequences of Non-Intervention for Infectious Disease in African Great Apes | PLOS ONE". PLOS ONE. 6 (12): e29030. doi: 10.1371/journal.pone.0029030 . PMC   3245243 . PMID   22216162.
  25. ↑ Cherry, J.D. The History of Pertussis (Whooping Cough); 1906–2015: Facts, Myths, and Misconceptions. Curr Epidemiol Rep 2, 120–130 (2015). https://doi.org/10.1007/s40471-015-0041-9
  26. ↑ Lv Z, Yin S, Jiang K, Wang W, Luan Y, Wu S, et al. (May 2023). "The whole-cell proteome shows the characteristics of macrolides-resistant Bordetella pertussis in China linked to the biofilm formation". Archives of Microbiology. 205 (6): 219. Bibcode:2023ArMic.205..219L. doi:10.1007/s00203-023-03566-0. PMC   10164027 . PMID   37148370.
  27. ↑ Locht C (2007). Bordetella: molecular microbiology. Wymondham: Horizon Bioscience. ISBN   978-1-904933-31-1. OCLC   159579443.
  28. ↑ [https://www.cdc.gov/vaccines/pubs/pinkbook/downloads/pert.pdf CDC Bordetella pertussis}
  29. ↑ Carbonetti NH (June 2007). "Immunomodulation in the pathogenesis of Bordetella pertussis infection and disease". Current Opinion in Pharmacology. Respiratory/Musculoskeletal. 7 (3): 272–278. doi:10.1016/j.coph.2006.12.004. PMID   17418639.
  30. ↑ Havers FP, Moro PL, Hariri S, Skoff T (2015). "Pertussis". In Atkinson W, Wolfe S, Hamborsky J (eds.). Epidemiology and Prevention of Vaccine-Preventable Diseases: The Pink Book (13th ed.). Centers for Disease Control and Prevention, Public Health Foundation.
  31. 1 2 Warfel JM, Beren J, Merkel TJ (September 2012). "Airborne transmission of Bordetella pertussis". The Journal of Infectious Diseases. 206 (6): 902–906. doi:10.1093/infdis/jis443. PMC   3501154 . PMID   22807521.
  32. ↑ Kline JM, Smith EA, Zavala A (August 2021). "Pertussis: Common Questions and Answers". American Family Physician. 104 (2): 186–192. PMID   34383446.
  33. ↑ Carbonetti NH (June 2016). "Bordetella pertussis: new concepts in pathogenesis and treatment". Current Opinion in Infectious Diseases. 29 (3): 287–94. doi:10.1097/QCO.0000000000000264. PMC   4846492 . PMID   26906206.
  34. 1 2 3 4 Kerr JR, Matthews RC (2000-03-03). "Bordetella pertussis Infection: Pathogenesis, Diagnosis, Management, and the Role of Protective Immunity". European Journal of Clinical Microbiology & Infectious Diseases. 19 (2): 77–88. doi:10.1007/s100960050435. ISSN   0934-9723. PMID   10746492.
  35. 1 2 3 4 Zouari A (21 Nov 2011). "The diagnosis of pertussis: which method to choose?". Critical Reviews in Microbiology. 38 (2): 111–121. doi:10.3109/1040841X.2011.622715. PMID   22103249.
  36. ↑ Bouchez V, Guillot S, Landier A, Armatys N, Matczak S, Toubiana J, et al. (2021-09-16). "Evolution of Bordetella pertussis over a 23-year period in France, 1996 to 2018". Eurosurveillance. 26 (37): 2001213. doi:10.2807/1560-7917.ES.2021.26.37.2001213. ISSN   1560-7917. PMC   8447829 . PMID   34533118.
  37. ↑ Nieves DJ, Heininger U (June 2016). "Bordetella pertussis". Microbiology Spectrum. 4 (3): 311–339. doi:10.1128/microbiolspec.EI10-0008-2015. ISBN   978-1-55581-944-6. PMID   27337481. S2CID   30621755.
  38. ↑ "ELISA classic - Bordetella pertussis | SERION Diagnostics". www.serion-diagnostics.de. Retrieved 2024-04-17.
  39. ↑ Organisation mondiale de la santé, World Health Organization (1998). Relevé épidémiologique hebdomadaire (Online) = Weekly epidemiological record. Organisation mondiale de la sante. OCLC   301147153.
  40. ↑ Finger H, von Koenig CH (1996). "Bordetell". In Baron S (ed.). Medical Microbiology (4th ed.). Galveston (TX): University of Texas Medical Branch at Galveston. ISBN   978-0-9631172-1-2. PMID   21413270.
  41. ↑ Sealey KL, Belcher T, Preston A (June 2016). "Bordetella pertussis epidemiology and evolution in the light of pertussis resurgence". Infection, Genetics and Evolution. 40: 136–143. Bibcode:2016InfGE..40..136S. doi:10.1016/j.meegid.2016.02.032. PMID   26932577.
  42. ↑ Carbonetti NH (June 2016). "Bordetella pertussis: new concepts in pathogenesis and treatment". Current Opinion in Infectious Diseases. 29 (3): 287–294. doi:10.1097/QCO.0000000000000264. PMC   4846492 . PMID   26906206.
  43. 1 2 Miguelena Chamorro B, De Luca K, Swaminathan G, Longet S, Mundt E, Paul S (2023-09-21). "Bordetella bronchiseptica and Bordetella pertussis: Similarities and Differences in Infection, Immuno-Modulation, and Vaccine Considerations". Clinical Microbiology Reviews. 36 (3): e0016422. doi:10.1128/cmr.00164-22. ISSN   0893-8512. PMC   10512794 . PMID   37306571.
  44. ↑ Wang J, Gao J, Fan H, Guo H, Yin Z, Dong M, et al. (April 2023). "Multiple rib and vertebral fractures associated with Bordetella pertussis infection: a case report". BMC Infectious Diseases. 23 (1): 212. doi: 10.1186/s12879-023-08189-w . PMC   10080936 . PMID   37024849.

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