Whooping cough, formally known as Bordetella pertussis, is a bacterium affecting the respiratory tract. While Bordetella pertussis is only pathogenic to humans, other species in the Bordetella family can infect animals, including pets, causing “kennel cough.” As implied by the name “whooping cough,” the infection is characterized by the whooping sound made during the frequent coughing fits. Whooping cough initially presents similarly to the common cold, with congestion, fever, and mild cough. After a week or two, the severe coughing fits set in and typically occur regularly for weeks, according to the Centers for Disease Control.
While the impacts of whooping cough can be significant, with lasting effects from the cough, it is thankfully preventable with a routine childhood vaccine. According to the World Health Organization, as of 2018, 86% of the target population had received the recommended three doses of the DTP vaccine. DTP vaccinates against diphtheria, tetanus, and pertussis and is typically administered to infants starting as early as 6 weeks of age. Vaccination in infancy is especially important as a B. pertussis infection can be especially dangerous for young babies. While the focus of vaccination efforts is on young children, there are vaccination options for adults. The main group of adults who are encouraged to receive these vaccinations are pregnant people, as the protection their bodies gain from the vaccine can be passed on to their baby via the placenta. According to the University of Oxford, the three doses of the vaccine should be completed by the 32nd week of pregnancy to ensure time for antibody production and transmission prior to delivery.
Figure 1: Graph of reported B. pertussis cases in the U.S. from 1922-2023 with indications of the timing of the introduction of pertussis vaccines. This graph shows the great decline of pertussis cases following the introduction of the DTP vaccine as well as the recent increases seen in the past 20 years. Source
After the introduction of the DTP vaccine in the late 1940s, a steep decline was seen up until the 1980s, according to the Centers for Disease Control (Fig. 1). This was followed by an increase that later peaked in 2012 due to an increase in reporting from healthcare professionals, and better diagnostics. They also partially attribute this increase to the fading immunity from the original widespread vaccinations. While these prevention mechanisms have helped us make great progress in whooping cough cases worldwide, the cellular mechanisms employed by the bacterium mean that those who are unvaccinated or partially vaccinated are left vulnerable to the effects of the infection.
Figure 2: Electron micrograph of Bordetella pertussis bacteria. Source
The causative agent of whooping cough, Bordatella pertussis, is a small ovoid Gram-negative bacterium that is transmitted in a host’s respiratory droplets and takes over the respiratory mucosa, the specialized lining of the nasal cavity and respiratory tract. B. pertussis uses multiple techniques to go about colonization. The bacteria form biofilms, groups of bacteria that adhere to a surface, in this case, the cells of the respiratory tract. They also use proteins, polysaccharides, and shorter oligosaccharides to aid in this adhesion and anchor the bacteria. Polysaccharides and oligosaccharides are made of monosaccharides, or “simple sugars.” Prior research from Ganguly et al. has found that the Bordetella pertussis polysaccharide allows for lung colonization. This led researchers to wonder if there was a similar structure impacting nasal colonization
While conducting research, a group at the University of Georgia found a nine-gene region that is responsible for making Bordetellae colonization oligosaccharide, or “b-Cool.” These findings are outlined in Su et al. First, they had to prove the significance of these genes. Using a mouse model, researchers infected mice with two strains of Bordetella bronchiseptica, the causative agent of kennel cough. Since B. pertussis is human-specific, and they were using a mouse model, they had to use an analog that could infect mice. It is important to note that b-Cool is found across Bordetellae, including B. pertussis. The first strain used was the wild-type strain, meaning no changes had been made to the genome. The second strain was the ∆b-Cool strain, a strain containing a deletion of the nine genes associated with b-Cool.
They nasally infected groups of mice with each of the strains and assessed the amount of infectious material at different timepoints in the tissues of the nose, trachea, and lungs. They found significance between the b-Cool and ∆b-Cool groups at timepoints from 6 hours to 3 days post infection in the nasal cavity (Fig. 3E). They found no significance in the trachea (Fig, 3B) or lungs (Fig. 3C) and no significance in the nose at 2 hours and at or after 7 days (Fig. 3E). This shows b-Cool’s importance in early nasal colonization and suggests a difference in the ability for this oligosaccharide to act in different tissues.
Figure 3: Figure from Su et al. showing the significant difference in B. bronchiseptica infectious material between the WT and ∆b-Cool strain nasal colonization in mice. In A, D, and E, we can see the significant difference between the two strains in the nasal cavity from the 6-hour to 3-day timepoints. This shows a disadvantage in the ∆b-Cool strain’s ability to colonize the nasal cavity. B and C show no significant difference between strains in the lung and trachea.
Su et al. performed multiple other experiments as part of this article. They found that airway mucins, a main component of mucus, seem to promote B. pertussis colonization. In environments lacking these mucins, there was no difference observed between the wild type and ∆b-Cool strains. They also found that the ∆b-Cool deficit in colonization observed in mice stood true with multiple mucus sources as long as mucins were present. In addition, they found that b-Cool is important for the transmission of B. pertussis. To test this, they exposed uninfected mice to infected mice via cohabitation. From this, they found a 100% transmission rate of the wild type strain and only a 30% transmission rate of the ∆b-Cool strain.
This study shows the significance of the Bordetellae b-Cool gene locus in transmission and colonization. This suggests that it is a good candidate for future research on the prevention of spread and infection of not only B. pertussis but also other Bordetella species. These findings also allow us to understand one of the mechanisms that the bacterium uses to infect us, by hijacking one of the immune system barriers, mucus. As this article was recently published in the fall of 2025, it is hard to say what advances may come from it. However, gaining a better understanding of how a pathogen infects us allows us to fight it better. So, when you hear about Bordetella pertussis, just remember to “b-Cool.”
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