Bordetella

From MicrobeWiki, the student-edited microbiology resource

A Microbial Biorealm page on the genus Bordetella

Classification

Higher order taxa

Bacteria; Proteobacteria; Betaproteobacteria; Burkholderiales; Alcaligenaceae; Bordetella

Species

B. pertussis, B. parapertussis, B. bronchiseptica, B. avium, B. petrii

NCBI: Taxonomy

Description and significance

Describe the appearance, habitat, etc. of the organism, and why you think it is important.

Genome structure

Describe the size and content of the genome. How many chromosomes? Circular or linear? Other interesting features? What is known about its sequence?


Cell structure and metabolism

Interesting features of cell structure; how it gains energy; what important molecules it produces.


Ecology

B. pertussis is a strict human pathogen that takes residence in the respiratory tract. B. pertussis is not found in animals, and it survives poorly in the environment. B. bronchiseptica was originally isolated in dogs but then was later found in other species of animals, including pigs, rabbits, and rats. In 1967, B. avium was isolated from young turkeys and by 1993 there were reports of it being isolated in cockatiel chicks. Recent research shows that this strain has been isolated in chickens, finches, noble macaws, Japanese quails, and ostriches. The optimal temperature of survival for all species of Bordetella is 35-37°C, therefore they are termed mesophiles because they survive best in moderate conditions.

Epidemiology

Prior to the 20th century, whooping cough was a terrible childhood disease. In 2005, it still accounted for about thirty-five thousand deaths per year worldwide. Seventy percent of these fatal cases occur in infants and children less than one year of age. There is no seasonal pattern in the spread of Bordetella. In the 1940’s, with the introduction of immunization for pertussis, the number of cases in the United States fell from 250,000 cases a year to less than 1 case out of 100,000 people. At one point there was a concern over vaccination reactions which led to a decrease in immunization rates and an increase in pertussis. The disease often goes unrecognized in adults which aids in the spread of the bacteria. In addition, outbreaks have been found to be associated with incomplete or reduced immunization. The vaccine formerly used was known as DTP and included antibodies for the diphtheria toxin (D), tetanus toxin (T), and pertussis (P). This vaccine has been replaced with the safer DTaP vaccine that causes fewer side effects. DTaP is an acellular vaccine that is genetically engineered to be immunogenic, inducing an immune response, but non-toxic. The vaccine is used for full primary immunization at 2, 4, and 6 months and boosters between 15-18 months and 4-6 years with additional boosters every 10 years.

Transmission of B. pertussis is most commonly spread from person-to-person through small droplets of respiratory secretions traveling in the air. In rare instances, B. pertussis can be transmitted by contact with freshly contaminated particles alone. Occurrence of pertussis may increase in summer and fall. However, as previously noted, research indicates that the spread of pertussis follows no seasonal pattern. Common sites of infection include schools and day care centers because parents, caregivers, and older siblings are “reservoirs” for B. pertussis. In adults, symptoms are generally mild so these individuals may not seek any treatment. By not getting medical attention, their disease is still highly contagious allowing for continued transmission of the disease to children.

The transmission of Bordetella in birds seems to be through contact. It does not seem to be an airborne disease because an infected bird in a cage next to an uninfected bird in a cage will not spread the disease. In the case of humans, Bordetella is an airborne disease and is highly contagious.

Pathology

Bordetella can be spread by airborne droplets and is highly contagious. The bacterium does not invade the cells of the respiratory tract nor do they spread to deeper tissues, instead Bordetella colonizes and multiplies on the mucus membranes of the respiratory tract. The bacteria adhere to the cilia of the bronchial epithelium via pili, pertactin, Fha, and the binding subunits of PT. The bacteria are able to immobilize the cilia and these ciliated cells are increasingly destroyed. The lack of cilia causes foreign matter to build in the lower airways, and coughing and inflammation results. Bordetella, as mentioned before, is gram-negative and therefore contains lipopolysaccharide in its outer membrane which is heat resistant. Bordetella is known to produce several endotoxins which include: pertussigen which interferes with the transfer of signals from cell surface receptors and is involved in the attachment of respiratory epithelia, adenylate cyclase toxin which increases cyclic AMP levels and inhibits immune effector cell functions, tracheal cytotoxin which causes the immobilization of the cilia, also known as ciliostasis, and the extrusion of ciliated epithelia, dermonecortic toxin which causes tissue destruction, and filamentous hemagglutinin which plays a role in attachment to the ciliated host epithelial cells. The pertussis toxin catalyzes ADP-ribosylation of the alpha-subunit of the inhibitory G protein Gi. This in turn prevents the exchange of GTP for GDP and uses Gi to block inhibition of adenylyl cyclase. It is not yet understood how the defect in the G-protein signaling can kill the ciliated epithelial cells. Pertussis is thought to occur in two stages. Colonization occurs first through the attachment of filamentous hemagglutinin structures and then the second stage begins with the prolonged coughing and whooping.

Current Research

Enter summarries of the most rescent research here--at least three required

References

[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Edited by student of Dr. Kirk Bartholomew