Bordetella pertussis
Forrest Lindsey

Bordetella pertussis is coccobacilli of the phylum proteobacteria that is gram negative and is an obligate aerobe. B.pertussis is also encapsulated and does not produce spores. Being an aerobe is advantageous being that it lives within the human respitory system. B. pertussis was identified as early as 1578 by Guillaume de Baillou, but earlier reports date back at least to the 12th century. B. pertussis was isolated in pure culture in 1906 by Jules Bordet and Octave Gengou. B. pertussis claim to fame is that it causes pertussis or whooping cough, a highly contagious disease of the respitory system that is characterized by a cough followed by a whooping sound.B. pertussis is one of the leading causes of vaccine preventable deaths worldwide, mostly occurring in infants in third world countries.

B. pertussis is highly fastidious and is only a pathogenic in humans. Transmission from one human to another occurs by direct contact or when the host coughs causing small aerosol droplets to disperse into the air to be inhaled by another. The initial infection results in colonization and quick multiplication on the mucous membranes of the respitory tract. Bacteremia or the presence of bacteria in the blood never occurs. Upon arriving in the respitory tract B. pertussis binds to the ciliated epithelial cells causing stasis of the cilia which enables the entry of bacteria to tracheal/bronchial ciliated cells. One of the first toxins expressed after infection is tracheal cytotoxin, which is a byproduct of the breakdown of the bacterial cell wall, usually this molecule is recycled but in B. pertussis it is released into the environment. Once released the toxin causes DNA replication to cease as well as paralysis of the cilia. The same toxins that cause the stasis of the cilia also inhibit the phoagocytic abilities of the host. The most important of the regulated toxins is adenylate cyclase toxin. This is present on the surface of B. pertussis cells and is delivered to the cytoplasm of host cells on contact. Immune cell functions are then inhibited by the resulting accumulation of 3’-5’ cyclic AMP. In humans an initial peribronchial lymphoid hyperplasia occurs, accompanied or followed by necrotizing inflammation and leukocyte infiltration in parts of the larynx, trachea, and bronchi. As of now there is no explanation of the characteristic whooping cough associated with the development of b. pertussis. Research is stunted because it’s solely a human pathogen and because of the limited opportunities to direct studies.

Although B. pertussis is susceptible in vitro to several antibiotics, such as tetracycline, erythromycin, and chloramphenicol, the efficiency of these drugs in patients during the beginning phases is not reliable. Treatment with erythromycin, which is usually considered the antibiotic of choice, will eliminate viable B. pertussis organisms from the respiratory tract within a few days. The treatment, however, has no influence on the course of the disease. Human hyper immune pertussis globulin is still used occasionally, but no data support its efficiency.

*Disclaimer - This report was written by a student participaring in a microbiology course at the Missouri University of Science and Technology. The accuracy of the contents of this report is not guaranteed and it is recommended that you seek additional sources of information to verify the contents.

 

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