by Melissa Clyburn                                                                                   

·        Pertussis, a highly contagious disease also known as whooping cough, causes uncontrollable, violent coughing (1).  Bordetella pertussis causes the disease, and is not found in any animal or environmental reservoirs, but resides in the mouth, nose, and throat of humans (1).  Pertussis is spread by airborne droplet contact transmission, in which an infected person sneezes or coughs, causing tiny droplets containing the bacteria to move through the air (1).  Pertussis is an upper respiratory infection that can affect all ages, but is predominantly found in infants and young children, that makes it very difficult for the victim to breathe, and can cause permanent disability in infants and even death (1). 

·        Bordetella pertussis is an aerobic, non-spore forming, Gram-negative coccobacillus (2) that colonizes the respiratory tract of humans, causing pertussis (3).  Pertussis is diagnosed by looking at clinical history, culturing Bordetella pertussis from nasal mucous, or using a polymerase chain reaction test (4).  This test is positive if genetic material from Bordetella pertussis matches the genetic material in the nasal mucous (4).  However, there is a quick method for identifying Bordetella pertussis that uses monoclonal antibodies against the bacterium’s virulence factors: lipo-oligosaccharide and peroxidase conjugate (5).  The test dries cells of Bordetella pertussis in a formalin-saline onto a nitrocellulose disk, the disk is placed in a filtration device, and then the monoclonal antibodies are added (5).  Afterwards, disk is washed in a peroxidase substrate solution and Bordetella pertussis is identified using a direct fluorescent-antibody assay (5).



·        Bordetella pertussis was named after its discoverer, Jules Bordet, who, in 1906, isolated the bacterium (7).

·        Pertussis is characterized by a series of stages.  The first stage, known as the catarrhal stage, mimics the common cold, and is classified by a runny nose, low fever, sneezing, and mild cough (4).  This stage lasts one to two weeks, while the second stage, known as the paroxysmal stage, lasts anywhere from four to ten weeks and is characterized by the high-pitched whoop preceded by a paroxysm of violent, rapid coughs (4).   This stage is the period of illness, in which most infants and young children may turn blue from lack of oxygen, can vomit after paroxysm, or die (4).  The final stage, known as the convalescent stage, can last from two to six weeks and is known as the recovery stage (4).  During this stage, the cough begins to disappear as paroxysms are less frequent, and the cough may disappear after two weeks (4).  Also during this stage the patient is at risk for recurrence (4) and most of the pertussis-related deaths are a result of a secondary bacterial infection, pneumonia (4).

·        While many microbiologists and researchers do not fully understand how Bordetella pertussis becomes pathogenic, there are several virulence factors associated with initial infection (8). Upon entrance into the respiratory tract, Bordetella pertussis colonizes in the host via filamentous hemagglutinin (FHA) and the pertussis toxin (9).  FHA, a large protein that forms filamentous structures on the cell surface, binds to galactose residues on the surface of the trachea’s ciliated epithelial cells (9).  The pertussis toxin, a protein composed of six subunits: S1, S2, S3, (2)S4, and S5, is also involved in adherence to the tracheal epithelium (9).  Some of these components function as adhesins, binding the bacteria to the host cell, while others utilize different receptors, such as binding to a glycolipid found specifically on tracheal epithelium, or binding to a glycoprotein found primarily on phagocytic cells (9).  Contributing to its virulence, Bordetella pertussis also produces its own toxins, such as invasive adenylate cyclase, a single polypeptide that enters epithelial cells, locally reduces phagocytic activity, and lyses red blood cells, thus initiating infection (9).  Lethal toxin, formerly called dermonecrotic toxin, is a protein that causes inflammation where Bordetella pertussis has colonized (9).  Tracheal toxin, a peptidoglycan fragment, destroys ciliated cells, stimulates the release of interleukin-1, and causes fever (9). 

·        Once infected, the individual receives antibiotics, usually erythromycin (2) for a designated time.  In order to control this disease, we must have better knowledge of Bordetella pertussis’ virulence and pathogenesis, we must be able to diagnose pertussis quickly, and help prevent pertussis outbreaks in infants and the population (10).

·        Although pertussis is considered to be an endemic illness, in the United States, pertussis epidemics occur every 3-5 years (10).  There are over 28,000 cases of pertussis each year since 2003; this is due to the treatment and preventative vaccination for infants and adults available in the United States (11), because globally there are between 20 and 40 million cases of pertussis each year (3).

·        Perhaps the best way to control and prevent pertussis is through vaccination.  The diphtheria and tetanus toxoids and acellular pertussis (DtaP) vaccine is an inactivated vaccine, a vaccine that does not contain live bacteria (12).  The DtaP vaccine has been licensed and in use since 1991, and is primarily used in pediatrics (12).  For teenagers and adults, an acellular vaccine was licensed in 2005, called tetanus toxoid-diptheria-acellular pertussis (Tdap) (12).  Because these vaccines are inactivated and the bacteria inside are not able to reproduce, several doses are needed to confer immunity (12).


                                                             Works Cited


1.  Illinois Department of Public Health.  “Health Beat: Pertussis.”  December 2006.  Accessed on 30 April 2007.  < >


2. Duckworth, Donna Ph. D, Richard Crandall PhD, and Richard Rathe M.D.  “Bordetella pertussis.”  13 April 1999.  Accessed on 30 April 2007.  < >


3.  “Preventable Diseases-Whooping cough.”  Sanofi Pastueur Corporate Website.  16 February 2007.  Accessed on 02 May 2007.  < >


4.  Stoppler, Melissa Conrad MD.  “Whooping Cough (Pertussis).”  21 December 2005.  Accessed on 29 April 2007.  < >


5.  G N Sanden, P K Cassiday, and J M Barbaree.  “Rapid immunodot technique for identifying Bordetella pertussis.”  J Clinical Microbiology. 1993 January. 31(1): 170–172.  Accessed on 04 May 2007.  < >


6.  Immunization Action Coalition “Pertussis: Photos.”  February 2007.  Accessed on 29 April 2007. < >  


7. Jules Bordet Institute.  “Biography: Jules Bordet.”  2005.  Accessed on 30 April 2007.   < >   


8. Bisgard, Kris, DVM, MPH.  “Guidelines for the Control of Pertussis Outbreaks: Chapter 1-Background.”  April 2000.  Accessed on 30 April 2007. < >


9.  Babu, M. Madan, J. Bhargavi, Ranajeet Singh Saund, and S. Kumar Singh.  “Virulence Factors of Bordetella Pertussis.”  Current Science.  80(12): 1512-1522.  25 June 2001.  Accessed on 03 May 2007.  < >


10.  Center for Disease Control and Prevention.  “Pertussis.”  13 October 2005.  Accessed on 01 May 2007.  < >


11.  Center for Disease Control and Prevention.  “Pertussis-United States, 2001-2003.”  MMWR Weekly. 54(50): 1283-1286.  23 December 2005.  Accessed on 04 May 2007.  < >


12.  Immunization Action Coalition “Pertussis Vaccine: Questions and Answers.”  February 2007.  Accessed on 03 May 2007. < >