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Whooping cough

Category: Illness or disabilities



Introduction and description


Pertussis, also known as whooping cough, is a highly contagious disease spread by the bacteria. B. pertussis - a small, aerobic gram-negative rod. B. pertussis produces:

multiple antigenic and biologically active products, including pertussis toxin (PT), filamentous hemagglutinin (FHA), agglutinogens, adenylate cyclase, pertactin, and tracheal cytotoxin. These products are responsible for the clinical features of pertussis disease. Immunity following B. pertussis infection does not appear to be permanent.

At one time it was considered a childhood disease.  Now however, there has been a general shift in the age distribution of pertussis toward older groups.

It has been around a very long time.  The earliest mention of pertussis, or whooping cough, is of an outbreak in Paris in 1414. This was published in Moulton’s The Mirror of Health, in 1640. Another epidemic of pertussis took place in Paris in 1578 and was described by a contemporary observer, Guillaume de Baillou.

Bahaodowle Razi, a Persian physician from the 15th century (AD), also reported two epidemics in Harat and one in Rey (in old Persia). He named it as Sorfe-ie-Am (meaning public cough).

 Pertussis was well known throughout Europe by the middle of the 18th century. Jules Bordet and Octave Gengou described in 1900 the finding of a new “ovoid bacillus” in the sputum of a 6-month-old infant with whooping cough. They were also the first to cultivate Bordetella pertussis at the Pasteur Institute in Brussels in 1906.



Whooping cough is an airborne disease which spreads easily through the coughs and sneezes of an infected person. People are infectious to others from the start of symptoms until about three weeks into the coughing fits.  The period of time between infection and the onset of symptoms is usually seven to ten days. It is rarely as long as 42 days.

  • First stage - Initially, symptoms are similar to those of the common cold with a runny nose, fever, and mild cough.
  • Second stage - This is then followed by weeks of severe coughing fits. Following a fit of coughing, a high-pitched whoop sound or gasp may occur as the person tries to inhale. 
    The cough may cause fainting, or vomiting after coughing. The cough from pertussis has been documented to cause “subconjunctival haemorrhages, rib fractures, urinary incontinence, hernias, and vertebral artery dissection.” Violent coughing can cause the pleura to rupture, leading to a pneumothorax.
    Fits can occur on their own or can be triggered by yawning, stretching, laughing, eating, or yelling; they usually occur in groups, with multiple episodes on an hourly basis throughout the day or night. This stage usually lasts two to eight weeks, or sometimes longer.
  • Third stage - A gradual transition then occurs to the convalescent stage, which usually lasts one to two weeks. This stage is marked by a decrease in paroxysms of coughing, both in frequency and severity, and a cessation of vomiting. A tendency to produce the "whooping" sound after coughing may remain for a considerable period after the disease itself has cleared up.

Thus this period of coughing fits may last for 10 or more weeks, hence the phrase "100-day cough".

Common complications include pneumonia, encephalopathy, earache, and seizures. Most healthy older children and adults fully recover, but those with comorbid conditions have a higher risk of morbidity and mortality.

Children less than one year old may have little or no cough and instead have periods where they cannot breathe.  Pertussis can cause severe paroxysm-induced cerebral hypoxia, and 50% of infants admitted to hospital suffer apneas.  Many children less than a year of age require hospitalization. Infection in newborns is particularly severe.

Pertussis is fatal in an estimated 1.6% of hospitalized US infants under one year of age. First-year infants are also more likely to develop complications, such as: pneumonia (20%), encephalopathy (0.3%), seizures (1%), failure to thrive, and death (1%).


 Diagnosis is by collecting a sample from the back of the nose and throat. This sample can then be tested by either culture or by polymerase chain reaction.


Pertussis is theoretically caused by the bacterium Bordetella pertussis.  But as we have seen above there are two stages of infection, with the second stage being much the nastiest part.  The bacteria can be recovered from the person only during the first three weeks of illness, rendering culturing and DFA useless after this period.  So from this we can deduce that the body may actually be capable of fighting the bacteria, eradicating it from the system.  Another clue, this time from Wikipedia.  According to Wikipedia “antibiotics may be used if started within three weeks of the initial symptoms, but otherwise have little effect in most people.”

Now perhaps they are ineffective because after that time the body has defeated the bacteria and is now having to compete with something far more nasty – and what that something is may be a virus.

It has long been known that Bordetella pertussis can harbour bacteriophage.  Bacteriophage are viruses that use the host bacteria like a Trojan horse to enter another host.  They are extremely tiny, very difficult as a consequence to detect:

For the first time Bordetella pertussis bacteriophage was isolated, and its presence was confirmed by electron microscopy and by agar layer titration. The lysogenic strains were activated by their treatment with mitomycin C in a dose of 4.5 mg/ml. The phage system of the Bordetella genus, heretofore unknown, has been revealed: Bordetella pertussis phage lyzed all the tested strains of Bordetella parapertussis (25 strains) and could be passaged in these strains. The phage formed turbid and transparent negative colonies 0.1 mm and 0.15 mm in size. The phage titer (e. g., in strain No. 3865) was 1 X 10(10). The lysogenic variants of Bordetella pertussis, capable of spontaneous release of the phage, were obtained. These variants were characterized by changes in some of their phenotypical properties, e.g., the increased content of certain toxic substances and increased virulence. PMID:  6251680

Bordetella pertussis bacteria are not 'friendly' bacteria, but on the other hand they are nowhere near as nasty as the phages they appear to harbour:

It has been the purpose of this paper to study molecular-biological features of the Bordetella bacteriophage interaction with the host cell during lysogeny and conversion as well as to determine the degree of homology between genomes of homologous and heterologous bacteriophages. Genomes of bacteriophages from B. pertussis 134, 41405 and B. bronchiseptica 214 were studied. Heteroduplex and restriction analyses revealed a heterogeneity of bacteriophage populations, and their DNAs were found to differ in size and position of inserts. As shown by blot hybridization, the bacteriophage genome is not inserted into the chromosome of the lysogenic cell but apparently exists as an autonomous plasmid replicon. It has been established that during conversion only a part of the phage genome is inserted into the chromosome of the recipient cell. PMID: 2904196

So there are a number of different types of bacteriophage that have used his bacteria and they do not harm their bacterial host.  Furthermore they are capable of living autonomously – in us for example.


Bordetella toxins

CDC Epidemiology and Prevention of Vaccine-Preventable Diseases - The Pink Book: Course Textbook - 13th Edition (2015)
Pertussis is primarily a toxin-mediated disease. The bacteria attach to the cilia of the respiratory epithelial cells, produce toxins that paralyze the cilia, and cause inflammation of the respiratory tract, which interferes with the clearing of pulmonary secretions. Pertussis antigens appear to allow the organism to evade host defenses, in that lymphocytosis is promoted but chemotaxis is impaired. Until recently it was thought that B. pertussis did not invade the tissues. However, recent studies have shown the bacteria to be present in alveolar macrophages

In other words one of the characteristics of the Bordetella pertussis is that it releases toxins.

Pertussis toxin and adenylate cyclase toxin are two important virulence factors of Bordetella pertussis, …… these two toxins, … are both able …. to enter mammalian cells, perform enzymatic activities and modify cell signaling events.  PMID: 20210554

One difference between the different species of Bordetella is that B. pertussis produces PT and the other species do not. Bordetella parapertussis shows the most similarity to B. pertussis and was therefore used for research determining the role of PT in causing the typical symptoms of whooping cough. Rat studies showed the development of paroxysmal coughing, a characteristic for whooping cough, occurred in rats infected with B. pertussis. Rats infected with B. parapertussis or a PT-deficient mutant of B. pertussis did not show this symptom; neither of these two strains produced PT.

PT is released from B. pertussis in an inactive form. …. The toxin causes several systemic effects, among which is an increased release of insulin, causing hypoglycemia.

So one effect of the toxin is hypoglycaemia – low blood sugar in simple terms.  The overall effect of this is that we will be exhausted and all we will want to do is lie down and go to sleep.

The toxin also modifies our immune system response and causes a very large increase in lymphocytes.  A lymphocyte is one of the subtypes of white blood cell in a vertebrate's immune system. They include natural killer cells (NK cells) (which function in cell-mediated, cytotoxic innate immunity), T cells (for cell-mediated, cytotoxic adaptive immunity), and B cells (for humoral, antibody-driven adaptive immunity). They are the main type of cell found in lymph, which prompted the name lymphocyte.

PT is also able to cross the blood–brain barrier by increasing its permeability.  There is more

…..PT inhibits early inflammatory responses in the respiratory tract, which reduces neutrophil influx in response to B. pertussis infection, potentially providing an advantage to the pathogen in this interaction. PMID: 18765723

But we also find that …………….

We have recently demonstrated that the binding subunit (B-oligomer) of pertussis toxin (PTX-B) deactivates CCR5 and inhibits entry of R5 human immunodeficiency virus type 1 (HIV-1) strains in activated primary T lymphocytes (M. Alfano et al., J. Exp. Med. 190:597-605, 1999). We now present evidence that PTX-B also affects a post-entry step of HIV-1 replication. While PTX-B inhibited fusion induced by R5 but not that induced by X4 envelopes, it blocked infection of T cells with recombinant HIV-1 particles pseudotyped with R5, X4, and even murine leukemia virus or vesicular stomatitis virus envelopes. It also suppressed HIV-1 RNA synthesis in cultures of infected peripheral blood mononuclear cells when new infections had been inhibited by zidovudine, and it reduced Tat-dependent expression of the luciferase reporter gene controlled by the HIV-1 long terminal repeat (LTR). Surprisingly, PTX-B did not affect expression from the cytomegalovirus promoter, nor did it reduce the basal (Tat-independent) expression from the LTR promoter. These results indicate that PTX-B inhibits HIV-1 infection at both the entry and the post-entry stages of viral replication, with the post-entry activity specifically affecting transcription or stability of Tat-stimulated HIV-1 mRNAs.  PMID:  10954581

Put simplistically it fights some viruses.  Superficially it appears to produce activities that guarantee its own survival long enough to release the toxins needed.  In effect it inhibits our immune response to it, but not to the viral pathogens.  All of which appear to point to an almost beneficial role for the toxin if the objective is to help fight viruses, including the phage viruses with which it is infected.

This leads one to ask the question is it really a toxin?

If the damage done is via the phages, then perhaps the toxin is being released by the bacteria to help us fight the phages.  This is pure hypothesis, but the toxin released appears to act in our defence, not against us.  If we lie down exhausted and sleep, the immune system can get to work, and if it results in the increase in lymphocytes, then these may be the troops needed to fight the phages – or even other viruses.


Vaccination - The strategy used by the medical profession to combat whooping cough is prevention by vaccination with the pertussis vaccine.  Initial immunization is recommended between six and eight weeks of age, with four doses to be given in the first two years of life.

Although childhood vaccination has dramatically reduced reported pertussis cases, the incidence of the disease has increased over the past 20 years, most notably in previously immunized adolescents and adults. Pertussis should be suspected in patients of all ages with cough who meet the clinical criteria for the disease. PMID:16913160

In other words, immunization does not confer lifelong immunity; furthermore, a 2011 CDC study indicated that protection may only last three to six years. Infection induces incomplete natural immunity that wanes over time.  The paper above also seems to imply that those who have been vaccinated stand a greater chance of catching the disease as their immunity fades, than those who have not been vaccinated.

It is as if Nature was trying to make sure we had the disease – however bizarre this may sound.

Antibiotics – the second part of the strategy used by the medical profession is the use of antibiotics

Preventative antibiotics are still frequently used in those who have been exposed and are at high risk of severe disease (such as infants)

Despite this, reported fatalities from pertussis in infants increased substantially from 1990-2010.



The World Health Organization recommended some while back, that a pertussis incidence of <1 case per 100,000 population be achieved in Europe by 2000. Available data indicate that this goal was not achieved, and the incidence is actually rising in some countries.

Although attempts are made to monitor the incidences of the disease, different case definitions, methods of diagnosis and reporting and surveillance systems make direct intercountry comparisons difficult, and pertussis is not a statutory notifiable disease in every country. Nevertheless the general consensus is that reported incidences are probably considerably lower than the actual incidence of pertussis; underreporting is common.

Prolonged cough may be the only clinical feature in adolescents or adults, who may present for diagnosis late (precluding laboratory confirmation) or not at all. When they do present, their condition is often misdiagnosed because, in part, clinicians continue to perceive pertussis as a childhood disease.

The consensus appears to be that despite generally high coverage with the DTP and DTaP vaccines, the incidence is increasing in the USA, Australia, Canada and Europe, possibly worldwide.

Despite underreporting, an increased incidence of infant, adolescent and adult pertussis has been observed worldwide since the introduction of widespread vaccination. This is of concern because adolescents and adults have been identified as a source of transmission of pertussis to very young infants who are unimmunized or partially immunized and thus more vulnerable to disease-related complications and higher mortality.  PMID: 15876918

All sorts of figures appear to be flying around about the incidence of the disease.  In one part of the Wikipedia description it says “An estimated 16 million people worldwide are infected per year. Most cases occur in the developing world, and people of all ages may be affected”, then using a different source they say “Worldwide, whooping cough affects around 48.5 million people yearly.  In 2013, it resulted in about 61,000 deaths – down from 138,000 deaths in 1990.”

Before vaccines, an average of 178,171 cases were reported in the U.S., with peaks reported every two to five years; after vaccinations were introduced in the 1940s, incidence fell but in 2012, rates in the United States reached a high of 41,880 people; this is the highest it has been since 1955 when numbers reached 62,786.  In the U.S. pertussis in adults has increased significantly since about 2004.

Despite high coverage rates for primary immunization in infants and children, pertussis continues to be a global concern, with increased incidence widely noted. PMID: 15876918

In conclusion


We do not believe that the bacterium Bordetella pertussis is as straightforward as it is described.  The toxin that it produces has an extremely complex activity which seems to be anti-viral in action.  As the bacteria is a host to viruses, some of this activity may be directed to the bacteriophage it contains, but if the research conducted on the toxins is correct then the toxin is a more general antiviral.  The fact that the symptoms in most people are not as severe as the full blown version indicate an almost protective role even though this may sound bizarre.

And to use antibiotics, if this is the case, is indeed unwise.  We may be killing a beneficial bacteria, whose side effects are only ever severe if the viral infection or infections against which it is fighting are severe.

Bordetella pertussis infection of the airways causes the disease pertussis (or whooping cough). The infection can be fatal in infants, but in older children, adolescents and adults usually results in a chronic cough of varying severity that persists long after clearance of the infection. The cause of the cough is unknown, but is presumably a result of the pathogenic effects of one or more of the various virulence factors produced by this bacterium. Accumulating recent evidence indicates that the majority of the virulence-associated effects of these factors is devoted to suppression and modulation of the host immune response, which can be skewed towards the recently described Th17 profile. Although the interplay between virulence factors and immune mechanisms might have evolved to benefit both partners in the host-pathogen interaction, it could also contribute to the severe disease pathology associated with this infection.  PMID: 17418639

References and further reading

  • Zh Mikrobiol Epidemiol Immunobiol. 1980 May;(5):85-90.  [Bordetella pertussis bacteriophage]. [Article in Russian]  Lapaeva IA, Mebel' SM, Pereverzev NA, Siniashina LN.
  • Zentralbl Bakteriol Mikrobiol Hyg A. 1988 Aug;269(2):147-55.  Bacteriophages of Bordetella sp.: features of lysogeny and conversion.  Holzmayer TA1, Karataev GI, Rozinov MN, Moskvina IL, Shumakov YL, Motin VL, Mebel SM, Gershanovich VN, Lapaeva IA.  1Gamaleya Institute of Epidemiology and Microbiology, USSR Academy of Medical Sciences, Moscow.
  • Iran Red Crescent Med J. 2015 Jul 1;17(7):e13454. doi: 10.5812/ircmj.13454. eCollection 2015.  The First Report of Epidemic Pertussis by Bahaodowle Razi From the 15th Century Anno Domini.  Yarmohammadi H1, Bahmani Kazeruni MH2, Soofi A3, Zargaran A4.
  • Pediatr Infect Dis J. 2005 May;24(5 Suppl):S10-8.  Epidemiology of pertussis.  Tan T1, Trindade E, Skowronski D.  1Feinberg School of Medicine, Division of Infectious Disease, Children's Memorial Hospital, 2300 Children's Plaza, Box 20, Chicago, IL 60614-3394, USA.
  • J Virol. 2000 Sep;74(18):8767-70.  The B-oligomer of pertussis toxin inhibits human immunodeficiency virus type 1 replication at multiple stages.  Alfano M1, Pushkarsky T, Poli G, Bukrinsky M.  1The Picower Institute for Medical Research, Manhasset, New York 11030, USA
  • Curr Opin Pharmacol. 2007 Jun;7(3):272-8. Epub 2007 Apr 5.  Immunomodulation in the pathogenesis of Bordetella pertussis infection and disease. Carbonetti NH1.   1Department of Microbiology & Immunology, University of Maryland School of Medicine, HH 324 Baltimore, MD 21201, USA. ncarbone@umaryland.edu

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