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Whooping Cough/Pertussis
Published in Charles Theisler, Adjuvant Medical Care, 2023
Whooping cough is a highly contagious respiratory tract infection which is more common in children than adults. It is caused by the bacterium Bordetella pertussis. In its early stages, pertussis appears to be nothing more than the common cold. After one to two weeks, more severe symptoms start to appear. In many people, whooping cough is marked by severe uncontrollable coughing fits followed by a high-pitched intake of breath that sounds like “whoop.” The coughing fit may be so severe as to obstruct breathing, cause vomiting, or even crack ribs.1 Despite vaccinations, worrisome outbreaks of whooping cough have been seen in the past decade.2
Beware of the Crocodiles
Published in Norman Begg, The Remarkable Story of Vaccines, 2023
One question that vexes vaccine researchers more than most is how to define the disease they are looking for. It sounds rather obvious – either you get the disease, or you don’t – but it’s a lot more complicated than that. Are you looking for all cases of the disease, including very mild ones, or do you just want to find the more serious ones? Do you need to have the diagnosis of all cases confirmed by laboratory tests? What about people who get the infection but have no symptoms? The effect of a vaccine will be different depending on how you define a case. Let’s consider the design of a trial against whooping cough vaccine as an example. If you just look for cases in which they had a cough, with a typical “whoop”, the effect of a vaccine would appear to be lower than if you only included people who also had those symptoms plus confirmation of the diagnosis by laboratory tests. Some of your cases of cough and whoop might not in fact be whooping cough, so the vaccine could not be expected to protect them. Only the cases with laboratory confirmation are true whooping cough. It pays to be strict in how you decide who is and who is not a case, as this gives you the best chance of finding out the true effect of the vaccine. Phase 3 trials nearly always require laboratory confirmation to be sure that a suspected case really is a case.
Paper 4
Published in Aalia Khan, Ramsey Jabbour, Almas Rehman, nMRCGP Applied Knowledge Test Study Guide, 2021
Aalia Khan, Ramsey Jabbour, Almas Rehman
Whooping cough is caused by Bordetella pertussis and treatment is essentially symptomatic. Erythromycin is useful in rendering a person non-infectious but does not alter the course of the disease. Children should be kept off school for 5 days after the start of medication.
Pertussis-like syndrome often not associated with Bordetella pertussis: 5-year study in a large children’s hospital
Published in Infectious Diseases, 2020
Qin Xiong, Shiying Hao, Lei Shen, Jian Liu, Tingting Chen, Guoqin Zhang, Yu-juan Huang
Pertussis, also called whooping cough, is an acute respiratory infectious disease caused by Bordetellapertussis (B. pertussis). Typical symptoms of pertussis are paroxysmal cough, inspiratory whoop, and post-cough vomiting. The course of the disease could last for 2 or 3 months [1,2]. Pertussis is more severe in infants less than 3 months. Paroxysmal cough can cause short breath or apnoea, which will increase the risk of life-threatening complications such as pneumonia, encephalopathy, and pulmonary hypertension [3]. A term pertussis-like syndrome (PLS) has been widely used as a clinical diagnosis for children presenting with symptoms and signs compatible with pertussis, but with indeterminate aetiology or without history of exposure to any confirmed pertussis case [4]. Pathogens of PLS include B. pertussis, other bordetella species, mycoplasma pneumonia, and chlamydia pneumonia, as well as other types of virus and bacteria [5–7].
Immune interference (blunting) in the context of maternal immunization with Tdap-containing vaccines: is it a class effect?
Published in Expert Review of Vaccines, 2020
Walid Kandeil, Miloje Savic, Maria Angeles Ceregido, Adrienne Guignard, Anastasia Kuznetsova, Piyali Mukherjee
Pertussis, also known as whooping cough, is a highly contagious respiratory disease caused by Bordetella pertussis. Although it can affect all ages, the number of complications and deaths from infection are highest in young infants under 2–3 months of age [1]. Maternal immunization with reduced antigen content tetanus-diphtheria-acellular pertussis (Tdap) vaccines has demonstrated to be a safe, effective, and successful strategy in preventing infant pertussis disease, since it can offer protection through transplacental transfer of maternal antibodies before the infants receive their primary vaccination [2–5]. At least 40 countries are currently recommending maternal immunization as part of their routine immunization schedules [6,7], including the United States (US) and the United Kingdom (UK) [8,9].
Immune surveillance for vaccine-preventable diseases
Published in Expert Review of Vaccines, 2020
Gerco den Hartog, Rob van Binnendijk, Anne-Marie Buisman, Guy A. M. Berbers, Fiona R. M. van der Klis
For many pathogens targeted by vaccines, first entry and infection happen at mucosal surfaces in the respiratory tract (e.g. B. pertussis, N. meningitidis, S. pneumoniae, Hib, measles) or the gastrointestinal tract (e.g. poliovirus, rotavirus). Disease symptoms may even be restricted to the respiratory tract, as is the case for whooping cough (B. pertussis) and pneumonia (S. pneumoniae). For these reasons in some studies antibody detection is carried out in oropharyngeal specimens such as saliva (also termed oral fluid), as these may be a better proxy for immune protection of the respiratory tract than antibodies in serum [78,85,86]. However, IgG antibody concentrations in saliva specimens are limited, equal, or less than 1% of what can be detected in serum. The relative proportion of IgA antibodies is higher because mucosal surfaces promote the production of protective IgA that can be secreted and neutralize pathogens before infection can occur [87–90]. Moreover, depending on the specific tissue, efficient transport of dimeric IgA can occur through the polymeric Ig receptor resulting in secretory IgA in the lumen of mucosal surfaces such as the respiratory tract [91,92]. Although memory IgA B cells could be detected 1-year post-MenC vaccination, local IgA antibodies induced by vaccination may decline relatively fast [93,94]. Assessing IgA antibodies after vaccination often proves challenging, because well-defined control sera or serum panels with defined concentrations and general knowledge regarding protective antibody concentrations are lacking.