At the end of the 12th century, St.Godric of Finchale reportedly cured a small boy of an intensive cough, providing the first documentation of the disease known to the western world today as whooping cough or Pertussis. However, there are also strong indications that a dreadful cough found its way onto the shores of Europe around the 16th century. Its mention is found in numerous texts that pinpoint its existence in Europe prior to the 17th century, however due to the fact that the majority of its symptoms are reflected in other diseases, the numerous terms that have been used to describe a cough are often not present in texts, primarily those that are associated with ailments that afflict children. Nonetheless, historians such as Robert Weston have been able to construct a timeline showing the mutations of the violent cough over time and casting a light on expanding populations and industrial activities of the 18th and 19th centuries that most definitely played a role in increasing the activity of the deadly cough (2012).
Pertussis, a Latin word for ‘intensive cough’ was first knowingly coined in a 1748 French translation of Robert James’ A Medicinal Dictionary (1745). Chyncough, kink, kinkhost and kninthoest are all medical term used to describe the disease in Europe, each word illustrating the characteristic cough (host), gasp (kik) or troubled breath (kuchen) that came along from Pertussis (Weston, 2012, p332). By the middle of the 16th century, it was noted in studies from London and Sweden that the disease mostly affected young infant children and that those who had caught the disease would not catch it again. Furthermore, by the 18th century and into the 19th century it was understood that epidemics would arise every four to five years, steadily increasing in strength as well as mortality with increases in population (ibid, p335).
Today, Pertussis is still prevalent as a disease although treatment by vaccines in recent decades has brought down the number of infected. Brought about by the Bordetella pertussis is an aerobic coccobacilli, rod-shaped and gram-negative bacterium which expels a toxin within the host. This blog post will be looking into the acute disease of Pertussis by analyzing it through the ‘Modern Classification of Disease’ (Finger, and von Koenig, 1996).
The disease is not hereditary; it is caught by the transmission of droplets, in which the bacterium settles on the respiratory mucosal lining of the infected host (Finger, and von Koenig, 1996). There is hereditary immunity which is passed down by the mother to infant. However, if the mother has received a vaccine against Pertussis the hereditary immunity is not as strong, if present at all. This is because the hereditary immunity is passed down through maternal antibiotics during childbirth and through the mother’s milk, whereas vaccinated mothers have fewer antibodies to pass to their children (Humphries, 2012).
Although it is possible for pregnant women to succumb to a Pertussis infection, there has been no evidence to support that it can be a congenital disease. Around the year 2000 a woman who had Pertussis during pregnancy, possibly resulting in the loss of her child was not found to have any Bordetella pertussis within her amniotic fluid (Haugen, Jenum, Scheie, Sund and Stray-Pedersen, 2000).
Genetics do not have an effect on catching the disease. In the year 1689, it was noted by Walter Harris that “fat and obese infants are more liable to [catch pertussis]” (Weston, 2012, p339). Being infected is more so a result of the surrounding environment, the health of the individual body and the health of the surrounding others (Humphries, 2012).
In the earliest noted cases of whooping cough, infants and young children have made up most of the infected. Youth and adults (age 25-44) have also been plagued by the violent cough (Weston, 2012); however, it has never been as common as in the past few decades. In terms of individuals who have received a vaccine against Pertussis, the body eventually erodes the vaccine’s effect, resulting in multiple vaccinations throughout a life (primarily in childhood and adolescence) (Donegan, 2000). If one received the vaccine in childhood and did not successively take it again, it is likely aided by poor health that they may be far more susceptible to catch the bacterium. Bordetella Pertussis infects those with weaker immune systems and those with lower antibody counts (Alphonso, 2012). Notwithstanding, young children, often below the age of six are the most likely to be infected (Cagney, MacIntyre, McIntyre, Pueech and Giammanco, 2006).
It can be stated that both males and females are equally affected by the bacterium Bordetella Pertussis, however, geographic location does have an effect (environmental, happiness, lifestyle and health care affecting this as well). In a study of 1054 infected children/adolescents in Australia, it was found that the gender difference was almost non-existent: 49.6% were males and 50.4% were female (Cagney, MacIntyre, McIntyre, Pueech and Giammanco, 2006).
Some research points to Pertussis outbreaks being more prevalent where people have not taken the vaccine, as a result, a religious exemption. In a 2000-2011 study in the state of New York in the United States of America, it was expressed that non-vaccinated individuals, especially children, brought about an increase in Pertussis outbreaks (cultural/religious sections of the city) (Blog, Easton, Halsey, Imdad, Shaw and Tserenpuntsag, 2013). Another American study from 1997, found that the Pertussis bacterium was more prevalent in poorer urban areas throughout the country (Davidson, Kafadar, Norris, Siegel, Steiner and Todd, 1997).
The primary organ system to be affected is the respiratory system. The Bordetella Pertussis bacterium enters the body through either the nose into the nasal cavity or by the mouth: both entries lead into the pharynx and onto the lower respiratory tract. The mucous membrane of the respiratory tract is ideal for the incubation and quick multiplication of the bacterial population, which often lasts a period of one to two weeks known as the catarrhal phase (Finger and von Koenig, 1996). The bacterium spreads to consume the larynx, trachea and lungs, causing mild fevers and feeling of nausea (Cherry and Mattoo, 2005). After the incubation phase, the disease spreads its infection into the host in the paroxysmal phase. The toxins bring about lymphoid hyperplasia within the larynx trachea and bronchi leading to acute inflammation of the areas which will all eventually succumb to necrosis; infiltration of leukocytes to the respiratory tract hastily occurs (Fingers and von Koenig, 1996). This phase often results in the expulsion of the mucous membrane as a result of the violent ‘whooping’ coughs and vomiting which brings about a decrease in the population of the bacterium as they have been devoid of their natural habitat inside the host’s respiratory tract. Apart from placing a strain on the body, the disease does not usually infect more than the respiratory system, however, there are two rare cases in which it does (ibid).
Pertussis encephalapathy is an uncommon complication of Pertussis that is associated with individuals who have been vaccinated and have been inflicted by the disease (from someone of from the vaccine), primarily females and individuals who have had family members inflicted by this type of Pertussis. There is still very little known as to why this complication occurs, however it has something to do with the whole-cell Pertussis vaccine. Symptoms include “acute encephalopathy. seizures, hypotonic-hyporeactive episodes, inconsolable crying, or anaphylactic reactions” (Gary, 2012). Bronchopneumonia Pertussis is another very rare case, one on which very little is written or researched. It is brought about by an increase in lymphocytes in the body, known as lymphocytosis.
The second phase of whooping cough brings about complications to the senses of the body. The constant, strained and violent coughing results in infections in the middle ear – between the tympanic membrane and the stapes. Moreover, the constant harping and mucosal inflammation brought on by the toxin can result in bleeding from the eyes as well as from the nose. Red dots also tend to occur on the skin of the face and of the chest as a result of minute blood vessels bursting during coughing sessions. More serious complications resulting from the coughing caused by the initial inflammation of the respiratory tract by the Bordetella Pertussis bacterium includes lung inflammation, pneumothoraxes – the entrapment of air between lung and chest, hernias, rectal prolapse, rib fractures and seizures often resulting from lowered brain function from the strain (Abbott, 2012).
The Pertussis toxin, in its glutaraldehyde – inactive state can bind to numerous cells within the body, including T-lymphocytes as well as to the cells lining the respiratory tract by grasping on to human cilia through the use of its binding protein filamentous hemagglutinin, which allows the toxic bacterium to bridge itself onto the “ciliary receptor” (Finger and von Koenig, 1996). The bacteria also bring about an increase in lymphocytes in the body resulting in leukocytosis. The Pertussis bacteria also bring about lymphoid hyperplasia into the larynx, trachea and bronchi leading to minor inflammation of the areas, eventually leading to necrosis. Other than blocking cell receptors, increasing lymphocytes and producing acute inflammation, no other changes occur in the cells or tissues as a direct cause of the Pertussis bacterium (ibid). The vaccine (acellular Pertussis vaccines) and in some cases the bacteria can lead to the inflammation of the brain, resulting in permanent brain damage. The Pertussis toxin which is used in the making of the vaccine is a “neurotoxin that is so reliable for inducing brain inflammation and brain damage that [it is] used to deliberately induce experimental autoimmune encephalomyelitis (EAE) in lab animals” (Mercola, 2012).
Chronic dehydration may ensue if hydration is not kept in check. Constant vomiting frequent diarrhea and cyanosis during coughing attacks all contribute to the possible acidification of the system and most prevalently the dehydration of the body (World Health Organization, 2013). Loss of appetite (from the constant coughing, from repeated vomiting and from pain) is common amongst children, this, however, leads to further dehydration, as well as contributing more to the possible acidic state of the body. As a result “adequate fluid intake, adequate nutrition and oxygen therapy, including mechanical ventilation” (Tidy, 2012) should be instated to combat the symptoms (ibid).
Allergies do not come about as a result of the disease, however, they do aid in its infiltration of the body. Cold stresses and pollen allergies increase “resistance to infection [as well as increase] capillary permeability” result in the host succumbing to illness far faster and stronger (Finger and von Koenig, 1996).
The most common deficiency to be seen amongst Pertussis patients is that of water loss – dehydration. It is attributed to regular regurgitations and diarrhea. Thi in hand leads to mineral and vitamin loss, by way of fluid loss, poor metabolism or excessive stress. If nothing is being absorbed through the gut as a result of both vomiting and diarrhea, the sick body will have more stress as a result of its deficiencies. Such circumstances bring about fever to assist in combating free radical damage in the body (Abbott, 2012).
The constant stress from painful coughing and vomiting even as a result of weight loss will contribute to the deficiency of vitamin c from within the body. Studies have shown that high doses of Vitamin C (along with cod liver oil) can prevent the dangerous development of the Pertussis disease, decreasing coughing especially amongst children who often have hoarser coughs. Additionally, vitamin C assists in neutralizing toxins within the bloodstream, although it will not kill the bacterium it does place neutrophils and phagocytes into action against them. What’s more, vitamin c is a fantastic antioxidant, aiding in the elimination of free radical and inflammation (Humphries, 2012).
All environmental exposure, be it workplace school or home are the same – except when looking at one who interacts and handles the vaccine on a daily basis. It is often encouraged that a child and those it interacts with being vaccinated, as the vaccine can only do so much and if someone loses to the child were to get infected, it is very likely that the child will be infected as well. Areas in first world countries with high percentages of individuals who refuse to be vaccinated can be dangerous for the rest of the general population who have had the vaccine. The reason why is that they have a greater chance of catching the Bordetella Pertussis toxin because people who have been vaccinated are the safest amongst other people who have been vaccinated (people who are not vaccinated, have the same chances). Underdeveloped and poor nations have high percentages of Pertussis outbreaks every four to five years. The World Health Organization, in a 2003 annual report, stated that of the 17.6 million cases of Pertussis that year, 90% of the cases came out of the developing world. It is quite possible to contract it anywhere as the toxin is both airborne and spreads through bacterial droplets (Manitoba: Communicable Disease Control Unit, 2007, p 2-3).
It is also interesting to note that in medical journals throughout the 1800’s whooping cough cases increased, almost to par with the increase in population and industrial activity. The more crowded and contaminated industrial areas got, the more children working in factories and the fewer time individuals spent outside in clean air, the more common it was to see Pertussis appear amidst the poor population throughout industrial Europe (Weston, 2012).
As was stated above, areas, where environmentally clean living standards are challenged as a result of poverty and population density, are far more susceptible than areas that have high standards of living. The lack of cleanliness may not bring about the disease; however, it will make it harder to treat it resulting in more individuals becoming susceptible to it. Furthermore, apart from the Pertussis toxin being airborne and infecting the host through either the external nose or the mouth, it can infiltrate the host by way of a flesh wound, ingestion of food that has the toxin in or on it, ” contact with non-intact skin [as well as] exposure to aerosols” (University of California, San Francisco, 2010).
The Bordetella Pertussis, a member of the ADP – ribosylating bacterial toxins, has a surface area of about 0.8 um by 0.4 um. It is a rod-shaped coccoid, Gram-negative, non-spore producing bacterium. This strict aerobe bacterium is organized either single or in minute groupings, however, they are unable to move as they are a nonmotile species (Finger, and von Koenig, 1996).
The Pertussis bacterium produces quite a few toxins including, “tracheal cytotoxin; pertussis toxin, an A-B toxin; and adenylate cyclase-hemolysin, a Repeats in ToXins [RTX] toxin” (Guison, 2009). These toxins, in a host, will inflict harm on the ciliated epithelial cells in addition to damaging alveolar macrophages and causing hyper-lymphocytosis. Apart from toxins, the bacterium also constructs adhesions which include “filamentous hemagglutinin, pertactin and 2 fimbrial proteins (FIM2 and FIIM3)” (ibid). The combination of toxins and adhesions make B Pertussis ideal in infiltrating host cells and eluding the host defences, resulting in it creating damage to the host’s respiratory tract (ibid).
The Pertussis toxins, also known as protein exotoxins, each have a specific subunit. These subunits can be one of two; the first carrying biological activity the second subunit allows for the complex to be bound to the host’s cell membrane. Upon attaching to a host cell, it attaches itself to the cell’s receptors using two dimmers thus disrupting the cells ability to defend itself (ibid).
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