CONTRARILY TO ILL CONCEIVED WISDOM… ANTIBIOTICS WORK AGAINST VIRUSES, In Several Ways:
Professor Didier Raoult’s research has demonstrated the antiviral property of the azithromycin antibiotic in the case of SARS2/Covid19. Moreover infections have been involved in a large proportion of COVID 19 deaths. By the way, bacterial co-infections are involved in 75% of influenza infections, according to the latest meta study from NCBI (extensively quoted below). Somehow, many Medical Doctors are unaware of this. (Jump to bottom for personal general conclusions, after all the science extracts…) Before the links, here is the truth, March 22:
CLOSED CASES: 112,174
Cases which had an outcome:
97,574 (87%): Recovered / Discharged
14,600 (13%): THIRTEENTH PERCENT DEATHS
Contrarily to what establishment propaganda is pretending, the death rate of COVID19 is getting worse. On OUTCOMES, the only relevant concept, the death rate is not one percent, as establishment propaganda insists it is, maximally lying, but thirteenth percent (13%). Ask 6,000 dead Italians.
Here are some links:
On antiviral antibiotic:
Novel antiviral properties of azithromycin in cystic fibrosis airway epithelial cells.
Schögler A et al. Eur Respir J. (2015)
Pharmacokinetic changes of antibiotic, antiviral, antituberculosis and antifungal agents during extracorporeal membrane oxygenation in critically ill adult patients.
Hahn J et al. J Clin Pharm Ther. (2017)
Azithromycin, a 15-membered macrolide antibiotic, inhibits influenza A(H1N1)pdm09 virus infection by interfering with virus internalization process.
Tran DH et al. J Antibiot (Tokyo). (2019)
And antibiotics work for influenza too:
There are 75% co-infections with bacteria in the case of flu, a meta-study in Frontiers in Microbiology, 23 June 2017, shows:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481322/
Here is from the last review paper:
“Abstract
Lower and upper respiratory infections are the fourth highest cause of global mortality (Lozano et al., 2012). Epidemic and pandemic outbreaks of respiratory infection are a major medical concern, often causing considerable disease and a high death toll, typically over a relatively short period of time. Influenza is a major cause of epidemic and pandemic infection. Bacterial co/secondary infection further increases morbidity and mortality of influenza infection, with Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus reported as the most common causes. With increased antibiotic resistance and vaccine evasion it is important to monitor the epidemiology of pathogens in circulation to inform clinical treatment and development, particularly in the setting of an influenza epidemic/pandemic.
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Introduction
From the Plague of Athens to the present day, infectious disease has beset mankind throughout history. Medical and socio-economic advances have substantially reduced this burden, the eradication of smallpox in 1979 (World Health Organization, 2017) and the remarkable successes against polio and parasitic Guinea worm disease being three examples of an extensive list. Respiratory tract infections, however, continue to be a major cause of morbidity and mortality worldwide (Lozano et al., 2012; Morse et al., 2012; Zumla et al., 2014). When combined, lower and upper respiratory infections are the fourth highest cause of global mortality (Lozano et al., 2012). Epi- and pandemic outbreaks of respiratory infection are a major medical concern, often causing considerable disease and a high death toll, typically over a relatively short period of time. The unpredictable nature of these outbreaks, in terms of their etiology and the reservoirs from which they emerge, the constant emergence of new antigenic variants by mutation, combined with transmission within potentially immunologically naïve populations facilitates the characteristic high proficiency of spread (Morse et al., 2012).
It is well established that both animals and humans can act as reservoirs of infection within which pathogens may adapt and evolve. Examples include Coxiella burnetii which typically causes Q fever in cattle, sheep and goats but can also infect humans (Eldin et al., 2017), the plague causing Yersinia pestis, infamously transmitted to humans by rats via a flea vector (Yang et al., 2016b), human immunodeficiency virus (HIV) which originated in non-human primates before spreading into the human population (Rupp et al., 2016) and of course the most common example, influenza, which circulates within and between swine, avian and human hosts (amongst others). This cross-species flow can lead to adaptations that result in an increased pathogenicity to susceptible hosts, creating the potential for localized outbreaks or global spread (Murphy, 1998; Karesh et al., 2012; Morse et al., 2012). Important evolutionary modifications can occur during the timespan of an individual infection, permitting new and evolved strains of pathogens to emerge at an increased rate (Karesh et al., 2012). The evolution of pathogens (particularly zoonotic pathogens which account for 60% of human infectious diseases), and development of pandemics and epidemics, can be described in ecological principles whereby changing environmental pressures or opportunities drive a pathogen to exploit new niches or hosts to survive and thrive. This evolution is influenced by a range of anthropogenic factors, which include population expansion, changing land use and habitat destruction, selective pressures of increased antimicrobial usage, vaccination, global trade and travel (Daszak, 2012; Karesh et al., 2012; Morse et al., 2012).
Pandemics are generally viral in cause. This is thought to be due to their high mutation rate, which is particularly true for RNA viruses such as influenza where high nucleotide substitution and poor proof reading leads to the accumulation of errors in newly synthesized RNA strands. Influenza can also undergo re-assortment during mixed infection. These factors can result in divergence of surface antigens, such as haemagglutinin (HA) and neuraminidase (NA), producing strains not recognized by the human immune system and not covered by extant vaccines (Holland et al., 1982; Webster et al., 1992; Chen and Holmes, 2006; Hampson and Mackenzie, 2006; Jones et al., 2008; Taubenberger and Morens, 2008; Dormitzer et al., 2011; Morse et al., 2012). For instance, influenza A is now known to have 18 subtypes of HA and 11 subtypes of NA (Li et al., 2012; Tong et al., 2012; Wu et al., 2014). This high mutation rate and the emergence of new strains can also make vaccine development and policy difficult to plan and carry out. Due to viral antigenic shift, yearly influenza vaccines are required so the population is sufficiently protected by the vaccine, however, vaccine composition is determined ∼8 months in advance of administration. This lag may allow new strains to emerge or for antigenic drift to result in a poor match between vaccine and the circulating strain of influenza. Furthermore as seen in the 2009 influenza pandemic, governments and public health departments face considerable difficulties in the production and distribution of vaccines when faced with sudden or unexpected outbreaks of newly emerged strains (Houser and Subbarao, 2015).
A common complication of respiratory viral disease can be secondary bacterial infection. Noting this association is important as it has clear implications for global health, principally because bacterial co/secondary infection is known lead to increased morbidity (Smith and McCullers, 2014). Co/secondary bacterial infection, as the name suggests, is a bacterial infection that occurs during or after an infection from another pathogen, commonly viruses. A number of viral infections (including infection from influenza virus, respiratory syncytial virus, parainfluenza virus and human metapneumovirus) can be complicated by co/secondary infection by a variety of bacteria including Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. This association leads to an increased severity of disease and sequela such as pneumonia (Smith and McCullers, 2014). In this review we dwell on influenza pandemics since the late 1800’s, focussing on the associations and complications that arise from secondary bacterial infection
Influenza
Influenza viruses are important zoonotic pathogens as they are highly contagious and one of the most prevalent causes of respiratory infection. Worldwide annual epidemics reportedly cause up to five million cases of severe illness, which result in 250,000–500,000 deaths per year. The majority of deaths caused by influenza occur in young children and people over 65 (World Health Organization, 2016). Reports suggest that each year up to 20% of the United States population may be infected by influenza…
There are three types of influenza virus, types A, B, and C, each differing in host range and pathogenicity (Taubenberger and Morens, 2008). Type A has been isolated from humans, avian, swine, horses, mink, dogs, seals, and ferrets (Jakeman et al., 1994; Taubenberger and Morens, 2008; Parrish et al., 2015), whilst type B has been isolated from humans, seals (Osterhaus et al., 2000) and ferrets (Jakeman et al., 1994), and type C from humans (Matsuzaki et al., 2002), swine and dogs (Youzbashi et al., 1996). Influenza A and B virions contain several structural antigens and three antigenic surface proteins; HA, NA, and M2/BM2 ion channels (Webster et al., 1992; Hampson and Mackenzie, 2006; Racaniello, 2009; Dormitzer et al., 2011). Influenza virus C only expresses one antigenic surface protein, haemagglutinin-esterase-fusion (HEF), and thus stimulates a lesser immune reaction than types A or B (Taubenberger and Morens, 2008; Racaniello, 2009). Influenza A is the fastest to evolve, at a rate 2–3 times faster than B, whilst C is the slowest…
Much is known about the havoc brought by a virus. Most spectacular is the destruction of the immune system within the lungs by the virus itself, which acts like HIV on steroids:
Throughout the past 300 years there have been 12 pandemics caused by influenza A; the most infamous being the 1918 ‘Spanish flu’ pandemic (Taubenberger and Morens, 2008). In the years between 1933 and 1957 there were nine influenza A (H1N1) epidemics and five influenza B epidemics. The worst of all these epidemics was the 1935–1936 influenza B epidemic that resulted in at least 55,000 deaths. This was closely followed by the 1943–1944 influenza A (H1N1) epidemic which caused 53,000 deaths (Glezen, 1996). Evidently, although influenza B doesn’t cause pandemics, it is still a cause for concern.
During an infection influenza virions attach to and enter host epithelial cells by the binding of viral HA to sialic acid on the host cell which instigates endocytosis and the movement of the virion into the cell within an endosome. The virus then uses/hijacks the host cells ‘machinery’ to replicate and transcribe viral RNA and produce more viral components (Samji, 2009). Progeny virions bud from the host cell, using the host cell membrane as a viral envelope, and go on to infect neighboring host cells (Nayak et al., 2009). As influenza infection develops the virus causes cell damage and death within the host’s airways and up-regulates the production of toxins, causing further destruction. Influenza cytotoxins for example causes necrosis of host cells (Conenello and Palese, 2007; Iverson et al., 2011). Influenza infection, particularly pandemic influenza infection, is known to generate an increased inflammation response within the host, as the body works to rapidly deliver immune cells to the site of infection. This inflammation is a response to the expression of cytokines and chemokines (de Jong et al., 2006; Kash et al., 2006; Kobasa et al., 2007; Rock and Kono, 2008). Virally induced decreased mucociliary activity, the dysfunction of immune cells and the reduction of phagocytosis reduces clearance of the virus from the host airways and the host’s ability to fight the virus (Brundage, 2006; Wu et al., 2011; Cauley and Vella, 2015). In an attempt to limit and control infection, the host immune system kills infected host cells. It does this in several ways, including; the production of perforin by Natural Killer (NK) cells which creates lesions/pores in cell membranes resulting in the induction of apoptosis, apoptosis from tumour necrosis factor (TNF) and FasL and the production of reactive oxygen species from macrophages and neutrophils causing oxidation of cellular lipids, proteins and DNA resulting in cell dysfunction and death (Topham and Hewitt, 2009; Kash et al., 2014; Kash and Taubenberger, 2015). Of course viral infection and/or interference with host processes can cause and direct the pathway of cell death, as is the case for necrosis. Host cell death, whether apoptosis, necrosis or pyroptosis, impacts on the severity and outcome of influenza disease in a variety of ways. Virally induced death of immune cells assist in the evasion of host defenses and hinders the clearance of the virus promoting the development of infection. Studies have shown a 90% reduction of alveolar macrophages in mice within a week of influenza infection, and evidence of necrosis in the remaining macrophages (Robinson et al., 2015). Necrosis and pyroptosis are pro-inflammatory due to their role in the release of cytokines. These cell death pathways allow for the rapid release of intracellular contents, including any viral components, from the infected host cell promoting host inflammatory responses and the formation of a cytokine storm which causes host tissue damage (Cundell et al., 1995; Rock and Kono, 2008; Lamkanfi and Dixit, 2010; Cauley and Vella, 2015). Furthermore infection with some influenza subtypes, for instance H1N1 and H5N1, typically result in lymphopenia, a state of abnormally low levels of lymphocytes, which has been associated with higher viral load. de Jong et al. (2006) found influenza infection caused lower levels of cytotoxic T cell lymphocytes, which would therefore negatively affect acquired immunity (de Jong et al., 2006; Cunha et al., 2009).
Bacterial Co-Infection and Secondary Infections
Laboratory, clinical and epidemiological research has made it abundantly clear that bacterial co/secondary infection can significantly increase the morbidity and mortality of viral infections (Gupta et al., 2008). UP TO 75% OF THOSE INFECTED WITH INFLUENZA THAT GO ON TO ACQUIRE PNEUMONIA, ARE CONFIRMED TO HAVE BACTERIAL CO-INFECTION (Zambon, 2001). Bacterial co/secondary infection of influenza infection appears to occur frequently. Studies have shown that up to 65% of laboratory confirmed cases of influenza infection exhibited bacterial co/secondary infection…
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INFLUENZA OFTEN OCCURS WITH A BACTERIAL CO-INFECTION, And CONSEQUENCES ARE MOST DREADFUL:
Various studies have shown the impact when H. influenzae co/secondarily infects with influenza, and some suggest a level of synergism. The effect of influenza and H. influenzae co-infection verses individual infection of both pathogens is tellingly different; Shope found that co-infection resulted in severe disease or death when on their own H. influenzae and influenza only caused mild infection or disease (Shope, 1931). More recently, Lee E.H. et al. (2010) undertook a similar study which provided comparable results and evidence that influenza and H. influenzae co-infection produces more epithelial cell destruction than single infection with either pathogen (Lee L.N. et al., 2010). Furthermore, they found individual infection caused mild bronchiolitis within 4 days of initial infection, from which the host lung was able to recover. Conversely, co-infection caused bronchial necrosis, bronchial inflammation and bronchitis within the same time period or less, and led to further complication such as epithelial erosion (Lee L.N. et al., 2010). It is now commonly accepted that co-infection results in more severe morbidity and poorer clinical outcome than infection of influenza or H. influenzae alone.
Synergies also occur during co-infection with other bacteria:
…In an act of synergism, S. aureus infection may actually assist influenza infection by increasing the infectivity of influenza; when the virion is being moved into the host cell within an endosome the low pH in the endosome causes a conformational change to the HA [HA(0)] allowing it to be cleaved by host proteases into two subunits [HA(1) and HA(2)]. This cleaving ‘activates’ the HA, mediating fusion between the virus and endosome membrane, ready for the opening of the M2 ion channel so the vRNP (viral ribonucleoproteins) can be released into the host cell where the viral RNA is replicated and transcribed. Several strains of S. aureus produce proteases that cleaves influenza HA; the more protease that is available, the more HA can be cleaved meaning more vRNP can get into host cells meaning overall more progeny virions (Tashiro et al., 1987; Steinhauer, 1999; Samji, 2009). This aspect contributes to the increased severity of disease caused by co-infection…
HOW DID THE FLU OF 1918 KILL? BACTERIAL PNEUMONIA, 95% CASES!
Historical Evidence of CO/Secondary Bacterial Infection During Major Influenza Pandemics
1918 Spanish Influenza Pandemic
The 1918 influenza pandemic was a result of influenza strain A (H1N1). It is considered the most devastating influenza pandemic ever recorded, infecting 50% of the world’s population and resulting in approximately 40–50 million deaths worldwide. India alone suffered 7 million deaths (Potter, 2001; Hilleman, 2002; Brundage, 2006; Michaelis et al., 2009). The main groups of individuals affected by this pandemic were those aged 20–40 years old, in addition to infants and those over 65. Ordinarily only young children and the elderly are the age groups most at risk from influenza, showing how distinctive pandemic strains can be (Potter, 2001). It is suggested that war time efforts meant that influenza easily spread through military camps, allowing the 20–40 years old age range to be more at risk than usual.
There are many published examples of co/secondary bacterial infections during the 1918 influenza pandemic, and pneumonia as a consequence of bacterial infection is estimated to have occurred in up to 95% of deaths during this pandemic (Morens et al., 2008). A majority of those deaths due to secondary S. pneumoniae infection (Brundage and Shanks, 2008; Morens et al., 2008). Many of the examples that detail co/secondary bacterial infection come from outbreaks within army camps…
1957 Asian Influenza Pandemic
This pandemic affected 40–50% of people worldwide. The cause was influenza strain A (H2N2) (Potter, 2001). Although global death toll estimates vary [between 1.5 million (Gatherer, 2009) and 2–4 million (Michaelis et al., 2009)], the death toll in the United States is accurately reported to have been 69, 800 (Klimov et al., 1999; Hilleman, 2002). Post-mortem cultures show evidence of bacterial infection in up to 80% of all severe and fatal cases (Hers et al., 1958; Morens et al., 2008; Gill et al., 2010)…
Conclusion
Viral infection aids bacterial infection in a number of ways, including unveiling/providing more sites for adhesion, impairing immune responses and causing cell and tissue destruction allowing for the spread of bacteria and development of invasive infection. Bacterial infection is then able to worsen clinical outcome and the severity of disease. Of course viral and bacterial co-infection can be mutually beneficial, further helping viral infection, which is bad news for public health. Although antibiotics can help reduce the impact of co/secondary bacterial infection, we still need to better understand the interactions between viruses, bacteria and their host, and to fully understand all mechanisms of disease. Particularly in light of increased antibiotic resistance and the ability of microbes to adapt and evade vaccine induced immunity.
The aim of this review was to emphasize the historical and continuing threat of influenza and to highlight the risk of bacterial co/secondary infection. Vaccines and antibiotics are readily available, however, with antibiotic resistance at an all-time high, vaccination is becoming even more vital in the fight against influenza epidemics and pandemics and the bacterial co/secondary infections commonly associated. It is important to examine the strains and types of bacteria and viruses being spread amongst and transmitted throughout the general public (or continue to in the case of influenza) to inform clinical treatment and development, particularly in the setting of an influenza epidemic or pandemic. As the threat from influenza is ever changing, we need to ensure we know what strains are circulating, which could cause issue and how they interact with other potential pathogens. This preparation also entails monitoring the changing epidemiology of bacterial pathogens associated with secondary infection, such as capsule switching which help S. pneumoniae evade immunity (Pai et al., 2005a,b).
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Some of these results above are many decades, even a century old… So why the insistence that antibiotics are useless in the case of flu? Well, in the USA, the food industry uses antibiotics massively, in the feed of animals, every day (this is now unlawful in Europe). But not just that, in the USA, antibiotics are used on plants, even “organic” plants… Refined studies have shown that antibiotics resistant mutations evolved in those food industry settings…
In other words, in the USA, antibiotics help profits grow everyday… The insistence that antibiotics should be avoided in humans maybe have originated as a coverup…
Patrice Ayme
Patrice Ayme's Thoughts 