Influenza Outbreak and Methicillin-Resistant Staphylococcus aureus (MRSA)

Specialization among infectious disease experts has prevented a deep understanding of the complexities of different pathogens that work cooperatively to cause serious and even fatal human infections. The anticipated human epidemic of an H5N1 influenza strain of avian origin should be a wake-up call to address this important issue. Influenza can make the body particularly susceptible to certain types of bacteria, which can therefore thrive; and could potentially become the driving force for an ongoing global pandemic. Prominent among these bacteria are the toxin-producing Staphylococcus aureus, some of which may be resistant to various antibiotics, including methicillin.

Pioneering research during the 1918 influenza epidemic clearly identified a component of the virus as the initial cause of illness. However, there is ample evidence that bacteria were responsible for “the severity of secondary pulmonary complications” and “common causes of death.” The idea of ​​a mixed infection is contained in the aforementioned letter written by a military doctor in 1919.

“Camp Devens is near Boston and has about 50,000 men, or had them before this epidemic broke out… This epidemic began about four weeks ago and has developed so rapidly that the camp is demoralized and all ordinary work it stops…until it’s over…These men start out with what looks like an ordinary bout of LaFrippe or Influenza, and when they’re taken to the hospital, they very quickly develop the slimiest type of pneumonia ever seen.Two hours after admission they have the mahogany spots on the cheekbones, and within a few hours you start to see the cyanosis spreading from the ears and spreading all over the face, until it is difficult to distinguish the colored men from the white ones.A matter of hours then until death comes, and it’s just a struggle for air until they drown, it’s horrible, one can bear to see one, two or twenty men die, but to see these poor devils them dropping like flies as it gets on my nerves. causing around 100 deaths per day, and still. There is no doubt in my mind that there is a new mixed infection here, but what I don’t know.”

Among the commonly cultured bacteria were Pneumococcus, Streptococcus, and Staphylococcus. Although H1N1 influenza virus has been recovered from victims of the 1918 epidemic, no formal study of possible toxin-producing bacteria from this period has been reported.

The vast majority of bacteria are essentially harmless to mankind. However, bacteria can become infected with their own sets of viruses, some of which can transfer the ability to produce toxins to otherwise relatively harmless bacteria. Bacterial viruses can also transfer the bacteria’s ability to resist certain types of antibiotics. The combination of toxin production capacity with antibiotic resistance is now occurring, especially among Staphylococcus aureus. Of great concern is a complex of toxins known as Panton-Valintine-Leucocidin or PVL. This toxin can easily disable the host’s inflammatory response by directly killing white blood cells (leukocytes). The toxin can also destroy healthy tissues if the bacteria that produce the toxin can enter the tissues. The PVL toxin was originally detected in antibiotic-sensitive bacteria.

Antibiotic resistance among bacteria is a consequence of genetic selection of surviving bacteria in patients treated with various antibiotics. These resistance genes become common, especially if they are carried by bacteria that infect viruses. The appearance of these bacteria is mainly observed in hospitals and other health centers. In fact, an important risk factor for hospital admission is acquiring a bacterial infection resistant to multiple antibiotics. The phenomenon is well documented among Staphylococcus aureus. Originally highly susceptible to penicillin-type antibiotics (known as beta-lactams and commonly represented by the antibiotic methicillin), many hospital-acquired Staphylococcus aureus are now resistant to methicillin. In addition, they are resistant to many other types of antibiotics commonly used in the hospital setting. Examples of resistance to the toxic “antibiotic of last resort” (vancomycin) are now showing up in Staphylococcus aureus and other bacteria in certain hospitals.

Staphylococcus aureus that produces the PVL toxin has begun to become resistant to antibiotics. Currently, most community-associated isolates are resistant to methicillin (CA-MRSA). Over time, they are likely to become resistant to a broader range of antibiotics simply by exchanging genetic information with hospital-associated bacteria (HA-MRSA). The only remaining barrier to severe systemic infection is the normally non-invasive quality of Staphylococcus aureus tissues. Influenza infection can provide that opportunity by destroying the cells that line the airways. Examples of fatal illnesses from a combination of regular influenza with CA-MRSA have been reported with little emphasis on a harbinger of what might occur in the face of an influenza epidemic and multi-antibiotic resistant PVL toxin-producing bacteria. Worse yet, this is just one example of the enormous risks posed by pathogens uniting in biological warfare against humanity and its animals.

What should be done? The most important thing is an all-out attack against the emergence of toxin-producing and/or multi-antibiotic resistant bacteria. There are financial incentives to develop additional antibiotics to replace those to which resistance has developed. This approach should give way to a more sensible approach to infection prevention through decontamination of areas where harmful bacteria reside.

The lack of awareness of decontamination strategies among public health and government officials is evident in their recommendations to simply wash hands with alcohol and short-acting oxidizing agents such as bleach. Much more preferable is to use agents such as phenols and their derivatives which can retain antibacterial activity for many months. Surveillance for toxin-producing and antibiotic-resistant bacteria must be in place in hospitals and settings where large numbers of people gather. Examples include prisons, schools, churches, sports facilities, and workplaces where skin trauma is likely to occur. A comprehensive hygiene program, such as that offered by Preventec Inc., in Atlanta GA, should be instituted at such facilities and its effects monitored.

The benefits of this type of program may well extend to other types of infectious agents, including viruses and fungi. An additional complication of the 1918 influenza epidemic was the subsequent onset of neurological diseases, including a Parkinson-like syndrome known as encephalitis lethargica. Underappreciated research implicated a herpes-like virus in this illness. Vaccination against swine flu triggered another set of neurological diseases, mainly Guillain Barre syndrome, which is also consistent with a process of activation of the virus. Viruses that are not effectively recognized by the immune system are prevalent within the community.

Called stealth-adapted viruses, they undoubtedly contribute to outbreaks of community-acquired infectious diseases with prominent neurological and/or psychiatric manifestations. Bacterial genes have been identified in cultures of sneak-adapted viruses and atypical bacteria have been isolated from patients infected with sneak-adapted viruses. The term viteria refers to viruses capable of crossing the genetic barrier between bacteria and human or animal cells.

They may have the genetic mix between bacteria and also help facilitate the transmission of stealthily adapted viruses to humans. Regular cleaning of environments that present a high risk of human infection with emerging viruses and bacteria will hopefully delay the onset of devastating diseases, such as the one humanity experienced with the 1918 pandemic. Additional information on this topic can be obtained by visiting http://www.s3support.com and [http://www.progressiveuniversity.org]

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