(01-12-2012 11:55 AM)fabietto Ha scritto: "Per favore registrati qui per vedere il link :-) "Il modo di alimentarsi ha qualche implicazione/interferenza su questa "simbiosi" virale? Questa intuizione/scoperta come si potrebbe manipolare a nostro vantaggio?
Citazione:L´Ebola uccide perché l´ospite non e´ quello giusto.
Come i virus dell'aviaria, della suina, etc. per i quali l'uomo non è "l'ospite giusto"?
Tu, Roberto, che sei un virologo, alla luce dell'epigenetica, come le vedi le vaccinazioni di profilassi?
P.S. Mi viene in mente, anche se è un batterio e non un virus, che Escherichia coli, normalmente non pericolosa per l'uomo, diventa un problema per via della "mutazione" causata, si presume, da un alimentazione sbagliata del ruminante e farmaci usati negli allevamenti.
Ciao, scusa per non aver risposto prima...impegni con i figli.
Allora andiamo per domanda
vaccinazioni...sono inutili e pericolose. e non e'certo una mia idea. molti illustri virologi e ricercatori la pensano come me. pericolosa per il contenuto di eccipienti che poi servono a creare uno stato infiammatorio/reazione al vaccino. Molti di questi contengono squalene e mercurio che sono neurotossici. Io stesso preparo isolati virali da iniettare in conigli per ottenere vaccini. Ebbene se non utilizzi un eccipiente come il Frued adiuvante, un carcinogenico, non ottieni un buon vaccino. Perche'? ..perche il corpo regisce al virus/epitopo virale e scatena la reazione immunologica che normalmente dopo 1-2 giorni va scemando.
Inoltre i vaccini non proteggono dal'infezione ma rendono il corpo pronto ad una reazione...ma non ti proteggono dall'infezione virale. Ci sono casi in cui soggetti deboli o con non ottimale reazione immunitaria, si sono ammalati di epatite etc dopo essersi fatta vaccinare. inoltre i virus mutano continuamente. Ricordo che 2 - 3 anni fa con l'aviaria..allora mandai un articolo sul Corriere della sera dicendo che era una burla, un modo di far fare soldi alle ditte farmaceutiche. Ricordo che ebbi una fruttuosa corrispondenza con la Rita Levi Moltalcini che la pensava come me.
Non ti puoi vaccinare contro l'influenza ...stagionale...ma che dicono? ti vaccini contro un virus che isoli, fai il vaccino e lo inietti e poi preghi che non muti. La mutazione avviene sia prima che durante l'infezione in corso.
Alla luce della epigenetica non tutti reagiscono allo stesso modo. Una volta si diceva prendi un po di vitamina C che fa bene. ma quanta? un grammo e stai bene dice tizio, caio dice 2 grammi etc. questo perche siamo diversi. e questa e'"il challenge"del futuro. La nutrigenomica,cosi come la terapia genomica mira a vedere il giusto dosaggio di medicinali e non, vitamine etc, per ogn'uno di noi.
Il modo di alimentarsi influenza sia il nostro corredo genetico, epigenetica, sia il nostro corredo batterico intestinale, che svolge molteplici attivita immunitarie. ritornero su questo con un nuovo post sulla epigenetica/flora batterica e cervello.
La storia che i batteri siano muati, E coli, in seguito all'uso stupido degli antibiotici e'non provata. io personalmente non ne sono convinto. Alcuni anni fa ricercatori russi, se non sbaglio, trovarono in mammut estratti dal permafrost, batteri resistenti a molti antibiotici.
Virus e batteri mutano molto di piu perche noi viviamo in modo diverso rispetto al paleolitico, e non perche ci alimentiamo diversamente, ma perche viviamo in "gruppi"che non sono piu di poche centinaia, dove l'incrocio e'anche molto alto, ma in citta di milioni di persono. Anche se non ti ammali il virus/batterio salta tra milioni di persone mutando. Poi con la facilita di spostamento, aerei, il gioco e'fatto.
Cerchero l'articolo che fu pubblicato su american scientific. Altri ricercatori hanno trovato giant virus resistenti ai batteri nelle alghe marine di milioni di anni fa. insomma i batteri mutano da soli...ma se li si forza, uso indiscriminato di antibiotici, mutano piu velocemente.
Pochi mesi fa c'e'stato un altro caso di cibi infettati dall'e coli in Olanda, salmone, prodotto su larga scala in Grecia. Io penso sia la produzione di massa che stimola i batteri. Se fai crescere colonie batteriche su una piasta con del media, e diventano molte i batteri muatno per "eliminare la conpetizione"e sopravvivere.
DISEASE IN HUMAN EVOLUTION: THE RE-EMERGENCE OF INFECTIOUS DISEASE IN
THE THIRD EPIDEMIOLOGICAL TRANSITION
by George J. Armelagos, Kathleen C. Barnes, and James Lin
For millions of years, humans and their ancestors suffered from diseases -- both the kind caused by
infectious pathogens (e.g., bacteria, viruses, parasites) and the kind caused by our own bodies as they age
and degenerate. Over this long period, humans constantly created new ways of living and eating, and
actual physical or genetic changes evolved to minimize the effects of these diseases. From the point of
view of a bacteria or virus, however, any shift in the physical makeup or behavior of its human host
represents not only an obstacle but also a challenge to be overcome. As a result, new diseases emerged
with each major change in the human way of life.
For nearly four million years, humans lived in widely dispersed, nomadic, small populations that
minimized the effect of infectious diseases. With the agricultural revolution about 10,000 years ago,
increasing sedentism and larger population groupings resulted in the first epidemiological transition in
which infectious and nutritional diseases increased. Within the last century, with the advent of public
health measures, improved nutrition and medicine, some populations in developed nations underwent a
second epidemiological transition. During this transition, infectious diseases declined and non-infectious,
chronic diseases, and degenerative conditions increased. Today, with the increasing use of antibiotics, we
are facing a third epidemiological transition, a reemergence of infectious disease, with pathogens that are
antibiotic-resistant and have the potential to be transmitted on a global scale. Populations that experienced
and those that never experienced the second epidemiological transition are both increasingly exposed to
"Emerging" pathogens are seen as new diseases, discovered when they have an impact on our adaptation
or survival. Even when we take a more holistic ecological perspective, it is often limited to a position that
considers emerging disease as the result of environmental changes that are only relevant to the present
situation as it affects humans here and now. This article argues that the emergence of new diseases has
been the human pattern since the origin of the hominids and accelerated with the shift to agriculture
10,000 years ago.
For most of their 4,000,000 years of evolutionary history, human populations lived in small, sparsely
settled groups. Population size and density remained low throughout the Paleolithic. Fertility and
mortality rates in small gathering-hunting populations would have to have been balanced for the
population size to remain small.
Demographic factors creating this stability are still a matter of discussion. Some demographers argue that
gatherer-hunters were at their maximum natural fertility, balanced by high mortality. Armelagos,
Goodman and Jacobs (1991) argue, however, that gatherer-hunters maintained a stable population with
controlled moderate fertility balanced by moderate mortality.
The demographic changes following the Neolithic may provide insights into the case for population
stability controlled by moderate fertility and mortality during the Paleolithic. Following the Neolithic
revolution, a dramatic increase in population size and density occurred. It was thought that the Neolithic
economy generated food surpluses that led to a better nourished and healthier population with a reduced
rate of mortality. Since populations were at their natural maximum fertility, there would have been a rapid
increase in population size.
The empirical evidence suggests an alternative scenario in the shift from gathering and hunting to
agriculture. The picture suggests a much bleaker picture of health. Instead of experiencing improved
- 2 -
health, there is evidence of a substantial increase in infectious and nutritional disease (Cohen and
Armelagos 1984). A paradox emerges if the traditionally accepted models of Paleolithic fertility and
mortality are correct. How can a population experiencing maximum fertility during the Paleolithic
respond with exponential growth in population when their health is deteriorating?
A consideration of the disease ecology of contemporary gatherer-hunters provides insights into the types
of disease that probably affected our gatherer-hunter ancestors. Polgar (1964) suggests that gathererhunters
had two types of disease to contend with in their adaptation to their environment. One class of
disease would be those organisms that had adapted to prehominid ancestors and persisted with them as
they evolved into hominids. Head and body lice (Pediculus humanus), pinworms, yaws, and possibly
malaria would be included in this group. Cockburn (1967) adds to this list most of the internal protozoa
found in modern humans and such bacteria as salmonella, typhi, and staphylococci.
The second class of diseases are the zoonotic, which have non-human animals as their primary host and
only incidentally infect humans. Humans can be infected by zoonoses through insect bites, by preparation
and consumption of contaminated flesh, and from wounds inflicted by animals. Sleeping sickness,
tetanus, scrub typhus, relapsing fever, trichinosis, tularemia, avian or ichthyic tuberculosis, leptospirosis,
and schistosomiasis are among the zoonotic diseases that could have afflicted earlier gatherer-hunters
Although early human populations were too small to support endemic (constantly present) pathogens,
they maintained some kind of relationships with the vectors that would later serve to perpetuate such
human host-specific diseases as yellow fever and louse-borne relapsing fever. Certain lice were
ectoparasites as early as the Oligocene, and the prehumans of the early Pliocene probably suffered from
malaria, since the Anopheles (mosquito) necessary for transmission of the disease evolved by the
Miocene era. Frank Livingstone, an anthropological epidemiologist, dismisses, however, the potential of
malaria in early hominids except in isolated incidences because of the small population size and an
adaptation to the savanna, an environment that would not have included the mosquitoes that carry the
The range of the earliest hominids was probably restricted to the tropical savanna. This would have
limited the pathogens that were potential disease agents. During the course of human evolution, the
habitat expanded gradually into the temperate and eventually the tundra zones. Hominids, according to
epidemiologist Frank Lambrecht, would have avoided large areas of the African landscape because of
tsetse flies and thus avoided the trypanosomes they carried. He also argues that the evolution of the
human species and its expansion into new ecological niches would have led to a change in the pattern of
trypanosome infection. While this list of diseases that may have plagued our gathering-hunting ancestors
is informative, those diseases that would have been absent are also of interest. The contagious community
diseases such as influenza, measles, mumps, and smallpox would have been missing. There probably
would have been few viruses infecting these early hominids, although Cockburn (1967) disagrees and
suggests that the viral diseases found in non-human primates would have been easily transmitted to
The First Epidemiological Transition:
Disease in Agricultural Populations
The reliance on primary food production (agriculture) increased the incidence and the impact of disease.
Sedentism, an important feature of agricultural adaptation, conceivably increased parasitic disease spread
by contact with human waste. In gathering-hunting groups, the frequent movement of the base camp and
frequent forays away from the base camp by men and women would decrease their contact with human
wastes. In sedentary populations, the proximity of habitation area and waste deposit sites to the water
- 3 -
supply is a source of contamination. While sedentarism did occur prior to the Neolithic period in those
areas with abundant resources, once there was the shift to agriculture, sedentary living was necessary.
The domestication of animals provided a steady supply of vectors and greater exposure to zoonotic
diseases. The zoonotic infections most likely increased because of domesticated animals, such as goats,
sheep, cattle, pigs, and fowl, as well as the unwanted domestic animals such as rodents and sparrows,
which developed (Polgar 1964) permanent habitats in and around human dwellings. Products of
domesticated animals such as milk, hair, and skin, as well as the dust raised by the animals, could
transmit anthrax, Q fever, brucellosis, and tuberculosis. Breaking the sod during cultivation exposed
workers to insect bites and diseases such as scrub typhus. Frank Livingstone showed that slash-and-burn
agriculture in west Africa exposed populations to Anopheles gambiae, a mosquito which is the vector for
Plasmodium falciparum, which causes malaria. Agricultural practices also create pools of water,
expanding the potential breeding sites for mosquitos. The combination of disruptive environmental
farming practices and the presence of domestic animals also increased human contact with arthropod
(insect) vectors carrying yellow fever, trypanosomiasis, and filariasis, which then developed a preference
for human blood. Some disease vectors developed dependent relationships with human habitats, the best
example of which is Aedes aegypti (vector for yellow fever and dengue), which breeds in stagnant pools
of water in open containers. Various agricultural practices increased contact with non-vector parasites.
Irrigation brought contact with schistosomal cercariae, and the use of feces as fertilizer caused infection
from intestinal flukes (Cockburn 1971).
The shift to agriculture led to a change in ecology; this resulted in diseases not frequently encountered by
forager populations. The shift from a varied, well-balanced diet to one which contained fewer types of
food sometimes resulted in dietary deficiencies. Food was stored in large quantities and widely
distributed, probably resulting in outbreaks of food poisoning. Intensive agricultural practices among the
prehistoric Nubians resulted in iron deficiency anemia as did the reliance on cereal grain, weaning
practices, and parasitic infestation. The combination of a complex society, increasing divisions of class,
epidemic disease, and dietary insufficiencies no doubt added mental stress to the list of illnesses.
Disease in Urban Populations
The development of urban centers is a recent development in human history. In the Near East, cities as
large as 50,000 people were established by 3000 BC. In the New World, large urban settlements were in
existence by AD 600. Settlements of this size increase the already difficult problem of removing human
wastes and delivering uncontaminated water to the people. Cholera, which is transmitted by contaminated
water, was a potential problem. Diseases such as typhus (carried by lice) and the plague bacillus
(transmitted by fleas or by the respiratory route) could be spread from person to person. Viral diseases
such as measles, mumps, chicken pox, and smallpox could be spread in a similar fashion. Due to
urbanization, populations for the first time were large enough to maintain disease in an endemic form.
Aidan Cockburn, a paleopathologist, estimated that populations of one million would be necessary to
maintain measles as an endemic disease. What was an endemic disease in one population could be the
source of a serious epidemic (affecting a large number of people at the same time) disease in another
group. Cross-continental trade and travel resulted in intense epidemics (McNeill 1976). The Black Death,
resulting from a new pathogen, took its toll in Europe in the 1300s; this epidemic eliminated at least a
quarter of the European population (approximately 25 million people).
The period of urban development can also be characterized by the exploration and expansion of
populations into new areas that resulted in the introduction of novel diseases to groups that had little
resistance to them (McNeill 1976). For example, the exploration of the New World may have been the
source of the treponemal infection (syphilis) that was transmitted to the Old World. This New World
infection was endemic and not sexually transmitted. When it was introduced into the Old World, a
different mode of disease transmission occurred. The sexual transmission of the treponeme created a
different environment for the pathogen, and it resulted in a more severe and acute infection. Furthermore,
- 4 -
crowding in the urban centers, changes in sexual practices, such as prostitution, and an increase in sexual
promiscuity may have been factors in the venereal transmission of the pathogen.
The process of industrialization, which began a little over 200 years ago, led to an even greater
environmental and social transformation. City dwellers were forced to contend with industrial wastes and
polluted water and air. Slums that arose in industrial cities became focal points for poverty and the spread
of disease. Epidemics of smallpox, typhus, typhoid, diphtheria, measles, and yellow fever in urban
settings were well documented. Tuberculosis and respiratory diseases such as pneumonia and bronchitis
were even more serious problems, with harsh working situations and crowded living conditions. Urban
population centers, with their extremely high mortality, were not able to maintain their population bases
by the reproductive capacity of those living in the city. Mortality outstripped fertility, requiring
immigration to maintain the size of the population.
The Second Epidemiological Transition: The Rise of Chronic and Degenerative Disease
The second epidemiological transition refers to the shift from acute infectious diseases to chronic noninfectious,
degenerative diseases. The increasing prevalence of these chronic diseases is related to an
increase in longevity. Cultural advances results in a larger percentage of individuals reaching the oldest
age segment of the population. In addition, the technological advances that characterize the second
epidemiological transition resulted in an increase in environmental degradation. An interesting
characteristic of many of the chronic diseases is their particular prevalence and 'epidemic'-like occurrence
in transitional societies, or in those populations undergoing the shift from developing to developed modes
of production. In developing countries, many of the chronic diseases associated with the epidemiological
transition appear first in members of the upper socioeconomic strata, because of their access to Western
products and practices.
With increasing developments in technology, medicine, and science, the germ theory of disease causation
developed. While there is some controversy about the role that medicine has played in the decline of some
of the infectious diseases, a better understanding of the source of infectious disease exists, and this
admittedly has resulted in increasing control over many infectious diseases. The development of
immunization resulted in the control of many infections and recently was the primary factor in the
eradication of smallpox. In the developed nations, a number of other communicable diseases have
diminished in importance. The decrease in infectious disease and the subsequent reduction in infant
mortality has resulted in greater life expectancy at birth. In addition, there has been an increase in
longevity for adults and this has resulted in an increase in chronic and degenerative diseases.
Many of the diseases of the second epidemiological transition share common etiological factors related to
human adaptation, including diet, activity level, mental stress, behavioral practices, and environmental
pollution. For example, the industrialization and commercialization of food often results in malnutrition,
especially for those societies in "transition" from subsistence forms of food provision to agribusiness. The
economic capacity to purchase food that meets nutritional requirements is often not possible. Obesity and
high intakes of refined carbohydrates are related to the increasing incidence of heart disease and diabetes.
Obesity is considered to be a common form of malnutrition in developed countries and is a direct result of
an increasingly sedentary lifestyle in conjunction with steady or increasing caloric intakes.
A unique characteristic of the chronic diseases is their relatively recent appearance in human history as a
major cause of morbidity. This is indicative of a strong environmental factor in disease etiology. While
biological factors such as genetics are no doubt important in determining who is most likely to succumb
to which disease, genetics alone cannot explain the rapid increase in chronic disease. While some of our
current chronic diseases such as osteoarthritis were prevalent in early human populations, other more
serious degenerative conditions such as cardiovascular disease and carcinoma were much rarer.
- 5 -
The Third Epidemiological Transition
Today, human populations are moving into the third epidemiological transition. There is a reemergence of
infectious diseases with multiple antibiotic resistance. Furthermore, this emergence of diseases has a
potential for global impact. In a sense, the contemporary transition does not eliminate the possible coexistence
of infectious diseases typical of the first epidemiological transition (some 10,000 years ago) in
our own time; the World Health Organization (WHO) reports that of the 50,000,000 deaths each year,
17,500,000 are the result of infectious and parasitic disease. WHO reports that 1.7 million have
tuberculosis and 30 million people are infected with HIV.
The emergence of infectious disease has been one of the most interesting evolutionary stories of the last
decade, and has captured the interest of scientists and the public. The popular media, with the publication
of books such as The Hot Zone and movies such as Outbreak, has captured the public's fascination with
emerging diseases as threats to human survival. There is genuine scientific concern about the problem.
David Satcher (Director of the Centers for Disease Control in Atlanta, GA) lists 22 diseases that have
emerged in the last 22 years, including Rotovirus, Ebola virus, Legionella pneumophila (Legionnaire s
Disease), Hantaan Virus (Korean hemorrhagic fever), HTLV I, Staphylococcus toxin, Escherichia coli
0157:h7, HTLV II, HIV, Human Herpes Virus 6, Hepatitis C, and Hantavirus isolates.
The emergence of disease is the result of an interaction of social, demographic, and environmental
changes in a global ecology and in the adaptation and genetics of the microbe, influenced by international
commerce and travel, technological change, breakdown of public health measures, and microbial
adaptation. Ecological changes such as agricultural development projects, dams, deforestation, floods,
droughts and climatic changes have resulted in the emergence of diseases such as Argentine hemorrhagic
fever, Korean hemorrhagic fever (Hantaan) and Hantavirus pulmonary syndrome. Human demographic
behavior has been a factor in the spread of dengue fever, and the source for the introduction and spread of
HIV and other sexually transmitted diseases.
The engine that is driving the reemergence of many of the diseases is ecological change that brings
humans into contact with pathogens. Except for the Brazilian pururic fever, which may represent a new
strain of Haemophilus influenzae, biotype aegyptius, most of the emerging diseases are of cultural origin.
The development of antibiotic resistance in any pathogen is the result of medical and agricultural
practices. The indiscriminate and inappropriate use of antibiotics in medicine has resulted in hospitals that
are the source of multi-drug resistant strains of bacteria that infect a large number of patients. Agricultural
use in which animal feed is supplemented with sub-therapeutic doses of antibiotics has risen dramatically
in the last half century. In 1954, 500,000 pounds of antibiotics were produced in the United States; today,
40,000,000 pounds are produced annually.
Recently, much attention has focused on the detrimental effects of industrialization on the international
environment, including water, land, and atmosphere. Massive industrial production of commodities has
caused pollution. Increasingly there is concern over the health implications of contaminated water
supplies, over-use of pesticides in commercialized agriculture, atmospheric chemicals, and the future
effects of a depleted ozone layer on human health and food production. At no other time in human history
have the changes in the environment been more rapid or so extreme. Increasing incidence of cancer
among young people and the increase in respiratory disease has been implicated in these environmental
Anthropogenic impact from technology has been the pattern since Neolithic times. Within the last 300
years, transportation has played a major role in disease patterns by bringing larger segments of humans
into contact with the pathogens at an accelerated rate. The emergence of disease in the New World upon
contact with Europeans was a consequence of large sailing ships that became a major mode of
- 6 -
transportation. Now it is possible for a pathogen to move between continents within a matter of hours. We
live in a time where there exists a virtual viral superhighway, bringing people into contact with pathogens
that affect our adaptation. The present pattern reflects an evolutionary trend that can be traced to the
beginning of primary food production. The scale has changed. The rates of emerging disease and their
impact can now affect large segments of the world population at an ever increasing rate, and we need to
be increasingly aware of the implications for today s human populations around the globe.
For further reading
Armelagos, G. J. Human evolution and the evolution of human disease. Ethnicity and Disease 1(1): 21-
Armelagos, G. J., A. H. Goodman, et al. The origins of agriculture: Population growth during a period of
declining health. Population and Environment 13(1): 9-22, 1991.
Cockburn, T. A. The evolution of human infectious diseases. In Infectious Diseases: Their Evolution and
Eradication, T. A. Cockburn, ed. Springfield, IL: Charles C. Thomas, 1967.
Cockburn, T. A. Infectious disease in ancient populations. Current Anthropology 12(1): 45-62, 1971.
Cohen, M. N. and G. J. Armelagos, eds. Paleopathology at the Origin of Agriculure. Orlando: Academic
Ewald, P. W. Evolution of Infectious Disease. New York: Oxford University Press, 1994.
McNeill, W. H. Plagues and People. Garden City: Anchor/Doubleday, 1976.
Polgar, S. Evolution and the ills of mankind. In Horizons of Anthropology, Sol Tax, ed. Chicago: Aldine,
Questo anche interessante
Wild sharks, redfish harbor antibiotic-resistant bacteria
Published: Wednesday, June 16, 2010 - 15:04 in Biology & Nature
(click to enlarge)
Photo by L. Brian Stauffer, U. of I. News Bureau.
Graphic produced by Diana Yates. Photo credits: Bull shark (NSW Department of Primary Industries); Lemon shark (drawing by Robbie Cada); Nurse shark (modified from photo by Joseph Thomas); Spinner shark (image by Dieno); Blacktip shark (modified from photo by Albert Kok); Smooth dogfish (image from U.S. Fish & Wildlife Service).Scientists have found antibiotic-resistant bacteria in seven species of sharks and redfish captured in waters off Belize, Florida, Louisiana and Massachusetts. Most of these wild, free-swimming fish harbored several drug-resistant bacterial strains. The study, published in the Journal of Zoo and Wildlife Medicine, found antibiotic-resistant bacteria in every fish species sampled.
The researchers also found multidrug-resistant bacteria in fish at nearly all of the study sites, said Mark Mitchell, a professor of veterinary clinical medicine at the University of Illinois and a senior author of the paper.
"Ultimately the idea of this study was to see if there were organisms out there that had exposures or resistance patterns to antibiotics that we might not expect," Mitchell said. "We found that there was resistance to antibiotics that these fish shouldn't be exposed to."
Among the animals sampled, nurse sharks in Belize and in the Florida Keys had the highest occurrence of antibiotic-resistant bacteria. These sharks feed on crustaceans, small fish and other animals living in shallow waters close to shore.
Random mutations may account for drug-resistant bacteria in marine environments, Mitchell said, but there is a lot of evidence for a human origin.
"The shark population in Belize, for example, is a big tourist area, so there are people in the water right there," he said. "The sampling site is not far from a sewage plant, and so all those exposures we think are playing a role."
Sewage also is a problem in the Atlantic coastal waters of the United States, he said. Previous studies have shown that sewage outflows can leak antibiotic-resistant bacteria into the environment.
In the new study, the researchers looked for and found bacterial resistance to 13 antibacterial drugs in the fish. Patterns of resistance varied among the sites.
Bacteria from sharks off Martha's Vineyard in Massachusetts and in offshore Louisiana were resistant to the fewest number of antibiotics, while sharks in the Florida Keys and Belize harbored bacteria that were resistant to amikacin, ceftazidime, chloramphenicol, ciprofloxacin, doxycycline, penicillin, piperacillin, sulfamethoxazole and ticarcillin.
Redfish in the Louisiana offshore site hosted more varieties of drug-resistance than sharks in the same waters. This may reflect differences in their age (the redfish were more mature than the sharks), feeding or migratory habits, Mitchell said.
While the presence of antibiotic-resistant bacteria in sharks and other fish does not necessarily harm them, Mitchell said, the findings point to a growing problem for human health.
"There are estimates of over 100,000 deaths from infections in hospitals per year, many of them from antibiotic-resistant organisms," Mitchell said. "And we're creating even more of these organisms out in the environment. … Unfortunately, as these things collect, there's probably a threshold at some point where there's going to be a spillover and it will start to affect us as a species."
People do eat sharks and redfish, Mitchell said, and now these fish represent a potential new route of exposure to drug-resistant bacteria. Sharks and redfish also are predators, and so may function as sentinels for human health.
"Some people might say, well, a bull shark in offshore Louisiana doesn't really have an influence on my health," Mitchell said. "But these fish eat what we eat. We're sharing the same food sources. There should be a concern for us as well."
Antibiotic resistance in the environment: a link to the clinic?
Gerard D Wright
M.G. DeGroote Institute for Infectious Disease Research, Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada L8N 3Z5
Available online 16 September 2010
"Per favore registrati qui per vedere il link :-) "
How to Cite or Link Using DOI
View full textPurchase $41.95Introduction: antibiotic resistance is a global phenomenonThe environmental antibiotic resistomeAntibiotic resistance in animalsConclusions: the clinical impact of environmental resistanceReferences and recommended readingAcknowledgmentsReferences
The emergence of resistance to all classes of antibiotics in previously susceptible bacterial pathogens is a major challenge to infectious disease medicine. The origin of the genes associated with resistance has long been a mystery. There is a growing body of evidence that is demonstrating that environmental microbes are highly drug resistant. The genes that make up this environmental resistome have the potential to be transferred to pathogens and indeed there is some evidence that at least some clinically relevant resistance genes have originated in environmental microbes. Understanding the extent of the environmental resistome and its mobilization into pathogenic bacteria is essential for the management and discovery of antibiotics
There is evidence that naturally occurring antibiotic resistance is common. The genes that confer this resistance are known as the environmental resistome. These genes may be transferred from non-disease-causing bacteria to those that do cause disease, leading to clinically significant antibiotic resistance.
In 1952 an experiment conducted by Joshua and Esther Lederberg showed that penicillin-resistant bacteria existed before penicillin treatment. While experimenting at the University of Wisconsin-Madison, Joshua Lederberg and his graduate student Norton Zinder also demonstrated preexistent bacterial resistance to streptomycin. In 1962, the presence of penicillinase was detected in dormant Bacillus licheniformis endospores, revived from dried soil on the roots of plants, preserved since 1689 in the British Museum. Six strains of Clostridium, found in the bowels of William Braine and John Hartnell (members of Franklin Expedition) showed resistance to cefoxitin and clindamycin. It was suggested that penicillinase may have emerged as a defense mechanism for the bacteria in their habitats, as in the case of penicillinase-rich Staphylococcus aureus, living with penicillin-producing Trichophyton. This, however, was deemed circumstantial. Search for a penicillinase ancestor has focused on the class of proteins that must be a priori capable of specific combination with penicillin. The resistance to cefoxitin and clindamycin in turn was speculatively attributed to Braine's and Hartnell's contact with microorganisms that naturally produce them or to random mutation in the chromosomes of Clostridium strains. Nonetheless there is an evidence that heavy metals and some pollutants may select for antibiotic-resistant bacteria, generating a constant source of them in small numbers.
facciamo il punto..
io vivo in una comunita molto densa quindi molti virus e batteri hanno molti ospiti. Vivo male in rapporto al mio corredo genetico, mi nutro male/non corretto rispetto al mio codice genetico, la mia flora batterica muta. mi becco un batterio che interaggisce con la mia flora batterica e...si scambiano per cosi dire informazioni. il batterio muta e per caso muta in un super bug...che in una piccola comunita della foresta amazzonica, uccide un paio di persone epoi sparisce..ma in una supercolonia umana come Milano si distribuisce e continua amutare.
Insomma come al solito non c'e'una sola risposta. e'l'insieme che conta.
(30-11-2012 06:42 PM)fabietto Ha scritto: "Per favore registrati qui per vedere il link :-) "Grazie Roberto,
leggendo la parte dei virus mi è venuto in mente, come un flash, che un certo Arnold Ehret (ho un certo disagio nel nominarlo) sosteneva che i virus in se non sono pericolosi e che in un organismo sano transitano indisturbati svolgendo dentro di noi svariate utili funzioni. Questi virus vengono paragonati a dei topi che nutrendosi della spazzatura ripuliscono il territorio (i virus il nostro organismo). Se la spazzatura e poca tutto va bene ma se tanta allora le tossine che scaturiscono da questo processo di pulizia non vengono espulse causando la malattia. Credo che Ehret si riferisse a Bechamp, infatti lui ha scoperto che i germi non sono la causa della malattia ma si occupano solo di decomporre i tessuti in degrado e sono prodotti dall'organismo; di fatto sono gli spazzini dell'organismo. Quindi quando noi, con i farmaci, uccidiamo i virus è come se uccidessimo i topi lasciando che la montagna di spazzatura continui a crescere. Così dopo che l'effetto del farmaco svanisce e i virus ritornano, si troveranno una super montagna di spazzatura da metabolizzare con un effetto ancora più drammatico per il nostro organismo. Lo stesso Pasteur in punto di morte disse ad un suo assistente: "Claude Bernard aveva ragione, il terreno è tutto, il microbo è nulla".
Anche un certo dr. Hamer disse: Se fossero i germi o i virus le cause delle malattie noi saremmo già morti perché ne abbiamo in gran quantità nel nostro organismo.
Articolo molto interessante
ZoekresultatenThe Neuroscience of the Gut: Scientific Americanwww.scientificamerican.com/article.cfm?id...gutIn cache - Vertaal deze pagina
U heeft dit openbaar een +1 gegeven. Ongedaan maken
19 Apr 2011 – For example, gut bacteria may have an influence on the body's use of ... way of phrasing it- how much of epigenetics is controlled by bacteria?