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This information is often anecdotal, may have been subject to bias, and may not satisfy modern scientific standards. Nevertheless, I believe that the researchers of those days tried to be conscientious and professional, and that their assessments are still valuable. The historical accounts as well as the limited evidence from more recent outbreaks discussed in this article agree that pneumonic plague is not easily transmitted from one person to another. Most modern experts agree with this interpretation [ 9 , 12 ], which was also strengthened by a mathematical model using data from published outbreaks that found an R 0 value i.

Perhaps the most convincing evidence of the low risk of transmission is the absence of any documented human-to-human transmission of plague in the Untied States since , long before effective antibiotics were available as prophylaxis for contacts. Antibiotic prophylaxis has been available since However, the diagnosis of plague often is delayed for several days, such as in the case of a patient in who was only diagnosed with plague 4 days after her death and after persons had been in contact with her [ 22 ].

It is unlikely that postexposure prophylaxis could have been responsible for prevention of all infections, if plague would be easily transmitted from person to person. The conclusion is that improved living conditions, better hygiene, better understanding of the disease, and a low underlying risk of infection must have been important factors for the absence of transmission.

The historical accounts I have cited show large differences in infection rates. These can probably be explained by differences in living conditions, hygiene, and observance of protective measures. There are no indications that differences in virulence or host factors could have played a role. Transmission apparently occurs through direct contact or through inhalation of airborne droplets expelled by coughing persons.

The very close contact required for transmission in clinical settings and the limited distance of spread demonstrated by experiments are indications that droplet nuclei do not play a significant role [ 23 ]. Patients in the early stage of pneumonic plague approximately the first 20—24 h apparently pose little risk [ 9 ]. This is likely because of the low counts of bacteria in their respiratory secretions and the general absence of coughing.

Antibiotic medication rapidly clears the sputum of plague bacilli, so that a patient generally is not infective within hours after initiation of effective antibiotic treatment [ 8 ]. This means that in modern times many patients may not reach a stage where they pose a significant risk to others. Simple protective measures can further reduce the risk of infection.

This is evidenced by the numerous outbreaks that stopped as soon as the population at risk realized that they were dealing with a contagious disease and before public health authorities took measures to control it. The main factors preventing transmission must have included avoidance of direct contact with patients, maintenance of a greater physical distance between caretakers and ill persons, reduction of the time caretakers spent with each patient, and perhaps implementation of better hygienic practices, such as hand washing.

In the Manchurian epidemics, a mask made of several layers of gauze seems to have protected almost all physicians who used it. What precautions should health care workers take while caring for suspected pneumonic plague patients? In the case of a bioterrorist event involving plague, the health care system of a region will be easily overwhelmed, especially if strict isolation is instituted indiscriminately for many patients. Strict isolation by itself can reduce a patient's chance of recovery [ 24 ]. Therefore, it is important to carefully triage patients according to which patients should be nursed with precautions, and it is important to reevaluate precautions for patients who may no longer pose a risk.

Protective measures, prophylaxis, and treatment of the patient should be commenced as soon as there is suspicion of pneumonic plague. However, the diagnosis of pneumonic plague should be confirmed by microbiological examination of respiratory secretions. If a bioterrorist event is suspected, it is also important to obtain an isolate to determine its antibiotic susceptibility, because the bacteria may have been engineered for resistance.

All of these guidelines agree on an approach that balances the risk of person-to-person transmission with limited health care resources, and they include the following recommendations:. Doxycycline, ciprofloxacin, chloramphenicol, and cotrimoxazole can be used for prophylaxis. If possible, the choice of drug should be guided by the antimicrobial resistance profile of the isolated strain. I would like to thank Kenneth Gage and Russell Enscore for helping to locate many of the historical publications, and Dr.

Erin Staples, for reviewing the historical plague surveillance data at the CDC. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Close mobile search navigation Article navigation. Clinical Aspects of Pneumonic Plague. Epidemiologic Data on Transmission of Pneumonic Plague. Collins, Colorado jkool cdc. Abstract Plague has received much attention because it may be used as a weapon by terrorists.

View large Download slide. Plague as a biological weapon: Working Group on Civilian Biodefense. Impediments to global surveillance of infectious diseases: Radiographic manifestations of plague in New Mexico, — A review of 42 proved cases. Richard Pearson Strong and the Manchurian epidemic of pneumonic plague, — Epidemiological and diagnostic aspects of the outbreak of pneumonic plague in Madagascar. Human plague associated with domestic cats—California, Colorado. Accessed 8 March Add comment Close comment form modal.

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Related articles in Web of Science Google Scholar. Related articles in PubMed Oral health is a mediator for disease severity in patients with behcet's disease: We also provide an overview of factors that are believed to contribute to the origin and global spread of emerging infectious diseases and offer suggestions that may serve as future prevention strategies, such as social mobilization, public health education, behavioral change, and communication strategies. Because there exists no comprehensive global surveillance system to monitor zoonotic disease emergence, the intervention measures discussed herein may prove effective temporary alternatives.

Contemporary pandemics and outbreaks of disease, such as the current H1N1 influenza pandemic, as well as the emergence of H5N1 influenza virus and severe acute respiratory syndrome SARS -associated coronavirus, serve as poignant reminders of our global vulnerability to emergent threats to human health and our current inability to predict or prevent such events.

However, despite the seemingly unpredictable nature of disease emergence, there are lessons to be learned from the origins of recently emerged diseases as well as those that have their origins in the more distant past, lessons that may offer clues as to how future infectious disease outbreaks and pandemics may be prevented. The challenge lies in using the accumulated, albeit incomplete, knowledge gained from emergent diseases of our past to identify practical solutions and strategies aimed at detecting and halting future threats.

Here, we review the field's current understanding of the origins of infectious diseases and the factors that contribute to their emergence. In particular, we highlight the importance of the zoonotic transmission of pathogenic agents from animals to humans, the favored mechanism by which emergent diseases have come to afflict humans throughout history [ 1—3 ]. Indeed, one key lesson from past pandemics is the pivotal importance of the human-animal interface.

Improving our understanding of this interface will be crucial to future pandemic prevention efforts. The majority of all human infectious diseases and pandemics have originated through the cross-species transmission of microorganisms from animals to humans, overwhelmingly in the Old World [ 1 , 3 ]. However, because most animal pathogens are not readily transmitted to humans [ 4 , 5 ], it follows that for an animal pathogen to become a specialized pathogen in humans, multiple variables must combine in a dynamic and as yet not fully understood process of cross-species transmission.

For an animal pathogen to become a successful human pathogen, it must evolve into a pathogen capable of not only infecting humans, but maintaining long-term human-to-human transmission without the need for reintroduction from the original animal host. This process can be categorized into five progressive stages reviewed by Wolfe et al [ 3 ]. Stage 1 involves animal microbes that are not present in humans under natural conditions, such as most malarial plasmodia. When a pathogen evolves such that it can be transmitted to a human under natural conditions but cannot support sustained human-tohuman transmission, it has entered stage 2.

Examples of such pathogens include tularemia bacilli, Nipah, rabies, and West Nile viruses. Transition from stage 2 and into stage 3 is defined by secondary transmission between humans. Stage 3 includes pathogens that undergo only a few cycles of secondary transmission between humans, such as Ebola, Marburg, and human monkeypox viruses, whereas stage 4 includes diseases that exist in animals but which undergo long sequences of secondary human-to-human transmission without the involvement of animal hosts, such as influenza A, Vibrio cholerae , and dengue virus.

Stage 5, in contrast, represents diseases that are exclusive to humans. Agents responsible for some of history's most troubling diseases belong to stage 5 and include pathogens such as human immunodeficiency virus HIV infection, smallpox, and tuberculosis [ 3 ]. The disease emergence model above provides a construct for how pathogens emerge from animals and illustrates the continuum of animal pathogen infectivity in the human population. However, relatively little is known about the factors that mediate transition from one stage to the next as a pathogen of animal origin scales the stages of this paradigm Figure 1 , ever increasing its ability to reside in the human population and be transmitted throughout it.

As we increase our interactions with animals through hunting, the trading of animal foods, animal husbandry practices, wet markets, and the domestication of animals or exotic pets, the probability of cross-species transmission dramatically increases. It is now generally accepted that the hunting and butchering of wild nonhuman primates in the early 20th century led to the introduction of simian immunodeficiency virus into the human population, giving rise to our modern day HIV pandemic [ 6 ].

In our own work, we have demonstrated that the traditional practice of hunting and butchering nonhuman primates continues to be a gateway for the zoonotic transmission of retroviruses. For instance, among central Africans reporting contact with nonhuman primate blood and body fluids through hunting, butchering, and keeping primate pets, we identified a wide array of primate T lymphotropic viruses [ 7 ], including 2 novel viruses: These results demonstrate that entry of pathogens into the human population via contact with nonhuman primates is an ongoing, dynamic process.

In fact, zoonotic transmission of viruses occurs on an astonishingly regular basis. Presumably, the likelihood of any one zoonotic agent becoming a human pathogen is dependent upon a number of factors.

Swine influenza - Wikipedia

Multiple introductions into the human population may be necessary before a zoonotic agent establishes itself as a human pathogen and the determinants of cross-species tropism are still ill defined, as are the factors that influence whether infection causes disease.

However, the frequency with which the human population is exposed to a potential zoonotic agent is likely to be an important determinant in disease emergence. The course that a pathogen of animal origin takes into the human population varies. The SARS outbreak originated from bats of the genus Rhinolophus , and its human emergence is believed to have been facilitated through intermediate hosts in the wet markets of southern China [ 9 , 10 ].

The current H1N1 influenza epidemic appears to have arisen in North America primarily through the reassortment of viruses of swine origin [ 11 , 12 ]. The species of animal that harbors the pathogen, the nature of human interaction with that animal, and the frequency of these interactions all likely modulate the risk of zoonotic transmission [ 3 ].

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Understanding this complex process will be important to combating future disease emergence. Therefore, further investigation into the interactions that humans have with animals as a potential reservoir of disease , and conditions that influence this interaction, is warranted.

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As an example, despite the fact that chimpanzees have an extremely small population size and human contact with them is infrequent, their close phylogenetic relationship to our own species likely played an important role in our acquiring HIV from chimpanzees, as did the nature of our relationship with them. Presumably, the odds of contracting HIV would have been much lower had humans not been engaged in hunting chimpanzees, a practice that offers many opportunities for exposure to zoonotic agents through contact with biological fluids and tissue.

The human-animal interface is fluid and our interaction with other species, and any potential zoonotic agents they may possess, is variable.

Swine influenza

The frequency and type of human-animal interaction fluctuates in response to other external factors that, in turn, influence the potential for transmission of zoonotic agents. The transmission from swine to humans is believed to occur mainly in swine farms, where farmers are in close contact with live pigs. Although strains of swine influenza are usually not able to infect humans, this may occasionally happen, so farmers and veterinarians are encouraged to use face masks when dealing with infected animals.

The use of vaccines on swine to prevent their infection is a major method of limiting swine-to-human transmission. Risk factors that may contribute to swine-to-human transmission include smoking and, especially, not wearing gloves when working with sick animals, thereby increasing the likelihood of subsequent hand-to-eye, hand-to-nose or hand-to-mouth transmission.

Influenza spreads between humans when infected people cough or sneeze, then other people breathe in the virus or touch something with the virus on it and then touch their own face. Germs spread this way. Diagnosis can be made by sending a specimen, collected during the first five days, for analysis. Recommendations to prevent spread of the virus among humans include using standard infection control , which includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers , especially after being out in public.

Experts agree hand-washing can help prevent viral infections, including ordinary and the swine flu infections. Also, avoiding touching one's eyes, nose or mouth with one's hands helps to prevent the flu. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms, such as a sudden fever, cough or muscle aches, should stay away from work or public transportation, and should contact a doctor for advice. Social distancing , another tactic, is staying away from other people who might be infected, and can include avoiding large gatherings, spreading out a little at work, or perhaps staying home and lying low if an infection is spreading in a community.

Public health and other responsible authorities have action plans which may request or require social distancing actions, depending on the severity of the outbreak. Vaccines are available for different kinds of swine flu. In the aftermath of the pandemic, several studies were conducted to see who received influenza vaccines.

These studies show that whites are much more likely to be vaccinated for seasonal influenza and for the H1N1 strain than African Americans [56] This could be due to several factors. Historically, there has been mistrust of vaccines and of the medical community from African Americans. Many African Americans do not believe vaccines or doctors to be effective.

This mistrust stems from the exploitation of the African American communities during studies like the Tuskegee study. Many people of lower socioeconomic status are less likely to receive vaccinations because they do not have health insurance. Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs, [57] an informal surveillance network in the United States is part of a world surveillance network.

As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required. Antibiotics are also used to treat this disease, which although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds. Since another subtype, pdmH1N1 , emerged globally and also in European pig population.

The prevalence varies from country to country but all of the subtypes are continuously circulating in swine herds. In the EU region whole-virus vaccines are available which are inactivated and adjuvanted.

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  • Vaccination of sows is common practice and reveals also a benefit to young pigs by prolonging the maternally level of antibodies. Several commercial vaccines are available including a trivalent one being used in sow vaccination and a vaccine against pdmH1N1 In vaccinated sows multiplication of viruses and virus shedding are significantly reduced. If a person becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster.

    They may also prevent serious flu complications.

    Zoonotic Disease Emergence

    For treatment, antiviral drugs work best if started soon after getting sick within two days of symptoms. Beside antivirals, supportive care at home or in a hospital focuses on controlling fevers, relieving pain and maintaining fluid balance, as well as identifying and treating any secondary infections or other medical problems. The agency issued these EUAs to allow treatment of patients younger than the current approval allows and to allow the widespread distribution of the drugs, including by volunteers. Swine influenza was first proposed to be a disease related to human flu during the flu pandemic , when pigs became ill at the same time as humans.

    Then, between and , new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In —, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. In in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm. The H1N1 form of swine flu is one of the descendants of the strain that caused the flu pandemic.

    Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. The flu pandemic in humans was associated with H1N1 and influenza appearing in pigs; [65] this may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests, in this case, pigs caught the disease from humans.

    He died the next day, and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced the cause of death was a new strain of swine flu. It was detected only from January 19 to February 9 and did not spread beyond Fort Dix.

    This new strain appeared to be closely related to the strain involved in the flu pandemic. Moreover, the ensuing increased surveillance uncovered another strain in circulation in the U. The vaccination program was plagued by delays and public relations problems. This resulted in a media outcry that linked these deaths to the immunizations, despite the lack of any proof the vaccine was the cause.

    According to science writer Patrick Di Justo, however, by the time the truth was known—that the deaths were not proven to be related to the vaccine—it was too late. Although whether a link exists is still not clear, this syndrome may be a side effect of influenza vaccines. As a result, Di Justo writes, "the public refused to trust a government-operated health program that killed old people and crippled young people. Overall, there were cases of GBS recorded nationwide by CDC surveillance, of which occurred after vaccination and before vaccination. In September , a swine flu virus killed one woman and infected others.

    A year-old woman, Barbara Ann Wieners, was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at a county fair in Walworth County, Wisconsin. Barbara died eight days later, after developing pneumonia. Her husband recovered from his symptoms. Influenza-like illness ILI was reportedly widespread among the pigs exhibited at the fair. Of the 25 swine exhibitors aged 9 to 19 at the fair, 19 tested positive for antibodies to SIV, but no serious illnesses were seen.

    The virus was able to spread between people, since one to three health care personnel who had cared for the pregnant woman developed mild, influenza-like illnesses, and antibody tests suggested they had been infected with swine flu, but there was no community outbreak. In , swine flu was found in pigs in four U.

    Within a year, it had spread through pig populations across the United States. Scientists found this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains. On August 20, , Department of Agriculture officers investigated the outbreak of swine flu in Nueva Ecija and central Luzon , Philippines.

    On July 27, , the Philippine National Meat Inspection Service NMIS raised a hog cholera "red alert" warning over Metro Manila and five regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga , even if these tested negative for the swine flu virus. Since November , 14 deaths as a result of swine flu in Northern Ireland have been reported. The majority of the victims were reported to have pre-existing health conditions which had lowered their immunity. This closely corresponds to the 19 patients who had died in the year prior due to swine flu, where 18 of the 19 were determined to have lowered immune systems.

    Because of this, many mothers who have just given birth are strongly encouraged to get a flu shot because their immune systems are vulnerable. Also, studies have shown that people between the ages of 15 and 44 have the highest rate of infection. Although most people now recover, having any conditions that lower one's immune system increases the risk of having the flu become potentially lethal.

    Swine flu outbreaks were reported in India in late and early As of March 19, the disease has affected 31, people and claimed over 1, lives. Researchers of MIT have claimed that the swine flu has mutated in India to a more virulent version with changes in Hemagglutinin protein. This has however been disputed by Indian researchers. There was another outbreak in India in The states of Maharashtra and Gujarat were the worst affected.

    More than people died of Swine flu in India in year till 26 August