he.lifepower.vip.avoori.com/9705-mujeres-solteras-la.php Therefore, there is considerable interest in the prevention of CA-MRSA infection among persons with recurrent infection and among close contacts of infected persons. At present, data are lacking on the efficacy of interventions to prevent CA-MRSA infection in persons who experience repeated infections or among close contacts of infected persons.
Some researchers have used nasal decolonization and decolonization of other body sites as a means to prevent CA-MRSA infection [ 21 , 23—25 ]. Decolonization strategies are based on robust literature involving this strategy to prevent health care-associated MRSA HA-MRSA infection, a context in which the model of pathogenesis is based on the tenet that infection is preceded by colonization [ 26 ].
However, there are data to suggest that stepwise progression of colonization to infection may not commonly occur in community settings. Recent data have suggested that nasal colonization may play a less important role in the pathogenesis of CA-MRSA infection and that, instead, skin-skin and skin-fomite contact could represent important transmission routes.
The ecologic niche for S. One-quarter to one-third of healthy persons harbor S. Although S. This idea is supported by studies that have revealed that, if S. Nasal S. The proof of principle demonstrating the importance of nasal colonization's role in the pathogenesis of S. This observation has spurred attempts to eradicate S.
Unfortunately, nasal decolonization strategies have limitations. Short-term eradication is generally successful, but patients are often later recolonized with the same strain [ 26 , 28 , 31 ]. This suggests that recolonization from sources exogenous to the nose can occur. Another limitation is that recolonizing strains are sometimes resistant to the previously used intranasal topical antibiotic [ 32 ].
The relationship between colonization and infection has been a fundamental tenet in the pathogenesis of S. Indeed, a common feature of outbreak and nonoutbreak i. This suggests that the strain was acquired from a nonnasal endogenous source or an environmental source. CA-MRSA infection among MSM has been associated with high-risk behaviors, including use of methamphetamines and other illicit drugs, high-risk sexual behavior, use of the Internet to find sexual contacts, occurrence of skin-abrading sex, and history of sexually transmitted infections [ 10 , 35—37 ].
Others have reported the occurrence of CA-MRSA infection in the buttocks and genitoperineal sites associated with heterosexual sexual activity [ 39 ]. In these outbreaks, players are believed to spread the infection through repeated skin-skin contact, especially contact between broken skin, which occurs in games and practices [ 33 ]. In theses outbreaks, CA-MRSA infection was associated with exposures to various contaminated fomites, including whirlpools, shared razors, and shared towels [ 7 , 33 ].
Other fomites implicated in outbreaks of sports team-associated CA-MRSA infection include benches, body suits worn by fencers, and even a bar of soap [ 6 , 33 , 42 ]. In non-sports team outbreaks, sauna benches have been implicated [ 34 ]. In nonoutbreak settings, close contact with a person who has a skin infection was also associated with CA-MRSA infection [ 43 ].
Because S. Environmental sources of S. In hospitals, S. One key component of the search-and-destroy method is aggressive environmental hospital ward cleaning, in which wards where MRSA has been isolated are closed and extensively cleaned [ 49 ]. Although the reason behind the success of the search-and-destroy method is almost certainly multifactorial e. Its success compared with other MRSA control measures lends credence to the notion that environmental sources are an important component of MRSA pathogenesis.
Clearly, the dynamics of community living differ markedly from the dynamics of health care settings. On the basis of CA-MRSA outbreak data, it is possible that infection pathogenesis relies much more on acquisition from environmental sources and less on antecedent nasal colonization. This model's role outside of outbreaks may not be as clear, because crowding living situations may not play a major role e. Taken in sum, data from outbreaks of CA-MRSA infection and from endemic infections suggest that antecedent nasal colonization may play a much less prominent role in the pathogenesis of CA-MRSA than was previously believed.
First isolated in [ 54 ], USA has been implicated in epidemiologically unassociated outbreaks in at least 38 US states figure 1 [ 5—7 , 10 , 20 , 33 , 39 , 42 , 52 , 54—68 ].
Although many USA infections occur in the context of outbreaks, many are sporadic and do not involve any well-defined populations [ 69 , 70 ]. Longitudinal analysis of S. This epidemic could be attributed entirely to the rapid dissemination of a single clone of this species: from 1 case involving USA in to cases involving USA in figure 2. Outbreaks of community-associated methicillin-resistant Staphylococcus aureus infection due to USA in the United States, as documented to date. Community-associated MRSA isolates were obtained from a clinical specimen from an outpatient or within the first 72 h after hospital admission.
Health care-associated MRSA isolates were obtained after 72 h of hospital admission or from patients residing in long-term care facilities.
Crowding and Disease Virulence David P. Clark Earlier thinking held that, given time, all diseases would adapt, to become no worse than measles and mumps. This Element is an excerpt from Germs, Genes, & Civilization: How Epidemics Shaped Who We Are Today () by David P. Clark. Available in.
The international spread of USA has been recently reported, with outbreaks of infection in Canada and many European countries [ 76—81 ]. Exportation of USA may be facilitated by a history of recent travel to the United States [ 76—77 ]. It is of interest that USA first gained a foothold in Canada among persons with a history of incarceration, illicit drug use, and homelessness [ 82 ]; the same risk factors were noted among the early patients infected with the USA strain described in the United States [ 5 , 54 , 55 , 73 ], suggesting that USA may emerge in the more marginalized populations with increased frequency of person-person contact.
However, this strain has clearly also established itself in nonmarginalized populations, such as healthy children [ 72 ]. The vast majority PVL-positive S. The role of PVL in disease pathogenesis is also controversial. Some animal studies have failed to find PVL as a major virulence factor [ 84 ], although others have found that it has a role in the pathogenesis of the pulmonary infection [ 85 ]. CA-MRSA, however, carries an allotype of SCC mec that is smaller in size than those typically found in nosocomial strains; this may impose only a slight cost to fitness, because it does not contain resistance genes other than mec A, which encodes an altered target penicillin-binding protein 2a.
Horizontal acquisition of ACME from the ubiquitous skin commensal Staphylococcus epidermidis may enhance the growth and survival of USA in the host—particularly on the human skin [ 89 ]. Compared with other CA-MRSA strains, USA strains may have features that are particularly well suited to cause disease, although these features are, at this time, poorly understood. The role of human host defenses against S.
Clearly, qualitative deficiencies in neutrophil function are associated with S. Other host factors associated with infection risk include antimicrobial peptides [ 94 ], although our current understanding of host response to S.
Skin integrity is also key to prevention of S. Many patients with CA-MRSA infection, however, have reported a breach in skin integrity that served as the portal of infection. For example, skin infections often resulted from activities that resulted in skin trauma, such as those resulting from physical contact sports [ 7 , 33 , 42 ], injection drug use [ 95 ], and shaving of the genital area before sexual activity [ 39 , 96 ].
Many children do not have recognized breeches in skin integrity before infection. Whether this means there was none or that these breeches were not recognized or recalled is not clear. Although longitudinal natural history studies have not been performed, epidemiologic and basic studies suggest that nasal colonization plays a less prominent role in the transmission and pathogenesis. For example, decolonization strategies that rely only on nasal decolonization may not be successful, because they do not address nonnasal colonization or decolonization of the patient's environs.
Rather than a stepwise progression of exposure to MRSA, followed by colonization, followed by infection, CA-MRSA acquisition may arise from a variety of forces that may result in either colonization or infection without preceding colonization.
In turn, colonization may lead to infection or infection to colonization. Financial support. 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. Sign In. Advanced Search. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents. Host Defenses against S. Reprints or correspondence: Dr. Carson St. Oxford Academic. Google Scholar. Binh An Diep. Article history. Cite Citation. Permissions Icon Permissions.
Abstract Community-associated methicillin-resistant Staphylococcus aureus MRSA infection is increasingly common worldwide and causes considerable morbidity and mortality. View large Download slide. Community-associated methicillin-resistant Staphylococcus aureus. Search ADS. Centers for Disease Control and Prevention. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus —Minnesota and North Dakota, — Community-acquired methicillin-resistant Staphylococcus aureus infections in south Texas children. Community-acquired methicillin-resistant Staphylococcus aureus and intrafamily spread of pustular disease.
Methicillin-resistant Staphylococcus aureus infections in correctional facilities—Georgia, California, and Texas, — Methicillin-resistant Staphylococcus aureus infections among competitive sports participants—Colorado, Indiana, Pennsylvania, and Los Angeles County, — A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns.
Community-acquired methicillin-resistant Staphylococcus aureus among military recruits. Outbreaks of community-associated methicillin-resistant Staphylococcus aureus skin infections—Los Angeles County, California, — Risk factors for community-associated methicillin-resistant Staphylococcus aureus skin infections among HIV-positive men who have sex with men. A prospective investigation of risk factors for community-acquired MRSA infection in a non-outbreak setting [abstract LB-7; oral abstract, late breaker].
Google Preview. Clinical presentation of community-acquired methicillin-resistant Staphylococcus aureus in pregnancy. Methicillin-resistant Staphylococcus aureus in community-acquired skin infections. Staphylococcal resistance revisited: community-acquired methicillin resistant Staphylococcus aureus —an emerging problem for the management of skin and soft tissue infections.
Characteristics of community-acquired methicillin-resistant Staphylococcus aureus in infants and children without known risk factors. Epidemiology and clonality of community-acquired methicillin-resistant Staphylococcus aureus in Minnesota, — Severe community-onset pneumonia in healthy adults caused by methicillin-resistant Staphylococcus aureus carrying the Panton-Valentine leukocidin genes.
Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles. Severe Staphylococcus aureus infections caused by clonally related community-acquired methicillin-susceptible and methicillin-resistant isolates. The host liquefies at death; release the viruses which are taken up by other hosts.
Many terminally killing pathogens have similar life histories In mammals; anthrax Bacilus anthracis is a case of mechanistic coupling In the late infection, bacterial density in the host grows to high levels and the high concentration of anthrax lethal toxin knocks out the immune system by destroying the macrophages. Anthrax oedema toxin causes the production of a high amount of cAMP in host cells, which disrupts the flow of ions and cellular functions leading to host death.
Transmission occurs primarily by spores which are released after the death of the host. From an evolutionary perspective, mechanistic coupling between transmission and extreme virulence strongly shapes the life history of parasites In the first major transmission episode parasite grows to maximum density and maximize the opportunities for successful transmission, consequently severely damages the host, and the chance of subsequent transmission rate is low. Reproductive success of a parasite is sometimes calculated by the number of newly infected hosts.
A long period of infection is beneficial to the parasite. A shorter infection period may be advantageous, if compensated by an increase in the infection rate to new hosts. This trade-off between the infection rate and the duration of infection determine the optimal parasite infectivity and duration of infection. A shorter infection period is associated with high virulence of the parasite.
Parasite evolution with this trade-off is the backbone of the adaptive theory. Anderson and May 15 proposed a theoretical framework for the evolution of parasites. An increase in the parasite-independent host mortality rate should lead to selection of parasites that kill their hosts rapidly and are more virulent Shorter life-span of the host often leads to a shorter infection period that in turn selects for rapidly replicating parasite. A long host life-span leads to selection of slower replicating parasites with low virulence.
These predictions have been tested with variable success Reduction in the mortality of transmission stages allows parasites to compensate for increased virulence and maintain infections in population previously too small to sustain them. Importantly, increase in the size of host population usually leads to increase in the incidence of parasite population In plants and invertebrates, host resistance is often defined as inability of the parasite to infect the host In vertebrates, host resistance is often the host ability to mount an effective immune response to clear the infection.
An increase in the recovery rate should select for more virulent parasites 28 as a higher recovery rate leads to a shorter duration of infection forcing parasites to evolve higher growth rate and virulence. Increased host resistance may select for high or low virulence depending on mechanisms of resistance Imperfect vaccines increase host resistance and allow replication and transmission of parasites leading to evolution of parasites with low or high virulence depending on the vaccine In epidemic infections the number of susceptible hosts is large and parasite strains infecting the hosts rapidly gain selective advantage In endemic diseases there is always dearth of susceptible hosts, so parasites infecting the maximum number of hosts will have selective advantage.
Thus, in endemic infections parasites maximize their basic reproductive number in case of directly transmitted diseases. Higher host densities and high rates of parasite transmission cause outbreaks of highly virulent parasites including influenza, cholera and HIV 32, Host immunodeficiency due to HIV infection may result from the within host, short-sighted evolution of the virus and may have nothing to do with the rate of virus transmission Duration of HIV infection is inversely correlated with the virus density in plasma of infected hosts early in the asymptomatic period of the infection Viral load is positively correlated with the probability of heterosexual transmission of HIV Such relationships indicate a positive correlation between HIV transmissibility and virulence for viral strains with different set points.
Adaptive theory assumes that only one parasite strain can occupy a given host. For example, Daphnia magna can be repeatedly infected with the same microsporidian parasite Humans infected with malaria often harbor several different strains of the parasite Theoretical results suggest that competition between different parasite stains within one host select for increased virulence because of the risk to share the host with a more virulent parasite strain.
The increase in the number of parasite strains occupying the same host may result from mutation 39 and co- or super infection Mixed-clone infections of mice with malaria parasite Plasmodium chabaudi result in higher maximum weight loss of the host 38 that correlates well with other measures of virulence in this experimental system Some observations of malaria infection in humans or trypanosome infection of bumblebee suggest that single infections may be as virulent as mixed infections During an acute infection, the probability of super infecting an already infected host is very low because of the short duration of infection.
Because of the short duration of infection, mutations are not likely to generate high diversity in the parasite population during the infection unless the mutation rate is extremely high.
The presence of different parasite strains in the initial inoculums is the most likely mechanism by which multiple infections may occur in acute infections. During chronic infections co-, super infection and mutation may lead to increased parasite diversity in infected hosts. Adaptive theory assumes that parasites evolve in populations of identical hosts. Higher levels of host heterogeneity would select for less virulent parasites. Spread of infections in host populations with low genetic diversity often results in high host moralities Many parasites when serially pass in new genetically identical hosts evolve to increase their virulence.
In accord with this increase, virulence generally decreases when it is measured in the original host. An increase in virulence of serially pass parasites may be simply due to strong selection for more rapid growth and not due to low genetic diversity of hosts Parasites causing acute infections in vertebrates evolve in the hosts that stochastically differ in their susceptibility to infection or their quality of the immune response. In the absence of heterogeneity parasites evolve to an intermediate growth rate but kill no host due to a high loss in total transmission when the parasite kills the host.
Thus, the analysis suggests that higher levels of stochastic heterogeneity should select for higher optimal level of parasite virulence. Since host mobility is not required and may be even deleterious for the transmission of vector-borne parasites, such parasites should on average be more virulent than parasites that are transmitted directly and that require host mobility for transmission Similar arguments are applied to water-borne infections causing diarrhea because they can spread from immobilized hosts Assuming a positive correlation between parasite transmissibility and virulence for directly transmitted and water-borne parasites, Ewald and De Leo 47 have found that parasites that can be transmitted directly through contact and indirectly through environment evolve higher virulence than parasites transmitted exclusively directly.
Since indirect transmission is not affected by the immobilization, there is no decrease in transmission rate with increasing virulence Ewald has suggested that high longevity of parasites in the environment should select for high virulence, because longer survival in the environment relaxes the parasite need for host and for transmission Parasite longevity does not affect the optimal level of parasite virulence for endemic infections transmitted exclusively indirectly Assuming that there is no trade-off between the parasite longevity in the environment and its virulence, the authors found that parasite longevity affects only the R0 of the infection but not optimal virulence.
However, results suggest that it is very difficult to make any general predictions on whether there is any relationship between the route of transmission and optimal virulence unless specific details of the infection are known.
In contrast with parasites, transmitted horizontally, it has been argued that vertically transmitted parasites should be less virulent because in this case transmission of the parasite is linked to the survival of the host Bull and coworkers in a series of elegant experiments have shown that increasing opportunities for horizontal transmission of a bacteriophage lead to selection of more virulent viral stains Finally, a comparative study suggests that vertically transmitted lice are less virulent than horizontally transmitted mites while infecting the same host species, rock doves Columba livia 50 While exclusively vertically transmitted parasites should evolve low virulence, even small rates of horizontal transmission may be sufficient for maintenance of highly virulent parasites that are transmitted vertically with high efficiency Thus the amount of vertical transmission may indicate of how virulent a parasite is but it needs not be the general rule.
Limited parasite dispersal favours lower parasite growth rates and, hence, reduced virulence because it decreases the direct benefit of producing offspring, and increases the competition for hosts experienced by both the focal individual and their relatives. This demonstrates that reduced virulence can be understood as an individual level adaptation by the parasite to maximize its inclusive fitness, and clarifies the links with virulence theory more generally Simple theory assumes that parasites evolve much faster than their hosts, but this may not be entirely correct since many host species may increase the rate of their evolution by reproducing sexually Clearly in the presence of parasites, hosts evolve to become more resistant to the infection and this in turn may affect parasite virulence.
Parasites may evolve to high or low virulence depending on particular properties of transmission and host connectivity In some cases, this is because such parasites infect hosts that are not normally transmitting the parasite to other hosts 2. Infections of this type include soil bacteria Clostridium tetani causing tetanus, and bacteria Clostridium botulinum causing botulism. Both parasites cause disease in humans by accident and toxin production by these bacteria most likely has evolved due to other reasons than to kill humans Similarly, hantaviruses, Niphavirus, and rabies may cause serious diseases but yet for neither of the infections there is detectable human to human transmission of the parasite 4.
It is possible, that such spill-overs may with time evolve to begin spreading from human to human without the requirement for the original hosts In that case, virulence of such an infection may evolve but how it will evolve would depend on many biological details of the within-host dynamics and epidemiological spread of the parasite. Levin and Bull 34 have suggested that virulence of such infections may be a result of the short-sighted, within-host parasite evolution.
Ebert 42 argues that within-host evolution of highly virulent parasite strains may be the direct cost of having high mutation rate required, for example, for evasion of the immune response. HIV persists for long periods of time in a given host and during that time it is faced with a constant pressure from the immune system.
High mutation rate might be one way of avoiding the recognition by the immune response A high mutation rate may have a cost of generating mutants that are able to end the infection by killing the host An increase in the mutation rate of such parasites should lead to an increased probability of disease occurrence and to an increased total transmission from hosts that have not developed the disease.
Decrease of the mutation rate should reduce the total transmission of parasites. Alternative explanation for the N. In summary, regardless of forces driving evolution of such parasites, within-host evolution may be an important factor affecting virulence of parasites which, when looked from a between-host viewpoint, may appear to be nonadaptive. Parasites have short lives and populations in comparisons to hosts.
Parasites are probably going to adapt to most prevalent gene complexes of their host, which means that there is, in general, a selective advantage to rare alleles and recombination. This principle states that since every improvement in one species will lead to a selective advantage for that species variation normally continuously lead to increase in fitness, in one species, or another.
Since in general different species are co-evolving, improvement in one species implies that it will get a competitive advantage on other species and thus, be able to capture a larger share of resources available to all. This means that fitness increase in one evolutionary system will tend to lead to fitness decrease in another system Evolution of virulence should be viewed from broad biological, epidemiological and clinical perspectives. Man made changes in the environment which facilitates zoonotic transfer of parasites should be urgently addressed. Burnet M, White DO.
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