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Related to Virulence: toxigenicity


The ability of a microorganism to cause disease. Virulence and pathogenicity are often used interchangeably, but virulence may also be used to indicate the degree of pathogenicity. Scientific understanding of the underlying mechanisms of virulence has increased rapidly due to the application of the techniques of biochemistry, genetics, molecular biology, and immunology. Bacterial virulence is better understood than that of other infectious agents.

Virulence is often multifactorial, involving a complex interplay between the parasite and the host. Various host factors, including age, sex, nutritional status, genetic constitution, and the status of the immune system, affect the outcome of the parasite-host interaction. Hosts with depressed immune systems, such as transplant and cancer patients, are susceptible to microorganisms not normally pathogenic in healthy hosts. Such microorganisms are referred to as opportunistic pathogens. The attribute of virulence is present in only a small portion of the total population of microorganisms, most of which are harmless or even beneficial to humans and other animals. See Opportunistic infections

The spread of an infectious disease usually involves the adherence of the invading pathogen to a body surface. Next, the pathogen multiplies in host tissues, resisting or evading various nonspecific host defense systems. Actual disease symptoms are from damage to host tissues caused either directly or indirectly by the microorganism's components or products.

Most genetic information in bacteria is carried in the chromosome. However, genetic information is also carried on plasmids, which are independently replicating structures much smaller than the chromosome. Plasmids may provide bacteria with additional virulence-related capabilities (such as pilus formation, iron transport systems, toxin production, and antibiotic resistance). In some bacteria, several virulence determinants are regulated by a single genetic locus. See Bacteria, Cellular immunology, Plasmid, Virus



the degree of pathogenicity of a given infectious agent (microbial or viral strain). Virulence varies both with the properties of the infectious agent and with the susceptibility (sensitivity) of the organism infected. The intensity of virulence is judged by the severity of the disease caused by a microbe or virus, and in experimental animals, by the lethal dose of the infectious agent. Virulence is deter-mined not only by the ability of the microorganism to penetrate into the organism of a susceptible animal and reproduce and spread within it, but also by whether the microbe (or virus) produces toxic products, or toxins. It is not a species characteristic of a microbe (virus), and it may vary widely from strain to strain. Change in virulence can be induced by artificial means, such as heating, irradiation, and use of chemical agents. These means are employed in the production of live vaccines. For this purpose the infectious agent is repeatedly passaged. (For example, street rabies virus is passaged through rabbit brains; this makes the virus less virulent for man, so that it can be used for vaccination against rabies.)



The disease-producing power of a microorganism; infectiousness.
References in periodicals archive ?
The role of PldA and PldB as virulence factor will be assessed using a murine model of respiratory tract infection.
Despite the characterization of numerous virulence factors, no single genetic feature currently defines EAEC or UPEC isolates.
Earlier research from Rock hinted at a connection between fatty acid synthesis and production of virulence factors, but this study is the first to establish the biochemical link and identify the mechanism involved.
In the era before antiretroviral therapy (ART), HIV virulence was measured directly by time to the development of AIDS and death.
Consequently, the virulence potential of the infecting pathogen may also vary, so that even bacteria with very low virulence capacity may cause extraintestinal infections in extremely compromised hosts (1).
It can enter the human system as a non-pathogen and can then increase its virulence to a pathogenic level.
The data suggest that strong adherence properties not only promote retention of strains on food processing equipment, but may also lead to enhanced invasion and replication in host tissues, causing greater virulence than less adherent strains.
Thus, with the exception of the tcpPH genes, the entire VPI is under the regulatory control of ToxT, emphasizing the importance of this virulence regulator to V.
In the present study for the mining of the regulatory sequence of virulence genes of M.
coli (EIEC) and causes dysentery that is indistinguishable from that due to Shigella species, with which it shares a large number of virulence determinants.
The researchers are investigating whether these sequences influence the bacterium's virulence or persistence.