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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 ?
Conclusions: These two multiplex PCRs when run simultaneously can provide vital information about methicillin resistance and virulence status of the isolate within a few hours as compared to several days needed by routine procedures.
faecium isolates carries high levels of resistance to many antimicrobials, is well equipped with virulence genes, and possesses the ability to form biofilm.
On the other hand, the presence of virulence factors in enterococci increase their pathogenicity and some of them related to antimicrobial resistance directly.
Key words: Adaptive immunity, Autophagy, Brucella spp, Innate immunity, Intracellular survival, Mechanism of evasion from host, Virulence factors.
Esp is found to be one of the important virulence factor to enhance the persistence of Enterococcus in urinary bladder during experimental urinary tract infections (7).
In response to irrational use of antimicrobials and the resulting resistance, researchers are turning to novel approaches to controlling infection using naturally-derived products in order to modulate the virulence of pathogens without the risk of them developing resistance.
7) Brucella evades macrophage killing via the c[beta]g, virB, and znuA virulence factors that lead to intracellular replication.
faecalis have been shown to contribute to the virulence of endocarditis in an animal model.
Besides these virulence factors, formation of biofilms is also a critical feature for the development of clinical infection.