Virulence


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Related to Virulence: toxigenicity

Virulence

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

McGraw-Hill Concise Encyclopedia of Bioscience. © 2002 by The McGraw-Hill Companies, Inc.
The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.

Virulence

 

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.)

KH. KH. PLANEL’ES

The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.

virulence

[′vir·ə·ləns]
(microbiology)
The disease-producing power of a microorganism; infectiousness.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
Gelatinase production as a virulence factor in causing endocarditis has been studied using animal models.
Virulence assays for plasma coagulase, phospholipase (Pz), protease (Prz), and hemolysin (Hz) production were carried out as per the methods of Deorukhkar and Saini.[sup][7] Assessment of biofilm formation was carried out as per the protocol of Yigit et al .[sup][9] In brief, single colony from SDA of the test sample was inoculated in saline and incubated at 37[degrees]C for 24 h.
The primers used for the detection of these virulence genes were synthesized by Sigma Aldrich, USA.
The current results show that the majority of isolates recovered from different area carried multiple virulence genes and these findings support the conception that different subsets of virulence genes exist in A.
For these strains, we determined the phylogroup/subgroup membership, the presence of the 11 virulence factors cited above, and the susceptibility to 6 antimicrobial drugs (amoxicillin, amoxicillin/clavulanic acid, cefotaxime, amikacin, ofloxacin, and cefoxitin).
coli virulence and biofilm formation genes were evaluated using quantitative reverse transcription PCR (qRT-PCR).
The virulence genes - toxA, exoS, lasB, algD, plcH and plcN - were amplified using previously reported primers.15 The primers were prepared through Macrogen (Korea).
The prevalence of traT and iss genes was 100% in both of respiratory and intestinal isolates while the percent of traT and iss genes in blood isolates were 100% and 50%, respectively whereas the prevalence of virulence genes in blood culture isolates which have (68.7%) and the occurrence of traT and iss genes observed in UTI isolates was 80 % and 60%, respectively (Table 1).
WGS confirmed this resistance profile by identifying several resistance genes in both isolates along with 18 virulence genes (Table 1).