The Ecology of Parasitism
Eric S. Loker, Bruce V. Hofkin in Parasitology, 2015
The previous section prompts us to a broader consideration of the factors that dictate parasite population sizes. This is an important issue that bears on how virulence evolves in parasites and on the likelihood that hosts will suffer from heavy infections. Recall from Chapter 1 that infectious disease biologists consider virulence to be a measure of the likelihood that an infectious agent causes disease or even fatality. Among ecologists and evolutionary biologists, virulence is considered to be the ability of a parasite to reduce its host’s fitness (see Chapter 7 for more discussion of virulence). One of the central issues is whether parasite populations are controlled by density-independent factors, such as temperature or rainfall, or whether density-dependent factors, such as competition with conspecifics or with other parasite species, play a prominent role. In the former case, it is likely that parasite population size will fluctuate considerably because density-independent factors are often unpredictable. In the latter case, with the operation of density-dependent mechanisms, it is likely that parasite populations fluctuate much less extensively. In this instance, the populations are regulated, implying they are stable or vary in size in a predictable way. In our discussion, we will refer to regulation of infrapopulation size; the factors regulating suprapopulation size are much harder to ascertain.
An Introduction to Parasitism
Eric S. Loker, Bruce V. Hofkin in Parasitology, 2023
Let us reconsider the notion of disease, pathology, harm, or damage caused by parasites. A term often used to embody this concept of harm is virulence. This term, which appears repeatedly throughout this book, is also defined differently depending on the discipline. Infectious disease biologists often consider virulence to be a measure of the likelihood that an infectious agent causes disease or even fatality. Among ecologists and evolutionary biologists, virulence is generally considered and measured differently; it is the ability of a parasite to reduce its host’s fitness. Fitness is a measure of the success of an individual in passing on its genes to future generations and is influenced by the individual’s ability to survive and to reproduce. A parasite might shorten its host’s life span and thereby affect the host’s eventual reproductive output, or the parasite might diminish its host’s reproductive output but not affect survival. If a parasite castrates or kills its host, it is considered to be especially virulent.
Pathobiology of Amebiasis
Roberto R. Kretschmer in Amebiasis: Infection and Disease by Entamoeba histolytica, 2020
Both for working on the pathogenesis of amebiasis, as well as for writing this chapter, our group has found it convenient to distinguish between the concepts of pathogenicity and virulence, which in the literature are often used interconvertibly. By pathogenicity we understand the capacity to cause disease of a given strain of amebas, so on the basis of this property we consider only two types of amebas: pathogenic and nonpathogenic. On the other hand, by virulence we refer to the degree to which pathogenicity is expressed, usually graded as low, intermediate and high, on the basis of arbitrary and subjective criteria. It follows that there can be no pathogenic amebas without virulence, or nonpathogenic amebas with some degree of virulence. We believe that this separation of the concepts of pathogenicity and virulence should be preserved as long as the mechanisms of both features are not completely and clearly delineated. Of course, we are fully aware that pathogenicity and virulence are not absolute properties of the parasite, but rather expressions of the specific host-parasite model under consideration, which also includes many important environmental conditions. Nevertheless, there are some indications that in human and in some experimental forms of amebiasis, pathogenicity, and virulence may depend more on the parasite than on the host.
Factors influencing the epidemiological characteristics of pandemic COVID 19: A TISM approach
Published in International Journal of Healthcare Management, 2020
S. Lakshmi Priyadarsini, M. Suresh
Virus virulence is the disease causing capability of a virus which depends on various factors like those allow it to replicate and spread inside a host by modifying host defenses, and breaking host cells and damaging tissues. It is this infectious potential of a pathogen which determines the severity of symptoms [7]. There are different types of Corona viruses reported over the years. Tissue tropism varies with the type of corona virus ie, alpha and beta corona viruses infect mammals; in contrast, gamma and delta corona viruses infect birds and fish, but some of them can also infect mammals [8]. The new 2019 novel Corona virus-2 or SARS-CoV-2 is identified as beta corona virus [9]. Virus virulence is basically due to its genes responsible for viral replication, genes which help to escape from host immune system, those which are involved in the transmissibility and genes coding toxic products in host cells. The current virus seems to be very contagious and has quickly spread globally [10].
Anti-virulence strategies for Clostridioides difficile infection: advances and roadblocks
Published in Gut Microbes, 2020
David Stewart, Farhan Anwar, Gayatri Vedantam
Anti-virulence strategies represent a rational approach to mitigate pathogens. The idea of targeting specific CD virulence factors, rather than the whole organism, is not new. As Koo et al.27 and Venuto et al.28 have reviewed, mechanisms to precisely target those factors and/or microbes have been, and continues to be, challenging. Indeed, the very definition of “virulence” factor is now debated, since context-dependent appreciation of infectious etiology now supports the idea of a pathogenic spectrum rather than static and easily identified causative factors of disease. Additionally, any “virulence” factors, especially surface-associated molecules in bacteria, fungi or parasites may also be harbored by – or conserved in – the commensal microbiota. Therefore, amelioration of disease-causing organisms must be accomplished with extreme precision so as not to disrupt the delicate homeostasis of the normal microbiome. Specifically for CD infections, much consideration has to be given to the likelihood that humans and animals can asymptomatically harbor the organism for years.29,30 Any intervention may have to be administered for extended time periods to ensure complete clearance of the organism; this warrants additional considerations of safety and tolerability. Finally, many at-risk patients may be immunocompromised;31,32 therefore, the most appropriate interventions are those that can be tolerated by these individuals as well.
Pathogenicity and virulence of human T lymphotropic virus type-1 (HTLV-1) in oncogenesis: adult T-cell leukemia/lymphoma (ATLL)
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Sanaz Ahmadi Ghezeldasht, David J. Blackbourn, Arman Mosavat, Seyed Abdolrahim Rezaee
The virulence of any infectious agent is mainly dependent on various factors, including genetic properties, dose of exposure, route of entry, growth efficiency, time required to cause symptoms or death, host physiological condition, and evading the host immune responses. Regarding HTLV-1 as an integrated virus in the host genome, different factors, such as the route of entry, acute infection, latency, polyclonal CD4+ T cell proliferation, and the inappropriate host responses, are mainly implicated in the pathogenesis of ATLL. Briefly, TAX is the main transcription regulatory factor in the early stage of colonization. In a cell-to-cell contact manner, it orchestrates the virus’ entry and spreading and potentiates the secretion of T cell growth factors, such as IL-1, and IL-2Ra, to promote infected cells toward the activation phase. At this phase and even after the virus colonization, the polyclonal population of infected cells is not malignant. Unlike the healthy uninfected primary T cells, they have auto-proliferation property, not needing IL-2 to be supplemented in the cell culture. Since Tax is an immunodominant protein, its expression decreases or suppresses at the latency stage; this process makes the virus latent to escape from the host immune responses [5,25–27].
Related Knowledge Centers
- Bacteria
- Cytokine Storm
- Enzyme
- Virulence Factor
- Pathogen
- Host
- Gene-For-Gene Relationship
- Fitness
- Bacterial Effector Protein
- Type III Secretion System