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An Introduction to Parasitism
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
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.
Introduction to Cells, DNA, and Viruses
Published in Patricia G. Melloy, Viruses and Society, 2023
We know that viruses can infect many kinds of host cells and can therefore have a range of effects on the host. We call the different species infected by a virus the “host range,” while the “tissue tropism” of a virus indicates the different tissues within a host that can become infected. These characteristics have a lot to do with how the virus gets inside the cells (Lostroh 2019). Sometimes the virus has no noticeable effect; sometimes it kills the host. However, all viruses have a mechanism to get their genome into the host cell and make many copies of the virus, and then eventually the new viral particles leave the host. The effect on the host in this process can be anticipated based on the virus’s virulence that is often expressed in adjective form as virulent. Virulence has to do with the ability to cause disease or its symptoms (Summers 2009). One might say that virulence tells you what the collateral damage might be to the host upon viral infection. However, many factors like the health of the patient prior to infection contribute to the disease outcome as well.
Epidemiology, Disease Transmission, Prevention, and Control
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
The environment influences human health favorably or unfavorably in many direct and indirect ways. We interact with all living things with which we have contact, i.e., plants, animals, and microorganisms, as well as with inanimate objects. Of particular importance to health are the organisms producing disease, the so-called pathogenic organisms. Pathogenicity refers to the organisms′ virulence and invasiveness, factors which determine their capability to produce disease. The higher the virulence, the higher will be the morbidity, mortality, and communicability of the infection and thus the epidemiological importance of the disease caused by the organism.
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].
Preterm infants at low risk for early-onset sepsis differ in early fecal microbiome assembly
Published in Gut Microbes, 2022
Sagori Mukhopadhyay, Jung-Jin Lee, Erica Hartman, Emily Woodford, Miren B. Dhudasia, Lisa M. Mattei, Scott G. Daniel, Kelly C. Wade, Mark A. Underwood, Kyle Bittinger
Understanding the dynamics of microbiome acquisition and development in LRE infants is specifically important in answering two clinical questions. First, is there molecular evidence of lower bacterial acquisition at birth that parallels the epidemiologically observed lower risk of EOS? Second, do the differences in birth environment and absence of routine antibiotic exposure after birth alter subsequent microbial ontogeny among preterm LRE infants compared to other preterm infants? To answer these questions, upon adopting the AAP delivery criteria-based approach for EOS risk assessment among the preterm infants,8 we enrolled a cohort of 48 VLBW infants and analyzed serial fecal samples as a marker of gut microbiome changes. We hypothesized that fecal samples obtained soon after birth from infants who met LRE criteria would have lower bacterial acquisition compared to infants born outside the pre-specified criteria (non-LRE). We also hypothesized that the microbiome composition would differ between the groups and that the difference would persist beyond the first three days after birth, a time period that is commonly used to demarcate differences in infection-causing colonization patterns among continuously hospitalized preterm infants.3 We assessed differences in virulence factors and antibiotic resistance genes in the two groups to further delineate differences arising from any compositional dissimilarities. Finally, we analyzed all study infants evaluated for late-onset bacteremia (onset >3 days after birth), to determine acute change in microbiome parameters with proven and suspected infection.
A case report: septic shock due to (tropical) pyomyositis and multiple metastatic embolisms caused by Panton Valentine Leukocidin-positive methicillin-sensitive staphylococcus aureus in a 12-year-old boy
Published in Acta Clinica Belgica, 2022
Valérie Vanbiervliet, Ignace Demeyer, Filip Claus, Kristien Van Vaerenbergh
Staphylococcus aureus (S. aureus) is an important human pathogen and it causes various types of infections, both in nosocomial and community setting. Based on methicillin susceptibility, it is divided into two major groups: methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA). Numerous virulence factors enable the organism to be a successful pathogen through different mechanisms of action. An important virulence factor is Panton-Valentine Leukocidin toxin (PVL). PVL is a membrane pore-forming protein responsible for cell leakage and cell death. PVL producing S. aureus causes more severe infections. Although commonly associated with community-acquired methicillin-resistant S. aureus (CA-MRSA), several outbreaks due to methicillin-susceptible S. aureus have been reported [1].