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Bacteria
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Many diseases of the oral cavity are caused by bacteria, especially bacteria that are indigenous to the mouth. These infections are among the most common bacterial infections of man. As the organisms causing them are not highly pathogenic, host factors play a role in whether disease develops following infection.
The patient with acute respiratory problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Host factors (e.g., individual resistance) and agent factors (e.g., virulence of organism) should be taken into account when considering individual susceptibility to infection. Although fit, healthy people can develop pneumonia, the following may increase risk: Smoking.Excessive alcohol intake.Presence of other conditions such as COPD, cancer and heart failure.Very young and older people.Weak immune system.Recent respiratory viral infection.Malnutrition/poor hydration.Treatment in intensive care.Increased susceptibility to inhalation – impaired consciousness, swallowing difficulties.
Cryptosporidium spp
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Differences in the virulence of various mammalian isolates of C. parvum and in their infectivity for laboratory and/or farm animals have been reported (see Ref. 2 for examples). It is possible that such differences in virulence may be responsible, at least in part, for differences in the severity of human cryptosporidiosis. Carefully controlled studies that eliminate differences in host factors such as immune status, genetic background, nutritional status, and general health are needed to define the virulence factors associated with Cryptosporidium spp.
Host factors subverted by Mycobacterium tuberculosis: Potential targets for host directed therapy
Published in International Reviews of Immunology, 2023
Rashi Kalra, Drishti Tiwari, Hedwin Kitdorlang Dkhar, Ella Bhagyaraj, Rakesh Kumar, Anshu Bhardwaj, Pawan Gupta
An alternate theory of disease causation as proposed by Pierre Jacques Antoine Bechamp (1816–1908), advocates that the human body’s “internal milieu” or “terrain” is responsible for development of disease post infection [187]. After several years of research, it is now well established that a wide range of “host factors” modulate the body’s “internal milieu” and influence disease susceptibility, treatment response and mortality rates. Therefore, host immunity is of paramount importance. In order to be a successful host, one should be able to tolerate damage caused by the pathogen and the immune system along with efficient pathogen clearance. This ability of tolerance is described as “host resilience” and is a relatively unexplored research niche [188,189]. The available treatment options predominantly target pathogen clearance; hence are antimicrobial in nature. However, proper attention has not been given to molecules that enhance host tolerance and target pathogens in a “non-microbial” fashion. Given this, there arises a need for understanding the host factors behind resilience for tailoring appropriate treatment options. It is believed that host molecules aiding M. tuberculosis during pathogenesis might be one of the factors responsible for this tolerance. Thus, detailed identification of the host molecules subverted by the pathogen for immune evasion is cardinal for pathogen clearance as well as for boosting the immune system in times of pandemics, such as the recent coronavirus (COVID-19). In the coming years, an investment of scientific efforts in this discipline will be required and is anticipated.
SARS-CoV-2 variants of concern and vaccine escape, from Alpha to Omicron and beyond
Published in Expert Review of Respiratory Medicine, 2022
Sean Wei Xiang Ong, Travis Chia, Barnaby Edward Young
Extrapolating from in vitro studies to predict the clinical consequences of different spike mutations is complicated by a number of factors. First, a range of different vaccines are in clinical use worldwide, and these induce antibody and cellular immune responses of varying quality and quantity [17]. Messenger RNA and viral vector vaccines have been associated with stronger and more sustained immunogenicity compared to inactivated vaccines, particularly with respect to T-cell responses. Correspondingly, the rate of waning immunity post-vaccination also varies greatly. Second, there are also important host factors, which determine the strength of immune response to vaccination, rate of waning, and susceptibility to symptomatic and severe infection [18]. These are highly correlated, such that advanced age, male sex, and comorbid conditions place individuals at highest risk of both severe infection intrinsically and a weaker vaccine-induced immune response, which further increases disease severity. Third, two years into the pandemic, successive outbreaks of ancestral and SARS-CoV-2 VOCs mean that immunity from prior infection varies in different regions of the world. Finally, vaccination has effects beyond the immune response. This includes reducing the viral loads and therefore transmissibility of SARS-CoV-2 in breakthrough infections. Vaccination may also modify behavior postvaccination and hence increase risk of exposure to SARS-CoV-2, for example, through public health measures, which privilege access to crowded indoor venues to vaccinated individuals.
Cytokine production and outcome in MDR versus non-MDR gram-negative bacteraemia and sepsis
Published in Infectious Diseases, 2021
Vasileios Karamouzos, Evangelos J. Giamarellos-Bourboulis, Dimitrios Velissaris, Theologia Gkavogianni, Charalambos Gogos
Our growing knowledge in the pathophysiology of sepsis, shifted the focus from the systemic inflammatory reaction caused by the causative agent to the aberrant response of the immune system leading to organ failure and death. The concept of sepsis was re-addressed by the third international consensus definitions for sepsis and septic shock resulting in defining sepsis as a life-threatening organ dysfunction caused by a dysregulated host response to infection [4]. This immune system dysregulation can be attributed to host factors like age, gender, genetic background and comorbidities. Although host factors are important, the role of the causative agent and its characteristics in inducing an abnormal immune reaction is not clear. Moreover, it may well be the case that the elicited host reaction may differ significantly in association with the resistance patterns of the offending organisms. In an animal study in the past, it was found that experimental infection by MDR P. aeruginosa led to death at a lower rate than susceptible P. aeruginosa whereas Klebsiella pneumoniae carrying plasmids encoding for resistance to carbapenem led to early death through plasmid-mediated immunosuppression [5,6]. However, similar data in humans are missing.