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    • As such PCR based procedures

    2018-10-29

    As such, PCR-based procedures have dominated research on the diagnosis and detection of Cryptosporidium over the last 25years, and in particular, because they have the added advantage of being able to provide information on the genotype or species of Cryptosporidium present in a clinical or environmental sample (Smith et al., 2006; Thompson and Ash, 2015). Such techniques are now replacing microscopy in many medical diagnostic laboratories, often in assays that are developed for the simultaneous detection of other enteric pathogens routinely screened for in clinical diagnostic laboratories, such as Giardia and Blastocystis (Cacciò et al., 2005). PCR-based tools have also proved to be of particular value in molecular epidemiological investigations by providing information on source of infection and the public health significance of isolates identified (Cacciò et al., 2005; Thompson et al., 2007). The most commonly targeted gene used for characterising species of Cryptosporidium is SSU-rDNA (Xiao, 2010). In addition to the development of diagnostic assays, much research has also been concerned with the molecular epidemiology of water- and food- borne outbreaks and particularly the ability to detect and differentiate between those species commonly infecting humans (C. hominis, C. parvum (= C. pestis; Slapeta, 2011)). This research has increased understanding of the possible transmission routes from the environment and co-habiting animals such as companion animals and livestock (Fayer et al., 2000; Hunter and Thompson, 2005). It has also resulted in the identification of ‘new’ genotypes and the subsequent proliferation of new species and host ranges identified (Slapeta, 2013; Xiao and Fayer, 2008). In addition to SSU-rDNA, molecular epidemiological investigations have identified additional Obeticholic Acid of value as genotyping tools including the 70kDA heat-shock protein (HSP70), the Cryptosporidium oocyst wall protein (COWP), and the internal transcriber region 1 (ITS-1) (reviewed in Thompson and Ash, 2015). For greater detail on possible transmission routes, intra-specific genotyping is required and the 60kDA glycoprotein is commonly used to provide negative feedback control level of discrimination (Lymbery and Thompson, 2011; Thompson and Ash, 2015).
    Zoonotic potential — a recently recognized human pathogen The first human case of Cryptospordium infection was described in 1976, and over the next 20years considerable circumstantial evidence accumulated of zoonotic exposure associated with farms and farm animals, riding stables, animal manure, and contaminated water (Fayer et al., 2000). Many of these early reports drew attention to the association of human infection with exposure to infected livestock, particularly young cattle or sheep, and there was often evidence of secondary spread within households or play-groups following such zoonotic exposure (Casemore et al., 1997; Thompson, 2003). Although farm workers and visitors to farms were considered to have contracted cryptosporidiosis by direct contact, indirect zoonotic transmission of Cryptosporidium of livestock origin via water was considered at that time to be the most important zoonotic source of human infection (Thompson, 2003). However, up until the early 1990s such conclusions were often only circumstantial, with presumptions being made that run-off from pasture used for cattle, was the pre-disposing factor. In 1991, analysis using restriction fragment length polymorphism (RFLP) revealed differences between Cryptosporidium of cattle and human origin (Ortega et al., 1991). In addition to confirming this result, subsequent molecular epidemiological studies demonstrated that humans were susceptible to infection with two genotypes of Cryptosporidium, one zoonotic (C. parvum (= C. pestis; Slapeta, 2011)), with cattle as its principal host, and the other host-specific for humans (C. hominis). This information was first put into an epidemiological context in 1997 in determining the source of contamination of the notorious Milwaukee outbreak (Peng et al., 1997), and subsequently in a series of outbreaks some of which were shown to be of zoonotic origin (Cacciò et al., 2005; Fletcher et al., 2012; Thompson, 2003).