Improved method for genotyping the causative agent of crayfish plague (Aphanomyces astaci) based on mitochondrial DNA

Parasitology ◽  
2019 ◽  
Vol 146 (8) ◽  
pp. 1022-1029 ◽  
Author(s):  
Diana Minardi ◽  
David J. Studholme ◽  
Birgit Oidtmann ◽  
Tobia Pretto ◽  
Mark van der Giezen

AbstractAphanomyces astacicauses crayfish plague, which is a devastating disease of European freshwater crayfish. The likely first introduction ofA. astaciinto Europe was in the mid-19th century in Italy, presumably with the introduction of North American crayfish. These crayfish can carryA. astaciin their cuticle as a benign infection.Aphanomyces astacirapidly spread across Europe causing the decline of the highly susceptible indigenous crayfish species. Random amplified polymorphic DNA-PCR analysis ofA. astacipure cultures characterized five genotype groups (A, B, C, D and E). CurrentA. astacigenotyping techniques (microsatellites and genotype-specific regions, both targeting nuclear DNA) can be applied directly to DNA extracted from infected cuticles but require high infection levels. Therefore, they are not suitable for genotyping benign infections in North American crayfish (carriers). In the present study, we combine bioinformatics and molecular biology techniques to developA. astacigenotyping molecular markers that target the mitochondrial DNA, increasing the sensitivity of the genotyping tools. The assays were validated on DNA extracts ofA. astacipure cultures, crayfish tissue extractions from crayfish plague outbreaks and tissue extractions from North American carriers. We demonstrate the presence ofA. astacigenotype groups A and B in UK waters.

Parasitology ◽  
2020 ◽  
Vol 147 (6) ◽  
pp. 706-714 ◽  
Author(s):  
John Rhidian Thomas ◽  
Chloe V. Robinson ◽  
Agata Mrugała ◽  
Amy R. Ellison ◽  
Emily Matthews ◽  
...  

AbstractThe spread of invasive, non-native species is a key threat to biodiversity. Parasites can play a significant role by influencing their invasive host's survival or behaviour, which can subsequently alter invasion dynamics. The North American signal crayfish (Pacifastacus leniusculus) is a known carrier of Aphanomyces astaci, an oomycete pathogen that is the causative agent of crayfish plague and fatal to European crayfish species, whereas North American species are considered to be largely resistant. There is some evidence, however, that North American species, can also succumb to crayfish plague, though how A. astaci affects such ‘reservoir hosts’ is rarely considered. Here, we tested the impact of A. astaci infection on signal crayfish, by assessing juvenile survival and adult behaviour following exposure to A. astaci zoospores. Juvenile signal crayfish suffered high mortality 4-weeks post-hatching, but not as older juveniles. Furthermore, adult signal crayfish with high-infection levels displayed altered behaviours, being less likely to leave the water, explore terrestrial areas and exhibit escape responses. Overall, we reveal that A. astaci infection affects signal crayfish to a much greater extent than previously considered, which may not only have direct consequences for invasions, but could substantially affect commercially harvested signal crayfish stocks worldwide.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura Martín-Torrijos ◽  
María Martínez-Ríos ◽  
Gloria Casabella-Herrero ◽  
Susan B. Adams ◽  
Colin R. Jackson ◽  
...  

AbstractThe oomycete Aphanomyces astaci is an emerging infectious pathogen affecting freshwater crayfish worldwide and is responsible for one of the most severe wildlife pandemics ever reported. The pathogen has caused mass mortalities of freshwater crayfish species in Europe and Asia, and threatens other susceptible species in Madagascar, Oceania and South America. The pathogen naturally coexists with some North American crayfish species that are its chronic carriers. Presumptions that A. astaci originated in North America are based on disease outbreaks that followed translocations of North American crayfish and on the identification of the pathogen mainly in Europe. We studied A. astaci in the southeastern US, a center of freshwater crayfish diversity. In order to decipher the origin of the pathogen, we investigated (1) the distribution and haplotype diversity of A. astaci, and (2) whether there are crayfish species-specificities and/or geographical restrictions for A. astaci haplotypes. A total of 132 individuals, corresponding to 19 crayfish species and one shrimp species from 23 locations, tested positive for A. astaci. Mitochondrial rnnS and rnnL sequences indicated that A. astaci from the southeastern US exhibited the highest genetic diversity so far described for the pathogen (eight haplotypes, six of which we newly describe). Our findings that A. astaci is widely distributed and genetically diverse in the region supports the hypothesis that the pathogen originated in the southeastern US. In contrast to previous assumptions, however, the pathogen exhibited no clear species-specificity or geographical patterns.


2006 ◽  
Vol 72 (6) ◽  
pp. 4347-4355 ◽  
Author(s):  
Sinisa Vidovic ◽  
Darren R. Korber

ABSTRACT The prevalence of Escherichia coli O157 associated with feedlot cattle in Saskatchewan was determined in a 10-month longitudinal study (3 feedlots) and a point prevalence study (20 feedlots). The prevalence of E. coli O157 at the three different sites in the horizontal study varied from 2.5 to 45%. The point prevalence of E. coli O157 among Saskatchewan cattle from 20 different feedlots ranged from 0% to a high of 57%. A statistically significant (P = 0.003) positive correlation was determined to exist between the density of cattle and the E. coli O157 prevalence rate. A significant correlation (P = 0.006) was also found between the E. coli O157 percent prevalence and the number of cattle housed/capacity ratio. All 194 E. coli O157 isolates obtained were highly virulent, and random amplified polymorphic DNA PCR analysis revealed that the isolates grouped into 39 different E. coli O157 subtypes, most of which were indigenous to specific feedlots. Two of the most predominant subtypes were detected in 11 different feedlots and formed distinct clusters in two geographic regions in the province. Antimicrobial susceptibility testing of the E. coli O157 isolates revealed that 10 were multidrug resistant and that 73 and 5 were resistant to sulfisoxazole and tetracycline, respectively.


2001 ◽  
Vol 18 (2) ◽  
pp. 227-237 ◽  
Author(s):  
Javier A Rodrı́guez-Robles ◽  
Glenn R Stewart ◽  
Theodore J Papenfuss

2021 ◽  
Vol 22 (10) ◽  
pp. 5100
Author(s):  
Paulina Kozakiewicz ◽  
Ludmiła Grzybowska-Szatkowska ◽  
Marzanna Ciesielka ◽  
Jolanta Rzymowska

The mitochondria are essential for normal cell functioning. Changes in mitochondrial DNA (mtDNA) may affect the occurrence of some chronic diseases and cancer. This process is complex and not entirely understood. The assignment to a particular mitochondrial haplogroup may be a factor that either contributes to cancer development or reduces its likelihood. Mutations in mtDNA occurring via an increase in reactive oxygen species may favour the occurrence of further changes both in mitochondrial and nuclear DNA. Mitochondrial DNA mutations in postmitotic cells are not inherited, but may play a role both in initiation and progression of cancer. One of the first discovered polymorphisms associated with cancer was in the gene NADH-ubiquinone oxidoreductase chain 3 (mt-ND3) and it was typical of haplogroup N. In prostate cancer, these mutations and polymorphisms involve a gene encoding subunit I of respiratory complex IV cytochrome c oxidase subunit 1 gene (COI). At present, a growing number of studies also address the impact of mtDNA polymorphisms on prognosis in cancer patients. Some of the mitochondrial DNA polymorphisms occur in both chronic disease and cancer, for instance polymorphism G5913A characteristic of prostate cancer and hypertension.


2017 ◽  
Vol 95 (8) ◽  
pp. 527-537 ◽  
Author(s):  
James W. Patterson ◽  
Anna M. Duncan ◽  
Kelsey C. McIntyre ◽  
Vett K. Lloyd

Ixodes scapularis Say, 1821 (the black-legged tick) is becoming established in Canada. The northwards expansion of I. scapularis leads to contact between I. scapularis and Ixodes cookei Packard, 1869, a well-established tick species in Eastern Canada. Examination of I. cookei and I. scapularis collected from New Brunswick revealed ticks with ambiguous morphologies, with either a mixture or intermediate traits typical of I. scapularis and I. cookei, including in characteristics typically used as species identifiers. Genetic analysis to determine if these ticks represent hybrids revealed that four had I. cookei derived mitochondrial DNA but I. scapularis nuclear DNA. In one case, the nuclear sequence showed evidence of heterozygosity for I. scapularis and I. cookei sequences, whereas in the others, the nuclear DNA appeared to be entirely derived from I. scapularis. These data strongly suggest genetic hybridization between these two species. Ixodes cookei and hybrid ticks were readily collected from humans and companion animals and specimens infected with Borrelia burgdorferi Johnson et al., 1984, the causative agent of Lyme disease, were identified. These findings raise the issue of genetic introgression of I. scapularis genes into I. cookei and warrant reassessment of the capacity of I. cookei and I. cookei × I. scapularis hybrids to vector Borrelia infection.


Author(s):  
George B. Stefano ◽  
Richard M. Kream

AbstractMitochondrial DNA (mtDNA) heteroplasmy is the dynamically determined co-expression of wild type (WT) inherited polymorphisms and collective time-dependent somatic mutations within individual mtDNA genomes. The temporal expression and distribution of cell-specific and tissue-specific mtDNA heteroplasmy in healthy individuals may be functionally associated with intracellular mitochondrial signaling pathways and nuclear DNA gene expression. The maintenance of endogenously regulated tissue-specific copy numbers of heteroplasmic mtDNA may represent a sensitive biomarker of homeostasis of mitochondrial dynamics, metabolic integrity, and immune competence. Myeloid cells, monocytes, macrophages, and antigen-presenting dendritic cells undergo programmed changes in mitochondrial metabolism according to innate and adaptive immunological processes. In the central nervous system (CNS), the polarization of activated microglial cells is dependent on strategically programmed changes in mitochondrial function. Therefore, variations in heteroplasmic mtDNA copy numbers may have functional consequences in metabolically competent mitochondria in innate and adaptive immune processes involving the CNS. Recently, altered mitochondrial function has been demonstrated in the progression of coronavirus disease 2019 (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Accordingly, our review is organized to present convergent lines of empirical evidence that potentially link expression of mtDNA heteroplasmy by functionally interactive CNS cell types to the extent and severity of acute and chronic post-COVID-19 neurological disorders.


Sign in / Sign up

Export Citation Format

Share Document