In less than five months, COVID-19 has spread from a small focus in Wuhan, China, to more than 5 million people in almost every country in the world, dominating the concern of most governments and public health systems. The social and political distresses caused by this epidemic will certainly impact our world for a long time to come. Here, we synthesize lessons from a range of scientific perspectives rooted in epidemiology, virology, genetics, ecology and evolutionary biology so as to provide perspective on how this pandemic started, how it is developing, and how best we can stop it. The origin of SARS-CoV-2 and COVID-19The novel human coronavirus (SARS-CoV-2), responsible for the current COVID-19 pandemic, was first identified in December 2019, in the Hubei province of China (Zhu et al., 2020). After SARS-CoV (severe acute respiratory syndrome coronavirus) and MERS-CoV (Middle East

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The ubiquitous protozoa Toxoplasma gondii is now the subject of renewed interest, due to the spread of oocysts via water causing waterborne outbreaks of toxoplasmosis in different parts of the world. This overview discusses the different methods for detection of Toxoplasma in drinking and environmental water. It includes a combination of conventional and molecular tools for effective oocyst recovery and detection in water sources as well as factors hindering the detection of this parasite and shedding light on a promising new molecular assay for the diagnosis of Toxoplasma in environmental samples. Hopefully, this attempt will facilitate future approaches for better recovery, concentration, and detection of Toxoplasma oocysts in environmental waters.

While a large number of laboratory methods for the detection of Cryptosporidium oocysts in faecal samples are now available, their efficacy for identifying asymptomatic cases of cryptosporidiosis is poorly understood. This study was carried out to determine a reliable screening test for epidemiological studies in livestock. In addition, three molecular tests were compared to identify Cryptosporidium species responsible for the infection in cattle, sheep and horses. A variety of diagnostic tests including microscopic (Kinyoun's staining), immunological (Direct Fluorescence Antibody tests or DFAT), enzyme-linked immunosorbent assay (ELISA), and molecular methods (nested PCR) were compared to assess their ability to detect Cryptosporidium in cattle, horse and sheep faecal samples. The results indicate that the sensitivity and specificity of each test is highly dependent on the input samples; while Kinyoun's and DFAT proved to be reliable screening tools for cattle samples, DFAT and PCR analysis (targeted at the 18S rRNA gene fragment) were more sensitive for screening sheep and horse samples. Finally different PCR primer sets targeted at the same region resulted in the preferential amplification of certain Cryptosporidium species when multiple species were present in the sample. Therefore, for identification of Cryptosporidium spp. in the event of asymptomatic cryptosporidiosis, the combination of different 18S rRNA nested PCR primer sets is recommended for further epidemiological applications and also tracking the sources of infection.

BackgroundHuman cryptosporidiosis is caused primarily by two species of apicomplexan protozoa, Cryptosporidium parvum and C. hominis. In cultured cell monolayers, the parasite undergoes two generations of asexual multiplication (merogony). However, the proportion of parasites completing the life-cycle is low and insufficient to sustain continuous propagation. Due to the intracellular location of meronts and later life-cycle stages, oocyst and sporozoites are the only forms of the parasite that can readily be isolated.ResultsResearch on the replicating forms of Cryptosporidium parasites and their interaction with the host cell remains challenging. Based on an RNA-Seq analysis of monolayers of pig epithelial cells infected with C. parvum, here we report on the impact of merogony on the host’s gene regulation. Analysis of the transcriptome of infected and uninfected monolayers demonstrates a significant impact of the infection on host cell gene expression. A total of 813 genes were differentially expressed. Functional terms significantly altered in response to infection include phosphoprotein, RNA binding and acetylation. Upregulation of cell cycle pathways indicates an increase in mitosis. Notably absent from differentially enriched functional categories are stress- and apoptosis-related functions. The comparison of the combined host-parasite transcriptome reveals that C. parvum gene expression is less diverse than the host cell transcriptome and is highly enriched for genes encoding ribosomal functions, such as ribosomal proteins.ConclusionsThese results indicate that C. parvum infection significantly changes host biological functions and provide new insight into gene functions driving early C. parvum intracellular development.Electronic supplementary materialThe online version of this article (10.1186/s13071-018-2754-3) contains supplementary material, which is available to authorized users.