scholarly journals Assays for monitoringToxoplasma gondiiinfectivity in the laboratory mouse

2019 ◽  
Author(s):  
Qiuling Wang ◽  
L. David Sibley

AbstractToxoplasmais a widespread parasite of animals including many rodents that are a natural part of the transmission cycle between cats, which serve as the definitive host. Although wild rodents, including house mice, are relatively resistant, laboratory mice are highly susceptible to infection. As such, laboratory mice and have been used to compare pathogenesis of natural variants, and to evaluate the contributions of both host and parasite genes to infection. Protocols are provided here for evaluating acute and chronic infection with different parasite strains in laboratory mice. These protocols should provide uniform standards for evaluating natural variants and attenuated mutants and for comparing outcomes across different studies and between different laboratories.

2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Kate L. Bowerman ◽  
Sarah C. L. Knowles ◽  
Janette E. Bradley ◽  
Laima Baltrūnaitė ◽  
Michael D. J. Lynch ◽  
...  

AbstractThe domestication of the laboratory mouse has influenced the composition of its native gut microbiome, which is now known to differ from that of its wild ancestor. However, limited exploration of the rodent gut microbiome beyond the model species Mus musculus has made it difficult to interpret microbiome variation in a broader phylogenetic context. Here, we analyse 120 de novo and 469 public metagenomically-sequenced faecal and caecal samples from 16 rodent hosts representing wild, laboratory and captive lifestyles. Distinct gut bacterial communities were observed between rodent host genera, with broadly distributed species originating from the as-yet-uncultured bacterial genera UBA9475 and UBA2821 in the families Oscillospiraceae and Lachnospiraceae, respectively. In laboratory mice, Helicobacteraceae were generally depleted relative to wild mice and specific Muribaculaceae populations were enriched in different laboratory facilities, suggesting facility-specific outgrowths of this historically dominant rodent gut family. Several bacterial families of clinical interest, including Akkermansiaceae, Streptococcaceae and Enterobacteriaceae, were inferred to have gained over half of their representative species in mice within the laboratory environment, being undetected in most wild rodents and suggesting an association between laboratory domestication and pathobiont emergence.


1994 ◽  
Vol 28 (2) ◽  
pp. 113-120 ◽  
Author(s):  
Felix R. Homberger ◽  
Peter E. Thomann

Pathogen-free sentinel mice were placed in 7 animal rooms with different housing conditions and were serologically screened for antibodies to mouse hepatitis virus (MHV), pneumonia virus of mice (PVM), Sendai virus, reovirus 3, Theiler's mouse encephalomyelitis virus (TMEV), ectromelia virus and Mycoplasma pulmonis by enzyme-linked immunosorbent assays, at intervals after introduction. The most commonly detected antibody was against MHV, which was found in mice from 4 rooms, followed by PVM antibody in mice from 3 rooms. Seroconversion to Sendai virus and TMEV was detected in mice from one room each. No seroconversion to any of the antigens was found in 2 rooms. The common criteria of these 2 rooms were that they housed pathogen-free animals from a single source and that the access to the rooms was, purposely or not, restricted to people who had no contact to other mice. The study demonstrated the importance of husbandry and hygienic regimen on the prevalence of infectious agents in laboratory mice.


1968 ◽  
Vol 46 (2) ◽  
pp. 135-140 ◽  
Author(s):  
Bro. Joseph Kavelaars ◽  
T. K. R. Bourns

Cercariae of Plagiorchis peterborensis sp. n. were obtained from Lymnaea stagnalis appressa, and the life cycle was completed using Aedes aegypti larvae and laboratory mice as experimental hosts. Description of the adult is based upon whole mounts and serial sections of 14-day-old worms. P. peterborensis resembles most closely P. muris, but differs in stylet shape, adult dimensions, and egg size.


2006 ◽  
Vol 87 (6) ◽  
pp. 1543-1556 ◽  
Author(s):  
David G. Besselsen ◽  
Melissa J. Romero ◽  
April M. Wagner ◽  
Kenneth S. Henderson ◽  
Robert S. Livingston

Random-source DNA samples obtained from naturally infected laboratory mice (n=381) were evaluated by PCR and RFLP analysis to determine the prevalence of murine parvovirus strains circulating in contemporary laboratory mouse colonies. Mouse parvovirus (MPV) was detected in 77 % of samples, Minute virus of mice (MVM) was detected in 16 % of samples and both MVM and MPV were detected in 7 % of samples. MVMm, a strain recently isolated from clinically ill NOD-μ chain knockout mice, was detected in 91 % of MVM-positive samples, with the Cutter strain of MVM (MVMc) detected in the remaining samples. The prototypic and immunosuppressive strains of MVM were not detected in any of the samples. MPV-1 was detected in 78 % of the MPV-positive samples and two newly identified murine parvoviruses, tentatively named MPV-2 and MPV-3, were detected in 21 and 1 % of the samples, respectively. The DNA sequence encompassing coding regions of the viral genome and the predicted protein sequences for MVMm, MPV-2 and MPV-3 were determined and compared with those of other rodent parvovirus strains and LuIII parvovirus. The genomic organization for the newly identified viral strains was similar to that of other rodent parvoviruses, and nucleotide sequence identities indicated that MVMm was most similar to MVMc (96.1 %), MPV-3 was most similar to hamster parvovirus (HaPV) (98.1 %) and MPV-2 was most similar to MPV-1 (95.3 %). The genetic similarity of MPV-3 and HaPV suggests that HaPV epizootics in hamsters may result from cross-species transmission, with mice as the natural rodent host for this virus.


2021 ◽  
Vol 9 ◽  
Author(s):  
Douglas F. Makin ◽  
Ella Agra ◽  
Manu Prasad ◽  
Joel S. Brown ◽  
Moshe Elkabets ◽  
...  

As cancer progresses, its impact should manifest in the foraging behavior of its host much like the effects of endo-parasites that hinder foraging aptitudes and risk management abilities. Furthermore, the lifestyle of the host can impact tumor growth and quality of life. To approach these questions, we conducted novel experiments by letting C57BL/6 laboratory mice, with or without oral squamous cell carcinoma, free range in a large outdoor vivarium. Our goals were to: (1) determine whether one could conduct experiments with a mouse model under free range conditions, (2) measure effects of cancer burden on foraging metrics, (3) compare tumor growth rates with laboratory housed mice, and (4) begin to sort out confounding factors such as diet. With or without cancer, the C57BL/6 laboratory mice dealt with natural climatic conditions and illumination, found shelter or dug burrows, sought out food from experimental food patches, and responded to risk factors associated with microhabitat by foraging more thoroughly in food patches under bush (safe) than in the open (risky). We quantified foraging using giving-up densities of food left behind in the food patches. The mice’s patch use changed over time, and was affected by disease status, sex, and microhabitat. Males, which were larger, consumed more food and had lower giving-up densities than females. Relative to cancer-free mice, mice with growing tumors lost weight, harvested more food, and increasingly relied on patches in the bush microhabitat. The tumors of free-ranging mice in the vivarium grew slower than those of their cohort that were housed in mouse cages in animal facilities. Numerous interesting factors could explain the difference in tumor growth rates: activity levels, stress, weather, food intake, diet, and more. To tease apart one of these intertwined factors, we found that tumors grew faster when mice in the laboratory were fed on millet rather than laboratory mouse chow. While just a start, these novel experiments and framework show how free-ranging mice provide a model that can test a broader range of hypotheses and use a broader range of metrics regarding cancer progression and its consequences for the host.


Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 157-160
Author(s):  
F Figueroa ◽  
E Neufeld ◽  
U Ritte ◽  
J Klein

Abstract Lehrach and his coworkers have isolated a series of DNA probes that specifically hybridize with different regions of mouse chromosome 17 within the t complex. The probes display restriction fragment length polymorphisms, RFLPs, which are specific for the t haplotypes in all laboratory mouse strains tested thus far. Some of these probes have been used to test wild mice populations for these t-associated DNA forms. It is demonstrated that populations from Germany, Switzerland, Italy, Greece, Yugoslavia, Australia, Costa Rica, and Venezuela contain chromosomes in which all the tested DNA loci display the t-specific polymorphisms. The frequency of mice carrying these chromosomes is as high as 31%. Wild mice from Israel and Spain, on the other hand, carry chromosomes displaying t-specific DNA forms only at one or two of the probed loci, while the other loci carry the wild-type (+) forms. These chromosomes thus resemble the partial t haplotypes known from the study of laboratory mice. One possible interpretation of these findings is that these DNA polymorphisms contributed to the assembly of the complete t haplotypes and that these haplotypes may have originated in the Middle East.


Author(s):  
Chia-Ming Su ◽  
Ying-Chien Cheng ◽  
Hurng-Yi Wang ◽  
Chia-Hung Hsieh ◽  
Cho-Hua Wan

Astroviruses are non-enveloped, positive-sense, ssRNA viruses and often associated with gastrointestinal diseases. Murine astrovirus (MuAstV) was first confirmed in a laboratory mouse colony in 2011. Although infected mice do not present significant clinical symptoms, the virus might interfere with research results. A recent surveillance has shown that MuAstV is highly prevalent in laboratory mice. The aims of the present study were to identify and characterize MuAstV strains as well as to investigate the prevalence rate of viral RNA in laboratory mice in Taiwan, and to estimate the origin and past population demography of MuAstVs. Based on molecular surveillance, MuAstV RNA was detected in 45.7 % of laboratory mice (48/105) from seven of nine colonies. Three fully sequenced MuAstV strains, MuAstV TW1, TW2 and TW3, exhibited 89.1−94.4 % and 89.1–90.0 % nucleotide identities with the reference strains MuAstV STL1 and STL2, respectively. Phylogenetic analyses of the partial regions of the RNA-dependent RNA polymerase (RdRp) and capsid protein (CP) genes of 18 Taiwan strains along with other astroviruses revealed that there are three distinct lineages of mouse astrovirus, MuAstV1, MuAstV2 and mouse astrovirus JF755422. The mutation rates of MuAstV1 were 2.6×10−4 and 6.2×10−4 substitutions/site/year for the RdRp and CP regions, respectively. Based on the above molecular clock, the colonization of MuAstV1 in laboratory mice was between 1897 and 1912, in good agreement with the establishment of ‘modern’ laboratory mouse facilities. Since its initial infection, the population size of MuAstV1 has increased 15–60-fold, probably consistent with the increased use of laboratory mice. In conclusion, MuAstV1 has been associated with modern laboratory mice since the beginning, and its influence on research results may require further investigation.


Parasitology ◽  
2009 ◽  
Vol 136 (12) ◽  
pp. 1581-1592 ◽  
Author(s):  
R. A. WILSON

SUMMARYSchistosomes infect the mammalian host by direct penetration of the skin and must then undergo a protracted migration to the site of parasitization, forSchistosoma mansonithe hepatic portal vasculature. This article reviews the work published roughly between 1976 and 1986 that clarified our understanding of the process in the laboratory mouse. A combination of histopathology, larval injection experiments and autoradiographic tracking revealed that migration involved one to several circuits of the pulmonary-systemic vasculature before chance delivery in cardiac output to splanchnic arteries that lead indirectly to the portal tract. The kinetics of migration through different capillary beds was established, with the lungs of naïve mice not the skin proving the greatest obstacle; a proportion of schistosomula entered the alveoli from where they did not recover. The ‘immunity’ displayed by mice with a chronic infection was shown to be an artefact of a ‘leaky’ hepatic portal system, generated as a result of egg-induced hepatic pathology. The blockade of pulmonary migration was exacerbated in mice vaccinated with irradiated cercariae by immune-mediated inflammatory foci that developed around lung schistosomula thus decreasing the proportion that matured, but parasite elimination was a prolonged process, not an acute cytolytic ‘hit.’


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