Risk for Mycobacterium celatum infection from ferret.
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ABSTRACT:
SUBMITTER: Ludwig E
PROVIDER: S-EPMC3166007 | biostudies-literature | 2011 Mar
REPOSITORIES: biostudies-literature
Publications
Risk for Mycobacterium celatum infection from ferret.
Ludwig Eva E Reischl Udo U Holzmann Thomas T Melzl Holger H Janik Dirk D Gilch Constanze C Hermanns Walter W
Emerging infectious diseases 20110301 3
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Project description:BackgroundEncephalitis is rarely caused by nontuberculous mycobacteria (NTM), which is generally not considered a highly virulent pathogen. However, NTM encephalitis in immunocompromised hosts occurs with varied clinical presentations, posing a diagnostic challenge in clinical practice. This study aims to describe an atypical case of NTM encephalitis caused by Mycobacterium celatum, which has not previously been reported to infect the central nervous system of immunocompromised hosts, mimicking autoimmune striatal encephalitis (ASE).Case presentationA 35-year-old immunosuppressed woman presented with prolonged fever for 4 months and rapidly progressive cognitive decline for 3 months. Neurological examination showed impaired cognition and parkinsonism. Laboratory testing was unremarkable. Her brain imaging on T2-weighted fluid-attenuated inversion recovery (T2/FLAIR) exhibited lesions involving basal ganglia and subcortical white matter in both hemispheres, mimicking ASE. Cerebrospinal fluid (CSF) analysis revealed mild pleocytosis with normal glucose and protein levels. CSF comprehensive microbiological studies and autoimmune panels were negative. ASE was suspected, and immunotherapies were given. Despite immunotherapies, her condition worsened with seizures, warranting a stereotactic brain biopsy to achieve a definite diagnosis. Her brain tissue pathology result was non-specific. However, we identified M. celatum from her brain tissue. Thus, the final diagnosis was M. celatum encephalitis. Therefore, we discontinued immunotherapies and started anti-NTM treatment, including isoniazid, rifampicin, ethambutol, and levofloxacin. After completing a 16-month treatment course, her clinical condition was stable, afebrile, and seizure-free.ConclusionsWe proposed that NTM invades the central nervous system and also triggers immune dysregulation, developing features resembling ASE. In case of suspicious autoimmune encephalitis with poor response to immunotherapies, a tissue biopsy should be performed to exclude chronic infection.
| S-EPMC11884120 | biostudies-literature
Project description:Clostridium celatum [ce.la'tum. L. adj. celatum hidden] has been known since 1974, when it was isolated from human feces. In 40 years, no association with human infection has been reported. In this work, we present two serious cases of infection with the anaerobic Gram-positive rod Clostridium celatum.
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Project description:whole genome sequence of Mycobacterium celatum
| PRJDB3515 | ENA
Project description:Ferret systemic coronaviral disease (FSCD) is a well-established cause of mortality in domestic ferrets. We describe herein novel findings in a case of FSCD that was diagnosed and medically managed following virus detection by immunohistochemical (IHC) staining of surgical biopsy samples. Hematologic changes in this ferret suggested spread of the virus to the bone marrow, which was confirmed by IHC staining of a postmortem sample. Genotyping of the virus indicated that the virus grouped with alphacoronaviruses and was most closely related to ferret enteric coronavirus (FRECV) MSU-2. Our clinical case demonstrates that a FRECV MSU-2-like ferret coronavirus associated previously with the enteric pathotype may cause systemic disease, including bone marrow involvement causing persistent pancytopenia.
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Project description:Direct sequencing of the 16S rRNA gene (16S rDNA) of Mycobacterium celatum isolates showed ambiguities, suggesting heterogeneity. Cloned 16S rDNA yielded two copies of the gene, which differed by insertion of a thymine at position 214 and by additional mismatches. Restriction fragment length polymorphism analysis confirmed the presence of two copies of 16S rDNA within the bacterial chromosome.
| S-EPMC104915 | biostudies-literature
Project description:Although initial observations of infections with the Zika virus describe a mild illness, more recent reports show that infections by Zika result in neurotropism. In 2015, substantial congenital malformations were observed, with numerous infants born with microcephaly in Brazil. To study the underlying mechanism and effects of the disease, it is critical to find suitable animal models. Rodents lack an immune system parallel to humans and also have lissencephalic brains, which are likely to react differently to infections. As the smallest gyrencephalic mammal, ferrets may provide an important animal model to study the Zika virus, as their brains share many characteristics with humans. To evaluate the prospect of using ferrets to study Zika virus infection, we injected seven pregnant jills with the PR strain subcutaneously on gestational day 21, corresponding to the initiation of corticogenesis. These injections resulted in mixed effects. Two animals died of apparent infection, and all kits were resorbed in another animal that did not die. The other four animals remained pregnant until gestational day 40, when the kits were delivered by caesarian section. We evaluated the animals using CT, MRI, diffusion tensor imaging, and immunohistochemistry. The kits displayed a number of features compatible with an infection that impacted both the brain and skull. The outcomes, however, were variable and differed within and across litters, which ranged from the absence of observable abnormalities to prominent changes, suggesting differential vulnerability of kits to infection by the Zika virus or to subsequent mechanisms of neurodevelopmental disruption.
| S-EPMC6593673 | biostudies-literature
Project description:Phase I human clinical studies involving therapeutics for emerging and biodefense pathogens with low incidence, such as the severe acute respiratory syndrome coronavirus (SARS-CoV), requires at a minimum preclinical evaluation of efficacy in two well-characterized and robust animal models. Thus, a ferret SARS-CoV model was evaluated over a period of 58 days following extensive optimization and characterization of the model in order to validate clinical, histopathological, virological and immunological endpoints. Ferrets that were infected intranasally with 10(3) TCID50 SARS-CoV showed higher body temperature (2-6 d.p.i.), sneezing (5-10 d.p.i.), lesions (5-7 d.p.i.) and decreased WBC/lymphocytes (2-5 d.p.i.). SARS-CoV was detected up to 7 d.p.i. in various tissues and excreta, while neutralizing antibody titers rose at 7 d.p.i. and peaked at 14 d.p.i. At 29 d.p.i., one group was challenged with 10(3) TCID50 SARS-CoV, and an anamnestic response in neutralizing antibodies was evident with no detectable virus. This study supports the validity of the ferret model for use in evaluating efficacy of potential therapeutics to treat SARS.
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Project description:BackgroundAlthough immune activation is associated with HIV acquisition, the nature of inflammatory profiles that increase HIV risk, which may include responses to M. tuberculosis (Mtb) infection, are not well characterized.MethodsWe conducted a nested case-control study using cryopreserved samples from persons who did and did not acquire HIV during the multinational Step clinical trial of the MRKAd5 HIV-1 vaccine. PBMCs from the last HIV-negative sample from incident HIV cases and controls were stimulated with Mtb-specific antigens (ESAT-6/CFP-10) and analyzed by flow cytometry with intracellular cytokine staining and scored with COMPASS. We measured inflammatory profiles with five Correlates of TB Risk (CoR) transcriptomic signatures. Our primary analysis examined the association of latent Mtb infection (LTBI; IFNγ+CD4+ T cell frequency) or RISK6 CoR signature with HIV acquisition. Conditional logistic regression analyses, adjusted for known predictors of HIV acquisition, were employed to assess whether TB-associated immune markers were associated with HIV acquisition.ResultsAmong 465 participants, LTBI prevalence (21.5% controls vs 19.1% cases, p = 0.51) and the RISK6 signature were not higher in those who acquired HIV. In exploratory analyses, Mtb antigen-specific polyfunctional CD4+ T cell COMPASS scores (aOR 0.96, 95% CI 0.77, 1.20) were not higher in those who acquired HIV. Two CoR signatures, Sweeney3 (aOR 1.38 (1.07, 1.78) per SD change) and RESPONSE5 (0.78 (0.61, 0.98)), were associated with HIV acquisition. The transcriptomic pattern used to differentiate active vs latent TB (Sweeney3) was most strongly associated with acquiring HIV.ConclusionsLTBI, Mtb polyfunctional antigen-specific CD4+ T cell activation, and RISK6 were not identified as risks for HIV acquisition. In exploratory transcriptomic analyses, two CoR signatures were associated with HIV risk after adjustment for known behavioral and clinical risk factors. We identified host gene expression signatures associated with HIV acquisition, but the observed effects are likely not mediated through Mtb infection.
| S-EPMC9064099 | biostudies-literature