Human ehrlichiosis: Hematopathology and immunohistologic detection of Ehrlichia chaffeensis

Dumler, J. Stephen; Dawson, Jacqueline E.; Walker, David H.

doi:10.1016/0046-8177(93)90087-w

Cited by 119 publications

(12 citation statements)

References 28 publications

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“…(32)(33)(34)(35)(36). Also consistent with HME and other pathogenic ehrlichioses, composite results of histology, ISH, and electron microscopy analysis of live mammalian rodent tissue performed in this study indicate that EmCRT infects a relatively small proportion of cells, which suggests that rather than cytopathic injury, pathogenesis is primarily a result of host immune response, leading to vascular leakage and toxic shock-like syndrome (30,37,38). These acute, severe disease outcomes contrast with the mild or asymptomatic, sublethal infections observed in laboratory mice infected with the type species isolate (E. muris AS145) obtained from a wild Japanese mouse, which may result in prolonged duration of infection (39,40).…”

Section: Discussionsupporting

confidence: 77%

Ehrlichia Isolate from a Minnesota Tick: Characterization and Genetic Transformation

Lynn

Burkhardt

Felsheim³

et al. 2019

Appl Environ Microbiol

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Ehrlichia muris subsp. eauclairensis is recognized as the etiological agent of human ehrlichiosis in Minnesota and Wisconsin. We describe the culture isolation of this organism from a field-collected tick and detail its relationship to other species of Ehrlichia. The isolate could be grown in a variety of cultured cell lines and was effectively transmitted between Ixodes scapularis ticks and rodents, with PCR and microscopy demonstrating a broad pattern of dissemination in arthropod and mammalian tissues. Conversely, Amblyomma americanum ticks were not susceptible to infection by the Ehrlichia. Histologic sections further revealed that the wild-type isolate was highly virulent for mice and hamsters, causing severe systemic disease that was frequently lethal. A Himar1 transposase system was used to create mCherry- and mKate-expressing EmCRT mutants, which retained the ability to infect rodents and ticks. IMPORTANCE Ehrlichioses are zoonotic diseases caused by intracellular bacteria that are transmitted by ixodid ticks. Here we report the culture isolation of bacteria which are closely related to, or the same as the Ehrlichia muris subsp. eauclairensis, a recently recognized human pathogen. EmCRT, obtained from a tick removed from deer at Camp Ripley, MN, is the second isolate of this subspecies described and is distinctive in that it was cultured directly from a field-collected tick. The isolate’s cellular tropism, pathogenic changes caused in rodent tissues, and tick transmission to and from rodents are detailed in this study. We also describe the genetic mutants created from the EmCRT isolate, which are valuable tools for the further study of this intracellular pathogen.

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Section: Discussionsupporting

confidence: 77%

Ehrlichia Isolate from a Minnesota Tick: Characterization and Genetic Transformation

Lynn

Burkhardt

Felsheim³

et al. 2019

Appl Environ Microbiol

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“…E. chaffeensis causes pancytopenia and hepatic dysfunction, which progress to a potentially fatal multiorgan system disorder that mimics toxic shock syndrome despite antibiotic treatment [5]–[8]. Ehrlichiae infect several myeloid cells, such as macrophages, monocytes, and dendritic cells, and thus cause systemic infection [2], [3], [9]–[12]. In mice, innocuous or fatal ehrlichial diseases that mimic different spectra of HME occur following infection with E. muris and Ixodes ovatus Ehrlichia (IOE), respectively [13]–[15].…”

Section: Introductionmentioning

confidence: 99%

TLR2 and Nod2 Mediate Resistance or Susceptibility to Fatal Intracellular Ehrlichia Infection in Murine Models of Ehrlichiosis

et al. 2013

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Our murine models of human monocytic ehrlichiosis (HME) have shown that severe and fatal ehrlichiosis is due to generation of pathogenic T cell responses causing immunopathology and multi-organ failure. However, the early events in the liver, the main site of infection, are not well understood. In this study, we examined the liver transcriptome during the course of lethal and nonlethal infections caused by Ixodes ovatus Ehrlichia and Ehrlichia muris, respectively. On day 3 post-infection (p.i.), although most host genes were down regulated in the two groups of infected mice compared to naïve counterparts, lethal infection induced significantly higher expression of caspase 1, caspase 4, nucleotide binding oligomerization domain-containing proteins (Nod1), tumor necrosis factor-alpha, interleukin 10, and CCL7 compared to nonlethal infection. On day 7 p.i., lethal infection induced highly significant upregulation of type-1 interferon, several inflammatory cytokines and chemokines, which was associated with increased expression levels of Toll-like receptor-2 (TLR2), Nod2, MyD88, nuclear factor-kappa B (NF-kB), Caspase 4, NLRP1, NLRP12, Pycard, and IL-1β, suggesting enhanced TLR signals and inflammasomes activation. We next evaluated the participation of TLR2 and Nod2 in the host response during lethal Ehrlichia infection. Although lack of TLR2 impaired bacterial elimination and increased tissue necrosis, Nod2 deficiency attenuated pathology and enhanced bacterial clearance, which correlated with increased interferon-γ and interleukin-10 levels and a decreased frequency of pathogenic CD8+ T cells in response to lethal infection. Thus, these data indicate that Nod2, but not TLR2, contributes to susceptibility to severe Ehrlichia-induced shock. Together, our studies provide, for the first time, insight into the diversity of host factors and novel molecular pathogenic mechanisms that may contribute to severe HME.

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“…Occasionally, small vessel occlusion and local ischemia may occur. In patients with ehrlichiosis, perivascular lymphohistiocytic infiltrates may be seen on histopathologic examination ( 16 ). …”

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confidence: 99%

Myocarditis after Trimethoprim/Sulfamethoxazole Treatment for Ehrlichiosis

Nayak¹,

Simon²

2013

Emerg. Infect. Dis.

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Human ehrlichiosis: Hematopathology and immunohistologic detection of Ehrlichia chaffeensis

Cited by 119 publications

References 28 publications

Ehrlichia Isolate from a Minnesota Tick: Characterization and Genetic Transformation

Ehrlichia Isolate from a Minnesota Tick: Characterization and Genetic Transformation

TLR2 and Nod2 Mediate Resistance or Susceptibility to Fatal Intracellular Ehrlichia Infection in Murine Models of Ehrlichiosis

Myocarditis after Trimethoprim/Sulfamethoxazole Treatment for Ehrlichiosis

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