Permeability of Coxiella burnetii to ribonucleosides

Miller, Jeffrey D.; Thompson, Herbert A.

doi:10.1099/00221287-148-8-2393

Cited by 12 publications

(14 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Biochemical studies of C. burnetii have focused on glutamate utilization (36), and genome analysis allowed identification of a probable glutamate uptake transporter (CBU2020). Unlike rickettsial and chlamydial species, C. burnetii does not possess any ATP͞ADP exchangers that enable these organisms to function as energy parasites by scavenging ATP from their host (37), confirming previous experimental observations (38). There are six transporters of unknown specificity belonging to a previously uncharacterized subfamily of the major facilitator superfamily, which seem to have undergone amplification in the C. burnetii lineage.…”

Section: Resultssupporting

confidence: 80%

Complete genome sequence of the Q-fever pathogenCoxiellaburnetii

Seshadri

Paulsen

Eisen

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

512

527

View full text Add to dashboard Cite

The 1,995,275-bp genome of Coxiella burnetii, Nine Mile phase I RSA493, a highly virulent zoonotic pathogen and category B bioterrorism agent, was sequenced by the random shotgun method. This bacterium is an obligate intracellular acidophile that is highly adapted for life within the eukaryotic phagolysosome. Genome analysis revealed many genes with potential roles in adhesion, invasion, intracellular trafficking, host-cell modulation, and detoxification. A previously uncharacterized 13-member family of ankyrin repeat-containing proteins is implicated in the pathogenesis of this organism. Although the lifestyle and parasitic strategies of C. burnetii resemble that of Rickettsiae and Chlamydiae, their genome architectures differ considerably in terms of presence of mobile elements, extent of genome reduction, metabolic capabilities, and transporter profiles. The presence of 83 pseudogenes displays an ongoing process of gene degradation. Unlike other obligate intracellular bacteria, 32 insertion sequences are found dispersed in the chromosome, indicating some plasticity in the C. burnetii genome. These analyses suggest that the obligate intracellular lifestyle of C. burnetii may be a relatively recent innovation.

show abstract

Section: Resultssupporting

confidence: 80%

Complete genome sequence of the Q-fever pathogenCoxiellaburnetii

Seshadri

Paulsen

Eisen

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

512

527

View full text Add to dashboard Cite

show abstract

“…This reference strain, isolated from a tick in 1935 (12), can cause Q fever in humans (3) and grows well in mouse models (14). It was grown in chicken eggs and purified by sucrose gradient centrifugation (20). Stocks were kept frozen at −80°C in sucrose phosphate glutamate buffer until use.…”

Section: Methodsmentioning

confidence: 99%

Early cytokine and antibody responses against Coxiella burnetii in aerosol infection of BALB/c mice

Schoffelen¹,

Self²,

Fitzpatrick³

et al. 2015

Diagnostic Microbiology and Infectious Disease

View full text Add to dashboard Cite

Coxiella burnetii, a Gram-negative intracellular bacterium, can give rise to Q fever in humans and is transmitted mainly by inhalation of infected aerosols from animal reservoirs. Serology is commonly used to diagnose Q fever, but the early cellular immune response –i.e. C. burnetii-specific interferon(IFN)-γ production in response to antigen challenge– might be an additional diagnostic. Detection of IFN-γ responses has been used to identify past and chronic Q fever infections, but the IFN-γ response in acute Q fever has not been described. By challenging immunocompetent BALB/c mice with aerosols containing phase I C. burnetii, the timing and extent of IFN-γ recall responses was evaluated in an acute C. burnetii infection. Other cytokines were also measured in an effort to identify other potential diagnostic markers. The data show that after initial expansion of bacteria first in lungs and then in other tissues, the infection was cleared from day 10 onwards as reflected by the decreasing number of bacteria. The antigen-induced IFN-γ production by splenocytes coincided with emergence of IgM phase II-antibodies at day 10 post-infection, and preceded appearance of IgG-antibodies. This was accompanied by the production of pro-inflammatory cytokines including IL-6, KC and IP-10, followed by MCP-1, but not by IL-1β and TNF-α, and only very low production of the anti-inflammatory cytokine IL-10. These data suggest that analysis of antigen-specific IFN-γ responses could be a useful tool for diagnosis of acute Q-fever. Moreover, the current model of C.burnetii infection could be used to give new insights into immunological factors that predispose to development of persistent infection.

show abstract

“…Nine Mile and M44 strains were used as purified stocks obtained by sucrose gradient centrifugation after growth in chicken eggs as previously described (Miller and Thompson 2002). The Henzerling, Priscilla, and K strain stocks were partially purified after growth on monolayers of the rabbit kidney cell line RK13 in tissue culture.…”

Section: Coxiella Burnetii Strainsmentioning

confidence: 99%

Virulence of PathogenicCoxiella burnetiiStrains After Growth in the Absence of Host Cells

Kersh

Oliver

Self

et al. 2011

Vector-Borne and Zoonotic Diseases

View full text Add to dashboard Cite

Coxiella burnetii is a gram-negative bacterium that causes the zoonotic disease Q fever. Traditionally considered an obligate intracellular agent, the requirement to be grown in tissue culture cells, embryonated eggs, or animal hosts has made it difficult to isolate strains and perform genetic studies on C. burnetii. However, it was recently demonstrated that the attenuated Nine Mile Phase 2 (NM2) C. burnetii strain will grow axenically in acidified citrate cysteine medium (ACCM) in a 2.5% oxygen environment. The current study was undertaken to determine whether more virulent C. burnetii strains could be grown in ACCM, and whether virulence would be maintained after passage. The ACCM medium supported an ?1000-fold expansion of Nine Mile Phase 1 (NM1), NM2, M44, and Henzerling strains of C. burnetii, whereas the Priscilla (Q177) strain expanded only 100-fold, and the K strain (Q154) grew poorly in ACCM. To determine if passage in ACCM would maintain the virulence of C. burnetii, the NM1 strain was grown for up to 26 weekly passages in ACCM. C. burnetii maintained in ACCM for 5 or 8 passages maintained full virulence in a mouse model, but NM1 passaged for 23 or 26 times was somewhat attenuated. These data demonstrate that virulent strains of C. burnetii can be successfully passaged in ACCM; however, some strains can lose virulence after extended passage, and other strains grow poorly in this medium. The loss of virulence in axenic culture was associated with some truncation of lipopolysaccharide chains, suggesting a possible mechanism for attenuation.

show abstract

Permeability of Coxiella burnetii to ribonucleosides

Cited by 12 publications

References 42 publications

Complete genome sequence of the Q-fever pathogenCoxiellaburnetii

Complete genome sequence of the Q-fever pathogenCoxiellaburnetii

Early cytokine and antibody responses against Coxiella burnetii in aerosol infection of BALB/c mice

Virulence of PathogenicCoxiella burnetiiStrains After Growth in the Absence of Host Cells

Contact Info

Product

Resources

About