Rickettsia australis infection

A murine model of a highly invasive vasculopathic rickettsiosis

Hui Min Feng, Julie Wen, David Walker

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

A mouse model of spotted fever group rickettsiosis, in which disease results from disseminated rickettsial infection of endothelial cells and vascular damage, was developed by intravenous inoculation of 6- to 8-week-old, male, Balb/c mice with Rickettsia australis. Animals developed progressively severe vasculitis, interstitial pneumonia, and multifocal hepatic necrosis. These lesions correlated with early disseminated infection of endothelial cells followed by growth and invasion of rickettsiae into perivascular cells. The dose of 2 × 106 organisms was uniformly lethal Serum interleukin- (IL) 1, IL-6, and interferon (IFN) increased by day 3 and tumor necrosis factor (TNF) on day 5. TNF, IL-6, and IFN declined on day 7. Spleen cells responded to Rickettsia australis antigen by producing IFN, TNF, IL-1, and IL-6 on day 5, followed by lower quantities of these cytokines on day 7. Despite the production of antibodies, IFN, TNF, IL-1, and IL-6, a lethal outcome occurred frequently. A decreased ability to secrete IL-2 suggests an element of infection-associated immunosuppression.

Original languageEnglish (US)
Pages (from-to)1471-1482
Number of pages12
JournalAmerican Journal of Pathology
Volume142
Issue number5
StatePublished - May 1993

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Rickettsia Infections
Rickettsia
Interferons
Interleukin-6
Tumor Necrosis Factor-alpha
Interleukin-1
Endothelial Cells
Infection
Interstitial Lung Diseases
Vasculitis
Immunosuppression
Antibody Formation
Interleukin-2
Fever
Necrosis
Spleen
Cytokines
Antigens
Liver
Growth

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Rickettsia australis infection : A murine model of a highly invasive vasculopathic rickettsiosis. / Feng, Hui Min; Wen, Julie; Walker, David.

In: American Journal of Pathology, Vol. 142, No. 5, 05.1993, p. 1471-1482.

Research output: Contribution to journalArticle

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