scholarly journals Associations between dogs that were serologically positive for Rickettsia conorii relative to the residences of two human cases of Mediterranean spotted fever in Piemonte (Italy)

2003 ◽  
Vol 60 (1) ◽  
pp. 13-26 ◽  
Author(s):  
A. Mannelli ◽  
M.L. Mandola ◽  
P. Pedri ◽  
M. Tripoli ◽  
P. Nebbia
Keyword(s):  
Spotted Fever ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever

scholarly journals Assessment of the Percentages of T-lymphocyte Subsets in the Peripheral Blood of Mediterranean Spotted Fever Patients

2020 ◽  
Vol 18 (2) ◽  
pp. 111-119
Author(s):  
Iv. Baltadzhiev ◽  
P. Pavlov
Keyword(s):  
T Cells ◽  
Disease Severity ◽  
T Lymphocyte ◽  
Lymphocyte Subsets ◽  
Spotted Fever ◽  
Healing Process ◽  
Cell Subset ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
T Lymphocyte Subsets

Purpose: Mediterranean spotted fever (MSF) is a rickettsial disease. The aim was to evaluate the host immunе response to Rickettsia conorii. Material and methods: 62 patients were assigned into three groups: with mild, moderate or severe clinical forms of MSF. Controls were 32 healthy individuals. The diagnosis of MSF was confirmed by the indirect immunofluorescence assay. Immunophenotyping was performed using Epics XL-MCL Coulter. Results: The percentage of immune competent (CD3+) cells decreased, whereas that of helper/inducer (CD3+CD4+) and suppressor/cytotoxic (CD3+CD8+) did not change compared to controls. All three T-cell subset percentages did not parallel the disease severity. Naïve T-cells (CD4+CD45RA+) showed reduced levels, whereas activated memory (CD4+CD45RO+) T-cells did not change significantly. The percentage of activated (CD3+HLA-DR+) T-cells increased regardless of the disease severity, till the rise of stimulatory molecules (CD38+total) matched the disease severity forms. The percentage of costimulatory CD28-molecules corresponded to the disease severity as their levels increased significantly in mild forms and showed an evident downward trend towards the severe ones. Conclusion: Reduced T-lymphocyte subsets are likely related to trans-migration into perivascular inflammatory foci. The increased percentage of T-lymphocytes armed with stimulatory molecules probably reflects the mobilization of cell-mediated immune response in the healing process.

scholarly journals Nonselective Persistence of a Rickettsia conorii Extrachromosomal Plasmid during Mammalian Infection

2016 ◽  
Vol 84 (3) ◽  
pp. 790-797 ◽  
Author(s):  
Sean P. Riley ◽  
Abigail I. Fish ◽  
Daniel A. Garza ◽  
Kaikhushroo H. Banajee ◽  
Emma K. Harris ◽  
...  
Keyword(s):  
Pathogenic Bacteria ◽  
Genetic Manipulation ◽  
Fluorescent Proteins ◽  
Spotted Fever ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
Extrachromosomal Dna ◽  
Content Type

Scientific analysis of the genusRickettsiais undergoing a rapid period of change with the emergence of viable genetic tools. The development of these tools for the mutagenesis of pathogenic bacteria will permit forward genetic analysis ofRickettsiapathogenesis. Despite these advances, uncertainty still remains regarding the use of plasmids to study these bacteria inin vivomammalian models of infection, namely, the potential for virulence changes associated with the presence of extrachromosomal DNA and nonselective persistence of plasmids in mammalian models of infection. Here, we describe the transformation ofRickettsia conoriiMalish 7 with the plasmid pRam18dRGA[AmTrCh]. TransformedR. conoriistably maintains this plasmid in infected cell cultures, expresses the encoded fluorescent proteins, and exhibits growth kinetics in cell culture similar to those of nontransformedR. conorii. Using a well-established murine model of fatal Mediterranean spotted fever, we demonstrate thatR. conorii(pRam18dRGA[AmTrCh]) elicits the same fatal outcomes in animals as its untransformed counterpart and, importantly, maintains the plasmid throughout infection in the absence of selective antibiotic pressure. Interestingly, plasmid-transformedR. conoriiwas readily observed both in endothelial cells and within circulating leukocytes. Together, our data demonstrate that the presence of an extrachromosomal DNA element in a pathogenic rickettsial species does not affect eitherin vitroproliferation orin vivoinfectivity in models of disease and that plasmids such as pRam18dRGA[AmTrCh] are valuable tools for the further genetic manipulation of pathogenic rickettsiae.

scholarly journals Demonstration of Rickettsia conorii-induced endothelial injury in vivo by measuring circulating endothelial cells, thrombomodulin, and von Willebrand factor in patients with Mediterranean spotted fever [see comments]

Blood ◽  
1993 ◽  
Vol 82 (7) ◽  
pp. 2109-2116
Author(s):  
F George ◽  
P Brouqui ◽  
MC Boffa ◽  
M Mutin ◽  
M Drancourt ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Spotted Fever ◽  
Clinical Manifestations ◽  
Endothelial Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
Von Willebrand ◽  
Willebrand Factor

The endothelial cell (EC) is the primary target for Rickettsia conorii (RC) in Mediterranean spotted fever (MSF). Clinical manifestations such as thrombosis and vasculitis are mediated by pathologic changes localized in blood vessels. To study the in vivo endothelial injury induced by RC, markers of endothelial damage, including circulating EC (CEC), plasmatic thrombomodulin (TM), and von Willebrand factor (vWF), were investigated in 12 patients with MSF. CEC were counted in whole blood by a new immunomagnetic separation assay using a specific anti-EC antibody, S-Endo 1. Plasmatic TM and vWF antigens were measured by enzyme-linked immunosorbent assay. High levels of CEC and cell fragments were found in patients with a severe or malignant form of MSF. Sequential studies of CEC showed a decrease from 162 +/- 454 cells/mL before treatment to 6 +/- 7 cells/mL during treatment and recovery. Mean plasma TM and vWF levels that were also elevated before therapy (TM, 106 +/- 27 ng/mL; vWF, 420% +/- 164%) decreased progressively (TM, 55 +/- 43 ng/mL; vWF, 148% +/- 26%) during treatment. The measurement of cellular and molecular markers of vascular damage such as CEC, plasmatic TM, and vWF contributes to the definition of the Rickettsia-induced endothelial injury in vivo.

Rickettsiosis

2015 ◽  
Author(s):  
Emmanuel A. Burdmann ◽  
Vivekanad Jha
Keyword(s):  
Serum Creatinine ◽  
Spotted Fever ◽  
Renal Involvement ◽  
Adverse Outcomes ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
Spotted Fever Group ◽  
Rocky Mountain Spotted Fever ◽  
Murine Typhus ◽  
Epidemic Typhus

Rickettsiae are obligate intracellular bacteria transmitted by arthropods to a vertebrate host. Clinically relevant rickettsioses have a similar clinical pattern, manifesting as an acute febrile disease accompanied by headache, articular and muscle pain, and malaise.Epidemic typhus is a worldwide distributed disease caused by the Rickettsia prowazekii, with a human louse as a vector. Data on epidemic typhus-related renal injury is extremely scarce.Murine typhus is caused by the Rickettsia typhi and has a rodent flea as the vector. It is one of the most frequent rickettsioses, and is usually a self-limited febrile illness. Proteinuria, haematuria, elevations in serum creatinine (SCr) and/or blood urea nitrogen (BUN) and AKI have been reported. The real frequency of renal involvement in murine typhus is unknown. Renal abnormalities recover after the infectious disease resolution.Scrub typhus, caused by the Orientia tsutsugamushi, has the Leptotrombidium mite larva as vector. It is endemic in the Tsutsugamushi triangle delimited by Japan, Australia, India, and Siberia. It can manifest either as a self-limiting disease or as a severe, life-threatening multiorgan illness. Early administration of adequate antibiotics is essential to prevent adverse outcomes. Proteinuria, haematuria, and acute kidney injury (AKI) are frequent.Tick-borne rickettsioses are caused by bacteria from the spotted fever group and have ticks as vectors. Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii. It is the most severe of the spotted fever rickettsial diseases, causing significant morbidity and lethality. RMSF occurs in North, Central, and South America. Renal impairment is frequent in severe forms of RMSF. Mediterranean spotted fever is caused by Rickettsia conorii, and is endemic in the Mediterranean area. It is usually a benign disease, but may have a severe course, clinically similar to RMSF. Haematuria, proteinuria, increased serum creatinine, and AKI may occur. Japanese spotted fever is caused by Rickettsia japonica. Lethal cases are reported yearly and AKI has occurred in the context of multiple organ failure.

Rickettsial keratitis in a Case of Mediterranean spotted fever

1992 ◽  
Vol 2 (1) ◽  
pp. 41-43 ◽  
Author(s):  
J. Alio ◽  
R. Ruiz-Beltran ◽  
I. Herrera ◽  
A. Artola ◽  
J.M. Ruiz-Moreno
Keyword(s):  
Differential Diagnosis ◽  
Corneal Ulcer ◽  
Spotted Fever ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
Infectious Keratitis ◽  
Corneal Infection ◽  
Documented Case ◽  
Corneal Ulcers

The first documented case of infectious keratitis (an ameboid-like corneal ulcer) caused by Rickettsia conorii is described. Corneal infection was probably caused by contamination through the tears during systemic rickettsial dissemination. Topical tetracyclin ointment was effective. Rickettsial keratitis should be considered in the differential diagnosis of ameboid-like corneal ulcers in areas where Mediterranean spotted fever is endemic.

scholarly journals A Case of Hemophagocytic Lymphohistiocytosis Associated With Mediterranean Spotted Fever in a Healthy 29-Year-Old Female

2020 ◽  
Vol 7 (10) ◽  
Author(s):  
Nour Karra ◽  
Rina Dolinski ◽  
Luiza Akria ◽  
Yevgeni Yampoulski ◽  
Jamal Awad
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Epigastric Pain ◽  
Spotted Fever ◽  
Initial Presentation ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
Cytokine Storm ◽  
Proper Treatment ◽  
Prompt Diagnosis

Abstract A 29-year-old female presented with fever, headache, and epigastric pain. Though her initial presentation was benign and nonspecific, she soon developed a full-blown cytokine storm with disseminated intravascular coagulation. She was diagnosed with hemophagocytosis secondary to Rickettsia conorii infection. A good outcome was achieved thanks to prompt diagnosis and proper treatment.

scholarly journals Demonstration of Rickettsia conorii-induced endothelial injury in vivo by measuring circulating endothelial cells, thrombomodulin, and von Willebrand factor in patients with Mediterranean spotted fever [see comments]

Blood ◽  
1993 ◽  
Vol 82 (7) ◽  
pp. 2109-2116 ◽  
Author(s):  
F George ◽  
P Brouqui ◽  
MC Boffa ◽  
M Mutin ◽  
M Drancourt ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Spotted Fever ◽  
Clinical Manifestations ◽  
Endothelial Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract The endothelial cell (EC) is the primary target for Rickettsia conorii (RC) in Mediterranean spotted fever (MSF). Clinical manifestations such as thrombosis and vasculitis are mediated by pathologic changes localized in blood vessels. To study the in vivo endothelial injury induced by RC, markers of endothelial damage, including circulating EC (CEC), plasmatic thrombomodulin (TM), and von Willebrand factor (vWF), were investigated in 12 patients with MSF. CEC were counted in whole blood by a new immunomagnetic separation assay using a specific anti-EC antibody, S-Endo 1. Plasmatic TM and vWF antigens were measured by enzyme-linked immunosorbent assay. High levels of CEC and cell fragments were found in patients with a severe or malignant form of MSF. Sequential studies of CEC showed a decrease from 162 +/- 454 cells/mL before treatment to 6 +/- 7 cells/mL during treatment and recovery. Mean plasma TM and vWF levels that were also elevated before therapy (TM, 106 +/- 27 ng/mL; vWF, 420% +/- 164%) decreased progressively (TM, 55 +/- 43 ng/mL; vWF, 148% +/- 26%) during treatment. The measurement of cellular and molecular markers of vascular damage such as CEC, plasmatic TM, and vWF contributes to the definition of the Rickettsia-induced endothelial injury in vivo.

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