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Tristan Ferry

Publications and source records attributed to Tristan Ferry.

9 recordsLinked to original sources

Comparative inflammatory properties of staphylococcal superantigenic enterotoxins SEA and SEG: implications for septic shock.

The severity of Staphylococcus aureus sepsis is positively associated with staphylococcal enterotoxin A (SEA) and negatively associated with the enterotoxin gene cluster (egc), which encodes five staphylococcal enterotoxins. We postulated that the variable, clinical severity of S. aureus sepsis might be a result of differences in the inflammatory properties of staphylococcal superantigens. We therefore compared the inflammatory properties of SEA with those of staphylococcal entérotoxin G (SEG), a member of the five egc superantigens. We found that SEA and SEG had similar superantigenic properties, as they induced CD69 expression on T lymphocytes and selective expansion of Vbeta subpopulations. Contrary to SEG, however, SEA induced a strong proinflammatory/Th1 response, including TNF-alpha and MIP-1alpha production. These results suggest that the association of SEA with the severity of S. aureus septic shock, characterized by a deleterious, inflammatory cascade, may be explained partly by the specific proinflammatory properties of this superantigen.

Antigens, CD↗

Toxin gene content of the Lyon methicillin-resistant Staphylococcus aureus clone compared with that of other pandemic clones.

The methicillin-resistant Staphylococcus aureus (MRSA) Lyon clone, detected throughout France, contains the enterotoxin A gene (sea), like other pandemic clones of clonal complex 8 (CC8). The egc locus was detected in MRSA pandemic clones of CC5, CC22, and CC45, occasionally with the toxic shock syndrome toxin 1 gene. The representative strain of the EMRSA-16 clone (CC30) harbored both sea and the egc locus.

Bacterial Toxins↗

Comparative prevalence of superantigen genes in Staphylococcus aureus isolates causing sepsis with and without septic shock.

BACKGROUND: Staphylococcus aureus superantigens are associated with the pathogenesis of toxic shock syndrome, but their involvement in septic shock is unknown. METHODS: We compared the distribution of 11 superantigen genes in S. aureus blood culture isolates obtained from patients with sepsis who did and did not have septic shock (19 and 61 patients, respectively), as well as from patients with suppurative infections (101 patients) and patients with colonization (25 patients). RESULTS: The prevalence of the enterotoxin A gene (sea) increased significantly with the severity of infection (P<.001), whereas the prevalence of the enterotoxin gene cluster (egc) decreased significantly (P=.009). CONCLUSION: Enterotoxin A (SEA) might play a key role in sea-positive S. aureus sepsis by triggering over-expression of inflammatory mediators associated with shock. Novel treatments targeting superantigens, especially the sea gene, might be beneficial in the treatment of S. aureus sepsis.

Adult↗

Virulence determinants in Staphylococcus aureus and their involvement in clinical syndromes.

Staphylococcus aureus is a major human pathogen responsible for a variety of toxin-mediated and suppurative diseases. About 50 staphylococcal virulence factors have been described to date. In this review, we examine the clinical implications of key staphylococcal virulence factors in toxin-mediated diseases, septic shock, and severe focal infections such as arthritis, infective endocarditis, pneumonia acquired during mechanical ventilation, and necrotizing pneumonia. Staphylococcal pathogenicity is sometimes due principally to a single virulence factor, as in toxic shock syndrome and necrotizing pneumonia. In contrast, several virulence factors are involved in other staphylococcal disease, such as septic shock. A better knowledge of the mechanism of action of each virulence factor involved in the different staphylococcal diseases could open the way to the use of specific inhibitors in the clinical setting.

Journal Article↗

Lupus-like presentation of parvovirus B19 infection.

OBJECTIVES: To describe 2 cases of parvovirus B19 (B19) infection mimicking systemic lupus erythematosus (SLE) and to identify all cases of SLE imitated by and/or associated with B19 in the medical literature. METHODS: A computer-assisted (PubMed) search of the medical literature from 1975 to 2003 was performed using the following key words: parvovirus, B19, SLE, lupus, antibodies, auto-immunity. RESULTS: Thirty-eight patients were identified: 35 women, 3 men; mean age = 28.8 years. Clinical manifestations were as follows: fever (24 patients); articular involvement (36 patients); cutaneous lesions (28 patients); lymphadenopathy (9 patients); hepato- and/or splenomegaly (6 patients); serositis (6 patients); renal involvement (4 patients); cerebral impairment (10 patients). Cytopenia was observed in 23 cases. Antinuclear antibodies were detected in 34 patients, anti-double-stranded DNA antibodies in 20 patients, anti-Sm antibodies in 4 patients, antinuclear ribonucleoprotein antibodies in 5 patients, anti-Ro-SSA antibodies in 4 patients, anti-La-SSB antibodies in 4 patients, and anticardiolipin and/or anti-beta2-glycoprotein I antibodies in 8 patients. Hypocomplementemia was found in 15 of 26 patients. In 19 cases, the B19 infection had a self-limiting course. In 6 cases, B19 infection occurred in a context of previously established SLE, simulating SLE exacerbation. In 6 observations, symptoms persisted several months after the viral infection. In 7 cases, the exact relationship between SLE and B19 could not be determined. CONCLUSIONS: B19 infection may present a clinical and serological tableau making it difficult to distinguish between a viral infection and the first episode of SLE. Although B19 may modulate the clinical and biological features of rheumatic disease, studies in large series do not support a causative role for B19 in the pathogenesis of SLE.

Adult↗

[Patients refused in admission to an intensive care unit. Prospective evaluation of the causes and outcome].

OBJECTIVES: To determine the reasons for refusing admission to an intensive care unit and the immediate outcome of the patients refused. METHOD: All patients triaged for admission to a medical intensive care unit ICU during a three-month period were studied prospectively. The frequency and reason for refused admission were studied. The immediate outcome of the refused patients, together with the time lapse before their subsequent management were determined. RESULTS: Out of 251 patients, 132 (53%) were refused admission. Primary reasons for refusal was lack of beds (92%). Nearly one patient out of 5 was not subsequently treated in an intensive care unit. CONCLUSION: Some refusals could have been avoided if the downstream networks (short-hospitalisation, re-habilitation centres.) had been able to accommodate the patients proposed. Moreover, by abandoning the strategy of wide admission to intensive care to the benefit of a selective triage of the patients proposed, a certain number of refusals would probably have been avoided. Nevertheless, there are obvious difficulties in the application of the latter method.

Aged↗

[Hypersensitive reaction to abacavir or syphilitic hepatitis?].

INTRODUCTION: Syphilis remains a current infection in France, with an increase in cases associated with the increase in sexual practices at risk. OBSERVATION: An HIV-seropositive homosexual male presented with a perturbed hepatic profile and roseola-like exanthema 15 days after starting treatment with Trizivir. Because of the combination of hepatitis and cutaneous eruption evoking hypersensitivity to abacavir, treatment was suspended, but no improvement was noted. The diagnosis of syphilitic hepatitis associated with roseola was made following a sero-conversion and improvement was obtained with benzathine-penicillin and the re-introduction of Trizivir without further problem. COMMENTS: This case report underlines the possibility of discovering syphilis when confronted with cholestatic and cytolytic hepatitis that regresses with penicillin and is isolated or associated with evocative cutaneous signs.

Adult↗