Short-course treatment with ceftriaxone for leptospirosis: a retrospective study in a single center in Eastern France.

Short-course (less than 7 days) antibiotic treatments have been rarely assessed in the management of leptospirosis. We analyzed the charts of patients hospitalized with confirmed and probable leptospirosis in a teaching hospital between 1994 and 2012. Of 89 patients with confirmed or probable leptospirosis, 21 patients (11 confirmed, 10 probable - 14 uncomplicated and 7 severe forms) admitted between 2001 and 2012 received ceftriaxone (1-2 g daily) for less than 7 days. Apyrexia was obtained within 2 days of treatment in all patients and no relapse was observed. These data support the hypothesis that short-course treatments of 3-6 days with ceftriaxone (1-2 g per day) may be an option in the treatment of uncomplicated and severe forms of leptospirosis responding quickly to therapy. This hypothesis deserves being confirmed in further clinical studies.

Low serum procalcitonin level accurately predicts the absence of bacteremia in adult patients with acute fever.

The ability of measurement of serum procalcitonin (PCT) levels to differentiate bacteremic from nonbacteremic infectious episodes in patients hospitalized for community-acquired infections was assessed. Serum samples were obtained from adult inpatients with fever to determine the serum PCT level, C-reactive protein (CRP) level, and erythrocyte sedimentation rate (ESR). Of 165 patients, 22 (13%) had bacteremic episodes and 143 (87%) had nonbacteremic episodes. PCT levels, CRP levels, and ESRs were significantly higher in bacteremic patients than in nonbacteremic patients (P<.001,.007, and.024, respectively). The best cutoff value for PCT was 0.4 ng/mL, which was associated with a negative predictive value of 98.8%. Area under the receiver operating characteristic curve was 0.83 for PCT, which was significantly higher than that for CRP (0.68; P<.0001) and ESR (0.65; P<.05). A serum PCT level of <0.4 ng/mL accurately rules out the diagnosis of bacteremia. The use of PCT assessment could help physicians limit the number of blood cultures to be processed and the number of antibiotic prescriptions.

The management of leptospirosis.

How to quickly identify patients who should be treated for leptospirosis is a challenge. The interest of polymerase chain reaction (PCR) assays is currently being evaluated and rapid tests which can be used outside of the specialised laboratory, have recently been developed. Leptospires are sensitive to many antibiotics and few clinical studies have been made to compare different treatment options. Doxycycline is standard therapy in early leptospirosis treatment and chemoprophylaxis. Intravenous penicillin has been considered the drug of choice in late and severe disease, although it is now challenged by ceftriaxone, which use is easier. Ciprofloxacin may be combined with standard therapy in uveitis. Adjunctive therapies proposed in the management of severe forms of leptospirosis and Jarisch-Herxheimer reactions, are reviewed.

Lipschütz genital ulceration: a rare manifestation of paratyphoid fever.

In 1913, a distinctive clinical entity of acute genital ulcer occurring in an adolescent girl with a non-venereal infectious aetiology was described by Lipschütz. Since the initial description, several aetiologies have been discussed, and among them, paratyphoid fever is very uncommon. After her return from a trip, a 25-year-old girl developed high fever and diarrhoea. Examination of the vulva revealed a genital ulcer. The rest of the general examination was normal. Blood cultures identified Salmonella paratyphi A, and a diagnosis of Lipschütz's ulcer associated with paratyphoid fever was made. Bacteriaemia was then treated with antibiotics and the vulvar ulceration rapidly disappeared. Lipschütz described a distinctive clinical entity of acute genital ulcers occurring in adolescents. To our knowledge, we report herein the second case associated with proved paratyphoid fever. The authors thus recommend that typhoid or paratyphoid fever should be included in the differential diagnosis of genital ulcerations.

A subset of functional effector-memory CD8+ T lymphocytes in human immunodeficiency virus-infected patients.

CD8(+) T cells provide protective immune responses via both cytolytic and non-cytolytic mechanisms in subjects infected with human immunodeficiency virus (HIV). In the present study, we investigated the CD28 expression of CD8(+) T cells present in the peripheral blood lymphocyte subset isolated from chronically HIV-infected subjects. Using flow cytometric analysis, a continuous spectrum of CD28 intensity ranging from negative to high, which could be separated into CD28-negative, intermediate (int) and high, was seen for CD8(+) T cells. Our study focused mostly on the CD28(int) CD8(+) T cells. The CD28(int) CD8(+) T cells are CD57(-) CD27(+) CD45RO(+) CD45RA(-) CCR7(low) CD62L(int). The proliferative capacity of CD28(int) CD8(+) T cells was intermediate between those of CD28(-) CD8(+) T cells and CD28(high) CD8(+) T cells. The CD28(int) CD8(+) T cells are specific for HIV, cytomegalovirus (CMV) and Epstein-Barr virus (EBV) antigens as measured by human leucocyte antigen pentamer binding and produce both intracellular interferon-gamma and tumour necrosis factor-alpha in response to their cognate viral peptides. The CD28(int) CD8(+) T cells have HIV-specific, CMV-specific and EBV-specific cytotoxic activity in response to their cognate viral peptides. These findings indicate that a subset of functional effector-memory CD8(+) T cells specific for HIV, CMV and EBV antigens may contribute to an efficient immune response in HIV-infected subjects.

CXCR4-mediated T cell apoptosis in human immunodeficiency virus infection.

Mechanisms of CXCR4-mediated T lymphocyte apoptosis in human immunodeficiency virus (HIV) infection are poorly understood. The authors used peripheral blood mononuclear cells isolated from HIV type 1-infected subjects and assessed both CD4(+) and CD8(+) T cell apoptosis in the presence and absence of CXCR4 blockade by AMD3100. Both CD4(+) and CD8(+) T cell apoptosis could be inhibited by CXCR4 blockade, mostly in acquired immunodeficiency syndrome subjects and more weakly in asymptomatic HIV-positive subjects, and depended only partially on the syncytium-inducing/non-syncytium-inducing viral envelope phenotype. Immune activation of CD8(+), but not CD4(+), T cells was CXCR4-dependent, resulting in increased T cell apoptosis. In the presence of monocyte-derived macrophages, CXCR4-mediated apoptosis targeted mostly CD8(+) T cells, with CD4(+) T cells being more weakly affected. Several immune and viral factors thus play a role in CXCR4-mediated T cell apoptosis in HIV infection: CD4/CD8 phenotype, viral envelope phenotype, T cell activation and T cell-macrophage intercellular contacts.