Francesco Scarlata

Asymptomatic Leishmania infantum/chagasi infection in blood donors of western Sicily

The purpose of this study was to evaluate whether the risk of transfusion-transmitted visceral leishmaniasis was present in an area of western Sicily where the incidence of the disease is higher than the regional average. From May to December 2005, 1449 blood donors from Agrigento district (Sicily, Italy) were screened for the presence of anti-Leishmania antibodies by an indirect immunofluorescent antibody test (IFAT). Blood samples from IFAT-positive donors were examined by PCR to detect Leishmania DNA. Anti-Leishmania antibodies were found in 11 (0.75%) cases, among which Leishmania DNA was detected from four (36.4%). Particular techniques to inactivate different pathogens would be considered mandatory in the case of immunosuppressed recipients.

Monocyte and Lymphocyte Apoptosis Resistance in Acute and Chronic Brucellosis and Its Possible Implications in Clinical Management

This study evaluated the level of susceptibility of monocytes and lymphocytes to spontaneously induced and CH11-induced apoptosis in 16 patients with Brucella infection. The expression of some immunological and apoptotic markers was evaluated. Before therapy, monocytes showed a high level of resistance to spontaneously induced or CH11-induced apoptosis in all patients. In patients with acute infection, this resistance persisted for 10-20 days after treatment was initiated, then decreased; in chronically infected patients, it persisted after 45 days of treatment. Lymphocytes were also more resistant to CH11-induced apoptosis. The level of activated CD8(+) T lymphocytes was high in patients with acute infection. The data indicate that the CD95-mediated apoptotic pathway is not involved in CH11 resistance. Lymphocytes are not infected by Brucella, so their resistance to apoptosis may be due to a soluble factor released by infected monocytes. The evaluation of levels of susceptibility to CH11-induced apoptosis in monocytes may be used to test the effectiveness of the therapy.

Treatment of Human Brucellosis with Rifampin plus Minocycline

Abstract In order to evaluate the efficacy and tolerability of a high intravenous dose of rifampin plus oral minocycline (administered daily for 3 weeks) for the treatment of acute brucellosis, we retrospectively reviewed the outcome of 239 consecutive patients (135 adults and 104 children) diagnosed and treated over a 17-year period in Italy. The combination used resulted in 100% response and a relapse rate lower than 2%. Fifty-two (30 adults and 22 children) (29.8%) complained of mild adverse effects including an increase in aspartate aminotransferase (>250 IU) observed in 12 cases and considered related to rifampin and in 11 cases a reversible hyperpigmentation of the tongue attributed to minocycline. A randomized prospective comparative study should be performed to confirm our encouraging results.

No Findings of Dental Defects in Children Treated with Minocycline

ABSTRACT Forty-one children <8 years of age treated for brucellosis with oral minocycline (2.5 mg/kg) twice daily for 3 weeks were recalled and examined to check for dental staining and defects. Dental staining and defects were found in 14 of 41 exposed children (34.1%) and in 30 of 82 matched controls (36.6%), respectively (P > 0.2).

Human toxocariasis: a report of nine cases.

Aim: Human toxocariasis is caused by infection with the larval stage of nematode parasites of dogs and cats, Toxocara canis or Toxocara cati. These helminths are not able to complete their life cycle in undefinitive hosts and so undergo aberrant migrations in the tissues causing a wide spectrum of signs and symptoms. Eosinophilia is often severe and sometimes represents the only sign of infection, except in ocular and neurological forms.

A case of Brucella endocarditis in association with subclavian artery thrombosis

Brucellosis is a common zoonosis, endemic in Mediterranean countries, and caused by bacteria of Brucella genus. Brucellosis is a systemic infection and the clinical presentation varies widely from asymptomatic and mild to severe disease. Cardiovascular complications are extremely rare. We present a case of arterial thrombosis in a previously healthy young patient with Brucella endocarditis. Careful attention must be paid to any sign or symptom of thrombosis in patients affected by brucellosis, regardless of the presence of endocarditis and cardiovascular risk factors.

Children, parents and Respiratory Syncytial Virus in Palermo, Italy: prevention is primary

A study was conducted to describe the characteristics of the Respiratory Syncytial Virus (RSV) infection cases occurring in the season 2006—7 in Palermo, Italy, and to evaluate the parents’ knowledge and behaviours concerning prevention and control of acute respiratory infections (ARIs). All children aged between 0 and 2 years, admitted for a lower respiratory tract infection (LRTI) between October 2006 and May 2007, were enrolled in the study. Data were collected about demographic and household characteristics. Furthermore, their parents were asked to compile a structured questionnaire on transmission, prevention and management of ARIs in children. A total of 198 children with a diagnosis of LRTI were enrolled. Ninety-eight (62.0%) of 157 were positive for RSV. Parents were generally aware of transmission of ARIs through sneezing and/or coughing, but less through contaminated objects or hands. Nationality, age and education level of parents and also the age of the patients proved to be associated with some self-reported knowledge and behaviours. Only 24 (12.3%) of the 195 respondents had received advice from GPs or paediatricians about good hygiene practices. It seems essential to implement public health interventions promoting behavioural changes aimed at the primary prevention of ARIs at the community level.

Visceral leishmaniasis, hypertriglyceridemia and secondary hemophagocytic lymphohistiocytosis.

cytokines, an upregulation of adhesion molecules and MHC I and II molecules on mono/macrophages, and an expansion of inflammatory monocytes. This exaggerated inflammatory response is responsible for necrosis and organ failure and results in uncontrolled proliferation and phagocytic activity of histiocytes [2]. Hypertriglyceridemia (fasting, greater than or equal to 265 mg/100 ml) is one of the current diagnostic criteria for HLH [2]. Several studies link hypertriglyceridemia to inhibition of lipoprotein lipase (LPL) by tumor necrosis factor-α (TNF-α), and TNF-α is a powerful autocrine and paracrine regulator of adipose tissue [3]. Indeed, many different sources of intense and prolonged T-lymphocyte/macrophage activation may be associated with dyslipidemia (particularly with hypertriglyceridemia) through inappropriate release of TNF-a, IFN-g, GM-CSF and respectively, of IL-1/IL-6, leading to adipose tissue lipolysis with increased VLDL secretion, decreased VLDL clearance, increased hepatic fatty acid synthesis, and suppression of fatty acid oxidation with HIV infection being the wellknown paradigm of this mechanism (possibly enhanced by some antiretroviral drugs). In PubMed there are at least 70 papers in which the association leishmaniasis/(hemophagocytic or haemophagocytic) is present. Leishmania parasites have been found to be the most common protozoan trigger of acquired HLH. In a multicenter prospective study conducted to determine the frequency of HLH syndrome in children with VL, ten children out of 24 (41 %) with VL developed HLH syndrome [4]. HLH incidence in European adult population is about 1/800,000/year, with a reported prevalence of parasitic infections of 2.4 % (53 out of 2197 subjects), and of Leishmania spp. of 0.77 % (17 out of 2197) as a trigger. The clinical picture of VL with HLH initially can be indistinguishable from HLH of other etiology, potentially Dear Sir,

Rickettsia typhi and Haemophagocytic Syndrome

We found the article by Pieracci et al. about Fatal FleaBorne Typhus in Texas very interesting. However, the diagnosis of secondary hemophagocytic lymphohistiocytosis (HLH) should also have been considered. HLH is a heterogeneous disorder that may be primary or secondary. The latter may be triggered by any severe infection, malignancy, or rheumatologic condition; it is diagnosed by five of eight of the following conditions: fever; splenomegaly; cytopenia (affecting 3 2 cell lineages); hypertriglyceridaemia and/or hypofibrinogenaemia; haemophagocytosis in the bone marrow, spleen, or lymph nodes; low or absent natural killer cell cytotoxicity; hyperferritinaemia; or elevated solubleCD25.HLH is considered adisorder due to a deficiency in cytolytic activity resulting in persistent activation of lymphocytesandhistiocytes. Thisexaggerated inflammatory response is responsible for necrosis and organ failure and results in uncontrolled proliferation and phagocytic activity of histiocytes. We found only a few articles describing cases of HLH in patientswithmurine typhus, butmanyarticles describe patients with severe or fatal forms of murine typhus in which a diagnosis of HLH should have been considered. Animal studies on the pathogenesis of infection with Rickettsia typhi, the causative agent ofmurine typhus, have shown that R. typhi enters macrophages, the major cellular source of tumor necrosis factor α (TNFα), interleukin 6 (IL-6), and interleukin 12 (IL-12). IL-6 and TNFα are critical for rapid response to tissue injury and infections, and induce the production of acute phase reactants in the liver, whereas IL-12 is the main inducer of interferon γ in natural killer and T cells. This cytokine assists in bacterial killing by activating macrophage bactericidal functions. Death ofR. typhi-infected CB17 severe combined immunodeficiencymice ismost likely due to overwhelming systemic inflammation driven by macrophages and other cells. HLH is a life-threatening syndrome. Liver involvement may be present with variable levels of transaminitis progressing to acute liver failure and coagulopathy; respiratory insufficiency represents a negative prognostic sign. HLH can be triggered by rickettsial diseases. It should remembered that the identification of hemophagocytosis in bone marrow aspirates represents only one of the criteria needed for the diagnosis of HLH and that a bone marrow aspirate lacking hemophagocytosis does not rule out the diagnosis. HLH should be suspected in every patient with rickettsial diseases, especially with respiratory distress or multiorgan dysfunction. Appropriate therapy (dexamethasone, cyclosporin, and etoposide) could save the patient in those cases inwhich the pathogen-direct therapyhasnotbeensufficientby itself tocontrol the disease.