An unusual presentation of pulmonary aspergilloma and review of available literature.

INTRODUCTION: Aspergilloma is a non-invasive form of pulmonary aspergillosis usually presenting as a clump of mold in pre-existing cavitary lung disease. Aspergillus related lung diseases have been classified into four types, whose manifestation is often related to previous lung diseases and host immunologic status. CASE REPORT: Cases of cavitary pulmonary aspergillosis without any evidence of pre-existing cavities, are rarely reported. We present here a case of pulmonary aspergillosis in which cavity formation appeared apparently after the establishment of infection. CONCLUSIONS: The occurrence of atypical presentations and the importance of recognizing these unusual cases of pulmonary aspergilloma is discussed.

Role of the innate immune system in host defence against fungal infections.

OBJECTIVE: The objective of this narrative review is to present a summary of current knowledge of host-fungal pathogen interaction focusing on the importance of the innate immune system in host defense against invasive fungal infections. In addition, the emergence of drug resistance in the treatment of invasive fungal infections has also been highlighted. MATERIALS AND METHODS: A literature review was conducted to identify articles documenting the role of the host innate immune system against fungal pathogen and the emergence of drug resistance in the treatment of invasive fungal infections. RESULTS: In this review, we provide an update from the most recent studies on the role of the host innate immune system against fungal pathogen and we also highlight the mechanisms that these pathogens use to evade the innate immune system. CONCLUSIONS: This review highlights the existence of different cellular mechanisms that, following the recognition of fungal PAMPS, induce the production of different sets of defense factors. The development of new diagnostic methods and antifungal drugs along with a better understanding of the host immune response are key approaches to controlling invasive fungal infections.

Protective role of IL-18 in host defenses against group B Streptococcus.

The aim of this study was to investigate the role of IL-18, a member of the IL-1 family, in group B Streptococcus (GBS) infection. Both in a neonatal and adult model of GBS infection, IL-18-deficient animals were significantly more susceptible to infection than WT animals. The lack of IL18 was associated with a marked reduction in IFN-γ-levels after bacterial stimulation but did not play a significant role in the recruitment of PMN to sites of GBS infection. Collectively, our data document a fundamental function of IL-18 signaling in boosting the host immune responses against GBS infection.

The interleukin-1ß/CXCL1/2/neutrophil axis mediates host protection against group B streptococcal infection.

Previous studies have indicated that group B streptococcus (GBS), a frequent human pathogen, potently induces the release of interleukin-1ß (IL-1ß), an important mediator of inflammatory responses. Since little is known about the role of this cytokine in GBS disease, we analyzed the outcome of infection in IL-1ß-deficient mice. These animals were markedly sensitive to GBS infection, with most of them dying under challenge conditions that caused no deaths in wild-type control mice. Lethality was due to the inability of the IL-1ß-deficient mice to control local GBS replication and dissemination to target organs, such as the brain and the kidneys. Moreover, in a model of inflammation induced by the intraperitoneal injection of killed GBS, a lack of IL-1ß was associated with selective impairment in the production of the neutrophil chemokines CXCL1 and CXCL2 and in neutrophil recruitment to the peritoneal cavity. Decreased blood neutrophil counts and impaired neutrophil recruitment to the brain and kidneys were also observed during GBS infection in IL-1ß-deficient mice concomitantly with a reduction in CXCL1 and CXCL2 tissue levels. Notably, the hypersusceptibility to GBS infection observed in the immune-deficient animals was recapitulated by neutrophil depletion with anti-Gr1 antibodies. Collectively, our data identify a cytokine circuit that involves IL-1ß-induced production of CXCL1 and CXCL2 and leads the recruitment of neutrophils to GBS infection sites. Moreover, our data point to an essential role of these cells in controlling the progression and outcome of GBS disease.

Topical distribution of initial paresis of the limbs to predict clinically relevant spasticity after ischemic stroke: a retrospective cohort study.

BACKGROUND: The degree of initial paresis relates to spasticity development in stroke patients. However, the importance of proximal and distal paresis in predicting spasticity after stroke is unclear. AIM: To investigate the role of topical distribution of initial limb paresis to predict clinically relevant spasticity in adults with stroke. DESIGN: Retrospective cohort study METHODS: Seventy-two first-ever ischemic stroke patients were examined. At the acute phase of illness, demographics and the European Stroke Scale motor items (maintenance of outstretched arm position, arm raising, wrist extension, grip strength, maintenance of outstretched leg position, leg flexion, foot dorsiflexion) were evaluated. At six months after the stroke onset, spasticity was assessed at the upper and lower limb with the modified Ashworth Scale. Clinically relevant spasticity was defined as modified Ashworth Scale ≥3 (0-5). RESULTS: The degree of initial paresis of the proximal muscles of the upper limb and the distal muscles of the lower limb showed the strongest association and the best profile of sensitivity-specificity in predicting clinically relevant spasticity at the upper and lower limb, respectively. Younger age showed higher risk for developing clinically relevant spasticity in the upper limb. CONCLUSIONS: Our findings support the hypothesis that the initial degree of proximal paresis of the upper limb and distal paresis of the lower limb as well as age may be considered early predictors of clinically relevant spasticity in adults with ischemic stroke. CLINICAL REHABILITATION IMPACT: Our findings further improve the role of initial paresis as predictor of spasticity after stroke.

Rehabilitation of brachial plexus injuries in adults and children.

Management of brachial plexus injury sequelae is a challenging issue in neurorehabilitation. In the last decades great strides have been made in the areas of early diagnosis and surgical techniques. Conversely, rehabilitation of brachial plexus injury is a relatively unexplored field. Some critical aspects regarding brachial plexus injury rehabilitation have to be acknowledged. First, brachial plexus injury may result in severe and chronic impairments in both adults and children, thus requiring an early and long-lasting treatment. Second, nerve damage causes a multifaceted clinical picture consisting of sensorimotor disturbances (pain, muscle atrophy, muscle weakness, secondary deformities) as well as reorganization of the Central Nervous System that may be associated with upper limb underuse, even in case of peripheral injured nerves repair. Finally, psychological problems and a lack of cooperation by the patient may limit rehabilitation effects and increase disability. In the present paper the literature concerning brachial plexus injury deficits and rehabilitation in both adults and children was reviewed and discussed. Although further research in this field is recommended, current evidence supports the potential role of rehabilitation in reducing both early and long-lasting disability. Furthermore, the complexity of the functional impairment necessitates an interdisciplinary approach incorporating various health professionals in order to optimizing outcomes.

Anti-idiotypic vaccination against group B streptococci.

We describe the antigenic properties of an anti-idiotypic single chain fragment variable (scFv) recombinant antibody mimicking the type III capsular polysaccharide of group B streptococci (GBS), an important cause of neonatal sepsis. This scFv could compete with the nominal antigen for binding to specific mouse or rabbit antibodies. Moreover, the scFv elicited, in mice, the production of antibodies which reacted against the type IlI polysaccharide and passively protected neonatal pups from GBS disease. Maternal immunization with the scFv also protected neonatal mice against GBS infection. Next, the scFv was expressed on the surface of the commensal bacterium Streptococcus gordonii. Intravaginal inoculation of mice with these recombinant bacteria induced significant elevations in serum titers of anti-GBS type III antibodies. Therefore, the expression scFv in commensal bacteria may be a convenient and effective way of delivering anti-idiotypic vaccines.