ABSTRACT
Pasteurellosis is a zoonosis often caused by cat or dog bites or scratches, or by direct exposure to their secretions. Pasteurella multocida is the main pathogen involved in infections through domestic animal bites; generally a local infection characterized by its particular virulence with consequent rapid onset. Serious infection has also been reported in persons affected by comorbidity without domestic animal bite injuries. Here we report the case of a woman with lower limb exudating vesicular skin ulcers affected by liver cirrhosis, bilateral knee arthritis, septicemia with positive blood culture and synovial fluid culture for Pasteurella multocida. The etiology of Pasteurella multocida must be borne in mind in cases of sepsis in immunodeficient individuals, such as the cirrhotic patient, as well as exposure to domestic animals.
Subject(s)
Immunocompromised Host , Liver Cirrhosis/complications , Pasteurella Infections/complications , Pasteurella multocida , Skin Ulcer/complications , Aged , Animals , Animals, Domestic/microbiology , Anti-Bacterial Agents/therapeutic use , Arthritis, Infectious/microbiology , Dogs , Fatal Outcome , Female , Humans , Liver Cirrhosis/microbiology , Lower Extremity , Opportunistic Infections/transmission , Pasteurella Infections/drug therapy , Pasteurella Infections/immunology , Sepsis/etiology , Skin Ulcer/microbiology , Synovial Fluid/microbiologyABSTRACT
The frequency of early-onset neonatal sepsis without prophylaxis is 1-5/1.000 live births. Since year '70 the most frequent causative microorganism is the group B Streptococcus (S. agalactiae, GBS), followed by Escherichia coli. The mortality rate is now reduced to 4% due to the improvement of neonatal intensive care. In the USA, the incidence of GBS early-onset neonatal sepsis has been markedly reduced by the application of the guidelines released by the Centers for Disease Control (CDC). This strategy, however, is not effective on occurrence of late-onset neonatal group B streptococcal disease. In Italy, the application of CDC guidelines is not customary, and different, often complex, protocols of obstetrical-neonatological integrated approach are applied. The frequency of infectious risk has made the GBS a paramount problem for the neonatologist, even for the legal responsibility issues resulting from the multiplicity of possible options. To reach the best level of protection of the newborn against early-onset GBS infection, the working group of providers of prenatal, obstetric, and neonatal care of the functional area of Cuneo issued an integrated protocol, in order to perform the GBS screening with the optimal culture method suggested by CDC guidelines in the highest possible number of pregnant women, and to standardize the obstetrical and neonatal management.
Subject(s)
Pregnancy Complications, Infectious/diagnosis , Streptococcal Infections/prevention & control , Streptococcus agalactiae , Adult , Age Factors , Algorithms , Anti-Bacterial Agents/pharmacology , Clindamycin/pharmacology , Clinical Protocols , Erythromycin/pharmacology , Female , Humans , Infant, Newborn , Intensive Care, Neonatal , Italy , Microbial Sensitivity Tests , Practice Guidelines as Topic , Pregnancy , Prevalence , Rectum/microbiology , Risk Factors , Streptococcal Infections/diagnosis , Streptococcal Infections/epidemiology , Streptococcal Infections/mortality , Streptococcal Infections/transmission , Streptococcus agalactiae/drug effects , Streptococcus agalactiae/isolation & purification , United States , Vagina/microbiologyABSTRACT
An early presentation of heparan N-sulphatase (SGSH) deficiency (mucopolysaccharidosis IIIA, MPS IIIA) with a prominent and isolated hepato-splenomegaly is described. Molecular analysis detected a nonsense mutation (Y40X) and two de novo missense mutations (E300V; Q307P).
Subject(s)
Codon, Nonsense , Mucopolysaccharidosis III/diagnosis , Mucopolysaccharidosis III/genetics , Mutation, Missense , Sulfatases/deficiency , Sulfatases/genetics , Echocardiography , Female , Hepatomegaly/diagnosis , Hepatomegaly/genetics , Humans , Infant , Piperazines/pharmacology , Purines , Sildenafil Citrate , Splenomegaly/diagnosis , Splenomegaly/genetics , Sulfones , Time Factors , Vasodilator Agents/pharmacologyABSTRACT
We report two cases of Acremonium fungemia with proven involvement of the skin and probably of the lung in patients who were both undergoing chemotherapy, one for mantle cell lymphoma and the other for acute lymphoblastic leukemia. Both patients failed amphotericin B deoxycholate treatment and were successfully treated with voriconazole with very mild toxicity.
Subject(s)
Acremonium/drug effects , Antifungal Agents/therapeutic use , Fungemia/drug therapy , Opportunistic Infections/drug therapy , Pyrimidines/therapeutic use , Triazoles/therapeutic use , Amphotericin B/pharmacology , Amphotericin B/therapeutic use , Antifungal Agents/administration & dosage , Antifungal Agents/pharmacology , Antineoplastic Agents/therapeutic use , Female , Fungemia/microbiology , Humans , Lymphoma, Mantle-Cell/complications , Lymphoma, Mantle-Cell/drug therapy , Middle Aged , Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications , Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy , Pyrimidines/administration & dosage , Pyrimidines/pharmacology , Triazoles/administration & dosage , Triazoles/pharmacology , VoriconazoleABSTRACT
The management of invasive aspergillosis in patients with hematological malignancies remains controversial. A major problem is how to manage patients who had invasive aspergillosis during remission induction and consolidation therapy and then undergo SCT. Indeed in these patients the mortality rate related to invasive aspergillosis recurrence remains unacceptably high. We report two cases of patients who underwent remission induction for AML, developed invasive aspergillosis during antifungal prophylaxis with itraconazole, failed amphotericin B deoxycholate and liposomal amphotericin B treatment, were successfully treated with voriconazole and eventually underwent SCT with voriconazole prophylaxis without reactivation of invasive aspergillosis.
