Cerebral venous sinus thrombosis and skull base osteomyelitis as manifestations of cat-scratch disease in a pediatric patient: A case report and literature review.

Cat-scratch disease (CSD) is caused by Bartonella henselae and usually presents with regional lymphadenopathy. Skull base osteomyelitis and cerebral venous sinus thrombosis are rarely reported, particularly in immunocompetent children. CSD should be considered in the differential diagnosis of any patient with persistent headaches in the setting of cat exposure.

Safety and immunogenicity of live attenuated and inactivated influenza vaccines in children with cancer.

BACKGROUND: The safety and immunogenicity of live, attenuated influenza vaccine (LAIV) has not been compared to that of the standard trivalent inactivated vaccine (TIV) in children with cancer. METHODS: Randomized study of LAIV versus TIV in children with cancer, age 2-21 years, vaccinated according to recommendations based on age and prior vaccination. Data on reactogenicity and other adverse events and blood and nasal swab samples were obtained following vaccination. RESULTS: Fifty-five eligible subjects (mean age, 10.4 years) received vaccine (28 LAIV/27 TIV). Both vaccines were well tolerated. Rhinorrhea reported within 10 days of vaccination was similar in both groups (36% LAIV vs 33% TIV, P > .999). Ten LAIV recipients shed virus; the latest viral shedding was detected 7 days after vaccination. Immunogenicity data were available for 52 subjects, or 26 in each group. TIV induced significantly higher postvaccination geometric mean titers against influenza A viruses (P < .001), greater seroprotection against influenza A/H1N1 (P = .01), and greater seroconversion against A/H3N2 (P = .004), compared with LAIV. No differences after vaccination were observed against influenza B viruses. CONCLUSIONS: As expected, serum antibody response against influenza A strains were greater with TIV than with LAIV in children with cancer. Both vaccines were well tolerated, and prolonged viral shedding after LAIV was not detected. CLINICAL TRIALS REGISTRATION: NCT00906750.

Life-Threatening Infectious Complications in Sickle Cell Disease: A Concise Narrative Review.

Sickle cell disease (SCD) results in chronic hemolytic anemia, recurrent vascular occlusion, insidious vital organ deterioration, early mortality, and diminished quality of life. Life-threatening acute physiologic crises may occur on a background of progressive diminishing vital organ function. Sickle hemoglobin polymerizes in the deoxygenated state, resulting in erythrocyte membrane deformation, vascular occlusion, and hemolysis. Vascular occlusion and increased blood viscosity results in functional asplenia and immune deficiency in early childhood, resulting in life-long increased susceptibility to serious bacterial infections. Infection remains a main cause of overall mortality in patients with SCD in low- and middle-income countries due to increased exposure to pathogens, increased co-morbidities such as malnutrition, lower vaccination rates, and diminished access to definitive care, including antibiotics and blood. Thus, the greatest gains in preventing infection-associated mortality can be achieved by addressing these factors for SCD patients in austere environments. In contrast, in high-income countries, perinatal diagnosis of SCD, antimicrobial prophylaxis, vaccination, aggressive use of antibiotics for febrile episodes, and the availability of contemporary critical care resources have resulted in a significant reduction in deaths from infection; however, chronic organ injury is problematic. All clinicians, regardless of their discipline, who assume the care of SCD patients must understand the importance of infectious disease as a contributor to death and disability. In this concise narrative review, we summarize the data that describes the importance of infectious diseases as a contributor to death and disability in SCD and discuss pathophysiology, prevalent organisms, prevention, management of acute episodes of critical illness, and ongoing care.

Murine typhus as a cause of cognitive impairment: case report and a review of the literature.

BACKGROUND: Murine typhus is a systemic febrile illness caused by Rickettsia typhi, a gram-negative, obligate intracellular bacterium. It is found worldwide, including in the United States, where cases are concentrated in suburban areas of Texas and California. The disease manifests with fever, headache, and rash. Central nervous system involvement is rare in both adults and children. Aseptic meningitis and meningoencephalitis are the most common neurological presentations, occurring in 2% to 5% of cases. Neurological dysfunction, including memory impairment and behavioral alterations, can occur and usually are reversible. Long-term deficits are considered rare even in untreated cases and have not been described in the pediatric population. METHODS: Single case report. RESULTS: We describe a previously healthy 17-year-old girl infected with R. typhi who developed meningoencephalitis that resulted in chronic cognitive impairment despite treatment. CONCLUSION: Murine typhus should be considered in the differential diagnosis of aseptic meningitis and meningoencephalitis. Early diagnosis and treatment can prevent death and long-term morbidity.

Seasonal and pandemic influenza: an overview with pediatric focus.

Influenza is an important cause of respiratory illness in children, who have the highest attack rates during the annual influenza outbreaks [60]. Clinical infection ranges from subclinical illness to complicated disease that affects multiple organs. Annual vaccination remains the most effective strategy for the prevention and control of influenza [2]. Recently developed antiviral drugs offer new approaches to the prevention and treatment of influenza.

Clinical and demographic characteristics of seasonal influenza in pediatric patients with cancer.

BACKGROUND: Changes in oncology care and the diagnosis and management of influenza over the past several decades may have altered the epidemiology and outcomes of influenza in pediatric oncology patients. METHODS: The clinical features and outcomes of 102 pediatric patients undergoing cancer therapy during 107 episodes of influenza between January 2002 and April 2009 were retrospectively ascertained. RESULTS: Median age at the time of influenza was 7.2 years (interquartile range: 3.8-11.2 years); 46% of patients were male. Nineteen patients (18%) were recipients of hematopoietic stem cell transplants. Patients' median absolute neutrophil and lymphocyte counts were 1300/µL (interquartile range: 500-2967/µL) and 360/µL (interquartile range: 180-836/µL), respectively. Twelve patients (11%) had coinfections with influenza and one or more other respiratory pathogens. Influenza prompted patients' hospitalization during 64% of episodes, and 75% received antiviral therapy. Complications occurred in 30% of infections and serious complications occurred in 7%. Three patients died, but no deaths were directly attributable to influenza. Most patients had delays in cancer therapy; the median delay was 5 days. Neutropenia, concurrent infection, increasing age and having received hematopoietic stem cell transplant increased the risk of serious complications. CONCLUSIONS: Advances in the management of pediatric cancer and influenza have not altered the epidemiology and outcome of influenza in oncology patients. Clinical features identify subgroups of patients with influenza who are at risk of poor outcomes and those with a good prognosis.

Oseltamivir-resistant influenza A and B viruses pre- and postantiviral therapy in children and young adults with cancer.

BACKGROUND: Immunocompromised patients are highly susceptible to influenza infection and can have prolonged viral shedding, which is a risk factor for the development of antiviral resistance. METHODS: We investigated the emergence of oseltamivir-resistant influenza variants in children and young adults with cancer during the 2002-2008 influenza seasons. The demographic and clinical features of influenza infections in 12 patients who had viral isolates obtained before and after oseltamivir therapy was initiated were studied. Antiviral susceptibilities were determined by the fluorescence-based neuraminidase (NA) enzyme inhibition assay and by sequencing genes encoding NA and matrix M2 proteins. RESULTS: The mean age of patients was 10.5 (range, 1.1-23.0) years. Ten patients had hematologic malignancies, 4 were recipients of hematopoietic stem cell transplants, and all patients were receiving immunosuppressive therapy. Eleven patients had prolonged respiratory symptoms and 8 had prolonged viral shedding. Serial viral isolates were available for 8 of 12 patients. Oseltamivir-resistant influenza viruses were isolated from 4 children (3 influenza A [H3N2] and 1 influenza B virus): before the initiation of antiviral therapy in 2 patients and during therapy in the other 2 patients. Three resistant influenza A (H3N2) viruses shared a common E119V NA mutation. One patient was infected with oseltamivir-resistant influenza B virus (IC50, 731.86 ± 155.12 nM) that harbored a N294S NA mutation, the first report of this mutation in influenza B viruses. CONCLUSIONS: Oseltamivir-resistant influenza viruses can exist before or rapidly emerge during antiviral therapy in immunocompromised individuals, and this has important implications for therapy and infection control.