The 2009 H1N1 influenza virus (formerly known as swine flu) first appeared in Mexico and the United States in March and April 2009 and has swept the globe with unprecedented speed as a result of airline travel. On June 11, 2009, the World Health Organization raised its pandemic level to the highest level, Phase 6, indicating widespread community transmission on at least two continents. The 2009 H1N1 virus contains a unique combination of gene segments from human, swine and avian influenza A viruses. Children and young adults appear to be the most affected, perhaps reflecting protection in the elderly owing to exposure to H1N1 strains before 1957. Most clinical disease is relatively mild but complications leading to hospitalization, with the need for intensive care, can occur, especially in very young children, during pregnancy, in morbid obesity, and in those with underlying medical conditions such as chronic lung and cardiac diseases, diabetes, and immunosuppression. Bacterial coinfection has played a significant role in fatal cases. The case of fatality has been estimated at around 0.4%. Mathematical modeling suggests that the effect of novel influenza virus can be reduced by immunization, but the question remains: can we produce enough H1N1 vaccine to beat the pandemic?

Herpes Simplex Encephalitis (HSE) is one of the commonest viral encephalitis and its recurrence is being increasingly reported were HSE relapse rate came up to 5%. Both herpes simplex virus (HSV) types can lead to encephalitis and it was established that HSV-1 is capable of nervous system invasion, latency, and recurrence. The recurrence of HSE used to be attributed to immunological compromise, but reports show many cases have no obvious immune system impairment. Further investigations revealed genetic predispositions to HSV infection that would explain the host vulnerability to its recurrence. In this review, we discuss the gene mutations that may predispose to recurrent HSE and the importance of early diagnosis and treatment.

The Bacillus Calmette-Guérin (BCG) vaccine contains live attenuated Mycobacte-rium bovis; was first used in humans to prevent tuberculosis (TB) in 1921. The World Health Organization (WHO) established the Expanded Program on Immunization in 1974 to ensure that all children have access to routinely recommended vaccines including BCG. Each year 120 million doses of BCG vaccine are administered worldwide. Intradermal BCG vaccine gives rise to a classic primary complex that consists of a cutaneous nodule at the site of injection and subclinical involvement of the regional lymph nodes, which is self-limiting and requires no treatment. However, ipsilateral regional lymph node enlargement may follow BCG vaccine and is consid-ered as the most common complication, some progress to suppuration. Rarely a disseminated BCG infection may develop in immunocompromised individuals resulting in a devastating outcome. Within the last decades, variable strategies have been applied in treating lymphad-enitis related to BCG vaccine, ranging from observation, anti-mycobacterial therapy, aspiration, incision and drainage to lymph node surgical excision. We are presenting these guidelines that intended to optimize and standardize management of various types of BCG related lymph adenitis in children. They are based upon the best avail-able evidence in literature beside our experience in this field.

Human metapneumovirus (hMPV) and the Netherlands human coronavirus (HCoV-NL63) have been isolated from children with respiratory tract infection. The prevalence of these viruses has not been reported from Saudi Arabia. We sought to determine whether hMPV and HCoV-NL63 are responsible for acute respiratory illness and also to determine clinical features and severity of illness in the hospitalized pediatric patient population. Prospective hospital-based study from July 2007 to November 2008. Nasopharyngeal specimens from children less than 16 years old who were suffering from acute respiratory diseases were tested for hMPV and HCoV-NL63 by reverse transcriptase-polymerase chain reaction. Samples were collected from July 2007 to November 2008. Both viruses were found among Saudi children with upper and lower respiratory tract diseases during the autumn and winter of 2007 and 2008, contributing to 11.1% of all viral diagnoses, with individual incidences of 8.3% (hMPV) and 2.8% (HCoV-NL63) among 489 specimens. Initial symptoms included fever, cough, and nasal congestion. Lower respiratory tract disease occurs in immunocompromised individuals and those with underlying conditions. Clinical findings of respiratory failure and culture-negative shock were established in 7 children infected with hMPV and having hematologic malignancies, myelofibrosis, Gaucher disease, and congenital immunodeficiency; 2 of the 7 patients died with acute respiratory failure. All children infected with HCoV-NL63 had underlying conditions; 1 of the 4 patients developed respiratory failure. hMPV and HCoV-NL63 are important causes of acute respiratory illness among hospitalized Saudi children. hMPV infection in the lower respiratory tract is associated with morbidity and mortality in immunocompromised children. HCoV-NL63 may cause severe lower respiratory disease with underlying conditions.

BACKGROUND AND OBJECTIVES: Stem cells from umbilical cord blood (CB) have increasingly become a viable alternate source of progenitor cells for hematopoietic cell transplantation (HSCT). Cytomegalovirus (CMV) is thought to contribute significantly to HSCT morbidity and mortality. DESIGN AND SETTING: Retrospective case-control study in patients at tertiary care center. PATIENTS AND METHODS: We determined the incidence, risk factors and outcomes for CMV infection and disease after unrelated cord blood transplantation (UCBT) in children. RESULTS: Between 2003 and 2007, 73 pediatric patients underwent UCBT and 68% of recipients were CMV seropositive. The overall incidence of CMV infection, early and late CMV infection was 58.9% (43/73), 62.8% (27/43), and 37.4% (16/43), respectively. In patients with early CMV infection, 6 of 27 (22%) patients progressed to develop CMV end-organ disease including pneumonitis and retinitis. High levels CMV antigenemia ≥70 infected cells by pp65 antigenemia assay + PMNs, P =.237) were associated with a higher risk of progression to CMV disease. The development of CMV infections was higher in CMV-seropositive recipients ( P <.001) and in those who developed graft-versus-host-diseases (GVHD) ( P <.001). Other risk factors for CMV infection include the use of high-dose corticosteroids ( P <.001) and older age of the recipient at the time of transplant ( P <.002). Late CMV infection was strongly associated with a previous history of early CMV infection ( P <.001). CONCLUSION: CMV infection is a significant complication in UCBT recipients in pediatric patients and is associated with an increase in transplant-related morbidity and mortality. Risk factors for CMV infections after UCBT include GVHD, use of corticosteroids, underlying diseases (hematologic malignancies) and older age. Late CMV infection was strongly associated with a previous history of CMV infection.