Neonatal adenoviral infection: a seventeen year experience and review of the literature.

OBJECTIVES: To describe the clinical manifestations and short-term outcomes of adenoviral infections in neonates and review all published cases to better determine impact and treatment outcomes. STUDY DESIGN: Retrospective cohort study of all neonates hospitalized at Children's Medical Center (CMC) and Parkland Memorial Hospital (PMH), Dallas, TX with laboratory-confirmed adenoviral infection from January 1,1995-December 31, 2012. Neonates were identified by review of the CMC Virology Laboratory's prospective database of all positive adenovirus tests performed in the inpatient and ambulatory settings, and at PMH, of a prospective neonatal database that included all neonatal intensive care unit admissions. Patients also were identified by discharge International Classification of Disease, 9th edition codes for adenoviral infection. The medical records were reviewed, and a review of the English literature was performed. RESULTS: During 17 years, 26 neonates had adenoviral infection (25, CMC; 1, PMH). The principle reasons for hospitalization were respiratory signs (88%) and temperature instability (65%). Five (19%) had disseminated disease and 4 (80%) of these infants died. Ribavirin or cidofovir treatment, as well as immune globulin intravenous, did not improve outcomes except in 1 neonate. Literature review (n = 72) combined with our data found that disseminated infection was associated with death (68% vs 21% with localized infection, P < .001). In addition, neonates <14 days of age were more likely to have disseminated disease (44% vs 12%, P = .004) and death (48% vs 8%; P < .001). CONCLUSION: Adenoviral infection in hospitalized neonates was associated with severe morbidity and mortality, especially when infection was disseminated and involved the respiratory tract. Development of new therapeutic strategies is needed.

Comparison of the effects of Puumala and Dobrava viruses on early and long-term renal outcomes in patients with haemorrhagic fever with renal syndrome.

AIM: The clinical course and outcome of patients with haemorrhagic fever with renal syndrome (HFRS) caused by Puumala (PUUV) and Dobrava viruses (DOBV) were analyzed and whether it left long-term consequences on kidney function after 10 years was evaluated. METHODS: Cross-sectional studies were conducted to test the kidney function and blood pressure of HFRS-affected patients and to follow them up 10 years after. Eighty-two PUUV- and 53 DOBV-induced HFRS patients and 14 and 31 participants 10 years after having contracted PUUV- and DOBV-related diseases, respectively were evaluated. RESULTS: Serum creatinine concentrations were 279.5 and 410 mcmol/L in PUUV and DOBV groups, respectively (P = 0.005). There were six and 13 anuric (P < 0.05), none and seven dialysis-dependant (P < 0.05), and nine and 18 hypotensive patients (P < 0.05) in PUUV and DOBV groups, respectively. After 10 years, glomerular filtration rates were 122.1 + or - 11.1 and 104.7 + or - 20.2 mL/min (P < 0.05) in PUUV and DOBV groups, respectively. CONCLUSION: During the acute phase, DOBV causes more severe renal impairment than PUUV infection. After 10 years follow up, renal function was found within normal limits, although after DOBV infection glomerular filtration rate (GFR) was significantly lower than after PUUV infection.

Serum thrombospondin-1 is altered in patients with hemorrhagic fever with renal syndrome.

Hemorrhagic fever with renal syndrome (HFRS) is a severe acute viral disease with pathological changes of impaired capillary and small vessels and thrombocytopenia. In this study, serum thrombospondin (TSP)-1 concentration in patients with HFRS was determined to explore its possible role in the pathogenesis of HFRS. The concentration of TSP-1 was measured using a competitive enzyme-linked immunoabsorbent assay. Significantly decreased levels of serum TSP-1 were observed in HFRS patients at febrile and hypotensive phases compared with those in the controls. The serum levels of TSP-1 in HFRS patients with more severe clinical types was reduced more profoundly than those in patients with milder clinical types at febrile and hypotensive phases, although the differences in TSP-1 were not significant. It was indicated that insufficient production or increased consumption of TSP-1, or both of these, may contribute to the impairment of capillary and small vessels and the development of hypotension at the early stage of HFRS, and the decreased degree may be associated with disease severity.

Lethal enterovirus-induced myocarditis and pancreatitis in a 4-month-old boy.

After inconspicuous pregnancy and birth, a 16-year-old mother presented her male baby 5 days later with severe diarrhoea and vomiting. During the following weeks, the child temporarily showed hypotension, hypothermia and increased body temperature, bradyarrythmia with apnoea, continuing diarrhoea, sometimes vomiting and developed signs of pancreatic insufficiency. Due to increasing loss of weight and obviously severe dystrophia, parenteral nutrition had to be initiated. All clinical investigations revealed no underlying disease. Numerous biopsies, mainly from the gastrointestinal tract were taken, but no relevant pathological findings were disclosed. The baby was found lifeless by his mother, 4 months after birth. According to the death certificate, the physicians regarded the lethal outcome as a case of sudden infant death syndrome (SIDS). Histological and immunohistochemical investigations of organ samples revealed signs of myocarditis, pancreatitis and focal pneumonia. Molecularpathological techniques were used to detect enterovirus RNA from tissue samples from the myocardium, liver and pancreas. Enteroviral myocarditis with concomitant pancreatitis was determined as cause of death.

Spectrum of hantavirus infection: hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome.

Hantaviruses chronically infect rodents without apparent disease, but when they are spread by aerosolized excreta to humans, two major clinical syndromes result: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Both diseases appear to be immunopathologic, and inflammatory mediators are important in causing the clinical manifestations. In HPS, T cells act on heavily infected pulmonary endothelium, and it is suspected that gamma interferon and tumor necrosis factor are major agents of a reversible increase in vascular permeability that leads to severe, noncardiogenic pulmonary edema. HFRS has prominent systemic manifestations. The retroperitoneum is a major site of vascular leak and the kidneys suffer tubular necrosis. Both syndromes are accompanied by myocardial depression and hypotension or shock. HFRS is primarily a Eurasian disease, whereas HPS appears to be confined to the Americas; these geographic distinctions correlate with the phylogenies of the rodent hosts and the viruses that coevolved with them.