Increased mortality from influenza infection in long-chain acyl-CoA dehydrogenase knockout mice.

We previously showed that the mitochondrial fatty acid oxidation enzyme long-chain acyl-CoA dehydrogenase (LCAD) is expressed in alveolar type II pneumocytes and that LCAD-/- mice have altered breathing mechanics and surfactant defects. Here, we hypothesized that LCAD-/- mice would be susceptible to influenza infection. Indeed, LCAD-/- mice demonstrated increased mortality following infection with 2009 pandemic influenza (A/CA/07/09). However, the mortality was not due to increased lung injury, as inflammatory cell counts, viral titers, and histology scores all showed non-significant trends toward milder injury in LCAD-/- mice. To confirm this, LCAD-/- were infected with a second, mouse-adapted H1N1 virus (A/PR/8/34), to which they responded with significantly less lung injury. While both strains become increasingly hypoglycemic over the first week post-infection, LCAD-/- mice lose body weight more rapidly than wild-type mice. Surprisingly, while acutely fasted LCAD-/- mice develop hepatic steatosis, influenza-infected LCAD-/- mice do not. They do, however, become more hypothermic than wild-type mice and demonstrate increased blood lactate values. We conclude that LCAD-/- mice succumb to influenza from bioenergetic starvation, likely due to increased reliance upon glucose for energy.

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.

Prolonged hypothermia following respiratory syncytial viral infection in infancy.

Following proven respiratory syncytial viral infection, a previously healthy 2 year old boy displayed notable persistent hypothermia-the lowest temperature being 34.2 degrees C. No obvious ill effects were observed.