Obesity is a significant risk factor for influenza virus infection. However, little is known about obesity and secondary bacterial coinfections; the major cause of morbidity and mortality. Obesity increases inflammation, alters immune response and decreases wound repair in the lungs of obese mice infected with influenza virus, all risk factors for bacterial colonization. Therefore, we questioned the effect of obesity on secondary bacterial pneumonia. Infection of lean and obese mice with a nonlethal dose of influenza virus followed by a nonlethal dose of Streptococcus pneumoniae resulted in 100% mortality in obese mice by day 3 post bacterial challenge with no loss of lean controls. No differences were observed in viral titers between groups; however, lung bacterial titers were significantly increased in obese animals. Histological analysis revealed widespread damage to the lungs of obese mice. Obesity increases the severity and mortality from influenza‐associated complications and secondary bacterial pneumonia may be greatly enhanced in an increasingly obese human population. Further study is necessary to determine the mechanisms of increased susceptibility to influenza, secondary bacterial infection and possible therapeutic strategies in this expanding risk group. Grant Funding Source : NIH NIAID contract number HHSN266200700005C and the American Lebanese Syrian Associated Charities (ALSAC)