BURKHOLDERIA PSEUDOMALLEI BIOFILM PLAYS A KEY ROLE IN CHRONIC INFLAMMATION IN C57BL/6 MICE.

Burkholderia pseudomallei is a causative agent of melioidosis. Clinical signs of melioidosis vary from acute septicemia to chronic inflammation or subclinical infection. This study investigated the role of B. pseudomallei biofilm in chronic inflammation in lungs of infected C57BL/6 mice. Low doses of B. pseudomallei H777 and its biofilm defective M10 mutant were fed intra-gastrically to C57BL/6 mice and inflammatory responses were investigated by histopathological techniques. Two hundred colony forming units (CFUs) of B. pseudomallei H777 induced chronic inflammatory responses in mice on day 20 post-infection, with discrete interstitial infiltration by mononuclear inflammatory cells. On day 40 postinfection, there were marked thickening of alveolar septa and congested capillaries, which increased in severity by day 60. On the other hand, mice infected with B. pseudomallei M10 showed less mononuclear infiltration. The results indicate that B. pseudomallei defective in biofilm production gave rise to less severe pathology, resulting a higher rate of survival in infected mice; and pulmonary melioidosis could be developed in C57BL/6 mice by intra-gastric feeding makes it a possible animal model of chronic human melioidosis.

Relapsed Melioidosis Model in C57BL/6 Mice.

BACKGROUND: Burkholderia pseudomallei are the causative agents of melioidosis, a disease that has a high relapse rate in endemic areas. The mechanism of relapse is unclear OBJECTIVE: This study aimed to establish relapsed melioidosis in C57BL/6 mice by induction with B. pseudomallei. MATERIAL AND METHOD: Low doses of B. pseudomallei H777 and its biofilm defective mutant (M10) were intra-gastric fed to C57BL/6 mice. All the infected mice had suppressed immune status by intra-peritoneal injection of hydrocortisone at 2.5 mg per mouse at day 60 post-infection. Inflammatory response to the infection was investigated by histo-pathological studies and monitoring bacterial counts in the blood and organs. RESULTS: All the infected mice were found to have a high infiltration of mononuclear cells at day 60 post-infection. The results showed high bacterial counts in the blood in both strains post-suppressed immune status after two days. The biofilm mutant and wild type strains produced relapse in C57BL/6 mice but the latter was responsible for significantly more severe inflammation than the biofilm mutant. CONCLUSION: Low immune status may cause relapsed melioidosis in hosts with chronic inflammation.