Host response to mixed anaerobic infection with Bacteroides melaninogenicus and Fusobacterium necrophorum

Infection ◽  
1983 ◽  
Vol 11 (1) ◽  
pp. 35-40 ◽  
Author(s):  
R. E. McCallum ◽  
Renate Urbaschek ◽  
B. Ditter ◽  
B. Urbaschek
2013 ◽  
Vol 62 (11) ◽  
pp. 1755-1759 ◽  
Author(s):  
Kentaro Nagaoka ◽  
Katsunori Yanagihara ◽  
Yosuke Harada ◽  
Koichi Yamada ◽  
Yohei Migiyama ◽  
...  

Anaerobic bacterial infection is often accompanied by abscess formation; however, few in vivo studies have been published with descriptive data specifically evaluating antimicrobial activity in the presence of abscesses. The aim of this study was to establish a murine model of anaerobic infection with abscess formation and to verify the utility of this model for evaluating the in vivo efficacy of an antimicrobial agent. A clinical isolate of Fusobacterium necrophorum was inoculated into the caudal vein of immunocompetent BALB/c mice at 108 c.f.u. per mouse. Changes in body weight, bacterial load and histopathology of key organs were evaluated. After inoculation, bacterial counts in the liver increased from 104 to 108 c.f.u. after 1–3 days, and liver abscess formation was observed on the day following infection. Abscess formation and bacterial growth were not observed in other organs. In this model, 3 days of treatment with 5 mg metronidazole kg−1 eradicated F. necrophorum in the liver; however, a reduction in bacterial load was not observed with 0.05 mg metronidazole kg−1. In this study, we established a novel murine model of F. necrophorum liver abscess via haematogenous infection that may be useful for investigating in vivo antimicrobial activity against anaerobic abscesses and understanding the pathogenesis of F. necrophorum infection.


2018 ◽  
Vol 3 (3) ◽  

Tonsillitis is a frequently encountered pathology in the outpatient setting, usually caused by viruses [1]. When bacterial, the most common causatory microbe is streptococcus group A [1]. Tonsillar and peritonsillar abscess (PTA) on the other hand are never viral, and are usually caused by streptococcus pyogenes, Streptococcus melleri, fusobacterium necrophorum and staphylococci [1,2]. The overall incidence of PTA is suggested to be 37/100,000 patients, with the highest incidence between ages 14-21 at 124/100,000 [3].


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