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J Med Microbiol 57 (2008), 210-217; DOI: 10.1099/jmm.0.47624-0
© 2008 Society for General Microbiology
ISSN 1473-5644

Histopathological and ultrastructural studies of a mouse lung model of Campylobacter jejuni infection

Nadia A. Al-Banna1, Thamradeen A. Junaid2, T. Chacko Mathew3, Raj Raghupathy1 and M. John Albert1

1 Department of Microbiology, Faculty of Medicine, Kuwait University, Kuwait

2 Department of Pathology, Faculty of Medicine, Kuwait University, Kuwait

3 Department of Medical Laboratory Sciences, Faculty of Allied Health Sciences, Kuwait University, Kuwait

Correspondence
M. John Albert
john{at}hsc.edu.kw

Received 11 September 2007
Accepted 24 October 2007

Campylobacter jejuni is a major cause of diarrhoea in humans. However, the pathogenesis of C. jejuni diarrhoea is poorly understood due to the lack of a good animal model of infection. Many animals have been tried with limited success, but a mouse lung model of infection has been found to be satisfactory previously; however, the lung pathology of this model has not been studied. For the purpose of characterizing the histopathological and ultrastructural lesions in the lung of the mouse pulmonary model of C. jejuni infection, C. jejuni strain 81-176 or sterile PBS was intranasally inoculated into BALB/c mice. The infection resulted in a mild illness only, and in an initial predominance of polymorphonuclear cells, followed by the accumulation of macrophages and later the prominence of epithelioid cells. Focal peribronchial pneumonia appeared on day 3, granuloma-like reaction on day 4 and bronchopneumonia on day 5 post-infection. These features developed until day 5 post-infection, but were less consistent afterwards when histopathology was monitored up to 9 days post-infection. Intracellular structures resembling bacteria were observed on days 3 and 5 post-infection, but not on day 7 post-infection. On days 3 and 5 post-infection, degenerative changes were also observed by transmission electron microscopy. The histological changes were not associated with acid-fast bacteria or any fungal elements. The infection was systemic as C. jejuni was isolated from blood and all organ homogenates (lung, spleen, liver, and small and large intestines) at 24 h post-infection. Thereafter, the organism was recovered from the intestine only, thus indicating its predilection for this location. This characterization of pathology should contribute to a better understanding of the animal model and pathogenesis of C. jejuni infection.

Abbreviations: BH, Brown and Hopps; PAS/D, periodic acid-schiff with diastase digestion; TEM, transmission electron microscopy; ZN, Ziehl–Neelsen.






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