Clostridium difficile infection and fecal bacteriotherapy

Introduction

Scanning electron micrograph of C. difficile bacteria obtained from the CDC Public Health Image Library.

By Rebecca Varnell

Endoscopic image of colon reveals presence of pseudomembranes caused by CDI. (Carrion et al. 2010).

Figure 4, The five genes endcoding toxin A and B as well as three regulatory gene products lie on a 19.6 KB pathogenicity locus. (Voth and Ballard 2005).

Figure 3. C. difficile spore exposure causes germination in hosts with certain primary bile salts such as taurocholate. After germination, vegetative cells grow and release toxins into the human host. Starvation induces sporulation and spores are spread through feces. Image courtesy of Seekatz and Young (2014).

Introduce the topic of your paper. What microorganisms are of interest? Habitat? Applications for medicine and/or environment?

Section 1

Include some current research, with at least one figure showing data.

Section 2

Include some current research, with at least one figure showing data.

Section 3

Include some current research, with at least one figure showing data.

References

[1] Nazarko, L. (2015). Infection control: Clostridium difficile. British Journal Of Healthcare Assistants, 9(1), 20-25.

Andres F Carrion et al. “Severe colitis associated with docetaxel use: a report of four cases,” World Journal of Gastrointestinal Oncology, 10 (2010): 390-394, accessed April 17, 2015, doi: 10.4251/wjgo.v2.i10.390.

Daniel E. Voth and Jimmy D. Ballard, “Clostridium difficile Toxins: Mechanism of Action and Role in Disease,” Clinical Microbiology Reviews 18 (2005): 249-263, date accessed April 19, 2015, doi: 10.1128/CMR.18.2.247-263.2005.

Daniel Paredes-Sabja et al. “Clostridium difficile spore biology: sporulation, germination, and spore structural proteins,” Trends in Microbiology 22 (2014): 406, accessed April 15, 2015, doi: 10.1016/j.tim.2014.04.003.