Pathophysiology of C. diff colitis

This week I will be writing about the pathophysiology of C. diff colitis. Basically, what that means is -- what does the little bugger do to make life so horrible?

Here is a visual with some scientific wording to help you understand if you are a visual learner.

Basically what is happening is the following: 

1. C. diff enters the gut usually through from consumption of fecal matter (which can occur unnoticeably) 
2. Without other gut flora to keep C. diff in check, the bacteria proliferates uncontrollably. As the bacteria grows, toxins are released. Most pathogenic C. diff strains release Toxin A and Toxin B. 
3. Toxin A and Toxin B work to cause inflammation (colitis) and to inflict mucosal damage, respectively. 
4. Destruction of the lining ultimately prevents absorption in the gut, leading to the diarrhea that is commonly seen in patients. Prolonged infection can ultimately lead to sepsis (infection of the blood), which can cause systemic organ failure. 

It is thought that there is a hyper-virulent  strain named NAP/BI/027. This strain is thought to cause more severe symptoms and faster acting, in terms of damaging the colon.

Interestingly, neonates, who are often carriers are the C. diff toxin,are aysmptomatic. It is believed that in addition to acquiring maternal antibodies in utero against the C. diff toxins, the immature gut cells of a neonate may lack the intestinal receptors for the C. diff toxins altogether. This prohibits the toxins from eliciting the immune response that ultimately destroys the mucosal lining of the gut.

Need I remind you? ALWAYS WASH YOUR HANDS! 

References

Lamont, T. J. (2015). Clostridium difficile in adults: epidemiology, microbiology, pathophysiology. Uptodate. Retrieved from  uptodate.com/home