Microbiology

NAP1 / 027 Clostridium difficile

NAP1 / 027 Clostridium difficile

Clostridium difficile NAP1/027

Also known as:
C. diff NAP1/027, C. difficile BI/NAP1/027

Industry of Interest: Healthcare

Classification: Bacteria

Microbiology: Clostridium difficile is a Gram-positive endospore forming rod. C. difficile is a common cause of antibiotic-associated diarrhoea and its incidence has increased dramatically in recent years, particularly in hospitals. This is thought to be as a result of a new hypervirulent strain called C. difficile NAP1/027 and from changes in the antibiotics usages (Tillotson and Tillotson, 2011). It is thought that C. difficile NAP1/027 produce 16 times more toxin A and 23 times more toxin B than C. difficile reference strains, and that this may be the reason for this strains increased disease severity and higher mortality rates (Carter et al., 2010).

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Biology

Habitat and transmission: It is an anaerobic microorganism that produces endospores in response to stress, which are difficult to eradicate from the environment and can be spread on via the hands of healthcare workers. Once established in the colon C. difficile NAP1/027 can produce toxins A and B, which lead to impairment of tight junctions in human gut epithelial cells causing the damaged cells to secrete fluid and become inflamed, resulting in diarrhoea (Carter et al., 2010).

Treatment and antibiotic resistance: Clinical presentations with this hypervirulent strain appear to be more serious than other less virulent C. difficile strains, resulting in increased morbidity and mortality. Until recently, vancomycin was heavily relied upon to treat C. difficile NAP1/027 infections; however its use has been reduced as a result of the increase in vancomycin-resistant bacteria such as vancomycin-resistant Staphylococcus aureus (VRSA) and vancomycin-resistant enterococci (VRE) (Carter et al., 2010). C. difficile NAP1/027 infection can establish when antibiotics, particularly clindamycin and cephalosporins are used (Tillotson and Tillotson, 2011). The antibiotics eradicate the normal microflora, which leaves C. difficile able to establish an infection. Alternative therapies such as novel antibiotics, monoclonal antibodies, a vaccine and novel biotherapeutics (faecal transplant) are being explored; however it is likely that a multi-faceted approach to prevention and treatment will be required (Tillotson and Tillotson, 2011).

Prevention and control: C. difficile being an endospore is particularly hardy and able to survive in the environment for extended periods of time.Good hand hygien, isolation of infected patients, , contact precautions and enhanced environmental decontamination have been shown to be effective in reducing the numbers of C. difficile in the environment. C. difficile is resistant to the effects of alcohol hand gels and as such healthcare workers should ensure they wash their hands thoroughly with soap and hot water. One study showed that the implementation of Bioquell hydrogen peroxide vapour (HPV) reduced the incidence of C. difficile infection in a US hospital (Boyce 2008).

Symptoms/Effects

Disease and symptoms: C. difficile infection generally only arises after use of antibiotic therapies (Carter et al., 2010). Clinical presentations are usually watery diarrhoea and occasionally pseudomembranous colitis, toxic megacolon, shock and even death. C. difficile NAP1/027 infections more likely to be recurrent and difficult to treat (Hookman and Barkin, 2009). Some of the risk factors for infection include prolonged hospital stay, serious underlying illnesses, reduced immune status and advancing age (Hookman and Barkin, 2009). Inflammatory bowel disease (IBD) is another possible risk factor for infection (Hookman and Barkin, 2009).

Technical

References:

Carter G.P., Rood J.I. and Lyras D. (2010)
The role of toxin A and Toxin B in Clostridium difficile associated disease. Past and present perspectives. Gut microbes. 1(1): 58-64.

Hookman P. and Barkin J.S. (2009) Clostridium difficile associated infection, diarrhea and colitis. World J Gastroenterol. 15(13): 1554-1580.

Tillotson G.S. and Tillotson J. (2011) Clostridium difficile—a moving target. F1000 Med Rep. 3:6.
 

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