Hospital acquired infections
Nosocomial (hospital acquired) infections are defined by the World Health Organisation as ‘an infection occurring in a patient during the process of care in a hospital or other health care facility which was not present or incubating at the time of admission’.
Nosocomial infections are detrimental to health care systems' fight against antibiotic resistance, as well as leading to costly hospital admissions and unnecessary deaths.
It is now well-known that hand-washing is fundamental to prevention of pathogen transmission. It is however, not the lone cause of transmission in hospital and health care settings.
A person can contract an infection from their own commensal bacteria via medical devices (i.e. catheter), the pathogenesis of which is owing to biofilm formation.
This is an area where LeMID microbiologists are actively engaged. One focus area is biofilms, which are a complex and dynamic community of multiple bacteria species embedded in secreted polysaccharide matrices.
Biofilms are an important mechanism for pathogenesis, Staphylococcus epidermidis for example, is associated with endocarditis post central line insertion. This is due to the strong adherence properties that allow biofilms to form on abiotic surfaces such as catheters.
Methicillin resistant Staphylococcus aureus (MRSA) is well-known antibiotic resistant pathogen that causes a high proportion of HCAIs and subsequently a high rate of mortality. The high prevalence of MRSA is partly due to high genetic variability that has resulted in multi drug and widespread antibiotic resistance (see our Antimicrobial Resistance page to find out more about LeMID research on combatting resistance).
Immune deficiency leaves individuals particularly susceptible to MRSA, however community acquired MRSA strains are able to infect immune-competent individuals independently of health-care settings.
An encapsulated gram negative bacteria that is known to cause disease in patients that are immunocompromised, meaning hospitals are an optimal place for acquiring this infective organism. Additionally, this bacterium is increasingly becoming antibiotic resistant and hence is contributing to high mortality rates.
C. difficile are a normal resident in the gut microbiome of young children and some adults, and will not cause disease in an immune competent person. When the balance shifts in the diverse system of the gut microbiome, C. difficile can multiply exponentially. The symptoms of diarrhea and fever are due to the abnormally high production of toxins by the vast number of C. difficile bacteria present. Visit the MRSA Action UK website for more information on C. difficile
There is an estimated 250,000 cases of CDI (C. difficile infection) annually in the USA.
C. difficile produce three major toxins: Toxin A, Toxin B and C. difficile binary toxin (CDT). These toxins play a part in disruption of the colon epithelium leading to inflammation and therefore the symptoms of C. difficile infection (diarrhea, and less commonly, pseudomembranous colitis and toxic megacolon).
Endospores are formed by C. difficile, these are tough structures and primarily protect the bacterium during exposure to sub-optimal conditions, thereby promoting survival. This means that in clinical settings the bacteria are more resilient to cleaning regimes.
NICE guidelines currently recommend Oral metronidazole for non-severe CDI and Oral vancomycin or fidaxomicin for sever CDI however these treatments do not protect a patient from recurrent infections. This factor motivates research into alternative therapies for infection caused by C. difficile from new antibiotics to riboswitch ligands, the use of fecal transplants to antibodies that target toxins.
A major focus of the research of Professor Martha Clokie is use of bacteriophage (phage) therapy to treat patients infected with C. difficile and to eliminate this pathogen from their systems.