Under the microscope, they appear as long, irregular (often drumstick- or spindle-shaped) cells with a bulge at their terminal ends (forms subterminal spores).

Under Gram staining, C. difficile cells are Gram-positive and show optimum growth on blood agar at human body temperatures in the absence of oxygen.

[8] Clostridioides difficile is an important emerging human pathogen; according to the CDC, in 2017 there were 223,900 cases in hospitalized patients and 12,800 deaths in the United States.

Toxin B (cytotoxin) induces actin depolymerization by a mechanism correlated with a decrease in the ADP-ribosylation of the low molecular mass GTP-binding Rho proteins.

[25] The bacterium also produces the chemical para-cresol, which inhibits the growth of other microbes in its vicinity and allows it to outcompete normal human gut flora.

[8] The emergence of a new, highly toxic strain of C. difficile, resistant to fluoroquinolone antibiotics, such as ciprofloxacin and levofloxacin, said to be causing geographically dispersed outbreaks in North America, was reported in 2005.

[27] The US Centers for Disease Control in Atlanta warned of the emergence of an epidemic strain with increased virulence, antibiotic resistance, or both.

Consequently, the World Health Organization advocates the use of soap in addition to alcohol solutions to limit the spread of the spores.

[34] Sporulation was shown to be significantly reduced after inactivation of C. diffiicile's DNA methyltransferase CamA,[35] raising the prospect of developing a drug that may inhibit this bacterium in a specific manner.

GI disturbances in carriers appear to trigger periods of increased shedding which may be an important factor for transmission.

The study estimated that 40% of cases began in nursing homes or community health-care settings, while 24% occurred in hospitals.

Additionally, carriage of C. difficile with high levels of toxins is common in young children, while disease is rare.

[38] Symptoms of C. difficile infection include diarrhea (at least three loose bowel movements a day), dehydration, abdominal pain that can be severe, loss of appetite, and nausea.

[40] C. difficile is often transferred from other patients through the hands of healthcare workers or from the overall hospital environment and acquired from ingesting the pathogen.

[41] As a consequence C. difficile is the most prevalent US healthcare infection, posing serious health risks and substantial care costs.

However, the levels of anti-TcdA and -TcdB IgG antibodies have not been able to discriminate healthy individuals from patients with C. difficile infection, meaning they have limited clinical use.

[46] This is further evidenced by the recovery of the toxin-specific Th17 cells and microRNA expression following Fecal microbiota transplant of patients with severe disease.

[46][47] New findings show that the loss of the interleukin-10 corresponds to higher levels of interleukin-22, which has been found to be important in a host's response to a C.difficile infection.

To confirm a CDI, a cytotoxin assay detects the cell's toxin B (ToxB) cytotoxicity in the fecal eluate.

PCR assays have a shorter turnaround time and a higher sensitivity range than the toxigenic stool culture.

[50] The vancomycin regimen has replaced the traditional use of metronidazole due to its greater efficacy, safety profile, and lower recurrence rates.

[51] In cases of fulminant CDI, adjuvant therapy with parenteral metronidazole plus oral vancomycin or fidaxomicin is suggested.

[52] Approximately 15-30%[53] of patients who successfully complete therapy of primary infection with metronidazole or vancomycin will experience a relapse.

[citation needed] When a patient is deteriorating or progressing to severe-complicated disease the addition of intravenous tigecycline merits considerations.

[56][57] Patients with high risk of relapse may also benefit from the addition of the monoclonal antibody bezlotoxumab to the standard of care.

Fecal matter transplants have also been found to be an effective and safe treatment option for children and young adults.

[64] In 2005, molecular analysis led to the identification of the C. difficile strain type characterized as group BI by restriction endonuclease analysis, as North American pulse-field-type NAP1 by pulsed-field gel electrophoresis and as ribotype 027; the differing terminology reflects the predominant techniques used for epidemiological typing.

[70] Clostridioides difficile has a highly diverse epigenome, with 17 high-quality methylation motifs reported so far, the majority pertaining to the 6mA type.

Methylation at one of these motifs - CAAAAA, was shown to impact sporulation, a key step in C. difficile disease transmission, as well as cell length, biofilm formation, and host colonization.