How C.<unk>  spreads<unk>  with C.<unk>  bacteria is responsible for C.<unk>  diarrhea. C.<unk>  Individual, drumstick-shaped C.<unk>  bacilli seen through scanning electron microscopy C.<unk>  colonies on a blood agar plate Clostridia are anaerobic motile bacteria, ubiquitous in nature, and especially prevalent in soil. Under the microscope, they appear as long, irregular (often drumstick- or spindle-shaped) cells with a bulge at their terminal ends. Under Gram staining, C.<unk>  cells are Gram-positive and show optimum growth on blood agar at human body temperatures in the absence of oxygen. When stressed, the bacteria produce spores that are able to tolerate extreme conditions that the active bacteria cannot tolerate. C.<unk>  may colonize the human colon without symptom; approximately 2–5% of the adult population are carriers, although it varies considerably with demographics. The risk of colonization has been linked to a history of unrelated diarrheal illnesses (e.g. laxative abuse and food poisoning due to Salmonellosis or Vibrio cholerae<unk> . Pathogenic C.<unk>  strains produce multiple toxins. The most well-characterized are enterotoxin (Clostridium<unk>  toxin A) and cytotoxin (Clostridium<unk>  toxin B), both of which may produce diarrhea and inflammation in infected people, although their relative contributions have been debated. Toxins A and B are glucosyltransferases that target and inactivate the Rho family of GTPases. 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. Another toxin, binary toxin, also has been described, but its role in disease is not fully understood. Antibiotic treatment of CDIs may be difficult, due both to antibiotic resistance and physiological factors of the bacteria (spore formation, protective effects of the pseudomembrane). The emergence of a new and highly toxic strain of C.<unk>  that is resistant to fluoroquinolone antibiotics such as ciprofloxacin and levofloxacin, said to be causing geographically dispersed outbreaks in North America, was reported in 2005. The U.S. Centers for Disease Control and Prevention in Atlanta warned of the emergence of an epidemic strain with increased virulence, antibiotic resistance, or both. C.<unk>  is transmitted from person to person by the fecal-oral route. The organism forms heat-resistant spores that are not killed by alcohol-based hand cleansers or routine surface cleaning. Thus, these spores survive in clinical environments for long periods. Because of this, the bacteria may be cultured from almost any surface. Once spores are ingested, their acid-resistance allows them to pass through the stomach unscathed. Upon exposure to bile acids, they germinate and multiply into vegetative cells in the colon. People without a history of gastrointestinal disturbances due to antibiotic use or diarrheal illness are less likely to become colonized by C.<unk> . In 2005, molecular analysis led to the identification of the C.<unk>  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. This strain is referred to as C.<unk>  BI/NAP1/027. Risk factors Antibiotics C.<unk>  colitis is associated most strongly with the use of these antibiotics: fluoroquinolones, cephalosporins, and clindamycin. Some research suggests the routine use of antibiotics in the raising of livestock is contributing to outbreaks of bacterial<unk> s such as C.<unk> . Healthcare environment People are most often infected in hospitals, nursing homes, or other medical institutions, although<unk>  outside medical settings is increasing. Individuals can develop the<unk>  if they touch objects or surfaces that are contaminated with feces and then touch their mouth or mucous membranes. Healthcare workers could possibly spread the bacteria or contaminate surfaces through hand contact. The rate of C.<unk>  acquisition is estimated to be 13% in those with hospital stays of up to two weeks, and 50% with stays longer than four weeks. Long-term hospitalization or residence in a nursing home within the previous year are independent risk factors for increased colonization. Acid suppression medication Increasing rates of community-acquired CDI are associated with the use of medication to suppress gastric acid production: H2-receptor antagonists increased the risk 1.5-fold, and proton pump inhibitors by 1.7 with once-daily use and 2.4 with more than once-daily use. Diarrheal illnesses People with a recent history of diarrheal illness are at increased risk of becoming colonized by C.<unk>  when exposed to spores, including laxative abuse and gastrointestinal pathogens. Disturbances that increase intestinal motility are thought to transiently elevate the concentration of available dietary sugars, allowing C.<unk>  to proliferate and gain a foothold in the gut. Although not all colonization events lead to disease, asymptomatic carriers remain colonized for years at a time. During this time, the abundance of C.<unk>  varies considerably day-to-day, causing periods of increased shedding that could substantially contribute to community-acquired<unk>  rates. Other As a result of suppression of healthy bacteria, via a loss of bacterial food source, prolonged use of an elemental diet increases the risk of developing C.<unk><unk> . Low serum albumin levels is a risk factor for the development of C.<unk><unk>  and when infected for severe disease. The protective effects of serum albumin may be related to the capability of this protein to bind C.<unk>  toxin A and toxin B, thus impairing entry into enterocytes.
Clostridioides difficile infection
Antibiotic-associated diarrhea
Irritable bowel syndrome
Campylobacteriosis
Gay bowel syndrome
Wilderness-acquired diarrhea
Factitious diarrhea
Cytomegalovirus colitis