On 1 October 2006, C. difficile was said to have killed at least 49 people at hospitals in Leicester, England, over eight months, according to a National Health Service investigation. Another 29 similar cases were investigated by coroners. A UK Department of Health memo leaked shortly afterward revealed significant concern in government about the bacterium, described as being "endemic throughout the health service"
On 27 October 2006, nine deaths were attributed to the bacterium in Quebec. On 18 November 2006, the bacterium was reported to have been responsible for 12 deaths in Quebec. This 12th reported death was only two days after the St. Hyacinthes Honoré Mercier announced the outbreak was under control. Thirty-one people were diagnosed with CDIs. Cleaning crews took measures in an attempt to clear the outbreak. C. difficile was mentioned on 6,480 death certificates in 2006 in UK. On 27 February 2007, a new outbreak was identified at Trillium Health Centre in Mississauga, Ontario, where 14 people were diagnosed with CDIs. The bacteria were of the same strain as the one in Quebec. Officials have not been able to determine whether C. difficile was responsible for the deaths of four people over the prior two months. Between February and June 2007, three people at Loughlinstown Hospital in Dublin, Ireland, were found by the coroner to have died as a result of C. difficile infection. In an inquest, the Coroners Court found the hospital had no designated infection control team or consultant microbiologist on staff.
Gitelman syndrome (GS) is an autosomal recessive kidney tubule disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. The disorder is caused by genetic mutations resulting in improper function of the thiazide-sensitive sodium-chloride symporter (SLC12A3, also known as NCC, NCCT, or TSC) located in the distal convoluted tubule of the kidney. The distal convoluted tubule of the kidney plays an important homoestatic role in sodium and chloride absorption as well as of the reabsorption of magnesium and calcium.Genetic mutations of NCC, lead to loss of function and subsequently, reduced transport of sodium and chloride via NCC. Secondary derangement of calcium, magnesium, and potassium concentrations are caused by secondary effects in the distal tubule and collecting duct. The effect is an electrolyte imbalance similar to that seen with thiazide diuretic therapy (which causes pharmacological inhibition of NCC activity).Gitelman syndrome was formerly considered a subset of Bartter syndrome until the distinct genetic and molecular bases of these disorders were identified. Bartter syndrome is also an autosomal recessive cause of hypokalemic metabolic alkalosis, but it derives from a mutations of a number of genes that reduce NKCC2 activity. NKCC2 is found in the thick ascending limb of the loop of Henle. Signs and symptoms
Affected individuals may not have symptoms in some cases.