29,000,000 people in the U.S. suffer from diabetes.  5% of the patients suffer from Type-1 diabetes (juvenile diabetes). Type-1 diabetes develops in childhood, and is thought to be an autoimmune disease, in which the immune system attacks the islet cells in the pancreas. Type-1 diabetes is known to develop after a severe acute infection. The scientific literature has postulated juvenile diabetes is caused by a Coxsackie virus, a rotavirus, a cytomegaly virus, mumps, or rubella.  Some Coxsackie viruses are believed to have an affinity for attacking the pancreas.  Most children are exposed to and acquire these common viruses; yet, most children do not develop type-1 diabetes.

Both chlamydia pneumonia and mycoplasma have been associated with type-1 diabetes. In mice, chlamydia pneumonia infected mast cells were found to significantly decrease beta-cell ATP and insulin production. (Intracellular chlamydia consumes ATP, and when the ATP is depleted consumes sugar for energy, causing fermentation.) The child who develops type-1 diabetes may have acute co-infections; and/or already have a weakened immune system, from chronic infections. Viruses may attach to the intracellular pathogens and/or parasites, which facilitates access to the pancreas.

Diabetes is defined by the effect—high blood sugar. More than one pathogen can cause the same effect—more than one bacteria, parasite, and virus, alone or in combination, may cause or trigger type-1 diabetes, by more than one mechanism.  The immune system is attacking the infectious pathogens in the pancreas.  Identifying the acute infection(s), which preceded the development of type-1 diabetes, and obtaining a history of current and prior infections, may help to identify triggering event(s) for type-1 diabetes.

Chlamydia pneumoniae Promotes Dysfunction of Pancreatic Beta Cells
http://europepmc.org/articles/PMC4533996