In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised persons (e.g., people with AIDS) the fatality rate is approximately 30%.Even in previously healthy children, measles can cause serious illness requiring hospitalization. One out of every 1,000 measles cases progresses to acute encephalitis, which often results in permanent brain damage. One to three out of every 1,000 children who become infected with measles will die from respiratory and neurological complications. Cause
Measles is caused by the measles virus, a single-stranded, negative-sense, enveloped RNA virus of the genus Morbillivirus within the family Paramyxoviridae.The virus is highly contagious and is spread by coughing and sneezing via close personal contact or direct contact with secretions. Measles is the most contagious transmissible virus known. It remains infective for up to two hours in that airspace or nearby surfaces. Measles is so contagious that if one person has it, 90% of non-immune people who have close contact with them (e.g., household members) will also become infected. Humans are the only natural hosts of the virus, and no other animal reservoirs are known to exist, although mountain gorillas are believed to be susceptible to the disease.
The fact that WPW patients are young and do not have structural heart disease, lead to using catheter ablation of the APs with the elimination of the atrial fibrillation as well as the episodes of re-entrant ventricular tachycardia. This elimination of the atrial fibrillation with ablation implies APs have some pathophysiologic role in the development of a-fib in the WPW patient.Functionally defined re-entry does not require the alternative anatomically defined circuit accessory pathways and it may not reside in just one location. Ventricular fibrillation (VF) following ventricular tachycardia (VT) may be described as a functionally defined re-entry problem caused by multiple mini re-entrant circuits spontaneously created within the ventricular myocardium. The original re-entrant circuit breaks down into multiple mini reentrant circuits. (VF becoming the grand finale of a single prolonged VT larger circus movement, propagating change in the "functional core" of the ventricular myocardium, dissipating mini reentrant circuits, exhibited as ventricular fibrillation.) Ischemia, electrolyte, pH abnormalities, or bradycardia are potential causes of functionally defined re-entry due to changes in the properties of the cardiac tissues functional core. (No accessory pathway required). For reentry to occur, the path length of circuit should be greater than the wave length (ERP × conduction velocity) of impulse. See also
AV reentrant tachycardia
AV nodal reentrant tachycardia

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