The temperature is generally too hot for the larvae to develop on the surface of the sand and the deeper sand does not have enough oxygen. This preferred ecological niche offers a way to decrease transmission among humans by investing in concrete grounds as opposed to the sand that is usually used in shacks and some favelas. Indeed, Nany et al. (2007) report that "In shacks with concreted ground being cleaned every day with water, Tunga [penetrans] larvae were hardly found. "In a longitudinal study conducted from March 2001 to January 2002, incidence of tungiasis was found to vary significantly with the local seasons of an endemic community in Brazil. In particular, the study found that "occurrence of tungiasis varies throughout the year and seems to follow local precipitation patterns. Maximum and minimum prevalence rates differed by more than a factor of three." The authors suggest that the correlation is due to the high humidity in the soil impairing larval development during the rainy season, as well as the more obvious reason that rain may simply wash away all stages of T. penetrans due its small size of 1mm.Acting as both biological vectors and definitive hosts, humans have spread Tunga penetrans from its isolated existence in the West Indies to all of Latin America and most of Africa via sea travel.
However, it is well known that MAS is usually associated with a triad of symptoms that include hypercalcemia, alkalosis, and acute kidney injury. In general, milk-alkali syndrome starts with excess calcium levels in the body (hypercalcemia), which causes the bodys pH to increase (become more alkaline) resulting in metabolic alkalosis and ultimately contributes to a decrease in renal function.Factors involved in the development of hypercalcemia include excess intestinal absorption of calcium, saturation of the bones buffering capacity for calcium, decreased renal excretion, and abnormal vitamin D metabolism. Underlying kidney disease is a risk factor for MAS, but even people with healthy kidneys can develop the syndrome.For a healthy individual, if calcium levels are high, the kidneys will decrease its production of calcitriol (active vitamin D) by reducing the hydroxylation of calcidiol (inactive vitamin D); lower calcitriol levels means a lower rate of calcium absorption in the small intestine, which eventually offsets the elevated calcium levels. However, excessive ingestion of calcium of more than 10-15 g per day has been reported to cause calcium levels too high for renal calcitriol suppression to control, resulting in net calcium absorption that ultimately causes hypercalcemia.Hypercalcemia affects the kidneys in multiple ways that altogether contributes to hypovolemia. Prolonged hypercalcemia can decrease glomerular filtration rate (GFR) via vasoconstriction, reduce creatinine clearance, and eventually cause renal insufficiency. Hypercalcemia also causes natriuresis by blocking the Na-K-Cl cotransporter (NKCC) in the medullary thick ascending limb of the loop of Henle, leading increased sodium excretion followed by water excretion that leads to hypovolemia.