The eponym Gee-Herter disease was sometimes used to acknowledge both contributions. Sidney V. Haas, an American paediatrician, reported positive effects of a diet of bananas in 1924. This diet remained in vogue until the actual cause of coeliac disease was determined.While a role for carbohydrates had been suspected, the link with wheat was not made until the 1940s by the Dutch paediatrician Dr Willem Karel Dicke. It is likely that clinical improvement of his patients during the Dutch famine of 1944 (during which flour was scarce) may have contributed to his discovery. Dicke noticed that the shortage of bread led to a significant drop in the death rate among children affected by coeliac disease from greater than 35% to essentially zero. He also reported that once wheat was again available after the conflict, the mortality rate soared to previous levels. The link with the gluten component of wheat was made in 1952 by a team from Birmingham, England. Villous atrophy was described by British physician John W. Paulley in 1954 on samples taken at surgery. This paved the way for biopsy samples taken by endoscopy.Throughout the 1960s, other features of coeliac disease were elucidated. Its hereditary character was recognised in 1965. In 1966, dermatitis herpetiformis was linked to gluten sensitivity. Social and culture
May has been designated as "Coeliac Awareness Month" by several coeliac organisations. Christian churches and the Eucharist
Speaking generally, the various denominations of Christians celebrate a Eucharist in which a wafer or small piece of sacramental bread from wheat bread is blessed and then eaten.
Subconjunctival migration of an adult worm to the eyes can also occur frequently, and this is the reason Loa loa is also called the "African eye worm." The passage over the eyeball can be sensed, but it usually takes less than 15 minutes. Eyeworms affect men and women equally, but advanced age is a risk factor. Eosinophilia is often prominent in filarial infections. Dead worms may cause chronic abscesses, which may lead to the formation of granulomatous reactions and fibrosis.In the human host, Loa loa larvae migrate to the subcutaneous tissue, where they mature to adult worms in approximately one year, but sometimes up to four years. Adult worms migrate in the subcutaneous tissues at a speed less than 1 cm/min, mating and producing more microfilariae. The adult worms can live up to 17 years in the human host. Cause
Transmission
Loa loa infective larvae (L3) are transmitted to humans by the deer fly vectors Chrysops silica and C. dimidiata. These carriers are blood-sucking and day-biting, and they are found in rainforest-like environments in western and central Africa. Infective larvae (L3) mature to adults (L5) in the subcutaneous tissues of the human host, after which the adult worms—assuming presence of a male and female worm—mate and produce microfilariae. The cycle of infection continues when a non-infected mango or deer fly takes a blood meal from a microfilaremic human host, and this stage of the transmission is possible because of the combination of the diurnal periodicity of microfilariae and the day-biting tendencies of the Chrysops spp.