In his autobiography [1] Karl May states that he became blind shortly after birth. The young boy could not see for four years and his eyesight returned only after treatment by two professors of medicine in Dresden. Several attempts to explain the nature of his blindness have been made in the past [2]. Such deprivation of one of the most important senses at an early age must have affected the child deeply. And so it did. It was the first link in the chain of events leading to the state of mind Karl May described many years later.
But what was this eye condition in medical terms? Some authors as Werner Raddatz in his book [3] brings up the possibility that the blindness could be traced to his father alcoholism. However Karl May writes: "I have never seen my father drunk." [4] Other statements have been made about the boy's blindness, assuming it was an eye infection [5]. Wollschlager named 'Ophthalmia neonatorum' and 'Ophthalmia pustularis', a perinatal eye infection, as being the cause of Karl May's childhood blindness [6].
This is what Karl May had written on his blindness: "I was born neither blind, nor burdened with some hereditary bodily defect. Father and mother were of quite strong, healthy constitution. Until their death they were never sick. To accuse me of atavistic weakness is malevolent, which I have quite definitely objected to. That I shortly after my birth became seriously ill, lost eyesight and was for full four years in bad health, was not the consequence of heredity, but of purely local conditions, the poverty, foolishness and the ruinous medicinal quackery to which I fell victim. As soon as I came into the hands of competent physicians, the eyesight returned to me and I became an extremely strong and resilient youngster, who was robust enough to take on anyone else." [7]
When Karl May's mother had gone to Dresden to study midwifery she also sought help for her son: "She acquired through her diligence and her quiet, deeply earnest character the patronage of both professors Grenser and Haase, and told them about me, her miserable, blind and yet mentally so lively boy. She was asked to bring me to Dresden to be treated by the two gentlemen. This had happened, and indeed with quite surprising success. I learned to see and returned, also for the rest recovered, home." [8]
From the description by Karl May it seems the treatment was painless and that his general condition also improved. Professors Grense and Haase at Dresden lectured midwifery and presumably also the perinatal care of the newborn babies. They certainly made the right diagnosis and cured Karl in a very short time. The two professors from Dresden did not use any surgical intervention; otherwise Karl May would have mentioned it. May had described the suffering of one of his sisters who had been affected by smallpox so badly that the doctor had to make an incision on her face to find the mouth so that she could drink. It seems the treatment of Karl May's eyes condition in Dresden had left him with no painful memory.
It is known that Karl May had not been drafted into the Army for compulsory military service because of poor eyesight. On the 6 December 1862 the military surgeon Dr. Horn found Karl May to be shortsighted [9]. It could have been in fact astigmatism, where - in May's case due to healed corneal ulcers - the warping of the cornea is out of the normal spherical contour. Examination of May's spectacles could help to solve this question. There are May's eyeglasses on display in the Radebeul museum. It is also of interest that G. Grosz, who visited Karl May in 1910, noticed his runny eyes as happens when one is exposed to the wind [10].
The World Health Organization program for the prevention of blindness [11] listed in 1996 the following conditions for intervention: Cataract, Trachoma, Vitamin A deficiency - xerophthalmia, Onchocerciasis, Glaucoma, Leprosy, Trauma, Diabetic Retinopathy, and Aging related Macular Degeneration.
Vitamin A deficiency - xerophthalmia, or the so-called 'blinding malnutrition', is the leading cause of childhood blindness in the world even nowadays. It is estimated that each year approximately 500.000 children go blind, and 70% of those due to vitamin A deficiency. Vitamin A deficiency is widely prevalent particularly in the developing world nowadays.
The earliest manifestations of this condition are night blindness and xerophthalmia or xerosis conjunctivae, which is a dry, thickened and pigmented bulbar conjunctiva. The pigmentation gives the conjunctiva a peculiar smoky appearance. Bitot's spots are glistening white plaques formed of desquamated thickened conjunctival epithelium, usually triangular in shape and firmly adherent to the underlying conjunctiva. When dryness spreads to the cornea it takes on a dull, hazy, lackluster appearance. Later the cornea undergoes necrosis and ulceration, so-called keratomalacia. The general condition of the child suffers as well; diarrhea is common, accompanied by loss of weight and frequent infections. Children between the ages of 1 and 5 years are most commonly affected.
Breast milk is virtually the only source of vitamin A the first few months for many infants. Without breast milk newborns can maintain optimal vitamin A nutriture for no more than a few weeks. Although vitamin A concentration in human milk is dependent on the mother's vitamin A status, vitamin A deficiency is rare among breastfed infants, even in parts of the world where vitamin A deficiency is endemic.
Measles, one of the six major childhood diseases, rapidly reduces blood levels of vitamin A and frequently precipitates xerophthalmia. Many studies have been done in the past decade confirming the impact of vitamin A deficiency on childhood growth, mortality and morbidity, including anemia and blindness [12].
The cause of vitamin A (Retinol) deficiency is a lack of pre-formed vitamin A, carotene and sometimes fat and oil in the diet. Retinol is chiefly found in milk, butter, cream, cheese, egg yolk, liver, kidneys and some of the fatty fish. Carotene is widely distributed among plant foods. It is found in green vegetables in association with chlorophyll, so that the green outer leaves of vegetables like cabbage and lettuce are good sources of carotene, while the inner leaves contain little or none. Other useful sources are yellow and red fruits and vegetables. All vegetable oils are devoid of vitamin A activity with the exception of red palm oil. The WHO guidelines on adequate consumption of vitamin A by children 6 to 24 months old are: approximately two tablespoons of cooked carrots or dark yellow squash, or 5 tablespoons of green vegetable daily for those still receiving breast milk.
Sufficient vitamin A-rich foods are often not available in some communities, particularly at certain times of the year. In other situations, vitamin A-rich foods may be available in the community but not be consumed in sufficient quantities by certain families for economic or cultural reasons, or they may be available in the family but not be eaten by young children or pregnant or lactating women. The whole question of vitamin A deficiency, the key resources in its prevention and elimination, the whole problem and the solution, has been studied in the past fifty years in detail globally. Even today more than a quarter of a million children six months to six years of age are estimated to go blind every year due to a deficiency of vitamin A, and some 14 million currently exhibit signs of clinical xerophthalmia ranging from dryness to severe ulceration's. [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24]
Karl May mentions in his biography bread, potatoes and apples, which were consumed in the family. In the third chapter of his book [25] - 'Without Youth 1847-1857' - he writes: "There were bad times then particularly for the poor inhabitants of that region, where my home was. Today people simply could not imagine how a poor man towards the end of the 1840's was starving there during his life. Unemployment, poor harvest, high prices, and revolution, these four words explain it all. We lacked almost everything what was necessary for the nourishment of the body. We begged of our neighbor, the innkeeper of 'Zur Stadt Glauchau', the midday leftovers of potato peels, to make use of the few scraps, which perhaps were still hanging there, for a hunger-soup. We were going to the 'Red Mill' to be given a few handfuls of bag-dust and chaff, from which we tried to make something resembling food. We have plucked orache from rubbish heaps, and wild lettuce from under the fences, to cook it and fill up the stomach with it. The leaves of the orache feel greasy. This gave when cooked two or three small rings of fat, which were swimming in the water. How nourishing and tasty it looked to us!..."
"When we were very diligent [weaving white gloves which used to be put on the hands of the deceased in the coffin] all of us together earned at the end of the week even twelve new pennies. What a capital! For that we got for five pennies beetroot syrup, which we spread on five bread rolls bought for three pennies; these were scrupulously cut into small pieces and passed around." [26]
As Karl May stated, he was born with normal eyesight, but shortly afterwards he could not see. He does not specify what time period was involved. The eye condition was treated with home remedies and no medical help was sought. This would indicate that the illness did not seem to be serious to the parents at the beginning, and even later on. May reported that this had been going on for four years.
We do not know whether the little boy was breast-fed by his mother, which would have given him protection from Vitamin A deficiency. Also we have no knowledge if he had measles, which would have lowered significantly the Vitamin A body stores. We may only speculate that one or the other condition contributed to Vitamin A deficiency in the boy. Xerophthalmia at the beginning does not look serious, and often had been treated with various ointments applied locally. This is what most probably happened to little Karl. There could have also been accompanying infection. From the sparse description Karl May gave on the food his family consumed, it is also clear that it was deficient in vitamins. Xerophthalmia is characterized by malfunction of the tear glands and could lead to permanent obstruction of the tear ducts with resulting watery eyes. G.Grosz observed this condition on Karl May in 1910.
Vitamin A deficiency with resulting Xerophthalmia seems to be the most acceptable explanation of Karl May's blindness when he was one to five years old. We can only speculate whether lack of maternal milk or concurrent measles infection contributed to the depleted level of Vitamin A in the child. What did make the condition worse was the low socio-economic status of the family.
References Please click on the hyperlinked reference numbers to return to your place in the text. [1] May, K.: 'Mein Leben und Streben.' Hildesheim-New York, 1997.
[2] Kluxen, G.: 'Die Ophthalmologie bei Karl May.' Der Augenarzt, Heft 2, March/April 1980, pp.114-118. Harder, R.: 'Die Erblindung - eine entscheidende Phase im Leben Karl Mays.' Mitteilungen der Karl-May-Gessellschaft' Nr.68/1968, pp.35-38.
[3] Raddatz, W.: 'Das Abenteuerliche Leben Karl Mays.' Sigbert Mohn Verlag 1968, p.13.
[4] May, K.: "Ich." Karl-May-Verlag Bamberg 1968, p.78.
[5] Vollmer, H.: 'Karl May's "Am Jenseits".' KMG-Presse Ubstadt 1983, p.17.
[6] Wollschlager, H.: 'Die sogenannte Spaltung des menschlichen Innern, ein Bild der Menschheitsspaltung ueberhaupt.' Jb KMG 1972, p.25.
[7] In (4), p.40.
[8] In (4), p.43.
[9] Wohlgschaft, Hermann: 'Grosse Karl May Biographie.' Igel Verlag Wissenschaft 1994, p.83.
[10] In (3), p.153.
[11] The WHO Programme for the Prevention of Blindness. International Eye Foundation, 7801 Norfolk Avenue, Bethesda, MD 20814, USA.
[12] Vitamin A Deficiency: Key resources in its prevention and elimination. Compiled by Jenny Cervinskas and Mashid Lofti; The Micronutrient Initiative, PO Box 8500, 250 Albert Street, Ottawa Ontario, Canada K1G 3H9; second edition January 1996.
[13] WHO Press Release 2 - 18 January 1994: WHO Report on Infant and Young Child Nutrition: Global Problem.
[14] Gujral, S.; Gopaldas, T.: 'Risk Factors of Nutritional Blindness and Determinants of a Successful Vitamin A Prophylaxis Program.' Indian Paediatric Journal, Feb. 1995, pp.199-205.
[15] Shankar, AV. et alii: 'Chronic Low Intakes of Vitamin A-rich Foods in Households with Xerophthalmic Children; a Case-control Study in Nepal.' Amer.Journ.Clin.Nutr., August 1996, pp.242-248.
[16] Katz, J. et alii: 'Impact of vitamin A supplementation on prevalence and incidence of xerophthalmia in Nepal.' Invest.Ophthalmol. Vis Sci., December 1995, pp.2577-2583.
[17] Wilson MR. Et alii: 'A population-based study of xerophthalmia in the extreme North Province of Cameroon, West Africa.' Arch. Ophthalmol. April 1996, pp.464-468.
[18] Rosen, DS. Et alii: 'Vitamin A deficiency and xerophthalmia in western Yemen.' Eur.J.Clin.Nutr. January 1996, pp.54-57.
[19] Kafwembe, EM, et alii: 'Socio-economic status and serum Vitamin A levels in Zambian children.' Centr.Afr.Jour.Med. March 1996, pp.70-72.
[20] Humphrey, JH. Et alii: 'Impact of neonatal Vitamin A supplementation on infant morbidity and mortality.' Journ.Paediat. April 1996, pp.489-496.
[21] Koo, W. et alii: 'Effect of different Vitamin A intakes on very-low-birth-weight infants.' Amer.Journ.Clin.Nutr. December 1995, pp.1216-1220.
[22] Hatchell, D. et alii: 'Herpetic keratitis in experimental Vitamin A deficiency.' Invest. Ophthalmol. Vis Sci., February 1987, pp.238-242.
[23] Twining, S. et alii: 'Effect of Vitamin A deficiency on the early response to experimental Pseudomonas Keratitis.' Investig. Ophthalmol. Vis Sci., March 1996, pp.511-522.
[24] Sommer, A. (Professor of Ophthalmology): 'Vitamin A Deficiency.' Oxford University Press 1996.
[25] In (1), pp.39-40.
[26] In (1), p.40.
