EFFECTS OBSERVED IN THE WHOLE ANIMAL 953 



as the mercurials, possess this action. Since the mercurials seem to lack 

 marked effects on glycolysis in intact tissues, one would not expect visual 

 disturbances if these are indeed due to glycolytic inhibition. Sorsby et al. 

 (1957) could detect no retinal degeneration in rats or rabbits given HgClg 

 or p-MB under conditions where lesions are produced by iodoacetate. How- 

 ever, in poisoning with certain organic mercurials there may be a marked 

 constriction of the visual field (Hunter et al., 1940). It is not known 

 whether this is a retinal effect or due to nerve degeneration. The sjaithesis 

 of rhodopsin from opsin and retinenci is blocked by 0.1 mM p-MB though 

 an action on opsin (Wald and Brown, 1951, 1952), and the synthesis of 

 iodopsin is likewise suppressed (Wald et al., 1955). The mercurial does not 

 alter rhodopsin directly but readily bleaches iodopsin. If this effect on the 

 regeneration of visual pigments occurs in vivo it has not been reported. 



For many years a rather uncommon disease of infants has been recog- 

 nized and called pink disease, infantile acrodynia, or erythredema, and is 

 characterized by a redness and swelling of the extremities and certain other 

 skin areas, along with photophobia, irritability, loss of reflexes, and muscular 

 hypotonia. Dr. Warkany of the Children's Hospital in Cincinnati in 1945 

 examined an infant suffering from this disease and found a urinary mercury 

 concentration of 360 ^g/liter. A summary of 20 cases showed that most 

 infants with pink disease had definitely elevated mercury levels — 75% 

 had more than 50 //g/liter and 10% more than 400 //g/liter ■ — whereas 

 most control infants showed undetectable levels (Warkany and Hubbard, 

 1948). It is now generally agreed that the majority of cases of pink disease 

 are due to mercury poisoning, which manifests itself somewhat differently 

 in infants than in adults although some of the neurological changes are 

 similar. The source of the mercury is usually calomel or mercury ointments. 

 Of the group of 54 studied by Zellweger and Wehrli (1951), around 80% had 

 been given such drugs, but in the remainder there was no obvious source 

 of mercury. The situation is probably more complex than believed originally. 

 Some of the symptoms may not be directly due to the mercury but are 

 predisposing conditions to mercury poisoning (Barrett, 1957). Thus a high 

 intestinal alkalinity, due in infants to faulty acid secretion in the stomach, 

 may accelerate the oxidation of calomel and increase its toxicity, and simul- 

 taneously reduce absorption of certain fatty acids, this latter possibly be- 

 ing responsible in part for the acrodynia. Since acrodynia in animals may 

 be induced by pyridoxine deficiency, there is also some possibility that the 

 mercury either inhibits some phase of pyridoxine metabolism or blocks a 

 pyridoxal-P enzyme to produce symptoms similar to deficiency. Since typi- 

 cal pink disease can occur in the absence of excess mercury intake or signifi- 

 cant urinary levels, one must assume that some basic metabolic disturbance 

 is the basis of this malady and that it can be brought about in various ways. 

 That aU the symptoms are not immediately due to mercury seems to be 



