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War Surgery and Medicine

Infective Hepatitis and Serum Jaundice

Infective Hepatitis and Serum Jaundice

The relationship of infective hepatitis to serum jaundice, postarsenical, and post-yellow-fever-vaccine jaundice remains a mystery. No laboratory animal has been found susceptible to infection with any of these varieties of jaundice.

Bigger (1943) has demonstrated that jaundice following antisyphilitic treatment was due to faulty sterilisation of syringes and needles contaminated with homologous serum jaundice virus. Sheehan (1944) and Salaman et al. (1944) and others have provided confirmation.

Dible and McMichael (1943) studied the histopathology of liver biopsy tissue from cases of arseno-therapy jaundice, and concluded that the appearances of the organ were more compatible with damage by an agent similar to that causing serum jaundice or epidemic hepatitis.

The relationship of serum jaundice to infective hepatitis presents a conundrum, for if it were eventually proved that the two were identical then the existence of subclinical, silent, blood-borne infective hepatitis would claim fresh significance.

Some believe that they are aetiologically different because infective hepatitis is spread by contact and has an incubation period of twenty-eight to thirty days, whereas clinical serum jaundice is normally caused by parenteral administration of icterogenic serum, and has an incubation period of eighty to a hundred days according to Paul et al. (1945), Steiner (1944), and Beattie and Marshall (1944). The latter also discovered that it was possible to reduce the incubation period of serum jaundice to thirty days by feeding infective serum. Evidence in favour of their identity has been provided by Sheehan (1944), who noticed that infective hepatitis virus may be conveyed from one man to another by unsterile needles and syringes used for aspirating blood, and that the ensuing malady assumed the character of typical serum jaundice after an incubation period of three months. Efforts to isolate virus from the faeces of serum jaundice cases by McCallum (1945) and Neefe, Stokes, and Gellis (1945) have been unsuccessful, and it therefore seems that the intestinal tract contents are not infective in serum jaundice.

Conclusions of the opposite kind have been reported by Paul et al. (1945), who found that three patients who had recovered from serum jaundice six months earlier, later proved susceptible to experimentally induced infective hepatitis. The latter have epitomised the present position by stating that the outstanding difference between serum jaundice and infective hepatitis rested in the length of the incubation period. Neefe, Stokes, and Gellis page 514 (1945) have commented that ‘Normal persons are much more likely to develop the disease when the agent is administered orally than when it is injected parenterally’, a fact which we regard as one of fundamental importance in the establishment of infective hepatitis as a primary pathological affection of the gut.

The two diseases may be closely related in that serum jaundice represents the artificial production of infective hepatitis in a proportion of instances: it cannot yet be said that all serum jaundice belongs to this category. The question of the aetiology of post-arsenical serum jaundice and infective hepatitis bristles with unsolved academic problems and practical obstacles to progress, but the subject is of as much interest in peace as in war and justifies intensive research into the pathogenesis of these icterogenic virus agents.