Thursday, October 4, 2007

Bed bugs, Insects, and Hepatitis B


Hepatitis B virus may be transmitted in two main ways. The first is by blood and some plasma derivatives, and by any procedure in which the skin or mucosa is penetrated by inadequately sterilised contaminated needles and instruments. Known modes of transmission of hepatitis B include tattooing, acupuncture, piercing of the ear and nose, scarification, ritual operations, and blood letting. The second main method of spread occurs non-parenterally, by intimate contact and by the sexual route. Both of these latter possibilities have been recognised more recently, but we now know that this list does not exhaust the epidemiological propensities of this infection: is, for instance, hepatitis B spread by mosquitoes and other blood-sucking arthropods, particularly in hot climates ? This
possibility has been studied for several years, but the results have been conflicting.[1] Hepatitis B surface antigen, a marker of the virus,[2] has been detected in several species of mosquitoes trapped in the wild or fed artificially on infected blood. Even
so, no convincing evidence has been obtained of either replication of the virus or persistence of the antigen in the

Bed bugs, on the other hand, live more intimately with man than mosquitoes, feed on blood, and could transfer blood and hepatitis B virus from one occupant of a bed to another. Indeed, hepatitis B surface antigen was detected in one of 18 pools of engorged bed bugs (species Cimex hemipterus) collected from brothels in the Ivory Coast.[3] In a laboratory
study two species of bed bugs-the common bed bug, C lectularius, and Rhodinus prolixus from South America-were fed artificially on blood from a patient with acute hepatitis B.[4] The surface antigen remained detectable in the bugs for over four weeks, and juvenile bugs fed on the antigen when in the fourth or fifth instar stage still retained it after moulting-the time when bugs usually start to search for a host and to refeed. In another study,[5] bed bugs of the species C hemipterus were collected on several separate occasions from bedding in village huts in Senegal. Hepatitis B surface antigen was detected in engorged and unengorged nymph and adult bed bugs, as well as in bugs kept alive without a blood meal for 30 days. Moreover, e antigen (a marker of infectivity of hepatitis B virus [2]) was found in one engorged and one unengorged bed bug.

Hence we might reasonably deduce that bed bugs feeding on the occupants of the same bed could increase the risk of hepatitis B infection. Blood-sucking bed bugs can regurgitate virus, and it might be present in their saliva; while two other modes of transmission of the virus might be by killing the insect during feeding, and by faecal extrusion of the unaltered virus by the bug after a meal of blood. By themselves these observations are insufficient evidence for accepting the bed bug as a vector of hepatitis B virus, but Jupp and McElligott [6] have now taken the story a step further. A colony of C lectularius was fed on blood containing hepatitis B surface antigen. Again, there was no evidence that the virus replicated in the bugs: the antigen persisted after one moult only (transstadial transmission) and it was not transmitted transovarially. Nevertheless, antigen was transmitted by adult bugs through a membrane into three out of 35 cannisters of antigen-negative blood and, as judged by the acquisition of hepatitis B surface antibody, to a rabbit by adult bugs and to two out of 10 guinea-pigs on which antigen-positive fourth and fifth nymphal instars had fed.

These findings indicate that bed bugs can transmit hepatitis B mechanically to non-permissive hosts, and it is reasonable to assume that transmission rates to susceptible primates might be high. Hence the question of transmission of hepatitis B by blood-sucking insects merits further investigation, especially since we could at least control this type of spread of this important infection.

[1] Viral Hepatitis, World Health Organisation Technical Report Series, No 570. Geneva, World Health Organisation, 1975.
[2] Zuckerman, A J, British Medical Journal, 1979, 2, 84.
[3] Brotman, B, Prince, A M, and Godfrey, H R, Lancet, 1973, 1, 1305.
[4] Newkirk, M M, Downe, A E R, and Simon, J B, Gastroenterology, 1975, 69, 982.
[5] Wills, W, et al, Lancet, 1977, 2, 217.
[6] Jupp, P G, and McElligott, S E, South African Medical-Journal, 1979, 2,54.

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