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Possible role of haematophagous insects in the transmission of type B hepatitis
368
CORRESPONDENCE
not megaloblastic anaemia. This left 17 megaloblastic anaemias due to other causes which will be reported separately. This was a very detailed study and the patients were followed for 18 months or more. In discussing megaloblastic anaemia Dr. Cook quotes East African and Zambian experience where the aetiology is dietary, and pregnant and post partum females are most commonly affected. Weight loss, intestinal symptoms and severe malabsorption are absent. He then claims that some of our cases undoubtedly fall into this category. In the abstract referred to we clearly say there was no statistical difference between the diets of our patients and matched controls. In practice a detailed dietary survey was carried out on patients and matched non anaemic controls and submitted to statistical analysis, which showed no difference. We emphasized that our patients had lost weight, had intestinal symptoms and evidence of severe malabsorption The sex incidence in our study was equal. 3 patients were post partum but it is well recognized that tropical sprue may first manifest itself at this time. It is noteworthy that 4 of our 17 non-tropical sprue megaloblastic anaemias were post partum. From this we submit that it is incorrect to infer that some of our patients have a megaloblastic anaemia due solely to poor diet. Reports of subclinical malabsorption in control populations in Africa (BANWELL et., al 1964; COOK and KAJUBI, 1966; COOK et al., 1969; HALSTEAD and SHEIR, 1969; FALAIYE, 1971; RHODES et al., 1971) emphasize that those studied were asymptomatic, and FALAIYE (1971) reports anaemia in asymptomatic Nigerians. Dr. Cook stresses that severe symptoms and megaloblastic anaemia are uncommon in tropical subclinical malabsorption but common in tropical sprue. This may be an oversimplification, as some consider subclinical malabsorption and overt tropical sprue merely to be at different points on the same spectrum (KLIPSTEIN et al., 1968; LINDENBAUM, 1973). Indeed convincing evidence has been produced that asymptomatic people and patients with hypoproteinanaemia without symptomatic tropical sprue, when investigated fully, are indistinguishable from tropical sprue. A proportion of these have been shown to improve small intestinal structure and function after conventional tropical sprue therapy (KLIPSTEIN et al., 1968). As elsewhere in Africa we see subclinical malabsorption in our normal population with changes in jejunal morphology and xylose malabsorption judged by Western criteria. We distinguish this entity from tropical sprue and it is difficult to understand how Dr. Cook, using his own criteria mentioned above, could suggest that some of our reported cases of tropical sprue are merely tropical enteropathy. Our abstract points out that all 24 tropical sprues had objective evidence of severe malabsorption and we mention symptoms of anaemia, weight loss, abdominal pain and diarrhoea. The details are that they all had weight loss and anorexia, 16 had abdominal pain or diarrhoea and 21 had severe megaloblastic anaemia (mean Hb. 5.4 g.). We further report remission on conventional therapy for tropical sprue, nine on tetracycline alone with no change of diet. Many presented with the classical symptoms and signs of chronic endemic tropical sprue, one died and autopsy revealed no other pathology. We therefore consider these patients to have proved symptomatic tropical sprue and we are regularly seeing similar cases in our practice in Rhodesia. We are, etc., G. E. THOMAS, D. J. CLAIN, University of Rhodesia. 4 April, 1975. REFERENCES BANWELL, J. G., HUTT, M. S. R. & TUNCLIFFE, R. (1964). E. Afr. med. J., 41, 46. COOK, G. C. (1974). Trans. R. Sot. trop. Med. Hyg., 68, 419. & KAJUEI, S. K. (1966). Lancet, i, 725. & LEE, F. D. (1969). J. Path. But., 98, 157. -> FALAIYE, J. M. (1971). Br. Med. J., 4, 454. HALSTEAD, D. H., WEIR, SOURIAL N. & PATHWARDHAN, V. N. (1969). Am. J. cl&. Nutr., 22, 744. KLIPSTEIN, F. A., SAMLOFF, I. M., SFVIARTH, G. & SCHENK, E. (1968). Ibid., 21, 1042. LINDENBATJM, J. (1973). Gastroenterology, 64, 637. RHODES, A. R., SHEA, N. & LINDENBATJM, J. (1971). Am. J. clin. Nutr., 24, 574.
POSSIBLEROLE OF HAEMATOPHAGOUSINSECTSIN THE TRANSMISSIONOF TYPE B HEPATITIS SIR,-Many recent studies have focused on the possible role of haematophagous insects in the transmission of type B hepatitis (HBV). SMITH et al. (1972) reported biological transmission by Culex pipiens futiguns, an observation which has not yet been confirmed. Most investigators believe that mosquitoes and other insects may act merely as mechanical or passive vectors of HBV (PRINCE et al., 1972; BYEOM et al., 1973; NEWKIRK et al., 1974). Working in a highly endemic area in Costa Rica, where the yearly incidence of hepatitis exceeds 150 per 100,000 in the absence of parenteral mechanisms of transmission (VILLAEEJOS et al., 1972), we have examined insects caught in the homes of chronic HBsAg carriers for the presence of the antigen. The population in the study area uses insecticides liberally; hence in 61 houses we were able to collect only 6 pools of fleas and a few reduviid bugs, but no Cymex. However, in and around the houses, 112 pools of Culex spp. and 18 pools of
CORRESPONDENCE
369
man biting Simuliidae were collected. All insect pools were examined by solid-phase radioimmuno-assay (Ausria I) Abbott Laboratories, North Chicago. The antigen was found in only one pool of Culex which contained blood engorged females; the other insect pools were consistently negative. These findings do not lend support to the hypothesis of active insect transmission of type B hepatitis; however, it is possible that squashing of infected mosquitoes on interrupted feeding may occasionally lead to transmission of the infection. Further, 8 groups of colony-reared Rhodnius prolixus were allowed to feed on HBsAg positive blood and killed at weekly intervals thereafter. The antigen was found in the stomach content and faeces of all insects during the first 2 weeks after the infecting feeding and it persisted up to 4 weeks in 50% of the reduviids. At no stage of the 6-week experiment did the haemolymph or the salivary glands contain detectable HBsAg, indicating that the virus does not proliferate in the insect. However, mechanical transmission by scratching insect faeces into the biting wound is possible. These results indicate that the bloodsucking insects investigated could play a certain role in the passive transmission of HBsAg, but probably are not biological vectors of hepatitis B virus. We are, etc., VICTOR M. vILL.4aEJos, ALBERTO Z~~IGA, ALVARO GUTI~RREZ
6 March, 1975
D., Louisiana State University, International Center for Medical Research and Training, Apdo. 10155 San Jose, Costa Rica.
REFERENCES BYROM, N. A., DAVISON G., DRAPER C. C. & ZUCKERMAN A. J. (1973). J. infect. Dis., 128, 259. NEWKIRK, M. M., DOWNE, A. E. R. & SIMON, J. B. (1974). Gastroenterology, 67, 817. PRINCE, A. M., METSELAAR, D., KAFUKO, G. W., MUKWAYA, L. G., LING, C. L. & OVERBY, L.
Lancet, ii, 247.
SMITH, J. A., AG~NBA, E. 0. & FRANCIS, T. I. (1972). Nature, 237, 231. VILLAREJOS, V. M., ARGUEDAS, J. A. & GUTII%EZ, A. (1972). Gastroenterology,
62, 199.
R. (1972).
CORRESPONDENCE
not megaloblastic anaemia. This left 17 megaloblastic anaemias due to other causes which will be reported separately. This was a very detailed study and the patients were followed for 18 months or more. In discussing megaloblastic anaemia Dr. Cook quotes East African and Zambian experience where the aetiology is dietary, and pregnant and post partum females are most commonly affected. Weight loss, intestinal symptoms and severe malabsorption are absent. He then claims that some of our cases undoubtedly fall into this category. In the abstract referred to we clearly say there was no statistical difference between the diets of our patients and matched controls. In practice a detailed dietary survey was carried out on patients and matched non anaemic controls and submitted to statistical analysis, which showed no difference. We emphasized that our patients had lost weight, had intestinal symptoms and evidence of severe malabsorption The sex incidence in our study was equal. 3 patients were post partum but it is well recognized that tropical sprue may first manifest itself at this time. It is noteworthy that 4 of our 17 non-tropical sprue megaloblastic anaemias were post partum. From this we submit that it is incorrect to infer that some of our patients have a megaloblastic anaemia due solely to poor diet. Reports of subclinical malabsorption in control populations in Africa (BANWELL et., al 1964; COOK and KAJUBI, 1966; COOK et al., 1969; HALSTEAD and SHEIR, 1969; FALAIYE, 1971; RHODES et al., 1971) emphasize that those studied were asymptomatic, and FALAIYE (1971) reports anaemia in asymptomatic Nigerians. Dr. Cook stresses that severe symptoms and megaloblastic anaemia are uncommon in tropical subclinical malabsorption but common in tropical sprue. This may be an oversimplification, as some consider subclinical malabsorption and overt tropical sprue merely to be at different points on the same spectrum (KLIPSTEIN et al., 1968; LINDENBAUM, 1973). Indeed convincing evidence has been produced that asymptomatic people and patients with hypoproteinanaemia without symptomatic tropical sprue, when investigated fully, are indistinguishable from tropical sprue. A proportion of these have been shown to improve small intestinal structure and function after conventional tropical sprue therapy (KLIPSTEIN et al., 1968). As elsewhere in Africa we see subclinical malabsorption in our normal population with changes in jejunal morphology and xylose malabsorption judged by Western criteria. We distinguish this entity from tropical sprue and it is difficult to understand how Dr. Cook, using his own criteria mentioned above, could suggest that some of our reported cases of tropical sprue are merely tropical enteropathy. Our abstract points out that all 24 tropical sprues had objective evidence of severe malabsorption and we mention symptoms of anaemia, weight loss, abdominal pain and diarrhoea. The details are that they all had weight loss and anorexia, 16 had abdominal pain or diarrhoea and 21 had severe megaloblastic anaemia (mean Hb. 5.4 g.). We further report remission on conventional therapy for tropical sprue, nine on tetracycline alone with no change of diet. Many presented with the classical symptoms and signs of chronic endemic tropical sprue, one died and autopsy revealed no other pathology. We therefore consider these patients to have proved symptomatic tropical sprue and we are regularly seeing similar cases in our practice in Rhodesia. We are, etc., G. E. THOMAS, D. J. CLAIN, University of Rhodesia. 4 April, 1975. REFERENCES BANWELL, J. G., HUTT, M. S. R. & TUNCLIFFE, R. (1964). E. Afr. med. J., 41, 46. COOK, G. C. (1974). Trans. R. Sot. trop. Med. Hyg., 68, 419. & KAJUEI, S. K. (1966). Lancet, i, 725. & LEE, F. D. (1969). J. Path. But., 98, 157. -> FALAIYE, J. M. (1971). Br. Med. J., 4, 454. HALSTEAD, D. H., WEIR, SOURIAL N. & PATHWARDHAN, V. N. (1969). Am. J. cl&. Nutr., 22, 744. KLIPSTEIN, F. A., SAMLOFF, I. M., SFVIARTH, G. & SCHENK, E. (1968). Ibid., 21, 1042. LINDENBATJM, J. (1973). Gastroenterology, 64, 637. RHODES, A. R., SHEA, N. & LINDENBATJM, J. (1971). Am. J. clin. Nutr., 24, 574.
POSSIBLEROLE OF HAEMATOPHAGOUSINSECTSIN THE TRANSMISSIONOF TYPE B HEPATITIS SIR,-Many recent studies have focused on the possible role of haematophagous insects in the transmission of type B hepatitis (HBV). SMITH et al. (1972) reported biological transmission by Culex pipiens futiguns, an observation which has not yet been confirmed. Most investigators believe that mosquitoes and other insects may act merely as mechanical or passive vectors of HBV (PRINCE et al., 1972; BYEOM et al., 1973; NEWKIRK et al., 1974). Working in a highly endemic area in Costa Rica, where the yearly incidence of hepatitis exceeds 150 per 100,000 in the absence of parenteral mechanisms of transmission (VILLAEEJOS et al., 1972), we have examined insects caught in the homes of chronic HBsAg carriers for the presence of the antigen. The population in the study area uses insecticides liberally; hence in 61 houses we were able to collect only 6 pools of fleas and a few reduviid bugs, but no Cymex. However, in and around the houses, 112 pools of Culex spp. and 18 pools of
CORRESPONDENCE
369
man biting Simuliidae were collected. All insect pools were examined by solid-phase radioimmuno-assay (Ausria I) Abbott Laboratories, North Chicago. The antigen was found in only one pool of Culex which contained blood engorged females; the other insect pools were consistently negative. These findings do not lend support to the hypothesis of active insect transmission of type B hepatitis; however, it is possible that squashing of infected mosquitoes on interrupted feeding may occasionally lead to transmission of the infection. Further, 8 groups of colony-reared Rhodnius prolixus were allowed to feed on HBsAg positive blood and killed at weekly intervals thereafter. The antigen was found in the stomach content and faeces of all insects during the first 2 weeks after the infecting feeding and it persisted up to 4 weeks in 50% of the reduviids. At no stage of the 6-week experiment did the haemolymph or the salivary glands contain detectable HBsAg, indicating that the virus does not proliferate in the insect. However, mechanical transmission by scratching insect faeces into the biting wound is possible. These results indicate that the bloodsucking insects investigated could play a certain role in the passive transmission of HBsAg, but probably are not biological vectors of hepatitis B virus. We are, etc., VICTOR M. vILL.4aEJos, ALBERTO Z~~IGA, ALVARO GUTI~RREZ
6 March, 1975
D., Louisiana State University, International Center for Medical Research and Training, Apdo. 10155 San Jose, Costa Rica.
REFERENCES BYROM, N. A., DAVISON G., DRAPER C. C. & ZUCKERMAN A. J. (1973). J. infect. Dis., 128, 259. NEWKIRK, M. M., DOWNE, A. E. R. & SIMON, J. B. (1974). Gastroenterology, 67, 817. PRINCE, A. M., METSELAAR, D., KAFUKO, G. W., MUKWAYA, L. G., LING, C. L. & OVERBY, L.
Lancet, ii, 247.
SMITH, J. A., AG~NBA, E. 0. & FRANCIS, T. I. (1972). Nature, 237, 231. VILLAREJOS, V. M., ARGUEDAS, J. A. & GUTII%EZ, A. (1972). Gastroenterology,
62, 199.
R. (1972).