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The susceptibility of golden hamsters to Brugia pahangi
736
TROJS~~IONS OF THE ROYAL SOCIETYOF TROPKXL MEDKXVE AND HYGIENE(1985) 79, CORRESPONDENCE
The susceptibility
of golden hamsters to Brugia Pahngi Various strains of golden hamster (Mesocricetus auratus) have been usid as experimental hosts for filarial worms (NEILSON, 1978; MALONE ec al., 1979; CRANDALL et al., 1982; SHIGENO et al., 1983; KIMURA et aE., 1984; CARRAWAY8~MALONE, 1985).
This work has shown that different strains of hamsters vary in their susceptibility to infection with filarial worms. This led us to test the susceptibility of six inbred strains of hamster to Brugia pahungi. Aedes aegypti mosquitoes were reared and infected as described by DENHAM (1982). Five or six male hamsters of the Blacks, DSN, BEC, CA, LGN and DS strains (Intersimian Ltd, Unit 83, Milton Trading Estate, Oxon, OX14 4RY, UK) were infected with 13-day-old infective larvae of B. pahangi. These were the only inbred strains of hamster currently bred in the UK. 50 larvae were injected subcutaneously in the inguinal region and 50 intraperitoneally. The syringes were then rinsed to determine the number of larvae uninoculated. Hamsters were autopsied 59 to 64 days later and the lymphatics, heart, lungs, testes and peritoneal cavities examined for the presenceof adult worms. Adult worm recoveries are shown in Table I in which percentage infection represents adult worm recoveries relative to the actual number of larvae administered. Most adult worms were recovered from the heart and lungs (70*8%), with 16.4% from the testes and spermatic cord lymphatics and 12.8% from the other lymphatics. The peritoneal cavity of hamsters was clearly an unfavourable site for worm development for despite a total of 1,471 larvae having been injected intraperitoneally into the hamsters no adults were recovered at autopsy. Adult worm recoveries were greatest for Blacks and DSN strains of hamster. However, worm recoveries were not significantly different from those of the other four strains of hamster. None the less, recoveries of adult worms related to the number of larvae injected subcutaneously for the Blacks strain of hamster (15.8%) and the DSN strain (14.8%) compare favourably with those found for the PD4 (16.8% and 25.4%; MALONE et al., 1979; CARRAWAY & MALONE, 1985) and APG (17.2%; SHICENO et al., 1983) strains. However, the worm recoveries from these strains of hamster &e considerably lower than that found for the GN strain of hamster (36.0%: SHIGENO et al.. 1983). The highest recoveriei of B. bahangi have been recorded in the CBN strain of hamster (74.8%; KIMURA et al., 1984). This was achieved by inoculating infective larvae into the testes, instead of subcutaneously. The high susceptibility of some inbred strains of hamster to B. pa/tat@ infections makes them useful models for the study of the immunology and pathology of filarial infections. However this model suffers from two main disadvantages. Firstly, little is known about the immunology of hamsters and, secondly, few immunological reagents are produced which are specilically designed for use with these animals. S. W. LINDSAY D. A. DENHAM
London School of Hygiene and Tropical Medicine, Keppel St., London WCIE 7HT
References _---_------
Carraway, J. H. & Malone, J. B. (1985). Brugiu pahangi: comparative susceptibility of the mongolian jird, Meriones unguiculatus, and the PD4 inbred hamster, Mesocricetus auratus. Experimental Parasitology, 59, 6% 73. Crandall, C. A., Neilson, J. T. M. & Crandall, R. B. (1982). Evaluation of inbred strains of hamsters as hosts for Brugia malayi. Transactions of the Royal Society of Tropical Medicine and Hygiene, 76, p. 277. Denham, D. A. (1982). The methodology of screening for filaricidal activity using Brugia pahangi. In: Animal Models in Parasitology. D. Owen (Editor) London: Macmillan, pp. 93-104. Kimura. E.. Shieeno, S., Sakamoto. M., Shimada, M. & Aoki, Y: (19g4). Studies on B&ia pahan@ in’inbred hamsters. 2. The intratesticular inoculation of infective larvae into CBN hamsters and some other rodents. Tropical Medicine, 26, 51-56. Malone, J. B., Taylor,, H. W. & Van Brackle, M. (1979). Greater susceptibihty of I’D-4 inbred hamsters to Brugia pahangi. Transactions of the Royal Society of Tropical Medicine and Hygiene, 73, p. 475. Neilson, J. J. M. (1978). Primary infections of Dipetalonema viteae in an outbred and five inbred strains of golden hamster. Journal of Parasitology, 64, 380-383. Shigenq, S., Yamashita, S., Takahashi, H., Kimura, E., Aoki, Y. & Nakajima, Y. (1983). Studies on Brugia pahangi in inbred hamsters. Susceptibility of inbred GN and APG hamsters. Southeast Asian Journal of Tropical Medicine and Public Health, 14, 407-412.
Accepted for publication 17th April,
1985.
The causative
organism of infantile kala-azar in bmt SCHNURer al. (1985) ask if Leishmania major is the
cause of infantile kala-azar in Egypt. The probable answer is that it is not and, without more evidence, it would be regrettable if the idea that it was became entrenched in the literature. These workers think that the appearanceof visceral leishmaniasis (VL) at El Aaamv. Alexandria. sueeests “recent importation of th< diskase”. However,“Fhere have been occasional reports of VL in Egypt (referencesin AZAB et al., 1984) with one remarkably early record by PHILLIPS (1904). Furthermore, recent serological surveys by RIFAAT et al. (1983b) and MORSY et al. (1984) suggest that VL is perhaps endemic, probably at a low level, in both Upper and Lower Egypt. VL is notoriously overlooked or confused with other diseases and it hardly seems necessary to postulate recent importation. According to SCHNURet al. (1985), “of the two types of parasite found in and near Alexandria so far [in dogs and brown rats], neither was like L. donovani or L. tropica.” Thev do not mention stock D3 isolated from a dog west of Alexandria by RIFAAT et al. f 1983a)which AZABet al. (1984) tvoed bv excreted factor and the electrophoretic mob& of GPI and found to be “indistinguishable from L. donovani (= L. infantum).”
Nor
do they
comment
on four
isolates from children which were provisionally characterized by the course of infection in hamsters and excreted factor and found to be similar to L. donovani (LRCL133) (MANSOUR et al., 1984). Perhaps SCHNURet al. (1985) have examined these isolates in
more detail and have reached different conclusions. However, if the provisional identifications are correct, the question whether or not L. major is the causative agent of VL in Egypt (and its undoubted presencein dogs) seems irrelevant. (L. major has, incidentally, been found in a dog by ELBIHARIet al. (1984) in Saudi Arabia). In posing their question, SCHNURet al. (1985) point out L. maior is both viscerotrooic and dermotronic in rodents. This tells us nothing about its tropism in*man. If L. major were a common causeof VL, why is it that this form of leishmaniasis is seldom, if ever, encountered in the major foci of zoonotic cutaneous leishmaniasis (ZCL)? It may be argued that it has been missed. But that surely cannot be said of the intensively studied foci in Turkmenia and Uzbekistan. Nor can it be said of the focus in the Al-Hassa oasis in Saudi Arabia where, in spite of more than 1,500 patients with ZCL seeking treatment each year (KILLICK-KENDRICK et al.. 1985). no autochthonous casesof VL have yet been diagnosed. The occasional patient in the oasis with this form of the diseasehas always had a history of a stay in the known VL focus in the south of the Kingdom bordering on the Yemen Arab Reoublic. If it is-meant to support the notion that L. major is the causeof VL in Eftvnt. it is misleadina to comment that, in houses in El Agamy, a proven-vector of L. major, P. papatasi, is 30 times more abundant than P. langeroni (see SCHNUR et al., 1985). P. pupatusi is highly endophilic whereas P. lungeroni is not. In sticky paper catchesin the samefocus, P. langeroni is more than twice as common as P. papatasi (seeBEIER et al.. 1984). Although P. lanrxmni is not a nroven vector of L. donovani or L. uinfantum, it is in a subgenus (Larrousius) in which there are seven vectors of doonovani-like parasites causing VL in man (P. “-1
,
ariasi. P. lonm‘cusbis. P. maior svriacus. P. orientalis. P. perniciosu~, p. imimoti’ and P. tobbi) (WHO;
1984). It seems more plausible to suggest that P. langeroni is the putative vector of a donouani-like
parasite causing VL in El Agamy than to propose that
L. major transmitted by P. pupatusi could be the
cause.If it were, one would expect many casesof ZCL in that focus. The old idea that Leishmania species in man are strictly dermotropic or viscerotropic is no longer tenable. In particular, there are a number of examples of normally viscerotropic parasites occasionally causing cutaneous lesions in man. Nevertheless, there is no hard evidence yet that L. major can cause VL in any focus and the importance of typing isolates of Leishmania from patients with VL is self evident. To understand the structure of the interesting focus at El Agamy, it is equally important to isolate and type parasites from dogs, wild mammals and sandflies. R.
KILLICK-KENDRICK
MRC External Scientific Staff, Department of Pure and Applied Biology, Imperial College, London, SW7 2AZ, UK. References
Azab, M. E., Rifaat, M. A., Schnur, L. F., Makhlouf, S. A., El-Sherif, E. & Salem, A. M. (1984). Canine and
TROJS~~IONS OF THE ROYAL SOCIETYOF TROPKXL MEDKXVE AND HYGIENE(1985) 79, CORRESPONDENCE
The susceptibility
of golden hamsters to Brugia Pahngi Various strains of golden hamster (Mesocricetus auratus) have been usid as experimental hosts for filarial worms (NEILSON, 1978; MALONE ec al., 1979; CRANDALL et al., 1982; SHIGENO et al., 1983; KIMURA et aE., 1984; CARRAWAY8~MALONE, 1985).
This work has shown that different strains of hamsters vary in their susceptibility to infection with filarial worms. This led us to test the susceptibility of six inbred strains of hamster to Brugia pahungi. Aedes aegypti mosquitoes were reared and infected as described by DENHAM (1982). Five or six male hamsters of the Blacks, DSN, BEC, CA, LGN and DS strains (Intersimian Ltd, Unit 83, Milton Trading Estate, Oxon, OX14 4RY, UK) were infected with 13-day-old infective larvae of B. pahangi. These were the only inbred strains of hamster currently bred in the UK. 50 larvae were injected subcutaneously in the inguinal region and 50 intraperitoneally. The syringes were then rinsed to determine the number of larvae uninoculated. Hamsters were autopsied 59 to 64 days later and the lymphatics, heart, lungs, testes and peritoneal cavities examined for the presenceof adult worms. Adult worm recoveries are shown in Table I in which percentage infection represents adult worm recoveries relative to the actual number of larvae administered. Most adult worms were recovered from the heart and lungs (70*8%), with 16.4% from the testes and spermatic cord lymphatics and 12.8% from the other lymphatics. The peritoneal cavity of hamsters was clearly an unfavourable site for worm development for despite a total of 1,471 larvae having been injected intraperitoneally into the hamsters no adults were recovered at autopsy. Adult worm recoveries were greatest for Blacks and DSN strains of hamster. However, worm recoveries were not significantly different from those of the other four strains of hamster. None the less, recoveries of adult worms related to the number of larvae injected subcutaneously for the Blacks strain of hamster (15.8%) and the DSN strain (14.8%) compare favourably with those found for the PD4 (16.8% and 25.4%; MALONE et al., 1979; CARRAWAY & MALONE, 1985) and APG (17.2%; SHICENO et al., 1983) strains. However, the worm recoveries from these strains of hamster &e considerably lower than that found for the GN strain of hamster (36.0%: SHIGENO et al.. 1983). The highest recoveriei of B. bahangi have been recorded in the CBN strain of hamster (74.8%; KIMURA et al., 1984). This was achieved by inoculating infective larvae into the testes, instead of subcutaneously. The high susceptibility of some inbred strains of hamster to B. pa/tat@ infections makes them useful models for the study of the immunology and pathology of filarial infections. However this model suffers from two main disadvantages. Firstly, little is known about the immunology of hamsters and, secondly, few immunological reagents are produced which are specilically designed for use with these animals. S. W. LINDSAY D. A. DENHAM
London School of Hygiene and Tropical Medicine, Keppel St., London WCIE 7HT
References _---_------
Carraway, J. H. & Malone, J. B. (1985). Brugiu pahangi: comparative susceptibility of the mongolian jird, Meriones unguiculatus, and the PD4 inbred hamster, Mesocricetus auratus. Experimental Parasitology, 59, 6% 73. Crandall, C. A., Neilson, J. T. M. & Crandall, R. B. (1982). Evaluation of inbred strains of hamsters as hosts for Brugia malayi. Transactions of the Royal Society of Tropical Medicine and Hygiene, 76, p. 277. Denham, D. A. (1982). The methodology of screening for filaricidal activity using Brugia pahangi. In: Animal Models in Parasitology. D. Owen (Editor) London: Macmillan, pp. 93-104. Kimura. E.. Shieeno, S., Sakamoto. M., Shimada, M. & Aoki, Y: (19g4). Studies on B&ia pahan@ in’inbred hamsters. 2. The intratesticular inoculation of infective larvae into CBN hamsters and some other rodents. Tropical Medicine, 26, 51-56. Malone, J. B., Taylor,, H. W. & Van Brackle, M. (1979). Greater susceptibihty of I’D-4 inbred hamsters to Brugia pahangi. Transactions of the Royal Society of Tropical Medicine and Hygiene, 73, p. 475. Neilson, J. J. M. (1978). Primary infections of Dipetalonema viteae in an outbred and five inbred strains of golden hamster. Journal of Parasitology, 64, 380-383. Shigenq, S., Yamashita, S., Takahashi, H., Kimura, E., Aoki, Y. & Nakajima, Y. (1983). Studies on Brugia pahangi in inbred hamsters. Susceptibility of inbred GN and APG hamsters. Southeast Asian Journal of Tropical Medicine and Public Health, 14, 407-412.
Accepted for publication 17th April,
1985.
The causative
organism of infantile kala-azar in bmt SCHNURer al. (1985) ask if Leishmania major is the
cause of infantile kala-azar in Egypt. The probable answer is that it is not and, without more evidence, it would be regrettable if the idea that it was became entrenched in the literature. These workers think that the appearanceof visceral leishmaniasis (VL) at El Aaamv. Alexandria. sueeests “recent importation of th< diskase”. However,“Fhere have been occasional reports of VL in Egypt (referencesin AZAB et al., 1984) with one remarkably early record by PHILLIPS (1904). Furthermore, recent serological surveys by RIFAAT et al. (1983b) and MORSY et al. (1984) suggest that VL is perhaps endemic, probably at a low level, in both Upper and Lower Egypt. VL is notoriously overlooked or confused with other diseases and it hardly seems necessary to postulate recent importation. According to SCHNURet al. (1985), “of the two types of parasite found in and near Alexandria so far [in dogs and brown rats], neither was like L. donovani or L. tropica.” Thev do not mention stock D3 isolated from a dog west of Alexandria by RIFAAT et al. f 1983a)which AZABet al. (1984) tvoed bv excreted factor and the electrophoretic mob& of GPI and found to be “indistinguishable from L. donovani (= L. infantum).”
Nor
do they
comment
on four
isolates from children which were provisionally characterized by the course of infection in hamsters and excreted factor and found to be similar to L. donovani (LRCL133) (MANSOUR et al., 1984). Perhaps SCHNURet al. (1985) have examined these isolates in
more detail and have reached different conclusions. However, if the provisional identifications are correct, the question whether or not L. major is the causative agent of VL in Egypt (and its undoubted presencein dogs) seems irrelevant. (L. major has, incidentally, been found in a dog by ELBIHARIet al. (1984) in Saudi Arabia). In posing their question, SCHNURet al. (1985) point out L. maior is both viscerotrooic and dermotronic in rodents. This tells us nothing about its tropism in*man. If L. major were a common causeof VL, why is it that this form of leishmaniasis is seldom, if ever, encountered in the major foci of zoonotic cutaneous leishmaniasis (ZCL)? It may be argued that it has been missed. But that surely cannot be said of the intensively studied foci in Turkmenia and Uzbekistan. Nor can it be said of the focus in the Al-Hassa oasis in Saudi Arabia where, in spite of more than 1,500 patients with ZCL seeking treatment each year (KILLICK-KENDRICK et al.. 1985). no autochthonous casesof VL have yet been diagnosed. The occasional patient in the oasis with this form of the diseasehas always had a history of a stay in the known VL focus in the south of the Kingdom bordering on the Yemen Arab Reoublic. If it is-meant to support the notion that L. major is the causeof VL in Eftvnt. it is misleadina to comment that, in houses in El Agamy, a proven-vector of L. major, P. papatasi, is 30 times more abundant than P. langeroni (see SCHNUR et al., 1985). P. pupatusi is highly endophilic whereas P. lungeroni is not. In sticky paper catchesin the samefocus, P. langeroni is more than twice as common as P. papatasi (seeBEIER et al.. 1984). Although P. lanrxmni is not a nroven vector of L. donovani or L. uinfantum, it is in a subgenus (Larrousius) in which there are seven vectors of doonovani-like parasites causing VL in man (P. “-1
,
ariasi. P. lonm‘cusbis. P. maior svriacus. P. orientalis. P. perniciosu~, p. imimoti’ and P. tobbi) (WHO;
1984). It seems more plausible to suggest that P. langeroni is the putative vector of a donouani-like
parasite causing VL in El Agamy than to propose that
L. major transmitted by P. pupatusi could be the
cause.If it were, one would expect many casesof ZCL in that focus. The old idea that Leishmania species in man are strictly dermotropic or viscerotropic is no longer tenable. In particular, there are a number of examples of normally viscerotropic parasites occasionally causing cutaneous lesions in man. Nevertheless, there is no hard evidence yet that L. major can cause VL in any focus and the importance of typing isolates of Leishmania from patients with VL is self evident. To understand the structure of the interesting focus at El Agamy, it is equally important to isolate and type parasites from dogs, wild mammals and sandflies. R.
KILLICK-KENDRICK
MRC External Scientific Staff, Department of Pure and Applied Biology, Imperial College, London, SW7 2AZ, UK. References
Azab, M. E., Rifaat, M. A., Schnur, L. F., Makhlouf, S. A., El-Sherif, E. & Salem, A. M. (1984). Canine and