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Cross-protection between the metacestodes of Mesocestoides corti and Taenia crassiceps in mice
Internorionol Journalfor Printed in Great Britain.
Parasitology
Vol. 14. No. Spp. 497-501,
1984. B
1984 Auslralian
002W7519/84 $3.oO+O.a) Per@nnon Press Ltd. Society for Parasitology
CROSS-PROTECTION BETWEEN THE METACESTODES OF MESOCESTOIDES CORTIAND TAENIA CRASSICEPS IN MICE MARIE NOVAK Department
of Biology,
University
of Winnipeg,
Winnipeg,
Manitoba,
Canada
R3B 2E9
(Received 29 August 1983; in revisedform 1 February 1984) Abstract-NOVAK M. 1984. Cross-protection between the metacestodes of Mesocestoides corti and Taenia crassiceps in mice. International Journal for Parasitology 14: 497-501. Infection with M. corti generated significant resistance against a challenge with T. crassiceps introduced either 2 or 6 weeks after primary infection. Challenge infection with T. crassiceps did not influence primary infection with M. corti. Infection with T. crassiceps protected significantly against challenge with M. corti given 2 weeks but not 6 weeks after the primary infection. Challenge infection with M. corti significantly suppressed primary infection with T. crassiceps. INDEX KEY WORDS:
Mesocestoides corti; Taenia crassiceps, metacestodes;
INTRODUCTION MICE develop a significant degree of resistance to a homologous challenge infection with Mesocestoides corti. This has been demonstrated by subcutaneous inoculations of tetrathyridia previous to intraperitoneal challenge (Kazacos, 1976) and by passive transfer of immune serum (Kowalski & Thorson, 1972) or sensitized spleen cells (Novak, 1977). Significant resistance in mice can also be generated to homologous intraperitoneal challenge with Tueniu crassiceps by previous subcutaneous implantation of cysticerci (Siebert, Good & Simmons, 1978a; Siebert & Good, 1980) or by sensitized lymph node cells (Anderson & Griffin, 1979). Although the mechanisms of resistance to homologous reinfections with these two parasites are poorly understood, the above studies indicate that both antibody and cellular components play a role in resistance to M. corti and
T. crassiceps. Since both these metacestodes elicit significant host resistance to homologous reinfections, it is possible that cross-protection may occur between these two proliferative larvae, which occupy a similar habitat, the peritoneal cavity of a mouse. The present study was designed to investigate this possibility.
MATERIALS AND METHODS Slciss-Webster female mice, 4 months old, were used. Groups of five mice were housed in wire-bottom cages at a temperature of 20°C and relative humidity of 50% and fed commercial food pellets and water ad libitum. The light cycle was 15 h simulated daylight and 9 h darkness. Mice infected with M. corti received, in all cases, 50 single tctrathyridia intraperitoneally each. Mice infected with T. crussiceps received 20 non-budding cysticerci each.
497
mice; cross-protection.
Primary infections were terminated 4, 6 and 10 weeks post infection (p.i.). Challenge infections with the heterologous parasite were performed either 2 or 6 weeks following primary infections and were always terminated 4 weeks p.i. At autopsy, the larvae were washed out of the peritoneal cavities of the mice and counted with the help of a dissecting microscope. Single and dividing (with at least two scoleces on one body) tetrathyridia in Mesocestoides infections and non-budders and budders (with bud primordia on the parental body) in Taenia infections were recorded. In the case of M. corti, estimation of the intensity of liver infection was made on the basis of the number of larvae per cm2 of the liver surface (Novak, 1972). Student’s t-test was used for statistical analysis. Probability levels greater than 5% were regarded as statistically not significant (NS).
RESULTS Mesocestoides challenged with Taenia Immunization of mice with Mesocestoides significantly reduced Tuenia burdens in challenged infections (Table 1). This reduction was more prominent at 2 than at 6 weeks of challenge, 93 and 75% respectively. The average number of cysticerci found in mice challenged 2 weeks p.i. was about 25% lower than the original inoculum (20 larvae per mouse). Obviously, some of the larvae did not get established, died and disintegrated. Those which were recovered were alive, but their growth was inhibited as only a few budders with very tiny bud primordia were present. The number of cysticerci in mice challenged 6 weeks after Mesocestoides infection slightly increased, when compared to the 2 weeks challenge infection, indicating that the asexual reproduction in this group was inhibited to a lesser degree. The tetrathyridial populations in mice challenged with cysticerci either at 2 or 6 weeks of infection were also
*M = moderate liver infection. +fp < 0.001. *p < 0.05. NS-not significant.
M
M. corti 10 15 T. crassiceps 4 14 challenge 6 weeks after M. corti infection M. corti/T. crassiceps 10/4 15 M
M
Liver* infection
challenge 2 weeks after M. corfi T. crassiceps 4 infection 15 M. corti/T. crassiceps 6/4 15
No. of mice
M
6
Duration of infection (weeks)
4 WEEKS
AFTER
Non-budders
Budders
Total
f S.E.
CHALLENGEOF MICE GIVEN T. crassiceps
CHALLE~~GEINFEC?I~NOF
Mean no. of Taenia cysticerci
CYSTKERCI RECOVERED PRI~R~~A
15
M. corii
Group
TABLE I-NUMBER OF TETRATHYR~DIA AND
Single
Dividing
Total
? S.E.
WEEKS
tetrathyridia
INFECTION OF A4. corti 2 OR 6
Mean no. of Mesocesfoides
A PRIMARY
after
corti
= light
NS-not
gp <
0.02.
to moderate
significant.
tp < om1. *p < 0.01.
*L-M
liver
infection 15 14
14
infection 15
15
mice
of
No.
infection;
challenge after T. crassiceps 4 10/4 M. corti 6 weeks corti T. crassiceps/M.
T. crassiceps
10
T. crassiceps 6 6/4
T. crassiceps/M crassiceps
challenge
(weeks)
infection
of
Duration
OF CYSTICERCI
4
2 weeks
2--NUMBER
M. corti
Group
TABLE
LL
AND
= very
;;
-
L-M
infection
Liver*
light
liver
;;;::
:::::
TETRATHYRIDIA
*
of
infection.
1 :;@;]NS
:
no.
::::I
Single
Mean
PRIOR
RECOVERED WEEKS
4 WEEKS
1;:;
:::I
: ‘::I]+
:
::j
Dividing
Mesocestoides
CHALLENGE INFECTION
:;;:;
::I::
tetrathyridia
AFTER
TO A CHALLENGE
: =;]NS
:
S.E.
:::;I
Total
f
*
COrfi
;;;:::
2;;::
4;:;]?
1 ;;;#;I
1
5
no.
:;;#:
;;::
of
INFECTION
Mean
A PRIMARY
Non-budders
OF MICE GIVEN OF M.
T.
CraSSiCefX
:JNS
1 ::#;]NS
1
Budders
Taeniacysticerci
OF
I;;:#;
5;:;]+
1 ::_3
1
Total
S.E.
2;;:;
k
2 OR 6
0
2 B 8.
3
1
I
500
MARIENOVAK
smaller (2.5 and 31% respectively) than those in controls and contained a lower number of larvae in the process of division. However, these differences were not (except between dividing larvae in the 6 weeks challenge group) statistically significant. The livers in controls and mice challenged with cysticerci at 2 or 6 weeks of infection were moderately infected with tetrathyridia. Taenia challenged with Mesocestoides Mice infected with Taenia and challenged 2 weeks later with Mesocestoides harbored significantly less than the Mesocestoides infected tetrathyridia controls (Table 2). This significant difference disappeared when mice were challenged 6 weeks p.i. In this latter challenge group, the reduction in the total intraperitoneal tetrathyridial biomass was only 20070, whereas it was 40% in the former challenge group. In both challenge groups of mice the asexual reproduction of tetrathyridia was severely impaired as indicated by the significant reduction in the number of dividing larvae. The livers of these challenged mice were very lightly infected whereas those of controls were light to moderate. Challenge infection also significantly reduced the number of Taenia cysticerci developing from a primary infection (Table 2). This reduction in the biomass of primary infection was much more pronounced when heterologous larvae were introduced 2 weeks rather than 6 weeks after primary infection, 75 and 37% respectiveiy. Though the Taenia populations from controls and challenged groups contained a similar the overall morphological number of budders, composition of these populations differed. Control populations contained large numbers of single larvae (non-budders) out of which many were small, freshly separated buds and the budding larvae in these populationswere covered with many buds of various sizes. In populations from challenged mice, the asexual reproduction of cysticerci was retarded. The budders had fewer and very small buds and the number of non-budders, including small individuals, was also low.
The present results revealed the existence of crossresistance between two proliferating cestode larvae, M. corti and T. crassiceps. Primary infection with either tetrathyridia of M. corti or cysticerci of T. crassiceps generated significant resistance against a challenge infection with the heterologous species. the degree of protection against the However, challenge infection varied according to the parasite species used in the primary infection and the time when the challenge infection was introduced. The finding that M. corfi, when introduced as a challenge infection, adversely affected the growth and proliferation of primary T. crassiceps pOpulations was unexpected and certainly deserves further
I.J.P.VOL. 14.1984
investigation. One of the possibilities which could be tested is the existence of substances released by tetrathyridia which might act as growth inhibitors. Various toxic or inhibitory substances secreted by the worms have been reported for cestodes. Hymertotepis diminuta releases substances with growth-inhibiting properties that affect other worms in the host intestine (Insler & Roberts, 1980a, b; Roberts & Insler, 1982). H. microstoma secretes toxic substances which produce lesions in the liver of the host (Simpson & Gleason, 1975). It has been observed that in M. corti infections in mice broad zones of necrotic hepatocytes develop in parasitized liver (Specht & Widmer, 1972; Novak, 1982). Whether these necrotic lesions are caused by toxic products secreted by tetrathyridia and if these secretions can act as growth inhibitors remains to be answered. Partial cross-protection was obtained also for other metacestodes such as Taenia hydatigena, T. ovis and E. granulosus by Heath, Lawrence & Yong (1979). There, prior infection with all combinations of heterologous species resulted in a lesser degree of immunity than that obtained for challenge infections with homologous species. The protection seemed to have acted on the establishment phase of development and did not influence cyst survival. Both metacestodes are known to provoke a dramatic inflammatory reaction (Freeman, 1964; Specht & Widmer, 1972; Mitchell & Handman, 1977; Siebert et al., 1978a, b; Siebert & Good, 1979; Novak, 1982) but more so in the case of AK corti infection, since this parasite invades host tissues, especially liver (Specht & Widmer, 1972; Novak, 1982). Conceivably, the cross-immunity observed in the present experiments, especially during the earlier challenge, arises to some degree from the nonspecific inflammation response evoked by one species acting nonspecifically against the other species present. Recently, similar mouse antibodies, with IgG and IgM in the greatest amounts, were demonstrated to be on the body surfaces of M. corti by Mitchell, Marchalonis, Smith, Nicholas & Warner (1977), Zodda & Thorson (1982) and on T. crassiceps by Siebert, Bhtz, Morita & Good (1981). However, the larvae of both species were found to be capable of rapid shedding of the host serum components attached to their tegument (Zodda & Thorson, 1982; Siebert er a/., 1981). Findings of this kind suggest that even if cross-reactive or specific antibodies to worm surface antigens are produced, the ability to shed surface bound antibodies by worms may be one of the means by which these metacestodes successfully survive in their immunologically active host.
I.J.P. VOL. 14. 1984
Cross-protection
between M. Corti and T. crassiceps
REFERENCES ANDERSON M. Y. D. & GRIFFIN Y. F. T. 1979. Taenia crassiceps in the rat: transfer of immunity and immunocompetence with lymph node cells. International Journal for Parasitology 9: 235-239. FREEMAN R. S. 1964. Studies on responses of intermediate hosts to infection with Taenia crassiceps (Zeder, 1800) (Cestoda). Canadian Journal of Zoology 42: 367-384. HEATH D. D., LAWRENCE S. B. & YONC W. K. 1979. Cross-protection between the cysts of Echinococcus granulosus, Taenia hydatigena and T. ovis in lambs. Research in Veterinary Science 27: 2 IO-2 12. INSLER G. D. & ROBERTS L. S. 198Oa. Developmental physiology of cestodes. XV. A system for testing possible crowding factors in vitro. Journal of Experimental Zoology 211: 45-54. INSLER G. D. & ROBERTS L. S. 1980b. Developmental physiology of cestodes. XVI. Effects of certain excretory products on incorporation of 3 H-thymidine into DNA of Hymenolepis diminuta. Journal of Experimental Zoology21l: 55-61. KAZACOS K. R. 1976. Immunization of mice against Mesocesfoides corri by subcutaneous inoculation of living tetrathyridia. Journalof Parasitology62: 161-163. KOWALSKI J. C. & THORSON R. E. 1972. Immunization of laboratory mice against tetrathyridia of Mesocesfoides corti (Cestoda) using secretory and excretory antigens and a soluble somatic antigen. Journal of Parasi/ology 58: 732-734. MIrTHELI. G. F. & HANDMA~ E. 1977. Studies on immune responses to larval cestodes in mice: a simple mechanism of nonspecific immunosuppression in Mesocesloides corti infected mice. Australian Journal of Experimental Biology and Medical Science 55: 6 1S-622. MI~~HELI. G. F., MARCHALONIS J. J., SMITH P. M., NICHOLAS W. L. & WARNER N. L. 1977. Studies on immune respones to larval cestodes in mice. Immunoglobulins associated with the larvae of Mesocesloides corri. Auskalian Journal of Experimenial Biology and Medwal Scrence 55: 187-2 11. NOVAK M. 1972. Quantitative studies on the growlh and multiplication of tetrathyridia of Mesocesroides corri Hoeppli, I925 (Ccstoda: Cyclophyllidea) in rodents. Canadian Journal of Zoology 50: 1189-l 196.
501
NOVAK M. 1977. Transfer of immunity to Mesocestoides corti infection by spleen cells. Journal of Parasifology 63: 587-588. NOVAK M. 1982. Histopathological changes in livers of mice infected with tetrathyridia of Mesocesfoides corti and exposed to different environmental temperatures. International Journal for Parasitology 12: 41-45. ROBERTS L. S. & INSLER G. D. 1982. Developmental physiology of cestodes. XVII. Some biological properties of putative “crowding factors” in Hymenolepis diminuta. Journal of Parasitology 68: 263-269. SIEFIER~ A. E. JR., GOOD, A. H. & SIMMONS Y. E. 1978a. Kinetics of primary and secondary infections with Taenia crassiceps metacetodes (Zeder, 1800) Rudolphi, 1810 (Cestoda: Cyclophyllidea). International Journal for Parasilology 8: 39-43. SIEBER~ A. E. JR., GOOD A. H. & SIMMONS J. E. 1978b. Ultrastructural aspects of early immune damage to Taenia crassiceps metacestodes. Iniernational Journal for Parasilology 8: 45-53. SIEBER~ A. E. JR. & GOOD A. H. 1979. Taenia crassiceps. Effect of normal and immune serum on metacestodes in vitro. Experimental Parasitology 48: 164-I 74. SlEaEar A. E. JR. & GOOD A. H. 1980. Tgenia crassiceps: Immunity to metacestodes in BALB/c and BDF, mice. Experimental Parasirology 50: 437-446. Sisstar A. E. JR., BLrrz R. R., MORITA C. T. & GOOD A. H. 1981. Taenia crassiceps: Serum and surface immunoglobulins in metacestode infections of mice. Experimental Parasitology 51: 418-430. SIMPSON G. F. & GLEASON L. N. 1975. Lesion formation in the livers of mice caused by metabolic products of Hymenolepis microsroma. Journal of Parasitology 6 1: 152-154. SP~~HJ D. & WIDMER E. 1972. Response of mouse liver LO infection with tetrathyridia of Mesocesroides (Cestoda). Journal of Parasitology 58: 43 l-437. ZODDA D. M. & THORSON R. E. 1982. In viva and in vifro studies demonstrating the presence and turnover of host substances on the tegument of Mesocestoides corri (Cestoda) tetrathyridia. Journal of Parasirology 68: 796-803.
Parasitology
Vol. 14. No. Spp. 497-501,
1984. B
1984 Auslralian
002W7519/84 $3.oO+O.a) Per@nnon Press Ltd. Society for Parasitology
CROSS-PROTECTION BETWEEN THE METACESTODES OF MESOCESTOIDES CORTIAND TAENIA CRASSICEPS IN MICE MARIE NOVAK Department
of Biology,
University
of Winnipeg,
Winnipeg,
Manitoba,
Canada
R3B 2E9
(Received 29 August 1983; in revisedform 1 February 1984) Abstract-NOVAK M. 1984. Cross-protection between the metacestodes of Mesocestoides corti and Taenia crassiceps in mice. International Journal for Parasitology 14: 497-501. Infection with M. corti generated significant resistance against a challenge with T. crassiceps introduced either 2 or 6 weeks after primary infection. Challenge infection with T. crassiceps did not influence primary infection with M. corti. Infection with T. crassiceps protected significantly against challenge with M. corti given 2 weeks but not 6 weeks after the primary infection. Challenge infection with M. corti significantly suppressed primary infection with T. crassiceps. INDEX KEY WORDS:
Mesocestoides corti; Taenia crassiceps, metacestodes;
INTRODUCTION MICE develop a significant degree of resistance to a homologous challenge infection with Mesocestoides corti. This has been demonstrated by subcutaneous inoculations of tetrathyridia previous to intraperitoneal challenge (Kazacos, 1976) and by passive transfer of immune serum (Kowalski & Thorson, 1972) or sensitized spleen cells (Novak, 1977). Significant resistance in mice can also be generated to homologous intraperitoneal challenge with Tueniu crassiceps by previous subcutaneous implantation of cysticerci (Siebert, Good & Simmons, 1978a; Siebert & Good, 1980) or by sensitized lymph node cells (Anderson & Griffin, 1979). Although the mechanisms of resistance to homologous reinfections with these two parasites are poorly understood, the above studies indicate that both antibody and cellular components play a role in resistance to M. corti and
T. crassiceps. Since both these metacestodes elicit significant host resistance to homologous reinfections, it is possible that cross-protection may occur between these two proliferative larvae, which occupy a similar habitat, the peritoneal cavity of a mouse. The present study was designed to investigate this possibility.
MATERIALS AND METHODS Slciss-Webster female mice, 4 months old, were used. Groups of five mice were housed in wire-bottom cages at a temperature of 20°C and relative humidity of 50% and fed commercial food pellets and water ad libitum. The light cycle was 15 h simulated daylight and 9 h darkness. Mice infected with M. corti received, in all cases, 50 single tctrathyridia intraperitoneally each. Mice infected with T. crussiceps received 20 non-budding cysticerci each.
497
mice; cross-protection.
Primary infections were terminated 4, 6 and 10 weeks post infection (p.i.). Challenge infections with the heterologous parasite were performed either 2 or 6 weeks following primary infections and were always terminated 4 weeks p.i. At autopsy, the larvae were washed out of the peritoneal cavities of the mice and counted with the help of a dissecting microscope. Single and dividing (with at least two scoleces on one body) tetrathyridia in Mesocestoides infections and non-budders and budders (with bud primordia on the parental body) in Taenia infections were recorded. In the case of M. corti, estimation of the intensity of liver infection was made on the basis of the number of larvae per cm2 of the liver surface (Novak, 1972). Student’s t-test was used for statistical analysis. Probability levels greater than 5% were regarded as statistically not significant (NS).
RESULTS Mesocestoides challenged with Taenia Immunization of mice with Mesocestoides significantly reduced Tuenia burdens in challenged infections (Table 1). This reduction was more prominent at 2 than at 6 weeks of challenge, 93 and 75% respectively. The average number of cysticerci found in mice challenged 2 weeks p.i. was about 25% lower than the original inoculum (20 larvae per mouse). Obviously, some of the larvae did not get established, died and disintegrated. Those which were recovered were alive, but their growth was inhibited as only a few budders with very tiny bud primordia were present. The number of cysticerci in mice challenged 6 weeks after Mesocestoides infection slightly increased, when compared to the 2 weeks challenge infection, indicating that the asexual reproduction in this group was inhibited to a lesser degree. The tetrathyridial populations in mice challenged with cysticerci either at 2 or 6 weeks of infection were also
*M = moderate liver infection. +fp < 0.001. *p < 0.05. NS-not significant.
M
M. corti 10 15 T. crassiceps 4 14 challenge 6 weeks after M. corti infection M. corti/T. crassiceps 10/4 15 M
M
Liver* infection
challenge 2 weeks after M. corfi T. crassiceps 4 infection 15 M. corti/T. crassiceps 6/4 15
No. of mice
M
6
Duration of infection (weeks)
4 WEEKS
AFTER
Non-budders
Budders
Total
f S.E.
CHALLENGEOF MICE GIVEN T. crassiceps
CHALLE~~GEINFEC?I~NOF
Mean no. of Taenia cysticerci
CYSTKERCI RECOVERED PRI~R~~A
15
M. corii
Group
TABLE I-NUMBER OF TETRATHYR~DIA AND
Single
Dividing
Total
? S.E.
WEEKS
tetrathyridia
INFECTION OF A4. corti 2 OR 6
Mean no. of Mesocesfoides
A PRIMARY
after
corti
= light
NS-not
gp <
0.02.
to moderate
significant.
tp < om1. *p < 0.01.
*L-M
liver
infection 15 14
14
infection 15
15
mice
of
No.
infection;
challenge after T. crassiceps 4 10/4 M. corti 6 weeks corti T. crassiceps/M.
T. crassiceps
10
T. crassiceps 6 6/4
T. crassiceps/M crassiceps
challenge
(weeks)
infection
of
Duration
OF CYSTICERCI
4
2 weeks
2--NUMBER
M. corti
Group
TABLE
LL
AND
= very
;;
-
L-M
infection
Liver*
light
liver
;;;::
:::::
TETRATHYRIDIA
*
of
infection.
1 :;@;]NS
:
no.
::::I
Single
Mean
PRIOR
RECOVERED WEEKS
4 WEEKS
1;:;
:::I
: ‘::I]+
:
::j
Dividing
Mesocestoides
CHALLENGE INFECTION
:;;:;
::I::
tetrathyridia
AFTER
TO A CHALLENGE
: =;]NS
:
S.E.
:::;I
Total
f
*
COrfi
;;;:::
2;;::
4;:;]?
1 ;;;#;I
1
5
no.
:;;#:
;;::
of
INFECTION
Mean
A PRIMARY
Non-budders
OF MICE GIVEN OF M.
T.
CraSSiCefX
:JNS
1 ::#;]NS
1
Budders
Taeniacysticerci
OF
I;;:#;
5;:;]+
1 ::_3
1
Total
S.E.
2;;:;
k
2 OR 6
0
2 B 8.
3
1
I
500
MARIENOVAK
smaller (2.5 and 31% respectively) than those in controls and contained a lower number of larvae in the process of division. However, these differences were not (except between dividing larvae in the 6 weeks challenge group) statistically significant. The livers in controls and mice challenged with cysticerci at 2 or 6 weeks of infection were moderately infected with tetrathyridia. Taenia challenged with Mesocestoides Mice infected with Taenia and challenged 2 weeks later with Mesocestoides harbored significantly less than the Mesocestoides infected tetrathyridia controls (Table 2). This significant difference disappeared when mice were challenged 6 weeks p.i. In this latter challenge group, the reduction in the total intraperitoneal tetrathyridial biomass was only 20070, whereas it was 40% in the former challenge group. In both challenge groups of mice the asexual reproduction of tetrathyridia was severely impaired as indicated by the significant reduction in the number of dividing larvae. The livers of these challenged mice were very lightly infected whereas those of controls were light to moderate. Challenge infection also significantly reduced the number of Taenia cysticerci developing from a primary infection (Table 2). This reduction in the biomass of primary infection was much more pronounced when heterologous larvae were introduced 2 weeks rather than 6 weeks after primary infection, 75 and 37% respectiveiy. Though the Taenia populations from controls and challenged groups contained a similar the overall morphological number of budders, composition of these populations differed. Control populations contained large numbers of single larvae (non-budders) out of which many were small, freshly separated buds and the budding larvae in these populationswere covered with many buds of various sizes. In populations from challenged mice, the asexual reproduction of cysticerci was retarded. The budders had fewer and very small buds and the number of non-budders, including small individuals, was also low.
The present results revealed the existence of crossresistance between two proliferating cestode larvae, M. corti and T. crassiceps. Primary infection with either tetrathyridia of M. corti or cysticerci of T. crassiceps generated significant resistance against a challenge infection with the heterologous species. the degree of protection against the However, challenge infection varied according to the parasite species used in the primary infection and the time when the challenge infection was introduced. The finding that M. corfi, when introduced as a challenge infection, adversely affected the growth and proliferation of primary T. crassiceps pOpulations was unexpected and certainly deserves further
I.J.P.VOL. 14.1984
investigation. One of the possibilities which could be tested is the existence of substances released by tetrathyridia which might act as growth inhibitors. Various toxic or inhibitory substances secreted by the worms have been reported for cestodes. Hymertotepis diminuta releases substances with growth-inhibiting properties that affect other worms in the host intestine (Insler & Roberts, 1980a, b; Roberts & Insler, 1982). H. microstoma secretes toxic substances which produce lesions in the liver of the host (Simpson & Gleason, 1975). It has been observed that in M. corti infections in mice broad zones of necrotic hepatocytes develop in parasitized liver (Specht & Widmer, 1972; Novak, 1982). Whether these necrotic lesions are caused by toxic products secreted by tetrathyridia and if these secretions can act as growth inhibitors remains to be answered. Partial cross-protection was obtained also for other metacestodes such as Taenia hydatigena, T. ovis and E. granulosus by Heath, Lawrence & Yong (1979). There, prior infection with all combinations of heterologous species resulted in a lesser degree of immunity than that obtained for challenge infections with homologous species. The protection seemed to have acted on the establishment phase of development and did not influence cyst survival. Both metacestodes are known to provoke a dramatic inflammatory reaction (Freeman, 1964; Specht & Widmer, 1972; Mitchell & Handman, 1977; Siebert et al., 1978a, b; Siebert & Good, 1979; Novak, 1982) but more so in the case of AK corti infection, since this parasite invades host tissues, especially liver (Specht & Widmer, 1972; Novak, 1982). Conceivably, the cross-immunity observed in the present experiments, especially during the earlier challenge, arises to some degree from the nonspecific inflammation response evoked by one species acting nonspecifically against the other species present. Recently, similar mouse antibodies, with IgG and IgM in the greatest amounts, were demonstrated to be on the body surfaces of M. corti by Mitchell, Marchalonis, Smith, Nicholas & Warner (1977), Zodda & Thorson (1982) and on T. crassiceps by Siebert, Bhtz, Morita & Good (1981). However, the larvae of both species were found to be capable of rapid shedding of the host serum components attached to their tegument (Zodda & Thorson, 1982; Siebert er a/., 1981). Findings of this kind suggest that even if cross-reactive or specific antibodies to worm surface antigens are produced, the ability to shed surface bound antibodies by worms may be one of the means by which these metacestodes successfully survive in their immunologically active host.
I.J.P. VOL. 14. 1984
Cross-protection
between M. Corti and T. crassiceps
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