Comprehensive Physiology Wiley Online Library
For Librarians For Authors Editors About

Parasite infections and gastrointestinal motility

Gilbert A. Castro

10.1002/cphy.cp060130

Source: Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Parasite‐Induced Alterations
1.1 Esophagus
1.2 Stomach
1.3 Small Intestine
1.4 Cecum, Colon, and Rectum
2 Basis For Motility Changes
2.1 Parasite‐Derived Substances
2.2 Gastrointestinal Hormone Imbalances
2.3 Inflammation
3 Summary
Figure 1.

Alterations in contractile activity of stomach and antroduodenal junction of sheep infected with Trichostrongylus axei and Chabertia ovina.

From Buéno et al. 11
Figure 2.

Duration of motor complex in antral part of abomasum and migrating myoelectric complex (MMC) in the duodenum of sheep infected with 2.5 × 103 L3 larvae of Haemonchus contortus.

From Bueno et al. 10. Reproduced with permission by Cambridge University Press, Copyright 1982
Figure 3.

Pressure recordings of migrating motor complex in jejunum from fasted control patient (A) and patient with Chagas’ disease (B) determined by manometry. Open‐tip catheters were 30 cm apart. Note slower propagation in infected patient.

From Oliveira et al. 58
Figure 4.

Velocity of propagation of migrating motor complex in jejunum from control patients and its reduction in patients with Chagas’ disease relative to megaorgan pathology. Open squares, megacolon; open circles, megaesophagus; open circle in square, megacolon and megaesophagus.

From Oliveira et al. 58
Figure 5.

Transit of chromatography beads through small intestine of mice 15 min after intragastric administration of marker. Segment 1 is duodenum and segment 12 is ileum. C, D5, and D9 represent, respectively, uninfected mice, mice infected for 5 days with Trichinella spiralis, and mice infected for 9 days with T. spiralis.

From Sukhdeo and Croll 74
Figure 6.

Transit of 51Cr through rat small intestine before infection with Trichinella spiralis (uninfected control), 3-5 days after primary infection (primary infection), 30 days after primary infection (immunized control), and 3-5 days after reinfection (immunized‐challenged). Percentage (mean ± SE) of radioactivity passing through or present in successive equal‐length segments of small intestine during 15‐min period after intraduodenal administration of marker is plotted as function of gut length. Slope of regression of percent radioactivity on gut length for primary infection is significantly different from other three groups.

From Castro et al. 18
Figure 7.

Percentage (mean ± SE) of 51Cr passing through given segment (segment 1, duodenum; segment 9, ileum) of small intestine of rats during 15‐min period immediately after its intraduodenal administration by an enterocutaneous catheter. Values are for uninfected (control) rats and rats at various times during infection with Nippostrongylus brasiliensis. Only at day 8 is transit increased over control value. Regression equations and statistical analysis of slopes are given in Table 1.

From Farmer 29
Figure 8.

Electromyograph tracing of dog infected with hookworms. Recording is continuous (left to right) from single electrode site in small intestine. Note unstable nature of spiking pattern as well as diminution of slow‐wave amplitude. Normal migrating myoelectric complexes were not evident until dog was treated to eliminate parasites. Horizontal bar, 1‐min interval.
Figure 9.

Recording of myoelectric activity from fasted dogs at seven sites on small intestine before (A) and 3 days after inoculation (B) with 2 × 104 Trichinella spiralis larvae/kg body wt. Note rapid movement of complex of spike potentials (circled) down the bowel.

From Schanbacher et al. 68
Figure 10.

Electrical spike activity in proximal small intestine of dog before infection with Trichinella spiralis (control), 3 days after primary inoculum of larvae (infected), 11 days postprimary inoculation (recovered), and 3 days after a secondary infection (challenged). Challenge infection was given 6 wk after primary inoculation. Percentage of slow waves with superimposed spikes for consecutive 2‐min intervals are plotted as function of time.

From Schanbacher et al. 68
Figure 11.

Frequency of migrating myoelectric complexes recorded in proximal small intestine before (open bars) and after (shaded bars) infection with Trichinella spiralis in rats. Values are means ± SE for number of recordings designated at base of the bars. Values for each animal were established by examining 60 min of myoelectric tracing. Asterisk, significant difference as compared with respective control values.

From Palmer et al. 63
Figure 12.

Histogram of fasted myoelectric pattern in rat in uninfected (control) state and 12 days after inoculation with infective Trichinella spiralis larvae. Infection disrupted normal phasic pattern of activity.

From Palmer et al. 63
Figure 13.

Migrating action potential complexes (MAPC) in 1‐hr interval from six rats infected with Trichinella spiralis. MAPC (inset) did not occur in uninfected control rats. Values are means ± SE.

From Palmer et al. 63
Figure 14.

Electromyograph recorded from four electrodes in proximal small intestine before and 6-12 min after intraduodenal challenge of rat immune to Trichinella spiralis. Challenge was with live larvae.

From Palmer and Castro 62
Figure 15.

FIG. 15. Slow wave and spiking activity in small intestine of rats immune to Trichinella spiralis and challenged with heat‐killed larvae on excretory‐secretory (ES) antigens and then rechallenged 90 min later with live larvae. All agents were administered intraduodenally. A: values are means ± SE. Asterisk indicates significant difference caused by rechallenge with live larvae compared with prechallenged state. B: values are means and 95% confidence interval for prechallenge group and means for other groups. Means excluded from 95% confidence interval are significantly different from prechallenge group. Only live larvae induced myoelectric changes.

From Palmer and Castro 62
Figure 16.

FIG. 16. Electromyogram of jejunum, ileum, and cecum of rabbit infected with Eimeria magna. On ninth day after inoculation with oocysts, spiking activity of small intestine was inhibited and frequency of spike bursts in cecum increased.

From Fioramonti et al. 33
Figure 17.

FIG. 17. Maximum (A and C) and graded responses (B and D) to acetylcholine (ACh) and serotonin (5‐HT) of isolated small intestinal segments from uninfected (open bar, open circle) rats and rats infected (hatched bar, filled circle) with Nippostrongylus brasiliensis. Segments were standardized for length and for region of intestine. Values are means ± SE. Number of animals per group are given at base of the bars.

From Farmer and Laniyonu 32
Figure 18.

FIG. 18. Relationship between applied tension and maximum developed tension, expressed as function of cross‐sectional area of smooth muscle in response to acetylcholine. Tension was measured in 2‐cm long small intestinal segments taken 20 cm from pylorus. Segments were from uninfected rats and rats infected with Nippostrongylus brasiliensis. Values are means ± SE for 3-5 observations per point. Asterisk indicates significant difference as compared with respective control (uninfected) values.

From Farmer et al. 31
Figure 19.

FIG. 19. Pressure changes in sigmoid colon and reaction of control and Chagasic patients with megacolon after intravenous administration of pentagastrin.

From Meneghelli et al. 55
Figure 20.

Transverse section of middle jejunum of noninfected pig (left) and pig harboring 49 adult Ascaris suis (right). Pigs were infected at 3 wk of age and were killed 8 wk later. Infection was induced by oral inoculation with 15‐day‐old Ascaris recovered from infected rabbits. This method of infection prevented extraintestinal stages of parasite from developing. Changes caused by infection were generalized and not restricted to area of worm localization in intestine.

From Stephenson et al. 72


Figure 1.

Alterations in contractile activity of stomach and antroduodenal junction of sheep infected with Trichostrongylus axei and Chabertia ovina.

From Buéno et al. 11


Figure 2.

Duration of motor complex in antral part of abomasum and migrating myoelectric complex (MMC) in the duodenum of sheep infected with 2.5 × 103 L3 larvae of Haemonchus contortus.

From Bueno et al. 10. Reproduced with permission by Cambridge University Press, Copyright 1982


Figure 3.

Pressure recordings of migrating motor complex in jejunum from fasted control patient (A) and patient with Chagas’ disease (B) determined by manometry. Open‐tip catheters were 30 cm apart. Note slower propagation in infected patient.

From Oliveira et al. 58


Figure 4.

Velocity of propagation of migrating motor complex in jejunum from control patients and its reduction in patients with Chagas’ disease relative to megaorgan pathology. Open squares, megacolon; open circles, megaesophagus; open circle in square, megacolon and megaesophagus.

From Oliveira et al. 58


Figure 5.

Transit of chromatography beads through small intestine of mice 15 min after intragastric administration of marker. Segment 1 is duodenum and segment 12 is ileum. C, D5, and D9 represent, respectively, uninfected mice, mice infected for 5 days with Trichinella spiralis, and mice infected for 9 days with T. spiralis.

From Sukhdeo and Croll 74


Figure 6.

Transit of 51Cr through rat small intestine before infection with Trichinella spiralis (uninfected control), 3-5 days after primary infection (primary infection), 30 days after primary infection (immunized control), and 3-5 days after reinfection (immunized‐challenged). Percentage (mean ± SE) of radioactivity passing through or present in successive equal‐length segments of small intestine during 15‐min period after intraduodenal administration of marker is plotted as function of gut length. Slope of regression of percent radioactivity on gut length for primary infection is significantly different from other three groups.

From Castro et al. 18


Figure 7.

Percentage (mean ± SE) of 51Cr passing through given segment (segment 1, duodenum; segment 9, ileum) of small intestine of rats during 15‐min period immediately after its intraduodenal administration by an enterocutaneous catheter. Values are for uninfected (control) rats and rats at various times during infection with Nippostrongylus brasiliensis. Only at day 8 is transit increased over control value. Regression equations and statistical analysis of slopes are given in Table 1.

From Farmer 29


Figure 8.

Electromyograph tracing of dog infected with hookworms. Recording is continuous (left to right) from single electrode site in small intestine. Note unstable nature of spiking pattern as well as diminution of slow‐wave amplitude. Normal migrating myoelectric complexes were not evident until dog was treated to eliminate parasites. Horizontal bar, 1‐min interval.



Figure 9.

Recording of myoelectric activity from fasted dogs at seven sites on small intestine before (A) and 3 days after inoculation (B) with 2 × 104 Trichinella spiralis larvae/kg body wt. Note rapid movement of complex of spike potentials (circled) down the bowel.

From Schanbacher et al. 68


Figure 10.

Electrical spike activity in proximal small intestine of dog before infection with Trichinella spiralis (control), 3 days after primary inoculum of larvae (infected), 11 days postprimary inoculation (recovered), and 3 days after a secondary infection (challenged). Challenge infection was given 6 wk after primary inoculation. Percentage of slow waves with superimposed spikes for consecutive 2‐min intervals are plotted as function of time.

From Schanbacher et al. 68


Figure 11.

Frequency of migrating myoelectric complexes recorded in proximal small intestine before (open bars) and after (shaded bars) infection with Trichinella spiralis in rats. Values are means ± SE for number of recordings designated at base of the bars. Values for each animal were established by examining 60 min of myoelectric tracing. Asterisk, significant difference as compared with respective control values.

From Palmer et al. 63


Figure 12.

Histogram of fasted myoelectric pattern in rat in uninfected (control) state and 12 days after inoculation with infective Trichinella spiralis larvae. Infection disrupted normal phasic pattern of activity.

From Palmer et al. 63


Figure 13.

Migrating action potential complexes (MAPC) in 1‐hr interval from six rats infected with Trichinella spiralis. MAPC (inset) did not occur in uninfected control rats. Values are means ± SE.

From Palmer et al. 63


Figure 14.

Electromyograph recorded from four electrodes in proximal small intestine before and 6-12 min after intraduodenal challenge of rat immune to Trichinella spiralis. Challenge was with live larvae.

From Palmer and Castro 62


Figure 15.

FIG. 15. Slow wave and spiking activity in small intestine of rats immune to Trichinella spiralis and challenged with heat‐killed larvae on excretory‐secretory (ES) antigens and then rechallenged 90 min later with live larvae. All agents were administered intraduodenally. A: values are means ± SE. Asterisk indicates significant difference caused by rechallenge with live larvae compared with prechallenged state. B: values are means and 95% confidence interval for prechallenge group and means for other groups. Means excluded from 95% confidence interval are significantly different from prechallenge group. Only live larvae induced myoelectric changes.

From Palmer and Castro 62


Figure 16.

FIG. 16. Electromyogram of jejunum, ileum, and cecum of rabbit infected with Eimeria magna. On ninth day after inoculation with oocysts, spiking activity of small intestine was inhibited and frequency of spike bursts in cecum increased.

From Fioramonti et al. 33


Figure 17.

FIG. 17. Maximum (A and C) and graded responses (B and D) to acetylcholine (ACh) and serotonin (5‐HT) of isolated small intestinal segments from uninfected (open bar, open circle) rats and rats infected (hatched bar, filled circle) with Nippostrongylus brasiliensis. Segments were standardized for length and for region of intestine. Values are means ± SE. Number of animals per group are given at base of the bars.

From Farmer and Laniyonu 32


Figure 18.

FIG. 18. Relationship between applied tension and maximum developed tension, expressed as function of cross‐sectional area of smooth muscle in response to acetylcholine. Tension was measured in 2‐cm long small intestinal segments taken 20 cm from pylorus. Segments were from uninfected rats and rats infected with Nippostrongylus brasiliensis. Values are means ± SE for 3-5 observations per point. Asterisk indicates significant difference as compared with respective control (uninfected) values.

From Farmer et al. 31


Figure 19.

FIG. 19. Pressure changes in sigmoid colon and reaction of control and Chagasic patients with megacolon after intravenous administration of pentagastrin.

From Meneghelli et al. 55


Figure 20.

Transverse section of middle jejunum of noninfected pig (left) and pig harboring 49 adult Ascaris suis (right). Pigs were infected at 3 wk of age and were killed 8 wk later. Infection was induced by oral inoculation with 15‐day‐old Ascaris recovered from infected rabbits. This method of infection prevented extraintestinal stages of parasite from developing. Changes caused by infection were generalized and not restricted to area of worm localization in intestine.

From Stephenson et al. 72
References
 1. Alizadeh, H., G. A. Castro, and W. A. Weems. Intestinal jejunal propulsion in the guinea pig during parasitism with Trichinella spiralis. Gastroenterology 93: 784-790, 1987.
 2. Alizadeh, H., G. A. Castro, and W. A. Weems. Onset and duration of intrinsic jejunal propulsive behavior induced by primary Trichinella spiralis infection (Abstract). Gastroenterology 90: 1324, 1986.
 3. Anderson, N., J. Hansky, and D. A. Tichen. Effects of a series of infections of Ostertagia circumcincta on gastric secretion of sheep. Parasitology 72: 1-12, 1976.
 4. Bach, M. K. Mediators of anaphylaxis and inflammation. Annu. Rev. Microbiol. 36: 371-413, 1982.
 5. Bell, R. G., D. D. McGregor, and L. S. Adams. Studies on the inhibition of rapid expulsion of Trichinella spiralis in rats. Int. Arch. Allergy Appl. Immunol. 69: 73-80, 1982.
 6. Binder, H. J., and M. Donowitz. Clinical trends and topics: a new look at laxative action. Gastroenterology 69: 1001-1005, 1975.
 7. Bowers, R. L., G. A. Castro, and N. W. Weisbrodt. Alterations in intestinal smooth muscle of the rat induced by Trichinella spiralis (Abstract). Gastroenterology 90: 1353, 1986.
 8. Brand, T. von. Carbohydrates II: metabolism of carbohydrates. In: Biochemistry of Parasites, edited by T. von Brand. New York: Academic, 1966, p. 79-156.
 9. Brasil, A. A peristalsis of the esophagus. Rev. Bras. Gastroenterol. 7: 21-31, 1965.
 10. Bueno, L., A. Dakkak, and J. Fioramonti. Gastro‐duodenal motor and transit disturbances associated with Haemonchus contortus infection in sheep. Parasitology 84: 367-374, 1982.
 11. Buéno, L., P. Dorchies, and Y. Ruckebusch. Analyse électromyographique perturbations motrices liées aus strongyloses gastrointestinales chez les ovins. C. R. Seances Soc. Biol. Fil. 169: 1627-1632, 1975.
 12. Bueno, L., Y. Ruckebusch, and P. Dorchies. Disturbances of digestive motility in horses associated with strongyle infection. Vet. Parasitol. 5: 253-260, 1979.
 13. Burks, T. F. Actions of drugs on gastrointestinal motility. In: Physiology of the Gastrointestinal Tract (1st ed.), edited by L. R. Johnson. New York: Raven, 1981, p. 495-516.
 14. Burns, T. W., J. R. Mathias, G. M. Carlson, J. L. Martin, and R. P. Shields. Effect of toxigenic Escherichia coli on myoelectric activity of small intestine. Am. J. Physiol. 235 (Endocrinol. Metab. Gastrointest. Physiol. 4): E311-E315, 1978.
 15. Burns, T. W., J. R. Mathias, J. L. Martin, G. M. Carlson, and R. P. Shields. Alteration of myoelectric activity of small intestine by invasive Escherichia coli. Am. J. Physiol. 238 (Gastrointest. Liver Physiol. 1): G57-G62, 1980.
 16. Castro, G. A. Spatial and temporal integration of host responses to intestinal stages of Trichinella spiralis: retro‐ and prospective views. In: Biochemistry of Parasites and Host‐Parasite Relationships, edited by H. Van den Bossche. Amsterdam: North‐Holland, 1976, p. 343-358.
 17. Castro, G. A. Immunological regulation of epithelial function. Am. J. Physiol. 243 (Gastrointest. Liver Physiol. 6): G321-G329, 1982.
 18. Castro, G. A., F. Badial‐Aceves, J. W. Smith, S. J. Dudrick, and N. W. Weisbrodt. Altered small bowel propulsion associated with parasitism. Gastroenterology 71: 620-625, 1976.
 19. Castro, G. A., J. J. Hessel, and G. Whalen. Altered intestinal fluid movement in response to Trichinella spiralis in immunized rats. Parasite Immunol. Oxf. 1: 259-266, 1979.
 20. Castro, G. A., C. A. Post, and S. A. Roy. Intestinal motility during the enteric phase of trichinosis in immunized rats. J. Parasitol. 63: 713-719, 1977.
 21. Clayton, H. M., and J. L. Duncan. Experimental Parascaris equorum infection of foals. Rev. Vet. Sci. 23: 109-114, 1977.
 22. Collins, S. M., and A. E. Fox. Gut inflammation alters calcium handling properties of intestinal smooth muscle (Abstract). Gastroenterology 86: 1052, 1984.
 23. Cook, R. W., J. F. Williams, and L. Lichtenberger. Hypergastric gastropathy in the rat due to Taenia taeniaformis infection: parabiotic transfer and hypergastrinemia. Gastroenterology 80: 728-734, 1981.
 24. Coulson, E. J. The Schultz‐Dale technique. J. Allergy 24: 458-473, 1953.
 25. Crompton, D. W. T., and A. Singhui. Intestinal responses of rats to Moniliformis (Acanthocephala) (Abstract). Parasitology 84: IXX, 1982.
 26. Dembinski, A. B., L. R. Johnson, and G. A. Castro. Influence of enteric parasitism on hormone‐regulated pancreatic secretion in dogs. Am. J. Physiol. 237 (Regulatory Integrative Comp. Physiol. 6): R232-R238, 1979.
 27. Dembinski, A. B., L. R. Johnson, and G. A. Castro. Influence of parasitism on secretin‐inhibited gastric secretion. Am. J. Trop. Med. Hyg. 28: 854-859, 1979.
 28. Duszynski, D. W., S. A. Roy, J. Stewart, and G. A. Castro. Intestinal transit time during infection with Eimeria nieschulzi in rats. J. Protozool. 25: 370-374, 1978.
 29. Farmer, S. G. Propulsive activity of the rat small intestine during infection with nematode Nippostrongylus brasiliensis. Parasite Immunol. Oxf. 3: 227-234, 1981.
 30. Farmer, S. G. Changes in responsiveness of intestinal smooth muscle to agonists in rats infected with Nippostrongylus brasiliensis (Abstract). Br. J. Pharmacol. 74: 199P, 1981.
 31. Farmer, S. G., J. M. Brown, and D. Pollock. Increased responsiveness to intestinal and vascular smooth muscle to agonists in rats infected with Nippostrongylus brasiliensis. Arch. Int. Pharmacodyn. Ther. 263: 217-227, 1983.
 32. Farmer, S. G., and A. A. Laniyonu. Effects of p‐chlorophenylaline on the sensitivity of rat intestine to agonists and on intestinal 5‐hydroxytryptamine during Nippostrongylus brasiliensis infection. Br. J. Pharmacol. 82: 883-889, 1984.
 33. Fioramonti, J., J. M. Sorraing, D. Licois, and L. Bueno. Intestinal motor and transit disturbances associated with experimental coccidiosis (Eimeria magna) in the rabbit. Ann. Rech. Vet. 12: 413-420, 1981.
 34. Fox, J. E. T., E. E. Daniel, C. R. De Faria, J. M. Rezendez, L. Rassi, J. De Renzendez, Jr., and V. P. Daniel. Relationship of functional changes to structural changes in megaesophagus of Chagas' disease. In: Gastrointestinal Motility, edited by C. Roman. Lancaster, UK: MTP, 1983, p. 51-58.
 35. Fox‐Robichaud, A. E., and S. M. Collins. Altered utilization of Ca++ by smooth muscle from inflamed gut (Abstract). Gastroenterology 88: 1386, 1985.
 36. Gabella, G. Hypertrophy of intestinal smooth muscle. Cell Tissue Res. 163: 199-214, 1975.
 37. Goyal, R. K. Does gastrin act via cholinergic neurons to maintain lower‐esophageal sphincter pressure (Letter to the editor)? N. Engl. J. Med. 291: 849-850, 1974.
 38. Huninnen, A. V. Studies on the life history and host‐parasite relation of Hymenolepis fraterna (H. nana var. fraterna Stiles) in white mice. Am. J. Hyg. 22: 414-443, 1935.
 39. Jarumilinta, R., and F. Kradolfer. The toxic effect of Entamoeba histolytica on leucocytes. Ann. Trop. Med. Parasitol. 58: 375-381, 1964.
 40. Justus, P. G., J. R. Mathias, J. L. Martin, G. M. Carlson, R. P. Shield, and S. B. Formal. Myoelectric activity in the small intestine in response to Clostridium perfringens A enterotoxin: correlation with histological findings in an in vivo rabbit model. Gastroenterology 80: 902-906, 1981.
 41. Koberle, F. Chagas' disease and Chagas' syndrome. The pathology of American trypanosomiasis. Adv. Parasitol. 6: 63-116, 1968.
 42. Koberle, F. The causation and importance of nervous lesions in American Trypanosomiasis. Bull. WHO 42: 739-743, 1970.
 43. Larsh, J. E. The relationship in mice of intestinal emptying time and natural resistance to. Hymenolepis. J. Parasitol. 33: 79-84, 1947.
 44. Larsh, J. E., and J. R. Hendricks. The probable explanation for the difference in the localization of adult Trichinella spiralis in young and old mice. J. Parasitol. 35: 101-106, 1949.
 45. Lee, D. L., and J. Martin. Changes in Nematodirus battus associated with the development of immunity to this nematode in lambs. In: Biochemistry of Parasites and Host‐Parasite Relationships, edited by H. Van den Bossche. Amsterdam: North‐Holland, 1976, p. 311-318.
 46. Leid, R. W., and J. F. Williams. Helminth parasites and the host inflammatory system. In: Chemical Zoology, edited by M. Florkin and B. T. Scheer. New York: Academic, 1979, vol. XI, p. 229-271.
 47. Lin, T. M., and L. J. Olson. Pathophysiology of reinfection with Trichinella spiralis in guinea pigs during the intestinal phase. J. Parasitol. 56: 529-539, 1970.
 48. Lushbaugh, W. B., A. F. Hofbauer, and F. E. Pittman. Proteinase activities of Entamoeba histolytica cytotoxin. Gastroenterology 87: 17-27, 1984.
 49. Lushbaugh, W. B., A. B. Kairalla, J. R. Cantey, A. F. Hofbauer, and F. E. Pittman. Isolation of cytotoxin‐enterotoxin from Entamoeba histolytica. J. Infect. Dis. 139: 9-17, 1979.
 50. Mathias, J. R., G. M. Carlson, G. Bertiger, J. L. Martin, and S. Cohen. Migrating action potential complex of cholera: a possible prostaglandin‐induced response. Am. J. Physiol. 232 (Endocrinol. Metab. Gastrointest. Physiol. 1): E529-E534, 1977.
 51. Mathias, J. R., G. M. Carlson, J. L. Martin, R. P. Schields, and S. Formal. Shigella dysenteriase I enterotoxin: proposed role in pathogenesis of shigellosis. Am. J. Physiol. 239 (Gastrointest. Liver Physiol. 2): G382-G386, 1980.
 52. McCoy, O. R. Rapid loss of Trichinella larvae fed to immune rats and its bearing on the mechanism of immunity. Am. J. Hyg. 32: 105-116, 1940.
 53. McGowan, K., C. F. Deneke, G. M. Thorne, and S. L. Gorbach. Entamoeba histolytica cytotoxin: purification, characterization, strain virulence and protease activity. J. Infect. Dis. 146: 616-625, 1982.
 54. McGowen, K., A. Kane, N. Asarkof, J. Wicks, V. Guerina, J. Kellum, S. Baron, A. R. Gintzler, and M. Donowitz. Entamoeba histolytica causes intestinal secretion: role of serotonin. Science Wash. DC 221: 762-764, 1983.
 55. Meneghelli, U. G., R. A. Godoy, R. B. Oliveira, J. C. M. Santos, Jr., and R. O. Dantas. Effect of pentagastrin on the motor activity of the dilated and nondilated sigmoid and rectum in Chagas' disease. Digestion 27: 152-158, 1983.
 56. Minick, C. R., G. E. Murphy, and W. G. Campbell. Experimental induction of athero‐arterio‐sclerosis by synergy of allergic injury to arteries and lipid‐rich diet. I. Effect of repeated injections of horse serum in rabbits fed a dietary cholesterol supplement. J. Exp. Med. 124: 635-652, 1966.
 57. O'Daly, J. A., and P. M. Aso. Trypanosoma cruzi, Lieshnania donovani and L. mexicana: extract factor that lyses mammalian cells. Exp. Parasitol. 47: 222-231, 1979.
 58. Oliveira, R. B., U. G. Meneghelli, R. A. De Godoy, R. O. Dantas, and W. Podovan. Abnormalities of interdigestive motility of the small intestine in patients with Chagas' disease. Dig. Dis. Sci. 28: 294-299, 1983.
 59. Olson, L. J. In vivo responses of small intestine of guinea pigs following challenge with sonicated Trichinella spiralis larvae. Program, American Society of Parasitologists, 42nd Annual Meeting, Tucson, Arizona, August 21-25, 1967, p. 41.
 60. Ovington, K. S., A. J. Bacarese‐Hamilton, and S. R. Bloom. Nippostrongylus brasiliensis: changes in plasma levels of gastrointestinal hormones in the infected rat. Exp. Parasitol. 60: 276-284, 1986.
 61. Padovan, W., R. A. Godoy, R. A. Dantas, U. G. Meneghelli, R. B. Oliveira, and L. E. A. Troncon. Lower oesophageal sphincter response to pentagastrin in Chagasic patients with megaoesophagus and megacolon. Gut 21: 85-90, 1980.
 62. Palmer, J. M., and G. A. Castro. Anamnestic stimulus‐specific myoelectric responses associated with intestinal immunity in the rat. Am. J. Physiol. 250 (Gastrointest. Liver Physiol. 13): G266-G273, 1986.
 63. Palmer, J. M., N. W. Weisbrodt, and G. A. Castro. Trichinella spiralis: intestinal myoelectric activity during enteric infection in the rat. Exp. Parasitol. 57: 132-141, 1984.
 64. Pesonen, E. Coronary wall thickening in children. Atherosclerosis 20: 173-187, 1974.
 65. Reeder, N. M., and L. C. Hamilton. Radiologic diagnosis of tropical diseases of the gastrointestinal tract. Radiol. Clin. N. Am. 7: 57-81, 1969.
 66. Russell, D. A., and G. A. Castro. Physiological characterization of a biphasic immune response to Trichinella spiralis in the rat. J. Infect. Dis. 139: 304-312, 1979.
 67. Saz, H. J. Facultative anaerobiosis in the invertebrates: pathways and control systems. Am. Zool. 11: 125-135, 1971.
 68. Schanbacher, L. M., J. K. Nations, N. W. Weisbrodt, and G. A. Castro. Intestinal myoelectric activity in parasitized dogs. Am. J. Physiol. 234 (Regulatory Integrative Comp. Physiol. 3): R188-R195, 1978.
 69. Smith, J. W., and G. A. Castro. Relation of peroxidase activity in gut mucosa to inflammation. Am. J. Physiol. 234 (Regulatory Integrative Comp. Physiol. 3): R72-R79, 1978.
 70. Spaet, T. H., M. B. Stemmerman, S. J. Veith, and I. Lejniecks. Intimal injury and regrowth in the rabbit aorta. Circ. Res. 36: 58-70, 1975.
 71. Sprinz, H. Morphological response of intestinal mucosa to enteric bacteria and its implication in sprue and Asiatic cholera. Federation Proc. 21: 57-64, 1962.
 72. Stephenson, L. S., W. G. Pond, M. C. Neisheim, L. T. Krock, and D. W. T. Crompton. Ascaris suum: nutrient absorption, growth and intestinal pathology in young pigs experimentally infected with 15‐day‐old larvae. Exp. Parasitol. 49: 15-25, 1980.
 73. Stirwalt, M. A. Skin penetration mechanisms of helminths. In: Biology of Parasites, edited by E. J. L. Soulsby. New York: Academic, 1966, p. 41-59.
 74. Sukhdeo, M. V. K., and N. A. Croll. Gut propulsion in mice infected with Trichinella spiralis. J. Parasitol. 67: 906-910, 1981.
 75. Symons, L. E. A. Pathology of infection of the rat with Nippostrongylus myris (Yokagawa). I. Changes in water content, dry weight and tissues of the small intestine. Aust. J. Biol. Sci. 10: 374-383, 1957.
 76. Symons, L. E. A. Digestion and absorption of maltose in rats infected by the nematode Nippostrongylus brasiliensis. Exp. Parasitol. 18: 12-24, 1966.
 77. Thorson, R. E. The stimulation of acquired immunity in dogs by injection of extracts of the esophagus of adult hookworms. J. Parasitol. 42: 501-504, 1956.
 78. Tichen, D. A. The role of hormones in the reactions of the host to enteric parasites. In: Parasites‐Their World and Ours, edited by D. F. Mettrick and S. S. Desser. Amsterdam: Biomedical, 1982, p. 245-247.
 79. Troncon, L. E. A., R. B. Oliveira, U. G. Meneghelli, R. O. Dantas, and R. A. Godoy. Fasting and food‐stimulated plasma gastrin levels in chronic Chagas' disease. Digestion 29: 171-176, 1984.
 80. Weems, W. A. Intestinal wall motion, propulsion, and fluid movement: trends toward a unified theory. Am. J. Physiol. 243 (Gastrointest. Liver Physiol. 6): G177-G188, 1982.
 81. Weems, W. A., and N. W. Weisbrodt. Comparison of colonic and ileal propulsive capabilities under conditions requiring hydrostatic work. Am. J. Physiol. 246 (Gastrointest. Liver Physiol. 9): G587-G593, 1984.
 82. Weinstein, P. P. Excretory mechanisms and excretory products of nematodes. In: Host Influence on Parasite Physiology, edited by L. A. Stauber. New Brunswick, NJ: Rutgers Univ. Press, 1960, p. 65-92.
 83. Weisbrodt, N. W., and G. A. Castro. Intestinal myoelectric activity of the dog during hookworm infection (Abstract). Federation Proc. 36: 595, 1977.
 84. Wolinsky, H. A new look at atherosclerosis. Cardiovasc. Med. 1: 41-54, 1976.
 85. Yeates, R. A., and B. M. Ogilvie. Nematode acetylcholinesterases. In: Biochemistry of Parasites and Host‐Parasite Relationships, edited by H. Van den Bossche. Amsterdam, North‐Holland, 1976, p. 307-310.
 86. Zwick, R., K. L. Bowes, E. E. Daniel, and S. K. Sarna. Mechanism of action of pentagastrin on the lower esophageal sphincter. J. Clin. Invest. 57: 1644-1651, 1976.

Contact Editor

Submit a note to the editor about this article by filling in the form below.

* Required Field

Article Title: Parasite infections and gastrointestinal motility
 

How to Cite

Gilbert A. Castro. Parasite infections and gastrointestinal motility. Compr Physiol 2011, Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation: 1133-1152. First published in print 1989. doi: 10.1002/cphy.cp060130