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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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
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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