Lethal effects of freezing Echinococcus multilocularis eggs at ultralow temperatures.

Methods for killing Echinococcus multilocularis eggs within stool or intestinal samples, without damaging the diagnostic value of the sample, would significantly reduce the risk of animal health providers acquiring alveolar hydatid disease. The first objective of this study was to determine whether E. multilocularis eggs located in fox intestines can survive storage at -70 C for at least 4 days. Results showed that none of 72,000 E. multilocularis eggs remained infectious to defined strains of mice under these conditions, yet, similar eggs recovered from nonfrozen carcasses stored at 4 C for the same time period were viable. The structural identities of adult worms and eggs were not significantly altered by the freezing and thawing processes. These results indicate that ultracold temperatures can be used to kill or inactivate E. multilocularis eggs, making them safe to handle when diagnosing this parasite in definitive hosts. The second objective of this study was to determine whether E. multilocularis eggs could survive freezing to -70 C if commonly used cryopreservation protocols were used. The use of the cryoprotectant solution, 5% dimethyl sulfoxide-35% saline-60% lamb serum, with a -1 C/min freezing rate was unable to prevent the eggs from being killed by freezing to -70 C. Rapid cooling by plunge freezing into liquid nitrogen was also lethal to E. multilocularis eggs. Only a few of the many potential cryopreservation protocols were tested in this study, so it is not yet possible to completely rule out the possibility of preserving these eggs at ultralow temperatures, but it does indicate that temperatures below -70 C are lethal to eggs even under favorable storage conditions.

Small intestinal transections decrease the occurrence of tapeworm-induced myoelectric patterns in the rat.

Abstract Luminal infection by the noninvasive tapeworm, H. diminuta, alters rat small intestinal myoelectric activity. The significance of continuity between small intestinal enteric nervous system (ENS) and that of both the stomach/pylorus and colon/caecum regarding the induction of tapeworm-altered myoelectric patterns was evaluated. A total of 32 rats were implanted with four serosal electrodes placed at sites in the duodenum through the mid-jejunum. Sixteen of the 32 rats underwent intestinal transections and anastomoses at both the duodenum and ileum. After recording myoelectrical activity of both normal and transected intestines, eight rats from each group (normal and transected) were infected with H.diminuta. Phase III frequency, duration of the migrating myoelectric complex (MMC), slow wave frequency, percentage of slow waves associated with spike potentials and the occurrence of the the two tapeworm-initiated myoelectric patterns, repetitive bursts of action potentials (RBAP) and sustained spike potentials (SSP), were measured. In infected rats, the frequency of the RBAP and SSP electric patterns were significantly reduced by the double transection. Intestinal transection did not affect the other changes caused by infection, such as decreased MMC phase III frequency and percentage of slow waves associated with spike potentials. In conclusion, a small intestinal ENS in continuity with other segments of the GI tract is required to generate maximal numbers of tapeworm-induced SSP and RBAP myoelectric activity in the small intestine of the rat.

Ileal mucosal mast cell, eosinophil, and goblet cell populations during Hymenolepis diminuta infection of the rat.

The population dynamics in the enteric connective tissues of eosinophils, mucosal mast cells (MMC), and in the mucosal epithelium of goblet cells were examined morphometrically in fixed ileal tissue of outbred Sprague Dawley rats during the first 32 days of infection with the tapeworm Hymenolepis diminuta. MMC and eosinophils were present in the lamina propria and submucosa; however, only eosinophils were also present in the muscularis externa. Eosinophilic infiltrate was first observed in the lamina propria at 15 days postinfection (dpi) and the numbers of eosinophils remained elevated through 32 dpi. Initial mucosal mastocytosis was detected on 6 dpi and MMC numbers continued to rise over the study period without reaching a plateau. Goblet cell hyperplasia occurred only at 32 dpi. In contrast to some intestinal nematode infections where these same 3 cell types are associated with the host's expulsion responses, H. diminuta is not lost by a rapid host response in the outbred Sprague Dawley rat strain used in these experiments. We suggest that either the induction of hyperplasia of these host effector cells in ileum tissue during H. diminuta infection is not capable of triggering parasite rejection mechanisms, or the function of the induced hyperplasia is necessary for some as yet unassociated physiological or tissue architecture change in the host's intestine.

Intestinal regrowth is amplified after jejunal but not ileal resection during tapeworm infection in the rat.

The ileum possesses functions required by a healthy individual that are not fully supplanted by the duodenum or jejunum. Evidence suggests that the ileum may also be necessary to maintain an enteric parasite-host interaction. We hypothesized that the ileum is essential to the survival of the lumen-dwelling, rat tapeworm, H. diminuta. Male rats were divided into three groups: those with ileal or jejunal resections and nonresected controls. Half of each rat group was infected with the tapeworm. After jejunal resection, the weight but not length of intestinal remnant (duodenum + ileum) in infected rats returned to that of control, nonresected intestine 29 days after surgery and tapeworm numbers were fully maintained. In contrast, after ileal removal intestinal length and weight of the remaining duodenum and jejunum in infected rats were significantly decreased and tapeworm survival diminished. Data indicates that intestinal growth following resection is amplified by tapeworm infection when the ileum remains but diminished when the ileum is removed. Furthermore, loss of the ileum results in decreased infection intensity and dry weight of the tapeworm.

Effect of surgical alteration of the rat gastrointestinal tract on the growth and development of Hymenolepis diminuta.

Eight groups of rats were used to study the involvement of the enteric (ENS) and central (CNS) nervous systems in the development of Hymenolepis diminuta using surgical intestinal transection, or CNS denervation, or both procedures. The transection procedure was used to isolate the ENS of the small intestine from either orad and/or caudal portions of the alimentary system, while the CNS denervation was used to eliminate direct visceral efferent inputs from the CNS. Nine days after the surgical procedures, all rats were infected with 35 cysticercoids of H. diminuta. On 20 days postinfection, the infection intensity, tapeworm dry weight, tapeworm morphology, intestine length, and intestinal wet weight were recorded. Only the combination of the duodenal and ileal transections with a CNS denervation reduced infection intensity and prevented the increased intestinal length normally observed in infected rats. In contrast, none of the various intestinal transection procedures alone or CNS denervation alone had any effect on the survival, ability to produce oncospheres or morphology of the tapeworms. In conclusion, tapeworm survival is decreased when both CNS and ENS inputs into the small intestine are altered or absent.

Myoelectric response of the small intestine to the orad presence of the tapeworm Hymenolepis diminuta.

During its 24-hr migratory cycle in the small intestine, Hymenolepis diminuta is located in the orad part of the small intestine during the early morning hours and then in the caudad part of the small intestine during the late afternoon and early evening. During the later period, tapeworm-induced alterations of interdigestive myoelectric activity, a correlate of smooth muscle contraction or intestinal motility, are most intense in the ileal region. The hypothesis tested was that the tapeworm-induced changes in intestinal motility are local responses of the intestine responding to the close proximity of the lumenally positioned tapeworm and to the nutritional state of the host. The small intestine was monitored before and for 20 days after infection using electrodes implanted on the serosa of the small intestine. Myoelectric recordings were analyzed for the frequency of the normal patterns of interdigestive myoelectric spiking patterns and the altered myoelectric spiking related to tapeworm infection. During the morning hours, when the tapeworms are situated in the orad small intestine, no changes were observed during the normal myoelectric pattern of the digestive phase in any region of the intestine. When examined after the conversion of the digestive to interdigestive phase of motility, only on day 10 postinfection was the interdigestive phase significantly altered. It was concluded that the presence of the tapeworm in the orad small intestine during the satiety stage of the rat causes no changes in the electric events of the small intestine, with the exception of day 10 postinfection. Because tapeworms in the orad small intestine do not induce the tapeworm-altered myoelectric activity observed in the afternoon and evening with caudally positioned tapeworms, tapeworm-altered motility is not simply a response of the small intestine to the local presence of the tapeworm.

Modulation of caudal intestinal permeability in the rat during infection by the tapeworm Hymenolepis diminuta.

Bidirectional movement of solutes between the intestinal lumen and systemic circulation is restricted by tissue barriers that may be altered under conditions such as intestinal infection. In a study using an in vitro everted sac preparation to assess small intestinal permeability in a lumen-to-serosa direction, 51Cr-EDTA movement was compared regionally in the jejunum and ileum of rats infected and uninfected by tapeworms. Whereas jejunal segments showed no significant differences in permeability to 51Cr-EDTA at 6, 15, or 32 days postinfection (dpi), ileal segments displayed an increased permeability on 15 and 32 dpi, but not 6 dpi. The alterations in permeability were not reversed 1 wk after removal of the tapeworm from the intestine. In conclusion, the strictly lumen-dwelling tapeworm infection allows increased movement of molecules from the lumen into ileal, but not jejunal, tissues by 15 dpi.

Ultrastructural and lectin-histochemical differences between the scolex/strobila and bladder teguments of the Taenia taeniaeformis strobilocercus.

The strobilocercus stage of the cat tapeworm Taenia taeniaeformis is surrounded by a single syncytial sheet of cytoplasm called the tegument. The outer membrane of the tegument covers both the scolex/strobila (S/S) and the bladder portions of the strobilocercus, but only the S/S region is resistant to intestinal digestion. It has been suggested that the glycocalyx, the surface-exposed glycoconjugates of the outer membrane, may serve to insulate underlying surface membrane components from digestion. In this study, we used lectin binding to test the hypothesis that the glycocalyx of the S/S is different from that of the bladder and that this may serve as the resistance mechanism of the S/S to digestion. Biotin-labeled lectins and an avidin-glucose oxidase detection system were applied to whole strobilocerci and to 1-microm epon-araldite plastic-embedded sections. Lectins bound to either both regions of the strobilocerci, to the S/S regions only, or did not bind at all. The restriction of some glycoconjugates to the glycocalyx of the S/S region only is consistent with our hypothesis.

Hymenolepis diminuta: praziquantel removal of adult tapeworms is followed by apoptotic down-regulation of mucosal mastocytosis.

The rat tapeworm, Hymenolepis diminuta, induces mastocytosis, hypertrophy of enteric smooth muscle, alteration of enteric myoelectric activity, and slowed enteric transit of the rat host's intestine. This report examines the resolution of both tapeworm-induced mastocytosis and tissue changes during the period following removal of the tapeworm with Praziquantel (PZQ). The dynamics of the mucosal mast cell (MMC) population following removal of the tapeworms was assessed by histochemical identification of MMC and morphometric techniques. As a possible mechanism of MMC population regulation, MMC apoptosis was examined over the same experimental period using the in situ nick end labeling of fragmented DNA (TUNEL). Shifts in MMC numbers were correlated with functional and morphological changes of the intestine following removal of the adult-stage tapeworm. Ileal tissues from rats infected 32 days with H. diminuta (the beginning of plateau phase of tapeworm-induced chronic mastocytosis) were harvested 1, 2, 3, and 4 weeks after the PZQ treatment. Control ilea were obtained either from rats which were never infected and never treated with PZQ or from rats infected with H. diminuta for 32 days but not treated with PZQ. In order to detect MMC and apoptosis, tissue sections of ileum were doubled stained sequentially with Astra blue for MMC granules followed by a modification of the TUNEL technique. No alteration in MMC numbers were observed in PZQ-treated animals until 3 weeks after the removal of the tapeworms. The decline of MMC occurred in the mucosa and submucosa. MMC numbers first approached uninfected control levels at 4 weeks posttreatment. Coincident with the decline in mucosal MMC numbers, the rate of MMC entering apoptosis also declined. Simultaneously, ileal smooth muscle layers, hypertrophied by infection, and mucosal structures began the process of involution and atrophy. Apoptosis of MMC in the submucosa and muscularis mucosa was not detected. In conclusion, H. diminuta-elicited mastocytosis and increased thickness of both mucosa and muscularis externa do not begin a decline toward control values until 3 weeks after the parasites are gone and normal intestinal motility is restored. These data are consistent with the lack of MMC mediation of altered motility, and the decline in the rate of MMC apoptosis at 3 weeks post-PZQ suggests that apoptosis may play an important role in the involution of tapeworm-induced mastocytosis.

Hymenolepis diminuta fractions but not previous tapeworm infection stimulate intestinal myoelectric alterations in vivo in the rat.

Infection of rats with the enteric, lumen-dwelling tapeworm Hymenolepis diminuta causes electric changes in host intestinal smooth muscle and decreased luminal transit. The mechanisms that stimulate host intestinal alterations during this nontissue invasive infection may include the tapeworm's biomass, its diurnal migratory behavior, a host immune-mediated response, or direct parasite stimulation of host motor activity. In vivo intestinal myoelectric activity was monitored to evaluate the following: (1) that reinfection with H. diminuta is influenced by host immune regulation and (2) that administration of tapeworm fractions to never-before-infected rats initiates an alteration of enteric smooth muscle activity. To address the first hypothesis, we determined that altered intestinal myoelectric activity patterns were no different and did not occur earlier in a second infection with H. diminuta than in a primary infection. The lack of either a change in myoelectric pattern or an earlier onset of intestinal myoelectric changes indicates that tapeworm-induced myoelectric activity is not anamnestically stimulated by host immunomodulatory mechanisms. Consistent with the second hypothesis, administration of either H. diminuta carcass homogenate or tegument-enriched fractions directly into the intestinal lumen of tapeworm-naive rats initiated myoelectric patterns previously characteristic of chronic H. diminuta infection. Additionally, the appearance of characteristic nonmigrating myoelectric patterns in uninfected rats administered tapeworm fractions indicates that a substance from H. diminuta acts as the triggering signal molecule for intestinal myoelectric alterations. These findings also indicate that neither the tapeworm's biomass nor its diurnal movement is required for initiation of H. diminuta-altered myoelectric patterns. We have shown that H. diminuta possess a signal molecule(s) that alters host enteric electric activity, and we suggest that these alterations may play an important role in the symbiotic rat-tapeworm interrelationship.

Hymenolepsis diminuta: mucosal mastocytosis and intestinal smooth muscle hypertrophy occur in tapeworm-infected rats.

The mechanisms mediating motility changes during noninvasive tapeworm infection have not been characterized. In contrast, host intestinal motility changes during invasive nematode infection are mediated by mucosal mast cells (MMC). The purpose of this study was to examine and the correlate onset of myoelectric alterations 8 days after initial tapeworm infection with changes in intestinal morphology, MMC numbers, and MMC secretory activity. Segments of the small intestine, the tapeworms normal habitat, along with stomach, colon, and bladder were taken from tapeworm-infected and control rats. Tissues were fixed and stained to identify MMC and for morphologic measurement. Tapeworm-infected and uninfected rats with chronically implanted intestinal electrodes were treated with ketotifen, a mast cell stabilizer, and in vivo myoelectric activity monitored. In tapeworm-infected rats, the muscularis externa, on day 20 postinfection, and crypts of Lieberkuhn, on day 26 postinfection, from the entire small intestine appeared thickened or deeper, respectively. Increased muscularis thickness was due to smooth muscle hypertrophy in both the circular and the longitudinal muscle layers. Mucosal mastocytosis was first observed on day 26 postinfection and occurred only in the ileum of tapeworm-infected rats. Pharmacologic stabilization of mast cells with ketotifen did not prevent onset of enteric myoelectric alterations during tapeworm infection. Stomach, colon, and bladder MMC numbers and tissue dimensions were not different between Hymenolepis diminuta-infected rats and uninfected controls. Initiation of myoelectric alterations 8 days after infection precedes and may be a contributing factor to the onset of both smooth muscle hypertrophy and mucosal mastocytosis. Taken together, our data indicate that mast cells are not an initiating factor nor chronic stimulus maintaining intestinal myoelectric alterations during H. diminuta infection.

Effect of tunicamycin on the uptake and incorporation of galactose in Hymenolepis diminuta.

The effects of tunicamycin (TM) on the uptake and incorporation of tritiated galactose into the tegumental membrane and carcass from adult Hymenolepis diminuta were examined to assess the potential usefulness of this inhibitor for studying the function of the tapeworm surface glycocalyx. Hymenolepis diminuta adults (11 days old) were preincubated for 1 hr, pulsed for 30 min with [3H]galactose and [14C]leucine, and chased for 2 hr; replicate experiments were conducted in which all media contained no TM or TM at 10 micrograms/ml. Tunicamycin significantly inhibited the incorporation of tritiated galactose into the tapeworm's carcass and 30,000-g tegumental membrane fraction. Incorporation of tritiated galactose into the tapeworm's tegumental surface membrane also was inhibited significantly when expressed relative to the incorporation of [14C]leucine. Tunicamycin did not affect the amounts of free, i.e., soluble, [3H]galactose or [14C]leucine recovered from the tapeworms not did it affect the short-term (2 min) uptake of [3H]galactose by tapeworms. Thus, the inhibitory effect of TM appears to be at the level of protein glycosylation rather than carbohydrate (galactose) transport. The data indicate that TM might be useful for producing tapeworm surface membranes with diminished carbohydrate moieties.

Tapeworm infection decreases intestinal transit and enteric aerobic bacterial populations.

Intestinal myoelectric patterns in rats are altered after chronic luminal infection with the tapeworm Hymenolepis diminuta. This study evaluates whether these altered patterns were associated with changes in intestinal fluid transit and endogenous enteric microbe levels. Luminal transit, measured throughout the small intestine during the interdigestive state, was significantly decreased during tapeworm infection. Reduced transit was regional, occurring in the same location as that of the tapeworm and maximal myoelectric alterations. In other experimental systems, aerobic and anaerobic bacterial overgrowth is associated with decreased transit; however, reduced transit during tapeworm infection was unexpectedly associated with decreased numbers of aerobic bacteria, whereas anaerobic bacterial populations remained unchanged. The lack of overgrowing endogenous microflora suggests that overgrowth is not responsible for tapeworm-stimulated alterations in host myoelectric patterns. We speculate that a tapeworm secretion could be responsible for both transit and motility changes while delayed intestinal transit could prevent tapeworm expulsion, aid the tapeworms' migration, and contribute to the digestion and absorption of nutrients by hosts and/or parasites.

Praziquantel treatment normalizes intestinal myoelectric alterations associated with Hymenolepis diminuta-infected rats.

Hymenolepis diminuta-associated alterations in rat intestinal myoelectric patterns are abolished following therapeutic administration of the anthelmintic praziquantel (PZQ). Host intestinal smooth muscle myoelectric patterns, reflecting smooth muscle contractility and intestinal phasic motility, were recorded using in vivo serosal electrodes, surgically implanted on the duodenum, jejunum, and ileum. Repeated electromyographic recording from unrestrained and unanesthetized rats began 5 days after electrode implantation surgery. Three initial control recordings from each rat confirmed the appearance of normal intestinal myoelectric patterns, characterized by the interdigestive migrating myoelectric complex (MMC). All animals were subsequently infected with H. diminuta and myoelectric recordings beginning after day 8 postinfection confirmed the appearance of diminished frequency of the MMC and 2 nonmigrating myoelectric patterns, i.e., repetitive bursts of action potentials and sustained spike potentials. PZQ was used to remove the tapeworms from rats 12 days after Hymenolepis diminuta infection, as intestinal myoelectric changes become maximal at this time in tapeworm-infected rats. PZQ administered to uninfected rats at either of 2 dose levels did not affect host interdigestive myoelectric activity. After removal of the parasite with PZQ, electromyographic recordings indicated a return to normal uninfected electrical patterns within 24 hr of drug treatment. We have demonstrated that the presence of Hymenolepis diminuta is necessary to induce and maintain abnormal intestinal myoelectric patterns. The altered motor properties of tapeworm-infected rat intestine and the rapid reconversion to preinfection myoelectric patterns provides a new and unique model to examine the regulatory mechanisms of intestinal motility and its control by luminal parasites.

Intestinal myoelectric alterations in rats chronically infected with the tapeworm Hymenolepis diminuta.

This study determined that intestinal myoelectric activity was profoundly altered during a strictly luminal, chronic, tapeworm infection. Chronically implanted bipolar electrodes were attached to five sites on the serosal surface of the rat small intestine. One was placed on the duodenum, three on the jejunum, and the fifth on the ileum. Electromyographic recording in nonfasted unanesthetized animals was begun at day 5 postsurgery. All electromyographic recordings were analyzed for slow wave (SW) frequency, phase III frequency, duration of phase III, and percentage of SW with spike potentials. Three initial control recordings prior to infection confirmed the presence of normal interdigestive motility characterized by the three phases (I, II, III) of the migrating myoelectric complex (MMC). Two nonpropulsive myoelectric alterations were observed in infected animals: the repetitive bursts of action potentials (RBAP) and periods of sustained spike potentials (SSP). Myoelectric activity from infected animals indicated decreased cycling of the interdigestive MMC. RBAP and SSP were more prevalent in the distal small intestine corresponding to tapeworm location. The percent of spike potential activity indicated that there was a reversal in the spike potential gradient on the small intestine. The number of spike potentials was maximal in caudal and minimal in oral intestine. We propose that overall localized increases in myoelectric spike potential activity represent increased contractility and decreased propulsion triggered by the presence of the tapeworm. These motility changes were surprising, since the tapeworm Hymenolepis diminuta does not penetrate the intestinal mucosa. This interaction between parasite and host may prevent expulsion of the tapeworm from the small intestine.

Hymenolepis diminuta: two morphologically distinct tegumental secretory mechanisms are present in the cestode.

The free-surface of the tapeworm's tegument was examined for morphological evidence of secretion after fixation by rapid freezing-freeze substitution and alternatively by immersion in low concentrations of glutaraldehyde maintained at room temperature. After low-aldehyde fixation, omega profiles were at the bases of tegumental microvilli, arguing for the participation of some of the ectocytoplasm's vesicles in secretion of their contents to the intestinal lumen. The almost instantaneous fixation provided by the rapid freezing-freeze substitution technique documents the constitutive production of 0.03 to 0.075-micron microvesicles from outpocketings from the plasma membrane of the tegumental brush border. Observed in secretory epithelial cells of other species, microvesicles are recognized as a secretory pathway for constituent molecules of surface membranes. We conclude that in addition to the primary route of merocrine exocytotic secretion provided by the fusion of the Golgi-derived, ectocytoplasmic vesicles at the bases of the brush border microvilli, tegumental microvesicles provide a second secretory pathway for endogenous macromolecules across the tegumental free surface.

The effect of dimethylsulfoxide on the tegumental brush border of the cestode Hymenolepis diminuta.

Dimethyl sulfoxide (DMSO), commonly used for cryoprotection or for the solvation of cytoskeleton-modifying drugs, causes changes in the topology of the plasma membrane of the tegumental brush border in the tapeworm Hymenolepis diminuta; however, relatively long exposures of high concentrations are required. In tapeworms treated with DMSO concentrations of greater than or equal to 1% in the present study, the interaction of the tegumental surface membrane with the underlying cytoskeleton may have been disrupted at focal points in the brush border, resulting in a partial loss of the membrane anchoring required for the structural integrity of the brush border. Blebbing of the tegumental surface was prominent only after exposure to 1% DMSO for 20 h in in vitro culture with RPMI 1640, and vesiculation of the membrane along the microvillar (microtriche) shafts, which may have been related to the in vitro conditions, was amplified by the presence of concentrations of greater than or equal to 1% DMSO in the incubation medium. The tegumental response to DMSO was not uniform but regional, consistently appearing to be more prevalent on the distal aspects of each proglottid rather than on the edge proximal to the scolex. Blebbing and vesiculation were not seen on the basal aspect of the tegument, including the basal ectocytoplasmic plasma membrane, the perikarya, and the internuncial processes. Microvillar core bundles of actin microfilaments persisted following 8 h in vitro exposure to all three concentrations of DMSO tested (0.1%, 1%, 5%); however, only in tapeworms that were treated in vitro with 5% DMSO for greater than or equal to 8 h did core microfilament bundles appear to lose the rigidly straight and parallel organization characteristic of control tapeworms that were incubated either in the absence of DMSO or with 0.1% DMSO. Other components of the brush border cytoskeleton (i.e., microvillar caps, junctional tubules, and tunics) appeared unaffected by DMSO except at foci where blebbing occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Development and dynamics of regional specialization within the syncytial epidermis of the rat tapeworm, Hymenolepis diminuta.

The epidermis of the tapeworm Hymenolepis diminuta is a highly organized syncytium, composed of an outer layer of continuous cytoplasm, or ectocytoplasm, and an inner layer of nucleated cell bodies, or perikarya. The perikarya are in direct cytoplasmic continuity with the ectocytoplasm via narrow plasmalemma-bound bridges called internuncial process. Although distinct structural and functional differences are apparent between ectocytoplasm and perikarya, all of the perikarya along the body of the cestode are morphologically similar, as are all regions of ectocytoplasm. However, immunocytochemically distinct subpopulations of perikarya and regionally defined areas of ectocytoplasm were identified along the tapeworm strobila by the use of monoclonal antibodies raised against a preparation of isolated tegument. The different types of perikarya and the regionally specialized areas of ectocytoplasm were organized in a topographically precise manner along the body of the parasite. Examination of labeling patterns after colchicine treatment suggests that different types of perikarya are specialized for biosynthesis of specific tegumental molecules and for turnover or recycling of tegumental material. Furthermore, it appears that a 52 kDa polypeptide synthesized by one population of perikarya is transported through the syncytium and ultimately resorbed by a different population of tegumental perikarya. These data suggest that the syncytial epidermis of parasitic platyhelminthes exhibits a more complex organization of function than previously appreciated.