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The human flea (Pulex irritans) and the dog louse (Trichodectes canis) can occasionally serve as intermediate hosts buy female viagra in united states online pregnancy 25 weeks. The gravid proglottids detach singly or in groups from the strobila or chain of segments or proglottids that make up the body of the cestode; they are mobile and pass to the exterior on their own or with the feces discount 100mg female viagra mastercard pregnancy 0-3 months. The proglottids disintegrate in the environ- ment order female viagra 100mg amex menopause sleep, releasing the eggs buy female viagra online now menopause age range, which must be ingested by the flea larvae to continue their development to adulthood. The eggs hatch in the intestine of the flea larva, and the embryos (oncospheres) penetrate the celomic cavity; there they turn into cysticer- coids. Hinaidy (1991) conducted a study in Austria of 9,134 fleas from 198 cats and 182 dogs, and found that 98. When a dog or cat ingests an infected flea, the cysticercoid is released in the small intestine through digestion, establishes itself in the mucosa, and becomes an adult parasite in about 20 days. In Latin America, the infection has been observed in Chile (17 cases), Argentina, Uruguay, Brazil, Venezuela, Guatemala, Mexico, and Puerto Rico. The infection is so rare in humans that, when single cases occur, they are reported in almost all coun- tries (Wijesundera and Ranaweera, 1989; Raitiere, 1992; Reid et al. The infection in cats is as prevalent as or more prevalent than in dogs, but is also variable. The Disease in Man: Because of its epidemiological characteristics, human dipy- lidiasis affects mainly infants and young children. The symptomatology consists of digestive disorders, such as diarrhea and colic, irritability, erratic appetite, and insomnia; the infection is often asymptomatic. In a series of patients studied in Chile (Belmar, 1963), abdominal distension was almost always seen. Elimination of motile proglottids is the sign usually noticed by the patients’ parents, and is some- times the only manifestation of the infection. The Disease in Animals: Dipylidiasis, like other cestodiases of dogs and cats, rarely has clinical manifestations. Anal irritation or itching has often been attributed to the movement of gravid proglottids in the anal area, because some infected animals rub themselves on the ground as if trying to scratch themselves; however, the presence of inflamed anal sacs, which also causes similar symptoms, has not been confirmed. Almost all cases of human infection are in very young children who live in homes with infected dogs or cats. The child accidentally eats the flea when kissing or biting the pet, or when the flea drops into his food or attaches itself to a wet pacifier. Diagnosis: In humans and animals, diagnosis is based on microscopic observa- tion of the gravid proglottids. These cestodes have, as a unique characteristic, two genital pores, one on each side of the proglottid. Each proglottid contains a large number of eggs typical of cestodes, but arranged in groups of 5 to 20 in sacs known as oviferous capsules. For observ- ing proglottids or eggs, better results are achieved by examining material collected from the perianal region than by examining the fecal matter. Control: Prophylactic measures consist of eliminating fleas from the home and cestodes from pets. While recommended, watching small children to keep them from ingesting fleas is difficult. A survey of helminths in domestic cats in the Pretoria area of Transvaal, Republic of South Africa. Part 1: The prevalence and com- parison of burdens of helminths in adult and juvenile cats. Rates of reinfection with Echinococcus granulo- sus, Taenia hydatigena, taenia ovis and other cestodes in a rural dog population in Uruguay. Gastrointestinal helminth parasites in stray cats from the mid-Ebro Valley, Spain. Ergebnisse parasitologischer Kotuntersuchungen von Equiden, Hunden, Katzen und Igeln der Jahre 1984–1991. Etiology: The agent of this disease is the hydatid or larval stage of the cestodes Echinococcus granulosus, Echinococcus multilocularis, Echinococcus oligarthrus, and Echinococcus vogeli. While other species and subspecies of Echinococcus have occasionally appeared in the literature, their taxonomic status is doubtful or uncer- tain. The adult cestode lives attached deep inside the mucosal crypts of the definitive host’s small intestine and is 3 to 6 mm long; it has 22 large hooks and 18 small hooks on the scolex and usually has just 3 proglottids, of which only the last is gravid. The gravid proglottid, containing several hundred eggs, detaches from the strobila, is expelled with the feces, and disintegrates in the environment. Each egg contains an embryo (oncosphere) with six hooks (hexacanth), which must be ingested by an intermediate host to continue its development. Intermediate hosts are sheep, bovines, swine, goats, equines, camelids (Asian and American), cervids, and man. The oncosphere is released in the small intestine of the intermediate host, passes through the intestinal wall, and is carried by the bloodstream to various organs, where it undifferentiates and then differentiates again to develop the larval stage, called the hydatid. After three weeks the hydatid measures 250 µm in diameter and has a central cavity. During the same period, brood capsules bud off from the germinative layer, and invaginated protoscolices, which constitute the infective agent of the parasite, develop within them. These capsules either adhere to the wall by means of a peduncle or float freely in the hydatid fluid. The capsules and the protoscolices that float freely in the hydatid fluid are known as “hydatid sand. In con- trast, daughter hydatids with a two-layer wall like that of the mother sometimes form inside the hydatid. As the larva develops and the tissues of the host are compressed, the host responds with a fibrotic reaction, surrounding the larva with dense connec- tive tissue, the adventitial layer. The most common localizations of these cysts are the liver (in about two-thirds of the cases) and the lungs (in about a fourth of the cases); on rare occasions they may become situated in some other organ, such as the kidneys, spleen, bones, and brain. The cycle is completed when a dog or other canid ingests the viscera of an intermediate host in which there are fertile hydatid cysts. The scolex attaches to the wall of the dog’s small intestine and develops into an adult cestode that begins to produce infective eggs 47 to 61 days after infection. A single cyst can give rise to thousands of adult cestodes because of the large number of sco- lices. For example, in Great Britain, two strains occur: an equine strain whose development cycle involves horses and dogs, and an ovine strain that circulates between sheep and dogs. In addi- tion to the differences in morphology and development in the different intermediate hosts, the two strains also differ in biochemical and physiological characteristics. Even though dogs are definitive hosts for both, it seems that the equine strain is not transmitted to sheep and vice versa. In Latin America, except around Santa María, Rio Grande do Sul, Brazil, horses are rarely affected by the larval form of E. In Australia, three strains are distinguished; one circulates between the dingo and macropodid marsupials (wallabies, kangaroos), and the other two (one continental and the other from Tasmania) circulate between dogs and sheep but differ in some biochemical, morphological, and biological properties (Thompson and Kumaratilake, 1982). Studies in the former Soviet Union have shown that the strain circulating between dogs and sheep is not infective for swine, and the strain circu- lating between dogs and swine is not transmitted to sheep. Recent molecular biol- ogy studies have confirmed the presence of four genotypes in Argentina: the ovine, circulating between sheep and humans; the ovine from Tasmania, circulating in sheep and humans; the porcine in swine; and the camelid in humans (Rozenzvit et al. The species are distinguished by subtle characteristics of the mature proglottid and by the number and shape of the hooks on the scolex. The natural definitive hosts are foxes, chiefly the arctic fox (Alopex lagopus) and the red fox (Vulpes vulpes). The intermediate hosts are wild rodents, primarily species of the genera Microtus, Clethrionomys, and Lemmus. Domestic dogs and cats may also serve as definitive hosts when they enter the cycle by feeding on infected wild rodents. The rodents develop the hydatid in the liver after ingesting eggs deposited with the fecal matter of definitive hosts; in about 60 days, the hydatid contains infective protoscolices. The vesicles are filled with a gelatinous liquid and generally lack protoscolices in humans. The absence of protoscolices seems to indicate that man is not a satisfactory host because, when a cyst is transplanted from man to a suitable rodent, the cyst begins to produce them. When a fox, dog, or cat ingests an infected rodent, the protoscol- ices give rise to the development of adult cestodes, which begin producing infective eggs that are eliminated in the fecal matter in about 33 days. The definitive hosts are wild felids such as pumas, jaguars, jaguarundis, and lynxes. The intermediate hosts are wild rodents such as the agouti Dasyprocta and possibly other rodents as well. This noninvasive cyst, which has multiple external compartments and abundant protoscolices, is generally called “polycystic. In some of these countries, the incidence has recently diminished notably because of control programs. Moreover, this species was identified recently in northeastern Mexico (Salinas-López et al. The highest infection rates are recorded in countries with livestock industries, especially sheep raising, in rural areas, and among people of limited economic and cultural means. Information on the prevalence of human hydatidosis is often based on doctors’ reports. Moreover, it is necessary to distinguish between the infection, which may be asymptomatic, and the disease, which, by definition, is symptomatic. The most reliable sources of infor- mation on the incidence of the disease are the hospital records of surgical opera- tions. In Latin America, the highest concentration of cases occurs in the Southern Cone of South America (Argentina, southern Brazil, the mountains of Peru, and Uruguay) (Arámbulo, 1997). In the 1960s, the annual incidence of surgical cases per 100,000 inhabitants was 1. However, these data paint an unrealistic picture, because prevalence refers to the total population of the country and not the rural population, which is the population at real risk for the infection.

The cycle of merozoite formation in the red blood cells takes 24 hours in some species (e purchase female viagra uk menstruation ovulation period. As the recurrent fevers of malaria coincide with the mass release of merozoites from the red cells order female viagra once a day menstrual cramps 9dpo, they occur daily or every third or fourth day generic 50 mg female viagra amex women's health raspberry ketone. Malaria is classified as quotid- ian order female viagra australia women's health fitness magazine uk, tertian, or quartan, respectively, according to the periodicity of these febrile attacks (Table 2). After several rounds of asexual reproduction in the erythrocytes, some merozoites become female cells, or macrogametocytes, and male cells, or microgametocytes, which are the infective forms for the vector. When an Anopheles mosquito ingests the gametocytes dur- ing a blood meal, they mature in the insect’s alimentary tract and become macroga- metes (ova) and microgametes (sperm). A sperm fertilizes each ovum, forming a motile zygote, the ookinete, which penetrates the epithelium of the insect’s midgut, is engulfed by a membrane, and forms an oocyst in the intestinal wall. Inside the oocyst, the zygote multiplies by successive mitosis to produce an enormous number of filamentous parasites, the sporozoites, which ultimately break out of the oocyst and are distributed in the hemocele of the insect. The sporozoites invade all of the mosquito’s tissues, and those that reach the salivary glands may be passed to a vertebrate host with the saliva of the insect at its next blood meal. Geographic Distribution: Although the prevailing opinion is that the plasmodia of simians originated in Southeast Asia, Escalante et al. Their current geographic dis- tribution coincides with that of their preferred hosts (Table 2). Occurrence in Man: Infection of man with plasmodia of nonhuman primates is considered very rare. The literature records only two confirmed human cases acquired under natural conditions: one caused by P. However, it was subsequently discovered that more than 90% of the adults in four tribes in northern Brazil had antibodies against P. After 170 serial passages, how- ever, the infection became so virulent that the passages were stopped (Collins and Aikawa, 1977). Although the level of para- sitemia in humans was low, the disease was moderately serious. The infection rate is close to 15% in howler monkeys of the genus Alouatta, spider monkeys of the genus Ateles, and capuchin or white monkeys of the genus Cebus. The prevalence of malaria has been reported to be 10% among simians in the Amazon region and 35% and 18% in the southeastern and southern regions of Brazil, respectively. Virtually all the parasites were detected in monkeys of the family Cebidae (Deane, 1992). Among nonhuman primates in Asia and Africa, the prevalence of the infec- tion seems to be high in areas with large numbers of monkeys and appropriate anopheline vectors. Conversely, there are areas with sparse monkey populations in both the New World and the Old World where the infection does not occur. The Disease in Man: Human malaria caused by plasmodia of simian origin resembles a mild and benign infection caused by human plasmodia (see Occurrence in Man). In general, the disease is of short duration, parasitemias are low, and relapses are rare. The Disease in Animals: In general, malaria in simians is a mild disease that resolves spontaneously in the parasite’s natural hosts. Source of Infection and Mode of Transmission: Malaria of both humans and nonhuman primates is transmitted by the bite of infected anopheline mosquitoes. Which species of mosquitoes transmit malaria of nonhuman primates in the forests of Africa, the Americas, and a large part of Asia is still not well known. However, the cycles of disease transmission in humans and nonhuman primates are generally independent of one another because the vectors of human plasmodia feed at ground level, while those of simian plasmodia feed in the treetrops. Nevertheless, in some regions of Brazil, such as the mountainous and wooded coastal areas of the state of Santa Catarina, A. In such conditions, human infection caused by simian plasmodia may occur naturally. In western Malaysia, a similar sit- uation exists: the vector is the same for the human and nonhuman cycles, and zoonotic infections may thus occur. However, the risk appears to be limited to those who live in or enter jungle areas, and it is unlikely that the infection could spread to other human communities. However, malariologists point out that the plas- modia of nonhuman primates pose little risk for the human population, since P. Diagnosis: Routine diagnosis in man and in monkeys is done by examining the parasite in thick blood films stained with Giemsa stain. Differentiation of the species of Plasmodium that infect nonhuman primates is based mainly on morphologic fea- tures of the parasite’s various stages of development. Another difficulty in diagnosis by microscopic examination of blood prepa- rations is the low parasitemia that occurs in nonhuman primates. To get around this difficulty, inoculation of blood into susceptible monkeys is recommended. Although serologic reactions are useful as a means of confirming malarial infection, they are rarely specific enough to identify the Plasmodium species involved. Control: Malaria experts agree that malaria of nonhuman primates does not con- stitute an obstacle for programs to control and eradicate human malaria. The human infection has been eradicated from some parts of Brazil, although high rates of infection in monkeys persist. Given the small number of confirmed cases of human infection by plasmodia of simian origin and the benign nature of the clinical mani- festations, special control measures are not justified. To prevent the disease, nonimmune persons who must go into the jungle should use insect repellents on exposed body parts and on clothing. Regular use of chemo- prophylaxis would be justified only if the nonimmune person had to live in an area where human malaria is endemic. A primate model for human cerebral malaria: Plasmodium coatneyi-infected rhesus monkeys. In: First Inter- American Conference on Conservation and Utilization of American Nonhuman Primates in Biomedical Research. Studies on transmission of simian malaria and on a natural infection of man with Plasmodium simium in Brazil. Sero-epidemiological stud- ies of malaria in Indian tribes of the Amazon Basin of Brazil. The evolution of primate malaria parasites based on the gene encoding cytochrome b from the linear mitochondial genome. A nonhuman primate model for human cerebral malaria: Rhesus monkeys experimentally infected with Plasmodium fragile. Plasmodium ovale: Observations on the parasite development in Saimiri monkey hepatocytes in vivo and in vitro in contrast with its inability to induce parasitemia. Hydrolytic enzymes of rhesus placenta during Plasmodium cynomolgi infection: Ultrastructural and biochemical studies. Although there are some 700 species that infect verte- brates and invertebrates, the species identified to date as parasites of man are Enterocytozoon bieneusi, Encephalitozoon intestinalis (formerly Septata intesti- nalis), Encephalitozoon hellem, Encephalitozoon cuniculi, and some species of the genera Nosema, Pleistophora, Trachipleistophora, and Vittaforma (Scaglia et al. Enterocytozoon causes intestinal infections almost exclusively, while Encephalitozoon may cause intestinal or systemic infections which may spread to various organs. Parasites of the genera Nosema, Pleistophora, Trachipleistophora, and Vittaforma are uncommon in man and do not affect the intestine (Field et al. Proof of the existence of isolates with genetic differences exists, at least within E. The genera Cryptosporidium, Isospora, and Cyclospora belong to a completely different phylum: Apicomplexa (formerly Esporozoa). Microsporidia are small intracellular protozoa that undergo a phase of asexual mul- tiplication—merogony—followed by a phase of sexual multiplication—sporogony— during which they produce spores, or oocysts, inside the infected cell. The spores are released from the host cell and are eliminated into the external environment, where they may infect other individuals. They are small, double-walled bodies measuring 1 µm to 3 µm which contain a parasitic cell, or sporoplasm, with one or two nuclei. At their anterior end, they have an extrusion apparatus, the polaroplast, which everts the polar tube or filament that is coiled around the polaroplast and sporoplasm within the spore. Infection takes place when the polar tube is extruded and penetrates the host cell, allowing the sporoplasm to pass through it and enter the host. Occurrence in Man: Microsporidiosis is one of the most frequent complications occurring in immunodeficient patients, but it is rare in immunocompetent individu- als. As of 1994, more than 400 cases had been recognized, most in immunodeficient patients. The parasites were detected in 60% of patients with chronic diarrhea but in only 5. Occurrence in Animals: Microsporidiosis occurs in a great number of vertebrate and invertebrate species, but as it is not generally pathogenic for vertebrates, its dis- covery is accidental, and there are thus no reliable statistics on its frequency. The clinical manifestations include chronic diarrhea with passage of watery or semi-watery stools numerous times (2–8) a day, but without evidence of intestinal hemorrhage; malabsorption with atrophy of the microvilli, which is aggravated by the ingestion of food; and subsequent progressive and irreversible weight loss. Although the causes of the intestinal disease are not well understood, it is presumed that it is due to loss of microvilli and enterocytes. Trachipleistophora hominis may affect the skeletal musculature, the cornea, and the upper respiratory tract (Field et al. The Disease in Animals: Most infections in vertebrates seem to be asympto- matic, except for E. Source of Infection and Mode of Transmission: The presence of microsporidia spores in the host stools and urine suggests that the infection could be transmitted by fecal or urinary contamination of the environment, especially water. Diagnosis: Diagnosis of microsporidiosis is difficult owing to the small size of the spores. Specimens are obtained, inter alia, from body fluids, feces, duodenal aspirates, urinary sediment, and corneal scrapings, and they are then stained using methods that facilitate microscopic examination.

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The efferent pathway probably involves vagal pre-enteric neurons and enteric final motor neurons purchase female viagra 50 mg women's health big book of exercises pdf free download. Gastric Secretomotor Neurons That Stimulate Acid Output Some secretomotor neurons govern gastric acid secretion [106] female viagra 50mg menopause type 7. These neurons are cholinergic and act on the parietal cells through muscarinic receptors buy generic female viagra 50 mg line breast cancer drugs. Projection studies indicate that the secretomotor neurons have cell bodies in the myenteric plexus close to the regions of mucosa that they innervate [107] order discount female viagra pregnancy gestation calculator. Gastric Vasodilator Neurons Gastric acid secretion and blood flow are enhanced when the vagus nerve is stimulated and these effects are reduced by muscarinic antagonists. In most exper- iments, it is not possible to determine whether vasodilation is due to a direct vascular action of cholinergic neurons in addition to a functional hyperemia consequent on the increased secretion [108]. The blood flow increase in the absence of secretory change was antagonized by atropine. The best documented motor neurons innervating enteric endocrine cells are those controlling release of gastrin, which is under the influence of vagal and of intrinsic gastric pathways [27]. Transmission from the final secretomotor neurons is mediated at least in part by gastrin-releasing peptide [111]. Hormone release from other entero-endocrine cells is also likely to be under neural control. The basal release of motilin is reduced by atropine and by tetrodotoxin, and stimulated by muscarinic agonists, suggesting that motilin cells receive an excitatory cholinergic input [113]. Innervation of Lymphoid Tissue (Peyer’s Patches), Lymphocytes and Mast Cells Lymphoid aggregations of the gastrointestinal tract, the most prominent being Peyer’s patches, have surrounding nerve fibers, but it is difficult to trace the fibers into the follicles [114, 115]. However, careful examination does reveal an inner- vation of the suprafollicular dome region, but not an innervation of the germinal centers, in porcine jejunal lymphoid aggregations [116, 117], human ileal Peyer’s patches [117] and follicles in the lamb small intestine [118]. Retrograde tracing from follicles reveals that they are innervated from submucosal ganglia [118]. In addition, receptors for transmitters of enteric neurons occur on lymphocytes that are scattered in the connective tissue (lamina propria) of the mucosa, and there are close approaches that suggest functional innervation of isolated lymphocytes within the connective tissue of the mucosa [119]. There are also close appositions between axons and mast cells in the mucosa [120]. Enteric Interneurons Studies of the projections of neurons within the gut wall have identified several types of interneurons. However, these are more difficult to investigate physiolog- ically than other neurons, because they can only be definitively studied by direct recording techniques, even though elegant divided organ bath methods have pro- vided insights into the properties of enteric interneurons [121]. Within the myenteric plexus, the interneurons form chains of like neurons that run both orally and anally [122–124]. In the guinea-pig small intestine, three classes of descending interneurons and one class of ascending interneuron have been identified. Detailed studies of synaptic connections indicate that the chains formed by two of the types of descending interneuron interconnect [125]. The somatostatin containing neurons have numerous branching, tapering, filamentous dendrites [123]. Recent evidence suggests that some classes of interneurons in the colon are mechanoceptive and that reflexes can be initiated when they are activated by stretch [126]. Neural Control of Gastrointestinal Muscle Activity The muscle layers of the gastrointestinal tract direct propulsion, mixing of contents, reservoir capacity (notably in the stomach) and expulsion of pathogens and noxious chemicals. In broad terms, the body of the esophagus is controlled through brain stem circuits located in the medulla oblongata and the stomach is controlled through the brain stem and vago-vagal reflexes. These circuits relay through the nucleus ambiguous, which contains the cell bodies of the motor neurons that innervate the striated muscle [127, 128]. Nevertheless, myenteric neurons do supply an innervation to about a third of the end-plates and thus, unlike motor endplates elsewhere, 3 The Enteric Nervous System and Gastrointestinal Innervation: Integrated. Thus the enteric nervous system seems to have a role in modulating peristalsis in the upper esophagus. The enteric innervation may have a greater role in young animals, because all motor endplates receive an enteric innervation at days 4–10 postnatal, after which there is partial withdrawal of innervation [135]. The nerve fibers that innervate the smooth muscle of the lower esophagus have their cell bodies in enteric ganglia. The enteric ganglia of the smooth muscle esophagus are directly innervated by pre-enteric neurons of the dorsal motor nucleus of the vagus, and lesion of this nucleus impairs the motility patterns of the smooth muscle esophagus [128]. However, sphincter relaxation still occurs in response to disten- sion following vagal block, indicating that a local reflex can be elicited [136]. This sphincter contraction is mediated by a vago-vagal reflex pathway that passes through the brain stem. Failure of this guarding results in reflux esophagitis and esophageal mucosal damage. Stomach A well-developed ganglionated myenteric plexus is found in the stomach, whose activity is significantly controlled through the vagus (see also above section “Vagal Efferent Pathways”). The stomach has a reservoir function; it increases volume as it fills, and relaxes prior to food arriving. It also has a function to mix the food with gastric juices and to push the liquefied products of gastric digestion into the duodenum. The fundus (proximal stomach) is primarily associated with the gastric reservoir function and the corpus-antrum (distal stomach) is associated with gastric mixing and antral propulsion [139]. Each antral contraction propels a small amount of liquid into the duodenum, while solid material is retained in the stomach [17]. Gastric Reservoir Function The pressure in the stomach does not increase as it is filled [140], implying that the muscle of the proximal stomach relaxes to accommodate the meal. In fact, relax- ation occurs before the food arrives, a phenomenon called receptive relaxation [141]. The relaxation that occurs when the pharynx or esophagus is distended occurs even when the esophagus is severed and no food reaches the stomach [142]. Relaxation of the proximal stomach also occurs if the gastric volume is increased, for example by distension with an intragastric balloon. A vagally mediated gastro-gastric reflex relaxation is also be elicited when distension is confined to the antrum [145]. In addition, there appears to be a small residual component of accommodation that is due to an intrinsic reflex [146]. Thus the stomach adjusts its volume both by relaxation and contraction, via vago-vagal reflexes. Gastric Peristalsis and Mixing (the Distal Stomach: Corpus and Antrum) Gastric peristalsis, which occurs in the body and antrum, is not prevented when the myenteric plexus is cut through or nicotine is given in a dose that blocks peristalsis in the intestine [147, 148]. Moreover, the frequency of peristalsis corresponds to the frequency of gastric slow waves in the muscle, indicating that gastric peristalsis is generated by the slow waves and, unlike peristalsis in the small intestine and colon, it does not require activity of excitatory neurons to be observed. The augmentation of the gastric contractions when the stomach is artificially distended with fluid is almost entirely through vago-vagal reflexes [149]. When the antrum, or the whole stomach, is extrinsically denervated, antral peristaltic con- tractions are smaller and emptying times are prolonged [149–151]. Moreover, the strengths of the antral contractions are sequentially reduced when the vagal branches entering the antrum are successively cut, from proximal to distal [152]. Nevertheless, a number of studies indicate that there is intrinsic activity of excitatory cholinergic neurons, even in the completely isolated stomach. The amplitudes, but not the frequen- cies of occurrence of contractile waves are reduced when transmission from excitatory neurons to the muscle is prevented by tetrodotoxin [156]. The effective- ness of the excitatory neurons is enhanced when the stomach is distended [156], presumably because their rates of firing are increased. After vagotomy, gastric distension causes very much weaker phasic contractions than are seen in the vagally innervated stomach [149]. The residual responses to distension are reduced by hexamethonium, indicating that there is a component of the enhancement of gastric peristaltic waves that is due to intrinsic reflexes. Furthermore, if the mus- carinic receptor agonist, carbachol, is applied to the isolated stomach in which all nerve-mediated events have been prevented by tetrodotoxin, gastric peristaltic waves are restored [156]. This suggests that neuronal circuits are not required to co-ordinate peristaltic movement, direct excitation of the muscle being sufficient. The structural organisation of the circuits that detect the state of the small intestine, integrate the information and direct the activities of motor neurons is known (Fig. Signals that trigger changes in patterns of movement in the small intestine have been identified. For example, fatty acids added to the luminal surface convert propulsive contractile activity to mixing movements, through a neural mechanism [159]. Conversion from one pattern to another can also be achieved with some drugs that target enteric neurons [160]. Similar component neurons have been identified in the small intestine of other species, including human, and in the large intestine. This is a simplified circuit diagram showing the major circuit features that have been identified. These synapse with descending (yellow) and ascending (green) interneurons, and connect with excitatory muscle motor neurons (blue) and inhibitory muscle motor neurons (purple) directly and via interneurons. Oxford: Blackwell 2006 Neural Control of Fluid Movement: Secretomotor and Vasomotor Reflexes It is essential that the movement of fluid between the lumen of the intestine and the body fluid compartments is regulated. More than two blood volumes cross the mucosal epithelial surface each day, and disruption of fluid transport regulation, such as occurs in cholera intoxication, is life-threatening. One reason for the large flux is that the absorption of sugars (monosaccharides) and amino acids is through cation-coupled transporters. Enteric reflexes, through activation of secretomotor neurons, return water and electrolyte to the lumen (Fig. Enteric secretomotor reflexes cannot act in isolation, they must be modulated to take into account whole body fluid balance.

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Comprehensive knowledge exists in the form of toolkits and guides to developing buy 100 mg female viagra visa menstrual zits, implementing and evaluating health communication activities [for example discount 100 mg female viagra with amex menopause numbers, 17-19] generic female viagra 50mg line menopause period changes. Resources such as these could usefully inform the development of a strategy for health communication activities for communicable diseases and provide a template for the development of initiatives order cheap female viagra online womens health fresno ca. Evaluation is particularly underdeveloped in the broader context of health communication and is scant in relation to health communication for the prevention and control of communicable diseases. Integral to the development of more formal evaluation is progress in identifying the indicators of success for health communication activities. Workforce Health communication competencies may be defined as the combination of the essential knowledge, abilities, skills and values necessary for the practice of health communication (adapted from [20]). It is clear that the complexities and the multidisciplinary nature of health communication involve a vast range of skills drawing from a number of disciplines including health, education, public health, health promotion, social marketing and information technology. Overall, stakeholders considered that education and training focused on health communication in the prevention and control of communicable diseases is currently underdeveloped across Member States [3]. Stakeholders identified that structured health communication training was required and suggested that European-level organisations should coordinate and facilitate such training. The research activity for health communication in communicable diseases in the European context is in a nascent stage of development. The lack of systematic evaluation of health communication for communicable diseases has resulted in a limited evidence base which could give rise to inefficient use of resources. Nevertheless, a body of evidence is emerging in relation to health communication, and some of it pertains to health communication for communicable diseases but much relates to non-communicable diseases. This evidence represents a resource that can be mined to establish its relevance and transferability to health communication for communicable diseases in the European context. The potential for capacity development for health communication in communicable diseases in Europe is manifest. Such organisations could provide the leadership and coordination required to advance the field of health communication for communicable diseases in a coordinated and strategic way. Paper presented at meeting organised by the Directorate General for Health & Consumers; 2011. Perceived priorities of key public health stakeholders in Europe on the use of health communication for the prevention and control of communicable diseases. Evidence review: social marketing for the prevention and control of communicable disease. A literature review on health information-seeking behaviour on the web: a health consumer and health professional perspective. A literature review of trust and reputation management in communicable disease public health. Health communication campaign evaluation with regard to the prevention and control of communicable diseases in Europe. A literature review on effective risk communication for the prevention and control of communicable diseases in Europe. Systematic literature review of the evidence for effective national immunisation schedule promotional communications. Systematic literature review to examine the evidence for the effectiveness of interventions that use theories and models of behaviour change: towards the prevention and control of communicable diseases. Health communication can take many forms, both written and verbal, and can be directed toward individuals, communities or entire nations. In addition, health communication is an integral component of health promotion, health protection, disease prevention and treatment and is recognised as a core competency in public health and health promotion practice, playing a pivotal role in achieving public health objectives. Health communication initiatives must use the most effective and efficient strategies for the promotion, protection and maintenance of health through the use of the best available evidence at practice and policy level. Public health practitioners, programme managers and policymakers need to be aware of what is known about the strengths, weaknesses and costs of health communication interventions aimed at the prevention and control of communicable diseases so that impacts can be enhanced and opportunities maximised for strengthening evidence-informed action. Without such knowledge and without clarity as to the strengths and weaknesses inherent in current practice, health communication’s contribution to the promotion of the public’s health is restricted. An examination of the strengths and weaknesses of health communication activities in the context of national, European and international evidence provides a useful basis from which to generate knowledge to inform capacity development in this key area of public health. To bring together stakeholders interested in health communication research focusing on communicable diseases via expert meetings, seminars and online forums. To facilitate the dissemination of the Translating Health Communication Project’s activities and evidence to promote good practices and innovations focusing on communicable diseases (adapted from [2]). A range of research activities were undertaken and completed during this three-year project, comprising both a synthesis of evidence [3-11] and primary information gathering [12]. The multiple research activities were designed to develop successively, with earlier research activities informing and supporting subsequent activities. This resulted in an explication of the state of current practice, consolidation of existing evidence, and an identification of future directions for the development of health communication for the prevention and control of communicable diseases. The aim of knowledge translation processes, frameworks and models is to maximise the benefits of research for health improvement by reducing the ‘know–do’ gap between knowledge creation and its application to policy and practice [13, 14]. These two components – knowledge creation and subsequent action – form the basis of the Knowledge-to-Action Framework [14]. The knowledge creation component consists of three phases: knowledge inquiry, knowledge synthesis, and knowledge tools/products. The action component comprises: problem identification; identifying appropriate knowledge; applying knowledge to the local context; assessing barriers to knowledge use; developing, tailoring and implementing interventions; monitoring the knowledge; evaluating outcomes; and sustaining the knowledge use. These two components and the phases within them interact dynamically throughout the knowledge translation process. Research activities in this project equate to phases in this Knowledge-to-Action process. Initial knowledge inquiry through primary information gathering activities was carried out to address Objective 1 of the project. Simultaneously a series of evidence reviews were undertaken synthesising current knowledge, addressing Objectives 2 and 3. In this introduction, information gathering and the synthesis of evidence are described in more detail. This research is intended to inform and support policymakers, practitioners and organisations involved in practice and the future development of this area for the European public health agenda. Primary information gathering Primary information gathering took place throughout the three years of the research project and was designed as an iterative, multi-method research process. A total of 65 participants completed the e-survey and 44 completed the telephone interviews. The data from these consultations informed a subsequent expert consultation which was undertaken to identify the perceived priorities for the efficacious use of health communication by public health bodies for communicable diseases [16]. The results of these research activities are reported in an aggregated report [12]. In addition, examples of health communication activities identified by key stakeholders during this phase were compiled, researched and distilled electronically to form a database for health professionals, researchers and academics working in the area [17]. Synthesis of evidence This component of the research project comprised of a series of evidence reviews: three rapid reviews of reviews of evidence, four literature reviews, and two systematic literature reviews. The topic areas of these reviews were: A rapid evidence review of interventions for improving health literacy [3]. Evidence review: social marketing for the prevention and control of communicable disease [5]. A literature review on health information-seeking behaviour on the web: a health consumer and health professional perspective [6]. A literature review of trust and reputation management in communicable disease public health [7]. Health communication campaign evaluation with regard to the prevention and control of communicable diseases in Europe [8]. A literature review on effective risk communication for the prevention and control of communicable diseases in Europe [9]. Systematic literature review of the evidence for effective national immunisation schedule promotional communications [10]. Systematic literature review to examine the evidence for the effectiveness of interventions that use theories and models of behaviour change: towards the prevention and control of communicable diseases [11]. The results of this analysis also formed the basis of a further level of stakeholder consultation. This general approach is more usually used in strategic planning at organisational level. Opportunities and challenges were identified in relation to the European practice context, as captured in the information gathering, including the expert consultations [12, 6, 18]. An organising framework was constructed through an iterative process resulting in the development of matrix templates2 against which project outputs were assessed. Initially it was envisaged that one matrix would capture all key issues across all project outputs but through undertaking the process it became apparent that, due to the wide range of outputs, this approach was not possible. The strengths and weaknesses matrix was developed in order to assess the strengths and weaknesses for each of the nine evidence reviews [3-11]. The main headings used in this matrix are clearly defined (see Appendix 2) and reflect the relevant key areas focused on across all of the reviews. Each of the reviews was assessed individually against this developed matrix template and are presented in separate tables in Chapter 1. The challenges and opportunities matrix was developed in order to assess the opportunities and challenges identified from the review of the primary information gathering phase of the project [12, 16] and aims to reflect what is currently happening in practice. The development of this matrix template was informed by some of the headings used in the e-survey questionnaire and telephone interview protocols.