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Pepsinogens of quail and chick, specific to adult proventriculus, were purified and their properties were compared. These two pepsinogens are similar in regard to enzymological characters, amino acid compositions, and immunological characters.
The present study is undertaken to describe the ultrastructure of Desportesius invaginatus (Nematoda, Acuariidae) for the first time in Egypt showing details that were not clearly defined before. This nematode is found in the proventriculus of Ardeola ibis ibis. The latter is known in Egypt as "Abu Erdan" and it is a very common and useful bird to Egyptian farmers. The pathogenecity of this nematode within their host was observed. The presence of such high number of worms raised the curiosity of the present author to see if they had the potential to cause any harm to such economically important birds to Egyptian farmers.
Cases of Libyostrongylus douglassii-associated proventriculitis in an adult female ostrich and two ostrich chicks occurring on two farms in different federal states of Germany are described. The adult bird was recently bought and kept under quarantaine conditions without contact to other animals of the herd. Without developing clinical signs of illness, the animal died. At necropsy, typical lesions of wireworm infection were found. The lining of the stomach had a moth-eaten appearance. Massive amounts of adult stages of trichostrongyloid nematodes were diagnosed in histological specimens of the proventricular mucosa and under the koilin layer of the ventriculus. The worms were isolated from the proventriculus and identified as L. douglassii. The feces of the bird contained high amounts of typical eggs of the worms with a medium size of approximately 70 x 40 microm. A polyphasic degeneration of heart and skeletal muscle was diagnosed in addition to the wireworm infection and interpreted to be a result of a malnutrition (Vit. E-/selenium deficiency). The ostrich chicks were reared on another farm and submitted for necropsy because of high mortality (8 out of 12 chicks died). A massive invasion of the proventricular mucosa with L. douglassi was macroscopically and histologically detected at necropsy of the anemic birds.
Mast cells in the digestive tract of the developing chick embryo were studied with histochemistry and electron microscopy (EM). The cells appeared in the esophagus, proventriculus and small intestine on about the 13th day of incubation, whereas mast cells in the tongue appeared earlier. The staining properties and ultrastructure of the mast cells varied with development. In 13- and 15-day embryos, mast cells showed a pale metachromasia with toluidine blue, and stained blue with Alcian Blue-Safranin O (AB-S). In the 18-day embryo, mast cells stained a deep purple with toluidine blue. Stained with AB-S, most of the mast cell granules stained blue, but some red granules were also seen in a few cells. In the newly hatched chick, the cells stained a strong reddish purple with toluidine blue. Stained with AB-S, a few cells contained only blue or red granules, but most contained both. Observations with the EM revealed that the internal structure of the granules varied with the stage of embryonic development. The basis for the changes in staining properties and ultrastructure of the mast cell in the developing chick embryo were discussed.
Chickens of 7 weeks or 20 weeks of age were divided into three groups according to their antibody status (high, low, absent) and were infected with a velogenic viscerotropic Newcastle disease virus. To follow patterns of viral replication, birds were necropsied at regular intervals up to 22 days and organs were sampled from each bird. In non-immune birds, virus could be isolated from all organs examined. In birds with antibody, virus was most frequently isolated from the proventriculus, cecal tonsil, bursa, and brain. However, because no one organ could be recommended for all situations, all four should be sampled for field diagnosis. In immune birds, although clinical signs were either mild or absent, widespread virus replication occurred up to 19 days post-challenge.
Two adenocarcinomas of the proventriculus and an adenocarcinoma of the ventriculus are described in psittacines. All birds had evidence of digestive tract dysfunction. Hemorrhage into the lumen of the digestive tract from the ulcerated surfaces of the tumors was evident in all birds, either clinically or at necropsy. Radiographic studies, including contrast films, were useful in two cases. Alcian blue and periodic acid-Schiff stains were helpful in determining the origin of the tumor in one case.
Studies of epithelio-mesenchymal recombination between the proventriculus and gizzard of 6-day chick embryos revealed that the proventricular mesenchyme can induce the morphogenesis of complex glands and cause the expression of embryonic pepsinogen in the gizzard endoderm, while the gizzard mesenchyme inhibits both of them.
Cyclopiazonic acid dissolved in corn oil was administered by gavage to broiler chicks (n = 80) daily, from the day of hatching for 23 days. Chicks were assigned to 3 groups (1, 2, or 4 mg of cyclopiazonic acid/kg of body weight); a control group was given corn oil. Each group was composed of 10 male and 10 female chicks. Surviving chicks were euthanatized and necropsied on day 24. Histologic examination revealed that the most common lesions consisted of necrosis and hemorrhage or hyperplasia of the mucosa of the proventriculus and hepatocellular vacuolation. Skeletal muscle degeneration, characterized by myofiber swelling or fragmentation accompanied by an infiltrate of macrophages and heterophils, was detected in the group given 4 mg/kg. This degeneration was associated with an increase of plasma creatine kinase activity. Focal hepatocellular and splenic necrosis also developed in the groups given 4 mg/kg.
A syndrome has occurred in broilers over the past several years in widespread localities, including Georgia, Arkansas, and Texas. Poor feed conversion and delayed marketing are the principle clinical features. Lesions consist of enlargement of the proventriculus, gizzard erosion and dilatation, and decreased spleen and bursa size. Trichothecenes were demonstrated in the rations sampled at several broiler facilities. The clinical features and gross and microscopic changes observed in the field syndrome were duplicated by feeding chicks multiple combinations of a trichothecene mycotoxin (T-2 toxin) with histamines and diamines for 6 to 8 weeks.
Examination of hematoxylin-and-eosin-stained sections of chicken esophagus and proventriculus revealed Cryptosporidium-colonized surface squamous and mucous gland columnar epithelial cells. This chicken also had malignant lymphoma (lymphosarcoma). The hypothesis that infection by Cryptosporidium sp. was either preceded by or followed by herpesvirus infection, immunosuppression, and neoplasia cannot be refuted. Clinicians and pathologists should be aware that esophageal and proventricular cryptosporidiosis can occur in chickens; they should also be aware that mild inflammation and necrosis can accompany parasitism.
Fusarium moniliforme culture material containing fumonisin B1 (FB1) was fed to white Pekin ducklings from 1 to 21 days of age. Four dietary treatments were prepared with 0, 100, 200, and 400 mg FB1/kg ration. Ducklings fed rations containing FB1 had a dose-dependent decrease in feed intake and weight gain. Increasing levels of FB1 in the ration were associated with increasing absolute organ weights of liver, heart, kidney, pancreas, and proventriculus. Liver sphinganine to sphingosine ratios increased significantly in ducklings fed FB1. Two of eight ducklings fed a ration containing 400 mg FB1/kg died prior to the termination of the experiment. Mild to moderate hepatocellular hyperplasia was evident in all ducklings fed FB1. Mild to moderate biliary hyperplasia was also noted in the liver sections of ducklings fed 400 mg FB1/kg in the ration. Ducklings, like other poultry, are relatively resistant to the toxic effects of FB1.
In situ analysis of the chicken cSox2 gene, a member of the transcription factor family containing an Sry-like high-mobility group (HMG) box, demonstrated localized expression in the embryonic endoderm. Transcripts of cSox2 appeared before commencement of morphogenesis and cytodifferentiation in the rostral gut epithelium from the pharynx to the stomach. The caudal limit of cSox2 expression coincided with that of the region competent for proventricular differentiation and to the rostral limit of the domain of CdxA, a homologue of Drosophila caudal. During morphogenesis, the level of transcripts of cSox2 decreased in epithelia invaginating into surrounding mesenchyme to form glandular or tubular structures, such as the primordia of the thyroid and lung, glandular epithelium of the proventriculus, and secondary bronchus of the lung. Tissue recombination experiments demonstrated that cSox2 expression is regulated by the underlying mesenchyme as well as morphogenesis and cytodifferentiation. The results suggest that cSox2 plays pivotal roles in generating morphologically and physiologically distinct types of epithelial cells in the gut.
This study was designed to establish the source of gut mesoderm's ability to induce regional pattern in the endoderm. The most obvious possibility is induction by the endoderm through epithelial-mesenchymal interaction. To test this experimentally, reciprocal quail/chick combinations were prepared of early proventricular endoderm (that is already known to be regionally determined) and presumptive small intestinal mesoderm. The combinations were cultured for 7 days to allow for 'programming' of the mesoderm by the endoderm. After removal of the proventricular endoderm the mesoderm was combined with young gizzard endoderm. It is known that gizzard endoderm can be provoked to develop in either a proventricular or a small intestinal direction by association with the appropriate mesoderm. Thus, by combining intestinal mesoderm 'programmed' by association with proventricular endoderm with gizzard endoderm, the subsequent differentiation of the gizzard endoderm would indicate whether or not the inducing ability of the intestinal mesenchyme had been altered. In addition to such experimental grafts, three types of control graft were prepared. The results of the experiment, based on the morphology of the grafts and the immunocytochemical analysis of selected endocrine cell types, showed that in the majority of cases the gizzard endoderm developed the features of small intestine, not those of proventriculus. This indicates that at the stages studied, endoderm does not act to program mesoderm with which it is associated. If this does occur, it must take place at an earlier stage, i.e., before the time of explantation of the presumptive small intestinal mesoderm (1.25 days of incubation).
The vagal neural crest adjacent to the first seven somites gives rise to both ganglionic and ectomesenchymal derivatives. Ganglionic derivatives are the neurons and supportive cells of the enteric nervous system (ENS), cardiac, and dorsal root ganglia. Ectomesenchymal derivatives are cells in the cardiac outflow tract and the mesenchymal components of thymus and parathyroids. Ectomesenchymal derivatives are formed by a segment of the vagal neural crest, from the level of the otic vesicle down to the caudal boundary of the third somite, called the cardiac neural crest. We performed neural crest ablations to study regional differences within the avian vagal neural crest with regard to the formation of the ENS. Ablation of the entire vagal neural crest from the mid-otic vesicle down to the seventh somite plus the nodose placode resulted in the absence of ganglia in the midgut (jejunum and ileum) and hindgut (colon). The foregut (esophagus, proventriculus, gizzard, and duodenum) was normally innervated. After ablation of the vagal neural crest adjacent to somites 3-5, ganglia were absent in the hindgut. Ablations of vagal neural crest not including this segment had no effect on the formation of the ENS. We surmise that the innervation of the hindgut in vivo depends specifically on the neural crest adjacent to somites 3-5, whereas innervation of the midgut can be accomplished by all segments within the vagal neural crest. The foregut can also be innervated by a source outside the vagal neural crest. To study intrinsic differences between various vagal neural crest segments regarding ENS formation, we performed chorioallantoic membrane cocultures of segments of quail vagal neural anlage and E4 chicken hindgut. We found that all vagal neural crest segments were able to give rise to enteric ganglia in the hindgut. When the neural crest of somites 6 and 7 was included in the segment, we also found melanocytes in the hindgut, suggesting that this segment is more related to trunk neural crest. Furthermore, we found that the vagal neural anlage from older embryos (> 18 somites) showed an increased potential to form enteric ganglia. This suggests that vagal neural crest cells that have been in prolonged contact with the neural tube in vivo, because of either late emigration or delayed migration, have an increased probability to form enteric ganglia.
The enteric nervous system is largely formed from the vagal neural crest which arises from the neuroaxis between somites 1-7. In order to evaluate the contribution of different regions of the vagal crest to the enteric nervous system, we marked crest cells by injecting somites 1-10 with a replication-defective spleen necrosis virus vector which contains the marker gene lacZ. After incubation in X-gal, lacZ-positive blue cells were found in the wall of the gut in three locations. Most were found at the peripheral edge of the developing circular muscle and within the developing submucosa, sites characteristic of developing ganglia. LacZ-positive cells in these ganglionic sites were always surrounded by HNK-1 immunostained cells, confirming their neural crest origin. LacZ-positive cells were also seen in a third location, the circular muscle layer of the esophagus and crop, and were separated from the HNK-1 positive ganglionic elements. These cells in the circular muscle are probably muscle cells derived from labeled mesodermal cells of the somite. Injection of somites 3, 4, 5, and 6 resulted in the largest percentage of preparations with lacZ-positive crest-derived cells and in the largest number of positive cells in the gut. After injection of these somites, lacZ-positive crest-derived cells were found in all regions of the gut from the proventriculus to the rectum. Very few positive crest-derived cells were found in the esophagus.(ABSTRACT TRUNCATED AT 250 WORDS)
The primary objective of this study was to establish the distribution of the progenitors of selected gut endocrine cell types at cranial somite levels. In addition, analysis of the material has provided new information about the location of the presumptive territories of certain gut regions and of the pancreas. Narrow transverse strips of full-thickness blastoderm two or three somites in length were excised at the levels of somites 1 to 5 of 8.5- to 18-somite chick embryos and cultured as chorioallantoic grafts to an age equivalent to 20 days of incubation. The grafts were analysed by immunocytochemistry, and their morphology was evaluated. Individual grafts exhibited up to five different types of gut morphology, including those of oesophagus, proventriculus, gizzard, pyloric region, small intestine, and pancreas. The morphologic survey yielded new information about the location, extent, or both, of the territories of the pyloric region, the small intestine, and the pancreas. In general, the progenitors of gut endocrine cell types identified were those expected for the different morphologic regions: in only a few instances were ectopic endocrine cell types detected. The available evidence points to the progenitors of bombesin/gastrin-releasing peptide cells being located cranial to somite 5 at the stages studied. Based on the morphology and the proportion of insulin cells, the development of pancreas in grafts appeared compromised compared with grafts of the intact dorsal pancreatic bud: this may relate to the likely exclusion of dorsal pancreatic bud mesoderm from the graft area. The results show that presumptive small intestinal endoderm in grafts can differentiate in the absence of homologous (i.e., small intestinal) mesoderm: this accords with the view that the primary source of positional information in the gut is in the endoderm.
Epithelial and endothelial tubes come in various shapes and sizes and form the basic units of many tubular organs. During embryonic development, single unbranched tubes as well as highly branched networks of tubes form from simple sheets of cells by several morphogenic movements. Studies of tube formation in the Drosophila embryo have greatly advanced our understanding of the cellular and molecular mechanisms by which tubes are formed. This review highlights recent progress on formation of the hindgut, Malpighian tubules, proventriculus, salivary gland, and trachea of the Drosophila embryo, focusing on the cellular events that form each tube and their genetic requirements.
The Eip28/29 gene of Drosophila is an example of a tissue- and stage-specific ecdysone-responsive gene. Its diverse patterns of expression during the third larval instar and a synopsis of those patterns in terms of expression groups have been reported previously. Here we have studied the expression (in transgenic flies) of reporter genes controlled by Eip28/29-derived flanking DNA. During the middle and late third instar, most tissues exhibit normal expression patterns when controlled by one of two classes of regulatory sequences. Class A sequences include only 657 Np of 5' flanking DNA from Eip28/29. Class B sequences include an extended 3' flanking region and a minimal (< or = 93 Np) 5' flanking region. The class B sequences include all those elements known to be important for ecdysone induction in cultured cells. They are sufficient to direct the normal premetamorphic induction of Eip28/29 in the lymph glands, hemocytes, proventriculus, and Malpighian tubules. This is consistent with our suggestion that Kc cells are derived from embryonic hematopoietic cells. It is remarkable that the epidermis requires only class A sequences. These are sufficient to up-regulate expression at mid-instar and to down-regulate expression at metamorphosis. It follows that the epidermis uses EcREs distinct from those that function in Kc cells. It is possible that the Upstream EcRE, which is nearly silent in Kc cells, is active in the epidermis.