Schistosoma - Wikipedia
THE BLOOD FLUKE AND THE SNAIL. They have a parasitic relationship, which is when one benifits and the other gets harmed. They live in Asia and africa. They get their start living in snails, which shed the parasites into the Getting blood flukes (the disease is known as schistosomiasis or .. 'There is hope on the border': In Tijuana, resilience endures among migrants. Schistosomiasis, also known as snail fever and bilharzia, is a disease caused by parasitic In tropical countries, schistosomiasis is second only to malaria among . The long-term manifestations are dependent on the species of schistosome, as the . They are considered equivalent in relation to efficacy against S. mansoni.
The mature larva makes its way into the body of the final host, man, through the skin or the mouth. The intestinal blood fluke S.
The eggs pass from the host with the feces. The larva enters the body of a snail any of several generathe intermediate host, and returns to a human host through the skin. Snails of the genus Oncomelania are the intermediate host. The adult occurs in the veins of the small intestine. Some eggs are carried in the bloodstream to various organs and may cause a variety of symptoms, including enlargement of the liver. Human hosts may die from severe infestations.
Flukes of detrimental economic significance to man include the widely occurring giant liver fluke of cattle Fasciola hepatica and the Chinese, or Oriental, liver fluke Opisthorchis sinensisor Clonorchis sinensis.
Man may become infested with this fluke by eating uncooked vegetables. The Chinese liver fluke infests a variety of mammals, including man. These mollusks also harbor blood flukes Schistosoma that develop into highly mobile cercaria that find human hosts and penetrate into their skin causing human schistosomaiasis.
The linkage of marsh fly larvae to snails was first reported by the French scientist E. Perris in and was proven a century later by Clifford O. Berga dedicated young scientist at Cornell University, who years later became a major professor for the graduate degree program of Lloyd Knutson, the senior author of this volume. Blood fluke eggs were found in Egyptian mummies from BC, and hematria was commonly found among soldiers reported by surgeons in Napoleon's army in Egypt — Schistosomes do not require a second intermediate host in their life cycles but mature in the blood vascular system of subject hosts, namely fishes, turtles, birds, and mammals, including humans.
Here, the life of sciomyzid flies is linked to snails, as these fly larvae must feed on snail tissue Roberts and Janovy, The chapters are organized by important subject areas of biological and ecological factors related to the linkage between sciomyzid flies and mollusks, focused on all aspects of morphological, ecological, and behavioral characteristics of larval development in their hosts.
This chapter is followed by a section describing the unique panorama of the marsh flies-schistosomes-human ecosystem that includes the natural enemies of snails and slugs, the malacophagy of Diptera, and their life cycle. In Chapters 5 through 8, the subject on the feeding behavior and competition of sciomyzid flies are presented in detail followed by Chapter 9 that is concerned with phenology, reproduction, and development of marsh flies.
Chapters 10 through 13 then present the core ecological resources related to population dynamics pp. A large portion of the book Chapters 14—17, pp.
Beginning with a comprehensive character analysis pertaining to morphology, physiology, and behavior related to adults, larvae, and eggs, the useful taxonomic keys adults and puparia are presented for the genera of different geographic regions, followed by a comprehensive treatment of the higher classification of marsh flies pp.
In the concluding remarks, the authors discuss the issues of character selection Section It may be important to visit the statement pertaining to taxonomic characters that states: The value of such non-adaptive characters in determining relationships of species and genera of Sciomyzidae might be questionable. That is later balanced by collagen degradation, fibrosis being the net result of both the intensity of infection and an imbalance toward collagen synthesis see Fig.
After treatment with drugs that kill the flukes, collagen tends to be resorbed; that occurs at a higher rate in early than in late infections. Studies of the hepatic microcirculation in experimentally infected animals have revealed that portal venous obstruction is caused not by the eggs alone but by the granulomas around them. Portal vein obstruction leads to portal hypertension, splenomegaly, and the development of esophageal varices. In spite of severe portal venous obstruction, the total liver blood flow remains within normal limits, as there is marked neovascular formation of arterial vessels in the areas of inflammation and fibrosis.
The liver parenchymal cells appear normal.
The spleen may become markedly enlarged and is firm in consistency, fibrotic, and congested. Hypersplenism may occur, with attendant anemia and pancytopenia. The acute clinical syndrome of Fasciola hepatica infection occurs during migration of the fluke lar vae in the liver parenchyma, with resultant inflammation and localized destruction of liver cells.
Once in the bile ducts, liver flukes of all species produce inflammation due to mechanical irritation and toxic secretions. Highly immunogenic predominant antigens have been found in the eggs of Opisthorchis. Studies in humans have revealed hyperplasia of the epithelial cells lining the biliary tract, periductal fibrosis, thickening of the duct wall, and dilation and obstruction of the duct lumen.
Secondary infection occurs due to biliary stasis, resulting in chronic recurrent, suppurative infections; cholangiocarcinoma also may occur. The intestinal fluke Fasciolopsis buski attaches to the duodenal and jejunal mucosa. Inflammation at the site of attachment may be followed by ulceration and even bleeding.
The flukes affect the secretion of intestinal fluids and mucus. The adults of the lung fluke Paragonimus are usually found just beneath the pleural surface, where they induce local necrosis, hemorrhage, inflammation and fibrous encapsulation. These flukes may also be found in other tissues including the brain.Schistomiasis or Bilharzia ( Schistosoma Habitat, Life cycle or disease)
In heavy infections a syndrome similar to that of chronic bronchitis occurs, with cough and sputum production, sometimes accompanied by intermittent hemoptysis. Cerebral lesions are characterized by necrosis and an eosinophilic granulomatous reaction. Host Defenses Schistosomes Host immune responses to infection with schistosomes are complex due to the developmental nature of multicellular-life cycle stages within the definitive host. The antigenic mosaic, presented to the host immune system by the infective cercariae, migrating schistosomula, adult worms and eggs, provides the basis for understanding the complexity of the host immune response as well as a paradigm for generating protective immunity through non-living vaccines.
Our understanding of host immunity to schistosomiasis has been generated from data collected from experimental models of infection and vaccination. Based on these data, immune responses to schistosomiasis can be summarized as either anti-egg or anti-worm.
Immune responses against antigens that are secreted by the egg stage include granulomatous hypersensitivity, antibody production, anti-fecundity, and transmission blocking immunity. Anti-worm immunity involves both cellular and humoral responses against adult worms and migrating larvae.
Some of these responses are characterized as protective and mediate resistance to reinfection. Granuloma formation around the parasite egg has been intensely studied by numerous investigators, because it plays a central role in the pathology of schistosomiasis.
Experimental models of granuloma formation involve parasite egg embolization into the lungs of rodents, followed by sequential analysis of granuloma size, and immune components. Natural infections of mice with experimentally-induced or genetic immune deficiencies, have been used to delineate the role of certain immune components in granuloma formation.
Schistosomiasis - Wikipedia
Finally, cytokine responses of egg-specific T cell clones, isolated and characterized from mice and humans, have provided additional information on the role of T helper subset responses to egg antigens. Recently, the cell mediated components of granuloma formation have been redefined based on cytokine profiles of CD4 helper T cell subsets.
Three major T helper subsets have been defined as Th0, Th1, and Th2 cells. Th0 subset secretes both sets of cytokines and appears as an intermediate undifferentiated subset.
The T helper subsets defined by these cytokines are Th0 and Th2. These data do not abrogate a role for Th1 helper cells in immunity to schistosome eggs, since adoptive transfer of murine Th1 T cell clones into naive recipient mice has demonstrated transfer of granulomatous hypersensitivity to eggs.
The cellular components in the Th1 T cell clone-induced granuloma were accompanied by Th2-like eosinophilia from probable Th2 subset recruitment into the granulomatous response by the egg-specific Th1 clone. These data illustrate the complexity of interacting cellular immune components in granuloma formation.
As a consequence of long term infection with schistosomiasis, granulomatous hypersensitivity, initiated by continual parasite egg deposition in tissues, undergoes immune modulation.
Several mechanisms appear to be responsible for granuloma modulation. The predominance of the Th2 helper subset and IL production renders Th1 helper subsets anergic or unresponsive to antigen. This unresponsiveness is due to IL downregulation of the expression of a macrophage costimulatory molecule, B7.
Absence of the B7 ligand prevents delivery of a costimulatory signal from the macrophage to the Th1 cell through the CD28 receptor which would normally activate Th1 cells. This evidence supports the premise that egg-specific undifferentiated Th cells become activated without essential costimulatory signals and therefore do not undergo clonal expansion and differentiation in models of chronic schistosomiasis.
Evidence for CD8 T cell involvement in granuloma modulation is based on adoptive cell transfer experiments in the mouse and characterization of some human soluble egg antigen-specific regulatory CD8 T cell lines and clones.
The exact mechanism for CD8 T cell involvement remains unclear.
Another manifestation of anti-egg immunity involves egg production, egg viability and egg excretion. Reduction in egg numbers, viability and egg excretion rates associated with specific anti-egg immune responses have been observed in both natural and vaccine models of schistosomiasis.
The immune etiology of these phenomena have been confirmed by several investigators, although the exact mechanisms require further elucidation. Experimental animals demonstrate some degree of resistance or susceptibility to a primary or single infection with schistosomes. The rat is an exceptionally resistant animal model demonstrating low numbers of developing worms even after a massive experimental exposure to thousands of cercariae.
Marsh Flies, Snails, and Blood Flukes: Biology of the Ecologically Connected
The mouse and hamster are at the other end of the spectrum, and develop a larger percentage of worms in response to smaller numbers of infective cercariae. Acquired resistance is the term used to describe protective immunity, which develops as a result of a primary immunizing infection against adult worms. Although the immune response against adult worms of a primary infection is only partially protective, when that immunity targets larval schistosomes of a secondary challenge infection for immune elimination, it is more evident.