Blood fluke and snail relationship quizzes

Schistosomes and Other Trematodes - Medical Microbiology - NCBI Bookshelf

blood fluke and snail relationship quizzes

Left: Distribution of the blood fluke Schistosoma haematobium (sub-Saharan Africa, Nile valley in Egypt and Freshwater snails ingest the eggs; the parasite ( and related flukes, above) undergoes .. Relationship between schistosomiasis and bladder cancer. Clin. 11, e1; quiz e doi: /kinenbicounter.info Biomphalaria snail shedding schistosome cercariae into the water. at risk of infection with urogenital and intestinal species of schistosomes. Fluke, also called blood fluke or trematode, any member of the invertebrate class The larval fluke develops in the body of a snail (chiefly of the genera Bulinus.

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.

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.

Flukes and snails.

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.

blood fluke and snail relationship quizzes

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. 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. Protective immunity in experimental models of resistance or vaccine models is not complete, as some challenge parasites always survive. Vaccine models of schistosomiasis have evolved from crude antigen-adjuvant mixtures or radiation-attenuated inocula to recombinant vaccines.

Advances in gene cloning and recombinant DNA technology have produced many defined antigen vaccines. All vaccine-candidate antigens induce protective immunity that is incomplete, i.

Partial protection, however, does reduce the number of surviving worms, therefore reducing the risk of severe disease. Cross-sectional and longitudinal studies of the clinical, parasitologic, epidemiologic and immunologic aspects of human schistosomiasis, utilizing endemic and hospitalized-based patients, have shown that peak prevalence and intensity of infection occur between the ages of 10 and 30 years. The chronic responses are in chronic schistosomiasis patients that are clinically classified as asymptomatic or symptomatic exhibiting hepatosplenic disease.

Immunologic differences have been documented in egg-specific cellular responses, granulomatous hypersensitivity, cytokine profiles and presence or absence of regulatory receptors or idiotypes on immune T and B cell receptors. Other longitudinal studies of endemic populations have analyzed the distribution of infection intensity before and after drug treatment and natural re-exposure to infective cercariae.

These studies have documented that younger people excrete more eggs than older individuals. Additionally, younger people regain heavy infections after treatment and re-exposure while older people do not become reinfected or are reinfected at low levels. The subset of individuals living in endemic areas with documented re-exposure with no evidence of reinfection, or low levels of infection, have been studied for evidence of protective immunity.

These studies have shown that anti-parasite IgE levels correlate with low egg output. The importance of the longitudinal endemic population studies cannot be overstated as these data will be used in the design and selection of endemic populations for future vaccine trials.

Hermaphroditic Flukes With respect to the hermaphroditic flukes, studies of Fasciola hepatica in experimental animals have revealed resistance to reinfection. Adoptive and passive transfer of resistance has been achieved with cells and serum.

blood fluke and snail relationship quizzes

Immunity has also been induced by nonliving vaccines. It is of interest that immunization with Fasciola antigens will induce resistance to Schistosoma infection and vice versa.

The defined antigen responsible for protective immunity in this model is a F hepatica12 kDa fatty acid binding protein and S mansoni 14 kDa fatty acid binding protein. Relatively little work in this area has been performed with the other trematodes.

Epidemiology Trematodes do not multiply directly in humans, but instead mate and produce large numbers of eggs that pass out of the body in the feces, urine, or sputum. Thus, the intensity of human infection is related largely to the rate of exposure to infective larvae—i. Mathematical models suggest that the intensity of infections in mammalian populations follows a negative binomial distribution, with most individuals having light to moderate infections.

In recent years, controlled studies have revealed that most infected individuals show no overt signs or symptoms of disease. Significant disease occurs mainly in the few individuals with a heavy burden of flukes. Three different species of human schistosome parasites are responsible for two hundred million infections. S japonicum is the only species that has significant animal reservoirs.

The distribution of all the flukes is limited by the distribution of their snail intermediate host. Fasciola hepatica occurs worldwide in ruminants and causes significant morbidity and mortality in sheep and cattle.

blood fluke and snail relationship quizzes

For the most part, human infection is sporadic; only a few hundred cases have been reported in the world literature, usually associated with ingestion of wild watercress. Fascioliasis in humans has almost always been identified during the acute migratory stage of infection; occasionally, worms are found in the bile ducts at surgery or autopsy.

Foci of chronic human fascioliasis have been found in rural areas of Peru. Clonorchis sinensis and O viverrini are common liver flukes of cats and dogs; they also infect many other mammalian hosts. Although humans are incidental hosts, millions of individuals are infected with these organisms.

blood fluke and snail relationship quizzes

Opisthorchis viverrini infection is widespread in Thailand. Infection with another species, O fe lineus, has been reported in many parts of Southeast Asia and Asia as well as Eastern Europe and the Soviet Union. Infection occurs after ingestion of raw or inadequately cooked freshwater fish saltwater fish do not carry these parasites. Fasciolopsis buski is a common parasite of humans and pigs in the Far East and Southeast Asia.

Infection results from consumption of the raw pods, roots, stems, or bulbs of certain water plants, often water chestnuts, and is related to the habit of peeling the metacercaria-infested hull of these vegetables with the teeth before consumption.

Paragonimus westermani has a cosmopolitan distribution among mammals; human infection is found largely in the Far East. Closely related species have been reported in Africa and in South and Central America. Paragonimiasis is transmitted by eating uncooked freshwater crayfish or crabs.

Diagnosis The anatomic locations of the symptoms and signs suggest a diagnosis of schistosomiasis or of disease caused by the liver, intestinal, urinary tract, or lung flukes. Except in the case of fascioliasis, the geographic history should be of particular value, because all other fluke infections of humans have relatively specific distributions. A careful dietary history is important in the case of the hermaphroditic flukes and provides relatively clear-cut evidence.

In diagnosing schistosomiasis, a history of significant contact with fresh water is of diagnostic value. Demonstrating the eggs of the parasite in the excreta provides the definitive diagnosis in all cases of fluke infection. A quantitative method is of great importance because of the relationship between the intensity of infection and the development of disease. The best method for doing this, which is equivalent in many ways to a concentration technique, is the Kato thick smear method, in which a 50 mg feces sample is placed on a slide covered with a plastic coverslip soaked in glycerol and is allowed to clear for 24 hr.

For S haematobium infections, Nucleopore filtration of 10 ml of urine is the simplest and most rapid method. Most immunodiagnostic methods are not specific or sensitive enough to assess these infections. Control A key control measure for all fluke infections is preventing egg-containing excreta from contaminating water sources. Another approach is to control snail populations, largely by the use of molluscicides. So we have the delightful job of collecting the larval stage, called miracidia, that hatch out from eggs.

How do we do this? We go into a school, collect stool samples from infected children and filter out the eggs.

blood fluke and snail relationship quizzes

We then put them in some water in sunlight and wait for them to hatch. I will explain this in more detail in a subsequent post on lab work. For now let's stick to the first stage: We visit state primary schools in the Mwanza region of Lake Victoria. To get to these schools we sometimes have to drive for hours through dirt tracks.

All sorts of obstacles occur but the most common one is this: On our way to a school, a herd of cattle, goats and sheep block our path. When we arrive we visit the head teacher and get a proper greeting from the school. The teacher then calls out our selected students - the ones we know are infected from a previous survey, more on this later.

Children were practicing singing, dancing and music on the day we arrived.

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Up close and personal, the kids stare at us. Eventually we do get them to smile. As well as our trusted driver — Mr Lenard. The team, Mr John, Mr Nagai and me. Getting our gloves on and our kit ready.

Me holding a football I am about to present to the headteacher as a present.

NaturePlus: Super-flies and parasites: The blood fluke story - visiting schools in Tanzania

Mr James is teaching the children how to give us a stool samples and most importantly to wash their hands afterwards!

We give the kids a container to put a stool sample, and some toilet paper. They run off to the latrines and come back with a full container. How they are able to poop on demand always amazes me. We label the containers with unique identification numbers for each child. And then go back in the lab to process the samples.

All the children in the school receive treatment a couple of weeks later. We always treat any infected child! Mr Nagai and Mr John handing out toilet paper to the kids.