New — Devil Worm — Is Deepest-Living Animal
New «Devil Worm» Is Deepest-Living Animal
- 1 New «Devil Worm» Is Deepest-Living Animal
- 2 Species evolved to withstand heat and crushing pressure.
- 3 Ivanov worm: photo and features of the life of a firefly
- 4 Animals That Can Be Found on the Shore of the Pacific Ocean
- 5 Video of the Day
- 6 Mammals
- 7 Shorebirds
- 8 Reptiles
- 9 Invertebrates
- 10 Invasive Species
- 11 Hookworm Disease
- 12 Background
- 13 Pathophysiology
Species evolved to withstand heat and crushing pressure.
PUBLISHED June 2, 2011
A «devil worm» has been discovered miles under the EarthвЂ”the deepest-living animal ever found, a new study says.
The new nematode speciesвЂ”called Halicephalobus mephisto partly for Mephistopheles, the demon of Faustian legendвЂ”suggests there’s a rich new biosphere beneath our feet.
Before the discovery of the signs of the newfound worm at depths of 2.2. miles (3.6 kilometers), nematodes were not known to live beyond dozens of feet (tens of meters) deep. Only microbes were known to occupy those depthsвЂ”organisms that, it turns out, are the food of the 0.5-millimeter-long worm.
«That sounds small, but to me itвЂ™s like finding a whale in Lake Ontario. These creatures are millions of times bigger than the bacteria they feed on,» said study co-author Tullis Onstott, a geomicrobiologist at Princeton University in New Jersey.
«Shocking» Worm Evolved For Harsh Depths
Onstott and nematologist Gaetan Borgonie of Belgium’s University of Ghent first discovered H. mephisto in the depths of a South African gold mine. But the team wasn’t sure if the worms had been tracked in by miners or had come out of the rock.
To find out, Borgonie spent a year boring deep into mines for veins of water, retrieving samples and filtering them for water-dwelling nematodes. He scoured a total of 8,343 gallons (31,582 liters) until he finally found the worm in several deep-rock samples.
What’s more, the team found evidence the worms have been there for thousands of years. Isotope dating of the water housing the worm placed it to between 3,000 and 12,000 years agoвЂ”indicating the animals had evolved to survive the crushing pressure and high heat of the depths.
«This discovery may not surprise passionate nematologists like Gaetan, but itвЂ™s certainly shocking to me,» Onstott said.
«The boundary of multicellular life has been extended significantly into our planet.»
Worm Inspires Search for Extreme Life
Onstott hopes the new devil worm will inspire others to search for complex life in the most extreme placesвЂ”both on Earth and elsewhere.
«People usually think only bacteria could exist below the surface of a planet like Mars. This discovery says, Hold up there!» Onstott said.
«We can’t negate the thought of looking for little green worms as opposed to little green microbes.»
Devil-worm study appears online June 1 in the journal Nature.
Ivanov worm: photo and features of the life of a firefly
Life of an Earthworm
What’s it like to be a worm? How would the world look, sound, and feel if you lived at ground level or below, if you couldn’t control your body temperature or even shiver when you were cold, and if you had no arms or legs and could only wiggle to move about?
Compare how your body does each of these things with how a worm does. Then do the journaling project at the end.
Seeing : Earthworms have no eyes, but they do have light receptors and can tell when they are in the dark, or in the light. Why is being able to detect light so important to a worm?
Hearing : Earthworms have no ears, but their bodies can sense the vibrations of animals moving nearby.
Thinking and feeling : Worms have a brain that connects with nerves from their skin and muscles. Their nerves can detect light, vibrations, and even some tastes, and the muscles of their bodies make movements in response.
Breathing : Worms breathe air in and carbon dioxide out, just like us, but they don’t have lungs. They can’t breathe through their mouth, and certainly can’t breathe through their nose because they don’t even have one! They breathe through their skin. Air dissolves on the mucus of their skin, so they MUST stay moist to breathe. If worms dry out, they suffocate. As fresh air is taken in through the skin, oxygen is drawn into the worm’s circulatory system, and the worm’s hearts pump the oxygenated blood to the head area. The movements of the worm’s body make the blood flow back to the back end of the body, and the hearts pump the blood forward again. Carbon dioxide dissolves out of the blood back to the skin.
Eating : Worms do not have teeth, but their mouths are muscular and strong. Nightcrawlers can even pull leaves into their burrows using their strong mouths. The front end of the worm, its prostomium , is pointed and firm, making it easy for worms to push their way into crevices as they eat their way through their burrows. (The mouth of the worm is just behind the prostomium.) Worms swallow pieces of dirt and decaying leaves, and the food passes through the pharynx , (located in body segments 1-6), the esophagus (segments 6-13), and into the crop, which stores food temporarily. The worm’s stomach is very muscular, so is called a gizzard . Like a bird’s gizzard, it grinds up the food, which then moves into the intestine . The intestine extends over two-thirds of the worm’s body length. In the intestine, food is broken down into usable chemicals which are absorbed into the bloodstream. Leftover soil particles and undigested organic matter pass out of the worm through the rectum and anus in the form of castings , or worm poop. Worm poop is dark, moist, soil-colored, and very rich in nutrients. That’s why farmers and gardeners like to have lots of worms in their soil.
Cleaning out the blood : Worms don’t have kidneys, but they have something serving the same purpose. Worms have nephridia to filter out the dead cells and other wastes that are sloughed into the blood. Wastes from the nephridia are eliminated through the same opening as the digestive wastes. Worm urine is more dilute than ours, but has ammonia as well as urea.
Heartbeats : Worms don’t have just one heart. They have FIVE! But their hearts and circulatory system aren’t as complicated as ours — maybe because their blood doesn’t have to go to so many body parts.
- First it grips the soil with some of its back setae so its back part can’t move.
- Then it squeezes its circular muscles, which makes its body get longer. Since the back of the body is gripping the soil, the front part of the body moves forward.
- Then the front setae grip the soil and the back setae let go.
- Then the worm squeezes its longitudinal muscles, which makes its body shorter. The back part moves forward.
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Animals That Can Be Found on the Shore of the Pacific Ocean
Video of the Day
The Pacific is the world’s largest ocean, spreading halfway around the world and comprising 48 percent of the world’s water. The great body of salt water is home to a vast array of creatures, many of which live on the shore. Animals living along Pacific beaches must be adapted to both wet and dry conditions as this area is underwater at high tide and exposed to the air at low tide.
Mammals that live on and near the Pacific coast include the California sea lion, harbor seal, northern elephant seal, Guadalupe fur seal, Northern fur seal and Hawaiian monk seal. These seals breed, raise young, and rest on shores from Alaska south to Mexico and also Hawaii.
Shorebirds that live along the coast of the Pacific Ocean include avocets, oystercatchers, phalaropes, plovers, sandpipers, stilts, snipes and turnstones. These birds are generally characterized by long, thin legs with little to no webbing on their feet for wading in shallow water. They also have long, thin bills for plucking prey such as worms, insect larva, amphipods, copepods, crustaceans and mollusks from rocks and sand.
Marine reptiles that are adapted to life on Pacific shores include eight species of marine turtles, several sea snakes, one unique lizard called the marine iguana and saltwater crocodiles. Marine reptiles live in places along coasts of tropical and southern temperate regions where ocean water is warm.
Pacific shoreline invertebrate species include sea anemones, barnacles, chitons, crabs, isopods, limpets, mussels, sea stars, snails and whelks. All of these creatures have adapted to a life of clinging to rocks and boat docks during high tides and low, and they can survive rough waves or tumbling out to sea and back.
Introduced species like the European green crab are wreaking havoc on native species of the Pacific coast. These crabs prey on and compete with other crabs, bivalves, gastropods like snails and slugs, and many other invertebrates.
Human hookworm disease is a common helminth infection that is predominantly caused by the nematode parasites Necator americanus and Ancylostoma duodenale; organisms that play a lesser role include Ancylostoma ceylonicum, Ancylostoma braziliense, and Ancylostoma caninum. Hookworm infection is acquired through skin exposure to larvae in soil contaminated by human feces (see the image below). Soil becomes infectious about 9 days after contamination and remains so for weeks, depending on conditions.
Worldwide, hookworms infect an estimated 472 million people. Although most of those affected are asymptomatic, [1, 2] approximately 10% experience anemia. Hookworms may persist for many years in the host and impair the physical and intellectual development of children and the economic development of communities.
Historically, hookworm infection has disproportionately affected the poorest among the least-developed nations, largely as a consequence of inadequate access to clean water, sanitation, and health education. The frequent absence of symptoms notwithstanding, hookworm disease substantially contributes to the incidence of anemia and malnutrition in developing nations.  It occurs most commonly in the rural tropical and subtropical areas of Asia, sub-Saharan Africa, and Latin America. 
Individual hookworm treatment consists of iron replacement and anthelmintic therapy. Community eradication has proven difficult, even with intensive, yearly, school-based programs. Part of the difficulty may be failure to clear infection from adults with high worm burden. Despite this, successful control and eradication of hookworms is a worthy goal for new methods that could offer huge economic and social benefits to much of Africa and Asia.
See Common Intestinal Parasites, a Critical Images slideshow, to help make an accurate diagnosis.
Hookworm life cycle
The life cycle of hookworms (see the image below) begins with the passing of hookworm eggs in human feces and their deposition into the soil. [4, 5]
Each day in the intestine, a mature female A duodenale worm produces about 10,000-30,000 eggs, and a mature female N americanus worm produces 5000-10,000 eggs (see the image below). After deposition onto soil and under appropriate conditions, each egg develops into an infective larva. These larvae are developmentally arrested and nonfeeding. If they are unable to infect a new host, they die when their metabolic reserves are exhausted, usually in about 6 weeks.
Larval growth is most proliferative in favorable soil that is sandy and moist, with an optimal temperature of 20-30°C. Under these conditions, the larvae hatch in 1 or 2 days to become rhabditiform larvae, also known as L1 (see the image below).
The rhabditiform larvae feed on the feces and undergo 2 successive molts; after 5-10 days, they become infective filariform larvae, or L3 (see the image below). These L3 go through developmental arrest and can survive in damp soil for as long as 2 years. However, they quickly become desiccated if exposed to direct sunlight, drying, or salt water. L3 live in the top 2.5 cm of soil and move vertically toward moisture and oxygen.
The L3 larvae are 500-700 µm long (barely visible to the naked eye) and are capable of rapid penetration into normal skin, most commonly on the hands or feet. Transmission occurs after 5 or more minutes of skin contact with soil that contains viable larvae. The skin penetration may cause a local pruritic dermatitis, also known as ground itch. Ground itch at the site of penetration is more common with Ancylostoma than with Necator.
The larvae migrate through the dermis, entering the bloodstream and moving to the lungs within 10 days. Once in the lungs, they break into alveoli, causing a mild and usually asymptomatic alveolitis with eosinophilia. (Hookworms are among the causes of the pulmonary infiltrates and eosinophilia [PIE] syndrome, along with Ascaris and Strongyloides species.)
Having penetrated the alveoli, the larvae are carried to the glottis by means of the ciliary action of the respiratory tract. During pulmonary migration, the host may develop a mild reactive cough, sore throat, and fever that resolve after the worm migrates into the intestines. At the glottis, the larvae are swallowed and carried to their final destination, the small intestine.
During this part of the migration, the larvae undergo 2 further molts, developing a buccal capsule and attaining their adult form. The buccal capsule of an adult A duodenale has teeth to facilitate attachment to mucosa, whereas an adult N americanus has cutting plates instead. A muscular esophagus creates suction in the buccal capsule.
Using their buccal capsule, the adult worms attach themselves to the mucosal layer of the proximal small intestine, including the lower part of the duodenum, jejunum, and proximal ileum (see the image below). In so doing, they rupture the arterioles and venules along the luminal surface of the intestine.
The adult worms release hyaluronidase, which degrades intestinal mucosa and erodes blood vessels, resulting in blood extravasation. They also ingest some blood. An anticoagulant facilitates blood flow by blocking the activity of factors Xa and VIIa. Adult worms also elaborate factors (eg, neutrophil inhibitory factor) that protect them from host defenses.
In 3-5 weeks, the adults become sexually mature, and the female worms begin to produce eggs that appear in the feces of the host.
Although N americanus infects only percutaneously, A duodenale can also infect by means of ingestion; however, in su Ancylostoma may also lie dormant in tissues and later be transmitted through breast milk. This ability to enter dormancy in the human host may be an adaptive response evolved to increase the chances of propagation. If all larvae were to mature promptly during dry seasons of the year, females would release eggs onto inhospitable soil. Eggs produced and released during the wet season have a much greater chance of encountering optimal soil conditions for further development.
Neither Necator nor Ancylostoma multiplies within the host. If the host is not reexposed, the infection disappears after the worm dies. The natural life span for an adult A duodenale is about 1 year, and that for an adult N americanus is 3-5 years.
Types of hookworm disease
Hookworm infection gives rise to the following 3 clinical entities in humans:
Classic hookworm disease — This is a gastrointestinal (GI) infection characterized by chronic blood loss that leads to iron-deficiency anemia and protein malnutrition; it is caused primarily by N americanus and A duodenale and less commonly by the zoonotic species A ceylonicum
Cutaneous larva migrans — This is an infection whose manifestations are limited to the skin; it is most commonly caused by A braziliense, whose definitive hosts include dogs and cats
Eosinophilic enteritis — This is a GI infection characterized by abdominal pain but no blood loss; it is caused by the dog hookworm A caninum
In cutaneous larva migrans, the infective larvae of zoonotic species such as A braziliense do not elaborate sufficient concentrations of hydrolytic enzymes to penetrate the junction of the dermis and epidermis. The larvae thus remain trapped superficial to this layer, where they migrate laterally at a rate of 1-2 cm/day and create the pathognomonic serpiginous tunnels associated with this condition. Larvae can survive in the skin for about 10 days before dying.
In eosinophilic enteritis, A caninum larvae typically enter a human host by penetrating the skin, though infection by oral ingestion is also possible. These larvae probably remain dormant in skeletal muscles and create no symptoms. In some individuals, larvae may reach the gut and mature into adult worms.
Why some individuals sustain A caninum development and then respond with a severe localized allergic reaction is unknown. Adult worms secrete various potential allergens into the intestinal mucosa. Some patients have been reported to experience increasingly severe recurrent abdominal pain, which may be analogous to a response to repeated insect stings.
Intestinal blood loss secondary is the major clinical manifestation of hookworm infection.  In fact, hookworm disease historically refers to the childhood syndrome of iron deficiency anemia, protein malnutrition, growth and mental retardation with lethargy resulting from chronic intestinal blood loss secondary to hookworm infection in the face of an iron deficient diet.
Hookworms ingest and digested some of the blood from the injured mucosa by means of a multienzyme cascade of metallohemoglobinases. Each Necator worm ingests 0.03 mL of blood daily, whereas each Ancylostoma worm ingests 0.15-0.2 mL of blood daily. Inhibited host coagulation due to a series of anticoagulants directed against factor Xa and the factor VIIa–tissue factor (TF) complex, as well as against platelet aggregation, further exacerbates blood loss.
The amount of blood loss and the degree of anemia are positively correlated with the worm burden, whereas hemoglobin, serum ferritin, protoporphyrin levels are significantly and negatively correlated with the number of worms.  Threshold worm loads for anemia differ nationally, with as few as 40 worms producing anemia in countries with low iron consumption.
Generally, the extent of hookworm infection may be categorized as follows:
Little is known about the innate immune response to metazoan in general and hookworms in particular.  Hookworm-derived pathogen-associated molecular patterns (PAMPS) of molecules are thought to react with receptors on dentritic cells or basophiles to stimulate interleukin (IL)–4 and initiate an immunological cascade resulting in a type 2 regulatory response from Th2 helper cells. This may be augmented by “alarmins” such as thymic stromal lymphopoietin (TSLP), IL-33, and IL-25 released from epithelial cells damaged by worms. These activate newly described innate lymphoid type-2 cells (ILC2) that provide early rise in protective TH2 cytokines IL-5 and IL-13.
Meanwhile, worm products inhibit IL-12 and TSLP induces basophil production of IL-4, both promoting differentiation of Th2 cells. The antiparasite Th2 cells produce more IL-4, IL-5, and IL-13, which cause B cell immunoglobulin G type 1 (IgG1) and immunoglobulin E (IgE) class switching. Antiworm IgE binds the parasite and actives mast cells, which release inflammatory molecules, while IL-5 promotes eosinophil expansion and activation and M2 macrophage differentiation, which damage and produce granulomas, respectively. Other effector molecules include transforming growth factor-beta (TGF-b), resistinlike molecule (RELM)–alpha, chitinases, and matrix metalloproteases, all of which damage or limit the parasite.
At the same time, this intense Th2 immune response must be regulated by the host to avoid immunopathology, and by the parasite to allow survival. Helminths enhance expression of T cell co-inhibitory molecules that include PD-1 and CTLA-4, and promote differentiation of tolerogenic dentric cells and T regulatory cells. T regulatory cells produce anti-inflammatory cytokines IL-10 and TGF-b. Hookworms also appear to secrete an inhibitor of natural killer cells, thereby suppressing production of interferon gamma and the Th2 response that would be expected to clear the parasite.
Since 1989 with David Strachan’s observation of a correlation between incidence of hay fever in children and low family size, the hygiene hypothesis has excited investigators as to a possible inverse relationship between helminth infections and allergic and autoimmune disease.
The increased prevalence of atopy, asthma, and food allergy in areas free of worm infestation has been cited as supportive of the hygiene hypothesis and has even prompted investigation of worms or worm products as therapy for such diseases. Similarly, areas of high hookworm endemicity have low rates of reaction to dust mite antigens. It is thought that worm-activated regulatory and counter-regulatory processes involving Th2 and T regulatory cells and cell products may paradoxically inhibit Th2 responses that in the absence of worms, cause reactions to potential allergens.
In the search for possible vaccine targets, investigators have focused on hookworm molecular inhibitors of coagulation factors Xa and VIIa-TF and metalloproteases that degrade hemoglobin and intestinal mucosal cells. The Sabin Vaccine Institute has developed a 2 antigen human hookworm vaccine comprising recombinant Necator antigens Na- GST-1 and Na- APR-1, each of which is required for hookworm use of host blood.  Another antigen, Ancylostoma -secreted protein 2 (ASP-2), appears necessary for chemokine receptor binding and invasion and has shown some promise in animal vaccine trials. The 3-dimensional structure of Na-ASP-2 has recently been reported and identified as a conserved tandem histidine motif necessary for catalytic or proteolytic activity.  Unfortunately, this vaccine produced urticarial reactions among previously infected recipients, and its development was halted.