text:
Arturo Álvarez (footballer, born 1985)

José Arturo Álvarez Hernández (born June 28, 1985) is a former professional footballer who played as a winger and forward. Born in the United States, he played for the El Salvador national team.

Professional
Álvarez did not play college soccer; instead, he joined MLS in 2003, signing a Project-40 contract, and was selected thirteenth overall in the 2003 MLS SuperDraft by the San Jose Earthquakes. In his first year, Álvarez scored his first MLS goal on June 14, 2003, against FC Dallas but would go on to get limited playing time. However, in January 2005 Álvarez was traded by San Jose with Richard Mulrooney and the #6 and #29 picks in the 2005 MLS SuperDraft to FC Dallas in exchange for Brad Davis, cash, and the #4 pick in the 2005 SuperDraft.

During the 2007 MLS Cup Playoffs, in the second leg of FC Dallas' Conference semifinal match with the Houston Dynamo, Álvarez was sent off for "violent conduct" after he kneed Brad Davis in the groin while out of bounds in the forty-seventh minute. Dallas went on to lose the tie 4–1, and the match 4–2 on aggregate.

Álvarez was traded to the new San Jose Earthquakes in July 2008 for allocation money and their first round draft pick in the 2009 MLS SuperDraft. In his debut, he scored the first goal of the match against the Los Angeles Galaxy in a match that ended 3–2. On November 24, 2010, Álvarez was selected in the tenth round of the 2010 MLS Expansion Draft by Portland Timbers but was immediately traded to Real Salt Lake for a 2nd round 2011 MLS SuperDraft pick.

The Salvadoran American made his debut with Real Salt Lake on March 15, 2011, when he entered in the 88th minuteof the first leg of the 2010–11 CONCACAF Champions League semifinals against Saprissa.

After the 2011 season, Real Salt Lake did not re-sign Álvarez. He opted to participate in the 2011 MLS Re-Entry Draft and was selected by Chivas USA on December 5, 2011. However, he instead signed a two-year contract with Portuguese first division club Paços de Ferreira. On March 18, 2012, he scored his first goal with his new team against Académica

On February 7, 2013, he was loaned to Hungarian club Videoton. He played well enough with the team that in June 2013 he signed a two-year contract to stay in Hungary. He was released in 2015.

On March 3, 2016, after a successful preseason trial with the club, Álvarez was signed by Chicago Fire to a one-year deal with one year option.

On December 10, 2017, Álvarez was traded by Chicago to his home town club, the Houston Dynamo, in exchange for a second-round selection in the 2019 MLS SuperDraft. Álvarez was mainly used as a sub and helped the Dynamo win the 2018 US Open Cup. He left the club again at the end of 2018.

On March 1, 2019, Álvarez announced his retirement from playing professional soccer.

United States
Álvarez represented the United States in various youth levels – U-17, U-18, and U-20. He also participated in various matches and training camps with the U-23 team.

El Salvador
Though Álvarez played on various United States national squads at the youth level, he was never called up to the senior national team. Being of Salvadoran descent, Álvarez was invited to play for the El Salvador national team by coach Carlos de los Cobos. On August 12, 2009, Álvarez made his debut for El Salvador in a World Cup qualifier against Trinidad and Tobago. On September 5, 2009, Álvarez started in a World Cup qualifier against his home country at Rio Tinto Stadium in Sandy, Utah. El Salvador fell, 2–1. On September 9, 2009, Álvarez played his first home game in Estadio Cuscatlán, in San Salvador, El Salvador against Costa Rica. El Salvador was victorious 1–0.

Honors
San Jose Earthquakes
 * MLS Cup: 2003

Videoton
 * Nemzeti Bajnokság I: 2014–15

Houston Dynamo
 * US Open Cup: 2018

title: Arturo Álvarez (footballer, born 1985)


text:
Alexander of Macedon (disambiguation)

Alexander of Macedon may refer to:

 * Alexander I of Macedon (died 454 BC), ruled from 498 to 454 BC
 * Alexander II of Macedon (died 368 BC), ruled from 370 to 368 BC
 * Alexander III of Macedon (356–323 BC), or Alexander the Great, ruled from 336 to 323 BC
 * Alexander IV of Macedon (323–310 BC), ruled as a child-king from birth to death
 * Alexander V of Macedon (died 294 BC), ruled with his brother Antipater from c. 297–294 BC
 * Alexander (son of Perseus), a child in the 160s

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Alexander of Macedon (disambiguation)


text: File:SmithsSingles.jpg

title: File:SmithsSingles.jpg


text:
Hymenolepiasis

Hymenolepiasis is infestation by one of two species of tapeworm: Hymenolepis nana or H. diminuta. Alternative names are dwarf tapeworm infection and rat tapeworm infection. The disease is a type of helminthiasis which is classified as a neglected tropical disease.

Symptoms and signs
Hymenolepiasis does not always have symptoms, but they usually are described as abdominal pain, loss of appetite, itching around the anus, irritability, and diarrhea. However, in one study of 25 patients conducted in Peru, successful treatment of the infection made no significant difference to symptoms. Some authorities report that heavily infected cases are more likely to be symptomatic.

Symptoms in humans are due to allergic responses or systematic toxaemia caused by waste products of the tapeworm. Light infections are usually symptomless, whereas infection with more than 2000 worms can cause enteritis, abdominal pain, diarrhea, loss of appetite, restlessness, irritability, restless sleep, and anal and nasal pruritus. Rare symptoms include increased appetite, vomiting, nausea, bloody diarrhea, hives, extremity pain, headache, dizziness, and behavioral disturbances. Occasionally, epileptic seizures occur in infected children.

Examination of the stool for eggs and parasites confirms the diagnosis. The eggs and proglottids of H. nana are smaller than H. diminuta. Proglottids of both are relatively wide and have three testes. Identifying the parasites to the species level is often unnecessary from a medical perspective, as the treatment is the same for both.

Complications
Abdominal discomfort and, in case of prolonged diarrhea, dehydration are possible complications.

In 2015 an unusual complication was noted in a man whose immune system had been compromised by HIV. He developed multiple tumors of malignant cell nests within his body that had originated from a tapeworm in his intestines.

Causes
Hymenolepis worms live in the intestines of rats and are common in warm climates, and are generally found in the feces of rats, which are consumed by their secondary hosts—beetles. The worms mature into a life form referred to as a "cysticercoid" in the insect; in H. nana, the insect is always a beetle. Humans and other animals become infected when they intentionally or unintentionally eat material contaminated by insects. In an infected person, it is possible for the worm's entire lifecycle to be completed in the bowel, so infection can persist for years if left untreated. H. nana infections are much more common than H. diminuta infections in humans because, in addition to being spread by insects, the disease can be spread directly from person to person by eggs in feces. When this happens, H. nana oncosphere larvae encyst in the intestinal wall and develop into cysticercoids and then adults. These infections were previously common in the southeastern USA, and have been described in crowded environments and individuals confined to institutions. However, the disease occurs throughout the world. H. nana infections can grow worse over time because, unlike in most tapeworms, H. nana eggs can hatch and develop without ever leaving the definitive host.

H. diminuta
The risk of human infection from H. diminuta is very low, since its main host is the rat. Also known as the rat tapeworm, H. diminuta adults live and mate in the bowels of rats. Eggs of H. diminuta are excreted by the rats in droppings, which are frequently consumed by beetles. Once inside the beetle, the eggs mature into a cysticercoid. The juvenile tapeworms claw their way out of the beetle gut into the circulatory system by means of their three pairs of hooks. There, they wait for a rat to ingest the host beetle, where they mature to adult form, lay eggs, and restart the entire cycle.

Beetle manipulation
H. diminuta has an effective mechanism for interspecies transfection. Beetles prefer to ingest rat droppings infected with tapeworm eggs, because of their odor. It is not known if the odor is produced specifically by the eggs or the droppings. H. diminuta also sterilizes its beetle host, if female. This is so the beetle does not waste energy in its reproductive system, allowing H. diminuta to further exploit the beetle's metabolic resources.

H. nana
H. nana is a tapeworm, belonging to the class Cestoidea, phylum Platyhelminthes. It consists of a linear series of sets of reproductive organs of both sexes; each set is referred to as a genitaluim and the area around it is a proglottid. New proglottids are continuously differentiated near the anterior end in a process called strobilation. Each segment moves toward the posterior end as a new one takes its place and, during the process, becomes sexually mature. The proglottid can copulate with itself, with others in the strobilla, or with those in other worms. When the segment reaches the end of its strobila, it disintegrates en route, releasing eggs in a process called apolysis.

Lifecycle
H. nana is the only cestode capable of completing its lifecycle without an intermediate host. It can, however, pass through an intermediate host, as well. The most common intermediate hosts for H. nana are arthropods (e.g. flour beetles). When an egg is ingested by the definitive host, it hatches and releases a six-hook larva called the oncosphere (hexacanth) which penetrates the villi of the small intestine and develops into a cysticercoid.

Infection
Transmission of H.nana occurs by the fecal-oral route. It also occurs by accidental ingestion of an insect containing the cysticercoid.

Screening for activity against H. nana
H. nana in mice is used because:
 * Human infection is easily maintained in mice.
 * Its armed scolex is similar to other pathogenic tapeworms.
 * It corresponds to other tapeworms in its sensitivity to standard anthelmintics,

Method:
 * 1) Mature worms are collected from infected mice.
 * 2) Terminal gravid proglottids are removed, crushed under coverslips, and eggs are removed.
 * 3) Eggs containing hooklets (mature) are counted.
 * 4) 0.2 ml stock soln. containing 1000 eggs/ml given to each mouse.
 * 5) Adult worms develop in 15–17 days.
 * 6) The test drug is given orally; mice are necropsied on the third day after treatment.
 * 7) A standard drug is given.
 * 8) The intestines are examined under a dissecting microscope for worms or scolices.
 * 9) The response is measured bt the number mice cleared.

Pathology
H. nana lodges itself in the intestines and absorbs nutrients from the intestinal lumen. In human adults, the tapeworm is more of a nuisance than a health problem, but in small children, many H. nana worms can be dangerous. Usually, the larvae of this tapeworm cause the most problem in children; they burrow into the walls of the intestine, and if enough tapeworms are present in the child, severe damage can be inflicted. This is done by absorbing all the nutrients from the food the child eats. Usually, a single tapeworm will not cause health issues. H. nana usually will not cause deaths unless in extreme circumstances and usually in young children or in people who have weakened immune systems. In some parts of the world, individuals who are heavily infected are a result of internal autoinfection.

Prevention
Good hygiene, public health and sanitation programs, and elimination of infected rats help to prevent the spread of hymenolepiasis. Preventing fecal contamination of food and water in institutions and crowded areas is of primary importance. General sanitation and rodent and insect control (especially control of fleas and grain insects) are also essential for prevention of H. nana infection.

Treatment
The two drugs that have been well-described for the treatment of hymenolepiasis are praziquantel and niclosamide. Praziquantel, which is parasiticidal in a single dose for all the stages of the parasite, is the drug of choice because it acts very rapidly against H. nana. Although structurally unrelated to other anthelminthics, it kills both adult worms and larvae. In vitro, the drug produces vacuolization and disruption of the tegument in the neck of the worms, but not in more posterior portions of the strobila. Praziquantel is well absorbed when taken orally, and it undergoes first-pass metabolism and 80% of the dose is excreted as metabolites in urine within 24 hours. Repeated treatment is required for H. nana at an interval of 7–10 days.

Praziquantel as a single dose (25 mg/kg) is the current treatment of choice for hymenolepiasis and has an efficacy of 96%. Single-dose albendazole (400 mg) is also very efficacious (>95%).

A three-day course of nitazoxanide is 75–93% efficacious. The dose is 1 g daily for adults and children over 12; 400 mg daily for children aged 4 to 11 years; and 200 mg daily for children aged 3 years or younger.

Prognosis
Cure rates are extremely good with modern treatments, but successful cure results may be of no symptomatic benefit to patients.

title: Hymenolepiasis


text:
Singles (The Smiths album)

""

Singles is the seventh compilation album by the English rock band the Smiths, pitched as a compilation of previously issued singles. It was released in February 1995 by the new owner of their back catalogue, WEA (Sire Records in the United States). Its highest British chart position was #5; it did not chart in the United States. Blender magazine listed the album among the "500 CDs You Must Own" on their website.

Background
WEA (now the Warner Music Group) acquired the entire Smiths back catalogue in early 1992. After re-releasing all of The Smiths' eight original albums (the four studio albums, the Rank live album and the three compilation albums issued while the band were still active) and releasing a newly-assembled two-volume best of compilation album (Best I and Best II) in 1992, they decided to celebrate The Smiths' reputation as a "singles band" by issuing a collection of the band's singles in 1995. Only the singles released in the UK were included.

Despite the album's title, the Singles versions of "Hand in Glove", "The Boy with the Thorn in His Side" and "Ask" were not the original single mixes. Similarly, "What Difference Does It Make?", "How Soon Is Now?", "That Joke Isn't Funny Anymore" and "Last Night I Dreamt That Somebody Loved Me" were the full-length album versions, that are on the original 12" singles, as opposed to the original single edits.

Cover
The cover features previously unused artwork designed by Morrissey, featuring singer and actress Diana Dors in a still from the 1956 film Yield to the Night.

Spin-off singles
WEA decided to promote the album in the UK by re-releasing the "Ask" single with its two original B-sides, "Cemetry Gates" and "Golden Lights". The single charted at #62. In the United States, Sire decided to release "Sweet and Tender Hooligan", a single of rarities, to promote the album, with a newly designed sleeve by Morrissey. It failed to chart.

The Smiths

 * Mike Joyce – drums
 * Johnny Marr – guitars, keyboards, harmonica, synthesized saxophone, string and flute arrangements
 * Morrissey – vocals
 * Andy Rourke – bass guitar, cello on "Shakespeare's Sister"

Additional musicians

 * Craig Gannon – rhythm guitar on "Panic" and "Ask"
 * Kirsty MacColl – backing vocals on "Ask"
 * John Porter – slide guitar on "Sheila Take a Bow"
 * Stephen Street – drum machine on "I Started Something I Couldn't Finish" and synthesized string arrangements on "Girlfriend in a Coma"

title: Singles (The Smiths album)


text:
M26 Modular Accessory Shotgun System

The M26-MASS (Modular Accessory Shotgun System) is a shotgun configured as an underbarrel ancillary weapon attachment mounted onto the handguard of a service rifle, usually the M16/M4 family of United States military, essentially making the host weapon a combination gun. It can also be operated as a stand-alone shotgun by attachment to a pistol grip/collapsible buttstock module. Rollout commenced in 2013, replacing the M500 shotguns in service.

Development

The M26-MASS is a lightweight underbarrel shotgun configured to be secured to a main rifle, developed by C-More Systems and manufactured by Vertu Corporation and originally marketed toward special operations forces. It attracted the interest of soldiers being deployed to Afghanistan who wanted a lightweight system that could eliminate the need to carry additional weapons.

The M26-MASS had been in development at the U.S. Army's Soldier Battle Lab since the late 1990s. The idea was to provide soldiers with lightweight accessory weapons which could be mounted underbarrel of the standard issue M16 rifle or M4 carbine. These would provide soldiers with additional capabilities, such as: door breaching using special slugs, very short-range increased lethality using 00 buckshot, and less-lethal capabilities using teargas shells, rubber slugs, rubber pellets, or other non-lethal rounds.

The original idea was based on the Knight's Armament Company Masterkey system, which dates back to the 1980s and originally comprised a shortened, tube-fed Remington 870 shotgun mounted under an M16 rifle or M4 carbine. The M26-MASS improved upon the original Masterkey concept with a detachable magazine option and more comfortable handling, thanks to a bolt-operated system which is manually cycled for reloading and is characterized by a bolt which must be moved backward to remove a spent case and forward to chamber a new cartridge. The relatively large bolt handle is located closer to the rear rather than the slide on the Masterkey pump shotgun, and thus is easier to cycle in combat. The handle can be easily attached on either side of the bolt. The detachable magazine offers quicker reloading and change of ammunition types.

The M26-MASS was chosen by the U.S. Military over the Masterkey as a breaching tool. Small numbers of M26-MASS shotguns were issued to U.S. troops in Afghanistan. The current contract calls for the delivery of 9,000 shotguns. In February 2012, the first unit was fully equipped with M26-MASS. At the same time the U.S. Army is in the process of replacing the M500s with the M26s.

War in Afghanistan
In May 2008, the Army announced it would procure 35,000 units. The first M26-MASS shotguns were procured and fielded to military police and engineer units in 2010. However, some units in both Iraq and Afghanistan were issued the M26-MASS in small quantities as early as 2003. Full initial fielding began in 2011.

Specifications

 * Caliber: 12 gauge
 * Operation: Manual Straight pull bolt-action.
 * Capacity: 3 or 5 round detachable box magazine.
 * Ammunition: 2.75 (70mm) and 3 in (76mm) lethal, non-lethal and breaching rounds.
 * Barrel length: 7.75 in (197 mm) with integral breaching stand-off adapter.
 * Under-barrel configuration:
 * Overall length: 16.5 in (419 mm)
 * Weight: 2 lb 11 oz (1.22 kg)
 * Stand-alone configuration:
 * Overall length: 24 in (610 mm) (stock collapsed)
 * Weight: 4 lb 3 oz (1.90 kg)

title: M26 Modular Accessory Shotgun System


text:
LSS

LSS may refer to:

Companies

 * LSS Data Systems, a medical software company
 * Lone Star Steel Company, a tubular steel mill in Lone Star, Texas

Schools

 * Lakeland School System, school district in Lakeland, Tennessee
 * Laurel Springs School, Ojai, California, United States
 * Lawrence Sheriff School, Rugby, Warwickshire
 * Langstaff Secondary School, Richmond Hill, Ontario
 * London School of Sound, school of music production based in London, United Kingdom

Other organizations

 * Law Society of Saskatchewan
 * Leicester Secular Society, the world's oldest Secular Society
 * Life Saving Society
 * Lithic Studies Society
 * Lincoln Square Synagogue, Manhattan, New York City
 * Lunds Studentsångförening, a Swedish male-voice choir

Science and technology

 * Large-scale structure of the universe
 * Large Space Simulator, Space simulator
 * Life Span Study of atomic bomb survivors, see Epidemiology data for low-linear energy transfer radiation
 * Linhard–Scharff–Schiøt theory in ion physics
 * LSS (gene), an enzyme
 * LSS (Lynxmotion Smart Servo), a series of hobbyist-grade smart actuators created by RobotShop Inc.
 * Landing Ship Stern Chute, a converted train ferry used early in WW2 as Dock landing ship
 * Lumbar spinal stenosis, a medical condition in which the spinal canal narrows
 * XM26 Lightweight Shotgun System

Other uses

 * L. S. Sheshagiri Rao, Indian writer and scholar of Kannada literature
 * Lean Six Sigma, a synergized managerial concept of Lean manufacturing and Six Sigma
 * Licentiate of Sacred Scripture, see Licentiate of Sacred Theology
 * Logistics Support System
 * Lone Star Showdown, the official rivalry between the Texas A&M Aggies and the Texas Longhorns
 * LSS (Last Song Syndrome), a 2019 Philippine film

title: LSS


text:
Cif

Cif is a French brand of household cleaning products owned by the British company Unilever, known as Jif in Australia, New Zealand, Japan, Middle East and the Nordic countries.

Cif was launched in France in 1965 and was marketed in competition against scouring powders such as Vim.

Name
Cif is sold under the names Jif, Vim, Viss and Handy Andy, depending on which of the 51 countries it is sold in.

In Sweden, and South Africa, the products were originally sold under the name Vim before this was changed to Jif, the launch name in the United Kingdom, Ireland, the Netherlands and Hong Kong.

In January 2001, the name in most of these countries was changed to Cif in order to align marketing and product inventories across the continent. Despite this, many in Ireland and Scotland continue to call the product Jif. The name change from Jif to Cif was confirmed by Unilever in December 2000.

In Belgium, Finland and Portugal, the product was known as Vim for quite some time, after which it became Cif. In Canada and India, it is still called Vim. Recently advertisements for Cif surface grease cleaner have started to appear in India, while the Vim name is still used for the kitchen dish cleaning product. In Germany, the cleaner's name is Viss. In Iraq it is still traded as Jif, with local Arabic and English writing.

In Norway, the product is traded as Jif and owned by Lilleborg, a part of Orkla ASA. Unilever had a decades long partnership with Lilleborg when they were given the exclusive rights to the brand Jif in Norway. Lilleborg registered the trademark in 1968. Without consent from Lilleborg, Unilever registered their trademark Cif in 1998 and started selling Cif products in 2018. Thereafter Lilleberg protested and two JIF vs CIF court cases followed. The court decided that Unilever was allowed to keep the brand Cif, but not allowed to sell Cif products in Norway.

In the United States, Cif Cream Cleaner is sold as a co-branded product with Scrub Daddy.

Products

 * Cif Bathroom Mousse
 * Cif Stainless Steel Cleaner
 * Cif Bathroom Cleaner
 * Cif Kitchen Cleaner
 * Cif Power Cream
 * Cif Cream Cleaner, a non-abrasive version

title: Cif


text:
Destroy What Destroys You

Destroy What Destroys You is an album by the American ska-punk band Against All Authority. It was recorded by the band in May 1995 without any affiliation to a label or studio. It was released in 1996 by Far Out Records. The original album contained 18 songs. it was expanded for the CD and cassette release to include four songs from the band's first 7" release, "Above the Law".

Track listing

 * 1)  "Lifestyle of Rebellion" – 1:51
 * 2)  "No Reason" – 2:19
 * 3)  "Conditioning" – 2:09
 * 4)  "Freedom" – 1:57
 * 5)  "Destroy What Destroys You" – 1:47
 * 6)  "It Really Sucks When..." – 1:33
 * 7)  "Bloodclot" – 1:35
 * 8)  "Another Fuck You Song" – 2:08
 * 9)  "No Government Can Give You Freedom" – 0:35 (mistitled as 30 Sec Song)
 * 10)  "Kickin' the Dog" – 1:36
 * 11)  "Sounds of the Underground" – 1:45
 * 12)  "Osuchowski's on the Loose" – 2:06
 * 13)  "Walking Revolution" – 2:33
 * 14)  "Disobey" – 1:36
 * 15)  "Chelsea Baby" – 1:53
 * 16)  "Corporate Takeover" – 1:58
 * 17)  "Hard as Fuck" – 2:13
 * 18)  "Centerfold" – 1:54
 * 19)  "We Won't Submit" – 2:27 (CD & cassette only)
 * 20)  "Above the Law" – 2:51 (CD & cassette only)
 * 21)  "Under Your Authority" – 2:42 (CD & cassette only)
 * 22)  "Court 22" – 2:17 (CD & cassette only)

Personnel

 * Danny Lore (bass guitar, lead vocals)
 * Joe Koontz (guitar, backing vocals)
 * Kris King (drums)
 * Tim Farout (trombone)
 * Joey Jukes (trumpet)
 * Tim Coats (saxophone)

Crew

 * Omar Angulo (artwork)
 * Greg Lee (mastering)

title: Destroy What Destroys You


text:
Gnathostomiasis

Gnathostomiasis, also known as larva migrans profundus, is the human infection caused by the nematode Gnathostoma spinigerum and/or Gnathostoma hispidum, which infects vertebrates.

Symptoms and signs
A few days after ingestion epigastric pain, fever, vomiting, and loss of appetite resulting from migration of larvae through intestinal wall to the abdominal cavity will appear in the patient. Migration of parasites in the subcutaneous tissues causing intermittent, migratory, painful, pruritic swellings is known as cutaneous larva migrans. Patches of edema appear after initial symptoms clear and are usually found on the abdomen. These lesions vary in size and can be accompanied by pruritus, rash, and stabbing pain. Swellings may last for 1 to 4 weeks in a given area and then reappear in a different location. Migration to other tissues causes visceral larva migrans and can result in cough, hematuria, ocular involvement, meningitis, encephalitis and eosinophilia. Eosinophilic myeloencephalitis may also result from invasion of the central nervous system by the larvae.

Causes
Human gnathostomiasis is infection by the migrating third-stage larvae of any of five species of Gnathostoma. The most common cause in Asia is G. spinigerum, and the most common cause in the Americas is G. binucleatum. G. hispidium and G. doloresi occur in East and Southeast Asia; the former has also been found in Eastern Europe. G. nipponicum occurs only in Japan and China. There is one unconfirmed report of G. malaysiae causing disease in humans.

Transmission
Gnathostomiasis is transmitted by the ingestion of third-stage larvae from raw or insufficiently cooked second intermediate or paratenic hosts such as freshwater fish, snakes, poultry, or frogs.

In Thailand and Vietnam, the most common cause appears to be consumption of undercooked Asian swamp eels (Monopterus albus, also called Fluta alba) which transmit G. spinigerum. Monopterus albus is an invasive species in North America, but no Gnathostoma infections in humans have yet been conclusively identified in the US.

It is unclear if humans can be infected from drinking water contaminated with infected copepods.

Intermediate host
The primary intermediate host is the minute crustaceans of the genus Cyclops. These crustaceans are then ingested by a second intermediate host, such as frogs and freshwater fish. Paratenic hosts are usually animals that prey on second intermediate hosts, such as snakes and birds.

Definitive host
The definitive hosts for gnathostomiasis include omnivorous or carnivorous mammals such as cats, dogs, tigers, leopards, lions, mink, opossums or raccoons. Humans are accidental hosts, not definitive hosts.

Incubation period
The incubation period for gnathostomiasis is 3–4 weeks when the larvae begin to migrate through the subcutaneous tissue of the body.

Morphology
The adult parasite is reddish-brown in color and has a globular cephalic dome that is separated from the rest of the body by constriction. The posterior portion of the nematode is smooth while the anterior half is covered with fine leaf-like spines. The head is round and contains 4 to 8 transverse rows of hooklets that are protected by a pair of fleshy lips. The males are shorter than the females, 11 - 25 mm compared to 25 - 54 mm respectively. Eggs are oval and have a mucoid plug at one end.

Life cycle in definitive hosts
Adult worms are found in a tumor located in the gastric wall of the definitive hosts and release eggs into the host's digestive tract. The eggs are then released with feces and in about a week hatch in water to develop into first stage larva. Larvae are then ingested by minute copepods of the genus Cyclops. Once entering the copepod, the larvae penetrate the gastric wall of their intermediate host and begin to develop into second-stage and even early third-stage larvae. The copepods are then ingested by a second intermediate host such as fish, frogs, or snakes. Within this second intermediate or definitive host the larva repeat a similar pattern of penetrating the gastric wall, but then continue to migrate to muscular tissue and develop into advanced third-stage larvae. These larvae then encyst within the musculature of the new host. If the cyst containing flesh of these hosts is ingested by a definitive host, such as dogs, and cats, the cysts are ingested and the larvae escape the cysts and penetrate the gastric wall. These released larvae travel to the connective tissue and muscle as observed before and after 4 weeks they return to the gastric wall as adults. Here they form a tumor and continue to mature into adults for the next 6–8 months. Worms mate and females begin to excrete fertilized eggs with feces 8–12 months after ingestion of cysts. They are passed out in the feces and eaten by another fish.

Life cycle in humans
Infection of humans by gnathostomiasis is accidental because humans are not one of the definitive hosts of the parasite and do not allow the parasite to complete its life cycle. Infection in humans follows ingestion of raw or insufficiently cooked infected intermediate hosts. The ingested third stage larva migrates from the gastric wall and its migration results in the symptoms associated with infection by gnathostomiasis. The third stage larvae don't return to the gastric wall preventing it from maturing into adult worms, leaving the life cycle incomplete. Instead the larvae continue to migrate unpredictably unable to develop into adults, so eggs are seldom found in diagnostic tests or human feces. This also means the number of worms present in humans is a reflection of the number of third stage larvae ingested.

Diagnosis
Diagnosis of gnathostomiasis is possible (with microscopy) after removal of the worm. The primary form of diagnosis of gnathostomiasis is the identification of larva in the tissue. Serological testing such as enzyme-linked immunosorbent assay (ELISA) or the Western blot are also reliable but may not be easily accessible in endemic areas.

CT scanning or MRI can be used to help identify a soft tissue worm and when looking at CNS disease it can be used to reveal the presence of the worm. The presence of haemorrhagic tracks on gradient-echo T2-weighted MRI is characteristic and possibly diagnostic.

Prevention
The best strategies for preventing accidental infection of humans is to educate those living in endemic areas to only consume fully cooked meat. The inability of the parasite to complete its life cycle within humans means that transmission can easily be contained by adequate preparation of meat from intermediate hosts. This is especially useful because of the difficulty and lack of feasibility inherent in eliminating all intermediate hosts of gnathostomiasis. So instead, individuals in endemic areas should avoid eating raw and undercooked meat in endemic areas, but this may be difficult in these areas.

The dish ceviche is native to Peru and a favorite of Mexico. It consists of onion, cubed fish, lime or lemon juice and Andean spices including salt and chili. The ingredients are mixed together and they are allowed to marinate several hours before being served at room temperature. Then in endemic areas in Southeast Asia there are traditional dishes associated with these areas that also include raw uncooked fish, such as koipla in Thailand, goi ca song in Vietnam, sashimi and sushi in Japan.

Acknowledging these cultural traditions, individuals in these cultural can be educated on methods of adapting their food preparation activities in order to remove the larvae without greatly altering these traditional dishes. For instance, meat should be marinated in vinegar for six hours or in soy sauce for 12 hours in order to successfully kill the larvae. In areas with reliable electricity, meat can be frozen at -20 degrees Celsius for 3–5 days to achieve the same results of killing the larvae present.

Treatment
Surgical removal or treatment with albendazole or ivermectin is recommended. The most prescribed treatment for gnathostomiasis is surgical removal of the larvae but this is only effective when the worms are located in an accessible location. In addition to surgical excision, albendazole and ivermectin have been noted in their ability to eliminate the parasite. Albendazole is recommended to be administered at 400 mg daily for 21 days as an adjunct to surgical excision, while ivermectin is better tolerated as a single dose. Ivermectin can also serve as a replacement for those that can't handle albendazole 200 ug/kg p.o. as a single dose. However, ivermectin has been shown to be less effective than albendazole.

Epidemiology
Endemic areas include Asia, Mexico, India and parts of South Africa. Originally believed to be confined to Asia, in the 1970s gnathostomiasis was discovered in Mexico, and found in Australia in 2011. Even though it is endemic in areas of Southeast Asia and Latin America, it is an uncommon disease. However, researchers have noticed recently an increase in incidence. This disease is most common in both Thailand and Japan. In Thailand, it is the most common cause of central nervous system parasitic infections. As of 2009, 23 cases in China were reported in Chinese literature. As of 2020, about 5,000 cases of Gnathostomiasis have been reported globally.

History
The first case of Gnathostoma infection was identified by Sir Richard Owen when inspecting the stomach of a young tiger that had died at London Zoo from a ruptured aorta. However it was not until 1889 that the first human case was described by Levinson when he found the Gnathostoma larva in an infested Thai woman. The lifecycle of G. spinigerum was described by Svasti Daengsvang and Chalerm Prommas from Thailand in 1933 and 1936. This delay in identification of the parasite in humans is due to the fact that humans are not a definitive host for this parasite making infection from this parasite rare. Gnathostomiasis infection is rare because the parasite must be digested when it has reached its third larvae stage, providing only a short time frame in which the parasite is capable of infecting humans. It is uncommon for the larvae to penetrate the skin of individuals exposed to contaminated food or water without ingestion.

title: Gnathostomiasis


text:
Fasciolosis

Fasciolosis is a parasitic worm infection caused by the common liver fluke Fasciola hepatica as well as by Fasciola gigantica. The disease is a plant-borne trematode zoonosis, and is classified as a neglected tropical disease (NTD). It affects humans, but its main host is ruminants such as cattle and sheep. The disease progresses through four distinct phases; an initial incubation phase of between a few days up to three months with little or no symptoms; an invasive or acute phase which may manifest with: fever, malaise, abdominal pain, gastrointestinal symptoms, urticaria, anemia, jaundice, and respiratory symptoms. The disease later progresses to a latent phase with less symptoms and ultimately into a chronic or obstructive phase months to years later. In the chronic state the disease causes inflammation of the bile ducts, gall bladder and may cause gall stones as well as fibrosis. While chronic inflammation is connected to increased cancer rates, it is unclear whether fasciolosis is associated with increased cancer risk.

Up to half of those infected display no symptoms, and diagnosis is difficult because the worm eggs are often missed in fecal examination. The methods of detection are through fecal examination, parasite-specific antibody detection, or radiological diagnosis, as well as laparotomy. In case of a suspected outbreak it may be useful to keep track of dietary history, which is also useful for exclusion of differential diagnoses. Fecal examination is generally not helpful because the worm eggs can seldom be detected in the chronic phase of the infection. Eggs appear in the feces first between 9–11 weeks post-infection. The cause of this is unknown, and it is also difficult to distinguish between the different species of fasciola as well distinguishing them from echinostomes and Fasciolopsis. Most immunodiagnostic tests detect infection with very high sensitivity, and as concentration drops after treatment, it is a very good diagnostic method. Clinically it is not possible to differentiate from other liver and bile diseases. Radiological methods can detect lesions in both acute and chronic infection, while laparotomy will detect lesions and also occasionally eggs and live worms.

Because of the size of the parasite, as adult F. hepatica: 20 – or adult F. gigantica: 25 –, fasciolosis is a big concern. The amount of symptoms depend on how many worms and what stage the infection is in. The death rate is significant in both cattle (67.55%) and goats (24.61%), but generally low among humans. Treatment with triclabendazole has been highly effective against the adult worms as well as various developing stages. Praziquantel is not effective, and older drugs such as bithionol are moderately effective but also cause more side effects. Secondary bacterial infection causing cholangitis has also been a concern and can be treated with antibiotics, and toxaemia may be treated with prednisolone.

Humans are infected by eating watergrown plants, primarily wild-grown watercress in Europe or morning glory in Asia. Infection may also occur by drinking contaminated water with floating young fasciola or when using utensils washed with contaminated water. Cultivated plants do not spread the disease in the same capacity. Human infection is rare, even if the infection rate is high among animals. Especially high rates of human infection have been found in Bolivia, Peru and Egypt, and this may be due to consumption of certain foods. No vaccine is available to protect people against Fasciola infection. Preventative measures are primarily treating and immunization of the livestock, which are required to host the live cycle of the worms. Veterinary vaccines are in development, and their use is being considered by a number of countries on account of the risk to human health and economic losses resulting from livestock infection. Other methods include using molluscicides to decrease the number of snails that act as vectors, but it is not practical. Educational methods to decrease consumption of wild watercress and other waterplants has been shown to work in areas with a high disease burden.

Fascioliasis occurs in Europe, Africa, the Americas as well as Oceania. Recently, worldwide losses in animal productivity due to fasciolosis were conservatively estimated at over US$3.2 billion per annum. Fasciolosis is now recognized as an emerging human disease: the World Health Organization (WHO) has estimated that 2.4 million people are infected with Fasciola, and a further 180 million are at risk of infection.

Humans
The course of fasciolosis in humans has 4 main phases: This phase may develop months or years after initial infection. Adult flukes in the bile ducts cause inflammation and hyperplasia of the epithelium. The resulting cholangitis and cholecystitis, combined with the large body of the flukes, are sufficient to cause mechanical obstruction of the biliary duct. In this phase, biliary colic, epigastric pain, fatty food intolerance, nausea, jaundice, pruritus, right upper-quadrant abdominal tenderness, etc., are clinical manifestations indistinguishable from cholangitis, cholecystitis and cholelithiasis of other origins. Hepatic enlargement may be associated with an enlarged spleen or ascites. In case of obstruction, the gall bladder is usually enlarged and edematous with thickening of the wall (Ref: Hepatobiliary Fascioliasis: Sonographic and CT Findings in 87 Patients During the InitialPhase and Long-Term Follow-Up. Adnan Kabaalioglu, Kagan Ceken, Emel Alimoglu, Rabin Saba, Metin Cubuk, Gokhan Arslan, Ali Apaydin. AJR 2007; 189:824–828). Fibrous adhesions of the gall bladder to adjacent organs are common. Lithiasis of the bile duct or gall bladder is frequent and the stones are usually small and multiple.
 * Incubation phase: from the ingestion of metacercariae to the appearance of the first symptoms; time period: few days to 3 months; depends on number of ingested metacercariae and immune status of host
 * Invasive or acute phase: fluke migration up to the bile ducts. This phase is a result of mechanical destruction of the hepatic tissue and the peritoneum by migrating juvenile flukes causing localized and or generalized toxic and allergic reactions. The major symptoms of this phase are:
 * Fever: usually the first symptom of the disease; 40 - 42 °C
 * Abdominal pain
 * Gastrointestinal disturbances: loss of appetite, flatulence, nausea, diarrhea
 * Urticaria
 * Respiratory symptoms (very rare): cough, dyspnoea, chest pain, hemoptysis
 * Hepatomegaly and splenomegaly
 * Ascites
 * Anaemia
 * Jaundice
 * Latent phase: This phase can last for months or years. The proportion of asymptomatic subjects in this phase is unknown. They are often discovered during family screening after a patient is diagnosed.
 * Chronic or obstructive phase:

Other animals
Veterinary clinical signs of fasciolosis are always closely associated with infectious dose (amount of ingested metacercariae). In sheep, as the most common definitive host, clinical presentation is divided into 4 types:
 * Acute Type I Fasciolosis: infectious dose is more than 5000 ingested metacercariae. Sheep suddenly die without any previous clinical signs. Ascites, abdominal haemorrhage, icterus, pallor of membranes, weakness may be observed in sheep.
 * Acute Type II Fasciolosis: infectious dose is 1000-5,000 ingested metacercariae. As above, sheep die but briefly show pallor, loss of condition and ascites.
 * Subacute Fasciolosis: infectious dose is 800-1000 ingested metacercariae. Sheep are lethargic, anemic and may die. Weight loss is dominant feature.
 * Chronic Fasciolosis: infectious dose is 200-800 ingested metacercariae. Asymptomatic or gradual development of bottle jaw and ascites (ventral edema), emaciation, weight loss.

In blood, anemia, hypoalbuminemia, and eosinophilia may be observed in all types of fasciolosis. Elevation of liver enzyme activities, such a glutamate dehydrogenase (GLDH), gamma-glutamyl transferase (GGT), and lactate dehydrogenase (LDH), is detected in subacute or chronic fasciolosis from 12 to 15 weeks after ingestion of metacercariae. Economical effect of fasciolosis in sheep consists in sudden deaths of animals as well as in reduction of weight gain and wool production. In goats and cattle, the clinical manifestation is similar to sheep. However, acquired resistance to F. hepatica infection is well known in adult cattle. Calves are susceptible to disease but in excess of 1000 metacercariae are usually required to cause clinical fasciolosis. In this case the disease is similar to sheep and is characterized by weight loss, anemia, hypoalbuminemia and (after infection with 10,000 metacercariae) death. Importance of cattle fasciolosis consist in economic losses caused by condemnation of livers at slaughter and production losses especially due to reduced weight gain.

In sheep and sometimes cattle, the damaged liver tissue may become infected by the Clostridium bacteria C. novyi type B. The bacteria will release toxins into the bloodstream resulting in what is known as black disease. There is no cure and death follows quickly. As C. novyi is common in the environment, black disease is found wherever populations of liver flukes and sheep overlap.

Cause
Fasciolosis is caused by two digenetic trematodes F. hepatica and F. gigantica. Adult flukes of both species are localized in the bile ducts of the liver or gallbladder. F. hepatica measures 2 to 3 cm and has a cosmopolitan distribution. F. gigantica measures 4 to 10 cm in length and the distribution of the species is limited to the tropics and has been recorded in Africa, the Middle East, Eastern Europe and south and eastern Asia. In domestic livestock in Japan, diploid (2n = 20), triploid (3n = 30) and chimeric flukes (2n/3n) have been described, many of which reproduce parthenogenetically. As a result of this unclear classification, flukes in Japan are normally referred to as Fasciola spp. Recent reports based on mitochondrial genes analysis has shown that Japanese Fasciola spp. is more closely related to F. gigantica than to F. hepatica. In India, a species called F. jacksoni was described in elephants.

Transmission
Human F. hepatica infection is determined by the presence of the intermediate snail hosts, domestic herbivorous animals, climatic conditions and the dietary habits of man. Sheep, goats and cattle are considered the predominant animal reservoirs. While other animals can be infected, they are usually not very important for human disease transmission. On the other hand, some authors have observed that donkeys and pigs contribute to disease transmission in Bolivia. Among wild animals, it has been demonstrated that the peridomestic rat (Rattus rattus) may play an important role in the spread as well as in the transmission of the parasite in Corsica. In France, nutria (Myocastor coypus) was confirmed as a wild reservoir host of F. hepatica. Humans are infected by ingestion of aquatic plants that contain the infectious cercariae. Several species of aquatic vegetables are known as a vehicle of human infection. In Europe, Nasturtium officinale (common watercress), Nasturtium sylvestre, Rorippa amphibia (wild watercress), Taraxacum dens leonis (dandelion leaves), Valerianella olitoria (lamb's lettuce), and Mentha viridis (spearmint) were reported as a source of human infections. In the Northern Bolivian Altiplano, some authors suggested that several aquatic plants such as bero-bero (watercress), algas (algae), kjosco and tortora could act as a source of infection for humans. Because F. hepatica cercariae also encyst on water surface, humans can be infected by drinking of fresh untreated water containing cercariae. In addition, an experimental study suggested that humans consuming raw liver dishes from fresh livers infected with juvenile flukes could become infected.

Intermediate hosts

Intermediate hosts of F. hepatica are freshwater snails from family Lymnaeidae. Snails from family Planorbidae act as an intermediate host of F. hepatica very occasionally.

Mechanism
The development of infection in definitive host is divided into two phases: the parenchymal (migratory) phase and the biliary phase. The parenchymal phase begins when excysted juvenile flukes penetrate the intestinal wall. After the penetration of the intestine, flukes migrate within the abdominal cavity and penetrate the liver or other organs. F. hepatica has a strong predilection for the tissues of the liver. Occasionally, ectopic locations of flukes such as the lungs, diaphragm, intestinal wall, kidneys, and subcutaneous tissue can occur. During the migration of flukes, tissues are mechanically destroyed and inflammation appears around migratory tracks of flukes. The second phase (the biliary phase) begins when parasites enter the biliary ducts of the liver. In biliary ducts, flukes mature, feed on blood, and produce eggs. Hypertrophy of biliar ducts associated with obstruction of the lumen occurs as a result of tissue damage.

Resistance to infection
Mechanisms of resistance have been studied by several authors in different animal species. These studies may help to better understand the immune response to F. hepatica in host and are necessary in development of vaccine against the parasite. It has been established that cattle acquire resistance to challenge infection with F. hepatica and F. gigantica when they have been sensitized with primary patent or drug-abbreviated infection. Resistance to fasciolosis was also documented in rats. On the other hand, sheep and goats are not resistant to re-infection with F. hepatica. However, there is evidence that two sheep breeds, in particular Indonesian thin tail sheep and Red maasai sheep, are resistant to F. gigantica.

Diagnosis
Most immunodiagnostic tests will detect infection and have a sensitivity above 90% during all stages of the diseases. In addition antibody concentration quickly drops post treatment and no antibodies are present one year after treatment, which makes it a very good diagnostic method. In humans, diagnosis of fasciolosis is usually achieved parasitologically by findings the fluke eggs in stool, and immunologically by ELISA and Western blot. Coprological examinations of stool alone are generally not adequate because infected humans have important clinical presentations long before eggs are found in the stools.

Moreover, in many human infections, the fluke eggs are often not found in the faeces, even after multiple faecal examinations. Furthermore, eggs of F. hepatica, F. gigantica and Fasciolopsis buski are morphologically indistinguishable. Therefore, immunonological methods such ELISA and enzyme-linked immunoelectrotransfer blot, also called Western blot, are the most important methods in diagnosis of F. hepatica infection. These immunological tests are based on detection of species-specific antibodies from sera. The antigenic preparations used have been primarily derived from extracts of excretory/secretory products from adult worms, or with partially purified fractions. Recently, purified native and recombinant antigens have been used, e.g. recombinant F. hepatica cathepsin L-like protease.

Methods based on antigen detection (circulating in serum or in faeces) are less frequent. In addition, biochemical and haematological examinations of human sera support the exact diagnosis (eosinophilia, elevation of liver enzymes). Ultrasonography and xray of the abdominal cavity, biopsy of liver, and gallbladder punctuate can also be used (ref: US-guided gallbladder aspiration: a new diagnostic method for biliary fascioliasis. A. Kabaalioglu, A. Apaydin, T. Sindel, E. Lüleci. Eur. Radiol. 9, 880±882 (1999) . False fasciolosis (pseudofasciolosis) refers to the presence of eggs in the stool resulting not from an actual infection but from recent ingestion of infected livers containing eggs. This situation (with its potential for misdiagnosis) can be avoided by having the patient follow a liver-free diet several days before a repeat stool examination.

In animals, intravital diagnosis is based predominantly on faeces examinations and immunological methods. However, clinical signs, biochemical and haematological profile, season, climate conditions, epidemiology situation, and examinations of snails must be considered. Similarly to humans, faeces examinations are not reliable. Moreover, the fluke eggs are detectable in faeces 8–12 weeks post-infection. In spite of that fact, faecal examination is still the only used diagnostic tool in some countries. While coprological diagnosis of fasciolosis is possible from 8- to 12-week post-infection (WPI), F. hepatica specific-antibodies are recognized using ELISA or Western blot after 2-4 week post-infection. Therefore, these methods provide early detection of the infection.

Prevention
In some areas special control programs are in place or have been planned. The types of control measures depend on the setting (such as epidemiologic, ecologic, and cultural factors). Strict control of the growth and sale of watercress and other edible water plants is important. Individual people can protect themselves by not eating raw watercress and other water plants, especially from endemic grazing areas. Travelers to areas with poor sanitation should avoid food and water that might be contaminated (tainted). Vegetables grown in fields, that might have been irrigated with polluted water, should be thoroughly cooked, as should viscera from potentially infected animals.

Humans
Several drugs are effective for fascioliasis, both in humans and in domestic animals. The drug of choice in the treatment of fasciolosis is triclabendazole, a member of the benzimidazole family of anthelmintics. The drug works by preventing the polymerization of the molecule tubulin into the cytoskeletal structures, microtubules. Resistance of F. hepatica to triclabendazole has been recorded in Australia in 1995 and Ireland in 1998.

Praziquantel treatment is ineffective. There are case reports of nitazoxanide being successfully used in human fasciolosis treatment in Mexico. There are also reports of bithionol being used successfully.

Nitazoxanide has been found effective in trials, but is currently not recommended.

Domestic animals
Only clorsulon and albendazole are approved for use in the treatment of domestic animals in the United States, but the available flukicides used worldwide also include triclabendazole, netobimin, closantel, rafoxanide, nitroxynil, and oxyclozanide; however, this list of available drugs has some drawbacks. Closantel, nitroxynil, and oxyclozanide are not effective against young liver flukes and should only be used to treat subacute and chronic infections. Triclabendazole is effective at killing flukes of any age, but over-use has resulted in increasing resistance to this drug, so it should only be used to treat early infections, with later stages treated with other fasciolicides. The timing of treatment is critical for success, and is determined by environmental factors and analysis of the expected distribution and prevalence of the disease. For example, in European countries that have large numbers of sheep, computerized systems predict when fascioliasis is most likely to make the biggest impact on sheep populations and how many sheep will most likely be affected. The predictions are dependent on guessing when environmental conditions that are most conducive to parasite multiplication will occur, such as amount of rainfall, evapotranspiration, and the ratio of wet to dry days in a particular month. If heavy infections are expected to occur, treatment for sheep should begin in September/October, then again in January/February, and finally in April/May; the amount of hatching fluke eggs is minimal during these times because they require a warm, wet environment, making treatment more effective.

Epidemiology
Human and animal fasciolosis occurs worldwide. While animal fasciolosis is distributed in countries with high cattle and sheep production, human fasciolosis occurs, excepting Western Europe, in developing countries. Fasciolosis occurs only in areas where suitable conditions for intermediate hosts exist.

Studies carried out in recent years have shown human fasciolosis to be an important public health problem. Human fasciolosis has been reported from countries in Europe, America, Asia, Africa and Oceania. The incidence of human cases has been increasing in 51 countries of the five continents. A global analysis shows that the expected correlation between animal and human fasciolosis only appears at a basic level. High prevalences in humans are not necessarily found in areas where fasciolosis is a great veterinary problem. For instance, in South America, hyperendemics and mesoendemics are found in Bolivia and Peru where the veterinary problem is less important, while in countries such as Uruguay, Argentina and Chile, human fasciolosis is only sporadic or hypoendemic.

Europe
In Europe, human fasciolosis occur mainly in France, Spain, Portugal, and the former USSR. France is considered an important human endemic area. A total of 5863 cases of human fasciolosis were recorded from nine French hospitals from 1970 to 1982. Concerning the former Soviet Union, almost all reported cases were from the Tajik Republic. Several papers referred to human fasciolosis in Turkey. Recently, serological survey of human fasciolosis was performed in some parts of Turkey. The prevalence of the disease was serologically found to be 3.01% in Antalya Province, and between 0.9 and 6.1% in Isparta Province, Mediterranean region of Turkey. In other European countries, fasciolosis is sporadic and the occurrence of the disease is usually combined with travelling to endemic areas.

Americas
In North America, the disease is very sporadic. In Mexico, 53 cases have been reported. In Central America, fasciolosis is a human health problem in the Caribbean islands, especially in zones of Puerto Rico and Cuba. Pinar del Río Province and Villa Clara Province are Cuban regions where fasciolosis was hyperendemic. In South America, human fasciolosis is a serious problem in Bolivia, Peru, and Ecuador. These Andean countries are considered to be the area with the highest prevalence of human fasciolosis in the world. Well-known human hyperendemic areas are localized predominately in the high plain called altiplano. In the Northern Bolivian Altiplano, prevalences detected in some communities were up to 72% and 100% in coprological and serological surveys, respectively. In Peru, F. hepatica in humans occurs throughout the country. The highest prevalences were reported in Arequipa, Mantaro Valley, Cajamarca Valley, and Puno Region. In other South American countries like Argentina, Uruguay, Brazil, Venezuela and Colombia, human fasciolosis appear to be sporadic, despite the high prevalences of fasciolosis in cattle.

Africa
In Africa, human cases of fasciolosis, except in northern parts, have not been frequently reported. The highest prevalence was recorded in Egypt where the disease is distributed in communities living in the Nile Delta.

Asia
In Asia, the most human cases were reported in Iran, especially in Gīlān Province, on the Caspian Sea. It was mentioned that more than 10,000 human cases were detected in Iran. In eastern Asia, human fasciolosis appears to be sporadic. Few cases were documented in Japan, Koreas, Vietnam, and Thailand.

Australia and the Oceania
In Australia, human fasciolosis is very rare (only 12 cases documented). In New Zealand, F. hepatica has never been detected in humans.

Other animals
A number of drugs have been used in control fasciolosis in animals. Drugs differ in their efficacy, mode of action, price, and viability. Fasciolicides (drugs against Fasciola spp.) fall into five main chemical groups:
 * Halogenated phenols: bithionol (Bitin), hexachlorophene (Bilevon), nitroxynil (Trodax)
 * Salicylanilides: closantel (Flukiver, Supaverm), rafoxanide (Flukanide, Ranizole)
 * Benzimidazoles: triclabendazole (Fasinex), albendazole (Vermitan, Valbazen), mebendazol (Telmin), luxabendazole (Fluxacur)
 * Sulphonamides: clorsulon (Ivomec Plus)
 * Phenoxyalkanes: diamphenetide (Coriban)

Triclabendazole (Fasinex) is considered as the most common drug due to its high efficacy against adult as well as juvenile flukes. Triclabendazole is used in control of fasciolosis of livestock in many countries. Nevertheless, long-term veterinary use of triclabendazole has caused appearance of resistance in F. hepatica. In animals, triclabendazole resistance was first described in Australia, later in Ireland and Scotland and more recently in the Netherlands. Considering this fact, scientists have started to work on the development of new drug. Recently, a new fasciolicide was successfully tested in naturally and experimentally infected cattle in Mexico. This new drug is called 'Compound Alpha' and is chemically very similar to triclabendazole. Countries where fasciolosis in livestock was repeatedly reported:
 * Europe: UK, Ireland, France, Portugal, Spain, Switzerland, Italy, Netherlands, Germany, Poland
 * Asia: Turkey, Russia, Thailand, Iraq, Iran, China, Vietnam, India, Nepal, Japan, Korea, Philippines
 * Africa: Kenya, Zimbabwe, Nigeria, Egypt, Gambia, Morocco
 * Australia and the Oceania: Australia, New Zealand
 * Americas: United States, Mexico, Cuba, Peru, Chile, Uruguay, Argentina, Jamaica, Brazil

On September 8, 2007, Veterinary officials in South Cotabato, Philippines said that laboratory tests on samples from cows, carabaos, and horses in the province's 10 towns and lone city showed the level of infection at 89.5%, a sudden increase of positive cases among large livestock due to the erratic weather condition in the area. They must be treated forthwith to prevent complications with surra and hemorrhagic septicemia diseases. Surra already affected all barangays of the Surallah town.

title: Fasciolosis


text:
Fasciolopsiasis

Fasciolopsiasis results from an infection by the trematode Fasciolopsis buski, the largest intestinal fluke of humans, growing up to 7.5 cm long.

Signs and symptoms
Most infections are light, almost asymptomatic. In heavy infections, symptoms can include abdominal pain, chronic diarrhea, anemia, ascites, toxemia, allergic responses, sensitization caused by the absorption of the worms' allergenic metabolites can lead to intestinal obstruction and may eventually cause death of the patient.

Cause
The parasite infects an amphibic snail (Segmentina nitidella, Segmentina hemisphaerula, Hippeutis schmackerie, Gyraulus, Lymnaea, Pila, Planorbis (Indoplanorbis)) after being released by infected mammalian feces; metacercaria released from this intermediate host encyst on aquatic plants like water spinach, which are eaten raw by pigs and humans. Water itself can also be infective when drunk unboiled ("Encysted cercariae exist not only on aquatic plants, but also on the surface of the water.")

Diagnosis
Microscopic identification of eggs, or more rarely of the adult flukes, in the stool or vomitus is the basis of specific diagnosis. The eggs are indistinguishable from those of the very closely related Fasciola hepatica liver fluke, but that is largely inconsequential since treatment is essentially identical for both.

Prevention
Infection can be prevented by immersing vegetables in boiling water for a few seconds to kill the infective metacercariae, avoiding the use of untreated feces ("nightsoil") as a fertilizer, and maintenance of proper sanitation and good hygiene. Additionally, snail control should be attempted.

Treatment
Praziquantel is the drug of choice for treatment. Treatment is effective in early or light infections. Heavy infections are more difficult to treat. Studies of the effectiveness of various drugs for treatment of children with F. buski have shown tetrachloroethylene as capable of reducing faecal egg counts by up to 99%. Other anthelmintics that can be used include thiabendazole, mebendazole, levamisole and pyrantel pamoate. Oxyclozanide, hexachlorophene and nitroxynil are also highly effective.

Epidemiology
F. buski is endemic in Asia including China, Taiwan, Southeast Asia, Indonesia, Malaysia, and India. It has an up to 60% prevalence in worst-affected communities in southern and eastern India and mainland China and has an estimated 10 million human infections. Infections occur most often in school-aged children or in impoverished areas with a lack of proper sanitation systems.

A study from 1950s found that F. buski was endemic in central Thailand, affecting about 2,936 people due to infected aquatic plants called water caltrops and the snail hosts which were associated with them. The infection, or the eggs which hatch in the aquatic environment, were correlated with the water pollution in different districts of Thailand such as Ayuthaya Province. The high incidence of infection was prevalent in females and children ages 10–14 years of age.

title: Fasciolopsiasis


text:
Hunter Mutual

Hunter Mutual was a credit union based in and serving the Upper Hunter Valley of New South Wales, Australia. It was established in 1968 as the Upper Hunter Local Government Employee's Credit Union. In 1971, it changed its name to the Upper Hunter Credit Union in 1971, and following a restructure of its operations in 2004, it took on the name Hunter Mutual. During the 1990s, when many major banks closed branches in small country towns, Hunter Mutual set up new branches areas within the Upper Hunter where this occurred.

Merger
In July 2009, a proposed merger between Hunter Mutual and the New England Credit Union was announced.

During December 2009, each credit union held their annual general meeting, with a majority of members (96% of Hunter Mutual members, 93% of NECU members) voting to approve the merger. The merger took effect on 1 January 2010, with Hunter Mutual members becoming members of New England Credit Union, with the two computer systems to be merged in March, followed by the introduction of NECU's product range and fee structure. The merged entity has retained all locations. The combined company is the largest inland credit union in Australia.

The plan was that the New England and Orana Credit Union arms of NECU were to be re-branded as New England Mutual and Orana Mutual, mimicking the Hunter Mutual name. All three also had the common name of the Community Mutual Group which was later rebranded as the Regional Australia Bank.

title: Hunter Mutual


text:
Talk:Achaea

Comments
"Achaea was originally settled by Greeks of Russian stock." This has probably been entered at Wikipedia in all earnestness. Wetman 09:28, 6 Oct 2004 (UTC)

 * anon edit of April 14; originally it read Achaea was originally settled by the Greek descendants of Russian stock. Remove, of course. dab 11:29, 6 Oct 2004 (UTC)

I think a disambiguation page might be needed? There is a MUD called Achaea, which is definitely not the same as this. Thank you! Tautaula (talk) 23:30, 4 May 2013 (UTC)

Name change
This article should be spelled "Achaia". The spelling "Achaea" is understandable, since Greek ai usually becomes Latin ae, but this is only when ai is a diphthong, which it is not in "Achaia" (hence the Greek being spelled with a dieresis). Furthermore, it was spelled "Achaia", not "Achaea", in Latin and, for example, Bible translators use "Achaia". — the Man in Question (in question)  05:14, 1 July 2012 (UTC)

Requested move

 * The following discussion is an archived discussion of a requested move. Please do not modify it. Subsequent comments should be made in a new section on the talk page. Editors desiring to contest the closing decision should consider a move review. No further edits should be made to this section.

The result of the move request was: not moved. Consensus is that the current title is the most common name. Jenks24 (talk) 14:23, 14 July 2012 (UTC)

Achaea → Achaia – The correct spelling of this article is "Achaia". It is true that Greek ai usually becomes Latin ae, and as the Latin form of words is almost invariably used in English, it is understandable to think that Greek Akhaia would become Latin (and therefore English) *Achaea. However, only Greek diphthong ai becomes Latin ae; in Achaia, the Greek ai represents two separate syllables—that is why it is written with a dieresis (¨) over the iota in Greek: αΐ. This means that in Latin (and therefore English) it is spelled Achaia—which it was:. Furthermore, the spelling "Achaia" is used in all major translations of the Bible: NIVKJVESVASVNASB. (P.S. Although it may seem odd, the people were nonetheless called "Achaeans", not "Achaians".) — the Man in Question (in question)  17:16, 2 July 2012 (UTC) See also:
 * Talk:Achaea (Roman province)
 * Talk:Achaea (Hellenic Parliament constituency)
 * Talk:Achaea (ancient region)

 * Comment this is about a modern region of Greece, so whatever the Bible says has no bearing on the modern region of Greece. The Bible hasn't been revised to take into account modern regions since it was codified (for a widespread version of the Bible, it would be the King James Version, for instance) -- 70.49.127.65 (talk) 22:03, 2 July 2012 (UTC)
 * Oh, I know the Bible hasn't been modernized in most places (though sometimes in some translations it is, for example use of "Negev"). I was just giving an example of an extremely widely circulated use of the "Achaia" spelling in English. The rationale I have is that "Achaea" is not proper Latin and, therefore, not proper English. — the Man in Question (in question)  07:05, 3 July 2012 (UTC)
 * Support the modern Greek area seems to be spelled as "Achaia", but the nom's rationale is faulty. -- 70.49.127.65 (talk) 22:16, 2 July 2012 (UTC)
 * Alternate On reflection perhaps Akhaia should be used instead. It's the form used by this earthquake page, and Wolfram Alpha -- 70.49.127.65 (talk) 02:37, 5 July 2012 (UTC)
 * As in the case of Chios, Acharnes, Chalandri, Chania, Chaidari, Polichni, and Cholargos, modern Greek place names with the letter chi are transliterated ch, not kh, by the vast majority of sources, including Wikipedia. — the Man in Question (in question)  07:18, 5 July 2012 (UTC)
 * Comment Achaia should redirect to Achaea (ancient region)? In ictu oculi (talk) 05:53, 3 July 2012 (UTC)
 * Good point, perhaps it should be a disambiguation page, like Macedonia. -- 70.49.127.65 (talk) 06:52, 3 July 2012 (UTC)
 * Not sure what you mean… I am saying that all the "Achaea" forms on Wikipedia should be converted to "Achaia", as "Achaea" is just a hypercorrective fiction invented by people who were not paying close enough to the rules of Greco-Roman transcription. — the Man in Question (in question)  07:09, 3 July 2012 (UTC)
 * That the primary usage in English of "Achaea" may be the ancient region (though it might not be the common name for the ancient region), and the modern region may use some other spelling, such as "Akhaia", so that "Achaia" might need to disambiguate between the ancient region and the modern region, such as how Macedonia disambiguates between the ancient kingdom and the modern republic. -- 70.49.127.65 (talk) 02:45, 5 July 2012 (UTC)
 * Ah, I see. Let me put this as simply as I can: Achaia really, truly, is spelled Achaia in all its manifold uses and incarnations. In making this page move nomination, I was not trying to push any viewpoint about how things should or shouldn't be transliterated: Achaea is, very simply, a spelling error (like spelling America as Amarica), and I wanted to correct the spelling error that was in the name of this article. — the Man in Question (in question)  07:18, 5 July 2012 (UTC)
 * That doesn't change whether a disambiguation page should be primary, since per Macedonia, the ancient region(s) can be competitive with the modern place(s), just what spelling such a page should use. -- 70.49.127.65 (talk) 04:32, 6 July 2012 (UTC)
 * I see. Well, I don't mind too much either way, but since the current page Achaea is concerned with the modern region of Achaia, it makes sense to me that it gets the undisambiguated name. Perhaps that should be another discussion after this one is sorted out. — the Man in Question (in question)  15:38, 6 July 2012 (UTC)
 * Oppose Although the reasoning for the transliteration Achaia is correct, it would be a clear violation of Naming conventions (use English) (and probably WP:OR) to ignore that Achaea is recorded as the only or most common spelling used in English according to most or all major dictionaries and other reference works. That naming convention specifically says do not substitute a systematically transliterated name for the common English form of the name, if there is one. All major dictionaries and other reference works seem to have only Achaea or list it first. They either don't have Achaia at all or only as an alternative: Oxford, Columbia, Britannica, American Heritage, Random House, Collins, Merriam-Webster. The spelling Achaia seems to be less rare when talking about the region after about 300 AD. Britannica has 35 hits for Achaea and 9 for Achaia, and these hits seem to illustrate this trend to use Achaia for the region after 300 AD. According to MOS we should use Achaea as the article title, but we should point out that the Greek government and the EU use the transliteration Achaia and Britannica uses Achaea and in addition Akhaï´a (stress on i) for the modern Greek word. --Espoo (talk) 14:12, 7 July 2012 (UTC)
 * As I said in the nomination, "Achaeans" is the correct transliteration (Achaia vs. Achaeans is an irregular but correct form, like Canada vs. Canadians), and therefore the dictionary spelling of "Achaean" cannot be taken into account in this discussion. Nonetheless, your point is an interesting one. A quick search on Google Books shows how much more common "Achaia" is than "Achaea": Achaia Achaea. (Though this of course does not distinguish between modern and ancient Achaia.) A search of Google News shows that "Achaia" is substantially preferred over "Achaea" for the modern region by news sources: Achaia Achaea. Presumably the dictionary preference of Achaea over Achaia is a back-formation of Achaeans. Dictionaries do not choose their headwords based on the "most common spelling used in English", they choose it based on previous editions, prescriptive judgments, and comparison to competitors. Therefore, it cannot be said that a dictionary records anything as the most or least common spelling unless the dictionary actually has a not to that effect. I would think that since "Achaia" is the preferred English spelling used by the European Union (as you cited above) and the United Nations, that would outweigh dictionary glosses (as far as placenames are concerned). Since it is a common English spelling (I would strongly argue the more common English spelling), it is not "a clear violation of Naming conventions (use English)" in any way. For the sake of clarity for anyone else reading this, dictionaries that list Achaia as the second spelling after Achaea: Collins, American Heritage, Webster's New World. Dictionaries that do not list the spelling Achaia: Oxford Abridged, Random House, and Columbia. Dictionaries that only list the Achaia spelling: New American Cyclopedia (the last sentence discusses the area in modern Greece) and the Catholic Encyclopedia. Needless to say, all Bible reference works give it as Achaia and only Achaia: Easton's, Smith's, Strong's, Nave's, and the International Standard Bible Encyclopedia. And Dorling Kindersley's Eyewitness Travel (Greece: Athens & the Mainland, 2011) uses the spelling Achaia…not that that matters too much. — the Man in Question (in question)  21:53, 7 July 2012 (UTC)
 * Dictionaries do not choose their headwords based on the "most common spelling used in English", they choose it based on previous editions, prescriptive judgments, and comparison to competitors. That is clearly wrong. Modern English dictionaries most definitely base their decisions on extensive databases of actual use and do not normally resort to prescription. Let's leave out Achaian/Achaean because that would unnecessarily complicate the issue. In any case, the following is not only pure speculation but also plain wrong: Presumably the dictionary preference of Achaea over Achaia is a back-formation of Achaeans. You left out Britannica in your confusing summary and forgot to point out that your additions are outdated reference works. My summary was much clearer as already stated: All major (up-to-date) dictionaries and other reference works have only Achaea or list it first. They either don't have Achaia at all or only as an alternative spelling. Let's please leave Bible spellings out because that's a completely different world and in any case fairly irrelevant for deciding what is the most common modern English spelling. Greek official usage determines EU and UN usage, so the latter two are not independent decisions, and in any case, neither they nor Greek official usage have precedence over well-established English usage as shown in reputable sources such as Britannica etc. See Burma for an example of not following local official and UN usage. --Espoo (talk) 22:41, 7 July 2012 (UTC)
 * Well, I don't feel like arguing anymore, but what I said about dictionaries is true, unfortunately; and I left out Britannica because it did not fall under any of the categories I mentioned, seeing as it used the "Akhaia" spelling as its secondary form. And yes, the Achaean to Achaea thing was certainly pure speculation, although your claim that it's "plain wrong" is founded in nothing, whereas my suggestion was at least based on logic. All in all, I am sorry you took so much offense at my response; my summary of the dictionary sources was meant to clarify which sources actually did include "Achaia" and to remove "Achaean" from the discussion since it is spelled and subsequently transliterated differently in Greek. I leave this discussion to everyone else now. Nothing like a great debate to find the truth. — the Man in Question (in question)  22:50, 8 July 2012 (UTC)
 * Strong oppose per Espoo, WP:COMMONNAME and simple recognizability. The modern province has been named after the historical geographical region, and is largely coterminous with it. Perhaps Elis will be moved to Ilis or Ilidha, Boeotia to Voiotia, and Alexandria to Iskandariyya? These terms, regardless of their phonetic accuracy or modern usage, are familiar to any English-speaking person with a knowledge of Classical literature and civilization in their present form, and are likely to remain so in the future. Constantine  ✍  10:35, 10 July 2012 (UTC)
 * Oppose per WP:COMMONNAME. -- Necrothesp (talk) 14:13, 12 July 2012 (UTC)
 * The above discussion is preserved as an archive of a requested move. Please do not modify it. Subsequent comments should be made in a new section on this talk page or in a move review. No further edits should be made to this section.

Hatnote
I have removed the hatnote for Achaea (ancient region). The disambiguation page list multiple articles, all of which could be considered an "ancient region", including: Achaea (ancient region), Achaea Phthiotis, Achaea (Roman province) and (tendentiously) Principality of Achaea. Attempting to further direct readers to these or the dab page from Achaea (ancient region) would clutter that page unnecessarily. Bernanke's Crossbow (talk) 16:39, 26 April 2021 (UTC)

Uninformative map
The map of Achaean municipalities shows only the numbers 1–5, which is worthless without the key buried in the article below. This map should surely be replaced by one with the names given explicitly, or the key should be given as a caption. 82.44.215.181 (talk) 13:52, 6 September 2022 (UTC)

title: Talk:Achaea


text:
Congenital syphilis

Congenital syphilis is syphilis that occurs when a mother with untreated syphilis passes the infection to her baby during pregnancy or at birth. It may present in the fetus, infant, or later. Clinical features vary and differ between early onset, that is presentation before 2-years of age, and late onset, presentation after age 2-years. Infection in the unborn baby may present as poor growth, non-immune hydrops leading to premature birth or loss of the baby, or no signs. Affected newborns mostly initially have no clinical signs. They may be small and irritable. Characteristic features include a rash, fever, large liver and spleen, a runny and congested nose, and inflammation around bone or cartilage. There may be jaundice, large glands, pneumonia (pneumonia alba), meningitis, warty bumps on genitals, deafness or blindness. Untreated babies that survive the early phase may develop skeletal deformities including deformity of the nose, lower legs, forehead, collar bone, jaw, and cheek bone. There may be a perforated or high arched palate, and recurrent joint disease. Other late signs include linear perioral tears, intellectual disability, hydrocephalus, and juvenile general paresis. Seizures and cranial nerve palsies may first occur in both early and late phases. Eighth nerve palsy, interstitial keratitis and small notched teeth may appear individually or together; known as Hutchinson's triad.

It is caused by the bacterium Treponema pallidum subspecies pallidum when it infects the baby after crossing the placenta or from contact with a syphilitic sore at birth. It is not transmitted during breastfeeding unless there is an open sore on the mother's breast. The unborn baby can become infected at any time during the pregnancy. Most cases occur due to inadequate antenatal screening and treatment during pregnancy. The baby is highly infectious if the rash and snuffles are present. The disease may be suspected from tests on the mother; blood tests and ultrasound. Tests on the baby may include blood tests, CSF analysis and medical imaging. Findings may reveal anemia and low platelets. Other findings may include low sugars, proteinuria and hypopituitarism. The placenta may appear large and pale. Other investigations include testing for HIV.

Prevention is by safe sex to prevent syphilis in the mother, and early screening and treatment of syphilis in pregnancy. One intramuscular injection of benzathine penicillin G administered to a pregnant woman early in the illness can prevent congenital syphilis in her baby. Treatment of suspected congenital syphilis is with penicillin by injection; benzylpenicillin into vein, or procaine benzylpenicillin into muscle. During times of penicillin unavailability, ceftriaxone may be an alternative. Where there is penicillin allergy, antimicrobial desensitisation is an option.

Syphilis affects around one million pregnancies a year. In 2016, there were around 473 cases of congenital syphilis per 100,000 live births and 204,000 deaths from the disease worldwide. Of the 660,000 congenital syphilis cases reported in 2016, 143,000 resulted in deaths of unborn babies, 61,000 deaths of newborn babies, 41,000 low birth weights or preterm births, and 109,000 young children diagnosed with congenital syphilis. Around 75% were from the WHO's African and Eastern Mediterranean regions. Serological tests for syphilis were introduced in 1906, and it was later shown that transmission occurred from the mother.

Signs and symptoms
Untreated early syphilis infections results in a high risk of poor pregnancy outcomes, including saddle nose, lower extremity abnormalities, miscarriages, premature births, stillbirths, or death in newborns. Some infants with congenital syphilis have symptoms at birth, but many develop symptoms later. Symptoms may include rash, fever, large liver and spleen, and skeletal abnormalities. Newborns will typically not develop a primary syphilitic chancre but may present with signs of secondary syphilis (i.e. generalized body rash). Often these babies will develop syphilitic rhinitis ("snuffles"), the mucus from which is laden with the T. pallidum bacterium, and therefore highly infectious. If a baby with congenital syphilis is not treated early, damage to the bones, teeth, eyes, ears, and brain can occur.

Neurosyphilis in newborns may present as cranial nerve palsies, cerebral infarcts (strokes), seizures or eye abnormalities.

Many newborns with congenital syphilis, 55% by some estimates, do not exhibit any symptoms initially, with signs and symptoms developing days to months later.

Early
This is a subset of cases of congenital syphilis. Newborns may be asymptomatic and are only identified on routine prenatal screening. If not identified and treated, these newborns develop poor feeding and runny nose. By definition, early congenital syphilis occurs in children between 0 and 2 years old.

Late
Congenital syphilis that is diagnosed after 2 years of age, either because it was not diagnosed earlier or because it was incompletely treated, is classified as late congenital syphilis. The signs of late congenital syphilis tend to reflect early damage to developing tissues that does not become apparent until years later, such as Hutchinson's triad of Hutchinson's teeth (notched incisors), keratitis and deafness.

Symptoms include:
 * Blunted upper incisor teeth known as Hutchinson's teeth, or mulberry molars
 * Deafness from auditory nerve disease
 * Frontal bossing (prominence of the brow ridge)
 * Hard palate defect
 * Inflammation of the cornea known as interstitial keratitis
 * Protruding mandible
 * Saber shins
 * Saddle nose (collapse of the bony part of nose)
 * Short maxillae
 * Swollen knees

Treatment (with penicillin) before the development of late symptoms is essential.

Clinical signs include:
 * Abnormal bone x-rays
 * Anemia
 * Cerebral palsy
 * Du Bois sign, shortening of the little finger
 * Enlarged liver
 * Enlarged spleen
 * Frontal bossing
 * Sensorineural hearing loss
 * Higouménakis' sign, enlargement of the sternal end of clavicle in late congenital syphilis, mostly on the right-hand side
 * Hutchinson's triad, a set of symptoms consisting of deafness, Hutchinson's teeth (centrally notched, widely spaced peg-shaped upper central incisors), and interstitial keratitis (IK), an inflammation of the cornea which can lead to corneal scarring and potential blindness
 * Hydrocephalus
 * Jaundice
 * Lymph node enlargement
 * Mulberry molars (permanent first molars with multiple poorly developed cusps)
 * Musculoskeletal deformities
 * Petechiae
 * Poorly developed maxillae
 * Pseudoparalysis
 * Rhagades, linear scars at the angles of the mouth and nose result from bacterial infection of skin lesions
 * Snuffles, aka "syphilitic rhinitis", which appears similar to the rhinitis of the common cold, except it is more severe, lasts longer, often involves bloody rhinorrhea, and is often associated with laryngitis
 * Sabre shins, malformation of the tibia
 * Skin rash or other skin changes such as rhagades

Death from congenital syphilis is usually due to bleeding into the lungs.

Transmission
Syphilis may be transmitted from mother to the fetus during any stage of pregnancy. It is most commonly transmitted via cross placental transfer of Treponema pallidum bacteria from mother to the fetus during pregnancy with transmission via exposure to genital lesions during childbirth being less common. The highest rate of transmission occurs in mothers with early syphilis (infection present for less than 1 year), which is responsible for 50-70% of infections, with syphilis being present for more than 1 year thought to be responsible for about 15% of transmission. It is not transmitted during breastfeeding unless there is an open sore on the mother's breast.

Diagnosis
Direct observation of Treponema pallidum from one of the lesions in the mother or infant is diagnostic and can be carried out using dark field microscopy, direct fluorescent antibody testing or immunohistochemical staining, however these tests are not readily available in many settings. Serological testing is more commonly carried out on the mother and the infant to diagnose maternal and congenital syphilis. In the mother, a serologic diagnosis of syphilis is made using a nontreponemal test for syphilis such as the Venereal Disease Research Laboratory test (VDRL) or Rapid plasma reagin (RPR) followed by a treponemal test, such as the Treponema pallidum particle agglutination assay (TP-PA) (the sequence of testing may be reversed with a treponemal test followed by a non-treponemal test in the reverse diagnostic sequence). Positivity of both tests indicates active syphilis or previous infection that was treated. Quantitative non-treponemal tests are monitored for disease activity and response to treatment, with RPR is expected to decrease by a factor of four compared to pre-treatment levels after successful treatment of syphilis in the mother. Failure of non-treponemal titers to decrease after treatment may indicate treatment failure or re-infection. A confirmed cure in the mother does not exclude the possibility of congenital syphilis as transmission to the fetus may have occurred prior to maternal cure.

Diagnosis of congenital syphilis in the fetus is based on a combination of laboratory, imaging and physical exam findings. Ultrasound findings associated with congenital syphilis intrauterine infection (which are seen after 18 weeks gestation) include fetal hepatomegaly (enlarged liver)(seen in greater than 80% of cases), anemia (as measured by the peak systolic velocity of the middle cerebral artery)(33%), placentomegaly(an enlarged placenta)(27%), polyhydramnios (an excess of amniotic fluid in the amniotic sac)(12%) and hydrops fetalis (edema in the fetus)(10%). The absence of these ultrasound findings does not rule out congenital syphilis in the fetus. These ultrasound abnormalities usually resolve several weeks after successful treatment of syphilis in the mother.

Immunohistochemical staining or nucleic acid amplification of the amniotic fluid may also aid in the diagnosis. Diagnosis of syphilis in the neonate may be challenging as maternal treponemal antibodies (as non-treponemal titers) can cross the placenta and persist in the infant for many months after birth in the absence of neonatal syphilis, complicating the diagnosis. The passively transferred non-treponemal titers should be cleared from the infant within 15 months of birth (with most titers being cleared by 6 months), and persistently elevated titers 6 months after birth should prompt investigation into neonatal syphilis including CSF analysis for neurosyphilis. Pleocytosis, raised CSF protein level and positive CSF serology suggest neurosyphilis. CSF VDRL is 50-90% specific for neurosyphilis. 60% of newborns with congenital syphilis also have neurosyphilis. Non-treponemal titers should be monitored in the newborns every 2-3 months to ensure an adequate response to treatment.

Treatment
If a pregnant mother is identified as being infected with syphilis, treatment can effectively prevent congenital syphilis from developing in the fetus, especially if she is treated before the sixteenth week of pregnancy or at least 30 days prior to delivery. Mothers with primary syphilis can be treated with a single dose of intramuscularly injected penicillin, whereas late-latent, secondary syphilis, or disease of an unknown duration is treated with once weekly penicillin injections for three weeks. The mother's partner should also be evaluated and treated.

The fetus is at greatest risk of contracting syphilis when the mother is in the early stages of infection, but the disease can be passed at any point during pregnancy, even during delivery. An affected child can be treated using antibiotics much like an adult; however, any developmental symptoms are likely to be permanent.

The greater the duration between the infection of the mother and conception, the better the outcome for the infant including less chance of stillbirth or developing congenital syphilis.

The Centers for Disease Control and Prevention recommends treating symptomatic or babies born to an infected mother with unknown treatment status with procaine penicillin G, 50,000 U/kg dose IM a day in a single dose for 10 days. Treatment for these babies can vary on a case-by-case basis. Treatment cannot reverse any deformities, brain, or permanent tissue damage that has already occurred.

A Cochrane review found that antibiotics may be effective for serological cure but in general the evidence around the effectiveness of antibiotics for congenital syphilis is uncertain due to the poor methodological quality of the small number of trials that have been conducted.

Up to 40% of pregnant women treated for congenital syphilis will develop a Jarisch-Herxheimer reaction, which is a temporary reaction that usually occurs within a few hours of starting penicillin and resolves by 24 hours. The reaction is characterized by cramping, fever, muscle aches and a rash. Treatment is supportive and fetal heart rate monitoring is recommended.

Epidemiology
Syphilis affects around one million pregnancies a year. In 2016, there were around 473 cases of congenital syphilis per 100,000 live births and 204,000 deaths from the disease worldwide. Of the 660,000 congenital syphilis cases reported in 2016, 143,000 resulted in deaths of unborn babies, 61,000 deaths of newborn babies, 41,000 low birth weights or preterm births, and 109,000 young children diagnosed with congenital syphilis. Around 75% were from the WHO's African and Eastern Mediterranean regions.

Cases of congenital syphilis in the United States have been rising since the early 2010s. The Centers for Disease Control and Prevention (CDC) reported 918 cases for 2017, which is more than twice the yearly incidence of the preceding four years. The incidence in the United States has increased by 754% from 2012 to 2021 with a higher incidence seen in those with a lower socioeconomic status, as well as Black people, Native Americans and Native Hawaiians. Reports in 2023 show a rise of more than 900 percent in Mississippi over the preceding five years.

History
Congenital syphilis was first described in Europe during the fifteenth century by the Spanish physician Gaspar Torrella. Nineteenth century physicians held the belief that congenital syphilis was contracted from contaminated semen at time of conception. Serological tests for syphilis were introduced in 1906, and it was later shown that transmission occurred from the mother.

title: Congenital syphilis


text:
Wikipedia:Articles for deletion/Israelis and anti-Palestinian racism

 * The following discussion is an archived debate of the proposed deletion of the article below. Please do not modify it. Subsequent comments should be made on the appropriate discussion page (such as the article's talk page or in a deletion review).  No further edits should be made to this page.

The result of the debate was - merged

Israelis and anti-Palestinian racism

 * Article has been merged with Zionism and racism. The debate below applies to an older version.

Not an encyclopedic article, just a bunch of quotes that supposedly represent the nation of "Israelis". We already have Zionism and racism, but by some twisted logic, if there is an article Arabs and anti-Semitism and Islam and anti-Semitism, then an article under this title also must exist. If you're in the area, check out neigborhoods of Umm al-Fahm or Nazareth, or see Beduins or Druze who proudly serve in the IDF. Israelis are not angels and 56 years of wars take their toll. There is some racism in any human society, but this preoccupation with demonizing Israel, of all states, is disturbing. Why don't we create Jews and anti-German racism or Jews and anti-Russian racism, that would explain a lot. ←Humus sapiens←Talk 10:02, 6 Oct 2004 (UTC)

 * Keep, maybe retitle to Racism in Israel or somesuch. I agree that the current article is gawdawful (a collection of quotations does not an encyclopedia article make), but I'll see what I can do to improve it. —No-One Jones (m) 12:34, 6 Oct 2004 (UTC)
 * Further comment: this article is partially redundant with Zionism and racism. I'm not sure if they should be merged or not. —No-One Jones (m) 12:44, 6 Oct 2004 (UTC) Merge the references, the external links, and the ==Discrimination in the facts== section into Zionism and racism and redirect; ditch the quotations. —No-One Jones (m) 12:56, 7 Oct 2004 (UTC)
 * Delete, redirect to Zionism and racism. I suspect that the relationship of Zionist racism and the type of Israeli racism we're talking about are close enough that they should share an article, although concievably Zionist racism is more broad, covering said racism in the diaspora. However, I am willing to be convinced otherwise. --Improv 16:38, 6 Oct 2004 (UTC)
 * Delete and re-direct. A series of quotes mined from various random Israelis in order to put Israel in a bad light is not an encyclopedia article.  Every country has racists. Jayjg 17:14, 6 Oct 2004 (UTC)
 * Delete. Incurably POV.   — Gwalla | Talk 02:12, 7 Oct 2004 (UTC)
 * "Incurably POV" says it best. Cannibalize, however, for any worthwhile quotes with which Zionism and racism might be adorned; then not redirect, but Delete. — Bill 12:25, 7 Oct 2004 (UTC)
 * Merge and redirect – What Jayjg said. – Smyth 12:36, 7 Oct 2004 (UTC)
 * I've merged and redirected it. —No-One Jones (m) 13:03, 7 Oct 2004 (UTC)
 * Delete redirect. Ambi 03:37, 10 Oct 2004 (UTC)
 * A: Why? B: The article has been merged and we therefore need to keep the history around. —No-One Jones (m) 14:29, 10 Oct 2004 (UTC)

 * The above discussion is preserved as an archive of the debate. Please do not modify it. Subsequent comments should be made on the appropriate discussion page (such as the article's talk page or in a deletion review). No further edits should be made to this page.


text:
User talk:143.127.3.10

Nomination of Rajesh Hukku for deletion
A discussion is taking place as to whether the article Rajesh Hukku is suitable for inclusion in Wikipedia according to Wikipedia's policies and guidelines or whether it should be deleted.

The article will be discussed at Articles for deletion/Rajesh Hukku& until a consensus is reached, and anyone, including you, is welcome to contribute to the discussion. The nomination will explain the policies and guidelines which are of concern. The discussion focuses on high-quality evidence and our policies and guidelines.

Users may edit the article during the discussion, including to improve the article to address concerns raised in the discussion. However, do not remove the article-for-deletion notice from the top of the article. -- Tamzin (she/they) | o toki tawa mi. 20:37, 3 June 2021 (UTC)

title: User talk:143.127.3.10


text:
User:Dushan Jugum

One day

 * New Zealand Wikipedians' notice board
 * Wikipedia library
 * Military history Tasks
 * WP:NPR
 * Category:All orphaned articles
 * Bump the lamp

Edit

 * Assessing articles
 * Good articles
 * Copy right check
 * "Find addition/removal" (also called "WikiBlame" after a feature from the very old Source Code Control System software). If dealing with very old edits, then a manual binary search works well

Quick link

 * Deletion sorting (WP:EDITATAFD)
 * Did you know
 * http://www.javascriptkit.com/script/script2/charcount.shtml
 * HOUND
 * Recentism

Format

 * EasyTimeline
 * User:Dushan Jugum/common.js

title: User:Dushan Jugum