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You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

What is the significance of the term 'Duplicated ureter' in the medical field?

Duplicated ureter or Duplex Collecting System is a congenital condition in which the ureteric bud, the embryological origin of the ureter, splits (or arises twice), resulting in two ureters draining a single kidney. It is the most common renal abnormality, occurring in approximately 1% of the population. Pathophysiology Ureteral development begins in the human fetus around the 4th week of embryonic development. A ureteric bud, arising from the mesonephric (or Wolffian) duct, gives rise to the ureter, as well as other parts of the collective system. In the case of a duplicated ureter, the ureteric bud either splits or arises twice. In most cases, the kidney is divided into two parts, an upper and lower lobe, with some overlap due to intermingling of collecting tubules. However, in some cases the division is so complete as to give rise to two separate parts, each with its own renal pelvis and ureter. Diagnosis Prenatally diagnosed hydronephrosis (fluid-filled kidneys) suggest post-natal follow-up examination. The strongest neo-natal presentation is urinary tract infection. A hydronephrotic kidney may present as a palpable abdominal mass in the newborn, and may suggest an ectopic ureter or ureterocele. In older children, ureteral duplication may present as: Urinary tract infection - most commonly due to vesicoureteral reflux (flow of urine from the bladder into the ureter, rather than vice versa). Urinary incontinence in females occurs in cases of ectopic ureter entering the vagina, urethra or vestibule. Classification Ureteral duplication is either of: Partial I.e., the two ureters drain into the bladder via a single common ureter. Partial, or incomplete, ureteral duplication is rarely clinically significant. Complete In which the two ureters drain separately. Complete ureteral duplication may result in one ureter opening normally into the bladder, and the other being ectopic, ending in the vagina, the urethra or the vulval vestibule. These cases occur when the ureteric bud arises twice (rather than splitting). Prevalence Duplicated ureter is the most common renal abnormality, occurring in approximately 1% of the population. It occurs in about 0.7% of healthy adults and in 2% to 4% of people with urinary tract issues. Race Duplicated ureter is more common in White Americans than in African-Americans. Sex Duplicated ureter is more common in females. However, this may be due to the higher frequency of urinary tract infections in females, leading to a higher rate of diagnosis of duplicated ureter. Complications A duplicated ureter increased the risk of: Hydronephrosis Urinary tract infection (UTI) Vesicoureteral reflux Incontinence See also Ureterocele Ectopic ureter Kidney development == References ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

Could you please explain the term 'Dandy–Walker malformation' in simple language?

Dandy–Walker malformation (DWM), also known as Dandy–Walker syndrome (DWS), is a rare congenital brain malformation in which the part joining the two hemispheres of the cerebellum (the cerebellar vermis) does not fully form, and the fourth ventricle and space behind the cerebellum (the posterior fossa) are enlarged with cerebrospinal fluid. Most of those affected develop hydrocephalus within the first year of life, which can present as increasing head size, vomiting, excessive sleepiness, irritability, downward deviation of the eyes and seizures. Other, less common symptoms are generally associated with comorbid genetic conditions and can include congenital heart defects, eye abnormalities, intellectual disability, congenital tumours, other brain defects such as agenesis of the corpus callosum, skeletal abnormalities, an occipital encephalocele or underdeveloped genitalia or kidneys. It is sometimes discovered in adolescents or adults due to mental health problems.DWM is usually caused by a ciliopathic or chromosomal genetic condition, though the causative condition is only identified in around half of those diagnosed before birth and a third of those diagnosed after birth. The mechanism involves impaired cell migration and division affecting the long period of development of the cerebellar vermis. The mechanism by which hydrocephalus occurs in DWM is not yet fully understood. The condition is diagnosed by MRI or, less commonly, prenatal ultrasound. There are other malformations that can strongly resemble DWM, and disagreement exists around the criteria and classifications used for the malformation.Treatment for most involves the implantation of a cerebral shunt in infancy. This is usually inserted in the posterior fossa, but a shunt in the lateral ventricles may be used instead or in conjunction. Endoscopic third ventriculostomy (ETV) is a less invasive option for patients older than 1 year. Posterior fossa shunts are most effective (80% of the time) but carry the highest risk of complications, while ETV is least effective but has the least risk of complications. The mortality rate is roughly 15%, mostly due to complications from hydrocephalus or its treatment, which can include subdural haematomas or infection. The prognosis after successful hydrocephalus treatment is usually good but depends on any associated condition and its symptoms. Those without hydrocephalus are treated based on any associated symptoms or condition.The prevalence of DWM is estimated at between 1 in 25,000 to 1 in 50,000. DWM is the cause of around 4.3% of cases of congenital hydrocephalus and 2.5% of all cases of hydrocephalus. At least 21% of those with DWM have a sibling with the malformation, and at least 16% have a parent with the malformation. The malformation was first described by English surgeon John Bland-Sutton in 1887, though it was named by German psychiatrist Clemens Ernst Benda in 1954 after American neurosurgeons Walter Dandy and Arthur Earl Walker, who described it in 1914 and 1942, respectively. Signs and symptoms Hydrocephalus The most frequent and prominent symptoms of DWM are those associated with hydrocephalus in the postnatal period. Hydrocephalus occurs in an estimated 80% of patients with classic DWM. This usually presents within the first year of life (85% of the time), most often within the first 3 months. Signs of hydrocephalus in infants include increasing head size, vomiting, excessive sleepiness, irritability, downward deviation of the eyes (known as "sunsetting eyes") and seizures. In contrast to classic DWM, only around 30% of those with Dandy–Walker variant (DWV), in which the posterior fossa is not enlarged, have hydrocephalus. Neurological Despite the hypoplastic cerebellar vermis, just over half of individuals with DWM (between 27% and 84%) do not appear to have significant intellectual disability or developmental delay. However, many of the genetic conditions associated with DWM can present with developmental delay and other brain anomalies. Agenesis of the corpus callosum has been found in between 5% and 17% of those with DWM. This does not seem to result in intellectual disability on its own, however. Other brain abnormalities known to be sometimes associated with DWM include grey matter heterotopia, pachygyria (fewer ridges in the brain), lissencephaly (shallower ridges), polymicrogyria, holoprosencephaly and schizencephaly. Individuals with these features tend to have developmental delay or seizures. Those without any other central nervous system abnormalities tend to have normal or close-to-normal intellectual development. A 2003 review found that moderate-to-severe intellectual disability and non-DWM brain abnormalities were only present in those with the most severe cerebellar vermis malformations (less than two fissures/three lobules in the vermis), and these comprised 16% of their sample. Hydrocephalus also affected all of these patients.In Dandy–Walker variant (DWV) and mega cisterna magna specifically, which are less severe malformations, there appears to be an increased rate of psychotic spectrum disorders such as schizophrenia, bipolar disorder, mania or catatonia. Associated anomalies A 2017 review found the following associations in patients with DWS (usually from an associated genetic condition or abnormality): 27% of patients had a congenital heart defect. These included patent ductus arteriosus, coarctation of the aorta, ventricular septal defect and atrial septal defect. In 2.7% of patients, heart failure was reported. 24% of patients had at least one ocular abnormality. These included cataracts, small eyes (microphthalmia), chorioretinal dysplasia/atrophy, optic nerve dysplasia/atrophy, a small cornea (microcornea) or corneal opacity (leukoma), short-sightedness (myopia) and coloboma (a hole in an eye structure). 16% of patients were diagnosed with a mental or behavioural disorder, with 6.4% also having a learning disability. 5.3% had either bipolar disorder or a psychotic spectrum disorder, and 2.1% had ADHD. Slightly more of these were found in Dandy–Walker variant (DWV) than in classic DWM, despite DWV being less common, at only around 20% of DWS diagnoses. Around 12% of patients had cancers or tumours arising from congenital genetic abnormalities. The most common were neurocutaneous melanosis (5.9%), hemangiomas (4.8%, including those with PHACE syndrome) and Wilms tumour (4.4%). 3.2% of patients had congenital melanocytic nevi, and 2.1% had tongue hamartoma. The melanocytic tumours in these cases are thought to relate to the same genetic errors in the development of the embryonic neural tube that lead to the DWM, since the subsequent embryonic neural crest gives rise to melanocytes, among other cells. 10% of patients had endocrine or metabolic disorders, and 2.7% had excessive hair growth (hypertrichosis). 9% of patients (almost all with classic DWM) had musculoskeletal abnormalities, which included scoliosis or kyphoscoliosis and arthrogryposis. 5.9% of patients had underdeveloped reproductive organs, such as hypoplastic genitalia or undescended testicles (cryptorchidism). 5.3% of patients had underdeveloped or polycystic kidneys.Occipital encephalocele may occur in DWM. This has generally been found at rates between 6 and 8%. It has been suggested to occur to compensate for the increased pressure in the posterior fossa during foetal life.Syringomyelia occasionally occurs with DWM, though it is not certain how often. One review reported an occurrence of 4.3% in a sample. This may be due to herniation of the bottom of the cyst through the foramen magnum (a similar mechanism to Chiari malformation). Alternatively, it may be a result of hydrocephalus, in which it forms as a "fifth ventricle" due to an enlarged central canal.Rarely, spina bifida has been found with DWM. When it is present, it is usually spina bifida occulta. Cause DWM is caused by any disruption to embryonic development that affects the formation of the cerebellar vermis. This is usually a genetic mutation that results in impaired cell migration and division. A large number of genetic conditions can result in the anomaly. In a large portion of DWM cases, the condition is identified in the person affected, however in most cases the cause is not identified. At least 21% of those with DWM have a sibling with the malformation, and at least 16% have a parent with the malformation. Ciliopathic genetic conditions A genetic condition is identified in around 33% of those diagnosed with DWM after birth. In a 2017 review, 4.3% were found to have PHACE syndrome, a condition involving brain, cardiovascular and eye abnormalities, while 2.3% had Joubert syndrome, a condition involving neurological and sometimes eye and kidney abnormalities. Anywhere from 21% to 81% of those with PHACE syndrome have DWM. Other comorbid genetic conditions that were found included oculocerebrocutaneous syndrome, oral-facial-digital syndrome, Coffin–Siris syndrome, Meckel–Gruber syndrome type 7 and Kallmann syndrome, among many others. DWM has also been associated with 3C syndrome, Rubinstein–Taybi syndrome, Marden–Walker syndrome, Sheldon–Hall syndrome, Shah–Waardenburg syndrome, Fryns syndrome,< Walker–Warburg syndrome, Fukuyama congenital muscular dystrophy, Ellis–van Creveld syndrome, Fraser syndrome, Aicardi syndrome, Cornelia de Lange syndrome,< Klippel–Feil syndrome and acrocallosal syndrome, among others. Many of these disorders are classified as ciliopathies, genetic disorders that affect the cellular primary cilia, thin cell projections made from microtubules that are believed to be crucial in signalling embryonic cell division and migration. DWM is one of the single largest predictors of a ciliopathic genetic disease.Other genes that have been linked to DWM include ZIC1, ZIC4, FOXC1, FGF17, LAMC1 and NID1. Chromosomal abnormalities In those who are diagnosed with DWM before birth on ultrasound, up to half are found to have a chromosomal abnormality, with the most common being Edwards syndrome (trisomy 18), at roughly 26% of prenatal DWM cases. 6.5% of those diagnosed with DWM after birth also have Edwards syndrome. Other chromosomal abnormalities that can lead to DWM include triploidy, Patau syndrome (trisomy 13), trisomy 9 and partial 3q deletion or duplication. The 3q24 region contains the ZIC1 and ZIC4 genes, known to be associated with DWM. External toxins Warfarin use during pregnancy has been known to lead to systemic defects in the fetus, including ocular dysgenesis, microcephaly, agenesis of the corpus callosum, skeletal abnormalities and heart defects. In 1985, it was also linked to DWM. Pathophysiology The cerebellum begins forming at the fifth week of embryonic development. It differentiates at the top of the metencephalon, while the pons (in the brainstem) differentiates at the bottom, separated by the fourth ventricle. The cerebellar hemispheres form from the rhombic lips on the forward surface of the fourth ventricle, which expand and roll over to fuse in the midline to form the cerebellar vermis by the 15th week. If this process does not complete, the cerebellar vermis will not form fully. This long period of development of the cerebellar vermis makes it particularly vulnerable to disruptions.In DWM, the fourth ventricle opens up into and is continuous with almost the entire posterior fossa subarachnoid space. Pathophysiology of hydrocephalus The reason why hydrocephalus occurs in DWM is not yet fully understood. The earliest authors had put it down it to blockage or narrowing of the foramina of Magendie and Luschka, the two apertures in the fourth ventricle that allow cerebrospinal fluid (CSF) to escape into the subarachnoid space of the posterior fossa. However, later studies found that these foramina are usually open in DWM. Hydrocephalus is also usually (80% of the time) not present at birth in those with DWM.The impairment to CSF flow may lie beyond the outlets of the fourth ventricle. Theories of abnormal development or inflammation of the arachnoid mater in the posterior fossa have been put forward. The arachnoid mater contains granulations necessary to return CSF from the subarachnoid spaces to the dural veins and circulation. Excisions of the cyst in DWM have not been able to show whether impaired arachnoid absorption is involved, since the subarachnoid space always takes days to weeks to fill up following excision.Aqueductal stenosis (narrowing of the passage between the third and fourth ventricles) does not seem to be a factor in DWM. It is usually open, and shunts placed in the posterior fossa cyst almost always drain all above ventricles. When it is present, it may be the result of compression from a herniated vermis or cyst or an associated developmental abnormality.It is known that once hydrocephalus has started, the compression by the posterior fossa cyst against the venous passages in the arachnoid mater is involved in the worsening pathology. Diagnosis Dandy–Walker malformation is diagnosed based on the characteristic neuroimaging findings. It can be diagnosed prenatally on ultrasound as early as 14 weeks of gestation, although it is usually diagnosed postnatally by MRI. It is diagnosed within the first year of life 41% of the time, normally due to increasing signs of hydrocephalus, but 28% of the time it is discovered in adolescence or adulthood due to mental health problems, such as psychosis or mood disorder. Criteria and classification The precise diagnostic criteria and classification systems of DWM are not agreed upon, and significant dispute exists as to which terms or criteria should be used. The core criteria of DWM are hypoplasia of the cerebellar vermis and an enlarged fourth ventricle and posterior fossa (the space behind the cerebellum), though the specific degree of hypoplasia or cystic enlargement for diagnosis of DWM is not agreed upon. Additionally, there are several similar conditions which have at various times been grouped with DWM on a continuum by some authors and separated as distinct by others, further complicating diagnosis.In 1976, Harwood-Nash and Fitz proposed the term Dandy–Walker variant (DWV) for a malformation in which the posterior fossa is not enlarged but the cerebellar vermis is hypoplastic. In 1989, Barkovich et al. proposed the term Dandy–Walker complex (DWC) to include classic DWM and DWV (under type A) plus a third malformation (under type B) in which the cerebellar vermis remains large enough to sit between the fourth ventricle and the cisterna magna beneath it, and instead it is mostly the cisterna magna that is enlarged. In this type, the hypoplasia of the cerebellar vermis does not reach past the horizontal midline of the fourth ventricle, and the posterior fossa is also not as large. The authors noted that this form would previously have been classified as simply mega–cisterna magna. In 1999, Calabró et al. first used the phrase Dandy–Walker continuum when referring to proposals that a condition known as Blakes pouch cyst falls under the umbrella of the Dandy–Walker complex proposed by Barkovich. Later authors would put these terms and systems under intense scrutiny and state that they added considerable confusion to the diagnosis of DWM. However, they remain commonly used.In 2011, Spennato et al. came up with a set of criteria based on Klein et al. (2003) that they considered necessary for diagnosis of DWM: The lower portion of the cerebellar vermis is absent to varying degrees (three quarters, one half or one quarter missing). The posterior fossa (the space behind the cerebellum) is enlarged, and its cerebrospinal fluid flow is continuous with that of the fourth ventricle. The rest of the cerebellar vermis is hypoplastic and is pushed upwards and rotated forwards due to the enlarged posterior fossa. The cerebellar hemispheres are pushed forwards and to the side by the enlarged posterior fossa. The angle at the centre of the cerebellar vermis (representing the location of the fastigial nucleus) is large, giving a flattened appearance to the bottom of the vermis, or the fastigial nucleus is absent entirely. The confluence of sinuses, part of the drainage system located at the far rear of the occipital lobe, is elevated due to the enlarged posterior fossa. (The adjacent cerebellar tentorium is also elevated.)Due to the inconsistency of the presence of hydrocephalus in DWM, Spennato and Klein suggested that it should not be considered a criterion for DWM. Kleins criteria differed from Spennatos mainly in that it required no apparent cerebellar hemisphere hypoplasia, but it may also have required the vermis to touch the tentorium or an absence of brainstem abnormalities. Methods DWM can be observed prenatally on ultrasound as early as 14 weeks of gestation, though an MRI scan is the most useful method for diagnosis. MRI can delineate the shape and extent of the malformation as well as assessing additional areas for malformations such as the cerebellar hemispheres, cerebral aqueduct or corpus callosum. Cardiac-gated phase-contrast MRI can observe the flow of cerebrospinal fluid (CSF) during systole and diastole of the heart. In true DWM, this will find a flow from the cerebral aqueduct to the posterior fossa and no flow between the cisterna magna and the space behind the cervical spinal cord.CT may also be used if MRI is unavailable, but it provides less detail. Klein et al. (2003) suggested that a suspected diagnosis based on CT or ultrasound should not be confirmed until an MRI is performed, due to the large number of conditions that can present highly similarly and confound diagnosis. Differential diagnosis DWM has a large number of conditions that can present highly similarly on imaging and confound diagnosis. Blakes pouch cyst Blakes pouch cyst (BPC), or persistent Blakes pouch, is a condition that arises when Blakes pouch, an invagination in the fourth ventricle that ruptures at around 4 months of gestation to form the foramen of Magendie (medial aperture), fails to rupture. This can lead to a dilated fourth ventricle and subsequent hydrocephalus of all four ventricles.In a Blakes pouch cyst, unlike in DWM: The cerebellum is not hypoplastic, though it may be compressed by the enlarged posterior fossa (mass effect). The posterior fossa is not enlarged. The cerebellar tentorium/confluence of sinuses is not raised. Hydrocephalus, when it occurs, involves all four ventricles.Some authors, however, consider Blakes pouch cyst part of a continuum with DWM (the "Dandy–Walker continuum"). Mega cisterna magna Mega cisterna magna is a condition in which the cisterna magna, the subarachnoid cistern below the fourth ventricle, is enlarged. It has been proposed to be due to a delayed rupture of Blakes pouch rather than a failed rupture.In mega cisterna magna, unlike in DWM: The cerebellum is not usually hypoplastic. The fourth ventricle is of relatively normal shape. Hydrocephalus is uncommon.There is debate as to whether this malformation is distinct from DWM or forms part of the "Dandy–Walker continuum". Posterior fossa arachnoid cyst An arachnoid cyst is a collection of cerebrospinal fluid (CSF) in the arachnoid mater. 10% of these occur in the posterior fossa.In a posterior fossa arachnoid cyst, unlike in DWM: The cyst is clearly localised in a specific location separate from the fourth ventricle outlets. The cerebellum is not hypoplastic, though it may be compressed by the cyst (mass effect). The CSF flow in the cyst is not continuous with that of the fourth ventricle. Hydrocephalus, if it occurs, is due to the cyst pressing on the cerebellum and compressing the cerebral aqueduct or fourth ventricle outlets. Treatment The main immediate goal of treatment is the control of hydrocephalus and the enlarged posterior fossa cyst, as these can lead to increased intracranial pressure and brain damage. A minority of those affected do not develop hydrocephalus and are treated based on any associated symptoms or condition. Hydrocephalus/cyst For hydrocephalus or the posterior fossa cyst, shunts are the mainstay of treatment. However, those with DWM have a higher rate of shunt-related complications than other patients with hydrocephalus (mainly due to the unconventional anatomy). One explanation for a failure of a shunt to reduce intracranial pressure in DWM has been that the cyst may herniate into the foramen magnum and form a scarring adhesion at the cervical junction, preventing it from shrinking again. If this occurs, a suboccipital decompression with duraplasty may be attempted.In DWM, it is not agreed whether a shunt should be placed in the fourth ventricle (a cystoperitoneal shunt, or CP shunt), the lateral ventricles (a ventriculoperitoneal shunt, or VP shunt) or both, due to conflicting studies on whether the cerebral aqueduct is affected by the malformation. However, a CP shunt almost always drains both the fourth and lateral ventricles in DWM, and according to strict definitions of the malformation, the aqueduct should be assumed open, though imaging is important to confirm this. Many authors therefore recommend the CP shunt as the logical option. However, it is associated with a high rate of complications, including shifting and overdrainage. Overdrainage can lead to subdural haematomas, a tethered spinal cord, due to scarring, or downward herniation of the cerebral hemispheres. Spennato et al. therefore recommend a flow-regulating or anti-syphon valve. On the other hand, VP shunts have a lower rate of complications than CP shunts and are recommended initially by some. However, they are less effective in DWM, and the elevated position of the tentorium should be considered before installing a VP shunt.In patients older than 1 year, endoscopic third ventriculostomy (ETV) may be considered as the first-line treatment. This less invasive procedure creates an artificial hole in the third ventricle to allow CSF to bypass any obstruction. It cannot be used on those with brain abnormalities such as agenesis of the corpus callosum, due to the risk of CSF escaping to other brain areas. A compressed brainstem is not a contraindication, however. ETV has a more modest success rate than shunts, as the hole often closes over. It is more likely to fail in younger patients (below 1 year), and its effects on the developing brain are not yet known. Cysts posterior to the cerebellum, presenting in children younger than 5 years, have been labeled developmental retrocerebellar cysts under a new classification in relation to the proposed neuroendoscopic management.Previously, craniotomy of the posterior fossa and excision of the cystic membrane was used, which was often unsuccessful in preventing cyst reformation and carried a degree of mortality. This may still be reserved for patients with repeated shunt failures/infections. Other Treatments for any other symptoms are generally focussed on the specific condition involved and may include supported education, physical therapy or other services. Genetic counselling may be offered to parents for future conceptions. Prognosis The prognosis is first and foremost dependent on the early and successful treatment of hydrocephalus, if present. The other significant factor affecting prognosis is the presence of a comorbid genetic condition or brain anomaly.Mortality rates from DWM are roughly 15%. In a study of Dandy–Walker variant (DWV), a mortality rate of 12.5% was observed. The most common cause of death is complications from hydrocephalus or its treatment. Untreated hydrocephalus can lead to increased intracranial pressure and brain damage. Shunts used to treat DWM have a moderate-to-good success rate, but they have a higher-than-average failure rate, which can result in failure to reduce the intracranial pressure or infection, such as meningitis. Complications from overdrainage such as subdural haematomas are also possible and can lead to mortality. Shunts in the fourth ventricle (cystoperitoneal shunts, or CP shunts) have a generally high rate of successful cyst and ventricle size reduction, especially in the cyst (at least 80%). With a shunt in the lateral ventricles (ventriculoperitoneal shunt, or VP shunt), studies have generally found a roughly 50% successful cyst size reduction rate, with successful ventricle size reduction roughly two thirds of the time.Other systemic or genetic conditions are often present with DWM, and each have their own significant effect on prognosis. Epidemiology The prevalence of DWM is estimated at between 1 in 25,000 to 1 in 50,000. DWM is the cause of around 4.3% of cases of congenital hydrocephalus and 2.5% of all cases of hydrocephalus.A 2017 review found that most patients (65%) were diagnosed with either "Dandy–Walker malformation" or "Dandy–Walker syndrome", while 20% were diagnosed with "Dandy–Walker variant" and 1.1% with "mega cisterna magna". History The malformation was first described in 1887 by English surgeon John Bland-Sutton as hypoplasia of the cerebellar vermis, an enlarged posterior fossa and hydrocephalus. In 1914, American neurosurgeon Walter Dandy and American paediatrician Kenneth Blackfan described the malformation as partial or complete absence of the cerebellar vermis, an enlarged fourth ventricle and hydrocephalus. In 1942, American physician John K. Taggart and Canadian–American neurosurgeon Arthur Earl Walker detailed the phenomenon extensively, ascribing the potential cause as underdevelopment of the foramina of Luschka and Magendie, now no longer believed to be significant.The term Dandy–Walker syndrome (DWS) was introduced by German psychiatrist Clemens Ernst Benda in 1954; he also used the term Dandy–Walker malformation once. In 1976, Harwood-Nash and Fitz proposed the term Dandy–Walker variant (DWV) for a malformation in which the posterior fossa is not enlarged but the cerebellar vermis is hypoplastic. In 1989, Barkovich et al. proposed the term Dandy–Walker complex (DWC) to include classic DWM and DWV (under type A) plus a third malformation (under type B) in which the cerebellar vermis remains large enough to sit between the fourth ventricle and the cisterna magna, and instead it is mostly the cisterna magna that is enlarged (sometimes diagnosed as "mega cisterna magna"). In 1999, Calabró et al. first used the phrase Dandy–Walker continuum when referring to proposals that a condition known as Blakes pouch cyst falls under the umbrella of the Dandy–Walker complex proposed by Barkovich. These additional terms are mostly discouraged by modern authors due to additional confusion and complexity to the diagnosis of DWM. References This article incorporates public domain material from the United States Government document: "Dandy-Walker Syndrome Information Page". Further reading Metry Phaces article in the Journal of Pediatrics, July 2001 E-medicine webpage definition Dandy–Walker Malformation article from Pan Arab Journal of Neurosurgery == External links ==

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I'm encountering the term 'Phentermine/topiramate' in medical literature. What's its definition?

Phentermine/topiramate, sold under the brand name Qsymia, is a combination drug of phentermine and topiramate used to treat obesity. It is used together with dietary changes and exercise. If less than 3% weight loss is seen after 3 months it is recommended the medication be stopped. The weight loss is modest. Effects on heart related health problems or death is unclear.Common side effects include tingling, dizziness, trouble sleeping, and constipation. Serious side effects may include suicide, abuse. Use is not recommended during pregnancy. Phentermine is a stimulant and appetite suppressant. Topiramate is an anticonvulsant that has weight loss side effects. The exact mechanism of action for both drugs is unknown.Phentermine/topiramate was approved for medical use in the United States in 2012. Approval was denied in Europe, due to concerns regarding safety. Medical uses In clinical trials, people treated with the highest dose of phentermine/topiramate ER in combination with a program of diet and exercise lost 10% to 11% of their body weight compared to 1% to 2% for those who received placebo. In addition, 62% to 70% of subjects receiving the recommended dose or top dose of phentermine/topiramate ER achieved ≥5% weight reduction by week 56 (ITT-LOCF) compared to 17% to 21% of those receiving a placebo.A Cochrane review on the long-term effects of weight-reducing drugs on people with hypertension found that phentermine/topiramate reduced body weight (when compared to orlistat, and naltrexone/bupropion) and also reduced blood pressure. Adverse effects In clinical trials, the most common adverse events which occurred at a rate ≥5% and ≥1.5 times placebo included paraesthesia (tingling in fingers/toes), dizziness, altered taste, insomnia, constipation, and dry mouth.In the U.S., the drug label contains warnings for increased heart rate, suicidal behavior and ideation, glaucoma, mood and sleep disorders, creatine elevation, and metabolic acidosis. Some of these warnings are based on historical observations in epilepsy patients taking topiramate. The FDA is requiring the company to perform a post-approval cardiovascular outcomes trial, due in part to the observation of increased heart rate in some people taking the drug in clinical trials. Pregnancy Phentermine and topiramate can cause fetal harm. Data from pregnancy registries and epidemiology studies indicate that a fetus exposed to topiramate in the first trimester of pregnancy has an increased risk of oral clefts (cleft lip with or without cleft palate). If a patient becomes pregnant while taking phentermine/topiramate ER, treatment should be discontinued immediately, and the patient should be apprised of the potential hazard to a fetus. Females of reproductive potential should have a negative pregnancy test before starting phentermine/topiramate ER and monthly thereafter during phentermine/topiramate ER therapy. Females of reproductive potential should use effective contraception during phentermine/topiramate ER therapy. Risk evaluation and mitigation strategy Phentermine and topiramate was approved with a risk evaluation and mitigation strategy (REMS) program to ensure that benefits of treatment outweigh the risks. Because of the teratogenic risk associated with phentermine/topiramate ER therapy, phentermine/topiramate ER is distributed via certified pharmacies. Contraindications Phentermine/topiramate ER is contraindicated in pregnancy, glaucoma, hyperthyroidism, during or within 14 days of taking monoamine oxidase inhibitors, and in patients with hypersensitivity or idiosyncrasy to sympathomimetic amines. Phentermine/topiramate ER can cause an increase in resting heart rate. History Phentermine and topiramate was developed by Vivus, a California pharmaceutical company. In December 2009 VIVUS, Inc. submitted a new drug application (NDA) to the FDA and on March 1, 2010, VIVUS, Inc. announced that the FDA accepted the NDA for review. In October 2010, the FDA announced its decision to not approve phentermine/topiramate ER in its current form and issued a Complete Response Letter to VIVUS due to lack of long-term data and concerns about side effects including elevated heart rate, major adverse cardiovascular events, and birth defects.The FDA expressed concerns about the potential for phentermine/topiramate ER to cause birth defects and requested that Vivus assess the feasibility of analyzing existing healthcare databases to determine the historical incidence of oral cleft in offspring of women treated with topiramate for migraine prophylaxis (100 mg).In October 2011, VIVUS resubmitted the NDA to the FDA with responses to the issues addressed in the CRL. The FDA accepted the NDA in November 2011.On September 18, 2012, Qsymia became available on the US market. References External links "Phentermine mixture with topiramate". Drug Information Portal. U.S. National Library of Medicine.

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Could you please explain the term 'Palmoplantar keratoderma' in simple language?

Palmoplantar keratodermas are a heterogeneous group of disorders characterized by abnormal thickening of the stratum corneum of the palms and soles. Autosomal recessive, dominant, X-linked, and acquired forms have all been described.: 505 : 211 Types Clinically, three distinct patterns of palmoplantar keratoderma may be identified: diffuse, focal, and punctate.: 505 Diffuse Diffuse palmoplantar keratoderma is a type of palmoplantar keratoderma that is characterized by an even, thick, symmetric hyperkeratosis over the whole of the palm and sole, usually evident at birth or in the first few months of life.: 505  Restated, diffuse palmoplantar keratoderma is an autosomal dominant disorder in which hyperkeratosis is confined to the palms and soles. The two major types can have a similar clinical appearance: Diffuse epidermolytic palmoplantar keratoderma (also known as "Palmoplantar keratoderma cum degeneratione granulosa Vörner," "Vörners epidermolytic palmoplantar keratoderma", and "Vörner keratoderma") is one of the most common patterns of palmoplantar keratoderma, an autosomal dominant condition that presents within the first few months of life, characterized by a well-demarcated, symmetric thickening of palms and soles, often with a "dirty" snakeskin appearance due to underlying epidermolysis.: 506  Diffuse nonepidermolytic palmoplantar keratoderma (also known as "Diffuse orthohyperkeratotic keratoderma," "Hereditary palmoplantar keratoderma," "Keratosis extremitatum progrediens," "Keratosis palmoplantaris diffusa circumscripta," "Tylosis," "Unna–Thost disease", and "Unna–Thost keratoderma") is inherited as an autosomal dominant condition and is present from infancy, characterized by a well-demarcated, symmetric, often "waxy" keratoderma involving the whole of the palms and soles.: 506–8 : 213 Focal Focal palmoplantar keratoderma, a type of palmoplantar keratoderma in which large, compact masses of keratin develop at sites of recurrent friction, principally on the feet, although also on the palms and other sites, a pattern of calluses that may be discoid (nummular) or linear. Focal palmoplantar keratoderma with oral mucosal hyperkeratosis (also known as "Focal epidermolytic palmoplantar keratoderma," "Hereditary painful callosities," "Hereditary painful callosity syndrome," "Keratosis follicularis," "Keratosis palmoplantaris nummularis", and "Nummular epidermolytic palmoplantar keratoderma") is an autosomal dominant keratoderma that represents a clinical overlap syndrome with pachyonychia congenita type I but without the classic nail involvement.: 510 Punctate Punctate palmoplantar keratoderma is a form of palmoplantar keratoderma in which many tiny "raindrop" keratoses involve the palmoplantar surface, skin lesions which may involve the whole of the palmoplantar surface, or may be more restricted in their distribution.: 505  Type 1: Keratosis punctata palmaris et plantaris (also known as "Autosomal-dominant hereditary punctate keratoderma associated with malignancy," "Buschke–Fischer–Brauer disease," "Davis Colley disease," "Keratoderma disseminatum palmaris et plantaris," "Keratosis papulosa," "Keratoderma punctatum," "Keratodermia punctata," "Keratoma hereditarium dissipatum palmare et plantare," "Palmar and plantar seed dermatoses," "Palmar keratoses," "Papulotranslucent acrokeratoderma," "Punctate keratoderma," "Punctate keratoses of the palms and soles," and "Maculosa disseminata") is a skin condition, an autosomal dominant palmoplantar keratoderma with variable penetrance, characterized clinically by multiple, tiny, punctate keratoses over the entire palmoplantar surfaces, beginning over the lateral edge of the digits.: 509 : 212–213  It has been linked to 15q22-q24. Type 2: Spiny keratoderma (also known as "Porokeratosis punctata palmaris et plantaris," "Punctate keratoderma," and "Punctate porokeratosis of the palms and soles") is an autosomal dominant keratoderma of late onset that develops in patients aged 12 to 50, characterized by multiple tiny keratotic plugs, resembling the spines on a music box, involving the entire palmoplantar surfaces.: 509  Type 3: Focal acral hyperkeratosis (also known as "Acrokeratoelastoidosis lichenoides," and "Degenerative collagenous plaques of the hand") is a late-onset keratoderma, inherited as an autosomal dominant condition, characterized by oval or polygonal crateriform papules developing along the border of the hands, feet, and wrists.: 509  It is considered similar to Costa acrokeratoelastoidosis. Ungrouped Palmoplantar keratoderma and spastic paraplegia (also known as "Charcot–Marie–Tooth disease with palmoplantar keratoderma and nail dystrophy") is an autosomal dominant or x-linked dominant condition that begins in early childhood with thick focal keratoderma over the soles and, to a lesser extent, the palms.: 513  Palmoplantar keratoderma of Sybert (also known as "Greither palmoplantar keratoderma," "Greither syndrome," "Keratosis extremitatum hereditaria progrediens," "Keratosis palmoplantaris transgrediens et progrediens" "Sybert keratoderma," and "Transgrediens and progrediens palmoplantar keratoderma") is an extremely rare autosomal dominant keratoderma (a skin condition involving horn-like growths) with symmetric severe involvement of the whole palmoplantar surface in a glove-and-stocking distribution.: 509  It was characterized by Aloys Greither in 1952. It was characterized by Virginia Sybert in 1988. An autosomal recessive form which is known as Mal de Meleda has been described. This is associated with mutations in the Secreted Ly-6/uPAR-related protein 1 (SLURP1) gene. Striate palmoplantar keratoderma (also known as "Acral keratoderma," "Brünauer-Fuhs-Siemens type of palmoplantar keratoderma," "Focal non-epidermolytic palmoplantar keratoderma," "Keratosis palmoplantaris varians," "Palmoplantar keratoderma areata," "Palmoplantar keratoderma striata," "Wachter keratoderma,": 778, 785  and "Wachters palmoplantar keratoderma") is a cutaneous condition, an autosomal dominant keratoderma principally involving the soles with onset in infancy or the first few years of life.: 509 Type 1: 148700: DSG1 Type 2: 612908: DSP Type 3: 607654: KRT1 Carvajal syndrome (also known as "Striate palmoplantar keratoderma with woolly hair and cardiomyopathy" and "Striate palmoplantar keratoderma with woolly hair and left ventricular dilated cardiomyopathy,") is a cutaneous condition inherited in an autosomal recessive fashion, and due to a defect in desmoplakin.: 811  Striate palmoplantar keratoderma, woolly hair, and left ventricular dilated cardiomyopathy has been described in both autosomal dominant and autosomal recessive forms, but only the recessive forms have a clear association with dilated cardiomyopathy.: 513  The skin disease presents as a striate palmoplantar keratoderma with some nonvolar involvement, particularly at sites of pressure or abrasion.: 513  Scleroatrophic syndrome of Huriez (also known as "Huriez syndrome," "Palmoplantar keratoderma with scleroatrophy," "Palmoplantar keratoderma with sclerodactyly," "Scleroatrophic and keratotic dermatosis of the limbs," and "Sclerotylosis") is an autosomal dominant keratoderma with sclerodactyly present at birth with a diffuse symmetric keratoderma of the palms and soles.: 513 : 576  An association with 4q23 has been described. It was characterized in 1968. Vohwinkel syndrome (also known as "Keratoderma hereditaria mutilans," "Keratoma hereditaria mutilans," "Mutilating keratoderma of Vohwinkel",: 213  "Mutilating palmoplantar keratoderma") is a diffuse autosomal dominant keratoderma with onset in early infancy characterized by a honeycombed keratoderma involving the palmoplantar surfaces.: 512  Mild to moderate sensorineural hearing loss is often associated. It has been associated with GJB2. It was characterized in 1929. Olmsted syndrome (also known as "Mutilating palmoplantar keratoderma with periorificial keratotic plaques," "Mutilating palmoplantar keratoderma with periorificial plaques" and "Polykeratosis of Touraine") is a keratoderma of the palms and soles, with flexion deformity of the digits, that begins in infancy.: 510 : 214  Treatment with retinoids has been described. It has been associated with mutations in TRPV3. Aquagenic keratoderma, also known as acquired aquagenic palmoplantar keratoderma,: 788  transient reactive papulotranslucent acrokeratoderma, aquagenic syringeal acrokeratoderma, and aquagenic wrinkling of the palms, is a skin condition characterized by the development of white papules on the palms after water exposure.: 215  The condition causes irritation of the palms when touching certain materials after being wet, e.g., paper, cloth. An association with cystic fibrosis has been suggested. The association with cystic fibrosis suggests an increased salt content in the skin. Genetics Epidermolytic palmoplantar keratoderma has been associated with keratin 9 and keratin 16.Nonepidermolytic palmoplantar keratoderma has been associated with keratin 1 and keratin 16. Treatment Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. Currently, the condition is incurable. See also Keratoderma List of cutaneous conditions References == External links ==

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Could you provide a brief overview of 'Angular cheilitis' in a medical context?

Angular cheilitis (AC) is inflammation of one or both corners of the mouth. Often the corners are red with skin breakdown and crusting. It can also be itchy or painful. The condition can last for days to years. Angular cheilitis is a type of cheilitis (inflammation of the lips).Angular cheilitis can be caused by infection, irritation, or allergies. Infections include by fungi such as Candida albicans and bacteria such as Staph. aureus. Irritants include poorly fitting dentures, licking the lips or drooling, mouth breathing resulting in a dry mouth, sun exposure, overclosure of the mouth, smoking, and minor trauma. Allergies may include substances like toothpaste, makeup, and food. Often a number of factors are involved. Other factors may include poor nutrition or poor immune function. Diagnosis may be helped by testing for infections and patch testing for allergies.Treatment for angular cheilitis is typically based on the underlying causes along with the use of a barrier cream. Frequently an antifungal and antibacterial cream is also tried. Angular cheilitis is a fairly common problem, with estimates that it affects 0.7% of the population. It occurs most often in people in their 30s to 60s, and is also relatively common in children. In the developing world, iron, vitamin B12, and other vitamin deficiencies are a common cause. Signs and symptoms Angular cheilitis is a fairly non specific term which describes the presence of an inflammatory lesion in a particular anatomic site (i.e. the corner of the mouth). As there are different possible causes and contributing factors from one person to the next, the appearance of the lesion is somewhat variable. The lesions are more commonly symmetrically present on both sides of the mouth, but sometimes only one side may be affected. In some cases, the lesion may be confined to the mucosa of the lips, and in other cases the lesion may extend past the vermilion border (the edge where the lining on the lips becomes the skin on the face) onto the facial skin. Initially, the corners of the mouth develop a gray-white thickening and adjacent erythema (redness). Later, the usual appearance is a roughly triangular area of erythema, edema (swelling) and breakdown of skin at either corner of the mouth. The mucosa of the lip may become fissured (cracked), crusted, ulcerated or atrophied. There is not usually any bleeding. Where the skin is involved, there may be radiating rhagades (linear fissures) from the corner of the mouth. Infrequently, the dermatitis (which may resemble eczema) can extend from the corner of the mouth to the skin of the cheek or chin. If Staphylococcus aureus is involved, the lesion may show golden yellow crusts. In chronic angular cheilitis, there may be suppuration (pus formation), exfoliation (scaling) and formation of granulation tissue.Sometimes contributing factors can be readily seen, such as loss of lower face height from poorly made or worn dentures, which results in mandibular overclosure ("collapse of jaws"). If there is a nutritional deficiency underlying the condition, various other signs and symptoms such as glossitis (swollen tongue) may be present. In people with angular cheilitis who wear dentures, often there may be erythematous mucosa underneath the denture (normally the upper denture), an appearance consistent with denture-related stomatitis. Typically the lesions give symptoms of soreness, pain, pruritus (itching) or burning or a raw feeling. Causes Angular cheilitis is thought to be multifactorial disorder of infectious origin, with many local and systemic predisposing factors. The sores in angular cheilitis are often infected with fungi (yeasts), bacteria, or a combination thereof; this may represent a secondary, opportunistic infection by these pathogens. Some studies have linked the initial onset of angular cheilitis with nutritional deficiencies, especially of the B (B2-riboflavin) vitamin and iron (which causes iron deficiency anemia), which in turn may be evidence of malnutrition or malabsorption. Angular cheilitis can be a manifestation of contact dermatitis, which is considered in two groups; irritational and allergic. Infection The involved organisms are: Candida species alone (usually Candida albicans), which accounts for about 20% of cases, Bacterial species, either: Staphylococcus aureus alone, which accounts for about 20% of cases, β-hemolytic streptococci alone. These types of bacteria have been detected in between 8–15% of cases of angular cheilitis, but less commonly are they present in isolation, Or a combination of the above organisms, (a polymicrobial infection) with about 60% of cases involving both C. albicans and S. aureus.Candida can be detected in 93% of angular cheilitis lesions. This organism is found in the mouths of about 40% of healthy individuals, and it is considered by some to be normal commensal component of the oral microbiota. However, Candida shows dimorphism, namely a yeast form which is thought to be relatively harmless and a pathogenic hyphal form which is associated with invasion of host tissues. Potassium hydroxide preparation is recommended by some to help distinguish between the harmless and the pathogenic forms, and thereby highlight which cases of angular cheilitis are truly caused by Candida. The mouth may act as a reservoir of Candida that reinfects the sores at the corners of the mouth and prevents the sores from healing. A lesion caused by recurrence of a latent herpes simplex infection can occur in the corner of the mouth. This is herpes labialis (a cold sore), and is sometimes termed "angular herpes simplex". A cold sore at the corner of the mouth behaves similarly to elsewhere on the lips, and follows a pattern of vesicle (blister) formation followed by rupture leaving a crusted sore which resolves in about 7–10 days, and recurs in the same spot periodically, especially during periods of stress. Rather than utilizing antifungal creams, angular herpes simplex is treated in the same way as a cold sore, with topical antiviral drugs such as aciclovir. Irritation contact dermatitis 22% of cases of angular cheilitis are due to irritants. Saliva contains digestive enzymes, which may have a degree of digestive action on tissues if they are left in contact. The corner of the mouth is normally exposed to saliva more than any other part of the lips. Reduced lower facial height (vertical dimension or facial support) is usually caused by edentulism (tooth loss), or wearing worn down, old dentures or ones which are not designed optimally. This results in overclosure of the mandible (collapse of the jaws), which extenuates the angular skin folds at the corners of the mouth, in effect creating an intertriginous skin crease. The tendency of saliva to pool in these areas is increased, constantly wetting the area, which may cause tissue maceration and favors the development of a yeast infection. As such, angular cheilitis is more commonly seen in edentulous people (people without any teeth). It is by contrast uncommon in persons who retain their natural teeth. Angular cheilitis is also commonly seen in denture wearers. Angular cheilitis is present in about 30% of people with denture-related stomatitis. It is thought that reduced vertical dimension of the lower face may be a contributing factor in up to 11% of elderly persons with angular cheilitis and in up to 18% of denture wearers who have angular cheilitis. Reduced vertical dimension can also be caused by tooth migration, wearing orthodontic appliances, and elastic tissue damage caused by ultraviolet light exposure and smoking.Habits or conditions that keep the corners of the mouth moist might include chronic lip licking, thumb sucking (or sucking on other objects such as pens, pipes, lollipops), dental cleaning (e.g. flossing), chewing gum, hypersalivation, drooling and mouth breathing. Some consider habitual lip licking or picking to be a form of nervous tic, and do not consider this to be true angular cheilitis, instead calling it perlèche (derived from the French word pourlècher meaning "to lick ones lips"), or "factitious cheilitis" is applied to this habit. The term "cheilocandidiasis" describes exfoliative (flaking) lesions of the lips and the skin around the lips, and is caused by a superficial candidal infection due to chronic lip licking. Less severe cases occur during cold, dry weather, and is a form of chapped lips. Individuals may lick their lips in an attempt to provide a temporary moment of relief, only serving to worsen the condition.The sunscreen in some types of lip balm degrades over time into an irritant. Using expired lipbalm can initiate mild angular cheilitis, and when the person applies more lipbalm to alleviate the cracking, it only aggravates it. Because of the delayed onset of contact dermatitis and the recovery period lasting days to weeks, people typically do not make the connection between the causative agent and the symptoms. Nutritional deficiencies Several different nutritional deficiency states of vitamins or minerals have been linked to AC. It is thought that in about 25% of people with AC, iron deficiency or deficiency of B vitamins are involved. Nutritional deficiencies may be a more common cause of AC in Third World countries. Chronic iron deficiency may also cause koilonychia (spoon shaped deformity of the fingernails) and glossitis (inflammation of the tongue). It is not completely understood how iron deficiency causes AC, but it is known that it causes a degree of immunocompromise (decreased efficiency of the immune system) which may in turn allow an opportunistic infection of candida. Vitamin B2 deficiency (ariboflavinosis) may also cause AC, and other conditions such as redness of mucous membranes, magenta colored glossitis (pink inflammation of the tongue). Vitamin B5 deficiency may also cause AC, along with glossitis, and skin changes similar to seborrhoeic dermatitis around the eyes, nose and mouth. Vitamin B12 deficiency is sometimes responsible for AC, and commonly occurs together with folate deficiency (a lack of folic acid), which also causes glossitis and megaloblastic anemia. Vitamin B3 deficiency (pellagra) is another possible cause, and in which other association conditions such as dermatitis, diarrhea, dementia and glossitis can occur. Biotin (vitamin B7) deficiency has also been reported to cause AC, along with hair loss (alopecia) and dry eyes. Zinc deficiency is known to cause AC. Other symptoms may include diarrhea, alopecia and dermatitis. Acrodermatitis enteropathica is an autosomal recessive genetic disorder causing impaired absorption of zinc, and is associated with AC.In general, these nutritional disorders may be caused by malnutrition, such as may occur in alcoholism or in poorly considered diets, or by malabsorption secondary to gastrointestinal disorders (e.g. Coeliac disease or chronic pancreatitis) or gastrointestinal surgeries (e.g. pernicious anemia caused by ileal resection in Crohns disease). Systemic disorders Some systemic disorders are involved in angular cheilitis by virtue of their association with malabsorption and the creation of nutritional deficiencies described above. Such examples include people with anorexia nervosa. Other disorders may cause lip enlargement (e.g. orofacial granulomatosis), which alters the local anatomy and extenuates the skin folds at the corners of the mouth. More still may be involved because they affect the immune system, allowing normally harmless organisms like Candida to become pathogenic and cause an infection. Xerostomia (dry mouth) is thought to account for about 5% of cases of AC. Xerostomia itself has many possible causes, but commonly the cause may be side effects of medications, or conditions such as Sjögrens syndrome. Conversely, conditions which cause drooling or sialorrhoea (excessive salivation) can cause angular cheilitis by creating a constant wet environment in the corners of the mouth. About 25% of people with Down syndrome appear to have AC. This is due to relative macroglossia, an apparently large tongue in a small mouth, which may constantly stick out of the mouth causing maceration of the corners of the mouth with saliva. Inflammatory bowel diseases (such as Crohns disease or ulcerative colitis) can be associated with angular cheilitis. In Crohns, it is likely the result of malabsorption and immunosuppressive therapy which gives rise to the sores at the corner of the mouth. Glucagonomas are rare pancreatic endocrine tumors which secrete glucagon, and cause a syndrome of dermatitis, glucose intolerance, weight loss and anemia. AC is a common feature of glucagonoma syndrome. Infrequently, angular cheilitis may be one of the manifestations of chronic mucocutaneous candidiasis, and sometimes cases of oropharyngeal or esophageal candidiasis may accompany angular cheilitis. Angular cheilitis may be present in human immunodeficiency virus infection, neutropenia, or diabetes. Angular cheilitis is more common in people with eczema because their skin is more sensitive to irritants. Other conditions possibly associated include plasma cell gingivitis, Melkersson–Rosenthal syndrome, or sideropenic dysphagia (also called Plummer–Vinson syndrome or Paterson–Brown–Kelly syndrome). Drugs Several drugs may cause AC as a side effect, by various mechanisms, such as creating drug-induced xerostomia. Various examples include isotretinoin, indinavir, and sorafenib. Isotretinoin (Accutane), an analog of vitamin A, is a medication which dries the skin. Less commonly, angular cheilitis is associated with primary hypervitaminosis A, which can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed or as a result from an excess intake of vitamin A in the form of vitamin supplements. Recreational drug users may develop AC. Examples include cocaine, methamphetamine, heroin, and hallucinogens. Allergic contact dermatitis Allergic reactions may account for about 25–34% of cases of generalized cheilitis (i.e., inflammation not confined to the angles of the mouth). It is unknown how frequently allergic reactions are responsible for cases of angular cheilitis, but any substance capable of causing generalized allergic cheilitis may present involving the corners of the mouth alone. Examples of potential allergens include substances that may be present in some types of lipstick, toothpaste, acne products, cosmetics, chewing gum, mouthwash, foods, dental appliances, and materials from dentures or mercury containing amalgam fillings. It is usually impossible to tell the difference between irritant contact dermatitis and allergic contact dermatitis without a patch test. Loss of lower facial height Severe tooth wear or ill fitting dentures may cause wrinkling at the corners of the lip that creates a favorable environment for the condition. This can be corrected with onlays or crowns on the worn teeth to restore height or new dentures with "taller" teeth. The loss of vertical dimension has been associated with angular cheilitis in older individuals with an increase in facial laxity. Diagnosis Angular cheilitis is normally a diagnosis made clinically. If the sore is unilateral, rather than bilateral, this suggests a local factor (e.g., trauma) or a split syphilitic papule. Angular cheilitis caused by mandibular overclosure, drooling, and other irritants is usually bilateral.The lesions are normally swabbed to detect if Candida or pathogenic bacterial species may be present. Persons with angular cheilitis who wear dentures often also will have their denture swabbed in addition. A complete blood count (full blood count) may be indicated, including assessment of the levels of iron, ferritin, vitamin B12 (and possibly other B vitamins), and folate. Classification Angular cheilitis could be considered to be a type of cheilitis or stomatitis. Where Candida species are involved, angular cheilitis is classed as a type of oral candidiasis, specifically a primary (group I) Candida-associated lesion. This form angular cheilitis which is caused by Candida is sometimes termed "Candida-associated angular cheilitis", or less commonly, "monilial perlèche". Angular cheilitis can also be classified as acute (sudden, short-lived appearance of the condition) or chronic (lasts a long time or keeps returning), or refractory (the condition persists despite attempts to treat it). Management There are four aspects to the treatment of angular cheilitis. Firstly, potential reservoirs of infection inside the mouth are identified and treated. Oral candidiasis, especially denture-related stomatitis is often found to be present where there is angular cheilitis, and if it is not treated, the sores at the corners of the mouth may often recur. This involves having dentures properly fitted and disinfected. Commercial preparations are marketed for this purpose, although dentures may be left in dilute (1:10 concentration) household bleach overnight, but only if they are entirely plastic and do not contain any metal parts, and with rinsing under clean water before use. Improved denture hygiene is often required thereafter, including not wearing the denture during sleep and cleaning it daily. For more information, see Denture-related stomatitis. Secondly, there may be a need to increase the vertical dimension of the lower face to prevent overclosure of the mouth and formation of deep skin folds. This may require the construction of a new denture with an adjusted bite. Rarely, in cases resistant to normal treatments, surgical procedures such as collagen injections (or other facial fillers such as autologous fat or crosslinked hyaluronic acid) are used in an attempt to restore the normal facial contour. Other measures which seek to reverse the local factors that may be contributing to the condition include improving oral hygiene, stopping smoking or other tobacco habits and use of a barrier cream (e.g. zinc oxide paste) at night.Thirdly, treatment of the infection and inflammation of the lesions themselves is addressed. This is usually with topical antifungal medication, such as clotrimazole, amphotericin B, ketoconazole, or nystatin cream. Some antifungal creams are combined with corticosteroids such as hydrocortisone or triamcinolone to reduce inflammation, and certain antifungals such as miconazole also have some antibacterial action. Diiodohydroxyquinoline is another topical therapy for angular cheilitis. If Staphylococcus aureus infection is demonstrated by microbiological culture to be responsible (or suspected), the treatment may be changed to fusidic acid cream, an antibiotic which is effective against this type of bacteria. Aside from fusidic acid, neomycin, mupirocin, metronidazole, and chlorhexidine are alternative options in this scenario. Finally, if the condition appears resistant to treatment, investigations for underlying causes such as anemia or nutrient deficiencies or HIV infection. Identification of the underlying cause is essential for treating chronic cases. The lesions may resolve when the underlying disease is treated, e.g. with a course of oral iron or B vitamin supplements. Patch testing is recommended by some in cases which are resistant to treatment and where allergic contact dermatitis is suspected. Prognosis Most cases of angular cheilitis respond quickly when antifungal treatment is used. In more long standing cases, the severity of the condition often follows a relapsing and remitting course over time. The condition can be difficult to treat and can be prolonged. Epidemiology AC is a relatively common condition, accounting for between 0.7 – 3.8% of oral mucosal lesions in adults and between 0.2 – 15.1% in children, though overall it occurs most commonly in adults in the third to sixth decades of life. It occurs worldwide, and both males and females are affected. Angular cheilitis is the most common presentation of fungal and bacterial infections of the lips. Etymology The term "angular cheilitis" is from Ancient Greek, χείλος meaning lip and -itis meaning inflammation. References == External links ==

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What is the significance of the term 'Ectopic ureter' in the medical field?

Ectopic ureter (or ureteral ectopia) is a medical condition where the ureter, rather than terminating at the urinary bladder, terminates at a different site. In males this site is usually the urethra, in females this is usually the urethra or vagina. It can be associated with renal dysplasia, frequent urinary tract infections, and urinary incontinence (usually continuous drip incontinence). Ectopic ureters are found in 1 of every 2000–4000 patients, and can be difficult to diagnose, but are most often seen on CT scans.Ectopic ureter is commonly a result of a duplicated renal collecting system, a duplex kidney with 2 ureters. In this case, usually one ureter drains correctly to the bladder, with the duplicated ureter presenting as ectopic.The embryology that explains the pathology of an ectopic ureter is a cephalad origin of the ureteral bud on the mesonephric duct. With an abnormally long common excretory duct, the ureter never becomes incorporated into the bladder, and, therefore, remains ectopic. In the female, the most common locations of an ectopic ureter are the bladder neck, urethra, or Gartners duct which lies between the urethra and the anterior vaginal wall. See also Ectopia (disambiguation) References == External links ==

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I'm curious about the meaning of the medical term 'Stimulant psychosis.' Can you give me some insights?

Stimulant psychosis is a mental disorder characterized by psychotic symptoms (such as hallucinations, paranoid ideation, delusions, disorganized thinking, grossly disorganized behaviour) which involves and typically occurs following an overdose or several day binge on psychostimulants; however, it has also been reported to occur in approximately 0.1% of individuals, within the first several weeks after starting amphetamine or methylphenidate therapy. Methamphetamine psychosis, or long-term effects of stimulant use in the brain (at the molecular level), depend upon genetics and may persist for some time.The most common causative agents are substituted amphetamines, including substituted cathinones, as well as certain dopamine reuptake inhibitors such as cocaine and phenidates. Signs and symptoms The symptoms of stimulant psychosis vary depending on the drug ingested, but generally involve the symptoms of organic psychosis such as hallucinations, delusions, or paranoia. Other symptoms may include mania, erratic behavior, agitation and/or aggression. Cause Substituted amphetamines Drugs in the class of amphetamines, or substituted amphetamines, are known to induce "amphetamine psychosis" typically when chronically abused or used in high doses. In an Australian study of 309 active methamphetamine users, 18% had experienced a clinical level psychosis in the past year. Commonly abused amphetamines include methamphetamine, MDMA, 4-FA, as well as substituted cathinones like a-PVP, MDPV, and mephedrone, though a large number of other closely related compounds have been recently synthesized. Methylphenidate is sometimes incorrectly included in this class, although it is nonetheless still capable of producing stimulant psychosis. The symptoms of amphetamine psychosis include auditory and visual hallucinations, grandiosity, delusions of persecution, and delusions of reference concurrent with both clear consciousness and prominent extreme agitation. A Japanese study of recovery from methamphetamine psychosis reported a 64% recovery rate within 10 days rising to an 82% recovery rate at 30 days after methamphetamine cessation. However it has been suggested that around 5–15% of users fail to make a complete recovery in the long term. Furthermore, even at a small dose, the psychosis can be quickly reestablished. Psychosocial stress has been found to be an independent risk factor for psychosis relapse even without further substituted amphetamine use in certain cases.The symptoms of acute amphetamine psychosis are very similar to those of the acute phase of schizophrenia although in amphetamine psychosis visual hallucinations are more common and thought disorder is rare. Amphetamine psychosis may be purely related to high drug usage, or high drug usage may trigger an underlying vulnerability to schizophrenia. There is some evidence that vulnerability to amphetamine psychosis and schizophrenia may be genetically related. Relatives of methamphetamine users with a history of amphetamine psychosis are five times more likely to have been diagnosed with schizophrenia than relatives of methamphetamine users without a history of amphetamine psychosis. The disorders are often distinguished by a rapid resolution of symptoms in amphetamine psychosis, while schizophrenia is more likely to follow a chronic course.Although rare and not formally recognized, a condition known as Amphetamine Withdrawal Psychosis (AWP) may occur upon cessation of substituted amphetamine use and, as the name implies, involves psychosis that appears on withdrawal from substituted amphetamines. However, unlike similar disorders, in AWP, substituted amphetamines reduce rather than increase symptoms, and the psychosis or mania resolves with resumption of the previous dosing schedule. Cocaine Cocaine has a similar potential to induce temporary psychosis with more than half of cocaine abusers reporting at least some psychotic symptoms at some point. Typical symptoms include paranoid delusions that they are being followed and that their drug use is being watched, accompanied by hallucinations that support the delusional beliefs. Delusional parasitosis with formication ("cocaine bugs") is also a fairly common symptom.Cocaine-induced psychosis shows sensitization toward the psychotic effects of the drug. This means that psychosis becomes more severe with repeated intermittent use. Phenidates Methylphenidate and its analogues (such as ethylphenidate, 4F-MPH, and isopropylphenidate) share similar pharmacological profiles as other norepinephrine-dopamine reuptake inhibitors. Chronic abuse of methylphenidate has the potential to lead to psychosis. Similar psychiatric side effects have been reported in a study of ethylphenidate. No studies regarding psychosis and 4F-MPH or isopropylphenidate have been conducted, but given their high DAT binding and cellular uptake activity, the possibility of stimulant psychosis remains. Caffeine There is limited evidence that caffeine, in high doses or when chronically abused, may induce psychosis in normal individuals and worsen pre-existing psychosis in those diagnosed with schizophrenia. Diagnosis Differential diagnosis Though less common than stimulant psychosis, stimulants such as cocaine and amphetamines as well as the dissociative drug phencyclidine (PCP, angel dust) may also cause a theorized severe and life-threatening condition known as excited delirium. This condition manifests as a combination of delirium, psychomotor agitation, anxiety, delusions, hallucinations, speech disturbances, disorientation, violent and bizarre behavior, insensitivity to pain, elevated body temperature, and hysterical strength. Despite some superficial similarities in presentation excited delirium is a distinct (and more serious) condition than stimulant psychosis. The existence of excited delirium is currently debated. Transition to schizophrenia A 2019 systematic review and meta-analysis by Murrie et al. found that the pooled proportion of transition from amphetamine-induced psychosis to schizophrenia was 22% (5 studies, CI 14%–34%). This was lower than cannabis (34%) and hallucinogens (26%), but higher than opioid (12%), alcohol (10%) and sedative (9%) induced psychoses. Transition rates were slightly lower in older cohorts but were not affected by sex, country of the study, hospital or community location, urban or rural setting, diagnostic methods, or duration of follow-up. Treatment Treatment consists of supportive care during the acute intoxication phase: maintaining hydration, body temperature, blood pressure, and heart rate at acceptable levels until the drug is sufficiently metabolized to allow vital signs to return to baseline. Typical and atypical antipsychotics have been shown to be helpful in the early stages of treatment. However, the benzodiazepines, temazepam and triazolam at 30 mg and 0.5 mg, respectively, are highly effective if aggression, agitation, or violent behaviour is apparent. In the instance of persistent psychosis after repeated use of stimulants, there are cases in which electroconvulsive therapy has been beneficial. This is followed by abstinence from psychostimulants supported with counselling or medication designed to assist the individual preventing a relapse and the resumption of a psychotic state. See also References == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

What does the medical term 'Cardiogenic shock' encompass?

Cardiogenic shock (CS) is a medical emergency resulting from inadequate blood flow due to the dysfunction of the ventricles of the heart. Signs of inadequate blood flow include low urine production (<30 mL/hour), cool arms and legs, and altered level of consciousness. People may also have a severely low blood pressure and heart rate. Causes of cardiogenic shock include cardiomyopathic, arrhythmic, and mechanical. CS is most commonly precipitated by acute myocardial infarction. People can have combined types of shock. Treatment of cardiogenic shock depends on the cause with the initial goals to improve blood flow to the body. This can be done in a number of ways—fluid resuscitation, blood transfusions, vasopressors, and ionotropes. If cardiogenic shock is due to a heart attack, attempts to open the hearts arteries may help. An intra-aortic balloon pump or left ventricular assist device may improve matters until this can be done. Medications that improve the hearts ability to contract (positive inotropes) may help; however, it is unclear which is best and at present there is no convincing evidence supporting inotropic or vasodilating therapy to reduce mortality in hemodynamically unstable patients. Norepinephrine may be better if the blood pressure is very low whereas dopamine or dobutamine may be more useful if only slightly low. Cardiogenic shock is a condition that is difficult to fully reverse even with an early diagnosis. With that being said, early initiation of mechanical circulatory support, early percutaneous coronary intervention, inotropes, and heart transplantation may improve outcomes. Care is directed to the dysfunctional organs (dialysis for the kidneys, mechanical ventilation for lungs dysfunction).Mortality rates have been decreasing in the United States. This is likely due to the rapid identification and treatment of the CS. Some studies have suggested that this possibly related to the increased use of coronary reperfusion strategies, like heart stents. Nonetheless, the mortality rates remain high. Multi-organ failure is associated with higher rates of mortality. Signs and symptoms The presentation is the following: Anxiety, restlessness, altered mental state due to decreased blood flow to the brain and subsequent hypoxia. Low blood pressure due to decrease in cardiac output. A rapid, weak, thready pulse due to decreased circulation combined with tachycardia. Cool, clammy, and mottled skin (cutis marmorata) due to vasoconstriction and subsequent hypoperfusion of the skin. Distended jugular veins due to increased jugular venous pressure. Oliguria (low urine output) due to inadequate blood flow to the kidneys if the condition persists. Rapid and deeper respirations (hyperventilation) due to sympathetic nervous system stimulation and acidosis. Fatigue due to hyperventilation and hypoxia. Absent pulse in fast and abnormal heart rhythms. Pulmonary edema, involving fluid back-up in the lungs due to insufficient pumping of the heart. Causes Cardiogenic shock is caused by the failure of the heart to pump effectively. It is due to damage to the heart muscle, most often from a heart attack or myocardial contusion. Other causes include abnormal heart rhythms, cardiomyopathy, heart valve problems, ventricular outflow obstruction (i.e. systolic anterior motion (SAM) in hypertrophic cardiomyopathy), or ventriculoseptal defects. It can also be caused by a sudden decompressurization (e.g. in an aircraft), where air bubbles are released into the bloodstream (Henrys law), causing heart failure. Diagnosis Electrocardiogram An electrocardiogram helps to establish the exact diagnosis and guides treatment, it may reveal: Abnormal heart rhythms, such as bradycardia (slowed heart rate) myocardial infarction (ST-elevation MI, STEMI, is usually more dangerous than non-STEMIs; MIs that affect the ventricles are usually more dangerous than those that affect the atria; those affecting the left side of the heart, especially the left ventricle, are usually more dangerous than those affecting the right side, unless that side is severely compromised) Signs of cardiomyopathy Echocardiography Echocardiography may show poor ventricular function, signs of PED, rupture of the interventricular septum, an obstructed outflow tract or cardiomyopathy. Swan-Ganz catheter The Swan–Ganz catheter or pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics. Biopsy When cardiomyopathy is suspected as the cause of cardiogenic shock, a biopsy of heart muscle may be needed to make a definite diagnosis. Cardiac index If the cardiac index falls acutely below 2.2 L/min/m2, the person may be in cardiogenic shock. Treatment Depending on the type of cardiogenic shock, treatment involves infusion of fluids, or in shock refractory to fluids, inotropic medications. In case of an abnormal heart rhythm immediate synchronized cardioversion or anti-arrhythmic agents may be administered, e.g. adenosine.Positive inotropic agents (such as dobutamine or milrinone), which enhance the hearts pumping capabilities, are used to improve the contractility and correct the low blood pressure. Should that not suffice an intra-aortic balloon pump (which reduces workload for the heart, and improves perfusion of the coronary arteries) or a left ventricular assist device (which augments the pump-function of the heart) can be considered. Mechanical ventilation or ECMO may be used to help stabilize people with severe or refractory cardiogenic shock until they can be given some type of definitive treatment, such as a ventricular assist device. Finally, as a last resort, if the person is stable enough and otherwise qualifies, heart transplantation, or if not eligible an artificial heart, can be placed. These invasive measures are important tools—more than 50% of patients who do not die immediately due to cardiac arrest from a lethal abnormal heart rhythm and live to reach the hospital (who have usually experienced a severe acute myocardial infarction, which in itself still has a relatively high mortality rate), die within the first 24 hours. The mortality rate for those still living at time of admission who develop complications (among others, cardiac arrest or further abnormal heart rhythms, heart failure, cardiac tamponade, a ruptured or dissecting aneurysm, or another heart attack) from cardiogenic shock is even worse around 85%, especially without drastic measures such as ventricular assist devices or transplantation.Cardiogenic shock may be treated with intravenous dobutamine, which acts on β1 receptors of the heart leading to increased contractility and heart rate. References External links Cardiogenic Shock by eMedicine

You are a conduit for medical education. Your task is to offer detailed explanations of medical terms, ensuring they are understandable and precise.

I'd like to learn more about the medical term 'Opisthorchiasis.' Can you provide some details?

Opisthorchiasis is a parasitic disease caused by certain species of genus Opisthorchis (specifically, Opisthorchis viverrini and Opisthorchis felineus). Chronic infection may lead to cholangiocarcinoma, a cancer of the bile ducts. Medical care and loss of wages caused by Opisthorchis viverrini in Laos and in Thailand costs about $120 million annually. In Asia, infection by Opisthorchis viverrini and other liver flukes affects the poorest people. Along with other foodborne trematode infections such as clonorchiasis, fascioliasis and paragonimiasis, opisthorchiasis is listed among the World Health Organizations list of neglected tropical diseases. Signs and symptoms Symptoms of opisthorchiasis are indistinguishable from clonorchiasis. About 80% of infected people have no symptoms, though they can have eosinophilia. Asymptomatic infection can occur when there are less than 1000 eggs in one gram of feces. Infection is considered heavy when there are 10,000-30,000 eggs in one gram of feces. Symptoms of heavier infections may include diarrhea, epigastric and right upper quadrant pain, lack of appetite, fatigue, yellowing of the eyes and skin and mild fever.These parasites are long-lived and cause heavy chronic infections that may lead to accumulation of fluid in the legs (edema) and in the peritoneal cavity (ascites), enlarged non-functional gallbladder and also ascending cholangitis, which can lead to periductal fibrosis, cholecystitis and cholelithiasis, obstructive jaundice, hepatomegaly and/or portal hypertension. Chronic opisthorchiasis and cholangiocarcinoma Both experimental and epidemiological evidence strongly implicates Opisthorchis viverrini infections in the etiology of a malignant cancer of the bile ducts (cholangiocarcinoma) in humans which has a very poor prognosis. Clonorchis sinensis and Opisthorchis viverrini are both categorized by the International Agency for Research on Cancer (IARC) as Group 1 carcinogens.In humans, the onset of cholangiocarcinoma occurs with chronic opisthorchiasis, associated with hepatobiliary damage, inflammation, periductal fibrosis and/or cellular responses to antigens from the infecting fluke. These conditions predispose to cholangiocarcinoma, possibly through an enhanced susceptibility of DNA to damage by carcinogens. Chronic hepatobiliary damage is reported to be multi-factorial and considered to arise from a continued mechanical irritation of the epithelium by the flukes present, particularly via their suckers, metabolites and excreted/secreted antigens as well as immunopathological processes. In silico analyses using techniques of genomics and bioinformatics is unraveling information on molecular mechanisms that may be relevant to the development of cholangiocarcinoma.In regions where Opisthorchis viverrini is highly endemic, the incidence of cholangiocarcinoma is unprecedented. For instance, cholangiocarcinoma represents 15% of primary liver cancer worldwide, but in Thailands Khon Kaen province, this figure escalates to 90%, the highest recorded incidence of this cancer in the world. Of all cancers recorded worldwide in 2002, 0.02% were cholangiocarcinoma caused by Opisthorchis viverrini. Cancer of the bile ducts caused by opisthorchiasis occurs in the ages 25–44 years in Thailand. A few cases have appeared in later life among U.S. veterans of the Vietnam War, who consumed poorly cooked fish from streams in endemic areas near the border of Laos and Vietnam. Diagnosis The medical diagnosis is usually established by finding eggs of Opisthorchis viverrini in feces using the Kato technique. Alternatively, an antigen of Opisthorchis viverrini can be detected by ELISA test. A polymerase chain reaction test that can be performed on faeces has been developed and evaluated in a rural community in central Thailand. Prevention Cholangiocarcinoma is typically incurable at diagnosis. Because of this, intervention strategies are focused on the prevention or treatment of liver fluke infection. Prevention can be accomplished through education (by persuading people not to consume raw or undercooked fish), but the ancient cultural custom to consume raw, undercooked or freshly pickled fish persists in endemic areas. One community health program, known as the Integrated Opisthorchiasis Control Program, has achieved success in the Lawa Lakes region south of Khon Kaen.Cooking or deep-freezing (-20 °C for 7 days) of food made of fish is an effective method of prevention. Methods for prevention of Opisthorchis viverrini in aquaculture fish ponds have also been proposed. Treatment Treatment of opisthorchiasis is usually accomplished with praziquantel. A single dose of praziquantel of 40 mg/kg is effective against opisthorchiasis (and also against schistosomiasis). Despite the efficacy of this compound, the lack of acquired immunity to infection predisposes humans to reinfection in endemic regions. In addition, under experimental conditions, the treatment of Opisthorchis viverrini-infected hamsters with praziquantel induced a dispersion of parasite antigens, resulting in adverse immunopathological changes following re-infection with Opisthorchis viverrini, a process which has been proposed to initiate and/or promote the development of cholangiocarcinoma in humans. Albendazole can be used as an alternative.A randomized controlled trial published in 2011 showed that tribendimidine, a broad-spectrum anthelmintic, appears to be at least as efficacious as praziquantel. Artemisinin was also found to have anthelmintic activity against Opisthorchis viverrini. Epidemiology Opisthorchiasis is prevalent where raw cyprinid fishes are a staple of the diet. Prevalence rises with age; children under the age of 5 years are rarely infected by Opisthorchis viverrini. Males may be affected more than females. The WHO estimates that foodborne trematodiases (infection by worms or "flukes", mainly Clonorchis, Opisthorchis, Fasciola and Paragonimus species) affect 56 million people worldwide and 750 million are at risk of infection. 80 million people are at risk of opisthorchiasis (67 million from infection with Opisthorchis viverrini in Southeast Asia and 13 million from Opisthorchis felineus in Kazakhstan, Russia, and Ukraine). In the lower Mekong River basin, the disease is highly endemic, and more so in lowlands, with a prevalence up to 60% in some areas of northeast Thailand. However, estimates using polymerase chain reaction-based diagnostic techniques indicate that prevalence is probably grossly underestimated. In one study from the 1980s, a prevalence of over 90% was found in persons greater than 10 years old in a small village near Khon Kaen in northeast Thailand in the region known as Isan. Sporadic cases have been reported from Malaysia, Singapore, and the Philippines. Although the overall prevalence has declined since initial surveys performed in the 1950s, an increase has occurred since the 1990s in some areas, possibly related to large increases in aquaculture. Research Using CRISP gene editing technology in animal models, researchers have been able to eliminate the genes responsible for symptoms of opisthorchiasis, which may lead to further research toward novel treatment and control of this disease and its sequelae. References == External links ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

I'm not familiar with the medical term 'Slipped capital femoral epiphysis.' Could you provide some insights?

Slipped capital femoral epiphysis (SCFE or skiffy, slipped upper femoral epiphysis, SUFE or souffy, coxa vara adolescentium) is a medical term referring to a fracture through the growth plate (physis), which results in slippage of the overlying end of the femur (metaphysis). Normally, the head of the femur, called the capital, should sit squarely on the femoral neck. Abnormal movement along the growth plate results in the slip. The term slipped capital femoral epiphysis is actually a misnomer, because the epiphysis (end part of a bone) remains in its normal anatomical position in the acetabulum (hip socket) due to the ligamentum teres femoris. It is actually the metaphysis (neck part of a bone) which slips in an anterior direction with external rotation. SCFE is the most common hip disorder in adolescence. SCFEs usually cause groin pain on the affected side, but sometimes cause knee or thigh pain. One in five cases involves both hips, resulting in pain on both sides of the body. SCFEs occurs slightly more commonly in adolescent males, especially young black males, although it also affects females. Whilst it can occur in any child, the major risk factor is childhood obesity. Symptoms include the gradual, progressive onset of thigh or knee pain with a painful limp. Hip motion will be limited, particularly internal rotation. Running, and other strenuous activity on legs, will also cause the hips to abnormally move due to the condition and can potentially worsen the pain. Stretching is very limited. Signs and symptoms Usually, a SCFE causes groin pain, but it may cause pain in only the thigh or knee, because the pain may be referred along the distribution of the obturator nerve. The pain may occur on both sides of the body (bilaterally), as up to 40 percent of cases involve slippage on both sides. In cases of bilateral SCFEs, they typically occur within one year of each other. About 20 percent of all cases include a SCFE on both sides at the time of presentation.Signs of a SCFE include a waddling gait, decreased range of motion. Often the range of motion in the hip is restricted in internal rotation, abduction, and flexion. A person with a SCFE may prefer to hold their hip in flexion and external rotation. Complications Failure to treat a SCFE may lead to: death of bone tissue in the femoral head (avascular necrosis), degenerative hip disease (hip osteoarthritis), gait abnormalities and chronic pain. SCFE is associated with a greater risk of arthritis of the hip joint later in life. 17–47 percent of acute cases of SCFE lead to the death of bone tissue (osteonecrosis) effects. Cause In general, SCFE is caused by increased force applied across the epiphysis, or a decrease in the resistance within the physis to shearing. Obesity is the by far the most significant risk factor. A study in Scotland looked at the weight of 600,000 infants, and followed them up to see who got SCFE. This study identified that obese children had an almost twenty times greater risk than thin children, with a dose-response- so the greater the weight of the child, the greater the risk of SCFE. In 65 percent of cases of SCFE, the person is over the 95th percentile for weight. Endocrine diseases may also contribute (though are far less of a risk than obesity), such as hypothyroidism, hypopituitarism, and renal osteodystrophy.Sometimes no single cause accounts for SCFE, and several factors play a role in the development of a SCFE i.e. both mechanical and endocrine (hormone-related) factors. Skeletal changes may also make someone at risk of SCFE, including femoral or acetabular retroversion, those these may simply be chronic skeletal manifestations of childhood obesity. Pathophysiology SCFE is a Salter-Harris type 1 fracture through the proximal femoral physis. Stress around the hip causes a shear force to be applied at the growth plate. While trauma has a role in the manifestation of the fracture, an intrinsic weakness in the physeal cartilage also is present. The almost exclusive incidence of SCFE during the adolescent growth spurt indicates a hormonal role. Obesity is another key predisposing factor in the development of SCFE.The fracture occurs at the hypertrophic zone of the physeal cartilage. Stress on the hip causes the epiphysis to move posteriorly and medially. By convention, position and alignment in SCFE is described by referring to the relationship of the proximal fragment (capital femoral epiphysis) to the normal distal fragment (femoral neck). Because the physis has yet to close, the blood supply to the epiphysis still should be derived from the femoral neck; however, this late in childhood, the supply is tenuous and frequently lost after the fracture occurs. Manipulation of the fracture frequently results in osteonecrosis and the acute loss of articular cartilage (chondrolysis) because of the tenuous nature of the blood supply. Diagnosis The diagnosis is a combination of clinical suspicion plus radiological investigation. Children with a SCFE experience a decrease in their range of motion, and are often unable to complete hip flexion or fully rotate the hip inward. 20–50% of SCFE are missed or misdiagnosed on their first presentation to a medical facility. SCFEs may be initially overlooked, because the first symptom is knee pain, referred from the hip. The knee is investigated and found to be normal. The diagnosis requires x-rays of the pelvis, with anteriorposterior (AP) and frog-leg lateral views. The appearance of the head of the femur in relation to the shaft likens that of a "melting ice cream cone", visible with Kleins line. The severity of the disease can be measured using the Southwick angle. Classification Atypical/Typical Loder classification Stable Unstable, practically defined as when the patient is unable to ambulate even with crutches Temporal Acute Chronic Acute-on-chronic Radiological Grade I = 0–33% slippage Grade II = 34–50% slippage Grade III = >50% slippage Treatment The disease can be treated with external in-situ pinning or open reduction and pinning. Consultation with an orthopaedic surgeon is necessary to repair this problem. Pinning the unaffected side prophylactically is not recommended for most patients, but may be appropriate if a second SCFE is very likely.Once SCFE is suspected, the patient should be non-weight bearing and remain on strict bed rest. In severe cases, after enough rest the patient may require physical therapy to regain strength and movement back to the leg. A SCFE is an orthopaedic emergency, as further slippage may result in occlusion of the blood supply and avascular necrosis (risk of 25 percent). Almost all cases require surgery, which usually involves the placement of one or two pins into the femoral head to prevent further slippage. The recommended screw placement is in the center of the epiphysis and perpendicular to the physis. Chances of a slippage occurring in the other hip are 20 percent within 18 months of diagnosis of the first slippage and consequently the opposite unaffected femur may also require pinning.The risk of reducing this fracture includes the disruption of the blood supply to the bone. It has been shown in the past that attempts to correct the slippage by moving the head back into its correct position can cause the bone to die. Therefore the head of the femur is usually pinned as is. A small incision is made in the outer side of the upper thigh and metal pins are placed through the femoral neck and into the head of the femur. A dressing covers the wound. Epidemiology SCFE affects approximately 1–10 per 100,000 children. The incidence varies by geographic location, season of the year, and ethnicity. In eastern Japan, the incidence is 0.2 per 100,000 and in the northeastern U.S. it is about 10 per 100,000. Africans and Polynesians have higher rates of SCFE.SCFEs are most common in adolescents 11–15 years of age, and affects boys more frequently than girls (male 2:1 female). It is strongly linked to obesity, and weight loss may decrease the risk. Other risk factors include: family history, endocrine disorders, radiation / chemotherapy, and mild trauma. The left hip is more often affected than the right. Over half of cases may have involvement on both sides (bilateral). See also Legg–Calvé–Perthes syndrome – another cause of avascular necrosis of the femoral head, seen in younger children than SCFE Hip dysplasia Drehmann sign – Clinical test examining for SCFE References == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

I'm encountering the term 'Keratosis follicularis' in medical literature. What's its definition?

Keratosis follicularis may refer to: Dariers disease Focal palmoplantar keratoderma with oral mucosal hyperkeratosisSee also: Isolated dyskeratosis follicularis Keratosis follicularis spinulosa decalvans

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I've come across the term 'Epirubicin' in a medical context, but I'm not sure what it means. Can you clarify?

Epirubicin is an anthracycline drug used for chemotherapy. It can be used in combination with other medications to treat breast cancer in patients who have had surgery to remove the tumor. It is marketed by Pfizer under the trade name Ellence in the US and Pharmorubicin or Epirubicin Ebewe elsewhere. Similarly to other anthracyclines, epirubicin acts by intercalating DNA strands. Intercalation results in complex formation which inhibits DNA and RNA synthesis. It also triggers DNA cleavage by topoisomerase II, resulting in mechanisms that lead to cell death. Binding to cell membranes and plasma proteins may be involved in the compounds cytotoxic effects. Epirubicin also generates free radicals that cause cell and DNA damage. Epirubicin is favoured over doxorubicin, the most popular anthracycline, in some chemotherapy regimens as it appears to cause fewer side-effects. Epirubicin has a different spatial orientation of the hydroxyl group at the 4 carbon of the sugar - it has the opposite chirality - which may account for its faster elimination and reduced toxicity. Epirubicin is primarily used against breast and ovarian cancer, gastric cancer, lung cancer and lymphomas. Medical uses Adjuvant therapy The aim of Epirubicin as adjuvanted therapy is to eradicate micro metastasis and prolong disease free survival. Vs standard adjuvant therapy The Standard adjuvant therapy is a combination of cyclophosphamide, methotrexate and fluorouracil (CMF). In comparison to this the Epirubicin therapy contains fluorouracil/epirubicin/cyclophosphamide (FEC). Three large randomized studies have directly compared the epirubicin-containing regimen fluorouracil/epirubicin/cyclophosphamide (FEC) with CMF in the adjuvant setting. Trial one and two contained premenopausal node-positive women with breast cancer, Trial three pre- and postmenopausal women with node-positive or negative breast cancer. It was discovered that FEC is at least as effective as CMF in premenopausal women with node positive- or negative breast cancer and that FEC produced no additional benefit in terms of 5-year relapse-free or overall survival. Dose response Researchers discovered a benefit for epirubicin 100 mg (FEC 100) over epirubicin 50 mg (FEC 50). Patients with FEC100 treatment of the study were relapse-free and an overall survival rate at 5 years higher as in FEC 50 treatment. They also compared epirubicin 90 mg/m2 (EC 90) with epirubicin 120 mg/m2 (EC 120). After a mean follow up of 27 months elapse-free survival of patients who received EC 120 was significantly longer than that of patients who received EC 90. The combination of Epirubicin and tamoxifen lead to an increase survival in node-positive postmenopausal women with hormone receptor-positive breast tumours. Advanced breast cancer First-line therapy Epirubicin monotherapy was shown to be therapeutically equivalent to doxorubicin monotherapy in patients who had to receive previous chemotherapy for advanced breast cancer. There are several Combination therapies: 1. FEC: fluorouracil + cyclophosphamide + epirubicin; 2. FAC: fluorouracil + cyclophosphamide + doxorubicin. The median survival rates markedly better than those achieved with epirubicin monotherapy. Additionally the FEC treatment seems to be less toxic. Second-line therapy Patients with advanced breast cancer who experience disease progression after first-line therapy may respond to subsequent chemotherapy regimens; however, response rates and durations are generally lower than those seen after initial treatment with these regimens (FEC and FAC). Dose escalation A reduced dose intensity leads to reduced response rates . Equimolar doses of epirubicin and doxorubicin have been shown to be therapeutically equivalent in patients with metastatic breast cancer. Additionally the administration of more dose intensive epirubicin-containing regimens to patients with metastatic breast cancer has been associated with improved response rates, but not increased overall survival. It is suggested that it is necessary to at least double the dose of chemotherapy to detect a clinically relevant effect. Pharmacology Mechanism of action The mechanism of action of epirubicin is similar to that of doxorubicin and other anthracycline drugs. The observed clinical differences between epirubicin and doxorubicin can be explained by the pharmacokinetic differences based on the different affinity to DNA and lipophilicity, as there is no indication that different mechanisms are involved in their activity.Epirubicin first forms a complex with DNA by intercalation of its planar rings between nucleotide base pairs. (Pharmacia & Upjohn Company LLC, 1999) This inhibits replication and transcription and triggers DNA cleavage by topoisomerase II. Epirubicin then stabilizes the topoisomerase II-DNA complex, resulting in irreversible DNA strand breakage, leading to cell death. Epirubicin is also capable of generating cytotoxic free radicals, which are very reactive against DNA, cell membranes and mitochondria.Epirubicin exhibits activity in all phases of the cell cycle, but maximal cell kill occurs during the S and G2 phases of the cell cycle. Pharmacokinetics The pharmacokinetic properties of epirubicin can be described by a 3-compartment model, with half-lives for the initial (alpha), intermediate (beta) and terminal (gamma) elimination phases of approximately 3 minutes, 1 hour and 30 hours, respectively. Only the latter differs substantially compared to doxorubicin, as the terminal elimination half-life of doxorubicin is estimated to be approximately 40-70% longer than that of epirubicin. The pharmacokinetics of epirubicin appear to be linear for doses in the range of 40 – 150 mg/m2.The volume of distribution of epirubicin is found to be high and variable (1 000- 1 500), but similar to those reported for doxorubicin. This indicates extensive distribution into the tissue. The total plasma clearance of epirubicin is approximately 45 to 50 L/h/m2, which is almost 2-fold higher than that of doxorubicin. Area under the plasma concentration versus time curve values (adjusted for dose) are 1.3 to 1.7 times higher for doxorubicin than epirubicin following single-dose intravenous administration. Epirubicin shows a 77% binding to plasma proteins, predominantly albumin, which is not affected by drug concentration. Metabolism Epirubicin is rapidly metabolized by the liver to relatively or totally inactive metabolites: epirubicinol, 2 glucuronides and 4 aglycones. As plasma levels of epirubicinol are lower than those of the unchanged drug and the metabolite has an in vitro cytotoxic activity 10% of that of epirubicin, it is unlikely to reach in vivo concentration sufficient for cytotoxicity. No significant toxicity has been reported for the other metabolites. Epirubicinol is the 13(S)-dihydro derivative formed via the reduction of the C-13 keto-group. Both the unchanged drug and epirubicinol can be conjugated with glucuronic acid, creating the 2 glucuronides. This glucuronidation pathway is unique to epirubicin metabolism in humans as epirubicin is the only anthracycline that serves as a substrate for beta-glucuronidation. This unique pathway might explain the better tolerability of this drug compared with doxorubicin.The 4 aglycones are formed by losing the amino sugar moiety through a hydrolytic process or redox process, creating the doxorubicin and doxorubicinol aglycones and 7-deoxy-doxorubicin and 7-deoxy-doxorubicinol aglycones, respectively. Excretion Epirubicin and its metabolites are primarily eliminated through biliary excretion. About 11 to 15% of the administered dose is eliminated as an unchanged drug, which makes up 6 to 7% of the excreted compounds, and metabolites. Side effects The most common side effects of the Epirubicin are alopecia, nausea/vomiting, cardiotoxicity, leukopenia, and stomatitis. Cardiotoxicity is a severe side effect and the exact pathway is still unknown. However, there is good evidence to suggest that cardiotoxicity is caused at least in part by the avid interaction of anthracyclines with iron, resulting in the formation of metal ion complexes. It was first observed in adult cancer patients as clinical congestive heart failure (CHF), characterized by pulmonary oedema, fluid overload, and effort intolerance, was initially reported in 1979 by Von Hoff et al. at 2.2% overall with a cumulative doxorubicin dose-dependent incidence of CHF of 3%, 7%, and 18% at 400, 550, and 700 mg/m2, respectively.There are a lot of adverse effects of epirubicin related with the dose-limiting. The major commun negative effects are fever, diarrhea, nausea and vomiting. More than 50% of patients without a right prophylactic antiemetics therapy experience nausea and vomiting the first 24 h after administration. That fact occurs if the epirubicin dose is between 50 to 75 mg/m2 single doses.Reversible alopecia and local cutaneous reactions are important adverse effects too. Those could be related with radiation recall and local reactions such as cellulitis, which cause development of tissue necrosis and pain if extravasation damage occurs.Another major adverse effects are cumulative dose-related cardiotoxicity and acute dose-limiting haematotoxicity. This last is related to mucositis, inflammation and ulceration in mouth or mucous membranes.Finally, the most adverse effect is secondary leukemia produced by breast cancer treated with epirubicin, particularly in those cases in which the patient receives concomitant alkylating agent therapy. Toxicity Epirubicins toxicity is according to the NCI-CTEP Common Toxicity Criteria, version 2.0. In some studies, patient toxicity reviews were obtained by a diary with the important information before and after each cycle of chemotherapy and their consequences.Common toxicities are neutropenia (<1 × 109 cells/L) without any death related and in lesser mesures anemia and thrombocytopenia.The most acute dose-limiting toxicity of epirubicin is bone marrow suppression, irreversible cardiotoxicity such as an important chronic cumulative dose-limiting toxicity illness and myelosuppression. The last one is associated with leukopenia, the decrease in the number of leukocytes (white blood cells) in the blood. Chemistry Epirubicin is a 4-epi-isomer of doxorubicin and a derivative of daunorubicin. As an anthracycline antibiotic it belongs to several chemical classes such as: aminoglycosides, tetracene quinones, p-quinones, primary alpha-hydroxy ketone and tertiary alpha-hydroxy ketones. Due to numerous ionisable groups, it has multiple pka (pKa1 = 9.17 (phenol); pKa2 = 9.93 (amine); pKa3 = 12.67 (hydroxyl)) and is soluble in a variety of solvents (DMSO 125 mg/mL; Ethanol 120 mg/mL; In water, 93 mg/L at 25 °C (est)). It has a melting point of 344.53 and a boiling point of 810.3±65.0 °C at 760 mmHg.Its shelf life (def. as the time it takes to degrade 10% from the initial concentration) has been documented as at least 14 and 180 days at 25 °C and 4 °C, respectively in a 0.9% sodium chloride solution in polypropylene syringes. Synthesis There are multiple ways of synthesizing epirubicin depending on which starting material is used as a precursor. Daunorubicin One pathway starts from Daunorubicin, a common byproduct found in fermentation, since it is relatively easily available and already structurally similar to the product (only requiring minor alterations). Firstly, the amine group is protected using trifluoroacetic acid to stop it from further reactions. Next the hydroxyl group needs to be changed from an equatorial position to an axial, this is achieved by firstly oxidizing an intermediate sulfoxy salt to a keto group (losing the optical center) followed by a stereo-specific reduction using sodium borohydride to give the hydroxide group in the axial position. Secondly, the focus shifts to carbon number 13 where it is necessary to add a hydroxide group which is achieved by bromination followed by a reaction with an alkali salt of formic acid and water to give the final product. There is an older variant of this pathway which involves first splitting the Daunorubicin, into daunomycin one and daunosamine methyl ether, using methanol. Analogous reactions are performed to get the two hydroxyl groups onto their positions and the rings are then recombined and the protecting groups released. The drawbacks are more chemicals are used and daunomycin one and daunosamine need to be separated first. 13-daunorubicinol The second pathway startsfrom 13-daunorubicinol (hydroxyl group on carbon 13 instead of Daunorubicins keto group). Firstly, the amine group is protected using trifluoroacetic acid then both the hydroxyl groups at positions 4 and 13 are oxidized simultaneously to keto groups again using DMSO, but a different alkylating agent. The reduction to alcohol is performed with a derivative of a borohydride of an alkali metal with formula MHBL3, where M=Li, Na, K; L=AlkO, AlkCOO, ArCOO. The subsequent halogenation is performed with a complex halogenating agent where an H or a chain of up to 4 carbons is combined with Cl, I or Br. The final hydrolysis is analogous to the one in the first pathway. Development history The first trial of epirubicin in humans was published in 1980. Upjohn applied for approval by the U.S. Food and Drug Administration (FDA) in node-positive breast cancer in 1984, but was turned down because of lack of data. In 1999 Pharmacia (who had by then merged with Upjohn) received FDA approval for the use of epirubicin as a component of adjuvant therapy in node-positive patients. Patent protection for epirubicin expired in August 2007. == References ==

You serve as a guide in the medical field. Explain medical terms thoroughly, ensuring the information is both insightful and comprehensible.

I'm seeking clarification on the medical term 'Pelvic kidney.' Could you explain it?

A pelvic kidney, also known as an ectopic kidney, is a normal kidney located in the pelvis, instead of the abdomen. This occurs when a kidney does not ascend from its original location in the pelvis to its final location during prenatal development. They usually present no symptoms, but can increase risk of certain illnesses and healthcare problems. Signs and symptoms Often, a person with a pelvic kidney will go through their whole life not even knowing they have a pelvic kidney. Complications Typically, the kidney functions normally despite being in the wrong location. However, it can develop complications. A pelvic kidney can make it more difficult to diagnose kidney infections and kidney cancer. The renal artery and the renal vein may be stretched if they remain attached to the normal locations on the abdominal aorta and the inferior vena cava, which can lead to illness. Causes In the development of the human embryo, the metanephric kidneys fail to ascend and usually remain at the brim of the pelvis. This clinical scenario may present no signs or symptoms and the kidneys may function normally. It is associated at times with Mullerian dysgenesis. Diagnosis A pelvic kidney is discovered on newborn kidney ultrasound screening. It may also be detected if complications arise later in life for this or a completely different reason, and during investigations. Epidemiology Between 1 in 2,200 and 1 in 3,000 people may have a pelvic kidney. History A pelvic kidney is also known as an ectopic kidney. == References ==

You are a conduit for medical education. Your task is to offer detailed explanations of medical terms, ensuring they are understandable and precise.

What is the significance of the term 'Mediastinal shift' in the medical field?

Mediastinal shift is the deviation of the mediastinal structures towards one side of the chest cavity, usually seen on chest radiograph. It indicates a severe asymmetry of intrathoracic pressures. Mediastinal shift may be caused by volume expansion on one side of the thorax, volume loss on one side of the thorax, mediastinal masses and vertebral or chest wall abnormalities. An emergent condition classically presenting with mediastinal shift is tension pneumothorax. It is also a useful indicator of malignant pleural effusion.Mediastinal shift may be detected on antenatal ultrasound in certain fetal conditions. == References ==

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I've come across the term 'Mazzotti reaction' in a medical context, but I'm not sure what it means. Can you clarify?

The Mazzotti reaction, first described in 1948, is a symptom complex seen in patients after undergoing treatment of nematode infestation, particularly with the medication diethylcarbamazine (DEC). Mazzotti reactions can be life-threatening, and are characterized by fever, urticaria, swollen and tender lymph nodes, tachycardia, hypotension, arthralgias, oedema, and abdominal pain that occur within seven days of treatment of microfilariasis. The Mazzotti reaction correlates with intensity of infection; however, there are probably multiple infection intensity-dependent mechanisms responsible for mediating this complex reaction.The phenomenon is so common when DEC is used for the treatment of onchocerciasis that this drug is the basis of a skin patch test used to confirm that diagnosis. The drug patch is placed on the skin, and if the patient is infected with the microfilaria of O. volvulus, localized pruritus and urticaria are seen at the application site. A case of the Mazzotti reaction has been reported after presumptive treatment of schistosomiasis and strongyloidiasis with ivermectin, praziquantel and albendazole. The patient had complete resolution of symptoms after intravenous therapy with methylprednisolone. == References ==

You act as a bridge between medical jargon and everyday language. Explain medical terms in a manner that is comprehensive yet approachable for non-experts.

Could you provide a brief overview of 'Child sexual abuse' in a medical context?

Child sexual abuse (CSA), also called child molestation, is a form of child abuse in which an adult or older adolescent uses a child for sexual stimulation. Forms of child sexual abuse include engaging in sexual activities with a child (whether by asking or pressuring, or by other means), indecent exposure (of the genitals, female nipples, etc.), child grooming, and child sexual exploitation, such as using a child to produce child pornography.Child sexual abuse can occur in a variety of settings, including home, school, or work (in places where child labor is common). Child marriage is one of the main forms of child sexual abuse; UNICEF has stated that child marriage "represents perhaps the most prevalent form of sexual abuse and exploitation of girls". The effects of child sexual abuse can include depression, post-traumatic stress disorder, anxiety, complex post-traumatic stress disorder, propensity to further victimization in adulthood, and physical injury to the child, among other problems. Sexual abuse by a family member is a form of incest and can result in more serious and long-term psychological trauma, especially in the case of parental incest.The global prevalence of child sexual abuse has been estimated at 19.7% for females and 7.9% for males. Most sexual abuse offenders are acquainted with their victims; approximately 30% are relatives of the child, most often brothers, fathers, uncles, or cousins; around 60% are other acquaintances, such as "friends" of the family, babysitters, or neighbors; strangers are the offenders in approximately 10% of child sexual abuse cases. Most child sexual abuse is committed by men; studies on female child molesters show that women commit 14% to 40% of offenses reported against boys and 6% of offenses reported against girls.The word pedophile is commonly applied indiscriminately to anyone who sexually abuses a child, but child sexual offenders are not pedophiles unless they have a strong sexual interest in prepubescent children. Under the law, child sexual abuse is often used as an umbrella term describing criminal and civil offenses in which an adult engages in sexual activity with a minor or exploits a minor for the purpose of sexual gratification. The American Psychological Association states that "children cannot consent to sexual activity with adults", and condemns any such action by an adult: "An adult who engages in sexual activity with a child is performing a criminal and immoral act which never can be considered normal or socially acceptable behavior." Effects Psychological Child sexual abuse can result in both short-term and long-term harm, including psychopathology in later life. Indicators and effects include depression, anxiety, eating disorders, poor self-esteem, somatization, sleep disturbances, and dissociative and anxiety disorders including post-traumatic stress disorder. While children may exhibit regressive behaviours such as thumb sucking or bedwetting, the strongest indicator of sexual abuse is sexual acting out and inappropriate sexual knowledge and interest. Victims may withdraw from school and social activities and exhibit various learning and behavioural problems including cruelty to animals, attention deficit/hyperactivity disorder (ADHD), conduct disorder, and oppositional defiant disorder (ODD). Teenage pregnancy and risky sexual behaviors may appear in adolescence. Child sexual abuse victims report almost four times as many incidences of self-inflicted harm. Sexual assault among teenagers has been shown to lead to an increase in mental health problems, social exclusion and worse school performance. A well-documented, long-term negative effect is repeated or additional victimization in adolescence and adulthood. A causal relationship has been found between childhood sexual abuse and various adult psychopathologies, including crime and suicide, in addition to alcoholism and drug abuse. Males who were sexually abused as children more frequently appear in the criminal justice system than in a clinical mental health setting. A study comparing middle-aged women who were abused as children with non-abused counterparts found significantly higher health care costs for the former. Intergenerational effects have been noted, with the children of victims of child sexual abuse exhibiting more conduct problems, peer problems, and emotional problems than their peers.A specific characteristic pattern of symptoms has not been identified, and there are several hypotheses about the causality of these associations.Studies have found that 51% to 79% of sexually abused children exhibit psychological symptoms. The risk of harm is greater if the abuser is a relative, if the abuse involves intercourse or attempted intercourse, or if threats or force are used. The level of harm may also be affected by various factors such as penetration, duration and frequency of abuse, and use of force. The social stigma of child sexual abuse may compound the psychological harm to children, and adverse outcomes are less likely for abused children who have supportive family environments. Posttraumatic stress disorder Child abuse, including sexual abuse, especially chronic abuse starting at early ages, has been found to be related to the development of high levels of dissociative symptoms, which includes amnesia for abuse memories. When severe sexual abuse (penetration, several perpetrators, lasting more than one year) had occurred, dissociative symptoms were even more prominent. Recent research showed that females with high exposure to child sexual abuse (CSA) develop PTSD symptoms that are associated with poor social functioning, which is also supported by prior research studies. The feeling of being "cut-off" from peers and "emotional numbness" are both results of CSA and highly inhibit proper social functioning. Furthermore, PTSD is associated with higher risk of substance abuse as a result of the "self-medication hypothesis" and the "high-risk and susceptibility hypothesis." Prolonged exposure therapy (PE) was found to decrease PTSD and depressive symptoms in female methadone using CSA survivors.Besides dissociative identity disorder (DID), posttraumatic stress disorder (PTSD), and complex post-traumatic stress disorder (C-PTSD), child sexual abuse survivors may present borderline personality disorder (BPD) and eating disorders such as bulimia nervosa. Research factors Because child sexual abuse often occurs alongside other possibly confounding variables, such as poor family environment and physical abuse, some scholars argue it is important to control for those variables in studies which measure the effects of sexual abuse. In a 1998 review of related literature, Martin and Fleming state "The hypothesis advanced in this paper is that, in most cases, the fundamental damage inflicted by child sexual abuse is due to the childs developing capacities for trust, intimacy, agency and sexuality, and that many of the mental health problems of adult life associated with histories of child sexual abuse are second-order effects." Other studies have found an independent association of child sexual abuse with adverse psychological outcomes.Kendler et al. (2000) found that most of the relationship between severe forms of child sexual abuse and adult psychopathology in their sample could not be explained by family discord, because the effect size of this association decreased only slightly after they controlled for possible confounding variables. Their examination of a small sample of CSA-discordant twins also supported a causal link between child sexual abuse and adult psychopathology; the CSA-exposed subjects had a consistently higher risk for psychopathologic disorders than their CSA non-exposed twins.A 1998 meta-analysis by Bruce Rind et al. generated controversy by suggesting that child sexual abuse does not always cause pervasive harm, that girls were more likely to be psychologically harmed than boys, that some college students reported such encounters as positive experiences and that the extent of psychological damage depends on whether or not the child described the encounter as "consensual." The study was criticized for flawed methodology and conclusions. The US Congress condemned the study for its conclusions and for providing material used by pedophile organizations to justify their activities. Physical Injury Depending on the age and size of the child, and the degree of force used, child sexual abuse may cause internal lacerations and bleeding. In severe cases, damage to internal organs may occur, which, in some cases, may cause death. Infections Child sexual abuse may cause infections and sexually transmitted diseases. Due to a lack of sufficient vaginal fluid, chances of infections can heighten depending on the age and size of the child. Vaginitis has also been reported. Neurological damage Research has shown that traumatic stress, including stress caused by sexual abuse, causes notable changes in brain functioning and development. Various studies have suggested that severe child sexual abuse may have a deleterious effect on brain development. Ito et al. (1998) found "reversed hemispheric asymmetry and greater left hemisphere coherence in abused subjects;" Teicher et al. (1993) found that an increased likelihood of "ictal temporal lobe epilepsy-like symptoms" in abused subjects; Anderson et al. (2002) recorded abnormal transverse relaxation time in the cerebellar vermis of adults sexually abused in childhood; Teicher et al. (1993) found that child sexual abuse was associated with a reduced corpus callosum area; various studies have found an association of reduced volume of the left hippocampus with child sexual abuse; and Ito et al. (1993) found increased electrophysiological abnormalities in sexually abused children.Some studies indicate that sexual or physical abuse in children can lead to the overexcitation of an undeveloped limbic system. Teicher et al. (1993) used the "Limbic System Checklist-33" to measure ictal temporal lobe epilepsy-like symptoms in 253 adults. Reports of child sexual abuse were associated with a 49% increase to LSCL-33 scores, 11% higher than the associated increase of self-reported physical abuse. Reports of both physical and sexual abuse were associated with a 113% increase. Male and female victims were similarly affected.Navalta et al. (2006) found that the self-reported math Scholastic Aptitude Test scores of their sample of women with a history of repeated child sexual abuse were significantly lower than the self-reported math SAT scores of their non-abused sample. Because the abused subjects verbal SAT scores were high, they hypothesized that the low math SAT scores could "stem from a defect in hemispheric integration." They also found a strong association between short-term memory impairments for all categories tested (verbal, visual, and global) and the duration of the abuse. Incest Incest between a child or adolescent and a related adult is known as child incestuous abuse, and has been identified as the most widespread form of child sexual abuse with a highly significant capacity to damage the young person. One researcher stated that more than 70% of abusers are immediate family members or someone very close to the family. Another researcher stated that about 30% of all perpetrators of sexual abuse are related to their victim, 60% of the perpetrators are family acquaintances, like a neighbor, babysitter or friend and 10% of the perpetrators in child sexual abuse cases are strangers. A child sexual abuse offense where the perpetrator is related to the child, either by blood or marriage, is a form of incest described as intrafamilial child sexual abuse.The most-often reported form of incest is father–daughter and stepfather–stepdaughter incest, with most of the remaining reports consisting of mother/stepmother–daughter/son incest. Father–son incest is reported less often; however, it is not known if the actual prevalence is less or it is under-reported by a greater margin. Similarly, some argue that sibling incest may be as common, or more common, than other types of incest: Goldman and Goldman reported that 57% of incest involved siblings; Finkelhor reported that over 90% of nuclear family incest involved siblings; while Cawson et al. show that sibling incest was reported twice as often as incest perpetrated by fathers/stepfathers.Prevalence of parental child sexual abuse is difficult to assess due to secrecy and privacy; some estimates state that 20 million Americans have been victimized by parental incest as children. Types Child sexual abuse includes a variety of sexual offenses, including: sexual assault – a term defining offenses in which an adult uses a minor for the purpose of sexual gratification; for example, rape (including sodomy), and sexual penetration with an object. Most U.S. states include, in their definitions of sexual assault, any penetrative contact of a minors body, however slight, if the contact is performed for the purpose of sexual gratification. sexual exploitation – a term defining offenses in which an adult victimizes a minor for advancement, sexual gratification, or profit; for example, prostituting a child, live streaming sexual abuse, and creating or trafficking in child pornography. sexual grooming – a term defining the social conduct of a potential child sex offender who seeks to make a minor more accepting of their advances, for example in an online chat room. Commercial sexual exploitation Commercial sexual exploitation of children (CSEC) is defined by the Declaration of the First World Congress against Commercial Sexual Exploitation of Children, held in Stockholm in 1996, as "sexual abuse by an adult accompanied by remuneration in cash or in kind to the child or third person(s)." CSEC usually takes the form of child prostitution or child pornography, and is often facilitated by child sex tourism. CSEC is particularly a problem in developing countries of Asia. In recent years, new innovations in technology have facilitated the trade of Internet child pornography.In the United Kingdom, the term child sexual exploitation covers any form of sexual abuse which includes an exchange of a resource for sexual activity with a child. Prior to 2009, the term commonly used to describe child sexual exploitation was child prostitution. The term child sexual exploitation first appeared in government guidance in 2009 as part of an attempt to promote an understanding that children involved in exploitation were victims of abuse rather than criminals. Because early definitions of child sexual exploitation were created to foster a move away from use of the term child prostitution, the concept of exchange, which made child sexual exploitation different from child sexual abuse, referred to financial gain only. However, in the years since the birth of the concept of child sexual exploitation, the notion of exchange has been widened to include other types of gain, including love, acquisition of status and protection from harm. Disclosure Children who received supportive responses following disclosure had less traumatic symptoms and were abused for a shorter period of time than children who did not receive support. In general, studies have found that children need support and stress-reducing resources after disclosure of sexual abuse. Negative social reactions to disclosure have been found to be harmful to the survivors well-being. One study reported that children who received a bad reaction from the first person they told, especially if the person was a close family member, had worse scores as adults on general trauma symptoms, post traumatic stress disorder symptoms, and dissociation. Another study found that in most cases when children did disclose abuse, the person they talked to did not respond effectively, blamed or rejected the child, and took little or no action to stop the abuse. Non-validating and otherwise non-supportive responses to disclosure by the childs primary attachment figure may indicate a relational disturbance predating the sexual abuse that may have been a risk factor for the abuse, and which can remain a risk factor for its psychological consequences.The American Academy of Child and Adolescent Psychiatry provides guidelines for what to say to the victim and what to do following the disclosure. Asa Don Brown has indicated: "A minimization of the trauma and its effects is commonly injected into the picture by parental caregivers to shelter and calm the child. It has been commonly assumed that focusing on childrens issues too long will negatively impact their recovery. Therefore, the parental caregiver teaches the child to mask his or her issues."In many jurisdictions, abuse that is suspected, not necessarily proven, requires reporting to child protection agencies, such as the Child Protection Services in the United States. Recommendations for healthcare workers, such as primary care providers and nurses, who are often suited to encounter suspected abuse are advised to firstly determine the childs immediate need for safety. A private environment away from suspected abusers is desired for interviewing and examining. Leading statements that can distort the story are avoided. As disclosing abuse can be distressing and sometimes even shameful, reassuring the child that he or she has done the right thing by telling and that they are not bad and that the abuse was not their fault helps in disclosing more information. Anatomically correct dolls are sometimes used to help explain what happened, although some researchers consider the dolls too explicit and overstimulating, which might contribute to non-abused children behaving with the dolls in one or more ways that suggest they were sexually abused. For the suspected abusers, it is also recommended to use a nonjudgmental, nonthreatening attitude towards them and to withhold expressing shock, in order to help disclose information. Treatment The initial approach to treating a person who has been a victim of sexual abuse is dependent upon several important factors: Age at the time of presentation Circumstances of presentation for treatment Co-morbid conditionsThe goal of treatment is not only to treat current mental health issues, and trauma related symptoms, but also to prevent future ones. Children and adolescents Children often present for treatment in one of several circumstances, including criminal investigations, custody battles, problematic behaviors, and referrals from child welfare agencies.The three major modalities for therapy with children and adolescents are family therapy, group therapy, and individual therapy. Which course is used depends on a variety of factors that must be assessed on a case-by-case basis. For instance, treatment of young children generally requires strong parental involvement and can benefit from family therapy. Adolescents tend to be more independent; they can benefit from individual or group therapy. The modality also shifts during the course of treatment; for example, group therapy is rarely used in the initial stages, as the subject matter is very personal and/or embarrassing. In a 2012 systematic review, cognitive behavior therapy showed potential in treating the adverse consequences of child sexual abuse.Major factors that affect both the pathology and response to treatment include the type and severity of the sexual act, its frequency, the age at which it occurred, and the childs family of origin. Roland C. Summit, a medical doctor, defined the different stages the victims of child sexual abuse go through, called child sexual abuse accommodation syndrome. He suggested that children who are victims of sexual abuse display a range of symptoms that include secrecy, helplessness, entrapment, accommodation, delayed and conflicted disclosure and recantation. Adults Adults who have been sexually abused as children often present for treatment with a secondary mental health issue, which can include substance abuse, eating disorders, personality disorders, depression, and conflict in romantic or interpersonal relationships.Generally, the approach is to focus on the present problem, rather than the abuse itself. Treatment is highly varied and depends on the persons specific issues. For instance, a person with a history of sexual abuse and severe depression would be treated for depression. However, there is often an emphasis on cognitive restructuring due to the deep-seated nature of the trauma. Some newer techniques such as eye movement desensitization and reprocessing (EMDR) have been shown to be effective.Although there is no known cure for pedophilia, there are a number of treatments for pedophiles and child sexual abusers. Some of the treatments focus on attempting to change the sexual preference of pedophiles, while others focus on keeping pedophiles from committing child sexual abuse, or on keeping child sexual abusers from committing child sexual abuse again. Cognitive behavioral therapy (CBT), for example, aims to reduce attitudes, beliefs, and behaviors that may increase the likelihood of sexual offenses against children. Its content varies widely between therapists, but a typical program might involve training in self-control, social competence and empathy, and use cognitive restructuring to change views on sex with children. The most common form of this therapy is relapse prevention, where the patient is taught to identify and respond to potentially risky situations based on principles used for treating addictions.The evidence for cognitive behavioral therapy is mixed. A 2012 Cochrane Review of randomized trials found that CBT had no effect on risk of reoffending for contact sex offenders. Meta-analyses in 2002 and 2005, which included both randomized and non-randomized studies, concluded that CBT reduced recidivism. There is debate over whether non-randomized studies should be considered informative. More research is needed.Sexual abuse is associated with many sub-clinical behavioral issues as well, including re-victimization in the teenage years, a bipolar-like switching between sexual compulsion and shut-down, and distorted thinking on the subject of sexual abuse (for instance, that it is common and happens to everyone). When first presenting for treatment, the patient can be fully aware of their abuse as an event, but their appraisal of it is often distorted, such as believing that the event was unremarkable (a form of isolation). Frequently, victims do not make the connection between their abuse and their present pathology. Prevention Child sexual abuse prevention programmes were developed in the United States of America during the 1970s. Some programme are delivered to children and can include one-to-one work and group work. Programmes delivered to parents were developed in the 1980s and took the form of one-off meetings, two to three hours long. In the last 15 years, web-based programmes have been developed. School-based education programs were evaluated in 2015 by Cochrane that demonstrated improvements in protective behaviors and knowledge among children. Offenders Demographics Offenders are more likely to be relatives or acquaintances of their victim than strangers. A 2006–07 Idaho study of 430 cases found that 82% of juvenile sex offenders were known to the victims (acquaintances 46% or relatives 36%).More offenders are male than female, though the percentage varies between studies. The percentage of incidents of sexual abuse by female perpetrators that come to the attention of the legal system is usually reported to be between 1% and 4%. Studies of sexual misconduct in US schools with female offenders have shown mixed results with rates between 4% to 43% of female offenders. Maletzky (1993) found that, of his sample of 4,402 convicted child sex offenders, 0.4% were female.According to research conducted in Australia by Kelly Richards on child sexual abuse, 35.1% of female victims were abused by another male relative and 16.4% of male victims were abused by another male relatives. Male relatives were found to be the most relevant predators in the case of both gender.In U.S. schools, educators who offend range in age from "21 to 75 years old, with an average age of 28".According to C.E. Dettmeijer-Vermeulen, Dutch national spokeswoman on human traffic and sexual violence against children, in the Netherlands, 3% of the convicted perpetrators are women, 14.58% of the victims are boys and "most victims were abused by a family member, friend or acquaintance." One in six perpetrators are underage. Typology Early research in the 1970s and 1980s began to classify offenders based on their motivations and traits. Groth and Birnbaum (1978) categorized child sexual offenders into two groups, "fixated" and "regressed". Fixated were described as having a primary attraction to children, whereas regressed had largely maintained relationships with other adults, and were even married. This study also showed that adult sexual orientation was not related to the sex of the victim targeted, e.g. men who molested boys often had adult relationships with women.Later work (Holmes and Holmes, 2002) expanded on the types of offenders and their psychological profiles. They are divided as follows: Situational – does not prefer children, but offend under certain conditions. Regressed – Typically has relationships with adults, but a stressor causes them to seek children as a substitute. Morally Indiscriminate – All-around sexual deviant, who may commit other sexual offenses unrelated to children. Naive/Inadequate – Often mentally disabled in some way, finds children less threatening. Preferential – has true sexual interest in children. Mysoped – Sadistic and violent, target strangers more often than acquaintances. Fixated – Little or no activity with own age, described as an "overgrown child". Causal factors Causal factors of child sex offenders are not known conclusively. The experience of sexual abuse as a child was previously thought to be a strong risk factor, but research does not show a causal relationship, as the vast majority of sexually abused children do not grow up to be adult offenders, nor do the majority of adult offenders report childhood sexual abuse. The US Government Accountability Office concluded, "the existence of a cycle of sexual abuse was not established." Before 1996, there was greater belief in the theory of a "cycle of violence", because most of the research done was retrospective—abusers were asked if they had experienced past abuse. Even the majority of studies found that most adult sex offenders said they had not been sexually abused during childhood, but studies varied in terms of their estimates of the percentage of such offenders who had been abused, from 0 to 79 percent. More recent prospective longitudinal research—studying children with documented cases of sexual abuse over time to determine what percentage become adult offenders—has demonstrated that the cycle of violence theory is not an adequate explanation for why people molest children.Offenders may use cognitive distortions to facilitate their offenses, such as minimization of the abuse, victim blaming, and excuses. Pedophilia Pedophilia is a condition in which an adult or older adolescent is primarily or exclusively attracted to prepubescent children, whether the attraction is acted upon or not. A person with this paraphilia is called a pedophile. In law enforcement, the term pedophile is sometimes used to describe those accused or convicted of child sexual abuse under sociolegal definitions of child (including both prepubescent children and adolescents younger than the local age of consent); however, not all child sexual offenders are pedophiles and not all pedophiles engage in sexual abuse of children. For these reasons, researchers recommend against imprecisely describing all child molesters as pedophiles.The term pedocriminality (De: Pädokriminalität; Fr: pédocriminalité) is a controversial term which originated in the 1980s and has been used by organisations such as UNICEF, UNHRC, the World Health Organization and the Council of Europe to refer to child sexual abuse and sexual violence used against children, child prostitution, child trafficking and the use of child pornography. The term "cyber-pedocriminality" has been used to refer to the activities of viewers of child pornography online. Recidivism Although reconviction data suggest that not many sex offenders reoffend, OJP reported that observed recidivism rates of sex offenders are underestimated of actual reoffending. Estimated rates among child sex offenders vary by surveys and it is difficult to estimate accurately. One study found that 42% of offenders re-offended (either a sex crime, violent crime, or both) after they were released. Risk for re-offense was highest in the first 6 years after release, but continued to be significant even 10–31 years later, with 23% offending during this time. A study done in California in 1965 found an 18.2% recidivism rate for offenders targeting the opposite sex and a 34.5% recidivism rate for same-sex offenders after 5 years.Because recidivism is defined and measured differently from study to study, one can arrive at inaccurate conclusions being made based on comparison of two or more studies that are not conducted with similar methodology. Other children When a prepubescent child is sexually abused by one or more other children or adolescent youths, and no adult is directly involved, it is defined as child-on-child sexual abuse. The definition includes any sexual activity between children that occurs without consent, without equality, or due to coercion, whether the offender uses physical force, threats, trickery or emotional manipulation to compel cooperation. When sexual abuse is perpetrated by one sibling upon another, it is known as "intersibling abuse", a form of incest.Unlike research on adult offenders, a strong causal relationship has been established between child and adolescent offenders and these offenders own prior victimization, by either adults or other children. Teachers According to a 2010 UNICEF report, 46% of Congolese schoolgirls confirmed that they had been victims of sexual harassment, abuse, and violence committed by their teachers or other school personnel. In Mozambique, a study by the Ministry of Education found that 70 percent of female respondents reported knowing teachers who use sexual intercourse as a necessary condition to advance students to the next grade. A survey by Promundo found that 16% of girls in North Kivu said they had been forced to have sex with their teachers. According to UNICEF, teachers in Mali are known to use "La menace du bic rouge" ("the threat of the red pen"), using the threat of bad grades to coerce girls into acquiescing to sexual advances. According to Plan International, 16% of children in Togo, for instance, named a teacher as responsible for the pregnancy of a classmate. Prevalence Global Based on self-disclosure data, a 2011 meta-analysis of 217 studies estimated a global prevalence of 12.7%–18% for girls and 7.6% for boys. The rates of self-disclosed abuse for specific continents were as follows: A 2009 meta-analysis of 65 studies from 22 countries found a global prevalence of 19.7% for females and 7.9% for males. In that analysis, Africa had the highest prevalence rate of child sexual abuse (34.4%), primarily because of high rates in South Africa; Europe showed the lowest prevalence rate (9.2%); and America and Asia had prevalence rates between 10.1% and 23.9%. Africa A ten-country school-based study in southern Africa in 2007 found 19.6% of female students and 21.1% of male students aged 11–16 years reported they had experienced forced or coerced sex. Rates among 16-year-olds were 28.8% in females and 25.4% in males. Comparing the same schools in eight countries between 2003 and 2007, age-standardised on the 2007 Botswana male sample, there was no significant decrease between 2003 and 2007 among females in any country and inconsistent changes among males.The prevalence of child sexual abuse in Africa is compounded by the virgin cleansing myth that sexual intercourse with a virgin will cure a man of HIV or AIDS. The myth is prevalent in South Africa, Zimbabwe, Zambia and Nigeria and is being blamed for the high rate of sexual abuse against young children.Child rape is on the rise in the war-ravaged eastern Democratic Republic of the Congo. Aid workers blame combatants on all sides, who operate with much impunity, for a culture of sexual violence. South Africa has some of the highest incidences of child rape (including the rape of babies) in the world (also see sexual violence in South Africa). A survey by CIET found around 11% of boys and 4% of girls admitted to forcing someone else to have sex with them. In a related survey conducted among 1,500 schoolchildren, a quarter of all the boys interviewed said that "jackrolling", a term for gang rape, was fun. More than 67,000 cases of rape and sexual assaults against children were reported in 2000 in South Africa, compared to 37,500 in 1998. Child welfare groups believe that the number of unreported incidents could be up to 10 times that number. The largest increase in attacks was against children under seven. The virgin cleansing myth is especially common in South Africa, which has the highest number of HIV-positive citizens in the world. Eastern Cape social worker Edith Kriel notes that "child abusers are often relatives of their victims – even their fathers and providers."A number of high-profile baby rapes appeared since 2001 (including the fact that they required extensive reconstructive surgery to rebuild urinary, genital, abdominal, or tracheal systems). In 2001, a 9-month-old was raped and likely lost consciousness as the pain was too much to bear. In February 2002, an 8-month-old infant was reportedly gang-raped by four men. One has been charged. The infant has required extensive reconstructive surgery. The 8-month-old infants injuries were so extensive, increased attention on prosecution has occurred. Asia In Afghanistan, some boys are forced to participate in sexual activities with men. They are also termed dancing boys. The custom is connected to sexual slavery and child prostitution.In Bangladesh, child prostitutes are known to take the drug Oradexon, an over-the-counter steroid, usually used by farmers to fatten cattle, to make child prostitutes look larger and older. Charities say that 90% of prostitutes in the countrys legalized brothels use the drug. According to social activists, the steroid can cause diabetes and high blood pressure and is highly addictive.In 2007, the Ministry of Women and Child Development published the "Study on Child Abuse: India 2007." It sampled 12447 children, 2324 young adults and 2449 stakeholders across 13 states. It looked at different forms of child abuse: physical abuse, sexual abuse and emotional abuse and girl child neglect in five evidence groups, namely, children in a family environment, children in school, children at work, children on the street and children in institutions. The studys main findings included: 53.22% of children reported having faced sexual abuse. Among them, 52.94% were boys and 47.06% girls. Andhra Pradesh, Assam, Bihar and Delhi reported the highest percentage of sexual abuse among both boys and girls, as well as the highest incidence of sexual assaults. 21.90% of child respondents faced severe forms of sexual abuse, 5.69% had been sexually assaulted and 50.76% reported other forms of sexual abuse. Children on the street, at work and in institutional care reported the highest incidence of sexual assault. The study also reported that 50% of abusers are known to the child or are in a position of trust and responsibility and most children had not reported the matter to anyone. Despite years of lack of any specific child sexual abuse laws in India, which treated them separately from adults in case of sexual offense, the Protection of Children Against Sexual Offences Bill, 2011 was passed the Indian parliament on May 22, 2012, which came into force from 14 November 2012.In Pakistan, sexual abuse of children is a problem in some madrassas. Child sexual abuse has also been reported in Madrassas across Bangladesh and India.The Kasur child sexual abuse scandal, which involved forced sex acts and an estimated 280 to 300 children, was termed the largest child abuse scandal in Pakistans history.In 2019, Pakistans Human Rights Minister, Shirin Mazari has said that Pakistan was ranked as the country with the largest numbers of child pornography viewers. Geo Pakistan, the Federal Investigation Agency, cyber-crime chief has said, "Child pornography is a business . . with those involved in the crime linked to international child pornography rings."In Taiwan, a survey of adolescents reported 2.5% as having experienced childhood sexual abuse.In Uzbekistan, the UK Ambassador Craig Murray wrote that the government, under president Islam Karimov, used child rape to force false confessions from prisoners. Pacific According to UNICEF, nearly half of reported rape victims in Papua New Guinea are under 15 years of age and 13% are under 7 years of age while a report by ChildFund Australia citing former Parliamentarian Dame Carol Kidu stated 50% of those seeking medical help after rape are under 16, 25% are under 10 and 10% are under 8.Additionally, a study found that men with a history of victimization, especially having been raped or otherwise sexually coerced themselves, were more likely than otherwise to have participated in both single-perpetrator and multiple-perpetrator non-partner rape. 57·5% (587/1022) of men who raped a non-partner committed their first rape as teenagers. United States and Europe Child sexual abuse occurs frequently in Western society, although the rate of prevalence can be difficult to determine. Research in North America has concluded that approximately 15% to 25% of women and 5% to 15% of men were sexually abused when they were children. In the UK, a 2010 study estimated prevalence at about 5% for boys and 18% for girls (not dissimilar to a 1985 study that estimated about 8% for boys and 12% for girls). More than 23,000 incidents were recorded by the UK police between 2009 and 2010. Girls were six times more likely to be assaulted than boys with 86% of attacks taking place against them. Barnardos charity estimates that two thirds of victims in the United Kingdom are girls and one third are boys. Barnardos is concerned that boy victims may be overlooked. A firm of solicitors that acts in many cases of child abuse has published a list of over twenty Childrens Homes and group actions that they have an interest in or for which they are lead solicitors.The estimates for the United States vary widely. A literature review of 23 studies found rates of 3% to 37% for males and 8% to 71% for females, which produced an average of 17% for boys and 28% for girls, while a statistical analysis based on 16 cross-sectional studies estimated the rate to be 7.2% for males and 14.5% for females. The US Department of Health and Human Services reported 83,600 substantiated reports of sexually abused children in 2005, while state-level child protective services reported 63,527 sexual abuse incidents in 2010. Including incidents which were not reported would make the total number even larger. According to Emily M. Douglas and David Finkelhor, "Several national studies have found that black and white children experienced near-equal levels of sexual abuse. Other studies, however, have found that both blacks and Latinos have an increased risk for sexual victimization".Surveys have shown that one fifth to one third of all women reported some sort of childhood sexual experience with a male adult. A 1992 survey studying father-daughter incest in Finland reported that of the 9,000 15-year-old high school girls who filled out the questionnaires, of the girls living with their biological fathers, 0.2% reported father-daughter incest experiences; of the girls living with a stepfather, 3.7% reported sexual experiences with him. The reported counts included only father-daughter incest and did not include prevalence of other forms of child sexual abuse. The survey summary stated, "the feelings of the girls about their incestual experiences are overwhelmingly negative." Others argue that prevalence rates are much higher, and that many cases of child abuse are never reported. One study found that professionals failed to report approximately 40% of the child sexual abuse cases they encountered. A study by Lawson & Chaffin indicated that many children who were sexually abused were "identified solely by a physical complaint that was later diagnosed as a venereal disease ... Only 43% of the children who were diagnosed with venereal disease made a verbal disclosure of sexual abuse during the initial interview." It has been found in the epidemiological literature on CSA that there is no identifiable demographic or family characteristic of a child that can be used to bar the prospect that a child has been sexually abused.Child marriage is often considered to be another form of child sexual abuse. Over 200,000 marriages involving minors were allowed between 2000 and 2015 in the US. These marriages were most often between an adult male and female minor. Child marriage in the United States is allowed in the majority of states as long as parental consent or judicial approval (typically for pregnancy) is given.In US schools, according to the United States Department of Education, "nearly 9.6% of students are targets of educator sexual misconduct sometime during their school career." In studies of student sex abuse by male and female educators, male students were reported as targets in ranges from 23% to 44%. In U.S. school settings same-sex (female and male) sexual misconduct against students by educators "ranges from 18 to 28% of reported cases, depending on the study"Significant underreporting of sexual abuse of boys by both women and men is believed to occur due to sex stereotyping, social denial, the minimization of male victimization, and the relative lack of research on sexual abuse of boys. Sexual victimization of boys by their mothers or other female relatives is especially rarely researched or reported. Sexual abuse of girls by their mothers, and other related and/or unrelated adult females is beginning to be researched and reported despite the highly taboo nature of female–female child sex abuse. In studies where students are asked about sex offenses, they report higher levels of female sex offenders than found in adult reports. This underreporting has been attributed to cultural denial of female-perpetrated child sex abuse, because "males have been socialized to believe they should be flattered or appreciative of sexual interest from a female." Journalist Cathy Young writes that under-reporting is contributed to by the difficulty of people, including jurors, in seeing a male as a "true victim".In the United Kingdom, reported child sex abuse has increased, but this may be due to greater willingness to report. Police need more resources to deal with it. Also parents and schools need to give children and adolescents regular advice about how to spot abuse and about the need to report abuse. Software providers are urged to do more to police their environment and make it safe for children. International law Child sexual abuse is outlawed nearly everywhere in the world, generally with severe criminal penalties, including in some jurisdictions, life imprisonment or capital punishment. An adults sexual intercourse with someone below the legal age of consent is defined as statutory rape, based on the principle that a child is not capable of consent and that any apparent consent by a child is not considered to be legal consent. The United Nations Convention on the Rights of the Child (CRC) is an international treaty that legally obliges states to protect childrens rights. Articles 34 and 35 of the CRC require states to protect children from all forms of sexual exploitation and sexual abuse. This includes outlawing the coercion of a child to perform sexual activity, the prostitution of children, and the exploitation of children in creating pornography. States are also required to prevent the abduction, sale, or trafficking of children. As of November 2008, 193 countries are bound by the CRC, including every member of the United Nations except the United States and South Sudan.The Council of Europe has adopted the Council of Europe Convention on the Protection of Children against Sexual Exploitation and Sexual Abuse in order to prohibit child sexual abuse that occurs within home or family. In the European Union, child sexual abuse is subject to a directive. This directive deals with several forms of sexual abuse of children, especially commercial sexual exploitation of children. History Child sexual abuse has gained public attention since the 1970s and has become one of the most high-profile crimes. While sexual use of children by adults has been present throughout history, public interest in prevention has tended to fluctuate. Initially, concern centered around children under the age of ten, but over time, advocates have attracted attention toward the sexual abuse of children between the ages of 11 and 17. Up until the 1930s, the psychological impact of sexual abuse was not emphasized, instead emphasis was placed on the physical harm or the childs reputation. Widespread public awareness of childrens sexual abuse did not occur until the 1970s in the West. Early writings The first published work dedicated specifically to child sexual abuse appeared in France in 1857: Medical-Legal Studies of Sexual Assault (Etude Médico-Légale sur les Attentats aux Mœurs), by Auguste Ambroise Tardieu, the noted French pathologist and pioneer of forensic medicine. Public concern Child sexual abuse became a public issue in the 1970s and 1980s. Prior to this point in time, sexual abuse remained rather secretive and socially unspeakable. Studies on child molestation were nonexistent until the 1920s and the first national estimate of the number of child sexual abuse cases was published in 1948. By 1968 44 out of 50 U.S. states had enacted mandatory laws that required physicians to report cases of suspicious child abuse. Legal action began to become more prevalent in the 1970s with the enactment of the Child Abuse Prevention and Treatment Act in 1974 in conjunction with the creation of the National Center for Child Abuse and Neglect. Since the creation of the Child Abuse and Treatment Act, reported child abuse cases have increased dramatically. Finally, the National Abuse Coalition was created in 1979 to create pressure in congress to create more sexual abuse laws. Second wave feminism brought greater awareness of child sexual abuse and violence against women, and made them public, political issues. Judith Lewis Herman, Harvard professor of psychiatry, wrote the first book ever on father-daughter incest when she discovered during her medical residency that a large number of the women she was seeing had been victims of father-daughter incest. Herman notes that her approach to her clinical experience grew out of her involvement in the civil rights movement. Her second book Trauma and Recovery coined the term complex post-traumatic stress disorder and included child sexual abuse as a cause.In 1986, Congress passed the Child Abuse Victims Rights Act, giving children a civil claim in sexual abuse cases. The number of laws created in the 1980s and 1990s began to create greater prosecution and detection of child sexual abusers. During the 1970s a large transition began in the legislature related to child sexual abuse. Megans Law which was enacted in 1996 gives the public access to knowledge of sex offenders nationwide.Anne Hastings described these changes in attitudes towards child sexual abuse as "the beginning of one of historys largest social revolutions."According to John Jay College of Criminal Justice professor B.J. Cling, "By the early 21st century, the issue of child sexual abuse has become a legitimate focus of professional attention, while increasingly separated from second wave feminism ... As child sexual abuse becomes absorbed into the larger field of interpersonal trauma studies, child sexual abuse studies and intervention strategies have become degendered and largely unaware of their political origins in modern feminism and other vibrant political movements of the 1970s. One may hope that unlike in the past, this rediscovery of child sexual abuse that began in the 70s will not again be followed by collective amnesia. The institutionalization of child maltreatment interventions in federally funded centers, national and international societies, and a host of research studies (in which the United States continues to lead the world) offers grounds for cautious optimism. Nevertheless, as Judith Herman argues cogently, The systematic study of psychological trauma ... depends on the support of a political movement." Media reporting and its quality Media reporting plays a crucial role in tackling the word-wide problem of child sexual abuse because it puts the issue on the public and political agenda. Media reporting can even contribute to the exposure and criminal investigation of sexual abuse cases in institutions. One notorious example is the Boston Globe coverage of the sex abuse scandal in the Catholic Archdiocese of Boston for which the newspaper received a Pulitzer Prize for Public Service in 2003. Another award-winning example is the Indianapolis Star coverage of the USA Gymnastics sex abuse scandal in 2016. Media reporting can be very beneficial by giving survivors a voice and informing the public.Media reporting can also violate the rights of abuse survivors and disseminate misleading and harmful messages. Content analyses of news reporting have revealed several quality issues such as a focus on sensationalized individual cases (so-called episodic framing) and neglect of thematic framing in the sense of contextualizing individual cases and pointing to the systematic problems that enable child sexual abuse. When media reporting on child sexual abuse is investigated, usual methodological approaches are the media content analysis and the media quality analysis. Here it is important to not only analyze text but also documentary and stock photos commonly used in media that report about child sexual abuse. Research shows that myths and stereotypes about child sexual abuse are disseminated through text and images alike. Several checklists and guidelines for journalist have been published by violence prevention and journalism organizations to help improve the quality of news reporting on child sexual abuse. Future media content and media quality analyses will show if and how the quality of news reporting on child sexual abuse will be improving over time in different countries and across different media systems. Civil lawsuits In the United States growing awareness of child sexual abuse has sparked an increasing number of civil lawsuits for monetary damages stemming from such incidents. Increased awareness of child sexual abuse has encouraged more victims to come forward, whereas in the past victims often kept their abuse secret. Some states have enacted specific laws lengthening the applicable statutes of limitations so as to allow victims of child sexual abuse to file suit sometimes years after they have reached the age of majority. Such lawsuits can be brought where a person or entity, such as a school, church or youth organization, or daycare was charged with supervising the child but failed to do so with child sexual abuse resulting, making the individual or institution liable. In the Catholic sex abuse cases the various Roman Catholic Diocese in the United States have paid out approximately $1 billion settling hundreds of such lawsuits since the early 1990s. There have also been lawsuits involving the American religious right. Crimes have allegedly gone unreported and victims were pressured into silence. As lawsuits can involve demanding procedures there is a concern that children or adults who file suit will be re-victimized by defendants through the legal process, much as rape victims can be re-victimized by the accused in criminal rape trials. The child sexual abuse plaintiffs attorney Thomas A. Cifarelli has written that children involved in the legal system, particularly victims of sexual abuse and molestation, should be afforded certain procedural safeguards to protect them from harassment during the legal process.In June 2008 in Zambia the issue of teacher-student sexual abuse and sexual assault was brought to the attention of the High Court of Zambia where a landmark case decision, with presiding Judge Philip Musonda, awarded $45million Zambian kwacha (US$13,000) to the plaintiff, a 13-year-old girl for sexual abuse and rape by her school teacher. This claim was brought against her teacher as a "person of authority" who, as Judge Musonda stated, "had a moral superiority (responsibility) over his students" at the time.A 2000 World Health Organization – Geneva report, "World Report on Violence and Health (Chap 6 – Sexual Violence)" states, "Action in schools is vital for reducing sexual and other forms of violence. In many countries a sexual relation between a teacher and a pupil is not a serious disciplinary offence and policies on sexual harassment in schools either do not exist or are not implemented. In recent years, though, some countries have introduced laws prohibiting sexual relations between teachers and pupils. Such measures are important in helping eradicate sexual harassment in schools. At the same time, a wider range of actions is also needed, including changes to teacher training and recruitment and reforms of curricula, so as to transform gender relations in schools." See also References Further reading Abagnalo, George (2001). Boy on a Pony. Moreland Press. ISBN 978-0-970-667700 (a groundbreaking novel exploring the subject of privileged sexual abuse of children within the healthcare system). Lew, Mike (2004). Victims No Longer: The Classic Guide for Men Recovering from Sexual Child Abuse (2nd ed.). Perennial Currents. ISBN 978-0-06-053026-6. Cynthia Crosson-Tower (2008). Understanding child abuse and neglect. Boston: Pearson/Allyn & Bacon. ISBN 978-0-205-50326-1. Asa Don Brown (2009). "Posttraumatic stress disorder in childhood". Family and Marriage Counseling. Lascaratos, J; Ascaratos J; Poulakou-Rebelakou, E (2000). "Child Sexual abuse: Historical cases in the Byzantine Empire (324–1453 A.D.)". Child Abuse & Neglect. 24 (8): 1085–1090. doi:10.1016/S0145-2134(00)00156-3. PMID 10983818. Durkin, KF; Clifton DB (1999). "Propagandizing pederasty: A thematic analysis of the on-line exculpatory accounts of unrepentant pedophiles". Deviant Behavior. 20 (2): 103–127. doi:10.1080/016396299266524. Zimring, Franklin E. (2009). An American Travesty: Legal Responses to Adolescent Sexual Offending. University of Chicago Press. ISBN 978-0-226-98358-5. External links Media related to Child sexual abuse at Wikimedia Commons American Academy of Child and Adolescent Psychiatry Facts for Families: Child Sexual Abuse Men who molest their sexually immature daughters: Is a special explanation required? Child Abuse: Sexual Abuse at Curlie 2017 child sexual abuse statistics from Darkness to Light

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I'm trying to expand my medical knowledge. Can you elucidate the term 'Campylobacteriosis'?

Campylobacteriosis is an infection by the Campylobacter bacterium, most commonly C. jejuni. It is among the most common bacterial infections of humans, often a foodborne illness. It produces an inflammatory, sometimes bloody, diarrhea or dysentery syndrome, mostly including cramps, fever and pain. Symptoms and signs The prodromal symptoms are fever, headache, and myalgia, which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by diarrhea (as many as 10 watery, frequently bloody, bowel movements per day) or dysentery, cramps, abdominal pain, and fever as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery.There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking acute appendicitis. Furthermore, Helicobacter pylori is closely related to Campylobacter and causes peptic ulcer disease. Complications Complications include toxic megacolon, dehydration and sepsis. Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub-febrile temperature and asthenia; eye damage, arthritis, endocarditis may develop if infection is untreated. Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in people who are elderly or immunocompromised.Some individuals (1–2 in 100,000 cases) develop Guillain–Barré syndrome, in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. This occurs only with infection of C. jejuni and C. upsaliensis. Other factors In patients with HIV, infections may be more frequent, may cause prolonged bouts of dirty brown diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance. In participants of unprotected anal intercourse, campylobacteriosis is more localized to the distal end of the colon and may be termed a proctocolitis. The severity and persistence of infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection. Cause Campylobacteriosis is caused by Campylobacter bacteria (curved or spiral, motile, non–spore-forming, Gram-negative rods). The disease is usually caused by C. jejuni, a spiral and comma-shaped bacterium normally found in cattle, swine, and birds, where it is nonpathogenic, but the illness can also be caused by C. coli (also found in cattle, swine, and birds), C. upsaliensis (found in cats and dogs) and C. lari (present in seabirds in particular).One effect of campylobacteriosis is tissue injury in the gut. The sites of tissue injury include the jejunum, the ileum, and the colon. C jejuni appears to achieve this by invading and destroying epithelial cells.C. jejuni can also cause a latent autoimmune effect on the nerves of the legs, which is usually seen several weeks after a surgical procedure of the abdomen. The effect is known as an acute idiopathic demyelinating polyneuropathy (AIDP), i.e. Guillain–Barré syndrome, in which one sees symptoms of ascending paralysis, dysaesthesias usually below the waist, and, in the later stages, respiratory failure.Some strains of C jejuni produce a cholera-like enterotoxin, which is important in watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism. Transmission The common routes of transmission for the disease-causing bacteria are fecal-oral, person-to-person sexual contact, ingestion of contaminated food (generally unpasteurized (raw) milk and undercooked or poorly handled poultry), and waterborne (i.e., through contaminated drinking water). Contact with contaminated poultry, livestock, or household pets, especially puppies, can also cause disease.Animals farmed for meat are the main source of campylobacteriosis. A study published in PLoS Genetics (26 September 2008) by researchers from Lancashire, England, and Chicago, Illinois, found that 97 percent of campylobacteriosis cases sampled in Lancashire were caused by bacteria typically found in chicken and livestock. In 57 percent of cases, the bacteria could be traced to chicken, and in 35 percent to cattle. Wild animal and environmental sources were accountable for just three percent of disease.The infectious dose is 1000–10,000 bacteria (although ten to five hundred bacteria can be enough to infect humans). Campylobacter species are sensitive to hydrochloric acid in the stomach, and acid reduction treatment can reduce the amount of inoculum needed to cause disease.Exposure to bacteria is often more common during travelling, and therefore campylobacteriosis is a common form of travelers diarrhea. Diagnosis Campylobacter organisms can be detected by performing a Gram stain of a stool sample with high specificity and a sensitivity of ~60%, but are most often diagnosed by stool culture. Fecal leukocytes should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of campylobacter organisms include antigen testing via an EIA or PCR. Prevention Pasteurization of milk and chlorination of drinking water destroys the organisms. Treatment with antibiotics can reduce fecal excretion. Infected health care workers should not provide direct patient care. Separate cutting boards should be used for foods of animal origin and other foods. After preparing raw food of animal origin, all cutting boards and countertops should be carefully cleaned with soap and hot water. Contact with pet saliva and feces should be avoided.The World Health Organization recommends the following: Food should be properly cooked and hot when served. Consume only pasteurized or boiled milk and milk products, never raw milk products. Make sure that ice is from safe water. If you are not sure of the safety of drinking water, boil it, or disinfect it with chemical disinfectant. Wash hands thoroughly and frequently with soap, especially after using the toilet and after contact with pets and farm animals. Wash fruits and vegetables thoroughly, especially if they are to be eaten raw. Peel fruits and vegetables whenever possible. Food handlers, professionals and at home, should observe hygienic rules during food preparation. Professional food handlers should immediately report to their employer any fever, diarrhea, vomiting or visible infected skin lesions. Treatment The infection is usually self-limiting, and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections. Antibiotics Antibiotic treatment only has a marginal effect on the duration of symptoms, and its use is not recommended except in high-risk patients with clinical complications.Erythromycin can be used in children, and tetracycline in adults. Some studies show, however, that erythromycin rapidly eliminates Campylobacter from the stool without affecting the duration of illness. Nevertheless, children with dysentery due to C. jejuni benefit from early treatment with erythromycin. Treatment with antibiotics, therefore, depends on the severity of symptoms. Quinolones are effective if the organism is sensitive, but high rates of quinolone use in livestock mean that quinolones are now largely ineffective.Antimotility agents, such as loperamide, can lead to prolonged illness or intestinal perforation in any invasive diarrhea, and should be avoided. Trimethoprim/sulfamethoxazole and ampicillin are ineffective against Campylobacter. In animals In the past, poultry infections were often treated by mass administration of enrofloxacin and sarafloxacin for single instances of infection. The FDA banned this practice, as it promoted the development of fluoroquinolone-resistant populations. A major broad-spectrum fluoroquinolone used in humans is ciprofloxacin.Currently growing resistance of the Campylobacter to fluoroquinolones and macrolides is of a major concern. Prognosis Campylobacteriosis is usually self-limited without any mortality (assuming proper hydration is maintained). However, there are several possible complications. Epidemiology Campylobacter is one of the most common causes of human bacterial gastroenteritis. For instance, an estimated 2 million cases of Campylobacter enteritis occur annually in the U.S., accounting for 5–7% of cases of gastroenteritis. Furthermore, in the United Kingdom during 2000, Campylobacter jejuni was involved in 77.3% in all cases of laboratory confirmed foodborne illness. About 15 of every 100,000 people are diagnosed with campylobacteriosis every year, and with many cases going unreported, up to 0.5% of the general population may unknowingly harbor Campylobacter in their gut.Unfortunately, the true incidence of campylobacteriosis is unknown in most countries, especially developing countries. The reasons are among others underreporting, difficulties with diagnosis and differences in reporting systems in different countries.A large animal reservoir is present as well, with up to 100% of poultry, including chickens, turkeys, and waterfowl, having asymptomatic infections in their intestinal tracts. Infected chicken feces may contain up to 109 bacteria per 25 grams, and due to the animals close proximity, the bacteria are rapidly spread to other chickens. This vastly exceeds the infectious dose of 1000–10,000 bacteria for humans.In January 2013, the UKs Food Standards Agency warned that two-thirds of all raw chicken bought from UK shops was contaminated with campylobacter, affecting an estimated half a million people annually and killing approximately 100. Outbreak In August–September 2016, 5,200 people fell ill with campylobacteriosis in Hastings, New Zealand after the local water supply in Havelock North tested positive for the pathogen Campylobacter jejuni. Four deaths were suspected to be due to the outbreak. It is suspected that after heavy rain fell on 5–6 August, water contamination from flooding caused the outbreak, although this is the subject of a government Inquiry. It is the largest outbreak of waterborne disease ever to occur in New Zealand. All schools in Havelock North closed for two weeks, with the Hastings District Council advising an urgent notice to boil water for at least one minute before consumption. This notice was lifted on 3 September, with the outbreak officially under control.According to Centers for Disease Control and Prevention, a multistate outbreak of human Campylobacter infection has been reported since 11 September 2017. In all, 55 cases were reported from 12 states (Florida, Kansas, Maryland, Missouri, New Hampshire, New York, Ohio, Pennsylvania, Tennessee, Utah, Wisconsin and Wyoming). Epidemiological and laboratory evidence indicated that puppies sold through Petland stores were a likely source of this outbreak. Out of 55 cases reported, 50 were either employees of Petland or had recently purchased a puppy at Petland, or visited there before illness began. Five people out of 55 cases reported were exposed to puppies from various sources.Campylobacter can spread through contact with dog feces. It usually does not spread from one person to another. However, activities such as changing an infected persons diapers or sexual contact with an infected person can lead to infection. Regardless of where they are from, any puppies and dogs may carry Campylobacter germs. References External links Campylobacter jejuni genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID