<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Central pontine myelinolysis and explain in detail? [/INST] Central pontine myelinolysis is a neurological condition involving severe damage to the myelin sheath of nerve cells in the pons (an area of the brainstem). It is predominately iatrogenic (treatment-induced), and is characterized by acute paralysis,  dysphagia (difficulty swallowing), dysarthria (difficulty speaking), and other neurological symptoms.
Central pontine myelinolysis was first described as a disorder in 1959. The original paper described four cases with fatal outcomes, and the findings on autopsy. The disease was described as a disease of alcoholics and malnutrition. Central pontine indicated the site of the lesion and myelinolysis was used to emphasise that myelin was affected. The authors intentionally avoided the term demyelination to describe the condition, in order to differentiate this condition from multiple sclerosis and other neuroinflammatory disorders.Since this original description, demyelination in other areas of the central nervous system associated with osmotic stress has been described outside the pons (extrapontine). Osmotic demyelination syndrome is the term used for both central pontine myelinolysis and extrapontine myelinolysis.Central pontine myelinolysis, and osmotic demyelination syndrome, present most commonly as a complication of treatment of patients with profound hyponatremia (low sodium), which can result from a varied spectrum of conditions, based on different mechanisms. It occurs as a consequence of a rapid rise in serum tonicity following treatment in individuals with chronic, severe hyponatremia who have made intracellular adaptations to the prevailing hypotonicity.

Signs and symptoms
Symptoms depend on the regions of the brain involved. Prior to its onset, patients may present with the neurological signs and symptoms of hyponatraemic encephalopathy such as nausea and vomiting, confusion, headache and seizures. These symptoms may resolve with normalisation of the serum sodium concentration. Three to five days later, a second phase of neurological manifestations occurs correlating with the onset of myelinolysis. Observable immediate precursors may include seizures, disturbed consciousness, gait changes, and decrease or cessation of respiratory function.The classical clinical presentation is the progressive development of spastic quadriparesis, pseudobulbar palsy, and emotional lability (pseudobulbar affect), with other more variable neurological features associated with brainstem damage. These result from a rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem.In about ten per cent of people with central pontine myelinolysis, extrapontine myelinolysis is also found. In these cases symptoms of Parkinsons disease may be generated.

Causes
The most common cause is overly-rapid correction of low blood sodium levels (hyponatremia). Apart from rapid correction of hyponatraemia, there are case reports of central pontine myelinolysis in association with hypokalaemia, anorexia nervosa when feeding is started, patients undergoing dialysis and burn victims. There is a case report of central pontine myelinolysis occurring in the context of refeeding syndrome, in the absence of hyponatremia.It has also been known to occur in patients suffering withdrawal symptoms of chronic alcoholism.  In these instances, occurrence may be entirely unrelated to hyponatremia or rapid correction of hyponatremia. It could affect patients who take some prescription medicines that are able to cross the blood-brain barrier and cause abnormal thirst reception - in this scenario the central pontine myelinolysis is caused by polydipsia leading to low blood sodium levels (hyponatremia).In schizophrenic patients with psychogenic polydipsia, inadequate thirst reception leads to excessive water intake, severely diluting serum sodium. With this excessive thirst combined with psychotic symptoms, brain damage such as central pontine myelinolysis may result from hyperosmolarity caused by excess intake of fluids, (primary polydipsia) although this is difficult to determine because such patients are often institutionalised and have a long history of mental health conditions.It has been observed following hematopoietic stem cell transplantation.Central pontine myelinolysis may also occur in patients prone to hyponatremia affected by:

Severe liver disease (e.g., cirrhosis)
Liver transplant
Alcoholism
Hypokalemia
People with serum sodium <105 mEq/L
Severe burns
Malnutrition
Anorexia nervosa
Severe electrolyte disorders
HIV/AIDS
hyperemesis gravidarum
Hyponatremia due to peritoneal dialysis
Wernicke encephalopathy

Pathophysiology
The currently accepted theory states that the brain cells adjust their osmolarities by changing levels of certain osmolytes like inositol, betaine, and glutamine in response to varying serum osmolality. In the context of chronic low plasma sodium (hyponatremia), the brain compensates by decreasing the levels of these osmolytes within the cells, so that they can remain relatively isotonic with their surroundings and not absorb too much fluid. The reverse is true in hypernatremia, in which the cells increase their intracellular osmolytes so as not to lose too much fluid to the extracellular space.With correction of the hyponatremia with intravenous fluids, the extracellular tonicity increases, followed by an increase in intracellular tonicity. When the correction is too rapid, not enough time is allowed for the brains cells to adjust to the new tonicity, namely by increasing the intracellular osmoles mentioned earlier. If the serum sodium levels rise too rapidly, the increased extracellular tonicity will continue to drive water out of the brains cells. This can lead to cellular dysfunction and central pontine myelinolysis.

Diagnosis
It can be diagnosed clinically in the appropriate context, but may be difficult to confirm radiologically using conventional imaging techniques.  Changes are more prominent on MRI than on CT, but often take days or weeks after acute symptom onset to develop </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Epiblepharon and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Chlamydia and explain in detail? [/INST] Chlamydia, or more specifically a chlamydia infection, is a sexually transmitted infection caused by the bacterium Chlamydia trachomatis. Most people who are infected have no symptoms. When symptoms do appear they may occur only several weeks after infection; the incubation period between exposure and being able to infect others is thought to be on the order of two to six weeks.  Symptoms in women may include vaginal discharge or burning with urination. Symptoms in men may include discharge from the penis, burning with urination, or pain and swelling of one or both testicles. The infection can spread to the upper genital tract in women, causing pelvic inflammatory disease, which may result in future infertility or ectopic pregnancy.Chlamydia infections can occur in other areas besides the genitals, including the anus, eyes, throat, and lymph nodes. Repeated chlamydia infections of the eyes that go without treatment can result in trachoma, a common cause of blindness in the developing world.Chlamydia can be spread during vaginal, anal, or oral sex, and can be passed from an infected mother to her baby during childbirth. The eye infections may also be spread by personal contact, flies, and contaminated towels in areas with poor sanitation. Infection by the bacterium Chlamydia trachomatis only occurs in humans. Diagnosis is often by screening which is recommended yearly in sexually active women under the age of twenty-five, others at higher risk, and at the first prenatal visit. Testing can be done on the urine or a swab of the cervix, vagina, or urethra. Rectal or mouth swabs are required to diagnose infections in those areas.Prevention is by not having sex, the use of condoms, or having sex with only one other person, who is not infected. Chlamydia can be cured by antibiotics with typically either azithromycin or doxycycline being used. Erythromycin or azithromycin is recommended in babies and during pregnancy. Sexual partners should also be treated, and infected people should be advised not to have sex for seven days and until symptom free. Gonorrhea, syphilis, and HIV should be tested for in those who have been infected. Following treatment people should be tested again after three months.Chlamydia is one of the most common sexually transmitted infections, affecting about 4.2% of women and 2.7% of men worldwide. In 2015, about 61 million new cases occurred globally. In the United States about 1.4 million cases were reported in 2014. Infections are most common among those between the ages of 15 and 25 and are more common in women than men. In 2015 infections resulted in about 200 deaths. The word chlamydia is from the Greek χλαμύδα, meaning "cloak".

Signs and symptoms
Genital disease
Women
Chlamydial infection of the cervix (neck of the womb) is a sexually transmitted infection which has no symptoms for  around 70% of women infected. The infection can be passed through vaginal, anal, or oral sex. Of those who have an asymptomatic infection that is not detected by their doctor, approximately half will develop pelvic inflammatory disease (PID), a generic term for infection of the uterus, fallopian tubes, and/or ovaries. PID can cause scarring inside the reproductive organs, which can later cause serious complications, including chronic pelvic pain, difficulty becoming pregnant, ectopic (tubal) pregnancy, and other dangerous complications of pregnancy.
Chlamydia is known as the "silent epidemic", as at least 70% of genital C. trachomatis infections in women (and 50% in men) are asymptomatic at the time of diagnosis, and can linger for months or years before being discovered. Signs and symptoms may include abnormal vaginal bleeding or discharge, abdominal pain, painful sexual intercourse, fever, painful urination or the urge to urinate more often than usual (urinary urgency).
For sexually active women who are not pregnant, screening is recommended in those under 25 and others at risk of infection. Risk factors include a history of chlamydial or other sexually transmitted infection, new or multiple sexual partners, and inconsistent condom use. Guidelines recommend all women attending for emergency contraceptive are offered chlamydia testing, with studies showing up to 9% of women aged <25 years had chlamydia.

Men
In men, those with a chlamydial infection show symptoms of infectious inflammation of the urethra in about 50% of cases. Symptoms that may occur include: a painful or burning sensation when urinating, an unusual discharge from the penis, testicular pain or swelling, or fever. If left untreated, chlamydia in men can spread to the testicles causing epididymitis, which in rare cases can lead to sterility if not treated. Chlamydia is also a potential cause of prostatic inflammation in men, although the exact relevance in prostatitis is difficult to ascertain due to possible contamination from urethritis.

Eye disease
Trachoma is a chronic conjunctivitis caused by Chlamydia trachomatis. It was once the leading cause of blindness worldwide, but its role diminished from 15% of blindness cases by trachoma in 1995 to 3.6% in 2002. The infection can be spread from eye to eye by fingers, shared towels or cloths, coughing and sneezing and eye-seeking flies. Symptoms include mucopurulent ocular discharge, irritation, redness, and lid swelling. Newborns can also develop chlamydia eye infection through childbirth (see below). Using the SAFE strategy (acronym for surgery for in-growing or in-turned lashes, antibiotics, facial cleanliness, and environmental improvements), the World Health Organization aims for the global elimination of trachoma by 2020 (GET 2020 initiative).

Joints
Chlamydia may also cause reactive arthritis—the triad of arthritis, conjunctivitis and urethral inflammation—especially in young men. About 15,000 men develop reactive arthritis due to chlamydia infection each year in the U.S., and about 5,000 are permanently affected by it. It can occur in both sexes, though is more common in men.

Infants
As many as half of all infants born to mothers with chlamydia will be born with the disease. Chlamydia can affect infants by causing spontaneous abortion; premature birth; conjunctivitis, which may lead to blindness; and pneumonia. Conjunctivitis due to chlamydia typically occurs one week after birth (compared with chemical causes (within hours) or gonorrhea (2–5 days)).

Other conditions
A different serovar of Chlamydia trachomatis is also the cause of lymphogranuloma venereum, an infection of the lymph nodes and lymphatics. It usually presents with genital ulceration and swollen lymph nodes in the groin, but it may also manifest as rectal inflammation, fever or swollen lymph nodes in other regions of the body.

Transmission
Chlamydia can be transmitted during vaginal, anal, or oral sex, or direct contact with infected tissue such as conjunctiva. Chlamydia can also be passed from an infected mother to her baby during vaginal childbirth. It is assumed that the probability of becoming infected is proportionate to the number of bacteria one is exposed to.

Pathophysiology
Chlamydiae have the ability to establish long-term associations with host cells. When an infected host cell is starved for various nutrients such as amino acids (for example, tryptophan), iron, or vitamins, this has a negative consequence for Chlamydiae since the organism is dependent on the host cell for these nutrients. Long-term cohort studies indicate that approximately 50% of those infected clear within a year, 80% within two years, and 90% within three years.The starved chlamydiae enter a persistent growth state wherein they stop cell division and become morphologically aberrant by increasing in size. Persistent organisms remain viable as they are capable of returning to a normal growth state once conditions in the host cell improve.There is debate as to whether persistence has relevance. Some believe that persistent chlamydiae are the cause of chronic chlamydial diseases. Some antibiotics such as β-lactams have been found to induce a persistent-like growth state.

Diagnosis
The diagnosis of genital chlamydial infections evolved rapidly from the 1990s through 2006. Nucleic acid amplification tests (NAAT), such as polymerase chain reaction (PCR), transcription mediated amplification (TMA), and the DNA strand displacement amplification (SDA) now are the mainstays. NAAT for chlamydia may be performed on swab specimens sampled from the cervix (women) or urethra (men), on self-collected vaginal swabs, or on voided urine. NAAT has been estimated to have a sensitivity of approximately 90% and a specificity of approximately 99%, regardless of sampling from a cervical swab or by urine specimen. In women seeking an sexually transmitted infection (STI) clinic and a urine test is negative, a subsequent cervical swab has been estimated to be positive in approximately 2% of the time.At present, the NAATs have regulatory approval only for testing urogenital specimens, although rapidly evolving research indicates that they may give reliable results on rectal specimens.
Because of improved test accuracy, ease of specimen management, convenience in specimen management, and ease of screening sexually active men and women, the NAATs have largely replaced culture, the historic gold standard for chlamydia diagnosis, and the non-amplified probe tests. The latter test is relatively insensitive, successfully detecting only 60–80% of infections in asymptomatic women, and often giving falsely-positive results. Culture remains useful in selected circumstances and is currently the only assay approved for testing non-genital specimens. Other methods also exist including: ligase chain reaction (LCR), direct fluorescent antibody resting, enzyme immunoassay, and cell culture.Rapid point-of-care tests are, as of 2020, not thought to be effective for diagnosing chlamydia in men of reproductive age and nonpregnant women because of high false-negative rates.

Prevention
Prevention is by not having sex, the use of condoms, or having sex with only one other person, who is not infected.

Screening
For sexually active women who are not pregnant, screening is recommended in those under 25 and others at risk of infection. Risk factors include a history of chlamydial or other sexually transmitted infection, new or multiple sexual partners, and inconsistent condom use. For pregnant women, guidelines vary: screening women with age or other risk factors is recommended by the U.S. Preventive Services Task Force (USPSTF) (which recommends screening women under 25) and the American Academy of Family Physicians (which recommends screening women aged 25 or younger). The American College of Obstetricians and Gynecologists recommends screening all at risk, while the Centers for Disease Control and Prevention recommend universal screening of pregnant women. The USPSTF acknowledges that in some communities there may be other risk factors for infection, such as ethnicity. Evidence-based recommendations for screening initiation, intervals and termination are currently not possible. For men, the USPSTF concludes evidence is currently insufficient to determine if regular screening of men for chlamydia is beneficial. They recommend regular screening of men who are at increased risk for HIV or syphilis infection. A Cochrane review found that the effects of screening are uncertain in terms of chlamydia transmission but that screening probably reduces the risk of pelvic inflammatory disease in women.In the United Kingdom the National Health Service (NHS) aims to:

Prevent and control chlamydia infection through early detection and treatment of asymptomatic infection;
Reduce onward transmission to sexual partners;
Prevent the consequences of untreated infection;
Test at least 25 percent of the sexually active under 25 population annually.
Retest after treatment.

Treatment
C. trachomatis infection can be effectively cured with antibiotics. Guidelines recommend azithromycin, doxycycline, erythromycin, levofloxacin or ofloxacin </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Developmental regression and explain in detail? [/INST] Developmental regression is when a child who has reached a certain developmental stage begins to lose previously acquired milestones. It differs from developmental delay in that a child experiencing developmental delay is either not reaching developmental milestones or not progressing to new developmental milestones, while a child experiencing developmental regression will lose milestones and skills after acquiring them. Developmental regression is associated with diagnoses of autism spectrum disorder, childhood disintegrative disorder, Rett syndrome, Landau-Kleffner syndrome, and neuro-degenerative diseases. The loss of motor, language, and social skills can be treated with occupational therapy, physical therapy, and speech therapy.

Associated Diagnoses
Developmental regression is typically a symptom of neurological disorder.

Autism Spectrum Disorder
Autism spectrum disorder is a developmental disorder in which a childs communication and social skills are affected. Children with autism spectrum disorder can experience a loss of their previously acquired language and social skills. This is often reported by the childs parents. Children can experience loss of vocabulary and language understanding, as well as no longer make eye contact or play social and imitative games when they previously had. They can also experience a loss of motor and basic skills like toileting or feeding themselves. In autism spectrum disorder, this regression occurs in the first few years of development.

Childhood Disintegrative Disorder
Childhood disintegrative disorder (CDD) is a developmental disorder in which children experience a regression of social language, and motor functioning skills. CDD was merged with autism spectrum disorder in the DSM-V in 2013. Children with CDD can experience a loss of expressive and receptive language skills, social and self-care skills, play skills, and/or motor skills. Regression commonly occurs at around 3 or 4 years old, but after at least two years of normal development and before age 10.

Rett Syndrome
Rett syndrome is a neurodevelopmental disorder caused by a genetic mutation. It occurs almost exclusively in girls. A child with Rett syndrome experiences a loss of previously had intentional hand skills, and can experience a loss of language skills. Children can also experience a loss of social skills and autism-like symptoms. The regression typically occurs between 1–4 years of age.

Landau-Kleffner Syndrome
Landau-Kleffner syndrome is a form of epilepsy associated with a loss of language skills. Those with LKS lose their ability to understand spoken language and to verbally express themselves. LKS typically has an onset of between the ages of 2 and 8 years old.

Neuro-degenerative diseases
Neuro-degenerative diseases (disorders like Batten disease) can result in a child losing previously acquired motor, language, and speech skills.

Signs and symptoms
Children with developmental regression lose developmental milestones they have previously gained. These can be motor, social, or language skills. The loss of motor skills could include loss of the ability to purposefully use hands, loss of the ability to feed oneself, loss of the ability to walk, loss of the ability to bathe oneself, and loss of the ability to dress oneself. The loss of social skills could include loss of the ability/desire to play, loss of the ability to make appropriate eye contact, and loss of interest in playing social games </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pashayan syndrome and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Fibrous dysplasia of bone and explain in detail? [/INST] Fibrous dysplasia is a disorder where normal bone and marrow is replaced with fibrous tissue, resulting in formation of bone that is weak and prone to expansion. As a result, most complications result from fracture, deformity, functional impairment, and pain. Disease occurs along a broad clinical spectrum ranging from asymptomatic, incidental lesions, to severe disabling disease. Disease can affect one bone (monostotic), multiple (polyostotic), or all bones (panostotic) and may occur in isolation or in combination with café au lait skin macules and hyperfunctioning endocrinopathies, termed McCune–Albright syndrome. More rarely, fibrous dysplasia may be associated with intramuscular myxomas, termed Mazabrauds syndrome. Fibrous dysplasia is very rare, and there is no known cure. Fibrous dysplasia is not a form of cancer.

Presentation
Fibrous dysplasia is a mosaic disease that can involve any part or combination of the craniofacial, axillary, and/or appendicular skeleton. The type and severity of the complications therefore depend on the location and extent of the affected skeleton. The clinical spectrum is very broad, ranging from an isolated, asymptomatic monostotic lesion discovered incidentally, to severe disabling disease involving practically the entire skeleton and leading to loss of vision, hearing, and/or mobility.Individual bone lesions typically manifest during the first few years of life and expand during childhood. The vast majority of clinically significant bone lesions are detectable by age 10 years, with few new and almost no clinically significant bone lesions appearing after age 15 years. Total body scintigraphy is useful to identify and determine the extent of bone lesions, and should be performed in all patients with suspected fibrous dysplasia.Children with fibrous dysplasia in the appendicular skeleton typically present with limp, pain, and/or pathologic fractures. Frequent fractures and progressive deformity may lead to difficulties with ambulation and impaired mobility. In the craniofacial skeleton, fibrous dysplasia may present as a painless “lump” or facial asymmetry. Expansion of craniofacial lesions may lead to progressive facial deformity. In rare cases, patients may develop vision and/or hearing loss due to compromise of the optic nerves and/or auditory canals, which is more common in patients with McCune-Albright syndrome associated growth hormone excess. Fibrous dysplasia commonly involves the spine, and may lead to scoliosis, which in rare instances may be severe. Untreated, progressive scoliosis is one of the few features of fibrous dysplasia that can lead to early fatality.
Bone pain is a common complication of fibrous dysplasia. It may present at any age, but most commonly develops during adolescence and progresses into adulthood.
Bone marrow stromal cells in fibrous dysplasia produce excess amounts of the phosphate-regulating hormone fibroblast growth factor-23 (FGF23), leading to loss of phosphate in the urine. Patients with hypophosphatemia may develop rickets/osteomalacia, increased fractures, and bone pain.

Pathophysiology
Fibrous dysplasia is a mosaic disease resulting from post-zygotic activating mutations of the GNAS locus at 20q13.2-q13.3, which codes for the α subunit of the Gs G protein-coupled receptor. In bone, constitutive Gsα signaling results in impaired differentiation and proliferation of bone marrow stromal cells. Proliferation of these cells causes replacement of normal bone and marrow with fibrous tissue. The bony trabeculae are abnormally thin and irregular, and often likened to Chinese characters (bony spicules on biopsy).Fibrous dysplasia is not hereditary, and there has never been a case of genetic inheritance from parent to child.

Diagnosis
On x-ray, fibrous dysplasia appears as bubbly lytic lesions, or a ground glass appearance. Computerized tomography (CT) or magnetic resonance imaging (MRI) scans may be used to determine how extensively bones are affected. CT can better demonstrate the typical "ground glass" appearance, which is a highly specific radiological finding, while MRI can show cystic areas with fluid contents. A bone scan uses radioactive tracers, which are injected into your bloodstream. The damaged parts of bones take up more of the tracer, which show up more brightly on the scan. A biopsy, which uses a hollow needle to remove a small piece of the affected bone for laboratory analysis, can diagnose fibrous dysplasia definitely.

Treatment
Treatment in fibrous dysplasia is mainly palliative, and is focused on managing fractures and preventing deformity </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Congenital hemolytic anemia and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Fibrofolliculoma and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Septic arthritis and explain in detail? [/INST] Acute septic arthritis, infectious arthritis, suppurative arthritis, osteomyelitis, or joint infection is the invasion of a joint by an infectious agent resulting in joint inflammation. Generally speaking, symptoms typically include redness, heat and pain in a single joint associated with a decreased ability to move the joint. Onset is usually rapid. Other symptoms may include fever, weakness and headache. Occasionally, more than one joint may be involved, especially in neonates and younger children. In neonates, infants during the first year of life, and toddlers, the signs and symptoms of septic arthritis can be deceptive and mimic other infectious and non-infectious disorders.In children, septic arthritis is usually caused by non-specific bacterial infection and commonly hematogenous, i.e., spread through the bloodstream. Septic arthritis and/or acute hematogenous osteomyelitis usually occurs in children with no co-occurring health problems. Other routes of infection include direct trauma and spread from a nearby abscess. Other less common cause include specific bacteria as mycobacterium tuberculosis, viruses, fungi and parasites. In children, however, there are certain groups that are specifically vulnerable to such infections namely preterm infants, neonates in general, children and adolescence with hematologic disorders, renal osteodystrophy and immune-compromised status. In adults vulnerable groups include an artificial joint, prior arthritis, diabetes and poor immune function.  Diagnosis is generally based on accurate correlation between history-taking and clinical examination findings and basic laboratory and imaging findings like joint ultrasound.In children septic arthritis can have serious consequences if not treated appropriately and timely. Initial treatment typically includes antibiotics such as vancomycin, ceftriaxone or ceftazidime. Surgery in the form of joint drainage is the gold standard management in large joints like the hip and shoulder. Without early treatment, long-term joint problems may occur, such as irreversible joint destruction and dislocation.

Signs and symptoms
Children
In children septic arthritis usually affects the larger joints like the hips, knees and shoulders. The early signs and symptoms of septic arthritis in children and adolescence can be confused with limb injury. Among the signs and symptoms of septic arthritis are: acutely swollen, red, painful joint with fever. Kocher criteria have been suggested to predict the diagnosis of septic arthritis in children.Importantly, observation of active limb motion or kicking in the lower limb can provide valuable clues to septic arthritis of hip or knee. In neonates/new born and infants the hip joint is characteristically held in abduction flexion and external rotation. This position helps the infant accommodate maximum amount of septic joint fluid with the least tension possible. The tendency to have multiple joint involvements in septic arthritis of neonates and young children should be closely considered.

Adults
In adults, septic arthritis most commonly causes pain, swelling and warmth at the affected joint. Therefore, those affected by septic arthritis will often refuse to use the extremity and prefer to hold the joint rigidly. Fever is also a symptom; however, it is less likely in older people. In adults the most common joint affected is the knee. Hip, shoulder, wrist and elbow joints are less commonly affected. Spine, sternoclavicular and sacroiliac joints can also be involved. The most common cause of arthritis in these joints is intravenous drug use. Usually, only one joint is affected. More than one joint can be involved if bacteria are spread through the bloodstream.

Prosthetic joint
For those with artificial joint implants, there is a chance of 0.86 to 1.1% of getting infected in a knee joint and 0.3 to 1.7% of getting infected in a hip joint. There are three phases of artificial joint infection: early, delayed and late.
Early – infection occurs in less than 3 months. Usual signs and symptoms are fever and joint pain, with redness and warmth over the joint operation site. The mode of infection is during the joint implant surgery. The usual bacteria involved are Staphylococcus aureus and gram negative bacilli.
Delayed – infection occurs between 3 and 24 months. There would be persistent joint pain, due to loosening of the implant. The mode of infection is during the implant surgery. Common bacteria are coagulase-negative Staphylococcus and Cutibacterium acnes.
Late – more than 24 months. It is usually presented with a sudden onset of joint pain and fever. The mode of infection is through the bloodstream. The bacteria involved are the same as those in septic arthritis of a normal joint.

Cause
Septic arthritis is most commonly caused by a bacterial infection. Bacteria can enter the joint by:

The bloodstream from an infection elsewhere (most common)
Direct penetration into the joint (arthrocentesis, arthroscopy, trauma)
A surrounding infection in the bone or tissue (uncommon, from osteomyelitis, septic bursitis, abscess).Microorganisms in the blood may come from infections elsewhere in the body such as wound infections, urinary tract infections, meningitis or endocarditis. Sometimes, the infection comes from an unknown location. Joints with preexisting arthritis, such as rheumatoid arthritis, are especially prone to bacterial arthritis spread through the blood. In addition, some treatments for rheumatoid arthritis can also increase a persons risk by causing an immunocompromised state. Intravenous drug use can cause endocarditis that spreads bacteria in the bloodstream and subsequently causes septic arthritis. Bacteria can enter the joint directly from prior surgery, intraarticular injection, trauma or joint prosthesis.

Risk factors
In children, although septic arthritis occurs in healthy children and adolescents with no co-occurring health issues, there are certain risk factors that may increase the likelihood of acquiring septic arthritis. For example, children with renal osteodystrophy or renal bone disease, certain hematological disorders and diseases causing immune suppression are risk factors for childhood septic arthritis.The rate of septic arthritis varies from 4 to 29 cases per 100,000 person-years, depending on the underlying medical condition and the joint characteristics. For those with a septic joint, 85% of the cases have an underlying medical condition while 59% of them had a previous joint disorder. Having more than one risk factor greatly increases risk of septic arthritis.
Age over 80 years
Diabetes mellitus
Osteoarthritis
Rheumatoid arthritis. Risk of septic arthritis increases with anti-tumor necrosis factor alpha treatment.
Immunosuppressive medication
Intravenous drug abuse
Recent joint surgery
Hip or knee prosthesis and skin infection
HIV infection
Other causes of sepsis

Organisms
Most cases of septic arthritis involve only one organism; however, polymicrobial infections can occur, especially after large open injuries to the joint. Septic arthritis is usually caused by bacteria, but may be caused by viral, mycobacterial, and fungal pathogens as well. It can be broadly classified into three groups: non-gonococcal arthritis, gonococcal arthritis, and others.
Non-gonococcal arthritis – These bacteria account for over 80% of septic arthritis cases and are usually staphylococci or streptococci. Such infections most commonly come from drug abuse, cellulitis, abscesses, endocarditis, and chronic osteomyelitis. Methicillin-resistant Staphylococcus aureus (MRSA) may affect 5 to 25% of the cases while gram negative bacilli affects 14 to 19% of the septic arthritis cases. Gram negative infections are usually acquired through urinary tract infections, drug abuse, and skin infections. Older people who are immunocompromised are also prone to get gram negative infections. Common gram negative organisms are: Pseudomonas aeruginosa and Escherichia coli. Both gram positive and gram negative infections are commonly spread through the blood from an infective source; but can be introduced directly into the joint or from surrounding tissue. It often affects older people, and often happens suddenly, involving only one joint. Joint aspiration cultures are positive in 90% of cases, while only 50% of blood cultures yield any organisms.
Gonococcal arthritis – Neisseria gonorrhoeae is a common cause of septic arthritis in people who are sexually active and under 40 years old. The bacteria is spread through the blood to the joint following sexual transmission. Other symptoms of disseminated gonococcal infection can include migration of joint pain, tenosynovitis and dermatitis. Synovial fluid cultures are positive in 25 to 70% of the cases while blood cultures are seldom positive. Apart from blood and joint cultures, swabs from urethra, rectum, pharynx, and cervix should also be taken. Polymerase chain reaction (PCR) is another useful way of identifying gonococcal infections if diagnosis is difficult and clinical presentation is similar to reactive arthritis.
Others – Fungal and mycobacterial infections are rare causes of septic arthritis and usually have a slow onset of joint symptoms. Mycobacterial joint infection most commonly affects hip and knee joints, caused by reactivation of past mycobacterial infections, with or without signs and symptoms of tuberculosis in lungs. Synovial fluid cultures will be positive in 80% of the cases. However, acid fast smears are not useful. Histology is not specific to myocobacterial infection as there are other granulomatous diseases that can show similar histology. Borrelia burgdorferi, a bacterium that causes lyme disease, can affect multiple large joints such as the knee. Confirmation of Lyme disease is done through enzyme-linked immunosorbent assay (ELISA) followed by confirmation using Western Blot test. It cannot be cultured from synovial fluid. However, PCR testing yields 85% positive result from synovial fluid. Viruses such as rubella, parvovirus B19, chikungunya, and HIV infection can also cause septic arthritis.
Prosthetic joint infection – Artificial joint infection are usually caused by coagulase negative Staphylococci, Staphylococcus aureus, and gram negative bacilli. Concurrent infections by multiple organisms is also reported in 20% of the cases. The risk factors of prosthetic joint infections are:  previous fracture, seropositive rheumatoid arthritis, obesity, revision arthroplasty, and surgical site infections.

List of organisms
Staphylococci (40%)Staphylococcus aureus – the most common cause in most age groups. Can be caused by skin infection, previously damaged joint, prosthetic joint or intravenous drug use.
coagulase-negative staphylococci – usually due to prosthetic joint
Streptococci – the second-most common cause (28%)Streptococcus pyogenes – a common cause in children under 5
Streptococcus pneumoniae
Group B streptococci – a common cause in infants
Haemophilus influenzae
Neisseria gonorrhoeae – the most common cause of septic arthritis in young, sexually active adults. Multiple macules or vesicles seen over the trunk are a pathognomonic feature.
Neisseria meningitidis
Escherichia coli – in the elderly, IV drug users and the seriously ill
Pseudomonas aeruginosa – IV drug users or penetrating trauma through the shoe
M. tuberculosis, Salmonella spp. and Brucella spp. – cause septic spinal arthritis
Eikenella corrodens – human bites
Pasteurella multocida, bartonella henselae, capnocytophaga – animal bites or scratches
Fungal species – immunocompromised state
Borrelia burgdorferi – ticks, causes lyme disease
Spirillum minus, Streptobacillus moniliformis– rat bites

Diagnosis
Septic arthritis should be considered whenever a person has rapid onset pain in a swollen joint, regardless of fever. One or multiple joints can be affected at the same time.Laboratory studies such as blood cultures, white blood cell count with differential, ESR, and CRP should also be included. However, white cell count, ESR, and CRP are nonspecific and could be elevated due to infection elsewhere in the body. Serologic studies should be done if lyme disease is suspected. Blood cultures can be positive in 25 to 50% of those with septic arthritis due to spread of infection from the blood. CRP more than 20 mg/L and ESR greater than 20 mm/hour together with typical signs and symptoms of septic arthritis should prompt arthrocentesis from the affected joint for synovial fluid examination.The synovial fluid should be collected before the administration of antibiotics and should be sent for gram stain, culture, leukocyte count with differential, and crystal studies. This can include NAAT testing for N. gonorrhoeae if suspected in a sexually active person.In children, the Kocher criteria is used for diagnosis of septic arthritis.

Differential diagnosis
The differential diagnosis of septic arthritis is broad and challenging. First, it has to be differentiated from acute hematogenous osteomyelitis. This is because the treatment lines of both conditions are not identical. Noteworthy, septic arthritis and acute hematogenous osteomyelitis can co-occur. Especially in the hip and shoulder joints their co-occurrence is likely and represents a diagnostic challenge. Therefore, physicians should have a high suspicion index in that regard. This is because in both the hip and shoulder joints the metaphysis is intra-articular which in turn facilitates the spread of hematogenous osteomyelitis into the joint cavity. Conversely, joint sepsis may spread to the metaphysis and induce osteomyelitis.
Acute exacerbation of juvenile idiopathic arthritis and transient synovitis of the hip both of which are non-septic conditions may mimic septic arthritis. More serious and life-threatening disorders as bone malignancies e.g. Ewing sarcoma and osteosarcoma may mimic septic arthritis associated with concurrent acute hematogenous osteomyelitis. In this regard, Magnetic resonance imaging may play an important role in the differential diagnosis.

Joint aspiration
In children, joint synovial fluid aspiration techniques aim at isolating the infectious organism by culture and sensitivity analysis. Cytological analysis of the joint aspirate can point to septic arthritis. However, a negative culture and sensitivity test does not rule out the presence of septic arthritis. Various clinical scenarios and technique-related factors may impact the validity of results of the culture and sensitivity. Additionally, results of cytological analysis, though important, should not be interpreted in isolation of the clinical settings.

In the joint fluid, the typical white blood cell count in septic arthritis is over 50,000-100,000 cells per 10−6/l (50,000-100,000 cell/mm3); where more than 90% are neutrophils is suggestive of septic arthritis. For those with prosthetic joints, white cell count more than 1,100 per mm3 with neutrophil count greater than 64% is suggestive of septic arthritis. However, septic synovial fluid can have white blood cell counts as low as a few thousand in the early stages. Therefore, differentiation of septic arthritis from other causes is not always possible based on cell counts alone. Synovial fluid PCR analysis is useful in finding less common organisms such as Borrelia species. However, measuring protein and glucose levels in joint fluid is not useful for diagnosis.The Gram stain can rule in the diagnosis of septic arthritis, however, cannot exclude it.Synovial fluid cultures are positive in over 90% of nongonoccocal arthritis; however, it is possible for the culture to be negative if the person received antibiotics prior to the joint aspiration. Cultures are usually negative in gonoccocal arthritis or if fastidious organisms are involved.If the culture is negative or if a gonococcal cause is suspected, NAAT testing of the synovial fluid should be done.Positive crystal studies do not rule out septic arthritis. Crystal-induced arthritis such as gout can occur at the same time as septic arthritis.A lactate level in the synovial fluid of greater than 10 mmol/L makes the diagnosis very likely.

Blood tests
Laboratory testing includes white blood cell count, ESR and CRP. These values are usually elevated in those with septic arthritis; however, these can be elevated by other infections or inflammatory conditions and are, therefore, nonspecific. Procalcitonin may be more useful than CRP.Blood cultures can be positive in up to half of people with septic arthritis.

Imaging
Imaging such as x-ray, CT, MRI or ultrasound are nonspecific. They can help determine areas of inflammation but cannot confirm septic arthritis.When septic arthritis is suspected, x-rays should generally be taken. This is used to assess any problems in the surrounding structures such as bone fractures, chondrocalcinosis, and inflammatory arthritis which may predispose to septic arthritis. While x-rays may not be helpful early in the diagnosis/treatment, they may show subtle increase in joint space and tissue swelling. Later findings include joint space narrowing due to destruction of the joint.Ultrasound is effective at detecting joint effusions.CT and MRI are not required for diagnosis; but if the diagnosis is unclear or the joints are hard to examine (ie.sacroiliac or hip joints); they can help to assess for inflammation/infection in or around the joint (i.e. Osteomyelitis), bone erosions, and bone marrow oedema. Both CT and MRI scans are helpful in guiding arthrocentesis of the joints.

Differential diagnosis
Crystal induced arthritis such as gout or pseudogout
Inflammatory arthritisRheumatoid arthritis
Seronegative spondyloarthropathy such as ankylosing spondylitis or reactive arthritis
Traumatic arthritis due to hemarthrosis, fracture or foreign body
Osteoarthritis

Treatment
Treatment is usually with intravenous antibiotics, analgesia and washout and/or aspiration of the joint. Draining the pus from the joint is important and can be done either by needle (arthrocentesis) or opening the joint surgically (arthrotomy).Empiric antibiotics for suspected bacteria should be started. This should be based on Gram stain of the synovial fluid as well as other clinical findings. General guidelines are as follows:

Gram positive cocci – vancomycin
Gram negative cocci – Ceftriaxone
Gram negative bacilli – Ceftriaxone, cefotaxime, or ceftazidime
Gram stain negative and immunocompetent – vancomycin
Gram stain negative and immunocompromised – vancomycin + third generation cephalosphorin
IV drug use (possible pseudomonas aeruginosa) – ceftazidime +/- an aminoglycosideOnce cultures are available, antibiotics can be changed to target the specific organism. After a good response to intravenous antibiotics, people can be switched to oral antibiotics. The duration of oral antibiotics varies, but is generally for 1–4 weeks depending on the offending organism.  Repeated daily joint aspiration is useful in the treatment of septic arthritis. Every aspirate should be sent for culture, gram stain, white cell count to monitor the progress of the disease. Both open surgery and arthroscopy are helpful in the drainage of the infected joint. During surgery, lysis of the adhesions, drainage of pus, and debridement of the necrotic tissues are done. Close follow up with physical exam & labs must be done to make sure the person is no longer feverish, pain has resolved, has improved range of motion, and lab values are normalized.In infection of a prosthetic joint, a biofilm is often created on the surface of the prosthesis which is resistant to antibiotics. Surgical debridement  is usually indicated in these cases. A replacement prosthesis is usually not inserted at the time of removal to allow antibiotics to clear infection of the region. People that cannot have surgery may try long-term antibiotic therapy in order to suppress the infection. The use of prophylactic antibiotics before dental, genitourinary, gastrointestinal procedures to prevent infection of the implant is controversial.Low-quality evidence suggests that the use of corticosteroids may reduce pain and the number of days of antibiotic treatment in children.

Outcomes
Risk of permanent impairment of the joint varies greatly. This usually depends on how quickly treatment is started after symptoms occur as longer lasting infections cause more destruction to the joint </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Benign paroxysmal vertigo of childhood and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Spastic quadriplegia and explain in detail? [/INST] Spastic quadriplegia, also known as spastic tetraplegia, is a subset of spastic cerebral palsy that affects all four limbs (both arms and legs).
Compared to quadriplegia, spastic tetraplegia is defined by spasticity of the limbs as opposed to strict paralysis. It is distinguishable from other forms of cerebral palsy in that those afflicted with the condition display stiff, jerky movements stemming from hypertonia of the muscles.Spastic quadriplegia, while affecting all four limbs more or less equally, can still present parts of the body as stiffer than others, such as one arm being tighter than another arm, and so forth. Spastic triplegia, meanwhile, involves three limbs (such as one arm and two legs, or one leg and two arms, etc.); spastic diplegia affects two limbs (commonly just the legs), spastic hemiplegia affects one or another entire side of the body (left or right); and spastic monoplegia involves a single limb.

Symptoms and signs
Spastic quadriplegia can be detected by the abnormal development of motor skills in children. Symptoms can present themselves as early as three months but are generally seen before the child reaches two years of age. Some warning signs include: a child of more than two months who has stiff legs that scissor and is unable to control his or her head, and a child of more than twelve months who has not developed the ability to crawl or stand.Spastic quadriplegia also presents a range of symptoms that affect the musculature. Many experience contractures, which are defined as joints that cannot be stretched or moved.  Clonus is another symptom that is characterized by alternating, rapid muscle contraction and relaxation. This presents itself as tremors and scissoring of the limbs. Distonia, or lasting muscle contractions and tightness, is also often experienced by those affected by spastic quadriplegia. These involuntary muscle contractions may affect the development of structural muscle around the hip and lead to hip dysplasia and dislocation, making it difficult to sit. The combination of these symptoms often makes it difficult for the patients to walk as well. Although the arms and legs of patients are often stiff, the neck is usually limp due to the lack of voluntary muscle control.

Causes
Spastic quadriplegia is generally caused by brain damage or disruptions in normal brain development preceding birth. According to the National Institutes of Health, there are four types of brain damage that can cause spastic quadriplegia. These include, damage to the white matter (periventricular leukomalacia), abnormal brain development (cerebral dysgenesis), bleeding in the brain (intracranial hemorrhage), and brain damage due to lack of oxygen (hypoxic-ischemic encephalopathy or intrapartum asphyxia).The white matter of the brain is especially vulnerable between the 26th and 34th weeks of maturation, and damage to the white matter can interfere with the brain’s ability to transmit signals to the rest of the body. Spastic quadriplegia can be caused by a condition known as periventricular leukomalacia which results in the formation of lesions and holes in the white matter of the brain.Prior to the 26th week of maturation, the fetal brain is particularly susceptible to various toxins whose effects can ultimately hinder normal development. Exposure of the brain to infectious agents is especially dangerous because they can trigger immune responses that activate cytokines and lead to inflammation of the brain. Some infections that have been linked to the development of spastic quadriplegia include meningitis, herpes, rubella, and encephalitis. A difference in blood types between the mother and the fetus can also initiate a problematic immune response and cause brain damage. Severe jaundice, can also lead to brain damage and spastic quadriplegia due to a buildup of bilirubin in the blood.Bleeding in the brain caused by fetal strokes, blood clots, weak and malformed blood vessels, or high maternal blood pressure may also lead to brain damage causing spastic quadriplegia. Maternal infection, most specifically pelvic inflammatory disease, has been shown to increase the risk of fetal stroke.Hypoxia, lack of oxygen to the brain, can also cause damage in the cerebral motor cortex and other brain regions </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bruns nystagmus and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pseudopelade of Brocq and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Manganese deficiency and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Lisch epithelial corneal dystrophy and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Carney complex and explain in detail? [/INST] Carney complex and its subsets LAMB syndrome and NAME syndrome are autosomal dominant conditions comprising myxomas of the heart and skin, hyperpigmentation of the skin (lentiginosis), and endocrine overactivity. It is distinct from Carneys triad. Approximately 7% of all cardiac myxomas are associated with Carney complex.

Presentation
The spotty skin pigmentation and lentigines occur most commonly on the face, especially on the lips, eyelids, conjunctiva and oral mucosa. Cardiac myxomas may lead to embolic strokes and heart failure and may present with fever, joint pain, shortness of breath, diastolic rumble and tumor plop. Myxomas may also occur outside the heart, usually in the skin and breast </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Chemical colitis and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is 3-Methylglutaconic aciduria and explain in detail? [/INST] 3-Methylglutaconic aciduria (MGA) is any of at least five metabolic disorders that impair the bodys ability to make energy in the mitochondria. As a result of this impairment, 3-methylglutaconic acid and 3-methylglutaric acid build up and can be detected in the urine.
3-Methylglutaconic acid is an organic acid.  The double carboxylic acid functions are the principal cause of the strength of this acid. 3-methylglutaconic acid can be detected by the presence of the acid function and the double connection that involves reactivity with some specific substances.

Genetics
The inheritance patterns of 3-methylglutaconic aciduria differ depending on the gene involved.

Types I and III are inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered. Most often, the parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene but do not show signs and symptoms of the disorder.
Type II is inherited in an X-linked recessive pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present in both copies of the gene to cause the disorder. Males are affected by X-linked recessive disorders much more frequently than females. A striking characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.
The inheritance pattern of 3-methylglutaconic aciduria type IV is unknown.

Diagnosis
Diagnosis is typically post-mortem.

Classification
There are five known subgroups of MGA; MGA type I, II, III, IV & V.

The characteristic features of 3-methylglutaconic aciduria type I include speech delay, delayed development of both mental and motor skills (psychomotor delay), elevated levels of acid in the blood and tissues (metabolic acidosis), abnormal muscle tone (dystonia), and spasms and weakness affecting the arms and legs (spastic quadriparesis). Fewer than 20 cases of 3-methylglutaconic aciduria type I have been reported.
Barth syndrome is a common name for 3-methylglutaconic aciduria type II. The main features of Barth syndrome include a weakened and enlarged heart (dilated cardiomyopathy), recurrent infections due to low numbers of white blood cells (neutropenia), skeletal problems, and delayed growth. The incidence of 3-methylglutaconic aciduria type II is approximately 1 in 200,000 male infants.
Costeff syndrome is another name for 3-methylglutaconic aciduria type III. This disorder is characterized mainly by the degeneration of the optic nerves, which carry information from the eyes to the brain. Sometimes other nervous system problems occur, such as an inability to maintain posture, poor muscle tone, the development of certain involuntary movements (extrapyramidal dysfunction), and a general decrease in brain function (cognitive deficit). The incidence of 3-methylglutaconic aciduria type III is about 1 in 10,000 newborns in the Iraqi Jewish population. This disorder is extremely rare in all other populations.
The signs and symptoms of 3-methylglutaconic aciduria type IV are variable and overlap with types I-III. The incidence of 3-methylglutaconic aciduria type IV is unknown.

Treatment
There is no known treatment or cure.

Epidemiology
3-Methylglutaconic aciduria seems to be  most prevalent amongst the Jewish population of Iraq. However, a high concentration of one type is found in the Saguenay-Lac-Saint-Jean region of Canada </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Waterhouse–Friderichsen syndrome and explain in detail? [/INST] Waterhouse–Friderichsen syndrome (WFS) is defined as adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection. Typically, it is caused by  Neisseria meningitidis.The bacterial infection leads to massive bleeding into one or (usually) both adrenal glands. It is characterized by overwhelming bacterial infection meningococcemia leading to massive blood invasion, organ failure, coma, low blood pressure and shock, disseminated intravascular coagulation (DIC) with widespread purpura, rapidly developing adrenocortical insufficiency and death.

Signs and symptoms
Waterhouse-Friderichsen syndrome can be caused by a number of different organisms (see below). When caused by Neisseria meningitidis, WFS is considered the most severe form of meningococcal sepsis. The onset of the illness is nonspecific with fever, rigors, vomiting, and headache. Soon a rash appears; first macular, not much different from the rose spots of typhoid, and rapidly becoming petechial and purpuric with a dusky gray color. Low blood pressure (hypotension) develops and rapidly leads to septic shock. The cyanosis of extremities can be extreme and the patient is very prostrated or comatose. In this form of meningococcal disease, meningitis generally does not occur. Low levels of blood glucose and sodium, high levels of potassium in the blood, and the ACTH stimulation test demonstrate the acute adrenal failure. Leukocytosis need not be extreme and in fact leukopenia may be seen and it is a very poor prognostic sign. C-reactive protein levels can be elevated or almost normal. Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Diastasis (pathology) and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Selenium deficiency and explain in detail? [/INST] Selenium deficiency occurs when an organism lacks the required levels of selenium, a critical nutrient in many species. Deficiency, although relatively rare in healthy well-nourished individuals, can have significant negative results, affecting the health of the heart and the nervous system; contributing to depression, anxiety, and dementia; and interfering with reproduction and gestation.

Signs and symptoms
Selenium deficiency in combination with Coxsackievirus infection can lead to Keshan disease, which is potentially fatal. Selenium deficiency also contributes (along with iodine deficiency) to Kashin-Beck disease. The primary symptom of Keshan disease is myocardial necrosis, leading to weakening of the heart. Kashin-Beck disease results in atrophy, degeneration and necrosis of cartilage tissue.  Keshan disease also makes the body more susceptible to illness caused by other nutritional, biochemical, or infectious diseases.
Selenium is also necessary for the conversion of the thyroid hormone thyroxine (T4) into its more active counterpart triiodothyronine (T3), and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage.

Causes
It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90).People dependent on food grown from selenium-deficient soil may be at risk for deficiency.  Increased risk for developing various diseases has also been noted, even when certain individuals lack optimal amounts of selenium, but not enough to be classified as deficient.For some time now, it has been reported in medical literature that a pattern of side-effects possibly associated with cholesterol-lowering drugs (e.g., statins) may resemble the pathology of selenium deficiency.

Diagnosis
Reference ranges
The European Food Safety Authority (EFSA) recommends a dietary allowance of 70 μg per day selenium intake for adults. In the US, the Dietary Reference Intake for adults is 55 µg/day. In the UK it is 75 µg/day for adult males and 60 µg/day for adult females. 55 µg/day recommendation is based on full expression of plasma glutathione peroxidase. Selenoprotein P is a better indicator of selenium nutritional status, and full expression of it would require more than 66 µg/day.

Epidemiology and prevention
Selenium deficiency is uncommon, but regions in China, Europe, Russia and New Zealand have low levels of selenium in croplands and diet. The worldwide prevalence of selenium deficiency is however predicted to rise under climate change due to the loss of selenium from croplands. These diseases are most common in certain parts of China where the intake is low because the soil is extremely deficient in selenium. Studies in Jiangsu Province of China have indicated a reduction in the prevalence of these diseases by taking selenium supplements. In Finland, selenium salts are added to chemical fertilizers, as a way to increase selenium in soils. Dietary supplements may utilize sodium selenite, L-selenomethionine or selenium-enriched yeast.

In non-human animals
In some regions (e.g. much of the northeastern and northwestern US and adjacent Canada, and the southeastern US), selenium deficiency in some animal species is common unless supplementation is carried out.   Selenium deficiency is responsible (either alone or together with vitamin E deficiency) for many of the cases of WMD ("white muscle disease"), evidenced at slaughter or during necropsy by whitish appearance of striated muscle tissue due to bleaching by peroxides and hydroperoxides </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Protothecosis and explain in detail? [/INST] Protothecosis, otherwise known as Algaemia, is a disease found in dogs, cats, cattle, and humans caused by a type of green alga known as Prototheca that lacks chlorophyll and enters the human or animal bloodstream. It and its close relative Helicosporidium are unusual in that they are actually green algae that have become parasites.  The two most common species are Prototheca wickerhamii and Prototheca zopfii. Both are known to cause disease in dogs, while most human cases are caused by P. wickerhami. Prototheca is found worldwide in sewage and soil. Infection is rare despite high exposure, and can be related to a defective immune system.  In dogs, females and Collies are most commonly affected.The first human case was identified in 1964 in Sierra Leone.

Cause
Prototheca has been thought to be a mutant of Chlorella, a type of single-celled green alga. However, while Chlorella contains galactose and galactosamine in the cell wall, Prototheca lacks these. Also, Chlorella obtains its energy through photosynthesis, while Prototheca is saprotrophic, feeding on dead and decaying organic matter.  When Prototheca was first isolated from slime flux of trees in 1894, it was thought to be a type of fungus </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Myhre syndrome and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Mesenteric pseudocyst and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Optic nerve glioma and explain in detail? [/INST] Optic nerve glioma (or optic glioma), a form of glioma which affects the optic nerve, is often one of the central nervous system manifestations of neurofibromatosis 1.Optic gliomas are usually pilocytic tumors, and can involve the optic nerve or optic chiasm. Optic gliomas are usually associated with neurofibromatosis type 1 in 30% of people with the condition.Optic nerve gliomas have low mortality but extremely high prevalence of vision loss & eye-bulging exophthalmos) in children. As of 2014, approximately 1000 cases had been reported.

Diagnosis
Optic nerve gliomas are diagnosed using magnetic resonance imaging (MRI) and CT scans. The tumor adopts a fusiform appearance, appearing wider in the middle and tapered at the ends. Enlargement of the optic nerve along with a downward kink in the mid-orbit is usually observed. While CT scans allow for optic nerve evaluation, MRI allows for intracranial evaluation to observe if the tumor has extended to other regions such as the optic chiasm & hypothalamus.

Treatment
The main goal of treating optic gliomas is to preserve vision for as long as possible </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Da Costas syndrome and explain in detail? [/INST] Da Costas syndrome (also known as "soldiers heart", cardiac neurosis, chronic asthenia, effort syndrome, functional cardiovascular disease, neurocirculatory asthenia, primary neurasthenia, subacute asthenia and irritable heart) is a psychiatric syndrome which presents a set of symptoms similar to those of heart disease. These include fatigue upon exertion, shortness of breath, palpitations, sweating, and chest pain.
While a physical examination does not reveal any gross physiological abnormalities, orthostatic intolerance has been noted. It was originally thought to be a cardiac condition, and treated with a predecessor to modern cardiac drugs. While the condition was eventually recategorized as psychiatric, in modern times, it is known to represent several disorders, some of which now have a known medical basis. For stress-related combat disorders generally, see post-traumatic stress disorder.
Historically, similar forms of this disorder have been noticed in various wars, like the American Civil War and Crimean war, and among British troops who colonized India. The condition was named after Jacob Mendes Da Costa who investigated and described the disorder in 1871.

Signs and symptoms
Symptoms of Da Costas syndrome include fatigue upon exertion, weakness induced by minor activity, shortness of breath, palpitations, sweating, and chest pain.

Causes
Da Costas syndrome was originally considered to be heart failure or other cardiac condition, and was later recategorized to be psychiatric. The term is no longer in common use by any medical agencies and has generally been superseded by more specific diagnoses, some of which have a medical basis.

Diagnosis
Although it is listed in the ICD-9 (306.2) and ICD-10 (F45.8) under "somatoform autonomic dysfunction", the term is no longer in common use by any medical agencies and has generally been superseded by more specific diagnoses.
The orthostatic intolerance observed by Da Costa has since also been found in patients diagnosed with chronic fatigue syndrome, postural orthostatic tachycardia syndrome (POTS) and mitral valve prolapse syndrome. In the 21st century, this intolerance is classified as a neurological condition. Exercise intolerance has since been found in many organic diseases.

Classification
There are many names for the syndrome, which has variously been called soldiers heart, cardiac neurosis, chronic asthenia, effort syndrome, functional cardiovascular disease, neurocirculatory asthenia, primary neurasthenia, and subacute asthenia. Da Costa himself called it irritable heart  and the term soldiers heart was in common use both before and after his paper. Most authors use these terms interchangeably, but some authors draw a distinction between the different manifestations of this condition, preferring to use different labels to highlight the predominance of psychiatric or non-psychiatric complaints. For example, Oglesby Paul writes that "Not all patients with neurocirculatory asthenia have a cardiac neurosis, and not all patients with cardiac neurosis have neurocirculatory asthenia." None of these terms have widespread use.

Treatment
The report of Da Costa shows that patients recovered from the more severe symptoms when removed from the strenuous activity or sustained lifestyle that caused them. A reclined position and forced bed rest were the most beneficial.Other treatments evident from the previous studies were improving physique and posture, appropriate levels of exercise where possible, wearing loose clothing about the waist, and avoiding postural changes such as stooping, or lying on the left or right side, or the back in some cases, which relieved some of the palpitations and chest pains, and standing up slowly can prevent the faintness associated with postural or orthostatic hypotension in some cases.
Pharmacological intervention came in the form of digitalis, a group of glycoside drugs derived from the foxglove (Digitalis purpurea), which is now known to act as a sodium-potassium ATPase inhibitor, increasing stroke volume and decreasing heart rate; at the time it was used for the latter effect in patients with palpitations.

History
Da Costas syndrome is named for the surgeon Jacob Mendes Da Costa, who first observed it in soldiers during the American Civil War. At the time it was proposed, Da Costas syndrome was seen as a very desirable physiological explanation for "soldiers heart". Use of the term "Da Costas syndrome" peaked in the early 20th century. Towards the mid-century, the condition was generally re-characterized as a form of neurosis. It was initially classified as "F45.3" (under somatoform disorder of the heart and cardiovascular system) in ICD-10, and is now classified under "somatoform autonomic dysfunction".
Da Costas syndrome involves a set of symptoms which include left-sided chest pains, palpitations, breathlessness, and fatigue in response to exertion. Earl de Grey who presented four reports on British soldiers with these symptoms between 1864 and 1868, and attributed them to the heavy weight of military equipment being carried in knapsacks which were tightly strapped to the chest in a manner which constricted the action of the heart </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Fontanelle and explain in detail? [/INST] A fontanelle (or fontanel) (colloquially, soft spot) is an anatomical feature of the infant human skull comprising soft membranous gaps (sutures) between the cranial bones that make up the calvaria of a fetus or an infant. Fontanelles allow for stretching and deformation of the neurocranium both during birth and later as the brain expands faster than the surrounding bone can grow. Premature complete ossification of the sutures is called craniosynostosis.
After infancy, the anterior fontanelle is known as the bregma.

Structure
An infants skull consists of five main bones: two frontal bones, two parietal bones, and one occipital bone. These are joined by fibrous sutures, which allow movement that facilitates childbirth and brain growth.

Posterior fontanelle is triangle-shaped. It lies at the junction between the sagittal suture and lambdoid suture. At birth, the skull features a small posterior fontanelle with an open area covered by a tough membrane, where the two parietal bones adjoin the occipital bone (at the lambda). The posterior fontanelles ossify within 6–8 weeks after birth. This is called intramembranous ossification.  The mesenchymal connective tissue turns into bone tissue.
Anterior fontanelle is a diamond-shaped membrane-filled space located between the two frontal and two parietal bones of the developing fetal skull. It persists until approximately 18 months after birth. It is at the junction of the coronal suture and sagittal suture. The fetal anterior fontanelle may be palpated until 18 months. In cleidocranial dysostosis, however, it is often late in closing at 8–24 months or may never close.  Examination of an infant includes palpating the anterior fontanelle.
Two smaller fontanelles are located on each side of the head, more anteriorly the sphenoidal or anterolateral fontanelle (between the sphenoid, parietal, temporal, and frontal bones) and more posteriorly the mastoid or posterolateral fontanelle (between the temporal, occipital, and parietal bones).During birth, fontanelles enable the bony plates of the skull to flex, allowing the childs head to pass through the birth canal. The ossification of the bones of the skull causes the anterior fontanelle to close over by 9 to 18 months. The sphenoidal and posterior fontanelles close during the first few months of life. The closures eventually form the sutures of the neurocranium. Other than the anterior and posterior fontanelles, the mastoid fontanelle and the sphenoidal fontanelle are also significant.

Closure
In humans, the sequence of fontanelle closure is as follows:
The posterior fontanelle generally closes 2 to 3 months after birth;
The sphenoidal fontanelle is the next to close around 6 months after birth;
The mastoid fontanelle closes next from 6 to 18 months after birth; and
The anterior fontanelle is generally the last to close between 12 and 18 months.

Clinical significance
The fontanelle may pulsate, and although the precise cause of this is not known, it is normal and seems to echo the heartbeat, perhaps via the arterial pulse within the brain vasculature, or in the meninges. This pulsating action is how the soft spot got its name – fontanelle is borrowed from the old French word fontenele, which is a diminutive of fontaine, meaning "spring". It is assumed that the term spring is used because of the analogy of the dent in a rock or earth where a spring arises.Parents may worry that their infant may be more prone to injury at the fontanelles. In fact, although they may colloquially be called "soft-spots", the membrane covering the fontanelles is extremely tough and difficult to penetrate.Fontanelles allow the infant brain to be imaged using ultrasonography. Once they are closed, most of the brain is inaccessible to ultrasound imaging, because the bony skull presents an acoustic barrier.

Disorders
Bulging
A very tense or bulging anterior fontanelle indicates raised intracranial pressure. Increased cranial pressure in infants may cause the fontanelles to bulge or the head to begin to enlarge abnormally. It can occur due to:
Craniosynostosis – premature fusion of the cranial sutures
Encephalitis – swelling (inflammation) of the brain, most often due to infections
Hydrocephalus – a buildup of fluid inside the skull
Meningitis – infection of the membranes covering the brain
Shaken baby syndrome

Sunken
A sunken (also called "depressed") fontanelle indicates dehydration or malnutrition.

Enlarged
The fontanelles may be enlarged, may be slow to close, or may never close, most commonly due to causes like:
Down syndrome
Hydrocephalus
Intrauterine growth restriction (IUGR)
Premature birthRarer causes include:
Achondroplasia
Apert syndrome
Cleidocranial dysostosis
Congenital rubella
Neonatal hypothyroidism
Osteogenesis imperfecta
Rickets

Third
Sometimes there is a third bigger fontanelle other than posterior and anterior ones in a newborn. In one study, the frequency of third fontanelles in an unselected population of newborn infants was 6.3%. It is very common in Down syndrome and some congenital infections. If present, the physician should rule out serious conditions associated with the third fontanelle.

Other animals
Primates
In apes the fontanelles fuse soon after birth </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bolivian hemorrhagic fever and explain in detail? [/INST] Bolivian hemorrhagic fever (BHF), also known as black typhus or Ordog Fever, is a hemorrhagic fever and zoonotic infectious disease originating in Bolivia after infection by Machupo mammarenavirus.BHF was first identified in 1963 as an ambisense RNA virus of the Arenaviridae family, by a research group led by Karl Johnson. The mortality rate is estimated at 5 to 30 percent. Due to its pathogenicity, Machupo virus requires Biosafety Level Four conditions, the highest level.During the period between February and March 2007, some 20 suspected BHF cases (3 fatal) were reported to the Servicio Departamental de Salud (SEDES) in Beni Department, Bolivia. In February 2008, at least 200 suspected new cases (12 fatal) were reported to SEDES. In November 2011, a second case was confirmed near the departmental capital of Trinidad, and a serosurvey was conducted to determine the extent of Machupo virus infections in the department. A SEDES expert involved in the survey expressed his concerns about the expansion of the virus to other provinces outside the endemic regions of Mamoré and Iténez provinces.

Epidemiology
History
The disease was first encountered in 1962, in the Bolivian village of San Joaquín, hence the name "Bolivian" Hemorrhagic Fever. When initial investigations failed to find an arthropod carrier, other sources were sought before finally determining that the disease was carried by infected mice. Although mosquitoes were not the cause as originally suspected, the extermination of mosquitoes using DDT to prevent malaria proved to be indirectly responsible for the outbreak in that the accumulation of DDT in various animals along the food chain led to a shortage of cats in the village; subsequently, a mouse plague erupted in the village, leading to an epidemic.

Vectors
The vector is the  large vesper mouse (Calomys callosus), a rodent indigenous to northern Bolivia. Infected animals are asymptomatic and shed the virus in excreta, thereby infecting humans. Evidence of person-to-person transmission of BHF exists but is believed to be rare.

Symptoms
The infection has a slow onset with fever, malaise, headache and myalgia, very similar to Malaria symptoms </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Abscess of thymus and explain in detail? [/INST]  </s>