In swine, three influenza A virus subtypes (H1N1, H3N2, and H1N2) are circulating throughout the world.[citation needed] In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. Most H3N2 virus isolates are triple reassortants, meaning that it contains genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.[citation needed]
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Systemic lupus erythematosus (SLE or lupus, pronounced s?’st?m?k ‘lu?p?s ??r???im?’to?s?s (help·info)) is a chronic autoimmune connective tissue disease that can affect any part of the body. As occurs in other autoimmune diseases, the immune system attacks the body’s cells and tissue, resulting in inflammation and tissue damage.[1]

SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remissions. The disease occurs nine times more often in women than in men, especially between the ages of 15 and 50, and is more common in those of non-European descent.[2][3][4]

SLE is treatable through addressing its symptoms, mainly with corticosteroids and immunosuppressants; there is currently no cure. SLE can be fatal, although with recent medical advances, fatalities are becoming increasingly rare. Survival for people with SLE in the United States, Canada, and Europe is approximately 95% at five years, 90% at 10 years, and 78% at 20 years.[4]

There are several types of lupus; in general, when the word lupus alone is used, reference is to systemic lupus erythematosus, as discussed in this article. Other types include:[1]

SLE is one of several diseases known as “the great imitators” because it often mimics or is mistaken for other illnesses.[7] SLE is a classical item in differential diagnosis,[2] because SLE symptoms vary widely and come and go unpredictably. Diagnosis can thus be elusive, with some people suffering unexplained symptoms of untreated SLE for years.

Common initial and chronic complaints are fever, malaise, joint pains, myalgias, fatigue, and temporary loss of cognitive abilities. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms (see below), however, they are considered suggestive.[8]

As many as 30% of sufferers have some dermatological symptoms (and 65% suffer such symptoms at some point), with 30% to 50% suffering from the classic malar rash (or butterfly rash) associated with the disease. Some may exhibit thick, red scaly patches on the skin (referred to as discoid lupus). Alopecia; mouth, nasal, and vaginal ulcers; and lesions on the skin are also possible manifestations.

The most commonly saught medical attention is for joint pain, with the small joints of the hand and wrist usually affected, although all joints are at risk. The Lupus Foundation of America estimates that more than 90 percent will experience joint and/or muscle pain at some time during the course of their illness.[9] Unlike rheumatoid arthritis, lupus arthritis is less disabling and usually does not cause severe destruction of the joints. Fewer than ten percent of people with lupus arthritis will develop deformities of the hands and feet.[9]

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Syringomyelia (IPA: /s??r??go?ma?’i?li?/) is a generic term referring to a disorder in which a cyst or cavity forms within the spinal cord. This cyst, called a syrinx, can expand and elongate over time, destroying the spinal cord. Since the spinal cord connects the brain to nerves in the extremities, this damage may result in pain, weakness, and stiffness in the back, shoulders, arms, or legs. In some cases paralysis occurs. Other symptoms may include headaches and a loss of the ability to feel extremes of hot or cold, especially in the hands. Each patient experiences a different combination of symptoms. These symptoms typically vary depending on the extent and, often more critically, to the location of the syrinx within the spinal cord.

Other, more common disorders share the early symptoms of syringomyelia. In the past, this has made diagnosis difficult. The advent of one diagnostic test, however, called magnetic resonance imaging or MRI, has significantly increased the number of syringomyelia cases diagnosed in the beginning stages of the disorder.

Syringomyelia has a prevalence estimated at 8.4 cases per 100,000 people,[1] or about 21,000 Americans, with symptoms usually beginning in young adulthood. Signs of the disorder tend to develop slowly, although sudden onset may occur with coughing, straining, or myelopathy. If not treated surgically, syringomyelia often leads to progressive weakness in the arms and legs, loss of hand sensation, and chronic, severe pain.

A watery, protective substance known as cerebrospinal fluid normally flows around the spinal cord and brain, transporting nutrients and waste products. It also serves to cushion the brain. Excess cerebrospinal fluid in the central canal of the spinal cord is called hydromyelia. This term refers to increased cerebrospinal fluid that is contained within the ependyma of the central canal. When the fluid dissects into the surrounding white matter, the term syringomyelia is applied. As these conditions coexist in the majority of cases, the term syringohydromyelia is applied. However, most physicians use the terms interchangeably.

A number of medical conditions can cause an obstruction in the normal flow of cerebrospinal fluid, redirecting it into the spinal cord itself. For reasons that are only now becoming clear, this results in syrinx formation. Cerebrospinal fluid fills the syrinx. Pressure differences along the spine cause the fluid to move within the cyst. Physicians believe that it is this continual movement of fluid that results in cyst growth and further damage to the spinal cord.

Generally, there are two forms of syringomyelia.

The first major form relates to an abnormality of the brain called an Arnold-Chiari malformation, named after the physicians who first characterized it. This is the most common cause of syringomyelia, where the anatomic abnormality causes the lower part of the cerebellum to protrude from its normal location in the back of the head into the cervical or neck portion of the spinal canal. A syrinx may then develop in the cervical region of the spinal cord. Because of the relationship that was once thought to exist between the brain and spinal cord in this type of syringomyelia, physicians sometimes refer to it as communicating syringomyelia. Here, symptoms usually begin between the ages of 25 and 40 and may worsen with straining or any activity that causes cerebrospinal fluid pressure to fluctuate suddenly. Some patients, however, may have long periods of stability. Some patients with this form of the disorder also have hydrocephalus, in which cerebrospinal fluid accumulates in the skull, or a condition called arachnoiditis, in which a covering of the spinal cord–the arachnoid membrane–is inflamed.

The second major form of syringomyelia occurs as a complication of trauma, meningitis, hemorrhage, a tumor, or arachnoiditis. Here, the syrinx or cyst develops in a segment of the spinal cord damaged by one of these conditions. The syrinx then starts to expand. This is sometimes referred to as noncommunicating syringomyelia. Symptoms may appear months or even years after the initial injury, starting with pain, weakness, and sensory impairment originating at the site of trauma.

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Syringomas are harmless sweat duct tumors, typically found clustered on eyelids, although they may also be found in the armpits, umbilicus, or vulva. They are skin-colored or yellowish firm rounded bumps, 1-3 mm in diameter, and are often confused with xanthelasma.

They may be removed with erbium or carbon dioxide lasers.

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Syndactyly (from Greek s??- = “together” plus da?t???? = “finger”) is a condition where two or more digits are fused together. It occurs normally in some mammals, such as the siamang but is an unusual condition in humans.

Syndactyly can be simple or complex.

Syndactyly can be complete or incomplete.

Complicated syndactyly occurs as part of a syndrome (such as Apert’s syndrome) and typically involves more digits and with complex syndactyly.

Fenestrated syndactyly means the skin is joined for most of the digit but in a proximal area there is gap in the syndactyly with normal skin. This type of syndactyly is found in amniotic band syndrome.

Simple syndactyly can be full or partial, and is present at birth (congenital). In early human fetal development, webbing (syndactyly) of the toes and fingers is normal. At about 16 weeks of gestation, apoptosis takes place and an enzyme dissolves the tissue between the fingers and toes, and the webbing disappears. In some fetuses, this process does not occur completely between all fingers or toes and some residual webbing remains.

Five types[1] of syndactyly have been identified in humans. The corresponding loci associated with these types and their common phenotypical expression are as follows:

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Sweet’s syndrome, or acute febrile neutrophilic dermatosis,[1] is a condition characterized by the sudden onset of fever, leukocytosis, and tender, erythematous, well-demarcated papules and plaques which show dense neutrophilic infiltrates on histologic examination.

It is named for Robert Douglas Sweet.[2][3]

Although it may occur in the absence of other known disease, Sweet’s syndrome is often associated with hematologic disease (including leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease).

A genetic association has been suggested,[4] but no specific genetic link has been identified.

Sweet, working in Plymouth in 1964, described a disease with four features: fever; leukocytosis; acute, tender, red plaques; and a papillary dermal infiltrate of neutrophils. This led to the name acute febrile neutrophilic dermatosis. Larger series of patients showed that fever and neutrophilia are not consistently present. The diagnosis is based on the two constant features, a typical eruption and the characteristic histologic features; thus the eponym Sweet’s syndrome (SS) is used.

Sweet’s syndrome can be classified based upon the clinical setting in which it occurs: classical or idiopathic Sweet’s syndrome, malignancy-associated Sweet’s syndrome, and drug-induced Sweet’s syndrome.[5]

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Sucrose intolerance, also called Congenital Sucrase-Isomaltase Deficiency (CSID)[1] or Sucrase-isomaltase deficiency,[2] is the condition in which sucrase, an enzyme needed for proper metabolization of sucrose, is not produced in the small intestine.

It is more common among the Inupiat.[3]

The result of consuming sucrose is excess gas production and often diarrhea and malabsorption.

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Succinic semialdehyde dehydrogenase deficiency (SSADHD), also known as 4-hydoxybutyric aciduria or gamma-hydoxybutyric aciduria, is a rare autosomal recessive disorder[1] of the degradation pathway of the inhibitory neurotransmitter ?-aminobutyric acid, or GABA. The disorder has been identified in approximately 350 families, with a significant proportion being consanguineous families.[2] The first case was identified in 1981 and published in a Dutch clinical chemistry journal that highlighted a patient that suffered from a number of neurological conditions such as delayed intellectual, motor, speech, and language as the most common manifestations. Later cases reported in the early 1990s began to show that hypotonia, hyporreflexia, seizures, and a nonprogressive ataxia were frequent clinical features as well.[3]

SSADH deficiency is caused by an enzyme deficiency in GABA degradation. Under normal conditions, SSADH works with the enzyme GABA transaminase to convert GABA to succinic acid. Succinic acid can then be utilized for energy production via the Krebs cycle. However, because of the deficiency, the final intermediate of the GABA degradation pathway, succinic semialdehyde, accumulates and cannot be oxidized to succinic acid and is therefore reduced to gamma-hydroxybutyric acid (GHB) by gamma-hydroxybutyric dehydrogenase. This causes elevations in GHB and is believed to be the trademark of this disorder and cause for the neurological manifestations seen.[2]

The symptoms of SSADH deficiency fall into three primary categories: neurological, psychiatric, and ocular. The most constant features seen are developmental delay, hypotonia, and mental retardation. Nearly half of patients seen manifest ataxia, behavior problems, seizures, and hyporreflexia.[2]

The age of onset ranges from newborn period to 25 years. Problems unique to neonates can include prematurity, lethargy, decreased sucking, respiratory difficulty and hypoglycemia. Gastrointestinal symptoms have been seen primarily in this population and are usually related to increased feeding.

Ocular problems related to the disorder include strabismus, nystagmus, retinitis, disc pallor, and oculomotor apraxia.[4]

Nearly half of the patients with SSADH deficiency have seizures. These include absence, tonic clonic, and convulsive status epilepticus. It is unclear whether decreased levels of GABA or elevated levels of GHB are responsible for these seizures but alterations in these neurotransmitters and their receptor binding or neurotransmitter transport is hypothesized to play a role in the pathogenesis of the seizures in this population.[5]

SSADH deficiency is inherited in an autosomal recessive fashion. Such diseases are caused by an error in a single DNA gene. Because the disease is autosomal, the defective gene is found on an autosome (chromosome 6), rather than the sex-linked 23rd chromosome. Being a recessive disorder, the disease can only be inherited from both parents since the disorder can only occur when a person has two copies of the gene.

It is believed that the genetic basis for SSADH deficiency resides in the SSADH human ALDH5A1 gene which maps to chromosome 6p22. More than 47 disease-causing mutations have been identified for the disorder, all of which lead to absence of functional proteins through missense, nonsense, or splicing errors; no hotspots have been identified. Consanguinity is frequent; this suggests the occurrence of rare disease causing alleles in the general population.[6]

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Strongyloidiasis is a human parasitic disease caused by the nematode (roundworm) Strongyloides stercoralis. Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.

The Strongyloides’ life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist:

Tropical and subtropical areas, but cases also occur in temperate areas (including the South of the United States). More frequently found in rural areas, institutional settings, and lower socio-economic groups.

Frequently asymptomatic. Gastrointestinal system symptoms include abdominal pain and diarrhea. Pulmonary symptoms (including Löffler’s syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. Blood eosinophilia is generally present.

Strongyloidiasis can become chronic and then become completely asymptomatic.

Strongyloidiasis resulting from persistent infection can greatly mimic peptic ulcer and gallbladder disease. Many individuals with persistent strongyloidiasis undergo treatment or surgery for both peptic ulcer and gallbladder disease and then they fail to respond to the surgery or treatment.

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Streptococcal pharyngitis or streptococcal sore throat (Strep throat AmE) is a form of group A streptococcal infection[1] that affects the pharynx and possibly the larynx and tonsils.

Streptococcal pharyngitis usually appears suddenly with a severe sore throat that may make talking or swallowing painful. In severe cases, breathing may be impaired.

Signs and symptoms may include:

Additional symptoms such as sinusitis, vaginitis or impetigo be present if the strep bacteria infects both the throat and a secondary location. For additional information on non-pharynx symptoms, see Group A Streptococcal (GAS) Infection.

There are several causes for pharyngitis, not just streptococcus bacteria. Productive coughing, nasal discharge, and red, irritated eyes in addition to fever and sore throat are more indicative of a viral sore throat than of strep throat, though a co-infection with a virus is possible and may explain the presence of these additional symptoms. A Rapid Strep Test or a throat culture may be undertaken to help clarify diagnosis.

The presence of marked lymph node enlargement along with sore throat, fever and tonsillar enlargement may also occur in infectious mononucleosis (glandular fever).[3]

A study of 729 patients with pharyngitis, in which 17% had a positive throat culture for group A streptococcus, identified the following four best predictors of streptococcus, also called the Centor criteria:[4]

Another study on 621 patients, assigned one point for each of the following symptoms:[6]

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