Category Archives: Ailmemts & Remedies

Mad Cow Disease

Other Names: Creutzfeldt-Jakob disease (CJD) or Bovine spongiform encephalopathy (BSE)

Description:
Mad cow disease is a degenerative brain disorder that leads to dementia and, ultimately, death. Symptoms of the disease is dementia-like brain disorders, such as Alzheimer’s. But mad cow disease usually progresses much more rapidly.

It captured public attention in the 1990s when some people in the United Kingdom developed a form of the disease after eating meat from diseased cattle.
Mad cow disease is thought to be due to an infection by a misfolded protein, known as a prion. Cattle are believed to have been infected by being fed meat-and-bone meal (MBM) that contained the remains of other cattle who spontaneously developed the disease or scrapie-infected sheep products. The outbreak increased throughout the United Kingdom due to the practice of feeding meat-and-bone meal to young calves of dairy cows. Cases are suspected based on symptoms and confirmed by examination of the brain. Cases are classified as classic or atypical, with the latter divided into H- and L types. It is a type of transmissible spongiform encephalopathy (TSE).

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The time between infection and onset of symptoms is generally four to five years. Time from onset of symptoms to death is generally weeks to months. Spread to humans is believed to result in variant Creutzfeldt–Jakob disease (vCJD)

Although serious, CJD is rare, and vCJD is the least common form. Worldwide, there is an estimated one case of CJD diagnosed per million people each year, most often in older adults.

Symptoms:
Mad cow disease is marked by rapid mental deterioration, usually within a few months. Initial signs and symptoms typically include:

  • Personality changes
  • Anxiety
  • Depression
  • Memory loss
  • Impaired thinking
  • Blurred vision or blindness
  • Insomnia
  • Difficulty speaking
  • Difficulty swallowing
  • Sudden, jerky movements

As the disease progresses, mental symptoms worsen. Most people eventually lapse into a coma. Heart failure, respiratory failure, pneumonia or other infections are generally the cause of death. Death usually occurs within a year.

In people with the rarer vCJD, psychiatric symptoms may be more prominent in the beginning, with dementia — the loss of the ability to think, reason and remember — developing later in the illness. In addition, this variant affects people at a younger age than classic CJD does and appears to have a slightly longer duration — 12 to 14 months.

Causes:
Mad cow disease is an infectious disease believed to be due to a misfolded protein, known as a prion. Cattle are believed to have been infected from being fed meat and bone meal (MBM) that contained the remains of other cattle who spontaneously developed the disease or scrapie-infected sheep products. The outbreak increased throughout the United Kingdom due to the practice of feeding meat-and-bone meal to young calves of dairy cows.

Prions replicate by causing other normally folded proteins of the same type to take on their misfolded shape, which then go on to do the same, leading to an exponential chain reaction. Eventually, the prions aggregate into an alpha helical, beta pleated sheet, which is thought to be toxic to brain cells.

The agent is not destroyed even if the beef or material containing it is cooked or heat-treated. Transmission can occur when healthy animals come in contact with tainted tissues from others with the disease. In the brain, the agent causes native cellular prion protein to deform into the misfolded state, which then goes on to deform further prion protein in an exponential cascade. This results in protein aggregates, which then form dense plaque fibers. Brain cells begin to die off in massive numbers, eventually leading to the microscopic appearance of “holes” in the brain, degeneration of physical and mental abilities, and ultimately death.

The agent can be transmitted to humans by eating food contaminated with it. The highest risk to humans is believed to be from eating food contaminated with the brain, spinal cord, or digestive tract though any tissue may be involved.

However, “classic”mad cow disease hasn’t been linked to contaminated beef.

Diagnosis:
Diagnosis of mad cow disease continues to be a practical problem. It has an incubation period of months to years, during which no signs are noticed, though the pathway of converting the normal brain prion protein (PrP) into the toxic, disease-related PrPSc form has started. At present, virtually no way is known to detect PrPSc reliably except by examining post mortem brain tissue using neuropathological and immunohistochemical methods. Accumulation of the abnormally folded PrPSc form of PrP is a characteristic of the disease, but it is present at very low levels in easily accessible body fluids such as blood or urine. Researchers have tried to develop methods to measure PrPSc, but no methods for use in materials such as blood have been accepted fully.[by whom?]

The traditional method of diagnosis relies on histopathological examination of the medulla oblongata of the brain, and other tissues, post mortem. Immunohistochemistry can be used to demonstrate prion protein accumulation.

In 2010, a team from New York described detection of PrPSc even when initially present at only one part in a hundred billion (10?11) in brain tissue. The method combines amplification with a novel technology called surround optical fiber immunoassay and some specific antibodies against PrPSc. After amplifying and then concentrating any PrPSc, the samples are labelled with a fluorescent dye using an antibody for specificity and then finally loaded into a microcapillary tube. This tube is placed in a specially constructed apparatus so it is totally surrounded by optical fibres to capture all light emitted once the dye is excited using a laser. The technique allowed detection of PrPSc after many fewer cycles of conversion than others have achieved, substantially reducing the possibility of artifacts, as well as speeding up the assay. The researchers also tested their method on blood samples from apparently healthy sheep that went on to develop scrapie. The animals’ brains were analysed once any signs became apparent. The researchers could, therefore, compare results from brain tissue and blood taken once the animals exhibited signs of the diseases, with blood obtained earlier in the animals’ lives, and from uninfected animals. The results showed very clearly that PrPSc could be detected in the blood of animals long before the signs appeared. After further development and testing, this method could be of great value in surveillance as a blood- or urine-based screening test for BSE or mad cow disease.

Treatmen:
No effective treatment exists for mad cow disease or Creutzfeldt-Jakob disease or any of its variants. A number of drugs have been tested and have not shown benefits. For that reason, doctors focus on alleviating pain and other symptoms and on making people with these diseases as comfortable as possible.

Prevention:
A ban on feeding meat and bone meal to cattle has resulted in a strong reduction in cases in countries where the disease has been present. In disease-free countries, control relies on import control, feeding regulations, and surveillance measures.

In UK and US slaughterhouses, the brain, spinal cord, trigeminal ganglia, intestines, eyes, and tonsils from cattle are classified as specified risk materials, and must be disposed of appropriately.

An enhanced BSE-related feed ban is in effect in both the United States and Canada to help improve prevention and elimination of BSE.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Bovine_spongiform_encephalopathy
https://www.mayoclinic.org/diseases-conditions/creutzfeldt-jakob-disease/symptoms-causes/syc-20371226

Clubfoot

Description:
Clubfoot describes a range of foot abnormalities usually present at birth (congenital) in which your baby’s foot is twisted out of shape or position. In clubfoot, the tissues connecting the muscles to the bone (tendons) are shorter than usual. Clubfoot is a fairly common birth defect.

Clubfoot can be mild or severe. Most babies who are born with clubfoot are healthy in all other ways; about 1 in 3 of them have it in both feet.

Clubfoot doesn’t cause pain, but if it’s not treated, it can make it hard for a child to walk without a limp. It’s easy to correct in most cases, so most children don’t have long-lasting effects. Doctors generally recommend treating it soon after birth.

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Doctors are usually able to treat clubfoot successfully without surgery, though sometimes children need follow-up surgery later on.

Symptoms:

If your child has clubfoot, here’s what it might look like:

  • The top of the foot is usually twisted downward and inward, increasing the arch and turning the heel inward.
  • The foot may be turned so severely that it actually looks as if it’s upside down.
  • The affected leg or the foot may be smaller than a normal foot by up to a half-inch.
  • The calf muscles in the affected leg are usually underdeveloped.
  • The foot may have a limited range of motion.
  • Despite its look, clubfoot itself doesn’t cause any discomfort or pain.

Most doctors can spot clubfoot simply by looking at your baby when he or she is born. If you have an ultrasound done late in your pregnancy, your doctor may notice it then.

Causes:
The cause of clubfoot is unknown (idiopathic), but it may be a combination of several factors.

There are many hypotheses about how clubfoot develops. Some hypothesis include: environmental factors, genetics, or a combination of both. Research has not yet pinpointed the root cause, but many findings agree that “it is likely there is more than one different cause and at least in some cases the phenotype may occur as a result of a threshold effect of different factors acting together.

Some researchers hypothesize, from the early development stages of humans, that clubfoot is formed by a malfunction during gestation. Early amniocentesis (11–13 wks) is believed to increase the rate of clubfoot because there is an increase in potential amniotic leakage from the procedure. Underdevelopment of the bones and muscles of the embryonic foot may be another underlying cause. In the early 1900s, it was thought that constriction of the foot by the uterus contributed to the occurrence of clubfoot.

Underdevelopment of the bones also affects the muscles and tissues of the foot. Abnormality in the connective tissue causes “the presence of increased fibrous tissue in muscles, fascia, ligaments and tendon sheaths”.

Genetics:
Mutations in genes involved in muscle development are risk factors for clubfoot, specifically those encoding the muscle contractile complex (MYH3, TPM2, TNNT3, TNNI2 and MYH8). These can cause congenital contractures, including clubfoot, in distal arthrogryposis (DA) syndromes.[6] Clubfoot can also be present in people with genetic conditions such as Loeys–Dietz syndrome.

Genetic mapping and the development of models of the disease have improved understanding of developmental processes. Its inheritance pattern is explained as a heterogenous disorder using a polygenic threshold model. The PITX1-TBX4 transcriptional pathway has become key to the study of clubfoot. PITX1 and TBX4 are uniquely expressed in the hind limb.

Risk Factors:

  • Gender. Two-thirds of babies with clubfoot are male.
  • Family history. Babies with a parent or sibling who had clubfoot are twice as likely to get it.
  • Lifestyle choices. If you smoke or use illegal drugs while you’re pregnant, you raise your baby’s chances of being born with it.
  • Other birth defects. In some cases, it’s linked with other another condition a baby is born with, such as spina bifida.
  • Environment. Smoking during pregnancy can significantly increase the baby’s risk of clubfoot

Too little amniotic fluid during pregnancy. This surrounds your baby in the womb. If there’s not enough, your baby’s chances of being born with clubfoot are higher.

Diagnosis:

Diagnosis of clubfoot deformity is by physical examination. Typically, a newborn is examined shortly after delivery with a head to toe assessment. Examination of the lower extremity and foot reveals the deformity, which may affect one or both feet. Examination of the foot shows four components of deformity.

  • First, there is a higher arch on the inside of the foot. This component of the deformity can occur without the other aspects of clubfoot deformity. In isolation, this aspect of the deformity is called cavus deformity.
  • Second, the forefoot is curved inward or medially (toward the big toe). This component of the deformity can occur without the other aspects of clubfoot deformity. In isolation, this aspect of the deformity is called metatarsus adductus.
  • Third, the heel is turned inward. This is a natural motion of the heel and subtalar joint, typically referred to as inversion. In clubfoot deformity, the turning in (inversion) of the heel is fixed (not passively correctable) and considered a varus deformity.
  • Fourth, and finally, the ankle is pointed downward. This is a natural motion of the ankle referred to as plantar flexion. In clubfoot deformity, this position is fixed (not correctable) and is referred to as equinus deformity.

A foot that shows all four components is diagnosed as having clubfoot deformity. These four components of a clubfoot deformity can be remembered with the acronym CAVE (cavus, forefoot adductus, varus and equinus).

The severity of the deformity can also be assessed on physical exam, but is subjective to quantify. One way to assess severity is based on the stiffness of the deformity or how much it can be corrected with manual manipulation of the foot to bring it into a corrected position. Other factors used to assess severity include the presence of skin creases in the arch and at the heel and poor muscle consistency.

In some cases, it may be possible to detect the disease prior to birth during a prenatal ultrasound. Prenatal diagnosis by ultrasound can allow parents the opportunity to get information about this condition and make plans for treatment after their baby is born.

Other testing and imaging is typically not needed. Further testing may be needed if there are concerns for other associated conditions.

Treatment:
Because your newborn’s bones, joints and tendons are very flexible, treatment for clubfoot usually begins in the first week or two after birth. The goal of treatment is to improve the way your child’s foot looks and works before he or she learns to walk, in hopes of preventing long-term disabilities.

Treatment options include:

  • Stretching and casting (Ponseti method)
  • French method:
  • Surgery

(Ponseti method :

Using the Ponseti method, the foot deformity is corrected in stages. These stages are as follows: manipulating the foot to an improved position and then holding it with a long leg cast, then removing the cast after a week, and then manipulating the foot again. The foot position usually improves over a course of 4–6 casts. The amount of casts varies from person to person to address each individual’s characteristic needs.

  • The initial cast focuses on aligning the forefoot with the hindfoot as Ponseti describes the forefoot as relatively pronated in comparison to the hindfoot. Supinating the forefoot and elevating the first metatarsal improves this alignment.
  • Subsequent casts are applied after stretching the foot with a focus on abducting the forefoot with lateral pressure at the talus, to bring the navicula laterally and improve the alignment of the talonavicular joint. In contrast to the Kite Method of casting, it is important to avoid constraining the calcanocuboid joint. With each additional cast, the abduction is increased and this moves the hindfoot from varus into valgus. It is important to leave the ankle in equinus until the forefoot and hindfoot are corrected.
  • The final stage of casting, is to correct the equinus. After fully abducting the forefoot with spontaneous correction of the hindfoot, an attempt is made to bring the ankle up and into dorsiflexion. For the majority of children, the equinus will not fully correct with casting and a procedure is done to facilitate this final aspect of the deformity correction. The procedure is a percutaneous achilles tendon release or tenotomy. Ponseti advocated for doing this in the clinic with a local anesthetic. For safety reasons, many centers perform this procedure with sedation or monitored anesthesia care. In this procedure, numbing medicine is applied, the skin is cleansed, and a small scalpel is used to divide the Achilles tendon. With a small scalpel there is minimal bleeding and no need for stitches. A small dressing is applied and a final clubfoot cast is applied with the foot in a fully corrected position. This cast is typically left in place for 3 weeks.

After correction has been achieved with casting, maintenance of correction starts with full-time (23 hours per day) use of a brace —also known as a foot abduction brace (FAB)—on both feet, regardless of whether the TEV is on one side or both, typically full-time for 3 months. After 3 months, brace wear is decreased and used mostly when sleeping for naps and at night-time. This part-time bracing is recommended until the child is 4 years of age.

Roughly 30% of children will have recurrence. A recurrence can usually be managed with repeating the casting process. Recurrence is more common when there is poor compliance with the bracing, because the muscles around the foot can pull it back into the abnormal position. Approximately 20% of infants successfully treated with the Ponseti casting method will have an imbalance between the muscles that invert the ankle (posterior tibialis and anterior tibialis muscles) and the muscles that evert the ankle (peroneal muscles). Patients with this imbalance are more prone to recurrence. After 18 months of age, this can be addressed with surgery to transfer the anterior tibialis tendon from its medial attachment (the navicula) to a more lateral position (the lateral cuneiform) to rebalance these muscle forces. While this requires a general anesthetic and subsequent casting while the tendon heals, it is a relatively minor surgery that corrects a persistent muscle imbalance while avoiding disturbance to the joints of the foot.

French method:
The French method for treatment of clubfoot is a conservative method of treatment of a newborn which requires daily physical therapy for the first two months. The goal of this treatment is to avoid future need of surgery, but the success rate varies and after release surgery may still be necessary. The treatment includes daily manipulations of the feet along with stretching of the feet, followed by taping in order to maintain the range of motion gains achieved at the end of each session. The French method differs from the Ponseti method in that the taping techniques allow some motion in the feet. Another focus is to strengthen the peroneal muscles which is thought to contribute towards long-term correction. After the two month mark physical therapy sessions can be weaned down to three times per week instead of daily until the child reaches six months old. Parents are required to continue on with home exercises and night splinting even after the program has achieved proper foot correction in order to maintain the correction. The Ponseti method is generally preferred.

Surgery:
If your baby’s clubfoot is severe or doesn’t respond to nonsurgical treatments, more-invasive surgery may be needed. An orthopedic surgeon can lengthen or reposition tendons and ligaments to help ease the foot into a better position. After surgery, your child will be in a cast for up to two months, and then need to wear a brace for a year or so to prevent the clubfoot from coming back.

Even with treatment, clubfoot may not be totally correctable. But in most cases, babies who are treated early grow up to wear ordinary shoes and lead full, active lives.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Clubfoot
https://www.mayoclinic.org/diseases-conditions/clubfoot/symptoms-causes/syc-20350860
https://www.webmd.com/a-to-z-guides/what-is-clubfoot#1

Herpangina.

Other Names: Mouth blisters or Hand-foot-and-mouth disease (HFMD).

Description:
Herpangina is often seen in the pediatric population, with occasional outbreaks among adult patients. They are both caused primarily by enteroviral infections. Herpangina presents as a stereotypical vesicular/ulcerative enanthem on the oropharyngeal mucosa. Usually, herpangina is produced by one particular strain of coxsackie virus A (and the term “herpangina virus” refers to coxsackievirus A) but it can also be caused by coxsackievirus B or echoviruses. Most cases of herpangina occur in the summer, affecting mostly children. However, it occasionally occurs in adolescents and adults. It was first characterized in 1920.

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HFMD is identified by a similar rash on the oral mucous membranes, with additional characteristic exanthem on hands and feet. Both syndromes are highly contagious. Although these syndromes are usually benign, their symptoms can cause significant temporary discomfort for patients and distress for their parents. Rarely, they can present as a more severe disease, and patients develop long-term sequelae.

Symptoms:
Symptoms include sudden fever with sore throat, headache, loss of appetite, and often neck pain. Within two days of onset an average of four or five (but sometimes up to twenty) 1 to 2 mm diameter grayish lumps form and develop into vesicles with red surrounds, and over 24 hours these become shallow ulcers, rarely larger than 5 mm diameter, that heal in one to seven days. These lesions most often appear on the tonsillar pillars (adjacent to the tonsils), but also on the soft palate, tonsils, uvula, or tongue.

A small number of lesions (usually 2 – 6) form in the back area of the mouth, particularly the soft palate or tonsillar pillars. The lesions progress initially from red macules to vesicles and lastly to ulcerations which can be 2 – 4 mm in size.

Causes:
Herpangina is usually caused by group A coxsackieviruses. However, it can also be caused by group B coxsackieviruses, enterovirus 71, and echovirus. These viruses are highly contagious and can easily spread from person to person, especially in schools and childcare centers.

People who are infected with herpangina are most contagious during the first week of infection.

Herpangina is typically transmitted through contact with fecal matter. The infection may also be spread through contact with droplets from an infected person’s sneeze or cough.

This means that you can get herpangina if you touch your mouth after touching something that’s contaminated with fecal particles or droplets from an infected person. The virus can live on surfaces and objects, such as countertops and toys, for several days.

Risk Factors:
Herpangina can affect anyone, but it most commonly occurs in children under age 5. It’s particularly common in children who attend school, childcare facilities, or camps. In the United States, the risk of developing herpangina is higher during the summer and fall.

Diagnosis:
The diagnoses of HFMD and herpangina are usually made clinically. In mild cases, no imaging or laboratory testing is required. Laboratory studies are usually obtained to gain additional information about complications such as dehydration or to rule out alternative diagnoses. Confirmatory testing is usually required only in complicated disease, for the collection of epidemiological data during epidemics, or to differentiate herpangina or HFMD from more serious diseases such as eczema herpeticum. Viral culture is the “gold standard” for confirmatory testing. Unfortunately, it can often take longer than 1 week to obtain culture results. This makes it an impractical test for clinical practice. Polymerase chain reaction (PCR) testing is fast and highly sensitive for enteroviruses. Samples may be obtained from the stool, mucocutaneous ulcers, vesicular fluid, or cerebrospinal fluid. Enzyme-linked immunosorbent assays (ELISA) are also available. ELISA testing for enteroviruses is generally less sensitive than PCR and should be utilized only in cases where PCR is not available.

Treatment:
Treatment is usually supportive only, as the disease is self-limiting and usually runs its course in less than a week.

Since herpangina is a viral infection, antibiotics aren’t an effective form of treatment. Instead, your doctor may recommend:

Ibuprofen or acetaminophen: These medications can ease any discomfort and reduce fever. Do not use aspirin to treat symptoms of a viral infection in children or teenagers. This has been linked to Reye’s syndrome, a life-threatening illness that results in sudden swelling and inflammation in the liver and brain.

Topical anesthetics: Certain anesthetics, such as lidocaine, can provide relief for a sore throat and any other mouth pain associated with herpangina.

Increased fluid intake: It’s important to drink plenty of fluids during recovery, especially cold milk and water. Eating popsicles can also help soothe a sore throat. Avoid citrus drinks and hot beverages, as they may make symptoms worse.
With treatment, symptoms should disappear within seven days with no lasting effects.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://www.ncbi.nlm.nih.gov/books/NBK507792/
https://www.healthline.com/health/herpangina#causes
https://en.wikipedia.org/wiki/Herpangina

Staphylococcal infection


Other Names:Stap infection

Description:
Staphylococcal infection is caused by staphylococcus bacteria, types of germs commonly found on the skin or in the nose of even healthy individuals. Sometime the bacterias may enter the body through cuts or abrasions which may be nearly invisible. Most of the time, these bacteria cause no problems or result in relatively minor skin infections.

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But staph infections can turn deadly if the bacteria invade deeper into your body, entering your bloodstream, joints, bones, lungs or heart. A growing number of otherwise healthy people are developing life-threatening staph infections.

Treatment usually involves antibiotics and drainage of the infected area. However, some staph infections no longer respond to common antibiotics.

Symptoms:
Staphylococcal infections can range from minor skin problems to endocarditis, a life-threatening infection of the inner lining of your heart (endocardium). As a result, signs and symptoms of staph infections vary widely, depending on the location and severity of the infection.

Skin infection:
Skin infections caused by staph bacteria include:

Boils. The most common type of staph infection is the boil, a pocket of pus that develops in a hair follicle or oil gland. The skin over the infected area usually becomes red and swollen.

If a boil breaks open, it will probably drain pus. Boils occur most often under the arms or around the groin or buttocks.

Impetigo. This contagious, often painful rash can be caused by staph bacteria. Impetigo usually features large blisters that may ooze fluid and develop a honey-colored crust.

Cellulitis. Cellulitis — an infection of the deeper layers of skin — causes skin redness and swelling on the surface of your skin. Sores (ulcers) or areas of oozing discharge may develop, too.

Staphylococcal scalded skin syndrome. Toxins produced as a result of a staph infection may lead to staphylococcal scalded skin syndrome. Affecting mostly babies and children, this condition features fever, a rash and sometimes blisters. When the blisters break, the top layer of skin comes off — leaving a red, raw surface that looks like a burn.

Food poisoning:
Staph bacteria are one of the most common causes of food poisoning. Symptoms come on quickly, usually within hours of eating a contaminated food. Symptoms usually disappear quickly, too, often lasting just half a day.

A staph infection in food usually doesn’t cause a fever. Signs and symptoms you can expect with this type of staph infection include:

  • Nausea and vomiting
  • Diarrhea
  • Dehydration
  • Low blood pressure

Septicemia:
Also known as blood poisoning, septicemia occurs when staph bacteria enter a person’s bloodstream. A fever and low blood pressure are signs of septicemia. The bacteria can travel to locations deep within your body, to produce infections affecting:

  • Internal organs, such as your brain, heart or lungs
  • Bones and muscles
  • Surgically implanted devices, such as artificial joints or cardiac pacemakers

Toxic shock syndrome:
This life-threatening condition results from toxins produced by some strains of staph bacteria and has been linked to certain types of tampons, skin wounds and surgery. It usually develops suddenly with:

  • A high fever
  • Nausea and vomiting
  • A rash on your palms and soles that resembles sunburn
  • Confusion
  • Muscle aches
  • Diarrhea
  • Abdominal pain

Septic arthritis:
Septic arthritis is often caused by a staph infection. The bacteria often target the knees, shoulders, hips, and fingers or toes. Signs and symptoms may include:

  • Joint swelling
  • Severe pain in the affected joint
  • Fever

Causes:
Some people carry staph bacteria on their skin or in their noses, but they do not get an infection. But if they get a cut or wound, the bacteria can enter the body and cause an infection.

Staph bacteria can spread from person to person. They can also spread on objects, such as towels, clothing, door handles, athletic equipment, and remotes. If you have staph and do not handle food properly when you are preparing it, you can also spread staph to others.

Staph bacteria are able to survive:

  • Drying
  • Extremes of temperature
  • Stomach acid
  • High levels of salt

Risk Factors:
Anyone can develop a staph infection, but certain people are at greater risk, including those who

  • Have a chronic condition such as diabetes, cancer, vascular disease, eczema, and lung disease
  • Have a weakened immune system, such as from HIV/AIDS, medicines to prevent organ rejection, or chemotherapy
  • Had surgery
  • Use a catheter, breathing tube, or feeding tube
  • Are on dialysis
  • Inject illegal drugs
  • Do contact sports, since you may have skin-to-skin contact with others or share equipment

Diagnosis:
The doctor will do a physical exam and ask the patient about the symptoms. Often, the doctor can tell if one has a staph skin infection by looking at it. To check for other types of staph infections, the doctor may do a culture, with a skin scraping, tissue sample, stool sample, or throat or nasal swabs. There may be other tests, such as imaging tests, depending on the type of infection.

Treatment:
Treatment for staph infections is antibiotics. Depending on the type of infection, one may get a cream, ointment, medicines (to swallow), or intravenous (IV). If you have an infected wound, your provider might drain it. Sometimes you may need surgery for bone infections.

Some staph infections, such as MRSA (methicillin-resistant Staphylococcus aureus), are resistant to many antibiotics. There are still certain antibiotics that can treat these infections.

Prevention:

Certain steps can help to prevent staph infections:

  • Use good hygiene, including washing your hands often
  • Don’t share towels, sheets, or clothing with someone who has a staph infection
  • It’s best not to share athletic equipment. If you do need to share, make sure that it properly cleaned and dried before you use it.
  • Practice food safety, including not preparing food for others when you have a staph infection
  • Always keep covered a cut or wound.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://www.mayoclinic.org/diseases-conditions/staph-infections/symptoms-causes/syc-20356221
https://en.wikipedia.org/wiki/Staphylococcal_infection

Ulcerative colitis

Description:
Ulcerative colitis is an inflammatory bowel disease (IBD) that causes long-lasting inflammation and ulcers (sores) in the digestive tract. Ulcerative colitis affects the innermost lining of the large intestine (colon) and rectum. Symptoms usually develop over time, rather than suddenly.

Ulcerative colitis can be debilitating and can sometimes lead to life-threatening complications. While it has no known cure, treatment can greatly reduce signs and symptoms of the disease and even bring about long-term remission.

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Symptoms
Ulcerative colitis symptoms can vary, depending on the severity of inflammation and where it occurs. The main symptom of ulcerative colitis is bloody diarrhea. There might be some pus in your stools, too.

Other problems include:

  • Crampy belly pain
  • Sudden urges to empty your colon right away
  • Not feeling hungry
  • Weight loss
  • Feeling tired
  • Fever
  • Dehydration
  • Joint pain or soreness
  • Canker sores
  • Eye pain when you look at a bright light
  • Too few red blood cells, called anemia
  • Skin sores
  • Feeling like you haven’t completely emptied your colon after you use the bathroom
  • Waking up at night to go
  • Not being able to hold your stools in
  • In some cases the symptoms can flare up, go away, and then come back again. Sometimes they might not bother you for weeks or years at a time.

Other gut diseases can have some of the same symptoms. Crohn’s disease causes inflammation, too, but it happens in other places in your digestive tract. Ulcerative colitis affects only your large intestine and only the inside lining. Irritable bowel syndrome has some of the same symptoms as UC, but it doesn’t cause inflammation or ulcers. Instead, it’s a problem with the muscle in your intestines.

Types:
Doctors often classify ulcerative colitis according to its location. Types of ulcerative colitis include:

  • Ulcerative proctitis. Inflammation is confined to the area closest to the anus (rectum), and rectal bleeding may be the only sign of the disease. This form of ulcerative colitis tends to be the mildest.
  • Proctosigmoiditis. Inflammation involves the rectum and sigmoid colon (lower end of the colon). Signs and symptoms include bloody diarrhea, abdominal cramps and pain, and an inability to move the bowels in spite of the urge to do so (tenesmus).
  • Left-sided colitis. Inflammation extends from the rectum up through the sigmoid and descending colon. Signs and symptoms include bloody diarrhea, abdominal cramping and pain on the left side, and unintended weight loss.
  • Pancolitis. Pancolitis often affects the entire colon and causes bouts of bloody diarrhea that may be severe, abdominal cramps and pain, fatigue, and significant weight loss.
  • Acute severe ulcerative colitis. This rare form of colitis affects the entire colon and causes severe pain, profuse diarrhea, bleeding, fever and inability to eat.

Causes:
The exact cause of ulcerative colitis is unknown. Previously, diet and stress were suspected, but now doctors know that these factors may aggravate but don’t cause ulcerative colitis.

One possible cause is an immune system malfunction. When your immune system tries to fight off an invading virus or bacterium, an abnormal immune response causes the immune system to attack the cells in the digestive tract, too.

Heredity also seems to play a role in that ulcerative colitis is more common in people who have family members with the disease. However, most people with ulcerative colitis don’t have this family history.

Risk factors:
Ulcerative colitis affects about the same number of women and men. Risk factors may include:

Genetic Factor: You’re at higher risk if you have a close relative, such as a parent, sibling or child, with the disease.

Age: Ulcerative colitis usually begins before the age of 30. But, it can occur at any age, and some people may not develop the disease until after age 60.

Race or ethnicity Factor. Although whites have the highest risk of the disease, it can occur in any race. If you’re of Ashkenazi Jewish descent, your risk is even higher.

Environmental factors:
Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis. They include:

  • Diet: As the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn’s disease. Few studies have investigated such an association; one study showed no association of refined sugar on the prevalence of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages.Specifically, sulfur has been investigated as being involved in the etiology of ulcerative colitis, but this is controversial.[24] Sulfur restricted diets have been investigated in patients with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.
  • Breastfeeding: Some reports of the protection of breastfeeding in the development of IBD contradict each other. One Italian study showed a potential protective effect.
  • One study of isotretinoin found a small increase in the rate of UC

Diagnosis:
Your doctor will likely diagnose ulcerative colitis after ruling out other possible causes for your signs and symptoms. To help confirm a diagnosis of ulcerative colitis, you may have one or more of the following tests and procedures:

  • Blood tests. Your doctor may suggest blood tests to check for anemia — a condition in which there aren’t enough red blood cells to carry adequate oxygen to your tissues — or to check for signs of infection.
  • Stool sample. White blood cells in your stool can indicate ulcerative colitis. A stool sample can also help rule out other disorders, such as infections caused by bacteria, viruses and parasites.
  • Colonoscopy. This exam allows your doctor to view your entire colon using a thin, flexible, lighted tube with an attached camera. During the procedure, your doctor can also take small samples of tissue (biopsy) for laboratory analysis. Sometimes a tissue sample can help confirm a diagnosis.
  • Flexible sigmoidoscopy. Your doctor uses a slender, flexible, lighted tube to examine the rectum and sigmoid, the last portion of your colon. If your colon is severely inflamed, your doctor may perform this test instead of a full colonoscopy.

*X-ray. If you have severe symptoms, your doctor may use a standard X-ray of your abdominal area to rule out serious complications, such as a perforated colon.

  • CT scan. A CT scan of your abdomen or pelvis may be performed if your doctor suspects a complication from ulcerative colitis. A CT scan may also reveal how much of the colon is inflamed.
  • Computerized tomography (CT) enterography and magnetic resonance (MR) enterography. Your doctor may recommend one of these noninvasive tests if he or she wants to exclude any inflammation in the small intestine. These tests are more sensitive for finding inflammation in the bowel than are conventional imaging tests. MR enterography is a radiation-free alternative.

Treatment:
Standard treatment for ulcerative colitis depends on the extent of involvement and disease severity. The goal is to induce remission initially with medications, followed by the administration of maintenance medications to prevent a relapse. The concept of induction of remission and maintenance of remission is very important. The medications used to induce and maintain a remission somewhat overlap, but the treatments are different. Physicians first direct treatment to inducing remission, which involves relief of symptoms and mucosal healing of the colon’s lining, and then longer term treatment to maintain remission and prevent complications. Acute severe ulcerative colitis requires hospitalisation, exclusion of infections, and corticosteroids.

For acute stages of the disease, a low fiber diet may be recommended.

Medicinal treatment:
Ulcerative colitis can be treated with a number of medications, including 5-ASA drugs such as sulfasalazine and mesalazine. Corticosteroids such as prednisone can also be used due to their immunosuppressive and short-term healing properties, but because their risks outweigh their benefits, they are not used long-term in treatment. Immunosuppressive medications such as azathioprine and biological agents such as infliximab and adalimumab are given only if people cannot achieve remission with 5-ASA and corticosteroids. Such treatments are used less commonly due to their possible risk factors, including but not limited to increased risk of cancers in teenagers and adults, tuberculosis, and new or worsening heart failure (these side effects are rare).

A formulation of budesonide was approved by the FDA for treatment of active ulcerative colitis in January 2013. Tofacitinib was approved for treatment of moderately to severely active ulcerative colitis in 2018 in the US, the first oral medication indicated for long term use in this condition. The evidence on methotrexate does not show a benefit in producing remission in people with ulcerative colitis. Off-label use of drugs such as ciclosporin and tacrolimus has shown some benefits. Fexofenadine, an antihistamine drug used in treatment of allergies, has shown promise in a combination therapy in some studies.[55][56] Opportunely, low gastrointestinal absorption (or high absorbed drug gastrointestinal secretion) of fexofenadine results in higher concentration at the site of inflammation. Thus, the drug may locally decrease histamine secretion by involved gastrointestinal mast cells and alleviate the inflammation.

Surgical Treatment:
Unlike in Crohn’s disease, the gastrointestinal aspects of ulcerative colitis can generally be cured by surgical removal of the large intestine, though extraintestinal symptoms may persist. This procedure is necessary in the event of: exsanguinating hemorrhage, frank perforation, or documented or strongly suspected carcinoma. Surgery is also indicated for patients with severe colitis or toxic megacolon. Patients with symptoms that are disabling and do not respond to drugs may wish to consider whether surgery would improve the quality of life.

Ulcerative colitis affects many parts of the body outside the intestinal tract. In rare cases, the extra-intestinal manifestations of the disease may require removal of the colon.

Another surgical option for ulcerative colitis that is affecting most of the large bowel is called the ileo-anal pouch procedure. This is a two- to three-step procedure in which the large bowel is removed, except for the rectal stump and anus, and a temporary ileostomy is made. The next part of the surgery can be done in one or two steps and is usually done at six- to twelve-month intervals from each prior surgery.

In the next step of the surgery, an internal pouch is made of the patient’s own small bowel, and this pouch is then hooked back up internally to the rectal stump so that the patient can once again have a reasonably functioning bowel system, all internal. The temporary ileostomy can be reversed at this time so that the patient is internalized for bowel functions, or, in another step to the procedure, the pouch, and rectal stump anastamosis can be left inside the patient to heal for some time while the patient still uses the ileostomy for bowel function. Then, on a subsequent surgery, the ileostomy is reversed and the patient has internalized bowel function again.

Alternative Treatment:
About 21% of inflammatory bowel disease patients use alternative treatments. A variety of dietary treatments show promise, but they require further research before they can be recommended.

  • Melatonin may be beneficial according to in vitro research, animal studies, and a preliminary human study.
  • Dietary fiber, meaning indigestible plant matter, has been recommended for decades in the maintenance of bowel function. Of peculiar note is fiber from brassica, which seems to contain soluble constituents capable of reversing ulcers along the entire human digestive tract before it is cooked.[80]
  • Fish oil, and eicosapentaenoic acid (EPA) derived from fish oil, inhibits leukotriene activity, the latter which may be a key factor of inflammation. As an IBD therapy, there are no conclusive studies in support and no recommended dosage. But dosages of EPA between 180 and 1500 mg/day are recommended for other conditions, most commonly cardiac.[81] Fish oil also contains vitamin D, of which many people with IBD are deficient.
  • Short chain fatty acid (butyrate) enema. The epithelial cells in the colon uses butyrate from the contents of the intestine as an energy source. The amount of butyrate available decreases toward the rectum. Inadequate butyrate levels in the lower intestine have been suggested as a contributing factor for the disease. This might be addressed through butyrate enemas.[83] The results however are not conclusive.
  • Herbal medications are used by patients with ulcerative colitis. Compounds that contain sulfhydryl may have an effect in ulcerative colitis (under a similar hypothesis that the sulfa moiety of sulfasalazine may have activity in addition to the active 5-ASA component). One randomized control trial evaluated the over-the-counter medication S-methylmethionine and found a significant decreased rate of relapse when the medication was used in conjunction with oral sulfasalazine.
  • Helminthic therapy is the use of intestinal parasitic nematodes to treat ulcerative colitis, and is based on the premises of the hygiene hypothesis. Studies have shown that helminths ameliorate and are more effective than daily corticosteroids at blocking chemically induced colitis in mice, and a trial of intentional helminth infection of rhesus monkeys with idiopathic chronic diarrhea (a condition similar to ulcerative colitis in humans) resulted in remission of symptoms in 4 out of 5 of the animals treated. A randomised controlled trial of Trichuris suis ova in humans found the therapy to be safe and effective, and further human trials are ongoing.
  • Aloe vera. Aloe vera gel may have an anti-inflammatory effect for people with ulcerative colitis, but it can also cause diarrhea.
  • Curcumin (turmeric) therapy, in conjunction with taking the medications mesalamine or sulfasalazine, may be effective and safe for maintaining remission in people with quiescent ulcerative colitis. The effect of curcumin therapy alone on quiescent ulcerative colitis is unknown.
  • Acupuncture. Only one clinical trial has been conducted regarding its benefit. The procedure involves the insertion of fine needles into the skin, which may stimulate the release of the body’s natural painkillers.
  • Exercise: Regular Yoga exercise & meditation is verymuch helpful and in most cases gives great relief to patient.(But it should be done under an expart)

Prognosis:
Patients with ulcerative colitis usually have an intermittent course, with periods of disease inactivity alternating with “flares” of disease. Patients with proctitis or left-sided colitis usually have a more benign course: only 15% progress proximally with their disease, and up to 20% can have sustained remission in the absence of any therapy. Patients with more extensive disease are less likely to sustain remission, but the rate of remission is independent of the severity of the disease.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://www.mayoclinic.org/diseases-conditions/ulcerative-colitis/symptoms-causes/syc-20353326
https://www.webmd.com/ibd-crohns-disease/ulcerative-colitis/what-is-ulcerative-colitis#1
https://en.wikipedia.org/wiki/Ulcerative_colitis
https://www.mayoclinic.org/diseases-conditions/ulcerative-colitis/diagnosis-treatment/drc-20353331