Tag: Epstein-Barr virus

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Epstein-Barr infection

Description: The Epstein-Barr virus, also called EBV, is an extremely common virus that infects most people at one time or another during their lifetimes. There are several forms of Epstein–Barr virus infection. Infectious mononucleosis, nasopharyngeal carcinoma, and Burkitt’s lymphoma can all be caused by the Epstein–Barr virus.

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It is best known as the cause of infectious mononucleosis (glandular fever). It is also associated with particular forms of cancer, such as Hodgkin’s lymphoma, Burkitt’s lymphoma, nasopharyngeal carcinoma, and conditions associated with human immunodeficiency virus (HIV), such as hairy leukoplakia and central nervous system lymphomas. There is evidence that infection with the virus is associated with a higher risk of certain autoimmune diseases, especially dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis, Sjögren’s syndrome, and multiple sclerosis.

Infection with EBV occurs by the oral transfer of saliva and genital secretions.

Most people become infected with EBV and gain adaptive immunity. In the United States, about half of all five-year-old children and 90 to 95 percent of adults have evidence of previous infection. Infants become susceptible to EBV as soon as maternal antibody protection disappears. Many children become infected with EBV, and these infections usually cause no symptoms or are indistinguishable from the other mild, brief illnesses of childhood. In the United States and other developed countries, many people are not infected with EBV in their childhood years. When infection with EBV occurs during adolescence, it causes infectious mononucleosis 35 to 50 percent of the time.

EBV infects B cells of the immune system and epithelial cells. Once the virus’s initial lytic infection is brought under control, EBV latently persists in the individual’s B cells for the rest of the individual’s life.

Symptoms:
Epstein-Barr virus infection generally causes a minor cold-like or flu-like illness, but, in some cases, there may be no symptoms of infection.Initial symptoms of infectious mononucleosis are fever, sore throat, and swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects. Although the symptoms of infectious mononucleosis usually resolve in 1 or 2 months, EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person’s life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. Reactivated and post-latent virus may pass the placental barrier in (also seropositive) pregnant women via macrophages and therefore can infect the fetus. Also re-infection of prior seropositive individuals may occur. In contrast, reactivation in adults usually occurs without symptoms of illness.

EBV also establishes a lifelong dormant infection in some cells of the body’s immune system. A late event in a very few carriers of this virus is the emergence of Burkitt’s lymphoma and nasopharyngeal carcinoma, two rare cancers. EBV appears to play an important role in these malignancies, but is probably not the sole cause of disease.

Most individuals exposed to people with infectious mononucleosis have previously been infected with EBV and are not at risk for infectious mononucleosis. In addition, transmission of EBV requires intimate contact with the saliva (found in the mouth) of an infected person. Transmission of this virus through the air or blood does not normally occur. The incubation period, or the time from infection to appearance of symptoms, ranges from 4 to 6 weeks. Persons with infectious mononucleosis may be able to spread the infection to others for a period of weeks. However, no special precautions or isolation procedures are recommended, since the virus is also found frequently in the saliva of healthy people. In fact, many healthy people can carry and spread the virus intermittently for life. These people are usually the primary reservoir for person-to-person transmission. For this reason, transmission of the virus is almost impossible to prevent.

The clinical diagnosis of infectious mononucleosis is suggested on the basis of the symptoms of fever, sore throat, swollen lymph glands, and the age of the patient. Usually, laboratory tests are needed for confirmation. Serologic results for persons with infectious mononucleosis include an elevated white blood cell count, an increased percentage of certain atypical white blood cells, and a positive reaction to a “mono spot” test.
Causes:
Epstein–Barr can cause infectious mononucleosis, also known as ‘glandular fever’, ‘Mono‘ and ‘Pfeiffer’s disease’. Infectious mononucleosis is caused when a person is first exposed to the virus during or after adolescence. Though once deemed “The Kissing Disease,” recent research has shown that transmission of EBV not only occurs from exchanging saliva, but also from contact with the airborne virus. It is predominantly found in the developing world, and most children in the developing world are found to have already been infected by around 18 months of age. Infection of children can occur when adults mouth feed or pre-chew food before giving it to the child. EBV antibody tests turn up almost universally positive.

Treatment:
There is no specific treatment for infectious mononucleosis, other than treating the symptoms. No antiviral drugs or vaccines are available. Some physicians have prescribed a 5-day course of steroids to control the swelling of the throat and tonsils. The use of steroids has also been reported to decrease the overall length and severity of illness, but these reports have not been published.

It is important to note that symptoms related to infectious mononucleosis caused by EBV infection seldom last for more than 4 months. When such an illness lasts more than 6 months, it is frequently called chronic EBV infection. However, valid laboratory evidence for continued active EBV infection is seldom found in these patients. The illness should be investigated further to determine if it meets the criteria for chronic fatigue syndrome, or CFS. This process includes ruling out other causes of chronic illness or fatigue.

Prognosis:
There is currently no specific cure for an Epstein-Barr virus infection. Treatment includes measures to help relieve symptoms and keep the body as strong as possible until the disease runs its course. This includes rest, medications to ease body aches and fever, and drinking plenty of fluids. People who are in good health can generally recover from an Epstein-Barr virus infection at home with supportive care, such as rest, fluids and pain relievers.

Prevention:
Treatment of most viral diseases begins with preventing the spread of the disease with basic hygiene measures. However, controlling the spread of the Epstein-Barr virus is extremely difficult because it is so common and because it is possible to spread the Epstein-Barr virus even when a person does not appear sick. Many healthy people who have had an Epstein-Barr virus infection continue to carry the virus in their saliva, which means they can spread it to others throughout their lifetimes. However, avoiding contact with another person’s saliva by not sharing drinking glasses or toothbrushes is still a good general disease prevention measure.

Regular exercise with healthy food habits and healthy life style is the best way of prevention.

Research:
As a relatively complex virus, EBV is not yet fully understood. Laboratories around the world continue to study the virus and develop new ways to treat the diseases it causes. One popular way of studying EBV in vitro is to use bacterial artificial chromosomes.  Epstein–Barr virus and its sister virus KSHV can be maintained and manipulated in the laboratory in continual latency. Although many viruses are assumed to have this property during infection of their natural host, they do not have an easily managed system for studying this part of the viral lifecycle. Genomic studies of EBV have been able to explore lytic reactivation and regulation of the latent viral episome.

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:
http://en.wikipedia.org/wiki/Epstein%E2%80%93Barr_virus
http://en.wikipedia.org/wiki/Epstein–Barr_virus_infection
http://www.healthgrades.com/conditions/epstein-barr-virus

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Guillain-Barre syndrome

Definition:
Guillain-Barre syndrome is an uncommon disorder in which your body’s immune system attacks your nerves. Weakness and numbness in your extremities are usually the first symptoms. These sensations can quickly spread, eventually paralyzing your whole body.

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The exact cause of Guillain-Barre syndrome is unknown, but it is often preceded by an infectious illness such as a respiratory infection or the stomach flu. Luckily, Guillain-Barre syndrome is relatively rare, affecting only 1 or 2 people per 100,000.

In its most severe form, Guillain-Barre syndrome is a medical emergency requiring hospitalization. There’s no known cure for Guillain-Barre syndrome, but several treatments can ease symptoms and reduce the duration of the illness.

GBS can cause symptoms that last for a few weeks. Most people recover fully from GBS, but some people have permanent nerve damage. In very rare cases, people have died of GBS, usually from difficulty breathing. In the United States, for example, an estimated 3,000 to 6,000 people develop GBS each year on average, whether or not they received a vaccination.

Guillain-Barre affects about 1,500 people every year in the UK, and about 150 develop CIDP. The exact mechanisms that cause the conditions aren’t clear, but about 60 per cent of those affected will have had a throat or intestinal infection, flu or major stress within the previous two weeks. This triggers the immune system, which then attacks the nerves.

It rarely occurs in first-degree relatives, but familial cases have been reported and genetic similarities noted. For example, a study of Japanese people with Guillain-Barre following an intestinal infection with the bacteria Campylobacter jejuni found they were more likely to have a rare version of the gene for an immune system chemical known as tumour necrosis factor.

Symptoms:
Guillain-Barre syndrome often begins with weakness, tingling or loss of sensation starting in your feet and legs and spreading to your upper body and arms. These symptoms may begin — often not causing much notice — in your fingers and toes. In some people, symptoms begin in the arms or even the face. As the disorder progresses, muscle weakness can evolve into paralysis.

Signs and symptoms of Guillain-Barre syndrome may include:

*Prickling, “pins and needles” sensations in your fingers, toes or both
*Weakness or tingling sensations in your legs that spread to your upper body
*Unsteady walking or inability to walk
*Difficulty with eye movement, facial movement, speaking, chewing or swallowing
*Severe pain in your lower back
*Difficulty with bladder control or intestinal functions
*Very slow heart rate or low blood pressure
*Difficulty breathing
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Most people with Guillain-Barre syndrome experience their most significant weakness within three weeks after symptoms begin. In some cases, signs and symptoms may progress very rapidly with complete paralysis of legs, arms and breathing muscles over the course of a few hours.

The disorder was first described by the French physician Jean Landry in 1859. In 1916, Georges Guillain, Jean Alexandre Barré, and André Strohl diagnosed two soldiers with the illness and discovered the key diagnostic abnormality of increased spinal fluid protein production, but normal cell count.

GBS is also known as acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis, French polio, Landry’s ascending paralysis and Landry Guillain Barré syndrome.

Canadian neurologist C. Miller Fisher described the variant that bears his name in 1956

Causes:
Many things can cause GBS; about two-thirds of people who develop GBS symptoms do so several days or weeks after they have been sick with diarrhea or a respiratory illness. Infection with the bacterium Campylobacter jejuni is one of the most common risk factors for GBS. People also can develop GBS after having the flu or other infections (such as cytomegalovirus and Epstein Barr virus). On very rare occasions, they may develop GBS in the days or weeks after getting a vaccination.

Click to see picture of Neuron Hand-tuned

Typically, Guillain-Barre develops as an autoimmune reaction following an acute infection. It’s not inherited, although it’s thought that genetic factors may make some people more likely to develop autoimmune conditions.

Risk Factors:
Anyone can develop GBS; however, it is more common among older adults. The incidence of GBS increases with age, and people older than 50 years are at greatest risk for developing GBS.

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Guillain-Barre may be triggered by:

*Most commonly, infection with campylobacter, a type of bacteria often found in undercooked food, especially poultry
*Surgery
*Epstein-Barr virus
*Hodgkin’s disease
*Mononucleosis
*HIV, the virus that causes AIDS
*Rarely, rabies or influenza immunizations

Diagnosis:
The diagnosis of GBS usually depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and electrodiagnostic tests of nerves and muscles (such as nerve conduction studies) are common tests ordered in the diagnosis of GBS.

*cerebrospinal fluid:
Typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100–1000 mg/dL), without an accompanying increased cell count pleocytosis. A sustained increased white blood cell count may indicate an alternative diagnosis such as infection.

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*Electrodiagnostics
Electromyography (EMG) and nerve conduction study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.

Diagnostic criteria Required:

*Progressive, relatively symmetrical weakness of two or more limbs due to neuropathy
*Areflexia
*Disorder course < 4 weeks
*Exclusion of other causes (see below)

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Supportive:
*relatively symmetric weakness accompanied by numbness and/or tingling
*mild sensory involvement
*facial nerve or other cranial nerve involvement
*absence of fever
*typical CSF findings obtained from lumbar puncture
*electrophysiologic evidence of demyelination from electromyogram

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Differential diagnosis:
*acute myelopathies with chronic back pain and sphincter dysfunction
*botulism with early loss of pupillary reactivity and descending paralysis
*diphtheria with early oropharyngeal dysfunction
*Lyme disease polyradiculitis and other tick-borne paralyses
*porphyria with abdominal pain, seizures, psychosis
*vasculitis neuropathy
*poliomyelitis with fever and meningeal signs
*CMV polyradiculitis in immunocompromised patients
*critical illness neuropathy
*myasthenia gravis
*poisonings with organophosphate, poison hemlock, thallium, or arsenic
*intoxication with Karwinskia humboldtiana leaves or seeds
*paresis caused by West Nile virus
*spinal astrocytoma
*motor neurone disease
*West Nile virus can cause severe, potentially fatal neurological illnesses, which include encephalitis, meningitis, Guillain-Barré syndrome, and anterior myelitis.

Treatment :
Supportive care with monitoring of all vital functions is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm. Early intubation should be considered in any patient with a vital capacity (VC) <20 ml/kg, a negative inspiratory force (NIF) that is less negative (i.e., closer to zero) than -25 cmH2O, more than 30% decrease in either VC or NIF within 24 hours, rapid progression of disorder, or autonomic instability.

Once the patient is stabilized, treatment of the underlying condition should be initiated as soon as possible. Either high-dose intravenous immunoglobulins (IVIg) at 400 mg/kg for 5 days or plasmapheresis can be administered, as they are equally effective and a combination of the two is not significantly better than either alone. Therapy is no longer effective two weeks after the first motor symptoms appear, so treatment should be instituted as soon as possible. IVIg is usually used first because of its ease of administration and safety profile, with a total of five daily infusions for a total dose of 2 g/kg body weight (400 mg/kg each day). The use of intravenous immunoglobulins is not without risk, occasionally causing hepatitis, or in rare cases, renal failure if used for longer than five days. Glucocorticoids have not been found to be effective in GBS. If plasmapheresis is chosen, a dose of 40-50 mL/kg plasma exchange (PE) can be administered four times over a week.

Following the acute phase, the patient may also need rehabilitation to regain lost functions. This treatment will focus on improving ADL (activities of daily living) functions such as brushing teeth, washing, and getting dressed. Depending on the local structuring on health care, a team of different therapists and nurses will be established according to patient needs. An occupational therapist can offer equipment (such as wheelchair and special cutlery) to help the patient achieve ADL independence. A physiotherapist would plan a progressive training program and guide the patient to correct functional movement, avoiding harmful compensations which might have a negative effect in the long run. There is also some evidence supporting physiotherapy in helping patients with Guillain–Barré syndrome regain strength, endurance, and gait quality,[23] as well as helping them prevent contractures, bedsores, and cardiopulmonary difficulties. A speech and language therapist would be essential in the patient regaining speaking and swallowing ability if they were intubated and received a tracheostomy. The speech and language therapist would also offer advice to the medical team regarding the swallowing abilities of the patient and would help the patient regain their communication ability pre-dysarthria. There would also be a doctor, nurse and other team members involved, depending on the needs of the patient. This team contribute their knowledge to guide the patient towards his or her goals, and it is important that all goals set by the separate team members are relevant for the patient’s own priorities. After rehabilitation the patient should be able to function in his or her own home and attend necessary training as needed.

Prognosis:
Most of the time recovery starts after the fourth week from the onset of the disorder. Approximately 80% of patients have a complete recovery within a few months to a year, although minor findings may persist, such as areflexia. About 5–10% recover with severe disability, with most of such cases involving severe proximal motor and sensory axonal damage with inability of axonal regeneration. However, this is a grave disorder and despite all improvements in treatment and supportive care, the death rate among patients with this disorder is still about 2–3% even in the best intensive care units. Worldwide, the death rate runs slightly higher (4%), mostly from a lack of availability of life support equipment during the lengthy plateau lasting four to six weeks, and in some cases up to one year, when a ventilator is needed in the worst cases. About 5–10% of patients have one or more late relapses, in which case they are then classified as having chronic inflammatory demyelinating polyneuropathy (CIDP).

Poor prognostic factors include: 1) age, over 40 years, 2) history of preceding diarrheal illness, 3) requiring ventilator support, 4) high anti-GM1 titre and 5) poor upper limb muscle strength

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:
http://www.bbc.co.uk/health/physical_health/conditions/guillainbarre1.shtml
http://www.riversideonline.com/health_reference/Nervous-System/DS00413.cfm
http://en.wikipedia.org/wiki/Guillain%E2%80%93Barr%C3%A9_syndrome
http://www.cdc.gov/flu/protect/vaccine/guillainbarre.htm

http://nursingcrib.com/nursing-notes-reviewer/guillain-barre-syndrome/

http://nursingcomments.com/tag/guillain-barre-syndrome/

http://www.ami20.com/tag/guillain-barre

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Glandular fever

Definition:
Glandular fever is a viral infection associated with a high fever.It’s also known as infectious mononucleosis or kissing disease (long ago it was realised that the infection was passed on through saliva – for example, by kissing).

It is a viral infection caused by the Epstein-Barr virus. Glandular Fever is often spread through oral acts such as kissing, which is why it is sometimes called “The Kissing Disease“. However, Glandular Fever can also be spread by airborne saliva droplets.

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Infectious Mononucleosis (IM) is an infectious, widespread viral disease caused by the Epstein-Barr virus (EBV), one type of herpes virus, to which more than 90% of adults have been exposed. Occasionally, the symptoms can reoccur at a later period. Most people are exposed to the virus as children, when the disease produces no noticeable symptoms or only flu-like symptoms. In developing countries, people are exposed to the virus in early childhood more often than in developed countries. As a result, the disease in its observable form is more common in developed countries. It is most common among adolescents and young adults.

Especially in adolescents and young adults, the disease is characterized by fever, sore throat and fatigue, along with several other possible signs and symptoms. It is primarily diagnosed by observation of symptoms, but suspicion can be confirmed by several diagnostic tests.

The syndrome was described as an infectious process by Nil Filatov in 1887 and independently by Emil Pfeiffer in 1889.
Symptoms:-
The following are mainly the symptoms of Glandular Fever:
*Headache
*Fever
*Sore throat/hard to swallow
*Tiredness, fatigue and malaise
*Enlarged lymph nodes
*Loss of appetite
*Muscle aches
*Tender enlargement of the glands (lymph glands or lymph nodes)
*Skin rash
*Sweating
*Stomach pain and enlarged spleen
*Enlarged liver
*Jaundice
*Depression
*Joint pain
*Swelling around eyes
*Orange urine (or discolored
*High blood pressure

Causes:
Glandular fever is caused by the Epstein-Barr virus. This can attack only two types of cell in the body: those in the salivary glands and white blood cells known as B lymphocytes (B-cells).

The most common way of spreading the virus is through the transmission of saliva from one person to another. Coughing, sneezing, and sharing drink bottles, eating utensils and other personal items can also spread the virus. In addition, the virus can also be spread through blood transfusion and organ transplantation.

Infection begins in the salivary glands, which release large amounts of the virus into the saliva. The infection spreads to the B lymphocytes, causing them to multiply, and causing the lymph glands to swell and become painful.

Once infected, the virus remains dormant in the body’s cells for the rest of a person’s life.

Diagnosis:–
The diagnosis of glandular fever or infectious mononucleosis is based on your physical symptoms, and will include a blood test and a throat swab. Your doctor will perform a blood test to determine abnormalities in the white blood cells. A throat swab will help determine if you have glandular fever.

The most commonly used diagnostic criterion is the presence of 50% lymphocytes with at least 10% atypical lymphocytes (large, irregular nuclei), while the person also has fever, pharyngitis and adenopathy. Furthermore, it should be confirmed by a serological test.  The atypical lymphocytes resembled monocytes when they were first discovered, thus the moniker “mononucleosis” was coined. Diagnostic tests are used to confirm infectious mononucleosis but the disease should be suspected from symptoms prior to the results from hematology. These criteria are specific; however, they are not particularly sensitive and are more useful for research than for clinical use. Only half the patients presenting with the symptoms held by mononucleosis and a positive heterophile antibody test (monospot test) meet the entire criteria. One key procedure is to differentiate between infectious mononucleosis and mononucleosis-like symptoms.

There have been few studies on infectious mononucleosis in a primary care environment, the best of which studied 700 patients, of which 15 were found to have mononucleosis upon a heterophile antibody test. More useful in a diagnostic sense are the signs and symptoms themselves. The presence of splenomegaly, posterior cervical adenopathy, axillary adenopathy, and inguinal adenopathy are the most useful to suspect a diagnosis of infectious mononucleosis. On the other hand, the absence of cervical adenopathy and fatigue are the most useful to dismiss the idea of infectious mononucleosis as the correct diagnosis. The insensitivity of the physical examination in detecting splenomegaly means that it should not be used as evidence against infectious mononucleosis.

In the past the most common test for diagnosing infectious mononucleosis was the heterophile antibody test which involves testing heterophile antibodies by agglutination of guinea pig, sheep and horse red blood cells. As with the aforementioned criteria, this test is specific but not particularly sensitive (with a false-negative rate of as high as 25% in the first week, 5–10% in the second and 5% in the third). 90% of patients have heterophile antibodies by week 3, disappearing in under a year. The antibodies involved in the test do not interact with the Epstein-Barr virus or any of its antigens. More recently, tests that are more sensitive have been developed such as the Immunoglobulin G (IgG) and Immunoglobulin M (IgM) tests. IgG, when positive, reflects a past infection, whereas IgM reflects a current infection. When negative, these tests are more accurate in ruling out infectious mononucleosis. However, when positive, they feature similar sensitivities to the heterophile antibody test. Therefore, these tests are useful for diagnosing infectious mononucleosis in people with highly suggestive symptoms and a negative heterophile antibody test. Another test searches for the Epstein-Barr nuclear antigen, while it is not normally recognizable until several weeks into the disease, and is useful for distinguishing between a recent-onset of infectious mononucleosis and symptoms caused by a previous infection. Elevated hepatic transaminase levels is highly suggestive of infectious mononucleosis, occurring in up to 50% of patients.

A fibrin ring granuloma may be present.

Diagnosis of acute infectious mononucleosis should also take into consideration acute cytomegalovirus infection and Toxoplasma gondii infections. These diseases are clinically very similar by their signs and symptoms. Because their management is much the same it is not always helpful, or possible, to distinguish between EBV mononucleosis and cytomegalovirus infection. However, in pregnant women, differentiation of mononucleosis from toxoplasmosis is associated with significant consequences for the fetus.

Acute HIV infection can mimic signs similar to those of infectious mononucleosis and tests should be performed for pregnant women for the same reason as toxoplasmosis.

Other conditions from which to distinguish infectious mononucleosis include leukemia, tonsillitis, diphtheria, common cold and influenza

Treatment:
Self care:
Infectious mononucleosis is generally self-limiting and only symptomatic and/or supportive treatments are used.  Rest is recommended during the acute phase of the infection, but activity should be resumed once acute symptoms have resolved. Nevertheless heavy physical activity and contact sports should be avoided to mitigate the risk of splenic rupture, for at least one month following initial infection or splenomegaly has resolved, as determined by a treating physician.

MedicationsIn terms of pharmacotherapies, non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen may be used to reduce fever and pain. Prednisone, a corticosteroid, is commonly used as an anti-inflammatory to reduce symptoms of pharyngeal pain, odynophagia, or enlarged tonsils, although its use remains controversial due to the rather limited benefit and the potential of side effects. Intravenous corticosteroids, usually hydrocortisone or dexamethasone, are not recommended for routine use but may be useful if there is a risk of airway obstruction, severe thrombocytopenia, or hemolytic anemia. There is little evidence to support the use of aciclovir, although it may reduce initial viral shedding. However, the antiviral drug valacyclovir has recently been shown to lower or eliminate the presence of the Epstein-Barr virus in subjects afflicted with acute mononucleosis, leading to a significant decrease in the severity of symptoms. Although antivirals are not recommended for patients presenting with simple infectious mononuscleosis, they may be useful (in conjunction with steroids) in the management of patients with severe EBV manifestations, such as EBV meningitis, peripheral neuritis, hepatitis, or hematologic complications. Antibiotics are not used as they are ineffective against viral infections. The antibiotics ampicillin and later the related amoxicillin   are relatively contraindicated in the case of any coinciding bacterial infections during mononucleosis because their use precipitates a non-allergic rash close to 99% of the time.

In a small percentage of cases, mononucleosis infection is complicated by co-infection with streptococcal infection in the throat and tonsils (strep throat). Penicillin or other antibiotics (with the exception of the two mentioned above) should be administered to treat the strep throat. Opioid analgesics are also relatively contraindicated due to risk of respiratory depression.
Prognosis:
Serious complications are uncommon, occurring in less than 5% of cases:

*CNS: Meningitis, encephalitis, hemiplegia, Guillain-Barré syndrome, and transverse myelitis. EBV infection has also been proposed as a risk factor for the development of multiple sclerosis (MS), but this has not been confirmed.

*Hematologic: Hemolytic anemia (direct Coombs test is positive) and various cytopenias; Bleeding (caused by thrombocytopenia).[

*Mild jaundice

*Hepatitis (rare)

*Upper airway obstruction (tonsillar hypertrophy) (rare)

*Fulminant disease course (immunocompromised patients) (rare)

*Splenic rupture (rare)

*Myocarditis and pericarditis (rare)

Once the acute symptoms of an initial infection disappear, they often do not return. But once infected, the patient carries the virus for the rest of his or her life. The virus typically lives dormantly in B lymphocytes. Independent infections of mononucleosis may be contracted multiple times, regardless of whether the patient is already carrying the virus dormantly. Periodically, the virus can reactivate, during which time the patient is again infectious, but usually without any symptoms of illness.  Usually, a patient has few if any further symptoms or problems from the latent B lymphocyte infection. However, in susceptible hosts under the appropriate environmental stressors the virus can reactivate and cause vague physical complaints (or may be subclinical), and during this phase the virus can spread to others. Similar reactivation or chronic subclinical viral activity in susceptible hosts may trigger multiple host autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s syndrome, antiphospholipid antibody syndrome, and multiple sclerosis. Such chronic immunologic stimulation may also trigger multiple type of cancers, particularly lymphoma—strongest cancer associations with EBV are nasopharyngeal carcinomas, Burkitt’s lymphoma, and Hodgkin’s lymphoma. EBV’s potential to trigger such a wide range of autoimmune diseases and cancers probably relates to its primary infection of B lymphocytes (the primary antibody-producing cell of the immune system) and ability to alter both lymphocyte proliferation and lymphocyte antibody production.

Prevention:
A vaccine against the Epstein-Barr virus is under development. The infection is most contagious during the feverish stage, when contact with others should be avoided.

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:
http://www.nativeremedies.com/ailment/glandular-fever-symptoms-info.html
http://simple.wikipedia.org/wiki/Glandular_fever
http://simple.wikipedia.org/wiki/Glandular_fever
http://www.bbc.co.uk/health/physical_health/conditions/glandularfever2.shtml

http://www.treatfast.com/mononucleosis-xidc18255.html

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Cytomegalovirus

Definition
Cytomegalovirus (say: si-toe-meg-ah-low-vi-russ), or CMV, is a very common virus. It  is a viral genus of the viral group known as Herpesviridae or herpesviruses. It is typically abbreviated as CMV: The species that infects humans it is commonly known as human CMV (HCMV) or human herpesvirus-5 (HHV-5), and is the best studied of all cytomegoloviruses. Within Herpesviridae, CMV belongs to the Betaherpesvirinae subfamily, which also includes the genera Muromegalovirus and Roseolovirus. It is related to other herpesviruses within the subfamilies of Alphaherpesvirinae that includes herpes simplex viruses (HSV)-1 and -2 and varicella-zoster virus (VZV), and the Gammaherpesvirinae subfamily that includes Epstein-Barr virus. All herpesviruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals. Other CMV viruses are found in several mammal species, but species isolated from animals differ from HCMV in terms of genomic structure, and have not been reported to cause human disease.

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People are usually infected by the time they are 2 years old or during their teenage years and carry the virus for life (usually in a dormant or inactive state). The majority of adults carry the virus by the time they are 40 years of age.

Many people are infected with CMV and don’t even know it because the virus rarely causes symptoms and usually does not cause long-term problems.

However, CMV can cause problems in people who have weak immune systems and in a newborn if the mother gets the infection during pregnancy.

Causes:
CMV gets into body fluids, such as saliva, blood, urine, semen and breast milk. A person is able to transmit (or “shed”) the virus to others only when it is active in his or her system (not dormant). It can be spread from one person to another through sexual contact and contact with blood and other body fluids. CMV can rarely be transmitted by blood transfusion or organ transplantation. In developed countries, blood supplies are screened for CMV when they’re to be used for those at greatest risk from the infection.

 Symptoms:

Usually, CMV does not cause symptoms or only causes mild symptoms. A few people will have symptoms that are similar to mononucleosis. Symptoms of CMV can include:

•Sore throat
•Swollen lymph nodes (lymph glands)
•Fever
•Headache
•Fatigue
•Weakness
•Muscle aches
•Loss of appetite


People who have weakened immune systems due to conditions like human immunodeficiency virus (HIV) or because they received an organ transplant and are taking immunosuppressant medicines may have severe symptoms. (Immunosuppressant medicines are medicines that lower or suppress the immune system.) Symptoms of severe CMV include:
•Blindness
•Pneumonia
•Diarrhea
•Bleeding ulcers in the esophagus (windpipe) or intestines
•Inflammation of the brain (encephalitis)
•Seizures

If a pregnant woman transmits CMV to her unborn baby, miscarriage, stillbirth or death of the newborn may occur. Newborns who survive are at an increased risk for hearing loss and mental retardation. However, only 1% of newborns who are infected with CMV during pregnancy experience problems from the virus. Most are born healthy, or with only mild CMV symptoms.

Who’s affected?
In most cases, CMV is harmless, but for some people infection can have disastrous consequences.

People with weakened immune systems (because of HIV, for example) can suffer serious illness. They may experience high fever for two or three weeks, accompanied by hepatitis and jaundice.

Other serious complications include pneumonia, inflammation of the brain (encephalitis) and blindness as a result of inflammation of the retina at the back of the eye.

CMV remains in the body for life. For those with strong immune systems, it remains inactive. If the immune system is weakened through illness or medical treatments, CMV may be reactivated, causing further medical problems and distress.

If a pregnant woman becomes infected with CMV for the first time, the virus may pass through the placenta and infect her unborn baby. If this happens early in pregnancy, the risk of miscarriage increases, as does the chance of the baby being born with malformations. For example, CMV infection in the womb is the leading cause of congenital deafness.

If the infection is contracted later in pregnancy, stillbirth and premature labour are more likely. A newborn baby may suffer severe illness shortly after birth – jaundice, enlargement of the liver and blood disorders.

Diagnosis:
CMV is diagnosed with a blood test.

CMV is more likey to cause vision problems in people who have weakened immune systems, so if you have conditions such as HIV or AIDS, your doctor may recommend that you visit an eye doctor to find out whether the virus has infected your eyes. Be sure to let your doctor know if you are having any painless blurring of your vision, “floaters” only in one eye, light flashes or areas of blindness. You should also let your doctor(s) know if you are experiencing frequent shortness of breath with flu-like symptoms, or if you are having problems hearing.

Treatment:
For otherwise healthy people, CMV usually doesn’t require treatment. If your immune system is weakened, your doctor may use one of several different medicines to treat CMV infection. However, because CMV is a virus, regular antibiotics won’t work against it. Antiviral drugs are usually prescribed, which slows the virus down (but cannot cure CMV).

If you are pregnant, your doctor may want to test you for CMV to determine if there is a risk for your unborn baby. If you do carry the virus, your doctor may suggest a test called amniocentesis, which collects a sample of the amniotic fluid for testing. It can help determine whether your unborn baby has CMV.

If you are pregnant and your baby has CMV, you doctor will likely check your baby once he or she is born for any problems or birth defects so they can be treated early. Treatable symptoms in newborns include pneumonia, hearing loss and inflammation of the eye.

Prevention:
In child care centers, as many as 70% of children ages 1 to 3 can shed the virus. Careful, frequent hand washing with soap and water may help prevent the spread of CMV.

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:
http://www.bbc.co.uk/health/physical_health/conditions/cmv1.shtml
http://familydoctor.org/online/famdocen/home/common/infections/common/viral/743.html
http://en.wikipedia.org/wiki/Cytomegalovirus
http://medippt.files.wordpress.com/2010/10/cytomegalovirus.jpg

http://health.allrefer.com/health/cmv-immunocompromised-host-cmv-cytomegalovirus.html

http://archive.microbelibrary.org/ASMOnly/Details.asp?ID=658

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Ailmemts & Remedies Pediatric

Bubble Boy Disease

Other Names: Severe combined immunodeficiency (SCID), or Boy in the Bubble Syndrome, (also known as “Alymphocytosis,” “Glanzmann–Riniker syndrome,” “Severe mixed immunodeficiency syndrome,” and “Thymic alymphoplasia”


Definition:
It is a genetic disorder in which both “arms” (B cells and T cells) of the adaptive immune system are crippled, due to a defect in one of several possible genes. SCID is a severe form of heritable immunodeficiency. It is also known as the “bubble boy” disease because its victims are extremely vulnerable to infectious diseases and some of them, such as David Vetter, become famous for living in a sterile environment.

CLICK & SEE THE PICTURES

David Vetter poses inside of his bubble in his Houston home in this Dec. 17, 1976

The body’s immune system fights against diseases and infections. The SCID syndromes are inherited disorders that result in severe defects in the immune system. White blood cells (which fight infection) are produced in the bone marrow by stem cells. In people with SCID, the bone marrow stem cells are absent or defective. This leaves the affected person open to any and all germs around him because he has no way to fight them off.

Prevalence:-
The most commonly quoted figure for the prevalence of SCID is around 1 in 100,000 births, although this is regarded by some to be an underestimate of the true prevalence; and a figure of about 1 in 65,000 live births has been reported for Australia.

Recent studies indicate that one in every 2,500 children in the Navajo population inherit severe combined immunodeficiency. This condition is a significant cause of illness and death among Navajo children. Ongoing research reveals a similar genetic pattern among the related Apache people.

Types:-
1. X-linked severe combined immunodeficiency:–
Most cases of SCID are due to mutations in the gene encoding the common gamma chain (?c), a protein that is shared by the receptors for interleukins IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21. These interleukins and their receptors are involved in the development and differentiation of T and B cells. Because the common gamma chain is shared by many interleukin receptors, mutations that result in a non-functional common gamma chain cause widespread defects in interleukin signalling. The result is a near complete failure of the immune system to develop and function, with low or absent T cells and NK cells and non-functional B cells.
The common gamma chain is encoded by the gene IL-2 receptor gamma, or IL-2R?, which is located on the X-chromosome. Therefore, immunodeficiency caused by mutations in IL-2R? is known as X-linked severe combined immunodeficiency. The condition is inherited in an X-linked recessive pattern.


2.Adenosine deaminase deficiency:-
The second most common form of SCID after X-SCID is caused by a defective enzyme, adenosine deaminase (ADA), necessary for the breakdown of purines. Lack of ADA causes accumulation of dATP. This metabolite will inhibit the activity of ribonucleotide reductase, the enzyme that reduces ribonucleotides to generate deoxyribonucleotides. The effectiveness of the immune system depends upon lymphocyte proliferation and hence dNTP synthesis. Without functional ribonucleotide reductase, lymphocyte proliferation is inhibited and the immune system is compromised.

3. Omenn syndrome:–
The manufacture of immunoglobulins requires recombinase enzymes derived from the recombination activating genes RAG-1 and RAG-2. These enzymes are involved in the first stage of V(D)J recombination, the process by which segments of a B cell or T cell’s DNA are rearranged to create a new T cell receptor or B cell receptor (and, in the B cell’s case, the template for antibodies).Certain mutations of the RAG-1 or RAG-2 genes prevent V(D)J recombination, causing SCID.

4.Bare lymphocyte syndrome:-
MHC class II is not expressed on the cell surface of all antigen presenting cells. Autosomal recessive. The MHC-II gene regulatory proteins are what is altered, not the MHC-II protein itself.

5.JAK3 :-  Janus kinase-3 (JAK3) is an enzyme that mediates transduction downstream of the ?c signal. Mutation of its gene also causes SCID.

6.Artemis/DCLRE1C:-
Mortan Cowan, MD, director of the Pediatric Bone Marrow Transplant Program at the University of California-San Francisco, noted that although researchers have identified about a dozen genes that cause SCID, the Navajo and Apache population has the most severe form of the disorder. This is due to the lack of a gene designated Artemis. Without the gene, children’s bodies are unable to repair DNA or develop disease-fighting cells.


Symptoms:
Chronic diarrhea, ear infections, recurrent Pneumocystis jirovecii pneumonia, and profuse oral candidiasis commonly occur. These babies, if untreated, usually die within 1 year due to severe, recurrent infections. However, treatment options are much improved since David Vetter.


You may click to see :
The list of signs and symptoms mentioned in various sources for SCID includes the 35 symptoms listed below:

Causes:
Click to see :New Genetic Cause Of Boy In The Bubble Syndrome :

New gene mutation found to cause ‘bubble boy disease’ :

How Gene Defects Cause Disease :

Diagnosis:
Several US states are performing pilot studies to diagnose SCID in newborns through the use of T-cell recombinant excision circles.[citation needed] Wisconsin and Massachusetts (as of February 1, 2009) screen newborns for SCID.

Despite these pilot programs, standard testing for SCID is not currently available in newborns due to the diversity of the genetic defect. Some SCID can be detected by sequencing fetal DNA if a known history of the disease exists. Otherwise, SCID is not diagnosed until about six months of age, usually indicated by recurrent infections. The delay in detection is because newborns carry their mother’s antibodies for the first few weeks of life and SCID babies look normal.

You may click to see :Diagnostic Tests for SCID :

Treatment:-
The most common treatment for SCID is bone marrow transplantation, which has been successful using either a matched related or unrelated donor, or a half-matched donor, who would be either parent. The half-matched type of transplant is called haploidentical and was perfected by Memorial Sloan Kettering Cancer Center in New York and also Duke University Medical Center which currently does the highest number of these transplants of any center in the world. David Vetter, the original “bubble boy”, had one of the first transplantations but eventually died because of an unscreened virus, Epstein-Barr (tests were not available at the time), in his newly transplanted bone marrow from his sister. Today, transplants done in the first three months of life have a high success rate. Physicians have also had some success with in utero transplants done before the child is born and also by using cord blood which is rich in stem cells.

More recently gene therapy has been attempted as an alternative to the bone marrow transplant. Transduction of the missing gene to hematopoietic stem cells using viral vectors is being tested in ADA SCID and X-linked SCID. In 1990, 12-year-old Ashanthi DeSilva became the first patient to undergo successful gene therapy. Researchers collected samples of Ashanthi’s blood, isolated some of her white blood peripheral T cells, and incorporated into them a virus engineered to contain a healthy immune system enzyme: adenosine deaminase (ADA) gene. These cells were then injected back into her body. She is now given a weekly shot of ADA that without would have her destined for a life of isolation. In 2000, the first gene therapy “success” resulted in SCID patients with a functional immune system. These trials were stopped when it was discovered that two of ten patients in one trial had developed leukemia resulting from the insertion of the gene-carrying retrovirus near an oncogene. In 2007, four of the ten patients have developed leukemias [11]. Work is now focusing on correcting the gene without triggering an oncogene. No leukemia cases have yet been seen in trials of ADA-SCID, which does not involve the gamma c gene that may be oncogenic when expressed by a retrovirus.

Trial treatments of SCID have been gene therapy’s only success; since 1999, gene therapy has restored the immune systems of at least 17 children with two forms (ADA-SCID and X-SCID) of the disorder.

You may click to see :Drugs and Medications used to treat SCID:
A new hope for gene therapy

Breakthrough for “Bubble Boy” 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:
http://en.wikipedia.org/wiki/Severe_combined_immunodeficiency#cite_note-Bolognia-0
http://rarediseases.about.com/od/immunedisorders/a/scid.htm
http://www.wrongdiagnosis.com/s/scid/intro.htm

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