Typical In Patients With Primary Ebv Infection example essay topic

ITI ON Infectious mononucleosis is a clinical syndrome that can be characterized by a multitude of symptoms. They include malaise, headache, fever, pharyngitis, pharyngeal lymphatic hyperplasia, lymphadenopathy, atypical lymphocytosis, and mild transient hepatitis. This disease occurs most often in adolescents and young adults. Mononucleosis is one of these diseases that are grouped into a class known as a viral infection; more specifically it is caused by the Epstein-Barr virus (EBV).

EBV is a herpes virus. In vito, EBV only infects human B-lymphocytes. This viral infection results in lymphocyte proliferation and immunoglobulin secretion. The virus usually remains dormant, but can be activated using certain chemicals or when subjected to certain bodily conditions.

To understand how this virus affects the body, we must first have a brief overview of the body and it's immune system. OVERVIEW The body's defense mechanisms can be split into two groups; non-specific and specific defense mechanisms. Non-specific mechanisms basically are the barriers that keep pathogens from penetrating the body. For example the epithelial membranes that cover the body, the strong acidity of the stomach killing pathogens before they have the opportunity to infect the system, these are just a couple, there are many others. Specific mechanisms help the individual acquire the ability to defend against specific pathogens by prior exposure to these pathogens. This is a function of the lymphocytes, which will be discussed later on in depth.

Mononucleosis affects the epithelium of the mouth where it is first introduced to the body, but that is the extent to which it is involved in the nonspecific defense mechanisms. The place where it does the most damage is the B-lymphocyte, which is a key component of specific immunity. To understand better what the infection does to the body we must look at the role of lymphocytes in the body briefly and how they do their work. B-lymphocytes are the ones that are affected directly upon when the body is subjected to this type of infection. Their role in the body is vital for immunity. They are grouped into five subclasses, depending upon some of the polypeptides in their makeup.

The basic role of B-lymphocytes is to secrete antibodies that they have made due to them coming into contact with an antigen. Each B-lymphocyte has two sites where specific antigens can combine, and this binding is what promotes the body's reaction to the infection. The B-lymphocyte is involved in what is called humoral immunity. This is when the cell secretes the antibodies but doesn't do the job directly. T-lymphocytes (T-cells) are the cells that actually do the fighting of the infections themselves.

There are three classes of T-cells. The first is called a Killer T-cell. The way that these cells work is that they have an antigen presented to them or they have found a rogue tissue cell. The way they can tell is by the protein vehicle that is left on the outside of the cell from when the virus entered it.

This is very important later on with regards to mononucleosis. It then injects a toxin called lympho toxin and this kills the cells from the inside out. Another way that it can kill is by using another protein called. It diffuses to the infected cell and inserts itself into the membrane and forms a pore, which causes there to be a hole in the membrane which screws up the sodium and potassium concentration gradient.

This kills the cell before the virus can be made completely. The second and third types of T-cells are ones that are called Helper T-lymphocytes and Suppressor T-lymphocytes. Helper T-cells are ones that stimulate the functions of B and Killer T-lymphocytes. Suppressor T-cells suppress this function as their name suggests. Now that there is a brief overview of how the body's defense mechanisms work, we can look at how mononucleosis, or more specifically EBV affects these cells.

PATHOGENESIS EBV first infects the epithelium of the mouth normally and then spreads to the sub epithelial circulating B-lymphocytes. The virus carries a gene similar to the human interleukin-10 gene, and the expression of this protein partially blocks the initial interferon, natural killer, and T-cytotoxic responses. The infection may be confined to epithelial and B-lymphocyte tissues, because only these cells have the EBV receptors. Tonsils and regional and systemic lymph nodes enlarge because of virus-infected B-lymphocytes and infiltration of sinuses with reactive, atypical T lymphocytes. Similar changes also occur in the spleen.

In patients with severe hepatitis, the portal areas may be infiltrated by mono nucleated cells. An area that is usually unaffected is the bone marrow. Early on in the illness, 1-2% of the circulating leukocytes may be EBV-infected B lymphocytes (Goldman and Bennett, 2000). The predominant atypical lymphocytes in the peripheral blood are reactive natural killer cells and T cells. EBV-infected B-lymphocytes can be detected by their expression of EBV nuclear proteins and latent infection membrane proteins. The antibody may be the direct product of EBV-infected B lymphocytes, or it may be produced as a result of lympho kines produced by EBV-infected or reactive lymphocytes.

After the patient recovers from acute infectious mononucleosis, the proportion of circulating B-lymphocytes infected with EBV is 1 in 10^5 to 10 ^6. Most of these lymphocytes express only a certain protein which is not recognized by immune cytotoxic T lymphocytes. These latently infected B lymphocytes are likely to be the site of virus persistence, since long-term suppression of virus replication does not decrease the number of circulating EBV-infected B lymphocytes, and after stopping of treatment the virus goes back to the epithelium of the mouth. Long after primary EBV infection, T lymphocytes, which can suppress or kill EBV-infected cells that express the right membrane proteins, continue to circulate in the peripheral blood. EPIDEMIOLOGY The usual mode of transmission for the EBV infection is by direct contact with the saliva of a previously infected person with the saliva of a non-infected person. Infection during infancy is usually due to contact with the food of an infected mother.

Infection in adolescence or in adulthood is usually by kissing. It has a long incubation period of around 30-50 days from the time you are exposed to it to the time when you actually get sick (Willis and Watkins, 1998). Once the saliva has been introduced to the virus, the virus then replicates in the epithelium of the mouth. The amount of the virus in the saliva is the highest right after primary infection and for months after. The viral replication occurs still many years after, and maybe even for life (Goldman and Bennett, 2000). When the virus follows this course, it then infects the tonsillar and peripheral blood B-lymphocytes.

This is the way that it can stay around for life, as it persists in the peripheral B-lymphocytes indefinitely. Previously infected people are immune to the development of infectious mononucleosis. But more that 90% of adults in all human populations have evidence of previous primary EBV infection and are carriers of the virus (Riccio, 2000). CLINICAL MANIFESTATIONS The syndrome of infectious mononucleosis was a distinctive clinical problem for at least 40 years before the discovery of it's exact cause (Goldman and Bennett, 2000).

Most infected non-immune adolescents and young adults develop malaise, headache, fever, pharyngitis, and lymphadenopathy lasting 1 to several weeks. Body temperatures may reach 40 degrees Celsius. Tonsillar or cervical lymph nodes may become enlarged, painful, and tender. Laboratory analysis has shown many things about the disease. Up to 40% of the peripheral lymphocytes are atypically large with an unusually large amount of cytoplasm and a large pale nucleus. Malaise or weakness may occur for several months.

Often rashes are typical in patients with primary EBV infection that are treated with penicillin or ampicillin. The majority of infected people recover from acute mononucleosis within 3-4 months. Persistent systematic, neurological, or cardiac problems are rare. Outside of the adolescent and young adult populations, primary EBV infection frequently most often does not result in the full infectious mononucleosis syndrome. In younger children, fever and pharyngitis from the primary EBV infection may be indistinguishable from upper respiratory tract infections caused by other viruses. In rare cases, severe, progressive, and sometimes fatal primary EBV infections occur in children with X-linked disease (Duncan's syndrome).

But also non-X-linked cases do occur. These children may have no obvious pre-existing immune deficiency, but the primary EBV infections leads to massive lymphocyte growth, fever, anemia, and hepatitis. The proliferating B-lymphocytes are EBV infected cells that express EBV-latent-infection-associated proteins. Very rare cases of chronic progressive primary EBV infection in otherwise normal young adults have been well documented. These few patients have had severe acute mononucleosis that persists with other clinical manifestations. Persistent active EBV infection has been proposed to be the cause of a more common chronic mononucleosis or chronic fatigue syndrome.

This syndrome is characterized by recurrent episodes of malaise and weakness, sometimes accompanied by pharyngitis, mild fever, and other complications. But there is little to support the initial hypothesis that EBV is a cause of this syndrome (Goldman and Bennett, 2000). DIAGNOSIS In normal adolescents the diagnosis of acute infectious mononucleosis can usually be made on clinical grounds and confirmed by the laboratory findings of atypical lymphocytosis and an antibody. The test most commonly used is the mononucleosis spot test.

This blood test detects the antibodies that the body makes to fight EBV. Because it takes awhile for the antibodies to develop, the doctor may need to repeat the test one or two weeks after you get the symptoms. At that time the test is about 85% accurate (Willis and Watkins, 1998). Other tests may included a complete blood count to see if your blood platelet count is lower than normal and if lymphocytes are abnormal, and a chemistry panel to see if liver enzymes are normal. A bacterial throat culture should be obtained in patients with extreme pharyngitis to rule out a streptococcal infection. The rapid antibody tests are more than 95% sensitive and 95% specific in an adolescent or young adult population (Dreher, 1997).

In patients with the absence of an antibody, EBV-specific serologic testing should be done (Goldman and Bennett, 2000). Specific serologic testing for EBV infection involves determining antibody levels to latently infected, early replication cycle, or late replication cycle viral proteins. This is usually done by microscopy or by enzyme-linked immunoassay. Those rare patients with chronically progressive EBV infection tend to have abnormally high levels of antibodies to some or many EBV antigens. TREATMENT No treatment is necessary for most EBV infections. Rest during the period of acute symptoms and slow return to normal activity are commonly advised.

Patients with enlarged spleens should restrict their involvement in sports to avoid traumatic rupture. Acetaminophen and aspirin can be used to treat fever and pharyngeal pain in most patients who have normal or only slightly abnormal liver function (Goldman and Bennett, 2000). CONCLUSION The body's defense mechanisms are great in most cases. But once in awhile they are fooled and in the case of mononucleosis or EBV, this has been done. As a person that has had the disease twice I can say that it is a very debilitating disease. The real kicker is that once you have it you are more susceptible to getting it again and again.

The body just can't recognize the antigens or the infection carrying B-lymphocytes because the protein vehicle is so well hidden in the protein membranes of the host cell. The Killer cells just aren't used to that and don't even know that the virus is there. So really it is a perfect viral infection in that it can't be detected until it is too late or the person has already had it.