Beijing 2008 Olympic Games

Beijing 2008 Olympic Games August 8-24, 2008.
Kenya’s 2008 Olympics: Top Medalists.


SPORT- MEDALS- ATHLETE- EVENT

Track &field: Gold- W.Bungei - Men’s 800m
Gold -P. Jelimo - Women’s 800m
Gold- N. Langat - Women’s 1500m
Gold -B. Kiprop Kipruto - Men’s 3000m
Gold -S. Wanjiru - Men’s Marathon
Silver- J. Jepkosgei - Women’s 800m
Silver- A. Kiprop - Men’s 1500m
Silver- E. jepkorir - Women’s 3000m
Silver- E. Kipchoge - Men’s 5000m
Silver- C. Ndereba - Women’s marathon
Bronze-A. Kirwa Yego- Men’s 800m
Bronze-R. Mateelong- Men’s 3000m
Bronze-E. Soi Men’s - 5000m
Bronze-M. Kogo - Men’s 10,000m

The total Medal haul from Beijing 2008 Olympics stands at 14;
5-Golds, 5-Silvers and 4-Bronze.

That brought Kenya’s Medals overall ranking at number 15th worldwide. Not a bad feat at all I would say! And For all the Men and Women, who sacrificed too much for our beloved country, let’s say, **ASANTENI SAANA! AND BRAVO**!

HIV/AIDS AND ITS EFFECTS ON SOCIETY 1

What is HIV/AIDS?

Introduction:

HIV- (human immunodeficiency virus) belongs to the retrovirus family (HIV-1 and HIV-2). Retroviruses are unique because they possess the enzyme reverse transcriptase. Reverse transcriptase allows the viral RNA genome to be replicated into DNA, rather than the usual RNA copies. The HIV attacks the immune system, the body’s natural defense system. Without a strong immune system, the body is unable to fight any disease that it encounters.

Both the virus and the infection it causes are all together referred to as HIV infection. The virus takes over certain immune system cells to make many copies of its own (replication). While many viruses can be controlled by the immune system, HIV targets and infects that same immune system i.e. cells that are supposed to protect the body from illnesses. These are a type of white blood cell called CD4 cells. HIV takes over CD4 cells and turns them into virus factories that produce thousands of viral copies. As the virus grows, it damages or kills CD4 cells, weakening the immune system, thus causing slow but constant damage to the body’s natural defense system of which at this stage is commonly called AIDS.

The virus may be passed from one person to another when infected blood, semen, or vaginal secretions come in contact with an uninfected person’s broken skin or mucous membranes. In addition, infected pregnant women can pass HIV to their baby during pregnancy or delivery, as well as through breast-feeding. People with HIV have what is called HIV infection. Some of these people will develop AIDS as a result of their HIV infection.


AIDS – (Acquired Immunodeficiency Syndrome):

Acquired – means that the disease is not hereditary but develops after birth from contact with a disease causing agent (in this case, HIV).
Immunodeficiency – means that the disease is characterized by a weakening of the immune system.
Syndrome – refers to a group of symptoms that collectively indicate or characterize a disease.

In the case of AIDS this can include the development of certain infections and/or cancers, as well as a decrease in the number of certain cells in a person’s immune system.

Acquired Immune Deficiency Syndrome is a set of symptoms and infections resulting from the damage to the human immune systems caused by the (HIV). This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. It is the condition diagnosed when there are a group of related symptoms that are caused by severe human immunodeficiency virus infection. AIDS makes the body vulnerable to life-threatening illnesses called opportunistic infections. But having HIV does not mean you have AIDS. Even without treatment, it takes a long time for HIV to progress to AIDS—usually 10 to 12 years. If HIV is diagnosed before it becomes AIDS, medicines can slow or stop the damage to the immune system. With treatment, many people with HIV are able to live long and active lives.

Immune system: (as pertains to the HIV/AIDS)

Your immune system is your body's natural defense against infection and illness. Specialized cells and organs all work in concert to protect your body and keeping your body away from diseases and thus healthy. Understanding these different parts of your immune system and how your immune system works will help to better understand HIV and AIDS. There will be more discussions dedicated to immune system in another entry.

Organs and Cells of the Immune System:

•Bone Marrow.
All the specialized cells of the immune system are formed in the bone marrow. Their formation is begun in bone marrow and then they move into the blood stream where they mature.
•Thymus.
This small but important organ produces T-cells. In addition, the thymus actually chooses which T-cells are best suited for the immune system. The remaining ones are eliminated by the body, assuring a healthy, effective immunity.
•Spleen.
You can think of the spleen as a filter for the blood. It catches foreign material in the blood and activates different types of immune system cells.
•Lymph Nodes.
The lymph nodes filter foreign material from the lymph fluid. Fluid that drains from various tissues in the body collects in the lymph system and passes through the nodes, being filtered as it passes.

•Cells-Leukocytes or WBCs.
The leukocytes are further subdivided into granulocytes (containing large granules in the cytoplasm) and agranulocytes (without granules). The granulocytes consist of neutrophils (55–70%), eosinophils (1–3%), and basophils (0.5–1.0%). The agranulocytes are lymphocytes (consisting of B cells and T cells) and monocytes. Lymphocytes circulate in the blood and lymph systems, and make their home in the lymphoid organs. For the sake of the topic we'll consider T-cells here.

T-Cells also called CD4 Cells:

T-Cells- There are two subsets of T-cells: CD4 cells and CD8 cells. CD4 cells secrete factors that activate other white blood cells that participate in the immune response. HIV attacks CD4 cells, damaging the body's ability to initiate the immune response.

CD8 cells are important in directly killing tumor cells, viral infected cells and some parasites. T/CD4 cells are also called “helper” cells. And in other words lead the attack against infections. While the T-8 cells (CD8) are called “suppressor” cells that end the immune response. CD8 cells can also be “killer” cells that kill cancer cells and cells infected with a virus.

It is important for people who are HIV+ to know their CD4 cells count as this can give a picture of the effectiveness or the status of their immune system.

Knowing how many functioning CD4 cells are circulating in the blood gives an idea of how strong the HIV+ person's immune system really is. A CD4 cells count measures the number of functioning CD4 cells in the body and therefore measures the health of the immune system.
The CD4 test ranges vary but Normal Values - In a healthy adult is typically 600 to 1200 cells per cubic millimeter of blood. And Between 600 and 350 - In an HIV+ person is considered "very good". And Between 350 and 200 - The immune system is weakened and therefore the HIV+ person may be at increased risk for infection and illness.

Signs and Symptoms:

Symptoms of infection with HIV can vary. Often a flu-like syndrome occurs in 50 to 80% of those who contract HIV within the first 2 - 6 weeks, including a combination of the following symptoms:
•Fever
•Sore throat
•Swollen lymph nodes
•Joint pain
•Muscle aches
•Rash
•Mouth ulcers
•Nausea
•Diarrhea
•Headache
After you are infected with HIV, you may remain relatively symptom-free for years or the disease may progress more rapidly. In this stage, the CD4 count may be below 500 per cubic millimeter. You may develop infections or chronic symptoms including:
•Swollen lymph nodes
•Diarrhea
•Weight loss
•Fever
•Cough and shortness of breath
•Low platelet count, which may manifest as easy bruising, bleeding gums, or nose bleeds
During the last stage of the disease, HIV infection may meet the official criteria for AIDS, which is the presence of an opportunistic infection (such as Pneumocystis carinii pneumonia, or PCP) or a CD4 count below 350-200 per cubic millimeter. At this stage, symptoms may include
•Pneumonia, including PCP
•Tuberculosis
•Night sweats
•Persistent fatigue
•Extreme weight loss and wasting, exacerbated by diarrhea. Up to 90% of HIV patients worldwide experience diarrhea
•Meningitis and other brain infections
•Fungal infections
•Syphilis
•Malignancies such as lymphoma, cervical cancer, and Kaposi's sarcoma (KS) (affects the skin and oral mucosa and may spread to the lungs. KS can actually occur in earlier stages of HIV as well).

****TO BE CONTINUED****

COMMON LIVER DISEASES(HEPATITIS)-SUMMARY

SUMMARY OF HEPATITIS; A, B, D, C, & E:

Hepatitis is a disease characterized by inflammation of the liver, usually producing swelling and, in many cases, permanent damage to liver tissues. A number of different agents can cause hepatitis, including infectious diseases, chemical poisons, drugs and alcohol. Viral hepatitis refers to a set of at least six viruses that are known to cause hepatitis: hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), hepatitis E (HEV), and hepatitis G (HGV). Recent scientific evidence also suggests the existence of other, as yet unidentified hepatitis viruses.
The most common types of viral hepatitis are hepatitis A, B, and hepatitis C. Both hepatitis B and C can lead to serious, permanent liver damage, and in many cases, death.
There are two primary types of viral hepatitis, food-borne and blood-borne hepatitis. The former, which is spread through contaminated food and water, does not cause chronic liver disease. By contrast, blood borne viral hepatitis may lead to long-term, persistent infections and chronic liver disease that has lethal consequences many years after infection.


Hepatitis A: is an acute liver disease caused by the hepatitis A virus (HAV), lasting from a few weeks to several months. It does not lead to chronic infection.
Transmission: Ingestion of fecal matter, even in microscopic amounts, from close person-to-person contact or ingestion of contaminated food or drinks.
Vaccination: Hepatitis A vaccination is recommended for all children starting at age 1 year, travelers to certain countries, and others at risk.

Hepatitis B: Is a liver disease caused by the hepatitis B virus (HBV). It ranges in severity from a mild illness, lasting a few weeks (acute), to a serious long-term (chronic) illness that can lead to liver disease or liver cancer.
Transmission: Contact with infectious blood, semen, and other body fluids from having sex with an infected person, sharing contaminated needles to inject drugs, or from an infected mother to her newborn.
Vaccination: Hepatitis B vaccination is recommended for all infants, older children and adolescents who were not vaccinated previously, and adults at risk for HBV infection.

Hepatitis C: is a liver disease caused by the hepatitis C virus (HCV). HCV infection sometimes results in an acute illness, but most often becomes a chronic condition that can lead to cirrhosis of the liver and liver cancer.

Transmission: Contact with the blood of an infected person, primarily through blood-blood/broken skin contact.
Vaccination: There is no vaccine for hepatitis C.

Hepatitis D- Is a serious liver disease caused by the hepatitis D virus (HDV) and relies on HBV to replicate.
Transmission: Contact with infectious blood, similar to how HBV is spread.
Vaccination: There is no vaccine for hepatitis D.

Hepatitis E- Is a serious liver disease caused by the hepatitis E virus (HEV) that usually results in an acute infection. It does not lead to a chronic infection. Hepatitis E is fairly common in many parts of the world.
Transmission: Ingestion of fecal matter, even in microscopic amounts; outbreaks are usually associated with contaminated water supply in regions with poor sanitation.
Vaccination: There is no currently approved vaccine for hepatitis E.

LIVER DISEASES(HEPATITIS) -PART THREE CONTINUES

Hepatitis C Virus

Introduction:

Although its means of transmission is fairly well documented, the hepatitis C virus itself largely remains a mystery. Hepatitis C is extremely small, even for a virus - it is only about 50 nanometers in diameter. A nanometer is one billionth of a meter - if you placed 200,000 hepatitis C viruses end to end, they would be only a single centimeter long. However, what is known about hepatitis C underscores the type of threat that it poses.

Hepatitis C is an RNA virus - which means that it mutates frequently. Once an infection has begun, hepatitis C creates different genetic variations of itself within the body of the host. The mutated forms are frequently different enough from their ancestors that the immune system cannot recognize them. Thus, even if the immune system begins to succeed against one variation, the mutant strains quickly take over and become new, predominant strains. As a result, the development of antibodies against HCV does not produce immunity against the disease like it does with most other viruses. More than 80% of the individuals infected with HCV will progress to a chronic form of the disease.

As a result of this, hepatitis C is usually not self-limited as a disease. In more than 85% of all cases, whether they progress to chronic liver disease or not, the infected individual carries the virus for life. This means that they also remain contagious for a lifetime, able to transmit the virus to others. And because of the long progression of the illness, even patients who will eventually die as a result of hepatitis C carry the virus for decades before it takes their lives. Most epidemics are self-limiting - they spread rapidly, but over a short period of time the affected population either dies or develops immunity to the disease, and it stops spreading. Not so with hepatitis C. Much like HIV and AIDS, it lasts a lifetime, and kills slowly - giving the virus plenty of time to spread.

There are six basic genotypes of HCV, with 15 recorded subtypes, which vary in prevalence in different regions of the world. Each of these major genotypes can differ significantly in their biological effects - in terms of replication, mutation rates, type and severity of liver damage, and detection and treatment options. However, these differences are not yet clearly understood.

The 21 current variations in genotype, complicated by the constant mutation of the virus within infected individuals, represents a major challenge for the development of treatments and vaccines against HCV - and even for reliable detection of the virus. There is no guarantee that a treatment, test, or vaccine against one strain will be effective against all of them. Moreover, individuals cured of one strain will be prone to re-infection by any of the other strains.

The infection is often asymptomatic, and can often lead to chronic infection and cause inflammation of the liver (chronic hepatitis). This condition can progress to scarring of the liver (fibrosis), and advanced scarring (cirrhosis). In some cases, those with cirrhosis will go on to develop liver failure or other complications of cirrhosis, including liver cancer. No effective vaccine against hepatitis C is available. The symptoms of infection can be medically managed, and a proportion of patients can be somewhat cleared of the virus by a course of anti-viral medicines. Although early medical intervention is helpful, people with HCV infection can experience mild symptoms, and consequently do not seek treatment. (Approximately 150-200 million or more) people are infected with hepatitis C world wide.

Although HCV is not known to efficiently be transmitted sexually, persons at risk for infection through injection drug use might seek care in STD treatment facilities, HIV counseling and testing facilities, prisons/and or correctional facilities, drug treatment facilities, and other public health settings where STD and HIV prevention and control services are available.

Sixty to 70% of persons newly infected with HCV typically are usually asymptomatic or have a mild clinical illness. HCV RNA can be detected in blood within 1–3 weeks after exposure. The average time from exposure to antibody to HCV (anti-HCV) seroconversion is 8–9 weeks, and anti-HCV can be detected in >97% of persons by 6 months after exposure. Chronic HCV infection develops in 70%–85% of HCV-infected persons; 60%–70% of chronically infected persons have evidence of active liver disease. The majority of infected persons might not be aware of their infection because they are not clinically ill. However, infected persons serve as a source of transmission to others and are at risk for chronic liver disease or other HCV-related chronic diseases decades after infection.

HCV is most efficiently transmitted through large or repeated percutaneous exposure to infected blood (e.g., through transfusion of blood from non screened donors or through use of injecting drugs). Although much less frequent, occupational, Perinatal, and sexual exposures also can result in transmission of HCV.

Since the clinical characteristics are similar for all types of acute viral hepatitis, the specific viral cause of illness cannot be determined solely on the basis of signs, symptoms, history, or current risk factors, but must be verified by specific serologic testing.

In most of the developed countries, the people at risks of HCV infection include; Current or former injection drug users, including those who injected only once many years ago, Recipients of clotting factor concentrates made before 1987 when more advanced methods for manufacturing those products were developed, Recipients of blood transfusions or solid organ transplants before July 1992 when better testing of blood donors became available, Chronic hemodialysis patients, Persons with known exposures to HCV such as health care workers after needle sticks involving HCV-positive blood recipients of blood or organs from a donor who tested HCV-positive Persons with HIV infection, Children born to HCV-positive mothers.

Is it possible for someone to become infected with HCV and then spontaneously clear the infection?

Yes. Approximately 15%–25% of persons clear the virus from their bodies without treatment and do not develop chronic infection; the reasons for this are not well known. HCV infection becomes chronic in approximately 75%–85% of cases.

Why most persons remain chronically infected with HCV?

A person infected with HCV mounts an immune response to the virus, but replication of the virus during infection can result in changes that evade the immune response. This may explain how the virus establishes and maintains chronic infection.

What are the chances of developing chronic HCV infection/liver disease, cirrhosis, or liver cancer or dying as a result of hepatitis C.?

For every 100 persons infected with HCV, approximately 75–85 will go on to develop chronic infection 60–70 will go on to develop chronic liver disease, 5–20 will go on to develop cirrhosis over a period of 20–30 years, 1–5 will die from the consequences of chronic infection (liver cancer or cirrhosis). And persons can become infected with a different strain of HCV after they have cleared the initial infection. Prior infection with HCV does not protect against later infection with the same or different genotypes of the virus. This is because persons infected with HCV typically have an ineffective immune response due to changes in the virus during infection.

For the same reason, no effective pre- or post exposure prophylaxis (i.e., immune globulin) is available. Currently there is no vaccine for hepatitis C available. Research into the development of a vaccine is still ongoing.

Transmission and Symptoms:

How HCV is transmitted:

HCV is transmitted primarily through large or repeated percutaneous (i.e., passage through the skin) exposures to infectious blood, such as Injection drug use. Receipt of donated blood, blood products, and organs (once a common means of transmission but now rare in most developed countries, Needle stick injuries in healthcare settings, Birth to an HCV-infected mother, HCV can also be spread infrequently through:
Sex with an HCV-infected person (an inefficient means of transmission),Sharing personal items contaminated with infectious blood, such as razors or toothbrushes (also inefficient vectors of transmission). Other healthcare procedures that involve invasive procedures, such as injections (usually recognized in the context of outbreaks)

Can HCV be spread during medical or dental procedures?

Yes, therefore Standard Precautions and other infection control practices should be followed routinely and consistently. There are However cases that HCV has been spread in healthcare settings when injection equipment, such as syringes, was shared between patients or when injectable medications or intravenous solutions were mishandled and became contaminated with blood. Healthcare personnel should understand and adhere to Standard Precautions, which includes safe injection practices and other guidance aimed at reducing blood borne pathogen risks for patients and healthcare personnel. If healthcare-associated HCV infection is suspected, this should be reported to state and local public health authorities.

Can HCV be spread within a household?

Yes, but does not occur very often. If HCV is spread within a household, it is most likely a result of direct, through-the-skin exposure to the blood of an infected household member.

Signs and symptoms of acute HCV infection:

Persons with newly acquired HCV infection usually are asymptomatic or have mild symptoms that are unlikely to prompt a visit to a healthcare professional. When symptoms occur, they can include; Fever, Fatigue, Dark urine, Clay-colored And approximately 20%–30% of those newly infected with HCV experience fatigue, abdominal pain, poor appetite, or jaundice. In those persons who do develop symptoms, the average time period from exposure to symptom onset is 4–12 weeks (range: 2–24 weeks).

Signs and symptoms of chronic HCV infection:

Most persons with chronic HCV infection are asymptomatic. However, many have chronic liver disease, which can range from mild to severe, including cirrhosis and liver cancer. Chronic liver disease in HCV-infected persons is usually insidious, progressing slowly without any signs or symptoms for several decades. In fact, HCV infection is often not recognized until asymptomatic persons are identified as HCV-positive when screened for blood donation or when elevated alanine aminotransferase (ALT, a liver enzyme) levels are detected during routine examinations.

Testing and Diagnosis HCV testing is recommended for anyone at increased risk for HCV infection, including:

Persons who have ever injected illegal drugs, including those who injected only once many years ago Recipients of clotting factor concentrates made before 1987, Recipients of blood transfusions or solid organ transplants before July 1992, Patients who have ever received long-term hemodialysis treatment.
Persons with known exposures to HCV, such as health care workers after needle sticks involving HCV-positive blood recipients of blood or organs from a donor who later tested HCV-positive

All persons with HIV infection. Patients with signs or symptoms of liver disease (e.g., abnormal liver enzyme tests), Children born to HCV-positive mothers (to avoid detecting maternal antibody, these children should not be tested before age 18 months)Several tests are performed for HCV infection,including; Screening tests for antibody to HCV (anti-HCV)enzyme immunoassay(EIA)enhanced chemiluminescence immunoassay (CIA)Recombinant immunoblot assay(RIBA)Qualitative tests to detect presence or absence of virus (HCV RNA polymerase chain reaction [PCR])Quantitative tests to detect amount (titer) of virus (HCV RNA PCR).
False-positive anti-HCV tests appear more often when persons at low risk for HCV infection (e.g., blood donors) are tested. Therefore, it is important to confirm a positive anti-HCV test with a supplemental test, such as RIBA (recombinant immunoblot assay), as most false positive anti-HCV tests are reported as negative on supplemental testing.

Persons with early HCV infection might not yet have developed antibody levels high enough that the test can measure which might result into a false negative. In addition, some persons might lack the (immune) response necessary for the test to work well. In these persons, further testing such as PCR for HCV RNA may be considered. A confirmed positive anti-HCV test is usually followed by other additional tests such as ALT (alanine aminotransferase, a liver enzyme). An elevated ALT indicates inflammation of the liver. The patient should be checked further for chronic liver disease and possible treatment. The evaluation should be performed by a medical doctor/ healthcare professional familiar with chronic hepatitis C. Also one can have a normal liver enzyme (e.g., ALT) level and still have chronic hepatitis C. It is common for patients with chronic hepatitis C to have liver enzyme levels that go up and down, with periodic returns to normal or near normal levels. Liver enzyme levels can remain normal for over a year despite chronic liver disease.

Management and Treatment:

HCV-positive persons should be evaluated (by referral or consultation, if appropriate) for presence of chronic liver disease, including assessment of liver function tests, evaluation for severity of liver disease and possible treatment, and determination of the need for hepatitis A and hepatitis B vaccination. A specialist can be consulted in the management of HCV-infected persons but, any physician who manages a person with hepatitis C should be knowledgeable and current on all aspects of the care of a person with hepatitis C; this can include some internal medicine and family practice physicians as well as specialists such as infectious disease physicians, gastroenterologists, or hepatologists.

Treatment for chronic hepatitis C:

Combination therapy with pegylated interferon and ribavirin is the treatment of choice, resulting in sustained virologic response (defined as undetectable HCV RNA in the patient's blood 24 weeks after the end of treatment) rates of 40%–80% (up to 50% for patients infected with genotype 1, and up to 80% for patients infected with genotypes 2 or 3). Combination therapy using interferon and ribavirin is approved for use in children ages 3–17 years in some countries. Treatment success rates are now being improved with the addition of polymerase and protease inhibitors to standard pegylated interferon/ribavirin combination therapy. At least six distinct HCV genotypes (genotypes 1–6) and more than 50 subtypes have been identified. It is necessary to do viral genotyping when managing a person with chronic hepatitis C. Because there are at least six known genotypes and more than 50 subtypes of HCV, genotype information is helpful in defining the epidemiology of hepatitis C and in making recommendations regarding treatment.

Knowing the genotype can help predict the likelihood of treatment response and, in many cases, determine the duration of treatment. Patients with genotypes 2 and 3 are almost three times more likely than patients with genotype 1 to respond to therapy with alpha interferon or the combination of alpha interferon and ribavirin. When using combination therapy, the recommended duration of treatment depends on the genotype. For patients with genotypes 2 and 3, a 24-week course of combination treatment is adequate, whereas for patients with genotype 1, a 48-week course is recommended. Once the genotype is identified, it need not be tested again; genotypes do not change during the course of infection. Super-infection is possible if risk behaviors (e.g., injection drug use) for HCV infection continue, but it is believed to be very uncommon.

Does chronic hepatitis C affect only the liver?

A small percentage of persons with chronic HCV infection develop medical conditions due to hepatitis C that are not limited to the liver. These conditions are thought to be attributable to the body's immune response to HCV infection. Such conditions can include;Diabetes mellitus, which occurs three times more frequently in HCV-infected persons, Glomerulonephritis, a type of kidney disease caused by inflammation of the kidney, Essential mixed cryoglobulinemia, a condition involving the presence of abnormal proteins in the blood, Porphyria cutanea tarda, an abnormality in heme production that causes skin fragility and blistering, Non-Hodgkins lymphoma, which might occur somewhat more frequently in HCV-infected persons, Counseling Patients.

Patients should be informed about the low but present risk for transmission with sex partners. Sharing personal items that might have blood on them, such as toothbrushes or razors, can pose a risk to others. Cuts and sores on the skin should be covered to keep from spreading infectious blood or secretions. Donating blood, organs,tissue, or semen can spread HCV to others. HCV is not spread by sneezing, hugging, holding hands, coughing, sharing eating utensils or drinking glasses, or through food or water. Patients may benefit from joining support group.

HCV-positive persons should be advised to avoid alcohol because it can accelerate cirrhosis and end-stage liver disease. Viral hepatitis patients should also check with a health professional before taking any new prescription pills, over-the counter drugs (such as non-aspirin pain relievers), or supplements, as these can potentially damage the liver.

Hepatitis C and Healthcare Personnel:

What is the risk for HCV infection from a needle stick exposure to HCV-contaminated blood?

After a needle stick or sharps exposure to HCV-positive blood, the risk of HCV infection is approximately 1.8% (range: 0%–10%).

Other than needle sticks, do other exposures, such as splashes to the eye, pose a risk to healthcare personnel for HCV transmission?

Although a few cases of HCV transmission via blood splash to the eye have been reported, the risk for such transmission is expected to be very low. Avoiding occupational exposure to blood is the primary way to prevent transmission of blood borne illnesses among healthcare personnel. All healthcare personnel should adhere to Standard Precautions. Depending on the medical procedure involved, Standard Precautions may include the appropriate use of personal protective equipment (e.g., gloves, masks, and protective eyewear).

What follow-up testing is recommended for healthcare personnel exposed to HCV-positive blood?

For the source, perform baseline testing for anti-HCV.For the person exposed to a HCV-positive source, perform baseline and follow-up testing, including baseline testing for anti-HCV and ALT activity and follow-up testing for anti-HCV (e.g., at 4–6 months) and ALT activity. If earlier diagnosis of HCV infection is desired, testing for HCV RNA may be performed at 4–6weeks. Confirmation by supplemental anti-HCV testing of all anti-HCV results reported as positive by enzyme immunoassay.

Pregnancy and HCV Infection:

Should pregnant women be routinely tested for anti-HCV?

No. Since pregnant women have no greater risk of being infected with HCV than non-pregnant women and interventions to prevent mother-to-child transmission are lacking, routine anti-HCV testing of pregnant women is not recommended. Pregnant women should be tested for anti-HCV only if they have risk factors for HCV.

What is the risk that an HCV-infected mother will spread HCV to her infant during birth?

Approximately 4 of every 100 infants born to HCV-infected mothers become infected with the virus. Transmission occurs at the time of birth, and no prophylaxis is available to prevent it. The risk is increased by the presence of maternal HCV viremia at delivery and also is 2–3 times greater if the woman is co-infected with HIV. Most infants infected with HCV at birth have no symptoms and do well during childhood. More research is needed to find out the long-term effects of Perinatal HCV infection.

Should a woman with HCV infection be advised against breastfeeding?

No. There is no evidence that breastfeeding spreads HCV. However, HCV-positive mothers should consider abstaining from breastfeeding if their nipples are cracked or bleeding.

When should children born to HCV-infected mothers be tested to see if they were infected at birth?

Children should be tested for anti-HCV no sooner than age 18 months because anti-HCV from the mother might last until this age. If diagnosis is desired before the child turns 18 months, testing for HCV RNA could be performed at or after the infant's first well-child visit at age 1–2 months. HCV RNA testing should then be repeated at a subsequent visit, independent of the initial HCV RNA test result.

LIVER DISEASES(HEPATITIS) -PART THREE

HEPATITIS B:

Hepatitis B virus (HBV) is a unique, coated DNA virus belonging to the Hepadnaviridae family of viruses, (partly double-stranded; icosahedral capsid with an envelope; virion-also called Dane particles as the main characteristics). It is not related to the hepatitis A virus or the hepatitis C virus. HBV primarily infect liver cells. The name of the family comes from hepa- meaning liver; dna- referring to deoxyribonucleic acid, the virus' genetic material; and viridae- meaning virus. Other viruses in this family can also cause hepatitis in certain animals e.g. mammalian and avian hepadnaviruses are known to exist. The Hepadnaviridae are very similar to one another. Accordingly, several animal models have been developed to study the hepatitis B virus and to evaluate new drugs to treat hepatitis B virus.The genes of the hepatitis B virus contain genetic codes to make a number of protein products, including hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg), hepatitis B e antigen (HBeAg), and DNA polymerase.

These four proteins are important because their tests are used to diagnose hepatitis B virus. The hepatitis B virus consists simply of a core particle (central portion) and a surrounding envelope (outer coat). The core is made up of the HBcAg, whereas the envelope is made up of the HBsAg. The core particle contains the hepatitis B virus DNA, HBeAg, and DNA polymerase. The HBeAg serves as a marker of the virus' ability to spread the infection. The DNA polymerase is an important part of the virus' uniqueness of its reproduction. Of relevant importance here is that, the human immunodeficiency virus (HIV) also reproduces using this same process. As a result, many drugs that have been developed to inhibit this process of reproduction to treat HIV infection may also be effective in treating chronic hepatitis B viral infection.

HOW HBV CAUSES INJURY TO THE LIVER:

The hepatitis B virus itself does not directly cause damage to the liver. Rather, the body's immune (protective) response to the virus (a foreign material) paradoxically causes the damage. Thus, in a hepatitis B viral infection, the body's immune response to the virus is responsible for both the elimination of the hepatitis B virus from the body and recovery from the infection. Yet, at the same time, the injury to the liver cells is caused by that same immune response to the hepatitis B virus in the liver cells.

Therefore, there is a balance between the protective and destructive effects of the immune system's response to the hepatitis B virus. How this balance is achieved determines the outcome in an individual infected with hepatitis B virus. Therefore, an acute hepatitis B viral infection can lead to recovery (the usual outcome), to acute liver failure (rarely), and sometimes to chronic infection. The chronic infection can result in a healthy carrier state (in which the affected person harbors the virus but remains healthy) or progress to cirrhosis (severe scarring, or fibrosis, of the liver) and its complications, including liver cancer.

TRANSMISSION:

Hepatitis B virus is spread or acquired through exposure to infected blood or the body's secretions. The highest concentrations of hepatitis B virus are found in the blood, semen, vaginal discharge, breast milk, and saliva. There are only low concentrations of hepatitis B virus in the urine and none in the feces. Therefore, hepatitis B is not spread through food or water or by casual contact. Furthermore, hepatitis B virus is no longer or rarely transmitted by blood transfusions in most countries because all blood for transfusion is screened (tested) to exclude contamination with hepatitis B virus. In much of the developing world, (sub-Saharan Africa, most of Asia, and the Pacific), most people become infected with HBV during childhood, and 8% to 10% of people in the general population become chronically infected. In these regions liver cancer caused by HBV figures among the first three causes death by cancer in men.

High rates of chronic HBV infection are also found in the Amazon and the southern parts of Eastern and Central Europe. In the Middle East and Indian sub-continent, about 5% are chronically infected.

TRANSMISSION –IN SUMMARY:

Hepatitis B virus is transmitted by contact with blood or body fluids of an infected person in the same way as human immunodeficiency virus (HIV), the virus that causes AIDS. However, HBV is 50 to 100 times more infectious than HIV.

The main ways of getting infected with HBV are

Perinatal (from mother to baby at the birth)

Child-to-child transmission

Unsafe injections and transfusions

Sexual contact.

Worldwide, most infections occur from infected mother to child, from child to child contact in household settings, and from reuse of non sterilized needles and syringes.

In many industrialized countries (e.g. Western Europe and North America, the pattern of transmission is different. In these countries, mother-to-infant and child-to-child transmission accounted for up to one third of chronic infections before childhood hepatitis B vaccination programmes were implemented.

Today however, the majority of infections in these countries are acquired during young adulthood by sexual activity, and injecting drug use. In addition, hepatitis B virus is the major infectious occupational hazard of health workers, and most health care workers have received hepatitis B vaccine. Hepatitis B virus is not spread by contaminated food or water, and cannot be spread casually in the workplace. High rates of chronic HBV infection are also found in the Amazon and the southern parts of Eastern and Central Europe. In the Middle East and Indian sub-continent, about 5% are chronically infected. In U.S., adolescents and young adults account for the majority of reported cases of hepatitis B infection. Sexual contact (intercourse) being the most common means of transmission. The virus also can be spread by hepatitis B virus-contaminated blood or body fluid in several different ways. These ways include intravenous drug use, skin-popping (injecting under the skin), tattooing, body piercing, and acupuncture using non-sterile instruments. Additionally, hepatitis B virus can be transmitted through the sharing of toothbrushes and razors. Finally, blood-sucking insects such as mosquitoes and bed bugs that are common in the tropics have reportedly spread hepatitis B virus.

Young children who become infected with HBV are the most likely to develop chronic infection. About 90% of infants infected during the first year of life and 30% to 50% of children infected between 1 to 4 years of age develop chronic infection. The risk of death from HBV-related liver cancer or cirrhosis is approximately 25% for persons who become chronically infected during childhood.

SYMPTOMS OF ACUTE HEPATITIS B:

Acute hepatitis B is the initial, rapid onset, short duration of illness that results from infection with hepatitis B virus. About 70% of adults with acute hepatitis B have few or no symptoms. The remaining 30% develop significant symptoms two to four months following exposure to the hepatitis B virus. This period of time between the exposure and the first symptoms is what is usually referred to as the incubation period. The most common symptoms of acute hepatitis B includes; fatigue, loss of appetite, nausea, and abdominal pain over the region of the liver. Jaundice (yellow skin) often accompanies these other symptoms. When this happens, the infection is commonly termed as acute icteric (jaundiced) hepatitis. Occasionally, individuals with acute hepatitis B develop the so-called prodromal symptoms. These are symptoms that start just the onset of the commonly showing symptoms. Sometimes, the prodromal symptoms resemble an allergic reaction, such as skin rash, pain and swelling of the joints, and low-grade fever. Other times, the prodromal symptoms resemble the symptoms of the flu. Rarely (in less than 0.5% of adults), individuals with acute hepatitis B can develop acute liver failure (fulminant hepatitis). These patients are extremely ill with the symptoms of acute hepatitis already described and the additional problems of confusion or coma (encephalopathy) and bruising or bleeding (coagulopathy). In fact, up to 80% of people with fulminant hepatitis can die within days to weeks.

DETERMINANT OF THE OUTCOME OF THE ACUTE HBV:

The individual's ability to eliminate (clear) the hepatitis B virus from the body and recover from acute hepatitis B depends on the strength of the body's immune response to the infection. The stronger the immune response, the greater is the likelihood of eliminating the virus and recovering. By the same token, however, the stronger the immune response, the more likely is the occurrence of acute liver injury and symptoms. On the other hand, a weaker immune response results in less liver injury and fewer symptoms. At the same time, however, the weaker immune response results in less viral elimination (clearance) and a greater likelihood of developing chronic hepatitis B viral infection. Indeed, most infants and children who acquire acute hepatitis B viral infection are asymptomatic, but their rate of developing chronic hepatitis B virus is greater than 95%. Most adults (about 95%), particularly those with acute, symptomatic, icteric hepatitis B (with jaundice), will recover completely from the infection within two to three months. They also will develop immunity, that is, protection from a subsequent hepatitis B viral infection. Moreover, these individuals rarely develop chronic liver disease. In contrast, those adults with few or no symptoms during their episode of acute hepatitis B, as compared to other adults with symptoms, are less likely to clear the infection and are more likely to develop chronic hepatitis B.

CHRONIC HEPATITIS B INFECTION:

The diagnosis of chronic hepatitis B can be made, by definition, only after six months from the onset of acute hepatitis B. It is often difficult to suspect the diagnosis of chronic hepatitis B based just on the patient's symptoms. The reason for this difficulty is that those individuals, who develop chronic hepatitis B, are usually the same individuals who had few or no symptoms to signal the onset of their acute hepatitis B.

Moreover, most individuals with chronic hepatitis B infection remain symptom free (asymptomatic) for many years, even up to two or three decades. During this time, the patient's liver blood tests usually are at most mildly abnormal and the inflammation and scarring (fibrosis) of the liver progresses little, if at all. Occasionally, however, these individuals with otherwise inactive chronic hepatitis B may develop flares (reactivation) of acute symptoms, elevated liver blood tests, and inflammation of the liver. These flares resemble acute hepatitis, but they can cause progression of the chronic liver scarring (fibrosis). They tend to occur in men who acquired the chronic infection at a young age.

At some point, however, the chronic hepatitis can progress to CIRRHOSIS (severe scarring, or fibrosis) of the liver. These patients then can develop the symptoms and signs (abnormal findings on physical examination) of cirrhosis. For example, they can become weak, fatigued, and susceptible to infections. They can also lose muscle mass, especially in the shoulders and upper legs. In fact, they can develop poor nutrition and weight loss from abnormal digestion, malabsorption, or abnormal liver metabolism of nutrients.

Thus, deficiencies can occur, for example, of vitamin A, which causes impaired vision at night, or of vitamin D, which causes thinning of the spine or hip bones (osteopenia). Patients with cirrhosis also often develop visible evidence (stigmata) of cirrhosis, including swollen breasts (gynecomastia), small (atrophic) testicles, red palms (palmar erythema), and characteristic dilated vessels on the skin (spider angioma).

ADVANCED LIVER CIRRHOSIS:

Ultimately, the progression of cirrhosis leads to what is commonly known as advanced cirrhosis, which is characterized by the development of certain complications. Advanced cirrhosis is sometimes referred to as cirrhosis or chronic liver failure. Some authorities also use the term, decompensated cirrhosis, as synonymous with advanced cirrhosis. Others, however, reserve the term, decompensated cirrhosis, for advanced cirrhosis that includes specifically any of the complications that result primarily from portal hypertension. (Some of the complications of advanced cirrhosis can have multiple causes.) This difference in terminology matters little because the important consideration in any particular case is to simply specify which of the complications of cirrhosis apply.

Accordingly, the complications of cirrhosis that indicate the presence of advanced cirrhosis are complications that include those resulting primarily from portal hypertension (fluid retention, encephalopathy, GI bleeding, hypersplenism, and the hepatorenal syndrome), as well as coagulopathy, jaundice, and the hepatopulmonary syndrome. Portal hypertension is the term for the increased pressure in the portal venous system that occurs in patients with advanced cirrhosis. (The portal venous system drains blood from the intestinal and abdominal organs to the liver.) The most common complications of cirrhosis that result primarily from portal hypertension are fluid retention, hepatic (liver) encephalopathy, and gastrointestinal (GI) bleeding. The retention of fluid leads to swollen ankles (edema) and a swollen abdomen( ascites).

Sometimes, the fluid in the abdomen becomes infected (spontaneous bacterial peritonitis), causing fever and abdominal pain. The hepatic encephalopathy causes drowsiness, confusion, and even coma. Widened (dilated) veins (varices) in the esophagus and stomach that burst can cause GI bleeding. As a result, the patient may vomit bright red blood or defecate dark (even tarry) blood. Some patients develop hypersplenism, a complication that is due, in part at least, to portal hypertension. These patients have an enlarged spleen (splenomegaly), decreased red blood cells (anemia), decreased white blood cells (leukopenia), and decreased platelets (thrombocytopenia). The anemia causes weakness; the leukopenia contributes to infections; and the thrombocytopenia impairs the clotting of blood. Patients with portal hypertension also can develop a serious problem with the functioning of their kidneys without actual damage to the kidneys themselves (hepatorenal syndrome).

In advanced cirrhosis also, other important complications can occur besides those due primarily to portal hypertension. For example, some patients are prone to easy bruising and bleeding, largely because the impaired function of the liver causes abnormalities in the blood clotting process (coagulopathy). Patients with advanced cirrhosis can also develop jaundice because the damaged liver is unable to adequately eliminate a yellow compound, called bilirubin. More rarely, some patients can develop difficulty with breathing because certain hormones released in advanced cirrhosis cause abnormal functioning of the lungs (hepatopulmonary syndrome).

LIVER CANCER (HEPATOCELLULAR CARCINOMA)-DUE TO ADVANCED CIRRHOSIS:

Finally, liver cancer can develop in chronic HBV infected patients as a complication of advanced cirrhosis. This primary (originating in the liver) cancer of the liver is most likely to occur in people with active hepatitis B virus reproduction. The way in which the cancer develops is not yet fully understood. It is thought, however, that the hepatitis B virus DNA somehow becomes incorporated into the liver cell DNA of the patient. The most common symptoms and signs of liver cancer are abdominal pain and swelling, an enlarged liver, weight loss, and fever. In addition, the liver tumors can produce and release a number of substances, including ones that cause increased red blood cells (erythrocytosis), low blood sugar (hypoglycemia), and high blood calcium (hypercalcemia). The most useful diagnostic screening tests for liver cancer are an alpha-fetoprotein blood test and an ultrasound imaging study of the liver.

HBV INVOLVEMENT OF ORGANS OUSTIDE THE LIVER-(EXTRA-HEPATIC):

Rarely, chronic hepatitis B infection can lead to disorders that affect organs other than the liver. The deposit of specific hepatitis B virus immune complexes in the various organs usually causes these disorders. A hepatitis B virus immune complex is the entity that results from the binding together of a hepatitis B virus antibody and a hepatitis B virus antigen. (An antigen is a substance that is foreign to the body and an antibody is a specialized protein that is produced by white blood cells in response to the antigen. Hepatitis B virus immune complexes that settle, or deposit, in the small arteries throughout the body can result in an inflammation of these vessels (vasculitis), called polyarteritis nodosa. This condition can cause a wide range of symptoms, including muscle weakness, nerve damage (neuropathy), deep skin ulcers, kidney problems with loss of protein in the urine, (proteinuria), and sometimes kidney failure, high blood pressure, unexplained fevers, and abdominal pain. The hepatitis B virus immune complexes can cause damage to the kidneys in yet another way. That is, the immune complexes can be deposited in the glomeruli(filtering elements) of the kidney, causing glomeronephritis, which is a different disease from polyarteritis nodosa.

DIAGNOSIS OF HBV:

Hepatitis B is diagnosed from the results of specific hepatitis B virus tests (serologies) that reflect the various components of the hepatitis B virus. These serological tests differ from the standard liver tests (such as the ALT and AST) that can become abnormal when the liver is damaged from whatever cause, including hepatitis B viral infection. HBsAg AND anti-HBs:

The diagnosis of hepatitis B infection is made primarily by detecting the hepatitis B surface antigen (HBsAg) in the blood. The presence of HBsAg means that there is active hepatitis B viral infection and the absence of HBsAg means that there is no active hepatitis B viral infection. Following an exposure to hepatitis B virus, HBsAg becomes detectable in the blood within four weeks. In individuals who recover from acute hepatitis B viral infections, the elimination, or clearance, of HBsAg occurs within four months after the onset of symptoms. Chronic hepatitis B viral infection is defined as the persistence of HBsAg for more than six months.

After the HBsAg is eliminated from the body, the antibodies to HBsAg (anti-HBs) usually appear. These anti-HBs provide immunity to subsequent hepatitis B viral infection. Likewise, individuals who are successfully vaccinated against hepatitis B virus have measurable anti-HBs in the blood.

Anti-HBc:

The hepatitis B core antigen can only be found in the liver and cannot be detected in the blood. The presence of large amounts of hepatitis B core antigen in the liver indicates an ongoing reproduction of the virus. This means that the virus is active. The antibody to hepatitis B core antigen, known as the hepatitis B core antibody (anti-HBc), however, is detectable in the blood. As a matter of fact, two types of anti-HBc antibodies (IgM and IgG) are produced.

IgM anti-HBc is a marker (indicator) for acute hepatitis B infection. The IgM anti-HBc is found in the blood during the acute infection and lasts for up to six months after the onset of symptoms. IgG anti-HBc develops during the course of the acute hepatitis B viral infection and persists for life, regardless of whether the individual recovers or develops the chronic infection. Accordingly, only the IgM type of anti-HBc can be specifically used to diagnose an acute hepatitis B viral infection. Moreover, determining just the total anti-HBc (without separating its two components) is not very helpful.

HBeAg, anti-HBe, AND PRE-CORE MUTATIONS:

Hepatitis B e antigen (HBeAg) and its antibody, anti-HBe, are useful markers to determine the likelihood of spread of the virus (transmissibility) by persons affected with chronic hepatitis B viral infection. Detecting both HBeAg and anti-HBe in the blood is usually mutually exclusive. Accordingly, the presence of HBeAg means ongoing viral activity and the ability to infect others, whereas the presence of anti-HBe signifies a more inactive state of the virus and less risk of transmission.

In some individuals infected with hepatitis B virus, the genetic material for the virus has undergone a particular structural change, called a pre-core mutation. This mutation results in an inability of the hepatitis B virus to produce HBeAg, even though the virus is actively reproducing. This means that even though no HBeAg is detected in the blood of people with the mutation, the hepatitis B virus is still active in these persons and they can infect others.

Hepatitis B virus DNA:

The most specific marker of hepatitis B virus reproduction is the measurement of hepatitis B virus DNA in the blood. You remember that DNA is the genetic material of hepatitis B virus. High levels of hepatitis B virus DNA indicate an ongoing reproduction of the virus and viral activity. Low or undetectable levels of hepatitis B virus DNA are associated with the inactive phase of hepatitis B viral infection. Several different laboratory tests (assays) are available to measure hepatitis B virus DNA.

The PCR- (polymerase chain reaction) is the most sensitive method (assay) for determining the level of hepatitis B virus DNA. This means that the PCR is the best method for detecting minute amounts of the hepatitis B virus marker. This method works by amplifying the material that is being measured up to a billion times for its detection. The PCR method, therefore, can measure as few as 50 to 100 copies (particles) of hepatitis B virus per milliliter of blood. This test, however, is actually too sensitive for practical diagnostic use.

The purpose of measuring hepatitis B virus DNA usually is to determine whether the hepatitis B viral infection is active or inactive (quiescent). This distinction can be made based on the amount of hepatitis B virus DNA in the blood. High levels of DNA indicate an active infection, while low levels indicate a dormant, or inactive, infection. Thus, patients with dormant disease have about a million viral particles per milliliter of blood, whereas patients with active disease have several billion particles per milliliter. Therefore, anyone who is HBsAg positive, even if the hepatitis B viral infection is inactive, will have detectable levels of hepatitis B virus DNA by the PCR method because it is so sensitive.

For practical purposes, hepatitis B virus DNA can be measured using a so-called hybridization method (assay), which is a less sensitive test than the PCR. Unlike the PCR method, the hybridization assay measures the viral material without amplification. Thus this test can detect hepatitis B virus DNA only when many viral particles are present in the blood, meaning that the infection is active. In other words, from a practical point of view, if hepatitis B virus DNA is detected with a hybridization assay, this means that the hepatitis B viral infection is active.

PREVENTION AND TREATMENT:

Liver cancer is almost always fatal, and usually develops between 35 and 65 years of age, when people are maximally productive and with family responsibilities. The loss of a mother or a father can be devastating to the entire family. In developing countries, most people with liver cancer die within months of diagnosis. In industrialized countries, surgery and chemotherapy can prolong life up to a few years. Chronic hepatitis B in some patients can be treated with drugs such as interferon or lamivudine, which can help some patients. However, interferon or lamivudine therapies are very costly and therefore few individuals can afford them and will never be available to most patients in developing countries due to their costs. Patients with cirrhosis are sometimes given liver transplants, with varying success. It is preferable to prevent this disease with vaccine than to try to cure it.
SAFETY AND EFFECTIVENESS OF THE HBV CACCINES:

The vaccine is given as a series of three intramuscular doses. It has been said that the vaccine is 95% effective in preventing children and adults from developing chronic infection if they have not yet been infected. In many countries where 8% to 15% of children used to become chronically infected with HBV, the rate of chronic infection has been reduced to less than 1% in immunized groups of children. And the reports are showing that. Since 1982, over one billion doses of hepatitis B vaccine have been used worldwide.

PREVENTION:

All countries have been urged by world bodies to add hepatitis B vaccine into their national immunization programmes. As of March 2000, 116 countries had included hepatitis B vaccine in their national programmes including most countries in Eastern and South- East Asia, the Pacific Islands Australia, North and South America,Western Europe and the Middle East. However, many low income countries in sub-Saharan Africa, the Indian subcontinent and in the Newly Independent States do not use the vaccine. The price of the hepatitis B vaccine has been one of the main obstacles to its introduction in many of these countries.

The Global Alliance for Vaccines and Immunization (GAVI) was created in 1999. It is a unique coalition of public and private institutions. The main mission of GAVI is to vaccinate as many children as possible against vaccine-preventable diseases. GAVI has introduced a new approach to international health funding: the Global Fund for Children's vaccines (GFCV). This fund will help 74 low-income countries including those in the sub-Saharan Africa, Asia and Southern America to reinforce their national vaccine programmes and introduce hepatitis B, yellow fever and haemophilus influenzae type b (Hib) vaccines into their national immunization programmes.

LIVER DISEASES-(HEPATITIS )CONTINUES

HEPATITIS A

Hepatitis A is caused by the viral hepatitis A or (HAV). It is an acute illness (acute viral hepatitis) that never becomes chronic. It was once referred to as "infectious hepatitis" because it could be spread from person to person like other viral infections. Infection with hepatitis A virus can be spread through the ingestion of food or water, especially where unsanitary conditions allow water or food to become contaminated by human waste containing hepatitis A (the fecal-oral mode of transmission). Hepatitis A typically is spread among household members and close contacts through the passage of oral secretions (intimate kissing) or stool (poor hand hygiene). It also is common to have infection spread to customers in restaurants and among children and large groupings if hand washing and sanitary precautions are not observed.

DESCRIPTION-SIGNS AND SYMPTOMS:

Hepatitis A is a liver disease caused by the hepatitis A virus. Good personal hygiene and proper sanitation can help prevent hepatitis A. Vaccines are also available for long-term prevention of hepatitis A virus infection in persons 12 months of age and older. Immune globulin(IG) is available for short-term prevention of hepatitis A virus infection in individuals of all ages.

Adults will have signs and symptoms more often than children.
• jaundice
• fatigue
• abdominal pain
• loss of appetite
• nausea
• diarrhea
• fever

LONG-TERM EFFECTS:

There is no chronic (long-term) infection. Once you have had hepatitis A, you cannot get it again.
About 15% of people infected with HAV will have prolonged or relapsing symptoms over a 6-9 month period.

TRANSMISSION:

HAV is found in the stool (feces) of persons with hepatitis A. HAV is usually spread from person to person by the fecal-oral route. Food borne transmission occurs when an HAV-infected food handler contaminates food during preparation or when food is contaminated during harvesting or processing before reaching the food service establishment or home( putting something in the mouth-even though it might look clean) that has been contaminated with the stool of a person with hepatitis A.

PERSONS AT RISK OF INFECTION:

Household contacts of infected persons, Sex contacts of infected individuals, persons especially children- living in areas with increased rates of hepatitis A, Men who have sex with men and Users of injection and non-injection drug.

PREVENTION:

Hepatitis A vaccine is the best protection. Short-term protection against hepatitis A is available from immune globulin(IG). It can be given before and within 2 weeks of coming in contact with HAV. Always wash your hands with soap and water after using the bathroom, changing undergarments, and before preparing and eating food.

VACCINATION:

Among the vaccines available are Havrix and Vaqta. Both contain inactive (killed) hepatitis A virus. For adults, two doses of the vaccine are recommended. After the first dose, protective antibodies develop in 70% of vaccine recipients in 2 weeks and more than 95% of recipients in 4 weeks. After two doses of the hepatitis A vaccine, immunity against hepatitis A infection is believed to last for many years.

Individuals at increased risk for acquiring hepatitis A and individuals with chronic liver disease (e.g., cirrhosis or chronic hepatitis C) should be vaccinated. Although individuals with chronic liver disease are not at increased risk for acquiring hepatitis A, they can develop serious (sometimes fatal) liver failure if infected with hepatitis A and, thus, they should be vaccinated.
Individuals at increased risk of acquiring hepatitis A are:
• Travelers to areas where hepatitis A is common
• Men who have sex with men who are infected
• Illegal drug users (either injection or non-injection drug use)
• Researchers working with hepatitis A or primates that are susceptible to infection with hepatitis A
• Patients with clotting factor disorders who are receiving clotting factor concentrates that can transmit hepatitis A
Some local health authorities or private companies may require hepatitis A vaccination for food handlers.

Because protective antibodies take weeks to develop, travelers to endemic areas should be vaccinated at least 4 weeks before departure. Immune globulin is recommended to be given in addition to vaccination if departure is prior to 4 weeks. Immune globulin provides quicker protection than the vaccines, but the protection is short-lived.

KENYA IS NOT FOR SALE

It is mind boggling to read this kind of garbage from the media that a full deputy- prime- minister of a coalition government is actually trying to justify corruption/and or a mismanagement-and in a not so covert way...... Deputy Prime Minister Uhuru Kenyatta also defended the Finance Minister saying that he was being subjected to a “lynching mob".

And also that there were actually some skin heads demonstrating. So I am not sure what the demonstrators were trying to prove- That embezzling/fleecing public assets are birth rights for some people/group? me think not. But will be interesting to see how this one spins out.

Actually two groups were demonstrating in support of Mr. Kimunya drawing mixed reactions from police as one was dispersed with teargas while the other marched to the hotel at the centre of the onslaught against the minister.

The first group, led by Lang’ata politician Stanley Livondo and comprising about 500 protesters, marched from the Arboretum grounds to the city centre before anti-riot police intercepted them. Waving placards, the group ignored an order from a senior police officer not to proceed to Parliament, forcing him to call for reinforcements. "You need a permit to have a procession and since you have not requested one, you should disperse,” said the officer.

Mr Livondo defied the order and urged the protesters to continue with their march.“You cannot stop us from conveying our message. These MPs who are accusing the minister are known to be corrupt and cannot throw stones at him,” he said. Mr Livondo accused Prime Minister Raila Odinga of pretending that he was not aware of the deal.

Mr Odinga has said he was briefed by Central Bank of Kenya governor Prof Njuguna Ndung’u as claimed by Mr Kimunya on Wednesday but added that at the time, there were conflicting statements from gorvernment officials about the sale of the hotel.

Meanwhile, the other group of demonstrators marched from Jevanjee Gardens to Mr Kimunya’s Treasury Building office. They chanted “Kimunya kaa Ngumu (Kimunya stay put!)” as they marched through the streets carrying placards. Some of their placards read “No Kimunya, No cabinet, MPs must be taxed, MPs are pretending.”

A spokesman, Mr Hosea Mwangi said the group comprised “concerned Nairobians” agitated by the fact that some of the MPs calling for Mr Kimunya’s resignation had been involved in mega scandals.“They are crucifying Kimunya because of his proposal to tax them. If he has done anything wrong, he should be allowed to tell his side of the story,” he said.

He accused the MPs of trying to divert Kenyans’ attention from more important issues by hounding Mr Kimunya. The demonstrators briefly gathered outside the Grand Regency where they chanted and danced before marching to the Freedom Corner at Uhuru Park.

Another blogger's perspective captured it best:

"THE ARROGANCE OF KIMUNYA- WITH THE SUPPORT OF THE KIKUYU MAFIA THE LIKES OF WAKINA UHURU KENYATTA IS DESPICABLE!!"


God complex is the self-delusion that one has a special mission to save the world. This delusion is engendered by extreme arrogance and absence of humility. It is a disease that afflicts the rich, the powerful and the privileged.

This complex is manifested in Finance minister Amos Kimunya.

When confronted by Parliament on Wednesday with a list of misdeeds, he responded by saying how he had rid the country of land-grabbers and tax dodgers, and how he had laid the institutional and legal structures to fight corruption. Mr Kimunya missed an opportunity to defend himself.

The minister is young, compared to most Kenyan political leaders, and well read, but completely naive in political leadership. Public service demands that the leaders live by the code they preach. It does not matter how many good laws one passes; it doesn’t matter how many anti-corruption institutions are set up — what matters is whether a leader abides by them.

Mr Kimunya’s public life betrays a man with contempt for systems he has set up. In the sale of Grand Regency Hotel to Libyans, if indeed they are, he broke every law applicable. He treated the hotel as casually as one would a ball-point pen.

But let us first have a look at what happened to world leaders with arrogance milder than Mr Kimunya’s so that we may realize how we have treated him with velvet gloves. David Blunkett was born blind, yet he rose to be a close and powerful confidante of British Prime Minister Tony Blair and held various Cabinet positions, including home affairs.

Socialite mistress

Mr Blunkett had a pretty and socialite mistress called Kimberley Quin, the editor of The Spectator magazine.

Ms Quin imported a Filipino nanny called Leoncia Casalme and, as required by law, she applied for a long-term work permit which takes about a year to complete. Ms Casalme qualified for the permit, but had to wait like everyone else for the process to complete its course.

Ms Quin, being the Home Affairs minister’s mistress, did not have such patience and on April 23, 2003, asked Mr Blunkett to fast-track the process.

Indeed, five days later, the permit was issued. When this fast-tracking was leaked to the media, the United Kingdom Parliamentary Committee on Standards censured him, and he quit.

In the US, Eliot Spitzer, a celebrity attorney-general for the New York state, went about his work with such gusto and chutzpah that he rid the city of economic crimes perpetrated by the large companies.

Wall Street was shaken to the ground and many were fined billions of dollars in plea bargains. In America, the law allows companies to in certain cases pay millions of dollars to avoid criminal investigations and prosecution, but on condition that one fixes up the problem.

New York was grateful and elected Mr Spitzer governor. In the same way he rid the city of economic crimes, he changed course to now deal with crimes personal: rid the city of prostitution.

It later transpired that while fighting the vice, the governor was member No 9 of an elite prostitution group, arrogantly called VIP Emperors Club. In shame, the governor resigned when he was hounded by the media.

Mr Blunkett and Mr Spitzer did not wait to be sacked or impeached respectively; they quit when their private peccadilloes were made public. Both men demanded from the public a high moral rectitude, yet they never lived by it.

They wanted to decouple their private lives from the public perceptions they had created. The false firewall was bound to fall and it did. And both men who had just begun national leadership and on the way to higher callings, have now disappeared into obscurity.

What did, or did not, Mr Kimunya do? At the outset, we must accept the fact that the entire truth and all the details surrounding the Grand Regency sale may never be told to the public.

Building the case:

But the information available to all is enough to build a case of impropriety on the part of the minister, Central Bank, National Security Intelligence Service and errant officers at Lands ministry.

The land Grand Regency is built on falls under the Registration of Titles Act, Cap 281, which is the clearest and most elaborate of the land laws. I have argued before in these columns that all land laws should be simplified and brought together within this Act.

This Act sets out the process of registering and deregistering land titles. The registrar of titles is the chief executive for properties falling under this Act and acts without any external interference.

Sections 59 and 60 of the Act allow him to recall and cancel a title deed obtained by deception, fraud, error, misrepresentations or by mistake, as has happened here.

Mr Kimunya says the land was sold for Sh2.9 billion to the Libyan government. We now know that the land was sold for Sh1.8 billion and that the buyer is a Kenyan company with Kenyan directors who have since disowned their signatures. And the minister insists that the sale is a government-to-government deal, yet this is not true.

The minister insists also that the land was sold for Sh2.9 billion even when the evidence is to the contrary. The sale agreement conveniently splits the transaction into two parts — the actual land and the hotel’s “movable assets”.

This dichotomy is false, fraudulent and misleading. Grand Regency was being sold as a going concern, yet the sale is a cannibalized one.

As a going concern, the hotel ought to have been sold at an all-inclusive price for the land, the building, the movable assets, the business goodwill, the reputation and all other intellectual property rights it has acquired.

If Grand Regency was being bought to be used as an office block, the dichotomy may make sense. No prestigious hotel has been sold the way Grand Regency has; the valuations are ridiculous, if not deceptive.

In law, land includes the physical land, the building on it and anything annexed to it. There is a legal doctrine — quicquid plantatur solo, solo cedit — that captures the entire meaning of land law.

This doctrine is that anything attached to land is part of the land. If, therefore, the wall paintings, beds, machines and kitchens at Grand Regency are firmly fixed on the floors and walls, then they are part of the land, and not separate, as the sale agreement implies. In making these false separations, the Government may have lost stamp duty worth more than Sh44 million. Who pocketed this money?

Once Grand Regency was surrendered to Central Bank, it became a public asset and its disposal was subject to the Public Procurement and Disposal Act, 2005, and the Privatization Act, 2005. Disposal of land is specifically identified as being a transaction that falls under these two Acts.

The law demands that the process of disposal include open tendering — invitation of tenders through advertisements and competitive bidding. Above all, the entire process is subject to the Cabinet’s control and vetting. Again, other than Mr Kimunya himself, every minister who has spoken has denied knowledge of the process.

And what was the National Security Intelligence Service doing at the lands offices overseeing the registration?

Normal land transactions take at times as long as three months, yet NSIS saw to it that the Grand Regency transfer was done in a day. Section 5 of the National Security Intelligence Service Act, 1998, clearly states that the security agency’s core and only duty is to protect Kenya from threats or potential threats.

When did the Grand Regency sale become part of the national security matrix? For the umpteenth time, I wish to say that NSIS is of no value to the country. We pay it Sh8 billion a year for its officers to idle till they misinterpret their mandate to think it includes running errands for politicians or dealing in properties sales. NSIS ought to be disbanded.

Throughout the entire process of the sale, Mr Kimunya was economical with the truth. The Public Officer Ethics Act, 2003, demands of him honesty, integrity, courtesy and respect to the public and the Government. But he violated every provision in the Act.

The sale shows that mandatory provisions of the Registration of Titles Act, Cap 281; the National Security Intelligence Service Act, 1998; the Central Bank of Kenya Act, Cap 491; the Anti-Corruption and Economic Crimes Act, 2003, and the Public Officer Ethics Act, 2003, were broken with impunity by Mr Kimunya, and with the tacit support of CBK governor Njuguna Ndung’u and NSIS director-general Michael Gichangi.

Mr Kimunya, Mr Ndung’u and Maj-Gen Gichangi must be indicted if the rule of law exists in this country.

In its absence, we will know that the law is two-tracked — for the powerful and the weak. We can only respect our systems if its top officers themselves respect them. Impunity that arises from political arrogance must end.