(d)*PREVENTION OF DENGUE*

-Vaccine development
There is no commercially available vaccine for the dengue flavivirus. However, one of the many ongoing vaccine development programs is the Pediatric Dengue Vaccine Initiative which was set up in 2003 with the aim of accelerating the development and introduction of dengue vaccine(s) that are affordable and accessible to poor children in endemic countries.Thai researchers are testing a dengue fever vaccine on 3,000–5,000 human volunteers after having successfully conducted tests on animals and a small group of human volunteers. A number of other vaccine candidates are entering phase I or II testing.

- Mosquito control

A field technician looking for larvae in standing water containers during the 1965 Aedes aegypti eradication program in Miami, Florida. In the 1960s, a major effort was made to eradicate the principal urban vector mosquito of dengue and yellow fever viruses, Aedes aegypti, from southeast United States.Primary prevention of dengue mainly resides in mosquito control. There are two primary methods: larval control and adult mosquito control.[citation needed] In urban areas, Aedes mosquitos breed on water collections in artificial containers such as plastic cups, used tires, broken bottles, flower pots, etc. Periodic draining or removal of artificial containers is the most effective way of reducing the breeding grounds for mosquitos.[citation needed] Larvicide treatment is another effective way to control the vector larvae but the larvicide chosen should be long-lasting and preferably have World Health Organization clearance for use in drinking water. There are some very effective insect growth regulators (IGRs) available which are both safe and long-lasting (e.g. pyriproxyfen). For reducing the adult mosquito load, fogging with insecticide is somewhat effective.[citation needed]
Prevention of mosquito bites is another way of preventing disease. This can be achieved by using insect repellent, mosquito traps or mosquito nets.
In 1998, scientists from the Queensland Institute of Medical Research (QIMR) in Australia and Vietnam's Ministry of Health introduced a scheme that encouraged children to place a water bug, the crustacean Mesocyclops, in water tanks and discarded containers where the Aedes aegypti mosquito was known to thrive. This method is viewed as being more cost-effective and more environmentally friendly than pesticides, though not as effective, and requires the continuing participation of the community.

Even though this method of mosquito control was successful in rural provinces, not much is known about how effective it could be if applied to cities and urban areas. The Mesocyclops can survive and breed in large water containers, but would not be able to do so in small containers of which most urban area have within their homes. Also, Mesocyclops are hosts for the guinea worm, a pathogen that causes a parasite infection, and so this method of mosquito control cannot be used in countries that are still susceptible to the guinea worm. The biggest dilemma with Mesocyclops is that its success depends on the participation of the community. This idea of a possible parasite bearing creature in household water containers dissuades people from continuing the process of inoculation, and without the support and work of everyone living in the city, this method would not be successful.

In 2004, scientists from the Federal University of Minas Gerais, Brazil, discovered a fast way to find and count mosquito population inside urban areas. The technology, named Intelligent Monitoring of Dengue (in Portuguese), uses traps with kairomones that capture Aedes gravid females, and upload insect counts with a combination of cell phone, GPS and internet technology. The result is a complete map of the mosquitoes in urban areas, updated in real time and accessible remotely, that can inform control methodologies. The technology was recognized with a Tech Museum Award in 2006.

In 2009, scientists from the School of Integrative Biology at The University of Queensland revealed that by infecting Aedes mosquitos with the bacterium Wolbachia, the adult lifespan was reduced by half. In the study, super-fine needles were used to inject 10,000 mosquito embryos with the bacterium. Once an insect was infected, the bacterium would spread via its eggs to the next generation. A pilot release of infected mosquitoes could begin in Vietnam within three years. If no problems are discovered, a full-scale biological attack against the insects could be launched within five years.

- Potential antiviral approaches
Dengue virus belongs to the family Flaviviridae, which includes the hepatitis C virus, West Nile and Yellow fever viruses among others. Possible laboratory-based modification of the yellow fever vaccine YF-17D to target the dengue virus via chimeric replacement has been discussed extensively in scientific literature. To date, however, no full scale studies have been conducted.

In 2006, a group of Argentine scientists discovered the molecular replication mechanism of the virus, which could be specifically attacked by disrupting the viral RNA polymerase. In cell culture and murine experiments, morpholino antisense oligomers have shown specific activity against Dengue virus.

In 2007 scientists' attenuated virus replication by interfering with activity of the dengue viral protease; subsequently, a project to identify novel protease disruption mechanisms has been launched.

(c)*TREATMENT OF DENGUE*

The mainstay of treatment is timely supportive therapy to tackle shock due to hemoconcentration and bleeding. Close monitoring of vital signs in critical period (between day 2 to day 7 of fever) is critical. Increased oral fluid intake is recommended to prevent dehydration. Supplementation with intravenous fluids may be necessary to prevent dehydration and significant concentration of the blood if the patient is unable to maintain oral intake. A platelet transfusion is indicated in rare cases if the platelet level drops significantly (below 20,000) or if there is significant bleeding. The presence of melena may indicate internal gastrointestinal bleeding requiring platelet and/or red blood cell transfusion.

Aspirin and non-steroidal anti-inflammatory drugs should be avoided as these drugs may worsen the bleeding tendency associated with some of these infections. Patients may receive paracetamol preparations to deal with these symptoms if dengue is suspected.

(b)*SYMPTOMS OF DENGUE*

The disease manifests as a sudden onset of severe headache, muscle and joint pains (myalgias and arthralgias—severe pain that gives it the nick-name break-bone fever or bonecrusher disease), fever, and rash. The dengue rash is characteristically bright red petechiae and usually appears first on the lower limbs and the chest; in some patients, it spreads to cover most of the body. There may also be gastritis with some combination of associated abdominal pain, nausea, vomiting, or diarrhea. Some cases develop much milder symptoms which can be misdiagnosed as influenza or other viral infection when no rash is present. Thus travelers from tropical areas may pass on dengue in their home countries inadvertently, having not been properly diagnosed at the height of their illness. Patients with dengue can pass on the infection only through mosquitoes or blood products and only while they are still febrile. The classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the disease (the so-called biphasic pattern). Clinically, the platelet count will drop until the patient's temperature is normal. Cases of DHF also show higher fever, variable haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate. DHF combined with a cirrhotic liver has been suspected in rapid development of hepatocellular carcinoma (HCC). Given that the Dengue virus (DEN) is related to the Hepatitis C virus, this is an avenue for further research as HCC is among the top five cancerous causes of death outside Europe and North America. Normally HCC does not occur in a cirrhotic liver for ten or more years after the cessation of the poisoning agent. DHF patients can develop HCC within one year of cessation of poisoning agent.

(a)*HISTORY OF DENGUE*

The first recorded potential case of dengue fever comes from a Chinese medical encyclopedia from the Jin Dynasty (265–420 AD). The Chinese referred to a “water poison” associated with flying insects.The first definitive case report dates from 1789 and is attributed to Benjamin Rush, who coined the term "breakbone fever" because of the symptoms of myalgia and arthralgia. The viral etiology and the transmission by mosquitoes were deciphered only in the 20th century. Population movements during World War II spread the disease globally. A pandemic of dengue began in Southeast Asia after World War II and has spread around the globe since then.

#(5)DENGUE FEVER

Dengue fever (pronounced UK: /ˈdɛŋɡeɪ/, US: /ˈdɛŋɡiː/) and dengue hemorrhagic fever (DHF) are acute febrile diseases, found in the tropics, and caused by four closely related virus serotypes of the genus Flavivirus, family Flaviviridae. It is also known as breakbone fever. It occurs widely in the tropics, including northern Argentina, northern Australia, and the entirety of Bangladesh, Barbados, Bolivia, Brazil, Cambodia, Costa Rica, Dominican Republic, Guyana, Honduras, India, Indonesia, Jamaica, Malaysia, Mexico, Pakistan, Panama, Paraguay, Philippines, Puerto Rico, Samoa, Singapore, Sri Lanka, Suriname, Taiwan, Thailand, Trinidad, Venezuela and Vietnam. Unlike malaria, dengue is just as prevalent in the urban districts of its range as in rural areas. Each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. Dengue is transmitted to humans by the Aedes aegypti or more rarely the Aedes albopictus mosquito, which feed during the day.

The WHO says some 2.5 billion people, two fifths of the world's population, are now at risk from dengue and estimates that there may be 50 million cases of dengue infection worldwide every year. The disease is now epidemic in more than 100 countries

(f)*MODE OF TRANSMISSION OF AIDS*

Modes of Transmission

HIV is transmitted only through the intimate exchange of body fluids, specifically blood, semen, vaginal fluid, and mother's milk (Dane and Miller 1990). HIV is sometimes passed from mother to fetus, or through breastfeeding (HIV levels in the bloodstream are typically highest when a person is first infected and again in the late stages of the illness. High-risk behaviors include unprotected anal and vaginal intercourse (without condom) and intravenous drug use. Before blood screening began in 1986, the virus was also being contracted from transfusions and blood-clotting agents.Read more:

(e)*TREATMENT OF AIDS*

There is currently no publicly available vaccine for HIV or cure for HIV or AIDS. The only known methods of prevention are based on avoiding exposure to the virus or, failing that, an antiretroviral treatment directly after a highly significant exposure, called post-exposure prophylaxis (PEP). PEP has a very demanding four week schedule of dosage. It also has very unpleasant side effects including diarrhea, malaise, nausea and fatigue.
Antiviral therapy
Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART. This has been highly beneficial to many HIV-infected individuals since its introduction in 1996 when the protease inhibitor-based HAART initially became available. Current optimal HAART options consist of combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of antiretroviral agents. Typical regimens consist of two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations are more aggressive for children than for adults. In developed countries where HAART is available, doctors assess the viral load, rapidity in CD4 decline, and patient readiness while deciding when to recommend initiating treatment.
Standard goals of HAART include improvement in the patient’s quality of life, reduction in complications, and reduction of HIV viremia below the limit of detection, but it does not cure the patient of HIV nor does it prevent the return, once treatment is stopped, of high blood levels of HIV, often HAART resistant. Moreover, it would take more than the lifetime of an individual to be cleared of HIV infection using HAART. Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to the plummeting of HIV-associated morbidity and mortality. In the absence of HAART, progression from HIV infection to AIDS occurs at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months. HAART is thought to increase survival time by between 4 and 12 years.
For some patients, which can be more than fifty percent of patients, HAART achieves far less than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART. The reasons for non-adherence and non-persistence are varied. Major psychosocial issues include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and thus hard to follow, with large numbers of pills taken frequently. Side effects can also deter people from persisting with HAART, these include lipodystrophy, dyslipidaemia, diarrhoea, insulin resistance, an increase in cardiovascular risks and birth defects. Anti-retroviral drugs are expensive, and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS.
Experimental and proposed treatments
It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly cost less, thus being affordable for developing countries, and would not require daily treatments. However, even after almost 30 years of research, HIV-1 remains a difficult target for a vaccine. Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. A number of studies have shown that measures to prevent opportunistic infections can be beneficial when treating patients with HIV infection or AIDS. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected. Patients with substantial immunosuppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.
Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.
In Berlin, Germany, a 42-year-old leukemia patient infected with HIV for more than a decade was given an experimental transplant of bone marrow with cells that contained an unusual natural variant of the CCR5 cell-surface receptor. This CCR5-Δ32 variant has been shown to make some cells from people who are born with it resistant to infection with some strains of HIV. Almost two years after the transplant, and even after the patient reportedly stopped taking antiretroviral medications, HIV has not been detected in the patient's blood.
Alternative medicine
Various forms of alternative medicine have been used to treat symptoms or alter the course of the disease. Current studies indicate that alternative medicine therapies have little effect on the mortality or morbidity of the disease, but may improve the quality of life of individuals with AIDS. The psychological benefits of these therapies are the most important use. Acupuncture has been used to alleviate some symptoms with no success and cannot cure the HIV infection. Several randomized clinical trials testing the effect of herbal medicines have shown that there is no evidence that these herbs have any effect on the progression of the disease, but may instead produce serious side-effects.
Morbidity and mortality among HIV-infected adults with adequate dietary nutritional intake is unaffected by multivitamin supplementation. A large Tanzanian trial in immunologically and nutritionally compromised pregnant and lactating women showed a number of benefits to daily multivitamin supplementation for both mothers and children. Dietary intake of micronutrients at RDA levels by HIV-infected adults is recommended by the World Health Organization. There is some evidence that vitamin A supplementation in children reduces mortality and improves growth. Daily doses of selenium can suppress HIV viral burden with an associated improvement of the CD4 count. Selenium can be used as an adjunct therapy to standard antiviral treatments, but cannot itself reduce mortality and morbidity.

(d)*PREVENTION OF AIDS*

The three main transmission routes of HIV are sexual contact, exposure to infected body fluids or tissues, and from mother to fetus or child during perinatal period. It is possible to find HIV in the saliva, tears, and urine of infected individuals, but there are no recorded cases of infection by these secretions, and the risk of infection is negligible.
Sexual contact
The majority of HIV infections are acquired through unprotected sexual relations between partners, one of whom has HIV. The primary mode of HIV infection worldwide is through sexual contact between members of the opposite sex.
During a sexual act, only male or female condoms can reduce the chances of infection with HIV and other STDs and the chances of becoming pregnant. The best evidence to date indicates that typical condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term, though the benefit is likely to be higher if condoms are used correctly on every occasion.
The male latex condom, if used correctly without oil-based lubricants, is the single most effective available technology to reduce the sexual transmission of HIV and other sexually transmitted infections. Manufacturers recommend that oil-based lubricants such as petroleum jelly, butter, and lard not be used with latex condoms, because they dissolve the latex, making the condoms porous. If necessary, manufacturers recommend using water-based lubricants.
il-based lubricants can however be used with polyurethane condoms.
The female condom is an alternative to the male condom and is made from polyurethane, which allows it to be used in the presence of oil-based lubricants. They are larger than male condoms and have a stiffened ring-shaped opening, and are designed to be inserted into the vagina.
The female condom contains an inner ring, which keeps the condom in place inside the vagina – inserting the female condom requires squeezing this ring. However, at present availability of female condoms is very low and the price remains prohibitive for many women.
Preliminary studies suggest that, where female condoms are available, overall protected sexual acts increase relative to unprotected sexual acts, making them an important HIV prevention strategy.
Studies on couples where one partner is infected show that with consistent condom use, HIV infection rates for the uninfected partner are below 1% per year. Prevention strategies are well-known in developed countries, but epidemiological and behavioral studies in Europe and North America suggest that a substantial minority of young people continue to engage in high-risk practices despite HIV/AIDS knowledge, underestimating their own risk of becoming infected with HIV.[92][93]
Randomized controlled trials have shown that male circumcision lowers the risk of HIV infection among heterosexual men by up to 60%. It is expected that this procedure will be actively promoted in many of the countries affected by HIV, although doing so will involve confronting a number of practical, cultural and attitudinal issues. However, programs to encourage condom use, including providing them free to those in poverty, are estimated to be 95 times more cost effective than circumcision at reducing the rate of HIV in sub-Saharan Africa.[95]
Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects.[96] However, one randomized controlled trial indicated that adult male circumcision was not associated with increased HIV risk behavior.
Exposure to infected body fluids
Health care workers can reduce exposure to HIV by employing precautions to reduce the risk of exposure to contaminated blood. These precautions include barriers such as gloves, masks, protective eyeware or shields, and gowns or aprons which prevent exposure of the skin or mucous membranes to blood borne pathogens. Frequent and thorough washing of the skin immediately after being contaminated with blood or other bodily fluids can reduce the chance of infection. Finally, sharp objects like needles, scalpels and glass, are carefully disposed of to prevent needlestick injuries with contaminated items. Since intravenous drug use is an important factor in HIV transmission in developed countries, harm reduction strategies such as needle-exchange programmes are used in attempts to reduce the infections caused by drug abuse.
Mother-to-child transmission (MTCT)
Current recommendations state that when replacement feeding is acceptable, feasible, affordable, sustainable and safe, HIV-infected mothers should avoid breast-feeding their infant. However, if this is not the case, exclusive breast-feeding is recommended during the first months of life and discontinued as soon as possible. It should be noted that women may breastfeed other children who are not their own; see wetnurse.

(c)*SYMPTOMS OF AIDS*

The symptoms of AIDS are primarily the result of conditions that do not normally develop in individuals with healthy immune systems. Most of these conditions are infections caused by bacteria, viruses, fungi and parasites that are normally controlled by the elements of the immune system that HIV damages.
Opportunistic infections are common in people with AIDS. HIV affects nearly every organ system.
People with AIDS also have an increased risk of developing various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the immune system known as lymphomas. Additionally, people with AIDS often have systemic symptoms of infection like fevers, sweats (particularly at night), swollen glands, chills, weakness, and weight loss. The specific opportunistic infections that AIDS patients develop depend in part on the prevalence of these infections in the geographic area in which the patient lives.

Main symptoms of AIDS.
Pulmonary infections

X-ray of Pneumocystis pneumonia (PCP). There is increased white (opacity) in the lower lungs on both sides, characteristic of PCP
Pneumocystis pneumonia (originally known as Pneumocystis carinii pneumonia, and still abbreviated as PCP, which now stands for Pneumocystis pneumonia) is relatively rare in healthy, immunocompetent people, but common among HIV-infected individuals. It is caused by Pneumocystis jirovecii.
Before the advent of effective diagnosis, treatment and routine prophylaxis in Western countries, it was a common immediate cause of death. In developing countries, it is still one of the first indications of AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200 cells per µL of blood.
Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to immunocompetent people via the respiratory route, is easily treatable once identified, may occur in early-stage HIV disease, and is preventable with drug therapy. However, multidrug resistance is a potentially serious problem.
Even though its incidence has declined because of the use of directly observed therapy and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent. In early-stage HIV infection (CD4 count >300 cells per µL), TB typically presents as a pulmonary disease. In advanced HIV infection, TB often presents atypically with extrapulmonary (systemic) disease a common feature. Symptoms are usually constitutional and are not localized to one particular site, often affecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system.
Gastrointestinal infections
Esophagitis is an inflammation of the lining of the lower end of the esophagus (gullet or swallowing tube leading to the stomach). In HIV infected individuals, this is normally due to fungal (candidiasis) or viral (herpes simplex-1 or cytomegalovirus) infections. In rare cases, it could be due to mycobacteria.
Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic infections; and uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, Mycobacterium avium complex (MAC) and viruses, astrovirus, adenovirus, rotavirus and cytomegalovirus, (the latter as a course of colitis).
In some cases, diarrhea may be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. It may also be a side effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting.
Neurological and psychiatric involvement
HIV infection may lead to a variety of neuropsychiatric sequelae, either by infection of the now susceptible nervous system by organisms, or as a direct consequence of the illness itself.
Toxoplasmosis is a disease caused by the single-celled parasite called Toxoplasma gondii; it usually infects the brain, causing toxoplasma encephalitis, but it can also infect and cause disease in the eyes and lungs. Cryptococcal meningitis is an infection of the meninx (the membrane covering the brain and spinal cord) by the fungus Cryptococcus neoformans. It can cause fevers, headache, fatigue, nausea, and vomiting. Patients may also develop seizures and confusion; left untreated, it can be lethal.
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus called JC virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis.
AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia. These cells are productively infected by HIV and secrete neurotoxins of both host and viral origin. Specific neurological impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection and are associated with low CD4+ T cell levels and high plasma viral loads.
Prevalence is 10–20% in Western countries but only 1–2% of HIV infections in India. This difference is possibly due to the HIV subtype in India. AIDS related mania is sometimes seen in patients with advanced HIV illness; it presents with more irritability and cognitive impairment and less euphoria than a manic episode associated with true bipolar disorder. Unlike the latter condition, it may have a more chronic course. This syndrome is less often seen with the advent of multi-drug therapy.
Tumors and malignancies

Kaposi's sarcoma
Patients with HIV infection have substantially increased incidence of several cancers. This is primarily due to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV) (also known as human herpesvirus-8 [HHV-8]), and human papillomavirus (HPV).
Kaposi's sarcoma (KS) is the most common tumor in HIV-infected patients. The appearance of this tumor in young homosexual men in 1981 was one of the first signals of the AIDS epidemic. Caused by a gammaherpes virus called Kaposi's sarcoma-associated herpes virus (KSHV), it often appears as purplish nodules on the skin, but can affect other organs, especially the mouth, gastrointestinal tract, and lungs. High-grade B cell lymphomas such as Burkitt's lymphoma, Burkitt's-like lymphoma, diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma present more often in HIV-infected patients. These particular cancers often foreshadow a poor prognosis. Epstein-Barr virus (EBV) or KSHV cause many of these lymphomas. In HIV-infected patients, lymphoma often arises in extranodal sites such as the gastrointestinal tract. [ When they occur in an HIV-infected patient, KS and aggressive B cell lymphomas confer a diagnosis of AIDS.
Invasive cervical cancer in HIV-infected women is also considered AIDS-defining. It is caused by human papillomavirus (HPV).
In addition to the AIDS-defining tumors listed above, HIV-infected patients are at increased risk of certain other tumors, notably Hodgkin's disease, anal and rectal carcinomas, hepatocellular carcinomas, head and neck cancers, and lung cancer. Some of these are causes by viruses, such as Hodgkin's disease (EBV), anal/rectal cancers (HPV), head and neck cancers (HPV), and hepatocellular carcinoma (hepatitis B or C). Other contributing factors include exposure to carcinogens (cigarette smoke for lung cancer), or living for years with subtle immune defects.
Interestingly, the incidence of many common tumors, such as breast cancer or colon cancer, does not increase in HIV-infected patients. In areas where HAART is extensively used to treat AIDS, the incidence of many AIDS-related malignancies has decreased, but at the same time malignant cancers overall have become the most common cause of death of HIV-infected patients. In recent years, an increasing proportion of these deaths have been from non-AIDS-defining cancers.
Other infections
AIDS patients often develop opportunistic infections that present with non-specific symptoms, especially low-grade fevers and weight loss. These include opportunistic infection with Mycobacterium avium-intracellulare and cytomegalovirus (CMV). CMV can cause colitis, as described above, and CMV retinitis can cause blindness.
Penicilliosis due to Penicillium marneffei is now the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia.
An infection that often goes unrecognized in AIDS patients is Parvovirus B19. Its main consequence is anemia, which is difficult to distinguish from the effects of antiretroviral drugs used to treat AIDS itself.

(b)*CAUSE OF AIDS*

AIDS is the most severe acceleration of infection with HIV. HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T cells (a subset of T cells), macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.
Once HIV has killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of blood, cellular immunity is lost. Acute HIV infection progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later to AIDS, which is identified either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of certain infections, as noted above. the absence of antiretroviral therapy, the median time of progression from HIV infection to AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2 months. However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years.
Many factors affect the rate of progression. These include factors that influence the body's ability to defend against HIV such as the infected person's general immune function. Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression than younger people.
Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression. The infected person's genetic inheritance plays an important role and some people are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5-Δ32 variation are resistant to infection with certain strains of HIV. HIV is genetically variable and exists as different strains, which cause different rates of clinical disease progression.

(a)*HISTORY OF AIDS*

AIDS was first reported June 5, 1981, when the U.S. Centers for Disease Control (CDC) recorded a cluster of Pneumocystis carinii pneumonia (now still classified as PCP but known to be caused by Pneumocystis jirovecii) in five homosexual men in Los Angeles. In the beginning, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus. They also used Kaposi's Sarcoma and Opportunistic Infections, the name by which a task force had been set up in 1981. In the general press, the term GRID, which stood for Gay-related immune deficiency, had been coined. The CDC, in search of a name, and looking at the infected communities coined “the 4H disease,” as it seemed to single out Haitians, homosexuals, hemophiliacs, and heroin users. However, after determining that AIDS was not isolated to the homosexual community, the term GRID became misleading and AIDS was introduced at a meeting in July 1982. By September 1982 the CDC started using the name AIDS, and properly defined the illness.
A more controversial theory known as the OPV AIDS hypothesis suggests that the AIDS epidemic was inadvertently started in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a poliomyelitis vaccine. According to scientific consensus, this scenario is not supported by the available evidence.
A recent study states that HIV probably moved from Africa to Haiti and then entered the United States around 1969.

#(4)AIDS [AOQUIRED IMMUNO DEFICIENCY SYNDROME]

Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system caused by the human immunodeficiency virus (HIV).
This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and breast milk.
This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, breastfeeding or other exposure to one of the above bodily fluids.
AIDS is now a pandemic. In 2007, it was estimated that 33.2 million people lived with the disease worldwide, and that AIDS killed an estimated 2.1 million people, including 330,000 children. Over three-quarters of these deaths occurred in sub-Saharan Africa, retarding economic growth and destroying human capital.
Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified in the early 1980s.
Although treatments for AIDS and HIV can slow the course of the disease, there is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries. Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS pandemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus.

(f)*TREATMENT OF HEPATITIS B*

Acute hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously. Early antiviral treatment may only be required in fewer than 1% of patients, whose infection takes a very aggressive course ("fulminant hepatitis") or who are immunocompromised. On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected individuals with persistently elevated serum alanine aminotransferase, a marker of liver damage, and HBV DNA levels are candidates for therapy.
Although none of the available drugs can clear the infection, they can stop the virus from replicating, and minimize liver damage such as cirrhosis and liver cancer. Currently, there are seven medications licensed for treatment of hepatitis B infection in the United States. These include antiviral drugs lamivudine (Epivir), adefovir (Hepsera), tenofovir (Viread), telbivudine (Tyzeka) and entecavir (Baraclude) and the two immune system modulators interferon alpha-2a and pegylated interferon alfa-2a (Pegasys). The use of interferon, which requires injections daily or thrice weekly, has been supplanted by long-acting pegylated interferon, which is injected only once weekly. However, some individuals are much more likely to respond than others and this might be because of the genotype of the infecting virus or the patient's heredity. The treatment works by reducing the viral load (the amount of virus particles as measured in the blood), which Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (hepatitis B immune globulin or HBIg). When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis B is reduced 95%. This treatment allows a mother to safely breastfeed her child.
On July 2005, researchers from A*Star and National University of Singapore identified an association between a DNA-binding protein belonging to the class of protein Heterogeneous nuclear Ribonucleoprotein K (hnRNP K) and HBV replication in patients. By controlling the level of hnRNP K may act as a possible treatment for HBV.

(e)*PREVENTATION OF HAPATITIS B*

Several vaccines have been developed for the prevention of hepatitis B virus infection. These rely on the use of one of the viral envelope proteins (hepatitis B surface antigen or HBsAg). The vaccine was originally prepared from plasma obtained from patients who had long-standing hepatitis B virus infection. However, currently, these are more often made using recombinant DNA technology, though plasma-derived vaccines continue to be used; the two types of vaccines are equally effective and safe.
Following vaccination Hepatitis B Surface antigen may be detected in serum for several days; this is known as vaccine antigenaemia. Vaccine is generally administered in either a two, three, or four dose schedules; and can be received by infants to adults. It provides protection for 85-90% of individuals, and lasts for 23 years.
Unlike Hepatitis A, Hepatitis B does not generally spread through water and food. Instead, it is transmitted through body fluids, from which prevention is taken to avoid: unprotected sexual contact, blood transfusions, re-use of contaminated needles and syringes, and vertical transmission during child birth. Infants may be vaccinated at birth.

(d)*SYMPTOMS OF HEPATITIS B*

Acute infection with hepatitis B virus is associated with acute viral hepatitis - an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few patients may have more severe liver disease (fulminant hepatic failure), and may die as a result of it. The infection may be entirely asymptomatic and may go unrecognized.
Chronic infection with Hepatitis B virus may be either asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer). Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of Membranous glomerulonephritis (MGN).

(c)*TRANSMISSION OF HAPATITIS B*

Transmission of hepatitis B virus results from exposure to infectious blood or body fluids containing blood. Possible forms of transmission include (but are not limited to) unprotected sexual contact, blood transfusions, re-use of contaminated needles & syringes, and vertical transmission from mother to child during childbirth. Without intervention, a mother who is positive for HBsAg confers a 20% risk of passing the infection to her offspring at the time of birth. This risk is as high as 90% if the mother is also positive for HBeAg. HBV can be transmitted between family members within households, possibly by contact of nonintact skin or mucous membrane with secretions or saliva containing HBV. However, at least 30% of reported hepatitis B among adults cannot be associated with an identifiable risk factor.

(b)*HISTORY OF HAPATITIS B*

The earliest record of an epidemic caused by Hepatitis B virus was made by Lurman in 1885. An outbreak of smallpox occurred in Bremen in 1883 and 1,289 shipyard employees were vaccinated with lymph from other people. After several weeks, and up to eight months later, 191 of the vaccinated workers became ill with jaundice and were diagnosed as suffering from serum hepatitis. Other employees who had been inoculated with different batches of lymph remained healthy. Lurman's paper, now regarded as a classical example of an epidemiological study, proved that contaminated lymph was the source of the outbreak. Later, numerous similar outbreaks were reported following the introduction, in 1909, of hypodermic needles that were used, and more importantly reused, for administering Salvarsan for the treatment of syphilis. The virus was not discovered until 1965 when Baruch Blumberg, then working at the National Institutes of Health (NIH), discovered the Australia antigen (later known to be Hepatitis B surface antigen, or HBsAg) in the blood of Australian aboriginal people. Although a virus had been suspected since the research published by MacCallum in 1947, D.S. Dane and others discovered the virus particle in 1970 by electron microscopy. By the early 1980s the genome of the virus had been sequenced, and the first vaccines were being tested.

(a)*PREVALENCE OF HARATITIS B*

The primary method of transmission reflects the prevalence of chronic HBV infection in a given area. In low prevalence areas such as the continental United States and Western Europe, where less than 2% of the population is chronically infected, injection drug abuse and unprotected sex are the primary methods, although other factors may be important. In moderate prevalence areas, which include Eastern Europe, Russia, and Japan, where 2-7% of the population is chronically infected, the disease is predominantly spread among children. In high prevalence areas such as China and South East Asia, transmission during childbirth is most common, although in other areas of high endemicity such as Africa, transmission during childhood is a significant factor. The prevalence of chronic HBV infection in areas of high endemicity is at least 8%

#(3)HEPATITIS B

Hepatitis B is a disease caused by hepatitis B virus (HBV) which infects the liver of hominoidae, including humans, and causes an inflammation called hepatitis. Originally known as "serum hepatitis", the disease has caused epidemics in parts of Asia and Africa, and it is endemic in China. About a third of the world's population, more than 2 billion people, have been infected with the hepatitis B virus. This includes 350 million chronic carriers of the virus. Transmission of hepatitis B virus results from exposure to infectious blood or body fluids containing blood.
The acute illness causes liver inflammation, vomiting, jaundice and—rarely—death. Chronic hepatitis B may eventually cause liver cirrhosis and liver cancer—a fatal disease with very poor response to current chemotherapy.The infection is preventable by vaccination.
Hepatitis B virus is an hepadnavirus—hepa from hepatotrophic and dna because it is a DNA virus—and it has a circular genome composed of partially double-stranded DNA. The viruses replicate through an RNA intermediate form by reverse transcription, and in this respect they are similar to retroviruses. Although replication takes place in the liver, the virus spreads to the blood where virus-specific proteins and their corresponding antibodies are found in infected people. Blood tests for these proteins and antibodies are used to diagnose the infection.

(f)*TREATMENT OF AVAIN FLUENZA "BIRD FLU"*

It's possible that antiviral medicines used to treat other types of flu may be effective in treating bird flu in humans. There is currently no vaccine to prevent bird flu in humans. Scientists are working on developing a vaccine, but it's difficult because the virus frequently mutates (changes).
-Medicines
The following antiviral medicines can reduce the severity of ordinary flu:
oseltamivir (Tamiflu)
zanamivir (Relenza)
If the medicines are administered early (within two days of symptoms starting) they should help to improve the chances of recovery in people who get bird flu.
-Vaccines
Currently available vaccines won't protect you against bird flu as they are not effective against the H5N1 strain of the virus. Although existing vaccines don't work against the H5N1 virus, they are being used to prevent poultry workers in affected countries from getting ordinary human flu. This reduces the risk that someone might catch human and bird flu at the same time, which would give the viruses the opportunity to merge and create a new virus capable of causing a pandemic.

(e)*PREVENTION OF AVIAN INFLUANZA "BIRD FLU"*

-1. Cullers and transporters should be provided with appropriate personal protective equipment:
Protective clothing, preferably coveralls plus an impermeable apron or surgical gowns with long cuffed sleeves plus an impermeable apron.
Heavy duty rubber work gloves that may be disinfected.
N95 respirator masks are preferred. Standard well-fitted surgical masks should be used if N95 respirators are not available.
Goggles.
Rubber or polyurethane boots that can be disinfected or protective foot covers that can be discarded. - 2. All persons who have been in close contact with the infected animals should wash their hands frequently with soap and water. Cullers and transporters should disinfect their hands after the operation.
-3. Environmental clean up should be carried out in areas of culling, using the same protective measures as above.
-4. All persons exposed to infected chickens or to farms under suspicion should be under close monitoring by local health authorities. It is recommended that oseltamivir be readily available for the treatment of suspected H5N1 respiratory infections in cullers and farm workers involved in the mass culling.
They should also be vaccinated with the current WHO recommended influenza vaccine to avoid simultaneous infection by human influenza and avian influenza and to minimize the possibility of a re-assortment of the virus's genes.
.Additional health monitoring of chicken cullers, others involved in the process and their family members should be carried out. These individuals should report any relevant health problems (respiratory complaints, flu-like illnesses or eye infections) to a health care facility. Persons at high risk for severe complications of influenza (e.g. immuno- compromised, over 60 years old, or with known chronic heart or lung disease) should avoid working with affected chickens. -5. Serological surveillance of exposed animal workers and veterinarians is encouraged. -6. In liaison with designated laboratories, full blood and post mortem specimens (intestinal contents, anal and oro-nasal swabs, trachea, lung, intestine, spleen, kidney, brain, liver and heart) of animals (including pigs) should be collected for investigation of new viral isolates.1 US NIOSH certified N-95, European CE P2, or comparable national/regional standards applicable to the country of manufacture. Higher level particulate respirators may also be used. -7 In the control of the outbreak of avian influenza in the Netherlands in 2003, N95 or equivalent respiratory protection was used. -8 For treatment, oseltamivir phosphate (Tamiflu®): 75 mg capsule twice daily, for 5 days. -9All concerned (persons at risk both environmentally and occupationally) should be vaccinated with the current WHO recommended influenza vaccine as soon as possible prior to anticipated risk exposure (2 weeks are required to develop preventive immunity by vaccination.). This does not specifically protect against H5N1.

(d)*SYMPTOMS OF AVAIN FLUENZA "BIRD FLU"*

The reported signs and symptoms of avian influenza in humans have ranged from eye infections (conjunctivitis) to influenza-like illness symptoms (e.g., fever, cough, sore throat, muscle aches) to severe respiratory illness (e.g. pneumonia, acute respiratory distress, viral pneumonia) sometimes accompanied by nausea, d
Back to TopSymptoms
Symptoms of avian flu infection in humans depend on the particular strain of virus. In case of the H5N1 virus, infection in humans causes more classic flu-like symptoms, which might include: -Cough (dry or productive)
-Sore throat
-Fever greater than 100.4°F (38°C)
-Difficulty breathing
-Diarrhea
-Runny nose
-Headache
-Malaise
-Muscle aches iarrhea, vomiting and neurologic changes

(c)*TRANSIMISSION OF AVIAN INFLUENZA "BIRD FLU"*

-Waterfowl act as a reservoir of avian influenza virus by carrying the virus in their intestinal tract and shedding it in their feces. Avian influenza viruses are spread to susceptible birds through inhalation of influenza particles in nasal and respiratory secretions and from contact with the feces of infected birds. -The main way that influenza viruses are spread is from person to person in respiratory droplets of coughs and sneezes. (This is called "droplet spread.") This can happen when droplets from a cough or sneeze of an infected person are propelled (generally up to 3 feet) through the air and deposited on the mouth or nose of people nearby. Though much less frequent, the viruses also can be spread when a person touches respiratory droplets on another person or an object and then touches their own mouth or nose (or someone else's mouth or nose) before washing their hand.
-A person can spread the flu starting one day before he or she feels sick. Adults can continue to pass the flu virus to others for another three to seven days after symptoms start. Children can pass the virus for longer than seven days. Symptoms start one to four days after the virus enters the body. Some persons can be infected with the flu virus but have no symptoms. During this time, those persons can still spread the virus to others.

(b)*HISTORY OF AVIAN INFLUENZA"BIRD FLU"*

-1997: In Hong Kong, avian influenza A (H5N1) infected both chickens and humans. This was the first time an avian influenza virus had ever been found to transmit directly from birds to humans. During this outbreak, 18 people were hospitalized and 6 of them died.
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-1999: In Hong Kong, cases of avian influenza A (H9N2) were confirmed in 2 children. Both patients recovered, and no additional cases were confirmed. The evidence suggested that poultry was the source of infection and the main mode of transmission was from bird to human. - 2003:Two cases of avian influenza A (H5N1) infection occurred among members of a Hong Kong family that had traveled to China. One person recovered, the other died. How or where these 2 family members were infected was not determined. Another family member died of a respiratory illness in China, but no testing was done. No additional cases were reported. -2003: Avian influenza A (H7N7) infections among poultry workers and their families were confirmed in the Netherlands during an outbreak of avian flu among poultry. More than 80 cases of H7N7 illness were reported (the symptoms were mostly confined to eye infections, with some respiratory symptoms), and 1 patient died (in a veterinarian who had visited an affected farm). There was evidence of some human-to-human transmission. - 2003: H9N2 infection was confirmed in a child in Hong Kong. The child was hospitalized but recovered.

(a)*CLASSIFICATION OF AVIAN INFLUENZA "BIRD FLU"*

Classification of Avian flu Virus
-Types of Flu viruses
In the orthomyxoviridae flu virus family, there are three types of flu viruses: type A, type B, and type C. The avian flu virus is a type A virus.
Type A viruses are the most dangerous. They can infect a wide range of organisms, including birds, humans, and pigs. There are also subtypes of type A viruses, classified by the type of surface proteins on the viruses. These viruses can also cause both local epidemics and global pandemics.

-Subtypes
Influenza viruses have two kinds of surface proteins: hemagglutinin and neuraminidase. There are different types of hemagglutinin (H) and neuraminidase (N) surface proteins. There are 16 types of H surface proteins and 9 types of N surface proteins (which are named H1, H2, N1, N2, etc.). An influenza virus always has one type of H surface protein, and one type of N surface protein.
Influenza virus subtypes are classified and named according to the types of H and N surface proteins on the virus. For example, a subtype named H6N4 would indicate that the virus has type 6 hemagglutinin surface proteins, and type 4 neuraminidase surface proteins.
There are many subtypes of influenza viruses that cause avian flu. The most notable of these avian flu virus subtypes is H5N1.
Different subtypes of virus, H7N2, H3N1, and H7N1.

-Strains
Within these subtypes, there are strains of viruses with slightly different genetic sequences, caused by random mutations in the viruses’ RNA over time. These mutations can cause small changes in the viruses’ characteristics, but if the strains have the same surface proteins, they are classified as the same subtype. These strains can be described as slight variations on the same virus.

#(2) AVIAN INFLUENZA "BIRD FLU" (H5N1)

For the H5N1 subtype of Avian influenza see H5N1.
Avian influenza, sometimes avian flu, and commonly bird flu, refers to "influenza caused by viruses adapted to birds."[1][2][3][4][5][6][7] Of the greatest concern is highly pathogenic avian influenza (HPAI).
"Bird flu" is a phrase similar to "swine flu," "dog flu," "horse flu," or "human flu" in that it refers to an illness caused by any of many different strains of influenza viruses that have adapted to a specific host. All known viruses that cause influenza in birds belong to the species influenza A virus. All subtypes (but not all strains of all subtypes) of influenza A virus are adapted to birds, which is why for many purposes avian flu virus is the influenza A virus (note that the "A" does not stand for "avian").
Adaptation is non-exclusive. Being adapted towards a particular species does not preclude adaptations, or partial adaptations, towards infecting different species. In this way strains of influenza viruses are adapted to multiple species, though may be preferential towards a particular host. For example, viruses responsible for influenza pandemics are adapted to both humans and birds. Recent influenza research into the genes of the Spanish flu virus shows it to have genes adapted to both birds and humans; with more of its genes from birds than less deadly

(f)*TREATMENT OF "SWIM FIU"*

-In swine
As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required. Instead veterinary efforts are focused on preventing the spread of the virus throughout the farm, or to other farms. Vaccination and animal management techniques are most important in these efforts. Antibiotics are also used to treat this disease, which although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds.
-In humans
If a person becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms). Beside antivirals, supportive care at home or in hospital, focuses on controlling fevers, relieving pain and maintaining fluid balance, as well as identifying and treating any secondary infections or other medical problems. The U.S. Centers for Disease Control and Prevention recommends the use of Tamiflu (oseltamivir) or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses; however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs. The virus isolates in the 2009 outbreak have been found resistant to amantadine and rimantadine.
In the U.S., on April 27, 2009, the Food and Drug Administration (FDA) issued Emergency Use Authorizations to make available Relenza and Tamiflu antiviral drugs to treat the swine influenza virus in cases for which they are currently unapproved. The agency issued these EUAs to allow treatment of patients younger than the current approval allows and to allow the widespread distribution of the drugs, including by non-licensed volunteers.

(e)*PREVENTION OF "SWINE FIU"*

Prevention of swine influenza has three components: prevention in swine, prevention of transmission to humans, and prevention of its spread among humans.
-In swine
Methods of preventing the spread of influenza among swine include facility management, herd management, and vaccination (ATCvet code: QI09AA03). Because much of the illness and death associated with swine flu involves secondary infection by other pathogens, control strategies that rely on vaccination may be insufficient.
Control of swine influenza by vaccination has become more difficult in recent decades, as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection when the virus strains match enough to have significant cross-protection, and custom (autogenous) vaccines made from the specific viruses isolated are created and used in the more difficult cases. Present vaccination strategies for SIV control and prevention in swine farms typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 isolates had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests that current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses. The United States Department of Agriculture researchers say that while pig vaccination keeps pigs from getting sick, it does not block infection or shedding of the virus.[8
Facility management includes using disinfectants and ambient temperature to control virus in the environment. The virus is unlikely to survive outside living cells for more than two weeks, except in cold (but above freezing) conditions, and it is readily inactivated by disinfectants. Herd management includes not adding pigs carrying influenza to herds that have not been exposed to the virus. The virus survives in healthy carrier pigs for up to 3 months and can be recovered from them between outbreaks. Carrier pigs are usually responsible for the introduction of SIV into previously uninfected herds and countries, so new animals should be quarantined. After an outbreak, as immunity in exposed pigs wanes, new outbreaks of the same strain can occur.
-In humans
Prevention of pig to human transmission
Swine can be infected by both avian and human influenza strains of influenza, and therefore are hosts where the antigenic shifts can occur that create new influenza strains.
The transmission from swine to human is believed to occur mainly in swine farms where farmers are in close contact with live pigs. Although strains of swine influenza are usually not able to infect humans this may occasionally happen, so farmers and veterinarians are encouraged to use a face mask when dealing with infected animals. The use of vaccines on swine to prevent their infection is a major method of limiting swine to human transmission. Risk factors that may contribute to swine-to-human transmission include smoking and not wearing gloves when working with sick animals.
Prevention of human to human transmission
Influenza spreads between humans through coughing or sneezing and people touching something with the virus on it and then touching their own nose or mouth. Swine flu cannot be spread by pork products, since the virus is not transmitted through food. The swine flu in humans is most contagious during the first five days of the illness although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days for analysis.
Thermal imaging camera & screen, photographed in an airport terminal in Greece. Thermal imaging can detect elevated body temperature, one of the signs of the virus N1H1 (Swine influenza).
Recommendations to prevent spread of the virus among humans include using standard infection control against influenza. This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in public. Chance of transmission is also reduced by disinfecting household surfaces, which can be done effectively with a diluted chlorine bleach solution.
Experts agree that hand-washing can help prevent viral infections, including ordinary influenza and the swine flu virus. Also avoiding touching eyes, nose and mouth with hands prevents flu. Influenza can spread in coughs or sneezes, but an increasing body of evidence shows small droplets containing the virus can linger on tabletops, telephones and other surfaces and be transferred via the fingers to the mouth, nose or eyes. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms such as a sudden fever, cough or muscle aches should stay away from work or public transportation and should contact a doctor for advice.
Social distancing is another tactic. It means staying away from other people who might be infected and can include avoiding large gatherings, spreading out a little at work, or perhaps staying home and lying low if an infection is spreading in a community. Public health and other responsible authorities have action plans which may request or require social distancing actions depending on the severity of the outbreak

(d)*SYMPTOMS OF "SWINE FLU"*

-In swine
In pigs influenza infection produces fever, lethargy, sneezing, coughing, difficulty breathing and decreased appetite. In some cases the infection can cause abortion. Although mortality is usually low (around 1–4%), the virus can produce weight loss and poor growth, causing economic loss to farmers. Infected pigs can lose up to 12 pounds of body weight over a 3 to 4 week period.
In humans

-In humans
Direct transmission of a swine flu virus from pigs to humans is occasionally possible (called zoonotic swine flu). In all, 50 cases are known to have occurred since the first report in medical literature in 1958, which have resulted in a total of six deaths. Of these six people, one was pregnant, one had leukemia, one had Hodgkin disease and two were known to be previously healthy. Despite these apparently low numbers of infections, the true rate of infection may be higher, since most cases only cause a very mild disease, and will probably never be reported or diagnosed.
According to the Centers for Disease Control and Prevention (CDC), in humans the symptoms of the 2009 "swine flu" H1N1 virus are similar to those of influenza and of influenza-like illness in general. Symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue. The 2009 outbreak has shown an increased percentage of patients reporting diarrhea and vomiting. The 2009 H1N1 virus is not zoonotic swine flu, as it is not transmitted from pigs to humans, but from person to person.
Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms but also a high likelihood of swine flu due to the person's recent history. For example, during the 2009 swine flu outbreak in the United States, CDC advised physicians to "consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the 7 days preceding their illness onset."A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab).

(c)*TRANSMISSION OF "SWINE FLU"*

-Transmission between pigs
Influenza is quite common in pigs, with about half of breeding pigs having been exposed to the virus in the US. Antibodies to the virus are also common in pigs in other countries.
The main route of transmission is through direct contact between infected and uninfected animals. These close contacts are particularly common during animal transport. Intensive farming may also increase the risk of transmission, as the pigs are raised in very close proximity to each other. The direct transfer of the virus probably occurs either by pigs touching noses, or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing are also an important means of infection. The virus usually spreads quickly through a herd, infecting all the pigs within just a few days. Transmission may also occur through wild animals, such as wild boar, which can spread the disease between farms.

-Transmission to humans
People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur.[ Vaccination of these workers against influenza and surveillance for new influenza strains among this population may therefore be an important public health measure. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study among others forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. Other professions at particular risk of infection are veterinarians and meat processing workers, although the risk of infection for both of these groups is lower than that of farm workers.
-Interaction with avian H5N1 in pigs
Pigs are unusual as they can be infected with influenza strains that usually infect three different species: pigs, birds and humans. This makes pigs a host where influenza viruses might exchange genes, producing new and dangerous strains. Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. H3N2 evolved from H2N2 by antigenic shift. In August 2004, researchers in China found H5N1 in pigs.

(b)*HISTORY OF "SWINE FLU"*

Swine influenza was first proposed to be a disease related to human influenza during the 1918 flu pandemic, when pigs became sick at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930. For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In 1997–1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2. In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm.
The H1N1 form of swine flu is one of the descendants of the strain that caused the 1918 flu pandemic. As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza. However, direct transmission from pigs to humans is rare, with only 12 cases in the U.S. since 2005. Nevertheless, the retention of influenza strains in pigs after these strains have disappeared from the human population might make pigs a reservoir where influenza viruses could persist, later emerging to reinfect humans once human immunity to these strains has waned.
Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. For example, this disease costs the British meat industry about £65 million every year.

(a)*CLASSIFICATION OF "SWINE FLU"*

-Influenza C
Influenza C viruses infect both humans and pigs, but do not infect birds. Transmission between pigs and humans have occurred in the past. For example, influenza C caused small outbreaks of a mild form of influenza amongst children in Japan and California. Due to its limited host range and the lack of genetic diversity in influenza C, this form of influenza does not cause pandemics in humans.
-Influenza A
Swine influenza is known to be caused by influenza A subtypes H1N1,[8] H1N2,[8] H2N3,[ H3N1, and H3N2. In pigs, three influenza A virus subtypes (H1N1, H1N2, and H3N2) are the most common strains worldwide. In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants, containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.
-Surveillance
Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs, there is an informal surveillance network in the United States that is part of a world surveillance network.
Veterinary medical pathologist, Tracey McNamara, set up a national disease surveillance system in zoos because the zoos do active disease surveillance and many of the exotic animals housed there have broad susceptibilities. Many species fall below the radar of any federal agencies (including dogs, cats, pet prairie dogs, zoo animals, and urban wildlife), even though they may be important in the early detection of human disease outbreaks.

#(1)SWINE INFLUENZA" Swime Flu"(H1N1)

Novel H1N1 flu, popularly known as swine flu, is a respiratory infection caused by an influenza virus first recognized in spring 2009. The new virus, which is officially called swine influenza A (H1N1), contains genetic material from human, swine and avian flu viruses.
Technically, the term "swine flu" refers to influenza in pigs. Occasionally, pigs transmit influenza viruses to people, mainly hog farm workers and veterinarians. Less often, someone infected occupationally passes the infection to others. You can't catch swine flu from eating pork. Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human influenza, often resulting only in the production of antibodies in the blood. If transmission does cause human influenza, it is called zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infection. The meat of an infected animal poses no risk of infection when properly cooked.
During the mid-20th century, identification of influenza subtypes became possible, allowing accurate diagnosis of transmission to humans. Since then, only 50 such transmissions have been confirmed. These strains of swine flu rarely pass from human to human. Symptoms of zoonotic swine flu in humans are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.

DISEASES

A disease or medical condition is an abnormal condition of an organism that impairs bodily functions, associated with specific symptoms and signs. It may be caused by external factors, such as invading organisms, or it may be caused by internal dysfunctions, such as autoimmune diseases.
In human beings, "disease" is often used more broadly to refer to any condition that causes pain, dysfunction, distress, social problems, and/or death to the person afflicted, or similar problems for those in contact with the person. In this broader sense, it sometimes includes injuries, disabilities, disorders, syndromes, infections, isolated symptoms, deviant behaviors, and atypical variations of structure and function, while in other contexts and for other purposes these may be considered distinguishable categories.