Monday, July 23, 2007
Saturday, July 21, 2007
Thursday, July 19, 2007
Japanese encephalitis ( previously known as Japanese B encephalitis to distinguish it from von Economo's A encephalitis) is a disease caused by the mosquito-borne Japanese encephalitis virus. The Japanese encephalitis virus is a virus from the family Flaviviridae. Domestic pigs and wild birds are reservoirs of the virus; transmission to humans may cause severe symptoms. One of the most important vectors of this disease is the mosquito Culex tritaeniorhynchus. This disease is most prevalent in Southeast Asia and the Far East.
Japanese encephalitis is the leading cause of viral encephalitis in Asia, with 30,000–50,000 cases reported annually. Case-fatality rates range from 0.3% to 60% and depends on the population and on age. Rare outbreaks in U.S. territories in Western Pacific have occurred. Residents of rural areas in endemic locations are at highest risk; Japanese encephalitis does not usually occur in urban areas. Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination, include China, Korea, Japan, Taiwan and Thailand. Other countries that still have periodic epidemics include Vietnam, Cambodia, Myanmar, India, Nepal, and Malaysia.
Japanese encephalitis has an incubation period of 5 to 15 days and the vast majority of infections are asymptomatic: only 1 in 250 infections develop into encephalitis.
Severe rigors mark the onset of this disease in humans. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between 38 and 41 degrees Celsius. Mental retardation developed from this disease usually leads to coma. Mortality of this disease varies but is generally much higher in children. Transplacental spread has been noted. Life-long neurological defects such as deafness, emotional lability and hemiparesis may occur in those who have had central nervous system involvement. In known cases some effects also include, nausea, headache, fever,vomiting and sometimes swelling of the testicles.
The causative agent Japanese encephalitis virus is an enveloped virus of the genus flavivirus; it is closely related to the West Nile virus and St. Louis encephalitis virus. Positive sense single stranded RNA genome is packaged in the capsid, formed by the capsid protein. The outer envelope is formed by envelope (E) protein and is the protective antigen. It aids in entry of the virus to the inside of the cell. The genome also encodes several nonstructural proteins also (NS1,NS2a,NS2b,NS3,N4a,NS4b,NS5). NS1 is produced as secretory form also. NS3 is a putative helicase, and NS5 is the viral polymerase. It has been noted that the Japanese encephalitis virus (JEV) infects the lumen of the endoplasmic reticulum (ER) and rapidly accumulates substantial amounts of viral proteins for the JEV.
Japanese Encephalitis is diagnosed by detection of antibodies in serum and CSF (cerebrospinal fluid) by IgM capture ELISA
Infection with JEV confers life-long immunity. All current vaccines are based on the genotype III virus. A formalin-inactivated mouse-brain derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanisation has led to control of the disease in Japan, Korea, Taiwan and Singapore. The high cost of the vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunisation programme.
In the UK, the two vaccines used (but which are unlicensed) are JE-Vax® and Green Cross. Three doses are given at 0, 7–14 and 28–30 days. The dose is 1ml for children and adult, and 0.5ml for infants under 36 months of age.
There is no specific treatment for Japanese encephalitis and treatment is supportive. There is no transmission from person to person and therefore patients do not need to be isolated.
Wednesday, July 18, 2007
State of the Epidemic
The first case of AIDS in Nepal was reported in 1988. Since then, the numbers have risen among the country’s 27 million people. By the end of 2005, more than 950 cases of AIDS and over 5,800 cases of HIV infection were officially reported, with three times as many men reported to be infected as women. However, given the limitations of Nepal’s public health surveillance system, the actual number of infections is expected to be much higher. UNAIDS estimates that 75,000 people were living with HIV at the end of 2005.
Nepal’s HIV epidemic is largely concentrated in high-risk groups, especially female sex workers (FSW), IDUs, MSM and migrants. Injection drug use appears to be extensive in Nepal and to overlap with commercial sex. Another important factor is the high number of sex workers who migrate or are trafficked to Mumbai, India to work, thereby increasing HIV prevalence in the sex workers’ network in Nepal more rapidly.
Nepal’s epidemic will continue to grow if immediate and vigorous action is not taken and will be largely driven by injection drug use and sex work. Major risk factors are as follows:
- Continued Spread among Injecting Drug Users
- Trafficking of Female Sex Workers
- Changing Values among Young People
- Low Awareness among Men Who Have Sex with Men (MSM)
Issues and Challenges: Priority Areas
Addressing the HIV/AIDS epidemic in Nepal requires immediate action and long-term continuity and sustainability. The following actions are essential:
- Emphasize HIV/AIDS as a development issue with continued high-level leadership. The epidemic cannot be tackled through medical/clinical interventions alone. HIV/AIDS prevention and control requires a multi-sectoral approach, involving sectors other than health, such as education, women’s affairs, information, law and order, defense, agriculture, labor and transport.
- Demonstrate the need for an expanded and coherent response. Also strengthen management for effective collaboration and coordination between public and private sectors, and improve implementation.
- Mobilize resources for scaling up responses for high risk groups. These include migrants, female sex workers, injecting drug users, and men who have sex with men.
- Scale up advocacy, behavioral change activities, and health promotion interventions for young people, mobile populations, female sex workers, IDUs, and men who have sex with men.
- Implement harm-reduction initiatives for IDUs and promote condom use in casual and commercial sex. Address opposition to scaling up harm-reduction measures such as the distribution of clean needles and syringes to IDUs.
- Strengthen biological and behavioral surveillance to enhance understanding of the extent and nature of HIV and STIs, sexual behaviors, and healthcare-seeking behaviors related to HIV and STIs.
- Encourage openness in addressing risky behaviors and to protect vulnerable populations. Denial and stigma of HIV and groups that are at high risk only hamper prevention efforts. Efforts to increase knowledge, reduce stigmatization, and promote positive attitudes and norms about safe sexual behaviors are critical.
- Provide comprehensive care for people living with HIV and AIDS, including widely available voluntary counseling and testing facilities, provisions for treating opportunistic infections, rolling out of quality structured treatment, and adherence to monitoring