Infectious Diseases
Mad Cow



Severe Acute Respiratory Syndrome (SARS)

newsweek cover:SARS photo


  • SARS coronavirus

Environmental Triggers:

  • Globalization of Travel and Trade
  • Chronic Disease Burden
  • Invasive Species


The epidemic of SARS appears to have started in Guangdong Province, China in November 2002. The first case of SARS was reportedly originated in Shunde, Foshan, Guangdong in Nov 2002, and the patient, a farmer, was treated in the First People's Hospital of Foshan (Mckay Dennis). The patient died soon after, and no definite diagnosis was made on his cause of death. Despite taking some action to control it, Chinese government officials did not inform the World Health Organization of the outbreak until February 2003. This lack of openness caused delays in efforts to control the epidemic, resulting in criticism of the People’s Republic of China from the international community. China has since officially apologized for early slowness in dealing with the SARS epidemic.

The first clue of the outbreak appears to be 27 November 2002 when Canada's Global Public Health Intelligence Network (GPHIN), an electronic warning system which is part of the World Health Organization's (WHO) Global Outbreak and Alert Response Network (GOARN), picked up reports of a "flu outbreak" in China through Internet media monitoring and analysis and sent them to the WHO. Importantly, while GPHIN's capability had recently been upgraded to enable Arabic, Chinese, English, French, Russian and Spanish translation, the system was limited to English or French in presenting this information. Thus, while the first reports of an unusual outbreak were in Chinese, an English report was not generated until 21 January 2003. Subsequently, the WHO requested information from Chinese authorities on 5 and 11 December. Despite the successes of the network in previous outbreak of diseases, it was proven rather defective after receiving intelligence on the media reports from China several months after the outbreak of SARS. Along with the second alert, WHO released the name, definition, as well as an activation of a coordinated global outbreak response network that brought sensitive attention and containment procedures (Dr. Heymann, 2003). However, by then although the new definitions do give nations a guideline to contain SARS, over five hundred deaths and an additional two thousand cases had already occurred worldwide.

In early April, there appeared to be a change in official policy when SARS began to receive a much greater prominence in the official media. Some have directly attributed this to the death of American James Earl Salisbury.[24] However, it was also in early April that accusations emerged regarding the undercounting of cases in Beijing military hospitals. After intense pressure, Chinese officials allowed international officials to investigate the situation there. This revealed problems plaguing the aging mainland Chinese healthcare system, including increasing decentralization, red tape, and inadequate communication.

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Human Immunodeficiency Virus (HIV)

HIV photo


  • lentivirus family

Environmental Triggers:

  • Bushmeat Hunting
  • Globalization of Travel and Trade
  • Habitat Conversion


Most people with dengue recover without any ongoing problems. The mortality is 1–5% without treatment, and less than 1% with adequate treatment; however severe disease carries a mortality of 26%. Dengue is endemic in more than 110 countries.It infects 50 to 100 million people worldwide a year, leading to half a million hospitalizations, and approximately 12,500–25,000 deaths.

UNAIDS and the WHO estimated that AIDS killed more than 25 million people between 1981, when it was first recognized, and 2005, making it one of the most destructive pandemics in recorded history. Despite improved access to antiretroviral treatment and care in many regions of the world, the AIDS pandemic claimed an estimated 2.8 million (between 2.4 and 3.3 million) lives in 2005 of which more than half a million (570,000) were children.

UNAIDS estimated that 33.3 million people were living with HIV at the end of 2009, up from 26.2 million people in 1999. They also estimated AIDS-related deaths in 2009 at 1.8 million people, down from a peak of 2.1 million in 2004, new infections at 2.6 million, down from a peak of 3.2 million in 1997, and the number of people in low- or middle-income countries receiving antiretroviral therapy in 2009 at 5.2 million, up from 4.0 million in 2008.

Sub-Saharan Africa remains by far the worst-affected region, with an estimated 22.5 million people currently living with HIV (67% of the global total), 1.3 million deaths (72% of the global total) and 1.8 million new infections (69% of the global total). However, the number of new infections declined by 19% across the region between 2001 and 2009, and by more than 25% in 22 sub-Saharan African countries during this period. Asia is the second-worst affected region, with 4.9 million people living with HIV (15% of the global total).

The latest evaluation report of the World Bank's Operations Evaluation Department assesses the development effectiveness of the World Bank's country-level HIV/AIDS assistance defined as policy dialogue, analytic work, and lending with the explicit objective of reducing the scope or impact of the AIDS epidemic.[172] This is the first comprehensive evaluation of the World Bank's HIV/AIDS support to countries, from the beginning of the epidemic through mid-2004. Because the Bank aims to assist in implementation of national government programmes, their experience provides important insights on how national AIDS programmes can be made more effective.

The development of HAART as effective therapy for HIV infection has substantially reduced the death rate from this disease in those areas where these drugs are widely available.[141] As the life expectancy of persons with HIV has increased in countries where HAART is widely used, the continuing spread of the disease has caused the number of persons living with HIV to increase substantially.

In Africa, the number of mother-to-child-transmission (MTCT) cases and the prevalence of AIDS is beginning to reverse decades of steady progress in child survival. Countries such as Uganda are attempting to curb the MTCT epidemic by offering VCT (voluntary counselling and testing), PMTCT (prevention of mother-to-child transmission) and ANC (ante-natal care) services, which include the distribution of antiretroviral therapy.

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West Nile Virus (WNV)

WNV transmission cycle photo


  1. Flaviviridae family
  2. Japenese encephalitis antigenic complex

Environmental Triggers:

  • Defaunation
  • Global Warming


Studies of phylogenetic lineages have determined that WNV emerged as a distinct virus around 1000 years ago. This initial virus developed into two distinct lineages, Lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an Africa zoonose. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary in 2008. Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa. A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans.

WNV has been posited as one of the possible causes of Alexander the Great's early death based on reports of avian deaths before his illness period.

WNV was first isolated from a feverish 37 year old woman at Omogo in the West Nile District of Uganda in 1937 during research on yellow fever virus. A series of serosurveys in 1939 in central Africa found anti-WNV positive results ranging from 1.4% (Congo) to 46.4% (White Nile region, Sudan). It was subsequently identified in Egypt (1942) and India (1953), a 1950 serosurvey in Egypt found 90% of those over 40 years in age had WNV antibodies. The ecology was characterized in 1953 with studies in Egypt and Israel. The virus became recognized as a cause of severe human meningoencephalitis in elderly patients during an outbreak in Israel in 1957. The disease was first noted in horses in Egypt and France in the early 1960s and found to be widespread in southern Europe, southwest Asia and Australia.

The first appearance of WNV in the Western hemisphere was in 1999 with encephalitis reported in humans, dogs, cats, and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus. The American outbreak began in the New York City area (specifically, College Point, Queens) and was later seen in New Jersey and Connecticut; the virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence.[53] The US virus was very closely related to a lineage 1 strain found in Israel in 1998. Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary Macaque, Macaca sylvanus, was the first non-human primate to contract WNV.[54] Both the US and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially corvidae—can be an early indicator of the arrival of the virus.

A high level of media coverage through 2001/2002 raised public awareness of WNV. This coverage was most likely the result of successive appearances of the virus in new areas, and had the unintended effect of increasing funding for research on this virus and related arthropod-borne viruses. Such research has expanded our understanding of viruses transmitted by mosquitoes.

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