270. EBOLA HAEMORRHAGIC FEVER

The Ebola virus causes severe viral haemorrhagic fever (VHF) outbreaks in humans.
Viral haemorrhagic fever outbreaks have a case fatality rate of up to 90%.
Ebola haemorrhagic fever outbreaks occur primarily in remote villages in Central and West Africa, near tropical rainforests.
The virus is transmitted to people from wild animals and spreads in the human population through human-to-human transmission.
Fruit bats of the Pteropodidae family are considered to be the natural host of the Ebola virus.
There is no treatment or vaccine available for either people or animals.

The Ebola virus can cause severe viral haemorrhagic fever (VHF) outbreaks in humans with a case fatality rate of up to 90%. Ebola first appeared in 1976 in two simultaneous outbreaks, in Nzara, Sudan, and in Yambuku, Democratic Republic of Congo (DRC). The latter was in a village situated near the Ebola River, from which the disease takes its name.

The Ebola virus is comprised of five distinct species: Bundibugyo, Ivory Coast, Reston, Sudan and Zaire.

Bundibugyo, Sudan and Zaire species have been associated with large Ebola haemorrhagic fever (EHF) outbreaks in Africa, while the Ivory Coast and Reston species have not. EHF is a febrile haemorrhagic illness which causes death in 25-90% of all cases. The Ebola Reston species, found in the Philippines, can infect humans, but no illness or death in humans has been reported to date.

Transmission

Ebola is introduced into the human population through close contact with the blood, secretions, organs or other bodily fluids of infected animals. In Africa, infection has been documented through the handling of infected chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines found dead or ill in the rainforest.

Later Ebola spreads in the community through human-to-human transmission, resulting from close contact with the blood, secretions, organs or other bodily fluids of infected people. Burial ceremonies where mourners have direct contact with the body of the deceased person can also play a role in the transmission of Ebola. Transmission via infected semen can occur up to seven weeks after clinical recovery.

Health-care workers have frequently been infected while treating Ebola patients. This has occurred through close contact without the use of correct infection control precautions and adequate barrier nursing procedures. For example, health-care workers not wearing gloves and/or masks and/or goggles may be exposed to direct contact with infected patients' blood and are at risk.

Among workers in contact with monkeys or pigs infected with Ebola Reston, several human infections have been documented and were clinically asymptomatic. Thus, the Ebola Reston virus appears to be less capable of causing disease in humans than the other Ebola species. However, the evidence available relates only to healthy adult males. It would be premature to conclude the health effects of the virus on all population groups, such as immuno-compromised persons, persons with underlying medical conditions, pregnant women and children. More studies of Ebola Reston virus are needed before definitive conclusions can be made about the pathogenicity and virulence of this virus in humans.

Signs and symptoms

EHF is a severe acute viral illness often characterized by the sudden onset of fever, intense weakness, muscle pain, headache and sore throat. This is followed by vomiting, diarrhoea, rash, impaired kidney and liver function, and in some cases, both internal and external bleeding. Laboratory findings show low counts of white blood cells and platelets as well as elevated liver enzymes.

People are infectious as long as their blood and secretions contain the virus. Ebola virus was isolated from seminal fluid up to the 61st day after the onset of illness in a laboratory acquired case.

The incubation period (interval from infection to onset of symptoms) varies between 2 to 21 days.

During EHF outbreaks, the case-fatality rate has varied from outbreak to outbreak between 25% and 90%.

Diagnosis

Differential diagnoses include, malaria, typhoid fever, shigellosis, cholera, leptospirosis, plague, rickettsiosis, relapsing fever, meningitis, hepatitis and other VHFs.

Ebola virus infections can only be diagnosed definitively in the laboratory by a number of different tests:
enzyme-linked immunosorbent assay (ELISA)
antigen detection tests
serum neutralization test
reverse transcriptase polymerase chain reaction (RT-PCR) assay
virus isolation by cell culture.

Tests on samples from patients are an extreme biohazard risk and should only be conducted under maximum biological containment conditions.

Treatment and vaccine

Severe cases require intensive supportive care. Patients are frequently dehydrated and in need of intravenous fluids or oral rehydration with solutions containing electrolytes.

No specific treatment or vaccine is yet available for EHF. New drug therapies have shown promising results in laboratory studies and are currently being evaluated. Several vaccines are being tested but it could be several years before any are available.

Natural host of Ebola virus

In Africa, fruit bats, particularly species of the genera Hypsignathus monstrosus, Epomops franqueti and Myonycteris torquata, are considered possible natural hosts for Ebola virus. As a result, the geographic distribution of Ebolaviruses may overlap with the range of the fruit bats.

Ebola virus in animals

Although non-human primates have been a source of infection for humans, they are not thought to be the reservoir but rather an accidental host like human beings. Since 1994, Ebola outbreaks from the Zaire and Ivory Coast species have been found in chimpanzees and gorillas.

Ebola Reston has caused severe VHF outbreaks in macaque monkeys (Macaca fascicularis) farmed in the Philippines and in imported monkeys in 1989, 1990 and 1996 to the USA and in 1992 in monkeys imported to Italy from the Philippines.

Since 2008, Ebola Reston viruses were detected during several outbreaks of a deadly disease in pigs. Asymptomatic infection in pigs has been reported and experimental inoculations tend to demonstrate that Ebola Reston cannot cause a disease in pigs.

Prevention

Controlling Ebola Reston in domestic animals

There is no animal vaccine available against Ebola Reston. Routine cleaning and disinfection of pig or monkey farms (with sodium hypochlorite or other detergents) is expected to be effective in inactivating the virus. If an outbreak is suspected, the premises should be quarantined immediately. Culling of infected animals, with close supervision of burial or incineration of carcasses, may be necessary to reduce the risk of animal-to-human transmission. Restricting or banning the movement of animals from infected farms to other areas can reduce the spread of the disease.

As Ebola Reston outbreaks in pigs and monkeys have preceded human infections, the establishment of an active animal health surveillance system to detect new cases is essential in providing early warning for veterinary and human public health authorities.

Reducing the risk of Ebola infection in people

In the absence of effective treatment and a human vaccine, raising awareness of the risk factors of Ebola infection and the protective measures individuals can take is the only way to reduce human infection and death.

In Africa, during EHF outbreaks, educational public health messages for risk reduction should focus on several factors.
Reducing the risk of wildlife-to-human transmission from contact with infected fruit bats or monkeys/apes and the consumption of their raw meat. Animals should be handled with gloves and other appropriate protective clothing. Their products (blood and meat) should be thoroughly cooked before consumption.
Reducing the risk of human-to-human transmission in the community arising from direct or close contact with infected patients, particularly with their bodily fluids. Close physical contact with Ebola patients should be avoided. Gloves and appropriate personal protective equipment should be worn when taking care of ill patients at home. Regular hand washing is required after visiting sick relatives in hospital, as well as after taking care of ill patients at home.
Communities affected by Ebola should inform the population about the nature of the disease and about outbreak containment measures, including burial of the deceased. People who have died from Ebola should be promptly and safely buried.
Precautionary measures are needed in Africa to avoid that pig farms infected through contact with fruit bats amplify the virus and cause EHF outbreaks.

For Ebola Reston, educational public health messages should focus on reducing the risk of pig-to-human transmission as a result of unsafe animal husbandry and slaughtering practices, and unsafe consumption of fresh blood, raw milk or animal tissue. Gloves and other appropriate protective clothing should be worn when handling sick animals or their tissues or when slaughtering animals. In the regions where Ebola Reston has been reported/detected in pigs, all animal products (blood, meat and milk) should be thoroughly cooked before eating.

Controlling infection in health-care settings

Human-to-human transmission of the Ebola virus is primarily associated with direct contact with blood and body fluids. Transmission to healthcare workers has been reported when appropriate infection control measures have not been observed.

Health-care workers caring for patients with suspected or confirmed Ebola virus should apply infection control precautions to avoid any exposure to the patient's blood and body fluids and/or direct unprotected contact with the possibly contaminated environment. Therefore the provision of health care for suspected or confirmed Ebola patients requires specific control measures and the reinforcement of standard precautions, particularly basic hand hygiene, the use of personal protective equipment, safe injections practices and safe burial practices.

Laboratory workers are also at risk. Samples taken from suspected human and animal Ebola cases for diagnosis should be handled by trained staff and processed in suitably-equipped laboratories.

269. Trypanosomiasis - Human African sleeping sickness.

Sleeping sickness occurs only in 36 sub-Saharan Africa countries where there are tsetse flies that can transmit the disease.
The people most exposed to the tsetse fly and therefore the disease are in rural populations dependent on agriculture, fishing, animal husbandry or hunting.
Trypanosoma brucei gambiense (T.b.g.) accounts for 95% of reported cases of sleeping sickness.
After continued control efforts, the number of cases reported in 2009 has dropped below 10 000 for first time in 50 years. This trend was maintained in 2010 with 7139 new cases reported.
Diagnosis and treatment of the disease is complex and requires

-Definition of the disease
Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne parasitic disease. The parasites concerned are protozoa belonging to the Trypanosoma genus. They are transmitted to humans by tsetse fly (Glossina genus) bites which have acquired their infection from human beings or from animals harbouring the human pathogenic parasites.

Tsetse flies are found just in sub-Saharan Africa though only certain species transmit the disease. For reasons that are so far unexplained, there are many regions where tsetse flies are found, but sleeping sickness is not. Rural populations living in regions where transmission occurs and which depend on agriculture, fishing, animal husbandry or hunting are the most exposed to the tsetse fly and therefore to the disease. The disease develops in areas ranging from a single village to an entire region. Within an infected area, the intensity of the disease can vary from one village to the next.

Forms of human African trypanosomiasis
Human African trypanosomiasis takes two forms, depending on the parasite involved:
Trypanosoma brucei gambiense (T.b.g.) is found in west and central Africa. This form currently accounts for over 95% of reported cases of sleeping sickness and causes a chronic infection. A person can be infected for months or even years without major signs or symptoms of the disease. When symptoms emerge, the patient is often already in an advanced disease stage where the central nervous system is affected.
Trypanosoma brucei rhodesiense (T.b.r.) is found in eastern and southern Africa. Nowadays, this form represents under 5% of reported cases and causes an acute infection. First signs and symptoms are observed a few months or weeks after infection. The disease develops rapidly and invades the central nervous system.

Another form of trypanosomiasis occurs mainly in 21 Latin American countries. It is known as American trypanosomiasis or Chagas disease. The causal organism is a different species from those causing the African form of the disease.

Animal trypanosomiasis
Other parasite species and sub-species of the Trypanosoma genus are pathogenic to animals and cause animal trypanosomiasis in wild and domestic animal species. In cattle the disease is called Nagana, a Zulu word meaning "to be depressed".

Animals can host the human pathogen parasites, especially T.b. rhodesiense; thus domestic and wild animals are an important parasite reservoir. Animals can also be infected with T.b. gambiense and act as a reservoir. However the precise epidemiological role of this reservoir is not yet well known. The disease in domestic animals, particularly cattle, is a major obstacle to the economic development of affected rural areas.

Major human epidemics
There have been several epidemics in Africa over the last century:
one between 1896 and 1906, mostly in Uganda and the Congo Basin
one in 1920 in a number of African countries and
the most recent epidemic occurred in 1970.

The 1920 epidemic was controlled thanks to mobile teams which organized the screening of millions of people at risk. By the mid 1960s, the disease had almost disappeared. After this success, surveillance was relaxed, and the disease reappeared in several areas over the last 30 years. The efforts of WHO, national control programmes, bilateral cooperation and nongovernmental organizations (NGOs) during the 1990's and the beginning of the 21st century stopped and reversed the upward trend of new cases.

Distribution of the disease
Sleeping sickness threatens millions of people in 36 countries in sub-Saharan Africa. Many of the affected populations live in remote areas with limited access to adequate health services, which hampers the surveillance and therefore the diagnosis and treatment of cases. In addition, displacement of populations, war and poverty are important factors leading to increased transmission and this alters the distribution of the disease due to weakened or non-existent health systems.
In 1986, it was estimated that some 70 million people lived in areas where disease transmission could take place.
In 1998, almost 40 000 cases were reported, but estimates were that 300 000 cases were undiagnosed and therefore untreated.
During epidemic periods prevalence reached 50% in several villages in the Democratic Republic of Congo, Angola and Southern Sudan. Sleeping sickness was the first or second greatest cause of mortality in those communities, ahead of even HIV/AIDS.
By 2005, surveillance was reinforced and the number of new cases reported on the continent was reduced; between 1998 and 2004 the number of both forms of the disease fell from 37 991 to 17 616. The estimated number of actual cases was between 50,000 and 70,000.
In 2009, after continued control efforts, the number of cases reported has dropped below 10 000 (9878) for first time in 50 years. This trend has been maintained in 2010 with 7139 new cases reported. The estimated number of actual cases is currently 30 000.

In 2000 and 2001, WHO established public-private partnerships with Aventis Pharma (now sanofi-aventis) and Bayer HealthCare which enabled the creation of a WHO surveillance team, providing support to endemic countries in their control activities and the supply of drugs free of charge for the treatment of patients.

The partnership was renewed in 2006 and recently in 2011. The success in curbing the number of sleeping sickness cases encouraged other private partners to sustain the WHO's initial effort towards the elimination of the disease as a public health problem.

Current situation in endemic countries
The prevalence of the disease differs from one country to another as well as in different parts of a single country.
In the last 10 years, over 70% of reported cases occurred in the Democratic Republic of Congo (DRC).
In 2010 only the DRC declared over 500 new cases per year.
Angola, Central African Republic, Chad, Sudan and Uganda declared between 100 and 500 new cases per year.
Countries such as, Cameroon, Congo, Côte d'Ivoire, Equatorial Guinea, Gabon, Guinea, Malawi, Nigeria, United Republic of Tanzania, Zambia and Zimbabwe are reporting fewer than 100 new cases per year.
Countries like Benin, Botswana, Burkina Faso, Burundi, Ethiopia, Gambia, Ghana, Guinea Bissau, Kenya, Liberia, Mali, Mozambique, Namibia, Niger, Rwanda, Senegal, Sierra Leone, Swaziland and Togo have not reported any new cases for over a decade. Transmission of the disease seems to have stopped but there are still some areas where it is difficult to asses the exact situation because the unstable social circumstances and/or remote accessibility hinders surveillance and diagnostic activities.

Infection and symptoms
The disease is mostly transmitted through the bite of an infected tsetse fly but there are other ways in which people are infected with sleeping sickness.
Mother-to-child infection: the trypanosome can cross the placenta and infect the fetus.
Mechanical transmission through other blood sucking insects is possible. However, it is difficult to assess the epidemiological impact of transmission.
Accidental infections have occurred in laboratories due to pricks from contaminated needles.

In the first stage, the trypanosomes multiply in subcutaneous tissues, blood and lymph. This is known as a haemolymphatic phase, which entails bouts of fever, headaches, joint pains and itching.

In the second stage the parasites cross the blood-brain barrier to infect the central nervous system. This is known as the neurological phase. In general this is when more obvious signs and symptoms of the disease appear: changes of behaviour, confusion, sensory disturbances and poor coordination. Disturbance of the sleep cycle, which gives the disease its name, is an important feature of the second stage of the disease. Without treatment, sleeping sickness is considered fatal.

Disease management: diagnosis
Disease management is made in three steps.
1.Screening for potential infection. This involves using serological tests (only available for T.b.gambiense) and checking for clinical signs - generally swollen cervical glands.
2.Diagnosing whether the parasite is present.
3.Staging to determine the state of disease progression. This entails examining cerebro-spinal fluid obtained by lumbar puncture and is used to determine the course of treatment.

Diagnosis must be made as early as possible and before the neurological stage in order to avoid complicated, difficult and risky treatment procedures.

The long, relatively asymptomatic first stage of T. b. gambiense sleeping sickness is one of the reasons why an exhaustive, active screening of the population at risk is required, in order to identify patients at an early stage and reduce transmission. Exhaustive screenings require a major investment in human and material resources. In Africa such resources are often scarce, particularly in remote areas where the disease is mostly found. As a result, many infected individuals may die before they can ever be diagnosed and treated.

Treatment
The type of treatment depends on the stage of the disease. The drugs used in the first stage of the disease are of lower toxicity and easier to administer. The earlier the disease is identified, the better the prospect of a cure.

Treatment success in the second stage depends on a drug that can cross the blood-brain barrier to reach the parasite. Such drugs are toxic and complicated to administer. Four drugs are registered for the treatment of sleeping sickness and provided free of charge to endemic countries.

First stage treatment:
Pentamidine: discovered in 1941, used for the treatment of the first stage of T.b. gambiense sleeping sickness. Despite non-negligible undesirable effects, it is in general well tolerated by patients.
Suramin: discovered in 1921, used for the treatment of the first stage of T.b. rhodesiense. It provokes certain undesirable effects, in the urinary tract and allergic reactions.

Second stage treatment:
Melarsoprol: discovered in 1949, it is used in both forms of infection. It is derived from arsenic and has many undesirable side effects. The most dramatic is reactive encephalopathy (encephalopathic syndrome) which can be fatal (3% to 10%). An increase in resistance to the drug has been observed in several foci particularly in central Africa.
Eflornithine: this molecule, less toxic than melarsoprol, was registered in 1990. It is only effective against T.b. gambiense. The regimen is strict and difficult to apply.
A combination treatment of nifurtimox and eflornithine has been recently introduced (2009). It simplifies the use of eflornithine in monotherapy, but unfortunately it is not effective for T.b. rhodesiense. Nifurtimox is registered for the treatment of American trypanosomiasis but not for human African trypanosomiasis. Nevertheless, after safety and efficacy data provided by clinical trials, its use in combination with eflornithine has been accepted and included in the WHO List of Essential Medicine, and it is provided free of charge for this purpose by WHO.

268. Ultraviolet radiation and human health

Skin cancer is caused primarily by exposure to ultraviolet (UV) radiation – either from the sun or from artificial sources such as sunbeds.
Globally in 2000, over 200 000 cases of melanoma were diagnosed and there were 65 000 melanoma-associated deaths.
Excessive sun exposure in children and adolescents is likely to contribute to skin cancer in later life.
Worldwide approximately 18 million people are blind as a result of cataracts, of these 5% of all cataract related disease burden is directly attributable to UV radiation exposure.
Sun protection is recommended when the ultraviolet index is 3 and above.

Ultraviolet radiation

Ultraviolet (UV) radiation is a component of solar radiation. UV radiation levels are influenced by a number of factors.
Sun elevation: the higher the sun in the sky, the higher the UV radiation level.
Latitude: the closer to the equator, the higher the UV radiation levels.
Cloud cover: UV radiation levels are highest under cloudless skies but even with cloud cover, they can be high.
Altitude: UV levels increase by about 5% with every 1000 metres altitude.
Ozone: ozone absorbs some of the UV radiation from the sun. As the ozone layer is depleted, more UV radiation reaches the Earth's surface.
Ground reflection: many surfaces reflect the sun's rays and add to the overall UV exposure (e.g. grass, soil and water reflect less than 10% of UV radiation; fresh snow reflects up to 80%; dry beach sand reflects 15%, and sea foam reflects 25%).

Health effects

Small amounts of UV radiation are beneficial to health, and play an essential role in the production of vitamin D. However, excessive exposure to UV radiation is associated with different types of skin cancer, sunburn, accelerated skin ageing, cataract and other eye diseases. There is also evidence that UV radiation reduces the effectiveness of the immune system.

Effects on the skin

Excessive UV exposure results in a number of chronic skin changes.
Cutaneous malignant melanoma: a life-threatening malignant skin cancer.
Squamous cell carcinoma of the skin: a malignant cancer, which generally progresses less rapidly than melanoma and is less likely to cause death.
Basal cell carcinoma of the skin: a slow-growing skin cancer appearing predominantly in older people.
Photoageing: a loss of skin tightness and the development of solar keratoses.

Effects on the eyes

Acute effects of UV radiation include photokeratitis and photoconjunctivitis (inflammation of the cornea and conjunctiva, respectively). These effects are reversible, easily prevented by protective eyewear and are not associated with any long-term damage.

Chronic effects of UV radiation include:
Cataract: an eye disease where the lens becomes increasingly opaque, resulting in impaired vision and eventual blindness;
Pterygium: a white or creamy fleshy growth on the surface of the eye;
Squamous cell carcinoma of the cornea or conjunctiva: a rare tumour of the surface of the eye.

Other health effects

UV radiation appears to diminish the effectiveness of the immune system by changing the activity and distribution of the cells responsible for triggering immune responses. Immunosuppression can cause reactivation of the herpes simplex virus in the lip ("cold sores").

Disease burden

Excessive exposure to UV radiation caused the loss of approximately 1.5 million DALYs (disability-adjusted life years) and 60 000 premature deaths in the year 2000.

Between 50% and 90% of skin cancers are due to UV radiation. In 2000, there were 200 000 cases of melanoma and 65 000 melanoma-associated deaths worldwide. In addition, there were 2.8 million cases of squamous cell carcinoma and 10 million cases of basal cell carcinoma.

Some 18 million people worldwide are blind as a result of cataracts; of these, as many as 5% may be due to UV radiation. Cataracts attributable to UV radiation are estimated to have caused the loss of about 500 000 DALY's in 2000.

Vulnerable groups

Children and adolescents are particularly vulnerable to the harmful effects of UV radiation. Excessive sun exposure in children is likely to contribute to skin cancer in later life. The mechanisms are unclear, but it may be that skin is more susceptible to the harmful effects of UV radiation during childhood.

A person's skin type is also important. Fair-skinned people suffer more from sunburn and have a higher risk of skin cancer than dark-skinned people. However, even though the incidence of skin cancer is lower in dark-skinned people, the cancers are often detected at a later, more dangerous stage. The risk of eye damage, premature ageing of the skin and immunosuppression is independent of skin type.

Protective measures

WHO recommends the following measures to protect against exposure to UV radiation.
Limit time in the midday sun.
Seek shade
Wear protective clothing such as a broad brimmed hat to protect the eyes, face and neck.
Wear sunglasses with side panels that provide 99 to 100 percent UV-A and UV-B protection.
Use and liberally reapply broad-spectrum sunscreen of sun protection factor (SPF) 30+ on skin areas that cannot be covered by clothes. Sun protection is best achieved by seeking shade and wearing clothes rather than applying sunscreens. Sunscreens should not be used for extending time spent in the sun, and people using sunscreen during sun tanning should voluntarily limit their time spent in the sun.
Avoid sunbeds: use of sunbeds before the age of 35 is associated with a 75% increase in the risk of melanoma. Unless under medical supervision, sunbeds or sunlamps should not be used. WHO recommends banning their use by people under 18 years old.
Protect babies and young children: always keep babies in the shade.

Encouraging children to take the simple precautions above will prevent both short-term and long-term damage while still allowing them to enjoy the time they spend outdoors. Parents and guardians should ensure that children are protected adequately.

Preventing vitamin D deficiency

While protection against over-exposure to UV radiation is the main health concern, UV in small amounts is essential to good health as it leads to the production of vitamin D in the body. Vitamin D strengthens the bone and musculoskeletal system. People who have very low sun exposure – such as those in institutional care or are housebound, people with deeply pigmented skin living in high latitudes or those who, for religious or cultural reasons cover their entire body surface when they are outdoors – should, in consultation with their doctor, consider oral vitamin D supplementation.

-WORLD HEALTH ORGANIZATION

267. Why should I donate blood?

Safe blood saves lives and improves health. Blood transfusion is needed for:
women with complications of pregnancy, such as ectopic pregnancies and haemorrhage before, during or after childbirth;
children with severe anaemia often resulting from malaria or malnutrition;
people with severe trauma following accidents; and
many surgical and cancer patients.

It is also needed for regular transfusions for people with conditions such as thalassaemia and sickle cell disease and is used to make products such as clotting factors for people with haemophilia.

There is a constant need for regular blood supply because blood can be stored for only a limited time before use. Regular blood donations by a sufficient number of healthy people is needed to ensure that safe blood will be available whenever and wherever it is needed.

Blood is the most precious gift that anyone can give to another person — the gift of life. A decision to donate your blood can save a life, or even several if your blood is separated into its components — red cells, platelets and plasma — which can be used individually for patients with specific conditions.

266. June 15 - Elder Abuse Awareness Day

Elder abuse is a significant public health problem. Each year, hundreds of thousands of adults over the age of 60 are abused, neglected, or financially exploited. In the United States alone, over 500,000 older adults are believed to be abused or neglected each year. These statistics are likely an underestimate because many victims are unable or afraid to tell the police, family, or friends about the violence.

There are six types of maltreatment that occur among people over the age of 60. These include:
•Physical Abuse
•Sexual Abuse
•Emotional Abuse
•Neglect
•Abandonment
•Financial Abuse

265. SMOKING KILLS

Cigarette smoking is the number one risk factor for lung cancer. In the United States, cigarette smoking causes about 90% of lung cancers.Tobacco smoke is a toxic mix of more than 7,000 chemicals. Many are poisons. At least 70 are known to cause cancer in people or animals. People who smoke are 15 to 30 times more likely to get lung cancer or die from lung cancer than people who do not smoke. Even smoking a few cigarettes a day or smoking occasionally increases the risk of lung cancer. The more years a person smokes and the more cigarettes smoked each day, the more risk goes up.

People who quit smoking have a lower risk of lung cancer than if they had continued to smoke, but their risk is higher than the risk for people who never smoked. Quitting smoking at any age can lower the risk of lung cancer.

Smoking can cause cancer almost anywhere in the body. Smoking causes cancer of the mouth, nose, throat, voicebox (larynx), esophagus, bladder, kidney, pancreas, cervix, stomach, blood, and bone marrow (acute myeloid leukemia).

264. Middle East respiratory syndrome coronavirus (MERS-CoV)

Middle East respiratory syndrome coronavirus (MERS-CoV). It is a new, emerging virus that is distantly related to the virus that caused SARS.

The first documented cases of MERS occurred in Jordan in early 2012. Globally, to date there has been a total of 55 cases confirmed by laboratory testing. Of these, 40 have occurred in KSA, and the rest have been reported from other countries in the Middle East (Qatar and the United Arab Emirates), from Tunisia in North Africa, and from France, Germany, Italy and the United Kingdom of Great Britain and Northern Ireland in Europe.

The overall number of cases is limited, but the virus causes death in about 60% of patients. So far, about 75% of the cases in KSA have been in men and most have occurred in people with one or more major chronic conditions.

There appears to be three main epidemiological patterns.

In the first pattern, sporadic cases occur in communities. At present, we do not know the source or how these people became infected.

In the second pattern, clusters of infections occur in families. In most of these clusters, there appears to be person-to-person transmission, but it seems that this transmission is limited to people who are in close contact with a sick family member.

The third pattern comprises clusters of infections in health care facilities. Such events have been reported in France, Jordan and KSA. In these clusters, the sequence seems to be that an infected person is admitted to hospital where that person then transmits the virus to other people in the health care facility.

Two important points need to be stressed.

First, there is no evidence of widespread person-to-person transmission of MERS-CoV. Where it has been suspected that the virus has been transmitted from person to person, it appears that there had been close contact between somebody who was sick and another person: a family member, a fellow patient or a health care worker.

Secondly, many fewer infections with MERS-CoV have been reported in health care workers in KSA than might have been expected on the basis of the previous experience of SARS. During the SARS epidemic, health care workers were at high risk of infection. The MERS-CoV is different from the SARS virus. Although the reason why fewer health care workers have been infected with MERS-CoV is not clear, it could be that improvements in infection control that were made after the outbreak of SARS have made a significant difference. In this context, infection control measures in KSA appear to be effective.

Currently, the diagnosis of MERS CoV relies heavily on clinical awareness combined with confirmatory testing for the presence of MERS-CoV by the polymerase chain reaction. No bedside test exists.

Treatment is primarily supportive and there are no convincing data that the use of potent antiviral agents, such as ribavirin and interferon, brings any benefit. The use of steroids in high doses should be avoided.

263. SARS-CoV

The SARS coronavirus, sometimes shortened to SARS-CoV, is the virus that causes severe acute respiratory syndrome (SARS). In April 16 of 2003, following the outbreak of SARS in Asia and secondary cases elsewhere in the world, the World Health Organization (WHO) issued a press release stating that the coronavirus identified by a number of laboratories was the official cause of SARS. Samples of the virus are being held in laboratories in New York, San Francisco, Manila, Hong Kong, and Toronto.

On April 12, 2003, scientists working at the Michael Smith Genome Sciences Centre in Vancouver, British Columbia finished mapping the genetic sequence of a coronavirus believed to be linked to SARS. The team was led by Dr. Marco Marra and worked in collaboration with the British Columbia Centre for Disease Control and the National Microbiology Laboratory in Winnipeg, Manitoba, using samples from infected patients in Toronto. The map, hailed by the WHO as an important step forward in fighting SARS, is shared with scientists worldwide via the GSC website. Dr. Donald Low of Mount Sinai Hospital in Toronto described the discovery as having been made with "unprecedented speed." The sequence of the SARS coronavirus has since been confirmed by other independent groups.

262. HORTON'S DISEASE

Giant-cell arteritis (GCA or temporal arteritis or cranial arteritis) or Horton disease is an inflammatory disease of blood vessels most commonly involving large and medium arteries of the head, predominantly the branches of the external carotid artery. It is a form of vasculitis.

The name (giant cell arteritis) reflects the type of inflammatory cell involved as seen on a biopsy.

The terms "giant-cell arteritis" and "temporal arteritis" are sometimes used interchangeably, because of the frequent involvement of the temporal artery. However, it can involve other large vessels (such as the aorta in "giant-cell aortitis". Giant-cell arteritis of the temporal artery is referred to as "temporal arteritis," and is also known as "cranial arteritis" and "Horton's disease."
It is more common in women than in men by a ratio of 2:1 and more common in those of Northern European descent, as well as those residing at higher latitudes. The mean age of onset is >55 years, and it is rare in those less than 55 years of age.

261. BROWICZ-KUPFFER CELLS

Kupffer cells, also known as Browicz-Kupffer cells and stellate macrophages, are specialized macrophages located in the liver lining the walls of the sinusoids that form part of the reticuloendothelial system (RES) (also called mononuclear phagocyte system).
The cells were first observed by Karl Wilhelm von Kupffer in 1876.The scientist called them "Sternzellen" (star cells or hepatic stellate cell) but thought, falsely, that they were an integral part of the endothelium of the liver blood vessels and that they originated from it. In 1898, after several years of research, Tadeusz Browicz, a Polish scientist, identified them, correctly, as macrophages.