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swine flu

diseasealso called swine influenza, influenza A(H1N1), hog flu, or pig flu

Main

a respiratory disease of pigs that can be transmitted to humans and that is caused by an influenza virus. The first flu virus isolated from pigs was influenza type A(H1N1) in 1930. This virus is a subtype of influenza that is named for the composition of the proteins hemagglutinin (H) and neuraminidase (N) that form its viral coat. Since the 1930s three other subtypes of flu viruses also have been isolated from pigs, including H1N2, H3N1, and H3N2. The emergence of H3N2 in pigs occurred in the late 1990s and is suspected of having been transmitted to pigs from humans. Although swine influenza viruses are similar to the influenza viruses that circulate among humans, swine viruses possess unique antigens (molecules that stimulate an immune response, primarily through the production of antibodies).

Symptoms and transmission


Between 25 and 30 percent of pigs worldwide carry antibodies to swine influenza viruses, which indicates that these animals have been exposed to swine flu. The disease is endemic in pigs in the United States, and in some regions of that country more than 50 percent of pigs carry antibodies to swine influenza viruses. Infection with any of these viruses causes a flulike illness in pigs, which typically occurs in the fall and early winter. Symptoms of infection include coughing (barking), fever, and nasal discharge, and illness generally lasts about a week. The virus is spread rapidly among pigs and is easily spread to birds and humans who come into contact with the pigs or contaminated food or bedding or who inhale infectious particles in the air. Humans infected with swine influenza virus may experience fever and mild respiratory symptoms, such as coughing, runny nose, and congestion. In some cases symptoms may be severe and include diarrhea, chills, and vomiting. Swine influenza virus rarely causes death in humans. The virus can be passed from human to human, primarily through inhalation of infectious particles or contact with an infected individual or a contaminated surface. This mode of transmission is rapid and increases the potential for outbreaks in humans.

Malaria
From Wikipedia, the free encyclopedia

Jump to: navigation, search Malaria is a vector-borne infectious disease caused by protozoan parasites. It is widespread in tropical and subtropical regions, including parts of the Americas, Asia, and Africa. Each year, there are approximately 350500 million cases of malaria,[1] killing between one and three million people, the majority of whom are young children in Sub-Saharan Africa.[2] Ninety percent of malaria-related deaths occur in Sub-Saharan Africa. Malaria is commonly associated with poverty, but is also a cause of poverty[3] and a major hindrance to economic development. Malaria is one of the most common infectious diseases and an enormous public health problem. The disease is caused by protozoan parasites of the genus Plasmodium. Five species of the plasmodium parasite can infect humans; the most serious forms of the disease are caused by Plasmodium falciparum. Malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae causes milder disease in humans that is not generally fatal. A fifth species, Plasmodium knowlesi, causes malaria in macaques but can also infect humans. This group of human-pathogenic Plasmodium species is usually referred to as malaria parasites. Usually, people get malaria by being bitten by an infective female Anopheles mosquito. Only Anopheles mosquitoes can transmit malaria, and they must have been infected through a previous blood meal taken on an infected person. When a mosquito bites an infected person, a small amount of blood is taken, which contains microscopic malaria parasites. About one week later, when the mosquito takes its next blood meal, these parasites mix with the mosquito's saliva and are injected into the person being bitten. The parasites multiply within red blood cells, causing symptoms that include symptoms of anemia (light-headedness, shortness of breath, tachycardia, etc.), as well as other general symptoms such as fever, chills, nausea, flu-like illness, and, in severe cases, coma, and death. Malaria transmission can be reduced by preventing mosquito bites with mosquito nets and insect repellents, or by mosquito control measures such as spraying insecticides inside houses and draining standing water where mosquitoes lay their eggs. Work has been done on malaria vaccines with limited success and more exotic controls, such as genetic manipulation of mosquitoes to make them resistant to the parasite have also been considered. [4] Although some are under development, no vaccine is currently available for malaria that provides a high level of protection[5]; preventive drugs must be taken continuously to reduce the risk of infection. These prophylactic drug treatments are often too expensive for most people living in endemic areas. Most adults from endemic areas have a degree of long-term infection, which tends to recur, and also possess partial immunity (resistance); the resistance reduces with time, and such adults may become susceptible to severe malaria if they have spent a significant amount of time in non-endemic areas. They are strongly recommended to take full precautions if they return to an endemic area. Malaria infections are treated through the use of antimalarial drugs, such as quinine or artemisinin derivatives. However, parasites have evolved to be resistant

to many of these drugs. Therefore, in some areas of the world, only a few drugs remain as effective treatments for malaria.

Contents
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1 Symptoms 2 Causes o 2.1 Malaria parasites 3 Mechanism o 3.1 Mosquito vectors and the Plasmodium life cycle o 3.2 Pathogenesis 4 Diagnosis o 4.1 Symptomatic diagnosis o 4.2 Microscopic examination of blood films o 4.3 Field tests o 4.4 Molecular methods o 4.5 Rapid antigen tests 5 Prevention o 5.1 Vector control o 5.2 Prophylactic drugs o 5.3 Indoor residual spraying o 5.4 Mosquito nets and bedclothes o 5.5 Vaccination o 5.6 Other methods 6 Treatment o 6.1 Antimalarial drugs o 6.2 Counterfeit drugs 7 History o 7.1 Evolutionary pressure of malaria on human genes 7.1.1 Sickle-cell disease 7.1.2 Thalassaemias 7.1.3 Duffy antigens 7.1.4 G6PD 7.1.5 HLA and interleukin-4 8 Society and culture o 8.1 Socio-economic effects 9 See also 10 References 11 External links

Symptoms

Main symptoms of malaria.[6] Symptoms of malaria include fever, shivering, arthralgia (joint pain), vomiting, anemia (caused by hemolysis), hemoglobinuria, retinal damage,[7] and convulsions. The classic symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting four to six hours, occurring every two days in P. vivax and P. ovale infections, while every three for P. malariae.[8] P. falciparum can have recurrent fever every 3648 hours or a less pronounced and almost continuous fever. For reasons that are poorly understood, but that may be related to high intracranial pressure, children with malaria frequently exhibit abnormal posturing, a sign indicating severe brain damage.[9] Malaria has been found to cause cognitive impairments, especially in children. It causes widespread anemia during a period of rapid brain development and also direct brain damage. This neurologic damage results from cerebral malaria to which children are more vulnerable.[10][11] Cerebral malaria is associated with retinal whitening,[12] which may be a useful clinical sign in distinguishing it from other causes of fever.[13]

Species

Appearance

Periodicity Persistent in liver?

Plasmodium vivax

tertian

yes

Plasmodium ovale

tertian

yes

Plasmodium falciparum

tertian

no

Plasmodium malariae

quartan

no

Severe malaria is almost exclusively caused by P. falciparum infection and usually arises 614 days after infection.[14] Consequences of severe malaria include coma and death if untreated young children and pregnant women are especially vulnerable. Splenomegaly (enlarged spleen), severe headache, cerebral ischemia, hepatomegaly (enlarged liver), hypoglycemia, and hemoglobinuria with renal failure may occur. Renal failure may cause blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine. Severe malaria can progress extremely rapidly and cause death within hours or days.[14] In the most severe cases of the disease fatality rates can exceed 20%, even with intensive care and treatment.[15] In endemic areas, treatment is often less satisfactory and the overall fatality rate for all cases of malaria can be as high as one in ten.[16] Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria.[17] Chronic malaria is seen in both P. vivax and P. ovale, but not in P. falciparum. Here, the disease can relapse months or years after exposure, due to the presence of latent parasites in the liver. Describing a case of malaria as cured by observing the disappearance of parasites from the bloodstream can, therefore, be deceptive. The longest incubation period reported for a P. vivax

infection is 30 years.[14] Approximately one in five of P. vivax malaria cases in temperate areas involve overwintering by hypnozoites (i.e., relapses begin the year after the mosquito bite).[18]

Causes

A Plasmodium sporozoite traverses the cytoplasm of a mosquito midgut epithelial cell in this false-color electron micrograph.

Malaria parasites
Malaria is caused by protozoan parasites of the genus Plasmodium (phylum Apicomplexa). In humans malaria is caused by P. falciparum, P. malariae, P. ovale, P. vivax and P. knowlesi.[19][20] P. falciparum is the most common cause of infection and is responsible for about 80% of all malaria cases, and is also responsible for about 90% of the deaths from malaria.[21] Parasitic Plasmodium species also infect birds, reptiles, monkeys, chimpanzees and rodents.[22] There have been documented human infections with several simian species of malaria, namely P. knowlesi, P. inui, P. cynomolgi,[23] P. simiovale, P. brazilianum, P. schwetzi and P. simium; however, with the exception of P. knowlesi, these are mostly of limited public health importance.[24] Although avian malaria can kill chickens and turkeys, this disease does not cause serious economic losses to poultry farmers.[25] However, since being accidentally introduced by humans it has decimated the endemic birds of Hawaii, which evolved in its absence and lack any resistance to it.[26]

Prevention

Anopheles albimanus mosquito feeding on a human arm. This mosquito is a vector of malaria and mosquito control is a very effective way of reducing the incidence of malaria.

Methods used to prevent the spread of disease, or to protect individuals in areas where malaria is endemic, include prophylactic drugs, mosquito eradication, and the prevention of mosquito bites. The continued existence of malaria in an area requires a combination of high human population density, high mosquito population density, and high rates of transmission from humans to mosquitoes and from mosquitoes to humans. If any of these is lowered sufficiently, the parasite will sooner or later disappear from that area, as happened in North America, Europe and much of Middle East. However, unless the parasite is eliminated from the whole world, it could become re-established if conditions revert to a combination that favors the parasite's reproduction. Many countries are seeing an increasing number of imported malaria cases due to extensive travel and migration. (See Anopheles.) There is currently no vaccine that will prevent malaria, but this is an active field of research. Many researchers argue that prevention of malaria may be more cost-effective than treatment of the disease in the long run, but the capital costs required are out of reach of many of the world's poorest people. Economic adviser Jeffrey Sachs estimates that malaria can be controlled for US$3 billion in aid per year. It has been argued that, in order to meet the Millennium Development Goals, money should be redirected from HIV/AIDS treatment to malaria prevention, which for the same amount of money would provide greater benefit to African economies.[46] The distribution of funding varies among countries. Countries with large populations do not receive the same amount of support. The 34 countries that received a per capita annual support of less than $1 included some of the poorest countries in Africa. Brazil, Eritrea, India, and Vietnam have, unlike many other developing nations, successfully reduced the malaria burden. Common success factors included conducive country conditions, a targeted technical approach using a package of effective tools, data-driven decision-making, active leadership at all levels of government, involvement of communities, decentralized implementation and control of finances, skilled technical and managerial capacity at national and sub-national levels, hands-on technical and programmatic support from partner agencies, and sufficient and flexible financing.[47

Typhoid fever
diseasealso called typhoid

Main

acute infectious disease caused by a specific serotype of the bacterium Salmonella typhi. The bacterium usually enters the body through the mouth by the ingestion of contaminated food or water, penetrates the intestinal wall, and multiplies in lymphoid tissue; it first enters into the bloodstream within 24 to 72 hours, causing septicemia (blood poisoning) and systemic infection. After an average 1014-day incubation period, the early symptoms of typhoid appear: headache, malaise, generalized aching, fever, and restlessness that may interfere with sleep. There may be loss of appetite, nosebleeds, cough, and diarrhea or constipation. Persistent fever develops and gradually rises, usually in a stepwise fashion, reaching a peak of 39 or 40 C (103 or 104 F) after 710 days and continuing with only slight morning remissions for another 1014 days. During about the second week of fever, when typhoid bacilli are present in great numbers in the bloodstream, a rash of small, rose-coloured spots appears on the trunk, lasts four or five days, and then fades away. The lymph follicles (Peyer patches) along the intestinal wall in which the typhoid bacilli have multiplied become inflamed and necrotic and may slough off, leaving ulcers in the walls of the intestine. The dead fragments of intestinal tissue may erode blood vessels, causing hemorrhage, or they may perforate the intestinal wall, allowing the intestines contents to enter the peritoneal cavity (peritonitis). Other complications can include acute inflammation of the gallbladder, heart failure, pneumonia, osteomyelitis, encephalitis, and meningitis. With a continued high fever the symptoms usually increase in intensity, and mental confusion and delirium may appear. By the end of the third week the patient is emaciated, abdominal symptoms are marked, and mental disturbance is prominent. In favourable cases, during about the beginning of the fourth week, the fever begins to decline, the symptoms begin to abate, and the temperature gradually returns to normal. If untreated, typhoid fever proves fatal in up to 25 percent of all cases. Patients with such diseases as cancer or sickle cell anemia are particularly prone to develop serious and prolonged infection with Salmonella. Most major epidemics of typhoid fever have been caused by the pollution of public water supplies. Food and milk may be contaminated, however, by a carrier of the disease who is employed in handling and processing them; by flies; or by the use of polluted water for cleaning purposes. Shellfish, particularly oysters, grown in polluted water and fresh vegetables grown on soil fertilized or contaminated by untreated sewage are possible causes. The prevention of

typhoid fever depends mainly on proper sewage treatment, filtration and chlorination of water, and the exclusion of carriers from employment in food industries and restaurants. In the early part of the 20th century, prophylactic vaccination using killed typhoid organisms was introduced, mainly in military forces and institutions, and contributed to a lowering of the incidence of the disease. Diagnosis of typhoid fever is made by blood culture, stool culture, and serological testing. The treatment of typhoid fever is with antibiotics, particularly chloramphenicol. Chloramphenicol begins to lower the patients fever within three or four days after beginning therapy, and there is progressive improvement thereafter. The drug treatment is continued for several weeks in order to prevent relapses. Typhoid bacteria can persist in the bile passages of patients for an indefinite period of time. These carriers can pass the infection to healthy persons if they practice poor hygiene or if they are food handlers. About 30 percent of persons infected with typhoid fever become transient carriers of the disease, excreting the causative bacteria in the stool or urine for weeks or months. About 5 percent remain long-term carriers, harbouring the microorganisms and shedding them for years. One of the most famous instances of carrier-borne disease in medical history was the case of Typhoid Mary (byname of Mary Mallon). Fifty-one original cases of typhoid and three deaths were directly attributed to her during the early 20th century.