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AISHWARIYA RAI

2012-09-27T20:51:00.002-07:00

DENGUE FEVER

2012-09-27T20:37:00.001-07:00

Dengue fever

Dengue fever (UK /ˈdɛŋɡeɪ/ or US /ˈdɛŋɡiː/), also known as breakbone fever, is an infectious tropical disease caused by the dengue virus. Symptoms include fever, headache, muscle and joint pains, and a characteristic skin rash that is similar to measles. In a small proportion of cases the disease develops into the life-threatening dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and blood plasma leakage, or into dengue shock syndrome, where dangerously low blood pressure occurs.
Dengue is transmitted by several species of mosquito within the genus Aedes, principally A. aegypti. The virus has four different types; infection with one type usually gives lifelong immunity to that type, but only short-term immunity to the others. Subsequent infection with a different type increases the risk of severe complications. As there is no vaccine, prevention is sought by reducing the habitat and the number of mosquitoes and limiting exposure to bites.
Treatment of acute dengue is supportive, using either oral or intravenous rehydration for mild or moderate disease, and intravenous fluids and blood transfusion for more severe cases. The incidence of dengue fever has increased dramatically since the 1960s, with around 50–100 million people infected yearly. Early descriptions of the condition date from 1779, and its viral cause and the transmission were elucidated in the early 20th century. Dengue has become a global problem since the Second World War and is endemic in more than 110 countries. Apart from eliminating the mosquitoes, work is ongoing on a vaccine, as well as medication targeted directly at the virus.

Signs and symptoms

Schematic depiction of the symptoms of dengue fever

Typically, people infected with dengue virus are asymptomatic (80%) or only have mild symptoms such as an uncomplicated fever.^[1]^[2]^[3] Others have more severe illness (5%), and in a small proportion it is life-threatening.^[1]^[3] The incubation period (time between exposure and onset of symptoms) ranges from 3–14 days, but most often it is 4–7 days.^[4] Therefore, travelers returning from endemic areas are unlikely to have dengue if fever or other symptoms start more than 14 days after arriving home.^[5] Children often experience symptoms similar to those of the common cold and gastroenteritis (vomiting and diarrhea),^[6] and generally have less severe symptoms than adults,^[7] but are more susceptible to the severe complications.^[5]

Clinical course

The characteristic symptoms of dengue are sudden-onset fever, headache (typically located behind the eyes), muscle and joint pains, and a rash. The alternative name for dengue, "break-bone fever", comes from the associated muscle and joint pains.^[1]^[8] The course of infection is divided into three phases: febrile, critical, and recovery.^[9]
The febrile phase involves high fever, often over 40 °C (104 °F), and is associated with generalized pain and a headache; this usually lasts two to seven days.^[8]^[9] At this stage, a rash occurs in 50–80% of those with symptoms.^[8]^[10] It occurs in the first or second day of symptoms as flushed skin, or later in the course of illness (days 4–7), as a measles-like rash.^[10]^[11] Some petechiae (small red spots that do not disappear when the skin is pressed, which are caused by broken capillaries) can appear at this point,^[9] as may some mild bleeding from the mucous membranes of the mouth and nose.^[5]^[8] The fever itself is classically biphasic in nature, breaking and then returning for one or two days, although there is wide variation in how often this pattern actually happens.^[11]^[12]
In some people, the disease proceeds to a critical phase, which follows the resolution of the high fever and typically lasts one to two days.^[9] During this phase there may be significant fluid accumulation in the chest and abdominal cavity due to increased capillary permeability and leakage. This leads to depletion of fluid from the circulation and decreased blood supply to vital organs.^[9] During this phase, organ dysfunction and severe bleeding, typically from the gastrointestinal tract, may occur.^[5]^[9] Shock (dengue shock syndrome) and hemorrhage (dengue hemorrhagic fever) occur in less than 5% of all cases of dengue,^[5] however those who have previously been infected with other serotypes of dengue virus ("secondary infection") are at an increased risk.^[5]^[13]
The recovery phase occurs next, with resorption of the leaked fluid into the bloodstream.^[9] This usually lasts two to three days.^[5] The improvement is often striking, but there may be severe itching and a slow heart rate.^[5]^[9] Another rash may occur with either a maculopapular or a vasculitic appearance, which is followed by peeling of the skin.^[14] During this stage, a fluid overload state may occur; if it affects the brain, it may cause a reduced level of consciousness or seizures.^[5] A feeling of fatigue may last for weeks afterwards.^[14]

Associated problems

Dengue can occasionally affect several other body systems,^[9] either in isolation or along with the classic dengue symptoms.^[6] A decreased level of consciousness occurs in 0.5–6% of severe cases, which is attributable either to infection of the brain by the virus or indirectly as a result of impairment of vital organs, for example, the liver.^[6]^[12]
Other neurological disorders have been reported in the context of dengue, such as transverse myelitis and Guillain-Barré syndrome.^[6] Infection of the heart and acute liver failure are among the rarer complications.^[5]^[9]

Cause

Virology

Main article: Dengue virus

A TEM micrograph showing dengue virus virions (the cluster of dark dots near the center)

Dengue fever virus (DENV) is an RNA virus of the family Flaviviridae; genus Flavivirus. Other members of the same genus include yellow fever virus, West Nile virus, St. Louis encephalitis virus, Japanese encephalitis virus, tick-borne encephalitis virus, Kyasanur forest disease virus, and Omsk hemorrhagic fever virus.^[12] Most are transmitted by arthropods (mosquitoes or ticks), and are therefore also referred to as arboviruses (arthropod-borne viruses).^[12]
The dengue virus genome (genetic material) contains about 11,000 nucleotide bases, which code for the three different types of protein molecules (C, prM and E) that form the virus particle and seven other types of protein molecules (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5) that are only found in infected host cells and are required for replication of the virus.^[13]^[15] There are four strains of the virus, which are called serotypes, and these are referred to as DENV-1, DENV-2, DENV-3 and DENV-4.^[2] All four serotypes can cause the full spectrum of disease.^[13] Infection with one serotype is believed to produce lifelong immunity to that serotype but only short term protection against the others.^[2]^[8]
The severe complications on secondary infection occurs particularly if someone previously exposed to serotype DENV-1 then contracts serotype DENV-2 or serotype DENV-3, or if someone previously exposed to type DENV-3 then acquires DENV-2.^[15]

Transmission

The mosquito Aedes aegypti feeding off a human host

Dengue virus is primarily transmitted by Aedes mosquitoes, particularly A. aegypti.^[2] These mosquitoes usually live between the latitudes of 35° North and 35° South below an elevation of 1,000 metres (3,300 ft).^[2] They bite primarily during the day.^[16] Other Aedes species that transmit the disease include A. albopictus, A. polynesiensis and A. scutellaris.^[2] Humans are the primary host of the virus,^[2]^[12] but it also circulates in nonhuman primates.^[17] An infection can be acquired via a single bite.^[18] A female mosquito that takes a blood meal from a person infected with dengue fever becomes itself infected with the virus in the cells lining its gut. About 8–10 days later, the virus spreads to other tissues including the mosquito's salivary glands and is subsequently released into its saliva. The virus seems to have no detrimental effect on the mosquito, which remains infected for life. Aedes aegypti prefers to lay its eggs in artificial water containers, to live in close proximity to humans, and to feed off people rather than other vertebrates.^[19]
Dengue can also be transmitted via infected blood products and through organ donation.^[20]^[21] In countries such as Singapore, where dengue is endemic, the risk is estimated to be between 1.6 and 6 per 10,000 transfusions.^[22] Vertical transmission (from mother to child) during pregnancy or at birth has been reported.^[23] Other person-to-person modes of transmission have also been reported, but are very unusual.^[8]

Predisposition

Severe disease is more common in babies and young children, and in contrast to many other infections it is more common in children that are relatively well nourished.^[5] Women are more at risk than men.^[15] Dengue can be life-threatening in people with chronic diseases such as diabetes and asthma.^[15]
Polymorphisms (normal variations) in particular genes have been linked with an increased risk of severe dengue complications. Examples include the genes coding for the proteins known as TNFα, mannan-binding lectin,^[1] CTLA4, TGFβ,^[13] DC-SIGN, and particular forms of human leukocyte antigen.^[15] A common genetic abnormality in Africans, known as glucose-6-phosphate dehydrogenase deficiency, appears to increase the risk.^[24] Polymorphisms in the genes for the vitamin D receptor and FcγR seem to offer protection against severe disease in secondary dengue infection.^[15]

Mechanism

When a mosquito carrying dengue virus bites a person, the virus enters the skin together with the mosquito's saliva. It binds to and enters white blood cells, and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing a number of signaling proteins, such as interferon, which are responsible for many of the symptoms, such as the fever, the flu-like symptoms and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow) can be affected, and fluid from the bloodstream leaks through the wall of small blood vessels into body cavities. As a result, less blood circulates in the blood vessels, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction of the bone marrow leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue fever.^[24]

Viral replication

Once inside the skin, dengue virus binds to Langerhans cells (a population of dendritic cells in the skin that identifies pathogens).^[24] The virus enters the cells through binding between viral proteins and membrane proteins on the Langerhans cell, specifically the C-type lectins called DC-SIGN, mannose receptor and CLEC5A.^[13] DC-SIGN, a non-specific receptor for foreign material on dendritic cells, seems to be the main point of entry.^[15] The dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is replicated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the cell's protein synthesis apparatus produces new viral proteins, and the viral RNA is copied. Immature virus particles are transported to the Golgi apparatus, the part of the cell where some of the proteins receive necessary sugar chains (glycoproteins). The now mature new viruses bud on the surface of the infected cell and are released by exocytosis. They are then able to enter other white blood cells, such as monocytes and macrophages.^[13]
The initial reaction of infected cells is to produce interferon, a cytokine that raises a number of defenses against viral infection through the innate immune system by augmenting the production of a large group of proteins mediated by the JAK-STAT pathway. Some serotypes of dengue virus appear to have mechanisms to slow down this process. Interferon also activates the adaptive immune system, which leads to the generation of antibodies against the virus as well as T cells that directly attack any cell infected with the virus.^[13] Various antibodies are generated; some bind closely to the viral proteins and target them for phagocytosis (ingestion by specialized cells and destruction), but some bind the virus less well and appear instead to deliver the virus into a part of the phagocytes where it is not destroyed but is able to replicate further.^[13]

Severe disease

Further information: Antibody-dependent enhancement

It is not entirely clear why secondary infection with a different strain of dengue virus places people at risk of dengue hemorrhagic fever and dengue shock syndrome. The most widely accepted hypothesis is that of antibody-dependent enhancement (ADE). The exact mechanism behind ADE is unclear. It may be caused by poor binding of non-neutralizing antibodies and delivery into the wrong compartment of white blood cells that have ingested the virus for destruction.^[13]^[15] There is a suspicion that ADE is not the only mechanism underlying severe dengue-related complications,^[1] and various lines of research have implied a role for T cells and soluble factors such as cytokines and the complement system.^[24]
Severe disease is marked by two problems: dysfunction of endothelium (the cells that line blood vessels) and disordered blood clotting.^[6] Endothelial dysfunction leads to the leakage of fluid from the blood vessels into the chest and abdominal cavities, while coagulation disorder is responsible for the bleeding complications. Higher viral load in the blood and involvement of other organs (such as the bone marrow and the liver) are associated with more severe disease. Cells in the affected organs die, leading to the release of cytokines and activation of both coagulation and fibrinolysis (the opposing systems of blood clotting and clot degradation). These alterations together lead to both endothelial dysfunction and coagulation disorder.^[24]

Diagnosis

Warning signs^[25]
Abdominal pain
Ongoing vomiting
Liver enlargement
Mucosal bleeding
High hematocrit with low platelets
Lethargy

The diagnosis of dengue is typically made clinically, on the basis of reported symptoms and physical examination; this applies especially in endemic areas.^[1] However, early disease can be difficult to differentiate from other viral infections.^[5] A probable diagnosis is based on the findings of fever plus two of the following: nausea and vomiting, rash, generalized pains, low white blood cell count, positive tourniquet test, or any warning sign (see table) in someone who lives in an endemic area.^[25] Warning signs typically occur before the onset of severe dengue.^[9] The tourniquet test, which is particularly useful in settings where no laboratory investigations are readily available, involves the application of a blood pressure cuff for five minutes, followed by the counting of any petechial hemorrhages; a higher number makes a diagnosis of dengue more likely.^[9]
The diagnosis should be considered in anyone who develops a fever within two week of being in the tropics or subtropics.^[14] It can be difficult to distinguish dengue fever and chikungunya, a similar viral infection that shares many symptoms and occurs in similar parts of the world to dengue.^[8] Often, investigations are performed to exclude other conditions that cause similar symptoms, such as malaria, leptospirosis, typhoid fever, and meningococcal disease.^[5]
The earliest change detectable on laboratory investigations is a low white blood cell count, which may then be followed by low platelets and metabolic acidosis.^[5] In severe disease, plasma leakage results in hemoconcentration (as indicated by a rising hematocrit) and hypoalbuminemia.^[5] Pleural effusions or ascites can be detected by physical examination when large,^[5] but the demonstration of fluid on ultrasound may assist in the early identification of dengue shock syndrome.^[1]^[5] The use of ultrasound is limited by lack of availability in many settings.^[1]

Classification

The World Health Organization's 2009 classification divides dengue fever into two groups: uncomplicated and severe.^[1]^[25] This replaces the 1997 WHO classification, which needed to be simplified as it had been found to be too restrictive, though the older classification is still widely used.^[25] The 1997 classification divided dengue into undifferentiated fever, dengue fever, and dengue hemorrhagic fever.^[5]^[26] Dengue hemorrhagic fever was subdivided further into grades I–IV. Grade I is the presence only of easy bruising or a positive tourniquet test in someone with fever, grade II is the presence of spontaneous bleeding into the skin and elsewhere, grade III is the clinical evidence of shock, and grade IV is shock so severe that blood pressure and pulse cannot be detected.^[26] Grades III and IV are referred to as "dengue shock syndrome".^[25]^[26]

Laboratory tests

Dengue fever may be diagnosed by microbiological laboratory testing.^[25] This can be done by virus isolation in cell cultures, nucleic acid detection by PCR, viral antigen detection or specific antibodies (serology).^[15]^[27] Virus isolation and nucleic acid detection are more accurate than antigen detection, but these tests are not widely available due to their greater cost.^[27] All tests may be negative in the early stages of the disease.^[5]^[15] PCR and viral antigen detection are more accurate in the first seven days.^[14] A PCR test that can run on equipment also used to diagnose influenza was introduced in 2012 and will make PCR testing more accessible.^[28]
These laboratory tests are only of diagnostic value during the acute phase of the illness with the exception of serology. Tests for dengue virus-specific antibodies, types IgG and IgM, can be useful in confirming a diagnosis in the later stages of the infection. Both IgG and IgM are produced after 5–7 days. The highest levels (titres) of IgM are detected following a primary infection, but IgM is also produced in secondary and tertiary infections. The IgM becomes undetectable 30–90 days after a primary infection, but earlier following re-infections. IgG, by contrast, remains detectable for over 60 years and, in the absence of symptoms, is a useful indicator of past infection. After a primary infection the IgG reaches peak levels in the blood after 14–21 days. In subsequent re-infections, levels peak earlier and the titres are usually higher. Both IgG and IgM provide protective immunity to the infecting serotype of the virus. In the laboratory test the IgG and the IgM antibodies can cross-react with other flaviviruses, such as yellow fever virus, which can make the interpretation of the serology difficult.^[8]^[15]^[29] The detection of IgG alone is not considered diagnostic unless blood samples are collected 14 days apart and a greater than fourfold increase in levels of specific IgG is detected. In a person with symptoms, the detection of IgM is considered diagnostic.^[29]

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2012-09-26T06:10:00.001-07:00

DENTAL PLAQUE

2012-09-26T04:47:00.000-07:00

Dental plaque is a biofilm, usually a pale yellow, that develops naturally on the teeth. Like any biofilm, dental plaque is formed by colonizing bacteria trying to attach themselves to a smooth surface (of a tooth).^[1] It has been speculated that plaque forms part of the defense systems of the host by helping to prevent colonization by microorganisms which may be pathogenic.^[2]
The oral cavity contains the only known anatomical aspect of the human body that does not have a regulated system of shedding surfaces: the teeth. This allows a numerous amount of microorganisms to adhere to the surface of teeth for long periods of time.^[3] These multiple species of bacteria become dental biofilm. Dental biofilm, more commonly referred to as dental plaque, is composed of about a thousand species of bacteria that take part in the complex ecosystems of the mouth. The natural, non-frequent regulation of tooth shedding plays a large role in making dental biofilm the most diverse biofilm in the human body despite the relatively small size of the teeth.
The human oral cavity is also called the human oral microbiome. This is because the human oral cavity can contain several environments at a given moment that could vary from tooth to tooth.^[4] Additionally it has been estimated that the number of bacteria that reside in the mouth is about 25,000 species of bacteria.^[5] This is in contrast to the previously estimated 700+species.^[4] Studies have found that out of the 25,000 species that exist in the oral cavity, about 1000 species can exist as part of the dental biofilm ecosystem.^[6] This is also in contrast to the previous estimate of more than 500 species as part of the dental biofilm.^[7] These 1,000 species have the ability to change their environment through a series of biotic relationships.
At first, the biofilm is soft enough to come off by using finger nail. However, it starts to harden within 48 hours, and in about 10 days the plaque becomes dental calculus (tartar) hard and difficult to remove.^{[citation needed]}
Dental plaque can give rise to dental caries (tooth decay)—the localised destruction of the tissues of the tooth by acid produced from the bacterial degradation of fermentable sugars^[2]—and periodontal problems such as gingivitis and chronic periodontitis.

Basic plaque formation

Microscopic view of some of the bacteria of which plaque is composed. Numbered ticks are 10 µm apart.

The mechanisms of plaque formation include:^[2]

Adsorption of proteins and bacteria to form a film on the tooth surface.
The effect of van der Waals and electrostatic forces between microbial surfaces and the film to create reversible adhesion to the teeth.
Irreversible adhesion due to intermolecular interactions between cell surfaces and the pellicle.
Secondary colonisers attach to primary colonisers by intermolecular interaction.
The cells divide and generate a biofilm.

Microorganisms

As previously mentioned there are about 1,000 out of the 25,000 species of bacteria that are involved with the formation of dental biofilm. Due to this fairly large number there is fierce competition among the bacteria present on dental biofilm for nutrients present in the mouth. Only about fifty percent of the 1,000 species have been cultured for study.^[6] Scientists at the Forsyth Institute in Cambridge, Massachusetts have begun the Human Oral Microbiome Project to identify bacteria and study the complex ecosystems of the mouth. On their website, one can find information about the identified organisms as well as the method being utilized to identify the organisms.

Environment

The ecological factors provided by the environment of the oral cavity are directly proportional to the species richness and species biodiversity of the microorganisms that reside on the teeth.^[3] The main ecological factors are pH, saliva, temperature and redox reactions.^[3]^[8] The majority of microbial organisms prefer neutral pH levels (pH 7). Saliva acts as a buffer, maintaining the pH in the mouth between 6.75 and 7.25.^[3] In addition to acting as a buffer, saliva is also a main source of nutrients for the thousands of bacteria (note: gingival crevicular fluid is also a nutrient source but a smaller one ). A two degree (ºC) change has been shown to drastically shift the dominant species in the plaque.^[8] The normal temperature of the mouth ranges from 35ºC to 36ºC (Marsh). Redox reactions are carried out by aerobic bacteria. This keeps the oxygen levels in the mouth at a semi-stable homeostatic condition. This allows other bacteria to survive, which will be discussed in the next section.^[8]

Biotic relationships

The microorganisms in the oral cavity live with one another in commensal or mutualistic symbiotic relationships.^[3] Typically, anaerobic bacteria would succumb to high levels of oxygen, but with the redox reactions discussed in the previous section they are able to survive. This commensal relationship allows a mixture of aerobic and anaerobic bacteria to live in the same area. The formation begins by the adsorption of early colonizers onto an acquired pellicle through chemical processes.^[9] An acquired pellicle is a layer of saliva that is composed of mainly glycoproteins and forms shortly after cleaning of the teeth or exposure of new teeth.^[9] These bound early colonizers manipulate the environment for the immediate benefit of other bacteria. Once the environment has been manipulated other bacterial colonizers are able to co-adhere to the early colonizers. This is done repeatedly resulting in layers of bacteria. Once new bacterial cells co-adhere to one another they gain the ability to communicate to one another. They are able to communicate to one another through a biochemical process called quorum –sensing.^[6] Quorum –sensing virtually allows all the bacteria to benefit from one another. This ability can allow a bacterium to feel the presence of other bacteria around it. Due to this communication, bacteria have the ability to change their genotype (and thus their phenotype) as a result of population concentration and/or environmental changes to remain as competent competitors.^[10] These relationships tend to exhibit homeostasis until there is some type of disruption in the ecosystem.
The most common reasons for ecosystem disruption are the ecological factors that were discussed in the environment section. The bacteria that exhibits the most fit plasticity for the change in environment dominates the given environment. Often, this could lead to opportunistic pathogens that lead to dental caries and periodontal disease. Pathogens that have the potential to cause dental caries flourish in acidic environments. Pathogenic bacteria that have the potential to cause periodontal disease flourish in a slightly alkaline environment.^[11]

Components of plaque

Plaque consists of microorganisms and extracellular matrix.
The microorganisms that form the biofilm are mainly Streptococcus mutans and anaerobes, with the composition varying by location in the mouth. Examples of such anaerobes include fusobacterium and actinobacteria.
The extracellular matrix contains proteins, long chain polysaccharides and lipids.
The microorganisms present in dental plaque are all naturally present in the oral cavity, and are normally harmless. However, failure to remove plaque by regular tooth brushing means that they are allowed to build up in a thick layer. Those microorganisms nearest the tooth surface ferment dietary sucrose; it is in this state that they start to produce acids.

Acids released from dental plaque lead to demineralization of the adjacent tooth surface, and consequently to dental caries. Saliva is also unable to penetrate the build-up of plaque and thus cannot act to neutralize the acid produced by the bacteria and remineralize the tooth surface.
They also cause irritation of the gums around the teeth that could lead to gingivitis, periodontal disease and tooth loss.
Plaque build up can also become mineralized and form calculus (tartar).

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2012-09-24T01:18:00.001-07:00

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DIYA AUR BAATI HUM 21 SEP 2012

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DIYA AUR BAATI HUM 18 SEP 2012 PART 4

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