CHIKUNGUNYA VIRUS IN INDIA

CHIKUNGUNYA VIRUS IN INDIA

Chikungunya is a relatively rare form of viral fever caused by an alpha virus (RNA Virus) that is spread by the bite of an infected Aedes aegypti mosquito. The virus is classified under arboviruses which are transmitted by arthropod vectors.

The name is derived from the Makonde word meaning “ that which bends up” in reference to the stooped posture developed as a result of the arthritic symptoms of the disease. The disease was first described in 1952 following an outbreak on the Makonde plateau along the border between Tanganyika and Mozambique.

Chikungunya virus was first isolated from Indian subcontinent in 1963 from Calcutta, since then there have been several reports of Chikungunya virus infection in different parts of India. The last outbreak of Chikungunya virus infection occurred in India in 1971. subsequently the virus had ‘disappreared’ from the subcontinent. However, recent reports of large scale outbreak of fever caused by Chikungunya virus infection in several parts of South India have confirmed the reemergence of this virus.

The symptoms of this infection include abrupt onset of fever, chills, headache and severe joint pain with or without swelling (usually the smaller joints), low back pain and rash. The symptoms are most often clinically indistinguishable from those observed in dengue fever. Therefore it is very important to clinically distinguish Dengue from Chikungunya virus infection. Unlike Dengue Hemorrhagic manifestations are relatively rare and as a rule shock is not observed in Chikungunya virus infection. Most often Chikungunya is a self limiting febrile illness. However, neurological complications such as meningoencephalitis and mother to child transmission has been observed.

The precise reasons for the reemergence of Chikungunya in the Indian subcontinent in not known. Although it is well recognized that reemergence of viral infection are due to a variety of social, environmental, behavioral and biological changes. The challenge faced during this large outbreak in the country has been the lack of rapid diagnostic facilities. Although, the National Institute of Virology at Pune, has been a great help in determining the etiology of the outbreak, relying on one institute in the country to render diagnostic help for case management would be a foolish task. It would be therefore desirable to ensure that several virology laboratories in the country are enrolled and networked to deliver rapid diagnosis in large outbreak such as this as well other emerging viral infections like Chandipura and Avian Influenza.

PRINCE.C.P
Lecturer in Microbiology

GLOBAL WARMING

WHAT IS GLOBAL WARMING?
Carbon dioxide and other gases warm the surface of the planet naturally by trapping solar heat in the atmosphere. This is a good thing because it keeps our planet habitable. However, by burning fossil fuels such as coal, gas and oil and clearing forests we have dramatically increased the amount of carbon dioxide in the Earth’s atmosphere and temperatures are rising.
The vast majority of scientists agree that global warming is real, it’s already happening and that it is the result of our activities and not a natural occurrence. The evidence is overwhelming and undeniable.
We’re already seeing changes. Glaciers are melting, plants and animals are being forced from their habitat, and the number of severe storms and droughts is increasing.
The number of Category 4 and 5 hurricanes has almost doubled in the last 30 years.
Malaria has spread to higher altitudes in places like the Colombian Andes, 7,000 feet above sea level.
The flow of ice from glaciers in Greenland has more than doubled over the past decade.
At least 279 species of plants and animals are already responding to global warming, moving closer to the poles.
If the warming continues, we can expect catastrophic consequences.
Deaths from global warming will double in just 25 years -- to 300,000 people a year.
Global sea levels could rise by more than 20 feet with the loss of shelf ice in Greenland and Antarctica, devastating coastal areas worldwide.
Heat waves will be more frequent and more intense.
Droughts and wildfires will occur more often.
The Arctic Ocean could be ice free in summer by 2050.
More than a million species worldwide could be driven to extinction by 2050.
There is no doubt we can solve this problem. In fact, we have a moral obligation to do so. Small changes to your daily routine can add up to big differences in helping to stop global warming. The time to come together to solve this problem is now – TAKE ACTION

malayalam kavitha

കക്കൊസില് തൂറാം

പട്ടരുകുട്ടി തൂറാന്‍ പോയി
കുണ്ടിയിന്മേല്‍ തേള്‍ കുത്തി
പട്ടരുകുട്ടി കരഞ്ഞു പോയി
പാവം പാവം പട്ടരുകുട്ടി .

prion diseases

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Entamoeba histolytica

Several protozoan species in the genus Entamoeba infect humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba, associated with intestinal and extra intestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.
Life Cycle:
Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ( : noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ( : intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ( : extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).
Geographic Distribution:Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.
Clinical Features:A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions).
Laboratory Diagnosis:Entamoeba histolytica must be differentiated from other intestinal protozoa including: E. coli, E. hartmanni, E. gingivalis, Endolimax nana, and Iodamoeba buetschlii (the nonpathogenic amebas); Dientamoeba fragilis (which is a flagellate not an ameba); and the possibly pathogenic Entamoeba polecki. Differentiation is possible, but not always easy, based on morphologic characteristics of the cysts and trophozoites. The nonpathogenic Entamoeba dispar, however, is morphologically identical to E. histolytica, and differentiation must be based on isoenzymatic or immunologic analysis. Molecular methods are also useful in distinguishing between E. histolytica and E. dispar and can also be used to identify E. polecki. Microscopic identification of cysts and trophozoites in the stool is the common method for diagnosing E. histolytica. This can be accomplished using:
§ Fresh stool: wet mounts and permanently stained preparations (e.g., trichrome).
§ Concentrates from fresh stool: wet mounts, with or without iodine stain, and permanently stained preparations (e.g., trichrome). Concentration procedures, however, are not useful for demonstrating trophozoites.
In addition, E. histolytica trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
Diagnostic findings:
§ Microscopy
§ Immunodiagnosis
§ Molecular methods for discriminating between E. histolytica and E. dispar
§ Morphologic comparison with other intestinal parasites
§ Bench aid for E. histolytica

Treatment:For asymptomatic infections, iodoquinol, paromomycin, or diloxanide furoate (not commercially available in the U.S.) are the drugs of choice. For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess), the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanide furoate



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