Tuesday, 4 March 2014

DMO'S CIRCULAR ON NETRABHISHYANDAM - MANAGEMENT

SUMMER STRIKES WITH DISEASES OF EYES DUE TO PITHA KOPA. INCIDENCE OF CONJUNCTIVITIS WERE REPORTED FROM SEVERAL PLACES. TO PREVENT AND CONTROL EYE DISEASES OF SUCH KIND, PLEASE FOLLOW THE TREATMENT PROTOCOL MENTIONED IN DMO'S CIRCULAR GIVEN BELOW-


Saturday, 1 March 2014

TASKFORCE MEETING HELD ON 24/02/2014 TOOK DECISIONS TO REVAMP..

 MEETING HELD UNDER THE CHAIRMANSHIP OF DMO(ISM) DR.RATHI.B.UNNITHAN, ON 24/02/2014 AND TOOK DECISIONS TO REVAMP ISM TASK FORCE. DISCUSSED ABOUT THE STRATEGY AND RESTRUCTURED ACTION PLAN FOCUSING ON MEASURES TO INCREASE 'VYADHIKSHAMATHWAM' (IMMUNITY) AND 1000 AWARENESS CLASSES NAMED AS "POORNASREE".

Monday, 24 February 2014

RECENT MEDICAL CAMPS


RECENT MEDICAL CAMPS-


1.   21/12/2014, GAD- THIRUVARPU- 
PREVENTIVE CAMP FOR JAPANESE ENCEPHALITIS

PARTICIPANTS-  

DR.EENA .D - GAD THIRUVARPU(CAMP CONVENER)
DR.SMITHA.T.V. - GAD  VELOOR

2.   22/12/2014, GAD-AYMANAM

PARTICIPANTS- 

DR.MIDHUN J.KALLOOR -NRHM GAD AYMANAM(CAMP CONVENER)
DR.TNTU JOSEPH-   NRHM GAD-KALLARA
DR.SMITHA.G.PANICKER- NRHM GAD THALAYOLAPARAMBU








Sunday, 16 February 2014


Now It is the turn of Japanese encephalitis. Low lying areas of Kottayam district  are prone to Japanese encephalitis where it has already reported one death in Thiruvarpu panchayath .The virus which- spreads through Culex mosquitoes, can be eliminated only by the body's immune system. A person suffers from high fever, convulsions and coma after being bitten by an infected mosquito. 


DMO DR.RATHI B.UNNITHAN VISITED JAPANESE ENCEPHALITIS REPORTED AREA IN THIRUVARPU PANCHAYATH, KOTTAYM AND AFTER A SURVEY,TOOK NECESSARY MEASURES TO CURB THE ILLNESS BY NATURAL REMEDIES WHICH BOOSTS OUR IMMUNE SYSTEM, SUPPLIED 'APARAJITHA DOOMA CHHORNAM' TO THE NEIGHBOURS OF THE  DECEASED AND ARRANGED A MEDICAL CAMP NEXT WEEK. THIS AREA IS AN ABODE OF MIGRATORY BIRDS WHICH MAY HAVE PLAYED A ROLE IN TRANSMISSION OF THE DISEASE..SHE HAD DISCUSSED THE MATTER WITH GRAMA PANCHAYATH PRESIDENT , WARD MEMBER ,ASHA WORKERS...







GEOGRAPHIC DISTRIBUTION OF J.E.


Japanese Encephalitis- in brief

Most human infections with JE virus are asymptomatic; <1% of people infected with JE virus develop clinical disease. Acute encephalitis is the most commonly recognized clinical manifestation of JE virus infection. Milder forms of disease, such as aseptic meningitis or undifferentiated febrile illness, can also occur. The incubation period is 5–15 days. Illness usually begins with sudden onset of fever, headache, and vomiting. Mental status changes, focal neurologic deficits, generalized weakness, and movement disorders may develop over the next few days.
  • The classical description of JE includes a parkinsonian syndrome with masklike facies, tremor, cogwheel rigidity, and choreoathetoid movements.
  • Acute flaccid paralysis, with clinical and pathological features similar to those of poliomyelitis, has also been associated with JE virus infection.
  • Seizures are common, especially among children.
  • Common clinical laboratory findings include moderate leukocytosis, mild anemia, and hyponatremia. Cerebrospinal fluid (CSF) typically has a mild to moderate pleocytosis with a lymphocytic predominance, slightly elevated protein, and normal ratio of CSF to plasma glucose.
The case-fatality ratio is approximately 20%–30%. Among survivors, 30%–50% have serious neurologic, cognitive, or psychiatric sequelae.
JE should be suspected in a patient with evidence of a neurologic infection (such as encephalitis, meningitis, or acute flaccid paralysis) who has recently traveled to or resided in an endemic country in Asia or the western Pacific. Laboratory diagnosis of JE virus infection should be performed by using a JE virus–specific IgM-capture ELISA on CSF or serum. JE virus–specific IgM can be measured in the CSF of most patients by 4 days after onset of symptoms and in serum by 7 days after onset. A ≥4-fold rise in JE virus–specific neutralizing antibodies between acute- and convalescent-phase serum specimens may be used to confirm the diagnosis. Vaccination history, date of onset of symptoms, and information regarding other flaviviruses known to circulate in the geographic area that may cross-react in serologic assays need to be considered when interpreting results.
Humans have low levels of transient viremia and usually have neutralizing antibodies by the time distinctive clinical symptoms are recognized. Virus isolation and nucleic-acid amplification tests are insensitive in detecting JE virus or viral RNA in blood or CSF and should not be used for ruling out a diagnosis of JE. Clinicians should contact their state or local health department or CDC at 970-221-6400 for assistance with diagnostic testing.
There is no specific antiviral treatment for JE; therapy consists of supportive care and management of complications.

Most human infections with JE virus are asymptomatic; <1% of people infected with JE virus develop clinical disease. Acute encephalitis is the most commonly recognized clinical manifestation of JE virus infection. Milder forms of disease, such as aseptic meningitis or undifferentiated febrile illness, can also occur. The incubation period is 5–15 days. Illness usually begins with sudden onset of fever, headache, and vomiting. Mental status changes, focal neurologic deficits, generalized weakness, and movement disorders may develop over the next few days.
  • The classical description of JE includes a parkinsonian syndrome with masklike facies, tremor, cogwheel rigidity, and choreoathetoid movements.
  • Acute flaccid paralysis, with clinical and pathological features similar to those of poliomyelitis, has also been associated with JE virus infection.
  • Seizures are common, especially among children.
  • Common clinical laboratory findings include moderate leukocytosis, mild anemia, and hyponatremia. Cerebrospinal fluid (CSF) typically has a mild to moderate pleocytosis with a lymphocytic predominance, slightly elevated protein, and normal ratio of CSF to plasma glucose.
The case-fatality ratio is approximately 20%–30%. Among survivors, 30%–50% have serious neurologic, cognitive, or psychiatric sequelae.
JE should be suspected in a patient with evidence of a neurologic infection (such as encephalitis, meningitis, or acute flaccid paralysis) who has recently traveled to or resided in an endemic country in Asia or the western Pacific. Laboratory diagnosis of JE virus infection should be performed by using a JE virus–specific IgM-capture ELISA on CSF or serum. JE virus–specific IgM can be measured in the CSF of most patients by 4 days after onset of symptoms and in serum by 7 days after onset. A ≥4-fold rise in JE virus–specific neutralizing antibodies between acute- and convalescent-phase serum specimens may be used to confirm the diagnosis. Vaccination history, date of onset of symptoms, and information regarding other flaviviruses known to circulate in the geographic area that may cross-react in serologic assays need to be considered when interpreting results.
Humans have low levels of transient viremia and usually have neutralizing antibodies by the time distinctive clinical symptoms are recognized. Virus isolation and nucleic-acid amplification tests are insensitive in detecting JE virus or viral RNA in blood or CSF and should not be used for ruling out a diagnosis of JE. Clinicians should contact their state or local health department or CDC at 970-221-6400 for assistance with diagnostic testing.
There is no specific antiviral treatment for JE; therapy consists of supportive care and management of complications.