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Sep25
RECENT ADVANCES IN TREATMENT OF AIDS /HIV PATIENTS
RECENT ADVANCES IN TREATMENT OF HIV/AIDS PATIENTS
-----DR.D.R.NAKIPURIA
AIDS is acquired immunodeficiency syndrome comprises of many symptoms and signs (different complains of patients and many thing evaluated by Doctor on examination)of Patient suffering from HIV,Hunam Immunedeficiency Virus.AS THE NAME SUGGEST OUR DEFENCE SYSTEM or Immune system is paralysed or made less responsive(measured in this infection by determining CD4 Count from Blood examination as a type of Lymphocyte fighting with invasion of HIV in our Body) whenever any infection of Bacteria,Virus,Fungus or parasite invade our body as a result infection can occur in any part of our body and as primary resistance from our Body System is weak,infection spreads more and more resulting in further growth of invading microbes and this HIV virus too(measured by Viral Load as Copies of Virus in Blood and susceptibility to drugs by sensitivity test).Therefore development of Anti Retro Virus (as HIV is Retrovirus) medicines has developed which once started raise immune system CD4 count by checking further growth of HIV virus and prevent infection by other Microbes(Oppurtinistic Infections) but as we know more and more about these medicines and their side effects and different Oppurtinistic Infections,WHO put some best guidelines when to start these medicines in HIV patients as in Year 2006 ART was to be started if CD4 count is below or 200 but in 2010 it is upto 350 But Amercan Journal suggest it upto 500 when patient is symptomatic or in stage I and II as per WHO staging(Patients with less grade of infections)but in stageIII and Stage IV patients or patients with severe form of disease or seriously ill as suffering from TB,Meningitis,Kidney or Cardiomyopathy,Chest or GI tract infections does not require any estimation of CD4 count as this is presumed and fact that their CD4 count is below 350 or 200 and ART or Better called HAART Medicines immediately.In case of TB patients ATT should be started after start of ART generally within 2-8 wks to avoid IRIS or any adverse reaction,those on HAART developing TB ,ART should be started immediately(with efavirenz except children below 03 yrs of age and first trimester pregnancy).In case of Pregnant Patient same module is practised ,in patients suffering with Hepatitis B or C patients,like TB, ART should be started immediately without any staging or delay of 2-8 wks.In case of Childrens too now same strategy is applied but here CD4 count varies according to age groups,we can start ART immediately in stage III and IV in infant or children upto 12 yrs of age but in Infants and children up to 2yrs of age no need of checking CD4 count start ART if patient is sytomatic or is diagnosed as HIV patients,even in infants now ART may be started if we strongly clinically suspect HIV (As Mother strongly positive or both parents positive or breast fed positive mother children etc) but in early age from 2-5 yrs reduction of CD4 count up to 750 or % of CD4 count below 25 but above 05 yrs criteria is 350 for stage I and II . In Developed countries Art is being started CD4 count upto 500 or less above 05 yrs and adult.CD4 count was previously estimated every 06 months but now at every 03 months and if it is not raising considered as immunological failure and Viral load to be done before starting therapy and also at 3-6 months to see copies below 5000/ml it is raising then drug sensitivity test is done and if not possible then IInd Line drug is started,if IInd line drug started then now a days IIIrd line drug is started.In pregnancy either mother exposed to AER earlier or not ART started in first trimester(avoiding Efavirez) with drug regime and is continued life long unlike nevirapine during labor or Zidovudine regime only,Zidovudine and Nevirapine found good in CD4 count between 250-350.
Now HAART medicines has been slightly modified,Two NRTIs and one NNRTIs is still practised to check drug resistance by Virus mutation but instead of dT4(Stavudine 30 or 40 as per wt above or below 60kg causing severe lididolysis or peripheral neuropathy,pancreatitis ) now3TC(Lamivudine)+AZT/ZDV(Zadivudine causing severe anaemia or neutropenia ) or 3TC + TDF(Tedofil,causing nephropathy and calcinosis ) or TDF + FTC (Emcritabine),AZT+ FTC(causing hepatitis) so 3TC+ AZT+NVP(causing hepatitis and stevenson Zhonson syndrome) or 3TC+AZT+EFV (Efavirenz)or 3TC+TDF+NVP(Nevirapine) or EFV is preferred ,even Simple FTC+NVP or FTC+ EFV is preferred.here Abacavir (ABC) or Diadanosine (ddi) is also used as NRTIS but combination like Stavudine+Zaduvidine,3TC+FTC or AZT+TDF or dt4+Abacavir is not used . Incase of Tuberculosis patients,Efavirenz is given not NVP except when patient is child below 03 yrs or Ist trimester pregnant or under Psychotic condition or medicines.If possible and patient can afford Rifabutine may be started in ATT instead of Rifampcin but mostly if patient is not renal compromised or under hepatic pathology simple ATT is good.In Resistant cases(increase in viral load,less cd4 count or drug resistance)IInd line drug of 03 drugs combination is started here one protease inhibitor(Liponavir(LPV) / Squanavir(SQR)/ Indinavir(IDV) /Atazanavir(ATV) /Fosamprenavir(FPV) / Darunavir(DRV) /Etarvine(ETV) with boosted Ritonavir(r)or plain Ritonavir(RTV) is used and along with this in TB patients with Rifampcin dose of protease inhibitor like Lopinavir+ boosted ritonavir(LPV/r) or Squanavir +Boosted Ritonavir or Indinavir + boosted Ritonavir is increased but with Rifabutine no dose adjustment is done.Instead of using NRTIS used in past as for dt4 or 3TC ,AZT + TDF or TDF + FTC or simply replacing 3TC by TDF or FTC or ABC or ddi is done,if any drug produce complication or side effect as mentioned above it is also replaced.In case of Hepatitis B TDF +3TC is used with NNRTIS or Protease Inhibitor.Revebrine and Pregylated Interferon is used with ART in Hepatits C patients.If after IInd line treatment CD4 count is increased third line treatment using one NNRTIS ,one Protease inhibitor as newly added ATV,DRVor FPV with Integrase inhibitor Raltegravir(RAL) is used.
Cotrimoxazole is added to prophylaxis below 350 to prevent malaria,bacterial,PNeumocystis Jivorecii or Campylobacter Diarrhoea and Toxoplasmosis.STD clinic for any sexual inflicted persons like commercial or flying sex worker (counselling and promoting use of condom )and treatment and screening of suspected highly prone patients like IDUs,drug users,(not sharing needle)migratory labours,Truck drivers etc., at target Intervention clinic is backbone to control it and every suspect should be submitted for HIV screening ,Similiarly every TB patient and in ICTC every Blood donor and PTCT pregnant mother is screened for HIV.Proper counselling of these patients with advise and regular follow up of these persons at primary or semi primary or assisting ART centre is must by doing off and on viral load and CD4 count examination. Every oppurtunistic infection should be controlled and here medicines shold be contined for a long time to prevent recurrence and continuation of ART medicine of great importance.Adhrence,compliance and continued taking medicines with proper counselling during IRIS or any other drug reaction is most important of HIV treatment.

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Author is an HIV specialist Doctor


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Sep17
PROSTATE SPECIFIC ANTIGEN TEST(AGE SPECIFIC)
Prostate cancer remains the most commonly diagnosed and the third leading cause of cancer deaths among men in western countries , but most men with the disease dont die from it. In the United States a man has 15.8% chance of being diagnosed with prostate cancer but the risk of dying is 2.8%. The American cancer society still recommends that men at high risk and those 50 and over should be screened. Prostate specific antigen (PSA) is a protein produced by the cells of prostate gland. The PSA test measures the level of PSA in blood. Because this antigen is produced by the body and can be used to detect diseases, they are also called biological markers or tumor markers.New studies show that men who have low prostate specific antigen at 60yrs of age , do not really need future screening. But what do you say to men who are 40, 50 or 55 ? All men should start having their PSA levels checked before the age of 60, then at 60 if the PSA is less than 1 nanogram / ml , they are at low risk of prostate cancer. According to researchers , PSA level at age 60 is a good predictor of who were at risk , and that low levels at age 60 means you are unlikely to benefit from subsequent PSA tests as your risk of metastasis or death from prostate cancer is very low.Conversely , men with high PSA reading- 2ng/ ml or above should be monitored and screened, as they are at higher risk. A digital rectal examination (DRE) and PSA levels are used for screening. PSA can be elevated in both benign and cancerous conditions of the prostate , and the level tends to increase with age. The use of age specific PSA reference ranges are suggested as more accurate. Men at risk and above 50 and over should talk with their doctors about the risk and benefits of screening.The American Cancer Society also stresses that in some cases - such as men over 50 who are not expected to live for another 10 yrs , such tests should not be offered because they will cause more harm than good with treatments that has unpleasant side effects such as incontinence and impotence which can greatly affect the quality of their lives.


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Sep10
DOCTORS ON STRIKE-HOW FAR IS THIS JUSTIFIED?
DOCTORS ARE ON STRIKE AT JODHPUR! WHOLE RAJASTHAN! AT SAFDARGANJ HOSPITAL! NOIDA!GAZIABAD! KOKATA! NORTH BENGAL MEDICAL COLLEGE! ----------SO MANY PATIENTS DIED! NO TREATMENT FOR POORS!PATIENTS ARE RETURNING HOME!MOVING TO PRIVATE CLINICS!GOVERNMENT HAS FAILED!-----THESE SLOGANS ARE COMMON ON ELECTRONIC MEDIA GIVING 24X7 NEWS AND PRINT MEDIA.EVEN AT ANY PLACE,HOME,OFFICE, CLUB,RESTURANTS,PARK,HOTELS,AMUSEMENT CENTRES OR LIBRARY ANY GENRAL PERSONS WILL BE OF VIEWS THAT MEDICAL IS A NOBLE PROFESSIONS,A PROFESSION TO SERVE THE HUMAN BEING ACCEPTING ALL SUFFERINGS TO THYSELF,SO DOCTORS AND ITS FAMILY MEMBERS LIKE NURSES,HOSPITAL STAFFS,PARAMEDICS, MEDICAL STUDENTS, TEACHERS, RESEARCH SCHOLARS,LAB ASSISTANTS, DIAGNOSTIC CENTRES ,HOSPITAL, PRIVATE CLINICS MEDICAL REPRESENTATIVES AND DRUG MANUFACTURERS AND RETAIL SELLERS SHOULD NEVER CALL FOR STRIKE CLOSING THEIR WORK COMPLETELY, ABSTAINING FROM EXAMINING,PRESCRIBING AND TREATING PATIENTS AT WHATEVER REASON AND WHATEVER COST OF PERSONAL OR COMMUNITY SUFFERINGS AS THEY ARE WORSHIPED LIKE GOD AND GENERAL PEOPLE SEE AN IMAGE OF GOD IN DOCTOR'S BODY.
SECONDLY FOR MAKING A GOVERNMENT DOCTOR,GOVERNMENT PAYS A HUGH MONEY COLLECTING FROM TAX PAYER'S POCKET SO DOCTORS HAVE NO RIGHT TO CEASE WORKS -MANY CHANNELS AND WRITERS ARE ADVISING GOVERNMENT TO BRING LAWS LIKE ASMA TO BAN DOCTOR'S STRIKE AND CEASEWORK AND PUNISH DOCTORS OPENLY FOR VIOLATION OF THEIR DUTY FOR PERSONAL OR COMMUNITY GAIN.
SUCH POPULISTIC AND GENERAL VIEWS ARE OFTEN SOUNDED BY LEADERS OF POLITICAL PARTIES AND SOCIAL WEFARE GROUPS WITHOUT GOING INTO DETAIL OF SUFFERINGS WHICH THE WHOLE MEDICAL WORLD UNDERGOES BEFORE SUBMITTING THEMSELVES TO THIS LAST PAINFUL WEAPON OF SUBMITTING THEMSELVES FOR STRIKE!OR CEASE WORK! EVEN DURING SUCH STRIKE MOSTLY DOCTORS KEEP OPENS EMERGENCY SERVICE BUT NUMBER OF PATIENTS IN GOVERNMENT AND SEMI GOVERNMENT CENTRES ARE SO MUCH THAT IT CANNOT TAKE LOAD OF PATIENTS SMOOTHLY ,SECONDLY MEDIA PEOPLE BECOMES SO ACTIVE THAT THEY START REPORTING NEWS OF DEATH AND SUFFERINGS SO MUCH FOCUSING THE STRIKE THAT IT APPEARS AS IF IT IS ALL BECAUSE OF STRIKE WHERE AS FACTS REMAIN THE SAME THAT SUCH KIND OF SUFFERINGS AND DEATH ARE COMMON IN THESE HOSPITALS BECAUSE OF LATE ARRIVALS OF SERIOUSLY ILL PATIENTS,INABILITY TO PROVIDE ADEQUATE MEDICINES,INVESTIGATIONS, TREATMENT FACILITIES TO THESE PATIENTS FREE BY GOVERNMENT WHO SPEND LESS THAN 3% OF GDP ON HEALTH WHEREAS 30% IS PAID FOR ARMY AND DEFENSE,AT MOST OF GOVERNMENT CENTRES ADEQUATE MEDICAL STAFFS,NURSES, PARAMEDICAL ASSITANTS AND HELPERS ARE LACKING,EVERYTHING IS LEFT ON TREATING DOCTORS AS THEY WILL MANGE EVERYTHING AND THEY ARE AT FAULT FOR EVERY MISTAKES OR LACK OF TREATMENT OR IF ANY COMPLICATION OR DEATH RESULT FROM TREATMENT .NOW A DAYS PEOPLE FROM EVERY CORNERS BLAME DOCTORS FOR SUCH PROBLEMS OF NOT GETTING GOOD TREATMENT OR DEVELOPING COMPLICATION OR DEATH AND FOR PROTESTING INSTEAD OF LAUNCHING PROTEST OR COMPLAINS THROUGH HOSPITAL OR POLICE OR ADMINISTRATION,TAKES LAW IN THEIR HAND AND TO MAKE ISSUE HIGHLIGHTED IN MEDIA AND EVEN POLITICAL PARTIES AND MANY CLUBS,NGO.S, SOCIAL WORKERS AND EVEN SOME MISCREANTS JOIN THESE PROTESTORS OPENLY AND ATTACK DOCTORS,NURSES,MEDICAL STUDENT, PARMEDICAL STAFFS AND MEDICINE SELLERS PHYSICALLY INFRONT OF EVERY BODY(MEDIA-WHO INSTEAD OF CONTROLLING SUCH JEHADI PROTESTORS REMAIN ENGAGED IN TAKING PHOTOGRAPHS AND TAKING BITES TO SELL THEIR NEWS TO EARN MONEY BY PUTTING MORE MASALA AND TARDKA AND PRESENTING THEMSELVES AS FIRST CHANNEL TO DICOVER IT AND TO GAIN MORE AND MORE TRP,POLICE; IS OFTEN CALLED FOR CONTROLLING LAW AND ORDER BUT MANY PLACES THEY DONOT REACH IN TIME BECAUSE MOSTLY CRIME IS COMMITTED BEFORE THEIR REACHING AT SPOT AND EVEN REACHING IN TIME,THEY MOSTLY REMAIN SILENT BECAUSE OF POLITICAL PRESSURE OR ATLEAST CONTOL DEMONSTATORS AND PROTESTORS WHO USE BAD UNPARLIAMENTARY LANGUAGES AND SLOGANS TO MALIGN "DOCTORS" AS SPEAKING IS OUR BASIC RIGHT,MOSTLY MOB BECOME FURIOUS BEFORE MEDICAL ADMINSTRATORS AND DOCTORS AND START DAMAGING HOSPITAL PROPERTY BY BRAKING RECEPTIONS,DIGNOSTIC CENTRES,OT, OPD LAUNGE,INDOOR INSTRUMENTS ,BEDS AND FUNITURES,AT SOME PLACES THEY PUT THESE ON FIRE BEFORE LAW PROTECTING FORCE IN NAME OF SHOWING AGONY ,GRIEVNCES AND SHOCK FOR DEATH OR MISS MANGEMENT OF THEIR NEAR ONES AS IF DOCTORS HAS CREATED THE ACCIDENT OR DISEASE TO THAT PERSON AND DOCTOR IS THE ONLY SOLE RESPONSIBLE FOR SUCH ACCIDENT.EVEN IN MOB GENERAL PEOPLE ALSO BECOMES PART OF THESE DEMOSTRATIONS THNKING THAT DOCTORS ARE CORRUPT,THEY EARN HUGH MONEY BY CHEATING GENERAL PEOPLE,MOVE IN GOOD CARS AND LIVE IN GOOD HOUSES BY TAKING COMMISSION FROM DRUG COMPANIES,DIAGNOSTIC CENTRES ILLEGAL PRACTICE FROM GOVERNMENT HOSPITAL TO PRIVATE HOSPITALS AND AS GNERAL PEOPLE ARE NOT GETTING GOOD SERVICE FOR THEIR HEALTH PROBLEMS AS GOVERNMENT CLAIMS AS IT IS FREE AND FAIR BUT PRACTICALLY DUE TO LESS INVESTMENT IT IS ALSMOST ABSENT ,SO DOCTORS BECOME EYESORE OF COMMON PEOPLE TOO AND POLITICIAN AND ADMINSTRATOR ALSO REMAIN SILENT AS THEY KNOW PUBLIC WANTS DEFAME AND DISREPUTE OF DOCTORS SO IF THEY SUPPORT DOCTORS IN SSUCH CRISIS PEOPLE AND MEDIA WILL DESTROY THEIR VOTE BANK AND IMAGE,SO DOCTORS ARE LEFT FOR BEATING AND PHYSICAL HURT IN OPEN DAY LIGHT.
EVEN GOD WILL BE BEATEN ON BASIS OF SOME FILTHY CHARGES WHERE HE IS NOT DIRECTLY INVOLVED OR WHERE DEATH OR COMPLICATION IS A PART AND PARCEL OF THE TREATMENT PROCEDURES WHERE LIFE AND DEATH ARE EXISTING SHARING SHOULDER OF EACH OTHER
,GOD WILL TOO REACT WHAT TO TALK OF THESE HUMAN BEINGS ,HOW ONE CAN ASPECT A FEARLESS GOOD TREATMENT BY DOCTORS WHEN WHOLE SOCIETY IS STANDING AGINST HIM FOR NOT PROVIDING GURANTED GOOD TREATMENT AND RECOVERY,DOCTORS ARE MOSTLY SHACKEN BY CONSUMER PROTECTION ACT,RTI ACT,VIGILANT AND INTROSPECTING MEDIA WHO IS ALWAYS IN HOSPITAL TO CLICK ANY STORY ON DOCTORS PATIENT TUSSEL OR ANY MISHAPPENING IN HOSPITAL TO EARN TRP AND IF SUCH SHOCKED AND TREMOROUS DOCTORS ARE BEATEN OPENLY,THEIR REPUTATION IS CHALLENGED SO OPENLY IN SOCIETY,THRE IS NO OPTION LEFT BUT TO ASK FOR PROTECTION AND FORM GOOD LAWS AND BRINGING STRICT ACTIONS AGAINST MISCREANTS SO THAT SUCH ACCIDENTS DONOT HAPPEN IN FUTURE BUT AS THIS IS A NORM IN OUR PRESENT SOCIO POLITICAL SYSTEM THAT UNLESS YOU PRESENT YOUR SELF IN A VERY SERIUOS UNPARLIAMENTARY MANNER NO BODY LISTENS TO YOU,EVEN PARLIAMENTS AND ASSEMBLY SHOWS US SOMANY ROUDY AND BREAKING MIKES,CHAIRS AND WINDOWS IN THESE HOUSES BY ELECTED MLSAS AND MPS AS GOVERNMENT DONOT LISTEN TO THEIR SIMPLE PROTEST.
EVRY DEATH IS PAINFUL ,NO DOCTORS WANT THAT SOMETHING WRONG OR COMPLICATION OR DEATH OCCURS TO HIS/HER PATIENTS (EVEN EVRY GENERAL PERSON ACCEPTS IT) BUT DURING SUCH ACT SUCH THINGS ARE FORGOTTEN AND AN ONE THEME AGENDA OF BRUTALLY ATTACKING DOCTOR'S AND THEIR FAMILY MEBERS OF MEDICAL WORLD PHYSICALLY AND DAMAGING HOSPITAL PROPERTY IS TAKEN,INSTEAD OF RECOMMENDING FOR PUNISHMENT OF THESE PEOPLE,POLITICAL LEADERS START SCORING THEIR GAIN AGANIST RULING PARTY FOR SUCH ACT,STRATS ENCOURAGING THEM MORE AND MORE AND RECOMMENDS FOR THEIR IMMEDIATE RELEASE EVEN CUGHT BY POLICE ,MEDIA SHOWS THEM AS GREAT PCIFIER,NGO'S ANS SOCIAL WORKERS, CLUB ALL COMES FOR THE RESCUE OF THESE TROUBLE SHOOTERS JUSTIFYING THEIR PROTEST AS NATURAL BECAUSE A HUMAN LIFE HAS BEEN LOST AND DECLARES "DOCTORS"AS CRIMINALS WHO HAS COMMITTED THE CRIME MAKING HIM RESPONSIBLE FOR EVERY SUCH MISDOING FORGETTING ALLOCATION OF MONEY,FACILITIES, INFRASTRUCTURES STAFF,WILL POWER,WORK CULTURE ETC., IN THESE HOSPITALS.
SO MANY TYPE OF CRIMES ARE COMMITTED IN OUR SOCIETY BUT IN MOST OF THEM MASS DOESNOT PARTICIPATE,INVESTIGATION AUTHORIITE S LIKE POLICE,CID,CBI AND STF WORKS AND EVEN PUBLIC OR MISCREANTS TRY TO SABOTAGE SUCH INVESTIGATIONS ,THEY ARE BOOKED AND TAKEN TO TASK BUT IN CASE OF MEDICAL INVOLVEMENT, "DOCTORS" HAVE BEEN MADE SOFT TARGET AS IF ANY BODY CAN HIT THEM PHYSICALLY AND DAMAGE THE HOSPITAL PROPERTY,NO EXELEMPARY PUNISHMENT IS IMPOSED (GOVERNMENT OF ANDHRA HAS BROUGHT A LAW TO ARREST AND RECOVER MONEY FROM MISCREANTS AND PROTESTOR DAMAGING HOSPITAL PROPERTY ) BUT SUCH LAW SHOULD BE PASSED BY OUR PARLIAMENT AND SUCH AN EXAMPLE SHOULD BE CITED BY ARRESTING AND RECOVERING FROM SUCH PROTESTORS THAT IN FUTURE NO BODY SHOULD TAKE LAW IN HAND,MEDIA SHOULD STOP SHOWING AND REPORTING SUCH INCIDENTS AS THEY ENCOURAGE MORE PEOPLE TO TAKE LAW IN THEIR HAND.BUT FACTS REMAIN THIS,MEDIA IS FREE! POLICE CANNOT ACT! POLITICIANS ARE WELL WISHERS OF PEOPLE,NGOS AND SOCIAL WORKERS ARE SERVING SOCIETY! POLICE CANOT BE CONTROLLED AND DISCIPLINED !ADMINISTRATION AND LAW MAKERS NEVER SOLVE PROBLEM BY SIMPLE WRITING, DEMANDS, DEMONSTRATIONS,PROTESTS UNTIL AN EXTREME STEP IS TAKEN IN THE FORM OF STRIKE OR CAESE WORK IS TAKEN ,THEN THEY RESPOND BY GIVING MERE CONSOLATIONS ,ARRANGING POLICE PICKETING AND SECURITY PROTECTION FOR FEW DAYS,AS THE TIME PASSES EVERYTHING AGAIN COMES TO SAME PREVIOUS STAGE, A NEW INCIDENT TOOK PLACE AND EVERY THING IS REPEATED IN THE SAME WAY.
THEREFORE,IT IS NEED OF TIME THAT OUR POLITICIANS ,ADMINISTRATORS,MEDIA AND PEOPLE SHOULD SIT TOGHTHER AND THINK'WHY DOCTORS ARE BOUND FOR STRIKING" ,SOLVE THEIR PROBLEM IN TIME,LISTEN TO THEIR REPRESENTATIONS AND JUSTIFIED DEMANDS (WHEN EVERY PARLIAMENTARIANS AND BUREAUCRATS ARE ENJOYING SO MUCH HIKED PAY AND FACILITIES,WHY DOCTORS WHO TREAT THE PATIENTS ARE PAID SO BADLY,WHY THEIR BASIC AMENTIES,FACILITIES ARE NOT IMPROVED, WHY MORE CAPITA IS NOT EXPENDITURES ON HEALTH,WHY FACILITIES OF BED,DIAGNOSTIC CENTRES,MEDICINES AND ADEQUATE STAFFS ARE NOT INCREASE IN HOSPITALS,WHY A PUBLIC RELATION OFFICERS IS NOT APPOINTED IN HOSPITALS WHO ACCEPTS ALL GRIEVANCES AND REPORT TO MEDIA AS WH IS AT FAULT FOR MISMANGEMENT OF PATIENTS AT HOSPITAL,WHY A DOCTOR IS MADE RESONSIBLE FOR ANY MISHAPPENING IN HOSPITAL?)CREATE SO MUCH AWARENESS IN PUBLIC THAT THEY UNDERSTAND ALL SUCH MIS HAPPENINGS AND NEVER RESORT FOR SUCH ACT OF TAKING LAW IN HAND.
THESE ARE BASIC QUESTIONS WHICH A GOD WILL ALSO LIKE TO BE RESOLVED BECAUSE MOST OF TIME HE IS NOT AT FAULT AND NO BODY ERRONEOUSLY BLAME HIM,SYSTEM IS POLLUTED AND AS HE IS DIRECTLY AT TOP IN HOSPITAL ,SO HE CANNOT BE BLAMED BECAUSE INDIRECT BOSSES ARE IN POLITICS AND ADMINISTRATIONS. EVERY GENRAL PEOPLE HAVE RIGHT TO COMPLAIN TO ADMINISTRATION,POLICE,JUDICIAL COURT,STRICT ACTION SHOULD BE TAKEN IF DOCTOR IS FOUND AT FAULT BY INVESTIGATIONS OF COMPETENT AUTHORITY ,OUR COURT SHOULD BE MADE RESPONSIVE FOR EARLY TRIAL AND JUDGEMENT ,ALL ADMINSTRATIONS AND POLITICIANS SHOULD SHARE THEIR DISCREPANCIES AND FAULTS(INSTEADING OF PASSING WHOLE BUCK TO "DOCTOR")AND RESORT TO DOCTOR'S PERSONAL OR COMMUNITY PROBLEMS AS SOON AS POSSIBLE SOTHAT SUCH A HARSH AND UNJUSTIFIED WEAPON OF PROTEST "STRIKE OR CAESE WORK " IS EVER TAKEN BY DOCTORS .EVEN DOCTORS SHOULD TAKE STERN MEASURES TO IMPROVE PATIENT DOCTORS RELATIONSHIP BY DOING SOME GOOD SOCIAL WORKS AS MANY DOCTORS ARE DOING INVOLVE MEDIA AND GENERAL PEOPLE IN POLITICIANS IN THESE PROGRAMMES SO THAT NOBLE WORK OF DOCTORS GET MAXIMUM EXPOSURE IN SOCIETY SO THAT GENERAL PEOPLE COMES IN SUPPORT OF DOCTORS AND HAVE TO BE REMAIN UNITED SO THAT GOVERNMENT AND ADMINISTRATIONS LISTEN TO DOCTORS ,NOW A DAYS SELF DEFENCE IS BEST DEFENCE RESPECTING LAWS OF OUR COUNTRY.SO MERE CRTICISM WILL NOT YIELD ANY RESULT,DOCTORS ARE MOST IMPORTANT MEMBERS OF SOCIETY WHO SPEND SO MANY VALUABLE TIME ABOUT 15 YRS MINIMUM TO BE A GOOD DOCTOR WHO HAS TO READ THROUGHT OUT LIFE AND UP TO DATE TO REMAN AS GOOD DOCTOR WITH VERY LOW PAYMENT INCOMPARISON TO MBA,IIT,BUREAUCRATS AND CEO OF MODERN COMPANIES AND A PROPER RESPECT AND RECOGNITION IS ESSENTIALS TO THEM AND OUR SOCIETY AND ADMINISTRATION SHOULD BRING ALL CHANGES IMMEDIATELY SOTHAT SUCH HOOGALINISM,VADILISM AND GOONDISM IS STOPPED IN OUR HEALTH ENVIORNMENT.
DR.D.R.NAKIPURIA
SILIGURI


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Sep04
NEW RURAL DOCTORS(BRHC)-HOW ARE THEY SAFE?
In UPA II Government ,some Minister are adamant to bring so much new conception in name of serving poor,rural,farmer and unemployed people of our country forgetting basic infrastructure, fasibilty, econmical viability ,its sustainibilty, acceptance,discimination against rich-poor,urban rural etc., and actual its performance in presence of open corruption,expoitation and tendency to earn money and poser forgetting basic Norm and value of Human life and society.Our present Central Health Minister Mr.Gulab Nami Azad first scapped MCI to grab such agency in Ministry clutch to regulate Medical Education,registration and giving license to run or open New Medical Colleges in INDIA ,an Industry of thousand of crores of Rupees.On May03,2010,Ministry bring "CLINICAL ESTABLISHMENT ACT" to regulate private Hospital and Clinics in name of better service to society and poor persons but Government own Hospital and agencies has been exlcuded from any improvement or screening or any desire or will for improvement as no body can check it whcih serve maximum number of people of our country and almost 90% of our poor people.Government agencies intervention and checking will increas more courruption by Babus and bureaucrats making Private hospitals more and more costly as Government cannot run without them as rich ,havenots,these babus,Politicians,Ministers hardly go to govt.hospitals for their treatment. secondly it is mostly run by Qualified Doctors who treat and cure these patients and if they are not relieved or are not treated well their reputation and complains with in present Laws is enough to deal this but Government wants supervision by Bureaucrats not expert in Medical science by bringing License system upbringing advance rich or MNC Centres to exist and closer of small units making Medical treatment more and more costly.
Similiarly "BACHELOR OF RURAL HEALTH CARE(BRHC) COURSE to produce Rural doctors has been prepared by MINISTER' S MCI on the basis of sending more and more Doctors in Rural areas as no Doctor wants to stay in rural areas,socially this theme may appear popuistic but infact it is faraway from true ,now a days under NRHM Scheme many Doctors are serving Rural areas because of good connectivity and communication facilities in rural areas,secondaly a discrimination between rural and urban people regarding dealing patients should not be done as it will not be accepted by rural people who will not like to get treated by these Rural socalled semieduca,if new medical colleges are open in rural areas where rural students should be admitted,or making compulsory of every physician toserve 02-3 years in rural areas as practised in MBBS course in Maharasthra befor getting final registration or before getting permannat service or promotion or adding more seats in medical colleges and giving it to strictly rural students could save our society from such ill educated doctors who need even a training of more than 4and 1/2 yrs to know better such advancing Medical science and where every body has got right to get best and equal oppurtunity atleast in field of Health and Education.When most of our youths are shifting to urban sides from villages because of lack of infrastructure and less development of Agriculture based Business and factories in rural areas and where farmers are doing day light suicide because of unability to run their livehood from agriculture and these Doctors willremain at rural areas appear only bubble declartaion.
On paper this syllabus is for the three-year course and this rural medical practitioners is ready in MCI premise. It promises to do away with what's "unnecessary" in the four-and-a-half-year MBBS course and prepare "hands-on" doctors at the primary level. The Medical Council of India (MCI), which has prepared the syllabus, has differentiated between BRHC and MBBS doctors by not allowing the former to use the prefix 'Dr' to their name. Instead, they will have BRHC suffixed to their name.
. This new category will be drawn from 10+2 students from rural areas/districts and 25 will be chosen district-wise after an exam. They will be trained at community colleges by practicing or retired doctors from nearby district hospitals. Their practice will be confined to that area and registration will be for one year only. The course will include 10 things: Community medicine, internal medicine, pediatrics, surgery, orthopedics, obstetrics and gynecology, ophthalmology, ENT, radio-diagnosis and dentistry. It will be divided into three phases. In the first, students will study the health problems of the community, basic principles of diagnosis and prevention of common rural aliments such as malaria, anemia, hookworm, kala-az ar, TB and diarrhoea. Phase II w ll involve taking patient history, basic clinical examination and management of diseases. They will be tied up with national health programmes. Phase III will deal with training to prevent basic health problems. The curriculum will do away with many unnecessary aspects in the MBBS course such as in pharmacy and anatomy.
Using "DR" is not trheatening to MBBS or any other practising Doctor as Educated Doctors know they got prestige and recognition respect from Society because of their knowledge not because of "DR"word as many teachers and many other practitioner use ths "DR" word before their name but such anme never disturb theri practice or reputation.
Secondly to produce Doctors without basic knowledge of Anatomy(Structure of Our Body Body parts and Organs ,Physiology(Function of our Body's different organs)Pathology(Basic cause of Disease)and Pharmacy(Knowing details of Medicines and their reaction) is like to fdrive an aircraft without knowledge of Airspacing,to drive car,bus,scooter without knowledge of driving and of road,it will kill all passengers and even persons on the road.
Therefore ,Government should think thrice to bring such populistic looking novice lucrative dreams in to action as instead of improving our society such programmes and course will destroy basic fabric of equality in our society and it will be a discovery of Atomic missiles which may give pride to humanity but may devast and finish whole Humanity if Blast takes place willingly or unwillingly.it is not a prestige issue for IMA or MBBS DOctors but it is a prestige for every citizen who has got a right to have good treatment and care whether he stays in rural or urban area.
dr.D.r.Nakipuria


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Aug20
CANCER-DEATH / DISABILTY / DRUG DEPENDANCE ----ARE THEY ASSOCIATED ?HOW TO FIGHT IT?
CACANCER-DEATH / DISABILTY / DRUG DEPENDANCE ----ARE THEY ASSOCIATED ?HOW TO FIGHT IT?

Cancer ,word it self fetches us to a very frieghtening and fearful meaning,if ,unfortunately somone in our family or society is being suspected or suffering from it and the word "CANCER" comes beore us in any way ,we start presuming very badly and gets completely shocked and nervous assuming that person concerned is very very seroius and his /her days are almost in counting scale and we became wholly sympathetic for that person forgetting every his/her adversary towards us and try to help the person as far as possibly by money,service or any other means if possible.But in real Biological sense "CANCER" is not that kind of Lion or Tiger that once you face it there is no hope of life and certainly it is not curable and we should be completely depressed and hopeless becauuse many "CANCERS" are now completely curable and life becomes as normal as it was without it ,only thing is that it should be detected as early as possible and treatment should be started as soon as possible.It is commonly believed that once Cancer means we,shall be never cured from this ,we have to take medicine regularly throughout the life,and we donot know when recurrence may occur and again mor discomfort or Death may come to us any time,person has to be in screening throughout the life moving to Hospital or doctor almost off and on throughout the life.Yes,for some persons these lines are true but in many cases these are simple myths ,Cancer once cured,never recurs or recur in so less percentage that one has nothing to worry,even follow up of symptoms noticing is important,that is with every disese once one suffers from cold or cough or diarrhoea one goes to Doctor,same way here one has to go to Doctor,no test or investigations are required and life becmes as normal as it was originally without Cancer,so nothing to worry,be happy,never get depressed or shcoked by this word,cancer, never loose heart face it at first meeting boldly and fight so well that finish it nipped into bud.As the modern science is growing and more and more reaseaches are done and treatment bieng enforced to treat Cancer by means of better chemotherapeutics or medicines with very less sideeffects,Monoclonal Antibodies,different caccines,interferons and Stem cell with development of Gene therapy ,better rays inform of Positron euipped with Ct scan and MRI or Tomography machine,Cyber knief,Brain Suits,or IMRT or Brachytherapy, Stereotactic Radiotherapy beside cobalt ,gamma and X-rt with linear acceletor and modern Surgical removl of cancer using ultrasound,ct scan,Laproscope and modern robotic Surgery with the facility of FNAC, TRUCUT BIOPSY,FROZEN BIOPSY and better detectection and control of micro metastases has made much advancement leading to almost curbing and controlling Cancer denovo.

In Medical Biology Cancer is defined "Uncontrolled Growth of Cells." that is if our finger which is shaped like a finger is constituted by Bone,Many MUscles,Tendon,Nerve and Blood and Lymphatic vessels covered by skin with hairs,sweat glnd and many type of receptors of pain,temperature,touch etc, type of tissues and each of these tissues are made up of many cells,like a brick which forms our house.if one or few cells starts dividing rapidly and excess cells are not destroyed ,first the shape of Finger will be destroyed and then whole finger will be deformed and gradually such growth will spread to hand and will deform and dysfunction it too.Normally in our body there is a check and balance of every Growth,excess and unrequired growth is destroyed or designed sothat a proper shape and function of every organ is established.But once this check and balance is destroyed such growth is called "CANCER" or "TUMOR" which may be localised to the organ where it was orginated or spread to adjoining organs or may spred by Lymph or Blood vessels to differnet distanorgan as cancer of leg spreading to Brain,Liver,Lung etc. and vice versa.if locally organised Tumor these are called "BENIGN CANCER OR GOOD TUMORS' as once excised they are mostly completely curable with use of Surgery or radiotherapy BUT THOSE TUMORS WHICH SPREAD FROM ORIGINATIONG ORGAN TO OTHER ORGANS ARE CALLED "metastatic tumors or bad tumors or growth" as they are once removed from a local place by radio or Surery may recur immediately or after months or years from distant place ,so they are taken care of by using Chemotherapy or Cancer Drugs which also kills normal cell too,so are some time very toxic killing Blood,Hairs,skin and many growing cells bringing so many side effects,some time so much that we have to stop these medicines as patient cannot bear them physically and economically resulting into icreased morbidity and mortality.Newer added Medicines like Interferons,Monoclonal Antibodies,Genetherapy,Stem cells and modern cancer drugs are very very costly being out of reach from many Patients of Developing countries.

Human body is made up of 60 trillion cells and different type of Tissues which after combinig form differnt organs and Organs form the Body .Till date if these Organs are working synchronically or working in order from each organ to another organ ,Life exists as their chronological or systemic or disciplined working toghther is hampered or this cycle is stopped by any meber organ of cycle ,all organs stars failig one after another and we say Death occured,we donot know which is starting point and which is end point,some say Brain,Some Say Heart but in real sense it is their working togher with each other mattrers,no one is superior,no one is inferior. Most of the cells except the cells in the brain re-live by the process of division and replacement. It can be simply understood that after a given time the old cell is replaced by new cell, exact replica of its predecessor. The renewal of the cells after a given time is a natural process but uncontrolled growth of cells is not natural.Even some cells grow abnormally ,to start with these are killed by Body Immunity as checking mechanism but if growth is excessive or Immunity is not reacting ,these became permanent and called Cancer.This is the reason that cancer is not recognised as an abnormal activity by the immune system of the body and therefore, cancer detection is very difficult unless it affects the performance of an organ or organs,symptoms or signs are attributed to the organ concerned if Eye means loss of vission,if Larynx means loss of voice etc.,but Cancer in itself does not have any symptoms. The first question which comes to anyone's mind is –If it is not a natural process then why does a cell start uncontrolled growth? The exact answer for this question is not yet known to humanity. The answer to this question lies in identifying the part of the cell, which is responsible for initiating the process of self replication and excessive reproduction. Presumably, it may be some section in the DNA, cell membrane or may be anything else either being stimulated by some external things like sunlight in cancer of skin Melanoma or heat,or application of some chemicals used locally or ingested inside but many times cause is not exactly known,some cancer runs in family and strong genetic basis is present for every Cancer either coming as sporidally mutation of gene in an Individual or by hereditary in family.Here lies the success of stem therapy or gene Modulation or therapy to treat cancer.

Surgery is the basic of treating most cancers of Abdominal organs,Hand,leg or extremities,lung,brain,breast and chest wall ,skin etc but surgery completely cannot remove the whole tumor as tumor might have spread to important organ completely as to Liver or pancreas ,we cannot completely remove these organs so after a good chunk removal we use radiotherapy to remove these cells or we can use radiotherapy initially to control thest tumors and then can resect them once their size is less or can use with surgery or after it to rmove any remaining tumor unvisiblt that time or because of important organ not removed in first chance.Some time for mouth ,tongue,cervix,breast cancer we use Raditherapy to burn these tumor in first instance and donot use surgery at all but may use surgey if tumor remains after 8-10 wks of radiotherapy or if tumor recurs at this site .Similiarly for cancer of Blood and connective tissue crmotherapy or Medicines are only needed no sugery or Raditherapy is needed,some time to make tumor resectable we use cheotherapy first but mostly we use it after surgery or radiotherapy to remove tumor completely from originationg sit and then removing any micro spread which occured to ant distant organ either dtectable or undeteable in first phase or recurrence phase.

Overall the subject is very vast and many reasearches are going on making Human life more safe and precious ,the days will come soon when Man will win over this demon completely and even today our victory should not be ubderestimated because we can completely overcome Cancer if it is detected and treated in early stage by present modern gadgets of Surgery,Chemotherapy and radiotherapy,many Ayush and otherwise natural healers and therapist claim many medicnes to cure them completely by showing or claiming their personal cases and experiences,in this regard this is advisable that please expose first your claim internationally by publishing papers in good modern Journals of modern Medicines or of your subject or therapy,simple assertions and personal claim may not be hold good for many other patients as aberrations are known in medical science so,please refer the patient to good medicl college or centre when you see any cancer patient,donot keep patient in your clutch only,allow them to get detected the Disease or cancer completely and then get started the therapy ,with this therapy you may add your medicines too if you are very confident or qualified otherwise for earning money if some false promises or trials are done on some patients of villages or slum or from poor uneducated class of our country by so many self claimed healers or doctors using any therapy is a heinous crime on the earth and please restrain from this and help the society to curb this fatal disease completely and in first instance.

Dr.d.r.Nakipuria

Ambika chikitshalya

29 agrasen road

siliguri-734005


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Aug18
SCAPPING MCI,DCI & NCI-GOVERNMENT'S POLICY DESERVES CRITICISM
UPA II GOVERNMENT UNDER LEADERSHIP OF MR.GULAM NABI AZAD ,A VETERAN POLITICIAN AND CLOSE TO MRS.SONIA GANDHI IS CONTINUOSLY STRIKING NAILS AND NAILS IN THE COFFIN OF MEDICAL PROFESSION ,FIRST ROBBING THE AUTONOMY OF "MEDICAL COUNCIL OF INDIA" BY BRINGING AN ORDINANCE THROUGH THE OFFICE OF PRESIDENT THROGH MEETING IN COUNCIL OF MINISTERS AFTER ARREST OF MR.KETAN DESIA ,PRESIDENT OF MCI THROUGH CBI N THE CHARGE OF ACCEPTING BRIBARY FOR ISSUING NO OBJECTION CERTIFICATES TO FEW PRIVATE MEDICAL COLLEGE IN PUNJAB.
GOVERNMENT IS NOW SAYING THAT DR.KOHLI,PRESIDENT OF "DENTAL COUNCIL OF INDIA" AND MR.R.DILIP BABU.PRESIDENT OF "NUSING COUNCIL OF INDIA" ARE TOO ENGAGED IN MALPRACTICE AND HAVE EARNED HUGH MONEY,CBI IS SEEKING PERMISSION TO IVESTIGATE THESE FOLLOWS AND CENTRAL HEALTH MINISTER WILL BRING AN ORDINANCE EITHER IN THIS PARLIAMENT SESSION OF OTHERWISE THROUGH COUNCILOF MINISTER'S MEETING ORDINANCE THRROUGH PRESIDENT'S OFFICE TO SCRAPE AUTONOMY OF THESE TWO COUNCILS AS DONE TO MCI.
AS INDIAN CITIZEN,NO BODY IS INTERESTED TO PROTECT THE CULPRIT IF PRESIDENT OR VICE PRESIDENT OR FEW MEMBERS OF THESE COUNCILS HAVE DONE ANY CORRUPTION THEN THEY MUST BE PUNISHED BUT LIKE 'SEBI,COMMON WEALTH GAME OR BCCI OR IPL OR OYMPIC OR FOOTBALL ASSOCIATIONS,CULPRIT CORRUPT OFFICIALS SHOULD BE REMOVED NOT THE WHOLE AUTONOMOUS BODY IF SUCH ACTION IS BEING DONE THEN OUR PARLIAMENT SHOULD DISSOLVE ALL THESE AUTONOMOUS BODIES AND PARLIAMENTARY COMMITTIES ON DIFFEREN MATTERS AND MINSTERS AND BUREAUCRATS OF THESE MINISTRY SHOULD BE MADE INCHARGE OF EVERY SUCH BODY BUT WE KNOW THAT IN THIS CASE CORRUPTION WILL REACH TO PEAK AND EVERYTHING WILL BE A POLITICAL PARTY GAME AND MANY SCAMS WILL EMERGE AND HARDLY ANY POLITICIAL WILL BE PUNISHED AS COMMON PRACTISE IN OUR COUNTRY. THE REASON SUCH BODIES ARE UNDER CHARGE OF CORRUPTION BECAUSE THEY HAVE FEW PRESIDENT AND MEMBERS WHO ARE THERE FOR MANY YEARS BY BLESSING OF POLITICAL BOSSES ,MANY POLITICIANS WHO NEVER PLAY ARE HEAD OF SPORTS AUTHORITIES ,FEW DOCTORS ARE RUNNING THESE MEDICAL COUNCIL FOR YEARS,IT IS NEEDED THAT OUR PARLIAMENT SHOULD MAKE RULE THAT NO PRESIDENT OR MEMBER SHOULD BE IN THESE COUNCIL FOR MORE THAN 03 YRS EITHER REPRESENTATIVE OF CENTRAL GOVERNMENT OR STATE COUNCIL OR REPRESENTATIVE OF UNIVERSITY OR ELECTED FROM ANY OTHER ASSOCIATIONS,PRESENCE OF FEW SUCH CORRUPT PERSONS CANNOT BLAME THESE IMPORTANT AUTONOMOUS BODIES NEEDED VERY MUCH FOR SMOOTH RUNNING OF OUR MEDICAL AND HEALTH EDUCATION.FEW UNTRAINED IAS OFFICERS AND SENI OR OTHERWISE EDUCATED POLITICIANS CANOT JUSTICE WITH THESE AUTONOMOUS BODIES,MERE SELECTION OF FEW EXPERTS BY THESE PERSONS WILL BRING THEIR WELL WISHERS AND CATORIE PEOPLE AND DEMOCRACY WILL BE STRANGULATED IN THESE ORGANISATION AS IF WE READ BELOW PARAGRAPHS WE SHALL KNOW HOW WISELY THE CONSTITUTION OF THESE ORGANISATION HAS BEEN WRITTEN .
MEDICAL COUNCIL OF INDIA,DENTAL COUNCIL OF INDIA AND NURSING COUNCIL OF INDIA ARE STATUTORY BODIES TO REGULATE MEDICAL,DENTAL AND NURSING EDUCATION AND SERVICE IN THE COUNTRY.MEDICAL COUNCIL OF INDIA WAS ESTABLISHED IN YEAR 1934 UNDER MEDICAL COUNCIL OF INDIA ACT 1933,IT WAS AMENDED POST INDEPENDENCE IN 1956.IT WAS FURTHER AMENDED IN YEAR 1958,1964,1993,2001 AND 2004.iN YEAR 2009 'MCI' CELEBRATED ITS PLATINUM JUBLEE IN YEAR 2009.IN YEAR 2002 HON'BLE SUPREME COURT CONSTITUTED A BODY OF THREE EMINENT DOCTORS DR.TANDON, DR.MRS.KANTHA AND DR.RANGABHASYA TTO MONITOR FUNCTIONING OF MCI AND THEY SUGGESTED THAT MCI SHOULD BE EMPOWERED MORE AND MORE BUT STILL GOVERNMENT REJECTS MANY ITS PROPOSAL TO START NEW MEDICAL COLLEGES BECCAUSE AS PER 1956 ACT,GOVERNMENT ONLY CONSTITUTES AND REGULATE MCI BY MAKING RULES .GOVERNMENT NOMINATES ITS 37 MEMBERS DIRECTLY CAN CONSTITUTE ANY ENQUIRY IF MCI IS NOT WORKING PROPERLY,CENTRAL GOVERNMENT REGULATE POST GRADUATION COURSE DIRECTLY AND MCI CANNOT START ANY MEDICAL COLLEGE WITHOUT PERMISSION FROM GOVERNMENT.MCI FINANCE IS AUDITED BY CONTROLLER AND AUDITOR GENERAL OF INDIA AND WHOLE MCI IS UNDER SCAN OF PARLIAMENTARY COMMITTEE OF HEALTH AND FAMILY WELFARE.
ITH HAS GOT MEMBERS FROM MEDICAL PRACTITIONERS FROM ALL OVER INDIA REGISTERED IN STATE MEDICAL COUNCIL ,BESIDES MEMBERS FROM STATES AND UNIVERSITIES.PRESIDENT AND VICE PRESIDENTS ARE ELCTED,BUT IT HAS A SEPARATE JURISTIC PERSONALITY ,IT IS NOT A MERE MOUTH PIECE OF GOVERNMENT,GOVERNMENT CANOT INTERFEE DIRECTLY INITS AFFAIS,REMOVE OFFICE BEARERS AND GUIDE AND SUGGEST THEM UNDER PRESSURE ,THIS THE REAL PROBLEM OF MCI AND GOVERNMENT ,NO DOUBT ITS OFFICE BEARERS HAVE DONE SOME MISTAKES BY ON THIS BOARD FOR YEARS AND MANIPULATION GOVERNMENT THROGH BACKDOOR INFLUENCING AND EARNING HUGH MAKING SUCH BODIES AS THEIR CORPORATE HOUSES BUT HERE IS A FAULT OF BBOTH MCI AND GOVERNMENT WHY GOVERNMENT FOLLOWED THERIR RECOMMENDATION AND ALLOWED THEM AT THESE PLACES FOR YEARS.THIS ORDINANCE 2010 IS FOR ONE YEAR AND HAVE STARTED A FIVE MEMBER BOARD OF GOVERNORS TILL NEW COUNCIL IS ELECTED.THIS ORDINANCE ITSELF IS CONTOVERSIAL FOR A STATUTORY BODY LIKE MCI AS ITS PARENT LAW DOESNOT PERMIT FOR SUCH DISSOLUTION ,GOVERNMENT OF INDIA HAS INTRODUCED A BILL IN PARLIAMENT ON 3RD MAY2010 "NATIONAL ACCREDITATION ANDREGULATORY FOR HIGHER EDUCATION INSTITUTIONAL BILL 2010"UNDER WHICH IN MANY UNLAWFUL CONDITION GOVERNMENT CAN DISSOLVE ANY STATUTORY EDUCATION BODY AFETER GIVING ENOUGH TIME TO REPRESENT.PREVIOUSLY FORMER HEALTH MINISTER DR.A RAMDOSS ALSO WANTED TO DISSOLVE MCI THROUGH AN ORDINANCE BUT PMO SEND IT TO PARLIAMENTARY COMMITTEE WHO REJECTED IT.
GOVERNMENT 'S HRD MINISTRY HAS BROUGHT A BILL NAMED AS "NATIONAL COMMISSION FOR HIGHER EDUCATION(NCHER) AND WANT MEDICAL EDUCATION LIKE ALL EDUCATION UNDER IT BUT HEALTH MINISTRY HAS ADVOCATED 'NATIONAL COUNCIL FOR HUMAN RESOUCE AND HEALTH(NCHRH) TO RETAIN MEDICAL EDUCATION UNDER THIS MINISTRY ,THERFORE WE CAN ASSUME HOW TWO DEPARTMENTS/MINISTERS ARE FIGHTING TO KEEP THIS GOLD MINE UNDER ITS REGULATION AND HERE INTEREST OF MEDICAL EDUCATION,SERVICE AND STATUS WILL BE COMPROMISED AND POLITICIANS AND BUREACRATS WILL EARN IN CRORES DISSOLVING THESE COUNCILS .AS PAST PRESIDENT OF THESE BODIES MIGHT EARNED HUGH EDUCATION IS ON SALE FOR STARTING NEW MEDICAL COLLEGE AND DENTAL COLLEGES AND NURSING COLLEGES WHERE A STUDENT HAVE TO PAY LAKHS IN WHITE AND LAKHS IN BLACK TO GET ADMISSION UNDER DIFFERENT QUOTAS IN GRADUATE COURESE AND CRORES FOR POST GADUATION IF SUCH HIGH FEES ARE BLOCKED BY GOVERNMENT CORRUPTION WILL GO AWAY FRO MEDICAL COLLG OR DENTAL COLLEGE OR NURSING COLLEGE.EVEN VERY WEAK STUDENTS ARE ADMITTED EITHER AS SPECIAL OR NRI QUOTA AND THESE WEAK REMAIN WEAK FOR YEARS AS THEY ALSO GET THROUGH BY BRIBERY IN THESE PRIVATE MEDICAL COLLEGE,GOVERNMENT SHOULD STOP ALL THESE THINGS AND STOPS COPMLETE CAPITATION AND BACK DOOR ENTRY FEE BUT THESE WILL NOT BE STOPPED BY GOVERNMENT BECAUSE OTHERWISE HOW THESE POLITICIANS AND BUREAUCRATS WILL EARN CRORES OF RUPEES.
THERFORE IT IS NEEDED THAT THESE COUNCILS ARE NOT DISSOLVED BUT SHOULD BE MADE MORE ACCOUNTABLE,TRANSPARENT AND FUNCTIONAL TO RAISE MEDICAL EDUCATION AND PRODUCE ENOUGH DOCTORS,DENTIST AND NURSES TO IMPROVE OUR HEALTH EDUCATION AND SERVICE TO OUR FELLOW CITIZENS AND TO CREATE MOR CHECK AND BALANCES SOTHAT NO BODY CAN BE HERE FOR YEARS AND USE IT AS ONE'S BUSINESS HOUSE OR CORPORATE BODY.
DR.D.R.NAKIPURIA
AMBIKA CHIKITSHALYA
29 AGRASEN ROAD
SILIGURI-734005,09434143550


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Aug13
NDM1-BACTERIA IN INDIA -IS REALLY THREAT ?
Recently just published Article in a prestigious and reputed Jounal of World fame "LANCET" by an Indian scientist on presence of NDM-1 Bacteria,originating from New Delhi, Called New Delhi Metallo-beta-Lactamase-1,a new Superbug ,is really a new threat to World and our country too.But the way it has been published with an inference at last paragraph issuing a warning to all coutries and persons of World to be ware of going to India as if it is only hub and concentrated centre of this newly discovered Gram Negative Bactria or called BUG and adding name of our capital "NEW DELHI" to its name only on the basis of one patient who got treatment from New Delhi before detection of this Bacteria from his blood in Sudan,having no knowledge whether he was carrying it before treatment in India and then sporidacally adding that it is also found in Pakistan,Bangladesh and even in UK raise seroius question regarding authencity of such publication funded by two multi national Drug companies who make medicines ,Antibiotics for killing Bacterias and secondly by maligning India to prevent Foregners coming to INDIA for Treatment leaving UK and European and America .This bacteria like all bacteria might be prevalet in all parts of World but as no research has been done carefully to identify it in various part of World cannot be accepted as it is found mainly in New Delhi /India/Pakistan/Bangladesh only.
If Journal like Lancet is also manipulated like this then our whole Humanity is under threat ,any body can get any thing published to control or manipulate any thing to market or defame any product but once it is coming to world of Health it is a really serious question for humanity as corruption,manipulation favourism or criticism like such will spoil our Human Enviornment of turst and belief completely.
Therefore ,it is not only limited to Our Politicians,Health Ministry Parliament,ICMR,Medical Associations and Doctors of India but of whole World should protest against it in India and whole world ,serois objection should be stated at WHO level as why such reports were published in this manner to malign the name of a country to check "MEDICAL TOURISM" and such efforts should be nipped in the bud today and even in future sothat Commerce and Market should atleast spare Health System for giving wrong informations otherwise whole Humanity will collapse.
But it does not mean that we shall not take precautions,we should take extra effort in sterilisation of our Operation Theatre,Post up Wards and Preop Wards and post Op care somuch clean and clear that such Bacteria never infect any patient whether Indian or from outside under our treatment.
we know that Bactrias are known for mutations to save its progeny from devastation by bringing change in ts plamid and cell wall proteins. esearchers and is resistant to all known antibiotics. These are not being killed by modern Carbopenams(meropenam)and other Beta Lactamase Inhibitors(Tazobactum,sulbactum,pipercillin) as a result more infection to wounds will come to a normal patients in our hospital and those compromised like diabetics,suffering from cancer,HIV,getting,immunosupressants for transplants, immunological disorders,on steroid,cancer chemotherapy,elderly and childrens.

Lancet Infectious disease journal reports 50 such cases. Most of them have carried this infection from India, Pakistan and Bangladesh. The superbug NDM-1 is named after the national capital, where a Swedish patient was reportedly infected after undergoing a surgery in 2008. It is much more dangerous than the notorious MRSA infection.
MDM-1 is an enzyme produced by certain bacteria, which allows them to neutralize the harmful effects of carbapenem one of the most powerful types of antibiotics. Currently no new types of antibiotics are in the development pipeline that will be effective against it. Enzymes such MDM-1 are produced by strands of DNA which bacteria are known to transfer between one another. Currently E Coli and Klebsiella Pneumoniae are the two bacteria who are host to MDM-1. What makes the superbug more dangerous is its ability to jump across different bacterial species. The superbug has the potential to get copied and transferred between bacteria, allowing it to spread rapidly. If it spreads to an already hard-to-treat bacterial infection, it can turn more dangerous.The current treatment option is to treat them with a cocktail of antibiotics. Most new antibiotics currently under development are effective only against gram positive bacteria like super bug MRSA. Unfortunately, bacteria that carry the NDM-1 enzymes are gram negative.

A joint study was led by Chennai-based Karthikeyan Kumarasamy, pursuing his PhD at University of Madras and UK-based Timothy Walsh from department of immunity, infection and biochemistry, department of medicine, Cardiff University. They found the bug in most of the hospitals in Chennai and Haryana with estimated prevalence of this infection 1.5%. They reported the superbug in 44 patients in Chennai, 26 in Haryana, 37 in the UK and 73 in other places across India, Pakistan and Bangaladesh.gram negative sepsis with culture report: resistant to all antibiotics. We have been seeing such cases in the last few years. Now we have a name for this disease. Many of the doctors are deying its existance and linking it to a move against medical tourism in India. But the ICMR, NICD should work on it and come out with guidelines for this infection as no one can deny the fact that we do see cases of gram negative sepsis with E Coli or Klebsiella with culture report resistant to all antibiotics.

Carbapenemases are carbapenem-hydrolyzing beta-lactamases that confer carbapenem resistance.while Class B enzymes require the presence of zinc for activity (and hence are referred to as metallo-beta-lactamases).Class B beta-lactamases: are also known as the metallo-beta-lactamases (MBLs), which are named for their dependence upon zinc for efficient hydrolysis of beta-lactams. As a result, MBLs can be inhibited by EDTA (an ion chelator), although they cannot be inhibited by beta-lactamase inhibitors such as tazobactam, clavulanate, and sulbactam.
Acquired MBLs consist of genes encoded on integrons residing on large plasmids that are transferable between both species and genera.In a hospital outbreak involving 62 patients (including 40 intensive care unit patients), for example, an MBL gene (bla IMP-4) spread among seven different gram-negative genera (Serratia, Klebsiella, Pseudomonas, Escherichia, Acinetobacter, Citrobacter, and Enterobacter).Laboratory detection of MBL-producing organisms can be especially difficult if the organisms carry "hidden" MBL genes; The MBL E-test (a commercially available assay) cannot consistently identify MBL-producing organisms that are truly resistant to carbapenems. Therefore, MBL-producing organisms should be considered carbapenem-resistant regardless of carbapenem susceptibility results.

Other identification methods take advantage of the zinc dependence of MBLs by using EDTA, which chelates the zinc. Combination disc tests using imipenem and EDTA discs or using two carbapenem discs (including one with EDTA incorporated) have been reported. A more sensitive MBL detection method uses an agar plate with three components: a double disc synergy test with imipenem and EDTA discs, a combined disc test comprising two imipenem discs (with one disc also containing EDTA), and an aztreonam disc to detect aztreonam susceptibility. Carbapenem susceptible isolates that are resistant to both ceftazidime and ticarcillin-clavulanate should be considered for MBL testin Genotypic identification using PCR amplification with primers specific for MBL genes (eg, blaVIM or blaIMP) is an accurate method for the detection of MBL-producing organisms.(Source uptodate)

Therfore,we are not against its finding but its conclusion and attribution to one country India ,more and more reseaches and studies are needed to confirm its real presence in World and how it comes and persist and before doing enough studies such publication with infernces in reputed journals should be avoided otherwise whole Humanity will be at stake and Market and commerce will win over our Human Value.
Dr.d.R.nakipuria
Teacher In North Bengal Medical College for undergarduate and Post Graduate
Ambika Multispeciality Hospital
29 Agrasen roadSiliguri-734005


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Aug10
The Prime Cause and Prevention of Cancer with two prefaces on prevention.
Revised lecture at the meeting of the Nobel Laureates on June 30, 1966 at Lindau, Lake Constance, Germany

by Otto Warburg Director, Max Planck-Institute for Cell Physiology, Berlin- Dahlem

Dr. Otto Warburg, twice Nobel Laureate, awarded the Nobel Prize for Physiology or Medicine in 1931 for his research on cellular respiration, explains:

“The growth of cancer cells is initiated by a relative lack of oxygen. Cancer cannot live in an oxygen-rich environment…Cancer has only one prime cause. It is the replacement of normal oxygen respiration of the body’s cells by an anaerobic (i.e., oxygen deficient) cell respiration.”

Going into greater detail in The Prime Cause and Prevention of Cancer, he writes: “…the cause of cancer is no longer a mystery, we know it occurs whenever any cell is denied 60% of its oxygen requirements.

Cancer, above all other diseases, has countless secondary causes. But, even for cancer, there is only one prime cause. Summarized in a few words, the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar. All normal body cells meet their energy needs by respiration of oxygen, whereas cancer cells meet their energy needs in great part by fermentation.

All normal body cells are thus obligate aerobes, whereas all cancer cells are partial anaerobes.” Compare Otto Warburg On The Prime Cause & Prevention of Cancer: Respiration of Oxygen in Normal Body Cells vs. Fermentation of Sugar in Cancer Cells.

Please download here the full Cancer Protocol of Otto Warburg (56 page pdf):
http://new-planet.net/pdf/O-Warburg-CancerProtocol.pdf


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Jul22
HAV & OTHER VIRAL INFECTIONS OF LIVER
HEPATITIS-A VIRUS (HAV)
INTRODUCTION:-
Known as Infectious Hepatitis. In 1973 this virus was detected in stool. In following years specific serologic assay & isolation of HAV in cell culture were done to study the epidemiology & prevention. Commonly transmitted by fecal-oral route via contaminated food or water. Incubation period is 2-6 weeks. In developing countries due to poor hygiene standard the incidence is high. Infection causes no clinical signs in >90% of children & offers lifelong immunity having special significance in indigenous population.It does not have a chronic stage & does not cause permanent liver damage. Vaccine is helpful in controlling out break.
VIROLOGY:-
Belongs to Picornaviridae family with genus Hepatovirus. HAV is icosahedral in shape without envelope, having diameter of 27- 28 nm. HAV survives exposure to ether, acid at pH 3, heat exposure at 60o C for 60 minutes but inactivated at 85 o C for 1 minute. HAV is capable of surviving sea water (4%), dried faeces at room temperature for 4 weeks(17%),in live oysters for 5 days(12%).Only one serotype of HAV is known & there is no antigenic cross-reactivity with B,C,D,E,F,& G. The HAV genome consists of positive sense RNA which is single stranded & linear. The HAVRNA has a long open reading frame consisting of 6681 nucleotides & covalently linked to a 5’ terminal protein& a 3’ terminal polyadenosine tract. HAV replication in cell culture takes weeks to months depending on metabolic activity of host cell. In the life cycle of the virus the 1st step is attachment to cell surface receptors, the location & function determine tissue tropism .Though exact mechanism of entry of HAV in to cell is not known probably through surrogate-receptor binding mechanism. A surface glycoprotein named HAVcr-1 has been identified as receptor for HAV. Experimental data suggest that HAVcr-1 not only serves as an attachment receptor but may facilitate un coating of HAV& its entry to hepatocytes. After entry of HAV the viral RNA is un coated , cell host ribosome bind to viral RNA forming polysomes & HAV is translated to large polyproteins which are organized to 3 regions:P1,P2,P3.The P1 encodes structural proteins VP1,VP2,VP3 &VP4.P2 & P3 encode non structural proteins associated with viral replication.
Numerous strains of HAV exists with variability of nucleotide sequences Human HAV strain have 4 genotypes (I,II,III,VII) where as simian have IV,V,VI genomes. But despite heterogeneity of nucleotide sequence the antigenic structure is maintained. HAV VP1/2 & 2C are thought to be responsible for virulence. Among many strains of HAV HM175 &CR326 are important as they are used for production of vaccine. Variation of HAV genome are responsible for fulminant hepatic failure (FHF) during acute HAV infection.
HAV can be inactivated by Chlorine treatment, formalin(0.35% 37C,72 hours),peracetic acid(2%,4 hours)beta-propiolactone(0.25%,1 hour), UV radiation(2΅w/cm2/min)
EPIDEMIOLOGY:-
In US the annual calculated rate is 93,000.The highest rate is among children between 5-14 years. But it can occur in any age. The epidemiological risk factors in US-unknown (57%), sexual or household contact (12%),
International travel(9%),male homosexual(8%),injection drug users(5%),child or employee in day care(1%),food & water borne(1%),other contacts(7%).
HAV infection usually follows one of the three epidemiologic patterns:-
1. In poor sanitary conditioned countries most children at an early age are infected showing 100% Anti-HAV antibody in their serum indicating sub clinical infection. Symptomatic infections has risen to 5 years & older groups. Differs in income groups. About 95% children of low income families are infected.
2. Second pattern is seen in industrialized countries where prevalence of Anti-HAV in children is 10% & adults 37%.
3. Third pattern is seen in closed or semi closed communities like South pacific. HAV infects entire population, which then become immune. Only new borne become susceptible.
TRANSMISSION:-
The primary route of transmission is fecal-oral route by either person to person contact or ingestion of contaminated food or water.
Rare routes:- Parenteral after blood transfusion, Injection users & non injection illicit drug users
Homosexual males
Detection of HAV & infectivity of secretions & excretions
Stool:- HAV detected during incubation & for several weeks after onset. HAV is found in 45% & 11% during 1st & 2nd weeks respectively. HAV-RNA (by PCR) is detectable up to 4-5 months.
Blood:- Viraemia present during incubation. Blood collected 3-11 days prior to onset causes post transfusion, Infection.
Bile:- Detected in Chimpanzees.
Urine:- Detected in viraemia phase. Urine contaminated with blood is infectious.
Nasopharyngeal secretion:- Unknown to human.
Semen, vaginal fluid:-Uncertain. HAV detected in viraemia phase.
Virus spread is common in poor sanitation & over crowding. Common source (e.g. water, restaurant) outbreaks are typical.
PATHOGENESIS:-
HAV once ingested survives gastric acid, pass to mucosa of small intestine & reaches liver via portal vein. Entering into hepatocytes by uncertain mechanism replicate in the cytoplasm (seen by E/M as fine granules) but not in the nucleus. HAV is distributed through out the liver. Though antigen is detected in lymphnodes, spleen, kidney they exclusivey replicate in hepatocytes. Once the virus is mature it reaches the systemic circulation via hepatic sinusoids & released to billiary tree through bile cannaliculi, pass into intestine & faeces. The hepatocyte injury is not clear as HAV is not cytopathic. Immunologically mediated cell damage is more likely. The anti HAV could result in hepatic necrosis duringmmunologically mediated elimination of HAV.
CLINICAL FEATURES:-
Incubation period is 2-4 weeks, rarely up to 6 weeks.
Course is usually acute self limiting, prolonged or relapsing, cholestatic phase but chronic infection does not occur. Mortality is low in healthy persons & morbidity is high in adults & older children.
More in men in all age groups.
HAV infection usually presents in 5 different clinical presentations:-
1.-Asymptomatic without jaundice
2.-Symptomatic with jaundice & self limited-8 weeks
3.-Cholestatic with jaundice lasting 10 weeks or more
4.-Relapsing with 2 or more bouts of acute infection over 6-10 weeks
5.-FHF
Children below 2 years are usually asymptomatic jaundice in 20%. Children over 5 years or more are symptomatic (80%).Symptoms are more in adolescent or adults. Cholestatic type is a rare variant where jaundice persists for long period & subjected to invasive diagnostic procedures. Relapsing course is observed in 10% cases where shedding of HAV in stool is detected. This variant is benign & resolve ultimately. Neither cholestatic nor relapsing variant has greater mortality & treatment is symptomatic. Unlike Hepatitis-E, HAV has no higher mortality in pregnant women.
Usual prodromal symptoms are fatigue, weakness, anorexia, nausea, vomiting, abdominal pain. Less common symptoms are fever, headache, arthralgia, myalgia, diarrhea. Dark urine precedes symptoms (90%).Symptoms may last for few days to 2 weeks & decrease after onset of jaundice. Right hypochondriac pain & mild tender hepatomegaly (85%), splenomegaly (15%), cervical lymphadenopathy (15%) may be noted.
Complete clinical recovery in 2 months (60%) & in 6 months (100%).
Overall prognosis is good in healthy adults.
Fulminant hepatic failure (FHF):-
FHF is rare in children, adolescent or young adults.
Case fatality in aged >49 years is 1.8%.
Usually manifest in 1st week of illness (55%) & first 4 weeks (90%).Rare after 4 weeks.
It is higher in hyperendemic area like India.
The increased among elderly, associated CLD.
Extra hepatic manifestations:-
Less frequent than HBV. Consists of evanescent rash(14%), arthralgia(11%), leukocytoclastic vasculitis, glomerulonephritis, arthritis which are due to immune complex mechanism.Cutaneous vasculitis are seen in legs & buttocks.Skin biopsy reveal presence of IgM anti HAV & complement in vessel wall. Vasculitis & arthritis are associated with cryoglobulinemia where cryoglobulin contains IgM antiHAV. Other extrahepatic manifestations include toxic epidermal necrolysis, fatal myocarditis, renalfailure,optic neuritis, transverse myelitis,polyneuritis, cholecystitis, thrombocytopenia, aplastic amaemia, red cell aplasia.
Auto immune hepatitis (AIH) after HAV: - HAV rarely trigger the onset of Type-1 AIH.
DIAGNOSIS:-
Acute HAV is to be differentiated from other causes of viral hepatitis, AIH & other causes of hepatitis by serological tests. Many times it may be difficult due to associated chronic HBV or HCV infection.
In acute HAV IgM-antiHAV antibody is positive from the onset of symptoms & usually remains +ve up to 4 months.In some low levels may be detected up to 1 year.IgG antiHAV antibody is detected at the onset & remain +ve through out life indicating a marker of previous infection.
HAV-RNA (by PCR) has been detected in stool, blood &liver. HAV-RNA is usually undetectable in FHF than non-fulminant hepatitis. It is suggested that detection of IgM antiHAV coupled with nondetectable or low titer of HAV-RNA may signal ominous prognosis & require liver transplant.
During acute phase the liver enzyme ALT is high.
TREATMENT &PREVENTION:-
High risk populations are targeted for vaccination. Childhood vaccination have a +ve effect in reducing incidence.
High risk groups:--
Healthy persons traveling to endemic area, occupation likelihood of exposure, family members of
Infected person, adopt infant or child from endemic area.
Persons with CLD.
Persons who are HIV +ve.
Homosexual man.
Users of injection & illicit drugs.
Clotting factor disorders.
Persons living in high or intermediate rate of HAV infection.
No specific treatment. Symptomatic treatment is the rule. Advise rest, avoid fatty food & alcohol, take balanced diet & proper hydration.
Attention of proper sanitation.
Role of Immune Globulin (IG):-Use of pre exposure prophylaxis is unnecessary due to availability of vaccine. In post exposure prophylaxis IG should be given within 2 weeks of exposure in a dose of 0.02 ml/kg IM.IG can cause fever, myalgia. IG can safely be given along with vaccine.
HAV vaccine: - Two inactivated HAV vaccine are available ,to be given IM in deltoid area.
HAVRIX & VAQTA are 2 vaccines derived from HAV grown in cell culture. They are purified, formalin inactivated & contains Alum as adjuvant. HAVRIX is prepared from HM175 strain & VAQTA from CR326 strain of HAV virus, Both are safe & immunogenic. Immunity lasts for 20 years or longer.
Common side effects are soreness at injection site (56%), headache (14%),malaise(7%). Some unexplained adverse reactions are neurologic, haematologic, &autoimmune syndrome.
A combination formula of HAV &HBV is available with excellent safety &efficacy (TWINRIX).
Dosing schedule-----
HAVRIX - 2-18 years 0.5ml 0,6-12 months.
>18 years 1 ml 0, 6-12 months.
VAQTA- 2-18 years 0.5 ml 0, 6-18 months.
>18 years 1 ml 0, 6-18 months.
TWINRIX- ≥ 18 years 1 ml 0, 1, 6 months.
PROGNOSIS:
Death usually occurs if patient is already suffering from other hepatitis like B,C & AIDS. Young children experience mild form whereas adults much severe form.

HEPATITIS-D VIRUS (HDV)

INTRODUCTION:
Hepatitis D(delta) virus was discovered by Rizzetto in 1977 as an unique nuclear antigen in hepatocytes of patients infected with HBV, when he observed a new antigen other than surface, core, & e antigen.
EPIDEMIOLOGY:
Distributed worldwide.5% of HBV carriers are infected with HDV with a burden of 15-20 millions. Highest prevalence in South America & Mediterranean basin. The incidence of HDV is declining in some countries due to screening of blood donors for HBsAg. However HDV remains among injection drug users. Among 3 genotypes of HDV(I,II,III) genotype-I is prevalent in Mediterranean countries, Africa, Europe, North –America. Different subtypes within this genotypes are seen in Africa. Genotype-II is seen in Japan &Taiwan with mild liver disease. Genotype -III is seen in South America associated with high mortality & a lesion in liver cell is called morula cells. Various genotypes of HDV & HBV may interact though their effect on HDV is not clear. But infection with HDV genotype III&HBV genotype F cause severe hepatitis. The mode of transmission of HDV is closely linked to HBV mainly parenteral route. Sexual transmission & familial clustering seen in endemic areas. In Asian population it is primarily in injection drug users. It is not clear why HDV is so frequent & lethal in Amazon basin, nonexistent in Asia & fairly benign in Greece & South pacific. Researchers suspect different HDV genotypes cause varying degrees of liver damage.
VIROLOGY:
The 1.7 kb single strand negative sense HDV-RNA genome shares many features with plant viroids.Unlike plant viroids HDVRNA encodes a protein hepatitis delta antigen (HDAg). The virion consists of HDV genome complexed with 70 copies of HDVAg in an envelope protein composed of lipid & HBsAg .The protein envelope contributed by HBV protects HDV-RNA-HDAg complex. Once HDV with its HBV envelope protein enters the host the HDV-RNA-HDAg complex migrates to the nucleus. Viral replication proceeds in the nucleus.
During translation two forms of HDAg are formed, short form (HDAg-S),long form(HDAg-L) the later having 19-20 more amino acids. The long & short forms have opposite effects on viral replication, the short form as facilitator, the long form as inhibitor. In states of high replication HDAg-S is produced.
HDV is classified as a single separate genus of Deltaviridae family. The consensus is that HDV is a satellite virus, which is a sub viral particle carrying distinct nucleic acid, usually RNA, requires helper virus for transmission & multiplication, differ in nucleic acid of helper virus. No other animal virus ha been identified as satellite virus. It is the smallest virus, unique virus & most virulent. The genetic information is stored in RNA where as in others it is stored in DNA.
TRANSMISSION:
Through blood & blood products like HBV. Unlike HBV sexual transmission is less though it can be transmitted by barrier free sexual activity. Homosexuals are prone but less than injection drug users. Vertical transmission is rare.
PATHOGENESIS:
Mechanism is not clear. HDV is not directly cytotoxic. Combined infection of HBV &HDV may have a direct cytotoxic effect or an enhanced immune response against two viruses. HDV may be related to immunological response s evidenced by presence of antibodies to liver-kidney microsome (anti-LKM), thymocytes, nuclear lamin C. The ability of HDV to cause hepatic necrosis is by expression of HBV. Blood is potentially infectious in all phases of acute & chronic infection, but most infectious prior to onset of illness & symptoms.
NATURAL HISTORY:
The incubation period varies from 21-90 days. Depending on HBV two types of HDV occurs.
1. Coprimary infection-Simultaneous infection of HDV &HBV.
2. Superinfection-HDV is superimposed on chronic HBV.
HDV infection has a varying influence on the course of HBV. The severity of HDV infection may vary with frequency of HDV in a population, with level of HBV viremia, with interaction of specific HBV &HDV genotypes.
Co primary infection:-Most often in injection drug users. As both resolve in most cases chronicity is <5%. Some data suggest enhanced risk of fulminant hepatitis & death.
Super infection:-Can lead to severe hepatitis & acute decompensation. There occur high levels of HDV viremia. As HDV replication inhibits HBV replication there occurs decline of HBV-RNA. Rarely disappearance of HBsAg & appearance of antiHBs occurs. Chronic HDV infection frequently occurs than confection (70%), characterized by persistent of HDV viremia & detectable HDV-RNA in serum. The persistent replication of HBV &HDV lead to progressive hepatitis & cirrhosis within years. More rapid course lead to end stage liver disease.
The clinical course of a triple infection HBV,HDV&HCV is dominated by HCV.The patients often have severe episode of acute hepatitis. The chronic stage slowly progress like HDV or HBV.
CLINICAL PRESENTATION:
Co infection typically manifest as self limiting acute hepatitis. Some show double peak of serum aminotransferase due to delay in HDV replication after HBV replication. Detectable serum IgM antiHBc, IgM antiHDV, HDV-RNA, HBV-DNA, HBsAg are seen. The enzymes return to normal after infection resolves.
HDV super infection manifest as acute hepatitis in a stable HBV carrier, mimicking spontaneous flare up of HBV infection. But presence of HDV-RNA and IgM anti HDV is the marker for super infection. As IgM anti HDV is seen in both co infection and super infection serologic finding of IgM anti HBc indicates co infection of HBV.
In association of HBV complicate acute liver failure, develop liver cancer and chronic infection. Combined mortality is 20%.Symptoms are similar to other viral infection, like fever, jaundice anorexia, malaise, dark urine, rash, nausea,arthralgia. But patients are more ill than HBV alone. Cirrhosis develops in 60-70% (higher than B or C ).
DIGNOSIS:
The useful markers are HDAg, antibody to HDAg(Anti HDV) , HDV RNA, and immunohistochemical starting of HDAg in liver.
• Detection of HDV-RNA by reverse transcriptase PCR(RT-PCR) is most reliable with 100% sensitively and earliest marker seen during the course without any other markers and high level is associated in severe cases. It also indicates efficacy of treatment and viral eradication. HDV RNA can be detected in liver by hybridization technique which is less sensitive than RT-PCR.
• HDAg is demonstrated in Liver cells by immunohistochemical staining but reliability decreases as disease become chronic. Presence of neutralizing antibody also interfere its detection.
• Detection of AntiHDV does not confer protection against HDV. Either IgM or IgG AntiHDV is detected. IgM appears in serum early and IgG later. IgM persists into chronic HDV infection and a marker of serious infection. As the disease turn to chronic the IgM changes from monomeric(S) form to multimeric (19S). IgG persists for a long time in immunocompetent person indicating chronic or previous infection.
TREATMENT:
Treatment of HDV is disappointing. Interferon is the only promising drug. Nucleoside analogs are not effective for HDV. Several clinical trials evaluated the efficacy of interferon in treating chronic HDV. Pegylated interferon treatment has not been reported. Nucleoside analogs like Lamivudine have not shown influence on HDV replication and not recommended. Co infections with HIV or HCV have poor rates of response. Usually Interferon alfa 9 million unites 3 times weekly for 1 year is recommended. Treatment for longer duration may be beneficial but to be considered on the basis of histologic severity, HDV-RNA response, and patient tolerability. Use of Pegylated interferon needs further study.
Advanced molecular biology may help to identify specific inhibitor of HDV replication. Prenylation (addition of prenyl lipid like farnesyl) of HDAg-L is a critical determinant of HDV particle assembly. In vitro it is shown that prenylation can abolish particle production.
PREVENTION:
Vaccination against HBV confers protection against HDV. Groups showing high rate of HDV infection should be vaccinated. Once HBV are eliminated HDV can not replicate without HBs antigen and also disappear. No vaccine is available against HDV. Super infection can be reduced by safer sex practice, avoiding blood or blood product contact and not sharing needles.

HEPATITIS-E VIRUS(HEV)
INTRDUCTION:
Hepatitis-E is a form of acute, icteric, self limited viral hepatitis caused by HEV. It was recognized in 1980 during epidemics at Delhi, Kashmir. Subsequently the virus and genomic sequence were identified. In retrospect study similar enterically transmitted hepatitis occurred in Europe in 18th and 19th centuries.
VIROLOGY:
It is a small RNA virus , 32-34 nm in diameter, unenveloped and icosahedral shape. HEV-RNA is 7.2 kilo bases in length, single and positive stranded 5-’capped and polyadenylated. It contains 3 open reading frames (ORSs). ORF1 encodes nonstructural protein, ORF2 encodes the viral capsid protein and ORF3 encodes a protein of unknown function. HEV attachment and entry to hepatocytes, its replication and release mechanism in unknown. The virus is classified to genus Hepatitis-E like virus and phylogenetically related to Togavirus. Geographically various isolates of HEV are isolated like genotype1 (Asian Strain), type-2(Mexico Strain). All genotypes share at least one major serologically cross-reactive epitope. Swine HEV is genetically different from Human HEV in India but similar in other parts.
EPIDERMILOGY:
Several epidemics have been found in different parts of the world. Overall attack rate is 1-15%, higher in adults (3-30%) than children (0.2-10%). The male female ratio varies from 1:1 to 4:1. High attack and mortality rate occur in Pregnant women. The nature of epidemics range from single peaked, short lived outbreaks to prolonged, multipeaked lasting for more than 1 year.
Classification of HEV genotypes:-
Genotype Geographical Origin
1 Asia
1A India, Myanmar, Nepal
1B China, Pakistan, Soviet Union
1C Africa
1D India
2 Mexico, Africa
3 U.S
4 China, Taiwan
5 Italy
6 ,7 Greece
8 Argentina
Prevalence rates of antiHEV, which is detectable in all geographical areas are higher among endemic (10-40%) than nonendemic (1-5%).
Reservoir:-Domestic animals like pigs have been reported. A number of rodents has also been identified. The disease is thought to be a zoonosis as animals like pigs & deer are the sourse.
TRANSMISSION:
Predominantly through fecal-oral route. Outbreaks usually occur following heavy rain or flood & in Summer due to increased contamination. Person to person contact is uncommon & secondary attack among household contact is 0.7-2.2%. Maintenance of continuous virus in endemic area are due to sub clinical HEV infection, animal reservoir harboring HEV- like viral agents & prolonged fecal shedding of virus. Sporadic hepatitis which is demographically & clinically similar to epidemic form accounts for 50-70% of acute cases in endemic areas. Some are related to travel to endemic areas. Occasionally it can be due to undercooked meat. One study shows HEV transmission through blood but data is inadequate. No evidence of parenteral or sexual transmission.
PATHOGENESIS:
Entering through oral route virus reaches liver through unknown mechanism. HEV can be detected in stool 1 week before the onset of illness & up to 2 weeks there after. HEVRNA is detected in serum for 2 weeks after the onset of illness in all patients. HEV antigen (HEVAg)is expressed in hepatocytes as early as 7 days after infection in >50% of cells. But the number decreases sharply when serum ALT is increased. The onset of elevation of ALT & histopathologic changes in liver correspond to the appearance of antiHEV (IgG,IgM) in serum. This suggests the liver injury may be due to immune mediated specially lymphocytes infiltrating liver have a cytotoxic/suppression immunophenotypes. Like other forms of hepatitis there occurs ballooned hepatocytes, acidophilic bodies, focal parenchymal necrosis, inflammatory infiltrates in the lobules, enlarged portal tracts. About 50% have cholestatic hepatitis characterized by canalicular bile stasis & gland like transformation of parenchymal cells with less marked hepatic degeneration & necrosis. In severe cases sub massive or massive necrosis & collapse of parenchyma are seen.
CLINICAL FEATURES:
The incubation period is 2—10 weeks.There are varying clinical presentations.
1.Acute icteric hepatitis:-Onset is insidious. Prodromal phase(1-4days) have flulike symptoms, fever, mild chill, abdominal pain, anorexia, nausea, vomiting aversion to smoking, clay coloured stool, dark urine, diarrhea, arthralgia, asthenia & transient macular rash.Prodromal symptoms disappears with onset of jaundice except dark urine, clay stool, & itching. On examination there is jaundice, soft tender mild hepatomegaly & splenomegaly. Laboratory tests show bilirubinuria, conjugated hyperbilirubinemia, marked elevation of aminotransferase &gamma glutamyl transpeptidase. Elevation of ALT may precede the onset & level does not correlate the degree of hepatic injury. Mild leucopenia with lymphocytosis occurs. Serum ALT & bilirubin normalize by 6 weeks. Ultrasonography shows mild hepatomegaly with increased parenchymal echogenicity, gall bladder edema, prominent portal venules &mild splenomegaly. Acute infection usually self limited. The case fatality is 0.5-4%. Chronic hepatitis or cirrhosis do not occur.
2. Cholestatic hepatitis:-In some cases there is persistent jaundice (2-6 months), itching, marked elevation of enzymes. Ultimately spontaneous resolution occurs.
3. Anicteric hepatitis:-Some have nonspecific viral like symptoms with raised enzymes without jaundice.
4. Asymptomatic & anicteric:-Occurs frequently in younger age groups.
5. Fulminant hepatic failure:-In small cases sub acute or fulminant hepatic failure occurs mostly in endemic areas.
Pregnant women particularly 2nd & 3rd trimester are frequently affected. Fulminant hepatic failure, abortion, stillbirth, neonatal deaths are increased. The cause of high incidence is unknown.
DIAGNOSIS:
1. Detection of HEV-RNA-Detected in stool & serum using PCR.
2. ELISA to detect immunoglobulin’s (IgM,IgG)-Presence of IgM antiHEV where as IgG antiHEV indicate convalescent phase or past infection. IgM appears early, lasting for 4-5 months, detected in 80-100% of cases during outbreaks. IgG appears few days after IgM and titer increases in convalescent phase & remain for 1-5 years.
TREATMENT & PREVENTION:
Acute infection is usually self limited requiring supportive treatment. In fulminant cases requires measures to decrease cerebral edema or liver transplant. In pregnancy no proved benefit of terminating pregnancy is seen. Hemorrhage due to deranged coagulation can be treated with fresh frozen plasma.
PREVENTION-In endemic areas depends on supplying clean water& strict sewage disposal. Boiling of water may reduce risk. Isolation is not indicated.
Role of immunoglobulin given in pre or post exposure is not proved. Occurrence of epidemics in endemic areas indicate that anti HEV is not fully protective or the antibody declines with time to non protective level.
Various trials of vaccine are in the process. An experimental HEVDNA vaccine tried in primates. Prospect of vaccine even having short term protection is needed for travelers & pregnant women.
HEPATITIS F VIRUS
It is a hypothetical virus linked to hepatitis. Several cases emerged in 1990 but reports not substantiated. In 1994 viral particles detected in stool of post transfusion nonA-nonE hepatitis and injection of these materials to Indian rhesus monkey caused hepatitis & named as hepatitis F or Toga virus. Further investigation failed to confirm the existence and it was delisted.
HEPATITIS G &GB AGENT INFECTION

INTRODUCTION:
Hepatitis G virus (HGV)& GB agents(GBV) are isolates of same virus. GBV has been identified as 3 different types e.g. GBV type A(GBV-A), GBV type B(GBV-B), GBV type C(GBV-C).About 96% homology of genome occurs between HGV&GBV-C indicating two strains of same virus. The term hepatitis G virus is questioned due to lack of association between GBV-C/HGV & acute or chronic hepatitis. For clarity GBV-C/HGV is referred as GBV-C.
VIROLOGY:
GBV-C is a positive strand RNA virus genome containing 9400 nucleotides encoding about 2900 amino acids, classified as a member of Flaviviridae family. GBV-C shares 44% &28% homology with GBV-A &GBV-B respectively. Though GBV-C is similar to HCV it is clearly distinct. One long open reading frame encodes a single large polyprotein with structural protein encoded at 5’ amino terminus & nonstructural protein encoded at 3’ carboxyl terminus. The structural proteins differ in GBV-C &HCV. Though there are 2 glycoproteins E1&E2 of GBV-C the difference of polymorphism inE2 accounts for less chronic viremia in GBV-C infection (25%) than HCV(50-70%). In contrast the nonstructural proteins of HCV &GBV-C are similar. HCV &GBV-C differ in tissue tropism. In contrast toHCV, GBV-C does not show hepatotropism. But like HCV it shows lymphotropic property as negative strand RNA are found in mononuclear cells, bone marrow & spleen. Due to its interaction inside lymphocytes there is some interaction between HIV &GBV-C.
EPIDEMIOLOGY & TRANSMISSION:
GBV-C is found world wide(2-5%). At least 5 genotypes identified according to geographical distribution.Genotype1 (West Africa), genotype2 (Europe, US), genotype3 (Asia), genotype4 (Southeast Asia), genotype5 (South Africa).
The development of antibodies to GBV-CE2 correlates with loss of viremia & suggest past exposure and clearance of GBV-C infection. Current & past infection is found among parenteral risk factors & voluntary blood donors. Frequent blood exposed patients are viremic and seropositive toE2 antibodies (50-70%). Past or current GBV-C infection may show normal ALT, posing a risk for transfusion transmission (raised ALT-exclusion criteria for donors). It can be transmitted sexually & vertically more frequently than HCV. Infected babies have no evidence of hepatitis or other sequlae. As
HCV& GBV-C are transmitted parentrally co infection is common. GBV-C viremia is seen in 20% of HCV infected persons where the rest 80% are seropositive toE2 antibodies. This suggests the high rate of natural clearance of GBV-C (75%) than HCV (25%). The virus can not be contacted through saliva, semen or any other body fluids other than blood.
CLINICAL FEATURES:
Though GBV-C is detected in many patients with non A to E acute or chronic hepatitis & may persists for years it does not cause liver (or any other) disease, even in immunocompromised patients. It does not modulate the course, response to therapy in HCV, HBV patients. It does not interfere liver transplant though the rate of viremia is more due to frequent transfusion. The duration of infection depends on age & immune status of the host. Childhood acquisition leads to chronic infection. In immunocompetent adults rapid viral clearance occurs. Chronic GBV-C hepatitis occurs in HIV patients. In contrast to HCV the development of antibodies toGBV-CE2 protects against reinfection. There is no clear association between GBV-C infection & HCC, nonHodgkins lymphoma, aplastic anemia, porphyria cutanea tarda or lichen planus.


DIAGNOSIS:
As it rarely causes human disease the diagnostic tests are reserved for research only. GBV-VRNA is detected by PCR. A test for antibody detection is also available.
GBV-C & HIV-It was observed that in HIV infected patients slow progression to AIDS & death correlated to GBV-C viremia. Co infected patients have better prognosis than HIV mono infected cases. In addition better antiretroviral therapy, rapid rise of CD4 count observed. The explanation of better response though not exactly known may be this virus prevents HIV from replicating frequently, thus extending the life span by inhibiting damage to the immune system.
TREATMENT:
As not associated with clinical disease, no treatment required. Those who are co infected with HCV treatment with interferon and ribavirin cause disappearance of GBV-CRNA from serum but reappeared in all cases after therapy completed.
TTV INFECTION

INTRODUCTION:-Identified in 1977 from a patient (initial-TT) in Japan who had acute post transfusion non A to G hepatitis.
VIROLOGY: TTV is a non enveloped, single stranded, negative polarity, circular DNA virus related to family of animal virus Circoviridae. The TTV genome is 3695 nucleotide long & contains at least 3 ORFs. Three messenger RNA (mRNA) are expressed by TTV. The protein product of largest mRNA (3kb long) functions as capsid protein. At least 16 genotypes have been identified with greater than 30% sequence divergence. TTV is believed to be hepatotropic as high viral level is seen in liver than serum. It also replicates in PBMCs and bone marrow cells.
EPIDEMIOLOGY & TRANSMISSION:-Found world wide & very common. Prevalence among blood donors are high.
Transmitted by all parenteral routes & high among hemophiliacs, IV drug users, haemodialysis & organ transplants. Also transmitted enterically (fecal-oral).
CLINICAL FEATURES:-In the first reported case there was acute hepatitis, viremia was detected 6 weeks after exposure &2 weeks before the rise of serum ALT.DNA was documented by PCR and ALT subsequently returned to normal. Viremia may persist for years in both immunocompetent & immunosuppressed persons. Most cases don’t have biochemical or histologic evidence of liver disease. It does not alter the natural history or response to treatment of HCV or HBVcases.
TREATMENT:--Protocol not studied. In a co infected HCV case treatment with PegIFN 6 of 10 cases cleared TTV viremia by end of therapy but majority relapsed within 6 months.

SANBAN, YONBAN, SEN &TTV LIKEMINI VIRUS (TLMV)
After discovery of TTV in 1997 similar viruses with small DNA genomes isolated in Japan. Sanban, Yonban and TLMV have been divided into 29 genotypes with diverge sequences. They are transmitted by parenteral & fecal oral route. None has been clearly associated with human liver disease so far.
In 1999 another virus identified in a HIV patient (initial SEN) which is a small, non enveloped, single stranded DNA virus, transmitted by parenteral &fecal oral routes. Vertical transmission may occur. No chronic infection occurs. Prevalence is high with parenteral risk factors particularly HCV co infection. Clinical significance of SEN virus is not clear. Fulminant course or CLD do not occur.
Most studies show no association between these viruses & human disease, nor any effect on course and response to treatment of chronic viral hepatitis.


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Jul22
OPPORTUNISTIC INFECTION IN HIV/AIDS
INTRODUCTION:
Opportunistic infections (OI) are the hall mark of immunodeficiency associated with HIV. They include opportunistic protozoan, fungal , bacterial , viral and other infections along with repeated episode of HIV infection. It is important to diagnose OIs, because acute infections are at times life threatening, effective prophylaxis result in better survival. The clinical manifestations are different than normal host. Various studies established the relationship between rising viral load and decreasing CD4+ count and progression of HIV. Timely chemoprophylaxis reduce the risk of OIs and effective ART therapy (anti retroviral) decreases viral load, restore immune function, reduce risk of OIs.

Certain patients in the developed and developing world do not have access to care or response to ART due to multiple reasons leading OIS as important cause of morbidity and mortality in HIV-1 infections. The therapy for OIs has changed substantially leading to new strategies for management.

CLASSIFICATION
AIDS (CDC classification category C diseases) is defined by the development of specified opportunistic infections or tumours. There is a correlation between CD4 count and HIV related infections.
TABLE – 1(CD4 COUNT AND ASSOCIATED INFECTIONS)
> 500 cells/mm3 Acute primary infection, Recurrent vaginal candidiasis
<500 cells /mm3 Pulmonary Tuberculosis, Pneumococcal pneumonia, Herpes Zoster, Oropharyngeal candidiasis, Extraintestinal salmonellosis, Lymphoid interstitial pneumonitis
<200 cells/mm3 Penumocystis carinii (jirovecii)pneumonia, Mucocutaneous herpes simplex, Cryptosporidium, Microsporidium, Oesophageal candidiasis, Miliary/extrapulmonary tuberculosis
<100 cells/mm3 Cerebral toxoplasmosis, Cryptococcal meningitis
<50 cells/mm3 CMV retinitis, CMV gastrointestinal diseases, Disseminated mycobacterium avium intracellulare
The Ols can be descried as per the system involved.
1. Pulmonary diseases seen in HIV (OIs)
• Bacterial: Streptococcus penumoniae, H. influenzae, Pseudomonas aeruginosa, Klebsiella penumoniae, Rhodococcus equi, Mycobacterium tuberculisis, Atypical mycobacteria
• Fungal: Penumocystis carinii (Jirovecii), Cryptococcus neoformans, H. Capsulatum, Coccidiodes emitis, Penicillium marneffi, Aspergillosis
• Viral - CMV, EBV, HSV, VZV
• Protozoal – Toxoplasma gondii, Strongyloides stercoralis
2. CNS
• C. Neoformans
• Toxoplasma Gondii
• JC Virus causing PML
• Others : Syphillis, M. tuberculosis, T. cruzi, HTLV – I infection, Acanthamoeba
3. G.I.T
• Fungus – Candidiasis, Histoplasma, Coccidioidomycosis, Penicillisis
• Bacterial – Salmonellosis, Shigella, Campyolobacter jejuni
• Virus EBV – (Oral Hairy leucoplakia)
CMV Colitis, Rotavirus, Adenovirus , HSV
• Protozoal infection : Cryptosporidiasis, Cyclospora, Micosporidiasis, E. histolytica, Isosporiasis, G. lamblia, C. difficile
4. Hepatobiliary – HBV and HCV infection
Fungus – C.immitis, Histoplasma
5. Genitourinary – Syphilis, candidiasis
6. Dermatological Condition
• Seborrheric dermatitis, Herpes simplex / Varicella zoster virus (VZV), Bacillary angiomatosis, Molluscum Contagiosum, Anogenital HPV (Human papilloma virus), Scabies, Syphilis, Fungal folliculitis rash (Fungal – Malassezia furfur), Dermatoplytic infections involving skin, nail
7. Cardiovascular
Cardiomyopathy – Cryptococcosus, Chagas disease, Toxoplasmosis
Pericardial Effusion - Tubercular
8. Rheumatological
Septic arthritis may be due to fungus C. neoformans, H. capsulatum, Sprorothrix schenckii, Systemic mycobacteria – M. haemophillum
9. Endocrine System
Adrenal gland involved in CMV, mycobacterial, cryptococcal, histoplasmosis
Thyroid – involved in P. carinii, CMV, toxoplasma, mycobacterial, cryptococcal
10. Haemopoetic System
Bone marrow suppressed by – Fungal, Mycobacterial and B19 parvovirus
11. Ophthalmic Disease
CMV Retinitis
HSV & VZV
P. Cariniii – Choroiditis
Toxoplasma - Chorioretinitis

Few common Ols are described in the paragraph following.


P.C.P. (Pneumocystis carnii pneumonia):
Very common infection and called as “ AIDS pneumonia”, occurring in 57% of children below 1 year and leading cause of interstitial plasma cell penumonia. It is a protozoan but closely related to fungi. The reservoir and mechanism of transmission is obscure but transmittd by direct air borne. The organism establishes in alveoli where it proliferates as an exracellular parasite producing interstitial oedema, hyaline membranes resulting in progressive hypoxemia and respiratory failure. The symptom tetrads are fever, cough, dyspnoea and tachypnea. Physical examination shows tachycardia, respiratory distress with accelerating tachypnoea and diffuse retraction without any specific auscultatory findings. Extrapulmonary penumocystitis involves L. node, spleen, liver, Thyroid, adrenal gland, kidney. Ophthalmic lesion of choroids, necrotising vasculitis resembling Burger’s disease, bone marrow hypoplasia, intestinal obstruction, heart. Associated with cystic lesion or calcification on CT or Ultrasound. Otic involvement cause polypoid in auditory canal.

Arterial blood gas analysis (ABG) shows progressive hypoxemia, respiratory failure. Chest X-ray shows signs of hyperinflation with peribronchial thickening , bilateral alveolar, interstitial in filtration, which spread outwards from hila. Further progression leads to bilateral airspace disease with air bronchogram, cavities, pleural effusion and spontaneous penumothorax, the last being characteristic.

The diagnosis is confirmed by Wright – Giemsa staining of induced sputum or Broncho-Alveolar Lavage (BAL). Trophozoites and intracystic trophozoites are seen. Prognosis is related to hypoxaemia (Alveolar – arterial O2 gradient - < 35 mm of Hg – Mild, 35-45 mm of Hg moderate and > 45 mm of Hg severe).

Treatment: The treatment is a medical emergency. The treatment of choice is Trimethoprim sulphamethoxazole (TMP-SMX) or Pentamidine. The other alterantive drugs used in adults are Dapsone – TMP, Clindamycin, Primaquine, Atovaquine.
TABLE – 2
Drug Schedule Remark
TMP-SMX 20mg of TMP/Kg/Day in 4 divided doses I/V for 21 days Restore to oral when patient responds
Pentamidine 4mg/Kg/Day,
Single Dose, I/V for 21 Days Reserved who cant tolerate TMP- SMX or no response after 7 days of therapy.
Dapsone – TMP
Clindamycin
Primaquine
Atovaquine
Mortality – 5-40% in treated and 100% in untreated cases.

PREVENTION:
Indication: All HIV infected children from 4 weeks to 12 months of life, in determinate status children from 4 weeks till HIV is excluded (4 months), HIV infected children above 1 year having CD4 count of < 500 (1- 5years) and < 200 (6-12 years). All children who have been treated for PCP.
TABLE – 3
Drug Schedule Side Effect
TMP-SMX • 150 mg of TMP/M2/day. Orally in two divided doses on 3 consecutive days of a week.
• 150 mg of TMP/M2/ day orally divided into 2 doses on 3 alternating days. Aplastic anaemia megaloblastic anaemia, Steven – Johnson’s Syndrome, Neutropenia, Thrombocytopenia
Dapsone 2mg/Kg/Day orally
(Max – 100mg) Methemoglobinemia
Haemolytic anaemia
Pentamidine (inhaled) 300mg of Pentamidine isoethionate inhaler every 28 days Cough, bronchospasm , increased risk of extra pulmonary PCP
Pentamidine (I/V) 4 mg/Kg /Day single dose I/V every 2-4 weeks Hypoglycemia, Hyperglycemia, Hypertension, Hypocalcaemia, rash

Rhodococcus Equi – Gram +ve pleomorphic acid – fast nonspore forming bacillus causing pulmonary or /and disseminated infection. Presents as fever cough. Chest X-ray show cavity or consolidation. Blood culture may be +ve treated with proper antibiotic.

TUBERCULOSIS:
In high prevalent areas primary and reactivation of tuberculosis is common due to depressed cell mediated immunity. Drug resistance is also common. The extensive tuberculosis is due to progressive depletion and dysfunction of CD4 cells with macrophage and monocyte dysfunction.

Clinically present as fever, cough, weight loss, night sweat, malaise. Extrapulmonary manifestation like CNS (meningitis), lymphadenopathy, hepatosplenomegaly, genitourinary, mastoid involvement occur. The disease may be extensive (miliary).

Diagnostic difficulty is due to unusual features (Tuberculin – ve) and extrapulmonary manifestation. History of contact, tuberculin test (induration > 5 mm), chest X-ray showing lobar or multilobar infiltration or diffuse interstitial lesion and hilar adenopathy are clue. Isolation of AFB from gastric lavage, BAL, sputum is gold standard test. The samples collected from pulmonary and extrapulmonary tissue subjected to culture and sensitivity to drugs as drug resistance is very high. PCR test on sputum , pleural fluid, CSF is highly sensitive and specific.

Treatment:
1st Line Drugs:
INH – 10-20 mg/kg/day (max 300mg)
Rifampicin – 10-20 mg/kg/day (max 600mg) – (May lower the concentration of antiretroviral drugs as it induces the action of hepatic cytochrome 450).
Pyrizinamide - 30 mg/kg/day
Ethambutol - 15 mg/kg/day
Streptomycin – 20-30 mg/kg/day IM
Rifabutin – 300mg for 4 months
2nd Line Drugs:
Ofloxacin, Ethionamide, Cycloserine, Capreomycin, PAS

Duration of Treatment:
• For pulmonary TB – 6-12 Months
• For extrapulmonary TB – Minimum 12 Months
• DOT (Directly Observed Therapy) may be given during initial phase.
• Children of Mx positive without any other lesion – INH & Rifampicin for 12 months.
• In MDR TB – 6-7 drugs depending on sensitivity for 12-15 months.
To start ART the CD4 count is a guideline (WHO recommendation).
• CD4 count < 200/L – Start ATT first and ART is started as soon as patient tolerate ATT (Takes 2-4 weeks).
• CD4 count 200 to 350/L – Start ATT and add ART after intensive phase –(8weeks).
• CD4 count > 350/L – Treat TB completely and defer ART.

NON-TUBERCULOSIS MYCOBACTERIAL INFECTIONS
Mycobaacterium avium complex (MAC) includes M. kansasii, M. Chelonei and M. fortuitum which are saprophytes present in soil, water, food and infect when CD4 count is below 50 cells/ml. Lung, liver, spleen and lymphnodes, bone marrow and GIT are the common sites. Incidence is less in India. Transmitted by inhalation or ingestion. Lung is an unusual site of infection.

Slow progressive clinically present as high fever, weight loss, anemia, abdominal pain, night sweat, diarrhoea, malaise, hepatomegaly, osteomyelitis, meningoencephalitis, intraabdominal and soft tissue abscesses.

Peripheral smear shows anaemia, neutropenia, chest X-ray shows nonspecific finding like focal, diffuse infiltration, cavity, hilar adenopathy. Culture of blood or tissue by Radiometric assay show +ve in two weeks. PCR can identify the species. Biopsy from liver, L. node or marrow shows AFB bacillus within macrophages.

For treatment Azithromycin (10 mg /kg/day – single dose), Clarithromycin (15 mg /kg/day – 2 divided dosees), Ethambutol (15-20 mg /kg/day – single dose), Rifabutin (5-10 mg /kg/day – single dose) Ciprofloxacin (20-30 mg /kg/day Orally– single dose) Amikacin are given. The regimen includes 2-4 drugs i.e Azithromycin or Clarithromycin with Ethambutol and/or Rifabutin and Ciprofloxacin or Amikacin. Immunomodulators like GM-CSF, G-CSF, Interferon gamma, interleukin –2 are helpful.

For primary prophylaxis any drug is given for periods depending on CD4 count (< 50 – 6years, <75 2 –6 years, < 500 – 1-2 years, < 750 – 12 months). Secondary prophylaxis in patients suffering from MAC is life long including at least two drugs.

TOXOPLASMA GONDII INFECTION
In children manifest as congenital toxoplasmosis and CNS manifestation. Pregnant Mother transmit to fetus.

Congenital toxoplasmosis present as low birth weight, microcephaly, hydrocephalus, hepatosplenomegaly and chorioretinitis. CNS toxoplasmosis present as fever, headache, seizures, psychosis, altered sensorium and focal meurological deficit as hemiparesis, ataxia, cranial nerve palsy, aphasia, cerebral edema, confusion, dementia, coma.
Demonstration of specific IgM and IgA antibodies in serum is diagnostic of congenital toxoplasmosis. CNS toxoplasmosis is diagnosed on clinical ground, presence of IgG antibodies and multiple ring enhancing granulomatous lesion on CT scan or MRI. Brain biopsy is definitive diagnosis.

TREATMENT
Sulphadiazine – Loading 100mg/kg followed by 85-120mg /kg/day in 2-4 divided doses. Pyrimethamine – 1-2 mg /kg/day for 2 days followed by 1 mg/kg/day for 2-6 months and 1 mg /kg/day up to 1 year. Folinic acid (calcium leukovorin) 5-10 mg /kg/day or alt days to prevent megaloblastic anaemia secondary to pyrimethamine. Prednisolone 1 mg/kg/daily orally in active chorioretinitis or CSF protein is > 1gm%. Clinadmycin (20 mg/kg/day in 4 divided doses), pyrimethamine, folinic acid is alternate regimen.
CNS Toxoplasmosis: - The drugs used are pyrimethamine and sulfadiazine or Trisulfapyrimidine. Folinic acid is given to prevent bone marrow suppression. Relapse is common which requires reinstitution of therapy.
An episode of CNS toxoplasmosis requires life long prophylaxis.

VIRAL INFECTIONS
The common viruses are Herpes Simplex Virus (HSV 1 & 2), Cytomegalo Virus (CMV), Varicella Zoster Virus (VZV), Epstein Barr Virus (EBV) and Human Herpes Virus type – 8 (HHV-8). The infections are often chronic, invasive and fatal with HIV infection.
1. HSV 1 & 2: HSV-1 is transmitted through contact with oral mucosa and salivary secretions. HSV2 transmitted sexually and present as anogenital lesion. When CD4 count is > 100/mm3 both present as recurrent self-limited cluster of orolabial ulcers, genital, anorectal ulcers. In lower CD4 count the vesicular lesions are found at other sites. In severe cases there are large, painful ulcer which slowly resolve. Stomatitis follow oral lesions and fissures and fistula follow rectal and genital ulcers. Bacterial infection may supervene. Advanced AIDS cases with low CD4 count may produce systemic HSV-infection producing oesophageal ulcer (odynophagia, chest pain)pneumonia, hepatitis, meningoencephalitis, ventriculitis, shock, sepsis like syndrome and transverse myelitis.
Diagnosis is based on typical clinical lesion, rising antibody titre, isolation of virus from culture, detecting HSV1 & 2 antigen from skin or mucosa by scraping and immunofluorescent stain. In suspected HSV encephalitis HSV DNA in CSF using PCR is useful.
Acyclovir is drug of choice. In neonates and severe HSV infection given in a dose of 30 mg/kg/day in 3 divided doses for 2-3 weeks. Primary gingivostomatitis or genital HSV are treated with oral Acyclovir 80mg/kg/day in 3 divided doses for 10 days. Famcyclovir or Valacyclovir in a dose of 750- 1500 mg/day in 3 divided dose may be used. Foscarnet in a dose of 120mg/kg/day on 2-3 divided doses in Acyclovir resistant cases.
For prophylaxis in HIV patients with frequent or severe relapse or slow healing lesion Acyclovir 200mg tid or 400mg bid orally is given.
2. Vericella Zoster Virus (VZV):
In immunocompromised patients causes greater morbidity and mortality. Clinically presents as fever with generalized pruritic rashes (typical). They may be chronic, recurrent, persistent (appearance of new lesion for > 1 month), sever in advanced cases. In chronic infection the skin lesion become verrucous or necrotic. In severe infection presents as high fever, numerous skin lesion, systemic involvement like pneumonia, encephalitis, hepatitis.
Demonstration of VZV antigen in skin lesion, isolation of virus from vesicle contents, rise in antibody during convalescence and VZV specific IgM antibody confirm the diagnosis. PCR is also extremely sensitive and specific.
In severe cases Acyclovir in a dose of 1500mg /M2/day in 3 divided doses for 7-10 days or till no new lesions appear whichever is later is given. In mild cases Acyclovir is given orally 80mg/kg/day in 4 divided doses.
HIV infected children exposed to chickenpox are given varicella zoster immunoglobulin (VZIM) within 96 hours in a dose of 1 vial/10kg (maximum 5 vials). For recurrent case daily Acyclovir is given.
3. Herpes Zoster:
It is a dormant form of VZV producing painful vesicular lesion affecting dermatomes in immunocompetent persons.
Clinically presents as multidermatomal infection, dessiminated Zoster, bilateral rash, retinitis, rarely penumonitis, consumptive coagulopathy, hepatitis, marked constitutional symptoms and encephalitis. Chronic and relapsing cases and post herpetic neuralgia are common.
Classical dermatomal distribution of painful, vesicular eruption is diagnostic. Confirmed by virus isolation and detection of viral antigen in the skin.
Severe cases or neurologic complications like Ramsey Hunt, Zoster Ophthalmicus, disseminated zoster require Acyclovir 30mg/kg/day in 3 doses I/V. Oral Acyclovir 80mg/kg/day in 4 divided doses hastens healing. Famciclovir and Foscarnet are drugs used in resistant or recurrent cases.

4. Cytomegalo Virus (CMV)
It is very common OIs and carry poor prognosis. Horizontally transmitted through saliva, sexual fluid, urines and vertically by infected mother. More than 90% of HIV pregnant mother are CMV – infected.
Clinical manifestations:-
a. Retinitis: - Chorioretinitis develops in CMV seropositive cases when CD4 count is < 50 cells/l. Blurred vision, floaters and flashes are nonspecific symptoms, which starts with one eye progressing to other. It is painless. It leads to visual loss and retinal detachment. Yellowish white area of retinal necrosis with perivascular exudates and haemorrhage at periphery is characteristic.
b. GI Manifestation :- Oesophagitis produce substernal pain, dysphagia and anorexia, Colonic involvement cuase diarrhoea, abdominal pain, weight loss , anorexia, fever, CMV hepatitis and gastritis are uncommon. In 5-10% cases of AIDs cause colitis.
c. Penumonitis – Cough, dyspnoea, hypoxaemia
d. Encephalitis – Produce sub-acute dementia complex.
Diagnosis:- Retinitis is diagnosed by Fundoscopy. GIT infections on mucosal biopsy shows inflammation and CMV inclusion bodies. On endoscopy oesophagitis shows small and confluent ulcers. Sigmoidoscopy of colon shows diffuse erythmatic, submucosal haemorrhage and multiple mucosal ulcer. Chest X-ray of pnumonitis shows diffuse interstitial infiltration and finding of inclusion bodies in lung tissues or BAL is supportive.

Serological test for CMV are less helpful.
Treatment: Ganciclovir 10mg/kg/day in 2 divided doses I/V over 2 hours for 14-21 days followed by life long maintenance therapy.
Or
Foscarnet – 180mg/kg/day in 3 divided doses I/V over 1-2 hours for 14-21 days followed by life long maintenance therapy with 90-120mg/kg/IV in a single daily dose.
Prophylaxis :- Regualr retinal examination at 4 – 6 weeks interval. Life long prophylaxis with Ganciclovir 5mg/kg/day IV 5 days per week.

Other viral infections:
1. Human Herpes Virus – 8 (HHV – 8): This DNA virus causes Kaposi sarcoma in seropositive cases. Although Ganciclovir , Foscarnet, Cidofovir are active in vitro their use in limited.
2. Progressive multifocal leukoencephalopathy by JC Virus : This is caused by polyoma Virus JC virus. Insidious onset with progressive features like congnitive dysfunction, dementia, seizure, ataxia, aphasia, cranial nerve palsy, hemiparesis, quadriparesis, Coma. CT scan shows single or multiple hypodense, non-enhancing lesion in cerebral, white matter. Confirmed by biopsy. No effective treatment. Majority dies within 3-6 months of symptoms.
3. Human Papilloma Virus (HPV): - Infection in anogenital tract resulting in transient infection, genital wart, condyloma, squamous cell cancer. Dignosed clinically and biopsy. No effective treatment.
4. Hepatitis C Virus (HCV): - High rate of HCV coinfection in HIV- I persons through drug user injection, mother to child or sexual route. HIV – I infection increases the progress of HCV infection leading to end stage liver disease. Acute HCV infection is symptomatic or mild symptomatic. Chronic infection leads to hepatocellular failure. A progressive form called fibrosing cholestatic hepatitis found in HIV- I infection. Anti viral treatment is considered in chronic HCV infection. Avoid alcohol. Two doses of Hepatitis A vaccination is advised.
5. Hepatitis B Virus (HBV): About 90% of HIV – I patients are +ve for some markers of HBV. It is associated with increased risk of chronic HBV. Symptoms of acute infection are nausea, vomiting, jaundice, abdominal pain, Chronic infection presents as fatigue hepatocellular failure. Testing for HBs Ag, Anti HBc, Anti-HBs are used. Detection of HBs Ag  6 months is chronic and should be tested for HbeAg and Antigen HBe. They are increased risk of carcinoma.
Avoid alcohol – Two doses of Hepatitis A vaccination and 3 doses of Hepatitis B vaccination is given. Antiviral treatment is given.
6. Hepatitis A Virus (HAV) – All susceptible, chronic HCV cases. Two doses of Hepatitis A vaccination given. Not seen so frequently
7. Influenza virus : All patients annually – inactivated trivalent influenca virus vaccine – 1 dose yearly. Oseltamivir – 75 mg orally – 4 tims or Rimantidine /Amantidine – 100 mg orally – 4 times are used.
8. EBV – When CD4 is < 300L cause oral hairy leukoplakia along tongue border and adjacent mucosa. Not a premalignant condition. Treated with topical podophyllin or systemic antiherpes virus infection.
9. Coinfection with hepatitis D, E, and G are also common.

Cryptosporidiosis: Protozoa parasite . Infects small and large gut and extra intestinal. In this group C.hominis (previously C. parvum) C. canis, C. felis, C. muris. C. meleagridis . Biliary tract involvement like papillary stenosis, sclerosing cholangitis are seen.
Microsporidiosis: Protists related to fungus, contains several groups of organism. Water borne in origin. Commonly manifest as diarrhoea. Rarely encephalitis, sinusitis, ocular manifestation, myositis and disseminated infection occur.
Bartonellosis: Bacterial infection causing Bacillary angiomatosis of skin. Organisms are B. henselae, B. quintana and others. Common among poor sanitation. Common when CD4 count is < 50 cells and chronic infection involving every organ but typical skin lesion which is papular, red, smooth surface, vascular and bleed on trauma. Diagnosed by biopsy. Serological test may be +ve before clinical disease. Treated with Erythromycin /Doxycycline/ Clarithromycin/Azithromycin for at least 3 months.
Syphilis: The impact of HIV – I infection on syphillis (Treponema pallidum) pathogenesis, severity , response to treatment and long term sequelae is not well documented. However the progress is hastened in immunocompromised state. A variety of rare presentation like lues maligna, an ulcer due to necrotising vasculitis. Most commonly presented as condylomata lata. VDRL is of ambiguous significance.
FUNGAL INFECTION:
A. Cryptococcal Infection: Cryptococcus neoformans – infects when CD4 count is <50. This unusual disease involves brain, meninges, skin, eye. Clinically may present as meningitis, meningoencephalitis. Pneumonia is seen in 50% of cases. Sepsis though rare is fatal. Post infective sequlae like hydrocephalus, seizure, ataxia, cranial nerve involvement is common. Uncommon presentation may be in skin (Molluscum contagiosum), L. node enlargement, palatal, glossal ulcer, myocarditis, prostitis, gastroenteritis.
In CSF fungus is detected by India ink stain, cryptococcal antigen (95-100% specificity and sensitivity), positive culture. A positive latex agglutination test from seum also used in pulmonary cases. CT Scan of brain may show granuloma (cryptococcomas). Chest X-ray may show poorly localized bronchopneumonia, nodular or lobar involvement, pleural effusion , hilar, mediastinal adenopathy.
Amphotericin B ( 0.5 – 1 mg/kg/day IV , once daily) with or without Flucytosine (50-150 mg/kg/day orally in 4 divided doses) for 14 days until clinical improvement is initial treatment. Fluconazole (6-12 mg/kg/day, orally) or Itraconazole (2-5 mg/kg/day, orally) up to 8-10 weeks is follow up therapy. Life long secondary prophylaxis with Fluconazole or Itraconazole or Amphotericin B is required.
B. Histoplasmosis: Dimorphic fungus Histoplasma capsulatum. By inhalation or reactivation of latent infection. Manifest as disseminated multiorgan disease – fever, fatigue, weight loss, respiratory symptoms. CNS, GIT, Skin Manifestation seen in < 10% of cases. Diagnosed by presence of antigen in serum or urine, fungal stain of blood or tissues. Chest X-ray in 50% show diffuse interstitial infiltration or diffuse nodularity. Bone marrow involvement is common causing anaemia, neutropenia, thrombocytopenia. Treated by Amphotericin-B 1mg/kg/daily followed by Iatraconazole.

C. Coccidioidomycosis: By C. immitis causing disseminated diseases or meningitis. Dissemianted present as generalized lymphadenopathy, skin nodule or ulcer, peritonitis, liver, bone and joint involvement. Local meningitis is 10% of cases. Diagnosed by culture or serology of serum or CSF. Pulmonary (nodules, cavity, pleural effusion, hilar adenopathy) and disseminated form is treated with Amphotericin B and meningitis is treated with Fluconazole.
D. Aspergillosis: By Aspegillus fumigatus causing two syndromes – Respiratory (pseudomembranous tracheitis, penumonitis), CNS infection (meningoencephalitis with vascular infarction). Diagnosed clinically and demonstration of organism. Treated with Amphotericin B or Variconazole.
E. Candida Infection: Oral candidiasis (thrush) and diaper skin are common. Thrush may be extensive. Painless, creamy white plaques over buccal , oropharyngeal, or tongue which can be easily scrapped off. Angular chelosis may be seen. Oesophageal candidiasis may present as substernal or abdominal pain, dysphagia, weight loss. Disseminated infection present as sepsis or shock. Vulvovaginal candidiasis present as creamy to white yellow vaginal discharge with mucosal burning or itching, dysuria, dysparenia. Vaginitis may be due to trichomonas or bacterias also.
Oral candidiasis are typical and confirmed by presence of pesudohyphae on KOH stained specimen. Oesophageal involvement is diagnosed by clinical, endoscopy and biopsy. Blood culture may be +ve.
For oral candidiasis Nystatin, Amphotericin-B and Azoles are used. Oral Azoles are used when topical application fails. For oesophageal candidiasis. Fluconazole and for disseminated Amphotericin B is the choice.
TABLE
Condition Drug Dose & Duration
Oral Candidiases • Nystatin – Suspension, Lozenge
• Amphotericine B oral Suspension
• Clotrimazole
• Fluconazole
• Ketoconazole
• Itraconazole • 1-2 Lak U orally 4 times – 14 day
• 1 mg orally 4 time – 14 day
• 10mg orally 4 times – 14 day
• 3-6 mg/kg orally once – 14 day
• 5-10mg/kg Orally once – 14 day
• 2-5 mg/kg Orally once – 14 day
Esophageal Candidiasis • Fluconazole
• Itraconazole
• Amphotericine – B • As Above
• As Above
• 0.5 – 1 mg/kg/daily IV – 14 days
Disseminated Candidiasis • Amphotericine – B • As Above

Oral Fluconazole is given as prophylaxis is recurrent cases.
E. Other Fungus: Cause meningoencephalitis – Naegleria, Achanthamoeba.

DERMATOLOGIC DISORDERS:
Seborrheic Dermatitis: Seen in 50% of HIV cases. Aggravated by Pityrosporium , a yeast like fungus. Ttopical antifungal treatment is useful.
Eosinophillic pustular folliculitis: Multiple urticarial perifollicualr papules associated with mite infection which respond to topical anthelminthics.
Norwegian scabies: Hyperketatotic psoriasiform lesion.
VZV: Reactivation in 20% cases of HIV, Visceral involvement is rare. Involve several dermatomes Acyclovir, Famciclovir, Foscarnet are used.
HSV: Recurrent oroabial, genital, perianal lesion as part of reactivation. Perirectal is associated with proctotis.
Molluscum Contagiosum: Flesh coloured umbilicated lesion, regress with ARV.
Erythematous Nodules: Due to Atypical microbacteria, fungus, bartonella, Aconthamoeba.

OPHTHALMIC DISEASES:
CMV retinitis: Painless, progressive visual loss with blurred vision. Retina shows perivascualr haemorrhage and exudates.
HSV & VSV: May cause bilateral necrosizing retinitis called Acute Retinal Necrosis Syndrome or Progressive Outer Retinal Necrosis (PORN). There is pain, keratitis, iritis , associated with orolabial HSV or trigeminal zoaster. Fundus shows pale gray periphery. Complicated by retinal detachment.
Other infections: P. carinii- Choroid lesion- Bilateral elevated yellow white plaque. Toxoplasma – Chorioretinitis associated with CNS lesion.

RECURRENT BACTERIAL INFECTIONS:
Recurrent bacterial infections within 2 years period is peculiar to HIV patients. The clinical presentation depends on the system involved.

TABLE
Site of infection Common Organism Clinical Manifestation Diagnostic Evaluation
Meningitis S. penumonia
H. influenzae
N. meningitides Fever, Headache, Vomiting, Altered sensorium, Neck rigidity CSF – examination and culture
Pneumonia S. penumonia
H. influenzae
Ps.aeruginosa
N. aosteroides Fever, cough, chest pain, tachypnea, crepitation Chest X-ray, Sputum Culture
Bacteremia S. penumonia
H. influenzae
Salmonella species Fever Or Hypothermia , Features of Multiorgan Dysfucntion Blood Culture
Oesteomyelitis Staphylococci Fever, pain, swelling or redness at local site Bone scan, Radiograph
Sinusitis S. penumonia
H. influenzae Persistent nasal discharge , fever, cough, Maxillary sinus – common Radiograph
Central venous catheter infection Staph aureus & epidermidis.
K. penumonae
Acinetonbacter species
Pseudomonas Species Redness and tenderness at local site Culture
Skin, ear and upper respiratory tract S. penumonia
H. influenzae
Group A beta fever, Haemolytic URTI Skin- Pyoderma
Ear- Pain, Discharge
URTI- Cough Culture from specimen

Treatment depends on culture sensitivity. Empiric broad spectrum antibiotic may be started taking into account the site of infection, nuetropenia, in dwelling catheter and other risk factors.

For prophylaxis immunization against organism and proper hygiene is to be maintained. Daily TMP-SMX may be used. Intervenous immunoglobulin monthly may boost the immunity.


DIARRHOEA:
Chronic diarrhoea is very common, which may be due to various organisms and side effects of drugs.
TABLE
Organism Species
Bacteria Salmonella, Shigella, Campylobacter, Clostridium difficile & MAC
Virus CMV, Adenovirus, HIV, HSV, Rota Virus
Protozoa Isopora belli, Cryptosporidium parvum, Microsporidia, E. histolytica, G. lamblia, Cyclospora
Fungi Histoplasma, Coccidiodomycosis, Penicilliosis

Peritonitis is seen in C.immitis.
Clinically presents as large watery stool, abdominal pain associated with fever, dehydration, anorexia, wasting and cachexia. Biliary tract involvement (cholangitis, cholecystitis) is seen in Isospora, Microsporidium, Cryptosporidium and Cyclospora.

DIAGNOSIS AND TREATMENT
Organism Diagnosis Treatment
Isospora Oocyst in stool after acid fast stain TMP SMX – 3-4 weeks Pyrimethamine with folinic acid
Cyclospora Oocyst in stool in acid fast stain Orally TMP SMX for 7 days
Microsporidia
Examiantion of concentrated stool,small intestine biopsy on EM or PCR Albendazole
Cryptosporidium
Stool examination in acid fast stain, Immunoflucoscent assay and stool ELISA Fluid supplementation, Paramomycin- Spiramycin, Azithromycin, Clarithromycin
E. histolytica Stool , trophozoite & Cyst, Serological test - +ve with tissue invasion, Endoscopy and biopsy For gut – Iodoquinol, diloxanide furoate, paramomycin
Invasive – Metronidazole, Dehydrometine
Hepatic – Chloroquine
G. lamblia Trophozoite and cyst in stool or duodenal aspirate, Giardia antigen in stool Metronidazole, Furazolidine, Tinidazole
Adenovirus Sigmoidoscopy – Patchy erythema & raised white lesion
Mucosal Biopsy – Intranuclear inclusion , Virus may grow Supportive treatment
Rotavirus ELISA in stool sample Supportive treatment
Camphylobacter Stool culture or blood culture.
Immunological test – IF, LA
Serology – ELISA for IgG, IgM, IgA level Azithromycin, Clarithromycin, Erythromycin, Ciporfloxacin, supportive therapy
Shigella Endoscopy – Deep mucosal ulcer and pseudomembrane
Stool Culture Ampicillin , cefixime, ceftriazone, Quinolones, Supportive care
Salmonella Stool Culture
LA and Fluorescence test
PCR Duration of treatment is 14 days
Cefotaxime /Ceftriaxone, Ciprofloxacin
Cl. difficile Stool Examination
Toxins detected by ELISA Supportive
Metronidazole
Vancomycin

Special Geographical OIs:
1. Penicilliosis: By dimorphic fungus Penicillium marneffei seen in Thailand, China. Infect when CD4 is less than 50 and high mortality if untreated. Presents as fever, weight loss, with skin, lymph node, bone marrow and hepatic involvement. Cutaneous lesions are papullar with central umbilication over face, ears and extremities. Fungus can be demonstrated. Treated with Amphotericin B for 2 weeks followed by Itraconazole for 10 weeks.
2. Leishmaniasis: It is an obligatory intracellular protozoa seen worldwide. May present as localized or diffuse cutaneous, mucosal or visceral disease, the last being common in AIDS (70%). Demonstration of Leishmania from lesion and antibody is diagnostic. Treated with pentavalent antimony.
3. Paracoccidiodomycosis: Dimorphic fungus P. brasiliensis, seen in central and South American. Few cases in HIV – I presenting multisystemic involvement. Treated with Amphotericin B or Azoles.
4. Isosporiasis: the Protozoa I.belli present in Caribbean & Africa and Worldwide. Presents as diarrhoea with systemic symptoms of fever, weight loss, abdominal pain. Treatment is supportive. Pyrimethamine or TMP-SMX are tried.
5. Chaga’s disease (American Trypanosomiasis): A flagellated protozoa T. cruzi. Among HIV-I infected persons with immunosuppression the reactivation is increased. Present as fever, headache, vomiting, seizure. Single or multiple ring enhancement in subcortical area (Vs toxoplasma – deeper). CSF may show increased cell and proteins. Organism found in blood or tissue. Treated with Benzimidazole (2.5 mg/kg BID) or Nifurtimox ( 2 mg/kg/QID) for 60 days followed by maintenance therapy for life with either drug in a dose of 5 mg /kg thrice a week.
6. Microsporidia: Small unicellular, obligate intracellular parasite, reside in the cytoplasm of enteric cells. The main species is Enterocytozoon bieneusi. Detected by light microscope with chromotobe bases stain. E/M of stain. In contrast to cryptococcal it is seen in other tissue like eye, muscle, liver . Albendazole is treatment.
7. Cryptosporidia: Symptoms range from self limiting, intermittent to sever life threatening diarrhoea. Assoiciated with nausea, vomiting, crampy abdominal pain. Associated with cholangitis and cholecystitis. Diarrhoea is non-inflammatory. Stool containing occyst stain with acid fast.

SUMMARY
• Opportunistic infections due to various organism are associated with HIV infection at some stage or other.
• They can be classified depending on the CD4 count or system involved.
• PCP is commonest form of pneumonia though there is a six-fold rise of pneumonia incidence due to other bacterias.
• The incidence, complications and resistance of M. tuberculosis is more in HIV cases. ATT is modified according to immune status of the patient.
• Atypical mycobacteria specially MAC incidence is common.
• Toxoplasma gondii infection of CNS leads to various clinical presentation.
• The common viral infections are HSV, CMV, VZV, EBV, HBV and HCV. CMV products commonly retinitis and GI complications.
• Fungal infections like candida, cryptococcal and histoplasma are common producing various complications.
• Dermatological and Ophthalmic complication due to various infections are vary often encountered.
• Due to low immune status recurrent bacterial infections give rise to varied clinical manifestations.
• Chronic diarrhoea due to multiple microogransim is a constant problem.
• Depending on the geographical distribution of some organism the infection predominantly seen.

CONCLUSION

With high prevalence of AIDS in developing and underdeveloped Countries the risk of OIs due to organisms is a menance. The clinical presentations are quite different than normal host. Wherever possible attempts are to be made to obtain tissue or specimen to establish a definitive diagnosis. Various studies have proved the relation between CD4 count and progression of HIV and OIs. Timely diagnosis and treatment and chemoprophylaxis have reduced the mortality and morbidity. Additional ART successfully decreases the organism load and restores the immune function reducing the development of OIs.

CLINICAL FOCUS
• OIs due to various microorganism go hand in hand with infection.
• The clinical presentation somewhat differ from normal host.
• Depending of CD4 count the HIV related infections are different.
• PCP is commonest infection in children and adult having high fatality if untreated.
• Depressing cellular immunity is responsible for high incidence of tubercular infection where the treatment modality depends on CD4 count.
• Atypical mycobacteria specially MAC is quite common giving rise to various systemic complications.
• Toxoplasma infection is another treatable neurological infection.
• Various viral infections are common out of which CMV carry poor prognosis as it involves multisystems.
• EBV produces hairycell leukoplakia.
• Incidence of HBV is about 90% of HIV cases,
• Fungal infections like Cryptococcus, Histoplasma present as disseminated multiorgan disease.
• Oral, oesophageal and vulvovaginal candidiasis are common and can be properly treated.
• CMV retinitis causes progressive permanent blindness.
• Recurrent bacterial infections are common giving rise tp various diseases.
• Chronic diarrhoea is very common, due to organism or drugs.


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