Ojokshaya kc023 gdg

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Evaluation of the comparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection), C.S.HANAMANTAGOUDARDepartment of Kayachikitsa, Post graduate studies and research center D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, Gadag - 582 103

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Ojokshaya kc023 gdg

  1. 1. “Evaluation of the comparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection)” By C.S.HANAMANTAGOUDAR As partial fulfillment of post graduation degree Ayurveda Vachaspati M.D. (Kayachikitsa) Under Rajeev Gandhi University of Health Sciences, Bangalore, Karnataka Guide Dr. K. Shiva Rama Prasad M.D. (Ayu) (Osm) M.A.(Astrology), {Ph.D (Astro-medicine)} Reader in Kayachikitsa Postgraduate Studies and Research Center, Department of KayachikitsaD.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE Gadag - 582 103 Post graduate studies and research center Department of Kayachikitsa 2004
  2. 2. This is to certify that the contents of this thesis entitled “Evaluation of thecomparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana inBhutabhishangaja Ojokshaya (HIV infection)” is has been worked out byC.S.HANAMANTAGOUDAR, under my supervision with close guidance. Even though this disease, Bhutabhishangaja Ojokshaya has been mentioned inAyurvedic texts, the aetiology, pathogenesis etc., needs further evaluation and research. Itis as developed and explained by C.S.HANAMANTAGOUDAR is unique and scientific andwill definitely help in elucidation of this disease in Ayurvedic and Modern scientific parlanceand further planning with the management. This work is applied, scientific and an original contribution in the field of research inAyurveda. I am fully satisfied with the work and recommend the dissertation to be put before theM.D. (Ayurveda Vachaspathi) Kayachikitsa panel of Rajiv Gandhi University of HealthSciences, Bangalore for adjudication. Guide Dr. K. Shiva Rama Prasad M.D. (Ayu) (Osm) M.A.(Astrology), {Ph.D (Astro-medicine)} Reader in Kayachikitsa Postgraduate Studies and Research Center, Department of Kayachikitsa
  3. 3. J.S.V.V. SAMSTHE’S D.G.M.AYURVEDIC MEDICAL COLLEGE POST GRADUATE STUDIES AND RESEARCH CENTER DEPARTMENT OF KAYACHIKITSA GADAG, 582 103 Certificate This is to certify that C.S.HANAMANTAGOUDAR has worked for his thesis on thetopic entitled “Evaluation of the comparative efficacy of Ojokalpa Rasayana andAmruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection)”. We here with forward this thesis for the evaluation and adjudication. Dr. V.Varadacharyulu Dr. G. B. Patil M.D.(K.C)(Osm), Principal Professor & H.O.D D.G.M. Ayurvedic Medical College, DEPT. KAYACHIKITSA Gadag DGMAMC, PGS&RC, Gadag
  4. 4. ACKNOWLEDGEMENT I take this glorious opportunity to acknowledge with the deep sense of gratitudeto my guide, Dr. K. Siva Rama Prasad, Reader, Department of Postgraduate Studiesand Research (Kayachikitsa), D.G.M.A.M.C., Gadag, for his valuable guidance andclose supervision during entire phase of the study. With profound sense of gratitude I express my sincere thanks to Dr. G. B. Patil,Principal, D. G. M. A. M. C, Gadag. For encouragement and facilities provided duringmy postgraduate studies. I am very much thankful to Father, Mother,Sister,Brother in law, Pavitra,Amritagouda and cousins for their affection and lots of co-operation. I wish to add my warmest thanks to my PG teaching faculty Dr. M. C. Patil, Dr.Shashidhara Doddamani, Dr. Kuber Sankh, Dr. R. V. Shetter, Dr.GirishDanappagoudar for their valuable suggestions and timely help which made me tocomplete this dissertation work successfully. I am very much thankful to Dr. B. G. Swami, Dr. K. S. Paraddi, Dr.C. S.Kudarikannur, Dr.V. M. Sajjan, Dr. V. M. Malagoudar, Dr. S. B. Govindappanavar, Dr.P.C. Chappanamath, for their encouragement and moral support during the study. I extend my gratefulness and sincere heartfelt gratitude to my colleagues,Dr. Shakuntala C. Garwad, Dr. Shankaragouda, Dr. U. V. Purad, Dr. Shyju O. Dr.mulki patil Dr. G.S. Hadimani Dr. Yasmeen Panibhandha Dr. Anilkumar Bacha, Dr.Sitaram prasad, and Dr. Vinay. Kulakarni , my friends Dr. Kallesha Murushillin and Dr.Vishwanatha Kokare, for their timely support during the course. I am very much thankful to all teaching and non teaching staff of college andspecial thanks for librarian Shri. V. M. Mundinamani and Mr. Surreban for their timelyhelp and co-operation during the study.
  5. 5. Index Evaluation of the comparative efficacy of Ojokalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection) Chapter-1 1 to 4Introduction Chapter-2 5 to 54Conceptual study – includes Shareera, Nidana, and Chikitsa indetail with respect to the disease in comparison tocontemporary medicine. Chapter-3 55 to 73Drug review – Ojokalpa Rasayana composition is discussedwith its pharmacological and pharmaco-dynamics. Chapter-4 74 to 81Material and methods Chapter-5 82 to 113Observation and results Chapter-6 114 to 130Discussion and conclusion Summary 131 to 136 Annexes References Bibliography case sheet
  6. 6. List of tables Table explanation Page Number1 Combination and proportions of Ojokalpa Rasayana 552 Guna Karmas of each drug of Ojo kalp rasayan 573 Age group incidences 824 Sex ratio incidences 835 Diet incidences 846 Religion incidences 857 Economic incidence 868 Occupational incidence 879 Marital status incidence 8810 Source of infection 8911 Chief complaints 9012 Associated complaints 9113 Changes Hemoglobin percentage (HB%) 9314 Erythrocyte Sedimentation Rate (ESR) 9415 Changes in Total Lymphocyte count 9516 Changes in white Blood corpuscles 9617 Changes in Weight 9718 Changes in Platelet count 9819 Changes in Kornefsky performance score 9920 Changes in general health condition 10021 Changes in CD4 count 10122 Changes in CD8 count 10223 Observations on Chronicity 10324 Observations on Ojo vyapat lakshana 10325 Observations on Ojo Vishramsha lakshana 10526 Observations on Ojokshaya lakshana 10527 Assessments criteria - Evaluation of the comparative efficacy 106 of Ojokalpa Rasayana in Bhutabhishangaja Ojokshaya28 Assessment Parameter study of group 1 10929 Assessment Parameter study Group 2 11030 Assessment Parameter Comparative study of Group 1 and 2 11131 Result in-group 1 11332 Result in-group 2 114
  7. 7. List of graphs Graph item Page number1 Age group incidences 822 Sex ratio incidences 833 Diet incidences 844 Religion incidences 855 Economic incidence 866 Occupational incidence 877 Marital status incidence 888 Result in-group 1 1139 Result in-group 2 114 List of Figures1 Life cycle of HIV 322 Structure of HIV 333 Ingredients of Ojokalparasayana 55
  8. 8. AcknowledgementI am deeply indebted to several people who have helped me during the study.I acknowledge my sincere gratitude to my guide Dr. K. Shiva Rama Prasad, Reader/Asst. Professor, Post-Graduate studies and Research Center in Kayachikitsa,D.G.M.A.M.C, Gadag, for his expert comments, critical analysis and affectionateencouragement, throughout the study.I am grateful to Dr. V. Varadacharyulu, H.O.D., Post-Graduate studies and ResearchCenter in Kayachikitsa, D.G.M.A.M.C, Gadag for inspiring me to take up thisdissertation subject and supporting me with timely guidance and encouragementWords are poor substitutes for my immense feelings of gratitude for Dr. G. B. Patil,Principal, DGMAMC, Gadag. I thank him for his ever inspiring encouragement,facilities provided and for his personal interest in overall supervision of this study.
  9. 9. I extend my immense gratitude to Dr. M.C. Patil, Dr. Raghavedra Shettar and Dr.Kuber Sankh, Dr. Shashidhar H. Doddamani, faculties of Post-Graduate studies andResearch Center in Kayachikitsa, D.G.M.A.M.C, Gadag.I scenically remember the co-operation and support extended by Dr. B.G. Swami, Dr.Chappanmath.P.C., Dr. V.M. Malagoudar, Dr.A.K.Panda, Dr.S.B.Govindappanavar,Dr. V.M. Sajjan, Dr. Gireesh Danappagoudar and Dr. C.S. Kudarikhannur, Dr K SParaddi, and all the staff of DGMAMC. I thank all my P.G. colleges for their constantsupport and co-operation.I am very much great full to my beloved father, mother, brother, sister, brother in lawAmrutagouda and Pavitra for their lots of affection and co-operation.I sincerely thank Mr. P.M. Nandakumar, statistician, for the statistical analysis of theresults and librarian V.M. Mundinamani and assistant librarian Sureban for theirtimely assistance.I honestly remember the co-operation and support of Dr.G.S.Hadimani, Dr.Shankaragouda, Dr. Srinivasa Reddy, Dr. A.P.Yasmin Dr. U. V. Purad, Dr.O.Shyju,and all the scholars of DGMAMC – PG branches. I thank all my P.G. colleagues andmy friends Dr Kallesha Moorashillin, Dr Vishwanatha Kokare for their constant helpand co-operation.I am very thankful to Sunil. L. Mundra, M.D., Natural Capsules Pvt. Ltd., Bangalorewho supplied Natural Vegetable and Gelatin capsules for the study. I am thankful toM/s R.Y.Shettar, Doddappa Billal and Dhanwantari Pharmacy who supplied mecomponents of my trail medicine. I am thankful to Hubli diagnostics, Hubli for theirconstant cooperation through out the study.With deep sense of gratitude I thank all the subjects who participated in this study. (C.S.Hanamantagoudar)
  10. 10. As we walk in so many centuries away from descent of Ayurveda many infectiousdiseases are emerging once again to remind us about their existence as urbanizationdeveloped. Among them since two decades sudden emerge of new epidemics such asSARS and AIDS/HIV, termed in Ayurveda as Bhootopaghataja Ojokshaya. This is veryvolatile disease-entity. The etymology of words, Bhoota and Upaghata developed form theword Bhootopaghata is, Bhoota denotes as Krimi or Virus and Upaghata means as infection.So exclusively the word Bhootopaghata indicates as viral infection. Every body believes that, the Ayurveda is the mother of all medical sciences. Allmedical knowledge’s of present world has authentic information about microbes anddiseases caused by them. Acharyas of Ayurveda have explained common means of gettinginfections long ago, such as sexual intercourse, physical contact, droplet infection, food andwater, sharing the-bed, cloth, ornaments. Ancient history revels and refers massiveinfectious conditions such as AIDS through excavations. Now a day it seems to bereminding as a simple dream is that “Health for all “. If we are not accumulating all of ourhuman resources, energies, intelligence not to allow any further spread of these infectiousdiseases such as HIV or SARS it will be havoc to the mankind. If not, according to theestimation one should wonder if the slogan “Health for all” turns out as “AIDS for all”. Thenumber of people infected by HIV would have crossed 50 million and till now there were 12million deaths due to ARC (aids related complications) in entire world. In India since thedetection of HIV infection since 1986, the epidemic has been frankly out of control. As ofnow an estimated 4-6 million HIV infected cases are present in India. Within this shortperiod it has emerged as one of the most serious public health problem in the country. Introduction to Bhutabhishangaja Ojokshaya 1
  11. 11. AIDS is a multi dimensional disease syndrome, affecting physical, mental, social andspiritual facets of the affected person. The virus HIV hampers the Immune system. Whereas in Ayurveda the immunity is termed as Ojas. So the vitiated Immune system is called asOjovikruti. Bhootopaghata is one of the causative factors for Ojovikruti. The unique featureof human immune-deficiency virus is that it attacks the basic defense mechanism of humanbeings and gradually destroys the system completely. Then body becomes playground forall types of microbes like viruses, bacteria, fungi, protozoa, to inter play. In absence of anycheck force the microorganisms that enter the body through various entry points. And freelymultiply to cause numerous infections, which may leads to life threatening. The Ojokshayais one among the Ojovikruti. Symptoms are also identical to the advanced AIDS sign andsymptoms for example Moorcha, Moha, Pralapa, Mrutyu, Mamsakshaya, etc. There forAcquired Immune Deficiency Syndrome can be termed as Bhootopaghata Ojokshaya. At the same time there is no specific treatment available for the AIDS /HIV infection.AZT the costly medicine is still in practice, which is use full for the preventing the ARC, andfurther duplication of HIV virus.Recent advances in medical treatment Recent advances in medical treatment have given scientists renewed strength in thestruggle against HIV-the virus that causes AIDS. Many of today’s scientists are using AZTand DDI as a source of treatment. AZT inhibits reverse transcription, which is vital for HIV toinfect its host. Since HIV is a retrovirus it must convert its RNA to DNA. AZT and DDI willstop this from occurring and thus stop the HIV virus from spreading. There are also manyscientists trying to use CD4 as a potential type of vaccine. CD4 is a membrane protein thatmany cells in our body use. Those cells include the immune system cells, blood cells, andthe nervous system cells. It has been found that HIV only infects cells with CD4. It is for thisthat HIV infects its host in only areas whose cells contain CD4 1. Introduction to Bhutabhishangaja Ojokshaya 2
  12. 12. Vaccine in trial The vaccine in “Evaluation of an HIV-1 DNA Vaccine Encoding a Modified Gag-Polin Uninfected Adult Volunteers (Contact: Grace Kelly, RN)” trial, VRC 4302, is classified as agenetic vaccine. Genetic vaccines contain the genes (hereditary material) which direct theproduction of the proteins of the HIV virus. VRC 4302 contains the gene for the Gag and Polproteins of HIV. It is important to know that you cannot catch HIV or AIDS from this vaccine.Volunteers will be randomized in a blinded manner to receive either active vaccine (at one of3 doses, 0.5mg, 1.5mg or 4.0 mg) or vehicle ("control") alone. Participants will receive VRC4302 by intra-muscular injection once a month for 3 months. The injection is given using aneedle-less injection device. A total of approximately 21 individuals will be evaluated.Volunteers will be evaluated over the course of one-year (approximately 15 visits).Present study - as Ojokalpa Rasayana .Present study is a comparative study to assess two Ayurvedic combinations ofimmune builders, Immuno-modulators and acts on Ojovikruti by preventing ARC. Foodsupplements of immune modulation through well-known herbo-mineral origin, AmrutaKayaKalpa Rasayan of Amruta pharmaceuticals Hyderabad, is compared with the trail drugcombination of Bilvadi Vati and Agnikumar Vati (Sahasrayoga) as Ojokalpa Rasayana. InSahasrayoga Bilvadi vati and Agnikumar vati are indicated for Chira Atisara and Ama-Atisara, Visarpa, Garavisha and Bhoota visha, symptoms, which are appearing in ARC.Limitations of the study This study is of only 3 months period and attempt is not made to see in vitro effect oftherapy on HIV virus. The total work dwells on inferences based on both subjective andobjective parameters such as KPS score and CD4 count. With this duration, sample size anddesign, it is not possible to conclude the exact role of Ayurvedic treatment but this is a good Introduction to Bhutabhishangaja Ojokshaya 3
  13. 13. beginning for further study. Serological test for HIV is not a criterion for assessment rather itis a diagnostic tool for inclusion of subjects. Viral load test (PCR) is not employed because of financial constrains, instead CD4enumeration, which is an internationally accepted surrogate marker of HIV status was undertaken.Study design So a rational combination was made to tackle cause of disease and management ofresultant condition under the shelter of Sahasra yoga. The Ojokalpa Rasayana, which hasOjovardhaka, Ama pachaka, jwarahara, and krimighna drugs in it. Recent researchers haveproved all the properties of individual drugs also. An attempt has been made to developnon-pharmacopeal methods of management of this condition by adopting Sadvritta(disciplines), do and don’ts prescribed by Charaka and other Acharyas 2. This dissertation begins with literary review of Ojokshaya and HIV infection and acomparative study of both. The basic physiology concerned with this disease, patho-physiology, causative factors, signs and symptoms, diagnostic tests involved are discussed. A detailed drug review has been done which speaks about the rationale behind thecombination. There is a chapter continued on materials and methods, which was adoptedfor this research work and in observation and results detail description of findings ofresearch are given. In discussion and conclusion, the possible mechanisms involved in thepharmacological intervention and subsequent improvement are discussed. There is a summary of over all work followed by the references and bibliography. It is a fond hope of people of this country that a successful drug will emerge out ofthis traditional knowledge and this is a humble effort to bring this much-cherished hope intoa reality. Introduction to Bhutabhishangaja Ojokshaya 4
  14. 14. The normal healthy state of such a body requires normalcy of several factors. Theyare Dosha, Agni, Dhatu, and Mala along with peaceful disposition of Atma, Indriya andMana 3. For this normal functioning body requires strength, which is called as Bala. Ayurveda describes human body as seat of Chetana (consciousness) and a productof panchabhoutic vikara, existing in equilibrium. When this equilibrium gets disturbed, thatresults in defective bodily tissues. This is the beginning of any disease 4. This normal strength in the body is called as Sleshma 5, which has synonym -“Ojas”.This Ojas is transformed from the parents to the progeny through Sukra and Sonita 6, whichforms the zygote and from that moment development of foetus continues. The strength of any living is disturbed either by internal humors viz. Vata, Pitta andKapha or exogenous factors such as bacteria and virus. The virology and bacteriology is notmuch discussed from the ancient literature but the existence was not denied. Thus thepresent study which is based on the existence of the “Bhuta” described from the Vedicliterature. The principle of the disease development commences either from the endogenous orexogenous factors. The endogenous factors are grouped as physical and psychological.The physicals are of three humors and the psychological are rajas and tamas. Theexogenous factors which gives rise the disease because of Achayapurvaka prakopaultimately has to land for the vitiation of Dosha. Thus the terminus of the disease is underthe influence of the Dosha triode. Conceptual study of Bhutabhishangaja Ojokshaya 5
  15. 15. Here in this concern discussed about the Ojas, Dosha and immunity as the virusmakes the deficiency of immunity and disturbs the Dosha triode.Ojas in general Man is a creature composed of millions of cells. A microbe is composed of only one.Yet, through out the ages, the microbes have had the upper hand in their ceaseless conflictwith man. The above sentence is narrated from Atharvaveda, which dates backs to 5000years. Ayurveda describes human body is seat of Chetana (consciousness) and a productof Panchabhoutika vikara, existing in equilibrium gets disturbed. That results in defectivebodily tissues. This is the beginning of any disease 7. The normal healthy state of a body requires normalcy of several factors they areDosha, Agni, and Dhatu, and Mala, Peaceful deposition of Atma, Indriya and Manas.8 fortheir normal functioning, body requires strength, which is called as Bala. The same normal 9.strength had synonym as Shlesma That is also known as Ojas. Ojokshaya is a broadunderstanding of immuno deficiency, depilated vigor and vitality. This Ojas is transformed 10from the parents to the pregnancy through Sukra and Shonita (Beeja of Purusha and Stri)at the time of zygote formation. Ojas is the essence of all the Dhatus. The Beeja isresponsible for the formation of particular organ or tissue, if it is vitiated, that results indeformity of the respective organ. If it develops undisturbed there will not be any deformityof the respective organ. There for it is clearly understood that every part of the healthy human body (Dhatuand Mala) develops according to the healthy state of the Beeja and Beejabhaga. There forthe essence of Dhatus as represented by Ojas of Pumbeeja and Stribeeja plays the majorrole in this mechanism. Conceptual study of Bhutabhishangaja Ojokshaya 6
  16. 16. Ojas depends upon healthy state of Kapha. Physiologically Kapha represents apotential sour of strength and resistance to disease and decay. Those are Bala and Ojas.These terms reflect to the force and power which resists the factors responsible for decayand disease. Bala may be Sahaja (inherited), Kalaja (seasonal) and Yuktikruta (acquired) 11.But these all are equally capable of resisting the diseases. As vyadhi kshamatva is a force 12antagonistic to virulence of diseases causative factors . Susruta clarified further stating 13Balam is Ojas . As long as Dhatus are strong and healthy and are conducting their normalfunctions which their essence i.e. Ojas being both qualitatively and quantitatively effective.The body will be strong enough to resist and counter the decay and degeneration caused byeither the natural processes or disease. So in this contest this is very essential that, to knowabout etymology and normal physiology of Ojas.Nirukti (Etymology) of Ojas ‘Ojas’ the word has its root in “uj”or “vaj” dhatu. That means confer or strong (Ugra) 14.Ojas is the subanta pratyaya of word Ojas, which means Deepti, Prakasha and BalamKalidas in Raghu vamsha kavya writes ‘Rudraoujasa’ with reference to the potency of Shiva15 .Paribhasha (Definition) of Ojas Ojas is the essence of all Dhatus. Ojas is nothing but the Bala or Strength of thebody, which is the ultimate end product of the seven Dhatus starting from Rasa and ending 16at Shukra . Chakrapani contradicts this opinion and says Ojas sustains the body but doesnot nourish it. The normal healthy state of a body requires normalcy of several facts. They areDosha, Agni, Dhatu and Mala, along with peaceful deposition of Atma, Indriya and Manas.For this normal functioning body requires strength which is called as Bala. The normalstrength is called as Shlesma, which has synonym of Ojas, This Ojas is transformed from Conceptual study of Bhutabhishangaja Ojokshaya 7
  17. 17. the parents to the pregnancy through Shukra and Shonita. Which is the essence of theDhatus. If a part of Beeja, which is responsible for the formation of particular organ or tissue,is vitiated, that results in deformity of the respective organ. If it develops undisturbed therewill not be any deformity of the respective organ. There for it is clearly understood that everypart of the healthy human body (Dhatu and Mala) develop according to the healthy state ofthe Beeja and Beejabhaga, there for the essence of Dhatus as represented by Ojas ofPumbeeja and Steebeeja plays the major role in this mechanism. Ojas depends upon healthy state of Kapha. Kapha in physiologically representspotential sours of strength and resistance to disease and decay of Bala and Ojas. Theseterms reflect to the force and power which resists the factors responsible for decay anddisease. Bala may be sahaj (inherited) kalaj (seasonal) and yuktikrita (acquired). But theseall are equally capable of resisting the diseases. As long as Dhatus are strong and healthyand conducting their normal functions with the essence i.e. Ojas being both qualitatively andquantitatively effective. The body will be strong enough to resist and counter the decay anddegeneration caused by either the natural processes or disease. So in this contest this isvery essential that, to know about etymology and normal physiology of Ojas.Formation of Ojas in the body 17 Ojas is the ‘Sara’ i.e. essence of all Dhatus . It is produced In the body as honey,Which is collected by bees from various flowers and fruits. Ojas is derived from all theSapta Dhatus in other words all the Dhatus contributes to its making. Ojas is the product ofthe prasada paka of Dhatvagni vyapara.That has the essence of all the Sapta Dhatus in it.Essentially Ojas depends on Ahara for its production and sustenance 18.Panchaboutic sangatan Apara Ojas is also known as slismika ojas and it is considered somatmak denotingthe predominance of Aap and prithvi mahabhootas 19. Conceptual study of Bhutabhishangaja Ojokshaya 8
  18. 18. 20Physical properties of Ojas Colour:-Whitish yellow or whitish red resembling the color of Ghee Taste:-Sweet like honey Odour:- smell like fried paddy or Laja gelatin Ojasthana: Ojas is present all over the body and in each cell of the body 21 Oja Karya 22 Dosha nigrahana Sthiropachita Mamsata Cheshtasu Apratighata Svara Varna prasadhana Karananam Atma karya pratipatti Preenitaha sarvadehinah Prana yatra pratishtita Consistency 23 Snigda(unctuous), Guru (heavy),24, Pichchila (gelatinous) 25 , Mridu 26, 27, 28 29 (smooth), Sheeta, or somatmaka (mild to touch), , Stira (stable), Shukla varnam, 30 Saram 31, Viviktam,32 Guru 33 Bahalam 34 , Madhu rasam,35.Lajagandhi. 36, Lohita peetakam, 37Ojas Poshana 38 Ojas is nurrished mainly by Ahara, from the Ahara–Ahara rasa- Rasa dhatu- Rakta-Mamsa-Medha-Asthi- Majjaa-Shukra dhatusClassification of Ojas 39 There are two classifications of Ojas, made by Charaka, Susruta, Chakrapani, andby all other acharyas. Those are 1) Para Ojas and Conceptual study of Bhutabhishangaja Ojokshaya 9
  19. 19. 2) Apara Ojas 40 These two types of Ojas have a direct bearing on body’s defense againstdegeneration and infection.Para Ojas Ojas marks the beginning of the formation of embryo. It is the essential nourishingfluid developed from the Rasa of the embryo. It enters the heart right at the stage of theletter’s initial formation and is permanently locates there, sustaining the life of fetus. Loss ofOjas amounts to the loss of life itself. Chakrapani comments that the above function pertainsto both the Ojas and further explains that Ojas plays a role in three different stages of the life 41of the fetus. It permeates to through Rasa in entire body and nourishes entire body andOjas is transported through the Ojovaha dhamanies. 42 1. At the time of conception it is the essence of Sukra and Shonit. 2. In the second stage it is the essence of the Rasa Sara, which provides nutrition to the embryo. 3. The third stage, when there is formation of various organs, Ojas manifests with its won action.Apara Ojas or Sleshmaka Ojas It performs the Tarpan action in the entire body. It is source of strength to theDhatus. Any loss in the quantity would cause sudden death. Commenting on function ofOjas Susruta has made a significant observation. Ojas permits entire body nourishes limbsand organs. In the absence or deficiency of Ojas in the body there will be wasting, decay,degeneration, and destruction of the body. This statement indicates the nutritive nature ofthe Apara Ojas in preventing the decay of the body. It is one of the ten seats of life. It givesfirmness to physical structures and gives strength to motor activity. Ojas spreads all over the Conceptual study of Bhutabhishangaja Ojokshaya 10
  20. 20. body. In the absence of it life does not exist. The seat of Apara Ojas is the ten dhamaniesconnected with Hrudaya 43. According to Vagbhata, the function of Apara Ojas is “Dehastitanibhandana”. Which 44means it keeps the physical fitness of the body. Chandranandana clarifies that it is theprotection of the body in all the states. Hemadri also states that the changes in the Ojas arethe root cause for all the changes in the body. Ojas is Bala, which is a potential source ofresistance to disease and decay. Bala controls the Doshas that cause disease. This iscalled Vyadhi kshamatva.45.Synonyms of Ojas The term Ojas has been stated in Ayurvedic classics represents Kapha, Bala,Shleshma, Rasa and Rakta.46Sleshma in normal state apart from other confers 47. 1. It gives Weight and bulk. 2. It gives Strength to perform work 3. It resists disease and decay. 4. Promotes durability, (preserves the body from decay) 5. Promotes healing process (Ropanam) 6. It promotes tissue building.Ojas vriddhi lakshanas Increase in Ojas results in vriddi of Bala, Varna, Agni, Medha, Ayu and Sukha.Decrease results in kshaya. 48Nidana of Ojokshaya The pathological state of Oja is called as Ojokshaya .49. Charaka and all otherclassics have described this Oja vikriti as Ojokshaya. Susruta has classified this condition in 50to three different stages as 1) Ojo Vishrams, 2) Ojo Vyapat, 3) Ojokshaya, The Nidana Conceptual study of Bhutabhishangaja Ojokshaya 11
  21. 21. which causes depletion of any Dhatu, can also causes depletion in the Ojas qualitatively andquantitatively. The factors influencing the Ojokshaya are as follows. 1) Ahar karana. 2) Vihar karana. 3) Manashika karana, 4) Aagantu karana.51Ahar karanas: - Alpaasha (mal nutrition) Anashana (starvation)Vihara karanas:- Vaata atapa shevana (expose to sun heat and winds) Ativyayama (excessive work beyond the capacity) Ativyavaya (excessive sex) Shonit ativartana (loss of blood) and Prajagara (keeping awake at night)Manashikakaranas: - Kopa, (anger) Shoka (grief) Chinta (worry) Bhaya (Phobia).Agantu karan: - “Sankramana” or “Upasarga” denote infection Krimi, Rakhsa, Rakshasa, yathudhana, Pishacha, Gandarva, Boota, Nishachar, presents different types of microbes, and Oja bhakshaka rajanichra. 52 Conceptual study of Bhutabhishangaja Ojokshaya 12
  22. 22. Many diseases like Rajayakshma, Abhishyanda, Kushta, jwara, Upadamsha,Pooyameha, Apatantraka,Visarpa, Masoorika, Rohini, are some examples of infectiousdiseases coming to the mode infection, Bootopaghat, due to bhuta, pishacha, Rakshasa,etc. Charaka has mentioned that the Ojas is the Ahara for rakshas and if they consume theOjas, which leads to depletion of Ojas. Here Rakshasa i.e. Rajanichara 53 can be correlatedto infectious organism which spreads through Prasanga (sexual contact), Gatra samsparsha(physical touch), Nishwas (droplet infection), Saha bhojana (eating together) and Sahashayyasana, (sharing bed).Nidanartkara Vyadhi for the Oja vikriti 54 55 56, Rajayakshma , Prameha Pandu Raktarsha, Raktatisara, Kshayaja kasa, 57Kshataja kasa, Sannipata jwara , are the diseases which causes Ojakshaya in there later 58stage. Susruta pointed such possibility while dealing Abhinyasa jwara where in he usedthe term Hataujas 59 indicating the Ojokshaya. The clinical futures are low or even sub normal temperature, sub comatose state,loss of voice, cracked tongue, dry ness of throat, suppression of stools, perspiration,micturition, hardness of chest, aversion to food, dull complexion, difficulty in breathing, anddelirium. Susruta observed that disturbance of Ojas to the various parts of the body isaffected either due to leakage or loss or obstruction to the Ojas carrying tiny shrotases inSannipataja jwara, such condition is called as Oja – Nirodhaja sannipata. Inertness of thelimbs, chills, fits, loss of consciousness, delirium, etc. The acute condition referred above illustrates how the pronounced loss of Ojascontributes to an extra –ordinary state of susceptibility to increased microbial / viral activityand to toxins produced by these agents. Other clinical conditions which are slow inprogression, chronic in nature, and cause profound Dhatuksaya (wasting of body tissues)occur due to metabolic abnormalities leading to diminished production of Ojas. This will Conceptual study of Bhutabhishangaja Ojokshaya 13
  23. 23. happen due to loss of structural integrity of Dhatu vaha srotas and obstruction in the supply 60system. Such other disease syndromes are Rajayaksma, Madhumeha, Ojomeha , Pandu,Sannipata jwara, and etc. Charaka has enumerated the pathological sequences very clearly while explainingthe Samprapti of Rajayaksma (both Anuloma and Pratiloma) in Charaka Chikitsa. Afterexplaining the manner in which nutrient materials are normally metabolized and assimilatedby the Dhatus he elaborates it further, due to the obstruction of srotas. As a result of adeficiency of nutrients Raktadi Dhatus, lowered functioning of dhatwagni and catabolicevents, the food ingested, which under goes pachana in kosta, is changed in to malas.Charaka in the Samprapti of Madhumeha observed that Vata by its ruksha guna. Charaka in the Samprapti of Madhumeha observed that Vata by its ruksha gunatransforms the Ojas, sweet in taste to astringent and transports it to the mutrashaya leadingto the causation of the condition known as Madhumeha. It is another disease whereOjokshaya is evident. Several other conditions creep in long with the main disease. Herethe Ojas produced in this person it self is vitiated 61. In case of Pandu roga the Samprapti is dominated by Pitta. The aggravated Doshavitiates the dhatus, which in turn loose their integrity and loss of normal colour, Bala(resistance) and Sneha, which are the gunas of Ojas are depleted by the dhosh-dhatusammurchana resulting the clinical features; impoverished Rakta, and medha dhatusleading shitilendriyata and vaivarnyata. Prameha, the urinary disorder is of two types. One caused due to endogenousfactors like Vatadi doshas, another one caused by exogenous or Agantuj factors likeindulgence in sex with the unfit and diseased partners. Agantuja prameha is infectious andcommunicable disease, transmitted through agamya, and dushita yoni samsarga (sexually Conceptual study of Bhutabhishangaja Ojokshaya 14
  24. 24. transmitted). In these pramehas Ojokshaya occurs as a consequence of the passage ofOjas – mixed with urine excessively. Here Ojokshaya takes place in two different ways 62. Dosh Dhatu kshayajanya Ojaksaya. (That is depletion of the Ojas, due to theendogenous factors such as dosh, dhatu.etc.) Aupasargika / agantuja meha janyaOjokshaya (depletion due to exogenous factors like infections etc). But there is lot ofdifference in treatment between above said two entities. In case of Madatyaya, that severely affects Ojas, Bala and Prana. Madya is havingqualities exactly opposite to that of Ojas. Hence the Vyadhikshamatva is affected in it’stotally. Krimi and Visha also lead to severe loss of Ojas.Ojovisramsha Ojas mixes with Rasa dhatu in Hriday, from there it circulates trough out the body viavarious srotases. In this condition, the circulating Ojas leads leaks out or oozes out from thetiny distributing channels as a result; this vital substance may not reach certain organs /parts of the body and leads to the following signs and symptoms.Ojovyapat It is a pathological condition of Ojas because of vitiation by the Dosha as a result, theOjas looses its physiological or normal qualities and properties as described to it, this vikrutaOjas prod uses the following laxanas.Ojokshaya This is the final stage of Ojo-vikriti represents the loss and wasting of Ojas.According to Susruta 63Ojo-visramsa i. Sandi visleshana (loss of firmness of the joints) ii. Gatrosada (inertness of the extremities) Conceptual study of Bhutabhishangaja Ojokshaya 15
  25. 25. iii. Doshachayana (disturbance) displacement of doshas from their own places iv. Kriyasannirodha (impairment of kaya vak-mano vyapara)Ojovyapat a. Stabdagatrata. (Heaviness and stiffness of the body and extremities.) b. Vata –shopha (oedema of vataja nature) c. Glani (malaise) d. Varna bheda (impairment of normal colour of the skin complexion) e. Tandra (drowsiness) f. NidraOjokshaya 1) Murcha (loss of conscious ness) 2) Mamsa kshaya (emaciation of mussels) 3) Moha (stupor) 4) Pralapa (delirium) 5) Marana (death)Kapha and vyadhikshamatva Health and longevity depends on the Balam as represented by kapha. Charaka hasexplained the same in the words “Baladisthanam Arogyam”. Bala denotes two vital aspectsof life process namely Vyayama Shakti. Vyadhikshamatva is further classified into threetypes – Sahaja, Kalaja and Yuktikrita.Sahaja Bala 64 The Sahaja Bala or resistance to the disease is stated to be prakriti. I.e. Inherentgenetic from of resistance existing in the individual body since birth and this also increases Conceptual study of Bhutabhishangaja Ojokshaya 16
  26. 26. along with the growth of the body elements i.e. Sapta dhatus .It comprehends both shariraand satwa i.e. body and mind.Kalaja Bala 65 Kalaja Bala is influenced by the factors like seasonal variations and age of theindividuals. Thus kalaja Bala is supposed to be dissipated at its lowest leveling the Adanakala comprising of Sishira.Vasanta and Greeshma ritus. On other hand Bala is stated to beconserved and at its high peek level in the visarga kala, inceasing over Varsha, Sharat andHemanta ritus. Those are known as Sheeta kala or cooler period.Yuktikrita Bala 66. Yuktikrita Bala refers to the body’s resistance against disease, which can beenhanced by appropriate nutrition such as meat, Ghee, etc. Restorative and Rasayanatherapy in keeping with the seasonal requirements, adaptation of swastha vritta principles ofAyurveda along with Achara Rasayana also contributes the growth of Yuktikrita Bala. Dalhana in his commentary on Bala lakshanas as explained by Susruta observesOjas and Bala as synonyms, especially with Chikitsa point of view. However they are distinctin the sense the former is the essence of all the dhatus and it has physical properties likeRoopa, Rasa, Veerya etc., the later has to be determined from the power to lift heavy weightand the capacity to bear heavy loads etc. it does not possess physical properties. 67 The Vyadhikshamatva is not the same merit/order in all constitutions. In other words-This Shakti varies from individual. The same is explained in the Charaka Samhita ”Na chasarva shareerani vyadhikshamatva samarthani bhavantani.” In the discussion on factors thatinfluence Bala, held between Punarvasu Atreya and Agnivesha is recorded in the chapterVividaashitiyapeeya in the Charaka sutra sthana. This discussion throws considerableamount of light on the views held on resistance to disease. Conceptual study of Bhutabhishangaja Ojokshaya 17
  27. 27. 68. Kapha is five types Those are Kledakakapha, Bodhakakapha, Tarpakakapha,Avalambakakapha and Shlesmakakapha. Each one is limited to some part or parts of bodyby their functions. They look after the functions of the Kapha locally and project the bodycollectively.The function of Kapha 69 The important functions, attributed to the Sleshma by the different Acharyas are, 1. Kapha is responsible for growth, weight, and bulk of the body. That is Brimhanam, and Gouravam. 2. It is Vrishya, a function relates to sexual stamina and productivity. 3. Sthairyam- it imparts stability and durability to the body and strength to the limbs. 4. It confers strength required to perform labors physical activity i.e. physical activity i.e. Vyayama Shakti. 5. It also provides the power to resist and overcome forces or factors, which bring about disease and decay popularly known as Vyadhikshamatva viz. Vyadhibala viroditva, Vyadhi utpadaka hetupratibhandakatvam.70. 6. Ropana- promotes healing process. 7. Ambukarma- Kapha being a repository of water, Makes this important fluid function to sub serve its vital secretary activities. 8. It has a function responsible of cohesion of various units and structures of the body.IMMUNE MECHANISM Defense mechanism of the body is classified in to two. 1. Immune 2. Non immune Conceptual study of Bhutabhishangaja Ojokshaya 18
  28. 28. Immunity gives the specific response to a foreign antigen or pathogen. Andgenerally takes longer time to materialize. Memory is the key feature of the immunitytowards the antigen. Non immune host defense is not antigen specific, without memory itresponses immediately and is call inflammation also. There are cellular immunity and humoral immunity in the immune system and foreach the active principles are Thymus-derived (T) lymphocytes, and Bone marrow derived(B) lymphocytes respectively. Although both “B” and “T” lymphocytes are derived fromcommon stem called Bone marrow. Neutrophills, Esinophills, Basophiles, Natural killer cells,monocytes, and macrophages, are the mediators for this immediate response as nonimmune substances. Non specific resistance represents a wide variety of body reactionsagainst a wide range of pathogens, specific resistance or immunity involves the productionof specific anti body against specific pathogen or its toxins. Non specific resistance todisease is occurring by - Mechanical factors like • Skin and mucous membrane. • Saliva, Lacrimation, and Sebum. Chemical factors like • Gastric juice. • Enzymes. Mucous produced by glands of stomach, Nasal secretion and tissue fluids. Anti microbial substances 1. Interferon. 2. Complement. 3. Proper din with adherence and ingestion phagocytic activity. Conceptual study of Bhutabhishangaja Ojokshaya 19
  29. 29. Specific resistance to the disease 1. Specific resistance to the disease is called Immunity. This destroys the particular antigen. 2. A detailed review of immunological process is desirable to understand the AIDS phenomena. Antigen and anti bodies Antigen is a chemical substance, which introduced at the time of production of antibodies. Antigen has 3 important characteristics. 1. Immunogenic. (This stimulates the formation of antibodies). 2. Reactivity(Reacts with antibodies) 3. Stimulation and reacting with antibodies. Vast majority of antigens are proteins, nucleoproteins, (nucleic acid plus proteins)lipoproteins, glycoprotein, and certain large polysaccharides. The entire microbe, such as a bacterium or virus or components of microbes may actinclude pollen, egg white, incompatible blood cells, and transplanted tissues and organs.The myriad of antigens in the environment provides many opportunities for the production ofantibodies by the body. Antibodies not form against with the whole antigen, at specificregions on the surface of the antigen, called antigenic determinant sites. Specific chemicalgroups of the antigen combine with the antibody. This combination depends up on the size and shape of the determinant. Site and themanner in that, it corresponds to the chemical structure of the antibody. Lymphocytes are key constituents of the immune system. In mammals, this systemhas the remarkable ability to produce antibodies against many millions of different foreignagents that invade the body. In addition, the immune system “remembers,” and a second Conceptual study of Bhutabhishangaja Ojokshaya 20
  30. 30. exposure to a foreign substance produces a more rapid and greater Hum oral immunity isimmunity due to circulating antibodies in the globulin fraction of the plasma proteins. It is amajor defense against bacterial infections. Cellular immunity is responsible for delayed allergic reactions and rejection oftransplants of foreign tissue. It constitutes a major defense against infections due to viruses,fungi, and a few bacteria such as the tubercular bacillus. It also helps to defend againsttumors. There have been spectacular advances in immunology in recent years, and the fieldis now large and complex. Only the fundamentals are presented here.Development of the Immune System During fetal development, Iymphocyte precursors come from the bone marrow.Those that populate in the thymus become transformed by the environment in this organinto the lymphocytes responsible for cellular immunity i.e.-Imphocytes. Lymphocytesresponsible for humeral immunity are B-lymphocytes. Four different varieties of T cells havebeen identified: helper / inducer T cells suppressor T cells, cytotoxic T cells (which are alsoknown as effectors T cells or killer cells), and memory T cells. The first 2 types are involvedin the regulation of antibody production by B cells derivatives, whereas the cytotoxic T cellsdestroy transplanted and other foreign cells. Cytotoxic and suppressor T cells have on theirsurface the glycoprotein CD8, which can be detected by monoclonal antibodies, so they arefrequently called T, cells. Helper / inducer T cells have on their surface the glycoprotein CD4and are therefore called T cells. CD8 is a co receptor for MHC class I molecules and CD4 isa co receptor for MHC class II molecules. Memory B and T cells are cells those have been exposed to an antigen and arereadily converted to effectors cells by a later encounter with the same antigen. Unlike otherlymphocytes, they persist in the body for months or even years. Conceptual study of Bhutabhishangaja Ojokshaya 21
  31. 31. Lymphocytes, macrophages, and other cells involved in immune responsescommunicate in part by hormone like chemical messengers called interleukins andcytokines.Major Histo – compatibility complex The genes of the major histo compatibility complex (MHC), which are located on theshort arm of human chromosome 6, encode glycoprotein that are located on the surface ofall cells and function in antibody processing and distinguishing self from non-self. They aredivided into 2 classes on the basis of tissue distribution and function. Class I antigens arecomposed of a 45-kilodalton heavy chain associated non-covalently with P, micro globulinencoded by a gene out side the MHC. Antigens can also be processed and presented to T4 cells by various types of cells inthe body in addition to macrophages. The other types of antigen presenting cells include theB cells themselves, the Langerahans cells of the skin, and specialized cells called dendriticcells in the lymph nods and spleen.Cellular Immunity T8 cells mediate cellular immunity. These cells are activated when they arepresented with antigens and MHC-1 proteins on the surfaces of antigen presenting cells.When also exposed to interleukin-2, they proliferate and differentiate into cytotoxic T cells.The cytotoxic T cells attack and destroy cells that have antigen, which activated them. Theykill by inserting pore-forming molecules (perforins) in the membranes of their target cells inthe same fashion as the complement system does. They may also act by including withinthe cells an as at undefined change that leads to death. Suppressor T cells, which developmore slowly then cytotoxic T cells, help terminate the immune response by dampening theimmune responses of T and B cells. This includes turning of the helper / inducer cells. Conceptual study of Bhutabhishangaja Ojokshaya 22
  32. 32. To ensure maximal specific T cells response the antigen is linked to molecularcomponents of the HLA system (by B cells, dendritic cells and macrophages) and presentedto T cell. The transformed blast cell undergoes progressive mitotic division and each cell ofthe resulting clone has the same specific immune potential. The subsequent T cell activitiestend to remain local at the site of the antigen concentration and this cell mediated immunity(CMI) is delayed, i.e. at least 24 hours are required for a significant local concentration ofsensitized T cells.T cell functions and mechanism Overall regulation of the immune response and reactions- this is effected by helper Tcells which promote, and suppressor T cells which inhibit immune reactions. In theperipheral blood, 2/3 of the T lymphocytes are helper and 1/3 suppressor. Using monoclonalantibodies, helper cells carry the CD4 surface antigen and suppressor cells the CD8.T cell effecter mechanisms:a). Cytotoxic T cells cause antigen-specific lyses by direct cell-to-cell contact.b). Natural killer cells, again cause lyses by direct cell to cell contact but usually the killingaction is non specific.c). Delayed hypersensitivity reactions are mediated by the release of lymphokines from thespecifically activated T cells. They promote a wide range of cellular activity associated withthe promotion and control of the immune response and the inflammatory reaction.Lymphokines and cytokines Lymphocytes, macrophages, and in some instances endothelial cells, neurons, glialcells, and other types of cells secrete many hormone like chemical messengers that effectthe immune response. The messengers secreted by lymphocytes and often calledlymphokines. However, since other cells produce them as well, it seems more appropriate to Conceptual study of Bhutabhishangaja Ojokshaya 23
  33. 33. call them cytokines. This field is growing very rapidly, and most of the cytokines are initiallynamed for other actions, e.g. B cell differentiating factor, B cell stimulating factor 2. There isa convention that once the amino acid sequence of a factor in humans is known its name ischanged to interleukin. Thus, for e.g. the name of B cell differentiating factor was changed to interleukin-4.However, nomenclature in this field remains somewhat confused and uncertain.Hemoglobin The red, oxygen-carrying pigment in the red blood cells of vertebrates isHemoglobin, Hemoglobin is a globular molecule made up of 4 sub units. Each sub unitcontains a hem moiety conjugated to a polypeptide. The average normal Hemoglobincontent of blood is 16g/dl in men and 14g/dl in women, all of it in red cells. In the body of a70- kg man, there is about 900gms of Hemoglobin, and 0.3gm of hemoglobin is destroyedand 0.3gm synthesized every hour.Platelets The platelets are small, granulated bodies 2-4 micrometers in diameter. There areabout 3 lakhs /µ liter platelets in circulating blood, and they normally have a half-life of about4 days. The megakaryocytes giant cells in the bone marrow, from platelets the pinching ofbits of cytoplasm and extruding them into the circulation. Platelet production is regulated bythe colony stimulating factors that cintroll the production of megakaryocytes. Between 60and 75% of the platelets that have been extruded from the bone marrow are in thecirculating blood, but the reminder are mostly in the spleen. Splenectomy causes anincrease in the platelet count (thrombocytosis). Non specific resistance represents a wide variety of body reactions against a wide ofpathogens. Specific resistance or immunity involves the production of specific antibodyagainst specific pathogen or its toxin. Conceptual study of Bhutabhishangaja Ojokshaya 24
  34. 34. Pathology in Bhutabhishanga Ojokshaya (HIV infection) The acquired immune deficiency syndrome (AIDS) was first recognized in the UnitedStates in the summer of 1981, when the centers for disease control and prevention (CDC)reported the unexplained occurrence of to diseases. At first Pneumocystis carinii pneumoniain five previously healthy homosexual men in Los Angeles was reported. Soon afterKaposi’s sarcoma in 26 previously healthy homosexual men in New York, and Los Angeleswere reported. Within months, the disease became recognized in male and female InjectionDrug Users (IDUs) and soon after, in recipients of blood transfusions and in hemophiliacs.As the epidemiological pattern of the disease was unfolded it became clear that a microbetransmissible by sexual contact or blood and blood products was the most likely etiologicagent for the epidemic. In 1983, Human Immuno Deficiency Virus (HIV) was isolated from apatient with lymph-adenopathy. In 1984 it was demonstrated clearly that this virus is thecausative agent of AIDS. During the early years of 1980’s the care of HIV-infected individuals in the UnitedStates was confined to restricted groups of physicians and hospitals, in urban areas, ofnorth eastern and western seaboards. But today, every practicing physician in this countryand other parts of the world is required to have some degree of familiarity with the work up,diagnosis, management, of HIV-infected individuals. HIV-infected individuals are presentingin increasing numbers to family physicians, obstetricians, gynecologists, pediatricians andsurgeons with clinical problems that may be directly or indirectly related to their HIV-infection.HIV infection in India The first case of HIV infection was identified in India in 1986 at Chennai. Duringthese days it was limited to female sex workers. Focus was shifted from Chennai to Mumbaias hundreds of female sex workers were found to have HIV infection. It is with truck drivers, Conceptual study of Bhutabhishangaja Ojokshaya 25
  35. 35. it started spreading from big cities to smaller ones. People, who travel from cities to city andthose who travel from villages to cities, were found to be more susceptible because ofunprotected, non-martial sexual contact. Even though thousands of people got infectedthrough blood transfusion during the first decade of epidemic, the heterosexual contact isthe major cause of spread. Every year 3 lakh Indians die due to AIDS. Since the beginning,amount of the death of the AIDS patients is 25 lakhs. It is second highest figurecommunicable diseases, which cause death.Definition of AIDS Any HIV-infected individual with CD4+T cell count of<200/microliter had AIDS bydefinition, regardless of the presence of symptoms or opportunistic diseases. The clinicalconditions like pulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer.While the definition of AIDS is complex and comprehensive, the clinician should not focuson presence of AIDS but should view HIV disease as a spectrum ranging from primaryinfection, with or without the acute syndrome, to the asymptomatic stage, and to advanceddisease. It is important to distinguish between being infected with HIV and having AIDS.People infected with HIV may take 5-7years or more to develop as AIDS. Some time it maybe sooner because of malnutrition and poor state of health, toxins and malnutrition out plaidfactors that stress the immune system probably cause AIDS. During this interval HIVinfected individuals may suffer from a variety of disorders and develop signs which aresuggestive of being infected with HIV. Mainly those symptoms are pain less swelling ofLymph nodes in the neck, Armpits and Groin, Fever, Night Sweats, Diarrhea, Loss of weightand infections such as Herpes, Pneumonia, etc. Conceptual study of Bhutabhishangaja Ojokshaya 26
  36. 36. Etiologic agent The etiologic agent of AIDS is HIV (the Human Immuno deficiency Virus), whichbelongs to family of (Heterogenous) human retroviruses and the subfamily of Lentiviruses.Lentiviruses cause disease in other animal species, including Sheep, Horses, Goats, Cattle,Cats and Monkeys. The four recognized human retroviruses belong to two distinct groups,i.e.HIV-1 and HIV-2. The most common cause of HIV disease throughout the world is HIV-1comprises several subtypes with different geographic distribution. HIV-2 was first identifiedin 1986 in West African patients and was originally confined to this region. Electron microscopy shows that the HIV virus is an icosahedra structure containingnumerous external spikes formed by the two major envelope proteins, the external Gp120and the transmembrane Gp41.The virion buds from the surface of the infected cellincorporates a variety of host proteins, including Major Histo-compatibility Complex (MHC)class I and II, antigens into its lipid bilayer. This virus contains two Snake like single strands of Ribose Nucleic Acid (RNA), slowin nature, having reverse transcriptase enzyme. Having size about 90-120 mm. this virus isa tiny, a thousand times smaller than the thickness of a hair. Looks like a roller upporcupine. This lies firmly wrapped up in a care which resembles a cone with a dimple at itsbase. This cone is protected by an envelop that has a knob like protein sticking out itssurface. HIV is free from live, when it is out side the body. It dies immediately in dry area.It can alive in blood at 4o c, about three weeks or till the cell disintegrates.Pathology and Pathogenesis The hallmark of HIV disease is a profound immunodeficiency resulting primarily froma progressive quantitative and qualitative deficiency of the subset of T lymphocytes referredto as helper or inducer T cells. This subset of T cells is defined phenotypicaly by thepresence on its surface of the CD4 molecule. This serve as the primary cellular receptor of Conceptual study of Bhutabhishangaja Ojokshaya 27
  37. 37. HIV it has recently been demonstrated that a co-receptor must be present together with CD4for effective fusion and entry of HIV-1 into its target cells. It is important appreciate that thepathogenic mechanisms of HIV disease are multi factorial and multi-phased and aredifferent at different stages of the disease. HIV has a number of mechanisms to evade elimination by the immune system. HIVhas as extraordinary ability to mutate, but this mechanism probably acts mainly after theestablishment of chronic infection and contributes to the maintenance of chronic. Since thetransmitted virus and the virus that initially becomes established as a chronic infection arerelatively homogeneous, the initial escape from immune system control likely involves othermechanisms. Molecular analysis of clono types has demonstrated that clones ofCD8+Cytolytic T Lymphocytes (CTLs) that expand greatly during primary HIV infection andlikely represent the high-affinity clones that would be expected to be more efficient ineliminating virus infected cells disappear after their initial burst of expansion.Viral Dynamics HIV-1 and HIV-2 are both viruses that belong to the same family, but vary in geneticmake up. HIV-1 was first discovered in 1983 in France and appears to be more preventionEurope and America. HIV-2 was first discovered in 1986 and is more prevalent in Africa.Both HIV-1 and HIV-2 have been detected in India and both leads to AIDS. It was originally thought that very little virus replication occurred during clinicallatency. However studies of lymphoid tissue using PCR analysis for HIV RNA and in sitehybridization for individual virus expressing cells clearly demonstrated that HIV replicationoccurs throughout the course of HIV infection, even during clinical latency. The availability ofsensitive PCR techniques leads to the demonstration that viremia present at all stages ofHIV disease. Conceptual study of Bhutabhishangaja Ojokshaya 28
  38. 38. The behavior of the HIV is very much similar to poison. The HIV is fragile, once thevirus is out side the body in a dry form, it dies immediately. When stored in blood banks at4oc, it can live for about 3 weeks or till the cell is integrates.Mode of Transmission Transmission is of two types, horizontal and vertical. HIV is transmitted byhomosexual and heterosexual contact. Blood, Blood products are the important routes ofinfection. Infection spreads from mothers to infants either intrapartum, perinatally, or viabreast milk. After more than 15 years of scrutiny, there is no evidence that HIV is transmittedby casual contact or that the virus can spread by insects, such as by a mosquito bite.1) Sexual transmission:- ♦ Homo sexual: More HIV infections occur in homo sexual and bisexual men (lesbianism) who have a large number of sexual partners the sexual practice often involves anal intercourse (anal sex) and fella tic with ejection of semen in to the mouth (oral sex). ♦ Hetero sexual: Multiple, Hetero sexual contacts often prostitutes. ♦ Blood and tissue liquids: i. Contaminated blood and blood based products, ii. Blood transfusion, iii. Semen and Sperm, iv. Brest milk, v. Urine, Tear, Saliva, CSF with visual blood containing, ♦ Contaminated instruments like needles, syringes, surgical and dental. ♦ Transplantation of tissues and organs, (Kidney, Cornea, Skin, Bone marrow) Conceptual study of Bhutabhishangaja Ojokshaya 29
  39. 39. ♦ Mother to child. Antenatal (In Uterus), Delivery (at birth), Postnatal (After birth by Breast feeding) HIV has been demonstrated in seminal fluid both within infected mononuclear cellsand in the cell free state. The virus appears to concentrate in the seminal fluid, particularly insituations where increased numbers of lymphocytes and monocytes are. The virus has alsobeen demonstrated in cervical smears and vaginal fluids. There is a strong association oftransmission of HIV with receptive intercourse. Owing to the fact that only a thin and fragilerectal mucosal membrane separates the deposited semen from potentially susceptible cellsin and beneath the mucosa this transmission takes place. Trauma associated with analintercourse provides at least two modalities of infection; direct inoculation into blood in casesof tears in the mucosa, and infection of susceptible target cells, such as langerhans cell, inthe mucosal layer in the absence of trauma. There is approximately a 20 fold greater chanceof transmission of HIV from a man to a woman than from a woman to a man through vaginalintercourse. This difference may be due to the prolonged exposure of the vaginal andcervical mucosa and endometrium to infected seminal fluid.2) Transmission by blood and blood products: HIV can be transmitted by blood products, both among individuals who sharecontaminated paraphemalia (needles and syringes) for injection drug use and in those whoreceive transfusions of blood and blood products. It is estimated that 90 to 100% individualswho were transfused with HIV-infected blood became infected. Transfusions of whole blood,packed red blood cells, platelets, leukocytes, and plasma are all capable of transmitting HIVinfection. The precautionary measures taken to check this: (1) the screening of all blood forp24 antigen and for HIV antibody body enzyme linked immuno-absorbent assay (ELISA), Conceptual study of Bhutabhishangaja Ojokshaya 30
  40. 40. with a confirmatory western blot where applicable; (2) the self-deferral of donors on thebasis of risk behavior.3) Occupational transmission of HIV: There is a small but definite occupational risk of HIV transmission among health careworkers, laboratory personnel, and potentially others who work with HIV infected specimens,particularly when sharp objects is used. It is estimated that 250,000 to 1 million health careworkers are stuck with needles or other sharp medical instruments in each year large.4) Maternal to fetal / infant transmission (vertical): HIV infection can be transmitted from an infected mother to her fetus duringpregnancy or during delivery. This is an extremely important form of transmission of HIVinfection in developing countries, where the proportion of infected women to infected men isapproximately 1:15) Transmission by other body fluids: There is no convincing evidence that saliva can transmit HIV infection, either throughkissing or through other exposures, such as occupationally to health care workers. But bloodcontaminated saliva and wet kissing will leads to HIV infectionEpidemiology of HIV infection HIV infection and AIDS is a global pandemic, with cases reported virtually from everycountry. The current estimate of the number of cases of HIV infection among adultsworldwide is approximately 22 million, and approximately 2.6 Million HIV-infected childrenhave been born since the start of the HIV pandemic, and approximately one half of thesehave developed AIDS and have died. The global projections for the number of HIV-infectedindividuals by the year 2000 range from 40 to 100 million. Conceptual study of Bhutabhishangaja Ojokshaya 31
  41. 41. Life cycle of HIV infection HIV is an RNA virus whose hallmark is the reverse transcription of its genomic RNAto DNA by the enzyme reverse transcriptase. The life cycle begins with the high affinitybinding of the Gp 120 protein via a portion of its VI region near N terminus to its receptor onthe host cell surface, the CD4 molecule. It has recently been demonstrated that the co-receptor that must be present together with the CD4 molecule for fusion and entry of T-celltropic strains of HIV-1 is a molecule termed CXCR4. Figure –1 Life cycle of HIV infection The reverse transcriptase enzyme, which is contained in the infecting Virions, thencatalyzes the reverse transcription of the genomic RNA into double-stranded DNA. The DNA Conceptual study of Bhutabhishangaja Ojokshaya 32
  42. 42. trans-located to the nucleus, where it is integrated randomly into the host cell chromosomesthrough the action of another virally encoded enzyme Integrate.Morphology of HIV Electron microscopy shows that the HIV virus is an icosahedral structure containingnumerous external spikes formed by the two major envelope proteins, the external gp 120and the transmembrane gp41. The Virion buds from the surface of the infected cellincorporates a variety of host proteins, including Major Histo-compatibility complex (MHC)class I and II, antigens into its lipid bilayer. Figure –2 Structure of HIV Glycoprotein Glycoprotein GP41 GP120 Fatty (Lipid Bilayer membrane Protein P18 Protein Reverse transcriptase P24 enzymeHIV genetics HIV-1 has genes that encode the structural proteins of the virus gag encodes theproteins that from the core of the Virion (including p24 antigen) I Pol encodes the enzymes Conceptual study of Bhutabhishangaja Ojokshaya 33
  43. 43. responsible for reverse transcription and integration and env encodes the envelopeglycoprotein. Molecular heterogeneity of HIV-1: Molecular analysis of various HIV isolates revealssequence variation over many parts of the viral genome.Types and Sub types There are two types of HIV-1 group M (major), which is responsible for most of theinfections in the world, and group O (outlier) a relatively rare viral form found at this time inCameroon, Gabon and France. The M group comprises at least light sequence subtypes, orclad, designated A to H.How does the HIV virus attack the immune system, Once the human immuno deficiency virus enters the body, it gets attacked to a typeof white blood cell called T lymphocytes. The RNA genetic material of the virus then getsconverted to DNA genetic material by an enzyme that the virus produces. This virus DNAthen gets incorporated in to the DNA of the T lymphocyte, and remains there for the lifetimeof individual. This infected cell knows becomes a virus factory producing more viruses whichbud out the cell, attack new T lymphocytes, and destroy them. Over a period of years, the Tcell count of the infected person drops to a critical level and the individual develops AIDS.Duration of an HIV infected person to develop AIDS. This depends on the mode of the HIV transmission and life styles of the HIV positiveperson. Persons those are infected through blood transfusion develop symptoms of anaverage from 3-5 years. With the other modes of transmission, when the dose of the virus isless, the person can remain healthy for 8-12 years or longer, if an HIV positive personimproves his or her quality of life by adopting safer sex, has a good nutrition, regularexercise, seeks immediate medical attention for any ill health. Avoids stress, continues to beactive he or she is likely to live longer. Conceptual study of Bhutabhishangaja Ojokshaya 34
  44. 44. The cytokine network in the HIV pathogenesis On perturbation of the immune system by antigenic challenge, the expressions ofcytokines increase to varying degrees. Cytokines that are important components of thisimmune regulatory network have been demonstrated to play a major role in the regulation ofHIV expression in vitro. A number of in vitro model systems of chronically infected monocyteor T cell lines, primary cultures of peripheral blood or lymph node mononuclear cells fromHIV-infected individuals, and acutely infected primary cell cultures have been used todemonstrate the role of cytokines in the regulation of HIV expression. Potent modulation ofHIV expression has been demonstrated either by manipulating endogenous cytokines or byadding exogenous cytokines to culture. Cytokines that induce HIV expression in one ormore of these systems include IL-1, IL-2, IL-3, IL-6, IL-12, TNF and TNF. Macrophagecolony stimulating factor (M-CSF) and granulocyte-macrophage colony stimulating factor(GM-CSF). Among these cytokines the most consistent and potent inducer of HIVexpression are the pro-inflammatory cytokines TNF IL- and IL-6. Interferon (INF) and(INF) 2, IL-4, IL-10 and INF 3 can either induce or suppress HIV expression, depending onthe system involved.Clinical manifestation of HIV infection HIV disease can be divided empirically on the basis of the degree ofimmunodeficiency into an early stage (CD4+T cell count 200 to 500/ micro liter), anintermediate stage (CD4+T cell count 200 to 500 /micro liter) and an advanced stage(CD4+T cell count < 200 / micro liter). Most AIDS defining opportunistic infections and truemalignancies occur in the advanced stage of disease, while neurological disease andKaposi’s sarcoma are not as strictly related to the degree of immunodeficiency. The twomajor classification systems for staging HIV disease are the CDC system and the Walter Conceptual study of Bhutabhishangaja Ojokshaya 35
  45. 45. reed medical center system; these are to be distinguished from the case definition for AIDS,which is used for surveillance purposes.Disease control classification system for HIV infection Group 1, Acute HIV syndrome Group 2, asymptomatic infection Group 3, Persistent genaralised lymph-adenopathy Group 4, other diseases • Constitutional disease • Neurological diseases • Secondary infectious diseases • Secondary neoplasms • Other conditionsThe acute HIV syndrome (acute Retro viral syndrome) About 50-70% of people infected with HIV usually develop acute viral fever flu likesyndrome called (ARS- acute retroviral syndrome), This occurs within 2-4 weeks after getting infected with HIV. The symptoms present are fever, body ache, and skin rashes. It is estimated that 50 to 70% of individuals with HIV infection experiences and acuteclinical syndrome approximately 2 to 4 weeks after primary infection. Varying degrees ofclinical severity have been reported, and it has been suggested that symptomatic sero-conversion leading to the seeking of medical attention indicates an increased risk for anaccelerated course of disease. Clinical findings occur along with a burst of plasma viremiaand p24 antigenemia. The syndrome is typical of an acute viral syndrome and has been linked to acuteinfections mononucleosis symptoms usually persist for 1 to several weeks and gradually Conceptual study of Bhutabhishangaja Ojokshaya 36
  46. 46. subside as an immune response to HIV develops and the levels of plasma viremiadecrease. Opportunistic infections have been reported during this stage of infection,reflecting the immunodeficiency that results from reduced numbers of CD4+T cells. Totallymphocyte and T cell subsets (CD4+ and CD8+) are initially reduced. An inversion of theCD4+/CD8+ T cell ratio occurs later because of the rise in the number of CD8+T cell subsets,as determined by T cell receptor analysis. The total circulating CD8+T cell levels usuallyremain some what depressed although there may be a slight rebound towards normal.Lymph-adenopathy occurs in approximately 70% of individuals with primary HIV infection.Most patients recover spontaneously from this syndrome and have a mildly depressedCD4+T cell count that remains stable for a variable period before beginning its progressivedecline. In most patients, primary infection with or without the acute syndrome is followed bya prolonged period of clinical latency.The asymptomatic stage Clinical latency although the length of time from initial infection to the development ofclinical disease varies greatly the median time is approximately 10 years. HIV disease withactive virus replication usually progresses during this asymptomatic period. Some patientscalled long term non-progressors, show little decline in CD4+T cells counts over an extendedperiod. These patients generally have extremely low levels of HIV RNA. In these patients,the appearance of an opportunistic disease may be the first manifestation of HIV infection.Some patients otherwise asymptomatic develop persist generalized lymph-adenopathyduring this time. With few exceptions, CD4+T cell counts fall progressively during thisasymptomatic period at an average rate of approximately 50 cells / micro liter per year.When the CD4+T cell count falls below about 200/micro liter, the resulting stage ofimmunodeficiency is severe enough to place the patient at high risk for opportunisticinfections and neoplasm and hence are clinically apparent disease. Conceptual study of Bhutabhishangaja Ojokshaya 37
  47. 47. Window period Even after a person is infected with HIV, he/she will remain healthy for some periodof time. Patient will have no complaints. In this time HIV tests will become negative for 6-12weeks after infection. In this period the person is highly infectious, viral load (number of virusin the body) is extremely high.Asymptomatic period After about 6 weeks of HIV infection, the HIV test will become positive. The HIVinfected person can remain healthy without any complaints for periods of up to 3-5 years.This period when the HIV test is positive but the person remains without symptoms orcomplaints is called the HIV positive asymptomatic period.HIV positive symptomatic period The HIV continues to multiply in the body.Early symptomatic disease At some point, usually after the CD4+T cell count has fallen below 500 /micro literpatients begin to develop signs and symptoms of clinical illness. Many of these problemscan be traced to minor opportunistic infections, not sufficiently indicative of a defect in cell-mediated immunity to be considered AIDS defining illness, while some of them appear to bedirect affects of long standing HIV infection. This stage of HIV infection has been given avariety of names in the past, among them pre-AIDS and AIDS-related complex (ARC),generalized lymph-adenopathy. This condition, defined as the presence of enlarged lymph nodes (1cm) in two ormore extra inguinal sites for more than 3 months without an obvious cause, it’s often theearliest symptom of HIV infection after primary infection. It is due to marked follicularhyperplasia. The nodes are generally discrete and freely moveable. This feature of HIV Conceptual study of Bhutabhishangaja Ojokshaya 38
  48. 48. disease, which may be seen at any point of time, is not associated with an increasedlikelihood of developing AIDS. Paradoxically a loss in lymph-adenopathy or a decrease in lymph nodes size may bea prognostic maker of disease progression. In the early and intermediate stages of HIVinfection, the main differential diagnosis is an idiopathic form of Kaposi’s sarcoma. Late in the course of disease, differential diagnosis expands to include lymphoma,mycobacterium infection, toxoplasmosis, systemic fungal infection and bacillary angiomatosis. Lymph node biopsy is not indicated in patients with early stage disease unlessthere are science and symptoms of systemic illness such as fever and weight loss, or unlessthe nodes begin to enlarge, become fixed or coalesce.Oral lesions Oral lesions, including fresh, hairy leukoplakia-and aphous ulcers, are particularlycommon during this phase. Thrush due to Candida infection and oral hairy leukoplakia, areusually indicate of fairly advanced immunologic decline, generally occurring in patients withfever than 300 CD4+T cells/ micro liter.Herpes zoster (shingles) This condition is seen in 10 to 20% of patients. This reactivation syndrome ofvaricella zoster virus indicates a modest decline in immune function and is often the firstclinical indication of immunodeficiency.Thrombocytopenia Thrombocytopenia also may be an early consequence of HIV infection.Approximately 3% of patients with HIV infection and CD4+T counts above 400/ micro literhave platelet count fewer than 150,000/ micro liter. This incidence increases to 10%.Thrombocytopenia is really a serious clinical problem in these patients. Conceptual study of Bhutabhishangaja Ojokshaya 39
  49. 49. Neurologic disease Clinical disease of the nervous system accounts for a significant degree of morbidityin a high percentage of patients. The neurologic problems that occur in HIV-infectedindividuals may be either primary to the pathogenic processes of HIV infection or secondaryto opportunistic infections or neoplasm.Opportunistic infections Opportunistic infections are late complications of HIV infection, for the most partoccurring in patients with less than 200 CD4+T cells per micro liter. While the causativeagents characteristically are opportunistic organisms, such as pneumocytis carimi,mycobacterium avium complex, CMV, and other organisms that do not ordinarily causedisease in the absence of a compromised immune system, they also include commonbacterial and mycobacterium pathogens. Opportunistic infections are the leading cause ofmorbidity and mortality I patients with HIV infection. Approximately 80% of AIDS patients dieas direct result of an infection other than HIV, with bacterial infections heading the list.Protozoal infections Pneumocystis carinii infection is one of the most common causes of infectionpatients generally present with fever and cough that is usually nonproductive or productiveof only scant amounts of white sputum. They may complain of a characteristic retro-sternalchest pain, which is usually course on inspiration and described as either sharp or burning.In more severe cases, patient usually notes dyspnoea on exertion, fatigue and weight loss.One may see a chest x-ray pattern with upper lobe cavity disease, reminiscent oftuberculosis.Protozoal diarrhea: Cryptosporidium is a well-known cause of Diarrhea in animals and may cause a self-limited Diarrheal infection in the immuno competent host. It is spread through fecal-oral Conceptual study of Bhutabhishangaja Ojokshaya 40
  50. 50. contact. In HIV-infected individuals, cryptosporidial infection may present in a variety ofways, ranging from a self-limited or intermittent diarrhea illness in patients in the earlystages of HIV disease to a severe, life treating Diarrhea in severely immuno deficientindividuals. Therapy is purely symptomatic at present. Patients can minimize their risk ofdeveloping cryptosporidiosis by avoiding contact with human and animal feces and by notdrinking water from lakes or rivers.Microsporidia The main species causing disease in humans is Enterocytozoon bieneusi. In contrastto Cryptosporidia, microsporidia have been noted in a variety of extra intestinal locations,including the eye, muscle, liver and cause conjunctivitis and hepatitis. As in the cause ofcryptosporidium, no effective therapy is known and treatment is purely symptomatic.Bacterial infections Bacterial infections are the leading cause of death in HIV infected individuals.Disseminated mycobacterial infection, particularly due to Mycobacterium avium complex(MAC) is the most common opportunistic bacterial infection. Mycobacterium fartuitum, mycobacterium chelonas, mycobacterium marinum,mycobacterium scrofulceum and mycobacterium haeneophilum all causes disseminateddisease and septic arthritis. Mycobacterium gardnae, generally a nonpathogenic in humans,and mycobacterium zeropi, a colonizer of water storage tanks, may cause disseminateddisease. Therapy of the latter organisms is extremely difficult.Tuberculosis M. Tuberculosis, one thought to be on its way to extinction in United States,experienced resurgence. Tuberculosis is a particularly important problem with HIV infection.HIV disease progresses more rapidly when associated with tuberculosis, the level of plasma Conceptual study of Bhutabhishangaja Ojokshaya 41
  51. 51. viremia increase during active tuberculosis and successful treatment of tuberculosis causesplasma viremia to fall back to baseline levels. Given the fact that, in contrast of HIV infection,with M. tuberculosis can be spread via respiratory droplets and close, non-sexual contact,this epidemic of tuberculosis probably represents the greatest health risk to the generalpublic and the health care profession associated with the HIV epidemic. Tuberculosis may be the earliest clinical sign of HIV infection. Patients present withfever, cough, and dyspnoea on exertion, weight loss, night sweats and a chest x-rayrevealing cavity apical disease of the upper lobes. Disseminated disease is more common with low CD4+T cell counts.Viral infections: Herpes virus infection: Human herpes virus infections present substantial problemsthroughout the course of HIV infection. Among the members of this group that areparticularly disabling of patients with HIV infection are CMV, Herpes simplex viruses,Varicella zoster, Epstein Barr virus and HIV-8. Cytomegalo virus infections: Retinitis, esophagitis, and colitis are the mostcommon manifestations of CMV infection in-patients with AIDS. Treatment for Cytomegalo: Three drugs-ganciclovir, foscarrnet and cidofavir arecurrently licensed for systematic treatment of CMV infection. Herpes simplex virus infection: Infection with herpes simplex virus (HSV) in HIVinfected individuals is associated with recurrent labial, genital, and peri anal lesions. As HIVdisease progresses and CD4+T cell count declines, these infections become more frequentand severe. Lesions often appear beefy red, are exquisitely painful and have a tendency tooccur high in the gluteal cleft. Treatment for Herpes simplex: The treatment for severe or recurrent HSV infectionis acyclovir. For most cases, 200mg is given orally five times per day 10 to 14 days. Conceptual study of Bhutabhishangaja Ojokshaya 42
  52. 52. Varicella-zoster virus infections: Varicella-zoster virus (VZV), the etiologic agent of chickenpox, assumes a latent forma dorsal root ganglia following primary infection. Reactivation is associated with shingles theappearances of shingles in any patient fewer than 50 years of age should be an indicationfor work up of an underlying immuno deficiency, particularly HIV. Skin infections like, Warts, Dermophytes, Folliculitis, Seborrohoic dermatitis, mayoccur. Toxoplasmic encephalitis, CMV Rinitis, Cryptococcal meningioencephalitis, bizarreneurological features will occur as complications.Treatment for VZV Treatment is with acyclovir and hyper immune globulin. Most physicians choose totreat it with high-dose oral or intravenous acyclovir or oral famciclovir.Treatment of Neoplastic diseases A variety of neoplastic and pre-malignant diseases occur with increased frequently inHIV-infected individuals. They are Kaposi’s sarcoma, lymphoma and intraepithelial dysplasiaof the cervix and anus. These diseases are significant contributors to the morbidity andmortality of patients with HIV infection.Kaposi’s sarcoma Kaposi’s sarcoma is a multi centric neoplasm consisting of multiple vascular nodulesappearing in the skin, mucous membranes and viscera. Diagnosis of Kaposi’s sarcoma isbased on biopsy of a suspicious lesion.Diagnosis of HIV infection The diagnosis of HIV infection depends on the demonstration of antibodies to HIVand or the direct detection of HIV or one of its components. The standard screening test forHIV is the enzyme linked immuno sorbent assay (ELISA). This solid phase assay is anextremely good screening test; with a sensitivity of over 99.5% most diagnostic laboratories Conceptual study of Bhutabhishangaja Ojokshaya 43
  53. 53. use a commercial ELISA kit that contains antigens from both HIV-1 and HIV-2 and that willdetect either. The most commonly used confirmatory test is the Western Blot. It takes advantage ofthe fact that multiple HIV antigens, having different molecular weights elicit the production ofspecific antibodies. These antigens can be separated on the basis of molecular weight, andantibodies to each component can be detected as discrete bands on the Western Blot. Anegative western blot is one in which no bands are present at molecular weightscorresponding to HIV gene products. In a patient with positive or indeterminate ELISA and anegative western blot, one can certainly that the ELISA reactivity was a false positive.List of some laboratory tests concerned to HIV/AIDS 1) Specific tests i. Serological tests by ELISA, Western blot and immunofluorescence test. ii. Antigen detection test using envelopand core proteins of HIV by recombinant DNA techniques. (HIV P24) iii. Virus isolation and culture in neoplastic T cell line. iv. Polymerase chain reaction (PCR) 2) Indirect tests a. CD4 and CD8 cell counts, reversal of CD4 to CD8 cell ratio b. Lymphopenia c. Lymph node biopsy d. Plate let count revealing thrombocytopenia e. Increased B2 microglobulinlevels Conceptual study of Bhutabhishangaja Ojokshaya 44

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