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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 Kayachikitsa

D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE


Gadag - 582 103

Post graduate studies and research center


Department of Kayachikitsa
2004

This is to certify that the contents of this thesis entitled Evaluation of the
comparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana in
Bhutabhishangaja

Ojokshaya

(HIV

infection)

is has

been

worked out

by

C.S.HANAMANTAGOUDAR, under my supervision with close guidance.


Even though this disease, Bhutabhishangaja Ojokshaya has been mentioned in
Ayurvedic texts, the aetiology, pathogenesis etc., needs further evaluation and research. It
is as developed and explained by C.S.HANAMANTAGOUDAR is unique and scientific and
will definitely help in elucidation of this disease in Ayurvedic and Modern scientific parlance
and further planning with the management.
This work is applied, scientific and an original contribution in the field of research in
Ayurveda.
I am fully satisfied with the work and recommend the dissertation to be put before the
M.D. (Ayurveda Vachaspathi) Kayachikitsa panel of Rajiv Gandhi University of Health
Sciences, 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

J.S.V.V. SAMSTHES

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 the
topic entitled Evaluation of the comparative efficacy of Ojokalpa Rasayana and
Amruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection).

We here with forward this thesis for the evaluation and adjudication.

Dr. V.Varadacharyulu
M.D.(K.C)(Osm),

Professor & H.O.D


DEPT. KAYACHIKITSA
DGMAMC, PGS&RC, Gadag

Dr. G. B. Patil
Principal
D.G.M. Ayurvedic Medical College,
Gadag

ACKNOWLEDGEMENT
I take this glorious opportunity to acknowledge with the deep sense of gratitude
to my guide, Dr. K. Siva Rama Prasad, Reader, Department of Postgraduate Studies
and Research (Kayachikitsa), D.G.M.A.M.C., Gadag, for his valuable guidance and
close 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 during
my 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.Girish

Danappagoudar for their valuable suggestions and timely help which made me to
complete 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 and
special thanks for librarian Shri. V. M. Mundinamani and Mr. Surreban for their timely
help and co-operation during the study.

Index
Evaluation of the comparative efficacy of Ojokalpa Rasayana in
Bhutabhishangaja Ojokshaya (HIV infection)
Chapter-1

1 to 4

Introduction
Chapter-2

5 to 54

Conceptual study includes Shareera, Nidana, and Chikitsa in


detail with respect to the disease in comparison to
contemporary medicine.
Chapter-3

55 to 73

Drug review Ojokalpa Rasayana composition is discussed


with its pharmacological and pharmaco-dynamics.
Chapter-4

74 to 81

Material and methods


Chapter-5

82 to 113

Observation and results


Chapter-6

114 to 130

Discussion and conclusion


Summary

Annexes
References
Bibliography
case sheet

131 to 136

List of tables
Table explanation

Page
Number

Combination and proportions of Ojokalpa Rasayana

55

Guna Karmas of each drug of Ojo kalp rasayan

57

Age group incidences

82

Sex ratio incidences

83

Diet incidences

84

Religion incidences

85

Economic incidence

86

Occupational incidence

87

Marital status incidence

88

10

Source of infection

89

11

Chief complaints

90

12

Associated complaints

91

13

Changes Hemoglobin percentage (HB%)

93

14

Erythrocyte Sedimentation Rate (ESR)

94

15

Changes in Total Lymphocyte count

95

16

Changes in white Blood corpuscles

96

17

Changes in Weight

97

18

Changes in Platelet count

98

19

Changes in Kornefsky performance score

99

20

Changes in general health condition

100

21

Changes in CD4 count

101

22

Changes in CD8 count

102

23

Observations on Chronicity

103

24

Observations on Ojo vyapat lakshana

103

25

Observations on Ojo Vishramsha lakshana

105

26

Observations on Ojokshaya lakshana

105

27

Assessments criteria - Evaluation of the comparative efficacy


of Ojokalpa Rasayana in Bhutabhishangaja Ojokshaya

106

28

Assessment Parameter study of group 1

109

29

Assessment Parameter study Group 2

110

30

Assessment Parameter Comparative study of Group 1 and 2

111

31

Result in-group 1

113

32

Result in-group 2

114

List of graphs
Graph item

Page number

Age group incidences

82

Sex ratio incidences

83

Diet incidences

84

Religion incidences

85

Economic incidence

86

Occupational incidence

87

Marital status incidence

88

Result in-group 1

113

Result in-group 2

114

List of Figures
1

Life cycle of HIV

32

Structure of HIV

33

Ingredients of Ojokalparasayana

55

Acknowledgement
I 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 affectionate
encouragement, throughout the study.
I am grateful to Dr. V. Varadacharyulu, H.O.D., Post-Graduate studies and Research
Center in Kayachikitsa, D.G.M.A.M.C, Gadag for inspiring me to take up this
dissertation subject and supporting me with timely guidance and encouragement
Words 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.

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 and
Research 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 S
Paraddi, and all the staff of DGMAMC. I thank all my P.G. colleges for their constant
support and co-operation.
I am very much great full to my beloved father, mother, brother, sister, brother in law
Amrutagouda and Pavitra for their lots of affection and co-operation.
I sincerely thank Mr. P.M. Nandakumar, statistician, for the statistical analysis of the
results and librarian V.M. Mundinamani and assistant librarian Sureban for their
timely 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 and
my friends Dr Kallesha Moorashillin, Dr Vishwanatha Kokare for their constant help
and co-operation.
I am very thankful to Sunil. L. Mundra, M.D., Natural Capsules Pvt. Ltd., Bangalore
who supplied Natural Vegetable and Gelatin capsules for the study. I am thankful to
M/s R.Y.Shettar, Doddappa Billal and Dhanwantari Pharmacy who supplied me
components of my trail medicine. I am thankful to Hubli diagnostics, Hubli for their
constant cooperation through out the study.
With deep sense of gratitude I thank all the subjects who participated in this study.

(C.S.Hanamantagoudar)

As we walk in so many centuries away from descent of Ayurveda many infectious


diseases are emerging once again to remind us about their existence as urbanization
developed. Among them since two decades sudden emerge of new epidemics such as
SARS and AIDS/HIV, termed in Ayurveda as Bhootopaghataja Ojokshaya. This is very
volatile disease-entity. The etymology of words, Bhoota and Upaghata developed form the
word 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. All
medical knowledges of present world has authentic information about microbes and
diseases caused by them. Acharyas of Ayurveda have explained common means of getting
infections long ago, such as sexual intercourse, physical contact, droplet infection, food and
water, sharing the-bed, cloth, ornaments. Ancient history revels and refers massive
infectious conditions such as AIDS through excavations. Now a day it seems to be
reminding as a simple dream is that Health for all . If we are not accumulating all of our
human resources, energies, intelligence not to allow any further spread of these infectious
diseases such as HIV or SARS it will be havoc to the mankind. If not, according to the
estimation one should wonder if the slogan Health for all turns out as AIDS for all. The
number of people infected by HIV would have crossed 50 million and till now there were 12
million deaths due to ARC (aids related complications) in entire world. In India since the
detection of HIV infection since 1986, the epidemic has been frankly out of control. As of
now an estimated 4-6 million HIV infected cases are present in India.

Within this short

period it has emerged as one of the most serious public health problem in the country.
Introduction to Bhutabhishangaja Ojokshaya

AIDS is a multi dimensional disease syndrome, affecting physical, mental, social and
spiritual facets of the affected person. The virus HIV hampers the Immune system. Where
as in Ayurveda the immunity is termed as Ojas. So the vitiated Immune system is called as
Ojovikruti. Bhootopaghata is one of the causative factors for Ojovikruti. The unique feature
of human immune-deficiency virus is that it attacks the basic defense mechanism of human
beings and gradually destroys the system completely. Then body becomes playground for
all types of microbes like viruses, bacteria, fungi, protozoa, to inter play. In absence of any
check force the microorganisms that enter the body through various entry points. And freely
multiply to cause numerous infections, which may leads to life threatening. The Ojokshaya
is one among the Ojovikruti. Symptoms are also identical to the advanced AIDS sign and
symptoms for example Moorcha, Moha, Pralapa, Mrutyu, Mamsakshaya, etc. There for
Acquired 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, and
further duplication of HIV virus.
Recent advances in medical treatment
Recent advances in medical treatment have given scientists renewed strength in the
struggle against HIV-the virus that causes AIDS. Many of todays scientists are using AZT
and DDI as a source of treatment. AZT inhibits reverse transcription, which is vital for HIV to
infect its host. Since HIV is a retrovirus it must convert its RNA to DNA. AZT and DDI will
stop this from occurring and thus stop the HIV virus from spreading. There are also many
scientists trying to use CD4 as a potential type of vaccine. CD4 is a membrane protein that
many cells in our body use. Those cells include the immune system cells, blood cells, and
the nervous system cells. It has been found that HIV only infects cells with CD4. It is for this
that HIV infects its host in only areas whose cells contain CD4 1.
Introduction to Bhutabhishangaja Ojokshaya

Vaccine in trial
The vaccine in Evaluation of an HIV-1 DNA Vaccine Encoding a Modified Gag-Pol
in Uninfected Adult Volunteers (Contact: Grace Kelly, RN) trial, VRC 4302, is classified as a
genetic vaccine. Genetic vaccines contain the genes (hereditary material) which direct the
production of the proteins of the HIV virus. VRC 4302 contains the gene for the Gag and Pol
proteins 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 of
3 doses, 0.5mg, 1.5mg or 4.0 mg) or vehicle ("control") alone. Participants will receive VRC
4302 by intra-muscular injection once a month for 3 months. The injection is given using a
needle-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 of
immune builders, Immuno-modulators and acts on Ojovikruti by preventing ARC. Food
supplements of immune modulation through well-known herbo-mineral origin, Amruta
KayaKalpa Rasayan of Amruta pharmaceuticals Hyderabad, is compared with the trail drug
combination of Bilvadi Vati and Agnikumar Vati (Sahasrayoga) as Ojokalpa Rasayana. In
Sahasrayoga Bilvadi vati and Agnikumar vati are indicated for Chira Atisara and AmaAtisara, 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 of
therapy on HIV virus. The total work dwells on inferences based on both subjective and
objective parameters such as KPS score and CD4 count. With this duration, sample size and
design, it is not possible to conclude the exact role of Ayurvedic treatment but this is a good

Introduction to Bhutabhishangaja Ojokshaya

beginning for further study. Serological test for HIV is not a criterion for assessment rather it
is a diagnostic tool for inclusion of subjects.
Viral load test (PCR) is not employed because of financial constrains, instead CD4
enumeration, which is an internationally accepted surrogate marker of HIV status was under
taken.
Study design
So a rational combination was made to tackle cause of disease and management of
resultant condition under the shelter of Sahasra yoga. The Ojokalpa Rasayana, which has
Ojovardhaka, Ama pachaka, jwarahara, and krimighna drugs in it. Recent researchers have
proved all the properties of individual drugs also. An attempt has been made to develop
non-pharmacopeal methods of management of this condition by adopting Sadvritta
(disciplines), do and donts prescribed by Charaka and other Acharyas 2.
This dissertation begins with literary review of Ojokshaya and HIV infection and a
comparative study of both. The basic physiology concerned with this disease, pathophysiology, causative factors, signs and symptoms, diagnostic tests involved are discussed.
A detailed drug review has been done which speaks about the rationale behind the
combination. There is a chapter continued on materials and methods, which was adopted
for this research work and in observation and results detail description of findings of
research are given. In discussion and conclusion, the possible mechanisms involved in the
pharmacological 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 of
this traditional knowledge and this is a humble effort to bring this much-cherished hope into
a reality.

Introduction to Bhutabhishangaja Ojokshaya

The normal healthy state of such a body requires normalcy of several factors. They
are Dosha, Agni, Dhatu, and Mala along with peaceful disposition of Atma, Indriya and
Mana 3. For this normal functioning body requires strength, which is called as Bala.
Ayurveda describes human body as seat of Chetana (consciousness) and a product
of panchabhoutic vikara, existing in equilibrium. When this equilibrium gets disturbed, that
results 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, which
forms the zygote and from that moment development of foetus continues.
The strength of any living is disturbed either by internal humors viz. Vata, Pitta and
Kapha or exogenous factors such as bacteria and virus. The virology and bacteriology is not
much discussed from the ancient literature but the existence was not denied. Thus the
present study which is based on the existence of the Bhuta described from the Vedic
literature.
The principle of the disease development commences either from the endogenous or
exogenous factors. The endogenous factors are grouped as physical and psychological.
The physicals are of three humors and the psychological are rajas and tamas. The
exogenous factors which gives rise the disease because of Achayapurvaka prakopa
ultimately has to land for the vitiation of Dosha. Thus the terminus of the disease is under
the influence of the Dosha triode.

Conceptual study of Bhutabhishangaja Ojokshaya

Here in this concern discussed about the Ojas, Dosha and immunity as the virus
makes 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 conflict
with man. The above sentence is narrated from Atharvaveda, which dates backs to 5000
years.
Ayurveda describes human body is seat of Chetana (consciousness) and a product
of Panchabhoutika vikara, existing in equilibrium gets disturbed. That results in defective
bodily tissues. This is the beginning of any disease 7.
The normal healthy state of a body requires normalcy of several factors they are
Dosha, Agni, and Dhatu, and Mala, Peaceful deposition of Atma, Indriya and Manas.8 for
their normal functioning, body requires strength, which is called as Bala. The same normal
strength had synonym as Shlesma

9.

That is also known as Ojas. Ojokshaya is a broad

understanding of immuno deficiency, depilated vigor and vitality. This Ojas is transformed
from the parents to the pregnancy through Sukra and Shonita

10

(Beeja of Purusha and Stri)

at the time of zygote formation. Ojas is the essence of all the Dhatus. The Beeja is
responsible for the formation of particular organ or tissue, if it is vitiated, that results in
deformity of the respective organ. If it develops undisturbed there will not be any deformity
of the respective organ.
There for it is clearly understood that every part of the healthy human body (Dhatu
and Mala) develops according to the healthy state of the Beeja and Beejabhaga. There for
the essence of Dhatus as represented by Ojas of Pumbeeja and Stribeeja plays the major
role in this mechanism.

Conceptual study of Bhutabhishangaja Ojokshaya

Ojas depends upon healthy state of Kapha. Physiologically Kapha represents a


potential 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 decay
and 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
antagonistic to virulence of diseases causative factors
Balam is Ojas

12

. Susruta clarified further stating

13

. As long as Dhatus are strong and healthy and are conducting their normal

functions 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 by
either the natural processes or disease. So in this contest this is very essential that, to know
about etymology and normal physiology of Ojas.
Nirukti (Etymology) of Ojas
Ojas the word has its root in ujor vaj dhatu. That means confer or strong (Ugra)
Ojas is the subanta pratyaya of word Ojas, which means Deepti, Prakasha and Balam

14.

Kalidas in Raghu vamsha kavya writes Rudraoujasa with reference to the potency of Shiva
15

Paribhasha (Definition) of Ojas


Ojas is the essence of all Dhatus. Ojas is nothing but the Bala or Strength of the
body, which is the ultimate end product of the seven Dhatus starting from Rasa and ending
at Shukra

16

. Chakrapani contradicts this opinion and says Ojas sustains the body but does

not nourish it.


The normal healthy state of a body requires normalcy of several facts. They are
Dosha, 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 normal
strength is called as Shlesma, which has synonym of Ojas, This Ojas is transformed from
Conceptual study of Bhutabhishangaja Ojokshaya

the parents to the pregnancy through Shukra and Shonita. Which is the essence of the
Dhatus. 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 there
will not be any deformity of the respective organ. There for it is clearly understood that every
part of the healthy human body (Dhatu and Mala) develop according to the healthy state of
the Beeja and Beejabhaga, there for the essence of Dhatus as represented by Ojas of
Pumbeeja and Steebeeja plays the major role in this mechanism.
Ojas depends upon healthy state of Kapha. Kapha in physiologically represents
potential sours of strength and resistance to disease and decay of Bala and Ojas. These
terms reflect to the force and power which resists the factors responsible for decay and
disease. Bala may be sahaj (inherited) kalaj (seasonal) and yuktikrita (acquired). But these
all are equally capable of resisting the diseases. As long as Dhatus are strong and healthy
and conducting their normal functions with the 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 by either the natural processes or disease. So in this contest this is
very essential that, to know about etymology and normal physiology of Ojas.
Formation of Ojas in the body
Ojas is the Sara i.e. essence of all Dhatus

17

. It is produced In the body as honey,

Which is collected by bees from various flowers and fruits. Ojas is derived from all the
Sapta Dhatus in other words all the Dhatus contributes to its making. Ojas is the product of
the 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 denoting
the predominance of Aap and prithvi mahabhootas 19.
Conceptual study of Bhutabhishangaja Ojokshaya

Physical properties of Ojas

20

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
Snigda(unctuous),
(smooth),

26,

Sheeta,

27,

23

Guru (heavy),24, Pichchila (gelatinous)

or somatmaka (mild to touch),

varnam, 30 Saram 31, Viviktam,32 Guru 33 Bahalam

28

25

, Stira (stable),

, Mridu
29

Shukla

34

, Madhu rasam,35.Lajagandhi.

36,

Lohita peetakam, 37
Ojas Poshana 38
Ojas is nurrished mainly by Ahara, from the AharaAhara rasa- Rasa dhatu- RaktaMamsa-Medha-Asthi- Majjaa-Shukra dhatus
Classification of Ojas 39
There are two classifications of Ojas, made by Charaka, Susruta, Chakrapani, and
by all other acharyas. Those are
1)

Para Ojas and


Conceptual study of Bhutabhishangaja Ojokshaya

2)

Apara Ojas 40

These two types of Ojas have a direct bearing on bodys defense against
degeneration and infection.

Para Ojas
Ojas marks the beginning of the formation of embryo. It is the essential nourishing
fluid developed from the Rasa of the embryo.

It enters the heart right at the stage of the

letters initial formation and is permanently locates there, sustaining the life of fetus. Loss of
Ojas amounts to the loss of life itself. Chakrapani comments that the above function pertains
to both the Ojas and further explains that Ojas plays a role in three different stages of the life
of the fetus. It permeates to through Rasa in entire body and nourishes entire body

41

and

Ojas 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 the

Dhatus. Any loss in the quantity would cause sudden death. Commenting on function of
Ojas Susruta has made a significant observation. Ojas permits entire body nourishes limbs
and 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 of
the Apara Ojas in preventing the decay of the body. It is one of the ten seats of life. It gives
firmness to physical structures and gives strength to motor activity. Ojas spreads all over the
Conceptual study of Bhutabhishangaja Ojokshaya 10

body. In the absence of it life does not exist. The seat of Apara Ojas is the ten dhamanies
connected with Hrudaya 43.
According to Vagbhata, the function of Apara Ojas is Dehastitanibhandana. Which
means it keeps the physical fitness of the body. Chandranandana

44

clarifies that it is the

protection of the body in all the states. Hemadri also states that the changes in the Ojas are
the root cause for all the changes in the body. Ojas is Bala, which is a potential source of
resistance to disease and decay. Bala controls the Doshas that cause disease. This is
called Vyadhi kshamatva.45.
Synonyms of Ojas
The term Ojas has been stated in Ayurvedic classics represents Kapha, Bala,
Shleshma, Rasa and Rakta.46
Sleshma 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. 48
Nidana of Ojokshaya
The pathological state of Oja is called as Ojokshaya .49. Charaka and all other
classics have described this Oja vikriti as Ojokshaya. Susruta has classified this condition in
to three different stages

50

as 1) Ojo Vishrams, 2) Ojo Vyapat, 3) Ojokshaya, The Nidana


Conceptual study of Bhutabhishangaja Ojokshaya 11

which causes depletion of any Dhatu, can also causes depletion in the Ojas qualitatively and
quantitatively. The factors influencing the Ojokshaya are as follows.
1) Ahar karana.
2) Vihar karana.
3) Manashika karana,
4) Aagantu karana.51
Ahar 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

Many diseases like Rajayakshma, Abhishyanda, Kushta, jwara, Upadamsha,


Pooyameha, Apatantraka,Visarpa, Masoorika, Rohini, are some examples of infectious
diseases 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 the
Ojas, which leads to depletion of Ojas. Here Rakshasa i.e. Rajanichara 53 can be correlated
to infectious organism which spreads through Prasanga (sexual contact), Gatra samsparsha
(physical touch), Nishwas (droplet infection), Saha bhojana (eating together) and Saha
shayyasana, (sharing bed).
Nidanartkara Vyadhi for the Oja vikriti
Rajayakshma

54

, Prameha

Kshataja kasa, Sannipata jwara


stage.

58

55

Pandu

56,

Raktarsha, Raktatisara, Kshayaja kasa,

57

, are the diseases which causes Ojakshaya in there later

Susruta pointed such possibility while dealing Abhinyasa jwara where in he used

the 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, and
delirium. Susruta observed that disturbance of Ojas to the various parts of the body is
affected either due to leakage or loss or obstruction to the Ojas carrying tiny shrotases in
Sannipataja jwara, such condition is called as Oja Nirodhaja sannipata. Inertness of the
limbs, chills, fits, loss of consciousness, delirium, etc.
The acute condition referred above illustrates how the pronounced loss of Ojas
contributes to an extra ordinary state of susceptibility to increased microbial / viral activity
and to toxins produced by these agents. Other clinical conditions which are slow in
progression, 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

happen due to loss of structural integrity of Dhatu vaha srotas and obstruction in the supply
system. Such other disease syndromes are Rajayaksma, Madhumeha, Ojomeha

60

, Pandu,

Sannipata jwara, and etc.


Charaka has enumerated the pathological sequences very clearly while explaining
the Samprapti of Rajayaksma (both Anuloma and Pratiloma) in Charaka Chikitsa. After
explaining the manner in which nutrient materials are normally metabolized and assimilated
by the Dhatus he elaborates it further, due to the obstruction of srotas. As a result of a
deficiency of nutrients Raktadi Dhatus, lowered functioning of dhatwagni and catabolic
events, 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 guna
transforms the Ojas, sweet in taste to astringent and transports it to the mutrashaya leading
to the causation of the condition known as Madhumeha. It is another disease where
Ojokshaya is evident. Several other conditions creep in long with the main disease. Here
the Ojas produced in this person it self is vitiated 61.
In case of Pandu roga the Samprapti is dominated by Pitta. The aggravated Dosha
vitiates 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-dhatu
sammurchana resulting the clinical features; impoverished Rakta, and medha dhatus
leading shitilendriyata and vaivarnyata.
Prameha, the urinary disorder is of two types. One caused due to endogenous
factors like Vatadi doshas, another one caused by exogenous or Agantuj factors like
indulgence in sex with the unfit and diseased partners. Agantuja prameha is infectious and
communicable disease, transmitted through agamya, and dushita yoni samsarga (sexually

Conceptual study of Bhutabhishangaja Ojokshaya 14

transmitted). In these pramehas Ojokshaya occurs as a consequence of the passage of


Ojas 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 the
endogenous factors such as dosh, dhatu.etc.) Aupasargika / agantuja meha janya
Ojokshaya (depletion due to exogenous factors like infections etc). But there is lot of
difference in treatment between above said two entities.
In case of Madatyaya, that severely affects Ojas, Bala and Prana. Madya is having
qualities exactly opposite to that of Ojas. Hence the Vyadhikshamatva is affected in its
totally. 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 via
various srotases. In this condition, the circulating Ojas leads leaks out or oozes out from the
tiny 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, the
Ojas looses its physiological or normal qualities and properties as described to it, this vikruta
Ojas prod uses the following laxanas.
Ojokshaya
This is the final stage of Ojo-vikriti represents the loss and wasting of Ojas.
According to Susruta 63
Ojo-visramsa
i. Sandi visleshana (loss of firmness of the joints)
ii. Gatrosada (inertness of the extremities)

Conceptual study of Bhutabhishangaja Ojokshaya 15

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.

Nidra

Ojokshaya
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 has
explained the same in the words Baladisthanam Arogyam. Bala denotes two vital aspects
of life process namely Vyayama Shakti. Vyadhikshamatva is further classified into three
types Sahaja, Kalaja and Yuktikrita.
Sahaja Bala 64
The Sahaja Bala or resistance to the disease is stated to be prakriti. I.e. Inherent
genetic from of resistance existing in the individual body since birth and this also increases
Conceptual study of Bhutabhishangaja Ojokshaya 16

along with the growth of the body elements i.e. Sapta dhatus .It comprehends both sharira
and satwa i.e. body and mind.
Kalaja Bala 65
Kalaja Bala is influenced by the factors like seasonal variations and age of the
individuals. Thus kalaja Bala is supposed to be dissipated at its lowest leveling the Adana
kala comprising of Sishira.Vasanta and Greeshma ritus. On other hand Bala is stated to be
conserved and at its high peek level in the visarga kala, inceasing over Varsha, Sharat and
Hemanta ritus. Those are known as Sheeta kala or cooler period.
Yuktikrita Bala 66.
Yuktikrita Bala refers to the bodys resistance against disease, which can be
enhanced by appropriate nutrition such as meat, Ghee, etc. Restorative and Rasayana
therapy in keeping with the seasonal requirements, adaptation of swastha vritta principles of
Ayurveda along with Achara Rasayana also contributes the growth of Yuktikrita Bala.
Dalhana in his commentary on Bala lakshanas as explained by Susruta observes
Ojas and Bala as synonyms, especially with Chikitsa point of view. However they are distinct
in the sense the former is the essence of all the dhatus and it has physical properties like
Roopa, Rasa, Veerya etc., the later has to be determined from the power to lift heavy weight
and 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 wordsThis Shakti varies from individual. The same is explained in the Charaka Samhita Na cha
sarva shareerani vyadhikshamatva samarthani bhavantani. In the discussion on factors that
influence Bala, held between Punarvasu Atreya and Agnivesha is recorded in the chapter
Vividaashitiyapeeya in the Charaka sutra sthana. This discussion throws considerable
amount of light on the views held on resistance to disease.

Conceptual study of Bhutabhishangaja Ojokshaya 17

Kapha is five types

68.

Those are Kledakakapha, Bodhakakapha, Tarpakakapha,

Avalambakakapha and Shlesmakakapha. Each one is limited to some part or parts of body
by their functions. They look after the functions of the Kapha locally and project the body
collectively.
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

Immunity gives the specific response to a foreign antigen or pathogen. And


generally takes longer time to materialize. Memory is the key feature of the immunity
towards the antigen. Non immune host defense is not antigen specific, without memory it
responses immediately and is call inflammation also.
There are cellular immunity and humoral immunity in the immune system and for
each the active principles are Thymus-derived (T) lymphocytes, and Bone marrow derived
(B) lymphocytes respectively. Although both B and T lymphocytes are derived from
common stem called Bone marrow. Neutrophills, Esinophills, Basophiles, Natural killer cells,
monocytes, and macrophages, are the mediators for this immediate response as non
immune substances. Non specific resistance represents a wide variety of body reactions
against a wide range of pathogens, specific resistance or immunity involves the production
of specific anti body against specific pathogen or its toxins. Non specific resistance to
disease 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

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 act
include pollen, egg white, incompatible blood cells, and transplanted tissues and organs.
The myriad of antigens in the environment provides many opportunities for the production of
antibodies by the body. Antibodies not form against with the whole antigen, at specific
regions on the surface of the antigen, called antigenic determinant sites. Specific chemical
groups of the antigen combine with the antibody.
This combination depends up on the size and shape of the determinant. Site and the
manner in that, it corresponds to the chemical structure of the antibody.
Lymphocytes are key constituents of the immune system. In mammals, this system
has the remarkable ability to produce antibodies against many millions of different foreign
agents that invade the body. In addition, the immune system remembers, and a second
Conceptual study of Bhutabhishangaja Ojokshaya 20

exposure to a foreign substance produces a more rapid and greater Hum oral immunity is
immunity due to circulating antibodies in the globulin fraction of the plasma proteins. It is a
major defense against bacterial infections.
Cellular immunity is responsible for delayed allergic reactions and rejection of
transplants 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 against
tumors.
There have been spectacular advances in immunology in recent years, and the field
is 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 organ
into the lymphocytes responsible for cellular immunity i.e.-Imphocytes. Lymphocytes
responsible for humeral immunity are B-lymphocytes. Four different varieties of T cells have
been identified: helper / inducer T cells suppressor T cells, cytotoxic T cells (which are also
known as effectors T cells or killer cells), and memory T cells. The first 2 types are involved
in the regulation of antibody production by B cells derivatives, whereas the cytotoxic T cells
destroy transplanted and other foreign cells. Cytotoxic and suppressor T cells have on their
surface the glycoprotein CD8, which can be detected by monoclonal antibodies, so they are
frequently called T, cells. Helper / inducer T cells have on their surface the glycoprotein CD4
and are therefore called T cells. CD8 is a co receptor for MHC class I molecules and CD4 is
a co receptor for MHC class II molecules.
Memory B and T cells are cells those have been exposed to an antigen and are
readily converted to effectors cells by a later encounter with the same antigen. Unlike other
lymphocytes, they persist in the body for months or even years.
Conceptual study of Bhutabhishangaja Ojokshaya 21

Lymphocytes, macrophages, and other cells involved in immune responses


communicate in part by hormone like chemical messengers called interleukins and
cytokines.
Major Histo compatibility complex
The genes of the major histo compatibility complex (MHC), which are located on the
short arm of human chromosome 6, encode glycoprotein that are located on the surface of
all cells and function in antibody processing and distinguishing self from non-self. They are
divided into 2 classes on the basis of tissue distribution and function. Class I antigens are
composed of a 45-kilodalton heavy chain associated non-covalently with P, micro globulin
encoded by a gene out side the MHC.
Antigens can also be processed and presented to T4 cells by various types of cells in
the body in addition to macrophages. The other types of antigen presenting cells include the
B cells themselves, the Langerahans cells of the skin, and specialized cells called dendritic
cells in the lymph nods and spleen.
Cellular Immunity
T8 cells mediate cellular immunity. These cells are activated when they are
presented 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. They
kill by inserting pore-forming molecules (perforins) in the membranes of their target cells in
the same fashion as the complement system does. They may also act by including within
the cells an as at undefined change that leads to death. Suppressor T cells, which develop
more slowly then cytotoxic T cells, help terminate the immune response by dampening the
immune responses of T and B cells. This includes turning of the helper / inducer cells.

Conceptual study of Bhutabhishangaja Ojokshaya 22

To ensure maximal specific T cells response the antigen is linked to molecular


components of the HLA system (by B cells, dendritic cells and macrophages) and presented
to T cell.
The transformed blast cell undergoes progressive mitotic division and each cell of
the resulting clone has the same specific immune potential. The subsequent T cell activities
tend 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 of
sensitized T cells.
T cell functions and mechanism
Overall regulation of the immune response and reactions- this is effected by helper T
cells which promote, and suppressor T cells which inhibit immune reactions. In the
peripheral blood, 2/3 of the T lymphocytes are helper and 1/3 suppressor. Using monoclonal
antibodies, 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 killing
action is non specific.
c). Delayed hypersensitivity reactions are mediated by the release of lymphokines from the
specifically activated T cells. They promote a wide range of cellular activity associated with
the promotion and control of the immune response and the inflammatory reaction.
Lymphokines and cytokines
Lymphocytes, macrophages, and in some instances endothelial cells, neurons, glial
cells, and other types of cells secrete many hormone like chemical messengers that effect
the immune response. The messengers secreted by lymphocytes and often called
lymphokines. However, since other cells produce them as well, it seems more appropriate to
Conceptual study of Bhutabhishangaja Ojokshaya 23

call them cytokines. This field is growing very rapidly, and most of the cytokines are initially
named for other actions, e.g. B cell differentiating factor, B cell stimulating factor 2. There is
a convention that once the amino acid sequence of a factor in humans is known its name is
changed 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 is
Hemoglobin, Hemoglobin is a globular molecule made up of 4 sub units. Each sub unit
contains a hem moiety conjugated to a polypeptide. The average normal Hemoglobin
content of blood is 16g/dl in men and 14g/dl in women, all of it in red cells. In the body of a
70- kg man, there is about 900gms of Hemoglobin, and 0.3gm of hemoglobin is destroyed
and 0.3gm synthesized every hour.
Platelets
The platelets are small, granulated bodies 2-4 micrometers in diameter. There are
about 3 lakhs / liter platelets in circulating blood, and they normally have a half-life of about
4 days. The megakaryocytes giant cells in the bone marrow, from platelets the pinching of
bits of cytoplasm and extruding them into the circulation. Platelet production is regulated by
the colony stimulating factors that cintroll the production of megakaryocytes. Between 60
and 75% of the platelets that have been extruded from the bone marrow are in the
circulating blood, but the reminder are mostly in the spleen. Splenectomy causes an
increase in the platelet count (thrombocytosis).
Non specific resistance represents a wide variety of body reactions against a wide of
pathogens. Specific resistance or immunity involves the production of specific antibody
against specific pathogen or its toxin.
Conceptual study of Bhutabhishangaja Ojokshaya 24

Pathology in Bhutabhishanga Ojokshaya (HIV infection)


The acquired immune deficiency syndrome (AIDS) was first recognized in the United
States 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 pneumonia
in five previously healthy homosexual men in Los Angeles was reported. Soon after
Kaposis sarcoma in 26 previously healthy homosexual men in New York, and Los Angeles
were reported. Within months, the disease became recognized in male and female Injection
Drug 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 microbe
transmissible by sexual contact or blood and blood products was the most likely etiologic
agent for the epidemic. In 1983, Human Immuno Deficiency Virus (HIV) was isolated from a
patient with lymph-adenopathy. In 1984 it was demonstrated clearly that this virus is the
causative agent of AIDS.
During the early years of 1980s the care of HIV-infected individuals in the United
States was confined to restricted groups of physicians and hospitals, in urban areas, of
north eastern and western seaboards. But today, every practicing physician in this country
and 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 presenting
in increasing numbers to family physicians, obstetricians, gynecologists, pediatricians and
surgeons with clinical problems that may be directly or indirectly related to their HIVinfection.
HIV infection in India
The first case of HIV infection was identified in India in 1986 at Chennai. During
these days it was limited to female sex workers. Focus was shifted from Chennai to Mumbai
as hundreds of female sex workers were found to have HIV infection. It is with truck drivers,
Conceptual study of Bhutabhishangaja Ojokshaya 25

it started spreading from big cities to smaller ones. People, who travel from cities to city and
those who travel from villages to cities, were found to be more susceptible because of
unprotected, non-martial sexual contact. Even though thousands of people got infected
through blood transfusion during the first decade of epidemic, the heterosexual contact is
the 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 figure
communicable diseases, which cause death.
Definition of AIDS
Any HIV-infected individual with CD4+T cell count of<200/microliter had AIDS by
definition, regardless of the presence of symptoms or opportunistic diseases. The clinical
conditions like pulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer.
While the definition of AIDS is complex and comprehensive, the clinician should not focus
on presence of AIDS but should view HIV disease as a spectrum ranging from primary
infection, with or without the acute syndrome, to the asymptomatic stage, and to advanced
disease.
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 may
be sooner because of malnutrition and poor state of health, toxins and malnutrition out plaid
factors that stress the immune system probably cause AIDS. During this interval HIV
infected individuals may suffer from a variety of disorders and develop signs which are
suggestive of being infected with HIV. Mainly those symptoms are pain less swelling of
Lymph nodes in the neck, Armpits and Groin, Fever, Night Sweats, Diarrhea, Loss of weight
and infections such as Herpes, Pneumonia, etc.

Conceptual study of Bhutabhishangaja Ojokshaya 26

Etiologic agent
The etiologic agent of AIDS is HIV (the Human Immuno deficiency Virus), which
belongs 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-1
comprises several subtypes with different geographic distribution. HIV-2 was first identified
in 1986 in West African patients and was originally confined to this region.
Electron microscopy shows that the HIV virus is an icosahedra structure containing
numerous external spikes formed by the two major envelope proteins, the external Gp120
and the transmembrane Gp41.The virion buds from the surface of the infected cell
incorporates 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), slow
in nature, having reverse transcriptase enzyme. Having size about 90-120 mm. this virus is
a tiny, a thousand times smaller than the thickness of a hair. Looks like a roller up
porcupine. This lies firmly wrapped up in a care which resembles a cone with a dimple at its
base. This cone is protected by an envelop that has a knob like protein sticking out its
surface. 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 from
a progressive quantitative and qualitative deficiency of the subset of T lymphocytes referred
to as helper or inducer T cells. This subset of T cells is defined phenotypicaly by the
presence on its surface of the CD4 molecule. This serve as the primary cellular receptor of
Conceptual study of Bhutabhishangaja Ojokshaya 27

HIV it has recently been demonstrated that a co-receptor must be present together with CD4
for effective fusion and entry of HIV-1 into its target cells. It is important appreciate that the
pathogenic mechanisms of HIV disease are multi factorial and multi-phased and are
different at different stages of the disease.
HIV has a number of mechanisms to evade elimination by the immune system. HIV
has as extraordinary ability to mutate, but this mechanism probably acts mainly after the
establishment of chronic infection and contributes to the maintenance of chronic. Since the
transmitted virus and the virus that initially becomes established as a chronic infection are
relatively homogeneous, the initial escape from immune system control likely involves other
mechanisms. Molecular analysis of clono types has demonstrated that clones of
CD8+Cytolytic T Lymphocytes (CTLs) that expand greatly during primary HIV infection and
likely represent the high-affinity clones that would be expected to be more efficient in
eliminating 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 genetic
make up. HIV-1 was first discovered in 1983 in France and appears to be more prevention
Europe 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 clinical
latency. However studies of lymphoid tissue using PCR analysis for HIV RNA and in site
hybridization for individual virus expressing cells clearly demonstrated that HIV replication
occurs throughout the course of HIV infection, even during clinical latency. The availability of
sensitive PCR techniques leads to the demonstration that viremia present at all stages of
HIV disease.

Conceptual study of Bhutabhishangaja Ojokshaya 28

The behavior of the HIV is very much similar to poison. The HIV is fragile, once the
virus is out side the body in a dry form, it dies immediately. When stored in blood banks at
4oc, 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 by
homosexual and heterosexual contact. Blood, Blood products are the important routes of
infection. Infection spreads from mothers to infants either intrapartum, perinatally, or via
breast milk. After more than 15 years of scrutiny, there is no evidence that HIV is transmitted
by 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

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 cells
and in the cell free state. The virus appears to concentrate in the seminal fluid, particularly in
situations where increased numbers of lymphocytes and monocytes are. The virus has also
been demonstrated in cervical smears and vaginal fluids. There is a strong association of
transmission of HIV with receptive intercourse. Owing to the fact that only a thin and fragile
rectal mucosal membrane separates the deposited semen from potentially susceptible cells
in and beneath the mucosa this transmission takes place. Trauma associated with anal
intercourse provides at least two modalities of infection; direct inoculation into blood in cases
of tears in the mucosa, and infection of susceptible target cells, such as langerhans cell, in
the mucosal layer in the absence of trauma. There is approximately a 20 fold greater chance
of transmission of HIV from a man to a woman than from a woman to a man through vaginal
intercourse. This difference may be due to the prolonged exposure of the vaginal and
cervical 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 share
contaminated paraphemalia (needles and syringes) for injection drug use and in those who
receive transfusions of blood and blood products. It is estimated that 90 to 100% individuals
who 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 HIV
infection. The precautionary measures taken to check this: (1) the screening of all blood for
p24 antigen and for HIV antibody body enzyme linked immuno-absorbent assay (ELISA),
Conceptual study of Bhutabhishangaja Ojokshaya 30

with a confirmatory western blot where applicable; (2) the self-deferral of donors on the
basis of risk behavior.
3) Occupational transmission of HIV:
There is a small but definite occupational risk of HIV transmission among health care
workers, 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 care
workers 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 during
pregnancy or during delivery. This is an extremely important form of transmission of HIV
infection in developing countries, where the proportion of infected women to infected men is
approximately 1:1
5) Transmission by other body fluids:
There is no convincing evidence that saliva can transmit HIV infection, either through
kissing or through other exposures, such as occupationally to health care workers. But blood
contaminated saliva and wet kissing will leads to HIV infection
Epidemiology of HIV infection
HIV infection and AIDS is a global pandemic, with cases reported virtually from every
country. The current estimate of the number of cases of HIV infection among adults
worldwide is approximately 22 million, and approximately 2.6 Million HIV-infected children
have been born since the start of the HIV pandemic, and approximately one half of these
have developed AIDS and have died. The global projections for the number of HIV-infected
individuals by the year 2000 range from 40 to 100 million.

Conceptual study of Bhutabhishangaja Ojokshaya 31

Life cycle of HIV infection


HIV is an RNA virus whose hallmark is the reverse transcription of its genomic RNA
to DNA by the enzyme reverse transcriptase. The life cycle begins with the high affinity
binding of the Gp 120 protein via a portion of its VI region near N terminus to its receptor on
the host cell surface, the CD4 molecule. It has recently been demonstrated that the coreceptor that must be present together with the CD4 molecule for fusion and entry of T-cell
tropic 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, then
catalyzes the reverse transcription of the genomic RNA into double-stranded DNA. The DNA

Conceptual study of Bhutabhishangaja Ojokshaya 32

trans-located to the nucleus, where it is integrated randomly into the host cell chromosomes
through the action of another virally encoded enzyme Integrate.
Morphology of HIV
Electron microscopy shows that the HIV virus is an icosahedral structure containing
numerous external spikes formed by the two major envelope proteins, the external gp 120
and the transmembrane gp41. The Virion buds from the surface of the infected cell
incorporates 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
GP120

Glycoprotein
GP41
Fatty (Lipid
Bilayer
membrane

Protein
P18
Protein
P24

Reverse transcriptase
enzyme

HIV genetics
HIV-1 has genes that encode the structural proteins of the virus gag encodes the
proteins that from the core of the Virion (including p24 antigen) I Pol encodes the enzymes
Conceptual study of Bhutabhishangaja Ojokshaya 33

responsible for reverse transcription and integration and env encodes the envelope
glycoprotein.
Molecular heterogeneity of HIV-1: Molecular analysis of various HIV isolates reveals
sequence 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 the
infections in the world, and group O (outlier) a relatively rare viral form found at this time in
Cameroon, Gabon and France. The M group comprises at least light sequence subtypes, or
clad, 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 type
of white blood cell called T lymphocytes. The RNA genetic material of the virus then gets
converted to DNA genetic material by an enzyme that the virus produces. This virus DNA
then gets incorporated in to the DNA of the T lymphocyte, and remains there for the lifetime
of individual. This infected cell knows becomes a virus factory producing more viruses which
bud out the cell, attack new T lymphocytes, and destroy them. Over a period of years, the T
cell 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 positive
person. Persons those are infected through blood transfusion develop symptoms of an
average from 3-5 years. With the other modes of transmission, when the dose of the virus is
less, the person can remain healthy for 8-12 years or longer, if an HIV positive person
improves his or her quality of life by adopting safer sex, has a good nutrition, regular
exercise, seeks immediate medical attention for any ill health. Avoids stress, continues to be
active he or she is likely to live longer.
Conceptual study of Bhutabhishangaja Ojokshaya 34

The cytokine network in the HIV pathogenesis


On perturbation of the immune system by antigenic challenge, the expressions of
cytokines increase to varying degrees. Cytokines that are important components of this
immune regulatory network have been demonstrated to play a major role in the regulation of
HIV expression in vitro. A number of in vitro model systems of chronically infected monocyte
or T cell lines, primary cultures of peripheral blood or lymph node mononuclear cells from
HIV-infected individuals, and acutely infected primary cell cultures have been used to
demonstrate the role of cytokines in the regulation of HIV expression. Potent modulation of
HIV expression has been demonstrated either by manipulating endogenous cytokines or by
adding exogenous cytokines to culture. Cytokines that induce HIV expression in one or
more of these systems include IL-1, IL-2, IL-3, IL-6, IL-12, TNF

and TNF. Macrophage

colony stimulating factor (M-CSF) and granulocyte-macrophage colony stimulating factor


(GM-CSF). Among these cytokines the most consistent and potent inducer of HIV
expression 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 on
the system involved.
Clinical manifestation of HIV infection
HIV disease can be divided empirically on the basis of the degree of
immunodeficiency into an early stage (CD4+T cell count 200 to 500/ micro liter), an
intermediate 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 true
malignancies occur in the advanced stage of disease, while neurological disease and
Kaposis sarcoma are not as strictly related to the degree of immunodeficiency. The two
major classification systems for staging HIV disease are the CDC system and the Walter

Conceptual study of Bhutabhishangaja Ojokshaya 35

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 conditions

The acute HIV syndrome (acute Retro viral syndrome)


About 50-70% of people infected with HIV usually develop acute viral fever flu like
syndrome 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 acute
clinical syndrome approximately 2 to 4 weeks after primary infection. Varying degrees of
clinical severity have been reported, and it has been suggested that symptomatic seroconversion leading to the seeking of medical attention indicates an increased risk for an
accelerated course of disease. Clinical findings occur along with a burst of plasma viremia
and p24 antigenemia.
The syndrome is typical of an acute viral syndrome and has been linked to acute
infections mononucleosis symptoms usually persist for 1 to several weeks and gradually
Conceptual study of Bhutabhishangaja Ojokshaya 36

subside as an immune response to HIV develops and the levels of plasma viremia
decrease. Opportunistic infections have been reported during this stage of infection,
reflecting the immunodeficiency that results from reduced numbers of CD4+T cells. Total
lymphocyte and T cell subsets (CD4+ and CD8+) are initially reduced. An inversion of the
CD4+/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 usually
remain 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 depressed
CD4+T cell count that remains stable for a variable period before beginning its progressive
decline. In most patients, primary infection with or without the acute syndrome is followed by
a prolonged period of clinical latency.
The asymptomatic stage
Clinical latency although the length of time from initial infection to the development of
clinical disease varies greatly the median time is approximately 10 years. HIV disease with
active virus replication usually progresses during this asymptomatic period. Some patients
called long term non-progressors, show little decline in CD4+T cells counts over an extended
period. 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-adenopathy
during this time. With few exceptions, CD4+T cell counts fall progressively during this
asymptomatic 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 of
immunodeficiency is severe enough to place the patient at high risk for opportunistic
infections and neoplasm and hence are clinically apparent disease.
Conceptual study of Bhutabhishangaja Ojokshaya 37

Window period
Even after a person is infected with HIV, he/she will remain healthy for some period
of time. Patient will have no complaints. In this time HIV tests will become negative for 6-12
weeks after infection. In this period the person is highly infectious, viral load (number of virus
in the body) is extremely high.
Asymptomatic period
After about 6 weeks of HIV infection, the HIV test will become positive. The HIV
infected 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 or
complaints 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 liter
patients begin to develop signs and symptoms of clinical illness. Many of these problems
can be traced to minor opportunistic infections, not sufficiently indicative of a defect in cellmediated immunity to be considered AIDS defining illness, while some of them appear to be
direct affects of long standing HIV infection. This stage of HIV infection has been given a
variety 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 or
more extra inguinal sites for more than 3 months without an obvious cause, its often the
earliest symptom of HIV infection after primary infection. It is due to marked follicular
hyperplasia. The nodes are generally discrete and freely moveable. This feature of HIV

Conceptual study of Bhutabhishangaja Ojokshaya 38

disease, which may be seen at any point of time, is not associated with an increased
likelihood of developing AIDS.
Paradoxically a loss in lymph-adenopathy or a decrease in lymph nodes size may be
a prognostic maker of disease progression. In the early and intermediate stages of HIV
infection, the main differential diagnosis is an idiopathic form of Kaposis sarcoma.
Late in the course of disease, differential diagnosis expands to include lymphoma,
mycobacterium infection, toxoplasmosis, systemic fungal infection and bacillary angio
matosis. Lymph node biopsy is not indicated in patients with early stage disease unless
there are science and symptoms of systemic illness such as fever and weight loss, or unless
the nodes begin to enlarge, become fixed or coalesce.
Oral lesions
Oral lesions, including fresh, hairy leukoplakia-and aphous ulcers, are particularly
common during this phase. Thrush due to Candida infection and oral hairy leukoplakia, are
usually indicate of fairly advanced immunologic decline, generally occurring in patients with
fever than 300 CD4+T cells/ micro liter.
Herpes zoster (shingles)
This condition is seen in 10 to 20% of patients. This reactivation syndrome of
varicella zoster virus indicates a modest decline in immune function and is often the first
clinical 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 liter
have 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

Neurologic disease
Clinical disease of the nervous system accounts for a significant degree of morbidity
in a high percentage of patients. The neurologic problems that occur in HIV-infected
individuals may be either primary to the pathogenic processes of HIV infection or secondary
to opportunistic infections or neoplasm.
Opportunistic infections
Opportunistic infections are late complications of HIV infection, for the most part
occurring in patients with less than 200 CD4+T cells per micro liter. While the causative
agents characteristically are opportunistic organisms, such as pneumocytis carimi,
mycobacterium avium complex, CMV, and other organisms that do not ordinarily cause
disease in the absence of a compromised immune system, they also include common
bacterial and mycobacterium pathogens. Opportunistic infections are the leading cause of
morbidity and mortality I patients with HIV infection. Approximately 80% of AIDS patients die
as 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 infection
patients generally present with fever and cough that is usually nonproductive or productive
of only scant amounts of white sputum. They may complain of a characteristic retro-sternal
chest 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 of
tuberculosis.
Protozoal diarrhea:
Cryptosporidium is a well-known cause of Diarrhea in animals and may cause a selflimited Diarrheal infection in the immuno competent host. It is spread through fecal-oral
Conceptual study of Bhutabhishangaja Ojokshaya 40

contact. In HIV-infected individuals, cryptosporidial infection may present in a variety of


ways, ranging from a self-limited or intermittent diarrhea illness in patients in the early
stages of HIV disease to a severe, life treating Diarrhea in severely immuno deficient
individuals.
Therapy is purely symptomatic at present. Patients can minimize their risk of
developing cryptosporidiosis by avoiding contact with human and animal feces and by not
drinking water from lakes or rivers.
Microsporidia
The main species causing disease in humans is Enterocytozoon bieneusi. In contrast
to 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 of
cryptosporidium, 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 disseminated
disease and septic arthritis. Mycobacterium gardnae, generally a nonpathogenic in humans,
and mycobacterium zeropi, a colonizer of water storage tanks, may cause disseminated
disease. 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

viremia increase during active tuberculosis and successful treatment of tuberculosis causes
plasma 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 general
public and the health care profession associated with the HIV epidemic.
Tuberculosis may be the earliest clinical sign of HIV infection. Patients present with
fever, cough, and dyspnoea on exertion, weight loss, night sweats and a chest x-ray
revealing 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 problems
throughout the course of HIV infection. Among the members of this group that are
particularly 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 most
common manifestations of CMV infection in-patients with AIDS.
Treatment for Cytomegalo: Three drugs-ganciclovir, foscarrnet and cidofavir are
currently licensed for systematic treatment of CMV infection.
Herpes simplex virus infection: Infection with herpes simplex virus (HSV) in HIV
infected individuals is associated with recurrent labial, genital, and peri anal lesions. As HIV
disease progresses and CD4+T cell count declines, these infections become more frequent
and severe. Lesions often appear beefy red, are exquisitely painful and have a tendency to
occur high in the gluteal cleft.
Treatment for Herpes simplex: The treatment for severe or recurrent HSV infection
is acyclovir. For most cases, 200mg is given orally five times per day 10 to 14 days.
Conceptual study of Bhutabhishangaja Ojokshaya 42

Varicella-zoster virus infections:


Varicella-zoster virus (VZV), the etiologic agent of chickenpox, assumes a latent form
a dorsal root ganglia following primary infection. Reactivation is associated with shingles the
appearances of shingles in any patient fewer than 50 years of age should be an indication
for work up of an underlying immuno deficiency, particularly HIV.
Skin infections like, Warts, Dermophytes, Folliculitis, Seborrohoic dermatitis, may
occur. Toxoplasmic encephalitis, CMV Rinitis, Cryptococcal meningioencephalitis, bizarre
neurological features will occur as complications.
Treatment for VZV
Treatment is with acyclovir and hyper immune globulin. Most physicians choose to
treat 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 in
HIV-infected individuals. They are Kaposis sarcoma, lymphoma and intraepithelial dysplasia
of the cervix and anus. These diseases are significant contributors to the morbidity and
mortality of patients with HIV infection.
Kaposis sarcoma
Kaposis sarcoma is a multi centric neoplasm consisting of multiple vascular nodules
appearing in the skin, mucous membranes and viscera. Diagnosis of Kaposis sarcoma is
based on biopsy of a suspicious lesion.
Diagnosis of HIV infection
The diagnosis of HIV infection depends on the demonstration of antibodies to HIV
and or the direct detection of HIV or one of its components. The standard screening test for
HIV is the enzyme linked immuno sorbent assay (ELISA). This solid phase assay is an
extremely good screening test; with a sensitivity of over 99.5% most diagnostic laboratories
Conceptual study of Bhutabhishangaja Ojokshaya 43

use a commercial ELISA kit that contains antigens from both HIV-1 and HIV-2 and that will
detect either.
The most commonly used confirmatory test is the Western Blot. It takes advantage of
the fact that multiple HIV antigens, having different molecular weights elicit the production of
specific antibodies. These antigens can be separated on the basis of molecular weight, and
antibodies to each component can be detected as discrete bands on the Western Blot. A
negative western blot is one in which no bands are present at molecular weights
corresponding to HIV gene products. In a patient with positive or indeterminate ELISA and a
negative 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

Evaluation of CD4 Count:


The relationship between clinical manifestations of HIV infection and CD4+T cell
count has made measurement of the latter quantity a routine part of the evaluation of HIV
infected individuals. CD4+T cells counts make a powerful set of tools for determining
prognosis and monitoring response to therapy while the CD4+T cell count provides
information on the current immunologic status of the patient. This measurement is done by
Flow Cytometry method.
Patients with CD4+T cell counts below 200/ul are at high risk of infection with
preumocytis carini, while patients with CD4+T cell counts below 100/microliter are at high
risk of infection with cytomegalovirus and mycobacterium avium-intracellular complex.
Patients with an initial diagnosis of HIV infection should have CD4+T cell measurements
performed approximately every 6 months and more frequently if a declining trend is noted.
At a minimum antiretroviral therapy is generally indicated when the CD4+T cell count falls
below 500/ul, and a declining CD4+T cell count may provide an indication for changing
therapy. Once the CD4+T cell count is 200/microliter these patients should be place on a
regimen for carini pneumonia (PCP) prophylaxis. All effective forms of antiretroviral therapy
to date have been associated with at least a transient increase in either CD4+T cell count.
Direct measurements of HIV RNA
Facilitated by techniques for the precise quantitation of small amounts of nucleic
acids, the measurement of serum or plasma levels of HIV RNA has become the most
commonly used approach for the direct detection of HIV. Two basic techniques are used the
reverse transcriptase PCR (RT-PCR) assay and the branched DNA (b DNA) assay. The RTPCR assay involves the PCR amplification of c DNA generated from viral RNA. The b DNA
assay involves the use of solid-phase nucleic acid capture system and signal amplification
through successive nucleic acid hybridization to detect small quantities of HIV RNA. Both
Conceptual study of Bhutabhishangaja Ojokshaya 45

assays generate date in the form of number of copies HIV RNA per milliliter and is positive
in >90% of patients. ALL effective forms of anti retroviral therapy to date have been
associated with a drop in levels of HIV RNA.
B2 Microglobulin levels
B2 microglobulin is an 11 Kda protein that is expressed on the surface of most
nucleated cells. Free B2 microglobulin can be measured in the serum and urine. Levels of
B2 microglobulin are elevated in a variety of conditions characterized by lymphocyte
activation and / or lymphocyte destruction among these or lympho-proliferative syndromes,
auto-immune diseases, and viral infections, including HIV infection.
MANAGEMENT OF HIV INFECTION IN PARLANCE
Prevention and controlling measures of HIV infection/AIDS
At present due to absence of preventive vaccine and curative drud, prevention and
control is the only cure for AIDS.
Counseling and Education
These are of paramount importance in providing patients with optimal overall care.
Patients must be educated about the potential transmission of their infection, including frank
discussions concerning sexual practices and sharing of intravenous needles.
The treating physician must not only be aware of the latest medications available for
HIV infection and its complications but most also educate patients concerning the history of
their illness and listen to their fears and concerns.
Education, counseling and behavior modification are the corner stones of an HIV
prevention strategy. Wide spread voluntary testing of individuals who practiced or are
practicing high-risk behavior, together with counseling of infected individuals, is
recommended. Information gathered from such an approach should serve as the basis for
behavior-modification programs, both for infected individuals who may be unaware of their
Conceptual study of Bhutabhishangaja Ojokshaya 46

HIV status and who could infect others for uninfected individuals practicing high-risk
behavior.

Promotion of voluntary blood donation and universal


testing of blood units for HIV

Condom promotion and its accessibility

Education to mother to prevent infant transmission

Avoiding transmission through infected syringes and


needles

Early detection and prompt treatment of sexually


transmitted diseases

Antiretroviral Therapy
The cornerstone of medical management of HIV infection is antiretroviral therapy.
Suppression of HIV replication is an important component in prolonging life. Nucleoside
analogues (reverse transcriptase inhibitors) are the ante retroviral agents. Ex, Zidovudine,
Didanosine, Zalcitabine, Lamivudine, stavudine.
Among them Zidovudine was the first drug approved for the treatment of HIV
infection. Patients treated with Zidovudine had increase in lymphocyte counts, including
CD4+T cell counts, declines in circulating levels of p24 antigen and weight gain. Initial
studies indicated that elevations of CD4+T cell counts from this approach.
Non-nucleus reverse transcriptase inhibitors
The non nucleoside reverse transcriptase inhibitors interfere with the function of the
viral enzyme reverse transriptase by binding to regions outside the active site and causing
conformational charges in the enzyme that render it inactive.
Two members of this class, Nevirapine and Delavirdine are currently available for
use.
Conceptual study of Bhutabhishangaja Ojokshaya 47

Protease inhibitors
The licensure of four separate HIV-1 inhibitors (Saquinavir, Ritonavir, Indinavir and
Nelfinavir) heralded a major change in the options available for antiretroviral therapy of HIV
infection. Unlike reverse transcriptase inhibitors, which interface with cellular DNA
polymerases as well as inhibiting the transcriptase of HIV-1; the HIV protease inhibitors are
exquisitely selective for the protease enzyme of HIV-1.
Vaccines
Given the fact that human sexual behavior is extremely difficult to change, the best
hope for preventing the spread of HIV infection rests with the development of a safe and
effective vaccine. This task is extremely problematic for number of reasons including the
high mutability of virus.
AYURVEDIC PERSPECTIVE OF HIV INFECTION AS BHUTABHISHANGA OJOKSHAYA
Samannya Samprapti 71
Indulgence in above said Nidana leads to aggravation of Vata, Pitta and Kapha,
ultimately it leads to Kapha kshaya. The aggravated doshas causes damage to
Ojovahasrotamsi leading to ojo visramsa (loss of Ojaswhen), when the further advancement
of the disease process continues the Doshas vitiate Ojas, causing qualitative change in
Ojas. The further advancement of the disease leads to depletion of Ojas both quantitatively
and qualitatively.
Vishesha Samprapti
Bhootopaghata janya Ojakshaya manifests in a different manner. The infectious
organisums (Bhoota) cause cell damage and entry of pathogen to the cell (Bootopaghata) is
the hallmark of this process. These pathogen causes srotorodha, which leads to Vata
vriddhi and vitiation of other doshas. From this stage onwards the pathological processes
continue like samanya Samprapti.
Conceptual study of Bhutabhishangaja Ojokshaya 48

Bhoota + Upaghata

Roga utpadaka jeevanu/vishanu, + Utpeedana

Pathogenic agent +destruction

HIV (in AIDS) +destruction

HIV-destruction (first stage) = Ojovisramsa,


(derangement with ordinary deficiency of Ojas or immunity)

HIV destruction (second) stage =Ojovyapat


(Diffusive Ojas or immunity disorders),

HIV- destruction (third stage) =Ojokshaya (complete loss of Ojas or immunity as found in
AIDS)

Results into death


Sankhya Samprapti
There are three types of Ojas vitiation mentioned as Ojovishramsh, Ojovyapat and
Ojokshaya. Even though there are explained as the types of Ojo vikriti. Practically they look
like the stage of Ojokshaya.
Kriyakala in Bhutabhishanga Ojokshaya (HIV infection)
Sanchaya
This period starts from the point of exposure to acute condition phase which take
minimum 10 days. In this phase virus grow silently in the lympha and lympha glands. In the
Conceptual study of Bhutabhishangaja Ojokshaya 49

Rasavaha srotas and in the Rasavaha srotomoola the virus aggravate doshas to creat some
symptom which is called prakopam.
Prakopam
This condition generally occurs within 10 -30 days after exposure and resolves in 321 days. The person develops an acute flu like ill ness with a verity of symptoms and signs
including lethargy. Malaise fever sore throat myalgio anorexia sweating orthalgia headache
diarrhea nausea generalized lymph-adenopathy. This phase is called acute condition phase
because prakupita doshas come out from their place and create abnormalities.
Pasaram and stanasamsraya
After prakopa doshas migrate in others path way. Then these dosha occupy places
other than their own place and circulate in channels other than their own. This stage of
dosha is called as stanasamsrayam.
These two stages of doshas can consider as a symptomatic perio phase. The acute
condition phase followed by asymptomatic period, which may last up to 10 year after the
acquisition of infection. During this phase patient is infective and the virus can be isolated for
peripheral blood lymphocytes. The number of functions of lymphocytes sub population is
however normal. Latest period a-symptomatic phase show some so0me signs of
opportunistic infections delayed healing of minor illness.
Of course this can be considered as Purvaroopa of AIDS. During this period
progressive weight loss, mild weakness, anorexia, generalized lymph-adenopathy, and
occasionally low-grade form etc. sign and symptoms observed.
Vyakti and Bheda
Presence of signs and symptoms is called Vyakti and difference from prakriti / nature
is called Bhedam. These two parts of stages of Samprapti can be included in the

Conceptual study of Bhutabhishangaja Ojokshaya 50

symptomatic infection phase. After the perio latency commonly manifests with weight loss
and weakness.
Accelerated weight loss in an HIV infected patient is sign of disease progression. No
specific cause of weight loss can be identified in most of the cases. Weakness and loss of
appetite are very frequently present. Fever is generally low grade may be accompanied by
night sweats and chills. AIDS patients have persistence diarrhea lasting more than one
month as one of the major complaints.
Among respiratory manifestations persistent cough of more than one months
duration is found in majority of patients. It may be due to pulmonary tuberculosis.
Pnemocytis cornii is common in western countries.
In addition to these symptoms the patient with AIDS may suffer from various
cutaneous, neurological, oral manifestations as well as tumors and lymph-adenopathy.
Upashayanupashaya 72
Depletion in Doshas and Dhatus as well as Ojas will make the person desire for such
foods and drinks, which will increases the depleted one. The foodstuffs so desired are called
Upashaya. E.g. Sneha, Sheeta and Madhura Rasa yukta dravyas like milk, sugar, ghee etc.
the Dravyas having opposite qualities like ruksha, Ushna, Katu and Kashaya Rasa Dravyas
are Anupashaya.
Vyavachedaka Nidana
It is also possible that Lakshanas of Visramsa /Vyapat/Kshaya may be felt in various
other clinical conditions apart from Ojokshaya. Sannipataja Jwara, Vishama jwara.
Rajayakshma and Kshata ksheena are the differential diagnosis of Ojokshaya.

Conceptual study of Bhutabhishangaja Ojokshaya 51

Samprapti ghataka
Nidana-

Mitya vihara, Pragnaparadha,

Dosha-

Three Dosha (specially Vata and Kapha)

Dushya-

Sapta dhatus, (Especially the Rasa, Rakta, Mamsa,


and Ojas)

Srotus-

All srotus

Srotodusti prakara-

Sangha, Atipravritti, Vimargagamana

Adhistana-

Sarva shareera

Agni-

Kyaya (Jataragni, Dhatvagni)

Rogamarga-

Madyama rogamarga

Satwa-

Heena

Bheda-

Raktaja vyadi

Vyadhiswaroopa-

Chirakari

Swabhava-

Dharuna

Sadhya-sadhyata-

Anupakram

Udbhava sthana-

Rakta vaha samsthana

Manas dosha -

Raja and Tama

In Prameha Nidana Charaka has explained the reasons for absence of disease and
causation of disease.
According to particular features of Aetiology, Doshas (innate pathogenic factors),
Dushyas (substratum of pathos) response occurs in the form of non-manifestation or other
wise of disorders.
That When these three factors do not combine together, or if combined together after
a long time, or informed or with out all the said symptoms. On the contrary the result will be
contrary. 73 Here the Vighata bhava as said by Charaka is innate immunity.
Conceptual study of Bhutabhishangaja Ojokshaya 52

Roopa (symptomatogy)
Charaka has described the Ojokshaya lakshanas as follows 74
Bhaya beeta (frightened)
Dowrbalya (severe fatigue)
Abheekshna (stress full)
Duschaaya (lost of luster)
Ruksha (ematiated and dry)
Vyatitendreeya (loss of sensory and motor functions)
Durmana (sorrowful)
Kshama (inability to talk)
Ojovardhaka Chikitsa
For the treatment of patients with HIV infection the physician requires not only a
comprehensive knowledge of the disease processes, but also the ability to deal with the
problems of a chronic, life-threatening illness. Specific antiretroviral therapy and
antimicrobial treatment and prophylaxis are critical measures in prolonging an acceptable
quality of life.
Since the disease is aggravated with the loss of immunity, the main theme of is to
increase Ojas in the body. The therapies used in Ayurveda for the same are 1) Rasayana (Rejuvenation therapy), which restores and prevents, the loss of
mental power, the loss of efficiency of functioning of sense organs, dimension of mental
vigor, and restoring of normal balancing of three Doshas establishing the most effective
interaction between the seven body constituents recovering the vitality.
2) Vajikarana (Aprodiasic therapy) helps to increase the physical potency and Oja,
vitality through increasing the quantity of Shukra dhatu, the last vital product of the seven
body constituents.
Conceptual study of Bhutabhishangaja Ojokshaya 53

Modern system of medicines like Lavimisole, Interferon, Cytokines, Interleukin,


Methotrexate, Cyclosorin, Gold salts.
3) Achara Rasayana and swasthavritta palana
Choice one sexual partner
Use of condoms during sexual penetration (vaginal, anal, or oral)
Avoid sex partners who have rashes redness, sores and
discharges.
Stay away from casual relation ships
Prevention of STDs would also reduce the risk of HIV
transmission.
Avoid blood transfusion as for as possible.
Do not share razors, syringes, needles, and blades.
Affected woman should avoid sex relation and next pregnancy.
Brahmacharya palana, like avoiding sexual stimulating thicking,
food, and circumstances, spiritual thinking
Public awareness campaigns for HIV
Anti retro viral therapy during pregnancy, delivery and postnatal
4) Bhootaghna therapy
Due to decrease of immunity, different pathogens grow over the body more easily
creates different signs and symptoms in the body. Through Bhootaghna therapy, the actual
causative organism and the other organism which are helping to improve the disease
process and producing different symptoms are ineffective.
5) Lakshanika Chikitsa
Anti-tussive, anti diarrhea, antipyretic, digestive, etc treatment has to follow
according to clinical features.
Conceptual study of Bhutabhishangaja Ojokshaya 54

Drug Review
The combinations for the evaluation in Bhutobhishanga Ojokshaya considered
are as follows in two groups. The first group patients receive Bilvadi vati fortified with
Agnikumar vati called as in the trial as Ojokalpa Rasayana, collected from the
Sahasrayoga. The second group receives Amrita kayakalpa Rasayana a patient
medicine available from market prepared from Amrut pharmaceuticals, Hyderabad.
Drug review of Bhutabhishangaja Ojokshaya 55

Ojokalpa Rasayana
The combination and proportions of Ojokalpa Rasayana is as follows:
Table -1
Sanskrit name

Latin name

Proportion

Bilva

Aegle marmelos

Three parts

Tulasi

Ocimum santum

Three parts

Haridra

Curcuma longa

Three parts

Daru Haridra

Berberis aristata

Three parts

Devadaru

Cedrus deodaru

Three parts

Shunti

Zingiber oficinalis

One part

Maricha

Pipper nigram

One part

Pippali

Pipper longum

One part

Amalaki

Phyluntus emblica

One part

Haritaki

Terminalia chebula

One part

Vibitaki

Terminalia bilirica

One part

Karanja

Pongomia glabra

Three parts

Tagara

Valerana wullichi

Three parts

Vidanga

Embelia ribes

Three parts

Agni kumar vati


Kusta

Saussurea lappa

Vacha

Acorus calamus

Musta

Cyperus rotundus

Vatsanabha

Aconitum ferox

Maricha

Pipper nigram

Ajamutra (Bhavana dravya)

Goat Urine

Three parts

Q.S.

Drug review of Bhutabhishangaja Ojokshaya 56

Contents of Amrit kaya kalp rasayan


1. .Suvarn bhasm

5mg

2. Mandurabhasm

5mg

3. Purnachandrodaya makardwaj

5mg

4. Abhraka bhasm (100 puti)

5mg

5. Lauve bhasma

5mg

6. Vangabhasma

5mg

7. Yashadabhasma

5mg

8. Jayapala

10mg

9. Jatiphala

2mg

10. Vidarikanda

50mg

11. Ashvaganda

25mg

12. Katukia

15mg

13. Punarnava

15mg

14. Gokshura

15mg

15. Shankpuspi

20mg

16. Yasti madu

20mg

17. Pippali

40mg

18. Shatavari

Q.S

19. Milk

Q.S

Function of the Amrita Kaya Kalpa rasayana compound.


Immuno modulation
Restorative tonic
Aphrodisiac
Nervin tonic and
Haematinic.

Drug review of Bhutabhishangaja Ojokshaya 57

Table-2
Guna Karmas of each drug of Ojo kalp Rasayana
Sanskrit name

Botanical
Name

Guna

Rasa

Veerya

Vipaka

Bilva

Aegle marmelos

Ruksha Laghu

Kashaya, Tikta

Ushna.

Katu.

Tulasi

Ocimum

Laghu, Ruksha.

Katu, Tikta.

Ushna,

Katu,

Rooksha,

Tikta, katu,

Ushna.

Katu.

santum
3

Haridra

Curcuma Longa

Laghu.
4

Daru Haridra

Berberis

Ruksha, Laghu,

Tikta, Kashaya,

Ushna,

Katu

Devadaru

Cedrusdeodaru

Laghu, Snigda.

Tikt katu.

Ushna.

Katu.

Shunti

Zingiber

Guru,

Katu,

Ushna,

Madhura

Oficinalis

Teekshna

Pipper Nigram

Laghu,

Katu.

Ushna.

Madhura.

Katu.

Anushna-

Madhura.

Mareecha

Ruksha

Teekshna.
8

Pippali

Pipper Longum

Laghu snigdha
Teekshna.

9
10

Amalaki
Haritaki

sheeta.

Phyluntus

Laghu, Ruksha,

Lavana

varjit

Sheeta.

Madhura.

Emblica

Sheeta

Pancha rasa

Terminalia

Laghu, Pramati

Lavana

Ushna,

Madhura.

Chebula

Ruksha,

Pancha rasa,
Ushna

Madhura,

Katu,

Ushna

Katu

Katu,

Ushna,

Katu,

Ushna,

Katu.

Ushna,

Katu,

varjita

lekhani,
11

Bibitaki

Terminalia

Ruksha, Laghu

Kashaya,

Pongomia

Laghu,

Tikt,

Glabra

Teekshna

Kashay

Valerana

Laghu, Snighda

Tikta,

Bilirica
12
13

Karanja
Tagara

wullichi
14

Vidanga

Embelia Ribes

Kashaya
Ruksha, Laghu,

Katu

Teekshna
15
16
17

Kusta
Vacha
Vatsanabha

Saussurea

Laghu, Ruksha,

Tikta,

Katu,

luppa

Teekshna,

Madhura

Acorus

Laghu, Teeksn,

Tikt, Katu

Ushna,

Katu

Calamus

Sara,

Aconitum ferox

Ruksha, Laghu

Madhura.

Ushna,

Madhura,

Sheeta,

Katu,

Ushna

Madhura,

Teekshna,
Vyavai, Vikashi
Yogavahi,
18
19

Musta
Ajamootra

Cyperus

Laghu, Ruksha,

Katu,

Tikta,

Rotundus

Grahi,

Kashaya,

Goat urine

Ruksha, Laghu,

Katu, Madhura,

Teekshna,

Tikta

Drug review of Bhutabhishangaja Ojokshaya 58

Method of medicine preparation


15 drugs are there in the Ojokalparasayana, among them Bilva, Tulasi,
Kharanja, are collected direct from the particular trees. Kusta, Triphala, Trikatu, Haridra,
Daruharidra, Devadaru, Tagara, Vidanga, Musta, Vatsanabha, Vacha, are taken from the
market. All drugs are taken in equal quantity and cleaned properly then made in to fine
powder separately. These fine powders are mixed together. This mixer soaked in to
Ajamootra and dried, this process has done for seven times. After drying the total drug
mixer sieved by cloth by that drug made in to fine powder. That powder filled in to Gelatin
capsules with quantity of 500mg. The Amruta Kayakalpa Rasayana is directly taken from
the company.
Laboratory test of Ojokalparasayana
1.

Loss on drying at 110oC.

2.395% w/w

2.

Ash value

7.68% w/w

3.

Acid insoluble ash

0.338% w/w

4.

PH of 10% (w/w) aqueous solution

5.

Solubility

Highly soluble in water and Alcohol.

6.

Tests for Alkaloids

7.

8.

a.

Mayers test

Positive

b.

Hagers test

Positive

Test of CArbohydrates
a.

Molish test

Positive (Carbohydrate present)

b.

Benedicts test

Positive (Reducing sugar present)

c.

Barfoedits test

Positive (Monosaccherides present)

0.4828 grams.

Average weight of Capsule

: 2 capsuls tid/day, after meals,

Dose
Anupana : Jala

Drug review of Bhutabhishangaja Ojokshaya 59

1) Bilva (Aegle marmelos)


Synonyms:- Shandily (peedahar), Malura

(increases the glamour), Sailusha,

Sriphala, Gandhgarbha, Sadaphala. Granthila, Kantaki


Chemical composition: -

Musilase, Pectin, Glucose (4.6%), Tinin (9%), Mermelosin,

Xanthotoxin, Umbelliferone, mermin, skimming, etc.


Karma: - Kapha Vata shamaka, Pittakara, Balavardhaka, Jwaraghna, Deepana,
Pachana, Grahi, Krimighna, Ruksh,Pittatisara

75,

mucuss membren Cronic dycentry and dyspepsia

Grahani

76

Kamala,77, use in debility of

78.

Research works Anthelmintic activity- 79

Antidiarrahoeal activity 80

Bilva powder in Atisara 81

Bilva powder in pravathika 82.

Bilva is also been used for treating giaradiasis 83

2) Tulasi (Ocimum santum)


Synonyms: - 1. Bhootaghni,
2. Apetha raakshsi
3. Devadundubi
Chemical compositions: - Pale yellow green essential oil, which becomes crystalline
over a period. It is called as Basil Camphor, Fenol (45.76%)
Karma: - Kapha vata shamaka, Pittavarda hara, Jantughna. Demulcent Expectorent
(Kasaghna)

Anti periodic Anti` catarrhal Fragrant and Aromatic used in Skin disease

Itches Ring worms, Leprocy, Broncitis (Swasaghna) and Diarrhea, Swedajanana,


Durgandha Nashaka. Acts on Heart and respiratory system, 84
3) Haridra (Curcuma Longa)
Synonyms:-Krumighna, Yostipreeya, Nisa, Yositpriya, Hattavilasini, Krmighni, Pita,
Kancani, Varavarnini, Gouri.
Drug review of Bhutabhishangaja Ojokshaya 60

Chemical compositions: -1% of volatile oil, Resin, Cur cumin is responsible for its
colour; Turmeric oil has a peculiar odour and taste. Curcumene, Curcumenone, curcone,
curdione, cineole, cineole, curzerenone, epiprocurcumenol, eugenol, camphene,
camphor, borneol, procurcumadiol, procurcumenol, curumins, ukonan A,B andD, sitosterol etc.
Karma:- Raktashodhaka, Twagdoshahara, Shothahara, Deepana, Grahi, Kaphagna,
Vatahara,

Pratishyaya,

Netrabhishanda,

Prameha,

Kaphaghna,

Kamala,

Yakritvikara,

Paryayika

jwara,

Krimi, Peenasa, Pandu, Vrinaropaka, Varnya,

Carminative and acts as vermicidal. 85


Vyanga 86 Slipada and Dadru kustha 87Pistameha 88
Research works
Antiseptic an ideal therapeutic agent in conditions of the biliary systems and
gallbladder due to suppressed staphylococcal infection. 89,
Curcuma powder has been found to increase appreciably the mucin content of
gastric juice in rabbits and thus may be useful in gastric disorder 90.

It was found that the antibacterial activity of C. longa against gram positive and gramnegative organism was less in degree as compared to penicillin and streptomycin 91

Anti-histamine or blockers, on isolated heart of guineapig, curcumin revealed a


depressant effect 92.

Its anti-inflammatory activity is investigated with reference to the inhibition of


activated proteases responsible for acute inflammatory process. The volatile oil of the
plant was found to inhibit tryspin as well as hyaluroniadase enzymes 93.

1.A clinical trial with C. longa was conduced in 114 patients of respiratory disease 94
The anti-inflammatory effect of volatile oil has been found to be greater than that of
hydrocortisone 95.
Three curcuminoids (curcumin I,II, III) were compared for their cytotoxic, tumor
reducing and anti-oxidant activities. Curcumin III was found to be more active than
Drug review of Bhutabhishangaja Ojokshaya 61

the other two in short term cytotoxic activity but inhibited the growth of tumor cells
(L929) in culture at similar concentration (IC 50-1 g. /ml). The curcuminooids also
inhibited lipid peroxidation. The amount needed for 50% inhibition was 20,14,11
micro/ml for curcumin I, II and III respectively 96.
4) Daru Haridra (Berberis)
Synonyms: - Daru nisa, Pita daru, Pacampaca, Katankateri, Parjani, Darvi
Chemical compositions: - B. Aristata Karachine (a protoberberine alkaloid),
taxilamine, berberine, palmatine, jatrorrhizine, and oxycanthine.
C. Fenestratum Berberine, berberrubine, jatrorrhizine. Palmattine, berlambine,
oxypalmatine etc,
Karma: - Balya, Poushtika, Deepana, Pachana, Grahi, Pittavirechaka, Jwarahara,
Swedala, Shleshmaghna, Phiranga, Apachi, Rasayana, Twagdoshahara, Vishamajwara,
Kupachana, Gandamala, Bhagandar, Pradar, Prameha, Pandu, Krimi, Peenasa, Meda
Rasayana Raktagami Used in Eyes liver Spleen and skin

97

Sveta pradara, Pistameha,

Vrddhi (kaphaja), Mutrakrcchra.


5) Devadaru (Cedrus deodaru)
Synonyms: -Bhoota hari, Indra daru, Drukilinam, Bhadradaru, Surabhuruha, Amaradaru,
Surahva, Bhadradri, Sura Kastha, Kilimam.
Chemical compositions:-It contains dark colored oil and Resin Essential oil from wood;
p-methylacetophenone, atlantone, sesquiterpenses ( and himochalene, himachalol
etc); stem bark; deodarin, toxifolin.
Karma: - Jwara, Jeerna, Amavata, Slipada, Jalodara, Kasa, Swasa, Atisara, Shotha,
Asmari, Kushtha Hara, Kandu, Amahara, Tandrahara, Vibanda, Adman, Peenasa, Hikka,
Prameha, Shleshma, Dustha vrina shodhana, Krimi, Anilahara, 98 Kasa 99 Sopha 100.
Research works

The alcoholic extract of the stem was found to have anticancer activity against
human epidermal carcinoma of the nasopharynx in tissue culture 101
Drug review of Bhutabhishangaja Ojokshaya 62

6) Shunti (Zingiber Oficinalis)


Synonyms:- Nagara, Srngavera, Visva, Visva bhesaja, Katubhadra, Mahousadha.
Chemical compositions:-1/5%Yellow volatile oil, ginjerol, gingerin, (pungent resin)
Carbohydretes, oil, and resin, is found just under the skin. Gingerol does not evoperates
with oil. -aurcumene, -D-curcumene, -bourbornene, d-borneal, citral, d-caphene
citronellol, geraniol, gingerol, and -Zingiberences, zingiberol, zingerone, gingerols,
paradol, gingerenone A, ginge glycolipis A,B, and C; (6) gingerdiol; gingerone B and C
etc
Karma:-Truptighna. Rochaka, Deepana, Pachana, Vatanulomana, Shopha, Arshoghna,
Raktarsha, Chardhi, Agnimandya, Ajeerna, Kostavata, Udarashoola,

Sandhivata,

Swasa, Kasa, Hikka. Pratishyaya, Samanyanda Sannipata Jwara, Jeerna Jwara, Kushta,
Pandu, Amavata, Vata Kapha hara, use in Vibhanda, Vrishya, Varnya,

Vamana,

Hridhya, Shoola, Slipada, Anaha,Udara, Seeta pitta, Grahani vikara, Guda keela hara,
Atisaara, 102 Jaladosa 103 Pratisyaya 104, Kaphaja Arasa 105, Murcha 106
Research works It has shown marked anti-inflammatory activity in rats, which is comparable to
prednisolone 107

Stem bark extract showed significant anti-inflammatory activity in rat 108,

The alcoholic extract showed some significant activity against E. coli, Proteus
vulgaris, S. typhimurium, Stap. Aurens and strep, Viridans 109

The aceton-extracts of Z. officinale, which contain essential oil and pungent


principles, caused an increase in the bile secretion. It is also reported that 6 gingerol
and 10 gingerol are mainly responsible for the chologosic effect of binger 110.

In a clinical study on Grahani roga, the effect of Z. officinale has been found
significant in term of control of number of motions, improvement of body weight,
appetite, Hb% etc 111.

Drug review of Bhutabhishangaja Ojokshaya 63

Acetone extract of ginger (100 mg/kg) significantly reduced serotonin (5-HT)- induced
hypothermia. At 750 mg/kg it significantly inhibited 5-HT-induced diarrhea 112.
A single case report (42F) on migraine headache reveals the efficacy of Z. officinale
in this condition 113.

Ginger juice produces anti-motion sickness action possibly by central and peripheral
anticholinergic and antihistaminic effect 114.

Shunthi was put to trial on 111 patients with Ghrahani roga. The effect of the
treatment was observed with in a short period. The regulation of bowel habits,
improvement in general health including anemia and body weight and improvement
in GL function was noted 115.

The antimicrobial activity of Z. officinale is reported 116.

The aqueous extract of ginger arrested with growth of M. tuberculosis in vivo 117.

Acetone extract of rhizomes of Z. officinale is attributed with the antioxidant property


118.

7) Mareecha (Pipper Nigram)


Synonyms:-krimihar Usana, Krsna, Dhanvantari, Dharmapattana, Vellaja, Sakanga,
Chemical compositions:-The thin pungent skin of the fruit contains piperin, A volatile
compound 5.9%, an aromatic oil 12% and 7% fatty acids, The fruit pulp has a letter
resin

called chavicin, starch, oil, gum, fats 1%, protein 7%, and alkaloids 4%,

Piperene, piperethine, Piperolein A and B, feruperine, dihydroferuperine,citronellol,


cryptone, dihydrocarveol, and - pinene, piperonal, camphene -caryophyllene, alanine, pipecolic acid, carotene, ascorbic acid, pipercide etc.
Karma:-Switra, Kilasa, Pama, Naktandya, Krimi, Hriddourbalya, Pratishaya, Shwasa,
Kasa, Shrtovrodha, Kapha vata shamaka, Shoola hara, Vrishya, use in ardita, Kustha
hara. Kasa 119, Pama 120, Sthoulya 121 rahani -122

Drug review of Bhutabhishangaja Ojokshaya 64

Research works

The fruit extract respond to be inhibitory to each. Coli, Acrobactor aerogens, L casei,
Staph, Faecalis, Staph, Aureus and Sh. Sonnei123,

The Essen. Oil inhibited vib, Cholerae, staph, Albus, C, Diphtheriae, Sh,
Dyscenteriae, Pr. Pyogener, strep pyogenes etc, 124.

Essential oil also inhibited B. subtilis, Stap aureus, Sal, Typhi, Sal, Paratyphi and
pestalotia Sp, 125,

Essential oil reported to be anti-fungal against Trich. Terrestre. Can. Albicans. Asp.
Niger etc. 126.

Its insecticide activity is reported 127,

Piperine exhibits antibacterial and anti-tumor activities against pseudo, Aeoginosa


and Alcaligenes F2518, Chem, 128
8) Pippali (Pipper Longum)
Synonyms:-Capala (giving instant action), Kana, Krsna, Kola, Capala, Tiksna Tandula,
Magadhi, Vaidehi, Usana, Soundi
Chemical compositions:-Resin, Volatil oil, starch, gum, fatty oil, inorganic matter, and
Resin-piperin 1-2% Essential oil, mono-and sesquiterpenses, caryophyllene (mainly),
piperine, piplartine, piperlogumine, piperloguminine, pipernonaline, piperudecalidine,
pipercide, sesamin, -sitosterol; foru aristolactams (capharanone B, aristolactum AII.
Piperlactum A and piperolactam B); five 4,5-dioxoaporphines etc
Karma:- Treedosha shamaka,

Ajeerna, Aruchi, Agnimandya, Vibanda, Udarshoola,

Arsha, use in Yakrit-Pleeha vikara, Krimi ,Hriddourballya, Pandu, Raktavikara, Kasa,


Shwasa, Hikka, Ballya. 129,Kamala 130 Rasayana 131Chardi132. Svasa 133
Research works

The pellitorine type of isobutylamide was reported to exhibit significant antitubercular


activity in vitro and the effect is about 20% of the potency of streptomycin 134

Drug review of Bhutabhishangaja Ojokshaya 65

The crude extract of P. longum and piplartine suppressed the ciliary movements of
the esophagus of frog. These findings suggest that its efficacy could be due to
suppression of cough reflex 135.

A preliminary study conduced on the effect of alcoholic extract of Pippali rasayana,


on serum proteins in rabbits showed a significant increase in body weight, serum
albumin and globulin ratio was also observed 136.

The milk extract was report to increase the rate of respiratory flow 137

Piperene revealed a hypotensive effect in dogs and also produced a non-specific


blockade of contractions induced by acetylcholine, histamine and serotonin in
isolated intestine of guinea pig and rat. It also had milk antipyretic activity 138.

Significant effect in controlling the frequency and severity of the asthmatic attack was
observed with P. longum powder in a clinical study 139.

The oil of P. longum fruit possessed anthelinintic activity 140.

9) Amalaki (Phyluntus Emblica)


Synonyms:-Amruta, Vrushya, Rochani, Kayasta. Abhaya, Amrta, Dhatri, Vayastha,
Vayassya, Vrsya, Tisyaphala, Sitaphala.
Chemical compositions:- Fruit Vit. C, phyllemblin, linolic acid, indole, acetic acid and
ayxubsm trigaloylglucose, terchebin, corilagin, ellagic acid, phyllemblic acid and salts.
Karma: -Dourbalya, Kshaya, Shotha, Shwasa, Kasa, Kusta, Visarphara, Soma roga
141

Prameha 142 Hikka 143

Research works

Anti-microbial activity- Emblica fruit found to have very potent anti-bacterial activity 144

Isolation of anti-microbial substace phyllemblin from the stem-gall callus is reported


145

Antioxidant activity- the long-lived belief that the therapeutic effect of Amla is due to
its rich vitamin C (L-ascorbic acid) content has thus been dispelled. The patent
vitamin C-like activity (antioxidative effect against reactive O2 species, Ros) of Amla
Drug review of Bhutabhishangaja Ojokshaya 66

fruits has now been located in the Low Mr (Mol. Wt. Less than 1000) hydrolysable
tannins. Four such compounds, emblicanin-A (1), emblicanin- B (2), puniglucomin
and penduculgin, have been isolated from the fruit pericarp 146.

Hepatoprotective activity- Dry powdered pulp of fruits (1.0g/kg) reduced the levels of
serum, aortic and hepatic cholesterol significantly in rabbits 147.

Rasayana activity Amalaki Rasayana is said to have growth promoting effect


(growth and longevity). The drug has no significant effect on the levels of serum
protein fractions, yet it raises the total protein level and increases the body weight.
The study also indicates that the increase in body weight is due to a positive nitrogen
balance 148
10) Haritaki (Terminalia Chebula)
Synonyms: - Amrta, Abhaya, Kayastha, Vayastha, Pathaya, Vijaya, Siva, Jaya,
Haimavati
Chemical compositions: -Gylic acid, Tinic acid, Niryas, Sharkar, albumin, calcium,
vitamin C, Fruits-

anthraquinone glycoside, chebulinic acid, tannic acid, terchebin,

vitamin C. Fruit kernel arachidic, behenic, lindeic, oleic, palmitic and stearic acids.
Karma: -Tridoshahara, Mukharoga, Arsha, Kamala, Yakrit Pliha, Krimi, Balapradhan,
Raktavikara, Pratishaya, Kasa, Swarabheda, Hikka, Kustha, Visarpa, kamalahara,
Twagsdoshhara, srotogamitva, vatanulomini, Medhya, Vatarakta hara, klibhya hara

149,

Ajirna, Prameha, Amlapitta, Upadamsa.


Research works

Study of in vitro antibacterial activity of extracts from the plants of T. chebula, E. Alba
and O. sanctum was carried out by the disk diffusion technique. All showed such
activity against human pathogenic Gram positive and Gram-negative bacteria. The
activity against Salmonella organisms was shown only by T. chebula; against shigella
organism by T. chebula and E. Alba, but not by O. sanctum. The widest spectrum of
antibacterial activity was shown by T. chebula. It was also most potent 150
Drug review of Bhutabhishangaja Ojokshaya 67

Various extracts prepared from the powdered fruits have been wide antibacterial and
anti-fungal spectrum 151.

It also inhibits growth of E. coli, the most common organism responsible for urinary
tract infection 152.

Ether extract showed higher antioxidant activity than BHA and BHT. Acid esters
present in phenolic fraction of extract were found most effective 153,
46 children with diarrhea wee given T. chebula and T. vulgare decoction. 57.17%
children were cured within 3 days of treatment 154.

Antioxidant property of T. chebula is reported. Alcoholic extract 10-20 fg/ml markedly


inhibitd lipid peroxidation of mouse liver and lung homogenate and mitochondria. The
above extracts effectively scavenge the oxygen free radical produced by V2 plus
light, and inhibit H2o2-induced red cell heamolyses. 20 fg/ml of extract significantly
inhibited chemiluminescene of human leukocytes induced by TPA (20ng/ml). The
extract (50fg/ml) also prevented DNA breaks of human leukocytes induced by TPA
and cigarette smoke condensate 155.

T. Chelaula inhibited HIV-1 proteas activity at a concentration of 25 microg/ml in the


flurogenic assay 156.
Aqueous extract of T. chebula (64-128 microg/ml concentrations) exhibited the most
prominent anti HBV activities 157.
11) Bibitaki (Terminalia Bilirica)
Synonyms:- Aksaphala, Kalidruma, Karsaphala,Bootawasa, (animals take shelterin its
shade
Chemical composition :-In fruitTinin 21.4%, B-sitostiral, Gylic acid, Eligic acid, Ethil
gylate, Chebulagic acid, Minital, Glucose, Gylactose, Fructose, Rimanose, In pulp
38.6%, greenish colored oil is present, Fruits Fructose, galactose, glucose, mannitol,
rhamnose, -sitosterol

Drug review of Bhutabhishangaja Ojokshaya 68

Karma: -Kapha pitta hara, Bhedhanam, Kasanashanam, Netrya, Keshya, Krimi


nashsana, Trisna-Chardi hara, Rasa, Rrakt, Mamsa, Medhaja dosham hanti, Madakara.
158

Svitra, Asmari, Kasa and Svasa, Atisara

Research works Out of 93 cases of cough and astma treated with T. bellerica, 22 showed complete
relief, 27 were significantly relieved, while 35 cases were moderately relieved. The
drug exhibited bronchodilatory, antispasmodic and antiasthamatic activities 159
The HIV-1 protease (PR) inhibitory activity was determined by using the fruit peal
methanol extract 160
T. Bellerica showed significant activity against both gram positive and gram-negative
bacteria. In addition it showed anti-fungal activity also 161.
12) Karanja (Pongomia Glabra)
Synonyms: - Karaja, Cirabilvaka, Naktamala, Gucchapuspaka, Ghrtapura, Snigdhapatra
Chemical compositions: - Fruit is having Pongamia oil 27-39%, Karangin, which is
Jantughn,

is

present.

Pongamol.

Karanjin,

pongapin,

3-methaoxypongapin,

pongaglabrne, kanjone, pongol, gamatin, lonchocarpin, isolonchocarpin, karanja


chromene, porgachromene, isopongaflavone, pongamol, glabrin, ovalitenone, kanugin,
cemethoxykanugin, pongamin, neglabrin etc.
Karma: - Kustaghna, Amavataghna, Krimighna, Vrinaropaka, Kasahara, Pachana,
Kanduhara, Parashrayi jeevanu nashaka, Dadru, Pama, Vicharchika, Visarpa Hara, Anti
septic, Used in Atisara Ama, Bhagandara, Raktarsha, Vidhradi.Kai 162, Granthi, visarpa,
Romasanjanana, Rakta Pitta.
Research works

The essential oil from leaves showed marked in vitro antibacterial activity against B.
antharcis, Ps. Mangiferae, sal. Typhi, B mycoides, B pumilus, Esch Coli, Sar, Lutea,
Stap, Aureus, Staph, Albus etc. 163.

The oil of P. pinnate showed antibacterial activity against several organisms 164
Drug review of Bhutabhishangaja Ojokshaya 69

Karanjin showed good antibacterial activity against M. tuberculosis H 37 Rv, leading to


complete inhibition of the growth of the organism at a concentration of 10 ppm. 165

The essential oil from P. Pinnata showed mild anti-fungal activity 166.

13) Tagara (Valerana wullichi)


Chemical compositions:-Valrianica acid present,
Karma: - Used in neurosis and Vatahara, Raktavisarana, Vatanadi, uttejaka,
Chetanakaraka,

Swapakaraka,

Vatanulomana,

Vedanastapaka,

Vranaropaka,

Apatantrakahara, Atatvabinivesha hara, Anti spasmodic Epilepsy 167.


14) Vidanga (Embelia Ribes)
Synonyms:-Jantu nashana, Jantughna, Krmighna, Citra, Tandula, Amogha, Vella,
Kairali, Tandula, Jantuhantri, Gahvara.
Chemical compositions:-Acid 2.5%, volatile oil, Stable oil coloring agent, tannin, resin,
Cristebin, kshara.
Karma: - Vata Kapha hara, Krimi hara, Carminative, Shoola, Aadmana, Udara, Shlesma,
and Use full in Agni mandya, Aruchi, arsha. 168,
15) Kusta (Saussurea luppa)
Synonyms:- Utapala, Kasmira, Vapya, Gada, Agada, Ama, Amauya, Kapalam,
Kouberam, Japyam, Tvakdohsa, Divya, Durnama, Padmaka, Paribhavya, Pakala,
Paribhadraka, Manusanjaka, Ramam, Ruk, Rogahva.
Chemical compositions: - Root contains 1.5%aromatic oil, Glucoside, Saussirin salt,
Tannin, Insulin 18%, Stabel oil, Nitrate, Glucose, Roots yield 3.5% ash. It contains large
quantity of manganese.
costuhactone,

alpha

Essential oil, costol, taraxas-terol, costunolide, dehydro

cyclocostunolide,

sitosterol,

sesquiterpenes,

Ar-curcumene,

isodihydrocostuslactone, costus-lactone etc


Karma:- Vata kapha hara, Shukrala, Visarpa, Kasa, Kustha, Hikka, Jwara,

169

Unmada

and Apasmara, 170 Sirahsula 171 Medhya Rasayana 172.

Drug review of Bhutabhishangaja Ojokshaya 70

Research works Kokate established anthelmintic activity of S. lappa, in 1986.

Two active component costunolide and Dc hydrocostus lactone, show strong


suppressive effect on the expression of Hepatitis B surface Antigen (HBS Ag) in
human hepatoma Hep 3 B cells, but have little effect on the viability of the cells. Both
fractions suppress HBSAg production by Hep 3 B cells in a dose dependent manner
with IC 50s of 1.0 and 2.0 micro H respectively. 173.

16) Vacha (Acorus Calamus)


Synonyms:-Rakshogni, Ugra gandha, Golomi, Sataparvika, Sandgrandha
Chemical compositions:-Rhizome bark has1.53.5% volatile oil which contains
Acorin, Eugenol, Asarone, Caffeine, and some amount of astringent matter are present
in Vacha. Acolamone, acorenone, acorgermacrone, acoramone, acorone, cis and transasarone, and ofasarone, azulene, cadalene, calacone, calacorene, calamene,
calamenol, calamone, calamenone, calamenene, calarene, - gurjunene, caphene,
eugenol, telekin, preisocalamendiol, acoric acid, calamen diol, calamenone etc.
Karma:-Vata Slesm hara, Ruja, Krimi, Shakrun-mootra vishodani, Buddi vivardanam,
Apasmara Hara, Mukha roga hara. 174Amalapitta 175 Apasmara 176, Sopha and Vrddi 177.
Research works Volatile oil from roots inhibited the growth of M. tuberculosis in a concentration of
10g /ml. it also inhibited the growth of gram-negative organisms in a concentration
of 0.4-0.6 mg/ml. the LD

50

for guinea pigs was found to be 0.6275 ml/100g body

weight 178.
17) Vatsanabha (Aconitum ferox)
Synonyms

Amrutam,

Ugravisha,

Garalam,

Nagam,

Nabhi,

Mahoushadha,

Amruta.Pranaharam, Maranam, Mahoushadham, Visham, Stokakam, Sthavaradyam,


Vatsanagam,

179-187

Drug review of Bhutabhishangaja Ojokshaya 71

Chemical compositions: Aconitine (toxin) Picroeconine, Benzoil, Econine and


Homonepelin. A. Ferox Roots contain toxic alkaloids, pseudoaconitine along with
bikhaconitine, chasmaconitine, indaconitine

188,

veratoryl pseudoaconitine and diacetyl

pseudoacontitine (Manske and Rodrigo, 1979). Two new alkaloids 2 (IH)- quinolinone
and 3,4- dihydro-6-hydroxy 2 (IH)- quinolone189. A new diterpenoid alkaloid 14-0
acetylsenbusine A; Vakognavine, Chasmaconitine, crassicauline A. falconericine,
bikhaconine, pseudoaconine, neoline, senbusine A. neoline, senbusine B, isotalatizodine
and

aconine

are

reported

190.

Four

lipoalkaloids

viz.,

liposeudo

aconitine,

lipoyunaconitine. Lipoindaconitine and lipobikhaconitine; and four-aconine viz., veratroy


lpseudaconine, anisoylyunaconine, benzoylindaconine and varatory ibikhaconine are
also reported 191.
Karma: -Vata Kapha hara, Pranadai, Rasayanam, Brimhana, Veery vardhana, Kustha,
shotha, Vishanashnama, Agni mandy, Swasa, Plihodhar, Jwara, Madhu meha,

192.

The

writhing response induced by acontine has been used for the measurement of analgesic
activity. The characteristic pattern of aconite-induced writhing response in albino mice
has been found to be similar to that induced by bradykinin. Acontine-induced writhing
response was found to be quicker than that induced by bradykinin, it lost for a longer
period and was consistently observed at 2 mg dose level. Analgesic agents 193 blocked
the response.
18) Musta (Cyperus Rotundus)
Synonyms: - Krodesta, Hima, Sugandhi, Varida, Gundra, Gangeya, Ghana, Megha,
Abda, Krodesta, Hima, Sugandhi, Varida, Gundra, Gangeya, Ghana, Megha, Abda.
Chemical compositions: -Cineol (+) copadiene, capaene cyperen I and II, cyperenone,
isopatchoulenone, cyperotudone, cyperol, cyperolone, -cyperone, copaene, cyperen I
and II, cyperenone, isopatcoulenone, cyperotundone, cyperol, cyperolone, cyperone,
(+) epoxyguaiene, isocyperol, isokobusone, kobusone, muystakon,e patchulene, (+)
rotundone, and -selinene, sugenul, -sitosterol etc.
Drug review of Bhutabhishangaja Ojokshaya 72

Karma: - Kapha Pitta Shamaka, Deepana, Pachana, Jwara, Aruchi, Jantughna,


Atisaraghni, Trisna hara, Sangrahi, 194 Jvara 195Atisara 196 Halimaka 197.
Research works Except cyperone other fraction like cyperene II, cyperol and I have shown antibacterial activity against a number of the organisms (More specifically against staph.
Urens) 198.
In a study C. rotundus is found to be more useful in GI conditions like amoebiosis
and giardiosis 199.
19) Ajamootra (Goat urine)
Synonyms: -Bastasya mootra,
Karma: -Treedoshagna, Alpa Vatakara, Shoola, Gulma, Visha, Shvasa, Kasa,
Nadivikara, Vishavikara, Kamala, Pandu, Shosha hara, Pleeharoga, Udararoga hara, 200.

Drug review of Bhutabhishangaja Ojokshaya 73

Materials and methods


The recent entry to the list of grave diseases is AIDS (Acquired Immuno deficiency
Syndrome), which is caused by Human Immuno deficiency Virus (HIV). It is a serious
disorder of the immune system, in which the bodys normal defense against infection breaks
down, leaving it vulnerable to host of life threatening infection including unusual
malignancies

201

. A long healthy life has been the cherished wish of man since ages, but

often many challenges are posed to this in the form of grave diseases. Ayurveda is able to
provide good health care by effectively managing the diseases from time to time 202.
Ayurveda describes a number of drugs with the proven or proposed immuno
modulating and immuno potentiating activities

203

. Recent findings of anti-viral activities of

many herbs have drawn the attention of the scientists to study the effect of Ayurvedic drugs
in HIV infection. A number of herbal drugs have been individually evaluated in the treatment
of HIV and AIDS related complex (ARC)

204

. According to estimation the number of people

infected by HIV would have crossed 50 million and till now there were 12 million deaths due
to AIDS in entire world. In India since the detection of HIV infection in 1986, the epidemic

Materials and Methods of Bhutabhishangaja Ojokshaya 74

has been frankly out of control. As of now an estimated 4 to 6 million HIV infected cases are
present in India.
The present study is designed to assess the therapeutic effect of Ojokalpa
Rasayana in HIV infected patients, which could be a safe, effective and economical drug
and compared with the market available Amrut Kaya Kalpa Rasayana

205

, which claims as

immuno-modulator.
Ojas is the essence of all Dhatus and also called as Bala, which is responsible for
Vyadhikshamatva or immunity against infections

206

. The condition in which Ojas gets

depleted is called Ojokshaya. Susruta explained the stages of the depletion of Ojas as Ojovisramsa, Ojovyapat and Ojokshaya 207.

Ojokshaya can be defined as qualitative and

quantitative lessening of Ojas. Ojas, the essence of all Dhatus, controls the vital functions
and immuno regulation. It is classified in to two types i.e. Para and Apara, out of which
Astabindu (Para) Ojas is depleted by the infection 208.
The symptomatology of the HIV infection resembles that of Ojokshaya. Clinical
stages of HIV infection is classified in to five stages on the basis of CD4 count. The anti
retro-viral drugs available now, act at different levels of the stages of the life cycle of HIV
and the combination therapy of them has shown to prolong the life span and to decrease
opportunistic infections and to increase CD4 cells count.
Ojokalpa Rasayana is an herbo-mineral compound rationally formulated on the
basis of Immunomodulatory effect, Antiretroviral and Antioxidant properties, Krimiharatwa
i.e. germ (Virus) killing property along with Rasayana (Tissue nourishment). Individual and
cumulated properties of yoga is carefully thought about from Bilwadi vati
Sahasrayogam added with Agnikumaravati

210

209

of

(Sahasrayogam), which is a jwarahara and

Bhuta (Virus) vishahara.

Materials and Methods of Bhutabhishangaja Ojokshaya 75

Objectives of the study


1. To evaluate the efficacy of Ojokalpa Rasayana and Amrut Kayakalpa Rasayana in
improving the clinical status of Ojokshaya with special reference to HIV infection
2. To assess the role Ojokalpa Rasayana and Amrut Kayakalpa Rasayana on CD4 cell
count, which is a marker of stages of the HIV infection along with viral load.
Source of data
a) Literary: Literary aspects of the study will be collected from standard Ayurvedic texts,
magazines and journals. The information regarding the disease will be updated from
Internet search along with authentic textbooks.
b) Drug: Ojokalpa Rasayana
The ingredients of Ojokalpa Rasayana will properly identified. The standard
manufacturing guidelines will be followed for the preparation. The combination and
proportion of Ojokalpa Rasayana is as follows.
1. Bilwa (Aegle marmelos) 211

1 Part

2. Tulasi (Ocimum sanctum) 212

1 Part

3. Karanja (Pongamia glabra) 213

1 Part

4. Tagara (Valeriana wallichii) 214

1 Part

5. Devadaru (Cedrus deodara)215

1 Part

6. Haridra (Curcuma longa) 216

1 Part

7. Daruharidra (Berberis aristata) 217

1 Part

8. Triphala (three Myrobalams) 218

1 Part

9. Trikatu 219

1 Part

10. Vidanga (Embelia ribes) 220

1 Part

11. Agnikumara vati 221

1 Part

Materials and Methods of Bhutabhishangaja Ojokshaya 76

The combination and proportion of Amrut Kayakalpa Rasayana

222

is as

follows.
Swarna Bhasma

1 mg

Makaradhwaja

2 mg

Abhrak Bhasma (100puti)

5 mg

Loha Bhasma (100puti)

5 mg

Vanga Bhasma

5 mg

Yashada Bhasma

5 mg

Moti pisti

5 mg

Kanta loha Bhasma

5 mg

Swarnamakshika Bhasma

5 mg

Jayaphala

10 mg

Shankhapushpi

20 mg

Ashwagandha

25 mg

Vidarikanda

50 mg

Katuki

15 mg

Punarnava

15 mg

Gokshura

15 mg

Yastimadhu

20 mg

Pippali

40 mg

Milk

Q.S.

Shatavari Kashaya

Q.S

b) Patients: Patients with Ojokshaya (HIV +ve) will be selected from O.P.D. of Post
Graduation and Research center of Sri D.G.M. Ayurvedic medical college & Hospital,
Gadag by preset inclusion and exclusion criteria.

Materials and Methods of Bhutabhishangaja Ojokshaya 77

The patients are included in the study after obtaining the informed
consent.
The identity of all the patients are kept confidentially.
All Patients undergone individually and couples together for special
counseling sessions before and after serological investigations and
periodically during the course of treatment.

Special instructions / advice given to patients:


To stop smoking alcohol and other habits which can super impose
infections or troubles systemic.
Not to indulge in strenuous work / exercise.
Not to take any other medication except the trail medication.
Not to indulge in sex with life partner and also extra marital.
To consume nutritious food
Avoiding out side food

Method of collection of data


a) Research design: As this disease is a grave condition & of high mortality rate and
there is no clinical evidence available for this particular yoga a prospective open
clinical trial was conducted. All the patients received the same medicine. Even though
a total of 25 patients were screened during this period, 20 patients were taken for the
study. A detailed pro-forma was prepared for case taking.
b) Sample size: A minimum of 20 patients
c) Exclusion criteria:
1. Patients below the age of 20 years and above the age of 50 years, pregnant and
lactating women will be excluded from the study.

Materials and Methods of Bhutabhishangaja Ojokshaya 78

2. The patients having diabetes mellitus and other systemic diseases will be
excluded and the patients with concomitant therapy will be excluded.
d) Inclusion criteria
1. The patients with the HIV infection diagnosed by serological test and Western
blot method will be taken in the study.
2. CD4 count ranging from 200 to 500/cu.mm.
3. Karnofsky Performance score 50 and above.
4. The patients are selected irrespective of Sex and race based on the clinical
signs & symptoms other than that of exclusive criteria,
e) Posology: 3-gm/24 hours or 50mg/Kg-body weight in divided dose orally
f) Study duration: 120 days
g) Follow up period: 60 days
h) Assessment of result: subjective as well as objective parameters are assessed.
1. General health condition (Grade)
2. Karnofsky performance score
3. Body weight.
4. Total WBC count.
5. Total count platelets.
6. Total count lymphocytes.
7. Erythrocytes sedimentation rate.
8. CD4 cell count
9. CD8 cell count.
10. CD4 : CD8 ratio

Materials and Methods of Bhutabhishangaja Ojokshaya 79

For the assessment grades were fixed depending upon the condition.
Overall assessment is made taking into consideration both subjective and
objective parameters.

Considering all the above parameters patients are graded in to four


groups depending upon the response to Ojokalparasayan. The over all
score was considered as 10 based on the subjective and objective
parameters excluding the dosha and ojas assessment. An exclusive
assessment is made for the Ayurvedic aspect. Out of 10 scores
depending upon the score of individual patient the grading was done as
follows:
Grade

Score range

Best responded

8 to 11

Moderately responded

5 to 8

Responded

2 to 4

Static / Not responded

0&1

i) Criteria for considering for dropouts:


Inability to attend two successive follow-ups.
Discontinuing medication for more than five days
j) Criteria for withdrawals:
Deterioration of condition, which needs hospitalization
Subsequence diagnosis of Aids related complications (ARC)
Investigation required for the Ojokshaya
All the patients were screened for HIV infection by using ELISA method. For the
assessment of HIV status all the patients were investigated, for CD4 cell count, erythrocyte
sedimentation rate, random blood sugar and total lymphocyte count total platelet count. CD4

Materials and Methods of Bhutabhishangaja Ojokshaya 80

cell count assay is conclusive of CDB cell count, total platelet count. CD4 cell count assay is
inclusive of CD8 cell count also. All the investigations are repeated after three months of trail
medication. Those patients who had respiratory system symptoms were investigated
radiological.
1. Screening tests

: Tri-dot

2. Confirmatory tests

: Western Blot

3. Other tests

: CD4 cell count - surrogate marker 223


: Erythrocyte Sedimentation Rate
: Haemoglobin %
: Random Blood Sugar
: Total Leukocyte Count
: Total platelet count
: Total Lymphocyte Count
: X-ray Chest (if necessary)
: Viral load 224 (subjected to the condition of
availability)

Materials and Methods of Bhutabhishangaja Ojokshaya 81

In this clinical study a total of 26 patients were reported either with known HIV status.
Those who indulged in risk factors of HIV infection also reported. Outs of all patients were
serologically diagnosed as having HIV infection. HIV status and intake of concurrent
therapy, A total of 18 patients were enrolled in this study as they fulfilled the inclusive
criteria. Out of these 26 patients 8 patients dropped out, during the trial study for various
reasons including subsequent diagnosis of opportunistic infections. Remaining 18 patients
have completed the total treatment schedule and follow up.
Total patients reported

26

Serological test positive

26

Excluded

Initially included

Withdrawal

Finally included for study

18 (9 patients in each group)

Each and every data pertaining to every patient was recorded in a well-designed
case taking perform. The final data is divided into 3 sections for better analysis and
convenience of observation.
1.

Data related to demography

2.

Data related to disease

3.

Data related to response to Ojokalparasayana and Amruta kayakalpa Rasayana.


Observations and Results Bhutabhishangaja Ojokshaya 82

1) Age group incidences


Table-3
Sl no

GROUP -1

Age (Years)

GROUP -2

20-30

Number of
patients
7

31-40

11.12

44.45

41-50

11.12

Total

%
77.77

Number of
patients
5

55.55

Maximum patients with ailment were found in 20-30 years group i.e. 7 (77.77%) in
group-1 and, (55.55%) in group-2. 31-40-age interval in-group-1 patients are 1 (11.11%) and
4 patients (44.44%) in group-2. And 41-50 age group observed with 1 patient (11.11%) in
group-1 and no patients in group-2 (0%). The data collected in the trail resembles with
international observations of HIV incidences in different age groups.
Graph -1

8
7
6
5
4
3
2
1
0

7
5
4

1
0

20-30

31-40

41-50

GROUP-1
GROUP-2

Observations and Results Bhutabhishangaja Ojokshaya 83

2) Sex ratio incidences


Table -4
Sl no

GROUP-1

Sex

Male

Female

Number of
patients
6
3

GROUP-2
%

66.66

Number of
patients
6

%
66.66

33.33

33.33

Maximum patients in this study are men and male verses female ratio is 2:1. This is
contradictory to the Indian data sex incidence. Which 1:1 this various can be due to the male
dominance in the local society with rural and illiteracy background. This observation
suggests that the lack of freedom and social stigma for female in India.

Graph -2

10
8

6
Female

4
6

GROUP-1

GROUP-2

Male

2
0

Observations and Results Bhutabhishangaja Ojokshaya 84

3) Diet incidences
Table -5
Sl no

Parameters

GROUP-1

Vegetarian

Number of
patients
0

Mixed diet

Total

GROUP-2
%

Number of
patients
0

100

100

In the study incidence among people of two different food habits, it was interesting to
note that all the patients (100%) consume mixed diet. But is also interesting to note that not
even a single vegetarian subject was seen in this study. As Ayurvedic concept speaks about
the role of predisposing factors, there must be a physiological or psychological impact of
non-vegetarian food that may be having a role to play in high incidence of HIV among nonvegetarians populations. And in further it was observed that patients who avoid nonvegetarian food during treatment improved a lot and deteriorated as they start consumption
of non-vegetarian food.
Graph -3

10
8
6
4

Mixed diet
Vegetarian

0
GROUP-1

GROUP-2

Observations and Results Bhutabhishangaja Ojokshaya 85

4) Religion incidences

Sl no

Table -6
GROUP-1

Religion

GROUP-2

Number of
patients

Number of
patients

Hindu

77.77

100

Muslim

22.23

Christian

Others

Total

An attempt was made to know the incidences in deferent religions groups. 7


patients of study for group-1 (77.77%) and all 9 patients (100%) in-group 2 are Hindu
patients attended. 2 patients reported (22.22%) as Muslim in group-1. This may be due to
religion ratio of local population or as earlier discussed more of non-vegetarian
consumption. On the contrary there is a study that claims less incidence of sexually
transmitted disease in subjects who under went circumcision 225.
Graph 4

10

9
7

8
6
4

0 0

0 0

th
er
s

GROUP-2

n
Ch
ris
tia

m
us
li
M

in
du

GROUP-1

Observations and Results Bhutabhishangaja Ojokshaya 86

5) Economic incidence
Table 7
S. No

GROUP-1

ECONOMIC
STATUS

Number

GROUP-2
%

Number

of patients

of patients

Poor

33.33

44.44

Middle Class

55.55

55.55

Higher Middle

11.11

Higher

Total

The maximum patients were in middle class 5 patients (55.55%) in each group of 1
and 2. Economically poor or B.P.L. patients are 3 (33.33%) and 4 (44.44%) in groups 1 and
2. Very less i.e. only one patient (11.11%) reported in higher middle class of group-1. It
doesnt reveal the clear status of economical status verses infection because the study was
made at district level and that too in small sample. It also reflects the easy acceptance of
infection to middle class and B.P.L. Class patients, as they are economically not strong to
consume immuno-potent food.
Graph 5

6
5

Poor

Middle Class

Higher Middle

Higher

2
1
1

0 0

0
GROUP-1

GROUP-2

Observations and Results Bhutabhishangaja Ojokshaya 87

6) Occupational incidence
Table - 8
Sl no

OCCUPATION

GROUP-1

GROUP-2

Sex Worker

Driver

11.11

Businessman

22.22

22.22

Service / Agriculture

33.33

44.44

Student

House wife

33.33

33.33

Total

In this study of incidence of HIV infection is in people of different occupation, it was


surprising to note that maximum 11% drivers, 22% business, 33.33% and 44.44% of service
/ Agriculture, in both 1, 2 group respectively. 33.33% house wives in-group 1 and 2. This is
an alarming signal for developing countries because they have high-density labour
population.
Graph - 6

5
4
3

2
1

Sex W orker
Driver
Businessman
Service
Student
House wife

1
0

0
0

0
GROUP-1

GROUP-2

Observations and Results Bhutabhishangaja Ojokshaya 88

7) Marital status incidence


Table - 9
Sl no

Marital Status

Group-1

Group-2

Married

Single

Divorced

Widower

2 Or 3 Marriages

Total

It is observed that the extramarital affairs are more in the married people. Neither
divorced nor widowers are reported with the HIV infection. In the study related to disease,
maximum number of male patients (100%) got the infection from heterosexual contact. This
data coincides with the international data. Women usually come in contact with disease
through their husbands. Even though the incidence charges are more among the patients
who got it from blood transmission or intra-venous injections, in almost got it with
heterosexual contact. It evidential for the high risk unsafe heterosexual practices in India.
Graph -7

9
8
7
6
5
4
3
2
1
0

8
Married
Single
Divorced
W idower
2 Or 3 Marriages

1
0 0 0

Group-1

0 0 0
Group-2

Observations and Results Bhutabhishangaja Ojokshaya 89

8) Source of infection
Table - 10
Sl

Infections

Before

After

Before

After

Anashana

Alpashana

Rooksha

Ahara

Pranita Ahara

Vatatapa Sevana

Ati Vyayama

Ati Vyavaya

Shonita Ativartana

10

Hetero Sexual

11

Prajagar

12

Kapa

13

Shoka

14

Chinta

15

Bhaya

16

Bhootopaghata

no

1) Anashana 7 (77%) and 3 (33%),


2) Alpashana 8 (88%) and 4 (44%),
3) Rooksha Ahar 5 (55%) and 4 (44%),
4) Pramita Ahara 0% and 1(11%),
5) Vataatapasevan 6(66%) each,
6) Ativyayama 5 (55%) and 6 (66%),
7) Ativyavaya 6(66%) and5 (55%)
8) Shonitaataitavartana 0 and 1 (11%),
9) Prajagar 4 (44%) and 5 (55%),
10) Kopa 5 (55%) and 2 (22%),

11) Shokha 6 (66%) each,


12) Chinta 9(99%) and 8 (88%),
13) Bhaya 6 (66%) and 5 (55%),
14) Bhootopaghata 9 (100%) seen in each
group,
15) Among these Vataatapasevan 1(11%),
Shokha

1(11%)

Bhootopaghata

9(100%) are continued in group 1 and


Bhya 1(11%) Bhootopaghata 9 (100%)
is continued in-group 2.

Observations and Results Bhutabhishangaja Ojokshaya 90

9) Chief complaints
Table -11
GROUP-1
Sl, no

Complaints

Loss Of Weight

General Weakness

Before

Group-2

After

Before

After

Loss Of Appetite

Fever

Inertia of the Body

Loss Of Complexion

Emaciation

Looseness Of Joints

Somnolence

10

Delirium/Conversion

Urethral Disease, Genital Ulcer, Genital Warts, Vegetal Candlings, Drowsiness,


Acne Valerian are not Seen At Any Cases. In group-1, two patients and in group-2, 1 patient
is not responded, in the symptoms of oral thrush, and 1 patient of group-1 is not respond in
White tongue.
1) Loss of weight 5 (55%) in each group, 2) General week ness (Glani) 9 (99%) and
8 (88%), 3) Loss of appetite (Aruchi) 1(11%) and 5 (55%), 4) Fever (Jwara) 9 (99%) and 7
(77%), 5) inertia of the body (Stabda gatrata) 5 (55%) each. 6) Loss of complexion,
(Vyatitendriya) 1 (11%) and 2 (22%), 7) Emaciation (Mamsakshaya) 7 (77%) and 4
(44%),8), 8) Looseness of joints (Sandhivislesha) 3 (33%) each, 9) Somnolence (Anidra) 2
(22%)each, 10) Delirium/ convulsions (Pralapa) 0% in each group found respectively. After
treatment these symptoms are not seen in both groups.
Observations and Results Bhutabhishangaja Ojokshaya 90

10) Associated complaints


Table -12
Group 1
Sl, No

Complaints

Group 2

Before

After

Before

After

Oral Thrush Vomiting

Bleeding Gums

Pain Abdomen

Dysphasia /Sore Throat

White tongue

Hairy tongue

Cough

Blood With Sputum

Breathlessness

10

Headach

11

Skin Eruption

12

Morlascum

13

Herpes Zoster

14

Giddiness

15

Palpitation

16

Burning Micturation

17

Diarrhea

18

Anal Itching

19

Cymphodenites

Observations and Results Bhutabhishangaja Ojokshaya 91

1) Oral thrush/ Vomiting/ Nausea 9 (99%) and 4 (44%),


2) Bleeding gums1 (11%) and 2 (22%),
3) Pain abdomen/distention 1 (11%) and 4 (44%),
4) Dysphasia/ Sore throat 5 (55%) and 2 (22%),
5)

White tongue4 (44%) and 3 (33%),

6) Hairy tongue 3 (33%) and 0%,


7) Cough 3 (33%) and 4 (44%),
8) Blood with sputum0% and 1(11%),
9) Breathless ness0% each in both group,
10) Chest pain 2 (22%) and 1 (11%),
11) Head ache 6 (66%) and 4 (44%),
12) Skin eruption1 (11%) each,
13) Moluscum0% and 1(11%),
14) Warts0% each in both group,
15) Herpes zoster 5 (55%) and 1(11%),
16) Giddiness 5 (55%) and 4 (44%),
17) Palpitation 2 (22%) and 5 (55%),
18) Burning micturation 2 (22%) and 0%,
19) Urethral discharge 0% each,
20) Diarrhea 3 (33%) in both group,
21) Anal isching0% and 1(11%),
22) Genital Ulcers 0% in both group,
23) Genital warts 0% in both group,
24) Veginal candidisis 0% in both group,
25) Drowsiness0% in both group,
26) Lymphedanitis 1 (11%) each,
27) Acne Vulgaris 0% in both group respectively.

Observations and Results Bhutabhishangaja Ojokshaya 92

DISCUSSION ON LABORATORY INVESTIGATIONS


11) Changes in Hemoglobin percentage (HB%)
Table -13
Group 1

Group -2

OPD No

Before

After

Difference

OPD

Before

After

Difference

216

14.2

12.8

-1.4

412

10

14

318

10.5

13

2.5

576

12.8

13

-2

561

10

10.8

0.8

4180

14.6

13

-1.6

2726

12

7.2

-4.8

5050

10.4

10

0.4

2784

11.0

7.0

-4

6421

12

13

3187

13.8

12.9

-0.9

6614

6.8

10.8

3427

13.5

11.0

-2.5

7187

12

11

-1

3434

12.8

13

0.2

8274

13.2

15

1.8

7221

10.2

10.2

8275

13

14

1.81

108

97.9

104.8

113.8

When studied hemoglobin % at individual level, in group-1 three patients (33%)


increased and in group-2 five patients (55%) reported increases. One (11%) patient is static
with hemoglobin % in group 1 and four patients (44%) in group-1 and three patients (33%) in
group-2 decreased hemoglobin %.
When compared inter group means of before after we found marked decrease of
10.1 mg in group-1 and 8.41 mg increase in group-2.

Observations and Results Bhutabhishangaja Ojokshaya 93

12) Changes in Erythrocyte Sedimentation Rate (ESR)


Table -14
Group - 1

Group - 2

OPD No

Before

After

Difference

OPD

Before

After

Difference

216

10

24

14

412

33

15

-18

318

30

32

576

25

25

561

40

68

28

4180

10

28

18

2726

25

82

57

5050

10.5

20

9.5

2784

20

64

44

6421

30

20

-10

3187

80

16

- 64

6614

38.1

35

-3

3427

80

38

- 42

7187

50

35

-15

3434

28

22

-6

8274

60

32

-28

7221

70

30

- 40

8275

77

24

-53

383

376

333.6

234

ESR of 1st hour measurement decreased in 4 patients (44.44%) in1st group and 6
patients (66.66%) in 2nd group. This is a good prognosis for the patients. 5 (55.55%) patients
of group-1 and 2 patients of group-2 show increase in the E.S.R., which is a bad prognosis.
One patient (11.11%) in the group-2 shows no change. But both groups exhibit decrease in
the mean values.

Observations and Results Bhutabhishangaja Ojokshaya 94

13) Changes in Total Lymphocyte count


Table -15
Group 1

Group - 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

3300

3500

200

412

900

2300

400

318

2200

4400

2200

576

1500

1000

-500

561

1100

1100

4180

1800

1700

-100

2726

1200

1000

-200

5050

1700

1463

-237

2784

1470

1300

-170

6421

1700

2400

700

3187

2600

2300

-300

6614

900

1000

100

3427

1400

1000

-400

7187

4600

3500

-1100

3434

1900

4000

2100

8274

2300

2550

250

7221

3200

2900

-300

8275

2700

2800

100

18370

21500

18100

18713

Total Lymphocyte count measurement decreased in 5 patients (55.55%) in 1st group


and 4 patients (44.44%) in 2nd group, which is a bad prognosis. 3 (33.33%) patients of
group-1 and 5 patients (55.55%) of group-2 show increase in the Total Lymphocyte count,
which is a good prognosis for the patients. One patient (11.11%) in the group-1 shows no
change. But both groups exhibit increase in the mean values. Total Lymphocyte count
increased in total 200-2200 in range at 1st group and 100-400 increased in 2nd group, after
treatment.

Observations and Results Bhutabhishangaja Ojokshaya 95

14) Changes in white Blood corpuscles


Table -16
Group - 1

Group - 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

8.2

7.8

-.4

412

6.5

8.3

1.8

318

5.8

7.5

1.7

576

8.9

7.5

1.4

561

5.6

5.6

4180

7.5

8.7

1.2

2726

6.3

4.9

-1.4

5050

13.5

6.2

-7.3

2784

10.7

9.6

-5.1

6421

10

8.7

1.3

3187

8.9

5.0

-3.9

6614

8.0

6.2

-1.8

3427

7.3

7.5

.2

7187

10.1

9.0

-1.1

3434

8.2

6.3

-1.9

8274

6.9

6.8

-1

7221

8.9

9.8

.9

8275

8.8

8.9

2.1

Total

69.9

64

80.2

70.3

It is significant that the viral activity is more in the samples and the fighting against
the infection is continuous. Thus the WBC counts doesnt show marked changes. Both
groups express the reduction in the mean values as minimum, which could be a good
prognosis.

Observations and Results Bhutabhishangaja Ojokshaya 96

15) Changes in Weight


Table -17
Group - 1

Group - 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

60

61

412

46

51

318

58

61

576

64

67

561

40

44

4180

65

66

2726

50

54

5050

48

53

2784

56

58

6421

51

52

3187

45

47

6614

37

40

3427

58

60

7187

56

61

3434

45

45

8274

73

73

7221

53

54

8275

57

61

Total

465

484

497

524

All the patients in the group-1 exhibit 1-2 Kg increase and group-2 even up to 5-Kg
weight increase. This is a good prognosis and expresses that the patient recovery is started.
Usually in the HIV+ves weight loss is a sign reversed with the present management. This
variation may be due to the various factors, including inclusion of proteins in the food and
Agni vardhaka herbs in the formula.

Observations and Results Bhutabhishangaja Ojokshaya 97

16) Changes in Platelet count


Table -18
Group - 1

Group - 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

2.05

2.14

0.9

412

1.5

1.52

.02

318

1.94

1.30

-.64

576

2.6

1.81

-.8

561

1.43

1.49

.06

4180

2.3

2.22

-.8

2726

1.07

1.26

.19

5050

1.95

2.10

+15

2784

2.23

2.60

0.37

6421

3.0

2.63

-37

3187

2.05

2.0

-.05

6614

1.36

1.20

-.16

3427

.81

1.5

+. 69

7187

2.5

3.5

1.5

3434

2.41

2.82

.41

8274

2.13

2.55

.42

7221

2.15

2.18

.03

8275

2.69

2.56

-.13

16.14

17.29

20.03

20.09

. Both groups express the reduction in the mean values of Platelet counts as
minimum, which could be a good prognosis.

Observations and Results Bhutabhishangaja Ojokshaya 98

17) Changes in Kornefsky performance score


Table - 19
Group - 1

Group - 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

90

90

412

80

90

10

318

80

90

10

576

90

90

561

90

90

4180

90

90

2726

80

90

10

5050

80

90

10

2784

80

90

10

6421

80

90

3187

80

90

10

6614

80

90

10

3427

80

90

10

7187

80

90

10

3434

90

90

8274

90

90

7221

80

90

10

8275

90

90

750

810

60

760

810

40

Kornefsky grade: - 6 (66%) increased by 10 grades and 3 (33%) were static in 1st group, 4
(44%) increased by10 grades and 5 (55%) were static in 2nd group. Kornofsky performance
score (KPS) is a widely accepted parameter for evaluation of HIV-AIDS. All patients (100%)
in this study have crossed the score 90, and none has reached score 80. This data is better
than Alka Despande study 1998. It interesting to note that, Despande administered the drug
for 1 year and the mean was 89, where as in this trial drug was administered for four months
and the mean KPS is 90 and 88. Therefore this drug is capable of controlling the
opportunistic infections, which indirectly helps for raise in CD4 cell count.

Observations and Results Bhutabhishangaja Ojokshaya 99

18) Changes in general health condition


Table 20
Group - 1

Group - 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

+1

412

318

+1

576

561

4180

2726

+1

5050

2784

+1

6421

3187

6614

3427

7187

3434

8274

7221

8275

13

20

15

22

General health condition: -7 (77%) increased and 2 (22%) static in both groups by 1 grade,
There was a significant improvement in GHC of all the patients, from lower grade to upper
grades like grade 2 and grade 3 after medicatioin. This result is quite similar with K.
Rajagopal

226

entitled and Alka Deshapande

227

entitled reference. The significant response

in general health condition may be due to the reduction in viral load, in plasma and reduction
in the viral replication.

Observations and Results Bhutabhishangaja Ojokshaya100

19) Changes in CD4 count


Table 21
Group - 1

Group 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

590

650

60

412

310

530

220

318

510

700

190

576

460

310

-150

561

320

320

4180

440

510

70

2726

410

310

-100

5050

480

203

-277

2784

520

410

-110

6421

410

430

20

3187

510

590

80

6614

290

320

30

3427

440

320

-120

7187

718

233

-485

3434

440

610

170

8274

580

490

-90

7221

630

580

-50

8275

590

350

-210

4370

4490

4278

3376

4 (44%) increased CD 4 cell count by 60-190, 4 (44%) decreased CD 4 cell count


and 1 (11%) were static in 1st group for CD 4 cell count, 4 (44%) increased CD 4 cell count
by 20-220 and 5 (55%) decreased CD 4 cell count in 2nd group.

Observations and Results Bhutabhishangaja Ojokshaya101

20) Changes in CD8 count


Table 22
Group - 1

Group - 2

OPD

Before

After

Difference

OPD

Before

After

Difference

216

1720

1800

80

412

320

1080

760

318

1030

2380

1350

576

590

390

-200

561

450

450

4180

820

680

-140

2726

430

390

-40

5050

710

899

189

2784

950

500

-450

6421

780

620

-160

3187

1110

1020

-90

6614

340

380

40

3427

540

380

-160

7187

1780

578

-1202

3434

890

2190

1300

8274

1030

840

-190

7221

1610

1420

-190

8275

1300

320

-980

8730

10530

7670

5787

CD 8 cell count: - 5 (55%) decreased, 3 (33%) increase in 1st group, 6 (66%) decreased and
3 (33%) increased in 2nd group,

Ratio of CD4 and CD

8:

- 5 (55%) increased, 3 (33%) decreased, 1, (11%) static in both

groups, This may be due to fast acting drugs, having better bio-availability and perhaps due
to its potent viral action.

Observations and Results Bhutabhishangaja Ojokshaya102

21) Observations on Chronicity


Table 23
Chronicity

Group-1

Group-2

Less Than 1 Year

1-2 Year

Above 2 Year

Total

Out of observations it was found that maximum number of patients appear with the 2
years and above chronicity. Out of two groups together only 4 cases found 1 - 2 years of
history and/or less then one year for 4 patients. It evidential that the disease does not have
any cure but it is only palliative and to be managed with the symptoms presented by the
patient and to attend the patient for the opportunistic or AIDS related complications.
22) Observations on Ojo vyapat lakshana
Table 24
GROUP-1
SL.NO

Symptoms

GROUP-2

Before

After

Before

After

Stabdagatrata

Gurugatrata

Vata Shopha

Varna Hani

Glani

Tandra

Nidra

Observations and Results Bhutabhishangaja Ojokshaya103

23) Observations on Ojo Vishramsha lakshana


Table 25
GROUP-1
SL.NO

GROUP-2

Symptoms

Before

After

Before

After

Gatra Sadana

Doshachavanama

Sandhi Vishlesha

Kriyasannirodha

24) Observations on Ojokshaya lakshana


Table 26
GROUP-1
SL.NO

Symptoms

GROUP-2

Before

After

Before

After

Bhaya

Chinta

Dushchata

Rooksha

Moorcha

Moha

Dourbalya

Vyatitendriya

Durmaan

10

Kshama

11

Mamsakshaya

12

Pralapa

A beneficial clinical out come cannot be expected unless there is an improvement in


status of Ojas. Because Ojas mediates the natural cellular immune response that lowers the
viral load and maintains the CD4 cell count,
Observations and Results Bhutabhishangaja Ojokshaya104

25) Observations on Vata vriddi lakshana


Karsha7 (77%) each, Karshna 6(66%) and 4(44%), Usnakamitwa 7 (77%) and 5 (55%),
Kampa 0% and 1(11%), Anaha 2 (22%) and 4(44%), Shakrit griha 7(77%) and 5 (55%),
Balabramsha3 (33%), Nidra bramsha 0% Pralapa 0%, Bhrama 0%, these symptoms are
seen before treatment in both groups respectively,in group I Karshata in 3 Patients (33%)
Karshnata in 3 (33%) Usnakamitva in 6 are seen after, and sdudy.in groupII ushnakamitva is
senn in 1 (11%) only,
26) Observations on Vata kshaya lakshana
Angasada 6 (66%) and 5 (55%), Alpabhasite Ahita 3 (33%) and 0%, Chesta heenta 2 (22%)
and 1(11%), Vyamoha 4 (44%) and 2 (22%), sleshmavriddi 2 (22%) and 1(11%), these
symptoms are seen before treatment and in group II angasad is seen in only one patient.
27) Observations on Pitta vriddi lakshana
Peeta mootrata, Peetanetrata, Peeta twak, Atikshuda, Atidaha, were not seen in both
groups before treatment,
28) Observations on Pitta kshaya lakshana
Pittakhaya lakshanas are seen as Mandagnin 2 (22%) and 1(11%), Shareerasheetatva 0%
in both groups, and Prabhahani 4 (44%) and 1 (11%), were seen before treatment and
these symptoms are not observed after treatment.
29) Observations on Kapha vriddi lakshana
gnisada 2 (22%) and 3 (33%), Praseka 0% in both groups, Alasya 7 (77%) and 6 (66%),
Gouravata 7 (77%) and 5(55%), Swetangata 1 (11%) and 0%, Sheetangata in both 0%, in
each group Shlatangata 4(44%), Shwasa 2 (22%) and 1(11%), Kasa 7 (77%) and 4 (44%),
Atinidrata 0% in both groups are seen before treatment and these are subsided after
treatment.
Observations and Results Bhutabhishangaja Ojokshaya105

30) Observations on Kapha kshaya lakshana


Bhrama 1(11%) and 3 (33%), Urahshunyata 1 (11%) in each, Shirah shunyata 0% and
1(11%), Hridrava 3 (33%) in each, Sandishitilya 2 (22%) and 5 (55%), these symptoms seen
before treatment and after treatment these are not seen.
31) Assessment of Result
The assessments criteria of the Evaluation of the comparative efficacy of
Ojokalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection) is as follows
Table 27

Total

Result

0
1
1
0
0
1
1
1
0
1
0
0
1
1
1
1
1
0
1
1
1
0
1
0
1
0
1
1
0
1
0
1
1
1
1
0
0
1
1
1
1
1
1
1
0
1
1
1
1
0
1
1
0
1
1
1
1
1
0
1
1
1
1
Group 2 Amritakayakalpa rasayana
1
1
1
1
0
0
1
1
0
1
0
0
1
1
1
1
0
1
0
1
1
1
1
1
0
0
1
0
0
0
1
1
1
1
1
1
1
0
1
1
1
0
0
1
0
1
1
1
0
0
1
0
1
1
1
1
1
0
1
0
1
1
1
1
1
1
0
0
1
1
1
1
Grade
Score range
Best responded
8 to 11
Moderately responded
5 to 8
Responded
2 to 4
Static / Not responded
0&1
BR= Best Responded, MR= Moderately Responded,
R = Responded, S = Static, NR = Not Responded

11.GHC

1
1
0
0
1
1
1
1
1

10.KFS

1
1
0
1
1
1
0
1
1

9.WEIGHT

1
2
3
4
5
6
7
8
9

8.RATIO

1
1
1
0
0
0
0
1
0

7.CD8

0
0
0
0
0
1
1
1
1

6.CD4

3.TLC

0
1
1
0
0
0
0
1
1

5.Platelet
count

2.ESR

1
2
3
4
5
6
7
8
9

4.WBC

1.Hb%

Group 1 Ojokalpa Rasayan

1
1
1
1
1
1
1
1
1

6
7
9
5
6
7
8
9
9

MR
MR
BR
MR
MR
MR
BR
BR
BR

1
1
1
1
1
1
1
1
1

9
8
7
5
10
8
7
9
9

BR
BR
MR
MR
BR
BR
MR
BR
BR

Observations and Results Bhutabhishangaja Ojokshaya106

Assessment Parameter study of group 1


Table 28

No

Parameter

Hemoglobin %

Erythrocyte sedimentation rate

Total leukocyte count

Before
12.0

Mean
S.D
S.E
t-Value
P value
Remarks
Difference
After
10.87
1.9
1.677
0.559
3.398
<0.01 Highly
significant

42.5

41.77

33.0

21.97

7.325

4.505

<0.005 Highly

2041.11

2388.89

652.22

856.3618

285.539

2.284

>0.05 Not

significant
significant
Highly
significant
Highly
significant
Highly
significant

White blood cell count

7.766

6.667

1.722

1.731

0.577

2.984

<0.002

Platelet count

1.793

1.921

0.3711

0.317

0.1056

3.514

<0.001

C.D.4 cell count

485.55

498.89

97.777

59.113

19.704

4.962

<0.005

C.D.8 cell Count

970.00

1170.0

406.66

536.702

178.9

2.273

>0.05 Not

Ratio

0.575

0.562

0.113

0.1017

0.033

3.433

<0.01 Highly

Weight

51.667

53.777

2.111

1.364

0.454

4.649

<0.005

10

Karnofskys performance score

83.333

90.00

6.666

5.00

1.666

4.00

<0.005

11

General health condition

1.444

2.222

0.777

0.440

0.146

5.32

<0.001

significant
significant
Highly
significant
Highly
significant
Highly
significant

Observations and Results Bhutabhishangaja Ojokshaya108

Assessment Parameter study Group 2


Table 29
No

Parameter

Hemoglobin %

Erythrocyte sedimentation rate

Total leukocyte count

Before
11.644

S.D
S.E
t-Value
P value
Remarks
Mean
Difference
After
12.644
1.666
1.414
0.471
3.537
<0.01 Highly
significant
Highly
significant
Highly
significant
Highly
significant
Highly
significant
Highly
significant
Highly
significant

37.066

26.00

17.166

15.862

5.287

3.246

<0.02

2011.11

2079.22

387.44

336.832

112.277

3.450

<0.01

White blood cell count

8.688

7.811

2.011

2.064

0.688

2.922

<0.02

Platelet count

2.225

2.232

0.482

0.474

0.158

3.051

<0.02

C.D.4 cell count

475.333

378.444

172.44

147.317

49.105

3.511

<0.01

C.D.8 cell Count

852.22

676.333

429.00

430.85

143.616

2.987

<0.02

Ratio

0.653

0.686

0.195

0.259

0.086

2.273

>0.05 Not

Weight

55.22

58.222

3.600

1.936

0.645

4.651

<0.005 Highly

10

Karnofskys performance score

84.44

88.888

4.444

5.27

1.756

2.53

<0.05

11

General health condition

1.666

2.222

0777

0.440

0.146

5.32

<0.001

significant
significant
Highly
significant
Highly
significant

Observations and Results Bhutabhishangaja Ojokshaya109

Assessment Parameter Comparative study of Group 1 and 2


Table 30
No

Parameter

Hemoglobin %

Erythrocyte sedimentation rate

Total leukocyte count

White blood cell count

Platelet count

C.D.4 cell count

C.D.8 cell Count

Ratio

Weight

10

Karnofskys performance score

11
General health condition

group

Mean

SD

1
2
1
2
1
2
1
2
1
2
1
2
1
2
1
2
1
2
1
2
1
2

10.877
12.644
41.777
26.00
2388.89
2079.22
6.667
7.811
1.921
2.232
498.89
378.44
1170.00
676.33
0.562
0.686
53.777
58.222
90.00
88.88
2.22
2.22

2.3936
1.6845
23.504
7.071
1362.39
848.85
1.612
1.158
0.567
0.683
157.356
120.112
85.155
275.032
0.234
0.248
6.887
10.133
0.0
3.33
0.66
0726

S.E
0.2659
0.561
7.834
2.357
454.13
282.95
0.537
0.386
0.189
0.227
52.45
40.375
268.38
91.677
0.078
0.0828
2.295
3.377
0.0
1.11
0.22
0.242

P.S.E

t-Value

P value

Remarks
Highly

0.6208

2.846

<0.02 significant

8.18

1.928

>0.05 significant

535.065

0.578

>0.05 significant

0.661

1.73

>0.05 significant

0.295

1.050

>0.05 significant

66.19

1.819

>0.05 significant

283.606

1.74

>0.05 significant

0.113

1.097

>0.05 significant

4.083

1.088

>0.05 significant

1.111

1.00

>0.05 significant

0.328

Not
Not
Not
Not
Not
Not
Not
Not
Not

Observations and Results Bhutabhishangaja Ojokshaya110

32) Statistical assessment of study

The effect of two groups in all parameters are the same there is a highly significant in
HB % when we compared two groups (P < 0.05) and all the after parameters and not
significant (P>0.05).
The group-1 is not significant in TLC and CD8 sell count (P>0.05) and after
parameters shows highly significant in-group II except ratio all the parameters are highly
significant (P>0.05).
Group-1 E.S.R. Platelet counts Kornefsky gradings and CD4 are highly significant
when compared to group 2 (P<0.05 and T values).
The WBC, Weight and General Health Condition are having same effect in both
groups (by comparing P and T values).
The parameter HB%, TLC and CD8 cell counts are highly significant in-group 2
compared with group 1.
Over all there is a more variation in group I.
In-group 2, HB% EWR, TLC, WBC and CD8 are having uniform effect and in group 1
platelet count CD4 and weight are having uninformed effect (by comparing co-efficient of
veriation).

Observations and Results Bhutabhishangaja Ojokshaya111

Result in-group 1
As mentioned that in the Table 27, group-1 has show the results with reference to
the grade declared in the study is as follows. The Best responded group is 4 patients
(44.44%) and moderately responded are of 5 (55.55%) patients. There was no patient who
doesnt respond for the treatment of Ojokalparasayana. Tabulation of group 1 is shown as
under in table-31 and the graphical form is displayed as under in the graph-8.
Table -31
Result category

Patients

Best responded

44.44

Moderately responded

55.56

Responded

Static

Not responded

Graph-8

Responded
0.00%

Moderately
responded
55.56%

Static
0.00%

Not
responded
0.00%

Best
responded
44.44%

Observations and Results Bhutabhishangaja Ojokshaya112

Result in-group 2
As mentioned that in the Table 27 group-1 has show the results with reference to the
grade declared in the study is as follows. The Best responded group is 6 patients (66.66%)
and moderately responded are of 3 (33.33%) patients. There was no patient who doesnt
respond for the treatment of Ojokalparasayana. Tabulation of group 2 is shown as under in
table-32 and the graphical form is displayed as under in the graph-9.
Table 32
Result category

Patients

Best responded

66.67

Moderately responded

33.33

Responded

Static

Not responded

Graph-9

Responded
0.00%

Moderately
responded
33.33%

Static
0.00%

Not
responded
0.00%

Best
responded
66.67%
Observations and Results Bhutabhishangaja Ojokshaya113

Discussion and conclusion


The aim of this study is understand the explanations, scientific background of the
traditional Ayurvedic literature and practices, to give practical guidelines for the Ayurvedic
modalities of treatment and approach to the HIV infected patient. Ayurveda has both
preventive and palliative methods of HIV management, as understood by the general study
of the literature. There are many facts yet to be unearthed. This is possible by profound
knowledge of Ayurveda with channeled efforts to explain the same in the light of modern
scientific knowledge by the way if scientific research on literature, drug efficacy and other
methods of Ayurvedic management.
The staggering worldwide growth of HIV pandemic is matched by the explosion of
information in the area of HIV virology, pathogenesis, and treatment of HIV disease
including the opportunistic infectious associated with it. The information related to HIV
disease is much greater than that for any other infectious disease or immunologic disorder.
It becomes almost impossible for health care personnel, to stay abreast of this literature.
This study deals with the present and most current available information regarding
prevalence of the disease, its pathogenesis, treatment and prevention.
The existence of microorganisms is well documented from the time of Atharva Veda
(5000 BC) and Ayurvedic texts too have vivid description of pathogens. On the country the
scientific community believes that the knowledge of microbiology evolved after 18th century.
The gap between these two periods is a vast one and it is difficult to know why such
knowledge did not grow further from the ancient times. One of the reasons may be because
Ayurveda gave more importance to host factor (Kshetra and Ambu) rather than the
pathogens (Beeja) factor.
Discussion and conclusion - Bhutabhishangaja Ojokshaya114

The second factor may be due to fewer incidences of infectious diseases in those
days. But with the changing times, these are sudden changes in environment due to
industrialization, deforestation, and pollution. Rapid explosion of population led us to usage
of chemical fertilizers, chemical medicines, pesticides, insecticides etc. this brought about a
devastating reduction in nutritional value of food products, human life span (Ayu) resistance
power (Vyadhi Kshamatva), and peace of mind (prasanna atma, indirya manah (is also
severely affected. This has lead to increased susceptibility of human beings, for infectious
diseases associated with emergence of new infectious organisms and their rapid growth.
So it is high time for all Ayurvedic practitioners to make necessary modifications in
their approach to infections diseases, in the light of changing scenario.
HIV is the etiological agent for the newfound immuno deficiency, which came to light
in 1981. This infection spectrum is ranging from primary infection with or without acute
syndrome are a symptomatic stage and to an advanced disease.
Immuno deficiency is refereed to as Ojokshaya in Ayurveda. Ojas is the essence of
sapthadhatus (all the bodily tissues) and it is responsible for vigor and vitality. It is the
protective mechanism against decay and degeneration, any depletion of Ojas can lead to
infection disease and death. There is clear description regarding the depletion of Ojas by
microorganisms. The resultant Ojokshaya also goes for different pathological stages like
microorganisms. The resultant Ojokshaya also goes for different pathological stages like
Ojovishramsha, vyapath and Kshaya. But in the concept of Ojokshaya we do not find a
stage similar to clinical latency. The reasonfor this may be perhaps in those days this
particular type of infections was not found or in those days there use to be a different
immunological response to same infection. Whatever we see as symptoms of Ojokshaya,
they are the general immuno deficiency symptoms.

Discussion and conclusion - Bhutabhishangaja Ojokshaya115

The HIV epidemic has occurred in waves in different regions of world. Each wave
having somewhat different characteristics, depending upon the demographics of the country
and region in question and the timing of the introduction of HIV into the population,
In the large-scale deaths some people used to survive and Acharyas have
recognized this phenomenon as Vyadhi Ksamatva and those died has Ojokshaya as a
predisposing factor.
Discussing the root cause of Janapadodhawamsa, it is said adarma (bad conduct)
is the reason for such fact transmission and fatality. When we analyze the basic cause
behind the origin of this disease and subsequent transmission, we understand bad conduct
of human beings unnatural behavior of man resulted in a disease called HIV infection.
HIV, a virus of green monkey of Africa started infecting human beings. The exact
methodology of this jump is highly debatable. But one this is sure, somewhere, some body
has behaved unnaturally and further spread speaks about the immoral conduct of a big
population of the world.
The transmission scenario of HIV has changed to heterosexual route as a
predominant cause from a homosexual route and intravenous drug use. The change has
been recognized in type of people, sex and their economical background. A disease of men
has infected equal number of women, a disease of cities in commonly seen in small villages,
a disease of rich and ducated is infecting most backward and uneducated population. Sex is
a basic instinct of human beings and the experience says these will not change even when
society doesnt permit is in unnatural means.
Susruta described communicable diseases in kusta chapter of Nidana stana. He has
given prasanga or sexual contact as the main cause of disease transmission. This gives us
an idea about the prevalence of sexually transmitted diseases in ancient period also. But we
do not find the reference of transmission of infection from mother to child, even though there
Discussion and conclusion - Bhutabhishangaja Ojokshaya116

are references about the congenital disorders and role of genetics in occurrence of
diseases. But there is a reference in Ayurveda about transfer of maternal Ojas to the foetus
in intra-uterine life. This is significant observation with regard to vertical transmission.
It is estimated that over 6 million Indians are HIV carriers, WHO and UNAIDS are the
internationally operating organizations, who do research on epidemiology of infection in
India NACO (National AIDS Control Organization) is working on same guidelines since
1987. In 1992 government of India HIV control project along with many N.G.Os.
But all the activities of government and non-governmental organizations involve only
modern medical professionals. Nowhere Ayurvedic doctor is involved in the AIDS control
program. On the contrary, Ayurveda is a popular medical science in India and the
unqualified quacks started exploiting people in the name of Ayurveda. WHO recognized the
importance of Ayurveda 3 decades ago and since then many modern medical professionals
and scientists are doing research on Ayurvedic drugs. But these are scattered ones, and run
by private people. But in most of these researches, there is no involvement of Ayurveidc
scholars. To succeed in developing a framework of Ayurvedic treatment modality, there
should be profound knowledge of Ayurveda along with scientific research methods.
Ojokshaya is not a disease dealt with in Nidanastana or Chikitsa stana of any Samhita. It is
not discussed as and Aristalakshana also rather it is a terminal condition of all debilitating
diseases, which cause death. Acharya Charaka and Susruta dealt in chapters where
general Vriddhi Kshaya Lakshanas of Dosha Dhatu and Mala are discussed. Ojokshaya is
pathological condition associated with kshataja kasa, grahani, jaja yaksma, sannipahaja
jwara raktasha, pandu, grahani, raktaatisara, and shosha, kshayaja kasa, many of which are
infectious diseases.
According Ayurveda, the Ahara (food) Vihara (activities) and Manasika vaikalya
(psychological disorder) are also causes Ojokshaya. Alpashana (malnutrition), Anasana
Discussion and conclusion - Bhutabhishangaja Ojokshaya117

(starvation) are said to be nutritional factors, which directly effect the bodys, defense
mechanism, against infection. In the modern parlance, it is a well-understood fact that
malnutrition is a common cause of immuno deficiency, because protein takes part in the
formation of antibodies. In Vihara (physical activities) Vatatapa sevana (exposing to wind
blow and hot sun) associated with Ativyayama (excessive work) lead to Ojokshaya. Extreme
heat and blows of wind cause severe exhaustion, which leads to immuno deficiency in long
run. This also speaks about the socioeconomic conditions of said population, which is
susceptible to this kind of Ojokshaya. The next cause, Ativyavaya or excessive indulgence
in sex is also a cause for Ojokshaya. Here modern medical understanding differs.
According to Ayurveda, Kshaya (emaciation) can result by two ways. The first type is
anulomakshaya second one pratiloma kshaya. Anulomakshaya is caused due to
malnutrition in which bodily tissues from Rasa, Rakta, Mamsa progressively undergo
depletion this is caused due to anashana, alpasana, vatatapa sevana type of causes.
Pratiloma kshaya is caused due to shukra kshaya (depletion of shukra dhatu) due to over
indulgence in sex. This is a reverse or opposite type of depletion of bodily tissues. According
to this principle loss of Shukra causes immuno deficiency and modern science doesnt relate
sex and immuno deficiency. Rather there are studies, which revel that sex does immuno
modulation. For this reason, ayurveda explains seasonal sexual schedule where as modern
science does not believe in this. This ayurveda has recognized brahmacharya (celibacy) as
one of the sub-pillars of the life where as modern science does not attach any importance to
celibacy in sustaining life.
Prajagara (sleeplessness) has been considered as a cause of Ojokshaya. Modern
science also believes in this and a good sleep increases ones immunity.
The next set of causes is manasika karanas (Psychological reason). They are kopa
(anger), shoka (grief), chinta (worry) and bhaya (phobia). In modern pariance the new
Discussion and conclusion - Bhutabhishangaja Ojokshaya118

branch of medicine, i.e. psycho-neuro-imunology speaks about the role of psychological


causes like stress etc, as causative factors for immunodeficiency. It is also proved that CD4
count depletes under stressful conditions and increases by meditation, chanting mantras.
Susruta explains about abhigata or injury as a cause of Ojokshaya. If we look it in
modern angle, apart from the tissue loss in injury, there is a scope or increased susceptibility
for infection after an injury. Very specifically an injury in sexual organs or anus is a high risk
factor for transmission of HIV infection.
When we a serve the signs and symptoms of Ojokshaya we lot of similarities in both
systems of medicine. Charaka does not explain the signs and symptoms of Ojokshaya,
whereas Susruta then explained different stages of Ojokshaya. The descriptions of Susruta
are more elaborate in this regard. He has classified the Ojovikruthi is in three stages as
vishramsha as a direct loss, vyapat as a vitiation, and Kshaya as depletion. But Charaka
has summarized them in one condition Ojokshaya and we dont get the advancing stages
of diseases. The symptomatologies given here are not in order, but marana or death
comes at the end.
When we see the modern classification of HIV disease there are 4 stages of HIV
infection, which results in death at the end. The first stage is primary infection or acute seroconversion stage. This happens after the primary infection followed by an incubation period
of 2-6 weeks in which 50% of individual feels acute viral syndrome characterized by high
fever, lymph adenopathy, myalgia etc. this lasts for 1-2 weeks, not responding to any line of
treatment. This is usually the uninvestigated phase of HIV infection. In many individuals this
stage may go unnoticed. During this phase there will be sever CD4 lymphopaenia. This
particular stage of HIV infection can not be correlated to the stages of Ojokshaya. This can
be correlated to sannipatika type of jwara, in which there will be a sudden depletion in Ojas,
which is limited to Ojo-visramsa. At this stage body repairs on its own with the help of Kapha
Discussion and conclusion - Bhutabhishangaja Ojokshaya119

(Bala), and this results in to the temporary reduction in Ojo-visramsa Lakshanas. But
because virus survives and camouflages, it enters in to chronic phase of infection and the
slow damage of Ojas continues.
In the II stage of HIV infection there will be occasional symptoms of fever, loss of
appetite, loss of body weight, asthenia, diarrhoea, cough etc. this stage can be compared to
Ojovishramsha stage with special reference to the sequence of symptomatology explained
in sannipataja Jwara where there ill be interns of limbs, chills, looseness of limbs, low grade
fever, body pain etc. it may not be as severe as a acute phase of sunnipathaja Jwara.
In the stage of III of HIV infection along with the above mentioned symptoms there
will be further immuno deficiency due to which many opportunistic infections like herpes
simplex, herpes zooster, oral Candidiasis, tuberculosis, hairy leukoplakia.
In second stage of Ojovikriti natural properties of Ojas under the influence of vitiated
Doshas goes for vyapath phase chih given rise to stabha gurugatrata, vatasopha,
varnabedha, glani, tandra and nidra

228

. Even though there is no mention of opportunistic

infection in Ojovyapat the symptomatology resembles as infectious conditions leading to


coma.
In the last stage of HIV infection there are, many neurological symptoms like
dementia and altered personality, convulsion, ataxia, visual impairment, neurologicval
deficits, hemiplegia followed by death. In Ojokshaya (3rd stage) there will be moorcha (loss
of consciousness) mamasakshaya (wasting of muscies) moha (stupor) Pralapa (delirium)
and vyathithendriyata (loss of motor and sensory perception) followed by marana (death)
this is in the strict sense of Susrutas classification of Ojokshaya stages.
None of the classics described the exact Samprapti of Ojokshaya. Regarding the
Samprapti of Ojokshaya, there are two different methodologies explained in different
contexts. The Ojokshaya occurred due to general causes apart from infection and that
Discussion and conclusion - Bhutabhishangaja Ojokshaya120

caused due to infection are of two different Samprapti. The description about general
Samprapti can be summarized as sited by Charaka in madhumeha

229

and panduroga

230

Vitiated Doshas (either Vata or Pitta) vitiate Dhatus, which later loose integrity and get
depleted and subsequently results in depletion of Ojas. This is also called as
Anulomakshaya. The autoimmune mechanism resembles this type of Ojovikriti. The
Samprapti of Ojokshaya caused by infection can be summarized with the available
references in the context of Rajayakshma

231

and Sannipata Jwara

232

. Here in the

individuals who have basic susceptibility for infection, when get infected due to already
discussed causes, get Bhootopaghata a damage of cells (carrying CD4 makers) followed by
abhishanga (penetration) and entry of viral materiel into the cell. This foreign toxic material
works like jangama visha (poison of animal origin) 233, but as virus is a live matter with RNA
genome instead of causing immediate death if replicates here getting sustenance from
bodily cells. Those cells where virus replicates become reservoirs of virus. This virus is
capable of causing srothorodha, raktadi Dhatu Kshaya. Due to the lowered functioning of
dhatwagni resulting inAma and apachaya (catabolic activity) due to the deficiency of
nutrition, which further leads of Ojokshaya 234.
The Ama so formed causes further Vata Vriddhi associated with Vikrita Pitta leads to
sannipathika Jwara. Vitiated Vata and Pitta cause damage to Dhatu vaha srotamsi and this
leads to Ojo-visramsa, vypth and Kshaya in due course of time. So in this way pathological
events following bhootopaghata correlate with modern understanding of HIV infection.
Sadhyasadhayata
Susruta has clearly said the Ojovishramasha and vyapth can be managed by
rasayana and vajeekarana Chikitsa along with appropriate diet, which increases Bala and
antagonistic to the causative factors of Ojokshaya

235

. Further it is said, as Ojokshaya will

not be reversed with rasayana or Vajikarana Chikitsa. The prognosis of diseases as


Discussion and conclusion - Bhutabhishangaja Ojokshaya121

explained in Ayurveda and modern science are similar as the early stages of HIV infection
can be managed with antiviral and immuno modulators and advanced stage will not improve
with any available treatment.
Chikitsa sutra
General management of Ojokshaya is by rasayana and Vajikarana, which are
Ojokara in nature

236

. But the management of Ojokshaya caused by infection needs an

additional line of treatment, which can be developed on the basis of Krimi Chikitsa an
explained in Charaka Vimana 7th chapter. Among 3 major principles of Krimi Chikitsa, the
prakriti vighata type suits the present context of HIV infection. This can be achieved by
usage of drugs having Krimi prakriti vagata property.
The Selection of drugs
Keeping the Samprapti of Ojokshaya in mind, there is a need for both Ojoskara
(immuno-stimulant) and Krimigna (anti-viral) and protecting and cures for the Aids related
complications along with potent action. The conceptualization of ideal drug should also
involved drugs having faster action and better cell penetration capacity. An attempt is made
in the formulation of Ojokalparasayana for the management of the HIV infection. The main
ingredients are Bilva, Tulashi, Haridra, Daru haridra, Devadaru, Trikatu, Triphala, Karanja,
Tagara. To get additive values and fortify the drug action Vidanga and Agnikumara vati. The
vidanga is krimighna and Agnikumara vati is anti-pyrexial. Ajamootra is used as Bhavana
dravya for the bilwadivati as directed in the text. The composition of Agni kumar vati is
Kusta, Vacha, Musta, Vatsanabha, Maricha. Therapeutic effect of Agni kumar vati is
jwarahara, Atisara shamaka and also prevents and cures upper respiratory tract infections.
Another drug undertaken for the comparison is Amruta kayakalpa Rasayana
established immuno-modulator, manufactured by a well-known company Amruta Herbs,
Hyderabad.
Discussion and conclusion - Bhutabhishangaja Ojokshaya122

Plan of the study


In this study a total is 9 patients each in two groups were included out of 26 cases
reported during this period for comparative clinical trial.
For the general analysis of overall condition of the subject, all the subjects were
investigated for hemoglobin percentage, Erythrocyte Sedimentation Rate. A total count was
carried out because of financial constraints. Instead CD4 and CD8 along with peripheral
lymphocyte and platelet counts are taken as surrogate makers of the immuno status. This is
in tune with internationally practiced research parameters.
All

the

patients

have

undergone

these

investigations

before

starting

Ojokalparasayana and Amruta kayakalparasayana that to soon after the completion of four
months schedule.
The effect of both Ojokalparasayana and Amruta kayakalparasayana on each of the
parameters was assessed with base line data. The Ayurvedic assessment was done with
detailed clinical analysis of Dosha status and Ojas status on the basis presenting symptoms
using darshana sparshana and prasna methodology. This was done before and soon after
completion of both trials on both compounds.
General observations
From the initial inclusion of 26 patients, 8 patients dropped out during the study. Due
to the decision by these patients to take medicine from a so-called AIDS specialist who had
released and advertisement in local newspaper, claiming a cure of HIV disease.
Maximum number patients in this study are men and male verses female ratio is 2:1.
This is contradictory to the Indian data sex incidence. Which 1:1 this various can be due to
the male dominance in the local society with rural and illiteracy background,
22% Muslim patients in the study may be due to religion ratio of local population and
there is a study that claims less incidence of sexually transmitted disease in subjects who
under went circumcision 237.
Discussion and conclusion - Bhutabhishangaja Ojokshaya123

The maximum patients were in middle class 55% followed by poor 33%, and 11% in
higher middle class reflect the socioeconomic status of the particular area. It also reflects the
easy acceptance of free treatment of middle class and poor class.
It is interesting to note that not even a single vegetarian subject was seen in this
study. As Ayurvedic concepts talk about the role of predisposing factors, there must be a
physiological or psychological impact of non-vegetarian food that may be having a role to
play in high incidence of HIV among non-vegetarians populations.
Coming to the study related to disease, maximum number of patients (100%) got the
infection from heterosexual contact. This data coincides with the international data.
Even though the incidence changes are more among the patients who got it from
blood transmission and intra-venous drug intake, but more patients got it from heterosexual
contact only. This clearly shows the high rate of unsafe heterosexual practices in our society
population.
Aids stages
Stages of HIV infection are well understood. It is a proven fact that HIV causes AIDS
and AIDS related complex. The mathematical and statically evaluated is often used to
explain the biological phenomena, through the years of studying the HIVI disease. The
investigation of CD4 and CD8 cells along with lymphocyte count is very much helpful in the
prediction of stages of HIV infection. CD4 count cell is a surrogate marker of immunodeficiency because lower HIV RNA level and higher CD4 cell counts correlates with long
time survivors in both adult and children

238.

In this study maximum patients were in early

symptomatic stage 0% in-group I and group II respectively followed by 88% in second stage
at both groups.

Discussion and conclusion - Bhutabhishangaja Ojokshaya124

Efficacy of Ojokalpa Rasayana


Ojokalpa Rasayana is said with so many cumulative properties with respect to the
ingredients included in it. Thus the properties are classified according to the Srotas in the
Ayurveda is as follows.
As Rasayana
Amalaki, Haritaki, Daruhariudra, Pippali, kusta and Vatsanabha are well-established
Rasayana dravyas in Ayurveda. These drugs act through rasadi dhatu ayanam i.e.
nourishing and fortifying the structural and functional aspect of individual tissue materials in
the body.
As Ama hara
Ama is one of the components of Vyadhi Samprapti. Thus Samprapti vighatana is
essential through Ama hara dravya. Ama in comparison as free radicals flown in blood to be
retarded and regulated otherwise they pretend the normal and unregulated functions in the
body. Thus the Ama hara dravyas are used in this combination are Devadaru, Shunti and
Hareetaki.
Some of the properties elicited by the pharmacologists are furnished here under.
As antioxident - Amalaki, Shunti and Haritaki
Anti tubercular - Pippali, Karanja and Vacha
Anti bacterial -Amalaki, vibhitaki, Karanja, Musta, Maricha and Haritaki
Anti fungal - Haritaki. Vibhitaki and Karanja
Pranavaha Srotas
Many patients repeatedly reported with the upper respiratory tract infections and in
late stages with the Tuberculosis (Rajayakshama). Tulasi, Devadaru, Shunit, Maricha,
Pippali, Amalaki, Haritaki, Vibhitaki, Karanja, Kusta and Vatsanabha combat these

Discussion and conclusion - Bhutabhishangaja Ojokshaya125

symptoms with the herbs in the composition. The bhavana dravya, Aja mutra is also a best
component to relieve dyspnoeas.
Annavaha Srotas:
Almost all dravyas have deepana and pachana effect, which makes sence to the
concept Agni Chikitsa is the modality management in the Ayurveda. Bilwa, Haridra,
Daruharidra, Shunti and Musta are reported with the Deepana and Pachana effect.
Main symptoms from the gastro-intestinal tract commonly reported are nausea and vomiting.
This is controlled with the Shunti, Pippali and Vibhitaki.
Pureeshavaha Srotas
Diarrhea is common symptom managed by the composition such as Bilwa, Tulasi,
Devadaru, Shunti, Vibhitaki, Musta and Haridra. All other conditions which develop from this
Srotas is also managed.
Rasavaha Srotas
Bilwa, Haridra, Daru haridra, Shunti, Pipplai, Kusta, Vatsanabha and Musta are the
best alliterative and anti pyrexial herbs included in the combination. These herbs not only
anti-pyrexial but also assists to potentiate the rasavaha sroto moola.
Raktavaha Srotas
Commonly observed skin conditions revile the inclusion of skin and its importance in
HIV infectious conditions. Few drugs included in the combination for the prevention and
curative aspect are Amalaki, Haritaki, Tulasi, Maricha, Vatsanabha, Karanja, Kusta,
Daruharidra, Shunti and Ajamutra.
Anemia (Pandu) is commonest complaint. Thus Haridra, Daru Haridra, Shunti and
Ajamutra are added to supplement the deficiencies in the formation of blood.

Discussion and conclusion - Bhutabhishangaja Ojokshaya126

Statistical evaluation
The clinical evaluation of Ojokalparasayana and Amruta kayakalparasayana was
conducted in 18 cases of Ojokshaya in two different groups due to the HIV infection. The
over all response is significant (P<0.001) in both subjective and parameters.
The effect of two groups in all parameters are the same there is a highly significant in
HB % when we compared two groups (P < 0.05) and all the after parameters and not
significant (P>0.05).
Recommendations for further study:
The following recommendations are made on the basis of the observations
made for further studies as well as to observe the limitations.
(a) Same yoga can be repeated by taking a large number of samples with
randomized control groups.
(b) The effect of Ojokalpa Rasayana can be studied along with Shodhana
therapy or individually as Bilwadivati and Agnikumara vati.
(c) The effect of Ojokalpa Rasayana can be studied on long duration to
evaluate its efficacy as antiretroviral therapy along with viral load
studies.
Limitations of the study:
Sample size is small to generalize the result.
Samples are selected incidentally.

As chosen drug is a compound form it is difficult to specify the action


of any individual herb and or to cumulative mode of action.

Discussion and conclusion - Bhutabhishangaja Ojokshaya127

Conclusion
AIDS is a multi dimensional disease syndrome, affecting physical, mental,
social and spiritual facets of the affected person.
The virus HIV hampers the Immune system. At the same time there is no
specific treatment available for the AIDS /HIV infection.
Susruta explains about abhigata or injury as a cause of Ojokshaya. Very
specifically an injury in sexual organs or anus is a high risk factor for
transmission of HIV infection.
The Ojokshaya occurred due to general causes apart from infection and
that caused due to infection are of two different Samprapti. So in this way
pathological events following bhootopaghata correlate with modern
understanding of HIV infection.
The prognosis of diseases as explained in Ayurveda and modern science
are similar as the early stages of HIV infection can be managed with
antiviral and immuno modulators and advanced stage will not improve
with any available treatment.
Among 3 major principles of Krimi Chikitsa, the prakriti vighata type suits
the present context of HIV infection.
In other words the management is
As antioxident - Amalaki, Shunti and Haritaki
Anti tubercular - Pippali, Karanja and Vacha
Anti bacterial -Amalaki, vibhitaki, Karanja, Musta, Maricha and
Haritaki
Anti fungal - Haritaki. Vibhitaki and Karanja

Discussion and conclusion - Bhutabhishangaja Ojokshaya128

The normal healthy state of such a body requires normalcy of several


factors. This normal strength in the body is called as Sleshma, which has
synonym -Ojas.

Ojas depends upon healthy state of Kapha. Kapha in physiologically


represents potential sours of strength and resistance to disease and
decay of Bala and Ojas.

HIV is transmitted by homosexual and heterosexual contact.


Transfusions of whole blood, packed red blood cells, platelets,
leukocytes, and plasma are all capable of transmitting HIV infection. It is
estimated that 90 to 100% individuals who were transfused with HIVinfected blood became infected.
Opportunistic infections are late complications of HIV infection, for the
most part occurring in patients with less than 200 CD4+T cells per micro
liter. Opportunistic infections are the leading cause of morbidity and
mortality in-patients with HIV infection.
This infection spectrum is ranging from primary infection with or without
acute syndrome are a symptomatic stage and to an advanced disease.
The Bhutabhighataja Ojokshaya is a syndrome, which is almost,
resembles the disease AIDS.
Etiological factors for the Bhutabhighataja Ojokshaya and AIDS are the
same.
The Ojokapla Rasayana found effective in Bhutabhighataja Ojokshaya i.e.
HIV+ve cases.

Discussion and conclusion - Bhutabhishangaja Ojokshaya129

The effect of two groups in all parameters are the same there is a highly
significant in HB% when we compared two groups (P < 0.05) and all the
after parameters and not significant (P>0.05).
The Ojokapla Rasayana group is not significant in TLC and CD8 sell
count (P>0.05) and after parameters shows highly significant in Amruta
Kayakalpa Rasayana group except ratio all the parameters are highly
significant (P>0.05).
Ojokapla Rasayana group E.S.R. Platelet counts Kornefsky gradings and
CD4 are highly significant when compared to Amruta Kayakalpa
Rasayana group (P<0.05 and T values).
The WBC, Weight and General Health Condition are having same effect
in both groups (by comparing P and T values).
The parameter HB%, TLC and CD8 cell counts are highly significant
Amruta Kayakalpa Rasayana group compared with Ojokapla Rasayana
group.
Over all there is a more variation in Ojokapla Rasayana group.
Amruta Kayakalpa Rasayana group, HB% EWR, TLC, WBC and CD8 are
having uniform effect and in Ojokapla Rasayana group platelet count CD4
and weight are having uninformed effect (by comparing co-efficient of
variation).

Discussion and conclusion - Bhutabhishangaja Ojokshaya130

Summary
Among them since two decades sudden emerge of new epidemics such as SARS and
AIDS/HIV, termed in Ayurveda as Bhootopaghataja Ojokshaya.
The etymology of words, Bhoota and Upaghata developed form the word Bhootopaghata
is, Bhoota denotes as Krimi or Virus and Upaghata means as infection. So exclusively
the word Bhootopaghata indicates as viral infection.
In 1983, Human Immuno Deficiency Virus (HIV) was isolated from a patient with lymphadenopathy.
HIV-infected individuals are presenting in increasing numbers to family physicians,
obstetricians, gynecologists, pediatricians and surgeons with clinical problems that may
be directly or indirectly related to their HIV-infection.
When we analyze the basic cause behind the origin of this disease and subsequent
transmission, we understand bad conduct of human beings unnatural behavior of man
resulted in a disease called HIV infection.
As of now an estimated 4-6 million HIV infected cases are present in India.
The first case of HIV infection was identified in India in 1986 at Chennai.
AIDS is a multi dimensional disease syndrome, affecting physical, mental, social and
spiritual facets of the affected person.
The virus HIV hampers the Immune system. At the same time there is no specific
treatment available for the AIDS /HIV infection.
Susruta explains about abhigata or injury as a cause of Ojokshaya. Very specifically an
injury in sexual organs or anus is a high risk factor for transmission of HIV infection.

Summary - Bhootopaghataja Ojokshaya131

Charaka does not explain the signs and symptoms of Ojokshaya, whereas Susruta then
explained different stages of Ojokshaya.
When we see the modern classification of HIV disease there are 4 stages of HIV
infection, which results in death at the end.
The first stage is primary infection or acute sero-conversion stage. This particular stage
of HIV infection can not be correlated to the stages of Ojokshaya.
The Ojokshaya occurred due to general causes apart from infection and that caused due
to infection are of two different Samprapti. So in this way pathological events following
bhootopaghata correlate with modern understanding of HIV infection.
The prognosis of diseases as explained in Ayurveda and modern science are similar as
the early stages of HIV infection can be managed with antiviral and immuno modulators
and advanced stage will not improve with any available treatment.
Among 3 major principles of Krimi Chikitsa, the prakriti vighata type suits the present
context of HIV infection.
In other words the management is
As antioxident - Amalaki, Shunti and Haritaki
Anti tubercular - Pippali, Karanja and Vacha
Anti bacterial -Amalaki, vibhitaki, Karanja, Musta, Maricha and Haritaki
Anti fungal - Haritaki. Vibhitaki and Karanja
Recent advances in medical treatment have given scientists renewed strength in the
struggle against HIV-the virus that causes AIDS.
AZT inhibits reverse transcription, which is vital for HIV to infect its host. AZT and DDI
will stop this from occurring and thus stop the HIV virus from spreading.
Those cells include the immune system cells, blood cells, and the nervous system cells.
It has been found that HIV only infects cells with CD4.
Summary - Bhootopaghataja Ojokshaya132

The vaccine in Evaluation of an HIV-1 DNA Vaccine Encoding a Modified Gag-Pol in


Uninfected Adult Volunteers (Grace Kelly, RN) trial, VRC 4302, is classified as a genetic
vaccine. Genetic vaccines contain the genes (hereditary material) which direct the
production of the proteins of the HIV irus. VRC 4302 contains the gene for the Gag and
Pol proteins of HIV.
Present study is a comparative study to assess two Ayurvedic combinations of immune
builders, Immuno-modulators and acts on Ojovikruti by preventing ARC.
This dissertation reviews literary review of Ojokshaya and HIV infection in comparison
The normal healthy state of such a body requires normalcy of several factors. This
normal strength in the body is called as Sleshma, which has synonym -Ojas.

Ojas depends upon healthy state of Kapha. Kapha in physiologically represents potential
sours of strength and resistance to disease and decay of Bala and Ojas.

Ojas is the Sara i.e. essence of all Dhatus.


Ojas is present all over the body and in each cell of the body.

It is of two varieties Para Ojas and Apara Ojas.


The term Ojas has been stated in Ayurvedic classics represents Kapha, Bala, Shleshma,
Rasa and Rakta and it resists disease and decay in further Promotes durability,
(preserves the body from decay)
Charaka has mentioned that the Ojas is the Ahara for rakshas and if they consume the
Ojas, which leads to depletion of Ojas.
Specific resistance to the disease is called Immunity.
Four different varieties of T cells have been identified: helper / inducer T cells
suppressor T cells, cytotoxic T cells (which are also known as effectors T cells or killer
cells), and memory T cells.

Summary - Bhootopaghataja Ojokshaya133

Antigens can also be processed and presented to T4 cells by various types of cells in
the body in addition to macrophages. The other types of antigen presenting cells include
the B cells themselves, the Langerahans cells of the skin, and specialized cells called
dendritic cells in the lymph nods and spleen.
T8 cells mediate cellular immunity. The cytotoxic T cells attack and destroy cells that
have antigen, which activated them. To ensure maximal specific T cells response the
antigen is linked to molecular components of the HLA system (by B cells, dendritic cells
and macrophages) and presented to T cell.
Cytotoxic T cells cause antigen-specific lyses by direct cell-to-cell contact.
Any HIV-infected individual with CD4+T cell count of<200/microliter had AIDS by
definition, regardless of the presence of symptoms or opportunistic diseases.
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.
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-1 comprises
several subtypes with different geographic distribution.
HIV is free from live, when it is out side the body. HIV has a number of mechanisms to
evade elimination by the immune system.
HIV-1 and HIV-2 are both viruses that belong to the same family, but vary in genetic
make up. Both HIV-1 and HIV-2 have been detected in India and both leads to AIDS.
However studies of lymphoid tissue using PCR analysis for HIV RNA and in site
hybridization for individual virus expressing cells clearly demonstrated that HIV
replication occurs throughout the course of HIV infection, even during clinical latency.

Summary - Bhootopaghataja Ojokshaya134

The availability of sensitive PCR techniques leads to the demonstration that viremia
present at all stages of HIV disease.
HIV is transmitted by homosexual and heterosexual contact.
Transfusions of whole blood, packed red blood cells, platelets, leukocytes, and plasma
are all capable of transmitting HIV infection. It is estimated that 90 to 100% individuals
who were transfused with HIV-infected blood became infected.
HIV has been demonstrated in seminal fluid both within infected mononuclear cells and
in the cell free state. There is a strong association of transmission of HIV with receptive
intercourse.
HIV infection can be transmitted from an infected mother to her fetus during pregnancy
or during delivery.
HIV is an RNA virus whose hallmark is the reverse transcription of its genomic RNA to
DNA by the enzyme reverse transcriptase. Life cycle of HIV infection
Opportunistic infections are late complications of HIV infection, for the most part
occurring in patients with less than 200 CD4+T cells per micro liter. Opportunistic
infections are the leading cause of morbidity and mortality in-patients with HIV infection.
Approximately 80% of AIDS patients die as direct result of an infection other than HIV,
with bacterial infections heading the list.
Tuberculosis is a particularly important problem with HIV infection. Tuberculosis may be
the earliest clinical sign of HIV infection. Disseminated disease is more common with low
CD4+T cell counts.
The diagnosis of HIV infection depends on the demonstration of antibodies to HIV and or
the direct detection of HIV or one of its components. The standard screening test for HIV
is the enzyme linked immuno sorbent assay (ELISA).

Summary - Bhootopaghataja Ojokshaya135

Patients with CD4+T cell counts below 200/ul are at high risk of infection with
preumocytis carini, while patients with CD4+T cell counts below 100/microliter are at high
risk of infection with cytomegalovirus and mycobacterium avium-intracellular complex.
The cornerstone of medical management of HIV infection is antiretroviral therapy.
Suppression of HIV replication is an important component in prolonging life.
Accelerated weight loss in an HIV infected patient is sign of disease progression.
Prevention of STDs would also reduce the risk of HIV transmission.
By running public awareness campaigns for HIV
T. Chelaula inhibited HIV-1 proteas activity at a concentration of 25 microg/ml in the
flurogenic assay.
The HIV-1 protease (PR) inhibitory activity was determined by using the fruit peal
methanol extract of Vibhitaki.
Objectives of the study
To evaluate the efficacy of Ojokalpa Rasayana and Amrut Kayakalpa Rasayana in
improving the clinical status of Ojokshaya with special reference to HIV infection
To assess the role Ojokalpa Rasayana and Amrut Kayakalpa Rasayana on CD4 cell
count, which is a marker of stages of the HIV infection along with viral load.
Drug: Ojokalpa Rasayana
General health condition (Grade), Karnofsky performance score, Body weight, Total
WBC count, Total count platelets, Total count lymphocytes, Erythrocytes sedimentation
rate, CD4 cell count, CD8 cell count and CD4: CD8 ratio are elicited in the patients
before and after the treatment.
This infection spectrum is ranging from primary infection with or without acute syndrome
are a symptomatic stage and to an advanced disease.

Summary - Bhootopaghataja Ojokshaya136

1. http://www.aidsnyc.org/network/trials/hiv.html
2. Charaka Samhita sutra 8/20-24
3. Susruta Samhita sutra 15/41
4. Charaka Samhita Shareera 6/3
5. Charaka Samhita sutra 17/117
6. Charaka Samhita sutra 30/9-11
7. Charaka Samhita Shareera 6/4
8. Susruta Samhita Sutra 15/41
9. Charaka Samhita Sutra 17/117
10. Charaka Samhita Sutra 30/9-11
11. Charaka Samhita Sutra 11/36
12. Charaka Samhita Sutra 28/7
13. Susruta Samhita Sutra 15/23.
14. Sanskrit-English Shabdakosha.
15. Viadhika Shabda Sindhu.
16. Astanga Hrudaya Sutra 11/37, Charaka Samhita Sutra 30/9-11.
17. Astanga Hrudaya Sutra 11/37
18. Charaka Samhita Sutra 17/75
19. Astanga Hrudaya Sutra 17/38
20. Charaka Samhita Sutra 17/74
21. Sharangadhara Samhita Purvakhanda 5/18 Gangadhara and Chakrapani (Charaka
Samhita Sutra 17/76)
22. Charaka Samhita Chikitsa 3/167, Susruta Samhita Sutra 15/20, Charaka Samhita
Soo 30/9, Astanga Hrudaya Sutra 11/37, indu
23. Susruta Samhita Soo15/21,
24. Charaka Samhita Chi24/31
25. Charaka Samhita Chi24/31,
26. Susruta Samhita Sutra 15/21, Charaka Samhita Chi24/31
27. Charaka Samhita Chi24/31
28. Susruta Samhita Sutra 15/21
29. Susruta Samhita Sutra 15/21, Charaka Samhita Chi24/31
30. Susruta Samhita Sutra 15/21,
31. Susruta Samhita Sutra 15/21
32. Susruta Samhita Sutra 15/21
33. Charaka Samhita Chikitsa 24/31,,
34. Charaka Samhita Chikitsa 24/31
I

Reference Bhutabhishanga Ojokshaya

35. Charaka Samhita Nidana 4/37


36. Charaka Samhita Sutra 17/75
37. Astanga Hrudaya Sutra 11/38,
38. Charaka Samhita Sutra 28/4
39. Charaka Samhita Sutra 30/7
40. Charaka Samhita Shareera 7/15, Charaka Samhita Sutra 30/9-11.
41. Susruta Samhita Sutra 15/22.
42. Charaka Samhita Sutra 30/8.
43. Charaka Samhita Shareera 7/15
44. Astanga Hrudaya Sutra 11/37
45. Astanga Hrudaya Sutra 1/95
46. Susruta Samhita Sutra 15/19, and 24 Sharangadhara Samhita Purvakhanda 15/18
47. Charaka Samhita Sutra 12/12, Susruta Samhita Sutra 15/4, 21/8, Astanga Hrudaya
11/3
48. Kasyapa Samhita Sutra 27/15-17.
49. Susruta Samhita Sutra 15/23.
50. Susruta Samhita Sutra 15/24
51. Charaka Samhita Sutra 17/73, Susruta Samhita Nidana 5/34, Astanga Hrudaya Sutra
11/39-40.
52. Charaka Samhita Shareera2/10
53. Vedonme Ayurveda
54. Susruta Samhita Uttara 39/41
55. Charaka Samhita Nidana 4/32,
56. Charaka Samhita Chikitsa 6/5
57. Susruta Samhita Uttara 39/41
58. Susruta Samhita Uttara 39/41, Charaka Samhita Nidana 4/32, Charaka Samhita
Chikitsa 6/5
59. Susruta Samhita Uttara 39/41
60. Bhaishajya Ratnavali Prameha Chikitsa
61. Charaka Samhita Nidana 4/37
62. Introduction to Kayachikitsa 258-259
63. Susruta Samhita Sutra 15/24
64. Charaka Samhita Sutra 11/36
65. Susruta Samhita Sutra 6/2
66. Charaka Samhita Sutra 11/25
67. Susruta Samhita Sutra 15/19
II

Reference Bhutabhishanga Ojokshaya

68. Susruta Samhita Sutra 2/14, Astanga Hrudaya 12/15.


69. Astanga Hrudaya 11/3
70. Charaka Samhita Sutra 28/7
71. Susruta Samhita Uttara 39/43-45
72. Kashyapa Samhita sutra 27/16
73. Charaka Samhita P.V.pp 269.
74. Charaka Samhita Sutra 17/73-78
75. Susruta Samhita Sutra Uttara 40
76. Vaidya madhava
77. Charaka Samhita Chikitsa 16
78. Bhava Prakasha Susruta Samhita Sutra- 46,Charaka Samhita Sutra 25
79. Marmelosin showed anthelmintic activity against ankylostomiasis (Lamba and
Bhargeva. 1969).
80. 1 Effect of Bael fruit in amoebiasis is reported (Verma, B.H.U., 1977.
81. Tupe, Ahmedanagar, 1992
82. Chandak, Nashik, 1986; Meshram, Raipur, 1996; Acharya, BHU, 1980; Desai V.G.
Bombay, 1927
83. Singh and Chatrurredi, 1981.
84. Bhava Prakasha, Charaka Samhita Sutra 27, Susruta Samhita Sutra 46
85. Bhava Prakasha, Dhanvantari Nighantu
86. Rasa Ratna Samuchaya
87. Vaidya Madhava and Bhava Prakasha
88. Susruta Samhita Chikista11
89. Ramaprasad and Sirsi, 1956, 1957a
90. Mukherjee et al, 1961
91. Basu, 1971.
92. Sinha et al., 1972
93. Tripathi et al., 1973
94. 71 cases of bronchitis, 13 cases of bronchiectasis, 18, cases of bronchial asthma
and 12 cases of tropical eosinophilia.
95. Katare, 1974
96. Anto R.J. et al., 1992
97. Dhanvantari Nighantu, Bhava Prakasha
98. Bhava Prakasha, Dhanvantari Nighantu, Susruta Samhita Sutra -45, Charaka
Samhita Chi-17
99. Astanga Hrudaya Chikitsa 3
III

Reference Bhutabhishanga Ojokshaya

100.

Susruta Samhita Chikitsa 23

101.

Dhar et al., 1968.

102.

Bhava Prakasha, Susruta Samhita Sutra 46, Ch Soo27, Vrind, Sho.

103.

Bhava Prakasha

104.

Susruta Samhita Uttara 24

105.

Susruta Samhita Chikitsa.6

106.

Bhava Prakasha

107.

Sharma and Singh, 1980.

108.

Ind. J. Pharmacol. 5:334, 1973

109.

Gugnani and Ezenwanze, 1985

110.

Miki et al., 1985

111.

Nanda et al., 1985.

112.

Huang et al., 1990

113.

Mustafa and Srivastava 1990

114.

Qian and Liu, 1992

115.

Nanda et al., 1993

116.

Limyati et al., 1994

117.

Usha and Saroja, 2000-2001

118.

Bandyopadhaya, 2001

119.

S.S.Ut. 52/18

120.

Vaidya madhava

121.

Ibid

122.

Astanga Hrudaya

123.

Subrahmanym et al., 1957

124.

Jain and Kar. 1971

125.

Rao and Nigam. 1976

126.

ain and Kar., 1972

127.

Chem. Abstr. 1984, 199, 48575 p

128.

Abstr, 1987.106,38300t),

129.

Bhavaprakasha , Charaka Samhita Soo-25and27, Susruta Samhita sutra 39,

Vanga sena
130.

Gadanigraha

131.

Vangasena

132.

Susruta Samhita Uttara 49/32

133.

Chakradatta

134.

Report of ICMR, 1967-68.


IV

Reference Bhutabhishanga Ojokshaya

135.

Banga et al., 1964

136.

Singh and Guru, 1972

137.

Dhanukar et al., 1981 and Nayampali et al., 1981.

138.

Neogi et al., 1971

139.

Fernandez et al., 1980 and Dhanukar et al., 1984

140.

Dcrux et al., 1980

141.

Gadanigraha

142.

(A.H.Ut. 40

143.

C.S.Ci. 17

144.

Vinayagamorthy, 1982.

145.

Jain et al., 1984.

146.

Ghosal et al., 1996

147.

Thakur, 1995

148.

Tewari et al; 1968.

149.

, Susruta Samhita Sutra 46, Bha pr, Ra Ni, Charaka Samhita Soo-25, Charaka

Samhita Chi 1, Dh Ni
150.

Sjuata and Kulkarni 1989.

151.

Inamdar et al., 1959

152.

singh R.H. et al; 1974, and Meera et al., 1999

153.

Chem. Abstr. 1993, 119, 269367c

154.

Sharma et al., 1984

155.

Fu Naiwu et al., 1992

156.

Xu H.X. et al., 1996

157.

Kin T.G. et al., 1999

158.

Bha Pr, Charaka Samhita Soo-27, Susruta Samhita soo,

159.

Trivedi et al; 1982.

160.

Kusumoto el al; 1992, and Valsaraj et al; 1996-97.

161.

Valsaraj et al; 1994

162.

Ni, Bha pr, Dh ni, Susruta Samhita Sutra 45-46

163.

Chaurasia and Jain, 1978

164.

patel and Trivedi, 1962.

165.

Ramaswamy and Sirsi, 1960, 1967.

166.

Jain and Agarwal, 1978

167.

Kayyadeva nighantu

168.

Bha pra, Susruta Samhita Soo-45, Ch Soo-25, Ra Ni, Su Chi

169.

Bha pra, Ra Va Ni, Charaka Samhita Sutra 25,


V

Ra Ma Va Ni,

Reference Bhutabhishanga Ojokshaya

170.

Charaka Samhita Chikitsa 10/25

171.

Sa.Sam. 3/11/62 and V.M.),

172.

Vaidya Madhava

173.

Chen, H.C. et al., 1995

174.

Dh Ni, Bha Pra, Susruta Samhita Sha.

175.

Gadanigraha

176.

Vangasena

177.

Vaidya Madhava and chakradatta

178.

Chopra et al., 1957

179.

Charaka Samhita , Chi 23/11, Dha Ni 7/111,

180.

Rasa tarangini 24/16

181.

Charaka Samhita, Chi 1/3/24-25.

182.

Susruta Samhita kalpa 2/5

183.

Ibid 2/12, Kustha

184.

Astanga Hrudaya Chikitsa 19/83Timira Astanga Ut 13/33, Gandamala

185.

Astanga Hrudaya Uttara 30/19, Nadivruna and Apachi

186.

Astanga Hrudaya Uttara 30/23, Akhu visha

187.

Astanga Hrudaya Uttara 38/32,

188.

loydia 1972, 35, 55

189.

Nat. Prod. Lett. 1993, 227: Chem. Abstr. 1994,121,175172b

190.

Phytochem, 1994, 36, 1527

191.

J. Nat. Prod. 1994, 57, 105

192.

Bha Pra, Ra Ni, R R S, -29

193.

Bhalla et al, 1969

194.

Bha Pra, Dha Ni, Ch Soo25, Vangasen.

195.

A.C.Ci.1

196.

Susruta Samhita Uttara 40

197.

Ibid

198.

Radomir et al., 1956.

199.

Yogendra Kumar, 1983.

200.

Dhanvantari, Raja, Bha Pra, Adarsha, Kaiyadeva, Madanapala,Nighantus/Mootra

Kandavisha, Poison

varga.
201.

Manual of HIV therapeutics, edited by William G. Powderly, M.D. published by

Lippincott Raven, New York, 1997


202.

Evaluation of the efficacy of ojovardhini yoga in Ojokshaya with special reference

to HIV infection by Dr. Sheetaram Prasad, 2002


VI

Reference Bhutabhishanga Ojokshaya

203.

Thatte, U.M. Dahanukar, S.A. Comparative study of immunomodualting activity of

Indian medicinal plants, Lithium carbonate and Glucan, 1988, October, (10) 639-44
204.

A survey of some Indian medicinal plants for anti human immuno deficiency virus

(HIV) activity, M. Premanathan et.al. The Indian journal of medicinal research, vol
112-9
205.

Ayurmedline, Vol-2, pp 556

206.

Astanga Hridaya sutra 11/37

207.

Susruta Samhita Sutra, 15/23-27, Edited by Vd. Jadavaji Trikamji Acharya,

published by Chaukhambha Orientalia, Varanasi, 1980


208.

Charaka Samhita Shareera 2/10, Edited by Vd. Jadavaji Trikamji Acharya,

published by Chaukhambha Sanskrit Samstan, Varanasi, 1984


209.

Sahasra yoga gutika prakarana

210.

Ibid, 189

211.

Indian materia medica, pp 45

212.

Ibid 856

213.

Ibid 1001

214.

Ibid 1260

215.

Ibid 295

216.

Ibid 414

217.

Ibid 187

218.

Bhavaprakasha poorva khanda haritakyadi varga 42

219.

Ibid 60-61

220.

Indian materia medica, pp 478

221.

Sahasrayoga Gutika prakarana

222.

Product index Amruta Drugs

223.

(a) Choi S, Lagakos SW, Schooley RT, Volberding PA. CD4+ lymphocytes are an

incomplete surrogate marker for clinical progression in persons with asymptomatic


HIV infection taking zidovudine. Ann Intern Med. 1993;118:674-680
(b) Volberding PA, Lagakos SW, Grimes JM, et al. A comparison of immediate with
deferred zidovudine therapy for asymptomatic HIV-infected adults with CD4 cell counts
of 500 or more per cubic millimeter. N Engl J Med. 1995;333:401-407
(c)Stein DS, Korvick JA, Vermund SH. CD4+ lymphocyte cell enumeration for
prediction of clinical course of human immunodeficiency virus disease: a review. J Infect
Dis. 1992;165:352-363
224.

Predictive value of viral load measurements in asymptomatic untreated HIV-1

infection, John.P.A, et.al. in AIDS 10 (3) pp 255-262, 1996


VII

Reference Bhutabhishanga Ojokshaya

225.

BMJ Nov. 2001

226.

Rajgopal K. Clinical evaluation of the efficacy of the an ayurvedic drug

formulation against HIV and AIDS in proceedings of seminar on Ayurvedic


management of AIDS and Cancer, Jamnagar, 1999.
227.

Evaluation of immuno potenntiating activity of a herbo mineral formulation PV-

150986 in HIV infection 1998,


228.

Susruta Samhita sutra 15/24

229.

Charaka Samhita Nidana 4/37

230.

Charaka Samhita Chikitsa 16/4-6

231.

Charaka Samhita Chikitsa 8/40-41

232.

Susruta Samhita Uttara 39/43-45

233.

Charaka Samhita Chikitsa 23/15

234.

Charaka Samhita Chikitsa 8/40-41

235.

Susruta Samhita sutra 15/28 Dalhana on it

236.

Ibid

237.

BMJ Nov. 2001

238.

Philips AN, Lee CA, Elford J, et al. Serial CD4 lymphocyte counts and

development of AIDS.lancet.1991: 337:389-392

VIII

Reference Bhutabhishanga Ojokshaya

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shashtri

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Dr.

Gorakhanatha

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Dravya Guna Vignanan II part by Dr. JLN Shashtri Ist edition 2004, published by
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Vaidhyaka shabdha sindu by Kaviraj Nagendranatha sen 3rd edition 1983,


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A Sanskrit - English dictionary by Shri Monier Monier Williams 1st edition 1993,
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Dhanvantari Nighantu by prof. Priyavruta Sharma, 1st edition 1982, published by


Chaukhambha orientalia Varanasi.
Bibliography- Bhutabhishanga Ojokshaya

11.

Madanapalana Nighantu

12.

Raj Nighantu by Dr. Indradeo, tripati, 2nd edition 1998, published by krishnadasa
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13.

Indian medicinal plants by K.R. Kirtikar and B.D. Basu 2nd edition published by
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14.

Kaiyadeva Nighantu pattya pattya vibhodhaka by Dr. Guruprasad Sharma 1st


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15.

Nighantu adarsha by Bapulal G. Vaidya 1st edition 1968, published by


Chakhamba Vidyabhavana Varanasi.

16.

Bhavaprakasha

of

Shri

Bhavamishra

vidhyotini

hindi

commentary

by

Bhaishajyaratna Pt. Shri Bramha Shankar Mishra. 5th edition 1988, published
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Kashyapa samhita Ayurveda linear shri. Satyapala Bhishagacharya, published


by Chaukhamba Sankrit Samsthana, Varanasi.

18.

Vedome Ayurveda by Vaidya Pt. Ramagopala Shashtri 1656 published by La


madana mohanalalal Ayurvedic Anusandhan Trust, Delhi.

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Sharangadhara Samhita by Pt. Parusharama Shastri Vidyasagar 3rd edition


1983, published by Chaukhambha Orientalia, Varanasi.

20.

Agnipuranaki Ayurvediya Anusandhana Samiksha By Vivekananda Pandeya 1st


edition 1997, published by Shri Satguru publications Delhi.

21.

Essentials of Basic Ayurveda concepts by prof. V.V.S. Shashtri 1st edition 1999,
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22.

Shareer kriya vignana by Dr. P.V. Sharma 4th edition 1982, published by
Chaukhambha Bharati Academy.

Bibliography- Bhutabhishanga Ojokshaya

ii

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Shabdha kalpa druma by Raja Radha Kanthadeva 1-5 Vol 3rd edition 1967,
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24.

Devidsons principles and practice of medicine 17th edition by CRW Edwards,


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Huchisons Clinical methods by Michelswsh published by W,B, Saunders 21st


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26.

Pharmocology and Pharmocotherapetic by R.S. Satuskar and S.D. Bhandarkar,


S.S. Ainapure 17th edition 2001 published by Popular prakashan Pvt. Ltd.
Mumbai.

27.

Tabers cyclopadic medical dictonery by Clyaton L. Thomus 17th edition 1993


published by Jeetendra P Vij for Jay Pee brothers medical publications pvt. Ltd.
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28.

Herrisons principles and internal medicinal by fauci, Braunwald and others.1-2


14th edition 1998 published by Mc-Graw-Hill Book company Singapore.

29.

Text book of Medical Physicology by Arthur C Guyton and John Hall 10th edition
2000, published by Harcourt. Asia pvt. Ltd.

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Grays anatomy by lawpence H Bennister and others, 38th edition 2000,


published by Charchil living stone, Edern Burgh London. Harcourt publishers.

31.

API textbook of medicine 6th edition 1999 by Gurumukha Sainani, published by


Association of physicians of India, Mumbai.

32.

Boyds textbook of pathology by AC Ratehie 9th edition 1-2 1990, published by


Lea and Sebrigy USA.

33.

Methods in Biostatics by B.K. Mahajan 6th edition 1997 published by Jay Pee
brothers medical publications pvt. Ltd. New Delhi.
Bibliography- Bhutabhishanga Ojokshaya iii

34.

Medical micro biology and immunology by Warren of Levingson and Erneast


Jawetz 3rd edition 1992 published by Prentice Hall International INC.

Bibliography- Bhutabhishanga Ojokshaya iv

Special case sheet for

Bhutabhishangaja Ojokshaya (HIV Infection)


PGCRC ,(KA YACH IK ITSA) , SHRI. D .G.M.AYUR VED IC MED ICA L COLLEGE, GADA G
G u id e:
C o - g u ide s:

Schola r:
C .S.Ha nama nta go ud ar

D r . Siva r ama Pras ad Ke tha makk a


D r . A sh ok K u m ar Pan da

1. Name of the Patient


2. Sex - M
F

Sl.No.
OPD No

3. Age -

IPD No

Years

Birth data:
Place of Birth
Date

4. Religion

District

Month

State

Year

Hindu

5. Occupation - Sex worker

Muslim

Driver

6. Economical status Poor


7. Marital Status - Married

Hours

Minutes

PM

Christian Other

Business

Service

Middle class
Single

AM

Time

Student

Household

Higher middle

Divorced

8. Address

Widow/er

Higher class
2/3 M a r r i a g e s

Phone:

Pin
Schedule initiation
9. Selection

Included

Excluded

10. Group

A) Ojokalpa Rasayana

11. Result

Responded

Schedule completion

B) AKK Rasayana

Not responded

Discontinued

INFORMED CONSENT
I

Son/Daughter/Wife of

am

exercising my free will, to participate in above study as a subject. I have been


informed to my satisfaction, by the attending physician the purpose of the clinical
evaluation and nature of the drug treatment. I am also aware of my right to quit the
treatment, at any time during the course.
Patient's Signature

1. CHIEF COMPLAINTS WITH DURATION


Sl.

Complaints

No
1

Loss of weight

General weakness (Glani)

Loss of appetite (Aruchi)

Fever (Jwara)

Internees of Body (Stabdhagatrata)

Loss of complexion (Vyadhitendriya)

Emaciation (Mamsa Kshaya)

Looseness of Joints (Sandhi Vislesha)

Somnolence (Anidra)

10

Delirium / Convulsions (Pralapa)

Duration
Less than 1 yr

1 to 2 years

2. ASSOCIATED COMPLAINTS
Annavaha Srotas

Rasavaha Srotas

Oral thrush/ Nausea/ Vomiting

Giddiness

Bleeding gums

Palpitation

Pain Abdomen / distention

Dysphagia / soar throat

Burning micturition

White tongue (Candidiasis)

Urethral discharge

Hairy tongue (leucoplakia)

Mutravaha Srotas

Pureeshavaha Srotas

Pranavaha Srotas

Diarrhea

Cough

Anal itching (Candidiasis)

Blood with sputum

Breathlessness

Genital ulcers

Chest pain

Genital warts

Headache

Vaginal Candidiasis

Prajanana Samstana

Raktavaha Srotas

Others

Skin eruptions

Drowsiness

Molluscum

Lymphdenitis

Warts

Acne Vulgaris

Herpes zoster

4
2

Above 2 years

3. HISTORY OF PRESENT ILLNESS


(a) How it was diagnosed?

Intentional / Accidental

(b) Mode of onset 1) Source of infection


Sexual exposure

Blood transfusion

Injections

2) Early symptoms
3) Later symptoms
(c) Mode of progress
Typical

Rapid

Longtime non progressive

(d) Suffering from any systemic disease?


Tuberculosis
Cancer

Diabetes Mellitus
Venereal diseases

4. HISTORY OF PAST ILLNESS

5. TREATMENT HISTORY

6. FAMILY HISTORY

Hypertension
Cardiac disease

7. PERSONAL HISTORY
a) Food habits

Vegetarian

Taste
preferred

Mixed diet

Sweet

Sour

Salty

Pungent

Bitter

Astringent

b) Sleep

Day

Night

Sound

c) Hygiene

Good

Unhygienic

d) Addictions

Tobacco

Disturbed

Alcohol

Drugs

e) Sexual behaviors
Heterosexual
Marital

Homosexual

Extra marital

Single

multiple

f) Blood transfusion Donor

Recipient

Frequency

g) Bowel habits

Loose

Constipated

Normal

h) Menstrual History Regular

Irregular

Amenorrhea

Menopause

8. EXAMINATION
a) Vitals
Temperature

F Pulse

Weight

Blood pressure

Height

Respiratory rate

Body-Mass Index

b) General
Built & Nutrition
Oral Cavity

well
Ulcers

Moderate
Hairy Leucoplakia

Poor
Coated

Lymph nodes enlargement


Epitroclear

Cervical

Supra clavicular

Axillary

Inguinal

Any other

c) Ayurvedic assessment
1. Hetu
Ahara

Vihara
B

Anashana
Alpashana

2. Dosha
Vata Vriddhi
B
Karshya
Karshnya
Ushnakamitwa
Kampa
Anaha
Shakritgraha
Balabhramsha
Nidrabhramsha
Pralapa
Bhrama

Anya
B

Vatatapa sevana
Ati Vyayama
Ati Vyavaya
Sonita a t i v a r t a n a
Prajagara

Pitta Vriddhi
B
Peetamootra
Peetanetra
Peetavit
Peeta twak
Atikshudha
Atidaha

Kapha Vriddhi
B
Agnisadana
Praseka
Alasya
Gowrava
Swetangata
Sheetangata
Shlathangata
Swasa
Kasa
Atinidra

Vata Kshaya
Pitta Kshaya
Kapha Kshaya
B
A
B
A
B
Angasada
Mandagni
Bhrama
Urah shoonyata
Alpabhshite
Shareera
sh
ee
ta
tw
am
Ahitam
Chesta heenata
Prabhahani
Shira shoonyata
Vyamoha
Hriddrava
Sleshma vriddhi
Sandhi saithilya
3. Lakshana
Ojo Vishramsha
Ojo Vyapat
B
A
B
Gatra sadanam
Stabdha gatrata
Dosha chyavanam
Guru gatrata
Sandhi vislesha
Vata shopha
Kriya sannirodha
Varna hani
Glani
Tandra
Nidra
Ojo Kshaya
Bhaya
Dowrbalya
Chinta
Vyathitendriya
Duschaaya
Durmana
Rooksha
Kshama
Moorcha
Mamsa kshaya
Moha
Pralapa
5

Koapam - Anger
Soka
Chinta
Bhaya
Bhootopaghgta

d) Systemic
1) Respiratory system
Shape of chest

Normal

Deformed

Trachea

Normal

Right Shift

Movements

Normal

Restricted

Left Shift

Auscultatory findings
Breath Sounds

Vesicular

Added sounds

Ronchi

Bronchial

Crepitation

Rub

(Advise X-ray chest / Sputum examination if required)


Report: -

2) Gastrointestinal tract
Tenderness
Organomegaly

Fluid

Mild

Moderate

Severe

Liver

Mild

Moderate

Severe

Spleen

Mild

Moderate

Severe

Thrill

Present

Absent

Shifting dullness

Present

Absent

Present

Absent

Abdominal Lump
(Advise U.S.G if required)
Report: -

3) Cardiovascular system

S1

S2

Murmur

(Advise E.C.G. if required)

4) Central Nervous System


Any neurological deficit, if so specify.
5) Genito-Urinary system

6) Any other (if any)

9. LABORATORY INVESTIGATIONS
HAEMATOLOGICAL
Hb%
Total Count Lymphocytes
Total Count Platelets
Total Count Leucocyte
E.S.R

gm/dl
/l
/l
/l
mm/1

Random Blood Sugar

st

Hour

DIFFERENTIAL COUNT
Lymphocytes
Neutrophils
Eosinophils
Basophils
Monocytes

mg/dl

SPECIAL INVESTIGATIONS
Elisa
HIV- I & II
Rapid (Tridot)
Western Blot
CD4 cell count
CD8 cell count
CD4 : CD8 Ratio
10. DIAGNOSIS

/mm 3
/mm 3
STAGE

11. ASSESSMENT CRITERIA


Parameter
General health
condition (Grade)
Total W.B.C Count
CD4 cell count
CD8 cell count
CD4 : CD8 ratio

Before

SUBJECTIVE
After
Parameter
Karnofsky
performance score
OBJECTIVE
Total Count
Platelets
Total Count
Lymphocytes
E.S.R.
Body weight

Before

After

PERIODICAL ASSESSMENT
Date

Baseline
Data
0 days

Date

st

2nd

3rd

Final

Assessment

Assessment

Assessment

Assessment

Follow up
Assessment-1

Follow up
Assessment-2

30 days

60 days

90 days

120 days

150 days

180 days

GH Sc or e
K P Sco re
Pulse Rate
B lo od P res su re
T e mpe ra t ur e
Re sp irat ory R a te
w eight
T LC
CD4
CD8
CD4:CD8

FINAL ASSESSMENT
ASSESSMENT CATEGORY

NOTES

S L .NO

1
2
3

Patients impression
Side effects
Investigators note

Guidelines for gradations in HIV positive cases


KARNOFSKY PERFORMANCE SCORE
S.No
1
2
3
4
5
6
7
8
9
10
11

Karnofsky performance score


Normal - no evidence of disease
Able to carry on normal activity
Normal activity with effort with some symptoms and
signs of disease
Cares for self, unable to carry on normal activity
Requires occasional assistance and medical care
Requires considerable assistance and frequent
medical care
Disable, requires special care and assistance
Severely disabled, hospitalization indicated
Very sick, active supportive treatment required
Morbid, fatal processes are progressing rapidly
Dead

IMPROVEMENT IN GENERAL HEALTH


Grade
0
1
2
3

Parameter for grading


Static / worsen
Mildly better
Moderately better
Much better

Score
100
90
80
70
60
50
40
30
20
10
00

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