Infection rn


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Infection rn

  1. 1. A STUDY ON AYURVEDIC PERSPECTIVE OF INFECTIOUS SKIN DISEASES WITH SPECIAL REFERENCE TO SUPERFICIAL MYCOSES Dissertation submitted to the Kannur University, Kerala, in partial fulfillment of the regulations for the award of the degree of DOCTOR OF MEDICINE (Ay) in Roganidana By Dr. Madhu P.M. B. A. M. S. Under the Supervision of Dr. R. Sreekumar M.D. (Ay) Professor & H.O.D., Department of Roganidana Govt. Ayurveda College Kannur DEPARTMENT OF POST GRADUATE STUDIES IN ROGANIDANA GOVERNMENT AYURVEDA COLLEGE, KANNUR – 670502 2005
  2. 2. CERTIFICATE This is to certify that this thesis envisages the outcome oforiginal thinking and observations made by Dr P.M.Madhu on “Astudy on ayurvedic perspective of infectious skin diseases withspecial reference to superficial mycoses” for the partial fulfillmentof the degree of Doctor of Medicine (Ayu.). This work has beencarried out under my direct guidance and supervision in thespeciality of Roganidana, Department of Roganidanam, Govt.Ayurveda College, Kannur. This thesis bears abundant evidence of original thoughts anddedicated work. It marks a distinct progress on scientific lines in thesubject. I strongly recommend and forward this thesis to be subjectedto the adjudicators.Forwarded: Guide:Dr B. Ambika, Dr.R.Sreekumar,Retired professor & H.O.D. Reader,Department of Roganidanam, Department of Roganidanam,Government Ayurveda College, Govt. Ayurveda college,Pariyaram, Kannur Pariyaram,Kannur
  3. 3. Á uÉÉXèûç qÉå qÉlÉÍxÉ mÉëÌiÉÌ·iÉÉ qÉlÉÉå qÉå uÉÉÍcÉ mÉëÌiÉÌ·iÉqÉç AÉ uÉÏUÉ uÉÏqÉï LÍkÉ uÉåSxrÉ qÉ AÉhÉÏ xjÉÈ ´ÉÑiÉqÉ qÉå qÉÉ mÉëWûÉxÉÏÈ AlÉålÉÉkÉÏiÉålÉ AWûÉåUɧÉÉlÉç xÉlSkÉÉÍqÉçç HiÉqÉç uÉÌSwrÉÉÍqÉ xÉirÉqÉç uÉÌSwrÉÉÍqÉ iÉlqÉÉqÉuÉiÉÑ iÉiÉç uÉ£üÉUqÉuÉiÉÑ;AuÉiÉÑ qÉÉqÉç AuÉiÉÑ uÉ£üÉUqÉç, Á vÉÉÎliÉÈ vÉÉÎliÉÈ vÉÉÎliÉÈMy words may rest in mind, and the mind in my words. It appears to methat they are the two pins of my knowledge that holds its wheels. May whatI have learnt not forsake me. I join day and night with what I have learnt. Ishall speak of the real, I shall speak the truth. May this protect me and maythis protect the teacher. Let us pray for an auspicious future. [Eithereya Upanishad]
  4. 4. We were the first batch of P.G.students in Kannur Ayueveda College. As anormal procedure for sample collection, we had published the informationabout the beginning of some special O.P.Ds in our hospital. For a largesample collection, this present subject was published as ‘skin diseases likeitching or discolouration.’ As a result, a large variety of patients sufferingfrom skin diseases came to our O.P. Senior doctors were broad mindedenough to give us the freedom for examination and selection of treatment.Thus we came to experience with a vast variety of dermatological cases bothas out patients and as inpatients. Most patients were economically poorvillage people. They came to us after a long run through many othermedicines. So it became our responsibility to heal the condition mosteffectively. Challenging cases made us to study about the scientific details.We were forced to discuss the problem among ourselves and among othersubject experts. Failures made us to reconstruct the pattern of treatment. Eachand every skin patients taught us new stories of Dermatology. Thus, slowlyand very slowly ….we started loving the branch of Dermatology verysincerely. …Hence, this thesis work is a humble dedication to varioussufferings of our patients, which really made us to think about our scopes andlimitations.
  5. 5. ContentsAcknowledgementsAbbreviationsList of tablesList of pictures Part 1Introduction1.1 Need and significance of the study1.2 Relevance of Ayurvedic study1.3 Ayurveda and infectious skin diseases1.4 About this thesis work1.5 Outline of the thesis Part 2Review of Literature-Modern review2.1 Infection- basic concepts 2.1.1 The sources of infection 2.1.2 Pathogenicity of microorganisms 2.1.3 Microorganisms 2.1.4 Normal flora 2.1.5 Fungus 2.1.6 Cell biology of fungi 2.1.7 Fungal metabolism2.2 Fungal Infection 2.2.1 Superficial mycoses 2.2.2 What causes fungal infection? 2.2.3 Tinea corporis 2.2.4 Tinea cruris 2.2.5 Tinea versicolar
  6. 6. 2.2.6 Tinea capitis 2.2.7 Tinea pedis 2.2.8 The ‘ID’reaction 2.2.9 Defense against fungi 2.2.10 Diagnosis 2.2.11 General treatment pattern 2.2.12 Prevention Part 3Skin and skin diseases3.1 The skin Anatomical and physiological aspects3.2 Twacha The Ayurvedic view 3.2.1. Role of various internal factors 3.2.2. Assessment of the health of skin3.3 Skin diseases and infectious skin diseases 3.3.1. Bacterial infection 3.3.2. Viral infection Part 4Review of Ayurvedic literature4.1. Vedic references 4.1.1 Krimiroga 4.1.2 General charecterestics 4.1.3 The effects of krimis4.2. Ayurvedic literature 4.2.1 Janapadodwamsa 4.2.2. Oupasargika 4.2.3 Graha 4.2.4. Krimi 4.2.5. Twak vikara and krimi 4.2.6. The Treatment principle
  7. 7. 4.2.7. Kshethravada and Beeja vada4.3. Theory of infection-A critical analysis 4.3.1. The web of causation-An Ayurvedic perspective 4.3.2. The spectrum of infectious diseases4.4. Ayurvedic perspective of Superficial mycoses 4.4.1 Assessment of the disease 4.4.2 Nidana-Viprakrishta and Sannikrishta 4.4.3 Poorvaroopa 4.4.4 Roopa 4.4.5 Samprapthi 4.4.6 Upasaya Part 5 Clinical study 5.1 Methodlogy 5.2 Observations & Analysis Part 6 Discussion 6.1 Discussion on theoretical aspect 6.2 Discussion on clinical examination 6.3 Discussion on test response 6.4 Discussion on statistical analysis Part7 Conclusion 7.1 Conclusion 7.2 Limitations 7.3 suggestions Summary Bibliography
  8. 8. Acknowledgement xÉuÉï ÌuÉZlÉWûUqÉç SåuÉqÉç xÉuÉï ÌuÉZlÉÌuÉuÉÎeÉïiÉqÉç xÉuÉï ÍxÉ̬ mÉëSÉiÉÉUqÉç uÉlSåWûqÉç aÉhÉlÉÉrÉMüqÉç At this unforgettable moment of successful fulfillment of an ambition, Ibow to my parents and to all my respectful teachers by whom I was able to thinkand work on such a divine medical science. I most sincerely convey thanks with best of my respects and gratitude to myhonorable Guide Dr. R Sreekumar. His guidance and valuable suggestions throughout the course of my study have helped in completing this thesis successfully. It gives me immense pleasure to express the heartfelt gratitude toDr.S.Rajeev, Associate Professor, Dept.of Dermatology, ACME Pariyaram, whohelped me a lot with valuable scientific guidance. I pay my sincere thanks to Dr.S.Jayadevan, Associate Professor, Dept.ofCommunity Medicine, ACME Pariyaram, who helped me a lot with valuableguidance on statistics. It is beyond the reach of my language to inscribe the profound gratitude, Ifeel for my department staff, colleagues and patients, who were always with me todiscuss various theoretical as well as practical issues confronted during the study. I would like to convey my heartfelt thanks to my beloved life companionand my little daughter, whose cooperation was always with me. I use this grateful event to convey my sincere thanks to all other teachers,friends and relatives, who have extended their direct or indirect co-operation formy dissertation.
  9. 9. AbbreviationsA. H. Su. - Ashtanga Hridya Sutra SthanaA. H. Chi. - Ashtanga Hridya Chikitsa SthanaA. H. Ni. - Ashtanga Hridya Nidana SthanaA. H. Sa. - Ashtanga Hridya Sharira SthanaA. S. Ni. - Ashtanga Sangraha Nidana SthanaA. S. Sa. - Ashtanga Sangraha Sharira SthanaA. S. Su. - Ashtanga Sangraha Sutra SthanaA. V - Adharva VedaCh.S. - Charaka samhithaCh. Chi. - Charaka Samhita Chikitsa SthanaCh. Ni. - Charaka Samhita Nidana SthanaCh. Sa. - Charaka Samhita Sharira SthanaCh. Su. - Charaka Samhita Sutra SthanaCh. Vi. - Charaka Samhita Vimana SthanaChak. - ChakrapaniDal. - DalhanaHar. - Harita SamhitaKa. Su. - Kashyapa Samhita Sutra SthanaMa. Ni. - Madhava NidanaMa.M.K. - Madhava Nidana Madhukosa vyakhyaSu. S - Susrutha SamhithaSu. Chi. - Sushruta Samhita Chikitsa SthanaSu. Ni. - Sushruta Samhita Nidana SthanaSu. Sa. - Sushruta Samhita Sharira SthanaSu. Su. - Sushruta Samhita Sutra Sthana
  10. 10. List of tables1. Layers of the skin2. Properties and functions of doshas3. Effects due to vitiated doshas4. Skin diseases due to Bacterial infection5. Skin diseases due to viral infection6. Sex wise distribution7. Age wise distribution8. Marital Status wise distribution9. Religion wise distribution10. Education wise distribution11. Occupation wise distribution12. Socio economical status wise distribution13. Habitat wise distribution14. Desatah wise distribution15. History of previous illness16. First choice of medication17. Dietary habit wise distribution18. Habit of excessive intake of some food item19. Appetite wise distribution20. Addiction wise distribution21. Bowel condition wise distribution22. Sleep pattern wise distribution23. Nature of cloth using24. Habit of using, soap, oil and powder25. Deha Prakriti wise distribution26. Sara wise distribution
  11. 11. 27. Sanhanana wise distribution28. Sattva wise distribution29. Satmya wise distribution30. Abhyavarana Sakti wise distribution31. Jarana Sakti wise distribution32. Vyayama Sakti wise distribution33. Kostha wise distribution34. Condition of sweat35. Nature of the skin36. Chief complaints reported by 75 patients of superficial mycoses37. Distribution of the types of superficial mycoses were like this38. Onset wise distribution39. Duration wise distribution40. Causes of aggravation of symptoms41. Occupation Exposed to sunlight42. History of emergence of the disease on exposure to43. Involvement of different Srotas44. Initial data45. After treatment period46. One month after treatment47. Two months after treatment48. Variations in total score49. Variations in symptom score –A comparison between the groups during follow –up50. Comparison of total score through the follow-up periods51. One way ANOVA test for TOTAL SCORE-Initial stage52. One way ANOVA test for TOTAL SCORE-Final stage53. Paired t test –group A54. Paired t test –group B55. Paired t test –group C
  12. 12. PART 1 Introduction ‘Infection’ is the most dreadful condition that the modern world has everseen. Many of the serious questions arisen by newly evolved infectious diseases,to the medical world remain unsolved even in this ultra scientific world. Now,each and every system of medicine is trying to evolve most effective method fortackling many infectious conditions. As research students of Ayurveda, it is ourduty to interpret the condition in the frame of Ayurveda and to evolve mostscientific and effective solutions after thorough observations and clinical trials.Attempting to give an Ayurvedic perspective on such an entity as ‘Infection’, onwhich the final word in modern research itself has not been out, is an arduous task.But, it is the utmost necessity of the present era. So, this work is a humblebeginning in this aspect.Considering various limitations of such a vast study, here ‘Infectious skindiseases’ form an example for infection, among which ‘superficial mycoses’ is thetypical sample for study. The cases are very common among our tropicalpopulation.1.1 Need and significance of the study One of the baffling problems of mankind since time immemorial is the skindisease, which manifest in variety of forms. Infectious diseases are the mostpredominant among them. About 10% of all the patients coming to a generalpractitioner consists infectious skin disease. To a dermatologist, nearly 40%consists of various types of infections (1). These are the figures from world widestatistical data.Considering the tropical condition, according to our hospital records, (Govt.Ayurveda college, Kannur O.P. Register 2003-2004) nearly 23% of all the cases
  13. 13. are contributed by Skin diseases. Among this, many cases were of ringworminfection. Enquiry in to details of this condition will open a wide vista of facts.For millennia, yeasts and fungi have enjoyed relatively good relations withhumans. Despite their abundance—they appear on plant leaves and flowers, soil,salt water, baked goods and beer, as well as in our gastrointestinal tracts and skinsurfaces—very few yeasts and fungi trigger disease in healthy people. But thescenario has changed very much now. Bacteria, the most common pathogenicorganism became almost yieldable to various potent antibiotics. Corticosteroidsplay miraculous game in infectious conditions. But the major advances inmedicine and technology has created a suppressive effect on the patient’s immunesystem, subjecting human body to various types of mere or fatal other infections.An increased number of several fungal infections have been observed during thelast two decades. This alarming increase in the fungal infections is seemed due tonew potent antibiotics and corticosteroids and up to a certain extent owing toenvironmental pollution (2).A survey of literature reveals that several saprophytic or plant pathogenic fungi areknown to become opportunistic pathogen in immunocompromised/immunosuppressed patients (3). Unfortunately, some medical advances have alsogiven rise to new problems. Organ transplantation, invasive surgery, implantationof prosthetic devices, and the use of immunosuppressive therapies have prolongedsurvival from some diseases but also resulted in compromised immunity andrendered previously normal individuals susceptible to microbes formerlyconsidered to be pure saprophytes.In tropical regions of Kerala, increasing prevalence of fungal infection is said to bedue to the climatic peculiarities and due to unhygienic practices of people. In arecent survey conducted at a rural area of ‘Kumble’ (Kasargod district) showed11.16% patients with dermatological problems. Of these patients, 43.41% hadcutaneous infections and 57.07% had non-infectious dermatoses. Fungal infectionwas the commonest infection seen (22.92%) and eczemas took an upper hand in
  14. 14. non-infectious group (32.19%) (4). According to laboratory of mycology and plantpathology, University of Rajasthan, Dermatophytoses poses a serious concern tothe sociologically backward and economically poor population of India. Fungicause both superficial and internal mycoses. The mycoses, normally not lethal, areunpleasant and difficult to cure, and cause considerable economic loss. Antibioticscan kill bacteria without much bad side effects, but as fungi contain cellularmachinery and proteins similar to our own, its hard to find agents to kill fungi thatdont have negative effects on us. By this fact, modern world find it more difficultthan Bacteria, to remove pathogenic fungi from our body (5).1.2 Relevance of Ayurvedic study Now, the ancient Indian medicine, ‘Ayurveda’ has become globallyacceptable with its unique concept of pure health. Many of the health seekersconsider it as their destiny of hope as it promise the holistic health. Living in a fastgoing and newly emerging world of modern science, the acceptance to Ayurvedais a surprising trend. So, by considering the significance of the situation, it is ourduty to present the concepts of Ayurveda in the frame of evidence based medicinewith clinical observations.According to the ‘General Guidelines for Methodologies on Research andEvaluation of Traditional Medicine’, published by WHO, there are various scopesfor unconventional medical fields, for research. Well established randomizedclinical trials provide the highest level of evidence for efficacy. Observationalstudies involving large number of patients may also be a very valuable tool for theevaluation of theories or efficacy of herbal medicines. According to the theoriesand concepts of traditional medicine, (as mentioned in Part1-section 1.3 of theguide line) the prevention, diagnosis, improvement and treatment of illness areoften based on the specific needs of the individual patient. So even a single casestudy itself is significant (6).
  15. 15. 1.3 Ayurveda and Infectious Skin Diseases Many of our traditional healers have much experience with various types ofinfectious skin disorders. Fascinating stories of long lasting results after Ayurvedictreatment really attract us towards this field of medicine. Complete cure, absenceof side effects, rare chances of recurrence etc are the main benefits. Success withAyurvedic treatment after so many other trials really signifies its magnanimity.But as a medical science, it has to be under the ground of evidence based clinicaltrials and under the criteria of statistical analysis. Other wise, the world will notaccept our theories or findings.1.4 About this thesis work Experience and practice have strong theories behind. We have the historyof various experiences from the classical books of Ayurveda. Our duty is to findout the theory behind each practice and generalize it with clinical trials andobservations. The attempt in this work is to observe and to understand ‘Superficialmycoses’ through the theories and clinical studies based on Modern as well asAyurvedic principles. To do that, it was felt necessary to first have an overview onsuperficial fungal infection, including the latest trends of research. This type of acompilation can throw light to many facts pertaining to mycology. A criticalanalysis through these facts reveals the necessity of a true intervention in this field.The research-oriented analysis through the olden pages of Ayurveda has drivenmuch information about this concept. There was a visible concept of infection inthose pages. Cases like that of ‘superficial mycoses’ were described in those oldendays. Based on these concepts, a thorough observational clinical study wasconducted among the patients. This thesis work contains the details of theseobservations and clinical interpretations.1.5 Outline of the thesis This is an observational clinical study, in which patients of superficialmycoses were randomly selected and grouped in to three categories. A clear cutMethodology was formulated as a first step of the study. Patients were selected
  16. 16. after thorough examination of their clinical symptoms and personal details.Diagnosis was purely based upon modern criteria. For the confirmation of fungi,scrapings were taken for microscopic study. First group was administered withExternal medicine, second group with Internal medicine and the third group withboth administrations. This is an ‘upasayathmaka’ study as the etiopathologicalaspects of the disease are still obscure. By comparative assessment of the degreeof symptomatic cure in all the three groups, here is an attempt to infer the degreeof pathological involvement. This thesis work tries to answer various questionsregarding the role of internal morbidity in the causation of infection.Follow up research works will really contribute for a concrete basis for the theoryof various infectious diseases in Ayurvedic perspective, which may lay morebeneficial milestones in the development of our science in modern scenario.References:1. Current science, vol.85, no1, 10 july2003, page302. Journal of investigative dermatology 116, 2, 313-318 (February, 2004)3. Journal of investigative dermatology 112, 3, 56-58 ( May, 2005) Mishra M, Mishra S, Singh PC, Mishra BC. Clinicomycological profile of superficial mycoses. Ind J Dermatol Venereol Leprol. 1998; 64:283-5. Huda MM, Chakraborty N, Sharma JN. Clinico-mycologicalStudy of superficial mycoses in upper Assam. Ind J Dermatol4. Pattern of skin diseases in an Indian village, Rao GS, Kumar SS, Sandhya Dermatology & Venereology Dept, KMC, Mangalore, Nov-20025. Current science, vol.85, no1, 10 july2003, page306. General Guidelines for Methodologies on Research and Evaluation of Traditional Medicine, Published by WHO, Geneva 2000.
  17. 17. PART 2 Review of the literature Modern review To study the Ayurvedic perspective of a disease, on which many studieshave already done by modern scientists, it is essential to have an up to dateknowledge of the present subject. So this chapter comprises the most recentknowledge about the infection, microorganism, fungal infection, superficialmycoses, their diagnostic methods and modern treatment schemes.2.1 Infection-Basic concepts The word infection originates from the Latin term, ‘infectio’ whichindicates the process of the successful invasion, establishment and growth ofmicroorganisms in the tissues of the host. The fate of infection alters depending onthe organism and patient. If the circumstances are suitable, this invasion causes aninfectious disease in the host. They are capable of transmission from one person toanother.2.1.1 The sources of infection The source of an infection refers to the habitat or growth area in the humanor animal reservoir and vehicle refers to objects that are contaminated or colonizedby microorganisms. As per the source, infections may be viewed as Endogenousor ExogenousEndogenous: It is from within the same individual. There are certain organisms,which live on the external and internal surfaces of the body, without causingdisease; such ability is called commensalisms. At times these act as pathogens andcause disease whenever bodily resistance is lowered.Exogenous: These are derived from human beings, animals or the soil (inanimatenature). The human carriers could be healthy convalescent and chronic.
  18. 18. 2.1.2 Pathogenisity of microorganisms The ability of certain microorganisms to establish an infective process isreferred to as pathogenesity. In practice, pathogenic mechanisms can besubdivided as follows1. Invasiveness: The ability to invade tissues.2. Evasiveness: the ability to evade host-defense mechanisms whilst invasion occurs.3. Virulence the ability of the micro organisms to produce tissue injuryDifferent microorganisms possess different pathogenicity. Depending on theirpathogenicity, the nature of disease also may have difference in presentation.Before explaining them, now we may go through the relevant aspects ofmicroorganisms.2.1.3 Microorganisms Universe is filled with a number of microorganisms. Earthly environmentalso harbours a variety of microorganisms. Each particular microorganismpossesses so many specific characters in their life cycle, transmission and inrelations. On the basis of their life-habits, organism may be classified assaprophytes or parasites.Saprophytism is the mode of life of free-living organisms, which obtain theirnourishment from soil and water. Saprophytes usually do not require a living host.Parasitism implies adaptation to life on or in the bodies of higher organisms. Theassociation may be of symbiosis, commensalisms or pathogenesis.2.1.4. Normal flora The normal skin of healthy persons contains so many classes ofmicroorganisms. Though there are a variety of microorganisms residing on humanskin, they remain harmless because of the relationship existing between the skinand its microflora. As the skin contains fats, proteins, nitrogeneous substances,minerals, by-products of keratinization and cutaneous appendages, they willprovide sufficient nutrition for the growth of microorganisms. The microbial flora
  19. 19. of each region of the skin seems to differ in detail from other regions. Climaticconditions, sweating, body hygiene and of course, skin disease besides a host ofother factors influences the composition of the microflora.Basic pattern of colonization of healthy human skin is different from others. Dryskin supports a low level of colonization, while moist areas and those wellsupplied with sebaceous glands are heavily populated. Within the genusStaphylococcus, 10 different species have regularly been isolated from normalskin. The normal flora of the skin appears to have several functions, of which themost important is probably defense against bacterial infection through bacterialinterference. It is almost certainly responsible for the production of free fatty acidsfrom skin lipids.Pityrosporum ovale is part of the normal skin flora in adults, but is rare in prepubertal children; it is generally found in greatest density in the scalp andproximal flexures. The proportion of the normal scalp flora represented by P.ovale is increased in adults with seborrhoeic dermatitis.The normal flora of the skin includes a number of morphologically distinctlipophilic yeasts. Pityriasis versicolor in most cases represents a shift in therelationship between a human and his or her resident yeast flora. Factorscontributing to the change are probably multiple.Most attention has been devoted to environmental factors and individual hostsusceptibility.The skin provides a dry, mechanical barrier from which contaminating organismsare constantly being removed by desquamation. Investigators have spreadorganisms on the skin surface, studied their disappearance and attempted toelucidate the factors concerned. It seems that more than 20% of normal subjectscarry some skin bacteria that produce antibiotics capable of inhibiting othermicroorganisms. On nearly one in 10 of normal human skins, these antibioticproducers actually predominate, in which case they appear to be helpful inprotecting against staphylococcal wound infection after surgery.
  20. 20. The normal human skin is colonized by huge numbers of bacteria that liveharmlessly as commensals on its surface and within its follicles. At times,overgrowth of some of these resident organisms may cause minor disease of theskin or its appendages. Apart from the arrival of these frankly pathogenicorganisms, a wide range of bacteria land more or less fortuitously on the skin, andlinger briefly in small numbers before disappearing, unable to multiply and thrivein this relatively inhospitable environment. Detailed quantitative studies ofpathogens and commensals, and investigations of epidermal replication and of theimmune capabilities of the host, are becoming feasible in a research setting. Thelessons they teach must be used to interpret the problems found in daily clinicalpractice, where such sophisticated methods are generally unavailable.Microorganisms of medical importance can be divided in to several large groups,including Bacteria, Virus, fungi and a number of organisms intermediate betweenthem. Study about these organisms became a serious subject of discussion,following the germ theory of disease causation. As our subject of discussion isabout Fungus, we may detail about that.2.1.5 Fungus All life on earth is divided into five kingdoms: Plants, Animals, Fungi,Protozoa, and Monera (bacteria). Fungi are neither plants nor animals; but are adifferent and more primitive kingdom whose differences provide the ability topoison the denizens of other kingdoms, including the species, Homosapiens.Fungi are the most widely distributed organisms on Earth. They are eukaryoticprotista. Many fungi are free-living in soil or water; others form parasitic orsymbiotic relationships with plants or animals, respectively. There are over200,000 fungal species and they make up a quarter of the biomass of the earth.There are 100,000 genera of the mold species, but only approximately 80 generaare known to cause illness. Their features can be classified on morphological,anatomical, ultra-structural, biochemical or based on sequences of nucleic acids.
  21. 21. 2.1.6 Cell biology of the fungiFigure 1 Their basic cellular unit is described as a hypha. This is usually a tubularcell, which is surrounded by a rigid, chitin-containing cell wall. The hypha extendsby tip growth, and multiplies by branching, creating a fine network called amycelium. Hyphae contain nuclei, mitochondria, ribosomes, Golgi and membrane-bound vesicles within a plasma membrane bound cytoplasm. The sub-cellularstructures are supported and organized by micro-tubules and endoplasmicreticulumNot all fungi are multicellular; some are unicellular and are termed yeasts. Thesegrow by binary fission or budding, creating new individuals from the parent cell.
  22. 22. 2.1.7. Fungal metabolism Fungi prefer moist habitats and they are largely mesophyllic, preferringtemperatures between 15°C and 35°C. The carbon needs of fungi for energymetabolism and biosynthesis has to be met heterotrophically by one of threelifestyles: -A) Parasitism of plants or animals (causing disease).B) Saprophytism, growing on dead animal, plant or microbial biomass.C) Symbiosis, growing together with algae, plants or insects.2.2 Fungal infections Fungal infections are caused by Fungi. Fungi may be contaminants,opportunistic invaders or pathogens. They can produce harmful effects because ofthe production of mycotoxins by evoking allergic reaction or by direct tissueinvasion. Fungal infections may be primary or superficial when it involves theskin and its appendages, or it may be deep mycosis with secondary manifestationson the skin. A third type of fungal infection is opportunistic infection, occurring inpatients with debilitating diseases.2.1.1 Superficial mycoses. Superficial mycoses are of two types-surface infections and cutaneousinfections. In the former, the fungi live exclusively on the dead layers of the skinand its appendages. They have no contact with living tissue and hence elicit noinflammatory response. The only changes produced are cosmetic effects. Tinea(pityriasis) versicolor, Tinea nigra and Piedra fall in to this group.In cutaneous infection, microorganism is generally confined to the cornified layerof the skin and its appendages but a variety of inflammatory and allergic responsesis induced in the host by the presence of the fungi and their metabolic products.The most important cutaneous infection is dermatophytosis caused by a group ofrelated fungi called the dermatophytes. Clinical surveys carried out in India haveshown ringworm as one of the most common infective organism. Their species
  23. 23. consist, trichophyton, microsporon and epidermophyton. Generally they are calledas Ringworm fungi, which are of three types according to the place they reside:Anthropophilic -reside on humanGeophilic -resides in soilZoophilic -resides on animalsAnthropophilic infections are often episodic in nature. They transmit from humanto human either by direct contact or indirectly by fomites. A relatively non-inflammatory infection often located in the covered area of the body. ChronicT.rubrum infection is the commonest example of non-suppurative lesions causedby anthropophilic species. Once the host skin is inoculated with the fungi undersuitable conditions, various stages follow. These area) Period of incubation,b) Enlargement,c) Refractory period andd) Stage of involution.Once the infection is established in the stratum cornium, two factors are importantin determining the size and duration of the lesion.1) The fungal growth rate must equal or exceed the epidermal turnover rate or the organism will be shed quickly.2) The inflammatory response at the rim of the annular lesions stimulates an increased epidermal turnover in an effort to shed the organism.2.2.2. What causes fungal infections? Fungal infections occur because the mold, mildew or yeast spores aretouched or inhaled and develop into an overgrowth in or on the body. Dependingon the conditions, these infections can be superficial or serious. Under conditionsof moisture, warmth and irritation, these fungi grow rapidly and may cause seriousillness.Superficial fungal infections can be caused by an overgrowth of existing fungi orcan be the result of contact with an infected person or contaminated surfaces and
  24. 24. objects. Fungal infections can be easily spread through bed sheets, towels andclothing. They can also spread from one part of the body to another by scratching.Systemic Fungal infections are often linked to the soil. Usually, they arecontracted when Fungi spores in the soil get inhaled when soil is dug up or blownaround in the air. They can be a chronic problem for people with suppressedimmune systems.Contact with a pathogen (fungal spore) alone will not be enough to cause a fungalskin infection. The fungal spore must be able to enter the skin (e.g. through minorskin lesions) in order for the fungal threads to multiply, and thus to bring about thetypical symptoms of reddening, itching, burning and flake formation on the skin.The sites most frequently affected in healthy people are the skin, hair and nails.Presumably infection is spread mainly a by air-borne spore. This is whyveterinarians do not want ringworm-infected animals to remain in their clinics orhospitals. If this is the case, all of us at one time must be exposed to infections byvarious ringworm fungi. Why is it then that few of us become infected? Why isinfection usually localized, e.g. ringworm of the scalp only occurs in part whilemost areas are not affected? Surely, there are enough spores produced that theentire scalp will be infected. Sometimes one person in a family, or animal in aherd, will get ringworm and it will not spread to others, whereas other times it ishighly contagious. There is a great deal to be learnedaboutringworm.Most people will be affected by a fungal infection, at least once during theirlifetimes. However, there are also some people whose risk of suffering a fungalskin infection is considerably higher. These high-risk groups include, for example, • People who are overweight (increased perspiration) • Sports persons (changing cubicles, showers) • People with metabolic disorders (diabetes mellitus) • People with weakened immune systems (AIDS) and with cancer • Pregnant women
  25. 25. • Elderly people • Young children and drug addicts are also at a higher risk of fungal skin infection.In general, a reduction in the bodys defense mechanism and a deficiency in theskins protective acidic coating (hydrolipid film) contribute to an increase in thesusceptibility to fungal infectionsThe estimated lifetime risk of acquiring a dermatophyte infection is between 10and 20 percent. Recognition and appropriate treatment of these infections reducesboth morbidity and discomfort and lessens the possibility of transmission.Dermatophyte infections are classified according to the affected body site, such astinea capitis (scalp), tinea barbae (beard area), tinea corporis (skin other thanbearded area, scalp, groin, hands or feet), tinea cruris (groin, perineum andperineal areas), tinea pedis (feet), tinea manuum (hands) and tinea unguium(nails).2.2.3. Tinea corporis (Ringworm of the body)The key characteristic of Tinea corporis is that the fungus involves the glabrous(relatively hairless) skin. The infection is limited to the stratum corneum of theepidermis. Vellus hair (the fine hair present on glabrous skin) may be invaded, andthe hair follicle may serve as a reservoir for the fungus. Tinea pedis, Tineamanuum, and Tinea cruris refer to Tinea corporis that is limited to the foot, hand,and groin, respectively. There is otherwise little special about them.History lesson:The term tinea has an interesting origin. A worm of a moth would sometimes growon a woolen blanket. The resulting round holes were similar to the rounded lesionsseen on the skin of patients. The genus name for the moth was Tinea, and thus thisname was used as part of the Latin binomials naming these infections.Epidemiology:Transmission of tinea corporis may occur from direct contact with infectedanimals (especially cats and dogs), infected humans, or contaminated fomites such
  26. 26. as furniture and clothing. Like many other fungal skin infections, warmth andhumidity favor the occurrence of this infection. Therefore, tropical and subtropicalregions have a higher incidence of tinea corporisClinical features:In hot humid climates, ringworm infection of the glabrous skin are much morecommon. Classically, the lesions are circinate and and this has lead to the termringworm .the lesion starts as an erythematous itchy papule which enlarges toform a ring. The centre is relatively normal and the borders are active, elevatedand may be vesciculopapular. The lesions may be single or multiple and eachlesion may enlarge up to 10 cm. Neighbouring lesions may become confluent.Aetiology and pathogenesis In India, T.rubrum accounts for the majority of cases of T.corporis.Theorganism invades the stratum corneum possibly aided by warm, moist, occlusiveconditions and resides in it. After about 1-3 weeks of incubation, it startsspreading centrifugally. The active advancing border has an increased epidermalturnover rate, presumably an attempt to shed the organism by exceeding the fungalgrowth rate. This defence mechanism is successful to a certain extent as there isrelative clearing of infection in the centre of the annular or polycyclic lesions.Temporary resistance to infection occurs in this area for a variable time; however,second waves in re-infection are commonly seen later. In addition to involvementof the stratum corneum, hair follicle involvement may also occur.2.2.4. Tinea cruris (Jock itch, ringworm of the groin) Tinea cruris is an acute or chronic infection of the groin, perineum, andperianal region.Epidemiology: This dermatophytoses is more commonly seen in men. According to Martinet al., the apparent reasons for this include:The temperature, humidity, and occlusion of the scrotum and groin area, especiallyrelated to the clothing, are ideal for the development of these fungi.
  27. 27. Men suffer more frequently from other dermatophytoses, particularly tinea pedis,and cross infection between sites is very common.Both direct contact between infected individuals and indirect contact withnonliving contaminated objects (towels, clothing, bed linens, urinals, and bedpans) are ways of transmission. Tropical climates and summer months intemperate regions appear to promote higher rates of this infection.Clinical manifestations: Tinea cruris presents with sharply demarcated lesions with a raisederythematous margin and thin dry epidermal scaling. Papulovesicular lesions mayalso be present but pustules such as those caused by candida are very unusual.Lesions classically involve the genitocrural area and medial upper thigh in asymmetrical fashion, but asymmetrical involvement may occur. The scrotum isusually minimally affected, and this is a distinct contrast with infections of thisarea by Candida (‘Intertrigo’). Extension to the pubic area, lower abdomen,buttock, and perianal areas occurs rarely but can be seen, especially ifTrichophyton rubrum is the causative agent. Patients complain initially of intensepruritus, but the lesions will become painful if maceration and superinfectionoccur. In addition to candidiasis ("intertrigo"), the differential diagnosis alsoincludes lichen simplex and erythrasma.During summer months, the prevalenceincreases due to the chances of accumulation of sweat.The infection is highly contagious and is usually transmitted through contaminatedtowels or the floors of bathrooms, showers, or hotel rooms. In many cases, patientswho present with tinea cruris also have tinea pedis, both caused by the samefungal species. Severe maceration may lead to subsequent bacterial superinfection. If the penis or scrotum is involved, the infection is probably due tocandidiasis rather than tinea.2.2.5 Tinea versicolor Tinea versicolor is an infection of the stratum corneum epidermidis wheresebaceous glands are present. Caused by the lipophilic yeast M. furfur (previously
  28. 28. called Pityrosporum orbiculare), it is not contagious and in most cases represents ashift in the relationship between a human and his or her resident yeast flora. Tineaversicolor commonly causes small round or oval macular areas ofhyperpigmentation or hypopigmentation. The back, chest, and shoulders areusually affected; facial involvement is particularly common in children. Hightemperature and humidity are predisposing factors involved with this condition.Patients most often have multiple, discrete macules or patches on the trunk thatmay coalesce into larger patches. The macule is characterized by fine, dustlikescaling with variations in skin color. The color of the macules ranges fromhyperpigmented in untanned white skin, to hypopigmented in tanned or dark skin.2.2.6 Tinea capitis Tinea capitis is the most common mycotic infection in children. Thepredominant age range affected is between 3 and 7 years. Initially, the areaaffected by tinea capitis is flat and scaly, but ultimately it becomes raised. Thecardinal clinical feature of this infection is the combination of inflammation withhair breakage and loss. Most patients who have any degree of inflammationultimately have retroauricular or posterior cervical lymphadenopathy2.2.7 Tinea pedis (Athletes foot, ringworm of the foot) Tinea pedis is a fungal infection of the feet, principally involving the toewebs and soles.Epidemiology: This infection is related to footwear and is considered to been a ‘new’dermatophytoses in that it began in association with use of footwear. Moreocclusive shoes are associated with higher chances of having tinea pedis. Contactwith bath or pool floors is another recognized risk factor and the rate of infectionincreases in relation with the number of people using the facilities. The infection ismore common during summer months and in tropical climates.
  29. 29. Clinical manifestations: Tinea pedis may present in several ways, varying from mild chronic scalingto acute lesions that are exfoliative, pustular, or bullous. 1. Tinea pedis: this form typically affects the toe webs and subdigital areas producing chronic scaling, fissuring and maceration. The 4th to 5th and 3rd to 4th interdigital areas are the most commonly affected. Some studies have implicated the interaction of dermatophytes with the mixed skin flora characteristic of this area in the pathogenesis of this infection . 2. Tinea pedis with a papulosquamous pattern ("moccasin-like"): as the name suggests, this form affects the soles and lateral aspects of the feet in a pattern suggestive of the skin covered were one wearing a moccasin. Scaling is the main process while inflammation is minimal. This type is usually bilateral and interestingly may present with concomitant involvement of one hand in a pattern called "one hand, two feet". 3. Vesicular or vesiculobullous tinea pedis: this form involves the instep and the mid-anterior aspect of the sole. It causes small, confluent vesicles or vesiculopustules surrounded by scaling. Scales may extend to the toewebs. Occasionally, large bullae appear. 4. Ulcerative tinea pedis: this type causes a more acute and symptomatic picture characterized by maceration and ulceration of large areas of the soles. White hyperkeratosis and a strong heady odor are characteristic. Bacterial superinfection, usually with gram-negative organisms, is frequent and should be taken into account at the time of treating this condition.Despite the previously detailed characterizations, it is not unusual to see apresentation in which there is overlap of two and even three of these clinicalvarieties. A correlation between lower extremity erysipelas and tinea pedis hasalso been established
  30. 30. Tinea pedis is regarded as a fungal infection of the feet that is caused bydermatophytes. In families, tinea pedis tends to spread throughout the household.It is communicable for as long as the infection is present. The differentialdiagnostic considerations include juvenile plantar dermatosis, dyshidrotic eczema,atopic and contact dermatitis, erythrasma (a superficial bacterial infection causedby Corynebacterium minutissimum), and other bacterial infections withstaphylococci, streptococci, or gram-negative organisms.The most common clinical form is an intertriginous dermatitis characterized bypeeling, fissures, itching, and maceration that affects the toe clefts. In T. rubruminfection, a squamous hyperkeratotic variety of tinea pedis may occur. Thisvariation is particularly chronic and resistant and affects the sole, heel, and side ofthe foot. Affected areas are pink and covered with fine, silvery white scales. If thefoot is extensively involved, the condition is called "moccasin foot"2.2.8. The ‘ID’ reaction Patients infected with a dermatophyte may show a lesion, often on thehands, from which no fungi can be recovered or demonstrated. It is believed thatthese lesions, which often occur on the dominant hand (i.e. right-handed or left-handed), are secondary to immunological sensitization to a primary (and oftenunnoticed) infection located somewhere else (e.g. feet). These secondary lesionswill not respond to topical treatment but will resolve if the primary infection issuccessfully treated2.2.9. Defense against fungi Defense against the fungi causing ringworm depends on both innate andacquired immune mechanisms, the latter requiring the intervention ofimmunological memory.Serum factors appear to be able to inhibit the growth of dermatophytes in vitro,and on cultured explants of skin. It is not entirely clear what is responsible for this,but unsaturated transferrin is one candidate, which inhibits the growth ofdermatophytes by binding to the hyphae. Its mode of action appears to be
  31. 31. independent of iron-binding capacity. In experimental infections of skin graftedonto nu/nu mice, there is evidence of increased turnover of epidermis, whichoccurs in the absence of effective T-lymphocyte-mediated defense.A further, potentially important mode of defense is provided by the presence offatty acids from sebaceous glands, which inhibit dermatophyte growth in vitro.This activity appears to reside in saturated fatty acids with chain lengths of 7, 9, 11and 13 carbon residues. It has been postulated that their presence on the skin inpost pubertal children may account for the spontaneous resolution of tinea capitisafter this age, and the rarity of new infections in adults. Undecenoic acidderivatives are a practical example where fatty acids have been used for thetreatment of dermatophytos.A further potential factor is the ability of commensal Malassezia yeasts forlipolysis, which may increase the pool of fatty acids available for inhibitoryactivity. Whatever the influence of these factors, it is clear that in experimentallyinfected mice the initial inflammatory changes occur as early in the process as 4hafter infection. This suggests that endogenous mechanisms may attract leukocytes,and the role of inflammatory mediators such as the eicosanoids, in this respectneeds to be investigated.It has also been found that dermatophytes are chemotactic, and that they canactivate the alternative pathway of complement activation. This has beendemonstrated for T. rubrum,T. mentagrophytes and fungi causing endothrix scalpinfections, such as T. violaceum. The production of cytokines, such as interleukin1 (IL-1), by keratinocytes has not been investigated in the mobilization ofneutrophil defenses.It has been shown that neutrophils, and to a lesser extent monocytes, can killdermatophyte conidia. This activity depend both on intra- and extra cellularmechanisms, and the generation of the respiratory burst is an important stage inthis process. Dermatophytes produce catalase and superoxide dismutase, whichmay act as defenses against the phagocyte myeloperoxidase system. By contrast,
  32. 32. there is little evidence that antibodies to dermatophytes are protective. Patientswith widespread infections, such as tinea imbricata, may have high antibody titers. The presence of elevated IgE in particular is associated with chronicity. Transferof specific serum containing a high titer of antibody to irradiated mice does notconfer immunity on recipients. It is still premature to rule out a role for antibody,as dermatophytes show some cytological changes when grown in the presence ofspecific antibody in vitro. There is, however, strong evidence that the developmentof cellular immunity via sensitized T-lymphocytes is a key factor inimmunological defense. Lymphocytes bearing T-helper phenotypic markers areresponsible for transferring immunity to infection to naïve recipient mice. Inhumans, the appearance of inflammation in ringworm correlates with thedevelopment of delayed-type skin reactivity to trichophytin.Chronic infections are associated with poor T-lymphocyte-mediated response tospecific fungal antigens, suggesting that depression of responses is responsible forthe poor clinical response. Other in vitro parameters of resistance, such asleukocyte-migration inhibition and leukocyte adherence, may also indicate that T-lymphocyte-mediated pathways are involved. Langerhans cells can act as antigen-presenting cells for dermatophyte antigens.The reasons for failure of immunity in persistent infections, and its relationshipwith chronicity, are still not well understood. There is an association between thepresence of atopy and chronic dermatophytosis, with a high proportion of thosewith persistent disease having atopy (usually asthma or hay fever) as well asimmediate-type hypersensitivity and raised IgE levels. It has been suggested thatmodulation of T-lymphocyte activity either locally or systemically may beresponsible.It has also been found that dermatophyte antigens, including those that containmannose residues, can reversibly suppress lymphocyte proliferation, but not theexpression of human leukocyte antigen (HLA)-DR Patients with persistentinfection have detectable levels of circulating antigen. Both are possible factors in
  33. 33. the regulation of immunity in dermatophytosis. Patients with dermatophytosis areusually otherwise healthy. However, altered or chronic infections have been notedin a number of patient groups, such as those with chronic mucocutaneouscandidosis, AIDS and patients on corticosteroid therapy or with endogenousCushings syndrome. In addition to these, there is the raised incidence of atopy inthose with chronic infection, suggesting that host factors may well determine theclinical course.2.2.10 Diagnosis Clinical wisdom of the physician remains the most important factor indiagnosis of superficial fungal infections. Historical data and predisposing factorsare also crucial to elicit. To confirm a diagnosis, physicians have essentially threetest options.Potassium hydroxide preparation The potassium hydroxide (KOH) preparation is the most rapid, convenient,and sensitive test for diagnosis. A sample of scale, nail, or hair is obtained with ascalpel or cotton swab. The active border or edge of a suspicious lesion is best forobtaining a specimen. The material is placed on a glass slide, and 10% to 20%KOH is added with or without dimethyl sulfoxide. (If dimethyl sulfoxide isincluded, heating is generally not necessary.) The skin or hair sample is placed ona slide with potassium hydroxide (KOH) solution and gently heated. This solutionslowly dissolves the skin cells but not the fungus cells. The fungus cells can thenbe seen with a microscope. Color stains may be used so that the fungus is easier tosee. Findings of a KOH test may include the following.Normal: No fungi are present in the skin or hair samples. Other tests may be done to determine the cause of the skin infection.Abnormal: Fungi are present in the skin or hair samples.
  34. 34. A positive KOH test shows numerous septate hyphae under microscopicexamination. Overall, the sensitivity of the KOH technique is 88%, but thesensitivity is less than 50% for tinea capitisWood’s light (Ultraviolet radiation) examination Examination under Wood’s lamp is used for the confirmation of thepresence of fungus. With ultraviolet light, Microsporum species, which causeabout 10% of tinea capitis, show a bluish green fluorescence under Woods light;the scaly lesions of pityriasis (tinea) versicolor fluoresce yellow to yellow-green.Fungal culture The standard fungal culture medium is Sabourauds dextrose agar.Appropriate agar choices include dermatophyte test medium and Mycosel andMyco-Biotic agars. Scale and affected nail or hair can be obtained by gentlyscraping a moistened area of involvement with a scalpel, cotton-tipped applicator,or toothbrush and placing the sample on the surface of the appropriate agar. Aphenol red indicator in the agar turns from yellow to red in the area surrounding adermatophyte colony. Malassezia furfur, the pathogen in tinea versicolor, grows invitro only with the addition of fatty acids to the medium and rarely needs to becultured. Fungal cultures are useful primarily in scalp and nail infections or whena diagnosis is in question, but the required incubation at room temperature for 2 or3 weeks is a disadvantage.2.3 General treatment options Modern treatment method against dermatophytes gives importance to thefungicidal action of medicines. For this purpose, they use both internal as well asexternal medications. Commonly used drugs are, Itraconazole, terbinafinehydrochloride, Ketoconazole, selenium sulfide and griseofulvin. Though theirpharmacokinetics slightly differs, all will cease the proliferation of fungus veryeffectively.Localized fungal infections, like tinea corporis, especially of recent origin,commonly responds to topical therapy applied twice daily, usually for about a
  35. 35. month. Topical terbinafine often works in a shorter time (e.g. 2 weeks). Oralantifungal medications may be required to treat dermatophyte infections in caseswhere the patient resists topical therapy (Noble SL, Forbes RC, Stamm PL.Diagnosis and management of common tinea infections. Am Fam Physician1998;58(1):163-781). Griseofulvin has been used successfully for treatment ofsuperficial dermatophyte infections for more than 30 years. It is best absorbedwhen taken with a fatty meal. In more widespread infections of recent onset, oralterbinafine or itraconazole will generally be preferred, and may be expected toclear the condition in about 2-3 weeks depending on the dose used. Withgriseofulvin, much longer-term treatment is needed, for up to several months withextensive infections.Modern treatment method against dermatophytes gives importance to thefungicidal action of medicines. For this purpose, they use both internal as well asexternal medications. Commonly used drugs are, Itraconazole, terbinafinehydrochloride, Ketoconazole, selenium sulfide and griseofulvin. Though theirpharmacokinetics slightly differs, all will cease the proliferation of fungus veryeffectively.Localized fungal infections, like tinea corporis, especially of recent origin,commonly responds to topical therapy applied twice daily, usually for about amonth. Topical terbinafine often works in a shorter time (e.g. 2 weeks). Oralantifungal medications may be required to treat dermatophyte infections in caseswhere the patient resists topical therapy (Noble SL, Forbes RC, Stamm PL.Diagnosis and management of common tinea infections. Am Fam Physician1998;58 (1):163-781). Griseofulvin has been used successfully for treatment ofsuperficial dermatophyte infections for more than 30 years. It is best absorbedwhen taken with a fatty meal. In more widespread infections of recent onset, oralterbinafine or itraconazole will generally be preferred, and may be expected toclear the condition in about 2-3 weeks depending on the dose used. With
  36. 36. griseofulvin, much longer-term treatment is needed, for up to several months withextensive infections.2.4. Prevention Several important steps can be taken to prevent fungal infections. Practicegood personal hygiene, skin should be kept clean and dry. Household sources offungus such; as showers, bathtubs, floors should be maintained by cleaningregularly with warm water and a disinfectant.If a member of the household has a superficial infection, be sure to keep sheets,towels and clothing separate and clean. Contact with a pathogen (fungal spore)alone will not be enough to cause a fungal skin infection. The fungal spore mustbe able to enter the skin (e.g. through minor skin lesions) in order for the fungalthreads to multiply, and thus to bring about the typical symptoms of reddening,itching, burning and flake formation on the skin. The sites most frequentlyaffected in healthy people are the skin, hair and nails.Fungal infections should be treated as soon as possible, in order to prevent anyfurther spread of the cause of the disease. For example, a fungal infection of thefoot that is not taken to be seen by a doctor in good time is allowed to develop intoa fungal infection of the nail. The treatment for this is much more difficult andtakes much longer. Fungal infections of the hand and feet usually need about 2 to5 weeks treatment (with complete re-growth of the new skin tissue in about 28days). Equally important: Even if the symptoms of the fungal infection havedisappeared (itching, reddening, burning, flaking, etc.), medical treatment must becontinued for another 1-2 weeks until healing is complete, in order to avoid therisk of the fungal skin infection flaring up again.Fungal skin infections love the damp and the warmth, so please follow these rulesof conduct to minimise the risk of repeated fungal infection:
  37. 37. • Do not wear clothes that prevent air circulation (synthetics). Do not wear trainers or rubber shoes for too long. • Wherever possible, wear clothes that can be boil washed (many fungal spores can easily withstand being washed at 60 degrees!). • Change your underwear every day, and especially after you have perspired heavily. • Do not walk barefoot in "risky" areas (changing cubicles, swimming pools, gymnasiums etc.). • Use a disinfectant foot bath as often as possible in public baths and showers. • Use mild skin cleansing substances rather than alkaline soaps. • Dry thoroughly after washing. Strengthen your immune system in general and keep your circulationworking wellReference:1 Text Book of Microbiology, Ananthanarayan & paniker, 7th edn.2. Text Book of Preventive and Social Medicine, K. Park, 14th Edn.3. Text book of Dermatology, edited by R.H.Champion,Cambridge.4. Textbook of Dermato-Epidemiology, Strachan D,Williams HC.5. Microbiology of Human Skin, Noble WC. London 1981.6. Medical Mycology, Chung KJ, Bennett JE. Philadelphia: 1992.7. Dermatology, Samuel L Moschella, Harry J Hurley.
  38. 38. PART 3 Skin and Skin diseases Before entering in to the details of Ayurvedic enquiry of the subject, it willbe better if we have an over all idea about the structure upon which the disease getmanifested. The basic structural and functional aspects of skin in modern as wellas in Ayurvedic perspective are discussed in this chapter.The SkinHuman skin is a biological marvel. Skin is the largest organ in the body. It formsthe outermost protective covering of our body. In Latin, skin means, the covering.The skin is composed of a superficial epithelial layer ‘the Epidermis’ & theunderlying connective tissue layers ‘The Dermis or corium’. Beneath the coriumthere is another connective tissue layer, rather loose in texture ‘The Hypodermis’or subcutaneous layer.The free surface of the epidermis is marked by a network of linear furrows &ridges of various sizes. In different body parts, the epidermal arrangement showswide variety.Epidermis:The epidermis, composed of epithelial cells is formed from the ectoderm of thefertilized ovum. It consists of 5 layers devoid of blood vessels, which from thebasal to the superficial are as follows – 1. Stratum basale or germinativum- Forms the lowest layer & consists of single row of columnar cells & is capable of continued cell division. As these cells multiply, they push up towards the surface & becomes part of the upper layers. The appendages of the skin are also products of this layer of cells.
  39. 39. 2. Stratum spinosum or malphigi -This prickle cell layer lies upon the basal layer & has 5 to 10 rows of polyhedral cells that fit close together. This layer involves most of the pathological conditions of the skin. 3. Stratum granulosum -It consists of about three rows of flattened rhombic granular cells. The granules vary in size & are highly reflectable. They consist of semisolid substance known as keratohyalin, which helps to form keratin. 4. Stratum lucidum -This layer is a thin clear strip of glistening, translucent, flattened cells without granules or nuclei. 5. Stratum corneum -The horny layer consists of several rows of flattened completely cornified horn cells containing a fatty & waxy material but no nucleus. The surface row of the cells appears as thin dry scales. This layer is thickest on the palms & the soles & thinnest on the eyelids & prepuce.Dermis: The dermis chiefly consists of white fibrous tissue, elastic fibers & nonstriped muscles & contains blood vessels, nerves, hair, sweat gland & sebaceousglands & nerve corpuscles. Finger like processes known as papillae projectupwards into the overlying epidermis followed by the reticular layer, which isformed of coarse, dense, interlining collegen fibres, a few reticular fibres &numerous classic fibres.The subcutaneous tissue or hypoderm resembles in its upper portion, the reticularlayer of the corium from which there is no distinct line of demarcation.Blood supply: There are two horizontal & parallel systems of plexuses which supply theskin. The plexus or network of blood vessels exists between the dermis & thesubcutaneous tissue. Its exact position can never be accurately described. Eacharteriole supplies an area of skin & each venous plexus associated with it drainsthe same area.
  40. 40. Nerve supply: The nerve supply of the skin is very complicated, & the pathway for themediation of sensations through the various nerves is very much under debate. Thevaried sensations arising from skin are derived from a diverse population ofcutaneous nerve endings or receptors. Thus tactile, temperature & pain sensationare each sub served by different groups of receptors.Lymphatic drainage of the skin:Numerous blind-ending lymphatic vessels terminate in the dermis near the base ofthe epidermis & drain deeply first into a dermal network in the papillary layer,then into another network at the junction of the dermis & superficial fascia. Deepto this zone, the lymph flows through wider channels provided with valves, intothe main lymphatic drainage of the area. The lymphatic drainage of the skin isquite profuse & free anastomosis appears to occur between vessels at all levels sothat there is free interchange of lymph between areas of the skin which areadjacent to each other.Function of the skin:1. Maintains thermoregulation2. Protects against mechanical injury3. Prevents entry of noxious chemical & micro-organisms4. Screens & reduces penetration of radiation5. Prevents loss of body contents6. Provides a frictional surface for grip7. Discourages microbial growth8. Restricts electrical conductivity9. Serves as the outpost of the sensory nervous system10. Serves as the outpost of the immune system11. Signal emotions via the autonomic nervous system12. Synthesises vitamin ‘D’
  41. 41. 3.2 Thwacha -The Ayurvedic View Acharya Sushruta has given the simile of development of cream, whileexplaining the origin of Tvacha. As, a layer of cream develops over the boiledmilk; in a similar fashion a layer Tvacha is thought to develop after thefertilization of ovum. (1)According to Charaka, the six layers of the Tvak are formed from the MamsaDhatu (2).Whereas, Vagbhata holds the opinion that the Tvak is formed from the Rakta.After the Paka of Rakta by its Dhatwagni, it gets dried up to form the skin, like thedeposition of cream on the surface of boiling milk. (3) There are six Bhavas(factors) which have been considered responsible in the formation of Garbha.Tvak is formed & nourished by Matrija Bhava.Acharya Vagbhata has stated 7 layers of skin. Formation of layers is due toParipaka of Rakta Dhatu by Ushma. Sharangdhara has also named the layersfollowing the Sushruta except the 7th layer. He has named this layer as ‘Sthula’,the site of Vidradhi. (4).Acharya Gangadhara (5) clarifies the difference of opinion between AcharyaCharaka & Sushruta that the third layer told by Charaka has two parts, superficial& deep. The superficial part is the third layer (sweta), while the deep part is thefourth layer (Tamra) as told by Sushruta. Thus fundamentally there is nodifference in the number of layers told by both Acharyas, Charaka & Sushruta.Acharya Vagbhata has stated seven layers of skin Arundatta & Hemadri havenamed them in compliance to Sushruta in their commentary (6).Tvacha & Mahabhuta Tvacha, though Panchbhautic, has Pruthvi Mahabhutadhikya (7). Tvacha isthe Indriya Adhisthana of Sparshanendriya which has Vayu Mahabhutadhikya (8)
  42. 42. Sparsha: Perception of tactile sensation is the function of Vata Dosha. Tvachaworks as a sensory organ (being Adhisthana of Sparshanendriya, Vata Dosha isthe main Dosha situated in Tvacha. (9) & is responsible for maintaining lusture ofthe skin. (10)Mala: Sweda is one of the Trimalas which maintains lusture & turgidity of theskin. (11)Layers of Skin: Acharya Sushruta has described seven layers of Tvak. Description of layersfrom above downwards is as follows –Name Thickness DiseasesAvabhasini 1/18th Vrihi Sidhma & PadmakantakaLohita 1/16th Vrihi Tilakalaka, Nyachcha & VyangaSweta 1/12th Vrihi Charmadala, Ajagallika & MashakaTamra 1/8th Vrihi Kilasa & KusthaVedini 1/5th Vrihi Kustha & VisarpaRohini 1 Vrihi Granthi, Arbuda, Galaganda, Apachi, SleepadaMansadhara 2 Vrihi Bhagandara, Vidradhi, ArshaDescription of skin according to Charaka – (12). No. Name Diseases take place 1 Udakadhara Contains Udaka means watery substance or lymph 2 Ashrukdhara Contains blood capillaries 3 3rd layer Manifestation of Sidhma & Kilas 4 4th layer Manifestation of Dadru & Kustha 5 5th layer Manifestation of Alaji & Vidradhi 6 6th layer Manifestation of Arunshi
  43. 43. 3.2.1 Role of various internal factors in maintaining the health of the skin: According to Ayurveda, functional activity of any part of the body ismaintained by different forms of Doshas, dooshyas malas and ojus. (13). Skin isnot an exemption from this. Let us analyze the role of each factor, in the integrityof normal skin.Doshas: By a broader generalization, functions of the body are three, viz. motion,transformation and growth including maintenance. ‘Motion’ connotes, apart fromthe external voluntary movements, all the kinetic processes taking place in everycell. This function is attributed to vata. ‘Transformation’ includes separation ofdifferent portions of nutrition and formation of the structure. This also causesgeneration of heat. These are related to pitta. Functions of kapha are more relatedto stability and repair of the compact structure of body parts. Ref-(14)The table given below explains this principleVata: Generally vatha dosha controls all the kinetics in dermal physiology. Eachsingle action will have the involvement of different properties in different degrees.Properties Possible functions in skinRuksha Keeping the necessary dryness (Soshana)Sita Keeping the necessary limits (Sthambhana)Laghu Keeping the Lightness (Langhana)Khara Keeping the Roughness& hardnessSukshma Spread of factors through srotusChala Motion of various factorsVisada Lack of flexibility of structural forms
  44. 44. Pitta: Generally pithadosha controls all the transformation processes inside thedermal system.Properties Possible functions in skinSasneha Keeping the normal moistureTikshna Penetration through minute channelsUshna Keeping the temperature, in normal levelLaghu Keeping the LightnessVisra Maintaining a smell to skinSara Flow of materialsDrava Discharging the enzymes and hormones at proper spots.Kapha: Generally kaphadosha controls all the nutritive and strengthening functionsin skin.Properties Possible functions in skinSnigdha Keeping the normal moisture (kledana)Sita Keeping the necessary limits (Sthambhana)Guru Providing the nutritive functions.Manda Necessary slowness in actionSlakshna Slimy discharges from various spots.Mritsna Slimy discharges.Stira Keeping the essential strength in the interconnections between the layers and among the components.Generally vitiation of Doshas will create some objective as well as somesubjective symptoms in the body. They are described by the following reference-Dosha vikrithi avastha (vitiated states) Effects due to the vitiated doshas (15)
  45. 45. Vatha Pitha Kapha1.Loosness (sramsa) 1.Burning sensation (daha) 1.Coldness (saithya)2.Dislocation (Bhramsa) 2.Heat (oushnya) 2. Whitish (Swaithya )3.Dilation (Vyasa) 3.Suppuration (paka) 3,Itching (kandu)4.Obstruction(sanga) 4.Perspiration (sweda) 4.Heaviness (gouravam)5.Seperation (bheda) 5.Softening (kleda) 5.Stability (sthairryam)6.exhaustion (sada) 6.Putrifaction (kodha) 6.Fixation (bandha)7.Excitation (Harsha) 7.Itching (kandu) 7.Rigidity (sthaimithya)8.Thirst (trisha) 8.Redness (ragam) 8.Hardness (kaadinya)9.Tremour (kampa) 9.Discharge (sravam) 9.Oedema (sopha)10.Round masses (vartha) 10.Fainting (moorcha) 10.Numbness (supthi)11.Pulsation (chala) 11.Intoxicated (mada) 11.Indigestion (apakthi)12.Pricking (toda) 12.Weakness (sadam) 12.Unctuousness (sneha)13.Aching (vyadha) 13.Pungent/sour tastes 13.Softening/exudation14.convulsions (cheshta) (katu/amla) (kleda )15.Tightness (veshtanam)16.Harshness (prusha)17.Non sliminess (visada)18.Porousness (sushira)19.Dusky redness (aruna )20.Dark (syamavarnatha)21.Astringenttaste(kashaya)22.Wasting (sosha)23.Piercing pain (soola)24.Numbness (supthi)25.Contraction (sancocha)26.Rigidity (sthambhana)27.Lameness (ghanjattha)
  46. 46. In the case of skin disease, Doshic predominance is assessed by some selectedfeatures from the above i.e. as far as Ayurveda is concerned, in the process ofdiagnosis, naming of the condition is not at all relevant than the doshapredominance of the stage. So assessment of the state of doshas should be givenprime importance in the process of diagnosis.Doshic predominance Any skin manifestation should be assessed on the basis of the doshapredominance.Vathika Syava,aruna, thanu, visarpini,thoda bheda,swapayuktha (Blackish,Reddish,Smooth,Spreading,Pain with numbness)Paithika Raga,osha, chosha, paridaha, dhoomayana, sweda, khshiprodhana, prapakabheditwa,krimijanma Kleda,sruthi.kodha (Reddish, Throbbing pain, Burning, hotness, sweating, sudden manifestation,spreading, origin of organisms, moisture,discharge, putrifaction)Kaphaja Uthsannatha, parimandalatha, kandu, chirothana,snigda, kadina, sopha (Rised,circular, Itching, longlasting, oily, hard,swelling)Dooshyas: As doshas are the Principal units of body functions, dooshyas are theSubunits. Each dooshya has a significant role in maintaining the structuralintegrity of the skin. We can elaborate this principle in this way-Rasa dhathu - Main part of the structure of skin,Raktha dhathu - Provides colour, nutrition and resistanceMamsa dhathu - Forms a slimy coatingMedo dhathu - Maintains an oily and balanced equilibrium
  47. 47. Asthi dhathu - Maintains the general firmness and formMajja dhathu - Forms the main source of unctuousness to the skinSukla dhathu - Forms the hereditary factor for skin (Ref-16)Mala: Among the malas, Sweada and Moothra are the main factors related withthe Skin. They can control the moisture content of the body which in turn cancontrol the moistness of the skin. In each membrane of the skin, moistness is veryessential for various transformations. So, vitiation of sweada causes effects onskin.(17 )Sweada is the form of excretion through the skin. So any obstruction in thisexcretion will cause malasanchaya at various levels of skin.Ojus: The principle of Ojus provides efficacy needed for all the processes ofdhathus. So, for the proper nutrition, resistance power and health of the skin, goodojus is essential. Diseases like AIDS, in which the status of ojus is reduced verymuch, various pathogenic organisms may invade in to the skin, causing variousinfectious skin diseases.3.2.2 Assessment of the health of skin (18) According to Ayurveda, ‘Sara’ is the principle, which forms the criteria forassessment of the health of different entities in body. By external appearance ofcertain parts, we can assess the health of associated organs. For the assessment ofthe health of skin and associated organs, we should take the criteria of ‘Twak sara’1. Snigdatha (Unctuousness)2. Slakshnatha (Smoothness)3. Mriduthwa (Softness)4. Prasannatha (Fairness)5. Sookshma, Alpa, Gambheera, Sukumara loma (minute, small, deep rooted andfair hairs)
  48. 48. 6. Saprabha (Lustrous)These are the assessment criterion. Optimum presence of all these factors incombination indicates good health of the skin. If any factor found in excess or indeficient, that indicate the reduction in skin health.Interpretation: According to Ayurvedic principles, formation of Twak (skin) is from theRakta. After the Paka of Rakta by its Dhatwagni, it gets dried up to form the skin,like the deposition of cream on the surface of boiling milk (19).So it has manyrelations with the organs of Rakthavahasrothas. Alterations in the functions of anyof these organs may precipitate deficient skin health.Yakrith (Liver) and Pleeha (Spleen) are the two main parts of Rakthavaha srothas.Liver maintains the major functions of detoxification and metabolism. Spleen isconcerned with the life of red blood cells. According to Ayurvedic principles, roleof these organs in dhathu parinama is very critical. The enzymes concerned withtheir functions can be correlated with the fractions of dhathwagni. Biochemicalaspects of these enzymes will prove their importance in maintaining many bodyfunctions. Lack or deficiency in these enzymes may block or alter certainmetabolic transformations, creating many abnormalities. In many skinmanifestations, this concept is very relevant. So, assessment of the health of skin,in other terms gives ideas about the health of internal organs of RakthavahaSrothas.In many contexts, we may notice the abnormalities in dhathwagni,leading toillhealth of the skin. For eg; medodhathwagnidushti happening in prameha leads tothe ill health of skin (20) resulting in prameha pidaka. (Carbuncles in Diabetes).Here a correlation with modern concepts proves the incidence of streptococcalbacterial invasion in to the skin due to the decrease in resistance power of skin.Actually, the abnormality happened inside the body makes the nest suitable forforeign microbial, and thus they enter in to the body.
  49. 49. 3.3 Skin Diseases Skin is the first organ of the body interacting with the environmentalagents like physical, chemical & biological agents. Variations in theenvironmental stimuli & natural ability of body to deal with these factors result inspontaneous remissions & relapses. Interaction with these factors results inspecific reaction pattern producing characteristic skin lesions in different parts ofthe body. Large community prevalence studies have demonstrated that between20-30% of the population have various skin problems requiring attention.(Davidson 18th Ed.) Skin is a mirror that reflects internal & external pathology &thus helps in diagnosis of diseases. In Dermatology, we can observe a wide arrayof skin manifestations with different names. In present day science, it is observedthat there are over 2000 skin disorders. Depending upon the etiology, they can beclassified into various groups such as, Genetic, Autoimmune, Allergic, Infectious,Traumatic, Developmental, Occupational Climatic etc. Skin diseases affect theindividual in 4 ways .i.e. Discomfort, Disfigurement, Disability and Death.Among the infectious diseases, include mainly Bacterial, Viral and Fungal skindiseases.3.3.1 Bacterial infection The normal human skin is colonized by huge numbers of bacteria that liveharmlessly as commensals on its surface and within its follicles. At times,overgrowth of some of these resident organisms may cause minor disease of theskin or its appendages. On other occasions, bacteria not normally found there maycolonize the epidermis and lead rapidly to disease. Major bacterial diseases of theskin-
  50. 50. Organism DiseaseCommensals Erythrasma,Pittedkeratolysis,Tricho mycosis axillarisStaphylococcal Erysipelas,Ecthyma,Folliculitis,Streptococcal Erysipelas,Cellulitis,Impetigo,EcthymaMycobacterial LupusvulgarisSpirochaetal syphilisThe normal human skin is colonized by huge numbers of bacteria that liveharmlessly as commensals on its surface and within its follicles. At times,overgrowth of some of these resident organisms may cause minor disease of theskin or its appendages. On other occasions, bacteria not normally found there maycolonize the epidermis and lead rapidly to disease. Apart from the arrival of thesefrankly pathogenic organisms, a wide range of bacteria land more or lessfortuitously on the skin, and linger briefly in small numbers before disappearing,unable to multiply and thrive in this relatively inhospitable environment.Bacteriological sampling will reveal the presence of these otherwise unsuspectedtransients. Organisms not normally considered as resident members of the skinflora may sometimes colonize and become established in modest numbers forrelatively long periods. Bacteria of this intermediate category have been labelledtemporary residents. Furthermore, certain sites such as the skin of the face may berepeatedly contaminated from the nostrils or mouth by Staphylococcus aureus orhaemolytic streptococci, giving the false impression that these organisms aremembers of the normal facial flora.3.3.2. Viral infection Normally, human skin contains no virus. For a virus to produce infection,it must gain entry into a susceptible cell within an appropriate host. Many viruses,in particular those producing systemic infection, enter the body via mucousmembranes after inhalation, ingestion or contact. The skin can act as a portal of
  51. 51. entry, but this usually depends on some break of the barrier function of theintegument, for instance a scratch or fissure, or by direct inoculation. Attachmentto the cell surface by means of a receptor is followed by entry of the virion into thecell, by pinocytosis or phagocytosis.About fungal infection, detailed discussion is done afterwards.Major viral diseases of the skin:Organism DiseaseHerpes virus hominis Herpes simplexVaricella zoster Herpes zosterHuman papilloma virus Viral wartsDNA pox virus Molluscum contagiosumPathogenesis of viral disease: For a virus to produce infection, it must gain entry into a susceptible cellwithin an appropriate host. Many viruses, in particular those producing systemicinfection, enter the body via mucous membranes after inhalation, ingestion orcontact. The skin can act as a portal of entry, but this usually depends on somebreach of the barrier function of the integument, for instance a scratch or fissure,or by direct inoculation. Attachment to the cell surface by means of a receptor isfollowed by entry of the virion into the cell, by pinocytosis or phagocytosis.Viruses differ in the range and type of cells which they can infect; host specificityand tissue tropism are hallmarks of viral infections. Poliovirus, for example, caninfect neurones and is called a neurotropic virus, and human papillomaviruses(HPV) have a tropism for epithelial cells. A cell in which a particular virus canreplicate is described as permissive for that virus. After entry into the cell, pre-existing cell enzymes remove or damage the capsid sufficiently for the nucleicacid to emerge. The next stage depends on the nature of the virus. In relativelysimple ones, like enteroviruses, the RNA acts as a messenger, is infectious on itsown and is immediately translatable by host ribosomes into viral proteins. More
  52. 52. complex RNA viruses, such as influenza, have non-infectious RNA, sometimescalled negative-strand RNA, which has to be transcribed into messenger RNA(mRNA) by a polymerase enzyme carried in the virus itself. RNA tumour virusescontain a reverse transcriptase enzyme which synthesizes DNA from the viralRNA template. DNA viruses are generally more complex and are able totranscribe mRNA from their DNA using either cell polymerase, for exampleadenoviruses, or viral polymerase, for example vaccinia. At the same time,replication of the viral nucleic acid also occurs. A variety of proteins, regulatory,enzymic and structural, are produced and these, together with the products of celldamage, probably contribute to the local and general response to the infection. Thetime required for new virus production in acute infections is measured in hoursand the number of new virions in thousands per cell. Newly produced virions caninvade adjacent cells or be carried via the bloodstream and so the infectionspreads. During this process the cell itself may be destroyed by a virus infection,for example enterovirus and herpes simplex, or damaged transiently, for examplemyxovirus. With time, an immune response develops against the virus particlesand processed viral proteins, which can lead to containment and clearance of theinfection. Not all virus infections end in this fashion. Some viruses infect cellswhich apparently remain normal and may multiply while virus replicationcontinues within, i.e. persistent infections. When persistently infected cellsproduce no infectious because the replication cycle is arrested, the virus is said tobe latent. From time to time, a latent virus can become active-reactivation, newvirions are produced and other cells are infected. This process can result in clinicalsigns and symptoms as in the case of cold sores (reactivated herpes simplex) andshingles (reactivated varicella-zoster). Other viruses cause cell proliferation, forexample poxviruses and human papillomaviruses. Viruses can also be implicatedin the process of carcinogenesis as in the development of cervical cancer andhepatoma.
  53. 53. A detailed compilation of the infectious skin diseases will be beyond the scope ofour study. So just after touching through the basic factors of these conditions, wemay move to the subject proper. About fungal infection, detailed discussion isdone afterwards.Analysis of these infectious conditions proves the following facts; • Depending upon the infective organism and its virulence, the signs and symptoms may have different forms • Underlying the pathogenesis of each clinical symptom, there are various complicated processes in side the body.In Ayurveda, descriptions about skin manifestations are seen mainly in thefollowing contexts-Kushtam, Dushtavranam, Visarpam, Swithram, Kshudraroga, Krimi,Seethapitham Romanthika, Udarddam, Vidradhi, Kodam, Grandhi, Masoorika,Vatharaktham etc.A clinical correlation between the similar conditions described in Modernmedicine will prove that many of the above diseases are infectious conditions. Butthere are no ample descriptions about the role of microorganisms in theseconditions. It may be because of the lack of deeper knowledge aboutmicroorganisms in those instrumentally insufficient olden days or because of theirway of approach i.e. giving more relevance to the platform and body factors whichare vitiated in the process of disease. This concept is detailed later.
  54. 54. Reference: 1 Su. Sha. 4/14 2 Ch. Chi. 15/16-17 3 A. H. Sha. 3/8 4 Sha. Pu. 5/22 5 Ch. Sha. 7/3 Gangadhara Tika 6 A. H. Sha. 3/8 7 Ch.Sha. 7/16 8 Ch. Su. 8/14 9 A.H. Su. 12/9 10 A.H. Su. 12/14 11 Su.Su. 15/17 12 Ch. Sha. 7/4 13. A.san.su19 14 A.san.su19 15. C.S-20/12, 15, 17 16.; A.San.Sa 17. 18. A.San.Sa.6-15 19. A. H. Sha. 3/8 20. Ch.Ni.4
  55. 55. PART 4 Review of Ayurvedic Literature Ayurveda contains so many declarative statements based on thecrystallization of accumulated experience and observation of natural phenomena.The conclusive statements made years ago could be the end result of theexperiments conducted by our ancestors. But the methods of derivation employedto arrive at the conclusion remain largely unclear and unknown to the latergenerations. Sincere research works are needed to explore the scientific background of many of these principles. As a basic step in this effort, collection of allthe ayurvedic references related with the subject is necessary.Infection –The Ancient Indian perspective4.1. Vedic references: Vedās, the ancient most written treatise of knowledge are having plenty ofreferences regarding the different aspects of the present context. AncientAyurvedic scholars had the sense of understanding of the concept of infection andits role in causing disease. This, we can observe at various portions of our classics.But these descriptions seem very vague and are filled with theistic ideas. Whilereading the classics of science, we should understand them with respect to theperiod in which they had written. They had made these observations during theperiod, when they had no microscopes or other sophisticated instruments. It is theneed of the time to interpret these concepts in terms of modern findings.There are ample descriptions pertaining to infectious disease and krimis orpathogenic micro organisms in Vedas and other ancient Indian literature such asRigveda, Adharvaveda, Sathapadhabhrahmana, thaithireeya, Aranyaka,ChandogyaUpanishad, Vishnupurana, Bhagvath purana, Mahabharatha,
  56. 56. Kamasoothra etc. Among these, Adharva Veda, which laid foundations forAyurveda contains much informations on.Basing on the descriptions available in the above ancient works, it appears thatduring Vedic period itself the ancient Hindus were well aware about the infectiousdisease innumerable varieties of pathogenic krimis (microorganisms) andcausation of disorders due to them, the clinical features and management ofinfectious diseases. In Vedas, much importance was given to Krimis (pathogenicorganisms) than in Ayurvedic texts. Krimi pisachas were regarded as one of thethree main aetiological factors of the diseases, the other two beings the toxicsubstances produced within the body and vatha, pitha and kapha. (1)4.1.1 Krimiroga From the days of Adharvaveda itself, there were discussions aboutmicroorganisms. In Vedas, many words were used to denote micro organisms. Theimportant among them are as follows: • KRIMI- Means which resides and nourish on raw flesh or which nourish on flesh and other tissues of the body. (2) • RAKSHASA- That which consumes the body; hence the body must be protected from these organisms. (3) • PISACHA- Means that which consumes raw flesh (4) • ASURA- Is that which causes death (5) • YAATHU- Spread in body and harm (6) • APSARA- Grow in water (7)Various types of Krimis are also described.4.1.2 General characteristics of Krimis or Microorganisms: In Vedic period itself, there were descriptions about the pathogenic andharmless varieties of micro organisms. Pathogenic Krimis are known as durnamaand the other one as sunama (commensals). Some cause Santhapa (Febrile) and