Abhijit Chakma; MD (Hom)*
We live in an era of rapidly changing global landscapes and local environments. It comes as no surprise, then, that several prominent recent examples of emerging or re-emerging diseases are caused by RNA viruses. Viruses with RNA as their genetic material can quickly adapt to and exploit these varying conditions because of the high error rates of the virus enzymes (polymerases) that replicate their genomes. However, a complex interplay of factors can influence disease emergence. In addition to virus genetic variation (mutation, recombination, and re-assortment), environmental factors (including ecological, social, health care, and behavioral influences) can play important roles. These can include (i) changing weather patterns and damming of rivers, which alters potential virus vector or host abundance and distribution, and (ii) tropical deforestation, which brings humans in close contact with these species-rich (hosts and their parasites) environments. Such factors, coupled with enormous increases in the human population during the last 50 years and urbanization in many developing countries, have greatly expanded the number of sampling events testing the fitness of RNA virus variants in different human cell backgrounds and potential transmission modes.
This change, together with the advances in the speed and volume of global transportation, combines to create increased opportunity for emergence and re-emergence of viral diseases. The incidence of emerging infectious diseases in humans has increased within the recent past or threatens to increase in the near future. Over 30 new infectious agents have been detected worldwide in the last three decades; 60 per cent of these are of zoonotic origin. Developing countries such as India suffer disproportionately from the burden of infectious diseases given the confluence of existing environmental, socio-economic, and demographic factors. In the recent past, India has seen outbreaks of eight organisms of emerging and re-emerging diseases in various parts of the country, six of these are of zoonotic origin.
Prevention and control of emerging infectious diseases will increasingly require the application of sophisticated epidemiologic and molecular biologic technologies, changes in human behavior, a national policy on early detection of and rapid response to emerging infections and a plan of action. WHO has made several recommendations for national response mechanisms. Many of these are in various stages of implementation in India. However, for a country of size and population of India, the emerging infections remain a real and present danger. A comprehensive national strategy on infectious diseases cutting across all relevant sectors with emphasis on strengthened surveillance, rapid response, partnership building and research to guide public policy is needed. A brief discussion is made below on few of the important viral diseases in India with scope of Homoeopathy in these diseases.
CHIKUNGUNYA
Introduction- A mosquito-borne (Aedes aegypti) viral disease associated with urban environments (recent outbreak in Delhi), similar to Dengue Fever; characterized by sudden onset of fever, rash, and severe joint pain usually lasting 3-7 days, some cases result in persistent arthritis. Spread by mosquitoes, the virus has been sweeping through southern India and islands in the Indian Ocean. But epidemics outside the tropics seem unlikely, scientists say, because the mosquitoes that carry the virus thrive mainly in hot, humid regions. The virus was first isolated from Tanzania (East Africa) in 1953, chikungunya (pronounced chick-en-GUN-ya) means “that which bends up” — an apt description of the victims, who are often doubled up with severe muscle and joint pain and suffering from fever, headaches, a rash, nausea and fatigue. The disease is rarely fatal, but the joint pain can last for weeks or months.
In India, this virus belonging to family Rhabdoviridae was isolated in 1965 in the Chandipura (Nagpur) region of India in two adult patients with febrile illness during an outbreak of febrile illness caused by chikungunya and dengue viruses. It was named as Chandipura (CHP) virus. Non-human primates act as a main reservoir of infection. After a quiescence of three decades, a resurgence of infection from southern and central parts of the country was reported in 2006. The first outbreak in India occurred in 1963 in Kolkata, followed by another in Chennai in 1964. The virus continued to circulate until 1973, when there was a small outbreak in Maharashtra. Subsequently, over more than three decades, India was possibly free of this virus. However, widespread reports from Andhra Pradesh, announced its reemergence in 2005. This was preceded by outbreaks due to this East/ Central/ South African strain of CHIKV, in the islands of the south-western Indian Ocean, starting with the Reunion Islands. Since 2006, the virus has spread across many parts of India, causing a few million cases, especially in Karnataka, Maharashtra, Kerala and Tamil Nadu, with additional reports from Orissa, Madhya Pradesh, Rajasthan, Gujarat and Delhi. Chikungunya is associated with joint pains lasting up to six months. Although deaths are not known to occur but the morbidity and disability caused due to chikungunya are enormous.
Causative agent- Chikungunya virus (CHIKV) infection, which has re-emerged in recent years, is caused by a single-stranded RNA virus belonging to the family Togaviridae, genus Alphavirus. It spreads by the bite of the Aedes mosquito.
Clinical presentation- The incubation period ranges from 1-12 days, but is usually 2- 3 days. The symptoms include-
- Fever of abrupt onset, with chills, headache, rash and myalgia. The fever lasts for 1- 7 days.
- Severe migratory polyarthalgia affecting various joints like those of the hands, wrists, ankles and feet.
- The symptoms may be indistinguishable from dengue virus infection, co-infection with which is also reported from India.
- Patients infected with the current strain have also presented with non- classical manifestations including hemorrhages, lymph node enlargement, jaundice and meningoencephalitis some of which may be associated with the new mutations.
- Chikungunya is a self limiting fever, though the arthralgia may persist for many months.
Diagnosis- The diagnostic tests during the viraemic phase (the first 2- 3 days of fever) include virus isolation in an Aedes mosquito- derived cell line or a reverse-transcription polymerase chain reaction (RT-PCR). CHIKV specific IgM antibodies, which appear around the fifth day and last for 1- 3 months, are most commonly detected by an IgMcapture enzyme linked immuno-sorbent assay (ELISA) or, in specialised virology laboratories, by the haemagglutination inhibition or neutralisation tests. In India, the CHIKV ELISA developed by the National Institute of Virology (NIV), Pune, is available in laboratories which are a part of the surveillance network of the National Vector- Borne Disease Control Programme (NVBDCP).
Homoeopathic perspective- In general, no specific medication or vaccine is available for this disease. Rest and mild exercise may improve the acute joint symptoms. Control of the vector is the main mode for prevention of transmission. Homoeopathy has shown a great result in symptom based treatment of chikungunya. Acute fever, joint pains are nicely managed by Homoeopathic medicines. This system has the potentiality to cure as well as to prevent chikungunya, based on its symptom totality.
The medicines are found to be very much effective in treatment of symptomatology of chikungunya disease are Aconitum napellus, Anthraquinone, Arnica Montana, Arsenicum album, Belladonna, Bryonia alba, Chininum sulphuricum, Eupatorium perfoliatum, , Gelsemium, Ignatia amara, Ledum palustre, Mercurius solubilis, Phosphorus, Plumbum metallicum, Pulsatilla pratensis, Rhus toxicodendron.
DENGUE FEVER
Introduction- A mosquito-borne (Aedes aegypti) viral disease associated with urban environments; dengue fever, also known as breakbone fever, is an infectious tropical disease caused by the dengue virus. It manifests as sudden onset of fever and severe headache; occasionally produces shock and hemorrhage leading to death in 5% of cases. Dengue is the most rapidly spreading mosquito borne viral disease in the world with wide clinical spectrum. In the last 50 years, incidence has increased 30-fold with increasing geographic expansion to new countries and, in the present decade, from urban to rural settings. An estimated 50 million dengue infections occur annually and over 2.5 billion people (about 40% of the world’s population) are now at risk from dengue. An estimated 500000 people with severe dengue require hospitalization each year, a large proportion of whom are children. About 2.5% of those affected die.
In India, the first epidemic of clinical dengue-like illness was recorded in Chennai in 1780 and the first virologically proved epidemic of dengue fever (DF) occurred in Kolkata and eastern coast of India in 1963-1964. The first major wide spread epidemic of dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS) occurred in 1996 involving areas around Delhi and Lucknow and then it spread to the whole country. India has become an endemic zone for DF and DHF/DSS outbreaks. In 2006, the country witnessed another outbreak of DF/DHF, with more than 12,000 reported cases. Among the NE States, Manipur has reported Dengue outbreak for the first time in 2007. The incidence of dengue is rising, progressively. Every year during the period of July-November there is an upsurge in the cases of DF and DHF.
Causative agent- It can be caused by any one of the four types of dengue viruses; DEN-1, DEN-2, DEN-3 & DEN-4. Aedes mosquitoes are the carrier of the dengue virus. These mosquitoes can be easily distinguished as they are larger in size and have black and white stripes on their body, so they are sometimes called tiger mosquitoes. The mosquito breeds in artificial accumulation of water, in and around human dwellings, such as water found in discarded tins, broken bottles, fire buckets, flower pots, coconut shells, earthen pots, tree holes etc. during & immediately after the rainy season. They usually bite during the daytime. The female Aedes aegypti usually becomes infected with dengue virus when it takes blood meal from a person during febrile (viremia) phase of dengue illness. After an extrinsic incubation period of 8 to 10 days, the mosquito becomes infected and the virus is transmitted when the infective mosquito bites and injects the saliva into the person.
Clinical presentation- DF is an acute viral infection characterized by high fever, severe headache & intense body ache. The period from the entry of virus through mosquito bite to appearance of first sign/symptoms is 3-10 days (commonly 5-6 days). An acute febrile illness of 2-7 days duration with two or more of the following manifestations:
- Severe headache
- Retro-orbital pain – Pain behind the eyes which worsens with eye movement
- Myalgia
- Arthralgia
- Rash – Flushing over chest and upper limbs
- Mild hemorrhagic manifestations (petechiae, mucous membrane bleeding)
- Fever and other symptoms often follow a ‘saddleback’ sequence that is a brief remission of fever after the third day followed by rise in temperature again after 1-2 days. The fever lasts for 5-7 days after which the recovery is usually complete. Fever may be associated with nausea and vomiting.
- After the incubation period, the illness begins abruptly and is followed by the three phases — febrile, critical and recovery. Patients typically develop high-grade fever suddenly. This acute febrile phase usually lasts 2–7 days and is often accompanied by facial flushing, skin erythema, generalized body ache, myalgia, arthralgia, headache, anorexia, nausea and vomiting. Mild haemorrhagic manifestations like petechiae and mucosal membrane bleeding (e.g. nose and gums) may be seen. The earliest abnormality in the full blood count is a progressive decrease in total white cell count, which should alert the physician to a high probability of dengue.
- In a small proportion of cases the disease develops into the life-threatening dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and plasma leakage, or into dengue shock syndrome, where dangerously low blood pressure occurs.
- Recovery from infection by one serotype provides lifelong immunity against that particular serotype. However, cross-immunity to the other serotypes after recovery is only partial and temporary. It can be more severe and fatal in children.
Diagnosis- Blood test for leukocyte, platelet & hematocrit are conducted to diagnose dengue fever and for assessment. Laboratory diagnosis of dengue is best made during the acute phase of the illness when dengue virus circulates in the blood and can be detected by assays to detect the viral RNA genome or soluble antigens or through serology.
General management & Homoeopathy in dengue fever- Homoeopathy has a long record of success in the treatment of epidemics and recent experiences in Brazil and India favor its usefulness in the management of dengue. The treatment is holistic and individualized and selection of homoeopathic medicines depends upon the individual response to infection, severity of disease and clinical presentation of the case. Homoeopathy has a potential to reduce the intensity of fever, headache, body ache, weakness, loss of appetite, nausea and other associated symptoms and, also reduce the probability of developing shock, hemorrhage and other complications. The homoeopathic intervention can be preventive for unaffected/high risk population (relatives, neighbors of diagnosed patient) as well as curative for persons already suffering from dengue.
Approach towards patients suffering from dengue involves detailed history taking including details of onset & nature of fever/illness, individual characterizing symptoms especially physical generals and mental and assessment for warning signs, and conditions in which, dengue is likely to be more severe. Assessment of hydration, hemodynamic status (pulse, systolic and diastolic blood pressure), checking for tachypnoea, pleural effusion, examination of rash and bleeding manifestations, assessment of abdominal tenderness, ascites and hepatomegaly are necessary. Encourage oral intake of oral rehydration solution (ORS), water, fruit juice, lime water, coconut water and other fluids containing electrolytes and sugar to replace losses from fever and vomiting. The following homoeopathic medicines can be used in dengue-
- In cases of classical dengue fever- Eupatorium perfoliatum is the remedy. It should be given in the third potency early 2-3 times daily to avoid haemorrhagic type, though rare. Other common medicines are Aconitum napellus, Arnica montana, Arsenic album, Belladonna, Bryonia alba, Ferrum phosphoricum, Gelsemium, Ipecacuanha, Natrum muriaticum, Nux vomica, Pulsatilla and Rhus toxicodendron which are prescribed on the basis of symptom similarity.
- For dengue hemorrhagic fever: In these cases, Homoeopathic System of Medicine has limited scope. Medicines can be given only as an add-on supportive therapy. The group of medicines usually indicated includes- Carbo vegetabilis, China, Crotalus horridus, Ferrum metallicum, Hamamelis, Ipecac, Lachesis, Millefolium, Phosphorus, Secale cornutum and Sulphuric acidum.
JAPANESE ENCEPHALITIS
Introduction– Japanese Encephalitis (JE) is an acute viral illness with high case fatality and long term complications. JE is a mosquito-borne (Culex tritaeniorhynchus) viral disease associated with rural areas in Asia. The vector breeds in large paddy fields and similar large water bodies. The vector is an outdoor rester and feeder. JE mainly affects animals and incidentally man, thus it is a zoonotic disease. JE is present in many areas of India and has caused serious epidemics in recent years. The disease has acquired serious magnitude in the states of Uttar Pradesh, Andhra Pradesh, West Bengal, Assam, Tamil Nadu, Karnataka, Kerala, Bihar, Goa, and Haryana. As a disease, it is a dreadful viral disease affecting mostly children. It fundamentally affects the brain and most patients die because of swelling of brain. It is only amenable to corticosteroids or dexamethasone therapy and has to be immediately undertaken, in spite of its harmful side-effects, to save life. When attacked, its symptoms are: (1) Stiffness of neck and body, convulsion and delirium with high fever and intense headache. (2) Nausea (3) Restlessness. (4) Pain in throat. (5) Numbness. (6) Trembling (7) Drowsiness. (8) Paralysis of eyelids. (9) Strabismus. (10) Stupefaction. (11) Unconsciousness. (12) Paralysis. Fortunately the National Institute of Vireology, Pune, India, has evolved a vaccine, 3 shots of which give immunity for a year against all strains of this disease.
Causative agent- It is caused by a group B arbovirus (Flavivirus) and transmitted by culicine mosquito.
Clinical presentation- The incubation period in man, following mosquito bite is not exactly known. Probably it varies from 5 – 15 days. Not all individuals bitten by infected mosquitoes develop disease. The course of the disease in man may be divided into three stages-
- Prodromal stage- Acute onset of fever, headache and malaise. The duration of this stage is usually 1 – 6 days.
- Acute encephalitic stage- High fever with nuchal rigidity, focal CNS signs, convulsions and altered sensorium progressing in many cases to coma.
- Late stage and sequelae- Stage of recovery with temperature becomes normal; neurological signs become stationary or tend to improve.
- The case fatality rate varies between 20 – 40%.
Diagnosis- The diagnosis is made primarily on the basis of the patient’s symptoms and the knowledge of the kinds of illnesses endemic to a particular geographic region. Immunofluorescence tests, where special viral markers react with human antibodies that have been tagged with a fluorescent chemical, are used to verify the disease. However, these results tend to be unavailable until week two of the infection. Other tests involve comparing the presence and quantity of particular antibodies in the blood or spinal fluid during week one with those present during week two of the illness.
General management & Homoeopathy in JE
There are no treatments available to stop or slow the progression of Japanese encephalitis. Only the symptoms of each patient can be treated. Fluids are given to decrease dehydration and medications are given to decrease fever and pain. Medications are available to attempt to decrease brain swelling. Patients in a coma may require mechanical assistance with breathing. Efforts were made by states and Govt. of India to contain JE outbreaks by instituting various public health measures including selective JE vaccination. Considering the value of vaccination in prevention of JE, the Centre launched a JE vaccination programme during 2006 for children between 1 and 15 years of age in 11 districts of the 5 states of Uttar Pradesh, Bihar, Assam, Karnataka and West Bengal with using single dose live attenuated SA-14-14-2 vaccine. The programme expanded to 27 districts in 9 states during 2008. Homoeopathy has a potential to reduce the intensity of fever, headache, body ache, neurological signs & symptoms and, also reduce the probability of developing altered sensorium, convulsions & coma. The homoeopathic intervention can be preventive for un-affected/high risk population (relatives, neighbors of diagnosed patient) as well as curative for persons already suffering from JE.
Homoeopathic treatment is wholly & solely guided by the symptom totality. The main homoeopathic remedies are ACON and BELL. They should be alternated in the 30th potency at short intervals according to the severity of the case. “Apis has been found to be an effective preventive (genus epidemicus). Children below 10- APIS 200 twice daily for two days; Children above 10 and adults: APIS 1M, once daily for three consecutive mornings. BELL 200 also acts as preventive. A dose on weekly basis has to be given for 4 to 8 weeks” (Dr. Harish Chand). Apart from these, the following medicines are also effective when the symptoms of the disease are present. The medicines are- Arnica montana, Arsenicum album, Bryonia alba, Causticum, Colchicum, Dulcamara, Ferrum phosphoricum, Gelsemium, Ledum palustre, Opium, Ranunculus bulbosus, Rhus toxicodendron, Stramonium, Taraxacum officinale, Veratrum album.
HEPATITIS C
Introduction- ‘About 250,000 people die of viral hepatitis in India annually’- Dr Ajit Sood, HoD, Gastroenterology at Dayanand Medical College and Hospital (DMCH), says “In particular, types B and C lead to chronic diseases in hundreds of millions of people and together, are the most common cause of liver cirrhosis and cancer. Hepatitis A and E are typically caused by ingestion of contaminated food or water. Hepatitis B, C and D usually occur as a result of prenatal contact with infected body fluids”. “Approximately 1 in 12 persons worldwide, or some 500 million people, are living with chronic viral hepatitis. In India, about 250,000 people die of viral hepatitis annually”. Professor S K Acharya, HoD of Gastroenterology at AIIMS, said studies reported from various parts of India estimate that about 20 million Indians are Hep B carriers and about 8 to 10 million may have silent Hep C virus infection.
Hepatitis- C virus was first identified in 1989, it has been shown to be the major cause of parenterally transmitted non-A, non-B (PT- NANB) hepatitis. The hepatitis C virus is a single-stranded RNA virus. This virus is mainly transmitted through transfusion of contaminated blood or blood products. Up to 50% of cases are related to intravenous drug users who share needles. The risk of sexual and maternal – neonatal transmission is small. For health care workers it is an occupational hazard requiring adherence to universal precautions. Traditional practices such as circumcision, tattooing and scarification with contaminated instruments can spread HCV infection. In India, screening for HCV has been made mandatory for all blood banks from July 1, 1997.
Interferon is the only drug that has been found effective in the treatment of HCV infection. However, treatment is very expensive thousands of dollars for the drug alone- and must be administered by injection several times a week for several months. For a number of technical reasons, the development of a vaccine to prevent HCV infection is unlikely for many years.
Clinical presentation- The incubation period averages 6 – 7 weeks, and clinical illness is often mild, usually asymptomatic with a high rate (more than 50%) chronic hepatitis, which may lead to cirrhosis of liver or liver cancer. Since it is known whether all PT-NANB hepatitis is due to HCB infection, the diagnosis of acute NANB hepatitis must first be established in persons with signs and symptoms consistent with acute hepatitis by ruling out acute HAV and HBV infections.
Diagnosis- Investigations include HCV antibody enzyme immunoassay or ELISA, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected. In chronic infections, there is elevated liver enzyme level. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.
Liver enzymes are variable during the initial part of the infection and on average begin to rise at seven weeks after infection. Liver biopsies are used to determine the degree of liver damage present.
Homoeopathy in HCV- Treatment of infective diseases especially viral is always a weak area in Homoeopathic field. Thus very less work done on this disease so far. A study shows that use of homeopathic medicine is increasing in its usage and popularity across North America in HCV infection. Few homoeopathic medicines are found in different literatures to be effective in hepatitis. The medicines are- Aranea ixobola, Chlorpromazinum, Lycopodium clavatum, Perhexilinum maleatum, Phosphorus.
H1N1
Introduction- Swine influenza, also called pig influenza, swine flu, hog flu and pig flu, is an infection caused by any one of several types of swine influenza viruses. Swine influenza virus (SIV) or swine-origin influenza virus (S-OIV) is any strain of the influenza family of viruses that is endemic in pigs. As of 2009, the known SIV strains include influenza C and the subtypes of influenza A known as H1N1, H1N2, H2N1, H3N1, H3N2, and H2N3. Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human flu, often resulting only in the production of antibodies in the blood. If transmission does cause human flu, it is called zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infection.
A new human H1N1 strain caused the 2009 pandemic. On June 11, 2009, the World Health Organization raised the worldwide pandemic alert level to Phase 6 for swine flu, which is the highest alert level. This alert level means that the swine flu had spread worldwide and there were cases of people with the virus in most countries. The pandemic level identifies the spread of the disease or virus and not necessarily the severity of the disease. Swine flu spread very rapidly worldwide due to its high human-to-human transmission rate and due to the frequency of air travel. In August 2010, the World Health Organization declared the swine flu pandemic officially over.
Clinical presentation- According to the Centers for Disease Control and Prevention (CDC), in humans the symptoms of the 2009 “swine flu” H1N1 virus are similar to those of influenza and of influenza-like illness in general. Symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue. The 2009 outbreak has shown an increased percentage of patients reporting diarrhea and vomiting. The most common cause of death is respiratory failure. Other causes of death are pneumonia (leading to sepsis), high fever (leading to neurological problems), dehydration (from excessive vomiting and diarrhea), electrolyte imbalance and kidney failure. Fatalities are more likely in young children and the elderly.
Diagnosis- Real time PCR as the method of choice for diagnosing H1N1. The oral or nasal fluid collection and RNA virus preserving filter paper card is commercially available. This method allows a specific diagnosis of novel influenza (H1N1) as opposed to seasonal influenza.
Homoeopathic perspective- After searching various literatures, few medicines found to be effective in H1N1. The medicines are mainly- Arsenicum album, Gelsemium, Influenzinum, Ipecacuanha.
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*Address for communication-
Dr. Abhijit Chakma, MD (Hom)
Research Scientist (H)
Regional Research Institute (H),
¼ Main Road, Colonel Chowmuhani,
Krishnanagar, Agartala- 799001
E-mail- dr.abhijit24@gmail.com
forget name disease,see body how it reacts to outside forces even to eyes of a person we do not like,at times we feel gone father was so good when alive did not care for him.viral is also some nature creation has its own power of attack,vital force has to be one above matched,homeopathy only science hathi mera sathy in crisis.every reaction starts with chill attempt to clear congestion.incubation period eupa per thirst so much even before chill,nat mur chill esp 11 am starts toes fingers lips nails blue,cedron severe chill profuse sweat with thirst,aranea hydrogenoid chill severe sweat absent spleen enlarged,gelsi shaking chill at back,lachesis chill so severe asks sit on my chest,arsenic so prostrated no clear indication except tongue clean as in ipecac with nausea.even common man can be told vital force good no remedy required chill then fever then sweat clears all attacks whether malaria viral etc.weak persons less weaponary to fight disease struggle at chill stage what to talk of fever which is boon to produce antibodies quickly,those brain washed by modern medicine take paracetamol end up in hospital admission,even some herbal tea could have avoided situation.