Common Viral Fever Epidemics in India

Dr.Suja Pillai, Dr.Aji Punnen, Dr.Rumsheed Necholi   
PG Scholars, Govt. Homeopathic  Medical College. Calicut
Moderator : Dr.K.R.Mansoor Ali . Lecturer, GHMC Calicut

Key words : Common Viral Fever Epidemics in India,Dengue fever, Dengue Haemorrhagic fever Japanese encephalitis,s Swine flu,Leptospirosis,Malaria, Chikungunya fever

SWINE INFLUENZA
Swine flu(hog flu,pig flu)  is a respiratory disease caused by  influenza Aviruses  that infect the respiratory tract of pigs and result in nasal secretions, a barking-like cough, decreased appetite, and listless behavior. Swine flu produces most of the same symptoms in pigs as human flu produces in people.

Swine influenza is common in pigs in the midwestern United States (and occasionally in other states), Mexico, Canada, South America, Europe (including the United Kingdom, Sweden, and Italy), Kenya, Mainland China, Taiwan, Japan and other parts of eastern Asia.

Transmission of swine influenza virus from pigs to humans is not common and properly cooked pork poses no risk of infection. When transmitted, the virus does not always cause human influenza and often the only sign of infection is the presence of antibodies in the blood, detectable only by laboratory tests.

 When transmission results in influenza in a human, it is called zoonotic swine flu. People who work with pigs, especially people with intense exposures, are at risk of catching swine flu. However, only about fifty such transmissions have been recorded since the mid-20th century when identification of influenza subtypes became possible.

History of swine influenza
o  The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs, this may reflect a zoonosis either from swine to humans, or from humans to swine.

o Although it is not certain in which direction the virus was transferred, some evidence suggests that, in this case, pigs caught the disease from humans.

o For instance, swine influenza was only noted as a new disease of pigs in 1918, after the first large outbreaks of influenza amongst people.

History of Influenza A virus in the human population:
The various types of influenza virus are clearly illustrated in the above figure. Solid squares show the appearance of a new strain causing recurring influenza pandemics. The dotted line indicates the unidentified strains.

The H1N1 form of swine flu is one of the descendants of the Spanish flu that caused a devastating pandemic in humans during 1918 -1919. It would have been persisting in pigs and was then circulated into humans during the 20th century, contributing to the normal seasonal epidemics of influenza.

This virus constantly changes its form, thereby eluding the protective antibodies that people may have developed in response to previous exposures to influenza vaccines. Every two or three years, the virus undergoes minor changes.

But at intervals, a bulk of world’s population has developed some level of resistance to these minor changes and it easily infect populations around the world, often infecting hundreds of millions of people whose antibody defenses are unable to resist it.

The 2009 flu outbreak in humans, known as “swine flu”, is due to a new strain of influenza A virus subtype H1N1 that contained genes most closely related to swine influenza. The origin of this new strain is unknown. However, the World Organization for Animal Health(OIE) reports that this strain has not been isolated in pigs. This strain can be transmitted from human to human, and causes the normal symptoms of influenza.

Pigs can become infected with human influenza and this appears to have happened during the 1918 flu pandemic and the 2009 flu outbreak

Classification
Of the three genera of influenza viruses that cause human flu, two also cause influenza in pigs, with Influenzavirus A being common in pigs and Influenzavirus C being rare. Influenzavirus B has not been reported in pigs. Within Influenzavirus A and Influenzavirus C, the strains found in pigs and humans are largely distinct, although due to reassortment there have been transfers of genes among strains crossing swine, avian, and human species boundaries.

Influenza A
Swine influenza is known to be caused by influenza A subtypes H1N1, H1N2,H3N1, H3N2 and H2N3 In pigs, three influenza A virus subtypes (H1N1, H3N2, and H1N2) are the most common strains worldwide. In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs.

History
Swine influenza was first proposed to be a disease related to human influenza during the 1918 flu pandemic, when pigs became sick at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930. For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In 1997-1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2  In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm.

The H1N1 form of swine flu is one of the descendants of the strain that caused the 1918 flu pandemic As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza.However, direct transmission from pigs to humans is rare, with only 12 cases in the U.S. since 2005  Nevertheless, the retention of influenza strains in pigs after these strains have disappeared from the human population might make pigs a reservoir where influenza viruses could persist, later emerging to reinfect humans once human immunity to these strains has waned.

Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. For example, this disease costs the British meat industry about £65 million every year.

Why is swine flu now infecting humans?
Many researchers now consider that two main series of events can lead to swine flu (and also avian or bird flu becoming a major cause for influenza illness in humans.

First, the influenza viruses (types A, B, C) are enveloped RNA viruses with a segmented genome; this means the viral RNA genetic code is not a single strand of RNA but exists as eight different RNA segments in the influenza viruses. A human (or bird) influenza virus can infect a pig respiratory cell at the same time as a swine influenza virus; some of the replicating RNA strands from the human virus can get mistakenly enclosed inside the enveloped swine influenza virus. For example, one cell could contain eight swine flu and eight human flu RNA segments. The total number of RNA types in one cell would be 16; four swine and four human flu RNA segments could be incorporated into one particle, making a viable eight RNA segmented flu virus from the 16 available segment types. Various combinations of RNA segments can result in a new subtype of virus (known as antigenic shift that may have the ability to preferentially infect humans but still show characteristics unique to the swine influenza virus It is even possible to include RNA strands from birds, swine, and human influenza viruses into one virus if a cell becomes infected with all three types of influenza (for example, two bird flu, three swine flu, and three human flu RNA segments to produce a viable eight-segment new type of flu viral genome). Formation of a new viral type is considered to be antigenic shift; small changes in an individual RNA segment in flu viruses are termed antigenic drift and result in minor changes in the virus. However, these can accumulate over time to produce enough minor changes that cumulatively change the virus’ antigenic makeup over time (usually years).

Second, pigs can play a unique role as an intermediary host to new flu types because pig respiratory cells can be infected directly with bird, human, and other mammalian flu viruses. Consequently, pig respiratory cells are able to be infected with many types of flu and can function as a “mixing pot” for flu RNA segments  Bird flu viruses, which usually infect the gastrointestinal cells of many bird species, are shed in bird feces. Pigs can pick these viruses up from the environment and seem to be the major way that bird flu virus RNA segments enter the mammalian flu virus population.

Transmission

Transmission between pigs
Influenza is quite common in pigs, with about half of breeding pigs having been exposed to the virus in the US. Antibodies to the virus are also common in pigs in other countries.

The main route of transmission is through direct contact between infected and uninfected animals.These close contacts are particularly common during animal transport. Intensive farming may also increase the risk of transmission, as the pigs are raised in very close proximity to each other. The direct transfer of the virus probably occurs either by pigs touching noses, or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing are also an important means of infection.The virus usually spreads quickly through a herd, infecting all the pigs within just a few days. Transmission may also occur through wild animals, such as wild boar, which can spread the disease between farms.

Transmission to humans
People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and Other professions at particular risk of infection are veterinarians and meat processing workers, although the risk of infection for both of these groups is lower than that of farm workers.

Signs and symptoms

In swine
In pigs influenza infection produces fever, lethargy, sneezing, coughing, difficulty breathing and decreased appetite. In some cases the infection can cause abortion. Although mortality is usually low (around 1-4%), the virus can produce weight loss and poor growth, causing economic loss to farmers. Infected pigs can lose up to 12 pounds of body weight over a 3 to 4 week period.

In Humans
Symptoms of Swine flu
According to Centre for Disease Control and Prevention (CDC), the symptoms of swine flu were similar to those of influenza and of influenza like illness. It includes fever, sore throat, body aches, headaches, chills and fatigue.

The 2009 outbreak has shown an increased percentage of patients reporting diarrhea and vomiting. In United States, CDC advised physicians to consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness.

The presumed pathophysiology indicates that influenza viruses bind through hemagglutin on to sialic acid sugars on the surfaces of epithelial cells, which typically affect the nose, throat and lungs of humans. The viruses are 80-120 nm in diameter

When to Seek Emergency Medical Care?

•  has difficulty breathing or chest pain
•  has purple or blue discoloration of the lips
•  is vomiting and unable to keep liquids down
•  has signs of dehydration such as dizziness when standing, absence of urination, or in infants, a lack of tears when they cry
•  has seizures (for example, uncontrolled convulsions)
•  is less responsive than normal or becomes confused

COMPLICATIONS

• Pneumonia
• Respiratory failure
• Convulsions

Infectious Period
Persons with swine influenza A (H1N1) virus infection should be considered potentially contagious for up to 7 days following illness onset.

Persons who continue to be ill longer than 7 days after illness onset should be considered potentially contagious until symptoms have resolved.

Children, especially younger children, might potentially be contagious for longer periods. The duration of infectiousness might vary by swine influenza A (H1N1) virus strain. Non-hospitalized ill persons who are a confirmed or suspected case of swine influenza A (H1N1) virus infection are recommended to stay at home (voluntary isolation) for at least the first 7 days after illness onset except to seek medical care.

DIAGNOSIS
Swine flu is presumptively diagnosed clinically by the patient’s history of association with people known to have the disease and their symptoms listed above.

Usually, a quick test (for example, nasopharyngeal swab sample) is done to see if the patient is infected with influenza A or B virus. Most of the tests can distinguish between A and B types. The test can be negative (no flu infection) or positive for type A and B.

If the test is positive for type B, the flu is not likely to be swine flu (H1N1).

If it is positive for type A, the person could have a conventional flu strain or swine flu (H1N1). Swine flu (H1N1) is definitively diagnosed by identifying the particular antigens associated with the virus type. In general, this test is done in a specialized laboratory and is not done by many doctors’ offices or hospital laboratories. However, doctors’ offices are able to send specimens to specialized laboratories if necessary

A confirmed case of swine influenza A (H1N1) virus infection is defined as a person with an acute respiratory illness with laboratory confirmed swine influenza A (H1N1) virus infection at CDC by one or more of the following tests:

• real-time RT-PCR
• viral culture
• four-fold rise in swine influenza A (H1N1) virus-specific neutralizing antibodies

RISK GROUPS
Household close contacts who are at high-risk for complications of influenza (persons with certain chronic medical condition

1. School children who are at high-risk for complications of influenza (persons with certain chronic medical conditions) who had close contact (face-to-face) with a confirmed or suspected case.
2. Travelers to Mexico who are at high-risk for complications of influenza (persons with certain chronic medical conditions, elderly).
3. Border workers
4. Health care workers or public health workers

Prevention
Prevention of swine influenza has three components: prevention in swine, prevention of transmission to humans, and prevention of its spread among humans.

Prevention in swine :Methods of preventing the spread of influenza among swine include facility management, herd management, and vaccination.

Vaccine
Control of swine influenza by vaccination has become more difficult in recent decades, as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection. Present vaccination strategies for SIV control and prevention in swine farms typically include the use of one of several bivalent SIV vaccines commercially available in the United States

Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests that current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses.

The United States Department of Agriculture researchers say that while pig vaccination keeps pigs from getting sick, it does not block infection or shedding of the virus.

Facility management; includes using disinfectants and ambient temperature to control virus in the environment. The virus is unlikely to survive outside living cells for more than two weeks, except in cold (but above freezing) conditions, and it is readily inactivated by disinfectants.

Herd management; includes not adding pigs carrying influenza to herds that have not been exposed to the virus. The virus survives in healthy carrier pigs for up to 3 months and can be recovered. carrier pigs for up to 3 months and can be recovered from them between outbreaks. Carrier pigs are usually responsible for the introduction of SIV into previously uninfected herds and countries, so new animals should be quarantined.

Prevention in humans
The transmission from swine to human is believed to occur mainly in swine farms where farmers are in close contact with live pigs. so farmers and veterinarians are encouraged to use a face mask when dealing with infected animals.

The use of vaccines on swine to prevent their infection is a major method of limiting swine to human transmission. Risk factors that may contribute to swine-to-human transmission include smoking and not wearing gloves when working with sick animals.

Prevention of human to human transmission
Influenza spreads between humans through coughing or sneezing and people touching something with the virus on it and then touching their own nose or mouth. Swine flu cannot be spread by pork products, since the virus is not transmitted through food.

Recommendations to prevent spread of the virus among humans include

• using standard infection control against influenza This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in public.
• Use of handkerchief while sneezing.
• Use of face mask while dealing with infected people
• Although the current trivalent influenza vaccine is unlikely to provide protection against the new 2009 H1N1 strain, vaccines against the new strain are being developed and could be ready as early as June 2009.
• Social distancing is another tactic. It means staying away from other people who might be infected and can include avoiding large gatherings, spreading out a little at work, or perhaps staying home and lying low if an infection is spreading in a community.
• Public health and other responsible authorities have action plans which may request or require social distancing actions depending on the severity of the outbreak.

Treatment
In swine
As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required. Instead veterinary efforts are focused on preventing the spread of the virus throughout the farm, or to other farms.

Vaccination and animal management techniques are most important in these efforts. Antibiotics are also used to treat this disease, which although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds.

In humans
If a person becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms).

Beside antivirals, palliative care, at home or in hospital, focuses on controlling fevers and maintaining fluid balance.

The U.S. Centers for Disease Controland Prevention recommends the use of Tamiflu (oseltamivir or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses, however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs.

The virus isolates in the 2009 outbreak have been found resistant to amantadine and rimantadine.

Prognosis

• In general, the majority (about 90%-95%) of people that get the disease feel terrible  but recover with no problems, as seen in patients in both Mexico and the U.S.
• Caution must be taken as the swine flu (H1N1) is still spreading and may become a pandemic.
• Young adults have not done well, and in Mexico, this group currently has the highest mortality rate, but this data could quickly change.
• People with depressed immune systems historically have worse outcomes.
• Another confounding problem with the prognosis of swine flu (H1N1) is that the disease is occurring and spreading in high numbers at the usual end of the flu season.
• Most flu outbreaks happen between November to the following April, with peak activity between late December to March
• This outbreak is not following the usual flu pattern.
• Because swine flu (H1N1)  does not seem to be following the usual flu disease pattern, any prognosis is speculative.
• The first traceable case in Mexico, termed “patient zero,” was a 5-year-old child in Veracruz who has completely recovered. Investigators noted that large pigfarms were located close to the boy’s home
• The first death in the U.S. occurred in a 23-month-old child who was visiting Texas from Mexico but apparently caught the disease in Mexico 

The World Health Organization has not, as of Apr. 29, declared a pandemic, but it has declared a phase 5 alert (a phase 5 WHO alert warns that a disease outbreak has occurred that is transmitted from person to person, is sustained in communities, and has spread to several nations). The WHO said it may consider declaring a pandemic (WHO stage 6) if the number of cases and nations affected increase; some scientists suggest that phase 6 is imminent.

Ten Swine Flu Lies Told by the Mainstream Media
The mainstream media is engaged in what we Americans call “bald faced lies” about swine flu. It seems to be true with this issue more than any other, and it became apparent to me recently when a colleague of mine — a nationally-syndicated newspaper columnist — told me their column on natural defenses for swine flu was rejected by newspapers all across the country. Many newspapers refused to run the column and, instead, ran an ad for “free vaccine clinics” in the same space.

The media, it seems, is so deeply in bed with the culture of vaccinations that they will do almost anything to keep the public misinformed. And that includes lying about swine flu vaccines.

There are ten key lies that continue to be told by the mainstream media (MSM) about swine flu and swine flu vaccines.

Lie #1 – There are no adjuvants used in the vaccines
I was recently being interviewed by a major U.S. news network when the reporter interviewing me came up with this humdinger: There are no adjuvants being used in the swine flu vaccines, he said!

I assured him that adjuvants were, indeed, a crucial part of the vaccine recipe, and they were being widely used by drug companies to “stretch” the vaccine supply. It’s no secret. But he insisted he had been directly told by a drug company rep that no adjuvants were being used at all. And he believed them! So everything being published by this large news network about swine flu vaccines now assumes there are no adjuvants in the vaccines at all.

Lie #2 – The swine flu is more dangerous than seasonal flu
This lie is finally starting to unravel. I admit that in the early days of this pandemic, even I was concerned this could be a global killer. But after observing the very mild impact the virus was having on people in the real world, it became obvious that this was a mild flu, no more dangerous than a seasonal flu.

The MSM, however, continues to promote H1N1 swine flu as being super dangerous, driving fear into the minds of people and encouraging them to rush out and get a vaccine shot for a flu that’s really no more likely to kill them than the regular winter sniffles. Sure, the virus could still mutate into something far worse, but if it does that, the current vaccine could be rendered obsolete anyway!

Lie #3 – Vaccines protect you from swine flu
This is the biggest lie of all, and the media pushes it hard. Getting a vaccine, they insist, will protect you from the swine flu. But it’s just flat-out false. Even if the vaccine produces antibodies, that’s not the same thing as real-world immunity from a live virus, especially if the virus mutates (as they often do).

As I pointed out in a recent article, statistically speaking the average American is 40 times more likely to be struck by lightning than to have their life saved by a swine flu vaccine. (http://www.naturalnews.com/026955_s…)

Lie #4 – Vaccines are safe
And how would any journalists actually know this? None of the vaccines have been subjected to real-world testing for any meaningful duration. The “safety” of these vaccines is nothing more than wishful thinking.

The MSM also doesn’t want you to know what’s in the vaccines. Some vaccines are made from viral fragments grown in diseased African monkeys. If that sounds incredible, read the true story here: http://www.naturalnews.com/026779_s…

Lie #5 – The vaccine isn’t mandatory
You hear this lie all the time: The swine flu vaccine shot is voluntary, they say. But it’s not true if you’re an employee at a place where vaccines are being mandated. Millions of Americans are now being told by their employers that if they don’t get vaccine shots, they will be effectively fired from their jobs. It’s especially true with health care workers, day care employees and school teachers.

Lie #6 – Getting a vaccine shot is a good bet on your health
In reality, a vaccine shot is far more likely to harm you than help you. According to one viral expert, the actual mortality rate of the swine flu virus is estimated to be as low as .007 percent (http://www.reuters.com/article/heal…). That means H1N1 swine flu kills less than one person in 100,000. Even if the vaccine works, let’s say, 10 percent of the time, you’d have to vaccine one million people to prevent one death from swine flu.

And in vaccinating one million people, you would inevitably harm or kill several people, simply from the vaccine side effects! Your net risk of death is increased by getting a swine flu vaccine.

Lie #7 – The vaccine isn’t made with “attenuated live virus”
When the swine flu vaccines were first being announced several months ago, they were described as being made with “attenuated live virus.” This was directly mentioned in CDC documents, among other places.

This term apparently freaked out the American news consumer, and it has since been all but erased from any discussion about vaccines. Now, journalists will actually argue with you and insist the vaccines contain no attenuated live viruses whatsoever.

Except they’re wrong. The vaccines are, indeed, made with “attenuated live viruses.” That’s how you make a vaccine: You take live viruses, then you weaken them (“attenuate”) and inject them into people.

Lie #8 – Wash, wash, wash your hands (to avoid exposure)
This idea of washing your hands a hundred times a day is all based on the assumption that you can avoid exposure to the swine flu virus. But that’s impractical. The virus is now so widespread that virtually everyone is certain to be exposed to it through the air if not other means. This whole idea of avoiding exposure to the swine flu virus is nonsense. The conversation should shift to ways to survive exposure via a healthy immune system.

Of course, hand washing is a very good idea in a hospital setting. Recent news reveals that doctors are too busy to wash their own hands, resulting in the rampant spread of superbugs throughout most large hospitals in first world nations.

Lie #9 – Children are more vulnerable to swine flu than adults
This is just a flat-out lie, but it makes for good vaccine sales. Vaccines are right now being targeted primarily to schoolchildren.

But the truth is that swine flu is extremely mild in children. “It’s mildest in kids,” says Dr Marc Lipsitch of Harvard University. “That’s one of the really good pieces of news in this pandemic.” Reuters actually had the guts to report this story, but most of the larger media outlets are still reporting that children are the most vulnerable.

Lie #10 – There is nothing else you can do beyond a vaccine and Tamiflu
This is where the media lies by omission. The mainstream media absolutely refuses to print just about any story that talks about using vitamin D, anti-viral herbs or natural remedies to protect yourself from swine flu. In the MSM, there are two options and only two: Vaccines and Tamiflu. That’s it. No other options exist in their fictional reality.

Why is the mainstream media so afraid to print the truth these days? Why can’t reporting on swine flu see the light of day… literally, with a mention of sunlight and vitamin D? Apparently, Big Pharma has such a tight grip on mainstream newspapers that no true story on swine flu can ever make it past the editor’s desk.

Killing stories, deceiving the public
It must really be depressing to work for the mainstream media. Even the reporters I know can’t stand it. The truth, they admit, rarely makes it into print.   

LEPTOSPIROSIS
Dr.Suja Pillai                                

Leptospirosis (also known as Weil’s disease, Weil’s syndrome, canicola fever, canefield fever, nanukayami fever, 7-day fever, “Fort Bragg fever,” and “Pretibial fever

Is a bacterial zoonotic disease caused by spirochaetes of the genusLeptospira that affects humans and a wide range of animals, including mammals, birds, amphibians, and reptiles

It was first described by Adolf Weil in 1886 when he reported an “acute infectious disease with enlargement of spleen, jaundice and nephritis.

TRANSMISSION

• Leptospirosis is transmitted by the urine of an infected animal and is contagious as long as it is still moist. Rats, mice  are important primary hosts.
• The type of habitats most likely to carry infective bacteria are muddy riverbanks, ditches, gulleys and muddy livestock rearing areas where there is regular passage of either wild or farm mammals.
• here is a direct correlation between the amount of rainfall and the incidence of leptospirosis, making it seasonal in temperate climates and year-round in tropical climates
• umans become infected through contact with water, food, or soil containing urine from these infected animals.
• his may happen by swallowing contaminated food or water or through skin contact.
• The disease is not known to be spread from person to person and cases of bacterial dissemination in convalescence are extremely rare in humans.

SYMPTOMS

• Leptospirosis is a biphasic disease that begins with flu-like symptoms(fever, chills, myalgias, intense headache). The first phase resolves, and the patient is briefly asymptomatic until the second phase begins.
• Characterized by meningitis, liver damage (causing jaundice), and renal failure; because of the wide range of symptoms the infection is often wrongly diagnosed This leads to a lower registered number of cases than there really are.
• Complications include meningitis, extreme fatigue, hearing loss, respiratory distress, azotemia, and renal interstitial tubular necrosis, which results in renal failure and often liver failure

DIAGNOSIS

• On infection the microorganism can be found in blood for the first 7 to 10 days and then moving to the kidneys.
• After 7 to 10 days the microorganism can be found in fresh urine.
• Hence, early diagnostic efforts include testing a serum or blood sample serologically with a panel of different strains. It is also possible to culture the microorganism from blood, serum, fresh urine.
• On infection the microorganism can be found in blood for the first 7 to 10 days and then moving to the kidneys.
• After 7 to 10 days the microorganism can be found in fresh urine.
• Hence, early diagnostic efforts include testing a serum or blood sample serologically with a panel of different strains. It is also possible to culture the microorganism from blood, serum, fresh urine.
• Serologi
  • cal testing, the MAT (microscopic agglutination test), is considered the gold standard in diagnosing leptospirosis.

 PREVENTION

• Proper waste disposal
• Rodent control by trapping.
• Use of rodenticides
• Fumigation
• Chemosterilants 

JAPANESE ENCEPHALITIS
Dr.SUJA PILLAI

Japanese encephalitis previously known as Japanese B encephalitis  is a disease caused by the mosquito-borne Japanese encephalitis virus.

• The Japanese encephalitis virus is a virus from the family Flaviviridae.
• Domestic pigs and wild birds are reservoirs of the virus
• One of the most important vectors of this disease is the mosquito Culextritaeniorhynchus
• The causative agent Japanese encephalitis virus is an enveloped virus of the genus flavivirus; it is closely related to the West Nile virus and St. Louis encephalitis virus.
• It has been noted that the Japanese encephalitis virus (JEV) infects the lumen of the endoplasmic reticulum and rapidly accumulates substantial amounts of viral proteins for the JEV.
• There is no transmission from person to person and therefore patients do not need to be isolated.

CLINICAL FEATURES

• Severe rigors mark the onset of this disease in humans. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days
• Neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between 38 and 41 degrees Celsius.
• Rapid onset of paralysis is characteristic
• Neurological function is regained gradually over 6-12 weeks .

DIAGNOSIS
Japanese Encephalitis is diagnosed by detection of antibodies in serum and CSF (cerebrospinal fluid) by IgM capture ELISA

PREVENTION

• Infection with JEV confers life-long immunity.
• In the UK, the two vaccines used (but which are unlicensed) are JE-Vax and Green Cross,
• Three doses are given at 0, 7–14 and 28–30 days. The dose is 1ml for children and adult, and 0.5ml for infants under 36 months of age.
• A new vaccine has been produced by Intercell biomedical ltd named IXIARO, and requires only 2 doses.

MALARIA
Malaria is one of the most common infectious diseases and an enormous public health problem. The disease is caused by protozoan parasites of the genus Plasmodium. 

Five species of the plasmodium parasite can infect humans; Plasmodiumfalciparum,Plasmodiumvivax, plasmodium ovale and plasmodium malarie . A fifth species,   p.knowlesi, causes malaria in macaques.

Usually, people get malaria by being bitten by an infective female Anopheles mosquito. Only Anopheles mosquitoes can transmit malaria.

SYMPTOMS

• The classic symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting four to six hours.
• Occurring every two days in P. vivax and P. ovale infections,
• Wile every three for P. malariae.
• P. falciparum can have recurrent fever every 36–48 hours or a less pronounced and almost continuous fever.
• For reasons that are poorly understood, but that may be related to high intracranial pressure, children with malaria frequently exhibit abnormal posturing, a sign indicating severe brain damage.
• Malaria has been found to cause cognitive impairments, especially in children.
• It causes widespread anemia during a period of rapid brain development and also direct brain damage.
• This neurologic damage results from cerebral malaria to which children are more vulnerable.

DIAGNOSIS
The most economic, preferred, and reliable diagnosis of malaria is microscopic examination of blood films.

Two sorts of blood film are traditionally used. Thin films allow species identification because the parasite’s appearance is best preserved in this preparation.

Thick films allow the microscopist to screen a larger volume of blood and are about eleven times more sensitive than the thin film, so picking up low levels of infection is easier on the thick film.

Antigen detection tests that require only a drop of blood.

Immunochromatographic tests (also called: Malaria Rapid Diagnostic Tests, Antigen-Capture Assay or “Dipsticks”) have been developed, distributed and fieldtested.

These tests use finger-stick or venous blood, the completed test takes a total of 15–20 minutes, and a laboratory is not needed.

PRINCIPLES OF VECTOR CONTROL
ANTI-LARVAL MEASURES 

ENVIRONMENTAL CONTROL

• Elimination of breeding places
• Filling and drainage operations
• Planned water management
• Provision of piped water supply
• Proper disposal of refuse
• Cleanliness in and around houses

 CHEMICAL CONTROL

• Use of larvicides
• Mineral oil
• Paris green
•  Synthetic insecticides

 BIOLOGICAL CONTROL : Gambusia fish

ANTI-ADULT MEASURES

• RESIDUAL SPRAYS
• SPACE SPRAYS
• GENETIC CONTROL

 PROTECTION AGAINST MOSQUITO BITES

• Use of mosquito nets
• Use of mosquito repellant cream
• Use of mosquito coils
• Use of screens

 Chikungunya fever
Dr. Rumsheed Necholi 

Chikungunya fever (CF) is a viral illness caused by an arbovirus transmitted by the Aedes mosquitoes. The disease was documented first time in the form of an outbreak in Tanzania. The name is derived from the ‘makonde’ dialect which means ‘that which bends up’, indicating the physical appearance of a patient with severe clinical features.

Causative agent
Chikungunya fever is caused by virus of same name (CHIK virus in short) which is an RNA virus that belongs to the Alphavirus genus of the Togaviridae, the family that comprises a number of viruses that are mostly transmitted by arthropods. The virus was first isolated in 1952-1953 from both man and mosquitoes  during an epidemic of fever that was considered clinically indistinguishable from dengue  fever in Tanzania.

It is a single stranded RNA virus, heat labile and sensitive to temperatures above 58 0 Celsius.two phyllogenetic -groups from Africa & one from Asia

Vector
Aedes aegypti is the common vector responsible for transmission in urban areas Where as Aedes albopictus has been implicated in rural areas.

The Aedes mosquito breeds in domestic settings such as flower vases, water-storage containers, air coolers, etc. and peri -domestic areas such as construction sites, coconut shells, discarded household junk items (tyres ,plastic and metal cans, etc.). The adult female mosquito rests in cool and shady areas in domestic and peri -domestic settings and bites during day time.

Epidemiology
In the South-East Asia Region, Chikungunya virus is maintained in the human population by a human-mosquito-human transmission cycle . A high vector density as seen in the post monsoon season accentuates the transmission.

Chikungunya fever epidemics display cyclical and seasonal trends. There is an inter-epidemic period of 4-8 years (sometimes as long as 20 years).

Outbreaks are most likely to occur in post-monsoon period when the vector density is very high. Human beings serve as the chikungunya virus reservoir during epidemic periods. During inter-epidemic periods, a number of vertebrates have been implicated as reservoirs. These include monkeys, rodents, birds, and other vertebrates

There is no significant sex predilection and the virus causes illness in almost all age groups.

CLINICAL PRESENTATION
CHIK virus causes a febrile illness in the majority of people with an incubation period of 2-4 days from the mosquito bite. Viremia persists for upto 5 days from clinical onset

 Commonest presenting features

• Fever (92%) usually associated with
• Arthralgia (87%),
• Backache (67%) and
• Headache (62%).

The fever varies from low grade to high grade, lasting for 24 to 48 hours  Fever rises abruptly in some , reaching 39-40 C, with shaking chills and rigor

ARTHALGIA. The joint pain tends to be worse in the morning, relieved by mild exercise and exacerbated by aggressive movements. The pain may remit for 2-3 days and then reappear in a saddle back pattern. Migratory polyarthritis with effusions may be seen in around 70% cases , but resolves in the majority. Ankles , wrists and small joints of the hand were the worst affected. Larger joints like knee  and shoulder and spine were also involved. There is a tendency for early and more significant involvement of joints with some trauma or degeneration .Occupations with predominant overuse of smaller joints predisposed those areas to be affected more. (eg. interphalangeal joints in rubber tappers, ankle joints in those standing and walking for a long time eg. policemen).

OTHER CLINICAL FEATURES
1. Transient maculopapular rash is seen in up to 50 % patients. The maculopapular eruption persisted for more than 2 days in approx

2. Intertriginous aphthous-like ulcers and vesiculobullous eruptions were noticed in some

3. A few persons had angiomatous lesions and fewer had purpuras

4. Stomatitis was observed in 25% and oral ulcers in 15% of patients

5. Nasal blotchy erythema followed by photosensitive  hyperpigmentation (20%) was observed

6. Exfoliative dermatitis affecting limbs and face was seen in around 5% cases

7. Epidermolysis bullosa was an observation in children

Most skin lesions recovered completely except in cases where the photosensitive hyperpigmentation persisted.

Photophobia and retro-orbital pain have been observed. Although rare in adults, children, particularly neonates have developed vomiting and/or diarrhoea and meningo-encephalitis. Neurologic manifestations such as encephalitis, febrile seizures, meningeal syndrome and acute encephalopathy were reported. Neuroretinitis and uveitis in one or both eyes have also been observed. The main ocular manifestation associated with the recent epidemic outbreak of chikungunya virus infection in South India included granulomatous and nongranulomatous anterior uveitis, optic neuritis, retrobulbar neuritis, and dendritic lesions. The visual prognosis generally was good, with most patients recovering good vision.

Laboratory diagnosis
The confirmation of Chikungunya fever is through any of the followings:

• Isolation of virus
• PCR
• Detection of IgM antibody
• Demonstration of rising titre of IgG antibody

IgM antibodies demonstrable by ELISA may appear within two weeks. It

may not be advisable to do the antibody test in the first week. In some persons it may take six to twelve weeks for the IgM antibodies to appear in sufficient concentration to be picked up in ELISA. Serological diagnosis requires a larger amount of blood than the other methods and uses an ELISA assay to measure Chikungunya-specific IgM levels. Results require 2–3 days and false positives can occur with infection via other related viruses such as O’nyong’nyong virus and Semliki Forest Virus No significant pathognomonic hematological finding is seen.

Leucopenia with lymphocyte predominance is the usual observation. Thrombocytopenia is rare. Erythrocyte sedimentation rate is usually elevated. C-Reactive Protein is increased during the acute phase and may remain elevated for a few weeks. A small proportion of patients have tested positive for rheumatoid factor during and after clinical episode.

Differential diagnosis
Fever with or without arthralgia is a very common manifestation of several other diseases. CHIK fever may not have the typical manifestations or it may co-exist with other infectious diseases like dengue fever or non infectious diseases like rheumatoid arthritis.

(1) Leptospirosis Severe myalgia localized to calf muscles with conjunctival congestion/ or subconjunctival haemorrhage with or without oliguria or jaundice in a person with history of contact to contaminated water might suggest Leptospirosis.

(2) Dengue fever Sever backpain with purpuras or active bleeding might suggest dengue fever. Confirmatory laboratory diagnosis is possible.

(3) Malaria Periodicity of fever and alteration of consciousness / seizures should prompt a diagnosis for malaria.

(4) Meningitis High fever with neck stiffness or alteration of consciousness should prompt a thought about meningitis. All cases of meningoencephalitis during an outbreak of CF must be suspected to have CF.

(5) Rheumatic fever is more common in the children and presents with fleeting (migratory) polyarthritis predominantly affecting the large joints. Modified Jones criteria should be the basis for diagnosis. Raised ASO titre and a history of recurrent sore throat are other points to be noted.

General management
1.Adequate rest in a warm environment; avoid damp surroundings. Heat may increase/worsen joint pain and is therefore best to avoid during acute stage.

2. Refrain from exertion. Mild forms of exercise and physiotherapy are recommended in recovering persons.

3. Cold compresses may help in reducing joint damage

4.Consume plenty of water with electrolytes (approximately 2 litres of home available fluids with salt in 24 hours). If possible ensure a measured urine output of more than a litre in 24 hours.

DENGUE FEVER
Also known as BREAK BONE FEVER or DANDY FEVER

AN ACUTE FEBRILE ILLNESS CHARACTERISED BY HIGH FEVER,SEVERE PAIN OF THE BONES & JOINTS,LYMPHADENOPATHY AND A CHARACTERISTIC RASH. Global incidence of dengue fever has grown dramatically in recent decades.Also known as DANDY FEVER –bz of having posture and gait of dandy(dandy-a man who give exaggerated attention to personal appearance)

Etiology
Dengue is caused by group B arbovirus ,50nm in size,4 distinct serotypes are present.Transmitted by Female AEDES  AEGYPTI mosquito-infective,8-14 days after infected meal.Reservoir of infection-MAN

Vector

1. Female AEDES AEGYPTI mosquito Called tiger mosquito-bz of white stripes on black body. The Aedes mosquito breeds in domestic settings such as flower vases, water-storage containers, air coolers, etc. and peri -domestic areas such as construction sites, coconut shells, discarded household junk items (tyres ,plastic and metal cans, etc.). The adult female mosquito rests in cool and shady areas in domestic and peri -domestic settings and bites during day time. They do not fly over long distance-< than 100 metre s.(this factor facilitates its eradication)

PATHOLOGY

 UNCOMPLICATED Dengue Fever-

• Endothelial swelling of small bld vessels
• Perivascular oedema
• Mononuclear cell infiltration

FULMINANT H’GIC DISORDER-AFTER 2^nd attack

1. Capillary dilatation
2. Raised permeability
3. Congestion of blood vessels
4. Organ h’gs- lungs ,brain ,kidney ,liver,myocardium
5. Hypovolaemic shock and Renal failure –blood loss and renal lesions
6. Lung shows oedema
7. liver-extensive damage
8. Skin-purpura,ecchymoses-mild trauma
9. Splenomegaly in some
10. Fibrinogen level in plasma reduced 

CLINICAL FEATURES

•  The incubation period 2 to 7 days
• Prodrome 2 days of malaise and headache
• Acute onset Fever, backache, arthralgias, headache, generalised pains (‘breakbone fever’), pain on eye movement, lacrimation , anorexia, nausea, vomiting, relative bradycardia , prostration, depression, Lymphadenopathy-posterior cervical,epitrochlear and inguinallymphnodes are mainly affected, scleral injection
• Fever  Continuous or ‘saddle-back’, with break on fourth or fifth day; usually lasts 7-8 days.

Rash
Transient macular in first 1-2 days. Maculo-papular, scarlet morbilliform from days 3-5 on trunk, spreading centrifugally and sparing palms and soles. May desquamate on resolution

Convalescence  Slow

The disease varies in severity,dengue fever may sometimes leads into dengue haemorrhgic fever,dhf is classified into 4 grades

•  GRADE 1 -fever + consti symptoms
•  GRADE 2 -Grade 1 + SPONTANEOUS BLEEDING FROM GUMS,SKIN & GIT
•  GRADE 3 – GRADE 2  +PROFOND SHOCK
•  GRADE 4 -& GR 3 KNOWN AS Dengue Shock Syndrome

PATHOGENESIS
1^st attack-sensitise the individual,2^nd attack-Ag Ab complex-attaches to macrophages and enters them,They multiply and 2^nd set of reactions occur-complement activation ,mast cell degranulation, activation of kinin system ,Anaphylotoxins such as C3a and C5a,other vasoactive peptides increase vascular permeability leading to- hypovolaemic shock,Complement activation-release of enzymes-thrombosis-platelet aggregation-intravascular coagulation-DIC, Plasma inhibitors of coagulation are also decreased.

CLINICAL FEATURES OF DENGUE HAEMORRHGIC FEVER
Children more affected,Abrupt onset of fever,Upper respiratory cattarh ,Cough,headache,nausea and vomiting,Abdominal pain,Myalgia and arthralgia absent,Petechial,maculopapular rash-forearm,forehead and leg,Cyanosis-pulmonary involvement,Convulsions and resp failure,Death due to extensive GIT h’ge-malena,haematemesis-circulatory failure.

LAB INVESTIGATIONS
Leucopenia is usual and thrombocytopenia common

The confirmation of DENGUE fever is through any of the followings:

1.  Isolation of virus
2. detection of dengue virus genomic sequences by Real-time  PCR
3.  Detection of IgM antibody
4.  Demonstration of rising titre of IgG antibody

GENERAL MANAGEMENT
Bed rest is advisable during a/c febrile phase.Oral fluid and electrolyte therapy recommended for pts suffering from vomitting,diarrhoea.High haematocrit value s/o significant plasma loss need parenteral fluid therapy.

Dr.Suja Pillai . Email : sujapillai8@gmail.com
Dr.Aji Punnen Email : ajipunnenkocheril@gmail.com
Dr.Rumsheed Necholi  Email : nrams3@gmail.com
PG Scholars, Govt. Homeopathic  Medical College. Calicut
Moderator : Dr.K.R.Mansoor Ali . Lecturer, GHMC Calicut