Lyme Disease- Borrelia

Not all joint pain are symtoms of arthritis, pain in joints pains leads to presence of Borrelia in blood. Today I would like to bring it to your notice, my experience with this bacteria during my stay in Norway.

A few weeks back I developed severe pain in joints without inflammation soon pain become unbearable, intensity of pain was so much that it became impossible to do day to day work including holding a cup of coffee. Fearing that I would be suffering from Arthritis we decided to diagnose it. One thing I really appreciate about my doctor is her diagnostics skill. It’s excellent. Doctor examined me with lot of questions. And her final question came to me “Were you bitten by any bug? I was not sure so she suggested me to go for Blood test and x ray.

To my surprise my blood samples showed presence of Borrelia not all people are aware of this organism and its effects on human so I take privilege of educating everyone about Borrelia.

Lyme disease is an infection that derives from a tick bite. The disease has a variety of symptoms, including changes affecting the skin, heart, joints and nervous system. It is also known as Borrelia or Borreliosis.

CAUSES

Lyme disease is caused by an infection from a micro-organism (Borrelia burghdor feri), itself transmitted by a bite from the wood tick, a blood-sucking parasite which normally lives on deer.

Borrelia burgdorferi, is a spirochete. Spirochetes are a group of phylogenetically-distinct bacteria that have a unique mode of motility by means of axial filaments (endoflagella). Spirochetes are widespread in viscous environments and they are found in the intestinal tracts of animals and the oral cavity of humans.
The wood tick is found in many areas, particularly in forests where deer are common. A tick will settle anywhere on a human body, but prefers warm, moist and dark places like the crotch or armpits.
When the tick has found a suitable place on the body, it sticks in its probe to draw up blood, exposing the host to the risk of infection.

SYMPTOMS

Simply seeing a tick somewhere on your body does not mean that you have contracted Lyme disease. Unfortunately, not everyone knows when they have been bitten, so consult your GP if you detect the following symptoms.

• A red spot around the location of the tick's bite. The spot will gradually grow bigger, often with a pale area in the middle. This symptom is called erythema migrans.
• Erythema migrans can also appear at other places on the body where the tick has not bitten. Some people get many red spots.
• Usually one to four weeks will pass between the bite and when erythema migrans appears.

Some patients with Lyme disease feel like they have caught influenza - the symptoms may be:

• drowsiness
• headaches
• mild fever
• joint and muscle pains
• swollen lymph glands.

COMPLICATIONS

Acrodermatitis chronica atrophicans
This is a condition that often develops in older women. Several years may pass from the tick bite until the development of this phenomenon. The symptoms usually involve changes in the skin around the tick bite, such as:

· swelling

· bluish or reddish discoloration of the skin.

Neuro borrelia
About 15 per cent of people with borrelia develop so-called neuro borrelia, between one and five weeks after the tick bite. The central nervous system is affected and the symptoms that result are very mixed and not specific.

• The symptoms often begin with back pain, typically between the shoulder blades and in the neck like a slipped disc. The pain worsens at night.
• Distorted feelings around the area of the bite. The nerves become numb, especially in the face. This may occur at any time up to four weeks after the pain began.
• Sometimes neuro borrelia may present itself as meningitis, with fever, headache and stiffness in the neck.
• In rare cases, the disease may become chronic, with a slowly developing destruction of the nervous system, numbing, partial hearing impairment and the development of dementia.
• Neuro borrelia demands immediate treatment, usually with an admission to hospital.

Inflammation of the joints or Lyme arthritis
This condition may present itself in days or, rarely, years after the bite, but it is very rare. The inflammation of the joints causes pain and swelling. Often, only one joint is inflamed and, rarely, more than three. The most commonly affected joint is the knee followed by the shoulder, elbow, foot, and hip. It has symptoms similar to arthritis.
When treated, the swelling will go away in about one to four weeks but it may return in later months or even years.

DIAGNOSIS

A diagnosis of Lyme disease is more likely if the patient remembers a tick bite and presents the doctor with the erythema migrans rash.

To make a firmer diagnosis the doctor may take a blood sample to determine whether the patient has developed an antibody towards Lyme disease in their blood. Antibodies can typically be found between two and four weeks after contracting the disease, but sometimes the antibodies do not appear for up to eight weeks. This means that the patient may have Lyme disease even though the antibody test is negative. On the other hand, a positive antibody test does not necessarily mean that Borrelia has recently been contracted. The antibodies may be found in the blood several years after an infection is over. Unfortunately, the antibody test is not a very efficient diagnostic tool: false-positive results are common.
If the doctor suspects neuro Borrelia then hospital admission is required for tests on fluids from the spinal canal. This is to determine whether Lyme disease has entered the nervous system.
In cases of chronic neuro borrelia the treatment may include a CT scan of the nervous system.

TREATMENT

• oral doxycillin (except in children), amoxicillin or cephalosporin antibiotics are the usual first choices.
• when antibiotics by injection are being given, then benzylpenicillin, cefotaxime and ceftriaxone are the usual choices.
• no particular choice and method is superior to another - the decision is made by the infectious disease specialist and is dependent on the individual circumstances.

PREVENTION

Removing leaves and clearing brush and tall grass around houses and at the edges of gardens may reduce the numbers of ticks that transmit Lyme disease. Reducing and managing deer populations in geographic areas where Lyme disease occurs may reduce tick abundance.

CDC recommends the following for personal protection from tick bites and Lyme disease:

Avoid tick-infested areas, especially in May, June, and July.

Wear light-colored clothing so that ticks can be spotted more easily. Tuck pant legs into socks or boots and shirt into pants or the area where pants and socks meet so that ticks cannot crawl under clothing.

Spray insect repellent containing DEET on clothes and on exposed skin other than the face, or treat clothes (especially pants, socks, and shoes) with permethrin, which kills ticks on contact.

Wear a hat and a long-sleeved shirt for added protection.

Walk in the center of trails to avoid overhanging grass and brush.

After being outdoors, remove clothing and wash and dry it at a high temperature; inspect body carefully and remove attached ticks with tweezers, grasping the tick as close to the skin surface as possible and pulling straight back with a slow steady force; avoid crushing the tick's body.

Preventive antibiotic treatment with erythromycin or doxycycline to prevent Lyme disease after a known tick bite may be warranted.

Cinnamon Is Lethal Weapon Against E. Coli O157:H7

When cinnamon is in, Escherichia coli O157:H7 is out. That's what researchers at Kansas State University discovered in laboratory tests with cinnamon and apple juice heavily tainted with the bacteria. Presented at the Institute of Food Technologists' 1999 Annual Meeting in Chicago on July 27, the study findings revealed that cinnamon is a lethal weapon against E.coli O157:H7 and may be able to help control it in unpasteurized juices.

Lead researcher Erdogan Ceylan, M.S., reported that in apple juice samples inoculated with about one million E.coli O157:H7 bacteria, about one teaspoon (0.3 percent) of cinnamon killed 99.5 percent of the bacteria in three days at room temperature (25 C). When the same amount of cinnamon was combined with either 0.1 percent sodium benzoate or potassium sorbate, preservatives approved by the Food and Drug Administration, the E.coli were knocked out to an undetectable level. The number of bacteria added to the test samples was 100 times the number typically found in contaminated food.

"This research indicates that the use of cinnamon alone and in combination with preservatives in apple juice, besides its flavoring effect, might reduce and control the number of E.coli O157:H7," concluded Ceylan, a Ph.D. graduate assistant. "Cinnamon may help protect consumers against foodborne bacteria that may be in unpasteurized juices and may partially or completely replace preservatives in foods to maintain their safety," he said.

"If cinnamon can knock out E.coli O157:H7, one of the most virulent foodborne microorganisms that exists today, it will certainly have antimicrobial effects on other common foodborne bacteria, such as Salmonella and Campylobacter," noted Daniel Y.C. Fung, Ph.D., professor of Food Science in the Department of Animal Sciences and Industry at K-State, who oversaw the research.

Last year, Fung and Ceylan researched the antimicrobial effects of various spices on E.coli O157:H7 in raw ground beef and sausage and found that cinnamon, clove, and garlic were the most powerful. This research led to their recent studies on cinnamon in apple juice, which proved to be a more effective medium than meat for the spice to kill the bacteria.

"In liquid, the E.coli have nowhere to hide," Fung noted, "whereas in a solid structure, such as ground meat, the bacteria can get trapped in the fat or other cells and avoid contact with the cinnamon. But this cannot happen in a free-moving environment."

Regardless of the K-State findings, people who are at greater than normal risk for foodborne diseases -- namely the elderly, young children, or immune-compromised would be urged to avoid drinking unpasteurized juices or unthoroughly cooked hamburgers, which may contain harmful microorganisms.

Source: ScienceDaily.com

Bacteria Fight Back

Biofilms Use Chemical Weapons To Neutralize Or Kill Attacking Amoebae

Bacteria rarely come as loners; more often they grow in crowds and squat on surfaces where they form a community together. These so-called biofilms develop on any surface that bacteria can attach themselves to. The dilemma we face is that neither disinfectants and antibiotics, nor phagocytes and our immune system can destroy these biofilms.

This is a particular problem in hospitals if these bacteria form a community on a catheter or implant where they could potentially cause a serious infection. Scientists at the Helmholtz Centre for Infection Research in Braunschweig have now identified one of the fundamental mechanisms used by the bacteria in biofilms to protect themselves against the attacking phagocytes.

The scientists are now publishing their findings in the PLoS One, together with colleagues from Australia, Great Britain and the USA -- the discovery being that biofilm bacteria use chemical weapons to defend themselves.

Until now, scientists have been unable to understand the root of the biofilm problem -- the inability of phagocytes to destroy these biofilms. Dr. Carsten Matz decided to investigate this problem. As a model for his investigation, this Braunschweig-based researcher decided to look at marine bacteria. They face constant threats in their habitat from environmental phagocytes, the amoebae, which behave in a similar way in the sea as the immune cells in our body: they seek out and feed on the bacteria. So long as bacteria are swimming freely and separately in the water, they are easy pickings for these predators. However, if they become attached to a surface and socialize with other bacteria, the amoebae can no longer successfully attack them. "The surprising thing was that the amoebae attacking the biofilms were de-activated or even killed. The bacteria are clearly not just building a fortress, they are also fighting back," says Carsten Matz.

The bacteria utilise chemical weapons to achieve this. A widespread and highly effective molecule used by marine bacteria is the pigment violacein. Once the defence system is ready, the biofilm shimmers a soft purple colour. If the attackers consume just a single cell of the biofilm -- and the pigment they contain -- this paralyses the attackers momentarily and the violacein triggers a suicide mechanism in the amoebae.

"I feel that these results could offer a change of perspective," says Carsten Matz. "Biofilms may no longer be seen just as a problem; they may also be a source of new bioactive agents. When organized in biofilms, bacteria produce highly effective substances which individual bacteria alone cannot produce." And the scientists hope to use these molecules to combat a specific group of pathogens: Human parasites that cause devastating infections such as sleeping illness and malaria. Amoeba are ancient relatives of these pathogens and thus biofilm-derived weapons may provide an excellent basis for the design of new parasiticidal drugs.

Source: ScienceDaily

Key Protein In Leptospirosis Bacterium Identified

Researchers at Weill Cornell Medical College have located a protein they believe is responsible for leptospirosis, a bacterial disease transmitted from animals to humans that infects a half-million people and leads to the death of up to 100,000 annually. The finding may help scientists create a vaccine to protect against the illness.

The protein is on the surface of the bacterium Leptospira interrogans, which causes leptospirosis.

"The disease is a major public health problem in urban slums of developing countries, such as Brazil," says Albert Ko, contributing researcher in the study and physician-scientist from the Division of International Medicine and Infectious Disease at the medical college.

The study, published recently in the Public Library of Science: Pathogens, shows that when a gene producing a protein called Loa22 is disrupted, the bacterium is rendered nonfunctional and unable to produce disease in guinea pigs. When the gene was reintroduced, the bacteria strains regained their virulence and ability to cause leptospirosis and death in guinea pigs.

In humans, leptospirosis is characterized by high fever, severe headache, chills, muscle aches, vomiting and may lead to jaundice, red eyes, abdominal pain, diarrhea or a rash. If left untreated, patients may develop kidney damage, meningitis, liver failure and respiratory distress, according to the Centers for Disease Control. Infection with the Leptospira bacteria can cause a severe pulmonary hemorrhage, which is associated with death in more than 50 percent of the cases with this syndrome.

Leptospira interrogans is found in the urine of infected animals, putting people who work with or are around such animals as cattle, pigs, horses, dogs, rodents and wild animals at greatest risk for infection. In cities in developing countries, large epidemics of rat-borne leptospirosis occur each year during the rainy season.

The disease is diagnosed through blood and urine testing. Treatment includes a course of oral or intravenous antibiotics.

Ko is stationed at Oswaldo Cruz Foundation/Brazilian Ministry of Health in Salvador, Brazil, as coordinator of a collaborative research and training program of infectious diseases and urban poverty.

Source: ScienceDaily

Bacteria-Killing Bandage

Biochemists Create Microbicidal Coating to Fight Hospital Infections

New bandages with microbicidal coating kill the most harmful bacteria on contact. The coating is washable and can also be used on hospital gowns and bed sheets, which will help reduce the risk of infection to all hospital patients and staff. Hospital infections are growing to epidemic proportions because they're passed from person to person. Now, researchers are working to wipe out these infections with a new bacteria-killing bandage.

Gary Smithson was hit head-on by a drunk driver. The accident put him in a wheelchair, but that is not what keeps him there. It's what happened in the ER -- hours after the crash -- that has made the past 10 years unbearable. During a routine check, doctors found an infection.

Gary is one of 20,000 Americans that leave the hospital each year with an infection they didn't come in with. Gregory Schultz, a biochemist at the University of Florida in Gainesville, is part of a team working to wipe out these super bugs. They've created a microbicidal coating that can kill the most harmful bacteria.

"The microbicidal agent -- that's the thing that kills the bacteria -- is permanently bonded on the surface of the fibers of the dressing," Schultz says.

The bandage on the left is not treated with the microbicidal coating. The area in red is infected with bacteria. Now, look at the bandage on the right. It is treated -- you can see there are no bacteria.

Chris Batich, a biomaterials expert at the University of Florida, says, "What we wound up with is a surface that you can wash. And whenever it touches bacteria, it kills the bacteria ... and keeps on killing them."

The microbicidal coating can also be used on hospital gowns and bed sheets, which will help reduce the risk of infection to all hospital patients and staff.

Because of his infection, Gary believes he will spend the rest of his life in wheelchairs he fixes in his shop. "It's completely changed the way I have to live," he says. Every day is a struggle against an invisible invader that Gary hopes won't claim any more innocent victims.

The bacteria-fighting agent can be used outside the hospital for soldiers in the field to help stop athletes foot. The cost of putting this agent on a bandage is about one cent.

BACKGROUND: University of Florida researchers have led the development of a new type of wound dressing that could keep dangerous antibiotic-resistant bacteria from spreading in hospitals, a problem that leads to thousands of deaths in the U.S. annually. Each year, nearly two million Americans contract infections while hospitalized.

HOW IT WORKS: The new wound dressing features a microbial coating that can be chemically bonded to gauze bandages, socks and even hospital bedding and gowns. This makes the material super-absorbent and pulls excess moisture away from the wound. The microbial coating blocks bacteria from reaching a wound and recolonizing there. It also kills the most common and harmful types of resistant bacteria that cause 70 percent of infections in hospitals, such as staph infections. The fabric can be made into clothing, such as antifungal socks and underwear that could help U.S. soldiers in the field who often don't have time to change or shower. Furthermore, the structure of the coating, and the complexity of the process, makes it nearly impossible for bacteria to become resistant to it. Other dressings use a process that allows molecules to diffuse into the air and into the wound, which can slow healing and increases the chance germs will develop resistance.

WHAT ARE STAPH INFECTIONS?

 Staph infections result when a bacteria called Staphylococcus aureus enters the body through an open cut or break in the skin. They usually produce pus. Minor staph infections include infections of hair follicles after shaving, or sties, which occur when the follicle surrounding the eyelashes causes a sore red bump in the eyelid. Staph infection is also behind most cases of food poisoning and can also lead to more life-threatening conditions, such as toxic shock syndrome, pneumonia, and infections of the heart of blood. Those in hospitals, with weakened immune systems, are especially vulnerable to staph infection.

 HOW WOUNDS HEAL: Controlling moisture and staving off infection are two of the most important aspects of wound healing. All wounds go through the same basic stages of healing. A cavity wound is when a large chunk of tissue has been removed, leaving a hole. Small cavity wounds can be closed with stitches, but larger cavities are more prone to infection and are left open to heal. In open healing, the wound "fills in" from the bottom by building new tissue. As it fills in, the sides of the wound also get new tissue. The sides must be kept from touching until the wound has filled in at least halfway, otherwise they can form bridges, trapping fluids in the wound. A healing wound should look bright red. In the active healing phase, cells multiply, connective tissue cells form collagen, and eventually small red fleshy masses of tissue begin to form. These masses keep growing and contracting until the cavity fills up completely.

Source: ScienceDaily

How Cranberry Juice Can Prevent Urinary Tract Infections

For generations, people have consumed cranberry juice, convinced of its power to ward off urinary tract infections, though the exact mechanism of its action has not been well understood. A new study by researchers at Worcester Polytechnic Institute (WPI) reveals that the juice changes the thermodynamic properties of bacteria in the urinary tract, creating an energy barrier that prevents the microorganisms from getting close enough to latch onto cells and initiate an infection.

The study, published in the journal Colloids and Surfaces: B, was conducted by Terri Camesano, associate professor of chemical engineering at WPI, and a team of graduate students, including PhD candidate Yatao Liu. They exposed two varieties of E. coli bacteria, one with hair-like projections known as fimbriae and one without, to different concentrations of cranberry juice. Fimbriae are present on a number of virulent bacteria, including those that cause urinary tract infections, and are believed to be used by bacteria to form strong bonds with cells.

For the fimbriaed bacteria, they found that even at low concentrations, cranberry juice altered two properties that serve as indicators of the ability of bacteria to attach to cells. The first factor is called Gibbs free energy of attachment, which is a measure of the amount of energy that must be expended before a bacterium can attach to a cell. Without cranberry juice, this value was a negative number, indicating that energy would be released and attachment was highly likely. With cranberry juice the number was positive and it grew steadily as the concentration of juice increased, making attachment to urinary tract cells increasingly unlikely.

Surface free energy also rose, suggesting that the presence of cranberry juice creates an energy barrier that repels the bacteria. The researchers also placed the bacteria and urinary tract cells together in solution. Without cranberry juice, the fimbriaed bacteria attached readily to the cells. As increasing concentrations of cranberry juice were added to the solution, fewer and fewer attachments were observed.

Cranberry juice had no discernible effect on E. coli bacteria without fimbriae, suggesting that compounds in the juice may act directly on the molecular structure of the fimbriae themselves. This reinforces previous work by the WPI team that showed that exposure to cranberry juice alters the shape of the fimbriae, causing them to become compressed. Using an atomic force microscope as a minute strain gauge, the team also showed that the adhesive force exerted by bacteria on urinary tract cells declined in direct proportion to the concentration of cranberry juice in the solution.

"Our results show that, at least for urinary tract infections, cranberry juice targets the right bacteria--those that cause disease--but has no effect on non-pathogenic organisms, suggesting that cranberry juice will not disrupt bacteria that are part of the normal flora in the gut," Camesano says. "We have also shown that this effect occurs at concentrations of cranberry juice that are comparable to levels we would expect to find in the urinary tract."

Camesano notes that unpublished work has shown that while cranberry juice has potent effects on disease-causing bacteria, those effects are transitory. "When we takes E. coli. bacteria that have been treated with cranberry juice and place them in normal growth media, they regain the ability to adhere to urinary tract cells," she says. "This suggests that to realize the antibacterial benefits of cranberry, one must consume cranberry juice regularly--perhaps daily."

For those watching calories, Camesano says other recent work in her lab has shown that the effects of regular cranberry juice cocktail and diet (sugar-free) cranberry juice are identical. "That's good news for people who do not like to consume a lot of sugary juice," she says.

Source: Sciencedaily.com

How Bacteria In Cows' Milk May Cause Crohn's Disease

Scientists at the University of Liverpool have found how a bacterium, known to cause illness in cattle, may cause Crohn's disease in humans.

Crohn's is a condition that affects one in 800 people in the UK and causes chronic intestinal inflammation, leading to pain, bleeding and diarrhoea.

The team found that a bacterium called Mycobacterium paratuberculosis releases a molecule that prevents a type of white blood cell from killing E.coli bacteria found in the body.  E.coli is known to be present within Crohn’s disease tissue in increased numbers.

It is thought that the Mycobacteria make their way into the body’s system via cows’ milk and other dairy products.  In cattle it can cause an illness called Johne's disease - a wasting, diarrhoeal condition. Until now, however, it has been unclear how this bacterium could trigger intestinal inflammation in humans.

Professor Jon Rhodes, from the University’s School of Clinical Sciences, explains: “Mycobacterium paratuberculosis has been found within Crohn’s disease tissue but there has been much controversy concerning its role in the disease.  We have now shown that these Mycobacteria release a complex molecule containing a sugar, called mannose.  This molecule prevents a type of white blood cells, called macrophages, from killing internalised E.Coli.” 

Scientists have previously shown that people with Crohn’s disease have increased numbers of a ‘sticky’ type of E.coli and weakened ability to fight off intestinal bacteria.  The suppressive effect of the Mycobacterial molecule on this type of white blood cell suggests it is a likely mechanism for weakening the body’s defence against the bacteria.

Professor Rhodes added: "We also found that this bacterium is a likely trigger for a circulating antibody protein (ASCA) that is found in about two thirds of patients with Crohn's disease, suggesting that these people may have been infected by the Mycobacterium."

The team is beginning clinical trials to assess whether an antibiotic combination can be used to target the bacteria contained in white blood cells as a possible treatment for Crohn’s disease.

Source:ScienceDaily