AED Pads – An answer to servere cardiac arrest

What is a Heart Attack (CVD)?

The heart, made up of specialized muscle cells known as myocytes, is a mechanical pump that propels blood through the circulatory system, thereby ensuring the delivery of oxygen and other essential elements to the body’s vital organs.  In order to perform this life-sustaining task, the heart itself requires a steady supply of oxygen, which it receives through the coronary arteries. An insufficient supply of blood and oxygen causes myoctye injury and cellular death.  This process is referred to as a heart attack, or in medical terms a myocardial infraction.

The death of myocytes has several important effects, which include:

  • Reduced heart performance and pumping efficiency
  • Reduced blood and oxygen supply to vital organs: the brain, kidneys, intestines, liver.
  • Increased irritability of the heart’s electrical system
  • Slowing, racing or erratic beating of the heart, each of which can be life-threatening.

In a majority of instances, a heart attack occurs when a blood clot, also referred to as a thrombus or the process of thrombosis, suddenly develops within a coronary artery. Coronary arteries themselves contain a buildup of plaque (deposits of fat-like substances) due to a process known as atherosclerosis.  When plaque bursts or ruptures, it leads to either partial or complete blockage of coronary artery blood flow and life-sustaining oxygen delivery to the heart muscle (myocardium). The blood vessel interprets, or perhaps more precisely misinterprets plaque breakage as a “breach of integrity” and a risk for serious bleeding.

Who is at Risk for a Heart Attack?

The development of coronary atherosclerosis represents a major and most common risk for a heart attack.  Though unique in their own right, atherosclerosis and thrombosis share common origins and are linked by genetic and environmental factors.  Thus, risk factors for atherosclerosis are also recognized for a heart attack. Atherosclerosis typically begins in the mid-to- late second and early third decades of life, with the accumulation of fatty material.

  • Traditional Risk Factors
  • High Blood Pressure
  • Tobacco Smoking
  • Diabetes Mellitus
  • Metabolic Syndrome
  • Overweight-Obesity
  • Inactivity
  • High Blood Cholesterol
  • Genetics and Family History of CHD

What can I do to reduce my risk for a heart attack?

The specific recommendations to prevent heart attack are:

  • Avoid exposure (Active or Passive)to tobacco smoke.
  • Maintain a healthy eating pattern.
  • Maintain blood pressure below 140/90 mmHg.
  • Lower cholesterol to appropriate level based on individual risk.
  • Perform at least 30 minutes of moderate-intensity physical activity on most (preferable all) days of the week.
  • Achieve and maintain an ideal body weight and abdominal circumference.
  • Maintain a normal fasting blood sugar (below 110 mg/dl).
  • Warning Signs of a Heart Attack, Rapid Response and Community Action

Heart attack pain is characteristically described as a deep, visceral sensation – an oppressive feeling or discomfort – located in the chest under the breast bone, and frequently expressed as choking, constricting, heavy, squeezing, pressure-like, vise-like or burning.

Rapid Response

The American Heart Association and National Heart Lung, and Blood Institute have launched a new “act in time” campaign that emphasizes the importance of calling 9-1-1 immediately at the onset of heart attack symptoms. Receiving immediate medical attention improves the chances of surviving a heart attack as well as of benefiting from a variety of medications and treatments designed specifically to minimize the extent of heart damage and facilitate recovery. Many physicians and doctors thus refers the use of AED Pads (Automated External Defibrillators). AEDs or automated external defibrillators are the electronic devices which can be handy in diagnosis of the potentially life threatening cardiac arrest of ventricular fibrillation and ventricular tachycardia in a patient or sportsperson. AED helps them treat through defibrillation, the application of electrical therapy which stops the arrhythmia, allowing the heart to reestablish an effective rhythm.

For more information on AEDs, AED Pads, AED Equipments, Automated External Defibrillators visit – http://www.aedlifepower.com/aed-pads.html

Food Safety FAQ Tips and Tricks for a Safe, Clean Kitchen

Food Safety – FAQ Tips and Tricks

Food Safety is very important and knowing about it can help keep you and your family healthy. Here are some answers, tips, and tricks, to frequently asked questions that you may have about food safety.

“What is the safe holding temperature for foods that are already cooked?”

If you have any potentially hazardous foods which are not served immediately after you are done cooking them, then they must be either cooled down to a temperature of less than 40 degrees, or held at 140 degrees or higher.

Food safety is all about keeping the foods you cook at the right temperatures, and not in the danger zone.

“What Happens if I do not hold the food at temperatures under 40 degrees or above 140 degrees?”

Foods that are held at a temperature that’s either under 40 or over 140, it is in what is called the Danger Zone.

This is not a good thing because if the food doesn’t get take care of in less than 2 hours, you run the risk of causing a food borne illness outbreak.

The amount of time spent in the danger zone does not reset if you decide to take it out again and return it to the danger zone.

This is because when it is in the danger zone it is growing bacteria and refrigerating your food doesn’t kill them, it just slows them down.

“What are foods that are considered to be potentially hazardous?”

This would include high protein food items such as poultry, milk, milk products, gravy, fish, shellfish, etc. These will all gladly support the growth of harmful bacteria causing a food borne illness.

“What is the difference between a food borne intoxication and a food borne infection?”

Certain bacteria under certain conditions produce chemicals and toxins in food which when ingested by a person, will cause a food intoxication.

A food borne infection is caused by the ingestion of food containing a bacteria, virus, or parasite that must multiply within the gastrointestinal tract before causing symptoms and problems.

This is why food safety is so important!

“What causes a food borne illness?”

Most of the time, the majority of food borne illnesses can be traced back to one or more of the following:

Food that has been cooked too far in advance to serving.

Food had poor refrigeration.

Food was not held at the correct temperature.

There was a lack of adherence to personal hygiene standards.

The person responsible was careless in the preparation of the product and the application of what was recommended to them.

“What is the best way to thaw frozen foods?”

If you have frozen food you are trying to thaw don’t use methods such as exposure to excessive heat, hot air, or hot water. Instead, thaw the frozen foods in the refrigerator.

This will take a little more time, but you will have a much better final product. For perfect thawing, 36-38 degrees is perfect.

You can even use their original wrappers and packaging to enhance uniform thawing and also reduce moisture loss.

“Is there a problem with pastries?”

Yes, cream puffs, custard filled pies and cakes, eclairs, and all products similar to those must be prepared and cooked under sanitary conditions, covered, cooled quickly, and refrigerated until they are served. They also must remain under refrigeration when serving.

“How should ice be handled when used as part of the meal being served?”

Ice that is intended to be served for human consumption in food or drinks must be made from potable drinking water only.

Ice should definitely be handled carefully like anything else and should be protected from contamination.

“Why are pastries so important to keep refrigerated?”

Pastries filled with dairy products and/or eggs, are highly perishable and provide ideal culture platform for pathogenic organisms to grow on. Only the quantity of food that will be consumed for the day should be prepared.

“What is the best method of freezing cooked foods for serving at a later date?”

Before you start freezing food that you’ve cooked, it’s important to cool it down quickly and as fast as you can so bacteria don’t grow.

Food Safety

A great way to do this is to place the containers of warm food into an ice bath, or another container filled with ice cubes and water. Wedge the containers into the ice and keep stirring the food occasionally.

Stirring ensures that the center of the food cools as well. As the mixture cools, a great way to find out the temperature is to use a thermometer.

This is the best way you know exactly when it gets to the right temperature to be wrapped labeled and placed in a freezer.

Angina pectoris: The Types, Causes and Risk factors

Angina pectoris, also known as Angina, a symptoms of  Ischemic heart disease, is defined as a condition of chest pain caused by poor blood flow through the blood vessels due to obstruction or spasm of the coronary arteries resulting of lack of blood that lead to lack of oxygen supply and waste removal. 

Types of Angina pectoris
1. Stable angina res
Stable angina is the chest pain occurred after physical activity or stress and may last up to 10 minutes. the symptoms may improve or go away when stop or slow down the exercise.

2. Unstable angina 
Unstable angina is a type of angina with chest pain occurs even at rest, with Crescendo angina and/or new-onset angina(1)

Symptoms
Beside chest pain or discomfort, patients with angina may also experience heaviness, tightness, squeezing, burning, or choking sensation of the chest and pain in the back, neck area, jaw, or shoulders. These are results of the pain perceived at a location other than the chest depending to the spinal level that receives visceral sensation.

Causes and risk factors 
A. Causes
A.1. Stable angina
Physical exertion is the most common cause of stable angina as a result of severely narrowed arteries of that interfere with the blood flow to the heart.

A.2. Unstable angina
Unstable angina is a condition of blood clots causes of  partially or totally block of an artery as a result of rupture of an artery. If severe case, large blood clot can increase the risk of cardiovascular diseases,
Blood clots may form, partially dissolve, and later form again. Angina can occur each time a clot blocks an artery.

B. Risk factors
1. Cigarette smoking
Men who are smokers are at higher risk to develop angina. According to the study of Framingham Heart Study, posted by Harvard University, indicated that those less than 60 years of age at angina onset who were nonsmokers or quitters during follow-up had a definite prognostic advantage over similarly aged continuing smokers. These results could not be explained by differences in coronary risk factors prior to symptom onset or by changes in factors other than smoking during follow-up. The findings suggest that stopping the cigarette smoking habit can improve both short-term and long-term prognosis in the younger patient and angina pectoris(2).

2. Obesity
in the study to evaluate the effects of moderate weight loss, in overweight patients with angina, on plasma coagulation, fibrinolytic indicies and pain frequency, at the University of Glasgow, researchers found that after the 12-week dietary intervention period, mean body weight fell by 3.5 (s.d. 2.6) kg or 4.3% (P=0.0001), range -11.7 to +1.7 kg. Mean angina frequency fell by 1.8 (s.d. 3.6) from 3.2 to 1.4 episodes/week (P=0.009) and plasma cholesterol by 0.4 (s.d. 0.7) from 6.3 to 5.9 mmol/l (P=0.0001). HDL cholesterol and triglyceride were unchanged. Of the coagulation and fibrinolytic factors, factor VII activity and RCA were significantly reduced by 5 (s.d. 20), IU/dl (P=0.04) and 1.3 (s.d. 1.3) arbitrary units (P=0.014), respectively(3).

3. Diabetes 
In the study of nineteen diabetic and 25 nondiabetic patients with exertional angina were exercised on a treadmill to measure anginal perceptual threshold, researchers at the Newham General Hospital found that the diabetic group had a longer anginal perceptual threshold (138 +/- 64 seconds vs 34 +/- 51 seconds, p less than 0.001), which correlated positively with the somatic pain threshold (r = 0.5, p = 0.03); patients with more prolonged anginal perceptual thresholds tended to have higher somatic pain thresholds. In the diabetic group anginal perceptual (r = -0.3, p = NS) and somatic pain (r = -0.4, p = 0.05) thresholds tended to increase as the ratio of peak to minimal heart rate during the Valsalva maneuver fell below 1.21, but these variables were unrelated in the nondiabetic group(4).

4. High cholesterol 
According to the study of The Heart Center of Chonnam National University Hospita of 34 stable angina pectoris (SAP) patients showed that these patients had unstable plaques (UPs) (61.6±9.2 years, 24 males, 12.8%). The percentage of plaque area in the minimum luminal area in high low density lipoprotein-cholesterol (LDL-C)/high density lipoprotein-cholesterol (HDL-C) ratio patients was significantly higher than in low LDL-C/HDL-C ratio patients (72.7±9.5% vs. 69.9±9.3%, p=0.035). An LDL-C/HDL-C ratio >2.0 was an independent predictor for UPs in SAP patients (odds ratio 5.252, 95% confidence interval 1.132-24.372, p=0.034)(5).

5. High blood pressure
Hypertension is associated to increased risk of Angina pectoris. In the study ofManagement of patients with hypertension and angina pectoris, reserachers showed thatin managing the patient with hypertension and angina pectoris, it is important to determine whether the angina occurs in the setting of hypertensive hypertrophic disease alone or coexists with coronary arterial stenoses(6).

6. Sedentary lifestyle and Unhealthy diet
Lifestyle with no or irregular physical activity is associated with increased risk of Angina pectoris. Diet high in saturated and trans fat with less fruits and vegetables enhances the building up of blood cholesterol of that increase the risk of angina.

7. Family history of early heart disease
If you have a family history of early heart disease, you are at higher risk to develop angina pectoris as family history of premature coronary artery disease increase the risk of an imbalance between myocardial oxygen supply and demand that may result of angina.

8.  Coronary artery disease
Coronary artery disease can cause decreased blood flow to the coronary arteries from the heart as a result of narrowing of the small blood vessels that supply blood and oxygen to the heart.

9. Other heart diseases
Increased blood flow for patients with preexisting ischemic heart disease may reduced the risk of angina pertoris, according to the study of Efficacy of early invasive strategy of diagnostics and treatment of unstable angina at the background of preexisting ischemic heart disease, indicated that detection of indications for myocardial revascularization in patients with unstable angina including those at medium and low risk confirms necessity of application of early invasive strategy as conventional strategy ensuring timeliness of pathogenetic treatment. Absence of indications to myocardial revascularization in a limited group of patients gives an opportunity to clarify diagnosis, prescribe drug therapy and prevent unjustified hospitalizations(7)

10. Previous heart attack
Heart attack victims may experience a diversity of symptoms, including chest pain, heaviness, tightness, squeezing, burning, or choking sensation of the chest and pain in the back, neck area, jaw, or shoulders.

11.  Age and lower socioeconomic status
According to the study of Dr. Sekhri N, and the research team at the Barts and the London NHS Trust, here is evidence of underutilisation of chest pain clinics by older people and those from lower socioeconomic status. More robust and patient focused administrative pathways need to be developed to detect inequity, correction of which has the potential to substantially reduce coronary mortality(8).

12. Etc.

For the series of Angina pectoris visit http://diseases-researches.blogspot.ca/p/angina-pectoris.html

For more health articles, please visit http://medicaladvisorjournals.blogspot.ca   

Sources can be found at http://medicaladvisorjournals.blogspot.ca/2012/08/angina-pectoris-types-causes-and-risk.html

My Daughter’s Open Heart Surgery

When my Raven was born she did not cry, even though it was via c-section and the umbilical cord was wrapped around her neck. She strained to open her eyes, gazing around the room with her hands cupped near her chin, quietly observing her new world. She would always be that way as she grew into a sweet, soft spoken little girl, who needed time to warm up to new situations, and would rather watch people than join them. She was always small, barely hitting the five percentile range at the doctor’s office and, while most happy when she was singing or dancing alone, she was painfully shy everywhere else. Everything, however, would change after she underwent heart surgery.

Raven had a loud heart murmur from day one and saw her first cardiologist before she was two weeks old. She was diagnosed with pulmonary stenosis, a condition that slowed the flow of blood from her heart to her lungs due to a thickening of her pulmonary valve and seemingly explained her murmur. While a bit worrisome, the defect was mild, requiring annual visits each summer, with a possibility of surgery in the future.

By age four Raven was my little sleeping beauty. Perpetually tired, slow, and sluggish, my little girl could only manage to find small bouts of energy throughout the day, but was constantly complaining about being tired, no matter how much she rested. During her annual appointment at Children’s Hospital in Seattle, her new cardiologist (her earlier one had retired) gave us some heavy, shocking news that would also explain her fatigue: the good news was that Raven’s pulmonary stenosis was now trivial at best and no longer a concern; the bad news was that a large hole was found on the backside of her heart via the routine sonogram. She had a condition called Atrial Septal Defect (ASD), in which part of the wall separating the upper chambers of the heart, called the atria, is missing, allowing oxygenated blood from the left atrium into the right atrium, mixing with oxygen-poor blood, and increasing the amount flowing to the lungs, which did not allow adequate oxygen to reach her other organs. It was concluded that Raven had had the condition since birth, resulting in her loud swishing murmur and, possibly, her low appetite and sleepiness.

The gap in the wall was big, but the surgeon wanted to try a minimally invasive surgery called cardiac catheterization, whereby a device would be guided through a vein in her groin up to her heart and secured on the wall. Our hope was that the hole was small enough to allow rims for the device to grab onto. If this young procedure (20 years) did not work or if the hole was too big, open heart surgery would be our only option to close it, a scary yet well documented highly invasive surgery with 50 years of success, but with the biggest risk out of the two surgeries of infection, blood loss, and death. I had a sinking feeling.

The day before Raven’s scheduled heart catheterization, she developed a high fever (103) and the surgery had to be rescheduled for September, five days before the first day of kindergarten. My seven year old son, Lucius, was distracted with second grade on the day his sister went to Seattle Children’s Hospital for what was supposed to be an overnight stay. After two hours of waiting to hear about Raven, the surgeon sat me down and gently explained what I had been fearing: Raven’s hole was nearly the size of her heart and a small camera that had been guided through a catheter in her vein and to her heart revealed no rims for the device to grab onto. She would need to have open heart surgery, which included bypass, where her heart would be drained of its blood and stopped while she was artificially kept alive, and a piece of her pericardium (sac that the heart sits in) was cut out and sewn over the hole in her heart. I knew that this was a necessary surgery that would give my daughter a better quality of life, but it was, nonetheless, a hard truth to swallow.

My sweet girl was required to lay flat for four hours after the minimally invasive surgery which only confirmed the need for an invasive surgery. She was exhausted, her mouth dry, and her tummy empty when I saw her next. She slowly nibbled on crackers and drank water from a straw while begging to go home or, at the very least, to sit up. I knew I would have to tell her later that the hole in her heart was too big and needed a bigger surgery to fix. As a parent who believes in being honest with her children, I needed to give myself a full day to come to terms with reality myself before delicately telling my five year old that we would be taking another trip back to Children’s Hospital.

One week later we were told that Raven’s surgery was scheduled for October 31st 2013, Halloween, and only four weeks away. In those weeks my husband and I talked openly with both our kids about the upcoming surgery nearly on a daily basis. My son knew more of the heavy details of surgery than my daughter, but she understand that her heart needed to be fixed so that her body would have more energy and she could grow strong and healthy; she knew that she would be asleep during the surgery and that afterwards would stay three to five days in the hospital with mommy by her side; she was aware that she would have a scar on her chest that would fade with each passing day; and, most importantly, she was given four weeks to get used to the idea before it happened. We celebrated Halloween on October 30th, trick-or-treating with a gaggle of other kids in the businesses of the Seattle Piers, and went to bed that night happy and ready for surgery.

I specifically requested an anti-anxiety pill to be given to Raven before being carried into surgery. We were given this option and grabbed at it since my five year had already been through a previous procedure only four weeks prior and had been so scared that she had to be held down by myself and three other doctors in order to administer the anesthesia. I wanted this experience, that would be scary for anyone, to be as pleasant as possible for my daughter. The medicine caused Raven to be calm and a little silly and, as I kissed her goodbye, she was happily carried away by a doctor, all the while informing him that she was here to fix her heart.

Stephen (my husband) and I were given updates every twenty minutes or so. The worst moment was when Raven was put on bypass. Knowing that my daughter’s heart was not beating and being cut into was almost unbearable. I tried to distract my nerves, but all I could do was clench my fists and remember to breathe, waiting for the next update. Twenty minutes later my husband’s cell phone rang and we were told that she was off bypass and her heart was beating. I was trembling with relief.

The ICU was meticulously sterile and everyone was required to Purell their hands before and after leaving Raven’s room, which I was grateful for since my biggest worry after surgery was infection. Raven looked particularly frail as she lay in the hospital bed, with three IV’s (including one that had to be sewn onto her neck), monitors, a fresh suture on her chest and a tube protruding from her abdomen that drained fluid from around her heart and into a bag. I remember thinking that as least the surgery; the hard part, was over.

Hours later Raven woke up screaming in pain and attempted to rip the tube sticking out of her abdomen out. I asked the nurse to do something about my daughter’s pain and she was quickly given morphine while I stroked her tear stained face and reassured her that everything was going to be alright. Our first and only night in the ICU was stressful, exhausting, and productive. Raven developed a slight fever for one hour, never to return. She was given x-ray’s, sonograms, and constantly had her vitals checked. We saw a nurse nearly every hour and, as her vitals progressed, she had two IVs removed, and was finally given something to eat. I did not get any sleep that first night, staying right by her bed in an uncomfortable chair, holding her hand and making sure that each time she woke up not in her bedroom, she felt me with her.

The next day Raven was given a full meal and moved out of the ICU and into a regular hospital room. Her catheter was removed and, for the first time since surgery, she walked on wobbly legs to the bathroom. Her recovery was fast and by the second night (!) she had been completely weaned off opiates and was simply taking Tylenol. After proving to herself that she could, in fact, walk, even with her drainage tube still trailing behind her, she insisted on walking everywhere. We walked the hallways, took a break, and she would eagerly but slowly walk to the play room a few floors and hallways away. She giggled when the nurse pushed her in a wheelchair to get her early morning X-rays and passed the time in bed by drawing pictures about bunny rabbits and butterflies and telling me stories about her new animal characters.

By the third day she had her complete appetite back and was suddenly craving milk. She also had her drainage tube removed and the hole in her abdomen sewn up, a painful ordeal that was made easier by the quick hands of the nurse practitioner. By that third and final night, Raven was so used to getting X-rays that she now posed for them, cracking the medical technicians up. Her final sonogram at Children’s Hospital revealed that the material taken from her heart’s sac was fitting in between her atrial valves just fine. Her heart was now without a defect and, to the delight of her cardiologist, her murmur was undetectable. Raven proudly informed all the nurses, doctors, and visitors that came to see her that her heart no longer went “whoosh, whoosh,” but now made a “bump, bump,” sound.

On the fourth morning of our stay at the hospital, having endured three nights and open heart surgery, my amazing five year old WALKED out of the hospital and got into the car like it was no thing!

Five days after leaving Children’s, Raven had her stitches removed from her abdomen (her chest wound was glued), revealing an air pocket where puss had gathered. The scar on her abdomen now looks like a beautiful tattooed belly button due to the infection.

Months following the surgery, Raven experienced bouts of depression, some nightmares, and a few bad headaches, but her chest never gave her problems. We decided to pull her out of kindergarten since she was a summer baby and give her the extra year to recover, emotionally more so than physically, and start kindergarten the next year, fresh and without open heart surgery getting in the way. After six months I was seeing some major changes: she had gained five pounds, her speech and drawings had improved dramatically, she no longer complained about being tired, and she had grown out of most of her clothes.

By the summer before kindergarten, my shy butterfly had blossomed into a sporty, high energized tiger that was assertive, demanding, and beaming with confidence. She had gained ten pounds since her surgery and shot up in height. Maybe surprising to some (but not to us), she talked openly about her heart surgery, about her experience at the hospital, and even about her scars in a positive light. For a now-six-year-old, she exemplifies bravery, resilience, and maturity. She had her chest cracked open, held apart, her heart drained, stopped, and cut into. She is not only my hero, she is a serious bad-ass who handled heart surgery like a boss and inspired the hell out of everyone around her! I hope to be more like my daughter when I grow up!

Molecular Mechanism of Drug resistance

Molecular Mechanism of Drug resistance

Drug resistance is the reduction in effectiveness of a drug in curing a disease or improving a patient’s symptoms. When the drug is not intended to kill or inhibit a pathogen, then the term is equivalent to dosage failure or drug tolerance. More commonly, the term is used in the context of diseases caused by pathogens.Pathogens are said to be drug-resistant when drugs meant to neutralize them have reduced effect. When an organism is resistant to more than one drug, it is said to be multidrug resistant.Drug resistance is an example of evolution in microorganisms. Individuals that are not susceptible to the drug effects are capable of surviving drug treatment, and therefore have greater fitness than susceptible individuals. By the process of natural selection, drug resistant traits are selected for in subsequent offspring, resulting in a population that is drug resistant.Multiple drug resistance or Multidrug resistance is a condition enabling a disease-causing organism to resist distinct drugs or chemicals of a wide variety of structure and function targeted at eradicating the organism. Organisms that display multidrug resistance can be pathologic cells, including bacterial and neoplastic (tumor) cells.Cross-resistance is the tolerance to a usually toxic substance as a result of exposure to a similarly acting substance. It is a phenomenon affecting e.g. pesticides and antibiotics.as an example rifabutin and rifapin cross react in the treatment of tuberculosis. Various microorganisms have survived for thousands of years by their being able to adapt to antimicrobial agents. They do so via spontaneous mutation or by DNA transfer. It is this very process that enables some bacteria to oppose the assault of certain antibiotics, rendering the antibiotics ineffective. These microorganisms employ several mechanisms in attaining multidrug resistance:

  • No longer relying on a glycoprotein cell wall
  • Enzymatic deactivation of antibiotics
  • Decreased cell wall permeability to antibiotics
  • Altered target sites of antibiotic
  • Efflux mechanisms to remove antibiotics
  • Increased mutation rate as a stress response

Many different bacteria now exhibit multidrug resistance, including staphylococci, enterococci, gonococci, streptococci, salmonella, Mycobacterium tuberculosis and others. In addition, some resistant bacteria are able to transfer copies of DNA that codes for a mechanism of resistance to other bacteria, thereby conferring resistance to their neighbors, which then are also able to pass on the resistant gene.

To limit the development of antibiotic resistance, one should:

  • Use antibiotics only for bacterial infections
  • Identify the causative organism if possible
  • Use the right antibiotic; do not rely on broad-range antibiotics
  • Not stop antibiotics as soon as symptoms improve; finish the full course
  • Not use antibiotics for most colds, coughs, bronchitis, sinus infections, and eye infections, which are caused by viruses.

It is argued that government legislation will aid in educating the public on the importance of restrictive use of antibiotics, not only for human clinical use but also for treating animals raised for human consumption.

Causes and risk factors

Schematic representation of how antibiotic resistance evolves via natural selection. The top section represents a population of bacteria before exposure to an antibiotic. The middle section shows the population directly after exposure, the phase in which selection took place. The last section shows the distribution of resistance in a new generation of bacteria. The legend indicates the resistance levels of individuals.

Antibiotic resistance can be a result of horizontal gene transfer, and also of unlinked point mutations in the pathogen genome and a rate of about 1 in 108 per chromosomal replication. The antibiotic action against the pathogen can be seen as an environmental pressure; those bacteria which have a mutation allowing them to survive will live on to reproduce. They will then pass this trait to their offspring, which will result in a fully resistant colony.

Several studies have demonstrated that patterns of antibiotic usage greatly affect the number of resistant organisms which develop. Overuse of broad-spectrum antibiotics, such as second- and third-generation cephalosporins, greatly hastens the development of methicillin resistance. Other factors contributing towards resistance include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by patients, the impregnation of household items and children’s toys with low levels of antibiotics, and the administration of antibiotics by mouth in livestock for growth promotion. Also unsound practices in the pharmaceutical manufacturing industry can contribute towards the likeliness of creation antibiotic resistant strains. Researchers have recently demonstrated the bacterial protein LexA may play a key role in the acquisition of bacterial mutations.

Drug resistance occurs in several classes of pathogens:

  1. bacteria—antibiotic resistance
  2. endoparasites
  3. viruses—resistance to antiviral drugs
  4. fungi
  5. cancer cells

Mechanisms

The four main mechanisms by which microorganisms exhibit resistance to antimicrobials are:

  1. Drug inactivation or modification: e.g. enzymatic deactivation of Penicillin G in some penicillin-resistant bacteria through the production of ?-lactamases. Antibiotic modification is the best known: the resistant bacteria retain the same sensitive target as antibiotic sensitive strains, but the antibiotic is prevented from reaching it. This happens, for example, with  lactamases the  lactamase enzymatically cleaves the four membered  lactam ring, rendering the antibiotic inactive. Over 200 types of  lactamase have been described (table). Most lactamases act to some degree against both penicillins and cephalosporins; others are more specific namely, cephalosporinases (for example, AmpC enzyme found in Enterobacter spp) or penicillinases (for example, Staphylococcus aureus penicillinase).  Lactamases are widespread among many bacterial species (both Gram positive and Gram negative) and exhibit varying degrees of inhibition by lactamase inhibitors, such as clavulanic acid.
  1. Alterations in the primary site of action may mean that the antibiotic penetrates the cell and reaches the target site but is unable to inhibit the activity of the target because of structural changes in the molecule. Enterococci are regarded as being inherently resistant to cephalosporins because the enzymes responsible for cell wall synthesis (production of the polymer peptidoglycan) known as penicillin binding proteins have a low affinity for them and therefore are not inhibited. Most strains of Streptococcus pneumoniae are highly susceptible to both penicillins and cephalosporins but can acquire DNA from other bacteria, which changes the enzyme so that they develop a low affinity for penicillins and hence become resistant to inhibition by penicillins.3 The altered enzyme still synthesises peptidoglycan but it now has a different structure.4 Mutants of Streptococcus pyogenes that are resistant to penicillin and express altered penicillin binding proteins can be selected in the laboratory, but they have not been seen in patients, possibly because the cell wall can no longer bind the anti-phagocytic M protein.
  1. Alteration of metabolic pathway: e.g. some sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.
  2. Quick Efflux: Active efflux is a mechanism responsible for extrusion of toxic substances and antibiotics outside the cell, this is considered to be a vital part of xenobiotic metabolism. This mechanism is important in medicine as it can contribute to bacterial antibiotic resistance.Efflux systems function via an energy-dependent mechanism (Active transport) to pump out unwanted toxic substances through specific efflux pumps. Some efflux systems are drug-specific while others may accommodate multiple drugs, and thus contribute to bacterial multidrug resistance (MDR).

There are three known mechanisms of fluoroquinolone resistance. Some types of efflux pumps can act to decrease intracellular quinolone concentration. In gram-negative bacteria, plasmid-mediated resistance genes produce proteins that can bind to DNA gyrase, protecting it from the action of quinolones. Finally, mutations at key sites in DNA gyrase or Topoisomerase IV can decrease their binding affinity to quinolones, decreasing the drug’s effectiveness.

Bacterial efflux pumps are proteinaceous transporters localized in the cytoplasmic membrane of all kinds of cells. They are active transporters meaning that they require a source of chemical energy to perform their function. Some are primary active transporters utilizing Adenosine triphosphate hydrolysis as a source of energy, while others are secondary active transporters (uniporters, symporters or antiporters) in which transport is coupled to an electrochemical potential difference created by pumping out hydrogen or sodium ions outside the cell.Bacterial efflux transporters are classified into five major superfamilies, based on the amino acid sequence and the energy source used to export their substrates:

  1. The major facilitator superfamily (MFS);
  2. The ATP-binding cassette superfamily (ABC);
  3. The small multidrug resistance family (SMR);
  4. The resistance-nodulation-cell division superfamily (RND); and
  5. The Multi antimicrobial extrusion protein family (MATE).

Of these only the ABC superfamily are primary transporters, the rest being secondary transporters utilizing proton or sodium gradient as a source of energy. While MFS dominates in Gram positive bacteria , the RND family is unique to Gram-negatives.

In the case of imipenem resistant Pseudomonas aeruginosa, lack of the specific D2 porin confers resistance, as imipenem cannot penetrate the cell. This mechanism is also seen with low level resistance to fluoroquinolones and aminoglycosides. Increased efflux via an energy-requiring transport pump is a well recognised mechanism for resistance to tetracyclines and is encoded by a wide range of related genes, such as tet(A), that have become distributed in the enterobacteriaceae.

Function

Although antibiotics are the most clinically important substrates of efflux systems, it is probable that most efflux pumps have other natural physiological functions. Examples include:

  • The E.coli AcrAB efflux system which has a physiologic role of pumping out bile acids and fatty acids to lower their toxicity.
  • The MFS family Ptr pump in Streptomyces pristinaespiralis appears to be an autoimmunity pump for this organism when it turns on production of pristinamycins I and II.
  • The AcrAB–TolC system in E.coli is suspected to have a role in the transport of the calcium-channel components in the E. coli membrane.
  • The MtrCDE system plays a protective role by providing resistance to faecal lipids in rectal isolates of Neisseria gonorrhoeae.
  • The AcrAB efflux system of Erwinia amylovora is important for this organism’s virulence, plant (host) colonization and resistance to plant toxins.

The ability of efflux systems to recognize a large number of compounds other than their natural substrates is probably because substrate recognition is based on physicochemical properties, such as hydrophobicity, aromaticity and ionizable character rather than on defined chemical properties, as in classical enzyme-substrate or ligand-receptor recognition. Because most antibiotics are amphiphilic molecules – possessing both hydrophilic and hydrophobic characters, they are easily recognized by many efflux pumps.

Impact on antimicrobial resistance

The impact of efflux mechanisms on antimicrobial resistance is large, this is usually attributed to the following:

  • The genetic elements encoding efflux pumps may be encoded on chromosomes and/or plasmids, thus contributing to both intrinsic (natural) and acquired resistance respectively. As an intrinsic mechanism of resistance, efflux pump genes can survive a hostile environment ( for example in the presence of antibiotics) which allows for the selection of mutants that over-express these genes. Being located on transpoable genetic elements as plasmids or transposons is also advantageous for the microorganisms as it allows for the easy spread of efflux genes between distant species.
  • Antibiotics can act as inducers and regulators of the expression of some efflux pumps.
  • Expression of several efflux pumps in a given bacterial species may lead to a broad spectrum of resistance when considering the shared substrates of some multi-drug efflux pumps, where one efflux pump may confer resistance to a wide range of antimicrobials.

Molecular epidemiology of resistance genes

Resistance in bacteria can be intrinsic or acquired. Intrinsic resistance is a naturally occurring trait arising from the biology of the organism for example, vancomycin resistance in Escherichia coli. Acquired resistance occurs when a bacterium that has been sensitive to antibiotics develops resistance this may happen by mutation or by acquisition of new DNA.

Mutation is a spontaneous event that occurs regardless of whether antibiotic is present. A bacterium carrying such a mutation is at a huge advantage as the susceptible cells are rapidly killed by the antibiotic, leaving a resistant subpopulation. Transferable resistance was recognised in 1959, when resistance genes found in shigella transferred to E coli via plasmids. Plasmids are self replicating circular pieces of DNA, smaller than the bacterial genome, which encode their transfer by replication into another bacterial strain or species. They can carry and transfer multiple resistance genes, which may be located on a section of DNA capable of transfer from one plasmid to another or to the genome a transposon (or “jumping gene”). Because the range of bacteria to which plasmids can spread is often limited, transposons are important in spreading resistance genes across such boundaries. The mecA gene found in MRSA may well have been acquired by transposition.7 Plasmid evolution can be complex, but modern molecular techniques can give an understanding (as is the case with the plasmids that contain the tetM gene and are found throughout the world in Neisseria gonorrhoeae).8

Bacteriophages (viruses that infect bacteria) can also transfer resistance, and this is frequently seen in staphylococci. When bacteria die they release DNA, which can be taken up by competent bacteria a process known as transformation. This process is increasingly recognised as important in the environment and is probably the main route for the spread of penicillin resistance in Streptococcus pneumoniae, by creation of “mosaic penicillin binding protein genes.

Origins of resistance genes

The origins of antibiotic resistance genes are obscure because at the time that antibiotics were introduced the biochemical and molecular basis of resistance was yet to be discovered. Bacteria collected between 1914 and 1950 (the Murray collection) were later found to be completely sensitive to antibiotics. They did, however, contain a range of plasmids capable of conjugative transfer.9 None of the Murray strains was resistant to sulphonamides, although these had been introduced in the mid-1930s; resistance was reported in the early 1940s in streptococci and gonococci.10 The introduction of streptomycin for treating tuberculosis was thwarted by the rapid development of resistance by mutation of the target genes. Mutation is now recognised as the commonest mechanism of resistance development in Mycobacterium tuberculosis, and the molecular nature of the mutations conferring resistance to most antituberculosis drugs is now known.11 Favourable mutations that arise in bacteria can be mobilised via insertion sequences and transposons on to plasmids and then transferred to different bacterial species.

In considering the evolution and dissemination of antibiotic resistance genes it is important to appreciate the rapidity of bacterial multiplication and the continual exchange of bacteria among animal, human, and agricultural hosts throughout the world. There is support for the notion that determinants of antibiotic resistance were not derived from the currently observed bacterial host in which the resistance plasmid is seen. DNA sequencing studies of  lactamases and aminoglycoside inactivating enzymes show that despite similarities within the protein studies of the two families, there are substantial sequence differences. 12 13 As the evolutionary time frame has to be less than 50 years it is not possible to derive a model in which evolution could have occurred by mutation alone from common ancestral genes. They must have been derived from a large and diverse gene pool presumably already occurring in environmental bacteria. Many bacteria and fungi that produce antibiotics possess resistance determinants that are similar to those found in clinical bacteria.10 Gene exchange might occur in soil or, more likely, in the gut of humans or animals. It has been discovered that commercial antibiotic preparations contain DNA from the producing organism, and antibiotic resistance gene sequences can be identified by the polymerase chain reaction.14

Genes either exist in nature already or can emerge by mutation rapidly. Rapid mutation has been seen with (a) the TEM  lactamase, resulting in an extension of the substrate profile to include third generation cephalosporins (first reported in Athens in 1963, one year after the introduction of ampicillin) and (b) the IMI-1 lactamase (reported from a Californian hospital before imipenem was approved for use in the United States).15 The selection pressure is heavy, and injudicious use of antibiotics, largely in medical practice, is probably responsible although agricultural and veterinary use contributes to resistance in human pathogens. The addition of antibiotics to animal feed or water, either for growth promotion or, more significantly, for mass treatment or prophylaxis (or both treatment and prophylaxis) in factory farmed animals, is having an unquantified effect on resistance levels.16 Bacteria clearly have a wondrous array of biochemical and genetic systems for ensuring the evolution and dissemination of antibiotic resistance.

Resistance mechanism to some important antibiotics

1.    ß-lactam resistance

ß-lactams belong to a family of antibiotics which is characterized by a ß-lactam ring. Penicillins, cephalosporins, clavams (or oxapenams), cephamycins and carbapenems are members of this family. The integrity of the ß-lactam ring is necessary for the activity which results in the inactivation of a set of transpeptidases that catalyze the final cross-linking reactions of peptidoglycan synthesis. Resistance to ß-lactams in clinical isolates is primarily due to the hydrolysis of the antibiotic by a ß-lactamase. Mutational events resulting in the modification of PBPs (penicillin binding proteins) or cellular permeability can also lead to ß-lactam resistance. ß-lactamases constitute a heterogenous group of enzymes. Several classification schemes have been proposed according to their hydrolytic spectrum, susceptibility to inhibitors, genetic localisation (plasmidic or chromosomal), gene or amino-acid protein sequence. The functional classification scheme of ß-lactamases proposed by Bush, Jacoby and Medeiros (1995) defines four groups according to their substrate and inhibitor profiles. Group 1 are cephalosporinases that are not well inhibited by clavulanic acid; group 2 penicillinases, cephalosporinases, and broad-spectrum ß-lactamases that are generally inhibited by active site-directed ß-lactamase inhibitors; group 3 metallo-ß-lactamases that hydrolyze penicillins, cephalosporins, and carbapenems and that are poorly inhibited by almost all ß-lactam-containing molecules; group 4 penicillinases that are not well inhibited by clavulanic acid. Subgroups were also defined according to rates of hydrolysis of carbenicillin or cloxacillin (oxacillin) by group 2 penicillinases. The classification initially introduced by Ambler (1980) and based on the amino-acid sequence recognizes four molecular classes designated A to D. Classes A, C, and D gather evolutionarily distinct groups of serine enzymes, and class B the zinc-dependent (“EDTA-inhibited”) enzymes. Fig : ß-lactamases

Commonly used B-lactam resistance markers in molecular biology

The bla gene encoding the TEM-1 ß-lactamase is the most encountered AmpR marker used in molecular biology (pBR and pUC plasmids). TEM-1 is a widespread plasmidic ß-lactamase that attacks narrow-spectrum cephalosporins, cefamandole, and cefoperazone and all the anti-gram-negative-bacterium penicillins except temocillin. Aminothiazol chephalosporins, cephamycins, monobactams and carbapenems are resistant to its action. It belongs to the Bush-Jacoby-Medeiros group 2b and the molecular class A. The TEM-1 enzyme was first reported from an E. coli isolate in 1965 and is now the commonest ß-lactamase found in enterobacteriaceae. Resistance in more than 50% of AmpR E. coli clinical isolates is due to TEM-1. Most extended-spectrum ß-lactamases (ESBLs) derive from TEM-1, TEM-2 and SHV-1 by mutations generating 1- to 4-amino-acid sequence substitutions.

2.    Aminoglycoside resistance

Aminoglycosides (Streptomycin, kanamycin, tobramycin, amikacin,…) are compounds that are characterized by the presense of an aminocyclitol ring linked to aminosugars in their structure. Their bactericidal activity is attributed to the irreversible binding to the ribosomes although their interaction with other cellular structures and metabolic processes has also been considered. They have a broad antimicrobial spectrum. They are active against aerobic and facultative aerobic Gram-negative bacilli and some Gram-positive bacteria of which staphylococci. Aminoglycosides are not active against anaerobes and rikettsia. Spectinomycin which is an aminocyclitol devoided of aminosugars is by extension included in the familiy of aminoglycosides. It also differs from them by its bacteriostatic ativity and by its way of action. Spectinomycin acts on protein synthesis during the mRNA-ribosome interaction and it does not lead to mistranslation like aminoglycosides do. Three mechanisms of resistance have been recognized, namely ribosome alteration, decreased permeability, and inactivation of the drugs by aminoglycoside modifying enzymes. The latter mechanism is of most clinical importance since the genes encoding aminoglycoside modifying enzymes can be disseminated by plasmids or transposons.

Ribosome alteration

High level resistance to streptomycin and spectinomycin can result from single step mutations in chromosomal genes encoding ribosomal proteins: rpsL (or strA), rpsD (or ramA or sud2), rpsE (eps or spc or spcA). Mutations in strC (or strB) generate a low-level streptomycin resistance.

Decreased permeability
Absence of or alteration in the aminoglycoside transport system, inadequate membrane potential, modification in the LPS (lipopolysacchaccarides) phenotype can result in a cross resistance to all aminoglycosides.
Inactivation of aminoglycosides
These enzymes are classified into three major classes according to the type modification: AAC (acetyltransferases), ANT (nucleotidyltransferases or adenyltransferases), APH (phosphotransferases). This classification was extensively reviewed by Shaw et al. (1993).

Commonly used aminoglycoside resistance markers in molecular biology

ant(3”)-Ia (synonyms: aadA, aad(3”)(9))confers resistance to streptomycin and spectinomycin. The gene has been found in association with several transposons (Tn7, Tn21, …) and is ubiquitous among gram-negative bacteria.aph(3′)-II (synonyms: aphA-2, nptII) confers resistance to Km (Kanamycin), Neo (Neomycin), Prm (Paromomycin), Rsm (Ribostamycin), But (Butirosin), GmB (GentamycinB). This gene is rarely found in clinical isolates. aph(3′)-II is associated with transposon Tn5 and observed in gram-negative bacteria and Pseudomonas sp. However, its relative abundance in environmental KanR isolates seems to be low (Recorbet et al., 1992; Leff et al., 1993; Smalla et al., 1993).aph(3′)-III (synonyms: nptIII) confers resistance to Km (Kanamycin), Neo (Neomycin), Prm (Paromomycin), Rsm (Ribostamycin), Lvdm (Lividomycin), But (Butirosin), GmB (GentamycinB). Amk (Amikacin) and Isp (Isepamicin) are also modified in vitro, but according to the susceptibility standards established by NCCLS resistance is only expressed at a low level by many strains. aph(3′)-III is commonly distributed among gram-positive bacteria but has also been observed in Campylobacter spp.
nptIII is not frequent in molecular biology but can be found on some Agrobacterium vectors for plant transformation (Bevan, 1984).

3.    Tetracycline resistance

Tetracyclines (tetracycline, doxycycline, minocycline, oxtetracycline) are antibiotics which inhibit the bacterial growth by stopping protein synthesis. They have been widely used for the past forty years as therapeutic agent in human and veterinary medicine but also as growth promotor in animal husbandry. The emergence of bacterial resistances to these antibiotics has nowadays limited their use. Three different specific mechanisms of tetracycline resistance have been identified so far: tetracycline efflux, ribosome protection and tetracycline modification.
Tetracycline efflux is achieved by an export protein from the major facilitator superfamily (MFS). The export protein was shown to function as an electroneutral antiport system which catalyzes the exchange of tetracycline-divalent-metal-cation complex for a proton. In Gram-negative bacteria the export protein contains 12 TMS (transmembrane fragments) whereas in Gram-positive bacteria it displays 14 TMS. Ribosome protection is mediated by a soluble protein which shares homolgy with the GTPases participating in protein synthesis, namely EF-Tu and EF-G. The third mechanism involves a cytoplasmic protein that chemically modifies tetracycline. This reaction takes only place in the presence of oxygen and NADPH and does not function in the natural host (Bacteroides). The two first mechanisms are the most widespread and most of their genes are normally acquired via transferable plasmids and/or transposons. These two mechanisms were observed both in aerobic and anaerobic Gram-negative or Gram-positive bacteria demonstrating their wide distribution among the bacterial kingdom. To date, about sixty-one tetracycline resistance genes have been sequenced and thirty-two classes of genes identified in non-producers and producers (Streptomyces). Each new class is identified by its inability to hybridize with any of the known tet genes under stringent conditions. A new nomenclature for the resistance determinants has been proposed for the future with the S. B. Levy group to coordinate the naming of the

Commonly used tetracycline resistance markers in molecular biology

Several tetracycline resistance determinants are currently used in molecular biology. The most encountered are the tetA genes of classes A (RP1, RP4 or Tn1721 derivatives), B (Tn10 derivatives) and C (pSC101 or pBR322 derivatives) encoding a tetracycline efflux system.These genes are regulated by a repressor protein (TetR). This feature has also been exploited to construct tightly regulated, high level mammalian expression systems by using the regulatory elements of the Tn10 tetracycline operon (Tet-OffTM and Tet-OnTM Expression Systems & Cell Lines,Clontech).The tetM gene from Tn916 which can be expressed both in Gram-positive and Gram-negative bacteria is also frequently used. Several Bacteroides/Escherichia shuttle vectors contain the tetQ gene. tetM and tetQ encode a soluble protein protecting the ribosome from the inhibiting effects of tetracycline. The distribution of these genes is given in the pages relating to the determinant classification.

Some Resistant pathogens

Staphylococcus aureus:

Staphylococcus aureus (colloquially known as “Staph aureus” or a Staph infection) is one of the major resistant pathogens. Found on the mucous membranes and the skin of around a third of the population, it is extremely adaptable to antibiotic pressure. It was the first bacterium in which penicillin resistance was found—in 1947, just four years after the drug started being mass-produced. Methicillin was then the antibiotic of choice, but has since been replaced by oxacillin due to significant kidney toxicity. MRSA (methicillin-resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now “quite common” in hospitals. MRSA was responsible for 37% of fatal cases of blood poisoning in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline and erythromycin.

Methicillin Resistant Staphylococcus Aureus (MRSA) is acknowledged to be a human commensal and pathogen. MRSA has been found in cats, dogs and horses, where it can cause the same problems as it does in humans. Owners can transfer the organism to their pets and vice-versa, and MRSA in animals is generally believed to be derived from humans.

This left vancomycin as the only effective agent available at the time. However, strains with intermediate (4-8 ug/ml) levels of resistance, termed GISA (glycopeptide intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus aureus), began appearing in the late 1990s. The first identified case was in Japan in 1996, and strains have since been found in hospitals in England, France and the US. The first documented strain with complete (>16 ug/ml) resistance to vancomycin, termed VRSA (Vancomycin-resistant Staphylococcus aureus) appeared in the United States in 2002.

A new class of antibiotics, oxazolidinones, became available in the 1990s, and the first commercially available oxazolidinone, linezolid, is comparable to vancomycin in effectiveness against MRSA. Linezolid-resistance in Staphylococcus aureus was reported in 2003.

CA-MRSA (Community-acquired MRSA) has now emerged as an epidemic that is responsible for rapidly progressive, fatal diseases including necrotizing pneumonia, severe sepsis and necrotizing fasciitis. Methicillin-resistant Staphylococcus aureus (MRSA) is the most frequently identified antimicrobial drug-resistant pathogen in US hospitals. The epidemiology of infections caused by MRSA is rapidly changing. In the past 10 years, infections caused by this organism have emerged in the community. The 2 MRSA clones in the United States most closely associated with community outbreaks, USA400 (MW2 strain, ST1 lineage) and USA300, often contain Panton-Valentine leukocidin (PVL) genes and, more frequently, have been associated with skin and soft tissue infections. Outbreaks of community-associated (CA)-MRSA infections have been reported in correctional facilities, among athletic teams, among military recruits, in newborn nurseries, and among active homosexual men. CA-MRSA infections now appear to be endemic in many urban regions and cause most CA-S. aureus infections.

Streptococcus and Enterococcus

Streptococcus pyogenes (Group A Streptococcus: GAS) infections can usually be treated with many different antibiotics. Early treatment may reduce the risk of death from invasive group A streptococcal disease. However, even the best medical care does not prevent death in every case. For those with very severe illness, supportive care in an intensive care unit may be needed. For persons with necrotizing fasciitis, surgery often is needed to remove damaged tissue. Strains of S. pyogenes resistant to macrolide antibiotics have emerged, however all strains remain uniformly sensitive to penicillin.

Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing worldwide. The major mechanism of resistance involves the introduction of mutations in genes encoding penicillin-binding proteins. Selective pressure is thought to play an important role, and use of beta-lactam antibiotics has been implicated as a risk factor for infection and colonization. Streptococcus pneumoniae is responsible for pneumonia, bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis.

Penicillin-resistant pneumonia caused by Streptococcus pneumoniae (commonly known as pneumococcus), was first detected in 1967, as was penicillin-resistant gonorrhea. Resistance to penicillin substitutes is also known as beyond S. aureus. By 1993 Escherichia coli was resistant to five fluoroquinolone variants. Mycobacterium tuberculosis is commonly resistant to isoniazid and rifampin and sometimes universally resistant to the common treatments. Other pathogens showing some resistance include Salmonella, Campylobacter, and Streptococci.

Enterococcus faecium is another superbug found in hospitals. Penicillin-Resistant Enterococcus was seen in 1983, vancomycin-resistant enterococcus (VRE) in 1987, and Linezolid-Resistant Enterococcus (LRE) in the late 1990s.

Pseudomonas aeruginosa

Pseudomonas aeruginosa is a highly prelevant opportunistic pathogen. One of the most worrisome characteristics of P. aeruginosa consists in its low antibiotic susceptibility. This low susceptibility is attributable to a concerted action of multidrug efflux pumps with chromosomally-encoded antibiotic resistance genes (e.g. mexAB-oprM, mexXY etc) and the low permeability of the bacterial cellular envelopes. Besides intrinsic resistance, P. aeruginosa easily develop acquired resistance either by mutation in chromosomally-encoded genes, or by the horizontal gene transfer of antibiotic resistance determinants. Development of multidrug resistance by P. aeruginosa isolates requires several different genetic events that include acquisition of different mutations and/or horizontal transfer of antibiotic resistance genes. Hypermutation favours the selection of mutation-driven antibiotic resistance in P. aeruginosa strains producing chronic infections, whereas the clustering of several different antibiotic resistance genes in integrons favours the concerted acquisition of antibiotic resistance determinants. Some recent studies have shown that phenotypic resistance associated to biofilm formation or to the emergence of small-colony-variants may be important in the response of P. aeruginosa populations to antibiotics treatment.

Clostridium difficile

Clostridium difficile is a nosocomial pathogen that causes diarrheal disease in hospitals worldwide. Clindamycin-resistant C. difficile was reported as the causative agent of large outbreaks of diarrheal disease in hospitals in New York, Arizona, Florida and Massachusetts between 1989 and 1992. Geographically dispersed outbreaks of C. difficile strains resistant to fluoroquinolone antibiotics, such as Cipro (ciprofloxacin) and Levaquin (levofloxacin), were also reported in North America in 2005.

Salmonella and E. coli

E. coli and Salmonella come directly from contaminated food. Of the meat that is contaminated with E. coli, eighty percent of the bacteria are resistant to one or more drugs made; it causes bladder infections that are resistant to antibiotics (“HSUS Fact Sheet”). Salmonella was first found in humans in the 1970s and in some cases is resistant to as many as nine different antibiotics (“HSUS Fact Sheet”). When both bacterium are spread, serious health conditions arise. Many people are hospitalized each year after becoming infected, and some die as a result.

Acinetobacter baumannii

On the 5th November 2004, the Centers for Disease Control and Prevention (CDC) reported an increasing number of Acinetobacter baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom were treated. Most of these showed multidrug resistance (MRAB), with a few isolates resistant to all drugs tested.

Summary:

We frequently refer to bacteria as being resistant to antibiotics, but rarely do we consider what that means. Even the most resistant bacterium can be inhibited or killed by a sufficiently high concentration of antibiotic; patients, however, would not be able to tolerate the high concentration required in some cases. Bacterial species vary tremendously in their susceptibility to an antibiotic for example, most strains of Streptococcus pneumoniae in Britain are inhibited by 0.01 mg/l of benzyl penicillin (the minimum inhibitory concentration), whereas for Escherichia coli 32-64 mg/l are required to inhibit growth, a level which cannot be achieved in the human body. This introduces the concept of clinical resistance, which is dependent on outcome and is all too often ignored. Clinical resistance is a complex concept in which the type of infecting bacterium, its location in the body, the distribution of the antibiotic in the body and its concentration at the site of infection, and the immune status of the patient all interact.

  • Antibiotic resistance should be defined in terms of clinical outcomes, not laboratory methods
  • Resistance occurs by means of four main mechanisms more than one may be present in a single bacterium
  • Resistance mechanisms have probably evolved from genes present in organisms producing antibiotics
  • Resistance genes occur not only in bacteria that carry disease but also in commensal bacteria, to which we are continuously exposed and which are found in food, the environment, and animals
  • The plethora of genetic mechanisms for evolution and reassortment of antibiotic resistance genes ensures that useful genes will be disseminated rapidly
  • Action must be taken to slow the rate of evolution and spread of antibiotic resistance genes, in which the biggest single factor is the amount of antibiotics used in human medicine and agriculture

Glamping Over Camping

The thought of cold, windy nights and the rain battering down centimetres from your head does not appeal to everyone. Sharing a shower (if you're lucky!) And a hole being the toilet is not everyone's cup of tea. Camping is certainly not the ideal getaway for some people, but many people like the thought of the idea but are not brave enough to chance it with the unpredictable elements. If this is you, then you may be pleased to hear that camping is evolving, in the shape of glamping.

Glamor camping provides a cheaper alternative for people seeking a break at a time when many people are making cut backs on their expenses. Glamping offers a holiday that is far cheaper and without the fuss or cost of traveling abroad. It can be enjoyed by all sorts of groups, families, friends and couples wanting a romantic getaway.

It is thought that glamping began at music festivals in the UK. Festival goers were disillusioned with ridiculously early start times to pitch their tents. Companies began offering luxury accommodation- for a festival at least- and would drop it off for you before building it. Another benefit of doing this at festivals was that Glamping saved you making numerous trips to and from the car with a heavy load on your back.

Glamping Holiday lets are not limited to festivals. Glamping has now expanded from festivals, with specific glamping sites popping up around the country each month. One of the wonders of glamping is the variety of accommodation you can find yourself staying in. They can be literally anything, such as a converted VW camper van, a tipi, a yurt, bell tents and huts, among many others.

There are many reasons why you should try glamping. The advantages of the glapping experience allows for people to be closer to the countryside and nature, unlike many hotels. And, unlike a lot of other camping opportunities, electricity is available in most of the accommodation so you do not feel like you're a cave man living in the Stone Age. Depending on your needs, you can enjoy your own toilet, shower and cooking facilities.

Holiday Lets are expecting glamping to really take off in the near future. Lots of people have traveled the world and stayed in luxury hotels, but not many have been glamping and stayed in a converted gypsy caravan! If this sounds like fun to you and you want a unique camping experience, give it a chance for a holiday to remember!

How to Make a Girl Come Quickly and Effortlessly

Imagine a sex life where regardless of how long it went for, or how hard you wanted to, you never reached orgasm.

It’d be pretty frustrating, right?

Sadly, that’s what about 70% of women go through every single day.

Many men are waking up to the fact that their partner isn’t getting the sexual satisfaction she craves, and to their credit, are seeking out a solution to the problem. However, many of you reading this article are probably still unsure of how to give a girl multiple, mind-blowing orgasms that she know she desperately needs.

That’s where I come in. In this article, I’m going to show you exactly how you can make your girl come quickly, easily, and effortlessly, using a simple, idiot-proof three-step formula.

Step 1: Build Sexual Tension

With all that goes on in our lives these days, it’s easy for us to lose touch with our inherent sexuality. For guys, this usually isn’t a big problem – we’re so highly sexually charged to begin with, that it doesn’t exactly take a lot for it to awaken.

Women, on the other hand, are a whole different story.

As opposed to men, who are generally more sexually charged the longer it’s been since they’ve had sex, women work the opposite way. That is to say, they are at their horniest when they are having regular orgasms.

In order to make a woman orgasm quickly and effortlessly, we have to re-awaken her sexuality. We do this first mentally, then physically. The mental component is called sexual tension.

Building sexual tension, whilst easy when you know how, is a whole subject in and of itself. For the purposes of this article, just understand that it involves getting a girl’s mind to be receptive to any sexual advances you make. Ways to do this may include light touching, a certain look, saying certain things, flirting, and much more.

Once you have built a decent amount of sexual tension, you can move on to the next step.

Step 2: Foreplay

Being able to perform powerful, arousing foreplay is one of the best skills a man can have in the bedroom.

If sexual tension is the key to awakening a woman’s mental sexuality, foreplay is the key to re-aquainting her body with her sexual side. Again, there really isn’t enough room in this article to be able to reveal the secrets to amazing foreplay, but essentially it revolves around “firing up” her nerves and putting her body in a highly sexually charged state.

 

Step 3: Direct Sexual Stimulation

If you have built sexual tension correctly, and have given your girl amazing foreplay, she’s 90% of the way to having amazing, powerful orgasms already.

Having said that, obviously the actual physical stimulation is still extremely vital in making her come.

Again, unfortunately, there just isn’t room in this article to give a thorough and in-depth explanation of how to use the clitoris, G-spot, and vaginal nerve endings in order to satisfy a woman’s sexual cravings. We don’t have the space to get into a discussion of primary and secondary stimulation, or the multitude of “hot spots” that are part of the female body, or how to use mental stimulation in tandem with physical stimulation in order to give her powerful, mind-blowing orgasms.

What you have just read is the basic skeletal outline of everything you need to know in order to make a girl come quickly and effortlessly. If you apply this roadmap, there is no doubt in my mind that your girl will have the most powerful orgasms of her life.

New research from Japan: Green tea fights blood and liver cancer, as well as pneumonia

(NaturalNews) Three new studies by Japanese scientists add even more evidence to what already is an astounding mountain of data showing green tea protects and heals the human body. All of the research is based on findings from the huge Ohsaki National Health Insurance Cohort Study in Japan which involved 41,761 Japanese adults between 40 and 79 years of age. None of the research subjects had a history of cancer when the study started and their diets, along with other lifestyle factors and any health problems they developed, were followed for about ten years.

In a study published in the September issue of the American Journal of Epidemiology, Dr. Toru Naganuma of Tohoku University School of Medicine in Senda and colleagues reported that drinking at least five daily cups of green tea was found to slash the risk of blood cancers by 42% and lymph system cancers by 48%. What’s more, these enormous reductions in cancer were consistent in both men and women and in people with various body mass sizes.

While Dr. Naganuma was looking at blood and lymph cancer rates, another research team in the Division of Epidemiology in Tohoku University’s Department of Public Health and Forensic Medicine was also searching the Ohsaki National Health Insurance Cohort Study and they discovered yet another link between green tea and cancer prevention. Their study, published in the September issue of the journal Cancer Causes and Control found that green tea consumption was inversely associated with the incidence of liver cancer. The study documented that the more green tea consumed, the more the risk plummeted — five cups or more offered the most protection from liver malignancies.

Yet another study of the Ohsaki data by scientists at the Tohoku University Graduate School of Medicine, published in the September edition of the American Journal of Clinical Nutrition, found a strong link between drinking green tea and protection against pneumonia in women. The researchers noted in their paper that experimental and animal studies have previously shown that catechins, antioxidant phytochemicals found abundantly in green tea, are active against infectious agents — so that could be a possible explanation for green tea’s apparent pneumonia-fighting ability.

They excluded any research participants who were missing information on their green tea consumption or who had reported a history of cancer, heart attack or stroke. In all, the scientists followed the research subjects’ health for over 12 years. The results showed, at least for women, a dramatic reduction in the risk of pneumonia for green tea drinkers. Once again, drinking five or more cups a day appeared to offer the most benefit.

NaturalNews has consistently reported on research demonstrating how green tea can help prevent and heal a spectrum of diseases and conditions. For example, green tea appears to prevent leukemia (http://www.naturalnews.com/026911_green_tea_EGCG_leukemia.html) and prostate cancer http://www.naturalnews.com/026872_Prostate_green_tea_cancer.html) Recently, scientists have found that green tea may help prevent and treat the bone-robbing condition known as osteoporosis, too (http://www.naturalnews.com/027194_green_tea_osteoporosis_disease.html).

10 Simple and Natural Home Remedies for Pneumonia

Pneumonia is a common illness that refers to an infection of the lungs. It occurs in all age groups, and is a leading cause of death among children and elderly people in chronic conditions. The major symptoms of pneumonia are productive cough resulting in mucus, chest pains, fever, chills and breathing shortness.

Here, in this article you will find home remedies for pneumonia. These home remedies are simple, easy to prepare and easy to follow. You will get benefited from these home remedies if followed as instructed below. These remedies can be taken along with your medication to improve your health and give relief from pneumonia symptoms.

1. Turmeric has several medicinal properties and is widely used in treating a number of ailments. It also helps in treating pneumonia. Other herbs such as black pepper, fenugreek and ginger are also beneficial for your lungs. You can take these herbs in raw or cooked form.

2. Sesame seeds are also helpful in treating pneumonia. Add 15 grams of sesame seeds in 250 ml water. Add a pinch of common salt, a teaspoon of linseed, and a tablespoon of honey in this mixture. Consume daily to expel phlegm from the bronchial tubes.

3. Ginger is a popular home remedy for treating most of the respiratory disorders. Take 10 ml juice of the fresh ginger, or one or two grams dried ginger powder along with honey two times daily.

4. Add a teaspoon of honey to a glass of lukewarm water. Drink it two or three times a day. This drink has very soothing effect and relieves symptoms.

5. Mix some camphor with warm turpentine oil and apply it on the chest. Gently massage to get relief from pneumonia.

6. The patient should be kept in a clean, hot and healthy room. Make sure that sunshine enters in the patient room.

7. Try to keep the chest and the feet of the patient warmer than the other parts of the body.

8. Do not take foods that may lead to constipation. It may aggravate the condition.

9. To get relief from chest pain and discomfort, take a teaspoonful of garlic juice.

10. Holy basil is also very useful in pneumonia. Take the juice of few fresh leaves of holy basil. Add a pinch of ground black pepper to this juice and consume at six hourly intervals.

Disclaimer: The reader of this article should exercise all precautionary measures while following instructions on the pneumonia home remedies from this article. Avoid using any of these products or ingredients if you are allergic to it. The responsibility lies with the reader and not with the website or the writer.

Copyright © Ryan Mutt, All Rights Reserved. If you want to use this article on your website or in your ezine, make all the urls (links) active.

Lyrical Dance – an Expression Driven Style of Dance

There are several aspects to the field of dance that make it quite an appealing art form to many. From ballet to jazz to tap, there is just so much there is to learn about dancing. However, for people who are more interested in expressing emotion through movement as opposed to learning set traditional techniques, there is the wonderful art of lyrical dance. While some element of technique is essential in lyrical dancing, what is more important is whether or not you are able to express what needs to be portrayed on stage.

Lyrical dance is a style that actually combines elements of the most popular traditional techniques like ballet, tap and jazz. However, it really is not that concerned with the physique of the dancer. The primary goal of a lyrical dancer is to have the ability to portray or convey the emotion behind the lyrics of a song. In some cases, lyrical dance can be performed to an instrumental piece of music, which also has some amount of emotion that needs to be interpreted and expressed by the dancer.

Lyrical dancers have to develop a certain level of maturity so they are able to express emotions through facial expressions and body movement. In a real sense, they are required to tell the story without including any spoken word and just focus on movement and facial interpretation.

Although the physique of the dancer is not the primary focus for the lyrical dance style, dancers do need to have a high degree of strength and flexibility because there are usually lifts and spins that could be considered complicated but necessary for the lyrical dancing style.

What is great about this type of dance is that you really do not need to start out at a young age. In fact, it is preferred that lyrical dancers are a little older because it is much easier for them to express their emotions than it is for young kids and teenagers.

It is still unclear where or when lyrical dance originated. However, it continues to be popular in certain arenas, especially theater and Broadway presentations. Although there are elements of different dance techniques involved in lyrical dance, many of the movements do not resemble any type of traditional dance technique. The way the body is required to bend and turn for lyrical dancing cannot usually be attributable to one technique or the other.

Generally, the choreography for lyrical dance involves partners who interpret ballads or love songs about how a relationship makes them feel. Although there are types of interpretive songs that are used for lyrical dance pieces other than love songs, positive love songs as well as songs about lost love are the most common types because they are usually filled with emotion.

If you have always wanted to become involved in dancing but never thought you would get the chance, you can consider lyrical dance because it caters to a wider age range and also relies on your ability to express yourself through facial emotions as well as body language.

Bronchitis Treatment – Patience Is Not A Virtue When It Comes To Bronchitis

A writer once said that every time medical science demonstrates that with proper resources and with proper treatment, diseases might be treated if they aren’t cured.

Bronchitis might be cured if you learn the ways for making yourself better. These information might also be very helpful for your caretaker.

Relieve the cough.

Since cough might be very annoying, you must find ways to stop coughing. The very effective action is drinking plenty of fluids [non-caffeinated] like water and juices. Studies reveal that water is a best expectorant for easing your cough and it’s thin like mucus.

If you’re a smoker, it’ll be recommended to you to discontinue smoking. Substances inside a cigarette have irritants which may contribute for the severity of the cough.

Get optimum rest.

The very best way for fighting these symptoms of bronchitis is to take ample amount of rest possible. By doing this, you’ll be able to possess more energy which you need for fighting the infections.

Try getting enough sleep. If you don’t sleep due to the inability to breathe normally, try increasing your bed’s head. When you do this, the nasal passages and sinuses would have better amount of drainage and it won’t induce a “tickle” inside the throat.
Use drugs which don’t need a prescription.

There are many recommended such medicines if you possess acute bronchitis. These drugs are given to decrease fever and any other discomfort pulled in by these kinds of symptoms.

1. Acetaminophen – a drug which is commonly used for relieving soreness of our body and fever as well.
2. Ibuprofen – this drug is given for individuals for giving aid to the fever which they possess.
3. Aspirin – a drug which is usually used like an “analgesic” for reducing minor pains, body aches etc. However, aspirins aren’t recommended being used by children unless they’re advised by their doctor.

If it can’t be prevented, there’re suggested and prescribed medications like the following:

1. betaz- agonists [inhaled] – this kind of medication will be usually prescribed if chronic cough is present. You or a caretaker must be very cautious of the side effects like trembling and tenseness.
2. Antibiotics – there’re some antibiotics which would be prescribed by doctors for treating individuals who’re in danger to develop various other complicated matters.

Chronic bronchitis does entail long-term treatment when compared to acute one. Medical findings reveal that there’s no cure for this chronic bronchitis. The prime objective for us to treat this kind of illness is by relieving you from these symptoms and by keeping off the complications.

Some doctors may recommend the consumption of antibiotics. But this is suited only for infections which recur. Also, the usage of steroids like Corticosteroids may sometimes be prescribed to those who may not act according to the recommended treatments. There’re few doctors who might not prescribe this kind of medication as it may lead to many side effects. Corticosteroid is used only when its needed.

If the chronic bronchitis is to be considered very severe then you’ll have to do “oxygen therapy.” This is a kind of therapy which administers oxygen as its therapeutic modality where the oxygen supply would be heightened. With the use of a nasal cannula or a mask, oxygen would be supplied to us.

Be well-informed about the disorder most especially its handling would give a lot of benefits. Read more about how bronchitis is treated. Most importantly, speak with your doctor and don’t fear to ask your queries if there are some vague terms which you couldn’t understand.

Treatment For Shoulder Dislocation Injuries

It is inevitable that with so much arm movement, somehow an injury involving the shoulders can happen. This can be due to a bad fall or simply, with the overuse of the joints near the shoulders. Simple activities such as carrying a heavy bag or extreme exercise or sports activities can lead to shoulder dislocation.

Dislocated shoulder brings extreme pain to the patient, and most often, leaves the patient in anguish for a couple of weeks. What’s worse, the pain a patient experiences can sometimes extend to the arms. Also, patients experience different sensations like tingles and numbness and if the condition worsens, the shoulder looks disfigured than it really is. Sometimes, a noticeable hallowed skin shows or has a swollen appearance.

Treating shoulder injuries entails rehabilitation of the entire arm. During rehabilitation, or what is called closed reduction treatment, doctors would sometimes swing or bend the injured arm to ease muscle contraction and to be able to reposition the arm right away. This can really be painful for the patient, thus, patients are administered pain killers and anti-inflammatory medicines prior to the treatment. In severe shoulder dislocation cases, an operation is the only solution to bring back the dislocated arm and joints together. This is called open reduction treatment.

Regardless of the treatment directed to the patient, doctors will definitely require them to wear braces or slings in order to avoid unnecessary movements on the injured arm. The length of time will primarily depend on the extent of the injury and the treatment applied on the arm. In most cases, continued rehabilitation exercises are needed for the arm to fully gain strength and muscle control until gradually, the pain subsides and the arm is back to normal.

Healing time for shoulder injuries usually takes three to five months. In several cases, former patients experience a repeat of the injury because either they did not complete the whole rehabilitation process or they took treatment and follow up instructions for granted. If this continues to happen, permanent damage to the joints and arms may occur. So, to avoid any forms of inconvenience, patients are advised to continually do some simple exercises and follow out-patient instructions as well.

Whiplash compensation – How much can I claim?

As with any other type of personal injury claim, whiplash compensation will vary substantially from one case to the next. When setting the value of whiplash claims, the courts must consider the severity of injuries and their impact on the claimants.

This process can include an examination of any relevant direct and indirect losses, such as medical expenses and loss of earnings. Therefore, it is impossible to accurately determine how much whiplash injury compensation can be awarded in any given case; furthermore, even when it may be possible to formulate a realistic expectation, the court retains the privilege to surprise all those concerned. Notwithstanding this, it is possible to outline a rough estimation as to what damages may be awarded in whiplash injury claims.

It is important to note that whiplash is a condition that is routinely categorised according to the severity of its symptoms. Some systems may adopt a simple classification for whiplash, such as: mild, moderate or severe. Other systems may require a more precise classification of whiplash on a scale of 0-4, with 0 denoting no physical symptoms and 4 describing a serious injury such as a fracture or dislocation.

Mild whiplash injury claims might be expected to attract compensation in the region of £1,000 to £4,500; moderate whiplash injuries can be worth up to £14,500; and compensation for severe whiplash injuries may be as high as £85,000 or more.

Whiplash claims are commonplace in traffic accidents, so obtaining the services of a specialist solicitor who is experienced in dealing such claims is vital in securing the maximum compensation available.

Diabetic Children's Camps

As any sufferer knows, there are two types of Diabetes, type I and type II. The latter is sometimes called adult acne diabetes, and over 90% of diabetics suffer this type.

It therefore takes no great leap of imagination to realize that the vast majority of diabetics are adults. But children can also suffer from diabetes, and for such kids, there are problems to face that are very different to those of their diabetic seniors.

For example, a child with diabetes will obviously need close monitoring, and a great deal of constant care and attention from parents. This in itself is not a problem, but it may mean that the child may never spend a night away from home, and it is not uncommon in these circumstances for a child to have never met another child of their own age with diabetes. Effectively, this is a very isolating period in a diabetic child's life.

For theses reasons, many countries are now establishing special camps for diabetic children, to address these problems, by bringing a higher degree of normality to the life of diabetic children. Such camps provide 24 hour professional medical supervision and care to all the children and are an extremely effective way to give young people living with diabetes a chance to be independent and learn about their condition with the support of their peers and trained health professionals.

They provide an enjoyable and safe camping experience in a supervised environment, and often focus, at least to some degree, on increasing the children's ability to manage their own condition. Such camping conditions also create an environment which allows the interaction between young people with diabetes that may otherwise be denied through geographical isolation.

These diabetes education and recreational camps are, of course, designed to be fun as well as educational. Typically, they will offer a wide range of sporting facilities, which allow participants to try out new sports and other recreational activities, particularly team based activities, that they may often be otherwise denied.

On the medical side, nothing is left to chance. Prior to camp, each participant is normally required to supply a detailed medical history and an indication of the management skills of the child. Based on this knowledge, the camp can then offer the child the opportunity to learn further self management skills and how to interact with other young people with diabetes under professional supervision.

Other people benefit too. Often, many of the "helpers" in such camps are volunteers, with little first hand knowledge of diabetes, and these people will learn a great deal from their exposure on a day to day basis to the children.

Even the health care professionals themselves can gain a valuable insight into the management and lifestyle of young people with diabetes that no textbook can provide. These people typically report that they do learn a lot, and even the most experienced educators say that they are moved by the realities of living day to day with these children

And, last but by no means least, the parents enjoy a break from the daily routine of caring for a young person with diabetes, with the real likelihood that their child will gain confidence and increase their self management skills.

Overcoming Childhood Nemsis

"Oh, mommy I want this for lunch," says a girl pointing to the Happy Meal in a McDonald's commercial on television. "Sure, darling. You can eat whatever you want," replied the mother as she grabs her daughter's hand to take her to the restaurant in Kahala. The following day, "Mommy, can we go to back to McDonald's for lunch today? I want that taro pie on the TV," the daughter said starring up at her mother. Surprised by her request, she smoked and took her there without a word. Halfway through that same day, "Mommy can we go back to McDonald's? I am getting hungry," said the daughter. The mother quickly knew what the problem was: her daughter's addiction to fast food. Hesitant and fearful of her daughter's reaction upon refusal, the mother ignored her conscience and responded, "Okay." The mother's decision to disregard her daughter's weight situation will jeopardize her daughter's adulthood.

Obesity is a devastating medical condition affecting all age groups. If one is overweight and the problem is left untreated in the early stage, he / she risks becoming obese in his / her adulthood. Obesity could prevent the child from participating in normal adolescent activities. Childhood obesity is prevalent through society even in an isolated community like Hawaii. This issue is often overlooked among children because he / she is still maturing. Society must address this issue in the early stage in order to reduce the problem.

Obesity is a mysterious problem that seems to arrise any time in a person's life. Overweight is medically defined to be in the body mass index (BMI) range of 25.0 and 24.9 and overweight is between 25.0 and 29.9 ("Overweight and Obesity"). Childhood obesity is an underestimated topic parents and doctors dismiss for its absence to be determined at an early age. Therefore, it is expected that the obese census has exponentially increased undetected in the past two decades. This low-state of awareness to react to a small problem will multiply making itself prevalent through society.

Childhood obesity is rapidly expanding towards every corner of the world. Hawaii, one of the most isolated communities, is greatly affected by the obesity epidemic due to cultural industrialization. In order for Hawaiian culture to stay connected with the rest of the society, it needed to change its old lifestyle to the fast-paced culture of modern society. In addition, Hawaii also needed to accept society's recommended fast foods into their culture that becoming a large target for obesity. Each year, the number of obese children in Hawaii has risen each subsequent year. In 2007, Hawaii's children obesity count was 28.5 percent ("Childhood Overweight and Obesity Trend"). Two years later, it has risen to about 33 percent; And the next two consecutive years it has risen to 38% (Segal). In four years, the number of obese children in Hawaii has increased by 33 percent. Hawaii's obese population is continuously growing and does not seem to stop in the future.

A major contributor for the rise is how parents raise their children. Parents are rarely at home to regularly monitor what foods their children eat and encourage daily exercise. A parent's participation in promoting a healthy behavior is a key factor in avoiding childhood obesity. Encouraging one's child to commit to healthy behavior is a significant variable to focus on for proper growth and development. However, in a fast-moving community like Hawaii, parents find it hard to instill these values ​​to our children. The first step to saving one's child from becoming obese is to guide them in distinguishing healthy foods. At home, children replicate behaviors, either good or bad, from an adult figure. Because parents are rarely present at home today, children have to follow different role models. Children often became attracted to the wrong crowd so learning the negative behaviors. To counteract this problem, parents should exemplify good values ​​and behaviors in front of their children like eating a well-rounded diet and drinking plenty of water. This discourages kids from consuming fatty foods and encourages healthier dieting. This front alone will not persuade children away from obesity. Parents must take the next step to by showing support along the way.

Eating healthy can only go so far without the right follow-up. A healthy diet is only the base of the solution; It needs the physical support to keep the treatment going. Parents should promote daily exercise. In hand with eating healthy helps, exercise helps speed up one's recovery from obesity. Obesity is typically caused from the imbalance of energy surplus. It is clear that by exercising, one is spending the excess calories from the food he / she eats. By being physically active, one is also building the muscle and confidence to feel good in public. Ultimately, exercise helps build character. With two of the three steps to preventing childhood obesity, the last step comes from the one giving the advice.

The last support needed is from one's parents. The best time to get in contact with one's parents is at dinner. During this event, parents should communicate with their child and hear what arises in their child's life. If a problem like feeling overweight happens, give them advice and show them what to do the following day. Do not punish or scold them for something that is out of their control. However, that also does not mean to ignore the problem. Parents are the best type of support because they are experienced and more knowledgeable of the problem. In addition, communication of the weight problem and commitment to overcoming it will create a strong relationship that will solve the problem. Taking these steps is not limited to only weight problems, but any situation.

With these tools at one's disposal, one should commit to practicing them regularly. Childhood obesity is a serious problem that involves the affected child and their parents. This issue should not be easily overlooked. A child and their parent should not be strangers towards each other on an issue like obesity. Parents should regularly check up on their children so that there are no obstacles preventing them from living a normal life. Children should frequently talk with their parents when a problem is bothering them. Children should listen to their positive role models and commit to their advice; It improves one's health which reflects very on society itself.