Viva For Your Health

The most common set of diseases facing Americans moving into their 40′s and beyond has been termed “metabolic syndrome”. Metabolic syndrome is a collection of disease symptoms that tend to occur together. These are excess body fat around your waist, high blood pressure, high LDL cholesterol, low HDL cholesterol, elevated triglyceride levels, and high fasting blood sugar.
As more Americans are carrying a high-deductible health plan along with a Health Savings Account, many say they are beginning to pay more attention to their health. Health Savings Accounts allow you to put aside pre-tax money to be used for future medical expenses. Because deposits grow tax-deferred and are not taxed for medical withdrawals, if you fund your account and stay healthy, you could have hundreds of thousands of dollars in your Health Savings Account by the time you retire.
The fundamental metabolic disturbance that seems to be common in almost all people who have metabolic syndrome is insulin resistance. Insulin is a hormone that your body uses to move the carbohydrate that you eat into your cells. If you are insulin resistant, your cells don’t respond well to insulin, and your pancreas has to produce higher amounts in order to keep your blood sugar from going too high. (Once your pancreas is no longer able to keep up with this increased demand, you become diabetic.) If you are insulin sensitive, your body is responding well to smaller amounts of insulin.
Fortunately, metabolic syndrome is almost entirely preventable. Avoid it, and you’ll greatly increase your chances of also avoiding cardiovascular disease, breast cancer, colon cancer, prostate cancer, stroke, and many other serious conditions. Though all the mechanisms behind the metabolic syndrome have not been worked out, the evidence is strong that combinations of several lifestyle strategies are very effective in preventing this condition.

Exercise
Exercising does more than just burn calories or build muscle. One of the most profound benefits of exercise is its effect on insulin sensitivity. When insulin is released in response to carbohydrate ingestion, glucose transporters come to the surface of the cell in order to carry the glucose into the cell. In muscles and fat cells this transporter is called Glut-4. Exercise itself helps Glut-4 to move through the cell membrane to the surface of your muscle cell, causing these cells to be much more insulin sensitive. Even a single bout of exercise will cause your muscles to respond more effectively to insulin.

Eat Low-Glycemic Foods
The glycemic index is a measure of how quickly a food raises our blood sugar. The high-glycemic carbohydrates in the American diet are primarily the “white foods” (bread, pasta, rice, white potatoes, and sugar). These foods cause many of the changes associated with metabolic syndrome, including lower HDL levels, and higher triglycerides. When a person eats these foods year after year, insulin levels remain chronically high. The result is that eventually the cells become less responsive to the insulin, in turn leading to increased risk of obesity, hypertension, heart disease, diabetes, and premature death. Low-glycemic carbohydrates include most fruits and vegetables. Eating a diet that limits or avoids high-glycemic grains, potatoes, and sugars, and includes more low-glycemic fruits and vegetables, fish, and lean meat can dramatically improve your insulin sensitivity.

Eat the Right Fat
We’ve talked in previous issues about the seemingly miraculous health benefits of fish oil. Fish oil improves insulin sensitivity. Eskimos, who consume high quantities of fish oil, rarely experience diabetes, even though they are often overweight. Though the mechanism by which fish oil works isn’t yet understood, many researchers believe that fish oil makes the cell membrane more “fluid”, enabling the Glut-4 transporters to more easily move to the surface of the cell in response to insulin. Everyone who does not eat fish on a regular basis should consider taking a high-quality fish oil.
Saturated fats and trans-fats, in contrast, make the cell membrane more stiff and inflexible, and also reduce insulin sensitivity. Saturated fats are found primarily in beef, pork, and dairy products and trans-fats are found in processed foods. Saturated fats should be minimized, and trans-fats should ideally be completely eliminated from your diet.

Eat Enough Protein
If you’re avoiding starches, you’ll need to replace those calories with something else – that should be lean protein. Protein satisfies your appetite more than any other macronutrient, it increases metabolism, and it will contribute to weight loss. The best proteins are lean meats like turkey breast and chicken breast, lean beef, fish, and eggs. And if you are overweight, nothing will improve your insulin sensitivity faster than losing some weight. In fact, weight loss significantly improves all aspects of metabolic syndrome. Eat the right foods, and your body will tend to normalize at the right weight without you having to count calories or starve yourself.

Take Action
Remember, just reading an article has never made anyone healthier. Though there are drugs available to treat some of the symptoms, doctors have no pharmaceutical cure for metabolic syndrome, and almost all individuals become more insulin resistant as they age. It is the lifestyle choices and the actions that you take today to improve your insulin sensitivity that will have a powerful impact on the length and quality of your life.
The characteristic that many people like about Health Savings Accounts (HSAs) is that they reward those who take responsibility for themselves. By putting aside money to pay for future medical expenses, you are being a responsible citizen, and deserve the tax benefits that an HSA offers. Make the same investment in your health, and you’ll not only have the good health to enjoy your retirement, but you’ll also have plenty of money in the bank as well.

Central Veterinary Laboratory in Kathmandu Tripureshwor Nepal

ABSTRACT:

Sudden death of broiler birds of above 40 days was suddenly increased in the month of August 2008 in Kathmandu valley. Birds which were presented for post-mortem examination in Central Veterinary Laboratory Tripureswor Kathmandu were usually found dead on their backs with wings out-stretched. Incidence of this condition recorded was between 1.5 to 2.5% of the flock. The mean mortality due to sudden death syndrome was 1.3 – 9.6% and mortality was peak after 6 week of age. Post-mortem necropsies of birds affected by Sudden Death Syndrome were well-fleshed with edema and general pulmonary congestion. Feed was present along the entire digestive tract and the gall bladder was empty. The liver and kidneys were slightly congested and have patchy subcapsular hemorrhage. The heart was containing clotted blood in the atria and the ventricles are most often empty. Microbial and Mycobial culture of tissue samples of liver, lung, spleen, Proventriculus revealed in majority of samples the growth of Penicillium and Aspergillus spp of fungus and E.coli and Staphylococcus spp of bacteria. On feed restriction, supplementation of glucose containing electrolyte, liquid toxin binder, Immunomodulaters, acidifier and antibiotic reduced the mortality. The condition seems to be related to fast growth rate . In extreme situations, feed restriction need to be practiced which will virtually eliminate sudden death syndrome. A practical approach seems to use diets with 5-7% reduction in nutrient density. Giving more space and supportive treatment with anti-stress medicine may be beneficial.

Key word:

Sudden death syndrome , broiler birds, Microbial and Mycobial culture, Penicillium and Aspergillus spp of fungus, feed restriction, glucose containing electrolyte, liquid toxin binder, Immunomodulaters, acidifier,

Background of outbreak of Sudden Death Syndrome in Kathmandu Valley.

During the first week of August 2008 there sudden increase in mortality of broilers of above 6 week age. Just before death birds appear normal and it is common to observe that these birds will be feeding, drinking or walking normally. Birds exhibit clinical signs such as extending their neck, squawk and start wing beating as well as leg extension before fall back on their back and birds used to die suddenly. Post-mortem necropsies of birds affected by Sudden Death Syndrome were well-fleshed with edema and general pulmonary congestion. Feed was present along the entire digestive tract and the gall bladder was empty. The liver and kidneys were slightly congested and have patchy subcapsular hemorrhage. The heart was containing clotted blood in the atria and the ventricles are most often empty.

Material and Methods:

1: Clinical Epidemiological observation of affected flocks.

2: Post-mortem examination and Microbial and Mycobial evaluation of tissue samples.

3: Evaluation of possible treatment and preventive measure

Epidemiology of Affected flock with sudden Death Syndrome in Month of August 2008:

Table: 1

Duration

no.of farm

Population at risk

Morbidity

Mortality

no.of samoles

First week

22

16620

4250

369

44

Second week

14

15450

1235

232

28

Third  week

20

10260

848

157

40

Fourth week

30

15700

2380

149

60

Total

86

58030

8713

907

172

Postmortem finding of SDS birds:

Postmortem finding of birds which died of sudden death syndrome revealed all birds were well-fleshed with edema and general pulmonary congestion. Feed was present along the entire digestive tract and the gall bladder was empty. The liver and kidneys were slightly congested and have patchy subcapsular hemorrhage. The heart with containing clotted blood in the atria and the ventricles were most often empty. The edematous lung was observed. There was milky fluid in proventricular gland and intact food particles were present in gizzard, spleenomegally to spleeno atrophy was observed in almost all birds which were examined.

Laboratory Finding of Mycobiota and Micro biota of Postmortem Tissue samples:A total 86 tissue samples of lung,liver,speen,peoventriculus gizzard,were collected during postmortem examination and were subjected for both bacterial and mycological culture in respective media for culture and identification laboratory findings of which is presented below.

Table: 2

Samples numbers

Bacterial spp isolated

Fungal spp.isolated

Positive no

negative no

86

E.coli,Streptococcus,Staphylococcus spp.

59

27

86

Aspergillus,Penicillium,Candida spp

58

28

172

117

55

Treatment and Preventive measure advised to rest of birds in flock:

All birds remaining in flocks were advised two restrict the feed up to 8-10% and feed to twice daily only. Along with this it was advised to supplement glucose containing electrolyte liquid toxin binders like toxolivum ,toxol, kokonil, immunomodulater like immunocare,and and simple broad-spectrum antibiotics were advised to provide in water while supplementation of multivitamin B complex was totally withdrawn .

Review of literatures:

Sudden Death Syndrome is an acute heart failure disease that affects mainly male fast growing chickens that seem to be in good condition. The birds suddenly start to flap their wings, lose their balance, sometimes cry out, and then fall on their backs or sides and die; usually all within a minute (Satya 1).Sudden Death Syndrome kills 0.1% to 3% of broilers in European Countries.  UK survey of broiler ascites and sudden death syndrome in 1993(The Welfare of Broiler Chicken 2). H.A. Upandra reported that  Broilers that die of sudden death syndrome show no specific abnormalities. Birds usually male, appear healthy and are often above average flock body weight. Just before death birds appear normal and it is common to observe that these birds will be feeding, drinking or walking normally. Birds exhibit clinical signs such as extending their neck, squawk and start wing beating as well as leg extension before fall back on their back. Hence some farmers call this condition as cases of heart attack. Death occurs within minutes. Post mortem examination fails to exhibit any specific lesion. Hence it is also considered as a Behavioral Disease. However many workers who recorded behavioral pattern of birds concluded that there is no single behavior pattern can be attributed to this condition.

Pathology of sudden death syndrome is studied many workers and they found that birds affected by sudden death syndrome are always well-fleshed with edema and general pulmonary congestion. Feed is present along the entire digestive tract and the gall bladder is usually empty. The liver and kidneys may be slightly congested and have patchy subcapsular hemorrhage. The heart may contain clotted blood in the atria and the ventricles are most often empty. The edematous lung observed in cases of SDS was thought to be the contributing factor of death but in all probabilities it is a normal observation in birds that on their back for some time.

A number of studies have been aimed at correlating changes in tissue mineral, electrolyte and fat content as it relates to Sudden Death Syndrome. Sudden Death Syndrome affected birds showed elevated levels of liver calcium and reduced iron in lungs and kidneys. A small but statistically significant reduction in the potassium content and an increase in sodium content of heart tissue are also reported in Sudden Death Syndrome birds. However it is not known if these changes are causative or the consequence of Sudden Death Syndrome.

Because female broilers have a much lower incidence of Sudden Death Syndrome and Leghorns of either sex rarely show the condition, a comparative study was made in male broiler birds using either female broilers or Leghorn birds as control in studying the blood parameters. Male birds consistently exhibited elevated levels of blood glucose, Blood uric acid and lactate dehydrogenase as compared to females birds. As far as blood electrolyte study is considered, Sudden Death Syndrome birds had higher levels of blood potassium. These data again pose the question of how to interpret biochemical profiles of Sudden Death Syndrome birds, because in most instances, birds have been dead for some time prior to blood sampling.

Other factors such as diet texture and restriction programs have been studied with a view to isolating causative agents in Sudden Death Syndrome . It is reported that feed restriction can reduce mortality due to Sudden Death Syndrome in broiler chicks but feed restriction can reduce the body weight of these birds. It is concluded that Sudden Death Syndrome can be prevented by growing birds at a slower rate.

Diet protein per se seems to have little effect on Sudden Death Syndrome . Relatively little research aimed at investigating the role of dietary aminoacids on incidence of SDS is taken up. Taurine is considered to be a non-essential amino-acids for poultry. While avian species are assumed to synthesize sufficient taurine, reduced cardiac taurine levels have been associated with heart tissue degeneration in turkeys. Furazolidone is known to cause heart muscle degeneration in turkeys and this is accompanied by reduction in tissue taurine levels. Feeding up to 0.2% taurine to broilers resulted in a small reduction in incidence of Sudden Death Syndrome.

Use of various sources of energy in the diet has also been suspected in affecting the occurrence of Sudden Death Syndrome. The replacement of carbohydrate by fat is suspected to be a factor. The occurrence of Sudden Death Syndrome seems to be increased by feeding hydrogenated fat such as coconut oil as compared to birds fed comparable levels of unsaturated sunflower oil.

Biotin has been singled out most frequently among vitamins as a possible factor in Sudden Death Syndrome. It is suggested that biotin may be an important factor in increasing the occurrence of Sudden Death Syndrome if it is complicated by the incidence of fatty liver and kidney syndrome. The Sudden Death Syndrome seems to be worse when biotin is marginal and other Vitamin B are in excess.

Among many drugs used in poultry the role of anticoccidial drugs perhaps have received more attention than other drugs. There is some evidence of higher Sudden Death Syndrome mortality when anticoccidial drugs are used. Historically the occurrence of Sudden Death Syndrome does coincide with the introduction of the ionophore anticoccidials. However the involvement of ionophores in Sudden Death Syndrome is far from clear and typical pathological lesion of ionophore toxicity have not been reported in Sudden Death Syndrome diagnosed birds.

It is obvious that there is no one treatment or preventive system for the control of SDS in broilers. The condition is undoubtedly related to fast growth rate and as such management techniques to reduce the early maximum genetic potential for growth after the best preventive measure. One of the most successful techniques used to hamper early growth rate is a step-down lighting programme. Broilers are subjected to reduced day light between 5-18 day of growth. This effectively reduces feed intake and so hampers early growth rate. In extreme situations, feed restriction can also be practiced and this will virtually eliminate Sudden Death Syndrome. A practical approach is to use diets with 5-7% reduction in nutrient density. Giving more space and supportive treatment with anti-stress medicine may be beneficial (H.A. Upandra). Sudden death syndrome in fast growing broiler chickens has been recognized as a patho-physiological entity for four decades, but its pathogenesis still remains unknown. More recent investigations provided evidence that link SDS to cardiac arrhythmia, but the mechanism triggering arrhythmogenesis and factors responsible for fatal outcome are poorly understood. In order to understand the chain of events leading to Sudden Death Syndrome in broilers, the present study focused on putative mechanisms that trigger arrhythmia and mechanisms that predispose the myocardium to fatal arrhythmia. Susceptibility of broilers to cardiac arrhythmia under stress conditions was evaluated using a simulated stress test with epinephrine. Detailed histopathological evaluation of the broiler heart was undertaken to identify structural features that may predispose the myocardium to fatal arrhythmia. The simulated stress challenge revealed that many broilers are highly susceptible to stress induced cardiac arrhythmia. In some broilers the stress challenge induced severe ventricular arrhythmia, and the life threatening nature of this arrhythmia was evidenced by the fact that several birds showing the most severe arrhythmic responses, died suddenly within several days after the stress challenge. Examination of hearts of broilers that died of Sudden Death Syndrome revealed microscopic lesions in the cardiomyocytes, and widespread changes in the sub-endocardial and mural His-Purkinje system (HPS). Immune staining for Caspase-3 confirmed that numerous Purkinje cells in the left ventricular myocardium from broiler chickens that died of SDS were undergoing apoptosis. The observed lesions suggest that the electrical stability of the myocardium was compromised. Taken together, our findings indicate that stress is a most likely trigger of cardiac arrhythmia in broilers, whereas the pathological changes seen in the myocardium and in the HPS in fast growing broilers provide a very conducive milieu for sustained ventricular arrhythmia. In cases where the electrical stability of the myocardium is compromised, even an episodic arrhythmic event may readily degenerate to catastrophic ventricular fibrillation and sudden death. We conclude that the combination of stress and changes in the cardiomyocytes and HPS are the key requisite features in the pathogenesis of SDS (4 A A Olkowski, C Wojnarowicz, S Nain, B Ling, J M Alcorn, B Laarveld). A condition of broiler chickens of unknown cause, possibly metabolic. It can be induced by lactic acidosis and about 70% of birds affected are males(5 www.thepoultrysite.com/diseaseinfo/146/sudden-death-syndrome-flipover ). Sudden death syndrome usually occurs in heavy, fast-growing and healthy-looking broilers. Most of the affected birds are males. The characteristic necropsy changes are seen in well-fleshed broilers with edema and generalized pulmonary congestion, recently ingested feed in the crop and gizzard, distended intestine with creamy content and empty gall bladder. The liver and kidneys are slightly enlarged and the latter have patchy areas of subcapsular hemorrhage. The heart contains clotted blood in the atria but the ventricles are often empty and the left ventricle in particular assumes a hypertrophied appearance (6 J.C. Ononiwu, R.G. Thomson, H.C. Carlson, and R.J. Julian). A syndrome specifically associated with broiler breeders. Clinical signs – Mortality ranging from 0.5 to 8% per week with most of the birds dying at feeding time. No evidence of respiratory infection. Commences as flock reaches about 5% production and being worst about 20-30% production. It is believed that this is most likely to be due to a mineral imbalance associated with low potassium as the flock comes into lay. Treatment including 3.5Kg/tonne of potassium carbonate has reduced the incidence (7 members.tripod.com/poultryworld/dis_dir.htm).

Result and Discussion:

All the birds remaining in all affected flocks responded to the above treatment management and there was marked improvement in controlling of the syndrome.As todays broiler birds are genetically so engineered that  they are suppose to achieve maximum body weight gain during the schedule period of 45days there is trend of using feed additives which  also exerts some health problem in broiler as well they causes the problem like tibial dyschondroplacia in heavey weight broiler  has been reported by many workers in Europe and elesewhere.As today universally a total of 30-35 grains are being contaminated with one or other toxigenic fungus whose deleterious effect on livestock and poultry health has been well documented were it causes sudden death also coincides with finding of this observation. Further more especially during hot humid season whish increases stress to birds as well as there is a conducive environment for the growth of mold and fungus also provides higher risk to the birds for the deleterious effect of mycotoxin  in broiler health.Still today so far in the management of mycotoxin and mycosis only there is practice of using toxinbinders only during feed formulation process in feed mills.Which alone is not suffient to minimize effect to fungal contamination during storage if poultry especially broilers of finisher age have to protected some management pattern need to be changed.

Conclusion and recommendation:

All clinical laboratory and epidemiological patterns observed in this investigation indicates that broilers in good body weight condition when not harvested timely and remain in poultry shade for prolong time due to the congestion of space enhances a stress factor. Along with this with increase in humidity and hot season favors the growth of mold and fungus in stored feeds there was increasing the risk of birds to mycosis. Under such circumstances birds are in danger to be affected by mycotoxicosis under such situation if a proper preventive measure to prevent the deleterious effect of mycotoxin is not under taken any time an unexpected syndrome may appear in poultry establishment. As this was a sudden mortality in broiler has been reported for first time finding of this invested need to be looked into.

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Reference:

1: Satya Feb 06: The Real Cost of Cheap Chicken by Joyce D’Silva www.satyamag.com/feb06/dsilva.html – Retrieved on 8 August 2008

2:The Welfare of Broiler Chicken ciwf.org.uk/publications/…/the_welfare_of_broiler_chickens_2000.pdf – Retrieved on 8 August 2008

3: SUDDEN DEATH SYNDROME:Dr. H.A. Upandra, Associate Professor, Dept. of Clinical Veterinary Medicine, Veterinary College, UAS, Bangalore: www.vetcareindia.com/halchal_sudden%20syndrome.htm – 15k – Retrieved on 8 August 2008

4: Res Vet Sci. 2007 Sep 26; : 17904171 (P,S,E,B,D) A study on pathogenesis of sudden death syndrome in broiler chickens.  A A Olkowski, C Wojnarowicz, S Nain, B Ling, J M Alcorn, B Laarveld : lib.bioinfo.pl/pmid:17904171 – 62k. Retrieved on 8 August 2008

5: Sudden Death Syndrome, ‘Flipover’ ThePoultrySite Quick Disease Guide www.thepoultrysite.com/diseaseinfo/146/sudden-death-syndrome-flipover- Retrieved on 8 August 2008

6 : Pathological Studies of “Sudden Death Syndrome” in Broiler Chickens

J.C. Ononiwu, R.G. Thomson, H.C. Carlson, and R.J. Julian

:www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1789498- Retrieved on 8 August 2008

7: THE A-Z POULTRY DISEASE INDEX: members.tripod.com/poultryworld/dis_dir.htm- Retrieved on 8 August 2008

Acknowledgement:

We would like to extend our sincier thanks to Dr.Dev Raj Adhikari SVO and incharge of Central Veterinary Hospital Tripureshwor, Kathmandu for providining early indication of problem. Our gratitude goes to the all broiler farmers of Kathmandu Valley for cooperating with this investigation team through out the observation period. Mr.Bal Bahadur Kunwar Srnior Vet.Technician and Mr.Bhimsen Adhikari Vet.Technician of Microbioly Unit of Central Veterinary Laboratory for their tedious work in lab for cultureing and processing of all samples deserves a special thanks. We would like to extend our heartfelt gratitude to Dr Esmeraldo M. Cabana, DVSM, MVSt (VPath) Veterinary Pathologist  Animal Health Laboratories

Diagnostic Services Branch Department of Primary Industries and Water, Australian Government service Tasmania.and  Dr.Lin, Tsang Long,Avian Pathologist and Dr.Hooser, Stephen B Head, Toxicology Sect. & Asst. Director,Animal Disease Diagnostic Laboratory Purdue University U.S.A for their continuous guidance through Email for this investigation and its documentation.Last but not least Dr.Poornima Manandhar chief of CVL Tripureshwor deserve a special thanks from this investigation team for her continuous inspiration