One of our most effective strategies to combat bacterial infections is rapidly becoming ineffective: more and more bacteria are developing resistance against commonly used antibiotics. This is a worrysome development, that, though been recognized for decades, seems to have worsened lately. It is perceived that the speed of resistance development has overhauled the rate of developing alternative drugs.

In attempts to stop this unwanted process, the use of antibiotics in veterinary medicine has become a focus of attention, especially in view of the broad range of drugs that are in use in both disciplines. The reasoning is that animals receiving antibiotics can also carry bacteria that are human pathogens (zoonoses), which develop resistance during treatment of the animal. When these resistant bacteria subsequently cause infections in patients these are hard to treat as a result of the resistance. This consequences to public health could be an increase in disease severity, complications, and even in mortality. This seemingly reasonable scenario has resulted in a demand to restrict the use of clinically relevant antibiotics in veterinary medicine. Here we would like to test the validity of the arguments used in the discussion by means of two selected examples. Further we would like to dig a bit deeper in the processes that result in resistance, and what can be done in a practical setting to prevent these.

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Campylobacter is our first example, since it is a common zoonotic pathogen that is mainly transmitted through food of animal origin. In many countries it is a more frequent cause of human diarrhoea than Salmonella. Campylobacteriosis is most often self-limiting, and only requires antibiotic treatment in patients at risk, or in severe cases. Up to 100% of poultry flocks can be found positive for C. jejuni. One single point mutation in the bacterial gene coding for gyrase is all that is needed for Campylobacter to become resistant to clinical concentrations of fluoroquinolones (Fq). The use of Fq in poultry husbandry results in a selection of resistant bacteria, but it should be noted that selection takes place when Fq is used in humans, too. Since human-to-human transmission is rare, a patient can be considered a ‘dead-end host’ for this pathogen. Transmission from poultry meat to humans is one of the most common sources of infection.

Since the use of Fq was introduced in both human and veterinary medicine, the frequency of Fq-resistence (FqR) in Campylobacter has rapidly increased. As a consequence, camylobacteriosis is not effectively treateble with Fq and erythromycin is now the first-choice antibioticum. The most common complication, Guillain-Barré-Syndrom (an autoimmune disease), is independent of antibiotic resistance. Countries have reported different frequencies of FqR in their Campylobacter populations but this doesn’t correlate with the relative frequency of clinical complications or mortality; these have also not increased in the past 15 years since FqR in Campylobacter is on the rise.

Case-control studies have reported that campylobacteriosis cases resulting from FqR infections were either more severe, or lasted longer, than infections with susceptible bacteria, but others who re-examined these data came to the conclusion that there was no difference (Wassenaar et al, 2007), and that conclusion was backed up by another, larger, epidemiological study (anonymous, 2002). Thus, although it is true that the use of Fq in poultry has resulted in development of resistance in Campylobacter, the impact of this resistance to human health is limited.

The second example deals with Salmonella in poultry, and here it is important to note that human salmonellosis is frequently treated with Fq, where the drug is shown to be effective (even though the majority of salmonellosis cases are self-limited and do not require antibiotic treatment). So far we have only observed a partial resistance (reduced susceptibility) against Fq in Salmonella isolated from poultry. These bacteria are still likely to respond to Fq treatment in a human patient, provided the antibiotic is used at the correct dose. Complete resistance has been established in the laboratory, and was observed in a few cases human isolates, but complete resistant Salmonella have so far not been isolated from animals. It may be that the complete resistance has a cost in fitness of the bacteria to survive and multiply in animals. It is therefore not correct to attribute the serious consequences of potentially life-threatening, though rare, complete Fq resistance in Salmonella to the use of Fq in the poultry industry.

As the two cases mentioned above illustrate, there is a disconnect in the argumentation: although the use of a specific antibiotic in veterinary medicine can result in resistance of zoonotic bacteria, it is not possible to attribute treatment failure in humans to these resistances. Zoonotic bacteria such as E. coli, Campylobacter, Salmonella, all show a complex epidemiology where particular serotypes, resistence types, Pathotypes and host specificity have to be taken into account, playing different roles depending on the species. It is impossible to assess the relative fraction of resistances that result from veterinary antibiotic use and separate these from consequences of human use (Wassenaar, 2005). Veterinary medicine is, however, fully responsible for resistances that are encountered in pathogens that exclusively or mainly infect animals, such as in animal isolates of M. avium paratuberculosis, Mycoplasma bovis, Streptococcus suis, Pasteurella multocida or Mannheimia haemolytica. Interestingly, for some of these pathogens, antibiotic resistance is not a major issue.

We must conclude that it is easy to blame veterinary use of antibiotics for resistances that produce untreatable human infections, but that it is impossible to give evidence that this blame is justified. Some would argue that ‘absence of evidence’ is not the same as ‘evidence of absence’, and that the precautionary principle would urge us to restrict the use of antibiotics in animals when these are of major importance in human treatment. Naturally, antibiotics should always be used with care, and only in cases where its use is justified. That applies to human as well as to animal treatment.

The conclusion of the above examples should not be that resistance in pathogenic bacteria is of no concern to human health. We experience a large number of serious pathogens becoming rapidly resistant to commonly used antibiotics, and the consequences of this development are severe.The importance of veterinary medicine in the selection of problematic resistances is relatively minor compared to the resistance problems encountered with nosocomial (hospital) infections or the resistances observed in exclusively human pathogens. For example, consider the serious multiple resistances in in Helicobacter pylori, Mycobacterium tuberculosis, or Neisseria gonorrhoe. For all these pathogens a serious increase in resistance causes acute problems, whereby multiple drug therapy or novel drugs provide only temporary solutions to treat their infections (Wassenaar & Silley, 2008).

The efforts to look for a veterinary source of resistances can have undesired consequences. Following detection of methicillin-resistant Staphylococcus aureus on fattening pigs, pork samples are now being checked for presence of MRSA. Though these are still research investigations, positive findings may eventually urge detection on a routine basis. Since life-threatening MRSA infections are mostly nosocomial and rarely result of foodborne contamination, any money spent on detection of MRSA in food could better be spent to avoid contamination and spread in hospitals. Likewise, concentrating our efforts on removal of resistant zoonotic bacteria from the food chain would be folly, as food safety is only improved when all zoonotic bacteria are being kept in check, whether they are resistent or not.

Our efforts to reduce resistance should concentrate on those occasions where these bacteria are selected for resistance, which is when they encounte antibiotics in whatever host. Let’s consider what happens to a bacterial population when an antibiotic is present. Resistance can result from single-point mutations or gene uptake, events that can take place any time. Therefore, we assume that in any bacterial population some cells are present that are resistant against a given antibiotic compound, even though the complete population would still be reported as ‘susceptible’. This simply means that the vast majority of the cells present are susceptable. An acute infection without antibiotic treatment would not change this minute proportion of resistant cells, as shown in the figure. When, however, antibiotics are being applied, this will for those cells that are resistant, and the longer the drug is present, the larger this fraction becomes, untill all remaining cells are resistant: the population has ‘developed resistance’.

It is a myth that short therapy will result in resistance and that longer treatment can prevent this. Quite in contrast, a therapy that is used longer than necessary will remove all susceptible bacteria (after all the resistant ones are, well, resistant). In case the treatment was stopped before this, some susceptible cells would remain present, and these could, without selective pressure (in another animal, in the environment, in another patient who is not taking the same drug), outgrow the resistant population. This route back towards increases susceptibility, of the bacterial population as a whole, is blocked when long treatment has effectively eliminated all susceptible organisms. A new mutation would be needed to reduce resistance in that case.

Figure. To the left is indicated in a schematic way how a self-limiting acute infection would progress without any antibiotic treatment. We assume that a minor population of resistant cells is already present at the onset of infection, and their proportion remains constant over time. Below the graph, the proportion of resistant cells in the population before and after treatment is shown. To the right is shown what happens if an antibiotic is given, either for a short or for a longer period: resistant bacteria are selected. This selection can be complete when therapy is extended over time.

Modern insights dictate that it is better to treat an acute infection short rather than long. Many scientific publications describe nowadays how short a therapy can be to be still effective (e.g. Rubinstein, 2007). These novel treatment regimes should be applied in medical practices now, as they can stop the resistance problem from going ever worse. Treatment duration should depend on the pathogen and type of infection, and should not be dictated by the size of the package. As a rule of thumb, an antibiotic can be stopped when a patient has been free of fever or symptoms for a certain period. This is already being practiced in hospitals, and should be advised by general practicioners treating the community as well. When the choice is between a longer treatment with a lower dose, or a shorter treatment with a higher dose, the latter is to be preferred if resistances are to be avoided, provided that side effects remain manageable. Long-term therapy and the increase of the dose during treatment should be avoided whenever possible.

In conclusion, the veterinary and human medicine can both contribute to reduce the problem of resistance, when they keep the use of antibotics as minimal as possible. When needed, an antibiotic should be used for a short time only, and be applied at the correct dose.

Literature:

Campylobacter Sentinel Surveillance Scheme Collaborators. (2002). Ciprofloxacin resistance in Campylobacter jejuni: case-case analysis as a tool for elucidating risks at home and abroad. J Antimicrob Chemother. 50: 561-568

Wassenaar TM. (2005). Use of antimicrobial agents in veterinary medicine and implications for human health. Critical Rev. Microbiob. 31: 155-169.

Wassenaar TM. and Silley P. (2008). Antimicrobial resistance in zoonotic bacteria: lessons learned from host-specific pathogens. Anim Health Res Rev. 9: 177-186.

Wassenaar, TM., Kist, M. and de Jong, A. (2007) Re-analysis of the risks attributed to ciprofloxacin-resistant Campylobacter jejuni infections. Int J Antimicrob Agents 30: 195-201.

Rubinstein E. (2007). Short antibiotic treatment courses or how short is short? Int J Antimicrob Agents S1:76-79.

Rajawali, Ya rajawali sang burung perkasa barangkali semua dari kita telah mengetahuinya. Rajawali termasuk hewan unggas berdarah panas yang mengerami telurnya. Ia menjaga dan merawat anak-anak nya dengan sangat baik hingga anak-anaknya mampu untuk terbang sendiri. Rajawali juga termasuk dalam golongan hewan pemangsa dengan makanan utama adalah mamalia kecil seperti tikus, tupai, ayam dan juga ikan yang ada di sungai serta hewan reptil seperti ular pun menjadi mangsa utama sang rajawali.

Rajawali memiliki sepasang kaki yang kuat dan kuku yang tajam yang digunakan untuk mencengkeram mangsanya. Paruh rajawali berbentuk bengkok tajam serta tak bergigi namun memiliki rahang yg kuat yang sanggup mengoyak daging mangsanya.

Rajawali selalu bertelur di atas puncak yang paling tinggi entah itu pepohonan maupun perbukitan. Rajawali selalu memilih tempat yg paling tinggi untuk menjaga telur-telurnya dari jangkauan hewan lain. Dalam beberapa minggu pertama setelah bayi rajawali lahir induk sang bayi rajawali bertanggung jawab mencarikan makanan untuk sang bayi dan menyuapi bayi rajawali dengan telaten dan penuh kasih sayang, Bayi rajawali umumnya akan menghabiskan masa beberapa minggu pertama mereka hanya dengan makan dan tidur di dalam sarang yang hangat dan nyaman. Kira-kira setelah melalu masa 1 hingga 2 bulan pertama tibalah saatnya bagi sang induk untuk mengajari bayi rajawali terbang,

Sang induk rajawali akan mengajari terbang dengan cara yang tidak lazim, sang induk akan terbang dengan kecepatan yang sangat tinggi menuju sarang dimana bayi rajawali berdiam lalu dengan sengaja menabrakkan tubuhnya ke sarang hingga sang bayi rajawali terlempar dari sarang. Saat itu juga dengan sigap sang induk rajawali akan merenggut bayi rajawali tersebut serta membawanya terbang tinggi. Setelah induk serta bayi rajawali berada di tempat yang cukup tinggi, tiba-tiba sang induk menjatuhkan bayi rajawali tersebut.
Maka mau tidak mau si bayi dengan reflek akan berusaha sekuat tenaga mengepak-ngepakan sayap mungilnya supaya bisa terbang. Tapi usaha itu sama sekali tidak membuahkan hasil, alhasil meskipun telah berusaha mengepak-ngepakan sayap dengan sekuat tenaga tetap saja si bayi rajawali tersebut akhirnya jatuh melayang meluncur dengan cepat ke bawah. Seketika itu juga begitu tubuh mungil bayi rajawali hampir menghunjam menyentuh tebing atau batuan dan seketika itu juga induk rajawali segera menyelamatkan anaknya dengan mencengkeram dan membawa kembali ke atas.

Pelajaran ini dilakukan induk rajawali bersama bayi rajawali berulang-ulang setiap hari hingga kirang lebih 2 minggu maka sayap bayi rajawali tersebut telah cukup terlatih hingga kemudian ia mampu terbang sendiri. Ketika anak rajawali telah mampu untuk terbang sendiri pada saat itu rajawali telah benar-benar mandiri dan berusaha untuk mencari makan sendiri lepas dari induknya.

Dalam kehidupan terkadang kita terlalu sering dimanjakan dalam zona nyaman (sarang rajawali) sehingga kita malas untuk keluar, malas untuk berkreasi, malas melakukan improvisasi, dan bahkan malas untuk berusaha dan bekerja keras dalam menggapai impian-impian kita. Seringkali dalam kehidupan kita, kita sering mengalami cobaan, masalah, rintangan, hambatan bagaikan sarang dimana sang bayi rajawali ditabrak dan mengalami guncangan yang sangat keras yang sanggup melemparkan kita hingga terpental keluar sarang (zona nyaman).

Banyak dari kita yang memilih untuk menyerah dan hampir pasti selalu menyalahkan faktor luar seperti : lingkungan yang tidak mendukung, tidak adanya dukungan orangtua dan lingkungan sekitar, tidak cukup pengalaman, kurang umur, terlalu tua,
berasal dari keluarga miskin, atasan yang egois dan tidak pernah mau mendengarkan opini kita, atau bawahan kita yg sulit diatur, bahkan puncaknya terkadang kita pun tidak segan-segan menyalahkan Tuhan sebagai penyebab semua masalah yang ada.

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*Rajawali Tidak Hanya Terbang, Tetapi Juga Melayang*

Satu hal yang paling membedakan keluarga rajawali (elang, garuda, dll) dengan burung yang lain adalah keluarga rajawali lebih banyak terbang dengan cara melayang, dengan membuka lebar kedua sayapnya dan menggunakan tenaga angin sebagai kekuatan pendorong bagi tubuhnya. Ini dilakukan rajawali untuk menghemat tenaga yang dikeluarkan mengingat rajawali adalah termasuk burung penjelajah dimana setiap harinya rajawali sanggup menempuh jarak hingga 400km atau bahkan lebih.

Kita manusia seringkali hanya mengandalkan kekuatan sendiri dalam melakukan suatu hal. Maka tidak heran jika manusia sering menemui serta mengalami berbagai macam keputus asaan, kelelahan, banyak membuang waktu dan banyak sekali mengalami kekecewaan di dalam kehidupan.

Belajar dari sang rajawali, maka hendaknya kita perlu juga terbang dengan mengandalkan sumber daya (resource) ataupun kekuatan-kekuatan yang ada di sekitar kita seperti waktu orang lain, tenaga orang lain, modal orang lain, kecakapan, ide atau bahkan kesempatan (opportunity) yang datangnya dari orang lain.

Dalam perspektif lain, terpaan angin juga bisa kita gambarkan sebagai masalah dan hambatan dalam kehidupan manusia. Rajawali selalu belajar untuk memperkuat sayap-sayapnya ketika terbang menerjang badai. Ketika kita manusia dihadapkan pada berbagai masalah dan hambatan dalam hidup hendaknya kita juga selalu bisa belajar menguatkan sayap-sayap mental, karakter serta kepribadian kita. Serta yang terpenting kita harus mencoba untuk bisa mensyukuri akan setiap masalah dan cobaan hidup yang kita alami.

*Rajawali Memiliki Pandangan Mata Yang Jauh*

Rajawali dikarunia sepasang mata yang luar biasa yang memiliki kekuatan atau jarak pandang hingga 10x lebih jauh dari mata manusia. Tidak heran dengan kekuatan mata seperti itu seekor rajawali sanggup mengintai mangsanya yang berjarak lebih dari 15km. Dengan kemampuan luar biasa seperti itu rajawali selalu bisa melihat dan mengintai mangsanya sehingga sangat jarang mangsa yang bisa lolos dari sergapan sang rajawali.

Selain memiliki pandangan yang jauh, rajawali juga sangat fokus terhadap calon mangsanya. Dengan kata lain pada saat rajawali telah menetapkan seekor buruan fokus pandangannya akan selalu ditujukan kepada calon mangsanya meskipun dihadapkan dengan berbagai halangan yang ada.

Kemampuan rajawali dalam melihat jauh ke depan bisa kita artikan dengan memiliki visi dan tujuan yang jelas. Dalam perjalanan menuju keberhasilan kita hendaknya harus membiasakan diri untuk selalu menetapkan tujuan yang ingin dicapai dalam hidup. Banyak orang yang telah menetapkan tujuan dan memiliki impian-impian di masa depan tetapi mengapa sebagian besar dari mereka pada akhirnya gagal untuk mewujudkannya? Karena pada dasarnya sebagian besar dari kita tidak memiliki tujuan yang jelas dan kita hanya menjalankan kegiatan sehari-hari tak lebih hanya sekedar rutinitas atau sekadar ritual demi menggugurkan kewajiban belaka.

Tujuan yang tidak jelas serta kurang terarah menyebabkan sebagian besar dari kita kurang bisa memperhitungkan kapan kita akan bisa menggapai impian-impian Yang paling menyedihkan adalah pada saat kita sudah tahu bahwa impian kita sudah tidak jelas, kita bisa dengan begitu mudahnya menggantikan impian itu dengan impian-impian yang lain demikian seterusnya sehingga tidak pernah adanya fokus dan persistensi dalam mewujudkan impian tersebut. Tujuan utama dalam melatih fokus ini adalah supaya kita tetap berada pada jalur yang tepat dalam
memperjuangkan tujuan dan impian kita.

*Perubahan Besar Dalam Kehidupan Rajawali*

Diantara semua jenis burung, rajawali adalah burung yang paling panjang usianya. Umur seekor rajawali pada umumnya bisa mencapai 70tahun. Akan tetapi, pada saat rajawali mulai memasuki umur 40tahun rajawali harus melakukan suatu perubahan yang menyangkut hidup dan mati. Paruhnya akan bertambah panjang, membengkok hingga mencapai dada sehingga tidak memungkinkan bagi rajawali untuk bisa memangsa makanan lagi. Cakarnya pun semakin tua, rapuh dan lemah hingga bulu sayapnya akan bertambah lebat dan berat sehingga rajawali tidak sanggup untuk terbang lagi. Di saat kritis itulah rajawali harus mau meluangkan waktu untuk memperbaharui dirinya sendiri. Rajawali hanya memiliki 2 pilihan pada saat itu : Mati Kelaparan atau Harus menjalankan dan melalui proses perubahan yang sangat menyakitkan. Untuk menjalani proses perubahan ini maka rajawali berusaha keras terbang menuju puncak gunung yang tertinggi.

Sampai di puncak gunung, rajawali harus mematahkan secara paksa paruh yang dimilikinya dengan cara membentur-benturkan paruh tersebut ke dinding batu yang keras hingga paruh tersebut sedikit demi sedikit terlepas dari mulutnya. Setelah paruh tersebut terlepas rajawali harus mau dengan sabar menunggu hingga perlahan-lahan paruhnya mulai tumbuh kembali. Rajawali juga harus mencabut cakarnya yang sudah tua dan lemah agar kuku yang baru bisa tumbuh kembali dan puncaknya rajawali akhirnya juga harus mencabuti semua bulu di seluruh tubuhnya.Dengan sabar rajawali harus mau menunggu proses re-generasi dan proses pembaruan tersebut dan mencari sinar matahari untuk mempercepat proses penyembuhan dirinya dan mempercepat pertumbuhan bulu-bulunya. Proses yang sangat menyakitkan ini dijalani rajawali dengan penuh kesabaran selama kurang lebih 6 bulan. Akan tetapi dengan proses perubahan yang teramat menyakitkan ini seekor rajawali sanggup untuk hidup lebih lama lagi hingga 30 tahun mendatang.

Sebenarnya proses perubahan yang dialami oleh rajawali tidaklah berbeda dengan proses perubahan yang dialami oleh manusia. Namun pada kenyataannya tidak banyak orang yang tahan dalam menjalani proses perubahan dalam hidup. People resist to change, ya pada dasarnya sebagian besar orang memiliki keengganan untuk berubah dikarenakan kebanyakan perubahan tersebut dirasa tidak nyaman dan amat
menyakitkan. Meskipun terkadang kita menyadari bahwa dengan melakukan perubahan tersebut kita akan bisa menjadi manusia yang lebih baik lagi.

Untuk itulah dalam momentum Bulan Ramadhan ini, dengan segala kerendahan hati saya ingin berbagi dan saling mengingatkan termasuk mengingatkan kepada diri saya sendiri melalui kisah singkat perjalanan hidup sang rajawali ini. Mari kita jadikan bulan ini sebagai momentum perubahan bagi diri kita. Momentum dimana kita belajar sesuatu yang baru dari falsafah hidup sang rajawali, belajar sesuatu yang baru yang mudah-mudahan bisa menjadikan kita sebagai pribadi yang lebih baik lagi selepas ramadhan.
Tak lupa pula di gerbang ramadhan ini saya memanjatkan permohonan maaf kepada rekan-rekan semua jika ada khilaf, sikap ataupun tutur kata yang kurang berkenan selama ini.

كُتِبَ عَلَى الَّذِينَ مِنْ قَبْلِكُمْ لَعَلَّكُمْ تَتَّقُونَ

Malam ini adalah menjelang 1 Ramadhan 1432 H, kami sekeluarga dan seluruh umat Muslim di seluruh negara dengan ijin Tuhan akan menunaikan Ibadah Puasa Ramadhan tahun 1432 H / 2011 M.

Untuk melengkapi keikhlasan, kami memohon maaf atas segala salah dan khilaf.Selamat menunaikan Ibadah Puasa, semoga berkah Ramadhan senantiasa menyertai kita sekalian.. Amiien

ABSTRACT

Sudden death syndrome (SDS) is a condition in which fast growing broiler chicks die suddenly with no apparent causes. It has developed in to a major problem for broiler industry in many parts of the world. Broiler chicken of all ages are affected starting as early as 2 days of age and continues up to marketable age. Peak mortality usually occurs between 3rd and 4th week of age with more affect being observed in male birds than the females. There is usually a short wing beating, convulsions prior to death. Majority of affected broilers are found dead lying on their backs. This condition is often referred to as "flip-over disease." Lung oedema is a prominent PM lesion. There is no proper treatment and preventive measures to control SDS.

The major factors include faulty management, nutrition, metabolic disorders and fast growth.

Keywords: Sudden Death Syndrome, Ascites, Metabolic disorders.

Introduction:

Sudden death syndrome (SDS) is a condition affecting fast growing broiler chicken especially males. The normal incidence is 1.5-2 % of the flock affecting birds from 21-28 days of age. Affected birds appear healthy, well fleshed and invariably have feed in their digestive tract. Death occurs within 1-2 minutes with birds most frequently being found dead on their backs. There are few changes in gross pathology. The heart may contain blood clots that are likely post-mortem in origin and ventricles are usually empty. Diagnosis is usually by exclusion of other diseases. Lungs are often oedematous. There are no specific changes in the tissues or blood profile. The condition is precipitated by fast growth rate and so conversely it can be prevented when ionophore anticoccidials are used or if the diet contains a readily available carbohydrate source such as glucose.

The condition can best be prevented or reduced in incidence by inducing a period of initial slow growth rate. This can be achieved by reducing day length, physical feed restriction and/or the use of low nutrient dense diets. However there is no proper treatment and preventive measures for control of SDS but incidence can be reduced by proper management techniques.

General signs:

Sudden death syndrome is a cause of mortality in apparently normal fast growing broiler chicken. Birds often males are usually found dead on their backs with wings outstretched. The condition rarely occurs in layer birds although there have been reports of similar type deaths in adult meat breeders. The disease is basically of a metabolic origin but genetic, environmental and nutritional factors also play an important role.

Broilers that die of SDS show no specific abnormalities. Birds usually healthy males an above average body weight are mostly affected. Immediately prior to death, they appear normal and are often seen feeding, drinking and walking. Birds extend their neck, squawk and due to wing beating and leg extension quickly work themselves onto their backs. Most poultry bird farmers describe the condition as a heart attack. Death occurs within minutes although birds can be revived with limited long-term success if they are vigorously massaged during the early stages of the attack.

Fig: Majority of affected broilers are found dead lying on their backs.

Gross pathology:

Dead birds are always well fleshed with oedema 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 enlarged and have patchy sub capsular haemorrhage. The heart may contain clotted blood especially in the atria, although the ventricles may appear slightly hypertrophied. The pathological lesions seen in SDS are associated with some type of vascular disturbance. The process likely starts with circulatory lesions manifested by increased capillary permeability followed by the congestion of many tissues. There seems to be some discrepancy regarding the occurrence of enlarged and/or haemorrhagic livers. Hypertrophied livers may relate to fatty liver and kidney syndrome showing pale fatty liver and in their birds. This suggests that the fatty liver syndrome may predispose to SDS, although a common diagnosis with an empty intestine since affected birds rarely eats as the condition progresses.

Tissue analysis:

A number of studies have been aimed at correlating changes in tissue mineral, electrolyte and fat extent. There is a small but statistically significant reduction in the K content and an increase in the Na+ content of heart tissue in the affected birds. SDS birds show elevated levels of liver Ca and reduced Fe in lungs and kidneys. The heart, lungs and especially the liver also exhibit reduced levels of dry matter. The elevated levels of liver Ca is of interest in relation to SDS condition occurring in broilers.

Blood profile:

Affected male birds consistency exhibit elevated blood glucose compared to female birds. Similarly there is increase in the blood uric acid and lactate dehydrogenase levels. Conversely the higher level of this enzyme suggests higher concentrations of substrate and so perhaps elevated lactate levels.

Factors responsible for sudden death syndrome:

A number of factors have been studied with a view to isolate causative agents in SDS. When reviewing these factors, it must be remembered that SDS is a condition exclusively seen in very fast growing birds. Most studies have investigated diet texture and composition as there are numerous nutritional and physiological factors which may lead to SDS. The level and type of fat in the diet has a significant influence on the incidence of SDS. Similarly sudden noising and high intensity lighting appears to increase the incidence of SDS. The possible factors which may be responsible for the occurrence of sudden death syndrome are as follows:

A) Nutritional causes:

a) Restriction programme:

Since SDS occurs only in fast growing birds that are assumed to be eating to near physical capacity. Physical feed restriction reduces the rate of mortality by 75% than the birds maintain on free choice feeding programme.

b) Diet texture:

In broilers pelleted feed is extremely used. It has significantly higher digestibility when compared to mash type feed. Thus there is fast growth among these birds. Hence incidence of sudden death syndrome is increased when birds are fed with pelleted diets. It has been observed that certain toxic substances by pelleting protein ingredients which predispose to SDS.

c) Diet composition:

The fast growing birds that are to be assumed to be eating to near physical capacity are prone to sudden death syndrome. Mortality due SDS is more than doubled when glucose is the predominant energy source compared to 2.1% mortality when fat is a major contributor or 2.5% when corn starch is used. A diet which is marginally deficient in the vitamin biotin may cause sudden unexpected death of young broiler chicken when exposed to stress.

d) Dietary protein and amino acids:

Dietary protein seems to have little effect on SDS. It has been observed that the meat meal supplies some unidentified factor that provides protection against SDS.

e) Dietary minerals and vitamin:

Sudden death syndrome may relate in some way to mineral availability suggesting a potential hypomagnesaemia tetany caused by nutrient interaction.

Sudden death syndrome incidence is increased when biotin pyridoxic acid and thiamine are marginally present in the diet. Biotin has perhaps been singled out most frequently as a possible factor in sudden death syndrome. Similarly SDS/fatty liver kidney syndrome seems to worse when biotin is marginal while as the other B-complex vitamins are in excess.

f) Lactate metabolism:

Lactate accumulates when there is inadequate oxygen for normal aerobic metabolism. Production of lactate rather than pyruvate due to anoxia leads to acidosis. Broilers receiving diet high in glucose flip within 30 minutes of dosing with lactic acid while birds receiving a diet high in corn-starch take over 1.5 hours to flip.

B) Managemental causes:

a) Lighting:

A period of short day length during early growth has recently been shown to be benefited in reducing SDS in broilers. There is about 30-60% reduction in incidence of SDS when broilers are subjected to 6 hours light from 3-4 days or various incremental programmes of 6 hour increasing to 23 hour over the 35 day period. Early growth rate is reduced because birds have less time to eat thus reducing the incidence of SDS.

b) Stock density:

Boiler chickens are generally reared at a considerably higher stocking density. Such rearing conditions may act on the birds as a stress causing functional disorders in their organs including the heart.

c) Pharmaceuticals:

Since heart function is obviously implicated in SDS a number of pharmaceutical products have been tested. Among them anticoccidial drugs when added to the diet cause more mortality due to SDS. It has been observed that SDS was substantially higher when birds are fed diets containing ionophores namely monensin and maduramicin ammonium. Generally ionophore compounds increase the movement of metal ions across the cell membranes.

C) Pathogenisis:

Stress is the main contribute towards the pathogenesis of SDS. When the course of disease is acute there is vascular disturbance which starts with circulatory lesions manifested by increased permeability of the peripheral circulatory system. This physiological permeability caused by short term increase in blood pressure is usually reversible. However when the stimulus surpasses the tolerance level, irreversible changes occur not only in the wall of the blood vessel but also in the tissue which they supply. In SDS death appears to be caused by heart damage which leads to lung oedema, so that the chicks are unable to breath sufficient fluid is lost from the circulatory system into the lung tissue spaces causing peripheral circulatory failure. The histological changes of intense congestion and oedema in the lungs result in the tissue parenchyma becoming separated from fresh blood supply leading to hypoxia. Vascular congestion is a constant feature of most of the tissue examined microscopically particularly the lungs where much of the effective air spaces are lost because of engorgement of pulmonary capillaries. Lymphocytic infiltration and inflammation involving the secondary bronchi and the presence of oedema in the alveoli considerably reduce gaseous exchange thus enhancing respiratory distress.

D) Diagnosis:

Diagnosis is based on the history of sudden death, gross and microscopic pathology and no evidence of other disease. Blood profile and tissue analysis has little role in confirmative diagnosis.

E) Prevention and control:

There is no single treatment or preventive measure to control the sudden death syndrome. The condition is undoubtedly related to fast growth rate and as such managemental technique to reduce the early maximum genetic potential for growth offer the best preventive scenario.

1) Broiler are most commonly fed diets in pelleted form to maximise feed consumption but if same diet in crumble form consume less to reduce early growth in chicks.

2) Use diets with 5-7% less nutrient density diet, thereby tampering early fast growth rate up to 18-120 days.

3) Feed a low protein/low energy diet during first 14 days to reduce the oxygen demand.

4) Protein supplements with soya bean meal, canola meal and fish meal which are not pelleted decrease the incidence of SDS.

5) All birds can be subjected to restricted feed up to 8-10% and fed twice daily only.

6) Supplement the birds with glucose containing electrolytes.

7) Feed liquid toxin binders and immunomodulators.

8) Provide only simples broad spectrum antibiotics through water.

9) Follow a step down lighting programme from 5-18 day period of growth.

There may be endless discussion on causative agent and mode of transmission of this lethal disease but one thing is for sure, there has definitely been a lacuna in Bio-security adherence.

This is high time for the poultry producers & others involved in this trade to strictly adhere to best bio-security measures at all cost and make it a priority for survival and growth of this promising industry.

Bio-security means doing everything you can to protect poultry from disease. As a poultry advisor or an owner, keeping your birds healthy is top priority.

Please remember "You are the best protection your birds have." If you follow the basic rules and make them your routine, you decrease the risk of disease entering your poultry flock and persisting in floor, pings and debris. Practicing Bio-security is an investment like premium in the health of your birds. Following steps are advised strictly to adhere:

01. MAKE SURE TO KEEP DISTANCE

• Restrict access to your poultry farm & premises.
• Allow only people who take care of birds to come into contact with them.
• Do not allow your caretakers to attend poultry exhibition & other farms.
• Maintain a record of visitors including purpose of visit, previous farm visited & next farms to be visited.
• Look for migratory birds/waterfowl & do not let them near farm at all.

02. PRACTICE "KEEP CLEAN"

• Keep a pair of shoes and a set of cloths to wear only in particular shed.
• Clean & disinfect shoes & launder cloth before work with the birds.
• Scrub shoes with long-handled scrub brush and disinfectant using Maxii-Guard – 4 QAC’s (Lipophilic) & hyhilic compound -Glutarldehyde.
• Wash your hands thoroughly with soap and disinfectant before entering.
• Trolley-car, Truck tires must be cleaned with disinfectant before entering.
• Keep cages, feeder water supply chain clean on daily basis.

03. CONTROL RODENT & PESTS

• Rodents are major vectors & reservoir of pathogenic bacteria & transmit the infection to other farms easily. So prevent their access to feed, water & shelter.
• Arrange prompt & secure disposal of dead birds & unused spilled feed.
• Inspect regularly for litter pests like "Lesser mealworm" or "Darkling beetles" (A.diaperinus).
• Arrange rodent baiting & trapping.

04. TREAT BEDDING/LITTER

• Use "Liiteron" while placement of new bedding materials.
• Do litter treatment at the interval of 40-50 days.
• Treated litter are better than fresh bedding materials which may be contaminated with bacteria, fungi & virus during handling, transportation & due to improper storage.

05. KNOW WARNING SIGNS

• Sudden increase in bird death of your flock.
• Sneezing, gasping for air, coughing and nasal discharge.
• Watery & green diarrhea.
• Lack of energy & poor appetite.
• Drop in egg production or soft or thin-shelled misshapen eggs.
• Swelling around the eyes, neck & head.
• Purple discoloration of the wattles, combs & legs.
• Tremors, ping wings, circling, twisting of the head & necks or lack of movement.

06. REPORT SICK BIRDS

• Call your local Veterinarians.
• Contact Regional Veterinary Laboratory for detail disease investigation.
• Early detection & reporting is the most important step in eradicating contagious disease outbreak.
• Be first to report suspected case to veterinary authorities.

07. PREVENT CROSS-CONTAMINATION

• Get correct disease diagnosis of any suspected bird of particular shed.
• Establish "High Risk Areas" of your poultry farms.
• Alter vehicle route & connection to prevent cross-contamination between farm sheds.
• Do misting or thermo-fogging (Terminal stage) with 1:1 solution of Maxii-Guard.

To make an effective bio-security program, one must follow the principal of on-farm HACCP (Hazard Analysis Critical Control Points).

Good bio-security plan is like chain, linked properly with each other in good condition. If even one link is broken, the "CHAIN" would not work. Therefore, review of Bio-security measure taken at farm level should be done at regular interval & improvement done as & when required with proper maintenance of record documentation.

Please remember "Bio-security" is the cheapest & most effective mode of disease control available for various disease threats to poultry industry.

Source : engormix.com

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