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Use of Antibiotics in Veterinary Medicine, a Hazard to Human Medicine?

Senin, 12 September 2011 11 komentar

Published on: 08/29/2011
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Author : Trudy M. Wassenaar and Heike Laubenheimer-Preuße (Molecular Microbiology and Genomics Consultants- MMGC)

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.

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Kategori:Informasi

Mohon Maaf Lahir dan Bathin

Senin, 5 September 2011 1 komentar

Kategori:Informasi

Marhaban ya Ramadhan

Minggu, 31 Juli 2011 2 komentar

يَا أَيُّهَا الَّذِينَ آمَنُوا كُتِبَ عَلَيْكُمُ الصِّيَامُ كَمَا

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

Kategori:Informasi

Sudden Death Syndrome in Broilers

Selasa, 19 Juli 2011 15 komentar

Published on: 06/21/2011
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Author : M. T. Banday (Sher-e-Kashmir);S. Islamuddin S. Shahnaz; Irfan A. Baba and S. Adil Hamid

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.

Baca selanjutnya…

Kategori:Informasi

Bio-Security for Safe & Profitable Poultry Farming

Selasa, 19 Juli 2011 12 komentar

Despite our strenuous prevention effort, notorious diseases create havoc in poultry industry. Time & again the dreaded virus have struck in poultry farms and threatened to collapse of poultry industry in affected areas.

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

Kategori:Informasi

Sistem clouse house

Rabu, 29 Juni 2011 1 komentar
Kategori:Informasi, Video

Watch “Chicken Farm Produces Eggs, Energy” on YouTube

Senin, 6 Juni 2011 2 komentar
Kategori:Informasi, Video