Fw: [BITES-L] bites Oct. 20/10 -- II

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Subject: [BITES-L] bites Oct. 20/10 -- II

bites Oct. 20/10 -- II

WISCONSIN: At least 20 people sick from outbreak

Investigation of an outbreak of viral gastroenteritis in an elderly nursing home Alpes-Maritimes, April-May 2008

DENMARK aims for 10 percent less antibiotics in pigs

EU to spend €250 million on animal disease control

Why don't the CHINESE eat Canadian food? Part II

NEW JERSEY: New sensor derived from frogs may help fight bacteria and save wildlife

IOWA State, USDA researchers discover eye test for neurological diseases in livestock

UK: Some Sokolow sausage products recalled

Decreasing Shigellosis-related deaths without Shigella spp.–specific Interventions, Asia

Plasmid-mediated Quinolone Resistance among Non-Typhi Salmonella enterica Isolates, USA

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WISCONSIN: At least 20 people sick from outbreak
20.oct.10
The Eagle
Jeremiah Tucker
http://www.wiscnews.com/saukprairieeagle/news/local/article_d7a57ef4-dc51-11df-854b-001cc4c002e0.html
Sauk Prairie Eagle
MERRIMAC -- A probe into the source of what investigators believe was an outbreak of norovirus at the Hillcrest on Lake Wisconsin restaurant earlier this month is ongoing, but one official said it's possible the source of the virus may never be discovered.
Jim Kaplanek, chief of food safety for the Wisconsin Department of Health Services, said norovirus spreads so quickly that it often is difficult to determine a source. It's possible that a member of the restaurant staff spread the illness, but it also could have originated with a patron that brought it into the establishment.
"Many times all we have is a best guess, there's no conclusive evidence," Kaplanek said, adding that it's difficult to determine where food-borne illnesses started. "In most cases, with food-borne illness, very rarely do you find a link between the people and the food."
Kaplanek said no food is being tested as part of the investigation, but the state is testing stool samples.

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Investigation of an outbreak of viral gastroenteritis in an elderly nursing home Alpes-Maritimes, April-May 2008
http://www.invs.sante.fr/publications/2010/epidemie_gastroenterites_ehpad_alpes_maritimes/rapport_epidemie_gastroenterites_ehpad_alpes_maritimes.pdf
In April 2008, several cases of acute gastroenteritis (GEA) among residents and staff of an elderly nursing home were reported to the health departmental authorities. An investigation was started. A case of GEA was defined as any person presenting with diarrhoea or vomiting, with or without abdominal pain or fever>38 °C. From April 18th to May 22nd 2008, 66 cases of GEA were identified. The attack rate was higher among residents (70%) than among the staff (18%). No case was transferred to the hospital. The same strains of noroviruses belonging to genogroup II, Bristol genotype (GGII-4) was found in stools cultures of two residents and a cook. Several informations are in favour of an outbreak of GEA caused by a norovirus: high attack rate; many cases over a short period; mild clinical; short duration of the disease; cases among residents and staff members; same strains of norovirus found in the faeces of two residents and a cook. It's difficult to determine if the outbreak origin is food or due to person-to-person transmission. Several elements show the important role played by the food: non-conformity due to a lack of hygiene and a failing manufacturing process; pathogenic agents isolated in a cook's samplings, ill at the beginning of the outbreak; attack rate of 79% in the beginning of epidemic among the persons benefiting from mixed meals; all mixed dishes analysed contamined.
This must reinforce that, facing an outbreak, strict control measures should be implemented quickly to minimise the occurrence of an epidemic.

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DENMARK aims for 10 percent less antibiotics in pigs
20.oct.10
VetsWeb
http://www.vetsweb.com/news/denmark-aims-at-10-percent-less-antibiotics-in-pigs-1547.html
The antibiotic use in the Danish pig production should be reduced by at least 10 percent in 2013.
In 2009, 11% more antibiotics were used in Danish pigs than the year before. This has to change according to Danish Agriculture Minister Henrik Høegh demands from the pig sector, who now demands the 10% reduction in the coming years.
This requirement is based on a new agreement with the parliament. The agreement also implies that mortality in sows should be reduced to 16 percent in 2013. Currently this is 24 percent.
According to Høegh, the objectives can be achieved by focusing on companies with the largest problems. A report by the Food and Veterinary Authority Fødevarestyrelsen shows that 20 to 25 percent of the total antibiotic consumption takes place at 10 percent of the farms. "Also the total sow mortality is affected by a relatively small proportion of the farms," said Høegh.
To achieve the new targets, certain limit standards are being introduced. If these are exceeded by the farmer, the farm will be checked more often by a veterinarian. The extra costs are for the farmer.

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EU to spend €250 million on animal disease control
15.oct.10
VetsWeb
http://www.vetsweb.com/news/eu-to-spend-€250-million-on-animal-disease-control-1530.html
Aiming to further strengthen the protection of human and animal health, the European Union earmarked today more than €250 million to support programmes to eradicate, control and monitor animal diseases in 2011.
The 138 annual or multi-annual programmes, which have been selected for EU funding, will tackle animal diseases that impact both human and animal health. More than half of the total sum will be used to finance programmes to eradicate 8 important animal diseases.
Focus on Eastern Europe
The total EU contribution to these programmes will be around €135 million. Following the success of the programmes in recent years, which have virtually eradicated rabies in the western part of the EU, most of the activity in 2011 will be focused towards the Member States in the eastern part of the continent and also includes some actions in Ukraine and Belarus. €24 million is allocated to rabies eradication in 12 Member States. Rabies is spread by infected wildlife and the programmes aim at producing immunity in the wildlife by orally vaccinating them with baits containing vaccine.
Zoonose control
Within this budget, diseases that might be transmitted to humans have been prioritised. Significant sums will be spent on the eradication of brucellosis, tuberculosis and rabies. For tuberculosis, €16 million is allocated to Ireland, €23 million to the UK, €7.5 million to Italy and €15 million for Spain. In 2011, over €23 million is allocated to control zoonotic salmonella in breeding and laying hens and in broilers (Gallus gallus) and turkeys (Meleagris gallopavo) in all 27 Member States.
Avian influenza surveillance
Member States will also continue to carry out surveillance for avian influenza in poultry and wild birds in 2011 with financial assistance from the EU towards laboratory testing and wild birds sampling costs. About €3.6 million are being made available from the EU budget.
TSE programmes
The Commission has agreed to make more than €86 million available from the EU budget to assist Member States in the monitoring of Transmissible Spongiform Encephalopathies (TSEs), and for BSE eradication and compulsory Scrapie eradication measures. The requests from Member States for BSE eradication, i.e. culling of cohorts of BSE-infected animals, have dropped in line with the major reduction in new BSE cases.
Reference Laboratories
SCoFCAH also endorsed another Commission proposal to allocate in 2011 €14 million to finance a network of European Union Reference Laboratories in the animal health and food safety area. These laboratories act as reference points for the Commission and Member States and are essential elements in the EU policy to ensure a high level of animal health and food safety throughout the European Union. The laboratories offer specialised advice in areas of animal health, food safety and residues. They also co-ordinate Laboratories in the Member States and ensure high standards by carrying out comparative trials on testing methods and standards.

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Why don't the CHINESE eat Canadian food? Part II
01.oct.10
Food Law
Ronald Doering
The big question in the news these days is whether the Chinese will buy part or all of Canada's Potash Corporation. Underly¬ing this is the recognition that China has a huge problem com¬ing at it: how to feed itself. With little arable land and a growing middle class — estimated by some to be 700 million by 2020 — China must increase crop yields and to do that they need a lot of fertilizer, i.e., Canadian potash. The more interesting question is: why don't the Chinese eat Canadian food?
I set out to answer that question in a column in the June 2007 issue of Food in Canada. At that time, Canadian processed food exports to China were minuscule. The release of recent statistics reveals that we are still doing no better.
Raw agricultural commodities have doubled in three years due entirely to increased exports of canola, barley, peas and flaxseed. I was president of the Canadian Food Inspection Agency when we received the historic breakthrough allowing pork into China, and thanks to Prime Minister Harper's work and announcement of June 24, 2010, we are back selling beef. But you still can't find Canadian food products in China's massive grocery stores.
In the 2007 article I concluded that the main reason Canada had missed the boat to the Chinese food market was because of the "timidity of Canadian companies that have been spoiled by the proximity of the U.S., combined with their lack of leadership and vision." Borrowing heav¬ily on Andrea Mandel-Campbell's analysis in her book Why Mexicans Don't Drink Molson, I concluded that we had squandered our early potential to export to China that came from our unprecedented wheat sales in 1960. Now, 50 years from that historic event and 40 years from our establishing of formal trade relations with China, our finished food exports are still pathetically low.
It would seem that three years later it is still because Canadian food manufacturers just don't even care to try. The only significant food company presence at Prime Minister Martin's trade mission to China in 2005 was some East Coast aquaculture companies. The Canada-China Business Council still estimates that one of the larg¬est untapped sectors that can benefit from the explosion of consumer demand is processed food. Yet, it still doesn't appear that any food companies are on the Board of Directors of the Council and they haven't even bothered to join as members, in spite of the fact that over 100 companies from most other sectors see the potential of this uniquely important business organization.
It's still not easy doing business in China, but the food compa¬nies of many other countries have concluded that the risk and work are well worth it consider¬ing the unprecedented growth in demand for safe, processed food.
Because Canadians can't eat much more food, growth in the food industry depends almost entirely on produc¬ing value-added products for export. As I concluded in 2007, if the Canadian food industry continues to miss the opportunities in China, they will have nobody to blame but themselves.
Thanks to Gowlings' trade law lawyer Ryan Kennedy for research help.
Ronald L. Doering, BA, LL.B, MA, LL.D, is a past president of the Canadian Food Inspection Agency. He practices food law in the Ottawa offices of Gowling Lafleur Henderson LLP, and can be reached at: Ronald.doering@gowlings.com

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NEW JERSEY: New sensor derived from frogs may help fight bacteria and save wildlife
19.oct.10
Princeton
Chris Emery
http://www.princeton.edu/engineering/news/archive/?id=3822
Princeton engineers have developed a sensor that may revolutionize how drugs and medical devices are tested for contamination, and in the process also help ensure the survival of two species of threatened animals.
To be fair, some of the credit goes to an African frog.
In the wild, the African clawed frog produces antibacterial peptides -- small chains of amino acids -- on its skin to protect it from infection. Princeton researchers have found a way to attach these peptides, which can be synthesized in the laboratory, to a small electronic chip that emits an electrical signal when exposed to harmful bacteria, including pathogenic E. coli and salmonella.
"It's a robust, simple platform," said Michael McAlpine, an assistant professor of mechanical and aerospace engineering at Princeton and the lead researcher on the project. "We think these chips could replace the current method of testing medical devices and drugs."
A paper outlining their development of the sensor was published online October 18 in the Proceedings of the National Academy of Science. The research was funded by the American Asthma Foundation and by the Air Force Office of Scientific Research.
The current testing method has a major drawback: It relies on the blood of the horseshoe crab, a species that is roughly 450 million years old. The horseshoe crab population has declined in recent years, and as a result, so too has the population of a bird that feasts on the crab.
The crab became desirable for testing because its immune system has evolved to cope with the constant threat of invasion from its bacteria-rich environment. Its blue-colored blood contains antimicrobial cells, known as amebocytes, that defend the crab against bacteria -- similar to the way the peptides protect the African frog's skin.
For almost 40 years, an aqueous extract made from horseshoe crab blood cells, called Limulus amebocyte lysate (LAL), has been used for testing drugs and medical devices for contamination.
In the era before the use of these animal extracts for testing, although drugs and medical devices were sterilized, they would sometimes cause patients to develop fevers due to an immune reaction to endotoxins, which are remnants of bacteria destroyed by the sterilization process. When a sample from a drug or device is added to LAL and the solution hardens into a gel, it indicates the sample is contaminated and not safe for human use.
New approach could help save animal populations
To produce LAL, the crabs are captured and roughly 30 percent of their blood drained before they are returned to the ocean. There is disagreement on how many crabs die as a result of the procedure, but their estimated mortality rate can be as high as 30 percent, according to the United States Geological Survey.
A conservative estimate puts the number of horseshoe crabs on the Atlantic Coast between New Jersey and Virginia at between 2.3 to 4.5 million, according to the Ecological Research & Development Group. In recent years, the populations of the horseshoe crab and shore birds that rely on them for food both have been in decline, with the red knot, a rust-colored species of shore bird, of particular concern.
Each spring the bird migrates 20,000 miles from the islands of Tierra del Fuego, off the southern tip of South America, to the Delaware Bay on the east coast of the United States. From April to May, the bird feasts on horseshoe crab eggs found on beaches, nearly doubling its body weight to sustain its health for the long flight south.
Studies have discovered a precipitous decline in the red knot population. One study by researchers at the University of Toronto found that the Tierra del Fuego population of red knots declined from 53,000 birds to 27,000 birds between 2000 and 2002.
The decline has been linked to the reduction in the number of horseshoe crabs, as a result of harvesting their blood for medical testing and their use as fishing bait for eel and conch.
In response, Delaware, Maryland and New York have limited the number of crabs that can be harvested each year to less than 150,000, and New Jersey has implemented a moratorium on harvesting the crabs. In 2009, since implementing the measures, the number of red knots visiting Delaware Bay was estimated at 24,000, up from 18,000 the year before, but still far lower than the population of 100,000 to 150,000 of two decades ago.
McAlpine and Manu Mannoor, a Princeton graduate student who worked on the project, hope that technology based on their electronic chip will eventually replace LAL as the standard for contamination testing, obviating the need for horseshoe crab blood and helping both the crabs and the red knots rebound.
At the same time, producing this new sensory device would not put pressure on the frog species. "No frogs were harmed in the making of this sensor," he said.

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IOWA State, USDA researchers discover eye test for neurological diseases in livestock
18.oct.10
Iowa State University
Jacob Petrich and Mike Krapfl
http://www.news.iastate.edu/news/2010/oct/TSEtest
AMES, Iowa -- The eyes of sheep infected with scrapie - a neurological disorder similar to mad cow disease - return an intense, almost-white glow when they're hit with blue excitation light, according to a research project led by Iowa State University's Jacob Petrich.
The findings suggest technologies and techniques can be developed to quickly and noninvasively test for transmissible spongiform encephalopathies, progressive and fatal neurological diseases such as mad cow disease in cattle and Creutzfeldt-Jakob disease in humans. Petrich, in fact, is working to develop a testing device.
The findings were published earlier this year in the journal Analytical Chemistry. The project was supported by a grant from the U.S. Department of Defense.
The research is the result of an accidental discovery while Petrich and his collaborators were developing a fluorescence spectroscopy device that's now used in slaughterhouses to test livestock carcasses for feces and possible E. coli contamination.
"One day we were testing the apparatus by shining light on the carcass and we saw the spinal cord glow - it fluoresced," said Petrich, professor and chair of Iowa State's chemistry department. "We saw the spinal cord through the skin. The light was pretty intense. It was an amazing result."
That sparked some new thinking: Maybe fluorescence technology could be used to test animals for transmissible spongiform encephalopathies such as bovine spongiform encephalopathy - what's often called mad cow disease. To reduce the risk of human exposure to the diseases, the brains and spinal cords of animals are removed during slaughter and processing. But there is no quick test to identify animals with the diseases.
And so Petrich and a team of researchers began studying the feasibility of a fluorescence test. The team included Ramkrishna Adhikary, an Iowa State graduate student in chemistry; Prasun Mukherjee, a former Iowa State graduate student and current post-doctoral associate in chemistry at the University of Pittsburgh; Govindarajan Krishnamoorthy, a former Iowa State post-doctoral research associate and current assistant professor of chemistry at the Indian Institute of Technology Guwahati; Robert Kunkle of the U.S. Department of Agriculture's National Animal Disease Center in Ames; Thomas Casey of the National Animal Disease Center; and Mark Rasmussen of the U.S. Food and Drug Administration's Center for Veterinary Medicine in Laurel, Md.
The researchers collected 140 eyeballs from 73 sheep. Thirty five of those sheep were infected with scrapie; 38 were not. The researchers took fluorescence readings from various parts of the eyes of all the sheep.
"The bottom line is the scrapie-positive retinas fluoresced like crazy," Petrich said. "And the scrapie-negative ones did not."
A previous study published in the journal Veterinary Pathology reported that the function and structure of retinas are altered in cattle infected with transmissible mink encephalopathy. Members of that study team included Iowa State researchers M. Heather West Greenlee, an associate professor of biomedical sciences in the College of Veterinary Medicine; Justin Greenlee, a collaborator assistant professor of biomedical sciences; and Juergen Richt, a collaborator associate professor of veterinary microbiology and preventive medicine.
Other studies have reported that lipofuscin, an intracellular fluorescent pigment, accumulates in the eyes of animals infected with the neurological diseases. Petrich and his team attribute the glow from scrapie-positive retinas to the elevated levels of lipofuscin.
Whatever the cause, Petrich said it's clear there are distinct differences in the fluorescence and spectroscopic signatures of retinas from sheep that were naturally infected with scrapie and those that were not. And so he and his research team think there's great promise for a diagnostic test based on that discovery.
That has Petrich starting to develop a device (he likes to call it a "gizmo") that could be used in meat plants to test the retinas of animals for signs of neurological diseases. He expects it will take several years to develop, build and test a useful device.
"What I like about this is it's really simple," Petrich said. "It's light in and light out."

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UK: Some Sokolow sausage products recalled
20.oct.10
Food Standards Agency
http://www.food.gov.uk/news/newsarchive/2010/oct/sokolow
Some Sokolów Home Black Pudding Sausage with a 'use by' date of 30 October 2010 has been recalled, because the product is contaminated with Listeria monocytogenes. The product is also sold under the name Grill Black Pudding Sausage. Listeria is a food bug that causes food poisoning.
The Agency has issued a Product Recall Information Notice advising that three wholesalers in the Doncaster area are recalling the affected products.
Product details
Details of products being recalled:
Sokolów Home Black Pudding Sausage
* Weight of packs varies
* Use by: 30 October 2010
* Batch code: 474M0916
Sokolów Grill Black Pudding Sausage
* Weight of packs varies
* Use by: 30 October 2010
* Batch code: 474M0916
M&K Polish Goods Ltd, Donney European Ltd and Expo Foods (Midlands) Ltd are recalling the affected product from consumers. Product recall notices will be displayed in stores that sell the products, explaining why the products have been recalled and how customers can get a full refund. Each company has produced their own point-of-sale notice. An example notice and image of the Sokolów Home Black Pudding Sausage product can be found at the link below.
No other Sokolów products are known to be affected.
About product withdrawals and recalls
If there is a problem with a food product that means it should not be sold, then it might be 'withdrawn' (taken off the shelves) or 'recalled' (when customers are asked to return the product). The Food Standards Agency issues Product Withdrawal Information Notices and Product Recall Information Notices to let consumers and local authorities know about problems associated with food. In some cases, a 'Food Alert for Action' is issued. This provides local authorities with details of specific action to be taken on behalf of consumers.
You can get FSA alerts about product recall and withdrawals either by email or SMS text. Visit the Get Alerts page at the link towards the bottom of this page to find out how.
You can also subscribe to our Really Simple Syndication (RSS) feed for food and allergy alerts. RSS is a format for distributing news content and is a simple way to keep up to date with the latest news on a website.
When we publish via RSS, you can automatically get the updated content via a 'news aggregator' or 'news reader'. Our RSS feed will contain a brief summary and link back to our web content. Click on 'What is RSS' on the left of this page for more details.

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Decreasing Shigellosis-related deaths without Shigella spp.–specific Interventions, Asia
01.nov.10
Emerging Infectious Diseases
Pradip Bardhan, A.S.G. Faruque, Aliya Naheed, and David A. Sack
http://www.cdc.gov/eid/content/16/11/1718.htm
Abstract
In 1999, a review of the literature for 1966–1997 suggested that ≈1.1 million persons die annually of shigellosis, including ≈880,000 in Asia. Our recent review of the literature for 1990–2009 indicates that ≈125 million shigellosis cases occur annually in Asia, of which ≈14,000 are fatal. This estimate for illnesses is similar to the earlier estimate, but the number of deaths is 98% lower; that is, the lower estimate of deaths is associated with markedly reduced case-fatality rates rather than fewer cases. Shigella spp.–related deaths decreased substantially during a period without Shigella spp.–specific interventions. We speculate that nonspecific interventions, e.g., measles vaccination, vitamin A supplementation, and improved nutrition, may have led to the reduced number of shigellosis-related deaths.
In 1999, Kotloff et al. reviewed the literature to estimate the global incidence of shigellosis. On the basis of studies published during 1966–1997, they estimated ≈1.1 million shigellosis-related deaths annually, resulting from ≈164.7 million cases. Of these, ≈163.2 million cases occurred in developing countries, ≈80% of which occurred in Asia (1). These high estimates of illness and death have increased interest in identifying interventions, including new vaccines, that might reduce these astonishing numbers (2–5).
Several changes have occurred that might have altered this incidence. Shigellosis might be increasing because of increasing populations in Shigella spp.–endemic areas; because of increasing resistance to antimicrobial drugs among shigellae, especially in S. dysenteriae type 1 (the Shiga bacillus) (6–8); or because of increasing rates of HIV infection and AIDS in many countries, which might be influencing shigellosis incidence. On the other hand, incidence might be decreasing because of improved nutrition in many countries, improved delivery of healthcare in some areas, and more widespread use of measles vaccine (9,10) and vitamin A supplementation (11), which might reduce the severity of intestinal infections. The availability of fluoroquinolones, often used without prescription, also might lead to changing treatment practices because families might use antimicrobial drugs earlier during diarrheal illness or for other illnesses (12).
Shigellosis incidence might also have changed because of the overall reduction in diarrhea-related deaths through case management, including rehydration therapy and proper feeding (13). Because shigellosis is not primarily a dehydrating condition, hydration is not critical for patients with dysentery. Nonetheless, the consistent use of oral rehydration therapy for diarrhea may reduce illness from the persistent effects of repeated episodes of diarrhea, which is common in developing counties.
Thus, at the request of the World Health Organization, we reviewed the literature for 1990–2009 to estimate the current incidence of shigellosis. The earlier study by Kotloff et al. attempted to extrapolate from data from developing countries; however, most of the data were from Asia. Because the epidemiology of shigellosis may differ in Africa, we restricted our review to studies in Asian populations.
Materials and Methods
Our review comprised studies identified through PubMed. The initial studies were identified by a computer search of the multilingual scientific literature published since 1990. Articles derived by using the keywords Shigella, dysentery, bacillary, and shigellosis were linked with a set of other articles obtained by using the keywords incidence, prevalence, public health, death rate, mortality, surveillance, burden, distribution, and permutations of the root word epidemiol-. We conducted searches for each Asian country, except Japan and Israel. The resulting cross-linked set contained 319 articles, which we culled to 164 articles that were relevant to the goal of the search. Additional sources were located through consultations with experts in the field, proceedings of expert meetings, and the ongoing Diarrheal Diseases Surveillance Programme of the International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B). To enable comparison over time, we adopted the methods of the previous review on shigellosis (1).
We created an algorithm to estimate the number of Shigella infections that occurred each year in Asia. In a preliminary step, the world's population was divided into 4 age strata (0–11 months, 1–4 years, 5–14 years, and >15 years). Published rates of diarrhea for each of the 4 strata were used to estimate the diarrheal disease incidence. An increase in the severity of a patient's illness influences the proportion of diarrheal episodes attributable to Shigella spp. This correlation can be presumed to strengthen as the proportion of Shigella infections increases because sampling progresses from cases of diarrhea detected by household surveillance to those among outpatients to persons admitted to hospital (14). Thus, we subdivided the total diarrheal disease incidence into these 3 settings: estimates of mild cases in persons who stayed at home; more severe cases needing care at a clinic but not hospitalization; and cases requiring hospitalization.
The total number of diarrhea cases attributable to shigellosis was calculated for the <1-year and 1–4-year age groups by multiplying the number of diarrhea cases in the 2 settings (community and treatment facilities) by the percentage of diarrhea cases from which Shigella spp. were isolated (Table 1). For older children and adults, we calculated total cases by multiplying the median percentages of diarrhea cases attributable to shigellosis in persons 5–14 years and >15 years of age by the number of diarrhea cases in these 2 age groups according to clinical setting (Table 2).
We adopted the estimates of Kosek et al. (15) to calculate the number of diarrhea episodes per person per year within countries in Asia (Table 1). These estimates were based on the review of 13 longitudinal studies of stable populations in 8 countries in Asia, where active surveillance was conducted during 1984–1995.
We estimated the proportion of diarrheal episodes in each stratum that can be attributed to shigellosis by analyzing only studies in which surveillance was conducted since 1990 and that used microbiologic confirmations to report the percentage of Shigella spp.–related diarrhea cases for the specified age group. An overall median percentage of shigellosis was then calculated for each stratum and multiplied by the total number of diarrheal cases in the stratum to derive the number of shigellosis cases in each stratum. In addition to the median, a weighted mean with 95% confidence intervals (CIs) was calculated for these analyses by using Freeman-Tukey transformed proportions. Weights used were equal to the inverse standard errors of these transformed proportions (18,19). The numbers of shigellosis cases were added to give an overall estimate of shigellosis-related illness. Case-fatality rates (CFRs) for persons hospitalized with Shigella infection at the ICDDR,B hospital were used to calculate age-specific rates of Shigella spp.–associated death. This hospital treats >100,000 diarrhea patients annually and is the same hospital used for CFRs in the earlier study.
Illness was expressed as episodes of diarrhea per person-year from which shigellae were recovered. Studies were included in the death estimates if deaths caused by Shigella spp. could be ascertained through active surveillance. The review comprised prospective and retrospective studies but not studies based on vital statistics only. Death was considered to have been caused by diarrhea only if diarrhea was listed as the primary cause.
Results
Approximately 3,938,020,000 persons resided in Asia during 2005. This estimate included 78,533,000 infants <1 year of age and 361,252,000 children 1–4 years of age (20,21).
Shigellosis Incidence
The median frequency of Shigella spp. isolation from diarrheal cases in the community in children 0–4 years of age was 4.4% (range 3.1%–13.4%; weighted mean 5.1%, 95% CI 4.4%–5.7%). Because only 1 study broke this rate down into the <1-year and 1–4-year ranges, the median of the 2 values for the combined range was calculated. The median frequencies of Shigella spp. isolation rates from persons with diarrhea reporting to the treatment facilities were 5.8% (range 2.4%–9.3%) among children <1 year of age and 9.4% (range 2.4%–23.5%) among children 1–4 years of age. The weighted mean of the combined group was 6.6% (95% CI 6.0%–7.2%). Details of these studies are found in Technical Appendix Tables 1, 2 [ 69 KB, 3 pages].
Approximately 39,669,000 (weighted mean 45,980,000, 95% CI 39,669,000–51,389,000) shigellosis cases occurred in children <5 years of age in the community and 6,671,000 (weighted mean 5,433,000, 95% CI 5,256,000–5,927,000) in treatment facilities, totaling 46,717,000 (95% CI 44,924,000–57,316,000) cases among Asian children <5 years of age annually. The proportions of cases with shigellosis are detailed in Technical Appendix Tables 1, 2 [ 69 KB, 3 pages].
The median percentage of diarrhea in the community was 4.0% (range 1.6%–13.5%; weighted mean 4.6%, 95% CI 4.0%–5.1%). The median percentages for patients treated at facilities were ≈11.6% (range 4.7%–17.3%) and ≈10.7% (range 4.1%–27%) respectively (weighted mean of the combined groups 8.3%, 95% CI 7.7–9.0%). (The proportions of shigellosis cases are detailed in Technical Appendix Tables 3 and 4 [ 69 KB, 3 pages].) Shigella infections among children 5–14 years of age and persons >15 years of age were ≈20,049,000 (95% CI 19,673,000–24,898,000) and ≈58,576,000 (95% CI 57,726,000–73,057,000), respectively.
We combined the number of shigellosis episodes in all age groups. The total annual number of shigellosis cases in Asia was ≈125 million (95% CI 122 million–155 million).
Shigellosis-associated Deaths
Median CFRs for hospitalized shigellosis patients <1 year and 1–4 years of age and patients >5 years of age were 0.89%, 0.01%, and 0 respectively (Table 3), according to data from the ICDDR,B hospital surveillance program during 1990–2007. The weighted means for patients <1 and 1–4 years of age were 0.8% (95% CI 0.5%–1.0%) and 0.1% (95% CI 0.02%–0.25%), respectively. No deaths were reported from large studies in other countries in Asia. By using median CFRs from Bangladesh for these age groups, we determined that ≈1,960 shigellosis deaths occurred in Asia among hospitalized patients annually (Table 3). By using the 95% CIs, we estimated that the number of deaths ranged from 1,347 to 2,595.
A study from Bangladesh found that only 17.8% of shigellosis-related deaths occurred in treatment facilities; another study from the Gambia reported that only 12% of deaths associated with Shigella infection among children occurred in a health center (23,24). Thus, the true number of shigellosis-associated deaths may be 6–8× higher than deaths recorded in the hospital records. Hence, the estimates of the in-hospital shigellosis-associated deaths were multiplied by a factor of 7 in all age groups to correct for out-of-hospital mortality. This increased the number of deaths in all age groups to ≈13,720 shigellosis-related deaths across all the age groups per year in Asia (Table 4).
Discussion
Our review calculated that ≈125 million cases of endemic shigellosis occur annually in Asia, of which ≈14,000 (0.011%) cases result in death. Children <5 years of age are at highest risk for Shigella spp.–related illness and death. Although this estimate suggests that shigellosis incidence is substantial and similar to the earlier estimate, the updated death estimate is 98% lower than the estimate by Kotloff et al. (1) that used data primarily from the 1980s. Assuming that the population of Asia is ≈80% of the total population of the developing countries, ≈130 million Shigella infections and ≈880,000 deaths occurred in Asia according to the earlier estimate.
With such a large difference in estimated incidences, one estimate may be more accurate than the other. Alternatively, Shigella spp.–related deaths may have decreased substantially since the 1980s, even in the absence of specific interventions against shigellosis. We believe the latter explanation best explains the large difference in estimates of deaths.
The major variable that was lower in our calculations was the CFR for hospitalized patients, especially children. In the earlier estimate, a CFR of 11% was used from the ICDDR,B hospital (24). Recent data from the same hospital indicate the rate is now ≈0.01% overall and only 0.89% for the youngest age group. A recent estimate from Africa found a CFR of <1% during an outbreak associated with S. dysenteriae, suggesting that this low CFR may not be limited to Asia (25).
The decrease in CFRs could be explained by >1 factor. Case management might have improved, strains might be less virulent, or children might be healthier when they become infected and therefore have less severe complications. Case management in the hospital is unlikely to have changed substantially, and in fact the increasing resistance of current strains to antimicrobial drugs makes case management more difficult. Case management in the home may have changed, however, because antimicrobial drugs are widely available, and families may purchase effective antimicrobial drugs, e.g., ciprofloxacin, and begin treatment earlier in the course of the illness (12). Virulence of infecting strains could be lower; infections with S. dysenteriae type 1 are unusual. During past epidemics with this serotype, however, the CFR for S. flexneri was as high as it was with S. dysenteriae type 1 (24). Thus, virulence is unlikely to explain the decrease in the number of deaths.
Improved health of children who become infected appears to best explain the decreased CFR. Nutritional status of children in Bangladesh has continued to improve slowly (26). Perhaps more essential is the high proportion receiving measles vaccine and vitamin A (27). Anecdotally, in children dying of shigellosis during the 1980s, postmeasles dysentery was often diagnosed, and measles increased the severity of diarrhea, including shigellosis (9,10). Measles with dysentery is rarely seen now in Bangladesh.
Our review has some limitations. Although we reviewed all available published data on shigellosis in Asia since 1990, few sites conduct active surveillance for this infection, and only one estimates CFRs. With this large population, extrapolating accurately to the entire continent might not be possible. Nevertheless, the same methods were used in this and the earlier review. The large multicenter study on shigellosis in Asia did not record any deaths, suggesting that fatalities from shigellosis are not common (22).
Second, the review included only Asia, and the situation in Africa is possibly (even likely) different (28). The higher rates of HIV infection and AIDS and malaria, different nutritional deficiencies, different rates of measles vaccination, and different health systems and civil disturbance might suggest higher Shigella spp.–related deaths in Africa. Unfortunately, until recently, no long-term surveillance for diarrhea has existed in Africa on which to base estimates.
Third, the data in the review were based on microbiologic diagnosis of Shigella infections. Although isolation of Shigella spp. from fecal samples is the most specific diagnostic test for shigellosis, the culture method has limited sensitivity because of the relatively fastidious nature of the organism. Adoption of improved specimen transport methods and newer and more sensitive molecular laboratory diagnostic methods (e.g., PCR) reportedly having high sensitivities may detect more infections (29) but is unlikely to alter the death estimates.
The remarkable 98% decrease in deaths from shigellosis in the absence of a Shigella spp.–specific intervention suggests that other nonspecific interventions have helped to lower Shigella spp.–specific deaths. These, we believe, include measles vaccine, vitamin A supplements, and overall improvement in nutrition. Although the ready availability of antimicrobial drugs encourages the development of antibiotic drug resistance because of frequent abuse, we cannot rule out the possibility that the rapid availability of these antibiotics (especially fluoroquinolones) also have benefited children with dysentery who may be receiving treatment more quickly than they previously did.
The findings from our review may provide lessons regarding other infectious diseases. Approximately 50% of deaths among children <5 years of age have malnutrition as an underlying cause (30). Also, malnutrition and infection are clearly related, with one leading to the other. By reducing rates of other common infections, e.g., measles, and improving the nutritional status, including micronutrient nutrition, of children, diseases from other infections, such as Shigella spp., may decrease.
The 4 species and numerous serotypes of Shigella spp. are a challenge for vaccine developers, but shigellosis remains high, and increasing resistance to antibiotic drugs continues to make treatment difficult. An effective Shigella spp. vaccine may have substantial benefits, but our study suggests that Shigella spp.–related deaths can be, and have been, substantially reduced with currently available interventions and that such interventions do not need to be Shigella spp. specific.
Acknowledgments
We gratefully acknowledge these donors who provide unrestricted support to the Centre's research: Australian International Development Agency, Government of Bangladesh, Canadian International Development Agency, Government of the Netherlands, Swedish International Development Cooperative Agency, Swiss Development Cooperation, and Department for International Development, UK. We also acknowledge statistical assistance of Richard E. Thompson.
This activity was funded by a grant from the World Health Organization and by core funds of the ICDDR,B.
Dr Bardhan is a senior scientist and physician at the International Centre for Diarrhoeal Disease Research, Bangladesh. He is involved in clinical care and clinical research.
References
Kotloff KL, Winickoff JP, Ivanoff B, Clemens JD, Swerdlow DL, Sansonetti PJ, et al. Global burden of Shigella infections: implications for vaccine development and implementation of control strategies. Bull World Health Organ. 1999;77:651–66.
Ashkenazi S, Passwell JH, Harlev E, Miron D, Dagan R, Farzan N, et al. Safety and immunogenicity of Shigella sonnei and Shigella flexneri 2a O–specific polysaccharide conjugates in children. J Infect Dis. 1999;179:1565–8. PubMed DOI
Kotloff KL, Taylor DN, Sztein MB, Wasserman SS, Losonsky GA, Nataro JP, et al. Phase I evaluation of delta virG Shigella sonnei live, attenuated, oral vaccine strain WRSS1 in healthy adults. Infect Immun. 2002;70:2016–21. PubMed DOI
Katz DE, Coster TS, Wolf MK, Trespalacios FC, Cohen D, Robins G, et al. Two studies evaluating the safety and immunogenicity of a live, attenuated Shigella flexneri 2a vaccine (SC602) and excretion of vaccine organisms in North American volunteers. Infect Immun. 2004;72:923–30. PubMed DOI
Altboum Z, Barry EM, Losonsky G, Galen JE, Levine MM. Attenuated Shigella flexneri 2a delta guaBA strain CVD 1204 expressing enterotoxigenic Escherichia coli (ETEC) CS2 and CS3 fimbriae as a live mucosal vaccine against Shigella and ETEC infection. Infect Immun. 2001;69:3150–8. PubMed DOI
Sack RB, Rahman M, Yunus M, Khan EH. Antimicrobial resistance in organisms causing diarrheal disease. Clin Infect Dis. 1997;24(Suppl 1):S102–5.
Bhattacharya SK, Sarkar K, Balakrish NG, Faruque AS, Sack DA. Multidrug-resistant Shigella dysenteriae type 1 in south Asia. Lancet Infect Dis. 2003;3:755. PubMed DOI
Dutta D, Bhattacharya MK, Dutta S, Datta A, Sarkar D, Bhandari B, et al. Emergence of multidrug-resistant Shigella dysenteriae type 1 causing sporadic outbreak in and around Kolkata, India. J Health Popul Nutr. 2003;21:79–80.
Koster FT, Curlin GC, Aziz KM, Haque A. Synergistic impact of measles and diarrhoea on nutrition and mortality in Bangladesh. Bull World Health Organ. 1981;59:901–8.
Mathur R, Mathur YN, Verma SD. An outbreak of shigellosis in central India: higher death rate in post-measles shigellosis. J Diarrhoeal Dis Res. 1989;7:28–9.
Mitra AK, Alvarez JO, Wahed MA, Fuchs GJ, Stephensen CB. Predictors of serum retinol in children with shigellosis. Am J Clin Nutr. 1998;68:1088–94.
Larson CP, Saha UR, Islam R, Roy N. Childhood diarrhoea management practices in Bangladesh: private sector dominance and continued inequities in care. Int J Epidemiol. 2006;35:1430–9. PubMed DOI
Victora CG, Bryce J, Fontaine O, Monasch R. Reducing deaths from diarrhoea through oral rehydration therapy. Bull World Health Organ. 2000;78:1246–55.
Ferreccio C, Prado V, Ojeda A, Cayyazo M, Abrego P, Guers L, et al. Epidemiologic patterns of acute diarrhea and endemic Shigella infections in children in a poor periurban setting in Santiago, Chile. Am J Epidemiol. 1991;134:614–27.
Kosek M, Bern C, Guerrant RL. The global burden of diarrhoeal disease, as estimated from studies published between 1992 and 2000. Bull World Health Organ. 2003;81:197–204.
Punyaratabandhu P, Vathanophas K, Varavithya W, Sangchai R, Athipanyakom S, Echeverria P, et al. Childhood diarrhoea in a low-income urban community in Bangkok: incidence, clinical features, and child caretaker's behaviours. J Diarrhoeal Dis Res. 1991;9:244–9.
Chen KC, Lin CH, Qiao QX, Zen NM, Zhen GK, Chen GL, et al. The epidemiology of diarrhoeal diseases in southeastern China. J Diarrhoeal Dis Res. 1991;9:94–9.
Rothman KJ, Greenland S. Meta-analysis. In: Modern epidemiology. 2nd ed. Philadelphia, Lippincott-Raven; 1998. p. 660–1.
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von Seidlein L, Kim DR, Ali M, Lee H, Wang X, Thiem VD, et al. A multicentre study of Shigella diarrhoea in six Asian countries: disease burden, clinical manifestations, and microbiology. PLoS Med. 2006;3:e353. PubMed DOI
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Bennish ML, Wojtyniak BJ. Mortality due to shigellosis: community and hospital data. Rev Infect Dis. 1991;13(Suppl 4):S245–51.
Guerin PJ, Brasher C, Baron E, Mic D, Grimont F, Ryan M, et al. Shigella dysenteriae serotype 1 in west Africa: intervention strategy for an outbreak in Sierra Leone. Lancet. 2003;362:705–6. PubMed DOI
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Caulfield LE, de Onis M, Blössner M, Black RE. Undernutrition as an underlying cause of child deaths associated with diarrhea, pneumonia, malaria, and measles. Am J Clin Nutr. 2004;80:193–8.
Tables
Table 1. Estimated annual number of diarrheal episodes in children 0–4 years of age, Asia, 1990–2009
Table 2. Shigella spp.–associated diarrhea in older children and adults, Asia, 1990–2009
Table 3. Case-fatality rates for hospitalized patients with Shigella infections, Asia, 1990–2009
Table 4. Estimated annual number of deaths and case-fatality rates for hospitalized persons with Shigella infection, Asia, 1990–2009

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Plasmid-mediated Quinolone Resistance among Non-Typhi Salmonella enterica Isolates, USA
01.nov.10
Emerging Infectious Diseases
Maria Sjölund-Karlsson, Rebecca Howie, Regan Rickert, Amy Krueger, Thu-Thuy Tran, Shaohua Zhao, Takiyah Ball, Jovita Haro, Gary Pecic, Kevin Joyce, Paula J. Fedorka-Cray, Jean M. Whichard, and Patrick F. McDermott
http://www.cdc.gov/eid/content/16/11/1789.htm
Abstract
We determined the prevalence of plasmid-mediated quinolone resistance mechanisms among non-Typhi Salmonella spp. isolated from humans, food animals, and retail meat in the United States in 2007. Six isolates collected from humans harbored aac(6′)Ib-cr or a qnr gene. Most prevalent was qnrS1. No animal or retail meat isolates harbored a plasmid-mediated mechanism.
Severe Salmonella enterica infections are commonly treated with fluoroquinolones (e.g., ciprofloxacin) (1). In the United States, the antimicrobial drug susceptibility of Salmonella spp. isolated from humans, food animals, and retail meats is systematically monitored by the National Antimicrobial Resistance Monitoring System (NARMS). This program is a collaborative effort of the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration Center for Veterinary Medicine (FDA-CVM) and the US Department of Agriculture (USDA). Antimicrobial susceptibility to fluoroquinolones among Salmonella spp. has been monitored since the program's inception in 1996.
Although fluoroquinolone resistance in Enterobacteriaceae is predominantly due to topoisomerase mutations, 3 plasmid-mediated mechanisms have been described that confer decreased susceptibility to ciprofloxacin: quinolone resistance proteins (Qnr), Aac(6′)-Ib-cr, and QepA efflux (2). The Qnr proteins protect the DNA-gyrase from quinolones, Aac(6′)-Ib-cr modifies quinolones with a piperazinyl group, and QepA is involved in active efflux (2). Because patients have experienced treatment failure when infected with Salmonella isolates that displayed decreased susceptibility to fluoroquinolones, plasmid-mediated mechanisms are clinically relevant (3).
A survey of 12,253 NARMS non-Typhi Salmonella (NTS) isolates collected from humans from 1996 through 2003 identified 10 (0.08%) qnr-positive isolates (4). A second survey of NARMS NTS collected from humans during 2004–2006 showed an increase in the proportion of isolates harboring plasmid-mediated quinolone resistance mechanisms. Among 6,057 isolates, 17 qnr-positive isolates and 1 aac(6′)-Ib-cr-positive isolate were detected, representing 0.3% of the NTS collected during that time (5).
The increase in plasmid-mediated quinolone resistance among NTS isolated from humans in the United States prompted further studies to determine continued presence among NTS of human origin and possible reservoirs of these mechanisms. In this study, we investigated plasmid-mediated quinolone resistance mechanisms among NARMS NTS isolated from humans, food animals, and retail meat in the United States in 2007.
The Study
In 2007, 54 NARMS-participating public health laboratories from all 50 states forwarded every 20th human isolate of NTS to CDC. Similarly, NTS isolated from retail meat (chicken breasts, ground turkey, ground beef, and pork chops) were submitted by 10 states that participated in CDC's Foodborne Diseases Active Surveillance Network (FoodNet) for analysis at FDA-CVM. NTS from food animals were obtained from carcass rinsates (chicken), carcass swab specimens (turkey, cattle, and swine), and ground products (chicken, turkey, and beef). Animal samples were collected by the Food Safety Inspection Service of the USDA from federally inspected slaughter and processing plants throughout the United States and sent to USDA facilities in Athens, Georgia, for further analysis.
At each agency, MICs were determined by broth microdilution (Sensititer; Trek Diagnostics, Westlake, OH, USA). Human, animal, and retail meat isolates of NTS that displayed decreased susceptibility to ciprofloxacin (MIC >0.25 mg/L) were included in our study. For each isolate, genomic DNA was prepared by lysing the bacteria at 95°C and collecting the supernatant after centrifugation. PCRs with previously described primers were used to screen isolates for qepA, aac(6′)-Ib-cr, and qnr genes (qnrA, B, C, D, S) (6–10). Positive controls were included for qepA (Escherichia coli TOP10 pAT851), qnrA (S. enterica serotype Montevideo AM28704), qnrB (S. enterica serotype Berta AM04589), qnrS (S. enterica serotype Bovismorbificans AM12888) and aac(6′)-Ib-cr (E. coli 36564). For isolates with positive results in the screening, amplicons were confirmed by direct sequencing by using a 3730 DNA Analyzer (Applied Biosystems, Foster City, CA, USA).
Among 2,165 isolates of NTS collected from humans in 2007, 51 (2.4%) displayed decreased susceptibility to ciprofloxacin. Among 320 NTS obtained from retail meat, 5 (1.6%) showed decreased susceptibility to ciprofloxacin, and among the 1,915 isolates obtained from animal sources, 5 (0.3%) showed such susceptibility. Six (11.8%) of the 51 human isolates carried a plasmid-mediated mechanism that affected quinolones; 5 isolates harbored a qnr gene, and 1 isolate contained the aac(6′)-Ib-cr gene (Table). None of the isolates harbored the qepA gene. Sequencing of the 5 qnr-positive isolates showed 3 qnrS and 2 qnrB variants among 4 serotypes (Beaudesert, Corvallis, Enteritidis, and Typhimurium) (Table). The aac(6′)-Ib-cr gene was found in an isolate of serotype Thompson, and sequencing confirmed the 2 point mutations (Trp102Arg and Asp179Tyr) characteristic of the ciprofloxacin-modifying variant. The MIC of ciprofloxacin among the qnr-positive isolates ranged from 0.25 mg/L to 0.5 mg/L, whereas the aac(6′)-Ib-cr–positive isolate displayed an MIC of 0.5 mg/L. All isolates from humans were susceptible to nalidixic acid (MIC range 8–16 mg/L). None of the isolates obtained from retail meat or those isolated from animal sources harbored plasmid-mediated mechanisms affecting quinolones. However, all retail meat and animal isolates with decreased susceptibility to ciprofloxacin were resistant to nalidixic acid (MIC >32 mg/L), which suggests the presence of topoisomerase mutations.
The 6 patients (3 male and 3 female) who were infected with a Qnr-producing or Aac(6′)-Ib-cr–producing Salmonella isolate had a median age of 18 (range 3–84 years). Three patients were available for interview. They reported gastrointestinal symptoms and had sought medical care for their condition. Two of the patients had received antimicrobial drug treatment (ciprofloxacin and cefdinir, respectively); none of the patients developed an invasive infection. Two patients reported a history of international travel to Mexico and Thailand, respectively.
Conclusions
Six (0.3%) NARMS NTS collected from humans in 2007 harbored a plasmid-mediated quinolone resistance mechanism, the same prevalence as in 2004–2006 (5). None of the isolates collected from animal and retail meat by the USDA and FDA in 2007 harbored these mechanisms. Among the human isolates, qnr genes predominated and qnrS1 was most prevalent. This gene has previously been described among NARMS human NTS and was first detected in an isolate of serotype Bovismorbificans collected in 2000 (4). The gene was later reported in 11 isolates (serotypes Corvallis, Enteritidis, Montevideo, Saintpaul, and Typhimurium) collected by NARMS during 2004–2006 (5).
That qnr genes could only be detected among Salmonella isolates obtained from humans warrants further exploration. One factor that could influence the number of Qnr-producing Salmonella isolates among humans in the United States is the extent of travel-associated infections. Two patients in this study had a history of international travel before illness onset. Another factor that could lead to the development of Qnr-producing Salmonella isolates is the in vivo transfer of resistance from other qnr-bearing Enterobacteriaceae.
Our study does not suggest that food animals and meat in the United States are major sources of Salmonella isolates that harbor plasmid-mediated quinolone resistance mechanisms. However, animals and food have been described as reservoirs for these mechanisms elsewhere. A high prevalence of Enterobacteriaceae with qnr and aac(6′)-Ib-cr have been reported among companion and food animals in the People's Republic of China and qnr-positive Salmonella isolates have been found in poultry in Europe (11,12). Thus, other food and meat sources, not investigated in the current study, may serve as reservoirs for these mechanisms.
Fluoroquinolone resistance among isolates of NTS has important public health implications because ciprofloxacin is commonly used to treat invasive infections of Salmonella spp. in adults. Although plasmid-mediated quinolone resistance mechanisms do not, by themselves, confer clinical resistance to ciprofloxacin, they may promote the selection of mutations that do (13). In addition, studies have shown that patients infected with isolates that display low-level fluoroquinolone resistance may respond poorly to treatment, prompting a reconsideration of MIC breakpoints in clinical medicine (3,14). To avoid further dissemination of plasmid-mediated quinolone resistance among Salmonella and other Enterobacteriaceae isolates in the United States, prudent use of antimicrobial agents in both human and veterinary medicine will be crucial. Continued surveillance for resistant bacteria among human, animal, and food sources remains critical.
Acknowledgments
We thank the NARMS participating public health laboratories, the Retail Foods Survey Working Group, and the Food Safety Inspection Service laboratories for submitting the isolates. We also thank the California and Virginia Divisions of Public Health for providing patient interviews; Kathryn Lupoli for serotype confirmations; and the National Veterinary Services Laboratories, Ames, Iowa, for serotyping the animal isolates.
This work was supported by an interagency agreement between CDC, USDA, and FDA-CVM.
Dr Sjölund-Karlsson is a research microbiologist with the National Antimicrobial Resistance Surveillance Team at CDC, Atlanta, Georgia. Her research interests include the genetic characterization of antimicrobial drug–resistant bacteria and the biological cost of antimicrobial drug resistance.
References
Guerrant RL, Van Gilder T, Steiner TS, Thielman NM, Slutsker L, Tauxe RV, et al. Practice guidelines for the management of infectious diarrhea. Clin Infect Dis. 2001;32:331–51. PubMed DOI
Robicsek A, Jacoby GA, Hooper DC. The worldwide emergence of plasmid-mediated quinolone resistance. Lancet Infect Dis. 2006;6:629–40. PubMed DOI
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Park CH, Robicsek A, Jacoby GA, Sahm D, Hooper DC. Prevalence in the United States of aac(6′)-Ib-cr encoding a ciprofloxacin-modifying enzyme. Antimicrob Agents Chemother. 2006;50:3953–5. PubMed DOI
Cattoir V, Weill FX, Poirel L, Fabre L, Soussy CJ, Nordmann P. Prevalence of qnr genes in Salmonella in France. J Antimicrob Chemother. 2007;59:751–4. PubMed DOI
Cavaco LM, Hasman H, Xia S, Aarestrup FM. qnrD, a novel gene conferring transferable quinolone resistance in Salmonella enterica serovar Kentucky and Bovismorbificans strains of human origin. Antimicrob Agents Chemother. 2009;53:603–8. PubMed DOI
Wang M, Guo Q, Xu X, Wang X, Ye X, Wu S, et al. New plasmid-mediated quinolone resistance gene, qnrC, found in a clinical isolate of Proteus mirabilis. Antimicrob Agents Chemother. 2009;53:1892–7. PubMed DOI
Ma J, Zeng Z, Chen Z, Xu X, Wang X, Deng Y, et al. High prevalence of plasmid-mediated quinolone resistance determinants qnr, aac(6')-Ib-cr, and qepA among ceftiofur-resistant Enterobacteriaceae isolates from companion and food-producing animals. Antimicrob Agents Chemother. 2009;53:519–24. PubMed DOI
Veldman K, van Pelt W, Mevius D. First report of qnr genes in Salmonella in The Netherlands. J Antimicrob Chemother. 2008;61:452–3. PubMed DOI
Martinez-Martinez L, Pascual A, Jacoby GA. Quinolone resistance from a transferable plasmid. Lancet. 1998;351:797–9. PubMed DOI
Crump JA, Barrett TJ, Nelson JT, Angulo FJ. Reevaluating fluoroquinolone breakpoints for Salmonella enterica serotype Typhi and for non-Typhi salmonellae. Clin Infect Dis. 2003;37:75–81. PubMed DOI
Table
Table. Characteristics of non-Typhi Salmonella enterica isolates harboring qnr or the aac(6′)-Ib-cr gene, collected through NARMS, 2007

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