Showing posts with label 2016. Show all posts
Showing posts with label 2016. Show all posts
Friday, December 23, 2016
Travel Associated Rabies in Pets and Residual Rabies Risk Western Europe Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Travel Associated Rabies in Pets and Residual Rabies Risk Western Europe Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Travel-Associated Rabies in Pets and Residual Rabies Risk, Western Europe - Volume 22, Number 7—July 2016 - Emerging Infectious Disease journal - CDC
Volume 22, Number 7—July 2016
Dispatch
Travel-Associated Rabies in Pets and Residual Rabies Risk, Western Europe
On This Page
- The Study
- Conclusions
- Suggested Citation
Florence Ribadeau-Dumas
, Florence Cliquet, Philippe Gautret, Emmanuelle Robardet, Claude Le Pen, and Hervé Bourhy
, Florence Cliquet, Philippe Gautret, Emmanuelle Robardet, Claude Le Pen, and Hervé BourhySuggested citation for this article
Abstract
In 2015, countries in western Europe were declared free of rabies in nonflying mammals. Surveillance data for 2001–2013 indicate that risk for residual rabies is not 0 because of pet importation from countries with enzootic rabies. However, the risk is so low (7.52 × 10?10) that it probably can be considered negligible.
Although western and northern Europe and most countries in central Europe have eliminated rabies in nonflying animals (https://zenodo.org/record/49670#) (1,2), alerts are regularly issued because of importation of rabid pets. Policy makers recommend postexposure prophylaxis (PEP) after exposure in Western Europe to bats or pet bites in areas with rabies alerts. However, the policy after exposure to these pets is unclear (https://zenodo.org/record/49670#).
Residual risk for rabies in pets in Western Europe is defined as no risk (no PEP necessary) or low risk (PEP recommended after exposure), depending on recommendations (e.g., no risk according to Public Health England and low risk according to the World Health Organization) (3). Thus, evaluation of residual rabies risk in western Europe caused by pet movement is needed. We evaluated residual rabies risk caused by pet movement in western Europe.
The Study
We calculated the risk that a given pet in western Europe is contagious for rabies on a given day by the equation
We describe factors associated with rabid pets (https://zenodo.org/record/49670#) and define pet transport as any noncommercial movement of a live cat, dog, or ferret and its owner or an authorized person across an administrative border.
During 2001–2013, a total of 21 animal rabies cases attributed to pets from rabies-enzootic countries were reported in western Europe (https://zenodo.org/record/49670#), which represented 1.6 pets/year and 23 days/year of potential contagiousness. Fifteen dogs and 1 kitten originated from rabies-endemic countries outside western Europe. Five dogs raised in western Europe acquired rabies outside this region. One dog subsequently infected 2 indigenous dogs in France (4). All pet owners were identified. All owners except 1 (a Spanish man living in a van) were official residents of western Europe. Circumstances that led to pet examination and rabies diagnosis were clinical suspicion (14 pets), bitten humans (3 pets), border quarantine (2 pets), and retrospective data (2 pets with indigenous secondary cases during the alert in France in 2008).
Average contagious period was 16 days/pet: 14 days in western Europe (8 days without signs of rabies and 6 days with signs of rabies) and 2 days before arriving in western Europe. For 1 dog, signs of rabies appeared before the animal entered western Europe. For each rabid animal, an average of 34 (range 0–187) persons and other animals received PEPs. The maximum value of this range corresponds to an alert in France in 2004. After this alert, 1,200 animals were tested and 759 were observed for 1 year. Human and pet vaccinations led to vaccine shortages that required importing of vaccines not authorized for use in France (5).
We identified animal origin and mode of entry into western Europe (Table 1). Most rabies cases originated in Morocco and were recorded in France. Three cases were imported from eastern Europe to Germany, 1 from The Gambia to France, and 1 from Sri Lanka to the United Kingdom. Customs officials could not identify any of 11 cases in animals transported mainly by road (e.g., after a ferry trip from Morocco to Spain, Portugal, or France). Seven pets were transported through other countries in western Europe before arriving in the country of diagnosis (https://zenodo.org/record/49670#). Six puppies and 1 kitten were transported by air, of which only 2 were identified by customs officials (in the United Kingdom and Germany).
Figure. European Union (EU) regulations (no. 998/2003 and no. 576/2013, http://eur-lex.europa.eu/legal-content/EN/TXT/?uri=CELEX:32013R0576) on movement of cats, dogs, and ferrets, 2003–2013. Before 2003, national rules applied (e.g., animal checked at destinations, rabies vaccination,...
Of 19 transported rabid pets, 8 (42%) had no rabies vaccination, pet passport, or health certificate. Only 6 were vaccinated (0/2 infected in France, 3/3 imported but raised in western Europe, 3/7 imported by air, and 0/8 imported by road). Most vaccinated pets did not comply with recommended age for vaccination (>12 weeks of age) or time between vaccination, serologic analysis, and transport. No reports mentioned valid rabies serologic analysis included in European Pet Movement Policy (Figure) for unlisted third countries (e.g., Morocco, the Gambia, Sri Lanka, or Azerbaijan) (6). Using data for 2001–2013, we calculated that, for contact on a given day with a pet in western Europe, the probability of the pet being contagious for rabies attributed to pet transport was 7.52 × 10?10 (Table 2).
We observed a significant correlation between number of contagious days for dogs in a country and number of tourists traveling from this country to Morocco (? = 0.73, p = 0.017). We found no correlation with other variables tested (total dog population, dog population density, number of dogs per inhabitant).
Conclusions
Risk for indigenous rabies has decreased in western Europe. During 2001–2013, because of appropriate control of imported rabid pets, only 4 indigenous cases of human rabies were reported (3 in recipients of organs from a donor infected in India and 1 from a rabid bat in Scotland) (https://zenodo.org/record/49670#). Since 2011, no indigenous rabies cases have been reported in terrestrial mammals in western Europe. Because of increased travel (7), rabies imported by trips to rabies-enzootic countries has increased, and travel became the main source of rabies in humans (1.46 patients/year) (8) and pets (1.6 rabid pets/year) in 2001–2013. However, because of improved surveillance, although the number of imported rabies cases increased, the number of secondary cases decreased (https://zenodo.org/record/49670#).
Illegal importation of rabid animals is not limited to western Europe (9) or dogs and cats (10). This finding highlights the need for a global approach for regulation of animal movement worldwide and strengthening real-time reporting for animal and human rabies.
Risk for dog rabies being reintroduced into the European Union from Morocco was estimated as 0.21 cases/year (11). However, we estimate that 1.1 pets/year are entering western Europe after being infected in Morocco. Morocco has become the main source of pet rabies in western Europe, often through Ceuta and Melilla (Spanish enclaves in northern Morocco). Because no prophylaxis or specific vaccinations are needed for travel to northern Africa, few travelers seek pretravel advice and most have little knowledge of pet rabies (12,13).
Lack of awareness also increases importation of human rabies. Despite an efficient policy for preventing entry of rabid pets, the United Kingdom reported the highest number of patients with imported rabies during the study period (https://zenodo.org/record/49670#). Patients returning to this country did not believe that a correct PEP was needed after exposure abroad. None of the transported rabid pets fully satisfied European Pet Movement Policy, which raised questions about how to improve the current regulation application. Increasing international travel, expansion of the Schengen area (26 countries in Europe that have a common visa policy) into rabies-enzootic countries in eastern Europe, and development of internet animal trade (source of illegal importation) (14) are new challenges for ensuring compliance.
Because bat rabies is more difficult to control than dog rabies, and some developing countries still have difficulties controlling rabies, eradication of rabies is not a realistic objective. Awareness should be increased, and current regulations for pet transport should be applied to reduce rabies importation and ensure that risk in western Europe remains low.
To avoid unnecessary and costly PEP and optimize resource allocation, it should be clearly stated which WHO recommendations, Public Health England recommendations, or other practices most relevant after pet exposure should be applied. Low risks (<10-–6) are usually considered acceptable or essentially 0 (3,15). The risk of a fatal car crash while traveling to PEP consultations was higher than the risk of rabies after exposure to a pet in France in 2001–2011 (3). The most pertinent policy in areas at low risk for rabies is probably that of the United Kingdom (i.e., no PEP outside alert areas that do not have asymptomatic animals or exposure to bats) (https://zenodo.org/record/49670#).
Dr. Ribadeau-Dumas is a physician and doctoral candidate in economics at Paris Dauphine University, Paris, France. Her research interests are infectious diseases, public health, health economics, and rabies.
Acknowledgment
We thank Karim Boubaker, Bernard Brochier, Laurent Dacheux, Juan Emilio Echavarria Mayo, Franco Mutinelli, Jacques-André Romand, and Reto Zanoni for providing information on rabies cases; Sylvie Tourdiat for providing assistance with formatting tables and the figure; and Delphine Libby-Claybrough for providing assistance with English editing.
References
- Cliquet F, Picard-Meyer E, Robardet E. Rabies in Europe: what are the risks? Expert Rev Anti Infect Ther. 2014;12:905–8. DOIPubMed
- Freuling CM, Hampson K, Selhorst T, Schröder R, Meslin FX, Mettenleiter TC, The elimination of fox rabies from Europe: determinants of success and lessons for the future. Philos Trans R Soc Lond B Biol Sci. 2013;368:20120142. DOIPubMed
- Ribadeau Dumas F, N’Diaye DS, Paireau J, Gautret P, Bourhy H, Le Pen C, Cost-effectiveness of rabies post-exposure prophylaxis in the context of very low rabies risk: a decision-tree model based on the experience of France. Vaccine. 2015;33:2367–78. DOIPubMed
- French multidisciplinary investigation team. Identification of a rabid dog in France illegally introduced from Morocco. Euro Surveill. 2008;13:pii: 8066.PubMed
- Servas V, Mailles A, Neau D, Castor C, Manetti A, Fouquet E, An imported case of canine rabies in Aquitaine: investigation and management of the contacts at risk, August 2004–March 2005. Euro Surveill. 2005;10:222–5.PubMed
- Regulation (EC) no. 998/2003 of the European parliament and of the council, 2003 [cited 2015 Apr16]. http://eur-lex.europa.eu/legal-content/EN/TXT/?uri=CELEX:32013R0576
- World Tourism Organization. UNWTO annual report 2014. Madrid: UNWTO 2015 [cited 2015 Jun 10].http://www2.unwto.org/annualreport2014
- Carrara P, Parola P, Brouqui P, Gautret P. Imported human rabies cases worldwide, 1990–2012. PLoS Negl Trop Dis. 2013;7:e2209. DOIPubMed
- Lankau EW, Tack DM, Marano N. Crossing borders: one world, global health. Clin Infect Dis. 2012;54:v–vi. DOIPubMed
- Metlin AE, Holopainen R, Tuura S, Ek-Kommonen C, Huovilainen A. Imported case of equine rabies in Finland: clinical course of the disease and the antigenic and genetic characterization of the virus. J Equine Vet Sci. 2006;26:584–7 .DOI
- Napp S, Casas M, Moset S, Paramio JL, Casal J. Quantitative risk assessment model of canine rabies introduction: application to the risk to the European Union from Morocco. Epidemiol Infect. 2010;138:1569–80. DOIPubMed
- Altmann M, Parola P, Delmont J, Gautret P. Knowledge, attitudes, and practices of French travelers from Marseille regarding rabies risk and prevention. J Travel Med. 2009;16:107–11. DOIPubMed
- Gautret P, Ribadeau-Dumas F, Parola P, Brouqui P, Bou
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Monday, December 19, 2016
Tropheryma whipplei as a Cause of Epidemic Fever Senegal 2010–2012 Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Tropheryma whipplei as a Cause of Epidemic Fever Senegal 2010–2012 Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Tropheryma whipplei as a Cause of Epidemic Fever, Senegal, 2010–2012 - Volume 22, Number 7—July 2016 - Emerging Infectious Disease journal - CDC
Volume 22, Number 7—July 2016
Research
Tropheryma whipplei as a Cause of Epidemic Fever, Senegal, 2010–2012
On This Page
- Materials and Methods
- Results
- Discussion
- Suggested Citation
Hubert Bassene, Oleg Mediannikov, Cristina Socolovschi, Pavel Ratmanov, Alpha K. Keita, Cheikh Sokhna, Didier Raoult, and Florence Fenollar
Suggested citation for this article
Abstract
The bacterium Tropheryma whipplei, which causes Whipple disease in humans, is commonly detected in the feces of persons in Africa. It is also associated with acute infections. We investigated the role of T. whippleiin febrile patients from 2 rural villages in Senegal. During June 2010–March 2012, we collected whole-blood finger-prick samples from 786 febrile and 385 healthy villagers. T. whipplei was detected in blood specimens from 36 (4.6%) of the 786 febrile patients and in 1 (0.25%) of the 385 apparently healthy persons. Of the 37T. whipplei cases, 26 (70.2%) were detected in August 2010. Familial cases and a potential new genotype were observed. The patients’ symptoms were mainly headache (68.9%) and cough (36.1%). Our findings suggest that T. whipplei is a cause of epidemic fever in Senegal.
Determining the etiologic causes of febrile illness in tropical settings provides public health and local community benefits. In the context of a decline in malaria cases in many parts of sub-Saharan Africa, the few studies that have been conducted in recent years to analyze the burden of bacterial infections used traditional blood cultures and identified typhoid fever and Streptococcus pneumoniae as the leading documented causes of nonmalarial bloodstream infections (1–3). However, this method does not enable the identification of intracellular organisms, and most causes of fever remain unknown. In 2008, we initiated a study of the etiologies of fevers of unknown origin in Africa, particularly in Senegal. Our preliminary studies showed the presence of previously known pathogenic microorganisms, such as Borrelia crocidurae, Rickettsia felis, R. conorii, and Coxiella burnetii, and the unexpected presence of Tropheryma whipplei (4–9).
T. whipplei was first considered to be an uncommon bacterium that causes Whipple disease, a rare chronic disease (10). However, T. whipplei is in fact a common bacterium associated with various conditions, such as acute infections (pneumonia and gastroenteritis) and chronic infections (classic Whipple disease and other infections without digestive involvement, including endocarditis and encephalitis) (10–19). T. whipplei can also be carried in human feces and, less commonly, in the saliva (20–23); carriage prevalence varies by the age and exposure of the population and by geographic area (21–30).
T. whipplei is highly prevalent in rural Senegal, where carriage rates reach 75% among children <2 years of age, and overall seroprevalence is 72% (21–26). In our preliminary study in Senegal, which was conducted in 2 villages (Dielmo and Ndiop) during December 2008–July 2009, we detected T. whippleibacteremia in 6.4% of the analyzed specimens (8). Bacteremia was significantly associated with cough, but no link to feces carriage was observed (8). However, our study had several limitations, such as a small number of febrile patients, no local control group of afebrile persons, and a short study period. In this same area, we recently showed that humans comprise the only source of T. whipplei among the populations in whom the bacterium is highly prevalent. Moreover, our findings showed that limited access to toilets and exposure to human feces was associated with the high prevalence of T. whipplei, suggesting that these conditions may facilitate fecal–oral transmission of the bacterium (31). To better characterize T. whipplei bacteremia, we extended our analysis, beginning in 2010, in this same area of rural Senegal to include the collection of >1,000 blood samples from healthy persons and ambulatory patients with acute fever.
Materials and Methods
We conducted the study during June 2010–March 2012 in Senegal’s rural Sine-Saloum area, a dry sahelian ecosystem with 2 typical seasons: dry (November–May) and rainy (June–October). We obtained written consent for every person included in the study. The National Ethics Committee of Senegal approved the study.
Participants
Study participants included 786 febrile patients at the healthcare center for the villages of Dielmo and Ndiop; 78% of the patients were <15 years of age, and the sex ratio was 1:1. For all patients with fever (defined as axillary temperature of >37.5°C), we conducted a medical examination, completed a questionnaire, and collected a whole-blood finger-prick sample (200-?L [4 drops]) (8). In parallel, we collected blood samples from a control group of 385 healthy, afebrile villagers; 62.5% of these study participants were <15 years of age, and the sex ratio was 1:1.
Molecular Analyses
DNA Extraction
For DNA extraction, we used a BioRobot EZ1 Workstation (QIAGEN, Courtaboeuf, France) according to the manufacturer’s instructions. Extraction was performed in Senegal, and specific quantitative real-time PCR (qPCR) was performed in France.
Specific qPCR
We used a 7900HT-thermocycler (Applied Biosystems, Foster City, CA, USA) with the QuantiTect-Probe PCR Kit (QIAGEN) to perform qPCR. First, we analyzed specimens for T. whipplei by using the primer pair Twhi3F (5?-TTG TGT ATT TGG TAT TAG ATG AAA CAG-3?)/Twhi3R (5?-CCC TAC AAT ATG AAA CAG CCT TTG-3?) and the specific Twhi3 probe (6-FAM-GGG ATA GAG CAG GAG GTG TCT GTC TGG-TAMRA). For specimens with positive results, we ran a second, confirmatory qPCR with the Twhi2F (5?-TGA GGA TGT ATC TGT GTA TGG GAC A-3?)/Twhi2R (5?-TCC TGT TAC AAG CAG TAC AAA ACA AA-3?) primer pair and the specific Twhi2 probe (6-FAM-GAG AGA TGG GGT GCA GGA CAG GG-TAMRA) (8,21). To validate the assays, we included positive (T. whipplei) and negative (PCR mix) controls in each run, as previously reported (8,21).
We considered samples to be T. whipplei–positive if qPCR results for the 2 specific genes were positive at a log-based fluorescence cycle threshold (Ct) of <38. We used qPCR for the ?-actin housekeeping gene, as previously described (7), to check the quality of DNA handling and blood specimen extraction; only positive samples were considered reliable.
Genotyping
We performed genotyping of T. whipplei as previously described (32). We attempted to amplify and sequence each of 4 multispacer sequences (TW133, ProS, SecA, and Pro184) from positive specimens. When sequences were obtained, we compared them with those available in the GenBank database and our internal laboratory database to determine their corresponding genotype.
Statistical Analyses
We performed statistical analyses by using Epi Info 6 software (http://www.cdc.gov/epiinfo/index.html); results with p<0.05 were considered statistically significant. The corrected ?2 test or the Fisher exact test was used where indicated.
Results
Prevalence of T. whipplei Bacteremia
A total of 786 febrile patients and 385 healthy controls were included in the study, among whom 36 (4.6%) and 1 (0.25%), respectively, were positive for T. whipplei DNA (p<0.00007). The positive control participant was a 13-year-old boy who had low concentrations of T. whipplei DNA (Ct of 36.85 and 37.99). The Ct for febrile patients ranged from 26.10 to 36.41 (mean ISD 33.40 ± 2.53).
Age Distribution
The prevalence of T. whipplei bacteremia was 4% (3/75) for febrile patients <12 months of age, 4.8% (12/250) for those 1–3 years of age, 4.2% (5/119) for those 4–6 years of age, 5.4% (9/167) for those 7–15 years of age, 2.7% (2/75) for those 16–29 years of age, and 5.2% (5/97) for those >30 years of age. Age data were not available for 3 patients. No significant differences in age distribution were observed.
Clinical Manifestations
Clinical data were available for 786 febrile patients (Table 1). The main symptoms in the 36 T. whipplei–positive febrile patients were headache (23 [68.9%]), cough (13 [36.1%]), rhinorrhea (8 [22.2%]), nausea (5 [13.9%]), vomiting (4 [11.1%]), and diarrhea (3 [8.3%]). No significant clinical differences were observed by Ct level.
Seasonality
Figure. Monthly prevalence ofTropheryma whippleibacteremia in Dielmo and Ndiop, Senegal, June 2010–March 2012. These 2 rural villages are located in the Sine-Saloum area, a dry sahelian ecosystem.
All 36 T. whipplei cases detected among the 786 febrile patients were in the 466 patients tested during the June–October rainy season; no cases were detected among the 320 febrile patients sampled during the November–May dry season (p = 0.0000001). Moreover, 33 (92%) of these 36 cases were diagnosed during the 2010 rainy season, and the other 3 were diagnosed during August 2011 (2 cases) and October 2011 (1 case) (Figure). The highest prevalence of T. whipplei bacteremia cases was detected during August, when 28 (30%) of 93 febrile patients were found to be positive (19 [28%] of 73 patients in Dielmo and 9 [45%] of 20 patients in Ndiop). In fact, the data were affected by the high prevalence of cases observed in August 2010, which seemed to be indicative of an outbreak.
In July 2010, T. whipplei infection was detected in 2 febrile patients, an 18-year-old boy in Dielmo (case detected July 24) and a 15-year-old girl in Ndiop (case detected July 27). In August 2010, a total of 29 febrile patients from Dielmo were tested; 17 (58.5%) of the 29 patients had samples (18 total samples) positive for T. whippleibacteremia. During the same month in Ndiop, 9 (69%) of 13 febrile patients had positive samples. In September 2010, 2 patients were positive in Dielmo and 1 in Ndiop, and in October, 2 patients were positive in Dielmo and none in Ndiop. For almost 1 year, all specimens from febrile patients were negative for T. whipplei. Then, in August 2011, only 2 patients were positive in Dielmo, and in October 2011, only 1 patient was positive in Ndiop.
Treatment and Follow-Up
Data about antimicrobial drug therapy was available for 33 patients, 23 of whom benefited from treatment with amoxicillin (18 patients), metronidazole (3 patients), or cotrimoxazole (2 patients). In Dielmo, 24 specimens from 23 patients were positive for T. whipplei; 1 patient was sampled twice 15 days apart, and both specimens were positive. For 17 patients, blood specimens were also sampled during other febrile episodes. Nine specimens from 5 patients were sampled from 15 days to 13 months before the positive sample was detected, and 43 specimens from 17 patients were sampled from 3 weeks to 16 months after the positive sample was detected; all of these samples were negative. Moreover, our previously published data (8) included test results for a 4-year-old boy who was diagnosed with T. whipplei bacteremia in January 2009 (19 months before August 2010). Four other blood specimens from this patient were tested 1 month before (1 sample) or 4, 11, and 15 months after (3 samples) the positive specimen was detected, and all were negative for T. whipplei.
In Ndiop, 12 specimens from 12 patients were positive. For 8 of these patients, blood specimens were sampled during other febrile episodes. The specimen for 1 patient was sampled 1 month before the positive sample, and 9 specimens from 6 patients were sampled from 7 weeks to 18 months after the positive samples; all of these specimens were negative. No data were available for these patients about antibody response against T. whipplei.
Genotyping
Because of the lack of specimens available for genotyping and the low sensitivity of genotyping, we could obtain multispacer sequences for only 8 patients at the time of the 2010 peak in T. whipplei bacteremia cases (Table 2). The T. whipplei genotype corresponds to the concatenation of the 4 spacers (TW133-ProS-SecA-Pro184); however, TW133 sequencing was not successful, so the corresponding spacer was not available (NA) for any of the patients. ProS sequence was obtained for 5 patients, SecA for 6 patients, and Pro184 for all patients. For 4 patients, 3 spacers were available, enabling the detection of the same multispacer sequence combination (NA-7-2-1) for the 4 patients. For another 4 patients, 2 spacers were available, enabling the detection of the NA-7-NA-1 combination for 2 of the patients and the NA-NA-2-1 combination for the other 2 patients. None of the potential combinations has previously been sequenced in Senegal. Moreover, the NA-7-2-1 combination has also not previously been detected in any other area of the world and is thus a new genotype. Overall, our data suggest that the same genotype was detected in Dielmo and Ndiop during the summer of 2010. However, T. whipplei genotyping was performed (sometimes only partially) for only 8 of 36 patients, so we can only suspect, but not confirm, that an epidemic clone was present and that an outbreak was ongoing at that time.
Affected Households
In Dielmo during the peak of the August 2010 outbreak, multiple persons in several households were positive for T. whipplei bacteremia: 4 of 6 persons in household no. 19, 3 of 4 persons in household no. 39, 2 of 2 persons in household no. 9, and 2 of 3 persons in household no. 14. In Ndiop, 2 of 2 persons in household no. 3 and 2 of 3 persons in household no. 8 were positive for T. whipplei bacteremia. Of note, during this time, the family in household no. 39 had a furnace in which they baked bread that they marketed locally. In December 2010, most of the family left the village and the furnace was shut down; no additional T. whipplei bacteremia cases were subsequently observed.
Discussion
We report the detection of T. whipplei DNA in the blood of patients in Dielmo and Ndiop, Senegal. The validity of our data is based on strict experimental procedures and controls, including rigorous positive and negative controls, used to validate test results. In addition, we confirmed each positive PCR result by the successful amplification of an additional specific DNA sequence, and we performed T. whipplei genotyping on several specimens. We also showed that the presence of T. whipplei in blood is significantly linked to the presence of fever; T. whipplei DNA was detected (at a low level) in the blood of only 1 afebrile person in the study area. Moreover, we included a control group of afebrile persons from the same area, thereby reinforcing the validity of our data. Indeed, several well-known pathogens have been detected in recently analyzed specimens from healthy persons. For example, Plasmodium falciparum has been detected in 32% of blood specimens from healthy, afebrile persons in Senegal (33); respiratory viruses, including influenza virus, have been detected in 12% of nasopharyngeal samples from symptom-free Hajj pilgrims (34); and S. pneumoniae has been detected in 6.3% of blood specimens from afebrile children in Tanzania (35). Thus, because of the significantly higher prevalence of T. whipplei among febrile patients compared with healthy controls, we suspect that this microorganism is a pathogenic agent.
The overall prevalence of T. whipplei bacteremia is 4.6%. However, in August 2010, we observed a peak in T. whipplei bacteremia cases in Dielmo and Ndiop, where T. whipplei was involved in more than half of the observed cases of fever. This peak corresponds to a short outbreak of T. whipplei bacteremia with 1 potential genotype. A similar new genotype was observed for the patients from Dielmo and Ndiop for whom genotyping was available at the time of the outbreak. To date, 35 different T. whipplei genotypes have been detected in Senegal, but only 1 common genotype has been detected in Dielmo and Ndiop, even though the villages are 5 km apart (25). All of the other genotypes detected in the Sine-Saloum area were specific to each village, including the 2 that were more prevalent: genotype 52 was detected in 54% of feces samples in Dielmo, and genotype 49 was detected in 28% of feces samples from Ndiop (25).
Several familial cases also occurred during this outbreak. The family in household no. 39 in Dielmo was 1 of the most affected families: 3 of 4 persons living in the home had fever and T. whipplei bacteremia. Genotyping was available for 2 of these patients, both of whom exhibited the same potential genotype. The family in household no. 39 was involved in the management of a traditional oven for preparing bread, which was thoroughly cooked and sold directly to other residents. Since the departure of the baker and his family, no other outbreaks have been observed, and the prevalence of T. whipplei bacteremia has dramatically decreased. Thus, this family may have contributed to spread of the outbreak on a daily basis in Dielmo and possibly on a weekly basis at traditional markets, which served as the main contact between villagers from Dielmo and Ndiop. Also of note, no toilet facilities were present in household no. 39, and a link between a lack of toilet facilities and the high detection of T. whipplei, mainly in feces, has previously been reported (31). Thus, we hypothesize that T. whipplei was transmitted to customers who bought bread contaminated with infectious feces (31). Overall, all of our data confirm human-to-human transmission of the bacterium (22,23,26,31).
One of the main symptoms among febrile patients with T. whipplei bacteremia is cough (36.1%). In our preliminary study of T. whipplei bacteremia, cough was also the main manifestation observed (36). Thus, T. whipplei could be involved in respiratory infections (13,14,36,37). However, the presence of cough in ?36% of febrile patients who were either T. whipplei–positive or –negative may also suggest that this symptom was poorly specific.
Of note, a 4-year-old patient had 2 febrile episodes associated with T. whipplei bacteremia 18 months apart (8); however, it was not possible to make a distinction between relapse and reinfection beca
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Porcine Bocavirus Infection Associated with Encephalomyelitis in a Pig Germany1 Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Porcine Bocavirus Infection Associated with Encephalomyelitis in a Pig Germany1 Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Porcine Bocavirus Infection Associated with Encephalomyelitis in a Pig, Germany1 - Volume 22, Number 7—July 2016 - Emerging Infectious Disease journal - CDC
Volume 22, Number 7—July 2016
Letter
Porcine Bocavirus Infection Associated with Encephalomyelitis in a Pig, Germany1
On This Page
- Letter
- Suggested Citation
Suggested citation for this article
To the Editor: In 2013, a 6-week-old female piglet kept in a flatdeck cage had coughing, growth retardation, and diarrhea and was taken to a local veterinarian in Hannover, Germany; the piglet was euthanized. After necropsy at the University of Veterinary Medicine in Hannover, histologic investigation found interstitial pneumonia; a mild, multifocal, lymphohistiocytic panencephalitis that affected the cerebrum and cerebellum, including brain stem and medulla oblongata; and a mild, multifocal, lymphohistiocytic panmyelitis. Results from screening for typical neurotropic viruses (classical swine fever virus, suid herpesvirus 1, rabies virus, teschovirus, porcine enterovirus 8, 9, and 10) were negative; Mycoplasma hyorhinis was detected by multiplex PCR (Institute of Virology, University of Veterinary Medicine Hannover) within the lung and pulmonary lymph nodes. Cerebral tissue from the pig was processed for viral metagenomics by random RNA and DNA virus screening and next-generation sequencing (NGS) with the 454 sequencing platform (GS Junior; Roche, Basel, Switzerland), as described (1), and 21,359 reads were obtained. Analysis by using blastn and blastx (2) showed 10 reads had >97% nt identity with porcine bocavirus (PBoV) KU14. No other viral sequences were detected.
By using primers based on sequence data of the PBoV, partially overlapping PCR amplicons were obtained to confirm and extend the NGS data of the isolate, which was named PBoV S1142/13 (1; GenBank accession no. KU311698). A total of 2,176 nt of PBoV S1142/13 were obtained, consisting of the partial nucleoprotein (NP) 1 and the nearly complete viral protein (VP) 1 gene. By using MAFFT version 7 (http://mafft.cbrc.jp/alignment/server/), we aligned the nearly complete VP1 gene of PBoV S1142/13 with various closely related members of the genusBocaparvovirus and built a maximum-likelihood tree by using the general time reversible plus invariable sites plus gamma distribution method, as determined by jModelTest 2.0 (3) and default parameters in MEGA6.06 (4). Results confirmed that PBoV S1142/13 was most closely related to PBoV KU14 (Figure, panel A). The partial genome of PBoV S1142/13 differed at 8 nt positions from PBoV KU14, resulting in 99.6% nt identity. Of these nucleotide differences, 4 resulted in an amino acid difference, including position 2733 (T?C on the basis of PBoV KU14 as a reference genome), which is part of the NP1 stopcodon of PBoV KU14. These results indicate that the stopcodon was located 39 nt farther downstream than for PBoV KU14. The other 3 aa differences were present in the VP1 protein; each of these differences was within the same group of amino acids as those detected in PBoV KU14.
For further substantiation of a potential cause-effect relationship of histologic (Figure, panel B) and NGS results, we performed fluorescent in situ hybridization (FISH) on formalin-fixed, paraffin-embedded central nervous system (CNS) sections of the diseased animal and of a control pig with no CNS lesions. We used an RNA probe specific for the obtained NP1 and VP1 sequences covering 1,153 nt (Affymetrix, Santa Clara, CA, USA) according to the manufacturer’s protocol, with minor variations (ViewRNA ISH Tissue 1-Plex Assay Kit and ViewRNA Chromogenic Signal Amplification Kit, Affymetrix). A probe specific for porcine ubiquitin (Sus scrofa ubiquitin C; GenBank accession no. XM_005657305; nt 2–890) served as a positive control.
Figure. Phylogenetic analysis and staining of porcine bocavirus (PBoV) from the spinal cord of a diseased pig, Hannover, Germany. A) Phylogenetic relationship of PBoV isolate S1142/13 (bold) with other bocaviruses. The nucleotide...
The spinal cord of the diseased pig showed diffuse intracytoplasmic and intranuclear PBoV-specific signals within scattered neurons adjacent to the histologically detected inflammatory lesions (Figure, panel C). The negative control and the nonprobe incubation lacked PBoV-specific signals. The porcine ubiquitin probe provided a strong intracellular and extracellular staining within the CNS of both pigs.
PBoV (genus Bocaparvovirus, family Parvoviridae) was first described in 2009 as porcine boca-like virus in pigs in Sweden with postweaning multisystemic wasting syndrome (5). PBoV is usually involved in respiratory and intestinal diseases in pigs (5) but has not been detected in the CNS. In the pig in our study, the lack of detection of other viral sequences by using NGS indicates the potential role of PBoV as a pathogen that triggers encephalomyelitis. FISH substantiated the NGS results and revealed neuronal intracytoplasmic and intranuclear PBoV-specific signals adjacent to the lesion, indicating intraneuronal transcription and replication (6). Nevertheless, a potential synergistic effect of M. hyorhinis on the PBoV pathogenesis cannot be ruled out. Similarly, co-infection of M. hyorhinis and porcine circovirus type 2 has been associated with enhanced inflammatory lesions in the lungs of pigs (7).
The CNS tropism of PBoV S1142/13 could result from various factors, including specific amino acid changes that enable the virus to pass the blood–brain barrier and infect neurons. Additional studies are necessary to elucidate a possible role of the amino acid differences between PBoV S1142/13 and PBoV KU14 in the tropism of these viruses.
Human bocavirus has recently been found in the cerebrospinal fluid of patients having encephalitis (8), and related human parvovirus 4 (9) and human parvovirus B19 (10) have been reported in human encephalitis. The correlation of PBoV-specific signals by using FISH for histologic detection of encephalomyelitis assigns PBoV a potential role in provoking CNS lesions. PBoV should be considered as a cause of encephalomyelitis but needs further investigation.
Vanessa M. Pfankuche, Rogier Bodewes, Kerstin Hahn, Christina Puff, Andreas Beineke, André Habierski, Albert D.M.E. Osterhaus, and Wolfgang Baumgärtner
Acknowledgments
The authors thank the Lower Saxony State Office for Consumer Protection and Food Safety, the Institute of Virology at the University of Veterinary Medicine Hannover, and the Friedrich-Loeffler-Institute in Jena for performing the routine diagnostic analyses of common porcine pathogens. The authors also thank Danuta Waschke, Kerstin Rohn, Bettina Buck, Caroline Schütz, and Kerstin Schöne for excellent technical assistance.
This study was in part supported by the Niedersachsen-Research Network on Neuroinfectiology of the Ministry of Science and Culture of Lower Saxony and by the COMPARE project and received funding from the European Union’s Horizon 2020 research and innovation program COMPARE (grant agreement no. 643476). V.M.P. received a scholarship from the Akademie für Tiergesundheit e.V. in Bonn, Germany.
References
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Figure
Suggested citation for this article: Pfankuche VM, Bodewes R, Hahn K, Puff C, Beineke A, Habierski A, et al. Porcine bocavirus infection associated with encephalomyelitis in a pig. Emerg Infect Dis. 2016 Jul [date cited]. http://dx.doi.org/10.3201/eid2207.152049
1Preliminary results from this study were presented at the 3rd International One Health Congress, March 15–18, 2015, Amsterdam, the Netherlands, and at the Conference of the German Veterinary Medical Association, March 8–10, 2015, Fulda, Germany.
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Restaurant Cooking Trends and Increased Risk for Campylobacter Infection Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Restaurant Cooking Trends and Increased Risk for Campylobacter Infection Volume 22 Number 7—July 2016 Emerging Infectious Disease journal CDC
Restaurant Cooking Trends and Increased Risk for Campylobacter Infection - Volume 22, Number 7—July 2016 - Emerging Infectious Disease journal - CDC
Volume 22, Number 7—July 2016
Research
Restaurant Cooking Trends and Increased Risk for Campylobacter Infection
On This Page
- Methods
- Results
- Discussion
- Suggested Citation
Anna K. Jones, Dan Rigby1, Michael Burton, Caroline Millman, Nicola J. Williams, Trevor R. Jones, Paul Wigley, Sarah J. O’Brien , Paul Cross1, and for the ENIGMA Consortium
, Paul Cross1, and for the ENIGMA ConsortiumSuggested citation for this article
Abstract
In the United Kingdom, outbreaks of Campylobacter infection are increasingly attributed to undercooked chicken livers, yet many recipes, including those of top chefs, advocate short cooking times and serving livers pink. During 2015, we studied preferences of chefs and the public in the United Kingdom and investigated the link between liver rareness and survival of Campylobacter. We used photographs to assess chefs’ ability to identify chicken livers meeting safe cooking guidelines. To investigate the microbiological safety of livers chefs preferred to serve, we modeled Campylobacter survival in infected chicken livers cooked to various temperatures. Most chefs correctly identified safely cooked livers but overestimated the public’s preference for rareness and thus preferred to serve them more rare. We estimated that 19%–52% of livers served commercially in the United Kingdom fail to reach 70°C and that predicted Campylobacter survival rates are 48%–98%. These findings indicate that cooking trends are linked to increasing Campylobacter infections.
Foodborne illness is very costly, comprising medical expenses, loss of earnings, and reduced quality of life. In the United States, the annual healthcare cost is ?$14 billion annually (1); in the United Kingdom, it is £1.8 billion (2). The foodborne illness most commonly responsible for these costs is campylobacteriosis (3–5). In the United States, cases increased by 13% between 2006–2008 and 2013 (6). In the United Kingdom, Campylobacteraccounted for over half of the estimated 500,000 cases of foodborne disease during 2011–2012 (3,7); in the United States, it accounts for 9% of foodborne disease cases annually (4).
Foods implicated as Campylobacter vehicles include poultry, red meat, milk, and water (7–11). Studies of outbreaks and sporadic cases have identified the principal source of infection as undercooked chicken meat (9–14). In the United Kingdom, increasing numbers of outbreaks are attributed to undercooked chicken livers (9) despite the fact that the UK Food Standards Agency (FSA) has provided guidelines for safely cooking them. These increased infections seem to have coincided with a trend among leading chefs to advocate minimal cooking of chicken livers, despite recommendations to maintain liver cores at 70°C for 2–3 minutes to ensure they areCampylobacter free (15).
Although the association between consuming chicken livers and infection with Campylobacter is well known (9), the underlying reasons for the changing epidemiology of outbreaks associated with chicken liver consumption are unclear. We hypothesized that the trend toward including rarer, pinker meat in the recipes of leading chefs and by mass media representation of meat cooking may be contributing to changes in the way chicken livers are consumed.
We therefore conducted an interdisciplinary investigation by using a combination of methods from social and biological sciences. Participants were selected from the UK population, and the study was conducted during 2015. Our study objectives were 1) to investigate the ability of chefs and members of the public to identify cooked chicken livers that meet FSA guidelines for safe cooking, 2) to elicit the preferences of chefs and the public regarding the rareness of chicken livers, and 3) to model the survival of Campylobacter in chicken livers sautéed to various core temperatures.
Methods
Participants
We recruited a quota-based sample of 1,030 members of the UK public via an online market research panel (http://www.researchnow.com). Quotas were used to ensure representativeness in terms of age groups and social class. The quota permitted an unequal split by sex (up to 70% women) because in the United Kingdom, food preparation at home is more commonly performed by women than men. We also recruited 143 chefs through face-to-face convenience sampling at culinary shows and competitions and by online culinary forums.
All participants gave informed consent. Respondents were debriefed on the purpose of the survey after completion and given the opportunity to withdraw their data. Ethical approval was obtained from the College of Natural Science Ethics Committee at Bangor University (CNS/2014/AJ1).
Preparation of Visual Aids
To prepare cooked chicken liver dishes to serve as visual aids, we used methods similar to those used in studies of hamburgers (16) and beefsteaks (17). A chef cooked 7 batches of chicken livers for various times, recorded the maximum core temperature for each batch, and arranged each batch on a plate for photography by a professional photographer. The process was repeated (without the temperature being recorded) for 3 other meats (duck breasts, lamb racks, and beef burgers).
Surveys of Preference and Knowledge
Figure 1. Chicken liver images, in order of cooking time/rareness, used in survey to determine preferences and knowledge of safe cooking practices among chefs and the public, United Kingdom.
To determine preferences and knowledge of safe cooking practices among chefs and members of the public, we used the images of cooked chicken livers as visual aids. The images were presented in surveys (online and print), arranged in order of cooking time/rareness (Figure 1). The surveys for chefs and the public were similar, except that the chefs were asked about serving preferences and the public was asked about eating preferences.
To avoid biases (such as social desirability bias) resulting from respondents perceiving the survey to be about food safety, we described the survey as being about food preferences. Respondents were first asked preference questions about 3 of the 4 meats (in random order) to obscure the focus on chicken livers and safety. Chefs were asked to indicate which chicken liver dish was cooked “the way you would like to serve it” and “the way you think most customers would like it.” Members of the public were asked which dish they would prefer if “eating out” and “eating at home.”
Respondents were subsequently asked which chicken liver dish (if any) was the first they thought would meet FSA safe cooking guidelines. Additional questions were asked about perceived trends and influences regarding cooking meat, dining habits, and demographic information such as class and age. Chefs provided additional information about their current position, such as their training and industry experience.
Campylobacter Survival
To prepare a suspension of Campylobacter for experimental inoculation, we streaked Camplyobacter jejuni M1 strain (sequence type 137, clonal complex 45) on Columbia agar base containing 5% defibrinated horse blood, incubated it at 37°C under microaerobic conditions for 48–72 h, and then inoculated it into Camplyobacter enrichment broth. After subculture for another 24 h, a bacterial suspension was prepared in maximum recovery diluent to an optical density of 600 nm (?109 CFU/mL). The culture broth was diluted in Camplyobacter enrichment broth to give a suspension of ?105 CFU/mL for inoculation into fresh chicken livers.
The fresh chicken livers were purchased in packs from supermarkets and sorted into batches of 4 with similar weights. The connective tissue was cut between the 2 liver lobes, with the weight of the larger lobe recorded and assigned for inoculation with Campylobacter broth suspension; 4 livers were assigned to each cooking batch. A 1-cm2 area of each liver was scored at its thickest point by using a sterile scalpel blade and injected with 100 ?L (?104CFU) of culture broth, corresponding to the highest levels of Campylobacter reported to be found in naturally contaminated livers (18).
For each cooking time, 10 g butter was heated in a frying pan over moderate to high heat on an electric cooktop; when the butter had finished frothing, the 4 inoculated liver lobes in the batch were added. The maximum core temperature of the largest and smallest liver in each batch was recorded. To determine the survival of the inoculated M1 strain of C. jejuni within the cooked livers, we placed each liver in a sterile petri dish and a 4–5-g portion around the scored inoculated region was removed and added to a Stomacher bag (Seward BA6040, Worthing, UK); 10 mL of Exeter broth was added to each bag before Stomaching (mechanical pounding of the outer surface of the bag to remove bacteria) for 1 min. The homogenized suspension was poured into a 20-mL universal container and incubated at 41°C under microaerobic conditions (Variable Atmosphere Incubator; Don Whitely Scientific, Shipley, UK) for 24 h, after which 1 loopful of broth was plated onto Campylobacter blood-free medium (modified charcoal cefoperazone deoxycholate agar, containing cefoperazone and amphotericin) at 41°C under microaerobic conditions for 48–72 h. We picked 1 typical Campylobacter colony from at least 1 plate in each batch and confirmed it as C. jejuni by PCR; for a cooked liver to be deemed positive, 1 isolate per batch was confirmed as C. jejuni positive (19).
Data Analyses
Figure 2. Campylobactersurvival in cooked (pan-fried) chicken livers, by cooking time and temperature. Error bars represent minimum and maximum temperatures reached.
We modeled the probability of survival for the 60 livers for which temperature and Campylobacterpresence/absence after cooking were recorded. We used logistic regression to model the relationship between the core temperature of the livers and the survival of Campylobacter. The probability of Campylobacter survival as a function of core temperature was modeled via estimation of a logit model, which captured the nonlinear temperature-survival relationship (Figure 2). Parameter estimates were obtained by using logistic regression (Stata logit command; StataCorp LP, College Station, TX, USA) on the binary variable indicating Camplyobacter survival (1 = survival, 0 = nonsurvival) in a sample of 60 cooked chicken livers. Temperature was the maximum core temperature recorded for the batch from which the chicken liver was taken. This model was used to assign predicted survival rates for each photographed chicken liver dish.
We used the Kolmogorov Smirnov 2-sample test to compare differences in the distribution of knowledge and preferences between groups (chefs and the public). We investigated within-person differences by using the Wilcoxon signed-rank test for paired data. Ordered logit models (20) were estimated to determine the effects of observable characteristics on respondents’ preferences for chicken liver rareness and their choices of FSA-compliant livers.
Results
Campylobacter Survival
We discuss the results of the Campylobacter survival experiment first because an understanding of those results is useful for interpreting the preferences and knowledge analyses. The relationship between core temperature and Campylobacter survival rate was inverse (Table; Figure 2). Of the 32 batches of 4 inoculated livers, the shortest cooking time was 1 minute, leading to a mean core temperature of 36°C and a 100% Campylobacter survival rate. At the maximum mean core temperature (72°C), Campylobacter survival rate was 8.3%.
The logistic model predicted a survival rate of 98% in liver with core temperature that reached 52°C (liver 1) and equivalent survival rates of 95% and 48% at core temperatures of 56°C and 66°C (livers 2 and 3). Liver 4 reached a maximum temperature of 70°C, but the temperature was not held for the recommended 2 minutes; predicted Campylobacter survival rate was 22%. Livers 6 and 7 met the FSA guidelines, and their predicted Campylobactersurvival rate was <0.001%.
Preferences and Knowledge of the Public
Of the 1,030 members of the public surveyed, 43.0% ate chicken livers and hence were asked to select the chicken liver dishes they preferred and which they thought met FSA guidelines. Half (49.3%) of all male respondents and 38.4% of all female respondents ate chicken livers. Rates of chicken liver consumption varied by age group: 18–34 years, 34.7%; 35–44 years, 44.7%; 45–54 years, 49.0%, 55–64 years: 51.5%; and >65: 42.9%. Chicken livers were eaten by half (51.0%) of respondents belonging to UK socioeconomic grouping ABC1 (upper, middle, and lower middle class) and 32.3% of those belonging to C2DE (working class and those at the lowest level of subsistence).
Figure 3. Rarest chicken livers visually identified by members of the public as complying with FSA cooking guidelines and associated core temperatures and probabilities ofCampylobacter survival in survey to determine preferences and...
Members of the public poorly identified whether a chicken liver met FSA guidelines for safe cooking (Figure 3). Thirty percent identified livers 1–3 as being safe to eat; the predicted rates of Campylobacter survival in these livers were 48%–98%. Another 22% thought that liver 4 (Campylobacter survival rate 22%) was safe to eat.
Figure 4. Proportion of public identifying which chicken liver dishes they preferred and which they believed complied with FSA cooking guidelines in survey to determine preferences and knowledge of safe cooking practices among...
No significant difference was found between the public’s choices of FSA-compliant livers and their preferences when dining out (p = 0.776, Wilcoxon signed-rank test; n = 386) (Figure 4); respondents were consistent between what they wanted to eat and what they thought was safe. Respondents showed a significant preference for pinker livers when eating out rather than at home (p = 0.007, Wilcoxon signed-rank test; n = 446). Paradoxically, respondents reported being more concerned about food safety when eating out than at home (p<0.001, Wilcoxon signed-rank test; n = 999).
Ordered logit results (not reported) identified no systematic differences in rareness preferences by respondent sex, age, or class. Livers that were more pink were preferred by respondents who described themselves as adventurous (p<0.030, n = 444) and who were less concerned about restaurant food safety (p<0.001, n = 444).
Perceptions and Knowledge of Chefs
Among the 143 chefs, of those who indicated their sex, 134 (88%) were male. Among the 141 who indicated their type of work, 31.9% worked in fine dining, 17% in contract catering, 11.3% in casual restaurants, 5.7% in pubs, and 19.1% in multiple kitchen types. The most commonly held position among 131 chefs who responded was head chef (54.0%), followed by chef trainer (11.5%), chef de partie (10.7%), commis chef (6.9%), and sous chef (6.1%).
Figure 5. Proportion of chefs identifying which chicken liver dishes they preferred and which they believed complied with FSA cooking guidelines in survey to determine preferences and knowledge of safe cooking practices among...
Chefs were much better than members of the public at
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