text:
Volume 13, Number 8—August 2007
[PDF - 5.16 MB - 151 pages]
Conference Summaries
Ecologic Immunology of Avian Influenza (H5N1) in Migratory Birds [PDF - 67 KB - 5 pages]
T. P. Weber and N. I. Stilianakis
The claim that migratory birds are responsible for the long-distance spread of highly pathogenic avian influenza viruses of subtype H5N1 rests on the assumption that infected wild birds can remain asymptomatic and migrate long distances unhampered. We critically assess this claim from the perspective of ecologic immunology, a research field that analyzes immune function in an ecologic, physiologic, and evolutionary context. Long-distance migration is one of the most demanding activities in the animal world. We show that several studies demonstrate that such prolonged, intense exercise leads to immunosuppression and that migratory performance is negatively affected by infections. These findings make it unlikely that wild birds can spread the virus along established long-distance migration pathways. However, infected, symptomatic wild birds may act as vectors over shorter distances, as appears to have occurred in Europe in early 2006.
Weber TP, Stilianakis NI. Ecologic Immunology of Avian Influenza (H5N1) in Migratory Birds. Emerg Infect Dis. 2007;13(8):1139. https://dx.doi.org/10.3201/eid1308.070319
Weber TP, Stilianakis NI. Ecologic Immunology of Avian Influenza (H5N1) in Migratory Birds. Emerging Infectious Diseases. 2007;13(8):1139. doi:10.3201/eid1308.070319.
Weber, T. P., & Stilianakis, N. I. (2007). Ecologic Immunology of Avian Influenza (H5N1) in Migratory Birds. Emerging Infectious Diseases, 13(8), 1139. https://dx.doi.org/10.3201/eid1308.070319.
Risk Factors for Colonization with Extended-Spectrum β-Lactamase–producing Bacteria and Intensive Care Unit Admission [PDF - 167 KB - 6 pages]
A. D. Harris et al.
Extended-spectrum β-lactamase (ESBL)–producing bacteria are emerging pathogens. To analyze risk factors for colonization with ESBL-producing bacteria at intensive care unit (ICU) admission, we conducted a prospective study of a 3.5-year cohort of patients admitted to medical and surgical ICUs at the University of Maryland Medical Center. Over the study period, admission cultures were obtained from 5,209 patients. Of these, 117 were colonized with ESBL-producing Escherichia coli and Klebsiella spp., and 29 (25%) had a subsequent ESBL-positive clinical culture. Multivariable analysis showed the following to be statistically associated with ESBL colonization at admission: piperacillin-tazobactam (odds ratio [OR] 2.05, 95% confidence interval [CI] 1.36–3.10), vancomycin (OR 2.11, 95% CI 1.34–3.31), age >60 years (OR 1.79, 95% CI 1.24–2.60), and chronic disease score (OR 1.15; 95% CI 1.04–1.27). Coexisting conditions and previous antimicrobial drug exposure are thus predictive of colonization, and a large percentage of these patients have subsequent positive clinical cultures for ESBL-producing bacteria.
Harris AD, McGregor JC, Johnson JA, Strauss SM, Moore AC, Standiford HC, et al. Risk Factors for Colonization with Extended-Spectrum β-Lactamase–producing Bacteria and Intensive Care Unit Admission. Emerg Infect Dis. 2007;13(8):1144. https://dx.doi.org/10.3201/eid1308.070071
Harris AD, McGregor JC, Johnson JA, et al. Risk Factors for Colonization with Extended-Spectrum β-Lactamase–producing Bacteria and Intensive Care Unit Admission. Emerging Infectious Diseases. 2007;13(8):1144. doi:10.3201/eid1308.070071.
Harris, A. D., McGregor, J. C., Johnson, J. A., Strauss, S. M., Moore, A. C., Standiford, H. C....Morris, J. (2007). Risk Factors for Colonization with Extended-Spectrum β-Lactamase–producing Bacteria and Intensive Care Unit Admission. Emerging Infectious Diseases, 13(8), 1144. https://dx.doi.org/10.3201/eid1308.070071.
Occupational Risks during a Monkeypox Outbreak, Wisconsin, 2003 [PDF - 231 KB - 8 pages]
D. R. Croft et al.
We determined factors associated with occupational transmission in Wisconsin during the 2003 outbreak of prairie dog–associated monkeypox virus infections. Our investigation included active contact surveillance, exposure-related interviews, and a veterinary facility cohort study. We identified 19 confirmed, 5 probable, and 3 suspected cases. Rash, headache, sweats, and fever were reported by >80% of patients. Occupationally transmitted infections occurred in 12 veterinary staff, 2 pet store employees, and 2 animal distributors. The following were associated with illness: working directly with animal care (p = 0.002), being involved in prairie dog examination, caring for an animal within 6 feet of an ill prairie dog (p = 0.03), feeding an ill prairie dog (p = 0.002), and using an antihistamine (p = 0.04). Having never handled an ill prairie dog (p = 0.004) was protective. Veterinary staff used personal protective equipment sporadically. Our findings underscore the importance of standard veterinary infection-control guidelines.
Croft DR, Sotir MJ, Williams CJ, Kazmierczak JJ, Wegner MV, Rausch D, et al. Occupational Risks during a Monkeypox Outbreak, Wisconsin, 2003. Emerg Infect Dis. 2007;13(8):1150. https://dx.doi.org/10.3201/eid1308.061365
Croft DR, Sotir MJ, Williams CJ, et al. Occupational Risks during a Monkeypox Outbreak, Wisconsin, 2003. Emerging Infectious Diseases. 2007;13(8):1150. doi:10.3201/eid1308.061365.
Croft, D. R., Sotir, M. J., Williams, C. J., Kazmierczak, J. J., Wegner, M. V., Rausch, D....Davis, J. P. (2007). Occupational Risks during a Monkeypox Outbreak, Wisconsin, 2003. Emerging Infectious Diseases, 13(8), 1150. https://dx.doi.org/10.3201/eid1308.061365.
Venezuelan Equine Encephalitis Virus Infection of Cotton Rats [PDF - 370 KB - 8 pages]
A. Carrara et al.
Venezuelan equine encephalitis virus (VEEV) is an emerging pathogen of equids and humans, but infection of its rodent reservoir hosts has received little study. To determine whether responses to infection vary among geographic populations, we inoculated 3 populations of cotton rats with 2 enzootic VEEV strains (Co97-0054 [enzootic ID subtype] and 68U201 [enzootic IE subtype]). The 3 populations were offspring from wild-caught cotton rats collected in a VEE-enzootic area of south Florida, USA; wild-caught cotton rats from a non–VEE-enzootic area of Texas, USA; and commercially available (Harlan) colony-reared cotton rats from a non–VEE-enzootic region. Although each population had similar early viremia titers, no detectable disease developed in the VEE-sympatric Florida animals, but severe disease and death affected the Texas and Harlan animals. Our findings suggest that the geographic origins of cotton rats are important determinants of the outcome of VEE infection and reservoir potential of these rodents.
Carrara A, Coffey LL, Aguilar PV, Moncayo AC, Da Rosa AP, Nunes MR, et al. Venezuelan Equine Encephalitis Virus Infection of Cotton Rats. Emerg Infect Dis. 2007;13(8):1158. https://dx.doi.org/10.3201/eid1308.061157
Carrara A, Coffey LL, Aguilar PV, et al. Venezuelan Equine Encephalitis Virus Infection of Cotton Rats. Emerging Infectious Diseases. 2007;13(8):1158. doi:10.3201/eid1308.061157.
Carrara, A., Coffey, L. L., Aguilar, P. V., Moncayo, A. C., Da Rosa, A. P., Nunes, M. R....Vasilakis, N. (2007). Venezuelan Equine Encephalitis Virus Infection of Cotton Rats. Emerging Infectious Diseases, 13(8), 1158. https://dx.doi.org/10.3201/eid1308.061157.
Source of Variant Creutzfeldt-Jakob Disease outside United Kingdom [PDF - 191 KB - 4 pages]
P. Sanchez-Juan et al.
We studied the occurrence of variant Creutzfeldt-Jakob disease (vCJD) outside the United Kingdom in relation to the incidence of indigenous bovine spongiform encephalopathy (BSE) and to the level of live bovines and bovine products imported from the UK during the 1980s and the first half of the 1990s. Our study provides evidence that a country's number of vCJD cases correlates with the number of live bovines it imported from the UK from 1980 to 1990 (Spearman rank correlation coefficient [rs] 0.73, 95% confidence interval [CI] 0.42–0.89, p<0.001). Similar correlations were observed with the number of indigenous BSE cases (rs 0.70, 95% CI 0.37–0.87, p = 0.001) and carcass meat imported from the UK from 1980 to 1996 (rs 0.75, 95% CI 0.45–0.89; p<0.001) Bovine imports from the UK may have been an important source of human exposure to BSE and may have contributed to the global risk for disease.
Sanchez-Juan P, Cousens SN, Will RG, van Duijn CM. Source of Variant Creutzfeldt-Jakob Disease outside United Kingdom. Emerg Infect Dis. 2007;13(8):1166. https://dx.doi.org/10.3201/eid1308.070178
Sanchez-Juan P, Cousens SN, Will RG, et al. Source of Variant Creutzfeldt-Jakob Disease outside United Kingdom. Emerging Infectious Diseases. 2007;13(8):1166. doi:10.3201/eid1308.070178.
Sanchez-Juan, P., Cousens, S. N., Will, R. G., & van Duijn, C. M. (2007). Source of Variant Creutzfeldt-Jakob Disease outside United Kingdom. Emerging Infectious Diseases, 13(8), 1166. https://dx.doi.org/10.3201/eid1308.070178.
Infection with Scedosporium apiospermum and S. prolificans, Australia [PDF - 325 KB - 8 pages]
L. Cooley et al.
Scedosporium apiospermum and S. prolificans are fungi of increasing clinical importance, particularly in persons with underlying diseases. We reviewed the records of 59 patients in Australia from whom Scedosporium spp. were isolated from June 30, 1997, through December 31, 2003. S. apiospermum was isolated predominantly from the respiratory tracts of 28 of 31 patients with underlying lung diseases and resulted in 2 infections and 1 death. The annual number of S. apiospermum isolates remained constant. S. prolificans was isolated from 28 patients only after November 1999. Eight patients with acute myeloid leukemia or hematopoietic stem cell transplants had invasive infection; 4 had fungemia and 6 died from infection. S. prolificans caused locally invasive infection in 2 immunocompetent patients and was found in the respiratory tract of 18 patients with underlying respiratory disease but did not cause fungemia or deaths in these patients. Scedosporium spp. showed distinct clinical and epidemiologic features.
Cooley L, Spelman D, Thursky K, Slavin M. Infection with Scedosporium apiospermum and S. prolificans, Australia. Emerg Infect Dis. 2007;13(8):1170. https://dx.doi.org/10.3201/eid1308.060576
Cooley L, Spelman D, Thursky K, et al. Infection with Scedosporium apiospermum and S. prolificans, Australia. Emerging Infectious Diseases. 2007;13(8):1170. doi:10.3201/eid1308.060576.
Cooley, L., Spelman, D., Thursky, K., & Slavin, M. (2007). Infection with Scedosporium apiospermum and S. prolificans, Australia. Emerging Infectious Diseases, 13(8), 1170. https://dx.doi.org/10.3201/eid1308.060576.
Genetic Diversity of Bartonella henselae in Human Infection Detected with Multispacer Typing [PDF - 187 KB - 6 pages]
W. Li et al.
We applied multispacer typing (MST) by incorporating 9 variable intergenic spacers to Bartonella henselae DNA detected in lymph node biopsy specimens from 70 patients with cat-scratch disease (CSD), in cardiac valve specimens from 2 patients with endocarditis, and in 3 human isolates from patients with bacillary angiomatosis, CSD, and endocarditis. Sixteen MST genotypes were found, 5 previously identified in cats and 11 new. Of the studied DNA, 78.7% belonged to 2 genotypes, which were phylogenetically organized into 4 lineages. Human strains were mostly grouped within 2 lineages, previously identified as Marseille and Houston-1. Our results suggest a greater genetic diversity in human-infecting B. henselae than what has previously been evaluated by using other genotyping methods. However, the diversity is not significantly different from that of cat strains. MST is thus a suitable genotyping tool for evaluating the genetic heterogeneity of B. henselae among isolates obtained from human patients.
Li W, Raoult D, Fournier P. Genetic Diversity of Bartonella henselae in Human Infection Detected with Multispacer Typing. Emerg Infect Dis. 2007;13(8):1178. https://dx.doi.org/10.3201/eid1308.070085
Li W, Raoult D, Fournier P. Genetic Diversity of Bartonella henselae in Human Infection Detected with Multispacer Typing. Emerging Infectious Diseases. 2007;13(8):1178. doi:10.3201/eid1308.070085.
Li, W., Raoult, D., & Fournier, P. (2007). Genetic Diversity of Bartonella henselae in Human Infection Detected with Multispacer Typing. Emerging Infectious Diseases, 13(8), 1178. https://dx.doi.org/10.3201/eid1308.070085.
Human Noroviruses in Swine and Cattle [PDF - 213 KB - 5 pages]
K. Mattison et al.
Human noroviruses are the predominant cause of foodborne gastroenteritis worldwide. Strains of norovirus also exist that are uniquely associated with animals; their contribution to the incidence of human illness remains unclear. We tested animal fecal samples and identified GIII (bovine), GII.18 (swine), and GII.4 (human) norovirus sequences, demonstrating for the first time, to our knowledge, that GII.4-like strains can be present in livestock. In addition, we detected GII.4-like noroviral RNA from a retail meat sample. This finding highlights a possible route for indirect zoonotic transmission of noroviruses through the food chain.
Mattison K, Shukla A, Cook A, Pollari F, Friendship R, Kelton D, et al. Human Noroviruses in Swine and Cattle. Emerg Infect Dis. 2007;13(8):1184. https://dx.doi.org/10.3201/eid1308.070005
Mattison K, Shukla A, Cook A, et al. Human Noroviruses in Swine and Cattle. Emerging Infectious Diseases. 2007;13(8):1184. doi:10.3201/eid1308.070005.
Mattison, K., Shukla, A., Cook, A., Pollari, F., Friendship, R., Kelton, D....Farber, J. M. (2007). Human Noroviruses in Swine and Cattle. Emerging Infectious Diseases, 13(8), 1184. https://dx.doi.org/10.3201/eid1308.070005.
High Prevalence of Tuberculosis in Previously Treated Patients, Cape Town, South Africa [PDF - 188 KB - 6 pages]
S. den Boon et al.
The tuberculosis (TB) notification rate is high and increasing in 2 communities in Cape Town, South Africa. In 2002, we conducted a prevalence survey among adults >15 years of age to determine the TB prevalence rate; 15% of households in these communities were randomly sampled. All persons living in sampled households were eligible for chest radiography and sputum examination. Of the 3,483 adults who completed a questionnaire, 2,608 underwent chest radiography and sputum examination. We detected 26 bacteriologically confirmed TB cases and a prevalence of 10.0/1,000 (95% confidence interval [CI] 6.2–13.8 per 1,000). We found 18 patients with smear-positive TB, of whom 8 were new patients (3.1/1,000, 95% CI 0.9–5.1/1,000). More than half of patients with smear-positive TB (10, 56%) had previously been treated. Such patients may contribute to transmission of Mycobacterium tuberculosis and the high TB prevalence rate. Successful treatment of TB patients must be a priority.
den Boon S, van Lill SW, Borgdorff MW, Enarson DA, Verver S, Bateman ED, et al. High Prevalence of Tuberculosis in Previously Treated Patients, Cape Town, South Africa. Emerg Infect Dis. 2007;13(8):1189. https://dx.doi.org/10.3201/eid1308.051327
den Boon S, van Lill SW, Borgdorff MW, et al. High Prevalence of Tuberculosis in Previously Treated Patients, Cape Town, South Africa. Emerging Infectious Diseases. 2007;13(8):1189. doi:10.3201/eid1308.051327.
den Boon, S., van Lill, S. W., Borgdorff, M. W., Enarson, D. A., Verver, S., Bateman, E. D....Beyers, N. (2007). High Prevalence of Tuberculosis in Previously Treated Patients, Cape Town, South Africa. Emerging Infectious Diseases, 13(8), 1189. https://dx.doi.org/10.3201/eid1308.051327.
Skin and Soft Tissue Infections Caused by Methicillin-Resistant Staphylococcus aureus USA300 Clone [PDF - 289 KB - 6 pages]
J. K. Johnson et al.
Until recently, methicillin-resistant Staphylococcus aureus (MRSA) has caused predominantly healthcare-associated infections. We studied MRSA infections and overall skin and soft tissue infections (SSTIs) in outpatients receiving care at the Baltimore Veterans Affairs Medical Center Emergency Care Service during 2001–2005. We found an increase in MRSA infections, from 0.2 to 5.9 per 1,000 visits (p<0.01); most were community-associated SSTIs. Molecular typing showed that >80% of MRSA infections were caused by USA300. In addition, SSTI visits increased from 20 to 61 per 1,000 visits (p<0.01). The proportion of SSTI cultures that yielded MRSA increased from 4% to 42% (p<0.01), while the proportion that yielded methicillin-sensitive S. aureus remained the same (10% to 13%, p = 0.5). The increase in community-associated MRSA infections and the overall increase in SSTIs in our population suggest that USA300 is becoming more virulent and has a greater propensity to cause SSTIs.
Johnson JK, Khoie T, Shurland S, Kreisel K, Stine O, Roghmann M. Skin and Soft Tissue Infections Caused by Methicillin-Resistant Staphylococcus aureus USA300 Clone. Emerg Infect Dis. 2007;13(8):1195. https://dx.doi.org/10.3201/eid1308.061575
Johnson JK, Khoie T, Shurland S, et al. Skin and Soft Tissue Infections Caused by Methicillin-Resistant Staphylococcus aureus USA300 Clone. Emerging Infectious Diseases. 2007;13(8):1195. doi:10.3201/eid1308.061575.
Johnson, J. K., Khoie, T., Shurland, S., Kreisel, K., Stine, O., & Roghmann, M. (2007). Skin and Soft Tissue Infections Caused by Methicillin-Resistant Staphylococcus aureus USA300 Clone. Emerging Infectious Diseases, 13(8), 1195. https://dx.doi.org/10.3201/eid1308.061575.
Classic Scrapie in Sheep with the ARR/ARR Prion Genotype in Germany and France [PDF - 311 KB - 7 pages]
M. H. Groschup et al.
In the past, natural scrapie and bovine spongiform encephalopathy (BSE) infections have essentially not been diagnosed in sheep homozygous for the A136R154R171 haplotype of the prion protein. This genotype was therefore assumed to confer resistance to BSE and classic scrapie under natural exposure conditions. Hence, to exclude prions from the human food chain, massive breeding efforts have been undertaken in the European Union to amplify this gene. We report the identification of 2 natural scrapie cases in ARR/ARR sheep that have biochemical and transmission characteristics similar to cases of classic scrapie, although the abnormally folded prion protein (PrPSc) was associated with a lower proteinase-K resistance. PrPSc was clearly distinct from BSE prions passaged in sheep and from atypical scrapie prions. These findings strongly support the idea that scrapie prions are a mosaic of agents, which harbor different biologic properties, rather than a unique entity.
Groschup MH, Lacroux C, Buschmann A, Lühken G, Mathey J, Eiden M, et al. Classic Scrapie in Sheep with the ARR/ARR Prion Genotype in Germany and France. Emerg Infect Dis. 2007;13(8):1201. https://dx.doi.org/10.3201/eid1308.070077
Groschup MH, Lacroux C, Buschmann A, et al. Classic Scrapie in Sheep with the ARR/ARR Prion Genotype in Germany and France. Emerging Infectious Diseases. 2007;13(8):1201. doi:10.3201/eid1308.070077.
Groschup, M. H., Lacroux, C., Buschmann, A., Lühken, G., Mathey, J., Eiden, M....Andreoletti, O. (2007). Classic Scrapie in Sheep with the ARR/ARR Prion Genotype in Germany and France. Emerging Infectious Diseases, 13(8), 1201. https://dx.doi.org/10.3201/eid1308.070077.
Babesia sp. EU1 from Roe Deer and Transmission within Ixodes ricinus [PDF - 305 KB - 3 pages]
S. Bonnet et al.
We report in vitro culture of zoonotic Babesia sp. EU1 from blood samples of roe deer in France. This study provides evidence of transovarial and transstadial transmission of the parasite within Ixodes ricinus, which suggests that this tick could be a vector and reservoir of EU1.
Bonnet S, Jouglin M, L'Hostis M, Chauvin A. Babesia sp. EU1 from Roe Deer and Transmission within Ixodes ricinus. Emerg Infect Dis. 2007;13(8):1208. https://dx.doi.org/10.3201/eid1308.061560
Bonnet S, Jouglin M, L'Hostis M, et al. Babesia sp. EU1 from Roe Deer and Transmission within Ixodes ricinus. Emerging Infectious Diseases. 2007;13(8):1208. doi:10.3201/eid1308.061560.
Bonnet, S., Jouglin, M., L'Hostis, M., & Chauvin, A. (2007). Babesia sp. EU1 from Roe Deer and Transmission within Ixodes ricinus. Emerging Infectious Diseases, 13(8), 1208. https://dx.doi.org/10.3201/eid1308.061560.
Pathogenic Hantaviruses, Northeastern Argentina and Eastern Paraguay [PDF - 193 KB - 4 pages]
P. Padula et al.
We describe the first, to our knowledge, cases of hantavirus pulmonary syndrome in northeastern Argentina and eastern Paraguay. Andes and Juquitiba (JUQ) viruses were characterized. JUQV was also confirmed in 5 Oligoryzomys nigripes reservoir species from Misiones. A novel Akodon-borne genetic hantavirus lineage was detected in 1 rodent from the Biologic Reserve of Limoy.
Padula P, Martinez VP, Bellomo C, Maidana S, San Juan J, Tagliaferri P, et al. Pathogenic Hantaviruses, Northeastern Argentina and Eastern Paraguay. Emerg Infect Dis. 2007;13(8):1211. https://dx.doi.org/10.3201/eid1308.061090
Padula P, Martinez VP, Bellomo C, et al. Pathogenic Hantaviruses, Northeastern Argentina and Eastern Paraguay. Emerging Infectious Diseases. 2007;13(8):1211. doi:10.3201/eid1308.061090.
Padula, P., Martinez, V. P., Bellomo, C., Maidana, S., San Juan, J., Tagliaferri, P....Almiron, M. (2007). Pathogenic Hantaviruses, Northeastern Argentina and Eastern Paraguay. Emerging Infectious Diseases, 13(8), 1211. https://dx.doi.org/10.3201/eid1308.061090.
Migrating Birds and Tickborne Encephalitis Virus [PDF - 331 KB - 4 pages]
J. Waldenström et al.
During spring and autumn 2001, we screened 13,260 migrating birds at Ottenby Bird Observatory, Sweden, and found 3.4% were infested with ticks. Four birds, each a different passerine species, carried tickborne encephalitis virus (TBEV)–infected ticks (Ixodes ricinus). Migrating birds may play a role in the geographic dispersal of TBEV-infected ticks.
Waldenström J, Lundkvist Å, Falk KI, Garpmo U, Bergström S, Lindegren G, et al. Migrating Birds and Tickborne Encephalitis Virus. Emerg Infect Dis. 2007;13(8):1215. https://dx.doi.org/10.3201/eid1308.061416
Waldenström J, Lundkvist Å, Falk KI, et al. Migrating Birds and Tickborne Encephalitis Virus. Emerging Infectious Diseases. 2007;13(8):1215. doi:10.3201/eid1308.061416.
Waldenström, J., Lundkvist, Å., Falk, K. I., Garpmo, U., Bergström, S., Lindegren, G....Olsen, B. (2007). Migrating Birds and Tickborne Encephalitis Virus. Emerging Infectious Diseases, 13(8), 1215. https://dx.doi.org/10.3201/eid1308.061416.
Avian Influenza (H5N1) Susceptibility and Receptors in Dogs [PDF - 359 KB - 3 pages]
R. Maas et al.
Inoculation of influenza (H5N1) into beagles resulted in virus excretion and rapid seroconversion with no disease. Binding studies that used labeled influenza (H5N1) showed virus attachment to higher and lower respiratory tract tissues. Thus, dogs that are subclinically infected with influenza (H5N1) may contribute to virus spread.
Maas R, Tacken M, Ruuls L, Koch G, van Rooij E, Stockhofe-Zurwieden N. Avian Influenza (H5N1) Susceptibility and Receptors in Dogs. Emerg Infect Dis. 2007;13(8):1219. https://dx.doi.org/10.3201/eid1308.070393
Maas R, Tacken M, Ruuls L, et al. Avian Influenza (H5N1) Susceptibility and Receptors in Dogs. Emerging Infectious Diseases. 2007;13(8):1219. doi:10.3201/eid1308.070393.
Maas, R., Tacken, M., Ruuls, L., Koch, G., van Rooij, E., & Stockhofe-Zurwieden, N. (2007). Avian Influenza (H5N1) Susceptibility and Receptors in Dogs. Emerging Infectious Diseases, 13(8), 1219. https://dx.doi.org/10.3201/eid1308.070393.
Molecular Epidemiology of Canine Parvovirus, Europe [PDF - 290 KB - 3 pages]
N. Decaro et al.
Canine parvovirus (CPV), which causes hemorrhagic enteritis in dogs, has 3 antigenic variants: types 2a, 2b, and 2c. Molecular method assessment of the distribution of the CPV variants in Europe showed that the new variant CPV-2c is widespread in Europe and that the viruses are distributed in different countries.
Decaro N, Desario C, Addie DD, Martella V, Vieira MJ, Elia G, et al. Molecular Epidemiology of Canine Parvovirus, Europe. Emerg Infect Dis. 2007;13(8):1222. https://dx.doi.org/10.3201/eid1308.070505
Decaro N, Desario C, Addie DD, et al. Molecular Epidemiology of Canine Parvovirus, Europe. Emerging Infectious Diseases. 2007;13(8):1222. doi:10.3201/eid1308.070505.
Decaro, N., Desario, C., Addie, D. D., Martella, V., Vieira, M. J., Elia, G....Buonavoglia, C. (2007). Molecular Epidemiology of Canine Parvovirus, Europe. Emerging Infectious Diseases, 13(8), 1222. https://dx.doi.org/10.3201/eid1308.070505.
Invasive Meningococcal Disease, Utah, 1995–2005 [PDF - 184 KB - 3 pages]
R. B. Boulton et al.
Trends in invasive meningococcal disease in Utah during 1995–2005 have differed substantially from US trends in incidence rate and serogroup and age distributions. Regional surveillance is essential to identify high-risk populations that might benefit from targeted immunization efforts.
Boulton RB, Alder SC, Mottice S, Catinella AP, Byington CL. Invasive Meningococcal Disease, Utah, 1995–2005. Emerg Infect Dis. 2007;13(8):1225. https://dx.doi.org/10.3201/eid1308.061406
Boulton RB, Alder SC, Mottice S, et al. Invasive Meningococcal Disease, Utah, 1995–2005. Emerging Infectious Diseases. 2007;13(8):1225. doi:10.3201/eid1308.061406.
Boulton, R. B., Alder, S. C., Mottice, S., Catinella, A. P., & Byington, C. L. (2007). Invasive Meningococcal Disease, Utah, 1995–2005. Emerging Infectious Diseases, 13(8), 1225. https://dx.doi.org/10.3201/eid1308.061406.
Outbreak of Sporotrichosis, Western Australia [PDF - 246 KB - 4 pages]
K. T. Feeney et al.
A cluster of sporotrichosis cases occurred in the Busselton-Margaret River region of Western Australia from 2000 to 2003. Epidemiologic investigation and mycologic culture for Sporothrix schenckii implicated hay initially distributed through a commercial hay supplier as the source of the outbreak. Declining infection rates have occurred after various community measures were instigated.
Feeney KT, Arthur IH, Whittle AJ, Altman SA, Speers DJ. Outbreak of Sporotrichosis, Western Australia. Emerg Infect Dis. 2007;13(8):1228. https://dx.doi.org/10.3201/eid1308.061462
Feeney KT, Arthur IH, Whittle AJ, et al. Outbreak of Sporotrichosis, Western Australia. Emerging Infectious Diseases. 2007;13(8):1228. doi:10.3201/eid1308.061462.
Feeney, K. T., Arthur, I. H., Whittle, A. J., Altman, S. A., & Speers, D. J. (2007). Outbreak of Sporotrichosis, Western Australia. Emerging Infectious Diseases, 13(8), 1228. https://dx.doi.org/10.3201/eid1308.061462.
Rotavirus G5P[6] in Child with Diarrhea, Vietnam [PDF - 234 KB - 4 pages]
K. Ahmed et al.
We detected rotavirus G5P[6] with a long RNA pattern in a Vietnamese child with diarrhea. Viral outer capsid protein VP7 and VP4 genes suggest that it likely originated from porcine rotavirus either by genetic reassortment or as whole virions. To our knowledge, this is the first report of human rotavirus G5 in Asia.
Ahmed K, Anh DD, Nakagomi O. Rotavirus G5P[6] in Child with Diarrhea, Vietnam. Emerg Infect Dis. 2007;13(8):1232. https://dx.doi.org/10.3201/eid1308.061038
Ahmed K, Anh DD, Nakagomi O. Rotavirus G5P[6] in Child with Diarrhea, Vietnam. Emerging Infectious Diseases. 2007;13(8):1232. doi:10.3201/eid1308.061038.
Ahmed, K., Anh, D. D., & Nakagomi, O. (2007). Rotavirus G5P[6] in Child with Diarrhea, Vietnam. Emerging Infectious Diseases, 13(8), 1232. https://dx.doi.org/10.3201/eid1308.061038.
Possible Autochthonous Malaria from Marseille to Minneapolis [PDF - 177 KB - 3 pages]
B. Doudier et al.
We report 2 cases of Plasmodium falciparum malaria in southern France in a French woman and an American man of Togolese origin who reported no recent travel to malaria-endemic countries. Both infections occurred after a stay near Marseille, which raises the possibility of autochthonous transmission. Entomologic and genotypic investigations are described.
Doudier B, Bogreau H, DeVries A, Ponçon N, Stauffer W, Fontenille D, et al. Possible Autochthonous Malaria from Marseille to Minneapolis. Emerg Infect Dis. 2007;13(8):1236. https://dx.doi.org/10.3201/eid1308.070143
Doudier B, Bogreau H, DeVries A, et al. Possible Autochthonous Malaria from Marseille to Minneapolis. Emerging Infectious Diseases. 2007;13(8):1236. doi:10.3201/eid1308.070143.
Doudier, B., Bogreau, H., DeVries, A., Ponçon, N., Stauffer, W., Fontenille, D....Parola, P. (2007). Possible Autochthonous Malaria from Marseille to Minneapolis. Emerging Infectious Diseases, 13(8), 1236. https://dx.doi.org/10.3201/eid1308.070143.
Waddlia chondrophila, a Potential Agent of Human Fetal Death [PDF - 298 KB - 5 pages]
D. Baud et al.
We investigated the zoonotic potential of Waddlia chondrophila, a new Chlamydia-like abortigenic agent in ruminants. Anti-Waddlia antibody reactivity was tested by immunofluorescence and Western blot. Waddlia seroprevalence was higher in women who had had sporadic and recurrent miscarriages than in control women (p<0.001). Waddlia spp. may represent a cause of human fetal loss.
Baud D, Thomas V, Arafa A, Regan L, Greub G. Waddlia chondrophila, a Potential Agent of Human Fetal Death. Emerg Infect Dis. 2007;13(8):1239. https://dx.doi.org/10.3201/eid1308.070315
Baud D, Thomas V, Arafa A, et al. Waddlia chondrophila, a Potential Agent of Human Fetal Death. Emerging Infectious Diseases. 2007;13(8):1239. doi:10.3201/eid1308.070315.
Baud, D., Thomas, V., Arafa, A., Regan, L., & Greub, G. (2007). Waddlia chondrophila, a Potential Agent of Human Fetal Death. Emerging Infectious Diseases, 13(8), 1239. https://dx.doi.org/10.3201/eid1308.070315.
Norovirus Detection and Genotyping for Children with Gastroenteritis, Brazil [PDF - 156 KB - 3 pages]
C. C. Soares et al.
During 1998–2005, we analyzed stool samples from 289 children in Rio de Janeiro to detect and genotype norovirus strains. Previous tests showed all samples to be negative for rotavirus and adenovirus. Of 42 (14.5%) norovirus-positive specimens, 20 (47.6%) were identified as genogroup GI and 22 (52.3%) as GII.
Soares CC, Santos N, Beard RS, Albuquerque MC, Maranhão AG, Rocha LN, et al. Norovirus Detection and Genotyping for Children with Gastroenteritis, Brazil. Emerg Infect Dis. 2007;13(8):1244. https://dx.doi.org/10.3201/eid1308.070300
Soares CC, Santos N, Beard RS, et al. Norovirus Detection and Genotyping for Children with Gastroenteritis, Brazil. Emerging Infectious Diseases. 2007;13(8):1244. doi:10.3201/eid1308.070300.
Soares, C. C., Santos, N., Beard, R. S., Albuquerque, M. C., Maranhão, A. G., Rocha, L. N....Gentsch, J. (2007). Norovirus Detection and Genotyping for Children with Gastroenteritis, Brazil. Emerging Infectious Diseases, 13(8), 1244. https://dx.doi.org/10.3201/eid1308.070300.
Atypical Q Fever in US Soldiers [PDF - 233 KB - 3 pages]
J. D. Hartzell et al.
Q fever is an emerging infectious disease among US soldiers serving in Iraq. Three patients have had atypical manifestations, including 2 patients with acute cholecystitis and 1 patient with acute respiratory distress syndrome. Providers must be aware of Q fever's signs and symptoms to avoid delays in treatment.
Hartzell JD, Peng SW, Wood-Morris RN, Sarmiento DM, Collen JF, Robben PM, et al. Atypical Q Fever in US Soldiers. Emerg Infect Dis. 2007;13(8):1247. https://dx.doi.org/10.3201/eid1308.070218
Hartzell JD, Peng SW, Wood-Morris RN, et al. Atypical Q Fever in US Soldiers. Emerging Infectious Diseases. 2007;13(8):1247. doi:10.3201/eid1308.070218.
Hartzell, J. D., Peng, S. W., Wood-Morris, R. N., Sarmiento, D. M., Collen, J. F., Robben, P. M....Moran, K. A. (2007). Atypical Q Fever in US Soldiers. Emerging Infectious Diseases, 13(8), 1247. https://dx.doi.org/10.3201/eid1308.070218.
Streptococcus sinensis Endocarditis outside Hong Kong [PDF - 284 KB - 3 pages]
I. Uçkay et al.
Streptococcus sinensis has been described as a causative organism for infective endocarditis in 3 Chinese patients from Hong Kong. We describe a closely related strain in an Italian patient with chronic rheumatic heart disease. The case illustrates that S. sinensis is a worldwide emerging pathogen.
Uçkay I, Rohner P, Bolivar I, Ninet B, Djordjevic M, Nobre V, et al. Streptococcus sinensis Endocarditis outside Hong Kong. Emerg Infect Dis. 2007;13(8):1250. https://dx.doi.org/10.3201/eid1308.070124
Uçkay I, Rohner P, Bolivar I, et al. Streptococcus sinensis Endocarditis outside Hong Kong. Emerging Infectious Diseases. 2007;13(8):1250. doi:10.3201/eid1308.070124.
Uçkay, I., Rohner, P., Bolivar, I., Ninet, B., Djordjevic, M., Nobre, V....Schrenzel, J. (2007). Streptococcus sinensis Endocarditis outside Hong Kong. Emerging Infectious Diseases, 13(8), 1250. https://dx.doi.org/10.3201/eid1308.070124.
PCR versus Hybridization for Detecting Virulence Genes of Enterohemorrhagic Escherichia coli [PDF - 1.91 MB - 3 pages]
R. S. Gerrish et al.
We compared PCR amplification of 9 enterohemorrhagic Escherichia coli virulence factors among 40 isolates (21 O/H antigenicity classes) with DNA hybridization. Both methods showed 100% of the chromosomal and phage genes: eae, stx, and stx2. PCR did not detect 4%–20% of hybridizable plasmid genes: hlyA, katP, espP, toxB, open reading frame (ORF) 1, and ORF2.
Gerrish RS, Lee JE, Reed J, Williams J, Farrell LD, Spiegel KM, et al. PCR versus Hybridization for Detecting Virulence Genes of Enterohemorrhagic Escherichia coli. Emerg Infect Dis. 2007;13(8):1253. https://dx.doi.org/10.3201/eid1308.060428
Gerrish RS, Lee JE, Reed J, et al. PCR versus Hybridization for Detecting Virulence Genes of Enterohemorrhagic Escherichia coli. Emerging Infectious Diseases. 2007;13(8):1253. doi:10.3201/eid1308.060428.
Gerrish, R. S., Lee, J. E., Reed, J., Williams, J., Farrell, L. D., Spiegel, K. M....Shields, M. S. (2007). PCR versus Hybridization for Detecting Virulence Genes of Enterohemorrhagic Escherichia coli. Emerging Infectious Diseases, 13(8), 1253. https://dx.doi.org/10.3201/eid1308.060428.
Multidrug-Resistant Bacteria in Southeastern Austria [PDF - 192 KB - 2 pages]
A. Badura et al.
Badura A, Feierl G, Kessler HH, Grisold A, Masoud L, Wagner-Eibel U, et al. Multidrug-Resistant Bacteria in Southeastern Austria. Emerg Infect Dis. 2007;13(8):1256. https://dx.doi.org/10.3201/eid1308.070283
Badura A, Feierl G, Kessler HH, et al. Multidrug-Resistant Bacteria in Southeastern Austria. Emerging Infectious Diseases. 2007;13(8):1256. doi:10.3201/eid1308.070283.
Badura, A., Feierl, G., Kessler, H. H., Grisold, A., Masoud, L., Wagner-Eibel, U....Marth, E. (2007). Multidrug-Resistant Bacteria in Southeastern Austria. Emerging Infectious Diseases, 13(8), 1256. https://dx.doi.org/10.3201/eid1308.070283.
Osteomyelitis of Parietal Bone in Melioidosis [PDF - 204 KB - 3 pages]
N. G. Miksić et al.
Miksić NG, Alikadić N, Lejko TZ, Andlovic A, Knific J, Tomažič J. Osteomyelitis of Parietal Bone in Melioidosis. Emerg Infect Dis. 2007;13(8):1257. https://dx.doi.org/10.3201/eid1308.070479
Miksić NG, Alikadić N, Lejko TZ, et al. Osteomyelitis of Parietal Bone in Melioidosis. Emerging Infectious Diseases. 2007;13(8):1257. doi:10.3201/eid1308.070479.
Miksić, N. G., Alikadić, N., Lejko, T. Z., Andlovic, A., Knific, J., & Tomažič, J. (2007). Osteomyelitis of Parietal Bone in Melioidosis. Emerging Infectious Diseases, 13(8), 1257. https://dx.doi.org/10.3201/eid1308.070479.
Chikungunya Fever, Andaman and Nicobar Islands, India [PDF - 159 KB - 2 pages]
S. P. Manimunda et al.
Manimunda SP, Singh SS, Sugunan AP, Singh O, Roy S, Shriram AN, et al. Chikungunya Fever, Andaman and Nicobar Islands, India. Emerg Infect Dis. 2007;13(8):1259. https://dx.doi.org/10.3201/eid1308.070193
Manimunda SP, Singh SS, Sugunan AP, et al. Chikungunya Fever, Andaman and Nicobar Islands, India. Emerging Infectious Diseases. 2007;13(8):1259. doi:10.3201/eid1308.070193.
Manimunda, S. P., Singh, S. S., Sugunan, A. P., Singh, O., Roy, S., Shriram, A. N....Vijayachari, P. (2007). Chikungunya Fever, Andaman and Nicobar Islands, India. Emerging Infectious Diseases, 13(8), 1259. https://dx.doi.org/10.3201/eid1308.070193.
Alistipes finegoldii in Blood Cultures from Colon Cancer Patients [PDF - 210 KB - 3 pages]
L. Fenner et al.
Fenner L, Roux V, Ananian P, Raoult D. Alistipes finegoldii in Blood Cultures from Colon Cancer Patients. Emerg Infect Dis. 2007;13(8):1260. https://dx.doi.org/10.3201/eid1308.060662
Fenner L, Roux V, Ananian P, et al. Alistipes finegoldii in Blood Cultures from Colon Cancer Patients. Emerging Infectious Diseases. 2007;13(8):1260. doi:10.3201/eid1308.060662.
Fenner, L., Roux, V., Ananian, P., & Raoult, D. (2007). Alistipes finegoldii in Blood Cultures from Colon Cancer Patients. Emerging Infectious Diseases, 13(8), 1260. https://dx.doi.org/10.3201/eid1308.060662.
Shiga Toxin–producing Escherichia coli, Idaho [PDF - 186 KB - 3 pages]
V. M. Lockary et al.
Lockary VM, Hudson RF, Ball CL. Shiga Toxin–producing Escherichia coli, Idaho. Emerg Infect Dis. 2007;13(8):1262. https://dx.doi.org/10.3201/eid1308.070189
Lockary VM, Hudson RF, Ball CL. Shiga Toxin–producing Escherichia coli, Idaho. Emerging Infectious Diseases. 2007;13(8):1262. doi:10.3201/eid1308.070189.
Lockary, V. M., Hudson, R. F., & Ball, C. L. (2007). Shiga Toxin–producing Escherichia coli, Idaho. Emerging Infectious Diseases, 13(8), 1262. https://dx.doi.org/10.3201/eid1308.070189.
Imported Chikungunya Infection, Italy [PDF - 169 KB - 3 pages]
A. Beltrame et al.
Beltrame A, Angheben A, Bisoffi Z, Monteiro G, Marocco S, Calleri G, et al. Imported Chikungunya Infection, Italy. Emerg Infect Dis. 2007;13(8):1264. https://dx.doi.org/10.3201/eid1308.070161
Beltrame A, Angheben A, Bisoffi Z, et al. Imported Chikungunya Infection, Italy. Emerging Infectious Diseases. 2007;13(8):1264. doi:10.3201/eid1308.070161.
Beltrame, A., Angheben, A., Bisoffi, Z., Monteiro, G., Marocco, S., Calleri, G....Viale, P. (2007). Imported Chikungunya Infection, Italy. Emerging Infectious Diseases, 13(8), 1264. https://dx.doi.org/10.3201/eid1308.070161.
Dyella japonica Bacteremia in Hemodialysis Patient [PDF - 151 KB - 2 pages]
P. Kiratisin et al.
Kiratisin P, Kowwigkai P, Pattanachaiwit S, Apisarnthanarak A, Leelaporn A. Dyella japonica Bacteremia in Hemodialysis Patient. Emerg Infect Dis. 2007;13(8):1266. https://dx.doi.org/10.3201/eid1308.061204
Kiratisin P, Kowwigkai P, Pattanachaiwit S, et al. Dyella japonica Bacteremia in Hemodialysis Patient. Emerging Infectious Diseases. 2007;13(8):1266. doi:10.3201/eid1308.061204.
Kiratisin, P., Kowwigkai, P., Pattanachaiwit, S., Apisarnthanarak, A., & Leelaporn, A. (2007). Dyella japonica Bacteremia in Hemodialysis Patient. Emerging Infectious Diseases, 13(8), 1266. https://dx.doi.org/10.3201/eid1308.061204.
Mycobacterium cosmeticum, Ohio and Venezuela [PDF - 195 KB - 3 pages]
R. C. Cooksey et al.
Cooksey RC, de Waard JH, Yakrus MA, Toney SR, Da Mata O, Nowicki S, et al. Mycobacterium cosmeticum, Ohio and Venezuela. Emerg Infect Dis. 2007;13(8):1267. https://dx.doi.org/10.3201/eid1308.061261
Cooksey RC, de Waard JH, Yakrus MA, et al. Mycobacterium cosmeticum, Ohio and Venezuela. Emerging Infectious Diseases. 2007;13(8):1267. doi:10.3201/eid1308.061261.
Cooksey, R. C., de Waard, J. H., Yakrus, M. A., Toney, S. R., Da Mata, O., Nowicki, S....Srinivasan, A. (2007). Mycobacterium cosmeticum, Ohio and Venezuela. Emerging Infectious Diseases, 13(8), 1267. https://dx.doi.org/10.3201/eid1308.061261.
Ecoregional Dominance in Spatial Distribution of Avian Influenza (H5N1) Outbreaks [PDF - 280 KB - 3 pages]
R. Sengupta et al.
Sengupta R, Rosenshein L, Gilbert M, Weiller C. Ecoregional Dominance in Spatial Distribution of Avian Influenza (H5N1) Outbreaks. Emerg Infect Dis. 2007;13(8):1269. https://dx.doi.org/10.3201/eid1308.070329
Sengupta R, Rosenshein L, Gilbert M, et al. Ecoregional Dominance in Spatial Distribution of Avian Influenza (H5N1) Outbreaks. Emerging Infectious Diseases. 2007;13(8):1269. doi:10.3201/eid1308.070329.
Sengupta, R., Rosenshein, L., Gilbert, M., & Weiller, C. (2007). Ecoregional Dominance in Spatial Distribution of Avian Influenza (H5N1) Outbreaks. Emerging Infectious Diseases, 13(8), 1269. https://dx.doi.org/10.3201/eid1308.070329.
Nephropathia Epidemica in Metropolitan Area, Germany [PDF - 192 KB - 3 pages]
S. S. Essbauer et al.
Essbauer SS, Schmidt-Chanasit J, Madeja EL, Wegener W, Friedrich R, Petraityte R, et al. Nephropathia Epidemica in Metropolitan Area, Germany. Emerg Infect Dis. 2007;13(8):1271. https://dx.doi.org/10.3201/eid1308.061425
Essbauer SS, Schmidt-Chanasit J, Madeja EL, et al. Nephropathia Epidemica in Metropolitan Area, Germany. Emerging Infectious Diseases. 2007;13(8):1271. doi:10.3201/eid1308.061425.
Essbauer, S. S., Schmidt-Chanasit, J., Madeja, E. L., Wegener, W., Friedrich, R., Petraityte, R....Ulrich, R. G. (2007). Nephropathia Epidemica in Metropolitan Area, Germany. Emerging Infectious Diseases, 13(8), 1271. https://dx.doi.org/10.3201/eid1308.061425.
Effect of Hurricane Katrina on Arboviral Disease Transmission [PDF - 316 KB - 3 pages]
J. A. Lehman et al.
Lehman JA, Hinckley AF, Kniss KL, Nasci RS, Smith TL, Campbell GL, et al. Effect of Hurricane Katrina on Arboviral Disease Transmission. Emerg Infect Dis. 2007;13(8):1273. https://dx.doi.org/10.3201/eid1308.061570
Lehman JA, Hinckley AF, Kniss KL, et al. Effect of Hurricane Katrina on Arboviral Disease Transmission. Emerging Infectious Diseases. 2007;13(8):1273. doi:10.3201/eid1308.061570.
Lehman, J. A., Hinckley, A. F., Kniss, K. L., Nasci, R. S., Smith, T. L., Campbell, G. L....Hayes, E. B. (2007). Effect of Hurricane Katrina on Arboviral Disease Transmission. Emerging Infectious Diseases, 13(8), 1273. https://dx.doi.org/10.3201/eid1308.061570.
Threat to Cefixime Treatment for Gonorrhea [PDF - 281 KB - 3 pages]
S. Yokoi et al.
Yokoi S, Deguchi T, Ozawa T, Yasuda M, Ito S, Kubota Y, et al. Threat to Cefixime Treatment for Gonorrhea. Emerg Infect Dis. 2007;13(8):1275. https://dx.doi.org/10.3201/eid1308.060948
Yokoi S, Deguchi T, Ozawa T, et al. Threat to Cefixime Treatment for Gonorrhea. Emerging Infectious Diseases. 2007;13(8):1275. doi:10.3201/eid1308.060948.
Yokoi, S., Deguchi, T., Ozawa, T., Yasuda, M., Ito, S., Kubota, Y....Maeda, S. (2007). Threat to Cefixime Treatment for Gonorrhea. Emerging Infectious Diseases, 13(8), 1275. https://dx.doi.org/10.3201/eid1308.060948.
"The Calf-Path" [PDF - 107 KB - 1 page]
"The Calf-Path". Emerg Infect Dis. 2007;13(8):1207. https://dx.doi.org/10.3201/eid1308.ad1308
"The Calf-Path". Emerging Infectious Diseases. 2007;13(8):1207. doi:10.3201/eid1308.ad1308.
(2007). "The Calf-Path". Emerging Infectious Diseases, 13(8), 1207. https://dx.doi.org/10.3201/eid1308.ad1308.
Vector- and Rodent-borne Diseases in Europe and North America: Distribution, Public Health Burden and Control [PDF - 204 KB - 1 page]
A. Barrett
Barrett A. Vector- and Rodent-borne Diseases in Europe and North America: Distribution, Public Health Burden and Control. Emerg Infect Dis. 2007;13(8):1278. https://dx.doi.org/10.3201/eid1308.070626
Barrett A. Vector- and Rodent-borne Diseases in Europe and North America: Distribution, Public Health Burden and Control. Emerging Infectious Diseases. 2007;13(8):1278. doi:10.3201/eid1308.070626.
Barrett, A. (2007). Vector- and Rodent-borne Diseases in Europe and North America: Distribution, Public Health Burden and Control. Emerging Infectious Diseases, 13(8), 1278. https://dx.doi.org/10.3201/eid1308.070626.
'To Market to Market…' and Risk for Global Disease [PDF - 172 KB - 2 pages]
P. Potter
Potter P. 'To Market to Market…' and Risk for Global Disease. Emerg Infect Dis. 2007;13(8):1279-1280. https://dx.doi.org/10.3201/eid1308.ac1308
Potter P. 'To Market to Market…' and Risk for Global Disease. Emerging Infectious Diseases. 2007;13(8):1279-1280. doi:10.3201/eid1308.ac1308.
Potter, P. (2007). 'To Market to Market…' and Risk for Global Disease. Emerging Infectious Diseases, 13(8), 1279-1280. https://dx.doi.org/10.3201/eid1308.ac1308.
Developing a Research Agenda and a Comprehensive National Prevention and Response Plan for Rift Valley Fever in the United States [PDF - 35 KB - 2 pages]
S. C. Britch and K. J. Linthicum
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text:
Spark Voices
Our scientific
platform & programs
About Gene Therapy
Inherited Retinal Diseases
Historical Stock Lookup
Spark team
Annual Report & Proxy
European Commission Approves Spark Therapeutics' LUXTURNA® (voretigene neparvovec), a One-time Gene Therapy for Inherited Retinal Disease Caused by Confirmed Biallelic RPE65 Mutations
LUXTURNA is first gene therapy for a genetic disease approved in both the U.S. and EU
LUXTURNA is first and only gene therapy approved in EU for patients with an inherited retinal disease (IRD)
Spark Therapeutics will manufacture and supply LUXTURNA for Novartis, while Novartis has exclusive rights to pursue development, registration and commercialization in all other countries outside the U.S.
PHILADELPHIA, Nov. 23, 2018 (GLOBE NEWSWIRE) -- Spark Therapeutics (NASDAQ:ONCE), a fully integrated, commercial gene therapy company dedicated to challenging the inevitability of genetic disease, today announced that the European Commission has granted marketing authorization for LUXTURNA® (voretigene neparvovec), a one-time gene therapy for the treatment of adult and pediatric patients with vision loss due to inherited retinal dystrophy caused by confirmed biallelic RPE65 mutations and who have sufficient viable retinal cells. RPE65-mediated inherited retinal disease (IRD) is a progressive condition leading to total blindness in most patients. This authorization is valid in all 28-member states of the EU, as well as Iceland, Liechtenstein and Norway. LUXTURNA is the first gene therapy for a genetic disease that has received regulatory approval in both the U.S. and EU.
"The historic approval of LUXTURNA in Europe furthers our mission to challenge the inevitability of genetic disease around the world. Following the launch of LUXTURNA in the United States earlier this year, this decision makes LUXTURNA the first gene therapy for a genetic disease approved in both the U.S. and EU, a promising milestone for the many people living with genetic disease around the world," said Ron Philip, chief commercial officer at Spark Therapeutics. "Having worked closely with the global IRD community on the development of LUXTURNA, we are proud to be able to share the first gene therapy treatment option for an inherited retinal disease (IRD) with appropriate patients in Europe, in collaboration with Novartis."
In January 2018, Spark Therapeutics entered into a licensing agreement with Novartis to commercialize LUXTURNA when approved in Europe and all other markets outside the U.S. Under the licensing agreement, Novartis has exclusive rights to pursue development, registration and commercialization in all countries outside the U.S. Upon the transfer of the marketing authorization from Spark Therapeutics to Novartis, Novartis can commercialize LUXTURNA in the EU/European Economic Area (EEA). Spark Therapeutics entered into a separate agreement with Novartis to manufacture and supply LUXTURNA to Novartis.
"Today's approval is momentous for patients given that there have been no pharmacological treatment options to date," said Christina Fasser, president of Retina International, an umbrella organization of more than 43 patient organizations worldwide promoting research to find treatments for inherited retinal degenerative diseases. "Access to this treatment has the potential to reduce the substantial physical, emotional and financial burden this disease has on patients and their families."
In September 2018, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion recommending approval of LUXTURNA. This decision was based on data from a Phase 1 clinical trial, its follow-up trial and a Phase 3 trial that together enrolled 43 participants with inherited retinal disease caused by mutations in both copies of the RPE65 gene. The Phase 3 trial was the first randomized, controlled gene therapy trial for a genetic disease. LUXTURNA is designated as an orphan medicinal product for the treatment of inherited retinal dystrophies.
LUXTURNA was approved by the U.S. Food & Drug Administration (FDA) in December 2017.
Clinical Trial Overview of LUXTURNA® (voretigene neparvovec)
The safety and efficacy of LUXTURNA were assessed in one open-label, dose-exploration Phase 1 safety study (n=12), a second open-label Phase 1 follow-on study to assess the safety of injection of the contralateral eye (n=11) and an open-label, randomized, controlled Phase 3 efficacy and safety study (n=31) in pediatric and adult participants (range 4 to 44 years) with biallelic RPE65 mutation-associated retinal disease and sufficient viable retinal cells.
Of the 31 participants enrolled in the Phase 3 study, 21 were randomized to receive subretinal injection of LUXTURNA and 10 were randomized to the control (non-intervention) group. One participant in the intervention group discontinued from the study prior to treatment and one participant in the control group withdrew consent and was discontinued from the study. All nine participants randomized to the control group elected to cross over to receive LUXTURNA after one year of observation. All participants in these studies planned to be followed for long-term safety and efficacy. LUXTURNA Phase 3 clinical trial data, including data from the intervention group of all randomized participants through the one-year time point, have been previously reported in The Lancet.
The efficacy of LUXTURNA in the Phase 3 study was established based on the binocular multi-luminance mobility test (MLMT) score change from baseline to one year. MLMT was designed to measure changes in functional vision as assessed by the ability of a participant to navigate a course accurately and at a reasonable pace at seven different levels of illumination, ranging from 400 lux (corresponding to a brightly lit office) to one lux (corresponding to a moonless summer night). Each light level was assigned a score ranging from zero to six, with a higher score indicating that a participant could pass MLMT at a lower light level. A score of negative one was assigned to participants who could not pass MLMT at a light level of 400 lux. MLMT score change was defined as the difference between the score at baseline and the score at one year with a positive score change indicating that a participant was able to complete MLMT at a lower light level. Additional clinical outcomes included white light full-field light sensitivity threshold (FST) testing and visual acuity, both averaged over both eyes.
LUXTURNA Phase 3 clinical study results showed a statistically significant difference between the intervention group (n=21) and control participants (n=10) at one year in mean binocular MLMT score change (intervention minus control group difference of 1.6; 95% CI, 0.72, 2.41; p=0.001). After crossing over to receive LUXTURNA, participants in the control group showed a similar response to those in the intervention group. This score change has been sustained for at least three years for the original intervention group and at least two years in the crossover group of the Phase 3 clinical study. In addition, participants who received LUXTURNA showed a statistically significant improvement from baseline to one year in white light FST averaged over both eyes (p<0.001) and first assigned eye MLMT change score (p=0.001) compared to the control group. The change in visual acuity from baseline to one year was not significantly different between the intervention and control participants.
Three ocular serious adverse events (SAEs) were reported in the clinical program. One SAE related to the surgical procedure in one eye of a Phase 3 participant, in which there was foveal thinning that resulted in unresolved loss of foveal function. One additional Phase 3 participant who continued into the long-term follow-up study reported an SAE of retinal detachment 4 years after vector administration assessed as related to the administration procedure. The third ocular SAE was reported in one eye of a Phase 1 participant in which the treatment for bacterial endophthalmitis led to elevated intraocular pressure and subsequent optic atrophy. There were three non-serious AEs of retinal deposits (subretinal precipitate) in three participants (three eyes) that were considered to be related to LUXTURNA. All three of these events were mild in intensity, transient in nature and resolved without consequences. No deleterious immune responses have been observed. The most common adverse reactions related to LUXTURNA reported in 5 percent or greater of the combined Phase 1 and Phase 3 trial participants included conjunctival hyperemia, cataract, increased intraocular pressure, retinal tear, dellen (thinning of the corneal stroma), macular hole, subretinal deposits, eye inflammation, eye irritation, eye pain and maculopathy (wrinkling on the surface of the macula).
Indication and Important Safety Information for LUXTURNA in the United States
LUXTURNA is an adeno-associated virus vector-based gene therapy indicated for the treatment of patients with confirmed biallelic RPE65 mutation-associated retinal dystrophy.
Patients must have viable retinal cells as determined by the treating physicians.
Warnings and Precautions
Endophthalmitis may occur following any intraocular surgical procedure or injection. Use proper aseptic injection technique when administering LUXTURNA and monitor for and advise patients to report any signs or symptoms of infection or inflammation to permit early treatment of any infection.
Permanent decline in visual acuity may occur following subretinal injection of LUXTURNA. Monitor patients for visual disturbances.
Retinal abnormalities may occur during or following the subretinal injection of LUXTURNA, including macular holes, foveal thinning, loss of foveal function, foveal dehiscence, and retinal hemorrhage. Monitor and manage these retinal abnormalities appropriately. Do not administer LUXTURNA in the immediate vicinity of the fovea. Retinal abnormalities may occur during or following vitrectomy, including retinal tears, epiretinal membrane, or retinal detachment. Monitor patients during and following the injection to permit early treatment of these retinal abnormalities. Advise patients to report any signs or symptoms of retinal tears and/or detachment without delay.
Increased intraocular pressure may occur after subretinal injection of LUXTURNA. Monitor and manage intraocular pressure appropriately.
Expansion of intraocular air bubbles Instruct patients to avoid air travel, travel to high elevations or scuba diving until the air bubble formed following administration of LUXTURNA has completely dissipated from the eye. It may take one week or more following injection for the air bubble to dissipate. A change in altitude while the air bubble is still present can result in irreversible vision loss. Verify the dissipation of the air bubble through ophthalmic examination.
Cataract Subretinal injection of LUXTURNA, especially vitrectomy surgery, is associated with an increased incidence of cataract development and/or progression.
In clinical studies, ocular adverse reactions occurred in 66% of study participants (57% of injected eyes), and may have been related to LUXTURNA, the subretinal injection procedure, the concomitant use of corticosteroids, or a combination of these procedures and products.
The most common adverse reactions (incidence ≥ 5% of study participants) were conjunctival hyperemia (22%), cataract (20%), increased intraocular pressure (15%), retinal tear (10%), dellen (thinning of the corneal stroma) (7%), macular hole (7%), subretinal deposits (7%), eye inflammation (5%), eye irritation (5%), eye pain (5%), and maculopathy (wrinkling on the surface of the macula) (5%).
Immunogenicity
Immune reactions and extra-ocular exposure to LUXTURNA in clinical studies were mild. No clinically significant cytotoxic T-cell response to either AAV2 or RPE65 has been observed. In clinical studies, the interval between the subretinal injections into the two eyes ranged from 7 to 14 days and 1.7 to 4.6 years. Study participants received systemic corticosteroids before and after subretinal injection of LUXTURNA to each eye, which may have decreased the potential immune reaction to either AAV2 or RPE65.
Treatment with LUXTURNA is not recommended for patients younger than 12 months of age, because the retinal cells are still undergoing cell proliferation, and LUXTURNA would potentially be diluted or lost during the cell proliferation. The safety and efficacy of LUXTURNA have been established in pediatric patients. There were no significant differences in safety between the different age subgroups.
Please see the full U.S. Prescribing Information for LUXTURNA here.
About Inherited Retinal Disease (IRD) Caused by Confirmed Biallelic RPE65 Mutations
Inherited retinal diseases (also known as inherited retinal dystrophies) are a group of rare blinding conditions caused by one of more than 220 different genes, often disproportionally affecting children and young adults. Based on Spark Therapeutics' assessment of available epidemiology data, the prevalent population in the U.S., Europe and select additional markets in the Americas and Asia/Pacific is up to approximately 6,000 individuals, in total, with biallelic RPE65 mutations.
People living with IRD due to biallelic RPE65 gene mutations nearly all progress to complete blindness. They often experience night blindness (nyctalopia) due to decreased light sensitivity in childhood or early adulthood and involuntary back-and-forth eye movements (nystagmus). As the disease progresses, individuals may experience loss in their peripheral vision, developing tunnel vision and eventually, they may lose their central vision as well, resulting in total blindness. Independent navigation becomes severely limited, and vision-dependent activities of daily living are impaired.
Gene therapy is an approach to treat or prevent genetic disease by seeking to augment, replace or suppress one or more mutated genes with functional copies. It addresses the root cause of an inherited disease by enabling the body to produce a protein or proteins necessary to restore health or to stop making a harmful protein or proteins, with the potential of bringing back function in the diseased cells and/or slowing disease progression. To deliver the functional gene into the cell, a vector is used to transport the desired gene and is delivered either intravenously or injected into specific tissue. The goal is to enable, through the one-time administration of gene therapy, a lasting therapeutic effect.
About Spark Therapeutics
At Spark Therapeutics, a fully integrated, commercial company committed to discovering, developing and delivering gene therapies, we challenge the inevitability of genetic diseases, including blindness, hemophilia, lysosomal storage disorders and neurodegenerative diseases. We have successfully applied our technology in the first FDA-approved gene therapy in the U.S. for a genetic disease, and currently have three programs in clinical trials, including product candidates that have shown promising early results in patients with hemophilia. At Spark, we see the path to a world where no life is limited by genetic disease. For more information, visit www.sparktx.com, and follow us on Twitter and LinkedIn.
Spark Therapeutics Cautionary note on forward-looking statements
This release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding the company's product LUXTURNA® (voretigene neparvovec). The words ''anticipate,'' ''believe,'' ''expect,'' ''intend,'' ''may,'' ''plan,'' ''predict,'' ''will,'' ''would,'' ''could,'' ''should,'' ''continue'' and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. We may not actually achieve the plans, intentions or expectations disclosed in our forward-looking statements, and you should not place undue reliance on our forward-looking statements. Any forward-looking statements are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in, or implied by, such forward-looking statements. These risks and uncertainties include, but are not limited to, the risk that the improvements in functional vision demonstrated by LUXTURNA in our clinical trials may not be sustained over extended periods of time. For a discussion of other risks and uncertainties, and other important factors, any of which could cause our actual results to differ from those contained in the forward-looking statements, see the "Risk Factors" section, as well as discussions of potential risks, uncertainties and other important factors, in our Annual Report on Form 10-K, our Quarterly Reports on Form 10-Q and other filings we make with the Securities and Exchange Commission. All information in this press release is as of the date of the release, and Spark undertakes no duty to update this information unless required by law.
Ryan Asay
Ryan.asay@sparktx.com
(215) 239-6424 Media Contact:
Monique da Silva
communications@sparktx.com
Source: Spark Therapeutics, Inc.
Spark Therapeutics, Inc.
Phone: 1-855-SPARKTX / +1 215-220-9300
© Spark Therapeutics, Inc.

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