Bacterial Causes of Empyema in Children, Australia, 2007–2009 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

 

Volume 17, Number 10—October 2011

Research

Bacterial Causes of Empyema in Children, Australia, 2007–2009

Article Contents

• Methods
• Results
• Discussion
• Acknowledgments
• References
• Figure 1
• Figure 2
• Table 1
• Table 2
• Table 3

Roxanne E. Strachan, Anita Cornelius, Gwendolyn L. Gilbert, Tanya Gulliver, Andrew Martin, Tim McDonald, Gillian M. Nixon, Rob Roseby, Sarath Ranganathan, Hiran Selvadurai, Greg Smith, Manuel Soto-Martinez, Sadasivam Suresh, Laurel Teoh, Kiran Thapa, Claire E. Wainwright, Adam Jaffé , and on behalf of the Australian Research Network in Empyema

Author affiliations: Sydney Children’s Hospital, Randwick, New South Wales, Australia (R.E. Strachan, A. Jaffé); Royal Hobart Hospital, Hobart, Tasmania, Australia (A. Cornelius); Centre for Infectious Diseases and Microbiology, Westmead, New South Wales, Australia (G.L. Gilbert, K. Thapa); John Hunter Hospital, Newcastle, New South Wales, Australia (T. Gulliver); Princess Margaret Hospital for Children, Perth, Western Australia, Australia (A. Martin); The Canberra Hospital, Canberra, Australian Capital Territory, Australia (T. McDonald, L. Teoh); Monash Institute of Medical Research, Melbourne, Victoria, Australia (G.M. Nixon); Alice Springs Hospital, Alice Springs, Northern Territory, Australia (R. Roseby); Royal Children’s Hospital, Melbourne (S. Ranganathan, M. Soto-Martinez); Children’s Hospital at Westmead (H. Selvadurai); Women’s and Children’s Hospital, Adelaide, South Australia, Australia (G. Smith); Mater Children’s Hospital, Brisbane, Queensland, Australia (S. Suresh); Royal Children’s Hospital, Brisbane (C.E. Wainwright)

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Abstract

An increase in the incidence of empyema worldwide could be related to invasive pneumococcal disease caused by emergent nonvaccine replacement serotypes. To determine bacterial pathogens and pneumococcal serotypes that cause empyema in children in Australia, we conducted a 2-year study of 174 children with empyema. Blood and pleural fluid samples were cultured, and pleural fluid was tested by PCR. Thirty-two (21.0%) of 152 blood and 53 (33.1%) of 160 pleural fluid cultures were positive for bacteria; Streptococcus pneumoniae was the most common organism identified. PCR identified S. pneumoniae in 74 (51.7%) and other bacteria in 19 (13.1%) of 145 pleural fluid specimens. Of 53 samples in which S. pneumoniae serotypes were identified, 2 (3.8%) had vaccine-related and 51 (96.2%) had nonvaccine serotypes; 19A (n = 20; 36.4%), 3 (n = 18; 32.7%), and 1 (n = 8; 14.5%) were the most common. High proportions of nonvaccine serotypes suggest the need to broaden vaccine coverage.

Empyema in children is a relatively uncommon disease that occurs in 0.7% of children with pneumonia (1).

Many organisms cause empyema in children; Streptococcus pneumoniae is the most common (2–6). Other important causes, which are becoming increasingly frequent in several countries, are methicillin-sensitive Staphylococcus aureus (MSSA) (2,7,8) and methicillin-resistant S. aureus (MRSA). The latter is particularly problematic in indigenous communities (9). Other commonly identified organisms include S. pyogenes, Haemophilus influenzae, Mycoplasma pneumoniae, Pseudomonas aeruginosa, and other Streptococcus spp (10). The identification of causative organisms is usually determined by standard blood or pleural fluid cultures. Cultures are limited in that the yield can be as low as 8% (11), possibly because of prior antimicrobial drug treatment. Molecular techniques, such as PCR, are more sensitive in detecting causative organisms than standard culture (11) but are not routinely employed in laboratories for clinical use.

The 7-valent pneumococcal conjugate vaccine (PCV7) (Prevenar; Wyeth, Philadelphia, PA, USA) was introduced in Australia for immunocompromised and indigenous children <2 years of age in 2001 and was added to the national immunization schedule for all children <2 years in 2005 (www.medicareaustralia.gov.au/public/services/acir/index.jsp). Of >90 pneumococcal serotypes, the 7 included in the vaccine were responsible for 50%–70% of invasive pneumococcal disease (IPD) in children in most populations at the time of its development (12).

Many reports from around the world suggest an increase in the incidence of empyema in children (1,6,13–19). The reasons for this increase are unknown but may be related to IPD caused by emergent nonvaccine replacement serotypes, particularly serotypes 1, 3, and 19A after the introduction of PCV7 (14–20).

However, this theory is controversial because several studies identified an increase in empyema prevalence before the introduction of PCV7 (5,21,22). Because no Australian data exist on the bacterial causes of empyema, it is difficult to determine whether incidence in Australia is similar to reported trends in North America (14,22), the United Kingdom (5,6,16,18,21), Spain (15,17), and France (13).

The aims of this study were to identify the bacterial causes of empyema in children by using molecular techniques and to assess the efficacy of PCV7 by using molecular typing of invasive pneumococcal disease serotypes. This information may be helpful in deciding which of the newer conjugate pneumococcal vaccines should be introduced into national vaccination programs.

Methods

full-text:
Bacterial Causes of Empyema in Children, Australia, 2007–2009 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

Suggested citation for this article: Strachan RE, Cornelius A, Gilbert GL, Gulliver T, Martin A, et al. Bacterial causes of empyema in children, Australia, 2007–2009. Emerg Infect Dis [serial on the Internet]. 2011 Oct [date cited]. http://dx.doi.org/10.3201/eid1710.101825

DOI: 10.3201/eid1710.101825

Multidrug-Resistant Tuberculosis, People’s Republic of China, 2007–2009 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

 

Volume 17, Number 10—October 2011

Research

Multidrug-Resistant Tuberculosis, People’s Republic of China, 2007–2009

Article Contents

• Methods
• Results
• Discussion
• Acknowledgments
• References
• Figure 1
• Figure 2
• Table 1
• Table 2

Guang Xue He¹ , Hai Ying Wang¹, Martien W. Borgdorff, Dick van Soolingen, Marieke J. van der Werf, Zhi Min Liu, Xue Zheng Li, Hui Guo, Yan Lin Zhao, Jay K. Varma, Christopher P. Tostado, and Susan van den Hof

Author affiliations: Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of China (G.X. He, H. Guo, Y.L. Zhao); University of Amsterdam, Amsterdam, the Netherlands (G.X. He, M.W. Borgdorff, M.J. van der Werf, S. van den Hof); Shandong Provincial Tuberculosis Control Center, Jinan, People’s Republic of China (H.Y. Wang, Z.M. Liu, X.Z. Li); National Institute for Public Health and the Environment, Bilthoven, the Netherlands (D. van Soolingen); KNCV Tuberculosis Foundation, The Hague, the Netherlands (M.J. van der Werf, S. van den Hof); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (J.K. Varma); Tsinghua University, Beijing (C.P. Tostado)

Suggested citation for this article

Abstract

We conducted a case–control study to investigate risk factors for multidrug-resistant tuberculosis (MDR TB) in the People’s Republic of China. Genotyping analysis was used to estimate the percentage of cases from recent transmission among 100 MDR TB case-patients hospitalized during April 2007–July 2009. Molecular subtyping of isolates showed that 41% of MDR TB strains clustered. Beijing genotype was found in 94% of the MDR TB isolates and 79% of the pan-susceptible isolates. In multivariate analysis, MDR TB was independently associated with Beijing genotype, retreatment for TB, symptoms lasting >3 months before first evaluation at the hospital, lack of health insurance, and being a farmer (vs. being a student). MDR TB was associated with Beijing genotype and lower socioeconomic status. A large percentage of MDR TB cases seemed to result from recent transmission. Early detection, effective treatment, and infection control measures for MDR TB are needed to reduce transmission.

Multidrug-resistant tuberculosis (MDR TB), defined as resistance to at least isoniazid and rifampin, has emerged as a global public health problem (1). The People’s Republic of China has the second greatest number of MDR TB cases in the world (2). According to the National Anti-Tuberculosis Drug Resistance Survey in 2007, an estimated 120,000 new MDR TB cases emerge annually in China, accounting for ≈24% of MDR TB worldwide (3). Although MDR TB represents only 8% of incident TB cases in China, controlling MDR TB is challenging because it is difficult to diagnose and treat (4). Thus, MDR TB is increasingly becoming a serious threat to TB control (3,5), and the recognition of extensively drug-resistant TB has furthered highlighted this threat (6,7).

The first pilot sites for the programmatic management of drug-resistant TB in China were established in October 2006. By the end of July 2010, similar management programs covered 41 prefectures/cities in 12 provinces in which ≈1,000 patients with MDR TB were treated with standardized treatment regimens recommended by the World Health Organization (8,9).

Mycobacterium tuberculosis acquires resistance to antimicrobial drugs through the selection of bacteria with mutations in resistance genes (10). Particular resistance genotypes, such as isoniazid-resistant strains from which the katG gene has been deleted, have been associated with decreased growth and persistence of M. tuberculosis in mice and guinea pigs (11). A recent molecular study suggests that drug-resistant strains of M. tuberculosis may be as transmissible as pan-sensitive strains (12). However, some isoniazid-resistant strains, such as those with a mutation at aa 315 of the katG gene, were as transmissible as drug-susceptible strains; these resistant, but equivalently transmissible, strains are typically associated with outbreaks (13–15).

In the past decade, many studies have evaluated the role of the Beijing genotype of M. tuberculosis in the worldwide TB epidemic (16,17). Beijing genotype strains are emerging in Southeast Asia, former Soviet republics, the Baltic states, and South Africa and are associated with multidrug resistance (17–22). In Europe, during 2003–2006, about half of MDR TB and extensively drug-resistant TB cases were caused by recent transmission, and 85% of those cases were caused by Beijing strains; during the same period, only 6%–7% of drug-susceptible TB cases in Europe were caused by Beijing strains (21,22). As the name suggests, Beijing genotype strains are particularly prevalent in China. In a survey of 10 provinces in China, the average percentage of Beijing genotype strains was 73%, but the percentage varied substantially by region, with the highest (93%) in the Beijing region (23).

Genotyping studies help elucidate transmission of TB by specific strains (17–20). Since 1993, IS6110 restriction fragment-length polymorphism typing has been considered the standard for studying the molecular epidemiology of TB (24). Although restriction fragment-length polymorphism typing has brought significant new insights into TB transmission, the method is technically demanding and time-consuming (23). Therefore, a new standard typing method using mycobacterial interspersed repetitive unit–variable-number of tandem repeats (MIRU-VNTR) in the genome was recently proposed for studying clustering and transmission (25). The analysis of regions of difference (RDs) in the genome of M. tuberculosis complex can be used to study the phylogeny of these bacteria; this approach can also be used as an alternative to the more complicated spoligotyping method for Beijing genotype strain identification (26,27).

We used the RD105 deletion detection method to identify Beijing genotype strains. We also used 24-locus VNTR typing to investigate MDR TB transmission in patients admitted to the largest TB hospital in Shandong Province during April 2007–July 2009. Our goal was to characterize the genotypes of different MDR TB strains and identify specific risk factors associated with MDR TB and MDR TB strain clustering. A study in TB patients in the same hospital during 2004–2007 showed a prevalence of MDR TB of 10.8% (28). Although the national guideline of the TB control program requests directly observed treatment, in which TB patients take all doses under supervision, another study in rural Shandong showed that most TB patients do not receive directly observed treatment (29), which poses a risk for drug resistance. In Shandong Province, the programmatic management of drug-resistant TB has been introduced only in 1 prefecture, starting in October 2008.

Methods

full-text:
Multidrug-Resistant Tuberculosis, People’s Republic of China, 2007–2009 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

Suggested citation for this article: He GX, Wang HY. Borgdorff MW, van Soolingen D, van der Werf MJ, Liu ZM, et al. Multidrug-resistant tuberculosis, People’s Republic of China, 2007–2009. Emerg Infect Dis [serial on the Internet]. 2011 Oct [date cited]. http://dx.doi.org/10.3201/eid1710.110546

DOI: 10.3201/eid1710.110546

¹These authors contributed equally to this article.

Pandemic (H1N1) 2009 among Quarantined Close Contacts, Beijing, People’s Republic of China - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

 

Volume 17, Number 10—October 2011

Research

Pandemic (H1N1) 2009 among Quarantined Close Contacts, Beijing, People’s Republic of China

Article Contents

• Methods
• Results
• Discussion
• Acknowledgments
• References
• Table 1
• Table 2
• Table 3
• Table 4

Xinghuo Pang¹, Peng Yang¹, Shuang Li, Li Zhang, Lili Tian, Yang Li, Bo Liu, Yi Zhang, Baiwei Liu, Ruogang Huang, Xinyu Li, and Quanyi Wang 

Author affiliations: Beijing Center for Disease Prevention and Control, Beijing, People’s Republic of China; Capital Medical University School of Public Health and Family Medicine, Beijing

Suggested citation for this article

Abstract

We estimated the attack rate of pandemic (H1N1) 2009 and assessed risk factors for infection among close contacts quarantined in Beijing, People’s Republic of China. The first 613 confirmed cases detected between May 16 and September 15, 2009, were investigated; 7,099 close contacts were located and quarantined.

The attack rate of confirmed infection in close contacts was 2.4% overall, ranging from 0.9% among aircraft passengers to >5% among household members. Risk factors for infection among close contacts were younger age, being a household member of an index case-patient, exposure during the index case-patient’s symptomatic phase, and longer exposure. Among close contacts with positive test results at the start of quarantine, 17.2% had subclinical infection. Having contact with a household member and younger age were the major risk factors for acquiring pandemic (H1N1) 2009 influenza virus infection. One person in 6 with confirmed pandemic (H1N1) 2009 was asymptomatic.

In early April 2009, human cases of infection with a novel influenza virus of swine origin, pandemic (H1N1) 2009 virus, were identified in the United States and Mexico, and this virus spread rapidly across the world (1–3). On June 11, 2009, the World Health Organization raised the pandemic level to 6, the highest level for pandemic alert (4).

Estimating attack rates is a major task in characterizing pandemic (H1N1) 2009. Some studies have reported attack rates of pandemic (H1N1) 2009 among household members and aircraft passengers (5–7). These studies suggested that the transmissibility of pandemic (H1N1) 2009 virus was low. These studies were conducted in outbreak settings, and attack rates were calculated on the basis of clinical diseases that included influenza-like illness (ILI) or acute respiratory illness (ARI) of close contacts rather than confirmed infection with pandemic (H1N1) 2009 virus. In addition, in these studies only symptomatic index and secondary cases were included. Although most infections of pandemic (H1N1) 2009 influenza virus produce ILI or ARI symptoms (8–12), subclinical infection can occur and can change the estimate of attack rate. In addition, the infectivity of asymptomatic case-patients has not been clearly defined (13).

Because of the high rates of illness and death among the initial case-patients with pandemic (H1N1) 2009 (14), the Chinese government decided to prevent and contain the rapid spread of disease through tracing and quarantine of persons who had close contact with persons with confirmed cases of pandemic (H1N1) 2009. Beijing, the capital of the People’s Republic of China, took strict containment and control measures through October 2009. The Beijing municipal government implemented border entry screening, ILI screening in hospitals, health follow-up of travelers from overseas, and quarantine and testing of close contacts to identify new introduction of cases and local transmission. Public health workers conducted epidemiologic investigation of all index case-patients (including those with subclinical infections) and traced and quarantined close contacts whose residence was within the jurisdiction of Beijing. We estimated the attack rate of pandemic (H1N1) 2009 virus infection and assessed risk factors or correlates for infection among different types of close contacts, including household members and aircraft passengers.

Methods

Confirmation of Index Cases

full-text:
Pandemic (H1N1) 2009 among Quarantined Close Contacts, Beijing, People’s Republic of China - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

Suggested citation for this article: Pang X, Yang P, Li S, Zhang L, Tian L, Li Y, et al. Pandemic (H1N1) 2009 among quarantined close contacts, Beijing, People’s Republic of China. Emerg Infect Dis [serial on the internet]. 2011 Oct [date cited]. http://dx.doi.org/10.3201/eid1710.101344

DOI: 10.3201/eid1710.101344

¹These authors contributed equally to this article.

Humans Infected with Relapsing Fever Spirochete Borrelia miyamotoi, Russia - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

 

Volume 17, Number 10—October 2011

Research

Humans Infected with Relapsing Fever Spirochete Borrelia miyamotoi, Russia

Article Contents

• Methods
• Results
• Discussion
• Acknowledgments
• References
• Figure 1
• Figure 2
• Figure 3
• Table 1
• Table 2
• Table 3

Alexander E. Platonov, Ludmila S. Karan, Nadezhda M. Kolyasnikova, Natalya A. Makhneva, Marina G. Toporkova, Victor V. Maleev, Durland Fish, and Peter J. Krause 

Author affiliations: Central Research Institute of Epidemiology, Moscow, Russia (A.E. Platonov, L.S. Karan, N.M. Kolyasnikova, V.V. Maleev); Municipal Clinical Hospital No. 33, Yekaterinburg, Russia (N.A. Makhneva, M.G. Toporkova); Yale School of Public Health and Yale School of Medicine, New Haven, Connecticut, USA (D. Fish, P.J. Krause)

Suggested citation for this article

Abstract

Borrelia miyamotoi is distantly related to B. burgdorferi and transmitted by the same hard-body tick species. We report 46 cases of B. miyamotoi infection in humans and compare the frequency and clinical manifestations of this infection with those caused by B. garinii and B. burgdorferi infection. All 46 patients lived in Russia and had influenza-like illness with fever as high as 39.5°C; relapsing febrile illness occurred in 5 (11%) and erythema migrans in 4 (9%). In Russia, the rate of B. miyamotoi infection in Ixodes persulcatus ticks was 1%–16%, similar to rates in I. ricinus ticks in western Europe and I. scapularis ticks in the United States. B. miyamotoi infection may cause relapsing fever and Lyme disease–like symptoms throughout the Holarctic region of the world because of the widespread prevalence of this pathogen in its ixodid tick vectors.

Borrelia miyamotoi, discovered in Japan in 1995, belongs to the relapsing fever group of Borrelia (1). Relapsing fever borreliae infections are characterized by influenza-like illness and >1 relapse episode of bacteremia and fever. B. miyamotoi is more distantly related to B. burgdorferi, a group of spirochetes that includes B. burgdorferi s.l. strains (B. afzelii; B. garinii; and B. burgdorferi s.s., the causative agent of Lyme disease) (2,3). In Eurasia and North America, B. miyamotoi is found in a small percentage of all species of ixodid tick vectors of B. burgdorferi, including Ixodes persulcatus (1,3,4), I. ricinus (5–7), I. scapularis (2,3,8,9), and I. pacificus (10). It is transmitted transovarially and transstadially by ticks and coexists with B. burgdorferi (2,3). Recently, we discovered B. miyamotoi in I. persulcatus and I. ricinus ticks in the European and Asian regions of Russia. In these areas, human ixodid tick-borne infections, including those caused by B. afzelii, B. garinii, and viral tick-borne encephalitis virus (TBEV; genus Flavivirus) are endemic and transmitted by the same tick species.

Despite the presence of B. miyamotoi in vector ticks, to our knowledge, human disease caused by this spirochete has not been definitively established. We previously noted presumptive B. miyamotoi infection in residents of central Russia with influenza-like illness but were uncertain whether their clinical manifestations were caused by co-infecting B. burgdorferi s.l. species (11–13). To confirm those findings and develop initial estimates of the prevalence and severity of B. miyamotoi infection, we conducted a comparative cohort study. We used improved antibody assays and PCRs to compare the relative frequency and clinical manifestations of B. miyamotoi infection with those of B. garinii infection in Russia and B. burgdorferi infection in the United States.

full-text:
Humans Infected with Relapsing Fever Spirochete Borrelia miyamotoi, Russia - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

Figure 1. Percentage of Ixodes persulcatus (I. p.) and I. ricinus (I. r.) ticks infected with Borrelia miyamotoi in Russia. The number of ticks that were tested is given in parenthesis. Star indicates...

Suggested citation for this article: Platonov AE, Karan LS, Kolyasnikova NM, Makhneva NA, Toporkova MG, Maleev VV, et al. Humans infected with relapsing fever spirochete Borrelia miyamotoi, Russia. Emerg Infect Dis [serial on the Internet]. 2011 Oct [date cited]. http://dx.doi.org/10.3201/eid1710.101474

DOI: 10.3201/eid1710.101474

Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus Infection in England and Scotland, 2009–2010 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

 

Volume 17, Number 10—October 2011

Research

Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus Infection in England and Scotland, 2009–2010

Article Contents

• Methods
• Results
• Discussion
• References
• Figure
• Table 1
• Table 2
• Table 3
• Table 4

Laurence Calatayud , Angie Lackenby, Arlene Reynolds, Jim McMenamin, Nick F. Phin, Maria Zambon, and Richard Pebody

 

Author affiliations: Health Protection Agency, London, UK (L. Calatayud, A. Lackenby, N.F. Phin, M.C. Zambon, R. Pebody); Health Protection Scotland, Glasgow, Scotland, UK (A. Reynolds, J. McMenamin)

Suggested citation for this article

Abstract

Oseltamivir has been widely used for pandemic (H1N1) 2009 virus infection, and by April 30, 2010, a total of 285 resistant cases were reported worldwide, including 45 in the United Kingdom. To determine risk factors for emergence of oseltamivir resistance and severe infection, a case–control study was conducted in the United Kingdom. Study participants were hospitalized in England or Scotland during January 4, 2009–April 30, 2010. Controls had confirmed oseltamivir-sensitive pandemic (H1N1) 2009 virus infections, and case-patients had confirmed oseltamivir-resistant infections. Of 28 case-patients with available information, 21 (75%) were immunocompromised; 31 of 33 case-patients (94%) received antiviral drugs before a sample was obtained. After adjusting for confounders, case-patients remained significantly more likely than controls to be immunocompromised and at higher risk for showing development of respiratory complications.

Selective drug pressure likely explains the development of oseltamivir resistance, especially among immunocompromised patients. Monitoring of antiviral resistance is strongly recommended in this group.

Neuraminidase inhibitors, antiviral drugs that limit replication of influenza A and B viruses (1), are recommended in the United Kingdom for treatment and prophylaxis of patients at higher risk for severe or complicated influenza virus infection (2). During the initial containment phase of the 2009 influenza pandemic, antiviral drugs were prescribed for all patients with confirmed infections and their close contacts. During the subsequent treatment phase of the pandemic, the drugs were recommended for persons with suspected influenza virus infections who were at high risk for severe disease (3).

Before the 2007–08 influenza season, the development of oseltamivir-resistant influenza was rare (4), mainly occurring among persons who were more likely to have prolonged virus shedding, such as children (5) and immunocompromised patients (6). Patients with subtype H1N1 oseltamivir-resistant strains had the same point mutation in the viral neuraminidase gene (H275Y) that is known to confer high-level resistance to oseltamivir (7), but the mutation was associated with reduced infectivity and replicative ability (8). During the 2007–08 season, transmissible influenza A (H1N1) viruses resistant to oseltamivir (with the H275Y mutation) emerged and became predominant over susceptible subtype H1N1 viruses (4,9). The influenza A pandemic (H1N1) 2009 virus was initially reported as fully susceptible to the neuraminidase inhibitors (oseltamivir and zanamivir) but resistant to adamantanes, having the S31N (serine to asparagine) mutation in the M2 ion channel (10).

On July 8, 2009, the World Health Organization reported the first sporadic cases of oseltamivir-resistant pandemic (H1N1) 2009 infection in Denmark; Japan; and Hong Kong Special Administrative Region, People’s Republic of China (11). By April 28, 2010, a total of 285 oseltamivir-resistant cases had been reported worldwide (12), including 45 in the United Kingdom. Three clusters each were reported from Wales (13); the United Kingdom; North Carolina, USA (14); and Vietnam (15). All of the pandemic (H1N1) 2009 oseltamivir-resistant viruses had the previously described H275Y mutation. No reassortment between the pandemic (H1N1) 2009 virus and the seasonal oseltamivir-resistant subtype H1N1 influenza strain has been detected (16–18), and all of the oseltamivir-resistant viruses have retained sensitivity to zanamivir.

This report describes the epidemiologic, clinical, and demographic characteristics of patients with oseltamivir-resistant pandemic (H1N1) 2009 virus infections in England and Scotland. It also identifies risk factors for severe infection and for the emergence of oseltamivir-resistant virus to inform modifications to current recommendations for the use of antiviral drugs for treatment and prophylaxis of influenza A pandemic (H1N1) 2009 virus infection.

Methods

full-text:
Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus Infection in England and Scotland, 2009–2010 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

Suggested citation for this article: Calatayud L, Lackenby A, Reynolds A, McMenamin J, Phin NF, Zambon MC, et al. Oseltamivir-resistant pandemic (H1N1) 2009 virus infection in England and Scotland, 2009–2010. [serial on the Internet]. 2011 Oct [date cited]. http://dx.doi.org/10.3201/eid1710.110117

DOI: 10.3201/eid1710.110117

Plasmodium knowlesi Malaria in Humans and Macaques, Thailand - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

 

Volume 17, Number 10—October 2011

Research

Plasmodium knowlesi Malaria in Humans and Macaques, Thailand

Article Contents

• Materials and Methods
• Results
• Discussion
• Acknowledgments
• References
• Figure 1
• Figure 2
• Table 1
• Table 2
• Table 3
• Table 4

Somchai Jongwutiwes , Pattakorn Buppan, Rattiporn Kosuvin, Sunee Seethamchai, Urassaya Pattanawong, Jeeraphat Sirichaisinthop, and Chaturong Putaporntip

Author affiliations: Chulalongkorn University, Bangkok, Thailand (S. Jongwutiwes, P. Buppan, R. Kosuvin, U. Pattanawong, C. Putaporntip); Naresuan University, Phitsanulok, Thailand (S. Seethamchai); Vector Borne Disease Training Center, Saraburi, Thailand (J. Sirichaisinthop)

Suggested citation for this article

Abstract

Naturally acquired human infections with Plasmodium knowlesi are endemic to Southeast Asia. To determine the prevalence of P. knowlesi malaria in malaria-endemic areas of Thailand, we analyzed genetic characteristics of P. knowlesi circulating among naturally infected macaques and humans. This study in 2008–2009 and retrospective analysis of malaria species in human blood samples obtained in 1996 from 1 of these areas showed that P. knowlesi accounted for 0.67% and 0.48% of human malaria cases, respectively, indicating that this simian parasite is not a newly emergent human pathogen in Thailand. Sequence analysis of the complete merozoite surface protein 1 gene of P. knowlesi from 10 human and 5 macaque blood samples showed considerable genetic diversity among isolates. The sequence from 1 patient was identical with that from a pig-tailed macaque living in the same locality, suggesting cross-transmission of P. knowlesi from naturally infected macaques to humans.

Plasmodium knowlesi circulates mainly among long-tailed macaques (Macaca fascicularis) and pig-tailed macaques (M. nemestrina) that inhabit a wide area of Southeast Asia (1). Microscopy-based detection of P. knowlesi has failed because morphologic features of young trophozoites of P. knowlesi resemble those of P. falciparum and characteristic band-shaped growing trophozoites resemble those of P. malariae (2–4). To date, the effective tool for diagnosing P. knowlesi infection is PCR specific for multicopy genes, such as small subunit rRNA and mitochondrial cytochrome b (3–5).

Human infections with P. knowlesi vary by geographic location (highest prevalence in Malaysian Borneo), but individual cases have been increasingly identified in countries in Southeast Asia (6). Our large-scale molecular-based survey of malaria in Thailand during 2006–2007 showed that P. knowlesi was widely distributed at a low prevalence (in 0.57% of all malaria cases identified) in several malaria-endemic areas bordering Myanmar, Cambodia, and Malaysia (7). Correct diagnosis of malaria has a major effect on malaria control in terms of treatment outcomes, disease transmission, and interpretation of efficiency of a given control measure.

Although malaria caused by P. knowlesi is generally benign and responsive to chloroquine treatment, severe and fatal cases similar to complicated P. falciparum malaria cases have been documented (6,8). To date, it has been unknown whether human infections with P. knowlesi in Thailand were caused by a new emergence of this parasite species or whether the parasite had been circulating cryptically with other human malaria parasites. Furthermore, it would be useful to explore spatiotemporal distribution of malaria species in humans and analyze genetic characteristics of P. knowlesi circulating among naturally infected macaques and humans. These data could lead to a better understanding of malaria transmission and provide information for a more effective malaria control policy at a nationwide level. Therefore, we sought to determine the prevalence of this simian malaria in malaria-endemic regions of Thailand.

Materials and Methods

Prospective Study and Sample Collection

Figure 1

Figure 1. Provinces of Thailand where blood samples were obtained and tested for malaria, 1996–2009. Tak: blue, n = 210 in 1996, n = 681 in 2006–2007, and n = 1,216 in 2008–2009;...

Most malaria infections in Thailand occur in forests or forest fringes along its borders with other countries, and malaria transmission exhibits a bimodal pattern that peaks in May–July and October–November (9,10). During October 2008–September 2009, venous or finger prick blood samples were obtained from 3,770 febrile persons (2,577 male and 1,193 female; mean age 27.4 years, range 1–87 years) who came to malaria clinics in northwestern (Tak Province, n = 1,354), eastern (Chantaburi Province, n = 401), and southern (Yala Province, n = 1,552, and Narathiwat Province, n = 463) Thailand (Figure 1). These 3,770 persons represented 12.4% of the 30,425 malaria cases in these areas during the study period (10). A total of 470 blood samples from these persons were negative for malaria parasites by microscopy (153 in Tak, 179 in Yala, and 138 in Narathiwat). The study was reviewed and approved by the Institutional Review Board of Faculty of Medicine, Chulalongkorn University.

full-text:
Plasmodium knowlesi Malaria in Humans and Macaques, Thailand - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

Suggested citation for this article: Jongwutiwes S, Buppan P, Kosuvin R, Seethamchai S, Pattanawong U, Sirichaisinthop J, et al. Plasmodium knowlesi malaria in humans and macaques, Thailand. Emerg Infect Dis [serial on the Internet]. 2011 Oct [date cited]. http://dx.doi.org/10.3201/eid1710.110349

DOI: 10.3201/eid1710.110349

Much have I travel’d in the realms of gold1 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC

Volume 17, Number 10—October 2011

About the Cover

Much have I travel’d in the realms of gold¹

Article Contents

• About the Cover
• References

Polyxeni Potter 

Author affiliation: Centers for Disease Control and Prevention, Atlanta, Georgia, USA

Suggested citation for this article

Rembrandt van Rijn (1606–1669) Aristotle with a Bust of Homer (1653) Oil on canvas (143.5 cm × 136.5 cm). The Metropolitan Museum of Art, New York, NY

 

“Know thyself” resonated with Rembrandt van Rijn. More than any other artist of his caliber at any time, he explored his own image in as many as 90 self-portraits, some 60 of them paintings, an extraordinary record of self-examination. He was so frank with his depictions he could not have been motivated by narcissism. He may have taken up portraiture for its connection to history painting, a lifelong interest. Portraits were very popular in the commercial market of his day, and his were much sought after in Holland. Whatever the motivation, his self-portraits captured much more than physical features. From youth to ripe old age they amounted to a spiritual autobiography, and since he never strayed more than a few miles from his native Leiden, the journey of discovery was an inward one.

Rembrandt’s life has been shrouded in mystery, largely because no written records exist beyond the usual certificates of birth, baptism, marriage, and death. He left no journal, and seven surviving letters from his hand concern routine transactions. But for an inventory of his possessions when near the end of his life he declared himself insolvent, the great artist left few clues about himself, save in his art, a brilliant legacy of more than 2,300 works, among them the famed Anatomy Lesson of Dr. Tulp, Night Watch, some of his self-portraits, and Aristotle with a Bust of Homer, on this month’s cover.

Aristotle with a Bust of Homer was commissioned by Don Antonio Ruffo, Sicilian nobleman, art collector, and patron of Rembrandt, without specific guidance, except to paint a philosopher. The meeting of the minds ensemble that ensued was the painter’s idea. A mixture of history and myth, the composition contains Rembrandt hallmarks: simplicity, quiet, character, empathy. While two figures are clearly present, a third one, Alexander the Great, appears indirectly, on the ornate pendant worn by Aristotle.

The philosopher is portrayed in his study as a distinguished figure, clad in finery reminiscent of the
Renaissance. A certain social rank, the markings of which appear in other works by Rembrandt, including some self-portraits, is present in the elegant attire and the sensitive ringed hands. Though not a military man, Aristotle seems decorated, the gold chain and medallion bestowed upon him by the warrior prince displayed prominently. Secure in his own stature, Aristotle seems lost in thought. He rests one hand on the bust as he casts brooding eyes on antiquity’s celebrated poet, “deep-brow’d” Homer, a figure much admired by Aristotle and revered by Alexander, Aristotle’s pupil, who carried everywhere he went a copy of The Iliad, annotated by his tutor.

This imaginary meeting of three ancient historical figures, a gathering of genius, shows not only the artist’s inventiveness and technical brilliance but also his thoughts on the subject. Asked to paint a generic philosopher, he was intrigued by his own choice, and “Like some watcher of the skies/when a new planet swims into his ken,” he did much more.

Homer is a legend. The exact period of his life has been debated, his very existence questioned. Skeptics have been so doubtful about him, it has been said in jest that the epic works were not created by him but by someone else with the same name. Still, Homer persists as poet of The Iliad and The Odyssey. Thought to have lived close to 3,000 years ago, he predated realistic portraiture. His image was invented much later and frequently copied, always sightless and bearded, often wearing a headband. Rembrandt likely relied on Hellenistic busts in his own collection for guidance.

The dark and stillness of the room and faint outline of books in back amplify the lighted face and figure of the philosopher. His depiction as a Renaissance man, be it artistic license or intentional anachronism, could not have been more apt. Aristotle knew and understood all that was known in his day, to which he contributed in spades. A man for whom no discipline was uninteresting or unattainable, he was as comfortable with the arts as he was with the sciences.

This extraordinary empirical man paused with humility in front of the revered poet, who explored the mysteries of the human heart. Homer’s world, a place of conflict and adversity against which humans were expected to show strength, courage, and perseverance paved the way for philosophy. His was too a world full of wonder and discovery: close calls, shipwrecks, natural catastrophes, lotus-eaters, Cyclops, Sirens, the bravest men, the most beautiful woman, the most faithful wife.

In Rembrandt’s portrait, the haunting eyes that surveyed the totality of human knowledge are unfathomable. Contemplation, the philosopher wrote in the Nicomachean Ethics, is the highest form of happiness, and of all pleasures in life, it is the most enduring and self-sufficient. Since the intellect (νους) is our most exalted attribute and what it grasps is the highest knowledge, contemplation must be the ultimate form of human activity. Equal to philosophical wisdom, it involves scientific understanding―the intuitive grasp of eternal first principles combined with demonstration.

Contemplation as guide to life has been interpreted in many ways. In the thousands of years since Homer, Aristotle, and Alexander, many have taken the philosopher’s call, and some have written modern Odysseys. More than 70,000 species of fungi alone have been described since Aristotle classified living things into animals and plants. His theory of spontaneous generation has been hotly debated. But his concept of emergence holds true: “The whole is not just the sum of its parts” because the emergent order will not arise if the parts simply coexist without interaction.

Complex interactions that Aristotle could not have anticipated, such as cell and solid organ transplantation and antimicrobial drug resistance, continue to stir up our biologic world. In this issue of Emerging Infectious Diseases, incidence of non-Aspergillus mold infections in hematopoietic cell and solid organ transplant recipients is increasing, and multiazole resistance in Aspergillus fumigatus associated with poor outcome in patients with invasive aspergillosis is now widespread in the Netherlands.

Long after Rembrandt painted Aristotle contemplating Homer, Nikos Kazantzakis wrote his version of The Odyssey. Having called modern humans to action against adversity and even against the inevitability of death, he engaged Homeric language to lead them in Aristotelian contemplation, not for any immediate resolution of perils in the world but as an end in itself: “I know not if I shall ever anchor.” Now the day’s work is done, “I collect my tools; sight, smell, touch, taste, hearing, intellect. Night has fallen …. I return like a mole to my home, the ground. Not because I am tired and cannot work. I am not tired. But the sun has set.”

References

1. Christian  JL. Philosophy: an introduction to the art of wondering. Belmont (CA): Wadsworth Cengage Learning; 2009.
2. Kazantzakis  N. The Odyssey: a modern sequel. New York: Simon and Schuster; 1958.
3. Park  BJ, Pappas  PG, Wannemuehler  KA, Alexander  BD, Anaissie  EJ, Andes  DR, Invasive non-Aspergillus mold infections in transplant recipients, United States, 2001–2006. Emerg Infect Dis. 2011;17:1855–64.
4. Van der Linden  JWM, Snelders  E, Kampinga  GA, Rijnders  BJA, Mattsson  E, Debets-Ossenkopp  YJ, Clinical implications of azole resistance in Aspergillus fumigatus, the Netherlands, 2007–2009. Emerg Infect Dis. 2011;17:1846–54.
5. Wallace  W. “The legend and the man,” in the world of Rembrandt: 1606–1669. New York: Time-Life Library of Art; 1968.

Suggested citation for this article: Potter P. Much have I travell’d in the realms of gold. Emerg Infect Dis [serial on the Internet]. 2011 Oct [date cited]. http://dx.doi.org/10.3201/eid1710.AC1710

DOI: 10.3201/eid1710.AC1710

Much have I travel’d in the realms of gold1 - Vol. 17 No. 10 - October 2011 - Emerging Infectious Disease journal - CDC