Atypical Pestivirus in Calves | CDC EID::Volume 17, Number 8–August 2011

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Atypical Pestivirus and Severe Respiratory Disease in Calves, Europe

Nicola Decaro, Comments to Author Maria Stella Lucente, Viviana Mari, Francesco Cirone, Paolo Cordioli, Michele Camero, Rossana Sciarretta, Michele Losurdo, Eleonora Lorusso, and Canio Buonavoglia

Author affiliations: Faculty of Veterinary Medicine of Bari, Valenzano, Bari, Italy (N. Decaro, M.S. Lucente, V. Mari, F. Cirone, M. Camero, R. Sciarretta, M. Losurdo, E. Lorusso, C. Buonavoglia); and Istituto Zooprofilattico Sperimentale di Lombardia ed Emilia Romagna, Brescia, Italy (P. Cordioli)

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Abstract
In 2010, a HoBi-like pestivirus was isolated from clinically affected calves in Italy. This European virus reproduced a milder form of disease under experimental conditions and was genetically related to previously reported HoBi-like strains. Isolation of this novel virus from a clinical outbreak may have implications for cattle health and prophylactic programs.

Genus Pestivirus (family Flaviviridae) includes Bovine viral diarrhea virus type 1 (BVDV-1) and Bovine viral diarrhea virus type 2 (BVDV-2), Classical swine fever virus (CSFV), Border disease virus (BDV), and other pestivirus species detected in wild ruminants (1,2). In 2004, an atypical pestivirus was isolated from a contaminated batch of calf serum originating from Brazil. This virus, named D32/00_HoBi, was proposed as prototype of a new pestivirus species, BVDV-3 (3). Although additional HoBi-like strains have been detected in South America (4), currently, there is a unique report of natural infection in cattle caused by a HoBi-like strain, Th/04_KhonKaen, which was isolated from a bovine serum sample collected during an epidemiologic survey for BVDV in Thailand (5). However, the virus was not associated with any evident clinical signs. Here we report the biologic and genetic characterization of a HoBi-like strain from Europe that was isolated from cattle during an outbreak of respiratory disease in Italy.

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Decaro N, Lucente MS, Mari V, Cirone F, Cordioli P, Camero M, et al. Atypical pestivirus and severe respiratory disease in calves, Europe. Emerg Infect Dis [serial on the Internet]. 2011 Aug [date cited]. http://www.cdc.gov/EID/content/17/8/101447.htm

DOI: 10.3201/eid1708.101447

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Nicola Decaro, Department of Veterinary Public Health, Faculty of Veterinary Medicine of Bari, Strada per Casamassima km 3, 70010 Valenzano, Bari, Italy; email: n.decaro@veterinaria.uniba.it

Aichi Virus Shedding in Patients with Diarrhea | CDC EID::Volume 17, Number 8–August 2011

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Aichi Virus Shedding in High Concentrations in Patients with Acute Diarrhea

Jan Felix Drexler, Sigrid Baumgarte, Luciano Kleber de Souza Luna, Monika Eschbach-Bludau, Alexander N. Lukashev, and Christian Drosten Comments to Author

Author affiliations: University of Bonn Medical Centre, Bonn, Germany (J.F. Drexler, M. Eschbach-Bludau, C. Drosten); Institute of Hygiene and the Environment, Hamburg, Germany (S. Baumgarte); Bernhard Nocht Institute for Tropical Medicine, Hamburg (L.K. de Souza Luna); and Chumakov Institute of Poliomyelitis and Viral Encephalitides, Moscow, Russia (A.N. Lukashev)

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Abstract
We assessed Aichi virus shedding in patients with gastroenteritis and negative test results for other viral and bacterial infections. High concentrations of up to 1.32 × 1012 RNA copies/g stool were found in 10 (2.0%) of 499 outpatients sampled in northern Germany, 2004. These data substantiate Aichi virus pathogenicity in humans.

The family Picornaviridae includes 12 established genera, and representatives of 5 of these have been found in humans (Enterovirus, Hepatovirus, Parechovirus, Cardiovirus, and Kobuvirus). Among those, human pathogenicity has been proven consistently only for enteroviruses (including polioviruses), hepatitis A virus, and parechoviruses. Several as-yet-unclassified picornaviruses have been found over the past few years in humans, termed cosavirus, klassevirus, and salivirus (1–3). For gastrointestinal pathogens, data on virus quantity in stool can exclude ingestion from nutritional sources of viruses that may be detected but do not replicate in the human gut. Prevalence studies with appropriate control groups and proof of the absence of co-infections with other pathogens are required to provide evidence in favor of human pathogenicity. For most of the novel viruses, these data are still awaited.

A novel human picornavirus termed Aichi virus (AiV; genus Kobuvirus), was described initially in 1991 (4) and epidemiologically linked with spontaneous and food-associated diarrhea in humans (5,6). Recently, it was also detected in sewage-polluted water (7). However, no quantitative data of AiV shedding have become available so far, possibly because of technical peculiarities such as high genomic GC content (≈60%) and strong RNA secondary structures, which may have contributed to a lack of sequence information and prevented more precise molecular detection. In this study, we analyzed well-established cohorts of patients with gastroenteritis and an appropriate control group. Stool samples from patients who had negative test results for other common viruses and bacterial infections showed high AiV shedding by highly sensitive real-time reverse transcription PCR (RT-PCR), thereby substantiating AiV human pathogenicity.

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Drexler JF, Baumgarte S, de Souza Luna LK, Eschbach-Bludau M, Lukashev AN, Drosten C. Aichi virus shedding in high concentrations in patients with acute diarrhea. Emerg Infect Dis [serial on the Internet]. 2011 Aug [date cited]. http://www.cdc.gov/EID/content/17/8/101556.htm

DOI: 10.3201/eid1708.101556

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Christian Drosten, Institute of Virology, University of Bonn Medical Centre, 53127 Bonn, Germany; email: drosten@virology-bonn.de

Canine Distemper in Rhesus Monkeys | CDC EID :: Volume 17, Number 8–August 2011

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Volume 17, Number 8–August 2011
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Canine Distemper Outbreak in Rhesus Monkeys, China

Wei Qiu,1 Ying Zheng,1 Shoufeng Zhang,1 Quanshui Fan,1 Hua Liu, Fuqiang Zhang, Wei Wang, Guoyang Liao, and Rongliang Hu Comments to Author

Author affiliations: Center for Disease Control and Prevention, Chengdu Military Region, Kunming, People's Republic of China (W. Qiu, Y. Zheng, Q. Fan, H. Liu, F. Zhang, W. Wang, G. Liao); and The Veterinary Research Institute of Academy of Military Medical Sciences, Changchun, People's Republic of China (S. Zhang, R. Hu)

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Abstract
Since 2006, canine distemper outbreaks have occurred in rhesus monkeys at a breeding farm in Guangxi, People's Republic of China. Approximately 10,000 animals were infected (25%–60% disease incidence); 5%–30% of infected animals died. The epidemic was controlled by vaccination. Amino acid sequence analysis of the virus indicated a unique strain.

Canine distemper is a highly contagious infectious disease of canine and feline species caused by canine distemper virus (CDV), a member of family Paramyxoviridae (1). Susceptible animals include dogs, wolves, jackals, foxes, mongooses, badgers, raccoon dogs, skunks, minks, and ferrets (2–6). Case-fatality rates for these animals has ranged from 30% to 80% and even to 100% of ferrets (7). Natural infection with CDV has occasionally been reported in bears, lesser pandas, and giant pandas (8–10). Monkeys are not generally considered susceptible but can be experimentally infected (11,12). In 1989, the first natural case of canine distemper in a monkey (Macaca fuscata) was reported (13). Recently, natural canine distemper infection was reported in a few monkeys in Beijing, People's Republic of China, with a description of the clinical signs and pathogenic changes (14). This outbreak most likely resulted from secondary transmission of CDV originating in a larger outbreak on a Guangxi breeding farm, where a similar disease had occurred 2–3 years earlier. Here we describe this larger outbreak and provide a more detailed epidemiologic analysis.

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Qiu W, Zheng Y, Zhang S, Fan Q, Liu H, Zhang F, et al. Canine distemper outbreak in rhesus monkeys, China. Emerg Infect Dis [serial on the Internet]. 2011 Aug [date cited]. http://www.cdc.gov/EID/content/17/8/101153.htm

DOI: 10.3201/eid1708.101153



1These authors contributed equally to this article.

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Rongliang Hu, Key Laboratory of Jilin Province for Zoonosis Prevention and Control and Laboratory of Epidemiology, Veterinary Research Institute, Academy of Military Medical Sciences, 1068 Qinglong Rd, Changchun 130062, People's Republic of China; email: ronglianghu@hotmail.com

Circulating Recombinant Coxsackievirus A16, China | CDC EID :: Volume 17, Number 8–August 2011

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Circulating Coxsackievirus A16 Identified as Recombinant Type A Human Enterovirus, China

Ke Zhao, Xue Han, Guanjun Wang, Wei Hu, Wenyan Zhang, and Xiao-Fang Yu Comments to Author

Author affiliations: First Hospital of Jilin University, Changchun, People's Republic of China (K. Zhao, X. Han, G. Wang, W. Hu, W. Zhang, X.-F. Yu); and Johns Hopkins University, Baltimore, Maryland, USA (K. Zhao, X.-F. Yu)

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Abstract
To determine the relationship of coxsackievirus A16 (CA16) to prototype CA16-G10, we conducted a phylogenetic analysis of circulating CA16 strains in China. Complex recombinant forms of CA16-related viruses involving multiple human enteroviruses, subgroup A (CA4, CA16, and enterovirus 71), are prevalent among patients with hand, foot, and mouth disease.

Coxsackievirus A16 (CA16) is a member of the family Picornaviridae, genus Human enterovirus (HEV). These viruses can be further divided into 4 subgroups on the basis of molecular typing: HEV-A, HEV-B, HEV-C, and HEV-D. The first, and prototype, CA16 strain, CA16-G10, was isolated in South Africa almost 60 years ago (1) and was subsequently sequenced in 1994 (2). CA16, along with enterovirus71 (EV71), CA2, and CA4, is a member of the HEV-A subgroup. CA16 is commonly associated with hand, foot, and mouth disease (HFMD) in children and sometimes causes aseptic meningitis, encephalitis, myocarditis, and poliomyelitis-like paralysis (3).

Enteroviruses related to HFMD have been endemic to Southeast Asia and the Pacific region for decades (4–7). Recently, a dramatic increase in HFMD prevalence has been reported in the People's Republic of China (8–10). Partial viral sequencing (e.g., of the viral protein [VP] 1 region), serologic characterization, or both, have shown that 10%–50% of viruses from HFMD patients are related to prototype CA16-G10, and thus they have been classified as CA16 strains (11). The relationship of circulating CA16-related viruses to CA16-G10 has not been well studied. Therefore, we conducted a serial phylogenetic analysis of existing and new CA16 sequences from northern, central, and southern China to examine whether CA16–G10 truly is the parental strain of circulating CA16 strains. As a result, we found that current CA16 strains in China, although still related to CA16–G10, are recombinant HEV-A.

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Zhao K, Han X, Wang G, Hu W, Zhang W, Yu X-F. Coxsackievirus A16 identified as circulating recombinant type A human enterovirus, China. Emerg Infect Dis [serial on the Internet]. 2011 Aug [date cited]. http://www.cdc.gov/EID/content/17/8/101719.htm

DOI: 10.3201/eid1708.101719

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Xiao-Fang Yu, Johns Hopkins University, Room E5148, 615 N Wolfe St, Baltimore, MD 21205-2103, USA; email: xfyu@jhsph.edu

Neurologic Disease in Mare with West Nile Virus | CDC EID :: Volume 17, Number 8–August 2011

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Fatal Neurologic Disease and Abortion in Mare Infected with Lineage 1 West Nile Virus, South Africa

Marietjie Venter, Comments to Author Stacey Human, Stephanie van Niekerk, June Williams, Charmaine van Eeden, and Frank Freeman

Author affiliations: University of Pretoria, Pretoria, South Africa (M. Venter, S. Human, C. van Eeden, S. van Niekerk, J. Williams); National Institute for Communicable Diseases, Sandringham, Johannesburg, South Africa (M. Venter); and Ceres Veterinary Hospital, Western Cape, South Africa (F. Freeman)

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Abstract
In 2010, lineage 1 West Nile virus was detected in South Africa in the brain of a pregnant mare that succumbed to neurologic disease and in her aborted fetus, suggesting an association with abortion in horses. All West Nile virus strains previously detected in horses and humans in South Africa were lineage 2.

West Nile virus (WNV), a mosquito-borne flavivirus, may cause outbreaks of febrile disease and encephalitis in humans and horses. Although <1% of human patients experience severe disease (1), up to 90% of symptomatic cases in horses result in neurologic disease with case-fatality rates of 30%–40% (2). In sheep, WNV infection may result in abortion, stillbirth, and neonatal death (3). In humans, transmission by transplacental route and breastfeeding has been described. Congenital WNV infection has been accompanied by bilateral chorioretinitis and severe malformation of the fetal central nervous system (4). We report a case of WNV with fatal neurologic disease and abortion in a horse.

Five genetic lineages of WNV exist, the major 2 being lineages 1 and 2 (5,6). Lineage 1 is distributed widely in North and South America, Europe, parts of Asia, North Africa, and Australia. Lineage 2 strains have been identified in humans and horses with febrile and neurologic disease in southern Africa and Madagascar (7) and recently emerged in central Europe causing encephalitis in birds, humans, and horses (7,8). WNV has become recognized as an important horse pathogen in South Africa with all cases positive by nucleic acid detection or virus isolation belonging to lineage 2 (6,7).

Bird deaths due to WNV are rare in South Africa, probably because of the long-term endemic nature of the virus, which limits their use in sentinel surveillance (9). A positive correlation exists between occurrence of symptomatic equine and human cases, which suggests equine outbreaks might predict disease risk for humans (3).

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Venter M, Human S, van Niekerk S, Williams J, van Eeden C, Freeman F. Fatal neurologic disease and abortion in mare infected with lineage 1 West Nile virus, South Africa. Emerg Infect Dis [serial on the Internet]. 2011 Aug [date cited]. http://www.cdc.gov/EID/content/17/8/101794.htm

DOI: 10.3201/eid1708.101794

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Marietjie Venter, Respiratory and Zoonosis Programmes, Department of Medical Virology, Faculty of Health Sciences, PO Box 2034, Pretoria 0001, South Africa; email: marietjiev@nicd.ac.za

WNV in Killer Whale | CDC EID :: Volume 17, Number 8–August 2011

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West Nile Virus Infection in Killer Whale, Texas, USA, 2007

Judy St. Leger, Comments to Author Guang Wu, Mark Anderson, Les Dalton, Erika Nilson, and David Wang

Author affiliations: SeaWorld, San Diego, California, USA (J. St. Leger, E. Nilson); Washington University School of Medicine, St. Louis, Missouri, USA (G. Wu, D. Wang); University of California at Davis, Davis, California, USA (M. Anderson); and SeaWorld, San Antonio, Texas, USA (L. Dalton)

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Abstract
In 2007, nonsuppurative encephalitis was identified in a killer whale at a Texas, USA, marine park. Panviral DNA microarray of brain tissue suggested West Nile virus (WNV); WNV was confirmed by reverse transcription PCR and sequencing. Immunohistochemistry demonstrated WNV antigen within neurons. WNV should be considered in cases of encephalitis in cetaceans.

West Nile virus (WNV) is a single-stranded RNA virus of the genus Flavivirus that is transmitted by mosquitoes. In humans and animals, WNV has been associated with a spectrum of clinical conditions from asymptomatic infections to sudden death. These have been identified in a variety of animal species. Among marine mammals, WNV infection has been reported in a harbor seal (Phoca vitulina) (1). We describe WNV infection in a killer whale (Orcinus orca) and seroprevalence in conspecific cohort and noncohort groups.

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St. Leger J, Wu G, Anderson M, Dalton L, Nilson E, Wang D. West Nile virus infection in killer whale, Texas, USA, 2007. Infect Dis [serial on the Internet]. 2011 Aug [date cited]. http://www.cdc.gov/EID/content/17/8/101979.htm

DOI: 10.3201/eid1708.101979

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Judy St. Leger, 500 SeaWorld Dr., San Diego, CA 92109, USA, email: judy.st.leger@seaworld.com

Pygmy Rice Rat as Potential Host of CASV | CDC EID :: Volume 17, Number 8–August 2011

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Pygmy Rice Rat as Potential Host of Castelo dos Sonhos Hantavirus

Elizabeth S. Travassos da Rosa, Daniele B. A. Medeiros, Márcio R.T. Nunes, Darlene B. Simith, Armando de Souza Pereira, Mauro R. Elkhoury, Marília Lavocat, Aparecido A.R. Marques, Alba Valéria Via, Paulo D'Andrea, Cibele R. Bonvicino, Elba Regina S. Lemos, and Pedro F.C. Vasconcelos Comments to Author

Author affiliations: Instituto Evandro Chagas, Ananindeua, Brazil (E.S. Travassos da Rosa, D.B.A. Medeiros, M.R.T. Nunes, D.B. Simith, A. de Souza Pereira, P.F.C. Vasconcelos); Fundação Nacional de Saúde, Brasília, Brazil (M.R. Elkhoury); Secretaria de Vigilância em Saúde, Brasília (M.R. Elkhoury, M. Lavocat); Secretaria de Saúde do Estado de Mato Grosso, Cuiabá, Brazil (A.A.R. Marques, A.V. Via); Fundação Oswaldo Cruz, Rio de Janeiro, Brazil (P. D'Andrea, C.R. Bonvicino, E.R.S. Lemos); Instituto Nacional de Câncer, Rio de Janeiro (C.R. Bonvicino); and Universidade do Estado do Pará, Belém, Brazil (P.F.C. Vasconcelos)

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Abstract
To study the dynamics of wild rodent populations and identify potential hosts for hantavirus, we conducted an eco-epidemiologic study in Campo Novo do Parecis, Mato Grosso State, Brazil. We detected and genetically characterized Castelo dos Sonhos virus found in a species of pygmy rice rat (Oligoryzomys utiaritensis).

Hantaviruses are RNA viruses (family Bunyaviridae, genus Hantavirus) distributed worldwide. In nature, these viruses are maintained in persistently infected rodents without disease manifestation. Hantaviruses are transmitted to humans through a respiratory route, mainly by inhalation of aerosolized, virus-infected particles in rodent excreta, such as feces, saliva, or urine. Hantavirus pulmonary syndrome (HPS) was first recognized in 1993 after an outbreak of acute respiratory distress syndrome associated with Sin Nombre virus occurred in the southwestern United States (1). In the same year, another hantavirus (Juquitiba virus) was identified in association with HPS cases in the state of São Paulo in southeastern Brazil (2).

Since 1993, molecular techniques have been used to identify New World hantaviruses in samples obtained from humans suspected of having hantavirus infection throughout the Americas and from captured rodents that test seropositive for hantavirus-specific immunoglobulin (Ig) G (3–5). Most known hantaviruses associated with rodent reservoir species have been identified in this way. However, for some hantaviruses, including Castelo dos Sonhos virus (CASV), the virus–host association remains unknown.

CASV was first identified in samples from a patient with HPS in 1995 and was the first hantavirus described in the Brazilian Amazon region (3). We report here data obtained during an eco-epidemiologic study conducted in the municipality of Campo Novo do Parecis, Mato Grosso State in central-western Brazil (Figure 1), including the identification of a possible rodent reservoir for CASV.

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Travassos da Rosa ES, Medeiros DBA, Nunes MRT, Simith DB, de Souza Pereira A, Elkhoury MR, et al. Pygmy rice rat as potential host of Castelo dos Sonhos hantavirus. Emerg Infect Dis [serial on the Internet]. 2011 Aug [date cited]. http://www.cdc.gov/EID/content/17/8/101547.htm

DOI: 10.3201/eid1708.101547

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Pedro F.C. Vasconcelos, Departamento de Arbovirologia e Febres Hemorrágicas, Instituto Evandro Chagas, Rodovia BR-316, Km 07, CEP 67030-000, Ananindeua, Pará, Brazil; email: pedrovasconcelos@iec.pa.gov.br