- Host Animals
- Hosts/Species Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Impact: Environmental
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- canine distemper
International Common Names
- English: hardpad disease
OverviewTop of page
Canine distemper is a highly contagious acute febrile disease caused by the canine distemper virus (CDV), which is a paramyxovirus closely related to the measles and rinderpest viruses. The disease has been known since at least 1760; it has a worldwide distribution, and occurs in a wide variety of terrestrial carnivores including Canidae (dog, fox, wolf, raccoon dog), Mustelidae (ferret, mink, skunk, wolverine, marten, badger, otter), Procyonidae (raccoon, coatimundi), Viverridae (palm civet), Ailuridae (red panda), Ursidae (bear), and large Felidae (lions, tigers, leopards, cheetahs), as well as a few other mammals such as Asian elephants and some primates. Domestic and feral dogs are considered to be the main reservoir host species. Closely related viruses cause a similar disease in seals (phocine distemper virus) and in porpoises and dolphins (cetacean morbillivirus). CDV is a serious threat to endangered wildlife and this threat is expected to increase with increased encroachment of humans (along with their dogs) into undeveloped areas of the world. Recent large outbreaks in nonhuman primates suggest the virus has adapted to these animals and that the potential exists for it to infect humans.
Host AnimalsTop of page
Hosts/Species AffectedTop of page
Canine distemper virus (CDV) is a multihost pathogen that infects a wide range of carnivores (i.e., members of the order Carnivora) (Deem et al., 2000; MacLachlan and Dubovi, 2011). Specifically, it has been reported from all species of the families Canidae (e.g. dog Canis familiaris, dingo C. familiaris dingo, fox (Vulpes spp., coyote Canis latrans, jackal (Canis), wolf Canis lupus) and Mustelidae (e.g. ferret Mustela putorius furo, skunk, badger, mink, weasel, otter (Lutrinae)), and in some members of the Procyonidae (e.g. raccoon Procyon lotor, lesser panda Ailurus fulgens, kinkajou Potos flavus), Hyaenidae (hyenas), Ursidae (bears) and Viverridae (palm civets), and the larger members of the family Felidae (lion Panthera leo, leopard P. pardus, cheetah Acinonyx jubatus, tiger P. tigris) (Deem et al., 2000). In addition, domestic cats (Felis catus) and pigs (Sus scrofa) have been experimentally infected with the virus (Appel et al., 1974).
In spite of these experimental studies, canine distemper is not a clinically recognized entity in domestic cats; however, large felids are susceptible to infection with CDV. CDV outbreaks with multiple mortalities were reported in lions, tigers, jaguars (Panthera onca), and leopards in zoos and wildlife safari parks in the United States and Europe in the late 1980s and early 1990s (Appel et al., 1994). Many reports of canine distemper in free-ranging large felids have been documented (reviewed in Kapil and Yeary, 2011); however, the most intensively studied have been the African lions of the Serengeti National Park, Tanzania, where in 1994, a large CDV epidemic caused fatalities in ~30% of the population, with antibodies found in 85% (Roelke-Parker et al., 1996). In addition to the lions, other carnivore species, including leopards, hyenas, bat-eared foxes (Otocyon megalotis), jackals, and domestic dogs were affected during the 1994 outbreak. It was demonstrated that feral domestic dogs living in or near the Serengeti probably served as the primary reservoir of CDV during outbreaks among large felids (Kapil and Yeary, 2011).
In developed countries that have higher vaccination rates among domestic dogs, various species of urban wildlife, such as raccoons, foxes, and skunks probably play a greater role in disease transmission.
Similar to other carnivorous species, members of the family Ursidae (bears) are susceptible to infection with CDV. For example, serological surveys have demonstrated antibodies to CDV in brown bears (Ursus arctos) from Italy (Francesco et al., 2015), grizzly bears (also U. arctos) from Alaska (Chomel et al., 1998), and black bears (U. americanus) from Maryland and California, USA (Bronson et al., 2014; Stephenson et al., 2015). In addition, in 2011, a wild black bear in Pennsylvania, USA, was found to have clinical disease (i.e., encephalitis and footpad hyperkeratosis) associated with CDV infection (Cottrell et al., 2013). Importantly for wildlife conservation efforts, in early 2015, several captive giant pandas (Ailuropoda melanoleuca) succumbed to CDV infection at a breeding centre in China. It is unclear whether panda handling practices contributed to the outbreak; however, it has been reported that the breeding centre also houses other rare animals and is close to a residential area where villagers keep unvaccinated dogs (Hvistendahl, 2015).
The disease has been reported in Asian elephants, Elephas maximus (Creevy, 2013).
Nonhuman primates have been experimentally infected with CDV resulting in encephalitis (Matsubara et al., 1985; Yamanouchi et al., 1977). More alarmingly, however, CDV appears to have expanded its natural host range to include nonhuman primates. The first outbreak of disease occurred in 1989 in Japan (Yoshikawa et al., 1989). Twenty-two Japanese macaques (Macaca fuscata) in the wild were captured and shown to have CDV infection; two of them later died of encephalitis. In 2006, a large CDV outbreak occurred at a breeding farm in Guangxi province in southern China (Qiu et al., 2011). Approximately 10,000 rhesus monkeys (M. mulatta) contracted the disease and 4250 died. Even after attempts to contain the outbreak and further spread of the virus with vaccination using inactivated suspensions made from the organs of dead animals, there continued to be ~100-200 cases per year during 2007 and 2008 (Qiu et al., 2011). In 2008, an animal centre in Beijing, China, experienced another CDV outbreak (Sun et al., 2010). This time, 20 rhesus monkeys showed clinical signs of disease and 12 died. Following these outbreaks in China, a CDV outbreak occurred in cynomolgus monkeys (M. fascicularis) in Japan in 2008; these monkeys were imported from China and phylogenic analysis of the genome of the virus isolated from them showed that it was closely related to the CDV strains associated with the outbreak in rhesus monkeys in China (Sakai et al., 2013a). Analysis of the cell receptors used by these strains indicated that the virus was able to use human immune and epithelial cell receptors, as well as monkey and canine ones, suggesting that CDV could potentially infect humans (Sakai et al., 2013b).
McCarthy et al. (2007), studying CDV from a variety of different hosts, found that molecular adaptation at known receptor-binding sites of the haemagglutinin gene was associated with independent instances of the spread of the virus to novel hosts.
In addition to terrestrial carnivores, various species of marine mammals have been affected by CDV or closely related viruses. Since 1988 several epizootics have been reported in a number of pinniped and cetacean populations living in different areas of the world (Guardo et al., 2005). In 1988, a major die-off affecting an estimated 17,000 to 23,000 harbour seals (Phoca vitulina) occurred in the North, Wadden, and Baltic Seas along the northern European coast. The affected seals exhibited clinical signs similar to those seen in dogs with distemper, and the seals that recovered had neutralizing antibodies to CDV. However, genetic typing of a morbillivirus isolated from the affected seals placed this virus in a separate species from CDV, now called phocine morbillivirus (MacLachlan and Dubovi, 2011) or phocine distemper virus. Additional epizootics occurred in 2000 in the Caspian Sea resulting in more than 10,000 deaths (Kennedy et al., 2000) and in 2002, again in northern Europe, resulting in an estimated 30,000 deaths (Jensen et al., 2002). Outbreaks of disease have not been limited to pinnipeds as dolphins and porpoises also have been affected. The first evidence of infection in cetaceans also dates back to 1988 when six harbour porpoises (Phocoena phocoena) were found stranded on the Irish coastline (Kennedy et al., 1988). Two years later, a large epizootic that resulted in the deaths of thousands of striped dolphins (Stenella coeruleoalba) occurred in the Mediterranean Sea (Domingo et al., 1990). Again, molecular typing indicated that the virus was a new species that was subsequently called cetacean morbillivirus. Epizootics of these marine mammal morbilliviruses have continued to occur sporadically, and it is now known that both phocine and cetacean morbilliviruses have a global distribution in the world’s oceans and seas (Duignan et al., 2014; Bressem et al., 2014).
DistributionTop of page
Canine distemper is distributed worldwide (Creevy, 2013); a detailed distribution table is not provided for this datasheet.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
PathologyTop of page
CDV, like other morbilliviruses, infects cells that express the species equivalent of the human CD150 (SLAM) (Tatsuo and Yanagi, 2002), which is present on thymocytes, activated lymphocytes, macrophages, and dendritic cells. Infection of these cells explains the immunosuppressive effects of the virus seen in clinical disease, which probably reflects virus-mediated destruction of immune cells. However, CD150-negative cells of the epithelia and the central nervous system (e.g., neurons and glial cells) are also affected by CDV, suggesting that viral infection of these cells occurs through a CD150-independent mechanism. Recently, the cellular adhesion molecule, nectin-4, was shown to be the epithelial receptor for CDV and other morbilliviruses such as measles virus; it is thought to play a role in neurovirulence in dogs (Muhlebach et al., 2011; Pratakpiriya et al., 2012).
Puppies with distemper develop pneumonia, conjunctivitis, rhinitis, and tracheitis. The lungs are typically oedematous, and microscopically there is bronchointerstitial pneumonia with necrosis of the epithelium lining the small airways and thickening of the alveolar walls (MacLachlan and Dubovi, 2011). In addition, secondary bacterial bronchopneumonia is common as a consequence of both virus-mediated immunosuppression and the inhibition of normal pulmonary clearance mechanisms. Lesions in the central nervous system of infected dogs can include any combination of demyelination, neuronal necrosis, gliosis, and nonsuppurative meningoencephalomyelitis. The occurrence and severity of these lesions can vary depending on the particular strain of virus and duration of infection. Cytologically, acidophilic inclusions may be seen in the nuclei and cytoplasm of infected astrocytes or in epithelial cells of various tissues (MacLachlan and Dubovi, 2011). Histologically, CDV produces necrosis of the lymphatic tissues, and thymic atrophy is a consistent postmortem finding in infected young puppies.
Pathologically, lesions of CDV infection in nondomestic carnivores are similar to those in domestic dogs (Deem et al., 2000).
DiagnosisTop of page
In domestic dogs, acute generalized CDV infection can often be diagnosed clinically, particularly if the animal is unvaccinated. Clinical diagnosis, however, can be complicated by the use of modified live vaccines as clinical distemper can occur in recently vaccinated puppies. In nondomestic species, the disease must be differentiated from other diseases with similar clinical signs, including rabies, feline panleukopenia, toxoplasmosis, parvovirus infection, lead poisoning, canine hepatitis, leptospirosis, and a variety of other viral infections.
Laboratory tests are necessary for a definitive diagnosis and to exclude other diseases with similar clinical manifestations. While virus isolation is possible, it is laborious as it requires co-cultivation of lymphocytes from the suspect animal with cell lines expressing the CD-150 (SLAM) receptor molecule (MacLachlan and Dubovi, 2011). Virus isolation is therefore not generally used as a routine diagnostic test. Alternatively, smears of conjunctival, tracheal, vaginal, or other epithelium can be examined by immunofluorescent assay (IFA); the buffy coat of blood, urine sediment, any swab containing epithelial cells, or bone marrow aspirates can be tested using reverse transcriptase PCR (RT-PCR) (Elia et al., 2006). An alternative test, particularly with antemortem skin biopies, is immunohistochemistry -- this can be done using formalin-fixed tissue which eliminates the need for fresh tissue (Haines et al., 1999). Postmortem sections of lung, intestine, stomach, kidney, brain, or bladder tissue can be collected at necropsy and tested by IFA, RT-PCR, or both. In animals displaying only neurologic manifestations, diagnosis can be made by examination of cerebrospinal fluid. Quantitative RT-PCR assays are available, including commercially (CDV Quant RealPCR™ Test from IDEXX Laboratories, Inc.), that can distinguish natural infection from the vaccine virus (modified live virus vaccine) (Wilkes et al., 2014). These assays would be of particular value in epidemiologic investigations or in outbreaks in non-canine species.
The serological status of an animal can be assessed using virus neutralization assays, enzyme-linked immunosorbent assays (ELISA), or IFA. For clinical canine distemper in the nondomestic animal, serologic tests are often unrewarding because most animals die before antibody titers are measurable (Deem et al., 2000). However, paired sera, taken 10-14 days apart, can be tested by viral neutralization assay or IFA.
In addition, ELISAs are available to detect serum IgG and IgM antibodies to CDV and CDV antigen. Detection of IgM indicates recent CDV infection unless the animal was vaccinated within 3 weeks of the test, and detection of IgG can indicate either vaccination or natural infection (Deem et al., 2000).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Other:All Stages||Sign|
|Digestive Signs / Diarrhoea||Other:All Stages||Sign|
|Digestive Signs / Vomiting or regurgitation, emesis||Other:All Stages||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Other:All Stages||Sign|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Other:All Stages||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Other:All Stages||Sign|
|General Signs / Tetraparesis, weakness, paralysis all four limbs||Other:All Stages||Sign|
|Musculoskeletal Signs / Forelimb spasms, myoclonus||Other:All Stages||Diagnosis|
|Musculoskeletal Signs / Hindlimb spasms, myoclonus||Other:All Stages||Diagnosis|
|Nervous Signs / Circling||Other:All Stages||Sign|
|Nervous Signs / Head tilt||Other:All Stages||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Other:All Stages||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Other:All Stages||Sign|
|Respiratory Signs / Coughing, coughs||Other:All Stages||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Other:All Stages||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Other:All Stages||Sign|
|Skin / Integumentary Signs / Hyperkeratosis, thick skin||Other:All Stages||Diagnosis|
Disease CourseTop of page
Transmission of canine distemper virus (CDV) is usually via aerosol or respiratory secretions and it is often passed from dog to dog by sneezing, coughing, or sharing food or water bowls. The virus typically gains entry to the respiratory tract and initially replicates in the local lymphatic tissue. Viraemia results in infection of all lymphatic tissues, which is followed by infection of respiratory, gastrointestinal and urogenital epithelium (Creevy, 2013). An acute, but transient, fever usually begins 3-6 days after infection, and is often accompanied by a low white blood cell count, especially of lymphocytes. The fever subsides for several days before a second round of fever begins approximately 11 or 12 days after infection and lasts for about 1 week. This second fever may be accompanied by serous nasal discharge, mucopurulent ocular discharge, lethargy, and anorexia. Gastrointestinal and respiratory problems may follow and these are typically complicated by secondary bacterial infections. Gastrointestinal involvement is manifest by vomiting and watery diarrhoea. Encephalomyelitis may occur in association with these signs, follow the systemic disease, or occur in the absence of systemic manifestations. Dogs with neurologic disease may develop hyperkeratosis (thickening) of the footpads and nose as result of epithelial damage caused by the virus. This manifestation in dogs gave rise to the term “hardpad disease” as an alternative common name for canine distemper. In dogs, less than half of the adult animals that are infected with CDV die from it; among puppies, however, the death rate can be as high as 80% (American Canine Association, undated).
Vaccinated adult dogs without a history suggestive of systemic canine distemper infection can suffer from chronic distemper encephalitis, involving ataxia, compulsive movements or incoordinated hypermetria. Although CDV has been detected in the brain in such cases, the dogs are not infectious, and replication-competent virus has not been isolated. The disease is caused by an inflammatory reaction associated with persistent CDV, but the mechanisms that trigger it are unknown (Creevy, 2013).
As lesions of CDV infection in nondomestic carnivores are similar to those in domestic dogs, and the same organ systems are affected (Deem et al., 2000), it is likely that the course of the disease is similar in other species; mortality rates are also similar.
EpidemiologyTop of page
Canine distemper occurs worldwide in domestic, captive, and free-ranging carnivores. Canine distemper virus (CDV) is highly contagious and the major route of transmission is through aerosol droplet spread (for example as a result of coughing, sneezing or barking) of respiratory secretions containing the virus; however, exposure to other body excretions (e.g., urine) can result in infection in susceptible hosts when aerosolized. Viral shedding may occur for 60-90 days after infection (Deem et al., 2000) and some infected dogs may shed virus for several months (Greene and Appel, 1990). Transplacental transmission of the virus has been documented in the domestic dog (Krakowka et al., 1977); however, the epidemiologic significance of this type of transmission, or whether it can occur in wildlife species, are unknown.
In many countries, unvaccinated feral domestic dogs probably serve as the primary reservoir of CDV. For example, the most intensively studied CDV outbreak has been in the African lions (Panthera leo) of the Serengeti National Park, Tanzania, where in 1994 a large CDV epidemic caused fatalities in ~30% of the population, with antibodies found in 85% (Roelke-Parker et al., 1996); in addition to the lions, other carnivore species, including leopards (Panthera pardus), hyenas (Hyaenidae), bat-eared foxes (Otocyon megalotis), jackals, and domestic dogs were affected during the 1994 CDV outbreak. The close similarity of viruses recovered from wild carnivores and domestic dogs suggest that a single dog variant was responsible for the outbreak (Carpenter et al., 1998). Also, it was documented that prolonged viral circulation occurred in high-density dog populations living adjacent to the park during 1992-1994. Thus, it was concluded that these dog populations were the most likely source of infection for the wildlife, including the lions, in the Serengeti park (Cleaveland et al., 2000).
While in many countries, unvaccinated feral domestic dogs are considered the primary reservoir of CDV, in western countries that have higher vaccination rates among domestic dogs, various species of urban wildlife - such as such as raccoons (Procyon lotor), foxes (Vulpes), and skunk - may play a greater role in the epidemiology of disease. In fact, wild raccoons were implicated in CDV outbreaks among captive lions, tigers (Panthera tigris), jaguars (P. onca), and leopards in zoos and wildlife parks in North America in the late 1980s and early 1990s (Appel et al., 1994).
Impact: EconomicTop of page
While there may be little economic impact of canine distemper in terms of agriculture, there is certainly impact associated with declines in wildlife populations or individuals. These impacts can be felt most significantly in zoos and wildlife parks around the world, in addition to the increased efforts, and cost of operations, of various wildlife conservation groups. Additionally, pet owners spend a significant amount of money each year obtaining canine distemper vaccination for their dogs (or other domestic pets susceptible to the disease).
Impact: EnvironmentalTop of page
Impact on Biodiversity
Canine distemper virus can have a significant effect on wildlife populations.
The most intensively studied CDV outbreak has been in the African lions (Panthera leo) of the Serengeti National Park, Tanzania. In 1994, a large epidemic, which had probably spread from domestic dogs (Cleaveland et al., 2000), caused fatalities in ~30% of the population (Roelke-Parker et al., 1996). By 1994, 85% of the Serengeti lion population had anti-CDV antibodies and the epidemic had spread north to lions in the Maasai Mara National Reserve in Kenya; by 1996, it was estimated that only 2,000 Serengeti lions remained (Roelke-Parker et al., 1996), although the population recovered quickly (Gilbert et al., 2014). In addition to the lions, other carnivore species, including leopards (Panthera pardus), hyenas (Hyaenidae), bat-eared foxes (Otocyon megalotis), jackals, and domestic dogs were affected during the 1994 CDV outbreak. Extinction of the endangered African wild dog (Lycaon pictus) in the Serengeti coincided with epizootic canine distemper in sympatric domestic dogs (Daszak et al., 2000).
As well as the species mentioned in the previous paragraph, studies cited by McCarthy et al. (2007) report mass mortalities in palm civets (Paguma larvata), red pandas (Ailurus fulgens), raccoons (Procyon lotor) and black-footed ferrets (Mustela nigripes); the last remnant wild population of the latter species (before more recent reintroductions), in Wyoming, USA, was reportedly extirpated by CDV. Timm et al. (2009) conclude that CDV was probably the cause of a precipitous decline in the population of the endangered Island Fox (Urocyon littoralis catalinae) on Santa Catalina island, California, USA (in contrast, elsewhere in California there is no evidence that disease has a significant impact on the endangered San Joaquin Kit Fox, Vulpes macrotis mutica [muticus], despite a high prevalence of antibodies to CDV – US Fish and Wildlife Service, 2010).
Gilbert et al. (2014) modelled the effects of CDV on Amur Tigers (Panthera tigris altaica), in which infection has recently been diagnosed, and concluded that the 50-year risk of extinction in their study area was between 6.3% and 55.8% higher (depending on the scenario used) in the presence of the virus than in its absence.
The Threatened Species table in the canine distemper virus datasheet lists some more species considered to be threatened by the virus.
Zoonoses and Food SafetyTop of page
While there is currently no definitive evidence of naturally acquired human CDV infection, there are several reasons to monitor the situation. CDV has a wide host range, and appears to have recently adapted to nonhuman primates as evidenced by several large outbreaks among multiple species (Qiu et al., 2011; Sakai et al., 2013a; Sun et al., 2010). Furthermore, it has been demonstrated that human cell surface molecules can serve as viral entry receptors for CDV (Bieringer et al., 2013; Otsuki et al., 2013; Sakai et al., 2013b). Lastly, due to the close relationship to, and immunological cross-reactivity with, measles virus (MV), some have suggested that when measles vaccination is stopped (due to the eventual eradication of MV), CDV might cross the species barrier to humans and emerge as a new human pathogen (Bieringer et al., 2013). Thus, it is prudent to be prepared with appropriate vaccines and therapeutics for use in humans in the event that CDV becomes a serious human pathogen.
Disease TreatmentTop of page
Treatment for canine distemper is mainly symptomatic and supportive, mostly aimed at limiting secondary bacterial infections, supporting fluid and electrolyte balance, and controlling neurologic manifestations. Some of these treatments can include broad-spectrum antibiotics, electrolyte solutions, parenteral nutrition, antipyretics, analgesics, and anticonvulsants (Creevy, 2013). If the time of exposure is known, hyperimmune serum or immune globulin can be given prophylactically immediately after exposure. Antivirals such as ribavirin, given alone or in combination with interferon-alpha, have been shown to be effective against CDV in vitro (Carvalho et al., 2014; Elia et al., 2008), but further evaluation of the clinical applicability of these drugs is needed. Treatment for acute neurologic manifestations of the disease is unfortunately often unsuccessful (Creevy, 2013).
Prevention and ControlTop of page
Canine distemper is best prevented by vaccination. A number of vaccines against canine distemper are available for dogs and other domestic and nondomestic animals (Deem et al., 2000). Currently domestic dogs are vaccinated with commercially available vaccines containing modified live virus (MLV). These viruses are attenuated by serial passage in tissue culture. Successful immunization of pups with MLV depends on the lack of maternal antibody interference. To attempt to overcome this issue, pups are vaccinated with MLV vaccine at 6 weeks old and at 3- to 4-week intervals until 16 weeks old (Creevy, 2013). Many varieties of MLV vaccine are available and should be used according to the manufacturers’ directions. MLV vaccines can produce disease in some immunosuppressed dogs. In addition, nondomestic species are often more susceptible to CDV than dogs. Thus, standard attenuated virus vaccines should not be used in nondomestic species. A recombinant canarypoxvirus-vectored vaccine is now available that is safe, does not contain live virus, and cannot cause distemper (Pardo et al., 1997). This product is recommended for nondomestic carnivore species and has been used for immunization of endangered species such as giant pandas (Ailuropoda melanoleuca) and black-footed ferrets (Mustela nigripes) (MacLachlan and Dubovi, 2011).
The virus is fragile and extremely susceptible to ultraviolet light, heat, desiccation, and common disinfectants such as formaldehyde, phenolic compounds and quaternary ammonium compounds. Also, it does not survive in the environment for more than a few hours at room temperature (~25°C); it can though survive for at least two weeks in shady environments at near-refrigeration temperatures (~5°C) (Shen and Gorham, 1980). Infected animals should be quarantined from other animals for several months due to the possibility of prolonged viral shedding during this time.
ReferencesTop of page
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11/08/15: Original text by:
Chris A. Whitehouse, U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, Maryland 21702, USA
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