porcine adenovirus PAV猪腺病毒 BioVector NTCC质粒载体菌种细胞基因保藏中心

porcine adenovirus PAV猪腺病毒

Etiology
• Porcine adenovirus (PAdV) is a non-enveloped DNA virus in the genus Mastadenovirus, family
Adenoviridae. There are currently three porcine species and five serotypes recognized: PAdV-A
(serotypes 1-3); PAdV-B (serotype 4); and PAdV-C (serotype 5).

Cleaning and Disinfection
• PAdVs can survive in the environment for days to weeks.
• Bleach, formaldehyde, alcohol and phenolic compounds are effective disinfectants for PAdV.
PAdV-5 (belonging to PAdV-C), has been successfully inactivated using 0.85% salt solution or
1M MgCl2 solution heated at 50°C for 1 hour. Heating to 56°C for greater than ten minutes can
also inactivate adenoviruses.

Epidemiology
• Adenoviruses are relatively host-specific and pigs are the only known hosts for PAdV.
Experimentally, human AdVs are able to infect pigs.
• PAdVs are not known to infect humans.
• The geographic distribution of PAdVs is not fully known, although the virus is suspected to be
widespread in domestic swine populations.
• Serological surveys from Canada and England in the 1960s–1970s indicated that up to 60% of
swine test positive for anti-PAdV antibodies. However, current seroprevalence data is lacking.
The virus rarely causes death.

Transmission
• The major routes of PAdV transmission are fecal-oral and inhalation. Virus has also been
detected in swine kidneys post-mortem, making exposure to urine a suspected route of
transmission. Because PAdV is stable in the environment, fomites are also a potential source of
virus.

Infection in Swine/Pathogenesis
• PAdV generally causes subclinical infections, and is commonly isolated from the gastrointestinal
tract of normal swine. However, PAdV can induce enteritis and has been isolated in association
with encephalitis, nephritis, respiratory disease, and reproductive disorders.

Diagnosis
• PAdV is easily cultured. PAdV can be detected in fecal and intestinal culture using negatively
stained, transmission electron microscopy (TEM). Immunofluorescence antibody (IFA) assays,
complement fixation, direct fluorescence antibody (FA), and gel diffusion precipitation tests are
all capable of detecting PAdV antigen and can be useful in confirming infection.
• A rise in anti-PAdV antibody in the presence of clinical disease is suggestive of clinical disease.
Serological methods include virus neutralization or indirect fluorescent antibody testing.

Immunity
• Most adult swine are seropositive to adenovirus and antibodies are presumably protective.
• There is no vaccine for PAdV. Information on cross-protection between strains is unavailable.

Prevention and Control
• There is no treatment for PAdV infection.
• Standard industry biosecurity practices should be in place to limit fecal contamination and virus
transmission.

Gaps in Preparedness
• PAdV is not thought to be a major threat to the United States swine industry. However, recent
seroprevalence data is lacking and further studies could help determine the potential impact of
PAdVs on swine production.

OVERVIEW
Porcine adenovirus (PAdV) is a ubiquitous virus with a worldwide distribution and is considered a low
grade pathogen in domestic swine. PAdV is a non-enveloped, DNA virus in the genus Mastadenovirus of
the family Adenoviridae. PAdV can be isolated from intestines during cases of moderate enteric disease,
but more commonly results in subclinical infections. Most adult swine are seropositive for anti-PAdV
antibodies, indicating that the virus is widespread but has a low incidence of disease. PAdV has also been
isolated in cases of nephritis and respiratory disease, and is thought to contribute to reproductive
disorders.
Currently, there are three porcine species and five serotypes in the Mastadenovirus genus. Porcine
adenovirus A is composed of porcine adenovirus serotypes 1-3 (PAdV 1-3). Serotype 4 (PAdV-4)
belongs to porcine adenovirus B and serotype 5 (PAdV-5) belongs to porcine adenovirus C. PAdV-4 is
the most commonly isolated serotype and has been associated with enteritis, nephritis, encephalitis and
pneumonia. Serotypes can be differentiated using cross-neutralization assays. PAdV is stable in the
environment for ten days. It is resistant to ether and chloroform but can be inactivated using 0.85% salt
solution or 1M MgCl2 solution heated to 50°C for 1 hour. Beach, formaldehyde, alcohol and phenolic
compounds are also effective disinfectants for PAdV.
PAdV is endemic in most conventional swine herds throughout the world and infection is mostly
asymptomatic. Swine are the only known hosts of porcine adenoviruses and there have been no reports of
zoonotic transmission from swine to humans; however, human adenoviruses have been able to
experimentally infect swine. Adenovirus was first isolated in swine in 1964 from a rectal swab of a pig
with diarrhea. Through the remainder of the 1960s and the 1970s, serological surveys in Canada and
England indicated many adult swine have anti-PAdV antibodies. However, the serologic prevalence of
PAdV has not recently documented and the current distribution of PAdV is unclear. PAdV-induced
clinical disease has been documented in several states in the United States, Belgium, Japan and the United
Kingdom.
Fecal-oral or fecal-nasal transmission of PAdV is most common. PAdV is stable in the environment, so
transmission via fomites is also likely. Once ingested, PAdV undergoes intranuclear replication, primarily
in the short blunt villous enterocytes and lymphoid tissue located in the distal jejunum and ileum. The
most common clinical sign associated with PAdV infections is intermittent, yellow, watery diarrhea.
Animals appear depressed, emaciated, and severely dehydrated. Occasionally diarrhea is accompanied by
vomiting. Post-mortem findings include thin walled distal small intestine and enlarged mesenteric lymph
nodes. Yellow, watery contents may be present in the small and large intestines. Upon histologic
examination, the villi are short and blunt in the distal jejunum and ileum. Intranuclear inclusion bodies are
present in the enterocytes of the affected villi.
PAdV is easily cultured in cell lines of porcine origin; primary and continuous kidney cells, primary
thyroid cells, and primary testicular cells are most commonly used. PAdV can be identified from fecal
and intestinal culture using negatively stained, transmission electron microscopy (TEM),
immunohistochemical staining or virus isolation. Alternatively, immunofluorescence antibody (IFA)
assays, complement fixation, direct fluorescence antibody (FA), and gel diffusion precipitation tests are
all capable of detecting PAdV antigen and can be useful in confirming infection. Although polymerase
chain reaction (PCR) assays have been developed for detection of PAdV in the environment, they are not
currently utilized in the clinical diagnosis of PAdV.
As PAdV rarely results in clinical illness, little information is available on immunity post-infection.
PAdV not considered to be a major threat to the United States swine industry; it is a low grade pathogen
and infections are generally asymptomatic. There is no specific treatment for PAdV-induced disease and
no vaccine is available.

LITERATURE REVIEW
1. Etiology
1.1 Key Characteristics
Porcine adenovirus (PAdV) is a non-enveloped, DNA virus with an icosahedral capsid, belonging to the
family Adenoviridae in the genus Mastadenovirus.
1 Adenovirus was first isolated in swine from a rectal
swab of a pig with diarrhea in 1964.2
1.2 Strain Variability
There are currently three recognized porcine species and five serotypes within the Mastadenovirus genus.
Serotypes can be differentiated using cross-neutralization assays.3
• Porcine adenovirus A is composed of porcine adenovirus 1-3 (PAdV 1-3). PAdV-1 and PAdV-3
have been isolated from diarrheic swine, and PAdV-2 and PAdV-3 have been isolated from
normal swine.
• Porcine adenovirus B has only one serotype, porcine adenovirus 4 (PAdV-4), 1 the most
commonly isolated serotype. PAdV-4 has been isolated from pigs with enteritis, nephritis,
encephalitis and pneumonia.4
• Porcine adenovirus C is comprised of porcine adenovirus 5 (PAdV-5).1 PAdV-5 has been isolated
from the brain of a newborn pig and from nasal secretions from pigs with respiratory disease.5,6
Recently, two novel PAdVs have been identified. Strain PAdV-WI was identified in swine facility pen
wash water and has been proposed as a prototype of a new Mastadenovirus species.7 A second strain,
PAdV-SVN1, was isolated in cultures of normal porcine urothelial cells (from the bladders of domestic
pigs), and has genetic similarity to PAdV-WI.8
Experimentally PAdVs have also been used in gene transfer research and as vectors in vaccine research.
5
For example, a recombinant PAdV-3 vector has been generated for potential gene transfer to human
cells.9 PAdV-3 and -5 have been investigated as vectors for transmissible gastroenteritis virus and
classical swine fever virus vaccines.10
2. Cleaning and Disinfection
2.1 Survival
Adenoviruses are able to survive in the environment for at least ten days.11 Following a manure spill,
porcine adenovirus was detectable 18 days later 5.6 km downstream.12 Heating to 56°C for greater than
ten minutes can inactivate adenoviruses.1
2.2 Disinfection
PAdV is stable in acidic conditions (pH 3–4) and not susceptible to ether or chloroform. Bleach,
formaldehyde, alcohol and phenolic compounds are effective disinfectants for PAdV. 2,6,11 PAdV-5 has
been successfully inactivated using 0.85% salt solution or 1M MgCl2 solution heated at 50°C for 1 hour.6
3. Epidemiology
3.1 Species Affected
Adenoviruses are relatively host-specific. Swine are the only known hosts for PAdV.5 Human
adenoviruses have been able to experimentally infect swine.13,14 The Mastadenovirus genus also includes
adenovirus species that infect humans, bovines, canines, equines, murines, ovines, and tree shrews. 1
6
3.2 Zoonotic Potential
There is no known zoonotic transmission of PAdV to humans.5
Adenoviruses generally have a specific
and restrictive host range.1
3.3 Geographic Distribution
In the 1960s–1970s, several serological surveys showed that PAdVs were widespread in Canada and
England. However, the serologic prevalence of PAdV has not documented recently and the current
distribution of PAdV is unclear.5 Natural PAdV-induced infections associated with nephritis have been
documented in the United States (Georgia and South Dakota)4 and Belgium.15 Natural PAdV-induced
infections associated with respiratory disease have been reported in Japan,6 and clinical enteritis has been
seen in the United States (Kentucky and Tennessee)16 and the United Kingdom.
2
3.4 Morbidity and Mortality
There is little data on adenovirus-related morbidity and mortality rates. Studies from England in the 1960s
reported seroprevalence rates of 25–53% and 50–60%.17,18 Serological surveys of swine in Quebec found
lower prevalence rates ranging from about 15% to 18%.19,20 In one documented PAdV-induced disease
outbreak, a morbidity rate of 30% was reported. Animals 14 days of age experienced diarrhea with
occasional vomiting and no sows showed clinical signs of infection.21 PAdV-induced infections rarely
result in death.
16
4. Transmission
Transmission of PAdV is primarily through fecal ingestion or inhalation.5 However, as PAdV has been
detected in kidneys post-mortem, urinary-oral and urinary-nasal should also be considered as viable
routes of transmission.4 PAdV is stable in the environment, so transmission via fomites is likely.5
5. Infection in Swine/Pathogenesis
Once ingested, PAdV undergoes intranuclear replication, primarily in the short blunt villous enterocytes
and lymphoid tissue located in the distal jejunum and ileum.3,5 In an experimental study, PAdV-3 viral
particles were detected 24 hours to 16 days post-inoculation in enterocytes. It was determined that
destruction of the epithelium and shortening of the villi correlated with the presence of PAdV-3 in the
nucleus of these cells. Viral antigen was found 24 hours and up to 45 days in some animals. However,
antigen detection at day 45 post-inoculation did not coincide with morphologic changes in the epithelium.
Tonsils were sporadically infected, and frequently at later stages, indicating a possible viremia of PAdV3.22
In experimental studies, diarrhea ensues three to four days post-inoculation and persists for three to six
days.21,22 During natural infection, diarrhea has been documented in some instances for three to five days
and others persisted for one to three weeks.16,21 Pre-weaned piglets one to four weeks of age are primarily
affected.16
5.1 Clinical Signs
The most common clinical sign associated with PAdV infections is intermittent, yellow, watery
diarrhea.16,21 Animals appear depressed, emaciated, and severely dehydrated.16 Occasionally diarrhea is
accompanied by vomiting.21 Natural infection usually occurs in piglets one to four weeks of age and
sows are not clinically affected by PAdV. Generally, PAdV-induced gastrointestinal disease is found
secondary to other clinical signs.
5
Rarely, nephritis is documented in association with PAdV. In reported cases, affected animals were four
to eight months of age. The presenting problem on these farms was chronic, purulent bronchopneumonia
and PAdV nephritis was an incidental finding that likely did not contribute to the clinical presentation.4
7
PAdV-5 has been isolated in cases of respiratory disease with sneezing, nasal discharge and coughing.6
PAdV is also thought to contribute to reproductive disorders, primarily those resulting in abortion.11
5.2 Postmortem Lesions
In clinical cases of PAdV-induced diarrhea, the wall of the distal small intestine is thin and mesenteric
lymph nodes enlarged.16,21 Yellow, watery contents can be present in the small and large intestines. 21
Upon histologic examination, the villi are short and blunt in the distal jejunum and ileum. Intranuclear
inclusion bodies are present in the enterocytes of the affected villi. Infiltration of the lamina propria in
these areas is made up of histiocytes, plasma cells, and lymphocytes.16,21
Animals experimentally infected with PAdV-3 strain 6618 had similar gross lesions as those found in
natural infections. This included thin intestinal walls with yellow watery contents. Mesenteric lymph
nodes were also enlarged and edematous. Occasionally, pulmonary lesions were found on apical lobes.
Similar lesions as those found in natural infections were also seen histologically including intranuclear
bodies in enterocytes of affected villi with infiltration of the lamina propria. Focal gliosis and nonpurulent perivasculitis was observed in the brain of some animals. The liver revealed some hepatocyte
vacuolization with neutrophilic infiltration. Lungs were congested with interstitial pneumonia and some
hydropic degeneration of bronchial epithelium.21
In documented cases of PAdV-induced nephritis, the connective tissue surrounding renal tubules
contained multifocal accumulations of lymphocytes and plasma cells. Some eosinophilic, necrotic
epithelial cells were present in the lumen of medullary tubules, and sloughed tubular epithelial cells
contained intranuclear bodies.4
6. Diagnosis
6.1 Clinical History
PAdV should be considered as a differential in cases of diarrhea in pre-weaning aged piglets.16
6.2 Tests to Detect Nucleic Acids, Virus, or Antigens
PAdV is easily cultured in cell lines of porcine origin; primary and continuous kidney cells, primary
thyroid cells, and primary testicular cells are most commonly used.5 Cytopathic effects can be seen two to
five days post-inoculation.3,5 Intranuclear bodies can be seen in infected tissue samples; however, PAdV
identification techniques should be used to confirm diagnosis.5,21 PAdV can be detected in fecal and
intestinal culture using negatively stained, transmission electron microscopy (TEM).4
Immunofluorescence antibody (IFA) assays, complement fixation, direct fluorescence antibody (FA), and
gel diffusion precipitation tests are all capable of detecting PAdV antigen and can be useful in confirming
infection.2-5,11 Although polymerase chain reaction (PCR) assays have been developed for detection of
PAdV in the environment, they are not currently utilized in the clinical diagnosis of PAdV.5
6.3 Tests to Detect Antibody
A rise in anti-PAdV antibody in the presence of clinical disease is suggestive of causation of clinical
disease.5 Serological methods include virus neutralization or indirect fluorescent antibody testing.
6.4 Samples
6.4.1 Preferred Samples
Preferred samples from diarrheic animals are the distal ileum and the jejunum.16,22 PAdV antigen has also
been successfully identified using fecal samples of infected animals.5
6.4.2 Oral Fluids
8
The use of oral fluids as a diagnostic specimen has not been evaluated for PAdV.
7. Immunity
7.1 Post-exposure
Viral antigen has been found in enterocytes up to 45 days post-infection, which is suggestive of long-term
shedding. PAdV has been successfully isolated from the brain, nasal tissue, pharynx, lung and intestine 48
days after experimental inoculation. Most adult serum and rectal swabs are positive for anti-PAdV
antibodies. 5,16
7.2 Vaccines
There is no vaccine for PAdV.
7.3 Cross-protection
Information on cross-protection between strains is unavailable.5
8. Prevention and Control
There is no specific treatment or vaccine for PAdV-induced infection.11 PAdV is a low grade pathogen
and rarely results in mortality. Swine industry biosecurity practices, including cleaning and disinfection,
should be in place to limit transmission of the virus.
9. World Organization for Animal Health (OIE) Terrestrial Animal Health Code
PAdV is not included in the 2015 OIE Terrestrial Animal Health Code. There are no restrictions for
importation of animals from countries or zones infected with PAdV.
10. Gaps in Preparedness
PAdV is a low grade pathogen that likely presents little threat to the swine industry. However, recent
seroprevalence data is lacking and further studies could help elucidate the potential impact of PAdVs on
swine production.

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