Download Further information on rat sialodacryoadenitis (SDA) virus

Further information on rat sialodacryoadenitis (SDA) virus transmission, effects, treatment, and other
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Lab Anim Sci 1990 Mar;40(2):138-43
Erratum in:

Lab Anim Sci 1991 Jun;41(3):291
Persistence of sialodacryoadenitis virus in athymic rats.
Weir EC, Jacoby RO, Paturzo FX, Johnson EA, Ardito RB.
Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06510.
To determine whether SDAV infection persists in athymic rats, weanling athymic rats and euthymic rats
were inoculated intranasally with 10(4) TCID50 of SDAV and examined periodically for up to 90 days.
Viral antigen and lesions characteristic of acute SDAV infection, including rhinotracheitis, bronchitis
and sialodacryoadenitis, were detected in both groups of rats during the first week. In euthymic rats,
tissues were under repair and viral antigen was undetectable by day 17, and tissues were histologically
normal by day 31 except for mild focal dacryoadenitis. In athymic rats, viral antigen and chronic active
inflammation of respiratory tract, salivary and lacrimal glands persisted through day 90. Inflammation
and viral antigen also were observed in the transitional epithelium of the renal pelvis and urinary bladder
as late as day 90. Virus was isolated from nasopharynx, lung, salivary gland and Harderian gland of
athymic rats through day 90. All euthymic rats seroconverted to SDAV by day 6, whereas all athymic
rats remained seronegative through day 31, and two of six were seropositive by day 90. As judged by
seroconversion of contact sentinels, six of six athymic rats shed virus through 6 weeks, and five of six
through 10 weeks. These results indicate that SDAV persists in athymic rats, and that normal T cell
function is required for host defenses against SDAV.
PMID: 2157091
Vet Pathol 1987 Sep;24(5):392-9
Exacerbation of murine respiratory mycoplasmosis by sialodacryoadenitis virus
infection in gnotobiotic F344 rats.
Schoeb TR, Lindsey JR.
Department of Comparative Medicine, School of Medicine, University of Alabama, Birmingham, AL.
To test the hypothesis that sialodacryoadenitis virus infection could exacerbate respiratory
mycoplasmosis in rats, four groups of 40 7- to 9-week-old gnotobiotic F344/N rats were given two
intranasal inoculations 7 days apart: Mycoplasma pulmonis, then sialodacryoadenitis virus; M. pulmonis
followed by sterile culture medium; medium initially, then virus; or two doses of medium. Immediately
and 3, 5, 10, and 20 days after the second inoculation, the nasal passages, middle ears, larynges,
tracheas, lungs, and salivary and lacrimal glands of four rats from each group were prepared for
histologic examination, and the respiratory organs from four other rats were collected for quantitative
culture of M. pulmonis and sialodacryoadenitis virus. To test statistically the effect of virus infection on
mycoplasmosis lesions, we determined indices of the severity of respiratory tract lesions by subjective
scoring. In rats given both organisms, indices of nasal and tracheal lesions were significantly (P less than
0.05) greater at 3 days and after than in rats given M. pulmonis alone, and middle ear, laryngeal, and
lung lesion indices were significantly greater at 5 days and after. Rats given both mycoplasma and virus
had significantly more mycoplasmal colony-forming units in the nasal passages at 3 days and after, and
in the larynges, tracheas, and lungs at 10 and 20 days, than rats given only mycoplasma. These results
show that sialodacryoadenitis virus infection can exacerbate respiratory mycoplasmosis in rats
under experimental conditions; therefore, the virus probably also contributes to expression of
naturally occurring mycoplasmosis.
PMID: 2823444
Lab Anim Sci 1990 Mar;40(2):144-9
Erratum in:

Lab Anim Sci 1991 Jun;41(3):292
Duration of protection from reinfection following exposure to sialodacryoadenitis virus
in Wistar rats.
Percy DH, Bond SJ, Paturzo FX, Bhatt PN.
Ontario Veterinary College, University of Guelph.
Wistar rats [Cr1:(WI)BR] were inoculated intranasally with approximately 10(3) median mouse lethal
infective doses of sialodacryoadenitis (SDA) virus. Animals were subsequently selected at random,
removed to a separate isolation room, and reinfected with SDA virus at 3, 6, 9, 12 or 15 months. Preand postinoculation serum samples were collected from all animals during the course of the study and
evaluated for antibody titers to SDA virus. All experimental, control and sentinel animals, following
inoculation with SDA virus, were necropsied and examined for lesions consistent with SDA. Salivary
gland lesions were minimal to absent in rats reinfected with SDA virus for up to 12 to 15 months after
the initial exposure and minimal to moderate in the respiratory tract at 12 or 15 months. SDA-associated
lesions were extensive in age matched control animals examined at each time period of reinfection with
SDA virus. Thus, prior exposure to SDA virus did protect against the development of typical salivary
gland lesions for up to 15 months. Recovered animals were evaluated for their ability to transmit the
virus following reinfection. Rats reinfected at 6 or 9 months were infectious to their naive cage
mates. The results indicate that reinfection with homologous rat coronavirus can occur as early as
6 months after the initial infection, and such rats can transmit the infection to contact controls.
PMID: 2157092
Vet Pathol 1986 May;23(3):278-86
Sialodacryoadenitis virus-associated lesions in the lower respiratory tract of rats.
Wojcinski ZW, Percy DH.
Eight- to 10-week-old outbred Wistar rats were inoculated intranasally with 10(2.9) medium mouse
lethal infective doses of sialodacryoadenitis (SDA) virus. Sham inoculated control rats and challenged
rats were killed at 1 day intervals for the first 8 days, then on days 10, 12, 14, and 20. Typical lesions
associated with SDA were seen microscopically in the salivary and lacrimal glands of inoculated
rats. In addition, laryngitis, tracheitis, bronchitis, bronchiolitis, and multifocal alveolitis were
present during the acute stages of the disease. Viral antigen was demonstrated in epithelial cells lining
airways by immunofluorescence microscopy. SDA virus was recovered from the lower respiratory tract
from days 2 to 6 post-inoculation (PI). Serum antibodies to SDA virus, but not to Sendai virus or
Mycoplasma pulmonis were present in rats tested at day 20 PI. These findings demonstrate that
during the acute stages of the disease, significant lesions do occur in the lower respiratory tract of
SDA virus-infected rats.
PMID: 3014706
Lab Anim Sci 1991 Jan;41(1):22-5
Chronic sialodacryoadenitis virus (SDAV) infection in athymic rats.
Hajjar AM, DiGiacomo RF, Carpenter JK, Bingel SA, Moazed TC.
Department of Comparative Medicine, School of Medicine, University of Washington, Seattle 98195.
Sialodacryoadenitis virus (SDAV) was detected in athymic rats subcutaneously implanted with human
tumor cell lines. Clinical signs included sneezing, dyspnea, weight loss and death. Necropsy
revealed both upper and lower respiratory tract disease from which Staphylococcus aureus,
Pasteurella pneumotropica and Pseudomonas aeruginosa were recovered. Histopathological changes
consisted of suppurative rhinitis and bronchopneumonia. Lesions characteristic of SDAV infection
were found in lacrimal and salivary glands, and viral antigens were detected in the salivary glands
and respiratory tract by immunohistochemistry. Submaxillary salivary gland. Harderian gland and
lung homogenates from affected athymic rats were inoculated intranasally into euthymic rats as a rat
antibody production test. All euthymic rats seroconverted to SDAV. Seroconversion to SDAV was
demonstrated in consecutive pairs of sentinel euthymic rats housed for 6 months with infected
athymic rats. Inoculation of supernatants of the original tumor cell lines into euthymic rats did not
result in seroconversion. The source of the virus was not determined. In this study, spontaneously
acquired SDAV infection persisted for at least 6 months in athymic rats.
PMID: 1849581
Can J Vet Res 1994 Jul;58(3):224-9
Coronavirus infections in the laboratory rat: degree of cross protection following
immunization with a heterologous strain.
Bihun CG, Percy DH.
Department of Pathology, Ontario Veterinary College, University of Guelph.
One hundred and twenty-one specific pathogen-free male Wistar rats eight to ten weeks of age were
used to evaluate the efficacy of Parker's rat coronavirus (PRC) in affording cross protection on
subsequent challenge with virulent sialodacryoadenitis (SDA) virus. Sixty-two animals were inoculated
intranasally on day 0 and 21 days later with approximately 10(2) median tissue culture infective doses
(TCID50) of the tenth passage of PRC replicated in L-2 cells. Animals were selected at random
postvaccination to evaluate the safety and efficacy of PRC by histopathology, immunohistochemistry
and serology. At three and six months postvaccination (PV), vaccinated and seronegative control rats
were inoculated intranasally with approximately 10(3) TCID50 doses of virulent SDA virus. Challenged
rats were then killed at 6, 10 and 14 days postchallenge and necropsied. Evaluations were based on
lesion indices in lacrimal and salivary glands and respiratory tract, the presence of viral antigen by
immunohistochemistry, and antibody response. Lesions were observed in rats killed PV, but in
general, they were significantly reduced compared with those present in seronegative animals
post-exposure to virulent SDA virus (p < or = 0.05). However, they were still considered to be an
unacceptable level for a routine vaccination procedure. Potvaccination antibody titers to rat
coronavirus were evident in all animals tested at three or six months prior to challenge with SDA
virus.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 7954126
Can J Vet Res 1995 Jan;59(1):60-6
Effect of time of exposure to rat coronavirus and Mycoplasma pulmonis on respiratory
tract lesions in the Wistar rat.
Schunk MK, Percy DH, Rosendal S.
Department of Pathology, Ontario Veterinary College, University of Guelph.
The effects of time of exposure on the progression of pulmonary lesions in rats inoculated with
Mycoplasma pulmonis and the rat coronavirus, sialodacryoadenitis virus (SDAV) were studied, using
six groups of 18 SPF Wistar rats (n = 108). Rats were inoculated intranasally as follows: Group 1, sterile
medium only; Group 2, sterile medium followed one week later by 150 TCID50 SDAV; Group 3, sterile
medium followed by 10(5.7) colony forming units of M. pulmonis; Group 4, SDAV followed one week
later by M. pulmonis; Group 5, M. pulmonis followed one week later by SDAV; Group 6, M. pulmonis
followed two weeks later by SDAV. Six rats from each group were euthanized at one, two and three
weeks after the final inoculation. In a separate experiment, six additional animals were inoculated in
each of groups 3, 5 and 6 (n = 18) and were sampled at five weeks after they had received M. pulmonis.
Bronchoalveolar lavage and quantitative lung mycoplasma cultures were conducted on two-thirds of the
rats. Histopathological examination and scoring of lesion severity were performed on all animals. Based
on the prevalence and extent of histopathological lesions, bronchoalveolar lavage cell numbers,
neutrophil differential cell counts and the isolation of M. pulmonis, the most severe disease occurred in
the groups that received both agents. There was no significant difference in lesion severity between the
groups receiving both agents other than in those examined during the acute stages of SDAV infection.
Based on these results, it is evident that SDAV enhances lower respiratory tract disease in Wistar
rats whether exposure occurs at one week prior to or at various intervals following M. pulmonis
infections.
PMID: 7704844
Vet Pathol 1995 Jan;32(1):1-10
Morphologic changes in the nasal cavity associated with sialodacryoadenitis virus
infection in the Wistar rat.
Bihun CG, Percy DH.
Department of Pathology, Ontario Veterinary College, University of Guelph, Canada.
A sequential study of lesions of the nasal cavity associated with sialodacryoadenitis virus (SDAV)
infection was made in the laboratory rat. Wistar rats were intranasally inoculated with approximately
10(3) TCID50 of the coronavirus SDAV. Transverse sections of four regions of the nasal cavity from
inoculated and control animals were examined by light microscopy and immunohistochemistry at 2, 4,
6, 8, 10, and 14 days postinoculation (PI). Lesions were observed in the following regions of the
upper respiratory tract: respiratory epithelium, transitional epithelium, olfactory epithelium,
nasolacrimal duct, vomeronasal organ, and the submucosal glands of the nasal passages. In
general, in structures lined by ciliated epithelial cells, there was focal to segmental necrosis with
exfoliation of affected cells and polymorphonuclear cell infiltration during the acute stages, progressing
to squamous metaplasia during the reparative stages. Repair in these regions was essentially complete by
14 days PI. In the olfactory epithelium and the vomeronasal organ, there was interstitial edema
with necrosis and exfoliation of epithelial cells and minimal to moderate inflammatory cell
response during the acute stages. Residual reparative lesions were still evident in the olfactory
epithelium, the columnar epithelium and neuroepithelium of the vomeronasal organ, and the
nasolacrimal duct at 14 days PI. Viral antigen was demonstrated by immunohistochemistry in all regions
during the acute stages of the disease, with the exception of the vomeronasal organ. In view of these
findings, infections of the respiratory tract with viruses such as SDAV could have significant
effects on functions such as olfaction and chemoreception for > or = 2 weeks postexposure in this
species.
PMID: 7725592
Vet Pathol 1995 Nov;32(6):661-7
Comparative severity of respiratory lesions of sialodacryoadenitis virus and Sendai
virus infections in LEW and F344 rats.
Liang SC, Schoeb TR, Davis JK, Simecka JW, Cassell GH, Lindsey JR.
Department of Comparative Medicine, University of Alabama at Birmingham, USA.
In several chronic diseases, lesions are more severe in LEW rats than in F344 rats.To determine whether
or not acute viral diseases also are more severe in LEW rats than in F344 rats, we inoculated 6-7-weekold LEW and F344 rats with 10(7.2) cell culture infective units of sialodacryoadenitis virus or 10(4.7)
infective units of Sendai virus. Twenty-four rats of each strain were given each virus. Lesions in nasal
passages, tracheas, intrapulmonary airways, and pulmonary alveoli in 6 or 12 rats inoculated with each
virus were assessed by scoring 5, 10, and 14 days after inoculation. Both viruses caused typical patchy
necrotizing rhinitis, tracheitis, bronchitis, and bronchiolitis, with multifocal pneumonitis, in rats
of both strains. Mean lesion indices for LEW rats given sialodacryoadenitis virus were significantly
different from those for F344 rats for nasal passages on days 10 (0.999 vs. 0.680) and 14 (0.736 vs.
0.278), bronchi on day 5 (0.479 vs. 0.361), and alveoli on day 5 (0.677 vs. 0.275). Lesion indices for
LEW rats given Sendai virus were significantly different from those for F344 rats for nasal passages on
days 10 (1.000 vs. 0.611) and 14 (0.778 vs. 0.583); trachea on day 10 (0.625 vs. 0.028); bronchi on days
5 (0.476 vs. 0.331), 10 (0.123 vs. 0.013), and 14 (0.038 vs. 0); and alveoli on days 5 (0.413 vs. 0.114)
and 10 (0.185 vs. 0.020). Thus, at the tested doses, both viruses caused more severe respiratory
tract lesions in LEW rats than in F344 rats.
PMID: 8592801
Arch Virol 1989;104(3-4):323-33
Replication of sialodacryoadenitis virus in mouse L-2 cells.
Percy D, Bond S, MacInnes J.
Department of Pathology, University of Guelph, Ontario, Canada.
Sialodacryoadenitis (SDA) is a naturally-occurring infection of the laboratory rat raused by the
coronavirus, sialodacryoadenitis virus (SDAV). The study of SDAV has been limited because there is
no widely available continuous cell line for the propagation of high titers of the virus. The purpose of
this study, therefore, was to compare the ability of SDAV to replicate in the permanent cell lines, LBC,
of rat origin, and the mouse cell lines. L-929 and L-2. Following 2 to 6 repeated passages of SDAV in
LBC cells, the virus could be readily propagated in LBC and L-2 cells, but not in L-929 cells. Similarly,
SDAV adapted to replicate directly in L-2 cells could be readily propagated in LBC, but not L-929 cells.
In LBC and L-2 cells, cytopathic effect (CPE), viral antigen, viral particles, and virus infectivity could
be demonstrated. Titers of up to 10(8.0) infectious viral particles/0.25 ml of culture fluid were obtained
at 48 hours in L-2 cells. Titers in LBC cells were one to two logs lower. When susceptible rats were
inoculated with eighth passage L-2 cell-adapted virus, they developed typical lesions of SDA. Virus
could be recovered from infected tissues and propagated in L-2 cells on first passage. The ability to
propagate SDAV to high titers in the widely available L-2 cell line should promote the study of
this virus and facilitate its comparison with other murine coronaviruses.
PMID: 2539798
Lab Anim Sci 1984 Jun;34(3):255-60
Comparison of strain susceptibility to experimental sialodacryoadenitis in rats.
Percy DH, Hanna PE, Paturzo F, Bhatt PN.
Wistar, Sprague-Dawley, and Long-Evans outbred rats, and the Fischer344 inbred strain were inoculated
intranasally with 10(3) TCID50 of sialodacryoadenitis virus at approximately 9 weeks of age. Paired
animals were killed at 2-day intervals post inoculation up to 2 weeks, then at 20 days. A comparison of
strain susceptibility to sialodacryoadenitis virus was made using the following criteria: histopathology,
immunofluorescent microscopy, serology and serum amylase activity. All four strains were susceptible
to sialodacryoadenitis virus. The disease was frequently subclinical, although typical lesions were
observed on histopathology. Focal bronchitis, bronchiolitis and pneumonitis were observed
histologically during the acute stages of the disease. Immunohistochemistry was performed on
trypsin-treated, paraffin-embedded sections, and viral antigen was readily demonstrated in salivary and
lacrimal glands during the early stages of the disease. A rise in serum amylase was observed, and it
was correlated with the first appearance of lesions in the salivary glands. Based on serology and
immunofluorescence microscopy, the appearance of detectable antibody to sialodacryoadenitis virus,
and the rate of viral clearance from infected glands, the course of the disease was similar in the four
strains studied.
PMID: 6205217
Vet Pathol 1989 May;26(3):238-45
Sequential changes in the harderian and exorbital lacrimal glands in Wistar rats
infected with sialodacryoadenitis virus.
Percy DH, Wojcinski ZW, Schunk MK.
Department of Pathology, Ontario Veterinary College, University of Guelph, Canada.
A sequential light and electron microscopic study of the exorbital and Harderian lacrimal glands was
done on 2.5- to 15-month-old Wistar rats exposed to sialodacryoadenitis (SDA) virus. Typical
coronaviral particles were readily demonstrated in cytoplasmic vesicles of Harderian and exorbital
glands examined at 6 days post-inoculation. Lesions were seen in a relatively high percentage of
lacrimal glands in infected animals of all ages, with no obvious age-related variations in the
incidence and extent of changes. Lesions frequently persisted for a longer interval post-exposure
in lacrimal glands than in salivary glands. The persistence of lesions commonly seen in Harderian
glands was attributed, at least in part, to the cytotoxic effects of porphyrin-containing secretions
released during the acute necrotizing stages of the disease. The persistence of lesions in some
lacrimal glands indicates that they are useful tissues for microscopic examination for the
retrospective provisional diagnosis of SDA. Persistent lesions also indicate that normal functions of
these glands may be compromised for up to several weeks following outbreaks of SDA.
PMID: 2548316
J Vet Med Sci 1991 Dec;53(6):1059-63
Antigenic heterogeneity of sialodacryoadenitis virus isolates.
Kojima A, Okaniwa A.
Safety Research Laboratory, Tanabe Seiyaku Co., Ltd., Osaka, Japan.
Seventeen field isolates of sialodacryoadenitis (SDA) virus had been isolated from the lung of rats with
clinical SDA during epizootics of SDA from 1976 to 1978 in the research laboratory. Based on their
neutralization patterns against antisera to strains 681, 930-10, Lu-3, Lu-4 and Lu-7, these isolates were
divided into 3 antigenic groups. The first group consisted of 8 isolates which were neutralized by 4 out
of 5 antisera at high serum dilution. The second group consisted of 6 isolates which were neutralized by
only 2 antisera at high serum dilution. The third group exhibited intermediate neutralization pattern and
3 isolates belonged to it. Considering the time course of virus isolation, it was concluded that three
antigenically different SDA viruses had been spread irregularly and ocassionally two had been
spread simultaneously in an animal house of rats during the several epizootics of SDA.
PMID: 1665081
Infect Immun 1977 Dec;18(3):823-7
Respiratory infection in mice with sialodacryoadenitis virus, a coronavirus of rats.
Bhatt PN, Jacoby RO, Jonas AM.
Sialodacryoadenitis virus (SDAV), a coronavirus of rats, evoked both serum neutralization and
complement fixation antibody responses when inoculated intranasally in mice. Weanling gnotobiotic
CD-1 mice inoculated intranasally with 10(3.0) mean tissue culture infective doses of SDAV remained
asymptomatic. Virus was recovered from the nasopharynx, trachea, and lung from day 2 to day 7.
Viral antigen was readily detected by indirect immunofluorescence in the lung but rarely in the
nasopharynx. Infected mice developed interstitial pneumonia. Susceptible mice contact exposed to
experimentally infected mice developed antibody to SDAV. Epizootiological studies indicated that
retired breeder mice can have complement-fixing antibody to SDAV and mouse hepatitis virus (MHV)
in the absence of MHV infection. These studies show that SDAV is infectious for mice and can be a
pathogen for the respiratory system. Thus, SDAV infection of mice may be responsible for
spurious seroconversions to MHV.
PMID: 201568
Can J Vet Res 1991 Jan;55(1):89-90
Experimental sialodacryoadenitis virus infection in severe combined immunodeficient
mice.
Percy DH, Williams KL, Croy BA.
Department of Pathology, Ontario Veterinary College, University of Guelph.
Mice with a severe combined immunodeficiency in B and T lymphocytes and natural killer cells (SCIDbeige) were inoculated intranasally with sialodacryoadenitis (SDA) virus, a coronavirus of rats. Animals
were killed at designated intervals and tissues were examined for evidence of viral infection by light
microscopy and immunofluorescence microscopy. Based on these criteria, there was no evidence that
these immunodeficient mice were susceptible to infection with SDA virus.
PMID: 1653101
Vet Pathol 1988 May;25(3):183-92
Depletion of salivary gland epidermal growth factor by sialodacryoadenitis virus
infection in the Wistar rat.
Percy DH, Hayes MA, Kocal TE, Wojcinski ZW.
Department of Pathology, Ontario Veterinary College, University of Guelph, Canada.
Male and female Wistar rats 2 to 15 months of age were inoculated intranasally with sialodacryoadenitis (SDA) virus and killed at 8 to 21 days post-inoculation (PI). Submandibular glands were
evaluated by light and electron microscopy, and levels of salivary gland epidermal growth factor (EGF)
were quantitated by cytochemistry and competitive radioreceptor assay. Apical granules in the epithelial
cells of the granular convoluted tubules (GCT) were selectively depleted during the acute and
convalescent stages of the disease. In addition, levels of immunoreactive EGF were reduced in
affected submandibular glands, especially at 8 to 14 days PI with SDA virus, but some evidence of
EGF depletion was seen at up to 3 weeks PI. A corresponding transient depletion of EGF receptor
reactive salivary EGF was seen between 1 and 3 weeks after experimental SDA infection. These
studies suggest that a clinical (or subclinical) infection with SDA virus could have significant effects on
experimental studies on EGF-dependent functions, including reproductive physiology and
carcinogenesis.
PMID: 2839922
Lab Anim Sci 1982 Dec;32(6):655-9
A subclinical epizootic of sialodacryoadenitis in rats.
Eisenbrandt DL, Hubbard GB, Schmidt RE.
An epizootic of sialodacryoadenitis was identified in 10-week-old rats 5 days after they were housed
with a group of older rats. The young rats generally did not develop the characteristic clinical signs
of sialodacryoadenitis, but they did have typical histologic lesions of sialodacryoadenitis in
Harderian, lacrimal, and salivary glands. The lesions were variable in distribution and severity, and
chronic lesions persisted in the Harderian glands of the rats.
PMID: 6298502
Invest Ophthalmol 1976 Jul;15(7):538-41
Keratoconjunctivitis associated with sialodacryoadenitis in rats.
Lai YL, Jacoby RO, Bhatt PN, Jonas AM.
A high incidence of keratoconjunctivitis was observed in a closed colony of inbred Lewis/Wistar rats.
Clinical signs including blinking, ocular discharge, circumcorneal flush, corneal opacity, ulceration,
pannus, hypopyon, and hyphema were observed at about three weeks of age. Acute disease subsided by
six weeks of age, but some lesions progressed to low-grade chronic keratitis. Six per cent of affected rats
developed megaloglobus, which usually appeared by three weeks of age. Lesions included focal or
diffuse interstitial keratitis, corneal ulceration, anterior synechia, and inflammatory exudate in the
anterior chamber. A high incidence of lenticular and retinal degeneration was associated with
megaloglobus. Most affected rats also had harderian dacryoadenitis. Sialodacryoadenitis virus (SDA)
was recovered from nasal washes, but not from affected eyes. Serological evidence indicated that
SDA virus infection was widespread in the colony.
PMID: 931700
Jikken Dobutsu 1978 Jul;27(3):283-7
Some clinical and epizootological observations of infectious sialoadenitis in rats.
Utsumi K, Maeda T, Tatsumi H, Fujiwara K.
Epizootological and clinical observation was made of infectious sialoadenitis ocurring at a rat facility.
The disease occurred mostly among animals 8 to 64 weeks of age without specific relevance with sex
and age, and clinical signs disappeared within 5 days after the onset. Morbidity rates and duration
of epizootics ranged from 13 to 100% and from 5 to 32 days, respectively. Most rats having severe
clinical signs of sialoadenitis showed decrease in food uptake, body weight loss and remarkable
disorders of estrous cycles.
PMID: 213299
J Leukoc Biol 1988 Aug;44(2):87-92
Inhibition of phagocytosis and interleukin-1 production in pulmonary macrophages
from rats with sialodacryoadenitis virus infection.
Boschert KR, Schoeb TR, Chandler DB, Dillehay DL.
Department of Comparative Medicine, University of Alabama, Birmingham 35294.
To test whether or not sialodacryoadenitis virus (SDAV) infection in rats affects pulmonary macrophage
function, we intranasally inoculated pathogen-free F344 rats with SDAV and collected alveolar and
interstitial macrophages 5 d later. We assessed Fc receptor-mediated attachment and phagocytosis by
phase-contrast microscopic examination of monolayers of alveolar and interstitial macrophages
incubated with zymosan, nonopsonized sheep erythrocytes, or erythrocytes opsonized with rabbit
antisheep-erythrocyte IgG. Alveolar macrophages from virus-infected rats had significantly (P less than
or equal to .05) lower indices of attachment and phagocytosis of opsonized erythrocytes than control
macrophages, but there was no difference in attachment of zymosan particles. Interstitial macrophages
were not affected. Alveolar macrophages from SDAV-infected rats produced significantly less
interleukin-1 than those from control rats, as assessed by testing supernatants from
lipopolysaccharide-stimulated macrophage cultures for induction of mouse thymocytes to take up
tritiated thymidine. Effects of SDAV infection on lung macrophages could increase host
susceptibility to other pathogens or complicate studies of respiratory tract immunity.
PMID: 2841399