II. Respiratory Viruses (Sendai and PVM)
III. Parvovirus (RV, H-1, and RPV-1)
IV. Rat Respiratory Virus (RRV)
A. Etiology: Coronavirus is an RNA virus with 2 strains identified to cause disease in rats. Rat coronavirus (RCV) causes respiratory infection while sialodacryoadenitis virus (SDAV) infects the upper respiratory tract, Hardarian and exorbital lacrimal glands, and the submandibular and parotid salivary glands. The SDAV strain causes clinical disease.
B. Transmission: RCV/SDAV is highly contagious and is spread by aerosol, direct contact, and fomites. No latent infection or carrier state occurs. The incidence of infection is high.
C. Clinical Signs: Viral infection is not fatal, and is
generally subclinical. Rats infected with SDAV may exhibit a porphyrin
oculonasal discharge. The submandibular salivary gland may be palpably
enlarged due to sialoadenitis (see photo). Dacryoadenitis may cause
exophthalmos, which can lead to keratitis and corneal ulcers. Symptomatic
rats are at a greater risk for inhalation anesthesia. Chronic exophthalmos
can result in exposure keratitis. 
D. Pathology: Lesions include enlarged submandibular and
parotid salivary glands, edematous cervical lymph nodes, swollen lacrimal
glands, and yellow-grey foci in Harderian glands (brown-red mottling of
the Harderian gland is normal due to porphyrin production). 
Histopathological examination of submandibular salivary glands reveals degenerative changes including acinar and ductal epithelial necrosis, interstitial edema, squamous metaplasia of ductular epithelium followed by proliferation of hyperchromatic acinar cells. Chronic lesions include replacement of acini with fibrous connective tissue and an infiltration of lymphocytes. Similar lesions are present in the lacrimal and Harderian glands. The sublingual salivary gland (mucous gland) is usually not affected.
E. Diagnosis: The most common diagnostic test is serologic screen for antibody and include ELISA and immunofluorescent antibody assays. Coronavirus PCR assays will help detect RCV or SDAV in acute infections. SDAV PCR samples include Hardarian gland or submandibular salivary gland, and while lung is the optimal RCV sample.
F. Control: No carrier state exists, and recovered rats are free of virus and are immune. Cessation of all breeding activity in a production colony for 60 days and concomitant removal of all suckling and weanling animals or intentional exposure of these young rats by frequent mixing will eliminate the infection in the colony. The immune status of the colony and of any new rats to be introduced should be monitored serologically.
II. Respiratory Viruses (Sendai Virus and PVM)
A. Etiology: Sendai virus is an RNA paramyxovirus of the parainfluenza type 1 group, and PVM is an RNA paramyxovirus of the pneumovirus group.
B. Transmission: The primary route of infection is by direct contact with infected animals during the first two weeks of infection when the virus is shed. The disease is usually enzootic in a colony in which susceptible animals are regularly introduced. The incidence of disease in research colonies is rare for Sendai virus and low for PVM.
C. Clinical Signs: Respiratory virus infections usually produce no clinical disease. Sendai virus is immunosuppressive and concomitant respiratory infections with the other respiratory pathogens of rats may occur.
D. Pathology: Gross and histologic lesions associated with uncomplicated respiratory virus infection are uncommon.
E. Diagnosis: Most respiratory virus infections are identified by screening sera by ELISA for anti-Sendai and for anti-PVM antibody.
F. Control: The viral infections are self-limiting. A constant introduction of naive rats will perpetuate infections in a colony. Cessation of all breeding activity in a production colony for 60 days and concomitant removal of all suckling and weanling animals or intentional exposure of these young rats by frequent mixing will eliminate virus infection in the colony.
III. Parvoviruses (RV, H-1, RMV, and RPV-1a)
A. Etiology: Parvoviruses are single stranded DNA viruses. Multiple species of parvoviruses in rats include Rat Virus (RV or Kilham rat virus), H-1 (Toolan's H-1 virus), Rat Minute Virus (RMV 1a, 1b and 1c) and Rat Parvovirus 1 (RPV-1a). Of these, RV is the only virus species reported to cause clinical disease in rats. The other parvoviruses are antigenically distinct from RV, and have not been associated with naturally-occurring disease. RMVs and RPV-1 cause subclinical, persistent infections in rats.
B. Transmission is primarily by direct contact or contact with fomites.
C. Clinical Signs: Parvovirus infections are usually subclinical. Clinical disease from RV has been reported when virus is introduced to a naive population. In newly infected breeding colonies, RV causes decreased fertility, fetal resorption, small litters, and runting of pups. RV infection in juvenile and young adult male rats resulted in lethal disease from hemorrhage and necrosis of brain and gonads.
D. Pathology: RV infects actively replicating cells and causes cytolysis. Lesions associated with RV infection include cerebellar hypoplasia, hemorrhagic infarction, thrombosis of multiple organ systems, focal necrosis, hypertrophy, and vacuolar degeneration of hepatocytes. No pathology has been associated with H-1 or RPV-1 infections.
E. Diagnosis: Serologic assays are used for virus identification. The ELISA and IFA are the most sensitive tests but cross-reactivity does occur among the parvovirus species, especially with the IFA. PCR assays can be used to identify and speciate parvovirus infection in rats.
F. Control: Eliminate seropositive rats and replace with parvovirus-free animals. Cesarean derivation has been used to produce rats free from parvovirus infection. Since parvoviruses can survive for weeks in the environment, environmental clean-up with parvovirocidal disinfectants is critical to prevent re-infection of clean rats. Any cells or other biologicals should be screened for the presence of parvovirus prior to use in animals.
A. Etiology: A respiratory disease has been identified in research rats and is believed to be caused by a virus tentatively identified as "Rat Respiratory Virus" or RRV. This agent has been cultivated from infected rat lungs and has been used to reproduce the disease, however, the taxonomic classification of the virus has not been completed.
B. Transmission: This virus is believed to be transmitted by direct contact and through fomites. RRV infection has been identified in rats from research colonies world-wide.
C. Clinical Signs: Rats show no clinical signs associated with RRV infection.
D. Pathology: The lesions associated with RRV are unlike those of other spontaneous rat viral infections and occur sporadically in rats from infected colonies. Gross pulmonary lesions include 1 to 4 mm grey flat to raised foci randomly distributed throughout all lung lobes at the peak of disease (A.). Microscopically, pulmonary lesions consisted of angiocentric inflammatory cell infiltrates which extended to the surrounding interstitum. The character of the inflammatory cell infiltrates and severity of lesions vary with age of rat. In rats 8-10 weeks of age, granulocytic (neutrophil and eosinophils) perivascular infiltrates are the predominant lesion. Peak lesions are observed in rats 10-12 weeks-old and include pyogranulomatous perivascular infiltrates with interstitial pneumonia characterized by thickening of neighboring alveolar septae with neutrophils, lymphocytes and macrophages and pneumocyte hyperplasia (B and C.). Lymphocytes, neutrophils, red blood cells and macrophages frequently accumulate in alveolar lumina. In some cases, advanced pneumonia resulted in consolidation of focal regions of the lung. Lungs from rats 18 weeks and older in age have perivascular lymphoid infiltrates and multifocal alveolar macrophage aggregates with minimal consolidation suggestive of lesion resolution.
E. Diagnosis: Current diagnostic strategies are limited by the incomplete characterization of the viral agent. Histopathological survey of 10-12 week-old is the most commonly used method. An IFA test is under development, and correlates well with histopathology for disease diagnosis.
F. Control: Comprehensive control measures have not been established
since there is so little known about the virus. Stocking of colonies with
RRV-free rats is possible, and isolation of these rats from other rodents
is important since there is some preliminary evidence that the rat may
not be the only susceptible rodent host to RRV infection. Rederivation
techniques have not been extensively evaluated for effectiveness in eliminating
disease.
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