Lab rats virus

Note: Always tell your treating physician about your research. Regardless of your symptoms, tell your physician about the work you do in the laboratory.

Summary Laboratory-reared rats and mice are specified pathogen-free and are typically accompanied by a health certificate when purchased from a University-approved source. Rat-Bite Fever The risk of rat-bite fever from Streptobacillus moniliformis or Spirillum minor inoculation into the bite wound is minimal due to the eradication of the causative agent from commercial rat colonies.

Campylobacter Transmission of campylobacter species from animals to humans is through the fecal-oral route. Prevention Wear Protective Clothing: Laboratory coat, disposable gloves preferably nitrile , bonnet and surgical mask are required when working in rodent housing and procedure areas.

Report injuries or illnesses to your supervisor and University Health Services. Injuries and Illnesses Report injuries or illnesses to your supervisor and University Health Services. Wiki Content. Explore Wikis Community Central. Register Don't have an account? Leo Dooley. Edit source History Talk 0.

This is Adam Davenport. Victor Gonzalez. Storyline Edit. Tasha wants Bree to be more ladylike and Leo to lay off video games. To these ends, Bree is permitted a slumber party while Donald is coerced into taking Leo on as a lab assistant. At the slumber party headed by the snobbish, elitist and ego-centric Stephanie , Chase sets out to prank them with Adam's aid. In the lab, Leo proves to be a deterrent to Donald's progress, so Donald assigns him the tedious duty of watching a computer download just to get him out of the way.

Bored, Leo decides to speed things up by dropping the firewall, which allows a virus to enter and corrupt Eddy. Now evil and in control, Viral Eddy traps and terrorizes the house inhabitants with intent to kill.

It's up to the boys to employ their computer gaming skills and set things right. Add content advisory. Did you know Edit. Clinical signs of infection are generally limited to mammary tumors, which may arise several months after infection, although distant metastases can also occur with subsequent organ compromise.

Most virus-induced tumors are adenocarcinomas While the mechanism of tumor induction is unknown, it is thought that MMTV induces hyperplastic nodules which eventually become neoplastic Mouse strains differ in their susceptibility to MMTV to the point that mouse strain selection can be used as a control measure Immunity involves both cellular and humoral components 47 , B cells are the primary targets of infection for MMTV.

However, for productive retroviral infection, T-cell stimulation through the virally encoded superantigen SAg is necessary. MMTV is used as a model for viral carcinogenesis. Natural infection of laboratory mice with MMTV will interfere with carcinogenesis studies and result in a shortened life span. Multiple biotypes have been reported While most species of rodents may harbor the organism , , reports of natural outbreaks are rare and are generally limited to rats and immunocompromised mice McGinn et al.

However, in that report the primary pathogen was not clearly established. Transmission is probably via direct contact and fomites Clinical disease, when apparent, is generally limited to lesions of the skin and adnexal structures, although ophthalmitis, conjunctivitis, and mastitis have also been reported Lesions are characterized by suppurative inflammation Natural infection of rats with P.

Staphylococcus aureus is a gram-positive, coagulase-positive coccus that commonly inhabits the skin, upper respiratory tract, and lower digestive tract of many animals, including laboratory rodents, in which it occasionally causes disease.

Transmission is direct, and entry into the body is via breaks in normal barriers. Disease frequently occurs following physiologic changes in the host e. A variety of clinical presentations have been reported in rats and mice. These include tail lesions, ulcerative dermatitis, and traumatic pododermatitis in rats; and facial abscesses, ulcerative dermatitis, preputial gland abscesses, and penile self-mutilation in mice Lesions are more severe in immunocompromised hosts.

In addition, rats inapparently infected during nonsterile surgical procedures are less active in open-field testing. Infected rats have alterations in the fibrinogen level in plasma, the glucose level in serum, total leukocyte counts, and wound histology scores The hallmark of S.

Most commonly, infection occurs in the skin and subcutaneous tissues, but it may also be found in the upper airways, lungs, conjunctiva, and other tissues. Immunity to S. Cell-mediated immunity may also be important and may secondarily contribute to the pathogenesis of some lesions Many of these may be degraded by phagocytic cells into other active products The effects of these products are numerous and include cell lysis ; increases in pulmonary microvascular permeability ; contractile dysfunction 50 ; shock and multiple-organ failure ; epidermolysis 18 ; and induction of excess sleep, fever, TNF, cytokine, IL-1, and IL-1 receptor antagonist Staphylococcal enterotoxins have been termed superantigens based on their ability to stimulate polyclonal proliferative responses of murine and human T lymphocytes In addition, infection with S.

Colonization of conventionally housed rodents is unavoidable. Natural infection of immunodeficient rodents can be prevented, but at great expense, by barrier facility housing. However, this may be necessary to prevent infection and to ensure accomplishment of specific research objectives. Natural infection of immunodeficient mice and rats could compromise a variety of studies involving these animals.

Corynebacteria are gram-positive, diphtheroid bacilli. Reports of hyperkeratosis in nude mice naturally infected with Corynebacterium spp. In the report by Richter et al. The authors of the latter report thoroughly described several aspects of an outbreak of hyperkeratosis in athymic nude homozygous and heterozygous mice, with hairlessness being a contributing characteristic.

Those authors found that transmission was accomplished via direct contact and via contaminated bedding and gloves Clinical signs included flaking of the skin, primarily along the dorsum, and, in some animals, pruritus. Pathologic changes were characterized as orthokeratotic hyperkeratosis and follicular keratosis; marked acanthosis; and mild neutrophilic, macrophage, and mast cell infiltration While reports of natural infection of mice with this Corynebacterium sp.

Nude mice naturally infected with this pathogen would be unsuitable for dermatologic and possibly other research projects.

While many species of mites infest wild rodents, only three species of nonburrowing mites are commonly found on laboratory mice and rats. Myobia musculi and Myocoptes musculinus infest mice, while Radfordia affinis infests rats Mice are much more commonly infested than are rats. The life cycles of all three mites are direct, with all stages egg, nymph, and adult present on the host.

Consequently, hairless mice are not susceptible. Life cycles require roughly 3 weeks for completion. Transmission is via direct contact. Once a facility is infested, eradication of the parasites is achievable but labor-intensive. Clinical signs vary in severity depending upon host factors and mite species.

C57BL and related strains are most susceptible to severe disease, due to overexuberant type 1 hypersensitivity reactions Infestation may be asymptomatic or may cause wasting; scruffiness; pruritus; patchy alopecia, which may be extensive; accumulation of fine bran-like material, mostly over affected areas; self-trauma to the point of excoriation or amputation; and secondary pyoderma 20 , , Lesions are most common on the dorsum, primarily on the back of the neck and interscapular region.

Pathologic changes include hyperkeratosis, erythema, mast cell infiltration, ulcerative dermatitis, splenic lymphoid and lymph node hyperplasia, and eventual secondary amyloidosis , , Mite infestation has reportedly caused secondarily amyloidosis; altered behavior ; selective increases in immunoglobulin G1 IgG1 , IgE, and IgA levels and depletion of IgM and IgG3 levels in serum; lymphocytopenia; granulocytosis; increased production of IL-4; and decreased production of IL-2 , These immunologic changes are consistent with a Th2-type response, with marked systemic consequences The primary importance of LCMV is as a zoonosis and as a contaminant of transplantable tumors and cultured cell lines , , , Natural infections of mice with LCMV are uncommon, and only mice and hamsters are known to transmit the infection, although rats and many other mammals and chickens are also susceptible , Along with implantation of infected tumors, transmission is via exposure of mucous membranes and broken skin to infectious urine, saliva, and milk and possibly via ingestion In addition, both transovarian and transuterine transmission occur in mice Patterns of infection differ depending on host and pathogen factors, including mouse strain and age, inoculum dose, route of inoculation, and virus strain , , Typical clinical patterns include the persistent tolerant infection, which follows in utero or neonatal infection.

Persistent infection of T-helper lymphocytes, viremia, and lifelong viral shedding occur Clinical signs include initial growth retardation and eventual immune complex glomerulonephritis accompanied by emaciation, ruffled fur, hunched posture, ascites, and, occasionally, death Pathologic features of this pattern, including ICG, stem from unabated B-cell activity, including production of pathologic amounts of anti-LCMV antibodies, lymphoid hyperplasia, and perivascular lymphocyte accumulation In contrast, T-cell activity is diminished.

Eventually, immune tolerance breaks down, resulting in chronic illness with widespread lymphocytic infiltration and vasculitis A second clinical pattern is that of the nontolerant infection This pattern occurs with acute infection of postneonatal mice. Viremia occurs without viral shedding. Infected mice either die or eliminate the virus, frequently without showing signs of disease Pathologic features of this pattern include necrotizing hepatitis and generalized lymphoid depletion Lymphocytic choriomeningitis is generally seen only following experimental intracerebral inoculation and is not a feature of natural infection Intestinal intraepithelial lymphocytes are also activated Virus-specific antibody is also induced Several investigators have reported effects of LCMV on research; however nearly all of this information comes from experimental infections Natural infection of laboratory mice would jeopardize human health and interfere with a variety of research endeavors, especially those involving the immune system and central nervous system CNS.

Multiple strains exist Mice and mouse cell cultures are the only hosts Rats are not susceptible. The major importance of LDEV is as a contaminant of transplantable tumors and of inocula of other infectious agents serially passaged in mice , , Transmission is via transplantation of contaminated tumors, cells, or serum but may also occur via direct contact, bite wounds, and transplacental or transmammary passage; however, given the short period when viral shedding occurs, the latter routes are less important , Clinical signs are limited to neurologic disorder in selected mouse strains that have been immunosuppressed Generally, however, there are no clinical signs of infection Pathologic changes have not been described in natural infections and are mainly in lymphoid organs in experimental infections.

Virus replication occurs for one cell cycle only in a small population of macrophages. The virus is therefore concentrated in organs with high macrophage populations Transient thymic necrosis, splenomegaly, and lymphocytopenia occur early in the infection LDEV causes persistent viremia, which induces antiviral antibodies and, eventually, circulating antigen-antibody complexes , which may result in a mild membranous glomerulonephritis The diagnostic hallmark of LDEV infection is elevation of lactate dehydrogenase LD levels in serum, which occurs due to reduced clearing of one LD isozyme Levels of other enzymes in serum are also elevated although not to the same extent.

Clearly, infection of laboratory mice with LDEV could seriously alter research results, especially where immune system function is involved, without any outward evidence of infection.

TMEV has been found infrequently in laboratory mice and even less often in rats Its primary importance is as a model of poliomyelitis, multiple sclerosis, and virus-induced demyelinating disease , Multiple strains exist and are classified according to virulence.

Because the virus naturally infects the intestinal mucosa, transmission is primarily fecal-oral, although the infection is not highly contagious. Viral shedding occurs for roughly 2 months In addition, transplacental transmission has been documented 2 , and mouse and rat cell cultures may be infected. Generally, no clinical signs of infection are observed.

However, viremia may disseminate virus from the intestine to many tissues, including the liver, spleen, and CNS, where spread via direct extension occasionally results in unilateral or bilateral flaccid paralysis of the hind limbs and, rarely, other neurologic signs , Mouse strains differ in their susceptibility to demyelinating disease , , which is usually induced via experimental inoculation. In addition, intraperitoneal inoculation results in acute myositis that progresses to a chronic inflammatory muscle disease which may be immune system mediated Clearing of the virus depends on the involvement of virus-specific cytotoxic T lymphocytes and IL-2 , Natural infection of mice has reportedly interfered with the study of other viral infections In addition, TMEV slows the conduction of spinal motor and somatosensory evoked potentials and could compromise studies involving the CNS.

Mouse adenoviruses are dsDNA viruses of the family Adenoviridae. Infections in the mouse, the principal host, have been reported only rarely. Infection of rats has been suspected based on serologic and morphologic studies Transmission of both strains is by contact.

MAd-1 has a systemic distribution pattern and may be shed in the urine for up to 2 years This ability of MAd-1 to persist cannot be explained by the model of reduced class I MHC-associated antigen presentation proposed for human adenoviruses Clinical signs have never been observed during natural infection with either strain.

Susceptible mice show symptoms of acute CNS disease, including tremors, seizures, ataxia, and paralysis. Light microscopic examination of CNS tissue revealed petechial hemorrhages, edema, neovascularization, and mild inflammation in the brain and spinal cord In other studies, pathologic lesions were most prominent in the kidneys, heart, spleen, adrenal glands, pancreas, liver, and intestines 52 , , , , MAd-2 may be shed in the feces for 3 weeks in immunocompetent mice and for at least 6 months in athymic mice In contrast to MAd-1, infection with MAd-2 is localized to the intestine, causes no clinical signs, and results in pathologic changes that are limited to intranuclear inclusions in crypt and villous cells of the small intestine Immunity to adenoviruses is primarily humoral.

Einarsson et al. Mouse adenovirus infection, while uncommon, may interfere with a variety of studies, particularly those involving the CNS, renal, and gastrointestinal systems.

Ectromelia virus is the causative agent of mousepox. It is a dsDNA virus in the family Poxviridae. Mice are the natural hosts. Rats may be transiently infected only experimentally Reports of natural infection in laboratory mice have become rare in the United States but continue to be common in Europe.

However, clinical mousepox was recently reported in mice at a U. The mice had been injected with contaminated, commercially produced pooled mouse serum Serologic surveys conducted in the United States occasionally reveal seropositive mice, further confirming that the agent is present.

Transmission is primarily via direct contact and fomites, with skin abrasions serving as portals of entry. Resistance to mousepox varies among mouse strains and is dependent upon multiple genes 76 , In these mice, clinical signs are evident in nearly all members of the colony and consist of foot swelling, pocks, lethargy, depression, and sudden death Following entry via broken skin, the virus replicates locally in skin and lymph nodes and then causes mild, primary viremia and spreads to the liver and spleen.

Massive replication in the macrophages of these organs results in a greater secondary viremia. The virus then localizes in many tissues but most prominently in the skin, conjunctiva, and lymph nodes Pathologic changes include massive splenic, lymph node, thymic, and hepatic necrosis; small intestinal mucosal erosions; and cytoplasmic inclusions in the skin and liver. Distal portions of the tail and limbs may necrose and slough, giving rise to the name ectromelia While virus persists for several months in the spleens of infected mice, it is shed in the feces for only about 3 weeks Multiple strains of ectromelia virus exist, with the Moscow strain being most virulent.

Natural infection of laboratory mice with ectromelia virus would severely compromise most research efforts involving mice. Relatively little is known of the natural biology of H-1 virus, and its significance is low in rats, the natural host, since natural infection does not cause clinical disease and effects on research are few The primary importance of H-1 virus is as a model for experimentally produced malformations in the CNS and skeletal system of rats Transmission is via exposure to infectious urine, feces, nasal secretions, and milk Natural infection with H-1 virus does not cause disease.

However, pathologic changes observed in experimental H-1 virus infection derive from the need for parvoviruses to infect replicating cells, wherein they are lytic Reports of H-1 virus affecting research are limited to hepatocellular necrosis in rats exposed to pathogens or chemicals causing liver injury and possibly to a reduction of the incidence of Yersinia -associated arthritis , , although in the latter studies other copathogens may also have been present.

In spite of the paucity of data incriminating H-1 virus as a confounder of research, natural infection of laboratory rats could alter studies of fetal development.

More is known of the natural biology of KRV than of H-1 virus. As with H-1 virus, rats are the natural host of KRV. Transmission is via direct contact with infectious urine, feces, nasal secretions, and milk or by contact with contaminated fomites.

The latter is probably more important than for many other rodent viruses, since parvoviruses are highly resistant to environmental extremes and are highly contagious. In addition, transplantable tumors and cell cultures may be infected , Rats may remain persistently infected for variable times depending upon their age at infection. Clinical signs of infection are rarely observed but have been reported in rats at day 13 of gestation Rats in that outbreak had reproductive anomalies, including increased fetal resorptions, as well as runting, ataxia, cerebellar hypoplasia, and jaundice of many offspring.

In another report, scrotal cyanosis, abdominal swelling, dehydration, and death occurred in young rats exposed to serologically positive adults Like other parvoviruses, KRV infects actively replicating cells and results in cell lysis and tissue destruction.

Therefore, KRV causes lesions primarily during fetal development and neonatal life. Infection may persist for variable times depending upon the age of the rat at infection, but it generally does not last beyond about 3 to 4 months Lesions may occur in multiple organs, including the CNS and gastrointestinal and reproductive systems ; they consist of focal necrosis, frequently in the liver; hemorrhage; and hypoplasia Lastly, KRV may alter leukocyte adhesion to rat aortic endothelium and may reduce the incidence of Yersinia -associated arthritis , , although in those three studies other copathogens may also have been present.

KRV could profoundly interfere with research involving a variety of body systems, especially if infection occurred during fetal development.

Minute virus of mice MVM is an ssDNA virus of the family Parvoviridae and therefore shares many biological features with other murine parvoviruses such as mouse parvovirus-1, H-1 virus, and Kilham rat virus. Like other parvoviruses, MVM is extremely contagious. Transmission is primarily via exposure to infectious feces and urine but may also be via fomites and via exposure to nasal secretions.

In addition, MVM is commonly found as a contaminant of transplantable tumors and mouse leukemia virus stocks , Multiple strains have been described. Mouse strains differ in their susceptibility to MVM 78 , 79 , ; however, there are usually no clinical signs with MVM infection, and natural infections cause no pathologic changes.

Experimental infection will, however, cause damage to multiple organs if infection occurs during fetal development or shortly after birth 78 , , While direct evidence of interference with research is limited to a report of myelosuppression , it can be surmised that MVM may interfere with research involving the immune system, since MVM I infection results in T-lymphocyte lysis and altered B- and T-lymphocyte activities and MVM p suppresses the growth of ascites tumors Mouse hepatitis virus MHV is probably the most important pathogen of laboratory mice.

Rats may also become infected but only as sucklings and only under experimental conditions It is extremely contagious and is transmitted primarily via aerosol, direct contact, fomites, and, experimentally, via transplantable tumors and transplacental passage , , Susceptibility, tissue tropism, clinical signs, and pathologic lesions are dependent on several host, environmental, and pathogen factors 30 , 70 , , Approximately 25 strains or isolates of MHV have been described and have been classified as either respiratory or enterotropic.

Recently, an outbreak of a highly hepatotropic strain of MHV was reported from a breeding colony of nude mice in Taiwan The presence or absence of the MHV receptor, a glycoprotein in the carcinoembryonic antigen family of the Ig superfamily, may determine tissue tropism Respiratory polytropic strains establish in the nasal mucosa, descend to the lungs, and disseminate hematogenously throughout the body or ascend along neurons to the CNS 35 , , , Intestinal involvement is usually absent.

Enterotropic strains may also become established in the nasal mucosa or in the intestinal tract and disseminate only locally to the liver, abdominal lymph nodes, and, in some cases, the CNS , Pulmonary involvement is uncommon. While polytropic strains have historically been considered more common, this situation is thought to have reversed 95 , Lesions are present for only 7 to 10 days following infection, are dependent upon strain of virus, and are characterized by multifocal necrosis.

Additionally, multinucleate syncytial giant cell formation occurs and may be associated with fragmentation and rearrangement of the Golgi apparatus Lesions due to polytropic strains may be observed in the olfactory mucosa, brain, lungs, and liver, while lesions due to enterotropic strains are generally, though not always, confined to the intestinal tract.

Lesions caused by either strain tend to be more severe and widespread in immunocompromised mice Most infections follow one of three clinical patterns Enzootic subclinical infection, commonly seen in breeding colonies, occurs when infection is endemic in the colony and is maintained only by the continual arrival of susceptible animals newborns.

No carrier state exists, although in a recent study viral RNA was detected in the liver up to 60 days after infection Adults are asymptomatic, and their young become asymptomatically infected by the time passively transferred maternal immunity wanes at weaning. Epizootic clinical infection occurs less commonly when the pathogen is introduced to a naive colony.

Adult infections are again usually asymptomatic. Clinical signs depend upon the virus and mouse strains and are most evident in infant mice; typically, they include diarrhea, poor growth, and death.

As the infection becomes established in the colony, the epizootic pattern is replaced with the enzootic pattern. Immunity to MHV is primarily but not entirely cell mediated; is partially protective between closely related virus strains; and is known to involve T lymphocytes, macrophages, IFN, and NK cells , , , , , Numerous reports document effects of natural or experimental infection with MHV on host physiology and research.

In immunocompromised mice, these effects include necrotic changes in several organs, including the liver, lungs, spleen, intestine, brain, lymph nodes, and bone marrow; differentiation of cells bearing T-lymphocyte markers; altered enzyme activities, bilirubin concentration, and antibody responses to sheep erythrocytes in serum; enhanced phagocytic activity of macrophages; rejection of xenograft tumors; impaired liver regeneration; and hepatosplenic myelopoiesis , Clearly, natural MHV infection of laboratory mice with MHV may affect a plethora of scientific studies and seriously compromise the value of these animals as research subjects.

Sialodacryoadenitis virus SDAV is a common, important, and highly contagious pathogen of laboratory rats. Transmission is via direct contact and fomites Infant mice, but not adult immunocompetent or scid mice, are susceptible to experimental infection 33 , , Natural infection of mice has not been reported Enzootic infection occurs in breeding colonies and is sustained only by the continual introduction of susceptible hosts newborns. Suckling rats develop transient conjunctivitis.

Weanlings and adults are asymptomatic Epizootic infection occurs when the agent is introduced to a fully susceptible population. Clinical signs are again transient, may vary in severity, and include cervical edema, sneezing, photophobia, conjunctivitis, nasal and ocular discharge, porphyrin staining, and corneal ulceration and keratoconus , Multiple strains of SDAV exist , and tissue tropisms differ somewhat among strains SDAV has a tissue tropism for tubuloalveolar glands of the serous or mixed serous-mucous types Therefore, inflammatory changes consisting primarily of diffuse necrosis are seen in the lacrimal including the Harderian glands and submandibular and orbital salivary glands.

Secondary damage may occur to structures of the eye. Cervical lymph nodes and the thymus may also be mildly necrotic.

Some strains of SDAV affect the respiratory tract, where pathologic changes may include patchy necrotizing rhinitis, tracheitis, bronchitis, and bronchiolitis, with multifocal pneumonitis 51 , , Virus is present in tissues for only about 1 week.

There is no carrier state, so clinical signs and pathologic changes are transient. In athymic rats, infection is more severe, is persistent, and may be fatal SDAV has been shown to alter estrous cycles, increase embryonic and postnatal mortality , cause depletion of epidermal growth factor in submaxillary salivary glands , cause anorexia and weight loss , , and reduce IL-1 production by alveolar macrophages Natural infections of laboratory rats with SDAV would be expected to interfere with studies involving the lacrimal, salivary, respiratory, ocular, olfactory, reproductive, and immune systems and to interfere with growth of infected newborns.

Corynebacterium kutscheri is a gram-positive bacillus that infects both mice and rats. Transmission is fecal-oral.