Infectious Diseases of Mice and Rats (1991) / Chapter Skim
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7. Digestive System
7. Digestive System
Pages 85-163
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From page 85... ...
There are approximately 21 infectious agents of the digestive system in mice and rats. Natural infections are usually due to varying combinations of these agents, and if clinical disease is present, careful judgments may be required in deciding which agents have causative relets)
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From page 86... ...
Order of importance for mice and rats. Agents listed in group I are undisputed important pathogens, but because of their high prevalence and known effects on research, mouse hepatitis virus and Spi'-onucleus muris in the mouse and sialodacryoadenitis virus and S
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From page 87... ...
* is a common subclinical infection of the submaxillary salivary glands and other tissues in wild mice.
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From page 88... ...
Further studies are needed to clarify the prevalence of MCMV in contemporary laboratory mice. In natural infections of wild mice, the salivary glands (particularly the submaxillary glands)
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From page 89... ...
are far more susceptible than their immunocompetent counterparts. The induction of natural killer cells and interferon early after infection are thought to be most important in non-specific defense against MCMV infection (Griffiths and Grundy, 19871.
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From page 90... ...
Virus isolation can be accomplished by using mouse embryo fibroblasts and other tissue culture systems (Osborn, 19823. Control Complete exclusion of wild mice from rodent facilities is essential.
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From page 91... ...
infections in laboratory rats. Acidophilic intranuclear inclusions thought to be due to CMV infection have been observed from time to time in the submaxillary salivary glands or kidneys of wild rats (Thompson, 1932; Kuttner and Wang, 1934; Syverton and Larson, 19471.
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From page 92... ...
Intranuclear inclusions typical of CMV infection were present in duct cells of the salivary glands, and clusters of virions typical of CMV were demonstrated in these cells by electron microscopy. Culture methods successfully detected virus in salivary glands of LEW rats for up to 12 months but in BN rats for only 5 months.
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From page 93... ...
Light and electron microscopy of salivary glands for inclusions and virions of CMV would also be of value. Latent infections can be activated by xirradiation or cyclophosphamide-induced immunosuppression, followed by attempted virus isolation by using, rat embryo fibroblasts (Bruggeman et al., 1983a)
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From page 94... ...
and transiently suppressed humoral response to sheep red blood cells during the weeks following infection (Bruggeman et al., 1985~. Experimental infection with RCMV (strain of Priscott and Tyrrell, 1982)
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From page 95... ...
The virus apparently occurs as a persistent, subclinical infection in the salivary glands with virus shedding in saliva (Cross et al., 1973; Osborn, 1982~. MTNI has been isolated on one occasion from mammary tissue of a lactating mouse, suggesting that it can be transmitted in milk (Morse, 19871.
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From page 96... ...
Necrosis and repair follow similar patterns in the lymph nodes and spleen. After neonatal infection, persistent infection of the salivary glands occurs, but the mice do not produce serum antibody (Cross et al., 1979~.
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From page 97... ...
reported two epizootics in which weanling rats had swollen, thickened necks and red porphyrin pigment along the eyelid margins. Microscopically, there was severe inflammation and edema of the submaxillary salivary glands and lIarderian glands (other lacrimal glands were not examined)
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From page 98... ...
Agent SDAV is an RNA virus, family Coronaviridae, genus Coronavirus. It is anti;,enically related to many other coronaviruses, including mouse hepatitis virus (MHV)
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From page 99... ...
and serous (parotid) salivary glands, lacrimal glands (Harderian, intraorbital, and exorbital)
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From page 100... ...
Pathology SDAV has a tissue tropism for tubuloalveolar glands of the serous or mixed serous-mucous types, with the submaxillary and parotid salivary glands, exorbital lacrimal. Harderian~ and intraorbital lacrimal glands being the major target organs.
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From page 101... ...
In routine health monitoring, it is recommended that histologic sections be taken of both Harderian glands and the submaxillary and parotid salivary glands of each animal. A presumptive diagnosis of SDAV infection often can be based on the characteristic histologic changes in these glands.
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From page 102... ...
19791. Interference with Research SDAV infection can seriously complicate studies involving the eyes, sail vary glands, lacrimal glands, or the respiratory tract of rats (Jacoby, 19861.
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From page 103... ...
Agent The term mouse hepatitis virus (MHV) is used to designate a large group of single-stranded RNA viruses belonging to the family Coronaviridae, genus Co'-onavirus.
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From page 104... ...
Direct contact, fomites, and airborne particles are all probably very important in transmission (Rowe et al., 1963; Robb and Bond, 1979; Barthold, 1986b) Transplacental transmission is of doubtful importance in natural infections (Piccinino et al., 1966)
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From page 105... ...
Infection is perpetuated among partially protected weanlings with little or no clinical disease (unless they are compromised immunologically such as by experimental procedures) (Manaker et al., 1961; Hierholzer et al., 1979; Ishida and Fujiwara, 1982; Barthold, 1986a,b)
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From page 106... ...
MHV infection consistently involves the nasal passages and lungs with dissemination to other organs by the blood vascular system; intestinal involvement, if present, is minimal. After experimental infection, the virus appears sequentially in nasal mucosa; then lungs; and then other organs including lymph nodes, thymus, spleen, bone marrow, brain, liver, and intestine.
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From page 107... ...
Syncytial giant cells can occur in lymph nodes, on mesothelial surfaces, and at other sites. Splenomegaly may occur because of compensatory myelopoiesis, and large numbers of myelopoietic cells may appear in the liver (Hirano et al., 1975b; Fujiwara et al., 1977; Tamura et al., 1977; Ward et al., 1977; Ishida et al., 1978; Furuta et al., 1979; Barthold, 1986a)
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From page 108... ...
The blunting of intestinal villi due to the loss of villous epithelium plus the presence of large, multinucleate syncytial giant cells in the mucosal epithelium of the small intestine, cecum, and/or ascending colon are virtually diagnostic. Lesions of MHV infection in other organs are usually nonspecific and often very subtle.
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From page 109... ...
Once MHV infection has been diagnosed in a facility, the affected population should be either promptly eliminated or quarantined in an area or facility completely away from patho;,en-free mice as MHV is highly contagious. Cesarean derivation followed by barrier maintenance has traditionally been recommended for rederivation of breeding stocks.
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From page 110... ...
In immunocompetent mice, MHV infection: a. Causes immunosuppression or immunostimulation durin, acute infection and chronic immunodepression in persistent infection (Virelizier et al., 19763.
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From page 111... ...
r. Subclinical infections (of MHV)
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From page 112... ...
syndromes. 1968-1988: Period of improving diagnostic methodology for distinguishing MRV and mouse hepatitis virus (MHV)
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From page 113... ...
, possibly mouse hepatitis virus (Kraft, 19825. The observation that increasing age and parity of dams in infected colonies was associated with protection of young can not be fully explained although it has now been shown that some degree of protection against infection (not disease)
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From page 114... ...
described intranuclear inclusions in the intestinal epithelium of infected mice that are compatible with inclusions now recognized as being due to mouse adenovirus-2 (Van der Veen and Mes, 1974; Luethans and Wagner, 1983; Hamelin et al., 1988~.
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From page 115... ...
Definitive diagnosis of diarrhea! disease due to MRV can be made by demonstration of lesions compatible with MRV infection in the small intestine, demonstration of MRV antigen in the intestine or feces, and isolation of the virus by usin, trypsinized primary monkey kidney cells (Tajima et al., 1984; Greenberg et al., 1986~.
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From page 116... ...
disease due to MRV (Morrey et al., 19841. Infant mice with MRV infection have increased mortality when challenged with enterotoxigenic Escherichia cold (Newsome and Coney, 1985J.
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From page 117... ...
The distal small intestine and colon contain fluid, poorly formed pellets, gas, and mucinous material (Vonderfecht et al., 19841. In histologic sections lesions are restricted to the small intestine and consist of villous epithelial necrosis, formation of epithelial syncytial cells, and villous atrophy.
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From page 118... ...
Reovirus-3 Significance Natural infections due to this virus have little significance for most studies with mice and rats but can interfere with studies involving transplantable tumors and in vitro test systems that use cells from these animals. The chief importance of reovirus-3 is that experimental infections with this agent, particularly in mice, provide a large number of models of human disease and test systems for studying the molecular biology of the virus.
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From page 119... ...
Also, experimental infection models using mice were used extensively in studies relating the molecular biology of reovirus- 1 and -3 to viral pathogenesis (reviewed by Sharpe and Fields, 1985~. Natural Infections and Disease 1960: Bennette (1960)
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From page 120... ...
. Mammalian reoviruses have been grown in a wide range of cells but most commonly in L cells and primary monkey kidney cells (Kraft, 1982~.
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From page 121... ...
. Natural infections caused by reoviruses in rodents are assumed to involve mainly the respiratory and gastrointestinal tracts as they do in people.
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From page 122... ...
Virus isolations can be performed with L cells or embryonic kidney cells (Kraft, 1982~. Transplantable tumors and cell lines can be screened for reoviruses by using tissue culture methods or the mouse antibody production test (Rowe et al., 1962~.
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From page 123... ...
Experimental infections of reovirus-3 have been reported to result in the followin, altered biological responses: a. Reduced pulmonary clearance of Staphylococcus aureus (Klein et al.
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From page 124... ...
evidence, but rats have been reported to be refractory to experimental infection with either MAd-1 or MAd-2 (Smith and Barthold, 19871. Epi ootiology The prevalence of these viruses in contemporary mouse and rat stocks is not well understood.
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From page 125... ...
Intraperitoneal, intracranial, or intranasal inoculation can produce a systemic fatal disease in suckling mice born to mothers without antibody (Hartley and Rowe, 1960; Heck et al., 1972; Wigand, 1980~. In 28-day-old mice inoculated intraperitoneally, most animals showed no clinical disease, although some became ill and 10 of 250 animals died (Van der Veen and Mes, 19731.
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From page 126... ...
Presumptive diagnosis of MAd-2 infection can be made by finding the characteristic intranuclear inclusions in histologic sections of intestinal epithelium (Cohen and de Groot, 1976; Ward and Young, 1976; Luethans and Wagner, 19831. A fluorescent antibody method has been used for the detection of MAd-2 antigen in the intestine (Takeuchi and Hashimoto, ~1 ~ ~ A 1976)
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From page 127... ...
suspensions of infected tissue can be passaged in immunocompetent mice given a concurrent dose of 100-200 mg/kg of cortisone acetate; and d. suspensions of infected tissue can be passaged in immunodeficient CBA/N-xid or C3.CBA/N-xid homozygous female or hemizygous male mice, with or without concurrent administration of cortisone (Waggle et al., 19811.
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From page 128... ...
Thus, a high concentration of spores in the animal environment, due to poor sanitation practices and crowding of animals, provides an ideal setting for the occurrence of clinical disease (Ganaway et al., 1971~. Very little is known about the epizootiology and natural history of B
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From page 129... ...
. The mesenteric lymph nodes usually are enlarged (Yamada et al., 1969; Jonas et al., 1970; Weisbroth, 1979; Ganaway et al., 1982; Tsuchitani et al., 19831.
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From page 130... ...
and enzyme-linked immunosorbent assay (Toriumi et al., 1986) tests have been used for the diagnosis of subclinical infections, but none of these tests is currently available commercially in the United States.
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From page 131... ...
The administration of cortisone or adrenocorticotropic hormone to animals with subclinical infection has provoked severe clinical disease (Kaneko et al., 1960; Fujiwara et al., 1963, 1973; Takagaki et al., 1966; Yamada et al., 1969)
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From page 132... ...
~ _ mice and rats during the first halt of the twentieth century teawaras en al., 1948; Habermann and Williams, 1958; Weisbroth, 1979J. More recently, clinical disease caused by these serotypes has virtually disappeared, while subclinical infections caused by weakly pathogenic S
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From page 133... ...
Epi ootiology The prevalence of S enteritidis in contemporary stocks of mice and rats is not well known, but there is evidence that subclinical infections due to weakly virulent strains of S
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From page 134... ...
must be questioned because diagnostic procedures were not done to rule out other causes or contributing agents such as mouse hepatitis virus infection. Followin;, ingestion of an infectious dose of the organism, clinical signs may appear after an incubation period of 2-6 days.
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From page 135... ...
enteritidis serotype typhimurium, O'Brien et al.
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From page 136... ...
Animals that survive a week or longer often appear emaciated, have hyperemia and thickening of the ileal and cecal walls, an empty or fluid-filled large intestine, multiple white or yellow foci in the liver, splenomegaly, enlarged mesenteric lymph nodes, and scanty fibrinous exudate in the peritoneal cavity. Chronic carriers usually do not have gross lesions (Buchbinder et al., 1935; Ratcliffe, 1949; Habermann and Williams, 1958; Maenza et al., 1970; Casebolt and Schoeb, 1988~.
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From page 137... ...
or exacerbate disease caused by S enteritidis.
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From page 138... ...
enteritidis infection is accomplished through barrier maintenance of rodent stocks. Particular attention must be given to the avoidance of Salmonella-contaminated food and water, and the exclusion of infected animals and wild rodents from the facility (Ganaway, 1982~.
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From page 139... ...
facultatively anaerobic rods, measuring 1.0 ,um wide x 2.0 to 6.0 Am long, which occur singly and in pairs, and grow on ordinary medium. They may be a normal inhabitant of the gastrointestinal tract in humans and other species.
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From page 140... ...
Suckling mice are more susceptible than adults. Mortality may reach 60% and rectal prolapse 15%.
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From page 141... ...
Interference with Research Cytokinetics of the mucosal epithelium in the large intestine is profoundly altered in infected mice. Susceptibility to the carcinogen 1,2dimethylhydrazine is increased, and the latent period for neoplasia induction is reduced (Barthold and Jonas, 19771.
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From page 142... ...
Hosts Laboratory and wild mice and rats, humans, and numerous other species (Palleroni, 1984~. Epi ootiology The organism is ubiquitous.
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From page 143... ...
, human carriers, and contact with infected rodents (either wild rodents or other laboratory animals) There is frequent shedding of the organism in infected.
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From page 144... ...
P aeruginosa can be completely eliminated from mice and rats by cesarean derivation followed by maintenance under gnotobiotic conditions (Trentin et al., 19661.
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From page 145... ...
when exposed to lethal doses of whole body irradiation (FIammond et am 1954, 1955; Vincent et al., 1955; Wensinck et al., 1957; Flynn, 1963a,b,c; Hammond, 1963; Hightower et al., 1966~. Similar early deaths in mice exposed to lethal irradiation have occasionally been attributed to other enteric bacteria including Enterobacter cloacae, Escherichia colt, Klebsiella pneumonia, and Proteus vulgaris (Matsumoto, 1980, 1982~.
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From page 146... ...
The majority of parasites that were commonplace in rodent colonies only a few decades ago have now been either eliminated or greatly reduced in prevalence through the application of cesarean derivation and barrier maintenance methodologies. Occasional exceptions may be encountered in conventional colonies that have never been rederived by cesarean section and in cesarean-derived stocks that have been contaminated by wild rodents.
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From page 147... ...
muris have been reported to have diarrhea, dehydration, rough hair coats, weight loss, listlessness, hunched posture, abdominal distension, and sporadic mortality (Sebesteny, 1969; Lussier and Loew, 1970; Boorman et al., 1973a; Csiza and Abelseth, 1973; Wagner et al., 1974; von Mattheisen et al., 1976; Flatt et al., 1978; Van Kruiningen et al., 1978; Eisenbrandt and Russell, 1979~. However, none of these studies excluded other possible causes such as mouse hepatitis virus infection.
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From page 148... ...
148 e~ c~ ._ o cc _ U2 c~ o o o c' v: o c~ ._ ~ , 0 c' ~ c.> O ~ ._ oc c~ 0 0 c~ ~ c.
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From page 149... ...
149 ~.O o ~ x ;5 E ,=`, x .= ~ O ~ ~ =~ O O~O ~0 = = e = O E 0 C ~ =~ = V: ~,~ = = ,,~ = ~ ¢~ ~, .= - c, O e O e E ~ ~ ~ = = ~ ,., E :, _ ~ s ~ ~ E O ~ D .= ~ ~ C~ ~ " '; ' 2; ~ 2 · ' " ~ 2 e Z v~ v: E ~ s: ~ 0 e O , _ _ ca \s C)
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From page 150... ...
Diagnosis Definitive diagnosis of disease caused by S muris requires exclusion of other possible causes of digestive tract disease, e.g., enterotrophic strains of mouse hepatitis virus.
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From page 151... ...
S mu-is can increase the severity and mortality of wasting syndrome (presumably due to mouse hepatitis virus)
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From page 152... ...
Clinical G muris infections in mice and rats are usually subclinical but can cause reduced weight gain, rough hair coats, and enlarged abdomens (Sebesteny, 1969; Roberts-Thomson et al., 1976b; Owen et al., 19791.
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From page 153... ...
muris, followed by barrier maintenance in the user facility. Cesarean derivation is required to eliminate the parasite from infected stocks.
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From page 154... ...
G muris infection can increase the severity and mortality of wastin, syndrome (presumably due to mouse hepatitis virus)
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From page 155... ...
Larval stages occasionally reach the mesenteric lymph nodes, liver, or lung where they incite a granulomatous inflammatory response (Flynn, 1973b; Hsu, 1979; Wescott, 1982~. This is reportedly a common occurrence in mice of the REM strain (C.
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From page 156... ...
Cesarean derivation and barrier maintenance are the most effective methods for eliminating the infection from infected rodent stocks (Flynn 1973b; Wescott, 19821. Interference with Research Infected rodents are deemed unsuitable for research use because of the potential for zoonotic infection and the fact that H
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From page 157... ...
Clinical signs have not been observed in rodents experimentally infected with S obvelata or S
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From page 158... ...
Control The use of cesarean derivation and barrier maintenance methods are effective (Phillips, 1960) , but subsequent reinfection of such stocks with Syphacia spp.
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From page 159... ...
The life cycle of A tetraptera differs from that of Syphacia obvelata and Syphacia muris in that it is 10-12 days longer, and the eggs of A
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From page 160... ...
Diagnosis The more common methods are demonstration of the distinctive eggs by fecal flotation (the cellophane tape method is of no value) and demonstration and identification of the adult worms in the colon at necropsy (Flynn, 1973c; Wescott, 1982~.
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From page 161... ...
. Control Infection with this amoeba is considered inconsequential, and control measures are not usually justified The infection can be eliminated by cesarean derivation and barrier maintenance.
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From page 162... ...
Clinical T muris infections are not known to cause clinical signs (Levine, 1974; Hsu, 1982~.
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From page 163... ...
Interference with Research No examples have been reported. Other Endoparasites Numerous other endoparasites have been reported from wild mice and rats and are encountered occasionally in animals maintained by conventional methods.
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