. After ex pos ure to a varian t of Citro bacter [reundii , suckling and adult mice developed transmissible murine coloni c hyper plasia of the same degree of seve rity . Muco sal hyperpl asia was most severe 2 to 3 weeks after inocu lation and then regressed . Suckling mice had a high morta lity because of seconda ry infla mmat ory and erosive changes . Severe hyper plasia was char acterized by mitotic activity along the ent ire crypt column and surface mucosa .Tra nsmissible m uri ne colo nic hyperplasia is a nat ura lly o ccu rr ing infectious di se ase of mi ce , cha ra cte rize d b y mu co sal hyp e rpl asia of th e d ista l col on . Erosio n a nd inf la m ma tio n ma y ac co m pa ny t he hyp e rpl asia. It is ca use d by a varia nt of Citrobacter [reundii [ I I. In a na tural o u tb re a k ret arded g ro wth , ruffle d fur , soft feces , o ccasio na l rect al pr ol a pse a nd mod erat e mort ality were see n in mic e a t th e lat e s uc kling a nd ea rly we an ling ag es. T he se signs we re se e n rarel y in a d u lts [3].T he ac tua l incid ence of tr an smi ssibl e mu rin e col on ic hyp erpl a sia in mouse co lo nies is difficult to d e termin e , since th e ine xp erien ced o bserve r ma y not not e the vag ue cl in ical signs a nd fre q uent lac k o f o bv io us gross le sion s . A num b e r o f po ssibl y rel at ed synd ro mes of mic e ha ve be en de scri be d b y o t he r la bo ra tories .T wo o f th ese la b orat orie s isol at e d varia nt s of C. fre undii a nd rep ro duce d co lo nic hyp e rpl a sia in experi me nt a lly in o cul a te d mic e [2 , 5 , 6 ]. T he pat ho lo gy de scribe d in th e se re po rts parti all y re sembl ed th at for tr an smissibl e murin e colonic hyp e rpl asia , b ut th ere a re diffe re nc es th at m ak e it di fficult to sta te t he y a re a ll th e sa me di se a se p roce ss . T hese d iffe re nces ma y be re al o r ma y b e ca use d b y vari at io n in co nd it io ns a nd tim e o f sa m p ling . T he ag es of mi ce a nd histo gen e sis o f th e lesion s were not given in re po rt s of ei t her the natu ral o r exp e rime n ta l di se ase . Ot he r possibl y rel at ed le sion s , of un d et e rmin ed ca us e , have bee n d escribe d [3 , 11] . T hese we re cl assi fied as co litis cystica [3 ] a nd ne opl asia [11] a n d had down growth of mu co sal e pi the lium into t he s u b m ucosa . E p ithe lia l d o wn gro wth ha s not bee n see n in tran smi ssible murin e col onic hyp erplasia o r o t he r hyp erpla st ic di se a se s kn o wn to be associa te d wit h C. freu ndii.Ou r stu dy exa mi ne s the path o gen e sis o f t his di se ase in N I H Sw iss m ice a nd co m pa res le sion s to th o se found by oth ers . Becau se of report ed clinical di fferences 223

Pathology, microbiology, and selected serum chemistries were evaluated in 144 male Fischer rats from 4 to 33 mo of age. The rats were reared and maintained under barrier conditions, which successfully excluded the introduction of major infectious disease agents throughout the entire study, including Mycoplasma pulmonis. A wide variety of pathology was found and tabulated, and many lesions were found to increase in severity and incidence with age. There was a high correlation of renal disease severity with increasing age, while alpha-1 globulin and cholesterol increased.

The virus that causes sialodacryoadenitis in rats has been isolated in mice and in primary cultures of rat-kidney cells and has been characterized as a heat-labile RNA virus that is sensitive to lipid solvents and is relatively stable at pH 3.0. This virus is antigenically related to the virus of hepatitis in mice and to coronavirus of rats. The range of hosts of this agent appears to be narrow. On the basis of available biologic characteristics, it has been placed in the coronavirus group.

The pathogenesis of sialodacryoadenitis was studied in gnotobiotic CD rats inoculated intranasally with the causal virus. Virus replication was detected sequentially in the nasopharynx, tracheobronchial tree, cervical lymph nodes, submaxillary and parotid salivary glands, exorbital gland, and Harderian gland. Acute rhinitis appeared within 2 days after inoculation, and salivary glands had lesions in 4 days. Early changes in salivary and exorbital glands were characterized by necrosis of ductal epithelium, which rapidly progressed to widespread acinar necrosis, marked inflammation, edema and total effacement of glandular architecture. Harderian glands also had massive necrosis of tubuloalveolar units. Repair in all glands was characterized by marked squamous metaplasia of tubuloalveolar units. Repair in all glands was characterized by marked squamous metaplasia of ducts. Neutralizing and complement-fixing antibodies were detected in 7 days, and there was a concomitant decrease in tissue-virus titers. There was no detectable evidence for hematogenous spread of virus or for retrograde infection by way of major salivary ducts.

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