Summary. Non-motile variants of Helicobacterpylori (strain 26695) occurred with a frequency of 1.6 (SD 0.4) x lo-* variants/cell/division cycle, and reversion to the motile form occurred with a frequency of < lo-' variants/cell/division cycle. The two forms remained > 90 YO pure for up to 50 cell divisions and differed only in the presence or absence of motility and flagella. Bacteria were recovered from nine of 10 gnotobiotic piglets inoculated orally with motile H. pylori, but from only two of eight inoculated with the non-motile variant. The motile form survived for 21 days in infected piglets, but the non-motile variant survived for only 6 days. Bacteria recovered from piglets inoculated with the non-motile variant were non-motile. These data support the hypothesis that motility is a colonisation factor for H . pylori.

Polycystic kidney disease in Persian cats culminates in chronic renal failure after a variable clinical course. An affected 6-year-old Persian cat was used to establish a colony of cats with polycystic kidney disease. In affected cats, cysts could be detected by ultrasonography as early as 7 weeks of age. Absence of cysts on ultrasound examination at 6 months of age was correlated with absence of polycystic kidney disease at necropsy. Both males and females were affected and, of progeny from affected x unaffected crosses, 42% were affected and 58% were unaffected. In affected x affected crosses, 73% of progeny were affected and 27% were unaffected. These results are compatible with autosomal dominant inheritance of this trait. Polycystic kidney disease in Persian cats resembles autosomal dominant polycystic kidney disease (ADPKD) in human beings, and represents a valuable animal model of the human disease.

A form of autosomal dominant polycystic kidney disease (ADPKD) similar in clinical features to human ADPKD occurs in the Persian cat. We characterized the morphologic and immunohistochemical features of this disease in a colony of affected cats. Complete postmortem examinations were performed on 11 normal and 22 affected cats ranging in age from 3 months to 10 years. Kidneys were evaluated by gross and histologic examinations, ultrastructure, lectin staining, bromodeoxyuridine immunochemistry for labeling index and immunochemistry for distribution of Na/K ATPase. Feline ADPKD was characterized by variable numbers of cysts in the renal cortex and medullar. Ultrastructural examination and lectin staining suggested that cysts arose from proximal and distal nephron segments. Bromodeoxyuridine labeling demonstrated increased proliferation of epithelium lining some cysts in young cats. Immunohistochemical staining showed variable translocation of Na/K ATPase from the basolateral membranes of cyst-lining cells to the cytoplasm or luminal membranes. Cystic renal disease commonly was associated with chronic tubulointerstitial nephritis and hepatobiliary hyperplasia and fibrosis. Focal hyperplasia of renal tubular epithelium, hepatic cysts, and cardiac lesions were present in some cats. Feline ADPKD shares many morphologic and pathogenetic features with human ADPKD.

Abstract. An outbrea k of vo m iting in a gro up of captive chee tahs (Acinonyx j ubat us) was inves tigated , and histologic examinati on revea led chro nic gastritis characterized by infiltration o f lymphocytes and nume rous pla sma cells and epithel ial erosio ns. Lymphoid follicles, globule leu kocytes, scatte red neutrophi ls, and (in on e ani ma l) abscessed gastric glands were incon sistent finding s. In addi tio n, necrop sy of three cheetahs revea led gastric mu cosal hyperplasia. T wo kinds of bacteria were identified in th e sto mac hs of infected cheetahs. Numerou s long, tightl y coi led motile Gastrospi rillum -like organis ms were seen in gastric mu cu s and in WarthinStarry-stai ned sections of m ucosa . T hese bacteria could not be cultured but were transmi tted to conventional mice in hom ogenates of gastric m ucosa from infected cheetahs. Ultrastructural exami natio n revea led helical filam ents on some of these bacteria. In add itio n, a sma ller Helicobacter sp. was isolated . Th is organism co uld be cultured in vitro und er m icroaeroph ilic co ndi tio ns. O ne or both of th ese bacterial species was proba bly respon sible for th e gastritis in these cheetahs.Key words: Bacteria; cheeta hs; gastritis; Gastrospirillum; Helicobacter pylori.In 1983 , a ba ct eri al organism now known as H elicobacter py lori was first isolated fro m th e sto machs of human pati ents with gastritis." This organism has since be en shown to be a co m m o n cause of gastritis and ha s be en associated with peptic ulcer di sease, gastric ca rcin oma , and a number o f othe r co nd it io ns .'>' Because of its association with peptic ulcer d isease, H. pylori has ev o ked a great deal of interest and stud y. Clinical trials have shown tha t erad icatio n of infection is asso ciated with healing of ulcers and that tr eatment for ulcers is in effecti ve in th e absen ce of bacterial era d ication ," suggesting that H. pylori is a n important fac to r in th e pathogenesis of human peptic ulc er di sea se.' > In addition to H. pylori, other gas tric bact eria ha ve been described in human beings.v-' but th ey are unco m mon and ha ve not been cult ured in vitro and thus cannot be taxonom icall y defin ed. They are m ost o fte n referred to as Gastrospirillum hominis or Gastrospir illum-like ba cteria (GLO). Like H. pylori, they may be as sociated with gastritis.s-" Bact eri a l ga stritis is po orl y docum ented in an imals. R ecent rep orts, however , suggest that gastri c ba ct eri a are relati vely co m m on and that gast ritis ca used by th ese ba cteria ma y ha ve been co m m o nly overloo ked in th e past. 12H. pylori-like o rganis ms ha ve been isolat ed fro m ferrets with gastritis a nd gastric ulce rsv -? and from macaques' a nd pigs" with gastritis. These ba ct eria are probably widespread in a nima ls, but their incidence and associa tio n with di sea se ha ve recei ved little a tte ntion. Althou gh th ey ha ve been incon sist entl y associat ed with hi stologic ga stritis, th ey have not previ ou sly been...

This study sought to determine if coccoid forms of Helicobacter pylori are virulent for gnotobiotic piglets. Coccoid forms were generated by maintaining broth cultures of H. pylori under microaerobic conditions for 16 days. The resulting cultures contained bacteria with a coccoid morphology that could not be cultured in vitro. Coccoid H. pylori did not colonize any of 6 gnotobiotic piglets that were inoculated, whereas bacillary H. pylori colonized 6 of 6 inoculated piglets. Piglets colonized by bacillary H. pylori developed lymphocytic gastritis, but no gastritis developed in piglets inoculated with coccoid H. pylori, and coccoid-inoculated piglets were sero-negative for H. pylori-specific antibody. Thus, coccoid H. pylori appears to be a degenerate nonviable morphologic phase.