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van der Waaij D, eds. Old Herborn University Monograph: Consequences of Antimicrobial Therapy for the Composition of the Microflora of the Digestive Tract. Herborn: Institute for Microbiology and Biochemistry, 1993:8–19. 88. Kager L, Ljungdahl I, Malmborg AS, Nord CE. Effect of tinidazole prophylaxis on the normal microflora in patients undergoing colorectal surgery. Scand J Infect Dis Suppl 1981; 26:84–91. 89. Heimdahl A, Nord CE, Okuda K. Effect of tinidazole on the oral, throat, and colon microflora of man. Med Microbiol Immunol (Berl) 1980; 168:1–10. 90. Adamsson I, Nord CE, Lundquist P, Sjostedt S, Edlund C. Comparative effects of omeprazole, amoxycillin plus metronidazole versus omeprazole, clarithromycin plus metronidazole on the oral, gastric and intestinal microflora in Helicobacter pylori-infected patients. J Antimicrob Chemother 1999; 44:629–640. 91. Buhling A, Radun D, Muller WA, Malfertheiner P. Influence of anti-Helicobacter triple- therapy with metronidazole, omeprazole and clarithromycin on intestinal microflora. Aliment Pharmacol Ther 2001; 15:1445–1452. 92. Brismar B, Edlund C, Malmborg AS, Nord CE. Ciprofloxacin concentrations and impact of the colon microflora in patients undergoing colorectal surgery. Antimicrob Agents Chemother 1990; 34:481–483. 93. Bergan T, Delin C, Johansen S, Kolstad IM, Nord CE, Thorsteinsson SB. Pharmacokinetics of ciprofloxacin and effect of repeated dosage on salivary and fecal microflora. Antimicrob Agents Chemother 1986; 29:298–302. 94. Brumfitt W, Franklin I, Grady D, Hamilton-Miller JM, Iliffe A. Changes in the pharmacokinetics of ciprofloxacin and fecal flora during administration of a 7-day course to human volunteers. Antimicrob Agents Chemother 1984; 26:757–761. 95. Ljungberg B, Nilsson-Ehle I, Edlund C, Nord CE. Influence of ciprofloxacin on the colonic microflora in young and elderly volunteers: no impact of the altered drug absorption. Scand J Infect Dis 1990; 22:205–208. 96. Rozenberg-Arska M, Dekker AW, Verhoef J. Ciprofloxacin for selective decontamina- tion of the alimentary tract in patients with acute leukemia during remission induction treatment: the effect on fecal flora. J Infect Dis 1985; 152:104–107. 97. Enzensberger R, Shah PM, Knothe H. Impact of oral ciprofloxacin on the fecal flora of healthy volunteers. Infection 1985; 13:273–275. 98. Krueger WA, Ruckdeschel G, Unertl K. Influence of intravenously administered ciprofloxacin on aerobic intestinal microflora and fecal drug levels when administered simultaneously with sucralfate. Antimicrob Agents Chemother 1997; 41:1725–1730. 99. Pecquet S, Ravoire S, Andremont A. Fecal excretion of ciprofloxacin after a single oral dose and its effect on fecal bacteria in healthy volunteers. J Antimicrob Chemother 1990; 26:125–129. 100. Holt HA, Lewis DA, White LO, Bastable SY, Reeves DS. Effect of oral ciprofloxacin on the fecal flora of healthy volunteers. Eur J Clin Microbiol 1986; 5:201–205. 101. Borzio M, Salerno F, Saudelli M, Galvagno D, Piantoni L, Fragiacomo L. Efficacy of oral ciprofloxacin as selective intestinal decontaminant in cirrhosis. Ital J Gastroenterol Hepatol 1997; 29:262–266. 102. Esposito S, Barba D, Galante D, Gaeta GB, Laghezza O. Intestinal microflora changes induced by ciprofloxacin and treatment of portal-systemic encephalopathy (PSE). Drugs Exp Clin Res 1987; 13:641–646. 103. Wistrom J, Gentry LO, Palmgren AC, et al. Ecological effects of short-term ciprofloxacin treatment of travellers’ diarrhoea. J Antimicrob Chemother 1992; 30:693–706. 104. Van Saene JJ, Van Saene HK, Geitz JN, Tarko-Smit NJ, Lerk CF. Quinolones and colonization resistance in human volunteers. Pharm Weekbl Sci 1986; 8:67–71. Modifying the Intestinal Microbiota with Antibiotics 367 105. van de Leur JJ, Vollaard EJ, Janssen AJ, Dofferhoff AS. Influence of low dose ciprofloxacin on microbial colonization of the digestive tract in healthy volunteers during normal and during impaired colonization resistance. Scand J Infect Dis 1997; 29:297–300. 106. Edlund C, Lidbeck A, Kager L, Nord CE. Effect of enoxacin on colonic microflora of healthy volunteers. Eur J Clin Microbiol 1987; 6:298–300. 107. Nord CE, Gajjar DA, Grasela DM. Ecological impact of the des-F(6)-quinolone, BMS- 284756, on the normal intestinal microflora. Clin Microbiol Infect 2002; 8:229–239. 108. Edlund C, Nord CE. Ecological effect of gatifloxacin on the normal human intestinal microflora. J Chemother 1999; 11:50–53. 109. Barker PJ, Sheehan R, Teillol-Foo M, Palmgren AC, Nord CE. Impact of gemifloxacin on the normal human intestinal microflora. J Chemother 2001; 13:47–51. 110. Garcia-Calvo G, Molleja A, Gimenez MJ, et al. Effects of single oral doses of gemifloxacin (320 milligrams) versus trovafloxacin (200 milligrams) on fecal flora in healthy volunteers. Antimicrob Agents Chemother 2001; 45:608–611. 111. Inagaki Y, Nakaya R, Chida T, Hashimoto S. The effect of levofloxacin, an optically- active isomer of ofloxacin, on fecal microflora in human volunteers. Jpn J Antibiot 1992; 45:241–252. 112. Edlund C, Sjostedt S, Nord CE. Comparative effects of levofloxacin and ofloxacin on the normal oral and intestinal microflora. Scand J Infect Dis 1997; 29:383–386. 113. Edlund C, Brismar B, Nord CE. Effect of lomefloxacin on the normal oral and intestinal microflora. Eur J Clin Microbiol Infect Dis 1990; 9:35–39. 114. Leigh DA, Emmanuel FXS, Tighe C, Hancock P, Boddy S, Pharmacokinetic studies on norfloxacin in healthy volunteers and effect on the fecal flora. 14th International Congress of Chemotherapy, Kyoto, Japan, 1985. 115. Pecquet S, Andremont A, Tancrede C. Selective antimicrobial modulation of the intestinal tract by norfloxacin in human volunteers and in gnotobiotic mice associated with a human fecal flora. Antimicrob Agents Chemother 1986; 29:1047–1052. 116. De Vries-Hospers HG, Welling GW, Van der Waaij D. Norfloxacin for selective decontamination: a study in human volunteers. Prog Clin Biol Res 1985; 181:259–262. 117. Meckenstock R, Haralambie E, Linzenmeier G, Wendt F. Die Beeinflussung der Darmflora du ¨ rch norfloxacin bei gesunden Menschen. Z Antimikr Antineoplast Chemother 1985; 1:27–34. 118. Edlund C, Bergan T, Josefsson K, Solberg R, Nord CE. Effect of norfloxacin on human oropharyngeal and colonic microflora and multiple-dose pharmacokinetics. Scand J Infect Dis 1987; 19:113–121. 119. Marco F, Gimenez MJ, Jimenez de Anta MT, Marcos MA, Salva P, Aguilar L. Comparison of rufloxacin and norfloxacin effects on fecal flora. J Antimicrob Chemother 1995; 35:895–901. 120. Pecquet S, Andremont A, Tancrede C. Effect of oral ofloxacin on fecal bacteria in human volunteers. Antimicrob Agents Chemother 1987; 31:124–125. 121. Edlund C, Kager L, Malmborg AS, Sjostedt S, Nord CE. Effect of ofloxacin on oral and gastrointestinal microflora in patients undergoing gastric surgery. Eur J Clin Microbiol Infect Dis 1988; 7:135–143. 122. Vollaard EJ, Clasener HA, Janssen AJ. Influence of pefloxacin on microbial colonization resistance in healthy volunteers. Eur J Clin Microbiol Infect Dis 1992; 11:257–260. 123. D’Antonio D, Pizzigallo E, Lacone A, et al. The impact of rufloxacin given as prophylaxis to patients with cancer on their oral and fecal microflora. J Antimicrob Chemother 1996; 38:839–847. 124. Inagaki Y, Yamamoto N, Chida T, Okamura N, Tanaka M. The effect of DU-6859a, a new potent fluoroquinolone, on fecal microflora in human volunteers. Jpn J Antibiot 1995; 48:368–379. Sullivan and Nord368 125. Ritz M, Lode H, Fassbender M, Borner K, Koeppe P, Nord CE. Multiple-dose pharmacokinetics of sparfloxacin and its influence on fecal flora. Antimicrob Agents Chemother 1994; 38:455–459. 126. van Nispen CH, Hoepelman AI, Rozenberg-Arska M, Verhoef J, Purkins L, Willavize SA. A double-blind, placebo-controlled, parallel group study of oral trovafloxacin on bowel microflora in healthy male volunteers. Am J Surg 1998; 176:27S–31S. Modifying the Intestinal Microbiota with Antibiotics 369 19 The Intestinal Microbiota of Pets: Dogs and Cats Minna Rinkinen Department of Clinical Veterinary Sciences, Faculty of Veterinary Medicine, University of Helsinki, Helsinki, Finland INTRODUCTION The knowledge of canine and feline intestinal microbiota is relatively scarce and based mainly on data from laboratory animals, on responses to dietary interventions, or on animals suffering from chronic intestinal disorders believed to be of bacterial nature. Most of the studies are performed on quite low numbers of animals that were often sacrificed and samples of intestinal material collected post-mortem (1,2). As obtaining fecal samples is much more feasible than sampling the contents of upper intestinal tract, most of the papers have focused on fecal microbiota, which may not be considered to represent the whole intestinal microecology. In addition, observations based on the cultivation of luminal contents may not reflect the microbiota adhered to mucosa. Most of the bacterial studies have been performed with traditional cultivation and characterization methods, which may have biased the identification and taxonomy of microbiota. In humans, it is estimated that only 40% of intestinal bacteria are culturable (3); a similar outcome can be expected also in dogs and cats. In addition, the bacterial taxonomy and nomenclature have changed during time, so bacteria identified in earlier studies may currently be re-classified under a different name. For a more in-depth description on the analysis of the intestinal microbiota, see the chapter by Ben-Amor and Vaughan in this book. Proximal small intestine harbors total bacteria of 10 6–8 CFU/ml of luminal content. The number of intestinal bacteria increases distally, reaching up to 10 14 CFU/g in feces. In the small intestine aerobic and facultative aerobic bacteria outnumber anaerobic bacteria (4). When moving aborally in the gut, anaerobic bacteria start to dominate and finally gain numbers as high as 10 10 of CFU anaerobic bacteria/g fecal material (5). DEVELOPMENT OF INTESTINAL MICROBIOTA IN DOGS AND CATS Although there is paucity of research data concerning the development of intestinal microbiota of dogs and cats, it can be considered to follow a similar pattern as known for 371 other mammals. Intestinal colonization is a gradual process starting immediately after birth. In newborn puppies and kittens the alimentary canal is sterile but is quickly inhabited by bacteria from birth canal and environment. The dam usually licks the newborn thoroughly thus transferring its own indigenous bacteria to her offspring. Within 24 hours the numbers of bacteria in various parts of the gastrointestinal tract of a newborn puppy are similar to those of an adult dog (2). The indigenous intestinal microbiota is considered an integral part of the host defense mechanisms. It forms a barrier against pathogen colonization and also influences the host’s immunological, biochemical, and physiological features (6). Once the microbiota has become established, it is relatively stable. Oral antibiotics may have a marked effect on the homeostasis of intestinal microbiota. However, these changes will be re-established relatively soon (7–9). Disturbances in the gut microbiota may result in diarrhea, malabsorption, and chronic intestinal inflammation (10). Acute diarrhea may be fatal as pathogens may invade the host’s tissues resulting in bacteremia and sepsis. Ageing has documented effects on the constitution of intestinal microbiota in dogs. Numbers of bifidobacteria and peptostreptococci diminish with ageing whereas Clostri- dium perfringens and streptococci are more prevalent in the large bowel of elderly dogs (1). CANINE AND FELINE GASTROINTESTINAL MICROBIOTA Gram-Positive Intestinal Bacteria Amongst Gram-positive bacteria residing in the gut, lactic acid bacteria (LAB) make up the largest and most important part of the intestinal microbiota. Although they have a significant protective function in the gut, the present knowledge of canine and feline Gram-positive intestinal microbiota is scant. Most of the canine LAB belong to the genera Streptococcus and Lactobacillus.Ina recent study, Streptococcus alactolyticus was found to be a predominant culturable LAB in jejunal and fecal samples of four beagle dogs. In addition, Lactobacillus animalis, L. reuteri, L. murinus, L. ruminus and S. bovis are reported to harbor in the gut (11,12). The presence of bifidobacteria in canine GI tract is controversial. Many papers report absence of bifidobacteria in the canine fecal samples (11,13), whereas others described bifidobacteria as a substantial part of canine fecal microbiota (14–17). Willard and co-workers isolated fecal bifidobacteria from dogs inconstantly and independent on the diet. It was concluded that bifidobacteria may be only sporadically present in the feces of healthy dogs (18). In healthy cats, the total number of duodenal microbiota is reported to range from 10 5 to 10 9 cfu/ml, most of the bacteria being anaerobic (10,19). The most common anaerobic isolates belonged to groups Bacteroides, Clostridium, Eubacteria and Fusobacteria, whereas Pasteurella spp were the most prevailing aerobic bacteria in feline proximal small intestine. In addition, Acinetobacter spp, Pseudomonas spp and Lactobacillus spp were detected in the duodenal samples of healthy cats (10,19). Lactobacilli were also isolated from feline fecal samples (20). Intestinal Pathogenic Bacteria Bacteria are seldom the sole pathogenic factor in canine and feline gastrointestinal disturbances. Some of the pathogens have been linked to clinical disease, but these pathogenic organisms are frequently isolated also in healthy individuals (21–26). Rinkinen372 Escherichia Coli Escherichia coli is a normal intestinal inhabitant in warm-blooded animals, including cats and dogs, although its clinical significance as canine and feline enteropathogen is not very well documented. Colonization is believed to take place within the first days of a newborn animal. Certain strains of E. coli may act as intestinal pathogens causing gastrointestinal infections. Enteropathogenic E. coli and enterotoxigenic E. coli are known to associate with canine diarrhea, especially in young dogs (27–30). However, these strains have been isolated from non–diarrheic animals, too (28,30,31). Enterohemorrhagic E. coli (EHEC) has been isolated occasionally from dogs. Most of these reports are from dogs living in contact with cattle. EHEC has never been documented in cats (24). Clostridia Clostridium perfringens Clostridium perfringens is an anaerobic, spore-forming bacillus associated with acute and chronic diarrhea in dogs and cats. However, the role of C. perfringens as an intestinal pathogen is questionable, as it commonly harbors in the intestinal tract of healthy dogs, too (23,32). C. perfringens produces toxins, which are classified in five toxigenic types (A–E). C. perfringens enterotoxin (CPE) is the best characterized virulence factor and coregulated with sporulation. All C. perfringens types can produce CPE, but type A strains are most frequently involved. CPE has been reported to cause nosocomial diarrhea, severe hemorrhagic enteritis, and acute and chronic large bowel diarrhea in dogs (33). On the other hand, CPE is also found in feces of non-diarrheic animals (23,32), although a significant association was present with diarrhea and detection of CPE (23). One study reports C. perfringens carrying ß2 toxin gene (cpb2) isolated from diarrheic dogs, suggesting ß2 toxin alone or together with CPE may play a role in canine clostridial diarrhea (34). Clostridium difficile C. difficile is associated with diarrhea in dogs, although it has been frequently isolated from dogs with no signs of diarrhea (23,35). C. difficile–related diarrhea in humans is principally associated with hospitalization and use of antimicrobials. In dogs, no significant association was found in the prevalence of C. difficile along with hospitalization and antibiotic administration, but increased carriage rate was observed in non-hospitalized dogs receiving antibiotics (23). Salmonella Both healthy and diarrheic dogs and cats may carry Salmonella. Prevalence in healthy dogs is reported to be between 1% and 38% (24,36). Furthermore, Salmonella isolation rates in dogs with clinical enteritis is reported low (21,25,37). The prevalence of Salmonella in canine fecal isolates examined has reduced during the past decades. This most likely reflects the change in feeding of dogs, as commercial pet foods have replaced raw meat and offal (36). Feeding bones and raw food diet yielded a 30% Salmonella isolation rate in stool samples of dogs consuming this type of diet. Feeding raw chicken and meat to dogs may therefore be a risk for potential transfer of Salmonella to humans, too (38,39). The Intestinal Microbiota of Pets 373 Salmonella is regarded relatively rare in cats, isolation prevalence varying between 0.8% and 18%; in most reports it is approximately 1%. Also cats may be asymptomatic carriers (22,24,40). An outbreak of Salmonella enterica serovar Typhimurium in cats was reported in Sweden, where salmonellosis was probably transmitted from wild infected birds hunted by the cats (41). Campylobacters Campylobacters are regarded as important zoonotic pathogens. Most of the human infections are food- or water-borne, but infections from pets may also be of concern, especially with immunocompromised people (42–44). Campylobacters have been associated with acute and chronic diarrhea in dogs and cats (43). However, as they are frequently isolated from both healthy and diarrheic animals, it is suggested they are not primary pathogens but more likely opportunistic microbes producing clinical signs in predisposing conditions, such as poor nutrition or housing, or high animal density (45,46). Young dogs seem to be more prone to carry campylobacters, carriage rate being up to 75% of dogs less than 12 months old, whereas the isolation rate in adult dogs was only 32.7% (47,48). Campylobacter shedding correlates clearly with diarrhea in young dogs, but for dogs older than 12 months there was no evident correlation with shedding and clinical disease. In cats, no significant association was found between campylobacteriosis and diarrhea in any age group (49,50). In cats and dogs, C. helveticus, C. jejuni, and C. upsaliensis are most prevalent Campylobacter strains. C. helveticus has been isolated in healthy cats and dogs (47,51,52). One study reported C. helveticus to inhabit 21.7% of the cats examined, being the most prevalent Campylobacter species isolated (47). In addition, C. coli, and C. lari have been isolated to lesser extent (43,45,48,50,53–55). However, the traditional phenotypic identification methods have been criticized for being unreliable when identifying thermo- philic campylobacters (56). The clinical relevance of these campylobacters is unclear. Campylobacter upsaliensis C. upsaliensis is a catalase-negative thermotolerant campylobacter recognized as an emerging human pathogen. In humans it is associated with gastroenteritis and bactere- mia (57). It was first isolated from canine feces (54) and some years later also from feline feces (58). It has been reported to be the most prevalent campylobacter in dogs (47,50,56) and cats (50,56). Thus, it is of interest whether household pets may comprise a reservoir for this zoonotic pathogen although human and canine strains are reported to be genotypically distinct (51). C. upsaliensis has been isolated from feces of both diarrheic and healthy dogs and cats. It is documented to infect puppies at approximately six weeks of age without causing a clinical disease when puppies were raised separately in a breeding kennel, presumably in acceptable conditions. Poor sanitation and high animal density are marked risk factors, increasing the carriage rate of C. upsaliensis up to 2.6-fold. These findings support the opportunistic nature of this organism as a canine and feline pathogen (51,59). Helicobacters Helicobacter spp. are Gram-negative, microaerophilic curved or spiral-shaped motile bacteria. Many gastric Helicobacter-like organisms (GHLO) are frequently found in cats Rinkinen374 and dogs. Virtually all dogs can be expected to harbor gastric GHLO (60,61), although most of the dogs are asymptomatic. Additionally, the clinical signs in dogs suffering from gastritis may persist despite the eradication of helicobacters. Therefore the role of GHLO as an etiological factor in canine gastritis is currently unclear (62,63). In dogs, H. felis, H. bizzozeronii, H. salomonis, “Flexispira rappini,” H. bilis, and “H. heilmannii” have been reported to inhabit the gastric mucosa. The human pathogen H. pylori has not yet been isolated in canine gastric biopsies. However, a recent paper reports presumably non-cultivable H. pylori, or a closely related Helicobacter in two dogs, results based on its 16S rRNA sequence (64). Unlike dogs, cats have been documented to acquire H. pylori, although very infrequently. Feline H. pylori infection has been suggested to be an anthroponosis, i.e., cats are infected by humans carrying H. pylori (63,65–67). In addition to GHLOs, dogs and cats are reported to have also enteric helicobacters. H. canis has been isolated from diarrheic cats and dogs (68,69), and H. marmotae from cat feces (70). MODIFYING THE INTESTINAL MICROBIOTA: PRE- AND PROBIOTICS First documented studies of dietary manipulation of canine and feline intestinal microbiota date back to the beginning of the twentieth century (71). Today, there is growing interest in modifying their gut microbiota towards what is considered a healthy composition, i.e., increase in LAB and bifidobacteria, and decrease in potential pathogenic bacteria (72). Many commercial pet foods now contain prebiotics (e.g., fructo-oligosaccharides, FOS). In addition, probiotics are also marketed for dogs and cats. Prebiotics Prebiotics are reported to have a variable impact on canine fecal and intestinal microbiota. Supplementing dogs’ food with FOS and mannanoligosaccharides increased ileal lactobacilli and fecal lactobacilli and bifidobacteria concentrations (73). Feeding short chain FOS to dogs increased the total number of fecal anaerobes and lowered the number of Clostridium perfringens (17,74). Similar outcome was achieved with arabinogalactan supplementation (15). On the other hand, no significant differences were noticed in the denaturing gradient gel electrophoresis analysis of fecal bacterial profiles when dogs were fed a diet containing 10% fiber (16), and another study revealed no significant effect of FOS supplementation on canine fecal Clostridium spp (18). FOS supplementation increased fecal lactobacilli and decreased numbers of E. coli in healthy cats, but did not alter the duodenal microbiota (75,76). This supports the notion that, as FOS are nondigestible fibers fermented in the proximal gut in humans (mainly in the large intestine) (77), also in cats FOS have only a minimal effect on the microbes residing in the proximal part of GI tract. In a study of eight cats, feeding lactosucrose increased fecal lactobacilli and bifidobacteria counts significantly, while numbers of clostridia and Enterobacteriaceace decreased significantly (78). Probiotics Currently, there are no commerically available probiotics fulfilling the species specificity criterion applied to probiotics as stated by Saarela and co-workers (79). Despite that, The Intestinal Microbiota of Pets 375 probiotics are utilized in pet animals in the hope to create beneficial alterations in the intestinal microbiota. Enterococcus faecium SF68 has been documented to enhance specific immuno- logical responses in young dogs (80) and E. faecalis FK-23 stimulated non-specific immune functions in healthy adult dogs (81). E. faecium is also reported to have an effect on canine enteropathogens. It significantly decreased the canine in vitro mucus adhesion of C. perfringens (82). This finding was supported also in vivo (83). On the other hand, E. faecium increased both the in vitro adhesion and fecal shedding of campylobacters (82,83). Pasupathy and co-workers (84) evaluated the effect of Lactobacillus acidophilus on the digestibility of food and growth of puppies. They concluded that Lactobacillus supplementation has a favorable effect during the active growth period, although differences between the study group and control group were not significant. CONCLUSION In the recent years the interest in canine and feline gastrointestinal microbiota has increased, resulting in a fair amount of documented information. However, the current knowledge of canine and feline gastrointestinal microbiota is still rather scarce. The growing interest in pre- and probiotics together with the novel microbiological methods has already made a scientific contribution to the field of small animal intestinal microbiology. With this trend likely to continue in the future, our knowledge of the canine and feline gastrointestinal microbiota and the factors related to its regulation will expand. REFERENCES 1. Benno Y, Nakao H, Uchida K, Mitsuoka T. Impact of the advances in age on the gastrointestinal microflora of beagle dogs. J Vet Med Sci 1992; 54:703–706. 2. Buddington RK. Postnatal changes in bacterial populations in the gastrointestinal tract of dogs. Am J Vet Res 2003; 64:646–651. 3. Tannock GW, Munro K, Harmsen HJM, Welling GW, Smart J, Gopal PK. Analysis of the fecal microflora of human subjects consuming a probiotic product containing Lactobacillus rhamnosus DR20. Appl Environ Microbiol 2000; 66:2578–2588. 4. Delles EK, Willard MD, Simpson RB, et al. Comparison of species and numbers of bacteria in concurrently cultured samples of proximal small intestinal fluid and endoscopically obtained duodenal mucosa in dogs with intestinal bacterial overgrowth. Am J Vet Res 1994; 55:957–964. 5. Davis CP, Cleven D, Balish E, Yale CE. Bacterial association in the gastrointestinal tract of beagle dogs. Appl Environ Microbiol 1977; 34:194–206. 6. Tannock GW. The normal microflora: an introduction. In: Tannock GW, ed. Medical Importance of Normal Microflora. London: Kluwer Academic Publishers, 1999:1–23. 7. Lode H, Von der Hoh N, Ziege S, Borner K, Nord CE. Ecological effects of linezolid versus amoxicillin/clavulanic acid on the normal intestinal microflora. Scand J Infect Dis 2001; 33:899–903. 8. Sullivan A ˚ , Edlund C, Nord CE. Effect of antimicrobial agents on the ecological balance of human microflora. Lancet Infect Dis 2001; 1:101–114. 9. Nord CE, Gajjar DA, Grasela DM. Ecological impact of the des-F(6)-quinolone, BMS-284756, on the normal intestinal microflora. Clin Microbiol Infect 2002; 8:229–239. 10. Johnston KL. Small intestinal bacterial overgrowth. In: Simpson KW, ed. The Veterinary Clinics of North America, Small Animal Practice. Saunders, Philadelphia: Progress in Gastroenterology, 1999:523–550. Rinkinen376 [...]... 127 2-Amino-3-carboxy-1,4-naphthoquinone (ACNQ), 287 Amino acid homeostasis, 53 Amino acid metabolism, 139–140 Aminoglycosides, 355–356 Amoxicillin, 336 Ampicillin, 336 Androgens, 143 Angiogenins, 104 Animal models, 253–265 Anthocyanins, 162 Antibiotic-associated diarrhea, 296, 318, 319 Antibiotics, 27, 94, 116, 189, 296, 335–363 Antibodies, 27 Antigen-presenting cells (APC), 96, 99, 112 Anti-rotavirus... morphology, motility, secretion and absorption in the digestive tract (102 ,103 ) The use of germ-free, gnotobiotic and conventional animals facilitated The Gastrointestinal Microbiota of Farm Animals 395 considerable progress in the knowledge of the complex ecological system of the gastrointestinal tract in birds (104 ) CONCLUSION The gastrointestinal microbiota plays a very important role in the physiology... The Gastrointestinal Microbiota of Farm Animals 391 log 10. cm−2 8 6 4 2 0 short-term continual Figure 1 Colonization of the jejunal mucosa of gnotobiotic piglets by Escherichia coli 08: K88 at short-term and continual preventive application of Lactobacillus paracasei (,) Control group E; (-) experimental group L-E Source: From Ref 76 jejunal mucosa of conventional piglets by 2.7 logarithm (4.75 log 10/ cm2)... fucose, 123 genome sequencing, 178 host-microbe interactions, 53, 181 PCR analysis, 64 B vulgatus, 3, 55, 64 Bacteroides, 52, 123, 208 Bacteroidetes, gene analysis, 2, 8 Batch-type simulators, 238 401 402 Beta-aspartylglycine, 279 Bifidobacteria, 52, 76, 286, 315 adults, 292–294 aging, 77, 78, 79–88, 95 colonization, 54, 76 diet, 55 immune response, 107 108 infants, 107 , 130, 291 large intestine, 42 mucus... nutrients from the small intestine of gnotobiotic and conventional chicks Br J Nutr 1982; 47:349–356 104 Vanbelle M, Teller E, Focant M Probiotics in animal nutrition: a review Arch Anim Nutr 1990; 40:543–567 Index Abomasum, 386 Acetate, 53, 324, 386 Achlorhydria, 30, 226 ACNQ See 2-amino-3-carboxy-1, 4-naphthoquinone Acquired immunity, 96 Actinobacteria, gene analysis, 2 Actinomyces israellii, 30 Acute... group-specific oligonucletide probes Results showed the Spirochetaceae, the Cytophaga-Flexibacter-Bacteroides assemblage, the Eubacterium rectale-Clostridium coccoides group and unknown cluster C of Clostridiaceae to be the largest populations in the equine gut, each comprising 10 30% of the total microbiota in each horse sampled Other detected notable populations were the BacillusLactobacillus-Streptococcus... Several useful in vitro methods are used to study gastrointestinal microbiota It seems that germ-free and gnotobiotic animals could represent, in conjunction with in vitro methods, a helpful base for the complex study of gastrointestinal ecosystem in farm animals REFERENCES 1 Salminen S, Boulez C, Boutron-Ruault M-C, et al Functional food science and gastrointestinal physiology and function Brit J Nutr... of acetate, butyrate and propionate increase from undetectable amounts in 1-day-old broilers to high concentrations in 15-day-old broilers (27) Facultative anaerobic microbiota (streptococci, lactobacilli and E coli) comprise the predominant microbiota of the small intestine and Salanitro and coworkers (28) found that the above-mentioned bacteria represent 60–90% of the isolated bacteria While the number... capture the total microbial community of complex anaerobic habitats such as the avian gastrointestinal tract Apajalahti and coworkers (31) analyzed broiler chickens from eight commercial farms in Southern Finland for the structure of their gastrointestinal microbial community by a non-selective DNA-based method, percent GCC-based profiling and, in addition, a phylogenetic 16S rRNA genebased study was carried... H, Kato S, et al Effect of lactosucrose (4G-beta-D-galactosylsucrose) on fecal flora and fecal putrefactive products of cats J Vet Med Sci 1993; 55:291–295 ´ ¨ ¨ 79 Saarela M, Mogensen G, Fonden R, Matto J, Mattila-Sandholm T Probiotic bacteria: safety, functional and technological properties J Biotechnol 2000; 84:197–215 380 Rinkinen 80 Benyacoub J, Czarnecki-Maulden GL, Cavadini C, et al Supplementation . 2001; 1 :101 –114. 9. Nord CE, Gajjar DA, Grasela DM. Ecological impact of the des-F(6)-quinolone, BMS-284756, on the normal intestinal microflora. Clin Microbiol Infect 2002; 8:229–239. 10. Johnston. the structure of their gastrointestinal microbial community by a non-selective DNA-based method, percent GCC-based profiling and, in addition, a phylogenetic 16S rRNA gene- based study was carried. Clostri- dium perfringens and streptococci are more prevalent in the large bowel of elderly dogs (1). CANINE AND FELINE GASTROINTESTINAL MICROBIOTA Gram-Positive Intestinal Bacteria Amongst Gram-positive

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