Etiology

Campylobacter is a genus of gram-negative, slender, curved, motile rods (1.5 to 5 µm × 0.2 to 0.5 µm) that are found singularly, in pairs, or in chains with three to five spirals (Fig. 37-1). The cells can also be curved, S = shaped, or gull-shaped. Campylobacter species have a single, nonsheathed polar flagellum and microaerobic growth requirements. Campylobacter jejuni is the organism routinely associated with diarrheal disease in dogs, cats, and humans, as well as other domestic, wild, and laboratory animals. Campylobacter coli, distinguished from C. jejuni on the basis of hippurate hydrolysis, is also isolated from diarrheic animals and humans. Other intestinal catalase-negative campylobacters, Campylobacter upsaliensis, Campylobacter helveticus, and Campylobacter lari, have been increasingly isolated from asymptomatic and diarrheic dogs and cats.* Results of further genetic analysis indicate that dogs may also be colonized with C. felis and Campylobacter showae in addition to other Campylobacter spp. previously identified by culture.⁷⁷ In addition to the isolation of multiple species of Campylobacter, genetic heterogeneity may also exist in individual Campylobacter species isolates from the feces of individual animals.^{3,324,325,330a} Web Table 37-1 summarizes the features of these Campylobacter species.

Epidemiology

Privately owned adult dogs and cats generally have a lower isolation rate of C. jejuni than strays or those maintained in kennels or catteries, laboratories, and animal shelters.4,193 C. jejuni has been isolated from 21% and 29% of diarrheic cats and dogs, respectively, compared with 4% of clinically healthy cats and dogs.¹¹⁴ In other studies the isolation rate from feces of mature dogs and cats with and without diarrhea has varied from 0% to 50%.^44,569 Prevalence of C. jejuni in clinically healthy dogs in one report was significantly greater (p less than 0.05) in dogs younger than 6 months old, in dogs living in high-density and cohabitation housing conditions for long periods, and in the autumn months.⁶⁰⁴ In a longitudinal study conducted in Denmark on 26 young (3 months to 1 year of age) pet dogs, C. jejuni was more prevalent in the feces of these dogs compared to those between 1 and 2 years of age.²⁴⁵ The authors also documented that dogs were often colonized with C. upsaliensis for up to 21 months of age. In Cheshire, England, high risk factors for carriage of C. upsaliensis by a dog included living with another dog that also carried C. upsaliensis; being small rather than medium-sized; being less than 3 years of age; living in a household that kept fish; being fed commercial dog treats; and being fed human food tidbits, particularly in the dog’s bowl.⁶⁵³ A higher prevalence of C. jejuni and other enteric bacteria has been found in dogs being fed raw meat.³⁶⁴ In clinically healthy or diseased dogs being evaluated at veterinary practices in the United Kingdom, C. upsaliensis isolation rate overshadowed that of C. jejuni, and most of the isolates were made from younger dogs.⁴⁵⁴

In a 6-year study, 64 of 227 commercially reared cats without clinical signs of diarrhea had microaerobic bacteria isolated from their feces.⁵³³ All the isolates were initially identified as Campylobacter-like organisms (CLOs) based on biochemical and phenotypic characteristics. DNA extractions from 51 of these isolates were subjected to the polymerase chain reaction (PCR) using primers specific for Helicobacter spp. and Campylobacter spp. Of these isolates, 92% (47 isolates) were positive for Campylobacter spp., 41% (21 isolates) were positive for Helicobacter spp., 33% (17 isolates) were positive for both genera, 59% (30 isolates) were positive only for Campylobacter spp., and 8%⁸ were positive only for Helicobacter spp. Sixteen of the 47 Campylobacter-positive cultures were positive for more than one species of Campylobacter. Based on a species-specific PCR assay, 83% of the isolates were identified as C. helveticus, 47% of the isolates were identified as C. upsaliensis, and 6% of the isolates were classified as C. jejuni. This study demonstrated that biochemical and phenotypic characteristics of microaerobic organisms in cat feces were insufficient to characterize mixed Helicobacter and Campylobacter infections. The finding of C. helveticus in a high percentage of the cats confirms the findings of a previous study in England in which the organism was cultured from the feces of healthy cats.⁵⁶⁵

In another investigation on co-infection with Campylobacter spp., enteric Helicobacter spp. and Anaerobiospirillum spp. in healthy or diarrheic dogs and cats, 27 animals (10%) were found to be infected with Campylobacter spp. and Helicobacter spp., and 8 dogs and 2 cats harbored all three genera.⁵⁰⁰ C. upsaliensis was the most frequently isolated species in dogs and C. helveticus from cats, whereas the isolation rates of C. jejuni were similar in both animals. The most frequent isolates were Helicobacter bilis (15.3%) followed by Helicobacter canis (12%) and finally Helicobacter cinaedi (6.2%). No statistically significant correlation between isolation of single or mixed infections and the presence of diarrhea was observed. In one report, 361 specimens were collected by rectal swab from cats and dogs in Ireland (179 cats and dogs in shelters and 182 cats and dogs in a university veterinary hospital); 163 of 361 (45.2%) of the pets surveyed were positive for Campylobacter spp. using a combination of culture techniques.¹ Specification results using DNA extraction and specific PCR confirmed that 50% of the isolates for C. upsaliensis and 41.9% were C. jejuni. A smaller percentage of isolates were C. coli (2.6%), C. lari (1.5%), and C. helveticus (1.1%). For 2.9%, identification among C. jejuni, C. lari, and C. coli could not be made.¹ In a study conducted in pet dogs and cats in Barbados, C. jejuni was cultured from 34 of 66 dogs (51.5%), whereas C. upsaliensis was isolated in 6 of 20 (30%) and C. helveticus in 10 of 20 (50%) of cats, respectively.⁶⁶⁵

Puppies and kittens appear more likely to acquire C. jejuni and show clinical disease, probably because of a lack of previous exposure and development of protective antibody. Studies of pups show that shedding of Campylobacter species ranges from less than 5% to as high as 90%.

As with most enteric microbial pathogens, fecal-oral spread with foodborne and waterborne transmission appears to be the principal avenue for infection. Suspected sources of Campylobacter infection include contaminated meat products, particularly poultry and unpasteurized milk.⁴⁰⁷ Asymptomatic carriers can shed campylobacters in their feces for prolonged periods and directly infect other animals or contaminate food products or water. Nosocomial infection of hospitalized animals occurs, as does exposure through other pets in a household (e.g., ferrets, hamsters, birds, rabbits) and rural farm animals that may shed the organism. Flies have also been incriminated in the spread of organisms.⁴²⁸

Pathogenesis

The severity of the disease depends on the number of organisms ingested by the host as well as previous exposure and development of protective antibody. Other enteric pathogens, such as parvovirus and coronavirus, Giardia organisms, or Salmonella organisms, may play a synergistic role.64,511 Environmental, physiologic, and surgical stresses may also exacerbate the severity of the disease. Blood and leukocytes in the feces, congestion, edema, mucosal ulcers, and occasional sepsis in humans suggest that the organism can be invasive. Experimental challenge in laboratory animals also indicates that the organism can be isolated from blood several days after challenge inoculation. Experimental infections of puppies and kittens with strains isolated from humans with diarrhea are less severe than those observed in the humans from which the organisms were isolated. Animals appear to be more resistant or better adapted to the pathogenic effects of various different C. jejuni isolates and usually only develop watery mucoid diarrhea.^372,478,478

A variety of virulence factors, such as enterotoxins, cytotoxins, or adherence or invasion properties, are expressed by different C. jejuni–coli isolates. A cytotoxin, referred to as cytolethal distending toxin (cdt), has been identified in C. jejuni; however, its role in production of intestinal disease is in the process of being determined. For example, wild-type C. jejuni containing cdt cause gastroenteritis in infected nuclear factor kappa B (NF-κB) deficient mice, whereas isogenic C. jejuni mutants lacking cdt do not induce disease.¹⁹⁶ In vitro, the cytotoxin causes distention of cell lines and cell-cycle arrest in the G₂M1 phase in the cell cycle.

An intriguing report in humans links the occurrence of acute onset of Campylobacter– or Salmonella-induced diarrhea to subsequent development of inflammatory bowel disease (IBD).²²⁵ Whether such an association occurs in dogs and cats is presently unknown.

Clinical Findings

Diagnosis

Therapy

The efficacy of antibacterial therapy and treatment of Campylobacter-associated diarrhea in the dog and cat is not known, nor is it known whether antibacterials effectively alter the course of enteric disease. However, in some dogs and cats with severe diarrhea, antibacterial therapy may be warranted. Antibacterial treatment of infected animals may be instituted to minimize exposure to people and other pets in the household. Fortunately, strains of Campylobacter isolated from animals and people are susceptible to several antimicrobial agents (Table 37-1). Erythromycin, the drug of choice for Campylobacter-induced diarrhea in people, may also be effective in the treatment of the disease in animals. Treatment of clinically affected cats and dogs has resulted in resolution of the illness and elimination of the organism as determined by Campylobacter-negative fecal culture results. However, failure to eliminate C. jejuni with oral erythromycin from ferrets housed in a research environment has also been noted.¹⁷² Erythromycin can also cause gastric irritation and vomiting in some animals.

Chloramphenicol has been given with mixed results to treat Campylobacter-associated diarrhea in dogs and cats. Treatment in dogs has resulted in abatement of clinical signs. However, the same organism has been reisolated after therapy has been completed. It is possible that these dogs developed an antibacterial-induced carrier state (as occurs in enteric Salmonella infections), experienced a protracted period of Campylobacter shedding, or became reinfected. Clinical improvement was noted in a diarrheic cat treated with chloramphenicol, and fecal culture results after completion of the treatment were negative for C. jejuni. C. jejuni–associated bacteremia and cholecystitis have been successfully treated with intravenous cefoxitin, a second-generation cephalosporin, or oral erythromycin (see Table 37-1) for 21 days, which resulted in complete resolution of all clinical and laboratory abnormalities.⁴⁴³

Several other antibacterials are active against Campylobacter strains isolated from dogs and cats. These strains show in vitro susceptibility to furazolidone as well as gentamicin, neomycin, clindamycin, and tetracycline. However, resistance in many strains to various tetracyclines and kanamycin is caused by plasmids that confer resistance and are transmissible within C. jejuni serotypes. Antimicrobial agents that are usually ineffective include penicillin, ampicillin, polymyxin B, trimethoprim, and vancomycin. In vitro resistance also develops to metronidazole and sulfadimethoxine.¹⁸³ Many Campylobacter strains produce β-lactamase, which accounts for the resistance to penicillin and ampicillin. Amoxicillin plus clavulanate appears to be effective in treating campylobacteriosis in humans.²⁴³ Before therapy is instituted, isolation and susceptibility tests should be done. Some animals continue to shed the organism despite antibacterial therapy. Quinolone antibacterials may be useful in eliminating C. jejuni and C. coli in asymptomatic carriers, but drug resistance to this class of antibacterials has severely impeded their use to treat Campylobacter infections.⁵⁴ Interestingly, in a human case-control study, therapy with a proton pump inhibitor, omeprazole, doubles the risk of acquiring Campylobacter enteritis.⁴¹⁹ The natural resistance imparted by gastric acid secretion has also been observed with other enteropathogens (see Salmonellosis).

Public Health Considerations

It is recognized that C. jejuni-coli is a leading cause of enteric disease in people and that puppies and kittens can serve as sources of infection for humans. The infectious dose of C. jejuni for humans is as low as a few hundred organisms. The disease is often severe in people and in addition to diarrhea may be characterized by vomiting, fever, and abdominal discomfort. Usually the incriminated pets have been suffering from diarrhea and have been recently acquired from pet stores or kennels. However, asymptomatic dogs and cats can also be a source of infection to people. Results of a survey conducted in Seattle, Washington, indicated that 6% of sporadic C. jejuni infections were linked to exposure to diarrheic kittens.¹⁹ Another study reported that 30% of the cases in university students were associated with healthy cats.¹⁶⁶ However, the major risk factor for acquiring C. jejuni enteritis is the consumption of raw or undercooked meat, particularly chicken.^{17,166,207,563,661}

In human infections associated with pets, findings of molecular diagnostic techniques have demonstrated the isolation of the same C. jejuni strain in both the pets and their owners.101,663 Therefore, veterinary practitioners should alert owners of the zoonotic implication of Campylobacter infection for other household members and stress the importance of exercising appropriate hygienic measures, especially when pets have diarrhea. An additional zoonotic risk is the development of Guillain-Barré syndrome, a demyelinating polyradiculoneuritis in people, which may occur after infection with C. jejuni. The antigens of peripheral nerves share epitopes with lipopolysaccharides of these bacteria.^408,440

C. upsaliensis has been isolated from a human with bloody diarrhea as well as his pet dog, which also had diarrhea. The plasmid profile of the two strains were identical, suggesting that C. upsaliensis infection may also be a zoonosis.²²³ C. upsaliensis was isolated from the blood and fetoplacental tissue of a woman with diarrhea who was 18 weeks pregnant and had been in contact with a cat that had a similar strain of C. upsaliensis isolated from its feces, also suggesting zoonotic transmission.²³⁹ Others have also reported C. upsaliensis gastroenteritis in humans who have had contact with pets.⁴⁵⁷ Human and canine isolates of C. upsaliensis have distinct ribotypes and plasmid profiles, suggesting that host-specific genotype differences may exist among strains of C. upsaliensis.⁵⁶⁶ However, these analyses or other molecular fingerprinting techniques must be used on suspected pet-associated C. upsaliensis zoonoses before the definitive transmission can be defined.

Campylobacter spp. and other enteropathogen infections have been prevalent in pets used in human health settings or as guide assistance dogs.235,357,357 The increased popularity of using dogs in hospital- or hospice-based settings as a recognized method of therapy has resulted in the recommendation for screening of these animals for zoonotic microorganisms including Campylobacter spp.^356,360

Etiology

Gram-negative, microaerophilic, curved to spiral-shaped bacteria isolated from gastric mucosa of humans and animals have created a great deal of interest because of their causal role in gastric disease.349,618 The genus Helicobacter includes 27 formally named species as well as other unnamed closely related organisms.* Once considered a predominantly sterile organ protected from microbial colonization by low gastric pH, the euchlorhydric stomach is now known to be colonized with gastric bacteria belonging to the genus Helicobacter (Web Table 37-2 and Fig. 37-2), whereas the hypochlorhydric stomach is resistant to their replication. These organisms possess a high level of urease activity that allows them to survive in an acidic environment. The type species Helicobacter pylori colonizes the stomach of 20% to 95% of human adult populations worldwide (see Fig. 37-2, A).²²⁶ H. pylori causes persistent, active, chronic gastritis and peptic ulcer disease in people and has been linked to the development of gastric adenocarcinoma and gastric mucosa-associated lymphoma.⁴⁵¹ H. pylori has also been isolated from inflamed gastric tissue of cats in a commercial cattery and can experimentally infect cats.^252,461

Other gastric helicobacters have been linked to gastritis in various mammalian hosts.167,257,420,435,666 Many of these infected animals have asymptomatic gastric inflammation. Additional species of gastric Helicobacter have been isolated from stomachs of various mammalian hosts, including dogs (Helicobacter rappini, Helicobacter felis, Helicobacter bizzozeronii, Helicobacter heilmannii-like, Helicobacter salomonis, Helicobacter bilis), cats (H. felis, H. heilmannii-like, Helicobacter pametensis, Helicobacter baculiformis sp. nov.),³¹ ferrets (Helicobacter mustelae), hamsters (Helicobacter aurati), cheetahs (Helicobacter acinonychis), dolphins, whales, harp seals (Helicobacter cetorum), and nonhuman primates (H. heilmannii-like). (See Web Table 37-2 and Fig. 37-2 for a summary of the gastric helicobacters infecting dogs and cats.)

Historically, Helicobacter spp. in dogs and cats have been described histologically as gastric spirilla.¹⁶⁷ Three morphologically distinct forms have been described in dogs and cats.^{29a,368,639,640} More than one of these morphologic types of bacteria can be seen in the stomach of one animal. Lockard type 1 is a bacterium with multiple bipolar, sheathed flagella entwined with periplasmic fibers, which appear to cover the entire surface of the organism (see Fig. 37-2, B). A similar organism was isolated from aborted ovine fetuses and was classified as Flexispira rappini.^320,439 This bacterium, reclassified as a Helicobacter species based on 16S RNA sequencing, has been isolated from the feces of asymptomatic mice, dogs, and cats as well as from the stomachs of dogs.^368,520 H. bilis, a member of the Flexispira taxa associated with hepatitis and IBD in mice, has also been cultured from the stomachs of dogs. Lockard type 2 also has periplasmic fibers, but they are most sparsely distributed on the organism and can appear singly or in groups of two, three, or four. This organism has been cultured from the feline stomach and has been named H. felis (see Fig. 37-2, C).⁴⁵⁶ The third type of organisms, called gastrospirilla, are the bacteria most commonly found in mammalian stomachs. These are also very tightly spiraled, but they have no periplasmic fibrils. On the basis of morphologic characteristics, it appears that the Lockard type 2 organism primarily is restricted to cats and dogs, whereas type 3 has been seen in cats, dogs, nonhuman primates, cheetahs, swine, and humans. The type 3 bacterium has been given various names in different hosts, including Gastrospirillum hominis and H. heilmannii (see Fig. 37-2, D).^255,551 Gastric helicobacters H. bizzozeronii and H. salomonis, H. felis, and Helicobacter cynogastricus²⁴² isolated from dogs have been formally named, based on defined biochemical and genetic analysis. H. bizzozeronii (see Fig. 37-2, E) has also been cultured from the inflamed gastric tissue of humans.¹⁸ By EM this organism lacks periplasmic fibers, in contrast to H. felis. This morphologic distinction is confounded with the observation of two gastric Helicobacter-like organisms (GHLOs). These GHLOs from dog stomachs lacking periplasmic fibers had genetic analysis compatible with H. felis.¹³⁰ H. salomonis (see Fig. 37-2, F) is a gastric helicobacter with unique molecular characteristics that has been isolated from dogs.^255,290 In cats, H. felis, H. pylori, H. pametensis (first isolated and characterized in birds), and H. heilmannii have been isolated or identified in gastric tissues. H. baculiformis, a novel species, has also been isolated from the gastric mucosa of a clinically healthy cat.³¹

Epidemiology

Although infected animals and humans mount a significant systemic IgG response to gastric organisms, the antibodies are not protective, and the organisms persist in the mucous layer or closely adhere to the gastric epithelium, protected from the gastric acidic milieu. The mechanisms of transmission are poorly understood. Gastric helicobacters have specific enteric tissue tropism and colonize only gastric and not intestinal epithelium. Fecal-oral transmission has been suggested, and gastric helicobacters have been isolated from feces of animals and humans.⁴⁵² H. mustelae was isolated from feces of ferrets, particularly when ferrets had drug-induced hypochlorhydria.¹⁹⁴ H. pylori has been isolated from feces of children from a third-world country as well as from infected adults from a more developed country.^312,599 Gastric helicobacters have been isolated from the environment in surface waters,²⁶² likely a result of fecal contamination. Indirect transmission in this manner might result in more widespread dissemination. One concern is that helicobacters are more resistant than coliforms to chlorination.

Oral-oral transmission is more likely and is supported by clinical observations of humans being infected by exposure to gastric secretions,⁴⁵² isolation of H. pylori from dental plaque and tissue, and nosocomial infection from improper disinfection of gastric pH probes and endoscopic equipment. Similar transmission routes are also probable for gastric Helicobacter in animals. Helicobacter spp. DNA has also been detected in the oral cavities of dogs.⁴⁸⁹ Vomitus containing gastric Helicobacter is another likely source for transmission.¹⁵² In pups, experimentally inoculated gastric helicobacters have been acquired during the lactation period, and puppies have infected each other.²⁵⁴ Cats naturally infected with H. pylori were screened by culture and PCR for the organism in salivary secretions, gastric juices, gastric tissues, and feces.¹⁹⁵ H. pylori was cultured, from salivary secretions (50%) and gastric fluid samples (91%), from cats. A PCR product specific for an H. pylori surface protein was amplified in 42% of feline dental plaque specimens and 80% of feline fecal specimens. Isolation of H. pylori from feline mucosal secretions suggests a zoonotic risk exists from personnel handling of H. pylori–infected cats in vivaria.²⁵² In comparison, H. pylori infection was not detected in stray cats,¹³³ which may reflect an anthroponosis in the closed commercial cattery where H. pylori was present in 100% of the animals. Additional studies using molecular, cultural, and histologic techniques are needed to ascertain whether H. pylori naturally colonizes dogs and cats.

The prevalence of gastric Helicobacter spp. infections in clinically healthy colony-raised dogs and cats in high population densities routinely approaches 100%, indicating the organisms’ unique ability to colonize the stomachs of numerous hosts selectively and efficiently.⁵³⁹ In laboratory-reared beagles, H. felis and other spiral helicobacters were observed in high numbers in the gastric glands of the fundic-pyloric junction and the cardia. These organisms were associated with lymphoid hyperplasia and parietal cell degeneration.^264,368 In pet dogs and cats a series of gastric biopsy samples were examined for the presence of GHLOs.²⁶⁸ GHLOs were observed in 82% of dogs and 76% of cats; the bacteria were present in the mucus of foveolar epithelia, gastric pits, and parietal cells. More lymphoid follicles are found in the stomachs of older random-source cats with high numbers of GHLOs in their gastric mucosae than in younger cats with lower numbers of GHLOs.⁴⁴⁴ A high prevalence of infection was observed, in association with histologic gastric inflammation, in 89.2% of stray cats.^27a Helicobacter spp. have been found in the oral cavity and stomach of stray cats; however, the species in the oral cavity did not always correlate with that found in the stomach.^584a

Pathogenesis

Chronic or chronic active gastritis resulting from oral inoculation of Helicobacter species has been experimentally produced in humans, germ-free pigs and dogs, specific-pathogen free cats, mice, and nonhuman primates with H. pylori; in ferrets with H. mustelae; in kittens with Helicobacter acinonychis and H. heilmannii and in germ-free dogs, specific-pathogen free dogs, mice, and rats with H. felis.¹⁶⁷ H. pylori–associated gastritis in humans consists of polymorphonuclear cells as well as mononuclear cell infiltrates and is classified as active chronic gastritis. Persistent H. pylori infections in humans (particularly children) and in the domestic cat also are often characterized by lymphoid aggregates and gastric lymphoid follicles.^174,253 Inflammation and associated lymphoid follicles were primarily located in the antrum, which corresponded to the heaviest concentration of H. pylori.²⁵² Ultrastructurally, the organisms were numerous in the gastric mucus, were less frequently adhered tightly to gastric epithelia, and formed pedestals between bacterial membranes and the epithelial microvilli.²⁵²

Gastric lymphoid elements had been considered a normal histologic finding in dogs and cats. However, experimental and clinical evidence suggests that they are the result of host responses to Helicobacter antigens.⁵⁴² The presence of GHLOs is often associated with a reduction in mucus content of surface epithelia, occasional intraepithelial leukocytes, and some degenerating glands. The gastritis observed in dogs and cats with non–H. pylori helicobacters is generally mild. Eosinophils in gastric mucosae of animals can also be a major component of the inflammation, particularly in the acute phase of the infection.^174,350,350 Neutrophils and eosinophilic infiltrates, interepithelial globule leukocytes, epithelial dysplasia, and upregulation of certain mucosal proinflammatory interleukin (IL)-1β and IL-8, and interferon-γ are noted in H. pylori–infected cats but not in uninfected control cats.^142,541,541 The degree of GHLO colonization and lymphoid follicles correlated well in cats but not in dogs. If the number of GHLOs in dogs was classified as high, then lymphoid follicles were more likely to be present. In high-grade GHLO infections, glandular degeneration was more pronounced in cats than dogs.^268,585,585 In other dogs³⁴³ the severity of gastritis correlated with infection but not with the clinical sign of vomiting. In other studies,¹²⁹ 100% of laboratory and shelter dogs and 67% of pet dogs were colonized with GHLOs that were morphologically consistent with H. heilmannii or H. felis. Regardless of the colonization intensity, all dogs had mild to moderate gastritis, and H. pylori was not isolated.

Experimentally, H. felis infection in dogs for 26 weeks did not correlate with number of H. felis observed and degree of inflammation or number of affected lymphoid follicles.⁵³⁸ Furthermore, the gastric secretory axis was not perturbed in H. felis–infected dogs or dogs naturally infected with GHLOs.⁵⁴⁰

Competitive inhibition, whereby the colonization by one organism suppresses proliferation of other helicobacters, may occur in gastric helicobacteriosis. This phenomenon has also been suggested to account for the rare occurrence of concurrent infection in humans and nonhuman primates with large gastric spiral organisms and H. pylori.119,120,263,349,571 Experimental inoculation of the feline H. pylori strain into naïve cats without gastric infection caused by GHLOs confirmed that H. pylori produces a persistent gastritis identical to that noted in cats naturally infected with H. pylori.¹⁷⁴ H. pylori was isolated on serial biopsies and at necropsy 7 months after inoculation from all cats.¹⁷⁴ Additional studies are required to ascertain whether duodenal and gastric ulcers have an infectious component in dogs and cats.¹⁷⁸