Discussion and conclusion
Gastric NHPH are highly present in dogs and cats, with prevalences ranging from 60 up to 100% [
21]. Evidence is accumulating that pets may serve as reservoir hosts for zoonotic NHPH [
3]. In several case studies, transmission of NHPH was expected to occur from dogs and cats to their owner [
8,
22‐
27]. Some studies even demonstrated presence of the same gastric species in the owner’s pets [
22,
23,
28] further supporting the zoonotic potential of NHPH. Although we did not investigate presence of
H. bizzozeronnii in the family dog, the patient most likely contracted infection through intense and close contact with the dog. Furthermore,
H. bizzozeronnii is the most prevalent gastric
Helicobacter species in dogs [
29‐
31], which further strengthens this hypothesis.
Nevertheless, in most case studies the specific NHPH species was not determined. One study described the isolation of
H. bizzozeronnii from the human gastric mucosa, highlighting its zoonotic potential [
26,
27]. Van den Bulck et al. demonstrated that
H. suis was the most prevalent NHPH species in human patients undergoing gastric biopsy (i.e. 37% of NHPH infected patients), followed by
H. salomonis (21%),
H. felis (15%),
H. heilmannii (8%), and
H. bizzozeronnii (4%). The low prevalence of
H. bizzozeronnii in these human gastric biopsies seems to be in contrast with its predominance in the canine stomach. This might be related to differences in colonization ability between gastric
Helicobacter spp, for example in their ability to adhere to the human gastric mucosa [
32].
The exact route of NHPH transmission from animals to humans is not yet clears [
3]. Several studies showed that living in close proximity to as well as intense contact with infected dogs, cats, and pigs leads to a significant risk of NHPH infection [
33,
34].
Helicobacter DNA has been detected in saliva and faeces from cats and dogs [
35], indicating that oral-oral and oral-faecal contact may be a route of transmission. In this case report, the dog was allowed to defecate in the house, which may have served as source of infection. Nevertheless, not all NHPH infected humans’ patients had contact with domesticated animals [
8,
24]. An additional transmission route might be contaminated water, as
Helicobacter spp. are able to survive in water for several hours [
36]. Finally, the role of wild mice as vector might be considered as well, as rodents are easily colonized by most NHPH [
3].
In humans, NHPH infections have been associated with a specific clinical sign like abdominal and/or epigastric pain, bloating, nausea, vomiting, dehydration, hematemesis, pyrosis, and dysphagia [
27]. On gastroscopy, chronic active gastritis, nodular gastritis, erythema, ulceration and/or MALT-lymphoma may be present [
8,
10,
12,
24,
37,
38]. Similarly, our patient showed signs of gastric disorders, as well as chronic active gastritis, mucosal erythema, and ulceration. It could be argued that these associations are incidental, in view of the low numbers of patients infected with NHPH. Nevertheless, experimental rodent models have shown that NHPH induce severe gastritis and MALT-lymphoma [
23,
39]. In our and other studies, both clinical signs as well as gastric anomalies resolved after clearance of NHPH infection, further underlying the causal relationship.
Treatment of NHPH infections in humans is difficult to determine due to the lack of randomized trials [
3]. In practice, treatment schemes successful in eradicating
H. pylori are used. Triple therapy consisting of a proton pump inhibitor (omeprazole or pantoprazole) and 2 antibiotics (clarithromycin + amoxcillin or metronidazole) has already been shown to be effective, similar to this case report [
40‐
42]. In some cases, NHPH were eradicated from the owner’s pet as well [
23]. Here, treatment of the dog in combination with improvement of hygienic standards may be considered as well to prevent reinfection. Furthermore, follow-up endoscopy 6–12 months after treatment would be suitable to confirm complete clearance of
H. bizzozeronii infection. The eradication could not be confirmed at this moment, although it was suggested by improvement of symptoms. Still, NHPH / Hp infections remain asymptomatic in > 80% of the patients having such gastric colonization. An urea breath test will not confirm the erradication, as it is often falsely negative in patients with NHPH.
Blaecher et al. showed a higher frequency of H. suis in human patients after H. pylori eradication, indicating that disappearance of H. pylori may create a niche for colonization of the human stomach by other pathogens, like NHPH. It can be advised to check for presence of these bacteria, especially when the patient shows persistent complaints in absence of H. pylori. Presence of NHPH can be implemented by histopathological analysis and/or by PCR on gastric biopsies.
In conclusion, for the first time, presence of a H. bizzozeronnii infection was shown in a young girl with gastric disorders in Mexico. This case report further emphasizes the zoonotic importance of NHPH. It can be advised to routinely check for presence of both H. pylori and NHPH in human patients with gastric complains.