







































 

 

 
1 

© 2024 Conscientia Beam. All Rights Reserved. 

One health approach on zoonotic helicobacter pylori in animals and man   

 

 

 Nourhan Eissa1+ 

 Maha A. 
Mohamed2 

 Rahma S. Shahban3 

 Salma M. 
Badrkhan4 

 Jana F. Mohamed5 

 Somaya A. 
Elsayed6 

 Ola H. Harb7 

 

1Department of Animal Hygiene and Zoonoses, Faculty of Veterinary 
Medicine, University of Sadat City, Egypt.  
Email: vet_noura@yahoo.com 
2Department of Biophysics, Faculty of Science, Cairo University, Egypt. 
Email: Mhmohamed2013@gmail.com   
3Department Zoology and Chemistry, Faculty of Science, Cairo University, 
Egypt.  
Email: rrsaid315@gmail.com    
4Faculty of Veterinary Medicine, Cairo University, Egypt. 
Email: Shamms951@gmail.com  
5Faculty of Physical Therapy, Cairo University, Egypt. 
Email: janafouad093@gmail.com  
6Department of Chemistry, Faculty of Science, Menoufia University, Egypt.  
Email: somayaelsayed@hotmail.com  
7Department of Bacteriology, Immunology and Mycology, Faculty of 
Veterinary Medicine, University of Sadat City, Egypt.  
Email: Ola.harb1373@vet.usc.edu.eg 

 

 
(+ Corresponding author) 

 ABSTRACT 
 
Article History 
Received: 21 October 2024 
Revised: 27 November 2024 
Accepted: 9 December 2024  
Published: 18 December 2024 
 

Keywords 
Control 
Diagnosis 
Epidemiology 
H. pylori 
Risk factors 
Zoonoses. 

 
Zoonotic disease-causing microbes are those naturally spread from animals to people, 
either directly or indirectly, with a serious hazard on the public health. Emerging 
zoonoses are mostly caused by travel, animal transhumance, population increase, and 
migration from rural to urban regions. Regarding the principal transmission route of 
Helicobacter pylori (H. pylori), one of the most global prevalent anthroponotic illnesses, 
not a lot of information is currently known. In the 20th century, H. pylori contribute to 
individuals stomach problems and cancer. Subsequently, an extensive amount of study 
has been conducted on the epidemiology of this intestinal infection, revealing that the 
likelihood of illness varies throughout individuals. This is a concise overview of the 
several epidemiological factors connected to zoonotic H. pylori infection. There are 
notable differences in the epidemiology of H. pylori in human and animal populations 
between developing and developed nations. Moreover, a multiplicity of consistent lines 
of evidence suggests that demographic data, different individual habits, socioeconomic 
position and living conditions are the main risk factors influencing the acquisition rate 
of H. pylori pathogen. These results are troubling since they are expected to change 
global demography and increase the number of people susceptible to H. pylori and its 
emergence. To reduce the danger to public health and the associated economic effects, 
stakeholders in the H. pylori management plan need to start merging technological, 
social, political, policy, and regulatory problems and working together. An active 
mitigation program offers the chance to address global health concerns and halt the 
development of zoonoses. 
 

Contribution/Originality: The current study provides an overall view on the zoonotic impact of H. pylori in 

different animals and humans as an aid in health education of the public about the danger of the disease, sources, 

reservoirs transmission modes, epidemiology, different diagnostic tools, methods of prevention and control. 

 

 

Animal Review 
2024 Vol. 11, No. 1, pp. 1-17. 
ISSN(e): 2409-6490 
ISSN(p): 2412-3382 
DOI: 10.18488/92.v11i1.4005 
© 2024 Conscientia Beam. All Rights Reserved. 

 
 
 

 
 
 
 

 

 
 
 
 

https://orcid.org/0000-0002-3622-6023
https://orcid.org/0000-0003-0936-9130
https://orcid.org/0000-0002-2082-7692
https://orcid.org/0000-0002-0407-1151
https://orcid.org/0009-0003-9056-0027
https://orcid.org/0009-0005-8079-5206
https://orcid.org/0009-0003-5606-1937
mailto:vet_noura@yahoo.com
mailto:Mhmohamed2013@gmail.com
mailto:rrsaid315@gmail.com
mailto:Shamms951@gmail.com
mailto:janafouad093@gmail.com
mailto:somayaelsayed@hotmail.com
mailto:Ola.harb1373@vet.usc.edu.eg
https://www.doi.org/10.18488/92.v11i1.4005


Animal Review, 2024, 11(1): 1-17 

 

 
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© 2024 Conscientia Beam. All Rights Reserved. 

1. INTRODUCTION 

Naturally, microorganisms that cause zoonotic illnesses can spread from animals to people. Human health is 

seriously threatened by the present zoonotic disease epidemic, especially for those with close contact with domestic 

or wild animals and reside in underdeveloped areas [1-13]. The main way for different illnesses transmission is 

spread, either directly or indirectly, from animals to humans. The main causes of the emergence of new zoonotic 

illnesses are changing patterns between rural and urban areas, animal transhumance, international travel, and 

climate change [1-13]. Two species of Campylobacter belong in the genus Helicobacter, according to Parija [14]. 

These are Campylobacter mustelae, also known as Helicobacter mustelae, and Campylobacter pylori, now known as 

Helicobacter pylori. There are currently 47 species recognized in the genus Helicobacter, a considerable increase from 

earlier estimates [15]. Based on ecological settings and phylogenetic analyses, this genus of bacteria are roughly 

classified into: stomach (GH) and enterohepatic (EHH) Helicobacter species [16].  

H. pylori, often known as Helicobacter pylori, is the species that has attracted the most attention from researchers. 

Up to 50% of people worldwide suffer from some of the most severe human illnesses, which are caused by H. pylori. 

But in recent years, new illnesses and perhaps zoonotic infections have increased the significance of the remaining 

GH. Reviews [17-19] have already addressed the evolution of these gastrointestinal species' taxonomy, 

epidemiology, and clinical significance. 

That being said, not much research has been done on EHH. But, there has been evidence linking EHH 

members to a range of human ailments, including acute gastroenteritis, inflammatory bowel disease, and problems 

related to the liver, gallbladder, and bile duct [19]. Since the most recent research on EHH has piqued interest, 

more investigation is required to ascertain the possible significance of these recently discovered ailments. Given 

this, the present review offers a brief of the current understanding of taxonomy, clinical relevance, and 

epidemiology of EHH with respect to animal hosts. 

 

2. ETIOLOGY 

Employing Helicobacter pylori as a model organism. Every single individual from the Helicobacter genus 

possesses the following physical traits: Fusiform bacteria do not create spores and have a size range of 0.2 to 1.2 to 

1.5 to 10 µm. They also generate cytochrome oxidase. In addition to having a helical, curved, microaerophilic, 

spiral, or rod-shaped structure where cells can become coccoid when exposed to air or become old cultures, they can 

also be gram-negative and feature periplasmic fibers. One or more sheathed or unsheathed flagella are what allow 

them to move. The majority of them grow well at 37 °C and are carbohydrate-free [20, 21]. 

 

2.1. TAXONOMY 

 

Table 1. Taxonomy of Helicobacter pylori according to Polaka, et al. [21]. 

Phylum: Campylobacterota  

Class: Campylobacteria  

Order: Campylobacterales 
Group:  Proteobacteria 
Subgroup:  Epsilon subgroup of Proteobacteria 
Family: Helicobacteraceae 
Genus:  Helicobacter 
Most known 
Pathogenic 
species:  

Helicobacter winghamensis, Helicobacter pullorum, Helicobacter canadensis, Helicobacter 
apodemus, Helicobacter hepaticus, Helicobacter cinaedi, Helicobacter equorum, Helicobacter 
trogontum, and Helicobacter mustelae are among the species of Helicobacter that are 
commonly found in the stomach. 

 

Table 1 presents that the taxonomic categorization of Helicobacter has been hampered by the limited function of 

the 16S rRNA gene, which is recognized as the "gold standard" gene for bacterial phylogeny. It is true to say that 



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16S rDNA is insufficient for identification of variant Helicobacteraceae species because of the potential for 

misidentification [22]. This is in line with the creation of mosaic molecules lacking phylogenetic information and 

the horizontal transport of 16S rRNA gene segments [23]. 

A greater number of identified pertinent phylogenetic markers have been examined to provide a more precise 

taxonomic evaluation of Helicobacter species. A few of these markers are gyrA, gyrB, cpn60, and atpA [23-26]. 

 

2.2. Virulence Factors 

Thanks to the identification and examination of more relevant phylogenetic markers, the taxonomic identity of 

Helicobacter species may now be ascertained with greater certainty. Several of these markers include gyrA and gyrB 

[23] cpn60 [24] and atpA [25].  

This gave information on the progression of the disease and assisted in identifying several virulence factors. 

Since then, efforts have been made to determine the genes responsible for the virulence mechanisms of 

enterohepatic species. The orthologues of Peb1 Campylobacter coli and Campylobacter jejuni, which are present in 

Helicobacter apodemus and Helicobacter hepaticus, have been shown to have an effect on adhesion [27].  

Additionally, it was shown that five EHH species—Helicobacter hepaticus, Helicobacter cinaedi, Helicobacter 

equorum, Helicobacter trogontum, and Helicobacter mustelae—carry H. pylori homologs, such as hor, hom, hop, and maybe 

horD and horG. They are referred to as "Hof-like outer membrane proteins" (OMPs). The bulk of OMPs, which are 

Hop proteins, have a porin or sticky quality that aids in the pathogens' adhesion to the mucosal surface [28].  

The existence of homologous genes is also established. These include virulent adhesin/OMPs flpA (fibronectin-

like protein A), enables adherence of EHH species to the extracellular intestinal fibronectin, and irgA (a virulence 

protein, is iron-regulated outer membrane protein), which appears in the enteric bacteria as Campylobacter spp., 

Escherichia coli, and Salmonella enterica [29]. 

The urease gene cluster in Helicobacter mustelae (ureABIEFGH; ureA2B2), cell-binding factor 2, gamma-

glutamyl transpeptidase, orthologs of systemic factor protein A (SfpA) and lipid A deacylase (LpxR), "immune 

evasion" genes (futA, futC, rfaJ), and the outer membrane protein phospholipase A (OMPLA) are additional factors 

linked to EHH. Additionally noted are genes associated with "secretion systems" (virB2, virB3, virB4, virB5, virB6, 

virB8, virB9, virB11, virD4, cag) and the HHGI1 type VI secretion system (icmF, hpc, vrgG). Additionally, it was 

found that the cag-PAI type IV secretion system (T4SS) is linked to the genes "Helicobacter apodemus" and 

"Helicobacter typhlonius". This route promotes cell division and proliferation, which in turn helps the bacterial gene 

cagA enter stomach and aid in H. pylori pathogenesis. The latter species' DNA was found to lack cagA, and its 

relationship to T4SS is still unclear [30]. The only known cytotoxin of this bacterial family, cytolethal distending 

toxin (CDT), is translated by a collection of genes named cdtA, cdtB, and cdtC, which occur in some species of EHH 

and other Gram-negative bacteria [31]. This toxin, which is made up of the three subunits CdtA, CdtB, and CdtC, is 

a heterotrimeric AB2 toxin [32].  

The active "A" component of the AB2 toxin, CdtB, is transported into cells by the combination of the two 

binding "B" subunits, CdtA and CdtC. CdtB is taken up from the host cell surface by the endoplasmic reticulum, the 

Golgi apparatus, and the nucleus in a clathrin-dependent manner after adhering to the cell surface [16]. CdtB is 

structurally and functionally similar to mammalian DNase I. In a cell, it could result in chromosomal DNA double 

strand breaks (DSBs). Moreover, CdtB has been shown to have phosphatase activity, which speeds up T-cell death 

[33]. 

Apoptosis and distention are the outcomes of the host cell cycle arrest that these two CdtB activities induce at 

the G2/M phase [33]. The existence of the toxin, its effects in vivo and in vitro, and the genes that encode it have 

all been reported by many EHH. Furthermore, a putative cytotoxin homologs that were resembled the vacA gene 

were found to be present in "Helicobacter winghamensis", "Helicobacter pullorum", "Helicobacter canadensis", and " 



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Helicobacter apodemus" [34]. Further investigation is required to ascertain the role this putative cytotoxin plays in 

virulence.  

Additional factors that have been linked to the pathogenicity of bacteria include the N-linked protein 

glycosyltransferase, similar to the general protein glycosylation (pgl) genes in Campylobacter jejuni. These genes 

facilitate attachment and entry into the epithelial cells of the host, even in vitro or in vivo. Additionally, the 

Campylobacter major protein (cmp), Helicobacter pullorum ortholog, is responsible for both activity and adhesion to 

the cultured cells, according to EHH. Pro-inflammatory cytokine release, the ability to resist complement protein 

degradation in vitro, and the durability of colonization in vivo are all linked to this [34]. 

 

2.3. ANTIBIOTIC RESISTANCE  

The global enormous issue of increasing antibiotic resistance among bacterial pathogens [8, 9] researchers 

began to study the mechanism of antibiotic resistance of different bacteria in a trial to evolve novel medications 

against them [8, 9]. However, the techniques of determining one's susceptibility to an EHH infection and 

managing the infection are not standardized. It is true that the Clinical and Laboratory Standards Institute (CLSI) 

does not currently have any guidelines available for evaluating the antibiotic susceptibility of Helicobacteria that are 

not Helicobacter pylori (NHPH).  

This is because Helicobacter is a species that has particular growth requirements, which makes it challenging to 

develop precise techniques for determining the Minimal Inhibitory Concentration (MIC) [22]. EHH species have 

also been compared to conventional antibiotics (b-lactams, tetracyclines, aminoglycosides, fluoroquinolones, 

phenicols, diaminopyrimidines, carbapenems, glycopeptides, and sulphonamides) used to treat Campylobacter sp. 

Infections [35, 36].  

Amoxicillin is commonly used in mixed therapy to treat EHH infections because it works by getting rid of H. 

pylori [37]. Despite the fact that other Helicobacter species benefit from this treatment, the scant information now 

available raises concerns over the antibiotic sensitivity of these species [38]. 

 

3. RESERVOIRS OF THE INFECTION 

3.1. Pet Animals  

In terms of carrying EHH, dogs are the companion animal that are exposed to the various examinations. 

However, it is hitherto how EHH reservoirs could affect the future zoonotic transmission. A limited culture-based 

studies presented Helicobacter cinaedi, Helicobacter bilis, and Helicobacter canis in feces of both healthy and diarrheal 

dogs offer most of the available EHH data in dogs [39]. The high incidence of these organisms in dogs implies that 

EHH might be a part of the canine microbiota, despite the lack of evidence demonstrating any beneficial or health-

promoting effects on their hosts [40]. 

Abundant research of bacteraemia due to Helicobacter canis in the immunosupressed individuals have been 

linked to close contact with infected dogs [41]. In addition, contact with infected cats also might be linked with 

Helicobacter canis [38]. 

 

3.2. Livestock (Farm Animals)  

Research on the connection between EHH and farm animals has been less extensive than that on 

Campylobacteria. Sheep are reservoirs for most zoonotic diseases, as evidenced by the recent isolation of Helicobacter 

canis from their manure [42]. Moreover, Egypt has provided phylogenetic evidence in favor of the theory that 

humans acquired Helicobacter canis from sheep [43]. In fact, a transmission dynamic might be linked to H. pylori, 

that fact is also showed in individuals with direct or indirect contact with sheep [44]. 

 

 



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3.3. Wildlife  

Initially, a significant quantity of EHH was found in the waste products of wild animals including rats and 

birds. Since EHH often affects numerous organs, it is unclear if these wild animals are true reservoirs for the 

sickness [45]. 

Both wild rats and laboratory animals harbor these infections [46]. Furthermore, several species of 

Helicobacter have been found in wild birds [47]. Research on the toxicity, clinical relevance, and zoonotic potential 

of most of these freshly found species remains necessary. 

 

4. TRANSMISSION OF H. PYLORI INFECTION 

Table 2 explains both the direct and indirect routes of H. pylori transmission in animals and man, where the 

direct (main) route is oral route while the indirect (secondary) route is via contact.  

 

Table 2. explains the transmission routes of H. pylori. 

Direct transmission route Indirect transmission route 

Mainly through ingestion of the pathogen (Oral 
transmission) via vomitus, feces, chopsticks, oral 
microbiota [48, 49]  

It is not a primary route. Occurs through contact 
with food, water, and animals have all been 
reported to contain H. pylori or its DNA [48].  

 

5. DETERMINANTS OF H. PYLORI EPIDEMIOLOGY (RISK FACTORS) 

All the associated risk factors of acquisition of H. pylori concerning host factors, environmental factors and even 

pathogenic factors, are already shown in Figure 1.  

 

 
Figure 1. shows the schematic draw on risk factors of H. pylori. 

 

6.1. Host Factors 

6.1.1. Age 

One of the most well-established and rarely contested features of the infection's epidemiology is the impact of 

age on the frequency of H. pylori infection. Age and prevalence have been found to be strongly correlated in both 

developed and developing nations [50].  

 



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The trend of adults having a higher frequency of infection than children has been partially explained by the 

birth cohort phenomenon, which was brought on by a greater prevalence in the past as a result of unsanitary living 

circumstances and inadequate sanitation [51]. 

 

6.1.2. Ethnic and Genetic Predisposition 

Helicobacter pylori seroprevalence has been observed to differ significantly among people of different racial and 

cultural backgrounds [52]. According to certain theories, Malaysian Chinese and Indian communities are more 

likely to contract H. pylori infection due to genetic predispositions [53]. Ethnicity has been identified by a number 

of New Zealand demographic groupings as a risk factor. Maori had an intermediate prevalence of H. pylori infection, 

while Europeans had the lowest prevalence. Ethnicity was a significant covariate even after consideration of other 

variables like age and even socioeconomic levels [54]. 

However, an American study discovered that while the prevalence of H. pylori infection was somewhat greater 

in Caucasians, it was almost the same in African Americans and Hispanic Americans. However, socioeconomic 

circumstances were blamed for the observed variance and ethnicity was rejected as a relevant component [55]. In 

conclusion, studies on monozygotic and dizygotic twins revealed a possible genetic component to the frequency of 

H. pylori infection [56]. 

 

6.1.3. Gender 

Studies evidenced that one sex/gender is more susceptible to infection than the other [2, 3, 9]. For example, it 

was shown that H. pylori infection was more among men than among women [57]. Additional investigation shows 

that the incidence of H. pylori illness is not gender-specific [58]. 

 

6.1.4. Interfamilial Relations 

The effect of interfamilial interactions on the H. pylori pathogen's transmission from adult to kid, particularly 

mother-to-child transmission, was the subject of earlier research [59]. Moreover, it was suggested that parents or 

siblings could contract the virus from sick children [60]. H. pylori disease has also been represented to be favorably 

influenced by family size; the likelihood of infection in a home rises with the number of children residing there [61]. 

Records of transfers between spouses were also kept [62]. 

 

6.1.5. Socioeconomic Factors 

The likelihood that an H. pylori infection will spread is apparently significantly influenced by socioeconomic 

position [63]. On the other hand, higher socioeconomic status of inhabitants may be linked with H. pylori lower 

prevalences in developed countries [53]. The linkage between increasing age and increased frequency of H. pylori in 

underdeveloped countries would be directly related to low socioeconomic position. It should go without saying that 

socioeconomic standing includes elements like living standards, sanitization, urbanization, and educational 

attainment in addition to social class and money [64]. When taken as a whole, these variables may raise the chance 

of contracting infectious diseases generally.    

 

6.1.6. Crowding Index (Density of Living) 

Living in close quarters, sharing a bed, and having more household contact have all been related to an 

increased risk of H. pylori infection [65]. One's current H. pylori status is influenced by their upbringing in close 

quarters, and having more children in the house increases an adult's risk of infection [66]. 

 

 

 



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6.1.7. Lifestyle Habits 

6.1.7.1. Breast-Feeding 

According to Dore, et al. [36] no statistical difference was shown in H. pylori seropositivity among children 

residing either urban or rural districts according to the infants' breastfeeding status. Nevertheless, a prospective 

population-based investigation on asymptomatic neonates in the Czech Republic found that children who had never 

been nursed had a higher incidence of H. pylori  [61]. However, children from low socioeconomic families in Lagos, 

Nigeria did not show any correlation or duration of H. pylori infection with exclusive nursing [62].  

It has been suggested that breastfeeding serves as a natural antibiotic, shielding infants from illness. So, if 

mothers' breath milk included more anti-H. pylori IgA than if it contained less, children were less likely to contract 

the virus [63]. 

 

6.1.7.2. Food 

Studies have shown that dairy products, particularly raw milk, contain H. pylori DNA, which is thought to be 

the primary food transmission mechanism [53]. Traditional cheese and ovine milk were shown to be the most often 

contaminated items by Dore, et al. [36] suggesting that milk consumed by humans may be affected. Similar 

outcomes were also represented for raw cow milk specimens from farms in America [53] Greece [64] and Japan 

[60].  

Significantly, it was discovered by Talaat Al Sherief and Thabet [65] that milk and dairy products were often 

the source of H. pylori strains that were resistant to antibiotics. Another notion about the potential reservoir of H. 

pylori is meat. It has been suggested that shepherds and their families may contract H. pylori from sheep [66]. 

Direct interaction with sheep and sheepdogs may be connected to it.   

Eating raw veggies can put a person at risk for H. pylori [53]. Because of tainted washing water, raw veggies 

may have included H. pylori. Thus, insufficient or nonexistent wastewater disinfection may enhance H. pylori 

persistence and is most likely a significant contributing factor to the chain of events that leads from people to 

bacteria. However, given the link between the condition and a lower socioeconomic standing, individuals with poor 

nutritional status may be more vulnerable to H. pylori infection [67]. 

 

6.1.7.3. Habits of Tobacco Smoking and Even Alcohol Drinking  

Research on the relationship between alcohol and tobacco use and H. pylori infection has produced a variety of 

results. Despite the fact that Gunathilake, et al. [68] showed no connection between alcohol or tobacco use and the 

development of H. pylori infection, smoking tobacco was found to be substantially linked to H. pylori seropositivity 

in adult Japanese persons [69]. Research conducted in Northern Ireland has revealed a favorable link between 

smoking and H. pylori infection. However, no significant correlation has been observed between alcohol use and 

smoking [70]. The higher stomach acidity caused by smoking may account for the unfavorable correlation between 

tobacco usage and illness. Moreover, it has been proposed recently that nonsmokers and heavy alcohol users may be 

less susceptible to H. pylori infection than the general population [71]. 

 

6.1.7.4. Close Contact with Animals 

Numerous research investigations looked at the processes by which various zoonotic bacteria could infect 

people as well as the toxicity of the bacteria in animals [1-13, 72]. EHH, however, has been given a considerable 

degree of zoonotic significance because it has been demonstrated that frequent and intimate human-animal contact 

is harmful [34]. 

 

 

 



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6.1.8. Occupation 

The risk of H. pylori in healthcare workers who work with patients has been the subject of numerous research. 

Hospital work with a direct patient contact has been found to be a substantial risk for infection in comparison with 

other jobs without such contact [73]. As a result, research revealed that nursing staff was more likely than 

technical and administrative professionals to have an H. pylori infection [74].  

 

6.2. Pathogen Factors 

6.2.1. Microbiota 

The makeup of the gut microbiota may be influenced by a wide range of factors, such as lifestyle choices, 

infections, diseases, and environmental pollutants [75]. In stomach cancer dysbiosis, helicobacter abundance and 

microbial diversity are both reduced [76]. Disease states have been associated with reduced microbial diversity; 

reports of this have been presented for inflammatory and malignant disorders [77]. According to Zhang [75] H. 

pylori affects the intestinal microbiota indirectly in addition to influencing the makeup of the stomach microbiota in 

the animal model. Moreover, the age-dependent immune responses of H. pylori-infected mice may influence the 

host's vulnerability to illness and infection [78]. An infant's microbiome may be significantly influenced by the 

shared microbiota of parents and children. 

 

6.2.2. Biological Risk Factors 

There are set of biological risk factors linked to increase the incidence of cancer among individuals. For 

example, viruses in humans account for 10% to 20% of cancer incidence globally. Numerous experimental and 

epidemiological investigations have verified the link between anal cancer and the papillomavirus of humans. 

Likewise, cancer of the upper and lower gastrointestinal tracts is probably caused by the Epstein-Barr virus (EBV) 

and the John Cunningham virus (JCV) [79]. In a similar vein, human carcinogenicity has been linked to parasite 

illnesses such as schistosomiasis, opisthorchiasis, and clonorchiasis [80]. 

Numerous bacteria have been connected to different neoplasms, such as Chlamydia pneumoniae, Salmonella typhi, 

and Streptococcus bovis; however, it is unclear how these bacteria may aid in the development of cancer [81]. 

Although H. pylori, Prevotella copri, and Propionibacterium acnes are critical factors for stomach cancer, a previously 

published case-control research [82] found that Lactococcus lactis acts as a protective factor against stomach 

cancer. The main biological agent for stomach cancer is H. pylori pathogen. Numerous studies that have looked at 

the various facets of this correlation have found a link between stomach cancer and H. pylori infection [83].  

 

6.3. Environmental Context 

6.3.1. Rural vs. Urban Living Conditions 

One of the variables increasing the acquisition of H. pylori in people in the world is the variation in living 

conditions between urban and rural areas. There were more children living in rural regions than in urban areas 

[68]. Socializing with dogs appears to have benefits, particularly in rural settings. In urban areas, the infection rate 

of H. pylori was substantially correlated with the parents' socioeconomic status, whereas in rural areas, there was no 

association between the head of the household's employment status and the incidence of infection [77].  

 

6.3.2. Water Hygiene 

Water may be a significant source of H. pylori contamination, according to a number of epidemiologic studies 

[78]. Due to the unsanitary distribution of water among the populace, waterborne infections—especially in poor 

nations—are the primary cause of H. pylori infections. In Japan, well water containing H. pylori DNA was tested 

positive for the infection by customers [79]. Accordingly, two studies—one from Portugal and the other from 



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Germany—found a favorable correlation between H. pylori infection and well water intake [43, 84]. Furthermore, it 

has been proposed that H. pylori contamination may exist in Japanese river water [82]. 

Public health is concerned about the possibility of live H. pylori infecting cells in water samples [83]. These 

results provide credence to the theory that water tainted with excrement could serve as a reservoir for the 

propagation of H. pylori. According to some theories, H. pylori's capacity to produce biofilm allows it to proliferate in 

natural water sources and water distribution networks [54]. When the temperature is over 20 °C, the optimal 

temperature range for H. pylori cultivability in water is fewer than ten hours [85]. The morphological 

transformation of bacteria into a rod shape, which is connected to the turnover of peptidoglycan (PG), is linked to 

the development of a culturable phenotype in water [54]. 

 Consequently, H. pylori undergoes a morphological transformation from a spiral form to a coccoid form and 

becomes a viable but not culturable (VBNC) pathogen few days after being injected into water [85]. 

 

7. EPIDEMIOLOGY OF H. PYLORI (GLOBAL DISTRIBUTION) 

In the past year, a lot of study has been done on the frequency of mutations associated with H. pylori and 

antibiotic resistance in patients with oncological illnesses (pancreatic cancer, colorectal cancer, gastric carcinoma, 

etc.). Alaridah, et al. [86] study Ma, et al. [87] examined 933 Jordanians' general population's awareness and 

information regarding H. pylori. Stomach cancer is highly prevalent among neoplasms in terms of occurrence in the 

country.  

68.7% of participants are ignorant as possible considerations for stomach cancer, despite this and the fact that 

63% of participants had a higher education degree [88]. In a different study, researchers looked at patients from 

over 360 US hospitals (18–65 years old, or 47,714,750 overall) to find out how much of a risk H. pylori infection had 

for colorectal cancer. Based on a large population-based analysis, the correlation between occurrence of colorectal 

cancer and H. pylori illness (OR 1.89, 95%CI: 1.69-2.10) has not been demonstrated before [88]. A different case-

control study carried out in the USA looked at five prospective cohorts to see if there was a connection between 

pancreatic cancer and H. pylori illness.  

Investigators declared that no significant relation was found between pancreatic cancer risk and H. pylori 

infection (OR 0.83, 95% CI: 0.65-1.06) [89]. The frequency of evolutions related to clarithromycin resistance and 

the connection between virulence factors and H. pylori infection were the subjects of a study carried out in Mexico. 

To get rid of H. pylori, a treatment strategy based on clarithromycin is required. The researchers discovered a 

greater than 15% frequency of mutations connected to clarithromycin resistance in addition to a linkage between 

23S rRNA gene alterations and cagA and vacA genotypes. A2143G (56%) and A2142C (25%) were the most 

prevalent alterations, according to Husnik, et al. [90].  

There are several challenges associated with H. pylori infection. For more than 40 years, a large number of 

studies on risk factors, vaccination prophylaxis, effective eradication therapy, and interruption of transmission 

pathways have been carried out. The World Gastroenterology Organization (WGO) updated its H. pylori guidelines 

by using the "cascade" technique, which distills the management basics on regional resources and expertise [91]. 

With a total population of 2,163, Alaridah, et al. [86] looked at 22 studies from 9 African countries to calculate the 

rate of H. pylori eradication in that continent, showing a pooled elemination rate of 79% (95% CI: 75%-82%), 

associated with a heterogeneity rate of 93.02%.  

An increased percentage of eradication (85%) was found in observational research as compared to randomized 

control trials (77%). Ivory Coast had the lowest eradication rate (22.3%) while Ethiopia had the highest (90%). The 

occurrence of H. pylori infection in Africa will be impacted by long-term eradication initiatives. Of the 1,160 cases 

included in a Pakistanian study conducted by Boustany, et al. [92] 48% were H. pylori positive. That research was 

carried out to reveal the frequency and various features of H. pylori. Higher incidence rates were seen among men 

between the ages of 20 and 40, the illiterate, diners at restaurants, users of municipal water systems, owners of pets, 



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and people who had interacted with animals. Additionally, a linkage was discovered between H. pylori prevalence 

and sociodemographic characteristics [94]. 

 

8. CLINICAL IMPORTANCE  

Different clinical signs can be recorded in cases infected with H. pylori either in animals or even humans as 

explained in Table 3. 

 

Table 3. Clinical manifestations of Helicobacteriosis in animals and man according to Lee, et al. [93] and Alarcón-
Millán, et al. [94]. 

In humans In animals 

Can induce:  

- Diarrhoea  

- Bacteraemia   

- Systemic disease 

- Development of neoplasia 

- Gastroenteritis  

- Proctocolitis 

- Cellulitis  

- Arthritis 

- Septicaemia  

- Inflammatory bowel disease (IBD) 

- Crohn’s disease (CD)  

- Ulcerative colitis (UC) 

- Hepatobiliar disease 

May be asymptomatic or may include:  

- Inflammatory bowel disease (IBD) 

- Biliary and liver diseases  

- Gastric, breast, colon, and liver cancers 

- Rectal prolapse  

- Ovine abortion 

- Vibrionic hepatitis in laying hens 

- Episodic diarrhoea in cats 
 
 
 

 

9. DIAGNOSIS OF H. PYLORI INFECTION 

There are many available direct and indirect diagnostic tools of zoonotic H. pylori available in both human and 

animals' fields as shown in Figure 2.  

 

 
Figure 2. Presents the available diagnostic tools of H. pylori according to Katelaris, et al. [95]. 

 



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10. TREATMENT OF H. PYLORI INFECTION 

There are many treatment lines concerning the treatment of H. pylori in animals and man as shown in Table 4.  

 

Table 4. Presents ideal conventional lines of medications used for H. pylori infection. 

Line of medication Drugs used References  

First and second line Clarithromycin, amoxicillin, 
clarithromycin,  
and proton pump inhibitor (PPI) 
bismuth-containing triple therapy 

Fekadu, et al. [96] 

Third line bismuth-based quadruple treatment 
amoxicillin, metronidazole,  
and PPI 
quinidine 
levofloxacin 
amoxicillin with high-dose PPI 
 
- Research suggest that eliminating 
H. pylori as soon as possible may 
help prevent stomach cancer. 

Awan, et al. [97] 
 
 
 
 
 
 
 
 
 
Awan, et al. [97] 

 

11. FUTURE ASPECTS 

In the purpose of shedding more light on the precise sources of infection and the part that animals play in the 

spread of disease, further case report studies are necessary. Given the significant risk that H. pylori poses to the 

public, we advise public health authorities to give priority to developing preventive interventions against H. pylori 

infection. 

 

12. CONCLUSION  

GH is more better understood than EHH, despite the fact that a substantial amount of data has just been 

gathered. To understand the role of EHH in human and animal sickness, a great deal of unresolved questions 

remain to be explored. The microbiological identification of EHH is one of the most crucial areas for advancement; 

there wouldn't be many clinical reports without better isolation and detection techniques. 

A thorough understanding of the range of species that act as EHH reservoirs is also essential. This will enable 

us to ascertain their epidemiology, pinpoint potential channels of transmission, and maybe initiate preventive 

measures to avert human infection. Similar opacity covers the specific pathologic pathways connected to EHH. 

Therefore, it is necessary to investigate animal models' infection in order to screen the different pathogenicity 

determinants. Moreover, future research should take these and other relevant factors into account in order to fully 

comprehend the risk that EHH actually poses to public health. There is hope that with all of the attention this class 

of bacteria has recently received, our knowledge of these freshly discovered microbes will advance dramatically in 

the years to come.  

 

13. ABBREVIATIONS 

°C, degree Celsius; µm, micrometer; CD, Crohnʼs disease; CDT, cytolethal distending toxin; CLSI, Clinical and 

Laboratory Standards Institute; cmp, Campylobacter major protein; DNA, deoxyribonucleic acid; DsBs, double 

strand breaks; EBV, Epstein-Barr virus; EHH, enterohepatic Helicobacter species; GH, gastric Helicobacter species; 

H. pylori, Helicobacter pylori; IBD, inflammatory bowel disease; IgA, immunoglobulin type A; irgA, iron-regulated 

outer membrane virulence protein; JCV, John Cunningham virus; LpxR, Lipid A deacylase; MIC, minimal inhibitory 

concentration; NHPH, non-Helicobacter pylori species; OMPLA, outer membrane protein phospholipase A; OMPs, 

outer membrane proteins; PCR, Polymerase Chain Reaction;   PG, Peptidoglycan, Pgl, protein glycosylation; PPI, 



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Proton Pump inhibitor; rDNA, ribodeoxyribonucleic acid; rRNA, ribosomal ribonucleic acid; SfpA, systemic factor 

protein A; UC, Ulcerative colitis; VBNC, viable but not culturable bacteria. 

 

Funding: This study received no specific financial support.    
Institutional Review Board Statement: Not applicable. 
Transparency: The authors state that the manuscript is honest, truthful, and transparent, that no key 
aspects of the investigation have been omitted, and that any differences from the study as planned have been 
clarified. This study followed all writing ethics. 
Competing Interests: The authors declare that they have no competing interests. 
Authors’ Contributions: Study design, scientific writing, data collection, overall revision, N.E.; data 
collection and scientific writing, M.A.M., R.S.S., S.M.B., J.F.M., S.A.E., O.H.H.; All authors have read and 
agreed to the published version of the manuscript. 

 

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