Helicobacter Pylori Bacteria

Running head: HELICOBACTER PYLORI BACTERIA 1

Helicobacter Pylori Bacteria

Oresteban Carabeo

Kaplan University

HELICOBACTER PYLORI BACTERIA 2

Helicobacter Pylori Bacteria

What are Helicobacter Pylori bacteria? Helicobacter Pylori (H. pylori) bacteria are a

predominant disease among various ethnic groups within the United States. Knowledge of H.

pylori risk factors, incidence, and prevalence among individuals can help disease prevention.

Clarifying the mechanisms of genetic exchange in H. pylori will create a better understanding of

diversity and development of genetic tools for study. Can a recombination and DNA transfer

contribute to H. pylori genetic variability and host adaptation to increase? Restriction-

modification (RM) systems are vital for bacteria to limit foreign DNA invasion. The H. pylori

are creating damage to the health of individuals globally, and it is important to combat this type

of bacteria by clarifying mechanisms of genetic exchange, DNA transfer recombination, and

restriction-modification systems, which can help with disease prevention.

Identifying Helicobacter Pylori bacteria will help the population with proper knowledge

about the disease along with the mechanisms for prevention. According to the Centers for

Disease and Control Prevention (CDC), H. pylori is a spiral-shaped bacterium found in the

gastric mucous layers of individuals that “causes more than 90% of duodenal ulcers and up to

80% of gastric ulcers” (2006, para. 1). Similarly, CDC discloses that H. pylori are acquired from

fecal to oral or oral-oral transmission, and it is estimated epidemiologically worldwide with

“70% in developing countries and 30%–40% in the United States and other industrialized

countries” (2015, para. 3). CDC (2006) stresses that this bacterium before it was discovered,

piquant foods, acid, stress, and lifestyle were creating ulcers in the population. Individuals were

given H2 blocker medications, and proton pumps inhibitor to treat ulcers by relieving the

symptoms and healing the gastric mucosal inflammation. H. pylori return in individuals when

acid suppression is being removed, which maintaining an appropriate antibiotic regimen can help


patients to eradicate the infection. These are the most common infection in the world among

older adults, African American, and Hispanics in the United States. H. pylori cause major

illnesses, such as chronic active persistent gastritis, atrophic in adults along with children,

duodenal, and gastric ulcer infections. Gastric cancer can develop in infected individuals along

with mucosal-associated-lymphoid-type (MALT) lymphoma (CDC, 2006).

Peptic ulcers develop by the H. pylori have symptoms on numerous individuals at some

point in their lifetime; the proper testing should be done on people along with diagnosis to help

identify the disease. CDC (2006) reveals that the American population is suffering from peptic

ulcer diseases with new cases each year, which adheres to one million ulcer-related in

hospitalizations. The most common ulcer symptoms in individuals are gnawing burning pain in

the epigastrium, and it occurs on an empty stomach, among meals, and in early hours of the

morning. Other ulcer symptoms may include nausea, vomiting, appetite loss, and bleeding in

individuals. People with an actual history of gastric and duodenal ulcers should be tested for H.

pylori. These testing and treatments are recommended for individuals who have been exposed

with gastric cancer recession or MALT lymphoma. It should be prudent for patients who are

bleeding or profound peptic ulcer diseases to retest after treatments. H. pylori are diagnosed by

serological tests that measure lgG antibodies for specific H. pylori to determine if a person is

contaminated. Similarly, the breath test is another method to diagnose H. pylori by given patients

a 13C labeled urea to drink. It is recommended as a reference method for diagnosis of H. pylori

the upper esophagogastroduodenal endoscopy (CDC, 2006).

Treatments regimens to eradicate H. pylori can help individuals by using the proper

antibiotics to prevent the infection, and it is important for people along with governmental

agencies to expose prevention measures around the globe. CDC (2006) notes that the H. pylori


therapy consists of 10 days to 2 weeks, which individuals have to take at least two effective

antibiotics. These are the H. pylori antibiotics for individual treatments, such as amoxicillin,

tetracycline, metronidazole, ranitidine bismuth citrate, and proton pump inhibitor. Another

excellent combination to combat H. pylori is the use of acid suppression by the H2 blocker,

which can help individuals with abdominal pain and nausea, which helps heal gastric mucosal

inflammation, and enhance antibiotic efficacy. On the one hand, people can use preventative

measures for H. pylori by washing their hands regularly, eating prepared food properly, and

drinking safe water from clean sources. On the other hand, governmental agencies can

collaborate with other organizations, such as academic institutions, and health industry to combat

H. pylori by conducting national campaigns. Informing the healthcare providers along with

consumers about H. pylori, stomach, and duodenal ulcers can help individuals understand about

the disease. Another form of prevention is by establishing an antimicrobial surveillance system

that can monitor H. pylori resistance changes through the United States (CDC, 2006).

According to the World Health Organization (WHO, 2008), H. pylori isolation from

human gastric mucosa was done in 1982 along with gastric adenocarcinomas that have change

the perception of these diseases for individuals. Notably, the development of atrophy and

metaplasia of the gastric mucosa is related to H. pylori infection, and it’s important to mention

that oxidative and nitrosative stress is the result along with inflammation of gastric

carcinogenesis. On the other hand, research and development have contributed to a vaccine,

such as Initiative for Vaccine Research (IVR), which will fight against pathogens of important

diseases, and economic problems within low-middle income nations. Similarly, the strategic

alignment of IRV activities along with objective 6, such as Global Vaccine Action Plan, country,


regional, and global research have developed innovations for vaccines immunization (WHO,

2008).

H. pylori have a genetic mechanism of exchange, which is important to clarify because it

will create an enhanced understanding of diversity and development of genetic utensils for study.

According to the National Center for Biotechnology Information (NCBI, 2001), the

incorporation of genetic material from other organisms is the acquisition and integration of

horizontal gene transfer (HGT), and genetic exchange transformation was first seen with

Streptococcus pneumoniae in 1928. Horizontal gene transfer is the main contributor to bacterial

diversity development. HGT exposes clinical interests because genes have encoding virulence

factors, antigen determinants, and antibiotic resistance. H. pylori show tremendous genetic

diversity, such as evidence gene variation on strains order, strain contents genetic differences, the

variety of some genes, and conserved sequence diversity of genes. The frequent genetic

exchange is frequently seen on H. pylori because it has a recombinational population structure.

Notably, the three traditional mechanisms of horizontal gene exchange are done through natural

transformation, conjugation, and transduction. Mechanisms of transformation are the exogenous

DNA taken up by bacteria, which the DNA develops genetically. Transformation mechanism is

studying more for DNA transfer in H. pylori (NCBI, 2001). NCBI informs that “approximately

75% of all H. pylori strains tested have been found to be capable of natural transformation by H.

pylori chromosomal DNA” (2001, para, 6).

NCBI (2001) stresses that most of the H. pylori are resistant to the natural transformation

of Escherichia coli, and it should be noted, H. pylori transport plasmids, which are isolated from

E. coli. Plasmids transformations occur at lower frequencies that are derived from heterologous

H. pylori strains. Transformation disparities within frequencies utilizing Chromosomal DNA


along with transporting DNA suggest that efficient homologous recombination saves

chromosomal markers. Similarly, transformation in DNA restriction is not as much of a factor

because the unrelated strain of a DNA from H. pylori is chromosomal and it's opposed to a

plasmid. Notably, transduction is not demonstrated yet in DNA transfer for H. pylori. On the

other hand, conjugation method usage for DNA mechanism for delivery have the advantages of

circumventing barriers that are restricted, which inhibits genetic exchange created by natural

transformation. The first significant barrier in H. pylori for genetic exchange is found in its

environmental gastric place. The second barrier for H. pylori is through genetic isolation by

inhibiting interspecies transfer in sequence amount of homology required for homologous

recombination. It seems like the strongest barrier for H. pylori is the restriction endonucleases on

a horizontal gene that exchanges through transformation. These type of restriction barriers could

be an obstacle for researchers trying to perform gene manipulation because it serves the

organism well with its natural environment for H. pylori. Lastly, clarifying genetic exchange

mechanisms for H. pylori could lead in understand diversity, which can help with the

development and genetic tools for studies (NCBI, 2001).

H. pylori genetic variability and host may increase in adaptation with a recombination

and DNA transfer. According to Fernandez-Gonzalez, and Backert (2014), H. pylori genetically

is one of the most diverse bacteria because of its recombination and DNA transfer that

contributes to the genetic variability, which enhances host adaptation. Genetic diversity in

bacteria have a strategic DNA transfer through conjugation, which uses a DNA fragment of cells

donor by transferring them to the recipient, and mechanisms mediated with conjugative

nucleoprotein complex. Notably, H. pylori Chromosomes DNA encode four T4SSs, such as

cagPAI genes, comB, tfs3, and tfs4 that promotes chronic infection. Similarly, the encoding


T4SS is interceded by the cagPAI injection from the effector protein CagA, proinflammatory

signaling, comB system, which involves environmental DNA acceptance. Functional presence of

XerD tyrosine recombinase with “5'AAAGAATG-3 border sequences as well as two putative

conjugative relaxases (Rlx1 and Rlx2), a coupling protein (TraG), and a chromosomal region

carrying a putative origin of transfer (oriT) suggest the presence of a DNA transfer apparatus in

tfs4” (Fernandez-Gonzalez, & Backert, 2014, para, 1). In addition, Fernandez-Gonzalez, and

Backert (2014) reveal that some extrachromosomal plasmids along with phages are present in H.

pylori strains, which genetic exchange between plasmids, and chromosomes are involved in

DNA events of genetic diversity (Fernandez-Gonzalez, & Backert, 2014).

According to Zhang, and Blaser (2012), RM systems are necessary for bacteria because it

limits foreign DNA invasion. H. pylori bacteria have a diverse strain-specific type II systems,

which apply to the strain-specific restriction of natural transformation. Genes were deleted with

the encoding of four active type II restriction endonucleases in H. pylori, which strains with

26695 using sacB-mediated counterselection. DNA donor transformation adheres to exogenous

cassettes, which are methylated with Escherichia coli that increases in the restriction

endonuclease-deficient (Red) strain by 1.7, 2.0 log10 for the cat, and aphA. Similarly, the

transformation was increased significantly for Red strain from DNA donor by other H. pylori

strains to the shared type II R-M system strain of 26695. The REd has a greater natural

transformation frequency that retains growth, such as DNA repair, spontaneous mutation

phenotypes, comparison with wild-type 26695, which indicates mutant construction, and genetic

engineering for H. pylori. Similarly, the four active type II restriction endonuclease genes are

hpyAII (HP1366), hpyAV (HP0053), hpyAIII (HP0091), and hpyAIV (HP1351) for H. pylori

wild-type 26695 strains (Zhang, & Blaser, 2012).


Zhang, and Blaser (2012) reveals that the four active type II restriction enzymes (RE)

genes have an instant downstream gene of distances, such as intergenic from 86 to 432 bp. It

should be noted that the mRNA-based analysis reveal expression of these instant downstream

genes. In addition, these genes in the REd strain was not different from the wild-type strain (<2-

fold), such as growth in by nutrient-rich, and to mid-log phases, which recommends removal of

the four RE genes because of its limited polar effect on their downstream genes. On the other

hand, H. pylori strains, such as 26695, have an active type II restriction-methylation systems and

restriction-methylation gene sequence leftovers on their genomes. The Phase variation inactivity

of restriction on genes are disappearing and reactivated to restore the endonuclease activity. The

REd strain tool can be useful in eliminating active type II R-M systems by applying selective

pressure for putative phase variable, such as restriction genes. The H. pylori evolution can be

done for research by the REd mutant strain, which can be useful in R-M systems.

In conclusion, H. pylori are creating health damages around the globe to individuals. The

best way to combat H. pylori is throughout clarifying genetic exchange mechanisms, such as

DNA transfer recombination, and restriction modification systems to help individuals with

disease prevention.


References

Centers for Disease Control and Prevention. (2006). Helicobacter pylori and peptic ulcer disease.

Retrieved from http://www.cdc.gov/ulcer/keytocure.htm

Centers for Disease Control and Prevention. (2015). Chapter 3 infectious diseases related to

travel. Retrieved http://wwwnc.cdc.gov/travel/yellowbook/2016/infectious-diseases-

related-to-travel/helicobacter-pylori

Fernandez-Gonzalez, E., and Backert, S. (2014). DNA transfer in the gastric pathogen

Helicobacter pylori. Journal of Gastroenterology, 49(4), 594-604. doi:10.1007/s00535-

014-0938-y

National Center for Biotechnology Information. (2001). Helicobacter pylori: Physiology and

genetics. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK2430/

World Health Organization. (2008). Helicobacter pylori. Retrieved from

http://www.who.int/immunization/topics/helicobacter_pylori/en/

Zhang, X.-S., & Blaser, M. J. (2012). Natural transformation of an engineered Helicobacter

pylori strain deficient in type II restriction endonucleases. Journal of

Bacteriology, 194(13), 3407–3416. http://doi.org/10.1128/JB.00113-12

http://doi.org/10.1128/JB.00113-12

http://www.who.int/immunization/topics/helicobacter_pylori/en/

http://www.ncbi.nlm.nih.gov/books/NBK2430/

http://www.cdc.gov/ulcer/keytocure.htm


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Helicobacter Pylori Bacteria