Analysis and disccusion of how Helicobacter Pylori (H.pylori) developed genetically and physically as a bacterium to be effective in affecting host cells. It has successfully affected 50% of host cells within the human population. Retrospective research of genomic advances and interactions of H.pylori migration between old and new world.
Helicobacter Pylori infect more than 50% of worlds population.HP causes gastritis,PUD,gastric cancer and MALT lymphoma.Variable invasive and noninvasive diagnostic modilities are available.Eradication of H.Pylori is possible with proper therapy.
Morphology and structure of H. pylori
Diagnosis of H. pylori infection
Transmission of H. pylori
Symptoms of H. pylori infection
Treatment and prevention
Pathogenesis of H. pylori
Helicobacter Pylori infect more than 50% of worlds population.HP causes gastritis,PUD,gastric cancer and MALT lymphoma.Variable invasive and noninvasive diagnostic modilities are available.Eradication of H.Pylori is possible with proper therapy.
Morphology and structure of H. pylori
Diagnosis of H. pylori infection
Transmission of H. pylori
Symptoms of H. pylori infection
Treatment and prevention
Pathogenesis of H. pylori
Helicobacter pylori associated Peptic ulcer diseaseS M Ali Hasan
Evidence-based clinical practice guidelines for H. pylori associated peptic ulcer disease based on
Japanese society of Gastroenterology, 2015
American College of Gastroenterology, 2017
The Maastricht V/Florence Consensus Report, 2018
Helicobacter pylori associated Peptic ulcer diseaseS M Ali Hasan
Evidence-based clinical practice guidelines for H. pylori associated peptic ulcer disease based on
Japanese society of Gastroenterology, 2015
American College of Gastroenterology, 2017
The Maastricht V/Florence Consensus Report, 2018
Acid peptic disease /dental courses /certified fixed orthodontic courses by I...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
00919248678078
The Japanese egg market trends and expectations- Hatta, H. Presented at DSM Customer Event: Exploring the benefits of feed carotenoids for egg quality, Village Neuf, France, 2013.
Helicobacter pylori as a food borne pathogen
the survival conditions of bacteria, mode of transmission, possible diseases and their prevention measures
Laboratory diagnosis of H. Pylori infection, Ola ElgaddarOla Elgaddar
A short presentation for the different laboratory techniques used in diagnosing Helicobacter Pylori infection. A special focus is given for the diagnostic performance of every test.
Helicobacter pylori and Peptic Ulcer diseaseDiaa Srahin
Case Study
Clinical Case Summary
History
Helicobacter pylori
Biochemical characteristics
Transmission
Epidemiology
Global incidence of H. pylori infection
risk factors for acquisition of H.pylori
Immune responses
Pathogenesis
Helicobacter pylori Virulence Factors
Clinical Presentation
Complications
Peptic Ulcer
Diagnosis
Treatment
Prevention
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
The IOSR Journal of Pharmacy (IOSRPHR) is an open access online & offline peer reviewed international journal, which publishes innovative research papers, reviews, mini-reviews, short communications and notes dealing with Pharmaceutical Sciences( Pharmaceutical Technology, Pharmaceutics, Biopharmaceutics, Pharmacokinetics, Pharmaceutical/Medicinal Chemistry, Computational Chemistry and Molecular Drug Design, Pharmacognosy & Phytochemistry, Pharmacology, Pharmaceutical Analysis, Pharmacy Practice, Clinical and Hospital Pharmacy, Cell Biology, Genomics and Proteomics, Pharmacogenomics, Bioinformatics and Biotechnology of Pharmaceutical Interest........more details on Aim & Scope).
All manuscripts are subject to rapid peer review. Those of high quality (not previously published and not under consideration for publication in another journal) will be published without delay.
Current Understanding of the Transmission, Diagnosis, and Treatment of H. pyl...AI Publications
H. pylori infection is a prevalent bacterial infection that affects the gastric mucosa of humans, with a prevalence ranging from 30% to 90%, depending on the region. The infection is a significant cause of gastritis, peptic ulcer disease, and gastric cancer. In this comprehensive review, we discuss the current understanding of the transmission, diagnosis, and treatment of H. pylori infection. We describe the risk factors and epidemiology of the infection, along with its pathogenesis, which involves multiple virulence factors that contribute to the colonization and survival of the bacteria in the acidic stomach environment. Diagnostic tests for H. pylori infection include invasive and non-invasive methods, with the choice of test depending on several factors. Treatment of H. pylori infection is aimed at eradicating the bacteria and preventing complications. Antibiotic-based triple or quadruple therapy, in combination with acid-suppressing agents, is the standard treatment, but antibiotic resistance is an emerging problem that needs to be addressed. This comprehensive review provides a useful resource for clinicians, researchers, and public health officials involved in managing H. pylori infection and its associated complications.
An ulcer is a sore in the lining of the stomach or duodenum (the first part of the small intestine). People of any age can acquire an ulcer. Women are affected just as often as men.
Similar to How Helicobacter Pylori can cause gastric ulcerations and how this can lead to cancers of the stomach - Piril Erel (19)
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Includes Summary Questions, Further Application questions and key definitions at the end of the slides
Slides aimed for teachers, but can be used as revision slides for students also.
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Analysis in to the Epidemiology and Pathophysiology of Respiratory Syncytial ...Pırıl Erel
Respiratory Syncytial Virus (RSV) places the heaviest clinical burden on paediatric wards in the UK and the US. It is in fact, a global issue with 3.4 million hospitalisations and approximately 66,000 deaths worldwide per annum (Bush et al., 2007) (Lambert et al., 2014). RSV is the leading cause, especially during the winter months, of severe respiratory infections in infants resulting in a rise in hospital admissions where 0.5-1% of infected babies die from respiratory failure. It is also a significant respiratory concern in the elderly population. (Agoti et al., 2014)
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It is important to understand RSV has been implicated with further acute and chronic illnesses therefore by considering the epidemiology and pathophysiology of RSV treatment may be implicated during early stages which can influence possible outcomes in the future.
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Slides specifically for AQA syallbus during A-Levels, this is for unit 1 - biology of disease - chapter 2 (specifically 2.1 and 2.4) I believe these chapters go hand in hand, I have made these for my students and they have found them very useful.
Slides aimed for teachers, but can be used as revision slides for students also.
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Analysis in to the Epidemiology and Pathophysiology of Respiratory Syncytial ...Pırıl Erel
Respiratory Syncytial Virus (RSV) places the heaviest clinical burden on paediatric wards in the UK and the US. It is in fact, a global issue with 3.4 million hospitalisations and approximately 66,000 deaths worldwide per annum (Bush et al., 2007) (Lambert et al., 2014). RSV is the leading cause, especially during the winter months, of severe respiratory infections in infants resulting in a rise in hospital admissions where 0.5-1% of infected babies die from respiratory failure. It is also a significant respiratory concern in the elderly population. (Agoti et al., 2014)
RSV has shown to have a willful ability to enter the host resulting in illness both by viral mechanisms and proteins encoded by RSV, dysregulating the synthesis of systemic immune response of the host. Alongside the infiltration of RSV, the heath status and genotype of the host will be a key factor in predetermining disease susceptibility and severity.
It is important to understand RSV has been implicated with further acute and chronic illnesses therefore by considering the epidemiology and pathophysiology of RSV treatment may be implicated during early stages which can influence possible outcomes in the future.
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Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
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under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
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heliosphere. By combining magnetic feld modelling and spectroscopic
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a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
Nutraceutical market, scope and growth: Herbal drug technologyLokesh Patil
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This presentation explores a brief idea about the structural and functional attributes of nucleotides, the structure and function of genetic materials along with the impact of UV rays and pH upon them.
How Helicobacter Pylori can cause gastric ulcerations and how this can lead to cancers of the stomach - Piril Erel
1. How helicobacter Pylori causes gastric
ulcerations and how this can be linked to
cancers of the stomach
By Piril Erel
2. Helicobacter Pylori
• 50% worlds population have
Helicobacter Pylori (H.
pylori) in upper
gastrointestinal track2.
• Most people infected by H.
pylori will show no
symptoms1.
• Infects gut2.
• H. pylori is a gram-negative
spiral shaped bacterium
• Detected in 19834.
3. H.pylori correlates much better
with socio- economic status than
race
Figure 1 : A worldwide geographic demonstration which illustrates the prevalence of
H.pylori around the world
4. H.pylori - The Almighty
• Flagella gives motility and
enables the bacteria to
grow under the mucosal
membrane3.
• Lipopolysaccharides and
membrane proteins adhere
to host cell receptors3.
• Urease enzyme is used to
combat the acidic
environment of the
stomach by producing
ammonia3.
Figure 2: This image shows the virulence factors of H.pylori and how it can
affect and survive in the human host.
5. How does H.pylori interact and
damage the intestinal mucosa?
• Vac A exotoxin causes injury
to the mucosal membrane3.
• Type IV secretion system
that uses a pillus to inject
effectors3.
• cagA causes actin
remodeling and inhibits
apoptosis3.
• Inhibits immune response by
inhibiting T cell activation
and proliferation3.
Figure 3: This image shows the various ways in which Vac A interacts with
epithelial cells and the various different ways it causes disruption
6. Sequelae
Figure 4: Proportions of individuals
with differing disease severity
• Association between H.pylori
infection and gastric cancer8.
• Infection causes H pylori associated
gastritis8.
• Increasing degenerative changes and
evolution towards atrophy8.
• Nine fold risk of developing
precancerous gastric conditions when
H.pylori positive patients were
compared with those without
infection8.
• Strong association with poor
socioeconomic conditions8.
7. Why does H pylori cause
cancer
This is not well understood, some ideas are:
• Chronic inflammatory response to infection pushes cells
in the stomach lining towards oncogenesis 11.
• Damage of the mucosal membrane due to inflammation
increases the carcinogenic effect of risk factors such as
high salt intake and smoking12.
• Recent research suggests CagA may lead to inactivation
tumor suppressor proteins like p5311.
This protein normally leads cells into apoptosis.
9. Signs
& Symptoms
• Indigestion: this can be caused
by an H pylori induced ulcer1.
Can be accompanied by:
• Dull and burning pain worse on
empty stomach, relieved briefly
by antacids, lasts for minutes
to hours and comes and goes
over days and weeks5.
• Weight loss, vomiting, trouble
in swallowing: can be caused
by H.pylori induced cancer1.
Figure 6: How helicobacter Pylori develops into an Gastric Ulcer
10. Diagnosis
• Blood test: antibody test
meaning that it is difficult to
tell whether the infection is
past or current5.
• Breath test: 14C labeled urea
drink, detection of the isotope
in exhaled CO2 will indicate
presence of urease secreted
by H pylori 5
• Biopsy taken during an
endoscopy, tissue sample
examined in the lab for
presence of H.pylori5.
• X ray examination after
barium meal (white chalky
liquid allowing soft tissues to
become visible on x-ray)5.
Figure 7: Carbon-14 Breath Test
11. Genome interactions
• H. pylori has infected humans since they
originated in the African continent6,7
• The bacterium has evolved with us
accumulating DNA changes as we migrated
across the world6,7.
• Where old world met new e.g. as in South
America, when European colonists arrived this
co-evolution was disrupted6,7
• Thus some individuals became infected with H.
pylori variants with differently evolved
ancestry6,7.
• This mismatch means that a harmless infection
can become cancer causing6,7
• The genomic sequence of the hosts compared
to that of the microbes can predict of the risk
of disease much better than when analysed
alone6,7.
• It was shown that people from Tumaco
Colombia find the majority of their DNA
ancestry and most of their H. pylori strains
come from Africa6,7
• The mountain population from Tuquerres is 67%
American/Indian and 31% European. Their H.
pylori are mostly from European which
replaced the native strains6,7.
• If the H. pylori strains have a different origin to
their hosts, they are more likely to cause
cancer6,7.
• Strains originating in Africa are mostly harmless
Africans, but caused cancer in people with a
largely American/Indian background6,7.
12. Treatment
• Double-dose PPI (e.g. 20 mg omeprazole) 10.
decreases the stomach's production of acid allowing damaged
tissue to heal. Examples of proton pump inhibitors include
Lansoprazole, Omeprazole, Pantoprazole and more.
• Plus two antibiotics; this increases treatment success
and antibiotic resistance9.
Omeprazole 20mg, metronidazole 400 mg & clarithromycin
250 mg TDS
Or, Omeprazole 20mg, amoxicillin 1 g and clarithromycin
500mg TDS
13. References
1. Information about Helicobacter Pylori. (2014). 1st ed. [ebook]
London: Core – the digestive disorders foundation, pp.2-5.
Available at:
http://www.nhs.uk/ipgmedia/national/core%20charity/assets/heli
cobacterpylori.pdf
2. Blaser, M. J. (2006). "Who are we? Indigenous microbes and the
ecology of human diseases". EMBO Reports 7 (10): 956–60.
3. Wikimedia, (2014). Helicobacter Pylori Virulence Factors. [image]
Available at:
http://upload.wikimedia.org/wikipedia/commons/9/9a/H_pylori_
virulence_factors_en.png
4. H.pylori & Peptic Ulcers. (2014). 1st ed. [ebook] Bethesda:
Clearinghouse, pp.1-6. Available at:
http://digestive.niddk.nih.gov/ddiseases/pubs/hpylori/hpylori_50
8.pdf
5. Yong, E/ (2014). Human-microbe mismatch boosts risk of
stomach cancer. [online] Available at:
http://www.nature.com/news/human-microbe-mismatch-
boosts-risk-of-stomach-cancer-1.14501 [Accessed 18 May.2014].
6. Kodaman, N., Pazos, A., Schneider, B., Piazuelo, M., Mera, R.,
Sobota, R., Sicinschi, L., Shaffer, C., Romero-Gallo, J., de Sablet,
T. and others, (2014). Human and Helicobacter pylori
coevolution shapes the risk of gastric disease. Proceedings of the
8. Forman, D. (1998). Helicobacter Pylori: the gastric cancer problem.
Gut, 43 (Suppl 1), p.33.
9. Uptodate.com, (2014). Helicobacter pylori infection and treatment.
[online[ Avaliable at: .http://www.uptodate.com/contents/helicobacter-
pylori-infection-and-treatment-beyond-the-basics
10. Patient.co.uk, (2014). Helicobacter Pylori [online] Available at:
http://www.patient.co.uk/doctor/helicobacter-pylori-pro
11. National Cancer Institute, (2014). Helicobacter pylori and cancer.
[online] Avaliable at:
http://www.cancer.gov/cancertopics/factsheet/Risk/h-pylori-cancer
12. J, B. and P,M. (2014). Helicobacter pylori and Gastric Cancer.
Digestive Disease, [online] 32(3). Available at:
http://ncbi.nlm.nih.gov/pubmed/24732191 [Accessed 18 May. 2014].
14. Image References
1. Helico.com. Epidemiology | The Helicobacter Foundation [Internet]. 2014 [23 April 2014].
Available from: http://www.helico.com/?q=Epidemiology
2. Upload.wikimedia.org. [Internet]. 2014 [23 April 2014]. Available from:
http://upload.wikimedia.org/wikipedia/commons/9/9a/H_pylori_virulence_factors_en.png
3. Cover T, Blanke S. Helicobacter pylori VacA, a paradigm for toxin multifunctionality.
Nature Reviews Microbiology. 2005;3(4):320--332.
4. Helico.com. Epidemiology | The Helicobacter Foundation [Internet]. 2014 [23 April 2014].
Available from: http://www.helico.com/?q=Epidemiology
5. Kim E, Hong K, Hong H, Hahm K. Detouring the undesired route of Helicobacter pylori-
induced gastric carcinogenesis. Cancers. 2011;3(3):3018--3028.
6. HealthTap. what is the effests of xycam 20mg on a developing peptic ulcer? [Internet].
2014 [23 April 2014]. Available from: https://www.healthtap.com/user_questions/326787-
what-is-the-effests-of-xycam-20mg-on-a-developing-peptic-ulcer
7. Static.groupon.hk, (2014). [online] Avaliable at:
https://static.groupon.hk/56/20/1328191622056.jpg [Accessed 18th May.2014]
Editor's Notes
Welcome to my presentation, Here I will be discussing how helicobacter pylori causes gastric ulcerations and how this can be linked to cancers of the stomach. I hope you enjoy the following slides
It affects around 50% of the world’s population. It’s one of the most common infections in the U.K. Unless it is treated, the infection will stay for the rest of an individuals life. Now this is due to the fact that H.pylori will not show any symptoms or problems caused by H.pylori and so will not even know that they are affected. However, further complications may indicate the presents of H.pylori in the gut and will then allow individuals to seek medical help.
Helicobacter Pylori is a gram-negative spiral shaped bacterium that grows in mucus layer that coats the inside of the human stomach. Gram-negative refers to the thin layer of peptidoglycan and presents of a outer membrane in the helicobacter cell wallHelicobacter was detected by Robin Warren who was a pathologist and a physician named Barry Marshall in Australia. Although many individuals did not believe Warren & Marshall as H.pylori did not show symptoms. Barry Marshall had decided to do something drastic and drank a solution of H.pylori and within 2 weeks developed acute symptoms which we will discuss later onNext Slide
The prevalence of H.Pylori infected varies widely by geographic area it can be seen that countries such as South America and Africa have the highest prevalence. This is due to the transmission of H.pylori. It is mostly transmitted through contamination of water and food which is much more likely to occur in 3rd world countries and when we compare these percentages with those such as The united states or united kingdom or even Australia, we can see here that the sanitization are much better and therefore the prevalence is much more lower.
Next Slide
There are 4 different steps that helicobacter pylori does in order to affect the human host. 1. Firstly there is the addition of Helicobacter Pylori to the host cell
2. Secondly, and most importantly helicobacter pylori minimizes the content of the acid in the stomach 3. it colonizes 4. and finally the degrades the epithelial cells
1 The addition of helicobacter pylori is enabled by the flagella which allows the bacterium to be motile and also permits the bacteria to propel itself through the gastric fluid, mucus layer and finally adheres itself to the epithelial lipopolysaccharides and membrane proteins, using this it interacts with epithelial cells of stomach
2 The hydrochloric acid keeps the pH of the stomach strongly acidic, between a pH of one and two, H.pylori is able to survive in acidic conditions but as the stomach pH is a little too acidic for the bacteria it uses an enzyme to raise the pH around the bacteria to a more survivable level. Urease enzyme is used where it will breakdown urea and water to produce carbon dioxide and ammonia. As we know that ammonia is a base and HCl is an acid this allows a neutralizing reaction making the pH of the stomach increase.
3This creates a microenvironment for the bacterium to survive this allows the colonization of more and more H.Pylori to thrive in this environmentNext Slide
Now the degradation of the epithelial cells occurs in many different ways:
The Vac A exotoxin causes injury to the mucosal membrane by inducing alterations in mitochondrial membrane permeability and apoptosis, it also stimulates pro-inflammatory signaling and increases the permeability of the plasma membrane.
Type IV secretion system uses a pillus to inject effectors such as Cytotoxin-associated gene A - cagA is a needle-like appendage that injects a toxin which remodels actin the cytoskeleton of the cell thereby disrupting the epithelial barrier and facilitating the passage of Vac A, it is also found to inhibit apoptosis.
These responses altogether inhibits immune response by T cell activation and proliferation so the body cannot produce an immune response against Helicobacter pylori and this is the development of gastric ulcerations
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So this image shows the proportions of individuals with differing disease severity The 50% of the worlds population who has helicobacter pylori is more susceptible in developing duodenal ulcers about 90% compared to the unaffected population. The development of gastritis is more likely when affected with the bacterium. There is a nine fold risk of developing precancerous gastric conditions when compared with individuals with and without the bacterium. Also almost all cases of gastric lymphoma is linked to helicobacter pylori being present in the human host. As discussed before the prevalence of helicobacter pylori in individuals and country is strongly associated with poor socioeconomic conditions.
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How helicobacter pylori leads to gastric cancer is not well understood but some ideas are put forward by scientist, it is unclear whether it is one specific cause or a collection of all of these effects of helicobacter pylori which increases the chance of gastric cancer. Long-term exposure to cagA toxin causes chronic inflammation and can induce oncogenesis, this inflammation leads to a damaged mucosal membrane and can increase the carcinogenic effect of risk factors leading to gastric cancer such as high salt intake and smoking. Recent research suggest that cagA may lead to inactivation and alteration of tumor suppressor proteins such as p53 which normally leads to apoptosis and therefore inactivation can promote the development and progression of gastric cancerNext Slide
80% of individuals who suffer with helicobacter pylori will experience chronic gastritis which is characterized by chronic inflammation of the stomach mucosa which is caused by injury to the gastric mucosa resulting from reflux of bile and pancreatic secretions into the stomach after adhesion of helicobacter pylori.15-20% of theses individuals will further develop chronic atrophic gastritis known as Type A or B gastritis is a process of chronic inflammation of the stomach mucosa leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. A duodenal ulcer can also develop due to the corrosive HCl in the stomach causing inflammation and ulcers to area of epithelial cells that are infected with helicobacter pylori. Furthermore 1% of these individuals can finally be presented with gastric carcinoma Next Slide
Indigestion is the main symptom of helicobacter pylori due to a induced ulcer however this symptom is common among many types of disorders, so can be difficult to link to helicobacter induced disorder. Indigestion can further be accompanied by dull and burning pain which is worse on an empty stomach and can be relieved by antacids very briefly. This burning pain can last for minutes to hours and comes and goes over days an weeks. Gastric carcinoma can present itself as weight loss, vomiting, dysphagia and anemia.Next Slide
Blood tests are used to measure antibodies to Helicobacter pylori. Antibodies are proteins made by the body’s immune system when it detects harmful substances such as bacteria. Blood tests for Helicobacter pylori can only tell if your body has Helicobacter pylori antibodies. It cannot however tell if you have a current infection or how long you have had it, this is because the test can be positive for years even if the infection is cured. As a result blood tests cannot be used to see if the infection has been cured after treatment. During breath tests the patient is asked to swallow a special substance that has urea labeled with carbon 14. Urea is a waste product the body produces as it breaks down protein. The urea used in the test has been made harmlessly radioactive. If Helicobacter pylori is present, the bacteria convert the urea into CO2, which is detected and recorded in your exhaled breath after 10 minutes. This test can identify almost all people who have Helicobacter pylori. A biopsy may also be taken from the stomach lining which is the most accurate way to tell if an individual has Helicobacter pylori.. To remove the tissue sample the patient undergoes an endoscopy. Common complications of helicobacter pylori infection are gastritis and ulcers. To check for ulcers, you may have a special stomach x-ray examination after a barium meal which becomes visible on x-rays.Next Slide
I found it interesting when doing my research about helicobacter pylori the origins and geographic distribution worldwide affecting 50% of the worlds population and genomic interactions universally. Helicobacter pylori was first originated in the African content and mutated across the world and has undergone genetic mutations along this spread. Where the old world met the new world the co-evolution was disrupted and helicobacter pylori was not dependent on infecting host cells in the African content. Individuals started to become infection with helicobacter pylori. Helicobacter pylori encountered new genetic material and evolved differently than compared to its origin. If an individual did not contain the resistant genomic sequence to helicobacter pylori it could become cancerous. Scientists in Tumaco Colombia had found the majority of their DNA ancestry and helicobacter pylori strains come from Africa. The mountain population from Tuquerres is 67% American/Indian and 31% European. Their helicobacter pylori are mostly from European which replaced the native strains. If the H.pylori strains have a different origin to their hosts, they are more likely to cause cancer. Strains originating in Africa are mostly harmless to Africans, but caused cancer in people with a largely American/Indian background
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Helicobacter pylori is treated with a double-dose Proton pump inhibitors such as omeprazole, lansoprazole and pantoprazole which decreases the stomach’s production of acid allowing damaged tissue to heal, this is accompanied with 2 antibiotics which increases treatment success and antibiotic resistance. These two antibiotics can either be metronidazole, clarithromycin and amoxicillinNext Slide