This course introduces learners to a variety of infectious diseases using a patient-centered, story-based approach. Through illustrated, short videos, learners will follow the course of each patient’s illness, from initial presentation to resolution. Integrating the relevant microbiology, pathophysiology and immunology, this course aims to engage and entice the learner towards future studies in microbiology, immunology and infectious diseases. The patient-centered videos included in this course were created as part of the Re-imagining Medical Education initiative, led by Charles Prober MD, Senior Associate Dean of Medical Education at the Stanford School of Medicine. This initiative was the first of its kind to explore the collaborative creation of foundational medical education online content by inter-institutional teams of faculty. The content presented in this course was created by faculty from Stanford University School of Medicine, in collaboration with The University of Washington School of Medicine, Duke University School of Medicine, UCSF School of Medicine, and The University of Michigan Medical School. Support for this initiative was provided by the Robert Wood Johnson Foundation and the Burke Family Foundation. PLEASE NOTE: Information provided in this course is for educational purposes only and is not intended to be used for diagnostic and/or treatment purposes.
Gastritis
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From the course by Stanford University
Stories of Infection
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From the lesson
Bacterial Infections Part 1
In Module Two, we will explore six infectious diseases caused by bacteria. We will see how factors like agricultural practices, prior infections, smoking history, and financial situations can play a role in infectious disease. By the end of this module, learners will be able to interpret the clinical presentation of these six infectious diseases and describe the relevant microbiology, pathophysiology, and immunology.
Meet the Instructors
Maya Adam, MDLecturer
Stanford School of Medicine
In this video, we'll be talking about the most common infection in the world.
Over half of the people on earth carry this bacterium in their stomachs.
This 52-year-old businessman,
who lives in Vancouver and commutes between Canada and Tokyo,
was one of the billions of people whose stomach is home to this remarkable microbe.
Mr. Akamatsu made an appointment to see his family physician in Vancouver
after six weeks of unusual stomach discomfort
just below his rib cage in the middle of his abdomen.
He also told his physician that he had been feeling nauseous almost daily
and had lost his usual appetite for food.
When he did manage to eat a proper meal,
he experienced significant belching and bloating.
He had lost a bit of weight, too, recently and this was his primary concern
and also the reason he had finally made time
in his busy schedule to seek medical attention.
Mr. Akamatsu's father had died two years ago from stomach cancer in Japan
and his father's early symptoms had been very similar to his own.
Towards the end of the history-taking, Mr. Akamatsu confided in his doctor
that he often lay awake at night, terrified he was going to die of stomach cancer.
Given this patient's history, including his family history,
the physician strongly suspected that Mr. Akamatsu was suffering
from symptoms associated with gastritis and perhaps a stomach ulcer.
He decided to order several tests, including a CBC to check for anemia,
as ulcers can cause gastrointestinal bleeding.
He also ordered a blood test for the antibodies to Helicobacter pylori,
as well as a stool antigen test for H.
pylori and tests to assess the function of his liver, kidneys, gallbladder and pancreas.
The results of these preliminary tests suggested an infection with H.pylori.
So Mr. Akamatsu was scheduled to undergo an endoscopy,
which would allow the medical team to visualize his GI tract
to look for evidence of gastric or duodenal ulcers
and to obtain biopsy specimens to confirm the infection with H.pylori,
as well as making sure that there was no evidence
of premalignant lesions or gastric cancer.
H.pylori is the strongest risk factor
for both peptic ulcers and gastric cancer, but in the majority of those infected,
there are no symptoms and H.pylori lives in the stomach as a commensal,
despite causing inflammation at the microscopic level.
It's a microbe that has evolved many strategies to survive in the stomach
and even to induce the immune system to tolerate it.
Exactly how the microbe is transmitted between hosts is unclear,
but transmission usually occurs in childhood
and in many developing countries, most children are infected by age 10.
Unlike many other infections that spread through the environment,
H.pylori requires close contact and is usually transmitted within families
from mothers to their children, or from one sibling to another.
The infection most likely occurs through the oral-oral
or gastric-oral route, when microbes are regurgitated from the stomach into the mouth.
Crowding and low socioeconomic environments are risk factors for transmission,
which is one of the reasons why the prevalence of this infection
is higher in under-resourced countries.
Interestingly, H.pylori doesn't seem to survive passage through the intestine
and although antigens from the bacteria can be readily detected in stool,
the bacteria can't be cultured from stool;
so transmission in contaminated food through the fecal-oral route is unlikely.
Once the bacteria have entered the host, they have to avoid being killed by the harsh
acidic environment of the stomach.
And amazingly, they persist throughout the lifetime of the individual,
because they've evolved several specialized survival strategies.
The bacteria have tufts of flagella and a sensory chemotaxis system
that allows them to navigate away from the acidic lumen of the stomach
and burrow into the protective mucus layer lining the stomach walls.
The stomach lumen contains hydrochloric acid,
with a pH that can be as low as one, but the stomach mucus
creates a protective buffering layer that prevents the epithelium from being destroyed.
Here is where H.pylori hides.
The microbe also protects itself from the acidity of the stomach by producing urease -
a powerful enzyme that catalyzes the breakdown of urea into ammonia and carbon dioxide.
The alkaline ammonia neutralizes the acidic environments,
conferring transient protection while the microbe finds its way to the epithelial surface.
Once H.pylori has burrowed through the mucus lining,
it senses metabolites from the epithelium that attract it.
And when it comes into contact with the epithelial cells,
it's able to adhere to these cells via specialized adhesion molecules
on the microbe's surface. Once attached, the bacteria produce a poreforming toxin
called VacA, that has multiple effects on the epithelium and the surrounding tissue.
The more virulent strains of H.pylori also have a specialized
micro injection needle called Cag - a type 4 secretion system that serves to poke
the epiphelial membrane and inject a microbial protein into the host cells.
This protein, called CagA, is a powerful signaling molecule
that affects the functioning of the epithelium.
The presence of CagA has been strongly associated with increased risks
of cancer in many studies.
The presence of the bacterium in close proximity to the epithelium
and the injection of CagA, results in the release of cytokines
that deploy immune cells like neutrophils and monocytes.
The host immune response is responsible for producing the widespread inflammation
that can result in many of the symptoms experienced by Mr.Akamatsu.
H.pylori strains are genetically diverse and can vary in their pathogenicity.
The human host also responds differently
to the infection, depending on the genetic background of the host
and also environmental factors, like diet or co-morbidities like smoking,
are also important determinants for the severity of the gastritis
and whether or not the gastric epithelium is likely to transform
into pre-cancerous and cancerous tissue.
Gastric cancer is the third most common cause of cancer-related death in the world
and it remains difficult to cure even in the most advanced countries,
mostly because patients typically present with advanced disease.
Mr. Akamatsu's endoscopy provided his medical team with a great deal of information
about what was causing his symptoms.
In addition to widespread inflammation of the gastric epithelium,
the gastroenterologist who performed the procedure
visualized a single gastric ulcer that measured 1.5 centimeters in diameter
in the region of the antrum of the stomach.
During the endoscopy, biopsy specimens were taken from Mr Akamatsu's gastric epothelium,
as well as the ulcer itself. Histological staining of the tissue specimens
confirmed the diagnosis of gastritis secondary to infection with H.pylori,
but there was no evidenceof pre-malignant lesions or malignant transformation.
In fact, most patients that develop antral or duodenal ulcers due to H.pylori,
usually don't go on to develop gastric cancer for unknown reasons.
Mr. Akamatsu was started on triple therapy, with a proton pump inhibitor
to reduce the secretion of acid into the lumen of his stomach,
as well as two anti-microbials to eradicate the H.pylori in his stomach.
This was followed up with eradication testing,
using stool antigen testing four weeks after he had completed his course of therapy.
Mr Akamatsu's symptoms resolved
and he returned to his busy work-travel schedule almost immediately.
Knowing that the H.pylori in his stomach had been eradicated
and that this was most likely the very same microbe
that had caused his father's stomach cancer, Mr. Akamatsu was once again
able to sleep through the night.
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