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.
Herpes Simplex Virus
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来自 Stanford University 的课程
Stories of Infection
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从本节课中
Viral Infections Part 2
In Module Five, we will explore five additional infectious diseases caused by viruses. We will also apply our knowledge of the immune system to explore the use of vaccines, and understand the history of the MMR vaccine. By the end of this module, learners will be able to interpret the clinical presentation of these five infectious diseases and describe the relevant microbiology, pathophysiology, and immunology.
与讲师见面
Maya Adam, MDLecturer
Stanford School of Medicine
Today we're going to be talking about a specific virus,
herpes simplex virus type 2, or HSV-2, that is best known for
causing symptomatic genital infection in about 10% of sexually active individuals.
What's less appreciated is that this virus is responsible for causing lifelong,
often clinically silent infection, in about 20 to 30% of adults.
If this silent infection is present in a pregnant woman, she can inadvertently
infect her baby at the time of delivery with potentially devastating consequences.
This newborn boy named Jack arrived 11 months after his parents were married.
His mother, Carey, had enjoyed a healthy pregnancy and
the delivery had gone smoothly.
Except for
the fact that Carey's obstetrician needed to perform a low forceps delivery
when the infant's heart rate fell during the final stages of birth.
Other than a few small abrasions on Jack's scalp where the forceps had
made contact with his skin, Jack appeared to be a perfectly healthy baby boy.
And the happy parents were able to bring him home within 48 hours of delivery.
At five days of age, Carey brought Jack to their new pediatrician's office for
a well-child visit.
A fourth-year medical student,
who was doing his pediatrics rotation at the clinic that month,
was given the task of performing a preliminary assessment of baby Jack.
During the physical exam,
the medical student noticed some small blisters on the baby's scalp in
the same areas where the forceps had caused minor trauma to the newborn's skin.
In his physical exam notes,
the medical student wrote vesicular rash on scalp, query herpes.
During the pediatrician's examination of baby Jack,
he also noticed the skin lesions on the baby's scalp.
But he suspected that this was a hospital-acquired bacterial infection
like bullous impetigo caused by Staphylococcus aureus.
He instructed the medical student to send a sample of fluid from inside
the blisters to the microbiology lab for gram stain and culture.
After two days, the results came back negative for bacterial infection.
Carey was notified by phone and
she reported that Jack's rash seemed to have resolved and that he was doing well.
Then three weeks later, Jack suffered a grand mal seizure, and
his parents rushed him to the emergency room.
The Physician who examined Jack
had no access to the medical records from his first well-child visit.
After a thorough examination and
an EEG, no identifiable cause could be found to explain the seizure.
So the medical team came to the conclusion
that this must have been a febrile seizure, despite the fact that
Jack's temperature wasn't elevated at the time of his seizure.
After Jack had a second seizure that night,
the infant was started on an anti-epileptic drug and
discharged after 48 hours of being seizure free on the medication.
At 2 months of age, Carey brought her son back to the pediatrician
who had examined him in the On the day of his first seizure.
Carey had noticed small, fluid-filled blisters on Jack's scalp again,
in the exact same location as the rash he'd had when he was just a few days old.
The pediatrician unroofed the blisters and sent the fluid for bacterial and
viral cultures and a PCR test for herpes.
The viral culture and PCR returned positive for
herpes simplex type 2 and confirmed the diagnosis of neonatal herpes.
The herpes simplex viruses are categorized into two types.
HSV-1 most commonly causes sores around the mouth and lips,
sometimes called fever blisters, or cold sores.
While HSV-2 is the most common cause of genital herpes.
Like the general population,
between 20 to 30% of pregnant women are infected with the HSV-2 virus.
And the majority are symptom free and may not even know they're carrying the virus.
Carey was one of these individuals.
HSV-2 can be transmitted in two ways.
Firstly, it can be transmitted horizontally between sexual partners,
most commonly by direct contact with the genitals of an infected individual.
And secondly, the virus can also be transmitted vertically from an infected
mother to her infant.
And this usually occurs when the infant comes into contact with
the virus during passage through the birth canal.
The HSV-2 preferentially infects epithelial cells
located in the mucosa or at sites of abrasion on the skin.
Following entry and colonization of the skin or mucosa,
the virus has evolved to exploit the cell biology of local neurons.
The virus enters and
travels up neuronal axons to local sensory ganglia in the peripheral nervous system.
Where it begins to establish latency in the ganglia
before returning back to the site of initial inoculation.
There the virus replicates, causing cell death and
the development of the small blisters that characterize herpes simplex infection.
But in many cases, the symptoms can be so mild that they may go unnoticed.
During the latent state in the sensory ganglia,
HSV is kept in check by the adaptive immune system.
Which tolerates the presence of the virus
in the immune privileged tissues of the nervous system.
The delicate balance needed to maintain the virus in its latent state
depends on a well-functioning immune system with ongoing immune surveillance.
When the immune system is weakened, the virus can reactivate and
cause symptoms in the infected adults.
But when a newborn like baby Jack is infected with the virus, the newborn's
immune system is too naive to control the infection in the first place.
After entering the body, the virus can disseminate to many organs,
including the central nervous system, causing encephalitis.
An infection of the brain that can lead to serious symptoms like seizures,
irreversible neurological damage, and death.
In Jack's case,
if his HSV infection had been correctly diagnosed at the first well-child checkup,
he could've received treatment with an antiviral medication that would have
prevented unchecked viral replication and the associated neurological damage.
Because the diagnosis of neonatal herpes was missed,
Jack began showing early signs of neurological damage.
And Carey was told that he would likely suffer from serious intellectual
disability.
In this case, the family decided to take legal action.
Newborns are at greatest risk of vertical infection with HSV-2 when
the mother acquires the virus for the first time late in the pregnancy.
This is partly because the mother's immune system doesn't have time to make
antibodies to the virus that could protect the newborn from infection at the time of
delivery.
Women with visible genital HSV-2 lesions at the time of delivery
are usually delivered by cesarean section before the rupture of the membranes,
to reduce the risk of infecting the newborn.
However, since the majority of infected pregnant women have no history
of symptoms or very mild symptoms, HSV-2 is often not suspected.
