Herpes simplex virus

Last updated: February 23, 2023

Herpes simplex virus

Pregnancy, childbirth, and the puerperium

Pregnancy, childbirth, and the puerperium

Preconception care: Clinical sciences
Antepartum fetal surveillance: Clinical sciences
Fetal aneuploidy screening: Clinical sciences
Maternal D alloimmunization (prevention): Clinical sciences
Antepartum care (first trimester): Clinical sciences
Antepartum care (second trimester): Clinical sciences
Antepartum care (third trimester): Clinical sciences
Cytomegalovirus (CMV), parvovirus B19, varicella zoster, and toxoplasmosis infection in pregnancy: Clinical sciences
Group B streptococcus (GBS) colonization in pregnancy: Clinical sciences
Herpes simplex virus infection in pregnancy: Clinical sciences
Abdominal trauma in pregnancy: Clinical sciences
Anemia in pregnancy: Clinical sciences
Approach to acute pelvic pain (GYN): Clinical sciences
Approach to diabetes in pregnancy: Clinical sciences
Approach to first trimester bleeding: Clinical sciences
Approach to hypertensive disorders in pregnancy: Clinical sciences
Approach to third trimester bleeding: Clinical sciences
Cholestasis of pregnancy: Clinical sciences
Diabetes in pregnancy (GDM, T1DM, and T2DM): Clinical sciences
Early pregnancy loss: Clinical sciences
Ectopic pregnancy: Clinical sciences
Fetal growth restriction: Clinical sciences
Gestational hypertension, preeclampsia, eclampsia, and HELLP: Clinical sciences
Hemoglobinopathies in pregnancy: Clinical sciences
Intraamniotic infection: Clinical sciences
Maternal D alloimmunization (management): Clinical sciences
Multifetal gestation: Clinical sciences
Nausea and vomiting of pregnancy: Clinical sciences
Placenta accreta spectrum: Clinical sciences
Placenta previa and vasa previa: Clinical sciences
Placental abruption: Clinical sciences
Therapeutic and induced abortions: Clinical sciences
Induction of labor: Clinical sciences
Intrapartum care (1st, 2nd, 3rd, and 4th stages): Clinical sciences
Intrapartum fetal heart rate monitoring: Clinical sciences
Late-term and postterm pregnancy: Clinical sciences
Pain management during labor: Clinical sciences
Prelabor rupture of membranes: Clinical sciences
Preterm labor: Clinical sciences
Protraction and arrest disorders: Clinical sciences
Shoulder dystocia: Clinical sciences
Vaginal birth after cesarean (VBAC): Clinical sciences
Approach to postpartum fever: Clinical sciences
Approach to postpartum hemorrhage: Clinical sciences
Perinatal depression and anxiety: Clinical sciences
Uterine atony: Clinical sciences
Immediate care of the well newborn: Clinical sciences
Approach to a rash in the well newborn and infant: Clinical sciences
Approach to anemia in the newborn and infant (destruction and blood loss): Clinical sciences
Approach to anemia in the newborn and infant (underproduction): Clinical sciences
Approach to birth injury (pediatrics): Clinical sciences
Approach to complications of prematurity (early): Clinical sciences
Approach to complications of prematurity (late): Clinical sciences
Approach to congenital infections: Clinical sciences
Approach to cyanosis (newborn): Clinical sciences
Approach to hypotonia (newborn and infant): Clinical sciences
Approach to jaundice (newborn and infant): Clinical sciences
Approach to respiratory distress (newborn): Clinical sciences
Approach to vomiting (newborn and infant): Clinical sciences
Neonatal respiratory distress syndrome: Clinical sciences
Alcohol, tobacco, cannabinoid, and substance use in pregnancy: Clinical sciences
Approach to prenatal teratogen exposure: Clinical sciences
Asthma in pregnancy: Clinical sciences
Chronic hypertension in pregnancy: Clinical sciences
Urinary tract infections and kidney stones in pregnancy: Clinical sciences
Venous thromboembolism in pregnancy: Clinical sciences
Anatomy clinical correlates: Female pelvis and perineum
Chlamydia trachomatis
Neisseria gonorrhoeae
Streptococcus agalactiae (Group B Strep)
Treponema pallidum (Syphilis)
Toxoplasma gondii (Toxoplasmosis)
Cytomegalovirus
Hepatitis B and Hepatitis D virus
Herpes simplex virus
HIV (AIDS)
Influenza virus
Parvovirus B19
Rubella virus
Varicella zoster virus
Congenital TORCH infections: Pathology review
Complications during pregnancy: Pathology review
Estrogens and antiestrogens
Progestins and antiprogestins
Uterine stimulants and relaxants

Flashcards

Herpes simplex virus

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Questions

USMLE® Step 1 style questions USMLE

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A 45-year-old man presents to the emergency department due to intense headaches and difficulty with bright lights. The patient developed new genital lesions about a week ago. Brain imaging shows no abnormalities. Lumbar puncture is performed, and the CSF profile shows pleocytosis with a predominance of lymphocytes and a normal CSF glucose concentration. Which is the most likely cause of this patient’s condition?  

Transcript

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Most of the time, when herpes simplex virus or HSV infects a person, there are no symptoms.

In fact, it also usually moves from one person to another in the absence of symptoms, so it can therefore it can move through a population silently.

Once in a while, though, it can cause symptoms, and typically those are in the form of skin and mucous membrane lesions which can be divided into infections “above the waist”—mostly involving the mouth and tongue, and those “below the waist”—involving the genitals.

There are two types of herpes simplex viruses—HSV1 and HSV2—both of which are part of a larger family of enveloped double-stranded DNA viruses: the herpesviridae family.

Generally speaking, HSV1 tends to cause infections above the waist and HSV2 tends to cause infections below the waist, but there’s a lot of crossover because both viruses can cause both types of infections.

Although herpes is most contagious when there are virus-filled lesions present, it can also spread by asymptomatic shedding which means that herpes viruses can be in saliva or genital secretions even when there are no signs of a cold sore or genital lesion.

Typically, when herpes virus lands on a new host, in other words a person that’s never had herpes before, it dives into small cracks in the skin or mucosa and binds to epithelial cell receptors, which triggers those cells to internalize the virus.

Once inside, the virus starts up the lytic cycle, which is where its DNA gets transcribed and translated by cellular enzymes which help to form viral proteins which are packaged into new herpes viruses which can leave to go off and infect neighbouring epithelial cells.

HSV1 and HSV2 also infect nearby sensory neurons, and travel up their axon to the neuron’s cell body to start up the latent cycle.

The sensory neurons of the face have their cell bodies in the trigeminal nuclei and those around the genitalia are located in the sacral nuclei.

So that’s ultimately where the herpes virus settles in—for life!

You see, the sensory neurons aren’t destroyed, instead, they become a permanent home for the herpes virus, and from time to time, the herpes virus makes a few viral copies of itself and sends those virus particles back down the axon so they can get released and infect epithelial cells.

Since the trigeminal and sacral nuclei serve just one side of the face or body, herpes vesicles and ulcers develop on the ipsilateral or same side as the affected nuclei.

This can happen over and over again throughout a person’s lifetime, with classic triggers being things like stress, skin damage, and viral illnesses.

Recurrent episodes are usually less severe than the primary infection, and sometimes there are no symptoms at all.

When there are symptoms, there might be a characteristic tingling or burning sensation, called a prodrome, one or two days before the blisters appear.

In oral and genital herpes, the primary infection is most often asymptomatic.

Having said that, in oral herpes when it does cause symptoms it usually affects children and it causes lesions on the palate, gums, tongue, lip, and facial area, as well as a fever and enlarged lymph nodes.

The lesions themselves are typically clusters of small, painful, fluid-filled blisters, that ooze and ulcerate, and then eventually heal after a few weeks.

In older children and adults, a common symptom is pharyngitis.

Most of the time, like primary infection, reactivation doesn’t cause any symptoms, but when it does, the most common pattern is having a handful of blisters at the vermillion border—the border of the lip—on one side of the face.

These blisters are typically smaller and heal over a week.

With genital herpes, primary infection can cause symptoms like ulcers and pustules which form on the labia majora, labia minora, mons pubis, vaginal mucosa, and cervix in women and on the shaft of the penis in men.