Herpes simplex virus

2,821,057views

Herpes simplex virus

Exam 2 - AHN 548

Exam 2 - AHN 548

The flu vaccine: Information for patients and families
Vaccinations
Vaccinations: Clinical
Protein synthesis inhibitors: Aminoglycosides
Antituberculosis medications
Protein synthesis inhibitors: Tetracyclines
Antimetabolites: Sulfonamides and trimethoprim
Miscellaneous cell wall synthesis inhibitors
Cell wall synthesis inhibitors: Penicillins
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Fluoroquinolones
Miscellaneous protein synthesis inhibitors
DNA synthesis inhibitors: Metronidazole
Mechanisms of antibiotic resistance
Bites and stings: Clinical
Antimalarials
Francisella tularensis (Tularemia)
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Hypersensitivity skin reactions: Clinical
Hypersensitivity pneumonitis
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Varicella zoster virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Parvovirus B19
Human papillomavirus
Poxvirus (Smallpox and Molluscum contagiosum)
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Hepatitis A and Hepatitis E virus
Hepatitis D virus
Influenza virus
Mumps virus
Respiratory syncytial virus
Measles virus
Human parainfluenza viruses
Dengue virus
Zika virus
West Nile virus
Yellow fever virus
Hepatitis C virus
Norovirus
Rotavirus
HIV (AIDS)
Human T-lymphotropic virus
Ebola virus
Rabies virus
Rubella virus
Eastern and Western equine encephalitis virus
Lymphocytic choriomeningitis virus
Hantavirus
Prions (Spongiform encephalopathy)
Protease inhibitors
Chlamydia pneumoniae
Chlamydia trachomatis
Coccidioidomycosis and paracoccidioidomycosis
Histoplasmosis
Blastomycosis
Pneumocystis jirovecii (Pneumocystis pneumonia)
Candida
Mucormycosis
Aspergillus fumigatus
Sporothrix schenckii
Cryptococcus neoformans
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Plasmodium species (Malaria)
Babesia
Giardia lamblia
Entamoeba histolytica (Amebiasis)
Cryptosporidium
Acanthamoeba
Naegleria fowleri (Primary amebic meningoencephalitis)
Toxoplasma gondii (Toxoplasmosis)
Trypanosoma brucei
Trypanosoma cruzi (Chagas disease)
Trichomonas vaginalis
Leishmania
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Anti-mite and louse medications
Pediatric lower airway conditions: Clinical
Pediatric infectious rashes: Clinical
Poliovirus
Knowledge Shot: What is acute flaccid myelitis, the polio-like paralyzing disease
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
Enterococcus
Streptococcus agalactiae (Group B Strep)
Streptococcus pneumoniae
Streptococcus viridans
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium tetani (Tetanus)
Clostridium difficile (Pseudomembranous colitis)
Bacillus anthracis (Anthrax)
Corynebacterium diphtheriae (Diphtheria)
Listeria monocytogenes
Infective endocarditis: Clinical
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Salmonella typhi (typhoid fever)
Shigella
Escherichia coli
Vibrio cholerae (Cholera)
Brucella
Yersinia pestis (Plague)
Neisseria gonorrhoeae
Mycobacterium tuberculosis (Tuberculosis)
Treponema pallidum (Syphilis)
Borrelia burgdorferi (Lyme disease)
Leptospira
Streptococcus pyogenes (Group A Strep)

Flashcards

Herpes simplex virus

0 of 25 complete

Questions

USMLE® Step 1 style questions USMLE

0 of 4 complete

Start
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

Watch video only

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.