Herpes Simplex Virus 1 & 2

Herpes simplex virus (HSV) is a double-stranded DNA virus belonging to the family Herpesviridae. Herpes simplex virus commonly causes recurrent infections involving the skin and mucosal surfaces, including the mouth, lips, eyes, and genitals. Typical mucocutaneous infections are characterized by an acute localized appearance of clusters of small, painful vesicles on an erythematous base. Although overlap exists, HSV-1 is classically associated with oropharyngeal lesions, whereas HSV-2 is mostly responsible for genital herpes, an STI. Systemic and severe infections including encephalitis, meningitis, and neonatal herpes may also occur. The diagnosis is made based on clinical presentation and history, which can be confirmed by the microscopic examination of a stained smear of a fresh vesicle, nucleic amplification test using PCR, direct immunofluorescence, or serologic tests. The therapy for mucocutaneous lesions is usually symptomatic, but antiviral therapies involving acyclovir, valacyclovir, or famciclovir are useful if given early, and are always part of the therapy for serious systemic infections.

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Classification

DNA virus classification flowchart

DNA virus identification:
Viruses can be classified in many ways. Most viruses, however, will either have a genome formed by DNA or RNA. Viruses with a DNA genome can be further characterized by whether that DNA is single or double stranded. If the viruses are covered by a thin coat of cell membrane (usually taken from the host cell), they are called “enveloped” viruses. If that coat is absent, the viruses are called “naked” viruses. Some of the enveloped viruses translate their DNA into RNA before it is incorporated into the host cell’s genome.

Image by Lecturio.

General Characteristics and Epidemiology

Basic features of herpes simplex virus

  • Taxonomy:
    • Family: Herpesviridae
    • Subfamily: Alphaherpesvirinae
    • Genus: Simplexvirus
  • DNA virus
    • Double stranded
    • Linear
    • Encodes approximately 70 proteins
  • Structure:
    • Core (contains genome)
    • Icosahedral nucleocapsid
    • Tegument (contains viral proteins and enzymes)
    • Envelope and glycoprotein spikes

Clinically relevant species

Two types have been recognized to cause infections:

  • HSV-1 (tropism for oral epithelium)
  • HSV-2 (tropism for genital epithelium)

Epidemiology

HSV-1:

  • Prevalent worldwide 
  • Affects approximately 66% of the population
  • Seroprevalence: 
    • Individuals 0–49 years of age: 
      • 47% in the US
      • Up to 90% in low-income countries
    • In children in the US:
      • 6–7 years: 26%
      • 12–13 years: 36%
  • No gender preference
  • Becoming more common as a cause of genital herpes
  • Most common cause of acute, nonepidemic viral encephalitis in the US

HSV-2:

  • Prevalent worldwide
  • More common in low-income countries
  • Seroprevalence: 
    • Individuals who are 14–49 years old in the US: approximately 16%
    • Increases with age and the number of sexual partners
    • Gender:
      • Women: 21%
      • Men: 12%
    • Race:
      • Non-Hispanic Blacks: 39% 
      • Non-Hispanic Whites: 12%

Neonatal herpes infection: 

  • A rare complication of maternal genital herpes infection
  • Occurs in about 1 in 3,200 deliveries in the US
  • Most likely to occur in women who acquire primary genital herpes infection and, thus, lack maternal antibodies at or near the time of delivery

Pathogenesis

Reservoir

Humans are the main reservoir.

Transmission

HSV-1:

  • Close contact with oral secretions of individuals who are actively shedding the virus
  • May also be transmitted via unapparent or asymptomatic lesions
  • Can be transmitted through oral sex to uninfected partners

HSV-2:

  • Sexual contact:
    • Risk is higher with male than with female source partners.
    • 70% of successful transmissions occur during periods of asymptomatic viral shedding.
  • Contact with infected secretions
  • Perinatal transmission:
    • Usually occurs during vaginal birth
    • In utero infections can occur in primary infections.

Pathophysiology

Primary infection:

  • Primary infection: 
    • Occurs in individuals with no preexisting antibodies for HSV-1 or HSV-2
    • Different from non-primary 1st-episode: a herpes infection in a patient with preexisting antibodies to the alternate serotype
    • Example: 1st episode of a perioral lesion of HSV-1 in a patient who has preexisting antibodies to HSV-2
      • Patients exhibit attenuated symptoms and signs similar to those in reactivation lesions, with fewer lesions and less severe systemic symptoms.
  • Virus must encounter mucosal surfaces or broken skin (intact skin is resistant). 
  • Virus attaches to and enters epithelial cells through interactions between the viral surface glycoproteins and cellular HSV receptors (e.g., nectin-1).
  • Vesicular lesions of the epidermis are produced → release of infectious virions during the lytic/reproductive phase

Lifetime latency:

  • Definition: the persistence of viral genomes in cells that do not produce infectious virus
  • Viral nucleocapsids are transported along sensory axons to the neuronal cell bodies → establishment of latent infection:
    • Trigeminal ganglia in oropharyngeal infections 
    • Sacral ganglia in genital infections
  • Virus remains latent in the nuclei of nerve cells.
  • Only latency-associated viral RNA transcripts (LATs) are synthesized (no viral proteins are produced). 
  • LATs appear to confer resistance to apoptosis by silencing lytic gene expression through heterochromatin formation, which prevents transcription.
  • HSV avoids cellular and humoral immune recognition by:
    • Inhibiting the class I MHC recognition pathway
    • Producing decoy receptors that bind the Fc domain of Igs and inhibit complement activation
    • Infecting dendritic cells that help in antiviral immune responses

Reactivation:

  • Signifies the transition of a virus from its latent state to lytic replication state in the nerve ganglia
  • The virus moves by anterograde axonal transport to epithelial cells at the original infected site.
  • Replication occurs within epithelial cells:
    • Formation of 1 or more typical clusters of vesicles
    • Can also be clinically unapparent and involve the asymptomatic shed of virions
  • Recurrent eruptions are usually: 
    • Less severe 
    • Occur less frequently over time
  • Occurs in immunocompetent individuals because HSV has multiple immune-evasion mechanisms
  • Factors favoring reactivation/frequency of reactivation:
    • Immunosuppressed states:
      • Transplant recipients
      • Patients with cancer
      • Patients with AIDS who have low CD4 counts (HSV requires intact cellular immunity to be normally contained)
    • Excessive sunlight
    • Febrile illnesses
    • Physical (e.g., dental procedures) or emotional stress 
    • Elderly
    • Unknown stimuli
pathogenesis of HSV-1 and 2 infections Herpes simplex virus

Diagram summarizing the pathogenesis of HSV-1 and -2 infections

Image by Lecturio. License: CC BY-NC-SA 4.0

Pathology

Herpes simplex viruses cause cytolytic infections that form the basis of all pathologic changes: necrosis of infected cells together with the inflammatory response

  • Gross: 
    • Grouped vesicles on an erythematous base
    • Later become pustules and form crusts that heal without scarring because cytopathic effects are limited to the epidermis
  • Microscopic:
    • Infected keratinocytes become multinucleated (from cell fusion) and acantholytic (separated from each other).
    • Distinct intranuclear inclusions (“Cowdry type A inclusions” = viral replication proteins and virions that push chromatin to the edge of the nucleus)
    • Epidermal necrosis or full-thickness acantholysis (causes blistering)
    • Dermal nerve twigs may have acute and chronic perineural inflammation with occasional Schwann cell hypertrophy and frank neuronal necrosis.

Diseases caused by HSV-1

A number of conditions are caused by HSV. The infections listed below are most commonly caused by HSV-1. Note: HSV-2 can also be (though often less commonly) associated with many of these diagnoses.

Asymptomatic infection

Only 20%‒25% of patients with HSV-1 antibodies have a positive clinical history of oral-labial or genital infections.

Oral infections

Gingivostomatitis:

  • Commonly caused in children by a primary infection
  • Signs and symptoms:
    • Fever
    • Painful vesicular lesions:
      • Occur on the oral and pharyngeal mucosa
      • Ulcerate rapidly
    • Gingivitis with extension to the lips and cheeks
    • Pharyngitis
    • Cervical lymphadenopathy
    • Systemic symptoms:
      • Fever
      • Malaise
      • Myalgias

Pharyngitis:

  • Commonly caused in adults by a primary infection
  • Signs and symptoms:
    • Pharyngeal edema and pain
    • Tonsillar exudate
    • Oral lesions:
      • Exudative
      • Ulcerative
    • Cervical lymphadenopathy
    • Systemic symptoms

Herpes labialis:

  • Recurrent reactivation infection
  • Signs and symptoms:
    • Prodrome:
      • Approximately 24 hours before the outbreak, painful lesions develop at the lip border (“vermilion border”).
      • Pain
      • Burning
      • Tingling
      • Pruritus
    • Lesions: 
      • Consist of vesicles or localized oral-labial ulceration (“cold sores” or “fever blisters”)
      • Decrease in pain after 24 hours
      • Healing and crust formation in 5–8 days
    • Rarely associated with systemic symptoms

Genital infection

  • Primary genital HSV-1 infections:
    • Bilateral genital ulcerations
    • Tender lymphadenopathy 
    • Fever 
    • Headache 
    • Myalgias
    • Autonomic dysfunction (urinary retention or constipation)
    • Sensory disturbances (hyperesthesia or anesthesia of the perineum)
  • Reactivation of genital HSV-1:
    • More common in the 1st year after infection 
    • Multiple recurrences are rare (unlike genital HSV-2 infections).

Other cutaneous manifestations

Herpetic whitlow: 

  • Infection of the finger from inoculation of the virus through a break in the skin 
  • Seen in: 
    • Children after autoinoculation
    • Adolescents in association with genital HSV
    • Healthcare personnel (dentists, home healthcare workers)
  • Signs and symptoms:
    • Single or cluster of vesicles:
      • Usually clear with erythematous base → can become turbid
      • Evolve into a shallow ulcer → crust
      • Gradually heal in 2–3 weeks
    • Burning or tingling pain
    • Flu-like symptoms can occur.
    • Differentiate from bacterial infections (paronychia), as surgical incision is not required.

Herpes gladiatorum: 

  • Skin infection of the face, neck, and arms of wrestlers and rugby players
  • Vesiculopustular rash → ulceration

Erythema multiforme: 

  • Immune-mediated disorder 
  • Signs and symptoms:
    • Cutaneous target lesions 
    • Mucosal erythema and erosions or bullae (painful)

Eczema herpeticum: 

  • HSV-1 infection superimposed on skin lesions from atopic dermatitis (particularly in patients on immunosuppressive therapy)
  • Signs and symptoms:
    • Pain and vesicular skin lesions
    • Can spread rapidly if untreated

Eye infections

Eye infections occur in < 5% of patients with HSV-1 infections, leading to vision loss and/or blindness.

Keratitis:

  • Infection of the corneal epithelium
  • Leading cause of corneal blindness in high-income countries 
  • Signs and symptoms:
    • Pain 
    • Foreign-body sensation
    • Visual blurring 
    • Tearing
    • Chemosis 
    • Conjunctivitis 
    • ↓ Corneal sensation 
    • Characteristic dendritic lesions of the cornea: 
      • Corneal ulcer with a branching pattern
      • Seen on slit-lamp examination
  • Recurrent infections are common. 
  • Stromal scarring can result.

Acute retinal necrosis:

  • Rare, potentially blinding, necrotizing retinitis 
  • Occurs in: 
    • Immunocompetent hosts
    • Pregnant women
    • Patients with an HIV infection
  • Signs and symptoms:
    • ↓ Vision 
    • Eye redness
    • Floaters
    • Photophobia
    • Some patients may have periorbital pain.

Conjunctivitis and blepharitis:

  • Unilateral
  • Vesicles on the lid margin 
  • Chemosis 
  • Edema of the eyelids 
  • Tearing

Chorioretinitis (posterior uveitis)

  • From disseminated HSV infections 
  • Seen in neonates or immunosuppressed individuals
  • Signs and symptoms:
    • Blurred, distorted, or loss of vision
    • Scotoma
    • Floaters

Neurologic syndromes

Encephalitis:

  • Usually unilateral, involving the temporal lobe and insular cortex (board exam question)
  • High rate of morbidity and mortality
  • Signs and symptoms:
    • Fever
    • Headache
    • Seizures
    • Focal neurologic signs
    • Impaired consciousness

Aseptic meningitis:

  • More commonly associated with HSV-2 infections
  • Signs and symptoms:
    • Fever
    • Headache
    • Photophobia
    • Meningismus

Other manifestations:

  • Bell’s palsy: temporary inability to control the facial muscles on the affected side of the face
  • Autonomic dysfunction: presents as urinary retention during a primary genital infection
  • Transverse myelitis: a demyelinating inflammation of both sides of 1 section of the spinal cord

Respiratory tract infections

Epiglottitis or laryngitis (herpetic croup): 

  • May occur in children
  • Self-limiting condition
  • Signs and symptoms: 
    • Nonproductive cough
    • Stridor 

HSV pneumonitis:

  • Rare
  • Usually occurs in immunocompromised patients
  • Considered an AIDS-defining condition
  • Occurs following tracheobronchitis
  • Signs and symptoms:
    • Dyspnea
    • Cough
    • Fever
    • Wheezing

Gastrointestinal disease

HSV esophagitis:

  • Usually seen in immunocompromised hosts
  • Considered an AIDS-defining condition 
  • Spread by either: 
    • Direct extension from the oropharynx 
    • Reactivation and spread through the vagus nerve to the mucosa
  • Signs and symptoms: 
    • Odynophagia 
    • Dysphagia 
    • Retrosternal chest pain 

Fulminant hepatitis: 

  • Rare 
  • Associated with disseminated disease
  • Caused by both HSV-1 and HSV-2
  • Only 30% of patients have typical skin lesions.

Diseases Caused by HSV-2

The conditions listed below are most commonly associated with HSV-2 infections. Again, keep in mind that HSV-1 can also be associated with many of these diagnoses.

Genital infection

Primary genital HSV-2 infections:

  • Average incubation period: 4 days (range 2–12 days)
  • Viremia is more common (24%) than in reactivation cases. 
  • Can be asymptomatic, or present with mild or severe symptoms:
    • Painful genital ulcers:
      • Clusters of 2–4-mm vesicles containing clear fluid
      • Become pustules that rupture → erosions or superficial ulcers with scalloped borders
      • Heal without scarring
    • Dysuria
    • Fever
    • Tender local inguinal lymphadenopathy
    • Headache 

Non-primary 1st episode infection (reactivation): 

  • Frequency of recurrences:
    • Earlier and more frequent recurrences if the primary infection had lasted > 5 weeks
    • More common with HSV-2 than HSV-1
    • More common in immunosuppressed patients
  • Signs and symptoms:
    • May be symptomatic or asymptomatic
    • Prodrome: mild tingling or shooting pains in the buttocks, legs, and hips
    • Fewer lesions and less severe systemic symptoms
Penile blisters herpes simplex-2

Penile blisters (arrows) due to a recurring herpes simplex-2 virus (HSV-2) infection

Image: “Penile blisters (arrows), due to a recurring herpes simplex-2 (HSV-2) virus infection” by CDC/ Susan Lindsley. License: Public Domain

Extragenital manifestations

  • Aseptic meningitis
  • Benign recurrent aseptic meningitis (Mollaret’s meningitis):
    • > 3 episodes of meningitis symptoms
    • Followed by spontaneous resolution
  • Sacral ANS dysfunction: causes urinary retention
  • Sacral radiculitis: 
    • Acute urinary retention with loss of sacral sensation
    • Occurs in severe primary infections
    • Transient, but requires catheterization
  • Hepatitis
  • Proctitis: more common in men who have sex with men (MSM)

Diagnosis

  • PCR:
    • Preferred method of diagnosis
    • Can be used to detect viral DNA
    • Can be used to identify HSV serotypes
    • Extremely high sensitivity (98%) and specificity (99%) 
    • Positive findings early in the course of illness 
    • Samples can be obtained from:
      • Unroofed vesicular lesions
      • Intraocular fluid (acute retinal necrosis)
      • Urethral, rectal, or cervical swabs
      • CSF 
      • Blood (useful for fulminant neonatal infections, hepatitis)
  • Viral cultures: 
    • Less sensitive than PCR
    • Depends on the quantity of virus
  • Tissue biopsy: 
    • Sites:
      • Skin
      • Lung
      • Liver
      • Esophagus
    • Can be diagnosed based on histologic appearance and confirmed using immunohistochemical or molecular methods
  • Tzanck smear:
    • Procedure:
      • Specimen is obtained by scraping the base of a vesicle.
      • Specimen is placed on a slide. 
      • Stained with Giemsa or toluidine blue
      • Typical cytopathic effects of HSV are observed.
    • Will show multinucleated giant cells
    • Low sensitivity and specificity
    • Cannot differentiate between HSV serotypes
  • Direct fluorescent antibody testing:
    • Rapid
    • Low sensitivity and specificity
  • Serologic testing: 
    • Limited applications
    • Titers do not correlate with positive cultures or the presence of lesions.
Image from a Tzanck smear Herpes simplex virus

Image from a Tzanck smear obtained from a penile lesion:
Multinucleated giant cells are seen, indicating a herpes infection.

Image: “Photomicrograph depicts a Tzanck stained penile lesion specimen” by CDC/ Joe Miller. License: Public Domain

Management

Medical therapy

Antivirals:

  • Mechanism of action: nucleoside derivatives that interfere with the synthesis of viral DNA by inhibiting viral DNA polymerase
  • Renal function should be monitored.
  • Uses:
    • Depends on severity (may not be needed for mild or minimally symptomatic infections)
    • Treatment of an active infection
    • Episodic therapy (started at the very 1st sign of prodromal symptoms)
    • Chronic suppression (for frequent or severe recurrences)
    • Reduces but does not eliminate viral shedding
  • Systemic options:
    • Acyclovir
    • Valacyclovir
    • Famciclovir
  • Topical options (for ocular infections):
    • Acyclovir
    • Ganciclovir
    • Trifluridine (more corneal toxicity)

Analgesics:

  • Lidocaine
  • Benzocaine

Immunosuppressed patients

  • Immunosuppressed patients may have more severe symptoms, higher risk of complications, and greater risk for developing drug-resistant HSV infections.
  • Treated with similar regimens as immunocompetent patients, but with higher doses for suppressive therapy
  • Patients who are HIV positive and not on antiretroviral therapy (ART) may be prone to immune reconstitution inflammatory syndrome (IRIS) when treated for HSV infections.
    • Clinical manifestations worsen initially after the initiation of ART.
    • Suppressive therapy may be given to prevent IRIS.

Prevention of new HSV infections

  • Herpes labialis: 
    • Avoid contact with saliva or saliva-contaminated fomites from family members and intimate partners (e.g., avoid kissing and sharing kitchen utensils and towels).
    • Healthcare workers: 
      • Universal precautions
      • Wear gloves during physical examination of a patient with active HSV lesions.
      • Eye and mouth protection when suctioning or during bronchoscopy
  • Genital herpes:
    • Barrier use for oral and genital sex is recommended.
    • Note: Precautions should be taken by pregnant partners who are HSV negative owing to the high risk of transmission to the neonate.
  • Herpes gladiatorum: 
    • Athletes must not participate in contact sports until all herpes lesions are in the dry, crust stage. 
    • Suppressive oral antiviral therapy has been suggested for all wrestlers regardless of HSV history, as it markedly reduces the risk of an outbreak (by 85%).

Comparison of Herpesviruses

The table presented below compares and contrasts HSV-1 and HSV-2:

Table: Comparision of herpes simplex viruses
SerotypeHSV-1HSV-2
Transmission
  • Respiratory secretions, saliva
  • Ubiquitous
  • 90% in childhood
  • Sexual contact, perinatal
  • 30% in adulthood
Lytic infectionMucoepithelial cellsMucoepithelial cells
LatencyTrigeminal gangliaSacral ganglia
Diseases
  • Gingivostomatitis
  • Herpes labialis
  • Keratitis
  • Conjunctivitis
  • Herpetic whitlow
  • Encephalitis
  • Hepatitis
  • Esophagitis
  • Pneumonitis
  • Herpes genitalis
  • Neonatal herpes
  • Aseptic meningitis
  • Proctitis

Comparison of viruses in the Herpesviridae family

The table below compares the 9 herpesviruses considered endemic in humans. There are 115 different total known species of herpesviruses, which are grouped into 3 families: 

  • Alpha (infect epithelial cells and produce latent infection in post-mitotic neurons)
  • Beta (infect and produce latent infection in various cell types)
  • Gamma (produce latent infection mainly in lymphoid cells)
Table: Comparison of the 9 herpesviruses considered endemic in humans
HHVCommon namePrimary target cellsLatency siteClinical presentation*
1
(alpha group)
HSV-1 Mucoepithelial cells Dorsal root ganglia
  • Gingivostomatitis
  • Keratitis
  • Herpetic whitlow
  • Encephalitis
  • Hepatitis
  • Esophagitis
  • Pneumonitis
2
(alpha group)
HSV-2
  • Genital herpes
  • Meningitis
  • Proctitis
3
(alpha group)
VZV
  • Chickenpox
  • Herpes zoster
4
(gamma group)
EBV
  • Epithelial cells
  • B cells
Memory B cells
  • Infectious mononucleosis
  • Hodgkin lymphoma
  • Burkitt lymphoma
  • Oral hairy leukoplakia
  • EBV-associated gastric cancer
5
(beta group)
CMV
  • Monocytes
  • Lymphocytes
  • Epithelial cells
Hematopoietic progenitor cells in bone marrow
  • CMV mononucleosis
  • CMV retinitis
  • CMV colitis
  • CMV encephalitis
6A, 6B
(beta group)
HHV-6 T cells Monocytes Roseola
7
(beta group)
HHV-7 T cells
8
(gamma group)
Kaposi’s sarcoma-associated herpesvirus
  • Lymphocytes
  • Epithelial cells
B cellsKaposi sarcoma
*Bold in “clinical presentation” column: AIDS-defining illnesses
VZV: varicella zoster virus

Differential Diagnosis

  • Recurrent aphthous ulcers (canker sores): a very common, probably immunologically related disease of the oral mucosa (and less commonly, the genital mucosa), manifesting as small, discrete, painful ulcers that heal within 1–2 weeks. Recurrent aphthous ulcers are not preceded by vesicles and occur only on mucosal surfaces. Diagnosis is clinical, although testing can be conducted to evaluate for associated conditions (e.g., nutritional deficiencies, inflammatory bowel disease). Management includes trigger avoidance, symptomatic therapy, and treatment of underlying etiologies.
  • Syphilis: a bacterial infection caused by the spirochete Treponema pallidum, which is usually spread through sexual contact. Primary syphilis can present with hard chancres that initially present as small red patches. Unlike the vesicles in HSV infections, these chancres (vesicles are absent) are painless. Diagnosis is made with serology, dark-field examination, and immunostaining on biopsy. Penicillin G is the antibiotic of choice.
  • Chancroid: an STI caused by Haemophilus ducreyi. Patients develop painful necrotizing genital ulcers and inguinal lymphadenopathy. Diagnosis is usually clinical, but PCR and cultures can be used for confirmation. Management is with macrolide antibiotics.
  • Other genital, anal, or perianal ulcers: noninfectious causes that are not STI related: yeast, trauma, carcinoma, aphthae, fixed drug eruption, and psoriasis.
  • Bacterial pharyngitis: an infection of the pharynx. Patients typically experience a sore throat and fever. Symptoms are not preceded by a grouped cluster of vesicles as those seen in HSV infections. Diagnosis can include rapid streptococcal screens to detect group A Streptococcus, bacterial cultures, and PCR to exclude HSV infections. Treatment includes penicillin or amoxicillin.
  • Enterovirus infections (e.g, herpangina): acute febrile illnesses mostly caused by coxsackievirus A and B, and enterovirus 71. Herpangina is associated with small vesicular or ulcerative lesions on the posterior oropharyngeal structures (enanthem). Clinical findings and PCR are used to make the diagnosis. Management is symptomatic.
  • Infectious mononucleosis: an infection caused by another herpesvirus, the EBV. Clinical manifestations include fever, tonsillar pharyngitis, and lymphadenopathy. Unlike HSV infections, mononucleosis is not usually associated with clusters of vesicles. Diagnosis is clinical and confirmed using heterophile antibody testing or serology. Management is supportive.
  • Stevens-Johnson syndrome (SJS): a rare, potentially lethal disease that attacks the skin and mucous membranes. Stevens-Johnson syndrome runs on a spectrum with the more severe form (toxic epidermal necrolysis (TEN)) and can be triggered by a reaction to a medication or to a preexisting bacterial or viral infection (including HSV) or illness. Patients present with a flu-like prodrome and the appearance of cutaneous bullae, followed by sloughing on the face, thorax, and mucous membranes. Diagnosis is clinical and the management is largely supportive.
  • Bacterial skin infections with superficial ulceration: infections that can mimic herpetic whitlow. Bacterial skin infections with superficial ulceration are not preceded by a vesicle and often involve subepidermal tissues. It is important to differentiate these conditions, as antibiotics and drainage are not necessary for herpetic whitlow.
  • Proctitis: besides HSV infections, the differential diagnosis in MSM includes Neisseria gonorrhoeae, Chlamydia, and T. pallidum infections. The presentation of proctitis can mimic inflammatory bowel disease. Diagnosis is by PCR, cultures, serology, dark-field examination, and immunostaining on biopsy.

References

  1. Wald, A., Johnston, C. (2020). Treatment and prevention of herpes simplex virus type 1 in immunocompetent adolescents and adults. UpToDate. Retrieved February 1, 2021, from https://www.uptodate.com/contents/treatment-and-prevention-of-herpes-simplex-virus-type-1-in-immunocompetent-adolescents-and-adults
  2. Miller, S. (2019). Herpesviruses. In Riedel, S, Morse, S.A., Mietzner, T., Miller, S. (Eds.), Jawetz, Melnick, & Adelberg’s Medical Microbiology, 28th ed, pp. 473–482.
  3. Corey, C. (2018). Herpes Simplex Virus Infections. In Jameson, J.L., et al. (Ed.), Harrison’s Principles of Internal Medicine, 20th ed. Vol 1, pp. 1345–1354.
  4. Frank, K.M., McAdam, A.J. (2020). Infectious Diseases. In Kumar, V., Abbas, A.K., Aster, J.C., (Eds.). Robbins & Cotran Pathologic Basis of Disease, 10 ed. pp. 354–355.
  5. Johnston, C., Wald, A. (2019). Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection. In Mitty, J. (Ed.), UpToDate. Retrieved May 24, 2021, from https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-simplex-virus-type-1-infection
  6. Saleh, D., Yarrarapu, S.N.S., Sharma, S. (2021). Herpes simplex type 1. [online] StatPearls. Retrieved May 24, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK482197/
  7. Mathew, Jr, J., Sapra, A. (2021). Herpes simplex type 2. [online] StatPearls. Retrieved May 24, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK554427/
  8. Ayoade, F.O., Balan, S., Todd, J.R. (2021). Herpes simplex. In Bronze, M.S. (Ed.), Medscape. Retrieved May 24, 2021, from https://emedicine.medscape.com/article/218580-overview

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