SEXUALLY TRANSMITTED DISEASES (STD) : Gonorrhea

Discussion
a. Etiology. Gonorrhea is caused by Neisseria gonorrhoeae .
b. Incidence. The highest incidence is in men between the ages of 20 and 24 years.

Clinical features
a. Local disease

i. Acute urethritis is the most common presentation in heterosexual men. Symptoms begin within 1 to 14 days of exposure and consist of dysuria and penile discharge. Three to ten percent of men with gonorrhea may be asymptomatic.
ii. Cervicitis. Primary gonorrhea in women is usually asymptomatic , and when symptoms do occur, they are usually mild and nonspecific. Up to 20% of women with primary gonorrhea develop pelvic inflammatory disease , and 33% to 81% of women with pelvic inflammatory disease have gonorrhea.
iii. Pharyngeal gonorrhea can be asymptomatic . The pharynx is colonized in 3% to 7% of heterosexual men, 5% to 20% of women, 10% to 25% of homosexual men and 39% to 96% of pregnant women.
iv. Anorectal gonorrhea is common in both heterosexual women and homosexual men and is often asymptomatic . When symptoms occur, they are usually mild pruritus and rectal discomfort .

b. Disseminated

Gonorrhea may complicate the disease course in 1% to 3% of patients with localized disease and is manifested most commonly as a monoarticular arthritis or pustular dermatitis syndrome .

Differential diagnoses

a. Gonococcal urethritis must be differentiated from nongonococcal urethritis caused by Chlamydia trachomatis .
b. Disseminated gonorrhea. N. meningitidis infection, acute rheumatic fever, and Reiter syndrome must be ruled out. Differential diagnoses for skin lesions include syphilis, HIV infection, and condyloma acuminata.
Evaluation. Gram stain and culture of discharges are the cornerstone of diagnosis. All patients evaluated for gonorrhea should also have blood drawn for syphilis serology.

Therapy

For uncomplicated cervicitis or urethritis:
a. Ceftriaxone (250 mg intramuscularly) and doxycycline (100 mg orally twice daily for 14 days, to cure possible concomitant Chlamydia infection) are the standard therapy.
b. Cefixime (400 mg orally in a single dose) is no longer an accepted alternative due to resistance.
c. Azithromycin, 2 g one-time dose, is an alternative for cephalosporin allergic patients.

Disposition

a. Uncomplicated gonorrhea is managed on an outpatient basis. All sexual contacts must be identified and treated, and HIV testing should be considered by the patient with his or her primary physician at a later date.
b. Patients with disseminated gonorrhea require hospitalization.

Management Snake Bites – Indication For Antivenom

DEFINITION

Injury resulting from snake biting a human.



TREATMENT

ACUTE GENERAL Rx

IN THE FIELD: For a suspected snakebite:

  • Transport immediately to nearest medical facility. No treatments in the field should delay travel to the nearest facility where an antivenom agent can be given if necessary.
  • Immobilize affected part below level of the heart.
  • Remove any constricting items. In cases of known elapid bites, compression has been advocated, especially in Australia, as a means of delaying neurotoxins, but use by those without specialized training is discouraged. However, crotalid bites are far more common in the U.S., and these frequently have tissuenecrosing venom, which will yield more damage with local pressure.
  • Do not apply ice; keep victim warm.
  • Avoid alcohol, stimulants (caffeine), or agents that can suppress mental status.

IN THE HOSPITAL:

  • Record vital signs: BP, HR, T, RR, and O2 sat
  • Establish intravenous access.
  • Obtain time of bite and description of snake if possible. Crotalids have a triangle-shaped head, nostril holes (pits), and elliptical pupils. The most dangerous of the crotalids is the rattlesnake, distinguished by its telltale rattle. Elapids, like the western and eastern coral snakes of the U.S., have brightly colored red, black, and yellow stripes.
  • Obtain and initiate reconstitution of appropriate antivenom. (Antivenoms are typically supplied in powder form and must be reconstituted before administration. If using older antivenoms, this process can take up to 1 hr, so it is recommended that it be initiated as soon as the patient arrives in the ED.)

C. Inspect site of bite for fang marks and local symptoms.

C. Delineate margins of erythema/edema with a marker.

C. Measure circumference of bitten part at two or more proximal sites and compare with unaffected limb; repeat every 15 to 20 min; assess for extension of erythema/ edema.

C. Conduct a neurologic examination.

C. Obtain past medical history; ask about allergies  to horse serum in those previously treated for snakebite.

  • If no signs of envenomation:
  1. Clean and immobilize affected part.
  2. Immunize against tetanus.
  3. For crotalid bites, observe patient for at least 8 hr. If, at the end of this interval, local and systemic sequelae are absent and lab values remain normal, the likelihood of significant envenomation is low, and the patient can be discharged from the acute setting. All definitive elapid bites should be treated. If elapid bite is only suspected, the patient must be monitored for up to 18 hr as symptoms can be delayed.

  • Patients who have progressive local symptoms or any systemic symptoms should be considered for antivenom. Crotalid envenomations without any progressive local or any systemic symptoms can be monitored for 12 to 24 hours, with repeat labs obtained 4 to 6 hours prior to discharge. If they have no new symptoms during that period of observation, they may be safely discharged. In  particular, copperhead bites often need no further interventions.

Once the decision is made to use antivenom:

  • Prepare epinephrine 0.5 to 1.0 mg (0.5-1 ml of a 1:1000 solution) to be administered subcutaneously (SQ) in case of a hypersensitivity reaction to the antivenom. The incidence of hypersensitivity reaction with sheep-based antivenom, now standard for crotalid envenomations, is estimated to be less than 0.15. This is much lower than that with horse serum antivenom previously used for crotalid and currently the standard for elapidad envenomations. Empiric prophylactic antihistamines or epinephrine have not been proved to prevent reactions.

ANTIVENOM TREATMENT OF CROTALID (RATTLESNAKE, PIT VIPER, COPPERHEAD, COTTONMOUTH)  ENVENOMATIONS:

  • Most centers now have sheep immunoglobulin– based antivenom (Crofab) for crotalid bites.

C. An initial IV loading dose of 4 to 6 vials (depending on the size and age of the patient and the severity of the bite) is infused over 60 min. The infusion should be given very slowly for the first 10 min to watch for allergic reaction. For patients with shock or serious active bleeding, use an intial dose of 8 to 12 vials.

C. If the patient has not responded after 1 hr, repeat the initial dose.

  • Relapse may occur in up to two thirds of patients after an initial response. Consequently, it is recommended that three maintenance doses—each consisting of 2 vials—be given at 6, 12, and 18 hr following the patient’s initial response to the loading dose.
  • The manufacturer of Crofab maintains a 24/7 hotline: 877-377-3784
  • Antivenin Crotalidae Polyvalent horse serum is no longer produced but may still be available at some pharmacies. It should be given as follows:

C. Progressive local or any systemic symptoms: 5 to 10 vials

C. Severe symptoms: 15 vials

C. Shock: 20 vials

TREATMENT OF NONNATIVE (EXOTIC) SNAKEBITES:

  • For bites by exotic or nonnative snakes, contact a Poison Control Center or your local zoo. (Zoos with exotic snakes are required to maintain a supply of snake-specific antivenom on their premises.)

Verrucae (Warts)

Warts are small, rough lumps or growths on your skin caused by the human papilloma virus (HPV). You can get them anywhere, but warts are most common on your hands, knees and feet.

Transmission is via direct contact, shared showers, or locker room floors.

SYMPTOMS. Plantar warts are sharp, well-defined hyperkeratotic lesions, either single or in clusters, with a smooth collar of thickened keratin. Plantar warts are painful as they grow inward because they exist on the plantar weight-bearing surface of the feet. Verrucae vulgaris are firm, rough papules or nodules that are 2–10 mm in diameter with punctate black dots within the lesion and appear on the rest of the body.

TREATMENT. Respond to numerous modalities; plantar warts may be treated with 30%–70% trichloroacetic acid, 40% salicylic acid, or taping with salicylic tape or duct tape for several days. Verrucae vulgaris may be treated with repeated cryotherapy with liquid nitrogen, 1% salicylic acid or lactic acid, or curettage with electrodessication.

PREVENTION. Routine usage of protective rubber slides/flip-flops in public showers or locker rooms.

Snake Bites – How Do You Treat A Snake Bites

Suspected Snake bites?

Injury resulting from snake biting a human.

Physical Finding and Clinical Presentation

  • In addition to local tissue injury, envenomation may affect the renal, neurologic, gastrointestinal, vascular, and coagulation systems. Symptoms vary widely depending on type of envenomation. Not all snakebites are poisonous, and not all bites lead to envenomation. Species-specific signs and symptoms following envenomation are discussed.

CROTALIDAE (PIT VIPERS)

Local Signs and Symptoms

 

  • Pain within 5 min
  • Edema within 30 min
  • Erythema of site and adjacent tissues/serous or hemorrhagic bullae, ecchymosis, and/or lymphangitis over the ensuing hours

If no edema or erythema is manifested within 8 hr after a confirmed crotalid snakebite, it is safe to assume envenomation did not occur. (Roughly 25% of cases do not involve envenomation.) In general, rattlesnake bites are more severe than those of the other snakes in the Crotalidae family.

Systemic manifestations may include:

  • Mild to moderate nausea/vomiting, perioral paresthesias, metallic taste, tingling of fingers or toes (especially with rattlesnake bites), and/or fasciculations (local or generalized)
  • Severe hypotension (due to increased vascular permeability), mental status change, respiratory distress, tachycardia, acute renal failure, rhabdomyolysis, and coagulopathies including intravascular hemolysis and disseminated intravascular coagulation.

ELAPIDAE (CORAL SNAKES):

  • Local symptoms are far less pronounced (little or no pain/swelling immediately after the bite).
  • Neurologic symptoms are more common due to neurotoxins in elapid venom.
  • Systemic symptoms predominate, but onset may be delayed for up to 12 hr. Examples include:
    1. Altered mental status and cranial nerve palsies featuring ptosis, dysphagia, or dysarthria
    2. Tremors
    3. Intense salivation, nausea, vomiting, or abdominal pain
    4. Loss of DTRs and respiratory depression (late manifestations)

Differential Diagnosis

  • Harmless snakebite
  • Scorpion bite
  • “Dry bite”
  • Insect bite
  • Cellulitis
  • Laceration or puncture wound
  • Necrotizing fasciitis

Workup

  • An estimated 25% of venomous snakebites do not result in envenomation, but all cases of suspected envenomation should be observed for 8 hr or longer
  • Check for signs of envenomation.
    1. Swelling, tenderness, redness, ecchymosis, or blebs at the bite site
    2. Elevated protime, decreased fibrinogen or platelets
    3. Systemic signs such as hypotension, bleeding complications, vomiting, diarrhea, angioedema, or neurotoxicity
  • Determine if patient has indications for antivenom. Continual reassessment is indicated throughout the observation period because severity of symptoms may change.

Laboratory Tests

  • For all suspected envenomations, obtain CBC (with peripheral smear and platelet count), DIC screen (PT/INR, PTT, fibrinogen, fibrin degradation products, d-dimer), ECG, serum electrolytes, BUN, Cr, and urinalysis. Serial measurements of hemoglobin, platelets, protime, and fibrinogen are needed to monitor for acute and delayed hematologic complications.
  • For more severe bites, consider LFTs, sedimentation rate, creatine kinase (rule out rhabdomyolysis), ABG, and type and crossmatch.
  • Other: consider chest radiograph in cases with severe envenomation or in patients over 40 years old with underlying cardiopulmonary disease; radiograph of bite site for retained fangs (poor sensitivity); head CT if concern is raised for intracranial hemorrhage

Treatment

IN THE FIELD: For a suspected snakebite:

  • Transport immediately to nearest medical facility. No treatments in the field should delay travel to the nearest facility where an antivenom agent can be given if necessary.
  • Immobilize affected part.
  • Remove any constricting items. Applying tourniquets, incising, and applying suction to the wound is discouraged. Tourniquets cause more local tissue damage due to tissue necrosing venom seen in crotalid bites and should not delay transport to a medical facility.
  • Do not apply ice; keep victim warm.
  • Avoid alcohol, stimulants (caffeine), or agents that can suppress mental status.

IN THE HOSPITAL

  • Record vital signs: BP, HR, T, RR, and O2 sat.
  • Establish intravenous access and initiate IV hydration with crystalloid if the patient is hypotensive.
  • Obtain time of bite and description of snake if possible. Crotalids have a triangle-shaped head, nostril holes (pits), and elliptical pupils. The most dangerous of the crotalids is the rattlesnake, distinguished by its telltale rattle. Elapids, like the western and eastern coral snakes of the U.S., have brightly colored red, black, and yellow stripes.
  • Obtain and initiate reconstitution of appropriate antivenom. (Antivenoms are typically supplied in powder form and must be reconstituted before administration. If using older antivenoms, this process can take up to 1 hr, so it is recommended that it be initiated as soon as the patient arrives in the ED.)
    1. Inspect site of bite for fang marks and local symptoms.
    2. Delineate margins of erythema/edema with a marker.
    3. Measure circumference of bitten part at two or more proximal sites and compare with unaffected limb; repeat every 15 to 20 min; assess for extension of erythema/edema.
    4. Conduct a complete neurologic examination.
    5. Obtain past medical history; ask about allergies to horse serum in those previously treated for snakebite.
  • If no signs of envenomation:
    1. Clean and immobilize affected part.
    2. Immunize against tetanus.
    3. For crotalid bites, observe patient for at least 8 hr. If, at the end of this interval, local and systemic sequelae are absent and lab values remain normal, the likelihood of significant envenomation is low, and the patient can be discharged from the acute setting. Some sources recommend observing patients with crotalid bites to the lower extremities for at least 24 hours because swelling in the larger compartments of the legs could be slower and less easily recognizable. All definitive elapid bites should be treated. If elapid bite is only suspected, the patient must be monitored for up to 18 hr as symptoms can be delayed.
  • Patients who have progressive local symptoms or any systemic symptoms should be considered for antivenom. Crotalid envenomations without any progressive local or any systemic symptoms can be monitored for 12 to 24 hours, with repeat labs obtained 4 to 6 hours before discharge. If they have no new symptoms during that period of observation, they may be safely discharged. Specifically, copperhead bites often need no further interventions.

TREATMENT OF NONNATIVE (EXOTIC) SNAKEBITES

  • For bites by exotic or nonnative snakes, contact a Poison Control Center or your local zoo. (Zoos with exotic snakes are required to maintain a supply of snake-specific antivenom on their premises.)

Complications

  • Allergic reactions were very frequent with horse serum antivenoms. CroFab from sheep serum should be preferentially used over equine serum if available.
  • Anaphylaxis occurs within 30 min and should be treated by immediately stopping the infusion to managing the symptoms of anaphylaxis, including epinephrine SQ or IM initially and IV if needed, diphenhydramine IV, and hydrocortisone IV. If the anaphylactic symptoms can be managed and the envenomation is severe, the infusion can then be resumed.
  • Delayed hematologic complications are common and can manifest up to 4 days post treatment. Most bleeding is self-limited but can rarely be severe, necessitating close follow-up.
  • Serum sickness occurs 7 to 14 days after antivenom administration and is characterized by fever, rash, arthralgias, and lymphadenopathy. It can be treated with prednisone 60 mg/d PO, tapered over 7 to 10 days.
  • Injuries also result from:
    1. Tourniquet placement on the field, which should be avoided
    2. Ice application (cryotherapy), which can worsen tissue damage

Actinomycosis or Lumpy jaw

Actinomycosis is an indolent, slowly progressive infection caused by anaerobic or microaerophilic bacteria, mostly from the genus Actinomyces, that normally colonize the mouth, vagina, and colon. Actinomycosis is characterized by the formation of painful abscesses, soft tissue infiltration, and draining sinuses.

CLINICAL

Actinomycosis can affect any organ. Although not typically considered as opportunistic pathogens, Actinomyces species capitalize on tissue injury or mucosal breach to invade adjacent structures in the head and neck regions. As a result, dental infections and oromaxillofacial trauma are common antecedent events. Characteristic manifestations include:

_ Cervicofacial disease

  • Occurs in the setting of poor dental hygiene, recent dental surgery, or minor oral trauma.
  • Painful soft tissue swelling commonly seen at the angle of the mandible.
  • Fever, chills, and weight loss
  • Trismus
  • Soft tissue facial infection with sinus tract or fistula formation.

_ Thoracic disease

  • Can involve the lungs, pleura, mediastinum, or chest wall.
  • Presumed secondary to aspiration of Actinomyces organisms in patients with poor oral hygiene.
  • Fever, cough, weight loss, and pleuritic chest pains are common symptoms.
  • Signs of pneumonia or pleural effusion may be present.

_ Abdominal Disease

  • Occurs most commonly after appendectomy, perforated bowel, diverticulitis, or surgery to the gastrointestinal tract.
  • Lesions develop most commonly in the ileocecal valve, causing abdominal pain, fever, weight loss, and a palpable mass.
  • Extension may occur to the liver, causing jaundice and abscess formation.
  • Sinus tracts to the abdominal wall can occur.

_ Pelvic disease

  • Commonly occurs by extension from abdominal disease of the ileocecal valve to the right adnexa (80% of cases).
  • Endometritis

CAUSES

_ Actinomycosis is most commonly caused by Actinomyces israelii. Other causes are A. naeslundii, A. odontolyticus, A. viscosus, and A. meyeri.

_ Actinomyces are gram-positive, non–sporeforming, filamentous, anaerobic or microaerophilic rods.

_ Actinomycosis infections are polymicrobial, usually associated with Eikenella corrodens, and Streptococcus, Bacteroides, Enterococcus, and Fusobacterium spp.

WORKUP

The workup includes obtaining specimens either by aspirating abscesses, excising sinus tracts, or tissue biopsies. All specimens should be set up to culture anaerobic bacteria and held at least 5 to 7 days.

MANAGEMENT

  • Incision and drainage of abscesses
  • Excision of sinus tract

_ Ampicillin 50 mg/kg/day in 3-4 divided doses x 4-6 wk; then Pen VK 2-4 g/day PO x 4-6 wk. In place of ampicillin, can also use penicillin 3-4 million units IV q4h for 4-6 wk.

_ In penicillin-allergic patients, erythromycin (500-1000 mg IV q6h), tetracycline or doxycycline (100 mg IV q12h), and clindamycin (900 mg IV q8h) are reasonable alternatives. Other alternatives include cetriaxone, imipenem, and piperacillin/tazobactam.

Avoid use of metronidazole, aminoglycosides, oxacillin, and cephalexin.

Human Immunodeficiency Virus management

THE ASYMPTOMATIC HIV-INFECTED PATIENT
● The human immunodeficiency virus, type 1 (HIV) causes a chronic infection that culminates, usually after several years, in acquired immunodeficiency syndrome (AIDS).
● Acute infection occurs 2 to 6 weeks from the time of viral transmission.  illustrates the kinetics of viral
load and immune response during the phases of HIV-1 infection.
● The acute infection most often is a mild, self-limited mononucleosis-like illness; pharyngitis, mucosal ulcerations
, rash , penile ulcer from sexual contact , splenomegaly, and lymphadenopathy commonly occur. Hepatitis and aseptic meningitis are occasionally seen.
● The p24 antigen and the HIV polymerase chain reaction (PCR) will be reactive ; positive HIV serology
usually first becomes positive 1 month later.

● CD4 cells subsequently decline an average of 75/mm3 per year, but the range is variable. Five percent of infected people are long-term nonprogressors; another 10% progress more rapidly.


CAUSE
● RNA retrovirus HIV-1  was probably derived from transmission of a simian immunodeficiency virus (SIV) from chimpanzees in Central Africa; a related virus HIV-2 was derived from an SIV found in Sooty Mangebey
monkeys from West Africa.
● HIV-1 is the predominant pathogenic retrovirus in human populations; HIV-2 has limited distribution (primarily in West Africa) and tends to be less rapidly immunosuppressive than HIV-1.
● Transmitted by sexual contact, shared needles, blood transfusion, or from mother to child during pregnancy, delivery, or breastfeeding.
● Primary target of infection: CD4 lymphocyte .
● Direct central nervous system (CNS) involvement: manifested as encephalitis , myelopathy, or neuropathy
in advanced cases
● Renal failure , rheumatologic disorders, thrombocytopenia, or cardiac abnormalities

DIFFERENTIAL DIAGNOSIS
● Acute infection: mononucleosis or other respiratory viral infections
● Late symptoms: similar to those produced by other wasting illnesses such as neoplasms, tuberculosis (TB), disseminated fungal infection, malabsorption, or depression
● HIV-related encephalopathy: confused with Alzheimer’s disease or other causes of chronic dementia; myelopathy and neuropathy possibly resembling other demyelinating diseases such as multiple sclerosis,

LABORATORY TESTS
Three HIV viral antibody screening tests currently are in use:
● ELISA
● Bound anti-HIV antibody is detected by antihuman antibody labeled with an enzyme. The use of recombinant proteins has reduced false-positive results (specificity, 99.9%).
● A false-negative finding may result when measured in the acute infection period (sensitivity, 99.9%).
● New rapid serologic-screening assays
● HIV-antigen–coated gelatin or latex particle agglutination assays. The single-use test can be performed rapidly but may be less sensitive and specifi c than standard ELISA tests.
● A oral salivary test called OraSure (sensitivity, 99.9%) is sent to a reference laboratory after being inserted into the
mouth for 2 minutes.
● Western blot confirmatory test  is performed when ELISA is positive.
● This test identifies specifi c viral antigens; it is positive when both core and envelope antigens are present.
● The result is indeterminate when either antigen is present; if unchanged when repeated in 6 months in more than
one laboratory, this is considered a false-positive result.

Management Strategies for the Asymptomatic Patient
● Initial testing: CD4 cell count and HIV viral load measured every 3 to 6 months to guide decisions regarding antiretroviral use and prophylaxis against PCP and MAC infection
● Other testing: identifi es previously acquired latent infections that may become reactivated because of loss of T cell
function but can be prevented by the use of specific agents
● Serology to Toxoplasma gondii (IgG):
● Clinical infection may be prevented by trimethoprimsulfamethoxazole (TMP-SMZ) used as prophylaxis for PCP.
● Venereal Disease Research Laboratories (VDRL) test:
● Lumbar puncture should be performed in patients with a confirmatory specifi c test (FTA).
● Treatment with intramuscular benzathine penicillin if the CSF fluid is normal, and intravenous penicillin for 10
days if the CSF VDRL test is reactive or CSF pleocytosis, protein elevation, or hypoglycorrhachia is present.
● PPD skin test showing induration of 5 mm or greater, or patients with exposure to someone with active tuberculosis
● Treatment with isoniazid 300 mg/day for 9 months or, in case of isoniazid-induced hepatitis, rifampin 600 mg PO qd (only for those not receiving protease inhibitors or nucleoside reverse transcriptase inhibitor agents) for 4 months

Herpes Zoster OR Shingles

Herpes zoster, or shingles, is the most common infection of the peripheral nervous system. It is an acute neuralgia confined to the dermatome distribution of a specific spinal or cranial sensory nerve root.

CAUSES. Reactivation of previous infection of dorsal root or sensory ganglion by varicella-zoster virus (which causes chickenpox).

CLINICAL. Vesicular rash confined to a radicular or cranial nerve sensory distribution; initial intense burning localized pain with vesicles appearing 72-96 hours later.

Usually one or several contiguous unilateral dermatomes (T5-L2), CN V (semilunar ganglion), or CN VII (geniculate ganglion).

Herpes Simplex

Herpes simplex is a viral infection caused by the herpes simplex virus (HSV). HSV-1 is associated primarily with oral infections, and HSV-2 causes mainly genital infections.

CLINICAL

_ Primary Infection

  • Symptoms occur from 3 to 7 days after contact (respiratory droplets, direct contact).
  • Constitutional symptoms include low-grade fever, headache and myalgias, regional lymphadenopathy, and localized pain.
  • Pain, burning, itching, and tingling last several hours.
  • Grouped vesicles, usually with surrounding erythema, appear and generally ulcerate or crust within 48 hr.
  • The vesicles are uniform in size (differentiating it from herpes zoster vesicles, which vary in size). Scattered erosions covered with exudate may be noted on genitals.
  • During the acute eruption the patient is uncomfortable; involvement of lips and inside of mouth may make it unpleasant for the patient to eat; urinary retention may complicate involvement of the genital area.
  • Lesions generally last from 2 to 6 wk and heal without scarring.

_ Recurrent Infection

  • Generally caused by alteration in the immune system; fatigue, stress, menses, local skin trauma, and exposure to sunlight are contributing factors.
  • A cluster of lesions generally evolves within 24 hr from a macule to a papule and then vesicles surrounded by erythema; the vesicles coalesce and subsequently rupture within 4 days, revealing erosions covered by crusts.
  • The crusts are generally shed within 7 to 10 days, revealing a pink surface.
  • Rapid onset of diffuse cutaneous herpes simplex (eczema herpeticum) may occur in certain atopic infants and adults.

DIFFERENTIAL DIAGNOSIS

_ Impetigo
_ Behçet’s syndrome
_ Coxsackie virus infection
_ Syphilis
_ Stevens-Johnson syndrome
_ Herpangina.
_ Aphthous stomatitis.
_ Varicella.
_ Herpes zoster

LABORATORY TESTS

  • Direct immunofluorescent antibody slide tests provide a rapid diagnosis.
  • Viral culture is the most definitive method for diagnosis; results are generally available in 1 or 2 days. The lesions should be sampled during the vesicular or early ulcerative stage; cervical samples should be taken from the endocervix with a swab.
  • Tzanck smear is a readily available test that will demonstrate multinucleated giant cells. However, it is not a highly sensitive test.
  • Pap smear will detect HSV-infected cells in cervical tissue from women without symptoms.
  • Serologic tests for HSV: immunoglobulin (Ig) G and IgM serum antibodies. Antibodies to HSV occur in 50% to 90% of adults. The presence of IgM or a fourfold or greater rise in IgG titers indicates a recent infection (convalescent sample should be drawn 2 to 3 wk after the acute specimen is drawn).

MANAGEMENT

Topical acyclovir, penciclovir, and docosanol are optional treatments for recurrent herpes labialis, but they are less effective than oral treatments.