Herpes Gladiatorum Pictures

Outline • A review of the previous e-lecture. • Viral Skin Infections. 1- HSV→ Serious conditions: Eczema Herpeticum, Erythema Multiforme, SJS/TEN. Not serious conditions: Herpes labialis and genital Herpes. 2- Herpes-caused infections: Herpetic whitlow and Herpes gladiatorum. 3- VZV: Chickenpox and Shingles. “The sheet was written based on our first lecture with the Doctor. The e-lecture is not included in this sheet, these are just some points the doctor mentioned as a review”. - Macule: Discoloration of the skin → Papule: Raised macule → Vesicle: Filled papule. Bulla: Larger papule → If the bulla breaks, it becomes a crust. - Ulcer: Losing part of the epidermis. - Cellulitis: Infection spreading into the subcutaneous tissue. - Necrotizing fasciitis: Infection involving superficial and deep fascia. - Myositis: Infection of the muscles. - Osteomyelitis: Inflammation of the bone. - Knowing the type of rash aids in determining the causative pathogen, whether it is bacterial, viral or fungal. - Almost all vesicular rashes are viral except a few rare ones. The doctor asked us to memorize it. - Rashes may be of a local problem in the skin, or as a systematic manifestation of a disease such as in salmonella. A- Herpes Simplex Virus - Herpes is a super-common infection that stays in your body for life. - Cutaneous manifestations of HSV infection include: The commonest presentation of HSV-1: Pharyngitis and gingivostomatitis, generally seen in children and young adults. General Features: Most viral infections show flu-like symptoms (Fever, malaise, chills, etc.). In addition, HSV is associated with difficulty in chewing and cervical lymphadenopathy. Also, ulcers and exudative lesions are found on the posterior pharynx and sometimes the tongue, buccal mucosa, and gums. - HSV disease is usually not life-threatening, self-limiting and is more a cause of discomfort than significant morbidity and mortality. However, uncommonly, HSV infections can be potentially fatal in certain conditions, which are: 1- Eczema Herpeticum: - It is an extensive cutaneous vesicular eruption that arises from pre-existing skin disease, usually Atopic Dermatitis (eczema). - Children with AD have a higher risk of developing Eczema Herpeticum, in which HSV-1 is the most common pathogen. Further explanation: HSV is not serious for those with no underlying dermatological problems. Patients with skin diseases (AD) can get critically ill after being infected virally (HSV-1) causing a “combination” of diseases called Eczema Herpeticum. - Eczema Herpeticum, is a form of Kaposi varicelliform eruption caused by viral infection, usually with HSV. Note: Kaposi varicelliform eruption is the name given to a distinct cutaneous eruption caused by some viruses (e.g. HSV). - Not all Eczema Herpeticum cases are severe. Only if a large area of the skin gets affected with Eczema Herpeticum, it can become severe, progressing to disseminated infection and death if untreated. Bacterial superinfection and bacteremia via the erupted vesicles are usually the complications that cause mortality. Note: Superinfection is a second infection after an earlier different one. - Skin eruptions, in general, are highly contagious, so it is important to inform the patient with Eczema Herpeticum to avoid contact with others. This is a case where the patient was misdiagnosed with impetigo during the initial treatment. It turned out that the patient actually suffered from Eczema Herpeticum. Diagnosis: a- It is important to first know the patient’s history whether they have/had dermatologic conditions (AD). b- Direct fluorescent antibody testing. It is accurate since it distinguishes between HSV-1, HSV-2, and varicella. Also, it is rapid requiring only several hours. However, it is expensive. c- Viral culture. Its results are accurate, reliable and can distinguish between different viruses. Also, it is a cheap method. However, results are slow requiring 2 days. d- Tzanck Smear. It is the cheapest method and results are immediate, but it requires a skilled and experienced observer to interpret the smear. To perform a Tzanck smear preparation: Scrapings from the base of a blister or erosion on a glass slide → Staining with Wright or Giemsa stain → examining under light microscopy for characteristic "Tzanck" cells (multinucleate keratinocytes). Tzanck cells can be seen in herpes, varicella, and CMV. e- PCR. It may be helpful when the cutaneous lesions are old or atypical and viral particles are few in number. However, it may give false positive results. f- Pathology lab can also help in the diagnosis, through the characteristics of the viral cytopathic changes of the epidermis and follicular epithelium present on H&E stained tissue. g- Immunohistochemistry (IHC), staining with antibodies can also help. Treatment: a- Systemic antiviral agents should be initiated as soon as a diagnosis of Kaposi varicelliform eruption is suspected. ➔ (Oral) Acyclovir is the preferred first-line treatment in healthy, immunocompetent pediatric patients. Usually with a high dose, a 5x/day for 710 days. ➔ (IV) Acyclovir, for patients with systemic involvement or in patients who are immunocompromised. ➔ Foscarnet is used in patients with acyclovir-resistant infection (last choice). Note: Foscarnet is rarely used (last choice), because it causes nephrotoxicity in 50% of the patients. But if the patient has a chance of mortality, then the risk is worth taking. ➔ Valacyclovir is efficacious and can be dosed only twice daily, an advantage over daily multiple dosing of acyclovir. However, it is cost-prohibitive (expensive). b- Trifluridine and Vidarabine, are two topical ophthalmic preparations, used for patients with ophthalmic involvement. Immediate ophthalmologic consultation is a must for any patient with potential ocular infection. c- Antibiotics are used in case of bacterial superinfection. 2- Erythema Multiforme: - HSV has been associated with up to 75% of cases of erythema multiforme. - Erythema multiforme is an acute, self-limiting and at times recurring skin condition (rash) thought to occur due to a hypersensitivity reaction against certain infections (HSV1) and medications (antibiotics). - Erythema multiforme is a term describing Target lesions (circular lesions often with a central blister and a symmetrical peripheral distribution). It usually shows on limbs as a result of type 4 hypersensitivity reaction, which is a cell-mediated response. “So Erythema Multiform is actually a rash of target lesions that appear due to cellular immunity’s response to HSV” - Features are often mouth, genital and eye ulcers and fever, these symptoms are in common with the symptoms of Steven-Johnson Syndrome (SJS). - The spectrum of the disease: “which is debated, refer to the note” Erythema Multiforme minor → Erythema Multiforme major → Steven-Johnson syndrome (SJS) → Toxic Epidermolysis Necrosis (TEN) being the most severe. Note: Since in Erythema Multiforme there is minimal mucous membrane association and <10% epidermal detachment, it is now considered to be a distinct condition from SJS and TEN. If there is 10% epidermal detachment this may indicate SJS, while if its >30% then its TEN. - Erythema Multiforme is frequently seen in adults between the ages of 20-40 years, with rash occurring 5-10 days after the onset of viral illness (flu-like symptoms). It happens over 3-5 days and persists for 1-2 weeks. - Urticaria Multiform (a benign cutaneous hypersensitivity reaction) is often misdiagnosed as Erythema Multiforme. However, Urticaria Multiform resolves within hours (unlike Erythema Multiforme which resolves within weeks). Causes: a- Idiopathic (50%), which means with no identifiable cause. b- HSV (>50%). It occurs 10 days after the acute eruption, or HSV may be the cause even without active lesions. c- Other infections such as Mycoplasma pneumoniae, VZV, HCV, CMV, and HIV. d- Drugs: Antibiotics and antiepileptic drugs are mostly involved (in SJS as well). Sulfa drugs, penicillin and ciprofloxacin. Treatment: a- Identifying and removing the causative agent (e.g. HSV, mycoplasma) or certain medication. b- Supportive care (pain meds, antihistamines, wound dressing, etc.) c- Antiviral therapy for HSV causes (oral acyclovir). d- Must tell the patient that if the bullae erupt, or systemic symptoms recur, they must return since it can be either SJS or TEN requiring medical emergency since it carries a mortality rate. “Not related to Erythema Multiforme” - Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are now believed to be variants of the same condition, distinct from Erythema Multiforme. Note: TEN is sort of a severe form of SJS. - SJS/TEN are rare, acute, serious, life-threatening and potentially fatal skin reactions. Complications are very serious and can result in multiple organ failures. - It begins with prodromal symptoms, then progresses to skin ulcerations that begin in the trunk, face and typically involves the mouth and eyes with genital sores as well. - The patient looks toxified (showing cyanosis, poor perfusion, etc.). Diagnosis: - Clinically linked to: Toxic looking patient and a positive Nikolsky sign. Note: Nikolsky sign is a method done by pushing a bullous over a normal skin with the finger. If the bullous affects the healthy skin, this indicates a positive Nikolsky sign and a severe activity of a bullous disease (e.g. SJS). - Biopsy confirms. From the biopsy, it shows a bullous formation where the epidermis is detached from the dermis. Treatment: Supportive-ICU admission (or burn unit) and some immune-based therapy show promise. - SJS mortality rate is 3%, while TEN mortality rate is 30% and up to 50%. - These are the causes of SJS and TEN: . As you can see, the causes are similar to Erythema Multiforme. However, in SJS and TEN, the causes are much more, and drugs are the main causative agents. Unlike in Erythema Multiforme where viruses are the main causative agents. After discussing serious skin infections, we will now discuss “normal” infections that are quite common. - The most frequent manifestation of HSV-1 reactivation. - More common in college students (37% at 1st yr college and 46% at the 4th yr in the US). - May be asymptomatic or present with symptoms that are milder and of shorter duration than primary infection (causing cold sores in about ¼ of college students). - Starts as mild prodromal symptoms (itch, burn, tingle, etc.), followed by the development of lesions within 48h and then they usually resolve within 5 days. - Immunosuppressed patients may experience severe mucositis, with spread to the skin surrounding the mouth. Note: The older and the more immunocompromised the patient is, the more severe the initial representation of the infection is. Pathophysiology: - Caused by HSV-1 more than HSV-2. However, HSV-2 is on the rise. - Transmission via mucous membranes (kissing), direct contact with open skin or sharing of fomites (towels, utensils, etc.) - After 2-20 days of HSV initial contact, symptoms may show. However, shedding is the first 2-4 days maximum. - After the 1st episode, the virus remains dormant in trigeminal ganglion and triggers again (recurrence) due to stressors such as: Fever, stress, sun exposure, trauma, immune suppression, hormonal changes (menses), fatigue (travel). - It shows grouped vesicles on an erythematous base, on the vermillion border (zone between the lip and the adjacent normal skin). If the patient scratches the vesicles, they will crust as shown in the 2nd image. Can cause gingivitis, lymphadenopathy, and ulcers on the tongue. - Symptoms of the first episode are usually severe with fever, lymphadenopathy, mouth or gingival ulcers. - Symptoms of the secondary episode (after recurrence), lesions that itch, burn, tingle in the first 12-36 hours, then vesicles erupt. It resolves in 7-14 days. Treatment: We can only reduce the symptoms’ duration, it does not remove the virus completely. a- The first episode → Acyclovir, reduces the lesions’ time to 4 instead of 10 days and the shedding to only 1 instead of 5 days. b- Recurrence → Oral Acyclovir, reduces eruption healing time by 2 days. Famciclovir or Valacyclovir can be used too. c- Topical treatment reduces healing time by one-day maximum. -------------------------------------------------------------------------------------------------------------- - Caused by HSV-2 (90%) and to a lesser extent HSV-1. It is very similar to Oral herpes except that genital Herpes affects the genital area and can be sexually transmitted. - It is the most common cause of genital ulcers (60-70% of STD ulcers). - It has a high prevalence in western countries (12% roughly) or 10-30% of sexually active people. 300k cases show a year in the US alone. - It is asymptomatic in the majority of patients (>2/3). The virus sheds asymptomatically, so without outbreak, the virus can be shedding in 10-20% of days. Primary infection: - May be associated with fever, malaise, and adenopathy. - HSV’s DNA migrates up the infected axon to the affected spinal cord sensory Ganglion and persists there life long, dormant until the next outbreak. Secondary infection (recurrence): - On periodic reactivation, HSV’s DNA migrates down the axon and erupts again. - The first infection is the worst, then subsequent outbreaks are typically less severe. - Vesicular eruption: It is similar to oral herpes, preceded by tingling, itch and burning lesions then vesicles erupt. Primary vesicles remain up to 2 weeks, while reactivation vesicles remain for 6-12 days. - HSV-1 genital herpes has milder and fewer outbreaks than HSV-2. - Lesions are seen around the genital area and the anal area. - In the early stages (more common clinically) normal vesicles are seen while in the later stages of the disease they seem to be crusted as vesicles erupt and some bacteria may enter. Diagnosis: a- Clinical pictures (symptoms and signs) are diagnostic. b- HSV PCR test. Treatment: - Antivirals for primary and recurrence. They do not cure but shorten the span of illness. - In pregnancy abstinence, vaccine (experimental) + antivirals are used. - As for measures for active lesions: loose clothing, ice pack or baking soda compression are used. Active lesions during pregnancy may require a C-section. - Topical antivirals and low dose anesthetics can be given. Genital Herpes during pregnancy: - It can be transmitted vertically and cause: 1- Neonatal HSV infections → Encephalitis or disseminated HSV infection in newborn. 2- Congenital HSV infection → Microcephalus, hydrocephalus or chorioretinitis. -------------------------------------------------------------------------------------------------------------- 1- Herpes gladiatorum: It is a mucocutaneous infection of surfaces such as chest, ears, face, and hands seen in rugby players and wrestlers. 2- Herpetic whitlow: - HSV infection of the finger which may result from: a- Auto-inoculation (existing oral or genital infection). b- Direct inoculation from some other environmental source. - Presents with vesicles/ulcers with or without regional lymphadenopathy. Diagnosis: Tzanck smear can be done Treatment: a- Prevent transmission (using a bandage). b- Antivirals in case of recurrent infection or immunocompromised. - Herpetic whitlow (viral) is different from Acute paronychia (bacterial). -------------------------------------------------------------------------------------------------------------- It is not a viral infection, but it is discussed to differentiate it from Herpetic Whitlow. - Paronychia occurs due to penetrating trauma (finger biting, manicure, etc.) where bacteria from skin (S. aureus) or from the mouth (S. pyogenes or Bacteroides) enter the tissue causing infection. - It is usually more common in females since finger biting is more amongst females. - Infection occurs 2-5 days after trauma, with pain at the site and local inflammation signs (red, hot, painful and tender). - Can progress to abscess formation and nail bed infection (serious), this requires systemic treatment. - Most differentiating feature from Whitlow is that in Paronychia the finger is more swollen, erythematous and painful with abscess formation. Treatment: a- Soak for 15 minutes in warm water or acetic acid soak (1:1). b- If there is abscess formation → Incision and drainage (I&D). c- Topical antibiotic for mild cases, e.g. Bacitracin, gentamicin, fluoroquinolone. d- Topical steroid to reduce inflammation (quicker healing). e- Systemic antibiotics for prolonged cases (suspect cellulitis or ingrown nail), must perform (I&D) and then give Cephalexin or Dicloxacillin as first-line therapy. f- As a second line therapy: TMP-SFX or doxycycline, especially if you suspect MRSA. Remember MRSA colonizes the nose, so biting can bring it easily to nail bed. . B- Varicella-zoster virus (Human herpes virus 3). - It causes Chickenpox where 90% of cases occur in children under 13 years of age. After that, the virus becomes dormant and its reactivation causes Shingles (Zoster). - Peak onset ages are 5-9 years old, while the peak outbreak time is January to May (cold season-fall). - Incubation is 10–14 days. Following incubation, the patient may have a 1-2 days febrile prodrome (an early symptom of a fever) before the onset of constitutional symptoms of malaise, itch, and anorexia. Then pruritic (itchy) red papules and vesicles rash arise (<5mm across). - Vesicles quickly pustulate and form scabs, which falls off 1-2 weeks after infection. They appear in successive crops 2–4 days, starting on the trunk and face and spreading centripetally. “This means the patient will have different stages of vesicles all over and not uniformly shaped vesicle” - Dermatomal distribution of chickenpox: Centripetal. - Generalized LAP (lymphadenopathy) is common. Transmission: a- Respiratory droplets. b- Through direct contact, where 90% is transmitted by direct contact in households. - Can also be transmitted vertically (transplacental). Complications of chickenpox: - May rarely involve the mucosa of the oropharynx and vagina. Other complications include secondary bacterial infection, pneumonitis, and encephalitis. - The disease may be severe in pregnancy and the immunocompromised. - If the virus affects a cranial nerve, it will become a serious problem. Treatment: - Usually, no antivirals used. Some guidelines depict oral antivirals in large households and in immunocompromised patients. - Reducing the itch through calamine lotion, oatmeal bath and giving antihistamine at bedtime. - Bacitracin for bacterial superinfection (impetigo) especially for crusted open lesions. -------------------------------------------------------------------------------------------------------------- Shingles - In Arabic, it is called fire belt, while in older medicine it is called a flame snake. - Shingles, or Herpes Zoster, is a localized recurrence of varicella virus. - Dermatomal distribution: It causes a unilateral vesicular eruption (band-like). Note: Shingles (zoster) are very painful and differ in their dermatomal distribution (band-like) in comparison to chickenpox (centripetal). - Thoracic and lumbar dermatomes are the most common site of infections, along with the cutaneous spinal nerve distribution. It is often preceded by 2–3 days of pain in the affected area. Note: A dermatome is an area of skin that is mainly supplied by a single spinal nerve. - In the US, 1 million case incidences show yearly. - Shingles often occur when a person's immune system is impaired. A weakened immune system can be part of the aging process; thus, the peak age is in older patients (50-80yrs). - Women, particularly during the menopause transition, have higher rates of shingles than men (60% are females), most likely due to hormonal changes to their immune response. Pathophysiology: - The virus infects dorsal root ganglionic cells and remains dormant, typically following a Varicella zoster infection (chicken pox). Reactivation occurs in states of reduced cell immunity (older age, immunosuppression and sometimes stress) causing shingles. - It is highly contagious. Avoidance of contact is a must until rash heals (days to few weeks). - Most commonly, preceding rash, fever, headache and numbing along the affected nerve root. The rash starts erythematous, maculopapular then clear distinct vesicles erupt. Vesicles turn cloudy after 3-5 days and crust by 10 days and may leave a residual scar. - Lymphadenopathy with tenderness is also a common finding. - Resolution may take 2–4 weeks. Diagnosis: - A rash develops 2-3 days after first symptoms appear and last for 2-4 weeks. - It follows a dermatomal distribution, proximal then distal to the dermatome. - Most common sites: Back T1, T2, and face. - The rash is described as erythematous maculopapular with clear vesicles that crust later. - PCR is the most sensitive and specific test to be done. Treatment: - Antivirals (within 3 days of onset is best) for patients less than 50 years old with more than 50 lesions or complication (e.g. facial, ophthalmic). - Pain management with NSAIDs and Opioids. If the pain persists, amitriptyline or gabapentin are used. - Steroids. -------------------------------------------------------------------------------------------------------------- Variants of shingles 1- Zoster Sine Herpete: Zoster without rash, this is uncommon, the pain, prodrome, and fever are all present with no (or little) rash seen. Here PCR can be very useful to diagnose it. 2- Ramsay Hunt syndrome (VZV of the facial nerve): Rapid onset with facial pain. If the cranial nerve 8 is involved → Tinnitus (ringing in the ears) and vertigo (dizziness). It is seen as a unilateral herpetic rash of ear pinna with a possibility of hearing loss. It causes peripheral facial paralysis (Bell's palsy). “check the figure in the nxt page” Management: Antivirals, corticosteroids, and painkillers. In this case, some doctors might brush this off thinking of this older patient as an old stroke patient and send them home. However, by looking at the ear you can see the rash indicating a Ramsay hunt syndrome. 3- Herpes Ophthalmicus: - It occurs when the virus is dormant in the trigeminal nerve ganglion. - It reactivates more in advanced age and immunocompromised patients (HIV, cancer, chemo or radiotherapy). It may also reactivate in systemic illness, or stress (much like typical shingles). - Hutchinson’s sign is where vesicles on the tip of the nose, or vesicles on the side of the nose, precedes the development of ophthalmicus herpes zoster. It increases the risk of ocular involvement by 2 folds. - Eye complications: Keratitis, iritis, episcleritis, and visual loss. - Recall the HSV-1 (mainly) also stays dormant in the trigeminal nerve ganglion where its reactivation manifests as Herpes labialis. Here, the zoster virus is dormant in the trigeminal nerve ganglion but its reactivation manifests as Herpes Ophthalmicus. Treatment: - Consult the ophthalmologist. - Antivirals: a- Acyclovir, 800 mg orally 5 times a day for 7-10 days. b- Valacyclovir, 1000mg 3 times a day for 1-2 weeks. c- Famciclovir, 500 mg 3 times a day for 7 days. - Anti-staphylococcal antibiotics. - Corticosteroids, only under the ophthalmology consultation, since they have a risk of corneal perforation. Kaposi Sarcoma (HHV8) - Form of Cancer, due to HHV8. It has no specific dermatomal distribution. If seen, must suspect an immunocompromised state, (e.g. HIV). Management is aimed at the cause of the immunocompromised state. Few Notes - Dermatological Distributions: 1- Chickenpox → Centripetal 2- Shingles → Band-like, proximal and distal to the affected dermatome. 3- Ramsay Hunt Syndrome → Unilateral rash of ear pinna. 4- Herpes Ophthalmicus → Hutchinson’s sign “rash on the tip of the nose” - Dormancy and Reactivation: 1- HSV becomes dormant in: a- Cranial nerve ganglion (trigeminal) → Reactivates as Oral Herpes. b- Sensory nerve ganglion → Reactivates as Genital Herpes. 2- VZV becomes dormant in: a- Dorsal root ganglia (mainly Thoracic and Lumber nerves) → Reactivates as Shingles. b- Cranial Nerves: Facial nerve → Ramsay Hunt Syndrome (hearing loss, vertigo, etc.). Trigeminal nerve → Herpes Ophthalmicus (Keratitis, iritis, visual loss, etc.).