1. Herpes simplex
Causative agent of herpes simplex is Herpesvirus hominis (HSV) that involves both skin and nerves. Ninety-nine percent of the patients do not have any clinical symptoms and signs after contamination. Those patients are described as in "carrier stage".

2. Herpes simplex virus (HSV)
Two antigenic types of this virus are type 1 and type 2. They cause localized infections:
Above the waist (Type 1)
Below the waist (Type 2)

3. First contact with HSV Infection usually occurs in childhood Infection
No clinical symptoms (99%)
CARRIER
Primary herpes simplex infections (1%)
CARRIER (Recurrent herpes simplex infections; 100%)

4. Primary herpes simplex infections
Primary herpetic gingivostomatitis
Primary herpes genitalis
Primary herpetic whitlow
Primary herpetic keratoconjunctivitis
Disseminated herpes simplex infection of newborn

5. Primary herpetic gingivostomatitis
Patients are mainly infants. Multiple vesicles appear in the mouth. After the bursting of vesicles, erosions occur secondarily. The whole oral mucosa is covered by multiple aphthae. Additionally meningitis and encephalitis may be seen besides high fever, malaise and general complaints.

6. Primary herpes genitalis
Patients are mainly adolescents. In this type primary herpes simplex entrance site of the HSV is genital area in the firstly contacting person with this virus. Painful grouped vesicles appear on the entrance area. Additionally meningitis and encephalitis may be seen besides high fever, malaise and general complaints.

7. Primary herpetic whitlow
It is seen most frequently in health personnel contacting oral mucosae. There are grouped vesicles on the entrance area as in other herpes simplex types.

8. Primary herpetic keratoconjunctivitis
One can initially see vesicles, then painful erosions after the bursting. Eyelids are also involved.

9. Disseminated herpes simplex infection of newborn
If maternal genital area has HSV type II, viruses may contaminate the neonate during the delivery. Visseral organs are also involved beside skin and mucosa. This is the most severe primary herpes simplex type and may be fatal.

10. HSV
According the accepted theory, virus shuttles periodically between entrance area and medulla spinalis in the 100% of the HSV infected persons. So, the virus periodically comes to entrance area and viral shedding occurs without clinical manifestation. Thus, the patient can contaminate other persons easily in this stage. Recurrent herpes simplex infections occur in the people exposed to predisposing factors during the viral shedding.

11. Recurrent herpes simplex infections
Recurrent herpes labialis
Recurrent herpes genitalis
Recurrent lumbosacral herpes simplex
Recurrent herpetic keratoconjunctivitis
Herpes encephalitis, menengitis

12. Recurrent herpes simplex infections
Usually same localization as primary infection
Pruritus replaces the pain of the primary infection

13. Recurrent herpes simplex infections
Predisposing factors are mainly
Acute infections
Stress
Excessive exposure to ultraviolet radiation
Menstruation

14. Recurrent herpes labialis
The first subjective symptom is pruritus. Grouped vesicles appearing on erythematous and edematous base follow it.

15. Recurrent herpes labialis
Painful lymphadenopathy may follow the onset of vesicles. Erosions occur after opening the vesicles and pustules, and crusts occur after drying these lesions. Crusts cover the erosions, and finally crust falls and recurrence ends.

16. Recurrent herpes genitalis
Similar to herpes labialis, grouped vesicles over an erythematous base appear.

17. Recurrent herpes genitalis
Vesicles burst and leave an erosion with intended borders.

18. Recurrent herpes genitalis
This erosion may also be covered with crust. It heals spontaneously in 5-7 days.

19. Recurrent herpes genitalis
Formerly this virus is considered as a carcinogen in women. But real carcinogen virus is Human papilloma virus (HPV) that infects frequently the women together with type 2 HSV.

20. Recurrent herpes genitalis
Neonates are under risk because they may be contaminated by HSV even if the pregnant mother does not have any genital lesion.

21. Recurrent herpes genitalis
Differential diagnosis must be made by syphilis if the patient has erosion in the genital area.

22. Recurrent lumbosacral herpes simplex
It is seen more frequently in females. Classical lesions of herpes are localized to the lumbosacral area.

23. Recurrent Herpetic Keratoconjunctivitis
It is rare and similar to primary herpetic keratoconjunctivitis.

24. Herpes encephalitis and menengitis
It is rare and due to recurrence of latent infection in the brain. Mortality is high.

25. Treatment Local acyclovir preparations are applied 5 times a day.
Acyclovir is administered by the oral route 5 x 200 mg for 7 days.
2 x 200 mg may be used for upto 1 year for recurrent infections.

26. Herpes zoster (Shingles)
This presentation occurs usually in adults previously infected with Varicella zoster virus due to reactivation.

27. Varicella-zoster virus (VZV)
VZV is an alpha herpes virus containing double strand DNA surrounded by enveloped icosahedral nucleocapsid.
VZV. Electron microscopic appearance.

28. Varicella-herpes zoster association
VZV causes two different diseases:
Varicella (Chickenpox) : In children
Herpes zoster (Shingles) : In adults

29. Varicella (Chickenpox)
It is a primary infection due to VZV encountered usually in children. In most countries, over 90% of the population is infected with VZV until age 15.
Clinical appearance of chickenpox

30. Latent virus and reactivation
Dorsal root ganglion
Skin
Dorsal root
2nd infection: herpes zoster (shingles)
1st infection: varicella
Sensory nerve
Spinal cord

31. Some factors playing role in viral reactivation
Spinal trauma
X rays to the spine
Chronic infectious diseases
Malignant diseases, especially Hodgkin disease and the treatments administered
Heavy metal intoxications and their treatment
PUVA
IDIOPATHIC

32. Dermatomes and the localization of shingles
Thoracic %55
Cranial %25
Lumber %14
Cervical %12
Sacral % 3
Generalized % 1
Cranial (only trigeminal dermatome is seen)
Cervical
Thoracic
Lumbar
Sacral

33. Subjective symptom: PAIN
Since there is nerve involvement, most cases are in pain (60-90%). Younger patients have less pain. Older patients have more severe and longer pain.

34. Progression of lesions
First maculopapular erythematous areas appear. On this base, grouped vesicles appear in hours. After 48 hours, the vesicles become pustules. After day 4, the lesions start to dry and are covered with crusts. In severe cases the vesicles may become necrotic.

35. Rash: Grouped vesicles
Most important feature of shingles is unilateral dermatomal involvement. Rarely one or two neighboring dermatomes may be affected.

36. Lesion characteristics
Since the vesicles are unilateral, the lesions end on the midline and do not cross over.
The appearance of a group of vesicles is not different than herpes simplex (except for the dermatomal distribution)

37. Postherpetic neuralgia
It is the continuation of dermatomal pain after the lesions have disappeared. The reason is unknown. It is thought to be due to changes in the nerves progressing from the peripheric pain pathways to the central nervous system.

38. Treatment
Acyclovir and its metabolites are used in treatment. Treatment should be initiated within 72 hours of onset of lesions:
Acyclovir: 7 days 5 x 800 mg
Valacyclovir: 7 days 3 x 1000 mg
Famcyclovir: 7 days 3 x 250 mg
Brivudin: days 1 x 125 mg

39. Other treatments Symptomatic: Wet dressings etc.
Analgesics: Opioids may be necessary
Corticosteroids: In special cases
Tricyclic antidepressants, anticonvulsives etc for PHN

40. Verrucae (Warts)
They are skin and mucosal papillomas caused by Human Papilloma Virus (HPV), are benign and may regress spontaneously.

41. Human papilloma virus (HPV)
It is a DNA virus of the group Papovavirus. Almost 100 serologic types exist and some are oncogenic.

42. Verrucae There are five morphologic types of verrucae:
Verruca vulgaris
Verruca plantaris
Verruca planus
Verruca filiformis
Verruca anogenitalis (Condylomata accuminata)

43. Verruca vulgaris
They are seen on the hands. Sharply bordered papules with hyperkeratosis are seen. They may spread by trauma (Koebner phenomenon).

44. Verruca plantaris
They are localized to the plantar area. They are painful and must be differentiated from calluses.

45. Verruca planus
They are seen on the face and hands. They are flat topped papules of several mm diameter. There may be hundereds of papules in one patient.

46. Verruca filiformis
They are seen usually in males. They are pedunculated and have string like prominences on top. The face, scalp, perinasal area and eyelids are especially affected.

47. Verruca anogenitalis
It is a venereal disease. It is seen as flat topped papules and pedunculated papillomas. When found in intertriginous areas they look like a rooster comb.

48. Treatment
The existence of many different shows that there is no ideal treatment.
Possibility of spontaneous remission should not be forgotten.
Electrocoagulation
Acid containing preparations
CO2 laser, cryotherapy, surgery vs.

49. Molluscum contagiosum
Causative agent is a Poxvirus. Pearl-like, hard nodules with a dimple at the top are seen.
Papules are mostly seen on the face and body in children, and genitals in young adults (sexually transmitted disease).

50. Molluscum contagiosum
It spreads easily with autoinoculation. ayca yayılır. Central dimple is an important diagnostic clue. If it is squeezed with a pair of forceps a white greasy mass is extruded.

51. Treatment
Curettage is an efficient method in treatment. Each lesion is curetted and iodine solution is applied. Electrocoagulation, cryotherapy with liquid nitrogen are also treatment methods.

52. Hand-Foot-Mouth Disease
Causative agent is Coxsackievirus and Enterovirus 71. Elementary lesion is an oval vesicle, based on an erythema. Palmo-plantar areas and mouth mucosa are involved.

53. Hand-Foot-Mouth Disease
It may cause epidemics especially in summer months. Vesicles in the mouth burst and look like aphtous ulcerations.

54. Hand-Foot-Mouth Disease
Lesions disappear in 8-10 days without complications. Treatment is usually unnecessary. If necessary, symptomatic treatment is used.

55. Web