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  1. 1. B Y A S H E N A F I G . 12/8/2022 1 Fungal and Viral infection
  2. 2. Fungal Infections 12/8/2022 2
  3. 3. o Dermatophytosis - "ringworm" disease of the nails, hair, and/or stratum corneum of the skin caused by fungi called dermatophytes. o Dermatomycosis - more general name for any skin disease caused by a fungus. 12/8/2022 3
  4. 4. THE SKIN PLANTS  Etiological agents are called dermatophytes - "skin plants". Three important anamorphic genera, (i.e., Microsporum, Trichophyton, and Epidermophyton), are involved in ringworm.  Dermatophytes are keratinophilic - "keratin loving". Keratin is a major protein found in horns, hooves, nails, hair, and skin.  Ringworm - disease called ‘herpes' by the Greeks, and by the Romans ‘tinea' (which means small insect larvae). 12/8/2022 4
  5. 5. Infections by Dermatophytes  Severity of ringworm disease depends on:- 1 strains or species of fungus involved 2 sensitivity of the host to a particular pathogenic fungus.  More severe reactions occur when a dermatophyte crosses non- host lines (e.g., from an animal species to man). Among dermatophytes there appears to be a evolutionary transition from a saprophytic to a parasitic lifestyle. 12/8/2022 5
  6. 6. called different names on basis of location of infection sites  tinea capitis - ringworm infection of the head, scalp, eyebrows, eyelashes  tinea favosa - ringworm infection of the scalp (crusty hair)  tinea corporis - ringworm infection of the body (smooth skin)  tinea cruris - ringworm infection of the groin (jock itch)  tinea unguium - ringworm infection of the nails  tinea barbae - ringworm infection of the beard  tinea manuum - ringworm infection of the hand  tinea pedis - ringworm infection of the foot (athlete's foot) 12/8/2022 6
  7. 7. Major sources of ringworm infection  Schools, military camps, prisons.  Warm damp areas (e.g., tropics, moisture accumulation in clothing and shoes). Historical note: More people were shipped out of the Pacific Theater in WWII back to U.S. because of ringworm infection then through injury.  Animals (e.g., dogs, cats, cattle, poultry, etc.). 12/8/2022 7
  8. 8. Diagnosis  Note the symptoms.  Microscopic examination of slides of skin scrapings, nail scrapings, and hair. Often tissue suspended in 10 % KOH solution to help clear tissue. Slides prepared this way are not permanent. These degrade rapidly due to presence of base.  Isolation of the fungus from infected tissue.  Proper treatment is dependent on diagnosis and prognosis. 12/8/2022 8
  9. 9. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT tinea pedis - Athletes' foot infection  between toes or toe webs (releasing of clear fluid) - 4th and 5th toes are most common.  Soreness and itching of any part of the foot.  Three causal agents, T. rubrum (source of inoculum comes from people with chronic infections, because fungus not long-lived in squames), T. mentagrophytes, and Epidermophyton floccosum (source of inoculum comes from long-lived arthrospores that reside in squames deposited in rugs and carpets (fomites). 12/8/2022 9
  10. 10. Cont…  Spread of disease correlated with introduction and generalized distribution of T. rubrum into Europe and America probably due to massive movement of peoples due to colonial occupation, slave trade, and World War II.  Origin of T. rubrum may have been SE Asia or Africa.  Fungi probably transmitted host to host through infected squames; flat, keratinised, dead cells shed from the outermost layer of a stratified squamous epithelium 12/8/2022 10
  11. 11. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT  Three Grades of Infection  Grade I - Subclinical  An itching between toes, skin may be soft and macerated, blistering my occur.  Treatment - keeping feet dry and clean, drying between the toes lightly each time you bathe to remove some skin. Application of fungicidal powders or ointments containing 1 salicylic acids to promote peeling of the skin 2 tonaftate or other topical fungicides. 12/8/2022 11
  12. 12. cont…  Grade II  Host is conscious of a burning sensation while walking and standing.  Soaks are recommended (paints or liquids) such as 1:4000 KMnO4 (stains the skin purple) or topical fungicides.  Remove clear liquid from blisters by having a doctor puncture near the base or unroofing the blister.  Dusting powder in morning to help keep feet dry. 12/8/2022 12
  13. 13. Tinea Pedis – Athlete’s Foot Infection 12/8/2022 13
  14. 14. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT  Grade III  A secondary bacterial infection sets in.  Patient should go to bed.  Use systemic antibiotics to fight bacterial infection.  Use of soaks and compresses.  After infection subsidies, go to treatments as for Grade I or II infections.  For persistent cases, (T. rubrum is usually the culprit), resort to systemic griseofulvin therapy or other antifungal systemic drugs (i.e., Lamisiltrademark or terbinafine HCl)  Griseofulvin is fungistatic, so it won't kill the fungus, just inhibit its growth. 12/8/2022 14
  15. 15. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT  Allergic reactions are sometimes associated with tinea pedis and other ringworm infections.  toxins get into blood stream and reaches a site other than the site of infection.  blistering occurs on fingers and hands.  in diagnosis, rule out allergic reaction to poison, detergents or other substances.  during diagnosis, look for tinea (pedis, often) on the body.  treat the primary site of infection where the antigen is being produced.  treat secondary site - blisters. 12/8/2022 15
  16. 16. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT tinea corporis - body ringworm  Generally restricted to stratum corneum of the smooth skin.  Symptoms result form fungi metabolites such as toxin/allergens.  Disease found throughout the world.  Produces concentric or ring-like lesions on skin, and in severe cases these are raised and may become inflamed.  All forms of tinea corporis caused by T. rubrum, T. mentagrophytes, T. tonsurans, M. canis, and M. audouinii are treatable with topical agent containing tolnaftate, ketoconazole, miconazole, etc...  Disease transmitted through infected scales hyphae or arthroconidia on the skin.  Also transmitted through direct contact between infected humans or animals, by fomites (any agent such a bedding or clothing capable of retaining a pathogen and transmitting to a new host). 12/8/2022 16
  17. 17. Tinea corporis – body ringworm 12/8/2022 17
  18. 18. Cont…  Transfer form on area to the body to another (from tinea pedis to tinea corporis).  Tinea Corporis normally resolves itself in several months.  T. verrucosum and T. violaceum infections require more vigorous treatment including cleaning of area to remove of scales and older fungicidal topical applications of ammoniated mercury ointment, 3 % salicylic and sulfuric acid, or tincture of iodine for several weeks.  Widespread tinea corporis and more severe types (lesions) require systemic griseofulvin treatment (about 6 weeks for effective treatment). 12/8/2022 18
  19. 19. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT tinea cruris - ringworm of the groin and surrounding region  More common in men than women.  Infection seen on scrotum and inner thigh, the penis is usually not infected.  Epidemics associated with grouping of people into tight quarters - athletic teams, troops, ship crews, inmates of institutions. 12/8/2022 19
  20. 20. Tinea Cruris – Jock Itch 12/8/2022 20
  21. 21. Cont…  Several causes of tinea cruris include T. rubrum (does not normally survive long periods outside of host), E. flocossum (usually associate with epidemics because resistant arthroconidia in skin scales can survive for years on rugs, shower stalls, locker room floors), T. mentagrophytes (usually of animal origin, such as rodents), and Microsporum gallinae (rarely seen - usually found on gallinaceous birds like turkeys and chickens).  Predisposing factors include persistent perspiration, high humidity, irritation of skin from clothes, such as tight fitting underwear or athletic supporters, pre-existing disease, such as diabetes and obesity. 12/8/2022 21
  22. 22. Cont…  Diagnosis  If lesion "weep", it is likely caused by a yeast, such as, Candida albicans, and not by a dermatophyte, especially if infections are seen in a woman.  KOH examination of skin scrapings.  Culture of dermatophyte from skin scrapings.  Treatment  Tolnaftate (Tinactin trademark) treatment protocol for tinea corporis.  Relief of symptoms occur within 3 days and treatment continued until all signs of disease are gone.  Area is sensitive so the other care needs to be taken into to add to irritation of region. 12/8/2022 22
  23. 23. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT  tinea unguium - ringworm of the nails  Tinea unguium or onchomycosis can take two forms:  Leukonychia mycotica - superficial white onychomycosis, invasion of fungus restricted to patches or pits on surface of the toenail.  Invasive subungual dermatophytosis - lateral or distal edges first involved, followed by establishment of the infection beneath the nail plate. Invasion of nail plates by dermatophytes.  Onychomycosis (infection of nails caused by non-dermatophytic fungi and yeasts)  Most commonly caused by T. rubrum, then E. floccosum or other Trichophyton species. 12/8/2022 23
  24. 24. Tinea Unguium – Nail Infection 12/8/2022 24
  25. 25. Cont…  Resistant to treatment, rarely resolves spontaneously.  Topical treatments - poor record of cure.  Ablation - surgical or chemical removal of nail.  Systemic griseofulvin therapy can lead to remission (usually a year or more of treatment required - results vary about 29 % cure rate).  Use of other systemic antifungal (i.e., Lamisiltrademark or terbinafine HCl).  Filing down the nail to paper thin consistency and soaking or painting with KMnO4 (1:4000), phenol, 10 % salicylic acid, or 1% iodine is useful adjunct to systemic griseofulvin treatment. 12/8/2022 25
  26. 26. CLINICAL MANIFESTATIONS OF RINGWORM SYMPTOMS AND TREATMENT tinea capitis - ringworm of the scalp, eyebrows and eyelashes  Caused by species of Microsporum and Trichophyton.  Fungus grows into hair follicle.  Using a Wood's lamp, on hair Microsporum species tend to fluoresce green while Trichophyton species generally do not fluoresce.  Lack of fluorescence does not mean it isn't Microsporum.  Subculture any strands of hair that fluoresce to help identify the causal agent.  Ectothrix infection - fragmentation of mycelium into conidia (called arthroconidia) around the hair shaft or just beneath the cuticle with destruction of the cuticle. This type of infection caused by M. audounii, M. canis, M. ferrugineum, T. mentagrophytes, T. verrucosum and T. megninii. 12/8/2022 26
  27. 27. Cont…  Endothrix infection - arthroconidia formation occurs by fragmentation of hyphae with the hair shaft with destruction of the cuticle. This type of infection caused T. tonsurans (most common cause), T. violaceum, T. rubrum, and T. gourvillii. All these pathogen species are anthropophilic.  "Gray patch ringworm" ectothrix common disease in children usually not associated with inflammation.  Zoophilic and geophilic dermatophytes infections on man associate with inflammation. Microsporum canis, T. verrucosum, and T. mentagrophytes (zoophilic); M. gypseum and M. fulvum (geophilic species). 12/8/2022 27
  28. 28. Tinea Capitis Gray Patch 12/8/2022 28
  29. 29. Treatment of Tinea Capitis  Ectothrix infections often resolve on their own.  Endothrix infections my become chronic and may continue into adulthood.  Topical treatments are ineffective (don't bother using tonaftate or topical griseofulvin)  Fungistatic agents are somewhat effective (miconazole, clotrimazole) in combination to systemic administration of griseofulvin.  Vigorous daily scrubs of scalp help removal of infectious debris. Do not use this treatment on patients with porphyria (an accumulation of blood pigment called porphyrins in blood stream and urine) or is hypersensitive to griseofulvin. 12/8/2022 29
  30. 30. Viral infection of the skin & mucous membrane 12/8/2022 30
  31. 31. Viral infection of the skin & mucous membrane  Viral diseases associated with maculopapular rash.  Viral disease associated with vesicular rash.  Human warts. 12/8/2022 31
  32. 32. Viral diseases associated with maculopapular rash  Measles.  Rubella (German measles),  Erythema infectiosum (slapped cheek or fifth disease).  Exanthem subitum (roseola infantum or sixth disease). 12/8/2022 32
  33. 33. Measles  Viral etiology : measles virus.  Family : paramyxoviridae,  Enveloped, with two glycoprotein spikes.  Hemagglutinine spikes are the main neutralizing Ag.  Also mediate adsorption of the virus to the host cell surface. 12/8/2022 33
  34. 34. Measles  Transmission : by inhalation of respiratory droplets.  IP : 10 – 14 days.  Target group : children. 12/8/2022 34
  35. 35. Clinical features  Prodromal : Fever, cough, mild conjunctivitis, nasal discharge. Lasting1-3 days.  Rash : maculopapular rash, first appear on the face then spread downward over the trunk and extremities.  The rash is red, become confluent, last 4 or 5 days, then disappears leaving brownish discoloration of the skin.  Recovery is usual. 12/8/2022 35
  36. 36. Clinical features of measles 12/8/2022 36
  37. 37. Prevention  Live attenuated vaccine (MMR).  Contains live attenuated measles, mumps and rubella virus strains.  Administered in one dose.  Protection; good immunity.  Contraindications: should not be given to pregnant women and immunocompromized. 12/8/2022 37
  38. 38. Treatment & lab. diagnosis  Treatment: there is no specific anti viral drug therapy.  Lab. Diagnosis : By detection of IgM-Ab to measles virus. 12/8/2022 38
  39. 39. Rubella (German measles)  Viral etiology: Rubella virus.  Family :Togaviridae.  Genus : Rubivirus.  The virus is enveloped, pleomorphic with helical nucleocapsid.  The viral genome is SS-RNA with positive polarity. 12/8/2022 39
  40. 40. Rubella  Transmission :By inhalation of respiratory droplets.  IP : 14 – 21 days.  Target group : children. 12/8/2022 40
  41. 41. Pathogenesis  After entry, the virus replicates in the epithelial cells lining the URT and invades sub-epithelial tissue.  The virus spreads by the blood stream to lymphoid tissues, followed by viremia.  The virus infects the endothelial cells of blood vessels in the skin, leading to the development of the maculopapular rash.  Virus-Ab complexes are thought to play a role in the development of the rash. 12/8/2022 41
  42. 42. Clinical features  Prodromal : Fever, cough, nasal discharge, mild conjunctivitis.  Rash : Maculopapular rash, first appears on the face then spreads downwards to trunk and limbs.  The rash is red, discrete, usually fades after 48 hr.  In nearly 50% of all infections there is no rash at all.  Rubella is characterized by enlargement of the post-auricular and sub-occipital lymph nodes. 12/8/2022 42
  43. 43. Clinical features of rubella 12/8/2022 43
  44. 44. Prevention , treatment & lab Diagnosis.  Vaccine : Live attenuated vaccine (MMR).  Treatment : There is no specific viral therapy.  Lab. Diagnosis : By detection of IgM-Ab rubella virus. 12/8/2022 44
  45. 45. Viral diseases associated with vesicular rash  HSV-1 infection.  HSV-2 infection.  Varicella (chickenpox).  Zoster. 12/8/2022 45
  46. 46. Family : Herpesviridae.  All herpes viruses are morphologically identical and have the same structure.  They consist of outer envelope and internal nucleocapsid  The viral genome is linear ds-DNA. 12/8/2022 46
  47. 47. Latency  The most important characteristic of herpes viruses is latency.  After resolution of primary infection, the virus remains latent inside the human body for life.  HSV-1, remains latent in the trigeminal ganglion.  HSV-2, remains latent in the sacral ganglion.  VZV, remains latent in the dorsal root ganglion. 12/8/2022 47
  48. 48. Pathogenesis  After entry ,the virus replicates locally in the skin at the site of entry.  Typical herpes lesions are developed.  The virus migrates up the neurons to the trigeminal ganglion and remain latent.  When the virus is reactivated, it travels through neurons to the same site where primary infection occurred. 12/8/2022 48
  49. 49. Transmission  By direct contact with herpes lesions.  By saliva. 12/8/2022 49
  50. 50. Clinical features 1- Gingivostomatitis:  Occurs primarily in children.  The disease is characterized by: Fever, localized pain, vesicles develop on the buccal mucosa and gums, vesicles ruptures to form ulcers.  The disease is self limiting, recovery is usual.  The virus remains latent in the trigeminal ganglion.  The disease usually lasts for 5-12 days. 12/8/2022 50
  51. 51. Gingivostomatitis 12/8/2022 51
  52. 52. Clinical features 2- Herpetic whitlow:  Vesicles and ulcers appear on the tips of the fingers.  Affects nurses and dentist. 12/8/2022 52
  53. 53. Clinical features 3- Kerato conjunctivitis:  Primary infection can involve both conjunctivitis and cornea.  Incase of conjunctivitis, there is localized pain, edema, preauricular adenopathy, lacrimation, vesicles and ulcers appear on the conjunctiva. 12/8/2022 53
  54. 54. Clinical features Keratitis:  Corneal infection varies from superficial that heal without damage to one affecting deeper parts of the eye.  Severe ulceration of the cornea may lead to blindness, usually unilateral.  Symptoms include: severe eye pain, photophobia, blurred vision and intense lacrimation. 12/8/2022 54
  55. 55. Recurrent infections 1- Herpes labiales (cold sores)  Usually milder disease, with short duration.  Few vesicles usually appear around the lips. 2- Keratitis:  Repeated ulceration of the cornea may lead to blindness. 12/8/2022 55
  56. 56. Herpes labialis 12/8/2022 56
  57. 57. Genital herpes  Both HSV-1 & HSV-2 can cause genital herpes.  About 90% of genital herpes are caused by HSV-2 and only 10% by HSV-1.  The signs and symptoms are similar in both cases. 12/8/2022 57
  58. 58. Transmission  Sexually, by direct skin contact with herpetic lesions, vesicle fluid and vaginal secretions.  From infected mother to neonate (neonatal herpes) mainly perinatally (during labor and delivery).  HSV-2 infects sexually active adults, especially those with multiple sexual partners. 12/8/2022 58
  59. 59. Pathogenesis  HSV-2 enters the body through the mucous membrane of the genitalia or through abraded or traumatized skin.  After entry, the virus replicate at the portal of entry.  After resolution of primary infection, the virus travels along the neurons to the sacral ganglion and remain latent for life.  The latent virus may reactivated under certain stimuli and recurrent herpetic infection occurs.  When the virus is reactivated, it travel backs from the sacral ganglion through nerve axons to the same site of primary infection. 12/8/2022 59
  60. 60. Primary genital herpes  Primary infection is usually asymptomatic.  Symptomatic infection is characterized by: localized pain, erythema, edema, inguinal lymph adenopathy, development of localized vesicular rash, vesicles ruptures to form ulcers.  Herpetic lesions appear on the external genitalia of males and females.  Lesions also appear inside vagina, urethra and cervix.  After resolution of primary infection, the virus travels from the genitalia via neurons to the sacral ganglion where it remains latent. 12/8/2022 60
  61. 61. Lab. diagnosis  Isolation of the virus in tissue culture, followed by identification of the virus.  Detection of Ig-M antibody to HSV-2.  Detection of the viral-DNA, using PCR. This method is limited to life threatening conditions, such as encephalitis. 12/8/2022 61
  62. 62. Prevention  There is no vaccine is available yet for HSV-2.  Prevention measures, by practicing safer sex (having one sexual partner). 12/8/2022 62
  63. 63. Treatment  Acyclovir, 400mg thrice daily for 10-days.  Famciclovir, 250 mg thrice daily for 5-days.  Valaciclovir, 1g, twice daily for 10-days. 12/8/2022 63
  64. 64. Varicella (chickenpox)  Caused by varicella-zoster virus (VZV).  The virus is transmitted by inhalation of respiratory droplets and by direct contact with the skin lesions.  Varicalla is a common childhood disease.  Varicella: is the primary illness.  Zoster: is the recurrent form of the disease. 12/8/2022 64
  65. 65. Pathogenesis  After entry, the virus replicates in the epithelial cells of the URT.  The virus spread by blood stream to the skin, where the typical vesicular rash occurs. 12/8/2022 65
  66. 66. Clinical features  IP : 14-21 days.  The disease starts with, fever, malaise, cough, headache, generalized vesicular rash.  The rash first appears on the trunk, then spreads to face and limbs.  The rash appears in successive waves.  Lesions progress from macules to papules to vesicles.  Vesicles ruptures to form ulcers.  The illness usually lasts for 4-7 days. 12/8/2022 66
  67. 67. Clinical features of varicella 12/8/2022 67
  68. 68. Vaccine  Live attenuated vaccine is available.  Administered in one dose.  Recommended for children 1-12 years, teenagers and adult who have not the diseases. 12/8/2022 68
  69. 69. Lab. diagnosis  Detection of Ig-M antibody.  Scraping from the base of the vesicles. 12/8/2022 69
  70. 70. Treatment  No anti-viral drug therapy is necessary for immunocompetent children.  Severe cases of chickenpox is treated with acyclovir. 12/8/2022 70
  71. 71. Zoster (shingles)  Zoster is localized vesicular rash.  It is a disease of elderly.  It is due to reactivation of VZV, which is latent in the dorsal root ganglion. 12/8/2022 71
  72. 72. Types of zoster 1- Thoracic zoster.  Reactivation of virus latent in the dorsal root ganglion, results in a segmental rash, extends from the mid of the back in a horizontal strip, round the side of the chest. 2- Ophthalmic zoster.  Reactivation of virus latent in the trigeminal ganglion results in a localized vesicular rash that involves the scalp, forehead, eye lids and may be cornea. 12/8/2022 72
  73. 73. Types of zoster 3- Ramsay Hunt syndrome.  Localized vesicular rash appears on the tympanic membrane and the external auditory canal.  Often there is a facial nerve palsy. 12/8/2022 73
  74. 74. Zoster 12/8/2022 74
  75. 75. Treatment  Acyclovir (zovirax), 800 mg,orally, five times daily for 5 to 7 days.  Famciclovir (Famvir), 500 mg, orally, three times daily for seven days.  Valacyclovir (valtrex), 1000 mg. orally, three times daily, for seven days. 12/8/2022 75
  76. 76. 10QQQQQ YOU 12/8/2022 76
  77. 77. REFERENCE  Standard treatment guideline for general hospital ,Third Edition, (2014).  J.DiPiro(pharm D), Talbert, Yee et al. Pharmacotherapy_ A Pathophysiologic Approach, Ninth Edition; (2014). 12/8/2022 77