Dermal Microbiology: Viral and Fungal Infections PDF

Dermal Microbiology: Viral, and Fungal Infections Beatrice Saviola Conflict of interest Disclosure In relation to this presentation, Dr. Saviola has no financial interests or other conflicts that need to be discloses. 2  Refer...

Dermal Microbiology: Viral, and Fungal Infections Beatrice Saviola Conflict of interest Disclosure In relation to this presentation, Dr. Saviola has no financial interests or other conflicts that need to be discloses. 2  References Warren Levinson Medical Microbiology, Chapter 37 Herpesviruses, Poxviruses, and Human Papilloma Virus Warren, Levinson, Medical Microbiology and Immunology, Chapter 47 Basic Mycology, Chapter 48 Cutaneous and Subcutaneous Mycoses, Chapter 50 Opportunistic Mycoses https://accessmedicine-mhmedical- com.proxy.westernu.edu/book.aspx?boo kid=3123#261979831  Objectives 1. After this lecture the student will be able to formulate the basic and clinical microbiology of various viruses and fungi that result in dermal infections. 2. After this lecture the student should be able to identify viral, or fungal infectious agents based on a clinical scenario and microbial characteristics. Localized viral infections of the skin Some viruses infect the skin, replicate locally and remain in that area. Examples of such viruses are: herpes simplex viruses, human papilloma viruses, mulluscum contagiosum virus. Families of DNA Viruses Herpes Simplex Virus Enveloped, icosahedral, DNA virus with ability to become latent within neurons, replicates in nucleus. Herpes Simplex type 1 and 2- they have a worldwide distribution, humans are only natural reservoir, and transmission is by direct contact. HSV-1-causes herpes labialis and is transmitted by oral secretions. HSV-2-causes genital herpes and is transmitted by genital secretions. HSV-1 and HSV-2 can infect the same tissues but have a predilection for those tissue indicated above. Spread of HSV to sensory neurons  Pathogenesis Local replication resulting in vesicular lesions Primary infection- frequently asymptomatic, gingivostomatitis and pharyngitis in children with HSV-1, Genital lesions in adolescents and young adults with HSV-2 Latent infections. Recurrence- stress, age, and damage of tissue such as sunburn can trigger recurrence and spread virus.  Factors affecting primary infection- Age- HSV-1 is acquired early, HSV-2 not until onset of sexual activity. Occupation- dentists et may get herpetic whitlow (on the finger). Sexual practices- incidence of HSV-2 correlates with # of sexual partners. Mother to neonate- newborns may acquire HSV-2 from mother perinatally through passage of infected birth canal. Manifestations in newborn- Infants infected at birth get a diffuse encephalitis. 60% die of overwhelming infection, and the majority of survivors are left with severe ocular and neurological sequelae. Prevention- Caesarian birth of children of infected mothers with lesions in the genital area at the onset of labor, and especially if it is the mother’s primary infection.  Tzank smear to look for syncytia formation. Cowdry type A inclusion bodies. There are antivirals that can inhibit replication of HSV, such as acyclovir, valacyclovir, and famciclovir  Warts (papilloma) Caused by Human Papilloma Virus (HPV) They are naked icosahedral dsDNA. There are numerous types with different site predilections and consequences of infection. They are very host specific. Usually passed by close personal contact; the role of fomites is uncertain Minor trauma may also be important.  Human papillomavirus infection and release of viral particles Gardasil vaccine available to prevent infection with 9 HPV types/9 valent (types 6, 11, 16, 18, 31, 33, 45, 52, 58) Previous vaccines: Quadrivalent of the most common HPV strains (6, 11, 16, and 18) that cause ano-genital warts and cervical cancer. For males and females. Ceravix protects females against HPV 16 and 18.  Molluscum contagiosum A Pox virus: DNA enveloped virus w/ complex capsid and membrane. REVIEW FOR BOARDS- virus replicates within cytoplasm. Transmitted by direct contact or fomites. Virus infects the basal cell layer and replicates. Lesions are smooth firm shiny flesh colored to pearly white hemispheric papules with umbilicated (depressed) centers confined to the skin and mucous membranes. Children, people living in tropical climates, and people with HIV tend to get lesions more often. Molluscum contagiosum- in a patient with AIDS Molluscum contagiosum (benign epidermal tumors), especially in people infected with HIV and children. Localized infection. Transmitted by direct contact or fomites. Virus infects the basal skin cell layer and replicates. Lesions are smooth firm shiny flesh colored to pearly white hemispheric papules with umbilicated centers confined to the skin and mucous membranes. Children, people living in tropical climates, and people with HIV tend to get lesions more often. Systemic viral infections of the skin (Mpox) Monkeypox A member of the poxvirus family, this virus may have a reservoir in rodents, but also infects primates. Two clades. Clade I and clade II with subclades. Clade I: outbreaks in Central and Eastern Africa. There was is an outbreak of clade II in the US and worldwide. Vaccinia virus protects against the virus. 2022-2023 outbreak: Outbreak peaked in August 2022, now lower case numbers. Spread through close or direct contact (can be intimate contact), prolonged face-face contact, and contact with fomites (inanimate objects) used or touched by the person with mpox. Virus is present in skin lesions, saliva, feces, and urine. Contact with skin lesions can transmit the virus. Vaccines effective protecting against Monkeypox: They are based on vaccinia virus JYNNEOS- replication-deficient vaccinia.  Fungi They are eukaryotic cells. With very few exceptions the natural habitat is water, soil or decaying vegetation. Only a few species are pathogenic for humans.  Yeasts- These are unicellular and reproduce by budding. Some also produce pseudohyphae. On solid media they grow as smooth colonies and look very much like bacteria. Yeasts and molds have a slower growth rate than bacteria. Molds- They form multicellular structures with hyphae being produced. They usually produce filamentous colonies on solid media. Fungi can switch between molds and yeast and this often happens in humans. Mold in the cold;yeast in the heat. Cell membrane and wall structure The cell membrane and wall are similar to gram positive bacteria in that there is a cell membrane surrounded by a cell wall. The fungal membrane contains Ergosterol. This is different than human cell membranes that have cholesterol. The cell wall contains Chitin in the inner most layer, then glucan, then mannoproteins. Unlike bacteria it contains no peptidoglycan.  KOH Preparation The skin is swabbed with 70% ETOH and allowed to air dry. The surface is scraped to remove skin scales or hair that contain the fungus. The specimen is treated with 10% potassium hydroxide to destroy tissue elements, specifically keratin (thus KOH is a clearing agent. One looks for branching hyphae or yeast cells. **In histological sample use periodic acid- Schiff stain. KOH (candida and microsporum)  Dermal fungal infections can be classified as follows: Superficial mycoses- limited to the outermost (cornified) layers of the skin and hair, no immune response. Cutaneous mycoses- infections that are deeper in the epidermis, hair, and nails, immune response. Subcutaneous- involving the dermis, subcutaneous tissues, muscle and fascia, increased destruction.  Superficial mycoses- these diseases are usually cosmetic in nature Pityriasis (tinea)Versicolor-Caused by lipophilic Malassezia furfur. Budding yeast and hyphae in skin scraping KOH prep and look for spaghetti and meatball appearance. The metabolism of fungus may inhibit melanin. Dimorphic. Tinea nigra-caused by Hortaea (Cladosporium) werneckii has a pigment that is melanin like. Dimorphic. Pityriasis or Tinea Versicolor  Tinea nigra Hortaea werneckii Cutaneous Mycoses-Dermatophytes Diseases of the skin, hair, and nail. They are generally restricted to the keratinized layers of the skin. These infections may evoke various immune reponses causing pathologic changes in the host that may be expressed in the deeper tissues of the skin. Monomorphic. Look for branching hyphae. These organisms express keratinases that can break down keratin. Spreads human to human. The clinical manifestations of the disease are referred to as ringworm, or tinea. tinea pedis: feet, tinea capitis: scalp, tinea manus: hands, tinea unguium: nails, tinea corporis: body.  Tinea pedis- athletes foot caused by Trichophyton rubrum, T. mentagrophytes, and Epidermophyton floccosum, common in adolescents and young males. Tinea Cruris- jock itch caused by T. rubrum and E. floccosum. Tinea unguium- infection of the nail plate caused by T. rubrum and T. mentagrophytes Tinea corporis- (ring worm) infection of the body skin found especially in children, it can be caused by any dermatophyte. Tinea manuum- infection of the palms of the hand, usually caused by T. rubrum. Tinea pedis Tinea unguium Tinea corporis  Candidiasis dermatomycosis This is caused by Candida albicans which is a dimorphic fungus with both yeast and mycelial forms. These fungi are part of the normal flora of mucous membranes. They have a limited ability to invade tissues and are considered opportunistic when invading blood and internal organs. Skin infections can occur however, and predisposing factors include : obesity, wetness, antibacterial therapy and cellular immune deficiencies. Not opportunistic. In infants, cutaneous candidiasis can result from diaper rash. Not opportunistic. Candida albicans: Pseudohyphae and true hyphae in tissues.  Subcutaneous Mycoses Sporotrichosis (Sporothrix schenckii) This is a dimorphic fungus. It is usually found in soil and decaying vegetation. It is usually introduced by accidental implantation. After inoculation, a small ulcer or subcutaneous nodule appears. The organism spreads through the lymphatics. Dimorphic- it is a mold in environment and a yeast in the human body. Sporotrichosis  Summary Superficial mycoses are limited to the cornified layer of the skin and cause little inflammation but are a cosmetic problem. Cutaneous mycoses go a little deeper into the epidermis and utilize keratinases to generate nutrients for themselves. They may elicit an immune response. Subcutaneous mycoses go deeper into the dermis, subcutaneous tissues, muscle and fascia.