Microbial Diseases of the Skin and Eyes PDF
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Summary
This document is a study of microbial diseases affecting the skin and eyes, covering objectives, etiological agents, diagnoses, and treatment for various conditions. It details different diseases like blepharitis, hordeolum, chalazion, periorbital cellulitis, acute and chronic dacryocystitis, conjunctivitis, ocular lymphogranuloma venereum, trachoma, and more. It also includes sections on the structure and function of the skin and relevant terms for skin conditions like vesicles, bullae, macules, papules, and pustules.
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MICROBIAL DISEASES OF THE EYES AND SKIN PHMP 211 (EYES) OBJECTIVES To Identify the different microbial disease affecting the skin and eyes To understand the mechanism of disease To identify the standard therapy. The Etiological agents that may affect the eys will vary dependin...
MICROBIAL DISEASES OF THE EYES AND SKIN PHMP 211 (EYES) OBJECTIVES To Identify the different microbial disease affecting the skin and eyes To understand the mechanism of disease To identify the standard therapy. The Etiological agents that may affect the eys will vary depending on the area and typ of tissue affected Disease spread may be divided into: Eyelids and tissue surrounding the eyes Conjunctiva Cornea Intraocular area Eyelids and tissue surrounding the eyes Blepharitis Etiological agent: Demodex folliculorum (a mite) followed by bacterial infection Staphilococcus aureus or Staphilococcus epidermidis Diagnosis: due to an allergic reaction to the mite which resides in the eyelash or the eyebrow Abscesses may form in and around the follicles, destroying the follicles, with the loss of lashes and the formation of ulcers. Treatment: Glucocorticoid for the allergic reaction There may be a history of itching and Doxycycline or Minocycline ( C/I in scaling of the lid since early children and pregnant) childhood. The patient describes an incessant urge to pull on the lashes in Azithromycin ( alternative) an attempt to remove the scales Hordeolum and Chalazion Etiological agents: Generally Staphylococcus aureus, but may also be caused by Pseudomonas aeruginosa and Proteus sp. Diagnosis: Obstruction of the orifice of a gland (Meibomian, Zeis, or Moll) seems to be the primary pathological event in the formation of hordeolum (Stye)-. A red nodule that is quite painful develops and is surmounted with a yellowish top as the lesion matures. The histopathology is typical of acute suppurative inflammation. ◼ Chalazion evolve from hordeolum that do not drain spontaneously or are not incised. ◼ There is usually persistent chronic inflammation, and granuloma formation may occur as sebaceous secretions are impounded. Treament: Erythromycin: for susceptible strains and for prevention of corneal and conjunctival infections Cephalexin: for acute hordoelum Doxycycline: may be added if there recurrent lesions or significant meibomitis Periorbital cellulitis Etiological Agent: Staphylococcus aureus ( most common) S. pneumoniae, H. influenzae Diagnosis: Characterized by acute eyelid erythema and edema Also known as periseptal cellulitis Treatment: Clindamycin as empirical therapy Doxycycline, cotrimoxazole: alternative therapy Acute Dacrocystitis Etiological agents: S. aureus, S. epidermidis, Streptococcus pneumoniae Diagnosis: This is an infection of the lacrimal sac, almost always secondary to obstruction of the lacrimal duct. occurs when both the upper and lower ends of the drainage system become partially or totally obstructed. The major symptom is pain in the tear sac area. There are also erythema, edema, a purulent discharge and epiphora Treatment Coamoxiclav, Sultamicillin, Levofloxacin Tobramycin opthalmic Tobramycin plus dexamethasone ophthalmic Chronic Dacrocysititis Etiological agents: Streptococcus pneumoniae Hemophilus influenzae Candida albicans Aspergillus sp. Actinomyces sp Chronic dacryocystitis is usually caused by a single site of partial or complete obstruction within the lacrimal sac or within the nasolacrimal duct. The infection is usually the result, and not the cause, of obstruction Obstruction may be due to: 1. Trauma 2. Tumors 3. Foreign bodies 4. Delayed canalization in neonates 5. Closure of canal in post menopausal women Conjunctiva Pink Eye Conjunctivitis Etiological agent: Haemophilus aegypticus and/or Moraxella lacunata Diagnosis: The only symptoms are conjunctivitis, either chronic or acute, and severe inflammation of the cornea. Diagnosis is via isolation of the organism ( a Gam-negative slender rod). Treatment: Topical sulfacetamide, erythromycin, ciprofloxacin, gatifloxacin or ofloxacin NEW agent: besifloxacin ◼ Opthalmic suspension Ocular Lymphogranuloma Venereum Etiological agent: Chlamydia trachomatis Diagnosis: This is a chlamydial disease transmitted to the fetus during passage down the birth canal. Inflammation begins about five days after birth and never results in follicle formation (thus, it differs from trachoma and inclusion conjunctivitis). Corneal scars, conjunctival scars, and micropannus formation occur. It is rarely a cause of blindness. There will be inclusions in the epithelial cells of the conjunctiva. Treatment: Azithromycin, Erythromycin Doxycycline (DOC) but caution in children Trachoma Caused by Chlamydia trachomatis This disease is limited to man, infecting only epithelial cells of the eye and possibly the nasopharynx; no systemic involvement has been described. It is found worldwide, and is the greatest single cause of blindness. Scarring of the conjunctiva may cause the eyelids to turn inward so that the lashes scratch the cornea Distortion of the structures of the external eye also interferes with normal lacrimal flow, growth of lashes, and function of glands; as a result, bacterial infections of trachomatous eyes are common Normal Tarsal Conjunctiva: Pink,smoth, thin and transparent. Over the whole area of the tarsal conjuctiva, there are large deep- lying blood vessels that run vertically (TF)Trachomatous Inflammation- follicular Presence of five or more follicles in the upper tarsal conjunctiva ◼ Follicles are round swellings that are paler than the surrounding conjunctiva, appearing white, grey or yellow ◼ O.5mm in diameter (TI)Trachomatous Inflammation-Intense Pronounced inflammatory thickening of the tarsal conjuctiva that obscures more than half of the normal deep tarsal vessels ◼ The tarsal conjunctiva appears red, rough and thickened, with numerous follicles which may be covered by the thickened conjuctiva Trachomatous scarring (TS) The presence of scarring in the tarsal conjunctiva Scars are visible as white lines or sheets in the tarsal conjunctiva. They are glistening and fibrous in appearance. Scarring, especially diffuse fibrosis, may obscure the tarsal blood vessels Trachomatous Trichiasis (TT) At least one eyelash rubs on the eyeball Evidence of recent removal of inturned eyelas should also be graded as trichiasis Corneal Opacity Easily visible corneal opacity over the pupil The pupil margin is blurred viewed through the opacity. Such corneal opacities cause significant visual impairment ( less than 6/18 or 0.3 vision) and visual acuity should also be measured Trachoma Treatment Based on WHO SAFE strategy: ◼ Azithromycin ◼ DOC for trachoma ◼ 1% tetracycline ointment ◼ Aternative for Azithromycin Viral Conjunctivitis Etiological agents: Adenovirus, types 3,7 and 8 Human Herpesvirus 1 (Herpes simplex 1 virus) Human Herpesvirus 2 (Herpes simplex 2 virus) Varicella-Zoster virus Cytomegalovirus Diagnosis Bilateral conjunctivitis which is usually self limited. It may be recurrent with herpesvirus. No constitutional symptoms are present Treatment: For Symptomatic relief ◼ Artifical tears ◼ Azalastine opthalmic ◼ Competes with H1 receptors ◼ Ketotifen ◼ Relatively selective H1 receptor antagonist that inhibits the release of mastcells Fungal Conjunctivitis Etiological agents ◼ Candida albicans, Sporothrix schenkii, Allescheria sp., Aspergillus sp., Mucor sp Diagnosis: An uncommon disease which can be acute or chronic. Often secondary to fungal infections of other parts of the body. Often aggravated by glucosteroids and initiated after antibiotic therapy. Diagnosed by isolation of the etiological agent Treatment ◼ Natamycin: Initial drug for fusarium disease ◼ Amphotericin B: First agent of choice for corneal infections due to yeast such as candida ◼ Azoles: For Fusarium, Aspergillus, Curvilaria and Candida ◼ Flucytosine: Active against Candida and Cryptococcus ◼ Voriconazole: DOC for aspergillus, Fusarium Blastomyces, Coccidiodes, Curvularia and other fungal infection Parasitic conjunctivitis River blindness Onchocerca vulvulus ◼ Onchocerciasis: transmitted by simulium blackflies ◼ Second leading cause of blindness in the world ◼ Treatment: ◼ Ivermectin: Drug of choice ◼ Moxidectin: a macrolytic lactone for 12 yrs and older, does not kill adult O. vulvulus ◼ Doxycycline: ▪ Adjunct therapy ▪ may be used to eliminate the endosybiotic bacteria Woblachia; this disrupts production of microfilariae by the adult female worm Loa loa African eye worm ◼ Transmitted by Chrysops deer fly ◼ Treatment: ◼ Diethylcarbamazine ◼ Available only through CDC ◼ Serves as inhibitor of arachidonic acid metabolism in microfilaria ◼ Albendazole ◼ For treatment of symptomatic loiasis with parasitemia of 8000 microfilariae/mL Cornea Ophthalmia neonatorum Etiological agent: Neisseria gonorrhoeae Diagnosis: The disease is contracted from a mother with gonorrhea as the fetus passes down the birth canal. Infection does not occur in utero. At one time about 10% of all cases of blindness in the United States was due to this disease. Corneal inflammation is the major clinical sign. Treatment: Erythromycin oral or ointment ◼ Systemic treatment is necessary Silver nitrate drops ( rarely used now) ◼ May be used to prevent disease Bacteria Keratitis Inflammation of the cornea Features: ◼ Rapid progression ◼ Corneal destruction may occur in 24-48 hours ◼ Corneal ulceration, stromal abscess formation, surrounding corneal edema and anterior segment inflammation Etiological agents: ◼ Streptococcus, Pseudomonas, Enterobacteriaceae ( Klebsiella, Enterobacter, Serratia and Proteus), Staphylococcus Treatment: Medical ◼ Tobramycin (14mg/mL) ◼ 1 drop every hour alternating with fortified cefazolin or vancomycin ◼ Fourth generation fluoroquinolones ◼ Moxifloxacin and Gatifloxacin ◼ Moxi: penetrates better than Gati ◼ New fluoroquinolone ◼ Besifloxacin ◼ Approved in 2009 for bacterial conjunctivitis Fungal Keratitis Aspergillus species is the most common isolate in fungal keratitis world wide, followed by Fusarium then penicillium More common in men than in women May be acquired through unhygienic contact lens use This may extend from the cornea to the sclera and intraocular structures May cause scleritis, endopthlamitis, panopthalmitis ◼ Very difficult to treat and may result to visual loss and loss of eye Treatment Ampothericin B: Drug of choice to treat patients with fungal keratitis caused by yeast Natamycin: for filamentous organisms ◼ The only commercially available topical opthalmic antifungal preparation ◼ Useful against Fusarium Surgical Treatment ◼ For unresponsive to treatment ◼ Some cases, even surgery will not restore vision ◼ May include corneal transplantation Intraocular Uveitis Nonpurulent uveitis seldom involves the entire uveal tract but may occur predominantly in the anterior segment (iritis, iridocyclitis) or the posterior segment (posterior uveitis, retinitis Common causes of Anterior uveitis: Mumps virus, Human Herpesvirus 3 (Varicella-Zoster virus), Rubella virus, Rubeola virus, Human Herpesvirus 1 (Herpes simplex 1 virus) Common causes of Posterior uveitis: Toxoplasma gondii (25% of all cases) Toxocara sp., Cryptococcus neoformans, Histoplasma capsulatum, Mycobacterium tuberculosis, Cytomegalovirus, Herpes simplex 1 virus, Human immunodeficiency virus MICROBIAL DISEASES OF THE SKIN AND EYES PHMP (SKIN) Structure and Function of the Skin The skin is a physical barrier against microorganisms. Moist areas of the skin support larger populations of bacteria than dry areas. Structure and Function of the Skin 1. Epidermis 2. Dermis Components: Keratin Sebum Perspiration Structure and Function of the Skin Epidermis The outer portion of the skin Composed of several layer of epithelial cells The outermost layer, the stratum corneum, consists of many rows of dead cells that contains a waterproofing protein called keratin Effective physical barrier against mo Structure and Function of the Skin Dermis The inner, relatively thick portion of skin Composed mainly of connective tissue The hair follicles, sweat gland ducts, and oil gland ducts in the dermis provide passage- ways through which microorganisms can enter the skin and penetrate deeper tissues. Structure and Function of the Skin Perspiration Provides moisture and some nutrients for microbial growth Also contains salt which inhibits many micro- organisms Contains the enzyme lysozyme, which is capable of breaking down the cell walls of certain bacteria; and antimicrobial peptides. Structure and Function of the Skin Sebum Secreted by oil glands A mixture of lipids (unsaturated fatty acids), proteins, and salts Prevents skin and hair from drying out Structure and Function of the Skin Mucous membrane a.k.a. mucosa Lines the body cavities that open to the exterior, i.e. gastrointestinal, respiratory, urinary, and genital tracts Consists of sheets of tightly packed epithelial cells attached at their bases to a layer of extracellular material called basement membrane Structure and Function of the Skin Many secretes mucus Other mucosal cells have cilia, i.e. respiratory system Often acidic Membranes of the eyes are mechanically washed by tears, and the lysozymes in tears destroys the cell walls of certain bacteria Normal Microbiota of the Skin Microorganisms that live on skin are resistant to desiccation and high concentrations of salt. Gram-positive cocci predominate on the skin. Washing does not completely remove the normal skin microbiota. Normal Microbiota of the Skin Members of the genus Cutibacterium metabolize oil from the oil glands and colonize hair follicles. Malassezia furfur yeast grows on oily secretions and may be the cause of dandruff. Normal Microbiota of the Skin The majority (90%) of skin microbiota consist of coagulase-negative Staphylococcus epidermidis. Microbial Diseases of the Skin Different Terms for Rashes and Lesions Vesicles are small fluid-filled lesions Bullae are vesicles larger than 1 cm Macules are flat, reddened lesions Papules are raised lesions Pustules are raised lesions containing pus Papules Bullae Vesicle Pustules Macules Bacterial Diseases of the Skin Staphylococcus Staphylococci are spherical gram-positive bacteria that form irregular grape-like clusters Divided into those that produce coagulase, and those that do not Coagulase-positive ◼ S. aureus Coagulase-negative ◼ S. epidermidis Staphylococcus Staphylococcus epidermidis Coagulase-negative Very common on the skin Generally pathogenic only when the skin barrier is broken or is invaded by medical procedures, e.g. insertion and removal of catheters into veins Staphylococcus Staphylococcus aureus Resident microbiota of the nasal passage Forms golden-yellow colonies Almost all pathogenic strains of S. aureus produce coagulase Some strains have impressive array of virulence factors and means of evading host defenses S. aureus infects the skin Blocks Resistant to chemotaxis of opsonization neutrophils It stimulates vigorous Produce Survive well inflammatory response toxins that kills within the phagocytic phagosome cells Macrophages and Neutralize the neutrophils are Cell wall is peptide lysozyme attracted to the site of defensin on resistant infection skin However, S. aureus evade host defense Staphylococcus Localized infections (sties, pimples, and boils) result from entry of S. aureus through openings in the skin. Staphylococcus Carbuncle is a furuncle which extensively damages neighboring tissues Produce a hard, round deep inflammation of tissue under the skin Patient can exhibit general illness with fever Staphylococcus Impetigo is highly contagious skin infection caused by Staphylococci. Characterized by isolated yellow pustules that become crusted. Staphylococcus Toxemia occurs when toxins enter the bloodstream; staphylococcal toxemias include scalded skin syndrome and toxic shock syndrome. Staphylococcus S. aureus produces exfoliative toxins: Exfoliatin A – causes localized, bullous impetigo Exfoliatin B – causes the systemic infection of scalded skin syndrome Staphylococcus Scalded skin syndrome is also characteristic of the late stages of toxic shock syndrome (TSS). Potential life-threatening condition, fever, vomiting, and a sunburn-like rash Followed by shock and sometimes organ failure (especially kidney failure) Caused by a staphylococcal toxin called TSST-1 Streptococcus Streptococci are gram-positive spherical bacteria usually grows in chains. Prior to division, the individual cocci elongate on the axis of the chain, and then the cells divide. Cause a wide range of disease conditions including meningitis, pneumonia, sore throat, otitis media, endocarditis, puerperal fever, and even dental caries. Streptococcus Streptococci are classified according to their hemolytic enzymes (hemolysin) and cell wall antigens. Hemolytic activity ◼ Alpha, beta, gamma Cell wall antigen ◼ Group A to T Streptococcus Streptococcus pyogenes Group A beta-hemolytic streptococci (GAS) produce a number of virulence factors: M protein, deoxyribonuclease, streptokinases, and hyaluronidase. Cause severe and rapid tissue destruction. Streptococcus Erysipelas Skin erupts into reddish patches with raised margins Can progress to local tissue destruction and even enter the bloodstream causing sepsis Usually appears first on the face High fever is common Streptococcus Necrotizing fasciitis Invasive group A streptococcal infection that destroys tissue and initially resembles TSS “Flesh-eating bacteria” Causes by pyrogenic toxins, streptococcal M- protein types (act as superantigens) Associated with streptococcal TSS Pseudomonas Pseudomonas aeruginosa Aerobic gram-negative rod Resistant to many antibiotic and disinfectant Can survive in any moist environment, traces of unusual organic matter such as soap films, cap liner adhesives Pseudomonas Diseases caused by P. aeruginosa include otitis externa, respiratory infections, burn infections, and dermatitis Produces an endotoxin and several exotoxins Other Bacteria Mycobacterium ulcerans Causes deep-tissue ulceration or Buruli ulcer Other Bacteria Cutibacterium acnes Formerly known as Propionibacterium acnes Its metabolic products (fatty acids) cause inflammatory acne Comedonal (mild) acne Inflammatory (moderate) acne Nodular cystic (severe) acne Viral Diseases of the Skin Warts Papillomaviruses cause skin cells to proliferate and produce a benign growth called a wart or papilloma. Warts are transmitted from one person to another by direct contact, even sexually. After infection, there is an incubation period of several weeks before the warts appear. Warts Warts may regress spontaneously or be removed chemically or physically. Nonpharmacologic Treatment Cryotherapy Electrodessication Acidtreatment Laser Warts Pharmacologic Treatment Salicylicacid Podofilox Imiquimod Bleomycin Variola Variola, also known as smallpox, is caused by an orthopoxvirus known as smallpox (variola) virus. Variola virus causes two types of skin infections: variola major and variola minor. Variola Smallpox is transmitted by the respiratory route, and the virus is moved to the skin via the bloodstream. The growth of the virus in the epidermal layers of the skin causes lesions that becomes pustular after 10 days or so. Variola Smallpox has been eradicated as a result of a vaccination effort by the World Health Organization. Varicella-Zoster Chickenpox (varicella) is a relatively mild disease when contracted, as it usually is, in childhood. It is the initial infection of a herpesvirus Varicellovirus. The species is varicella-zoster, or officially, human herpesvirus (HHV-3). Varicella-Zoster HHV-3 is transmitted by the respiratory route and is localized in skin cells after about 2 weeks. The infected skin is vesicular for 3 to 4 days. Complications of chickenpox include encephalitis and Reye’s syndrome. Varicella-Zoster Shingles Characterized by a vesicular rash along the affected cutaneous sensory nerves. After chickenpox, the virus can remain latent in nerve cells and subsequently activate as shingles. Varicella-Zoster Treatment HHV-3 can be treated with acyclovir. An attenuated live vaccine is available. Herpes Simplex Herpes simplex viruses (HSV) can be separated into two identifiable groups: HSV-1 (or human herpesvirus 1) HSV-2 (or human herpesvirus 2) Herpes Simplex Cold sores Herpes simplex (HSV-1) infection of mucosal cells Painful, short-lived vesicles that occur near the outer red margin of the lips https://www.verywellhealth.com/stages-of-a-cold-sore-outbreak-4173005 Herpes Simplex HSV-1 is transmitted primarily by skin contact, oral and respiratory routes. The virus remains latent in nerve cells, and cold sores can recur when the virus is activated. Herpes Simplex Herpes encephalitis occurs when herpes simplex viruses (HSV-1 and HSV-2) infect the brain. Treatment Acyclovir has proven successful in treating herpes encephalitis. Measles Measles (Rubeola) Caused by measles virus An extremely contagious viral disease transmitted by the respiratory route Vaccination (MMR vaccine) against measles provides effective long-term immunity Measles After the measles virus has incubated (10-12 days) in the upper respiratory tract, the following signs and symptoms appear. Symptoms (like fever) similar to common cold. Macular lesions appear on the skin. Koplik’s spots appear on the oral mucosa. ://phil.cdc.gov/PHIL_Images/20040908/4f54ee8f0e5f49f58aaa30c1bc6413ba /6111_lores.jpg Measles Complications of measles include middle ear infections, pneumonia, encephalitis, and secondary bacterial infections. Rubella Rubella (German measles) The rubella virus is transmitted by the respiratory route and causes a red rash and light fever. Congenital rubella syndrome can affect a fetus when a woman contracts rubella during the first trimester of her pregnancy. Rubella Vaccination with live, attenuated rubella virus provides immunity of unknown duration. Other Viral Diseases Fifth disease Also known as erythema infectiosum Causes by human parvovirus B19 Characterized by symptoms similar to mild influenza and a slapped-cheek facial rash that slowly fades Roseola Mild, very common childhood disease caused by HHV-6 and HHV-7 Other Viral Diseases Hand-foot-and-mouth disease An infection in young children in day care, preschool, and kindergarten Caused by several enteroviruses Spread by contact with mucous or saliva of an infected person Characterized by sore throat, then rashes appearing on hands, feet, mouth, tongue, and interior cheeks Fungal Infection Fungal infections or mycoses cause a wide range of diseases in humans. 1. Superficial Infection 2. Cutaneous Infection 3. Subcutaneous Infection 4. Deep mycosis Superficial Fungal Infection Pityriasis versicolor Common superficial mycosis, which is characterized by hypopigmentation or hyperpigmentation of skin of the neck, shoulders, chest, and back Due to Malassezia furfur which involves only the superficial keratin layer Superficial Fungal Infection Black Piedra A superficial mycosis due to Piedraia hortae which is manifested by a small firm black nodule involving the hair shaft Superficial Fungal Infection White Piedra Due to Trichosporon beigelii is characterized by a soft, friable, beige nodule of the distal ends of hair shafts Superficial Fungal Infection Tinea Nigra Most typically presents as a brown to black silver nitrate-like stain on the palm of the hand or sole of the foot and and is caused by Phaeoannellomyces werneckii Cutaneous Fungal Infection Dermatophytoses Caused by fungi (Microsporum, Trichophyton, and Epidermophyton) that colonize the outer layer of the epidermis cause dermatomycoses Also known as ringworm, or tinea These fungi grow on keratin-containing epidermis, such as hair, skin, and nails Name Common Name Location Tinea pedis Athlete’s foot Feet Tinea unguium Onchomycosis Nails Tinea corporis Ringworm Arm, legs, and trunk Tinea cruris Jock itch Groin area Hands and palm Tinea manuum area Tinea capitis Scalp Tinea barbae Barber’s itch Facial hair Tinea faciei Face fungus Face Athletes’ foot Onychomycosis (Tinea unguium) Ring worm (Tinea corporis) Tinea cruris (jock itch) Tinea capitis Tinea barbae Tinea faciei Cutaneous Fungal Infection Diagnosis is based on the microscopic examination of skin scrapings or fungal culture. Cutaneous Fungal Infection Dermatomycoses Cutaneous infections due to other fungi, the most common of which are Candida albicans. C. albicans causes infections of mucous membranes and is a common cause of oral thrush and vaginitis. Subcutaneous Fungal Infection Sporotrichosis Results from a soil fungus (Sporothrix schenckii) that penetrates the skin through a wound Common among gardeners or people working with soil Subcutaneous Fungal Infection Chromoblastomycosis Subcutaneous mycosis characterized by verrucoid lesions of the skin Most common causes are: Fonsecaea pedrosoi (Pedroso’s disease) Fonsecaea compacta (Fonseca’s disease) Cladosporium carionii (Cladosporiosis) Phialophora verrucosa Subcutaneous Fungal Infection Madura foot (mycetoma) Chronic infection of the skin and underlying tissues by both bacteria (actinomycetoma) and fungi (eumycetoma). Suppurative and granulomatous subcutaneous mycosis Occur most often in farmers, hunter-gatherers, and field laborer Parasitic Infestation of the Skin Scabies Scabies Involves intense local itching Caused by a tiny mite Sarcoptes scabiei burrowing and laying eggs in the skin The mite is transmitted by intimate contact https://www.nhs.uk/conditions/scabies/ Scabies Mite lives ~25 days, but by that time eggs have been laid and hatched Diagnosis Microscopic examination of skin scrapings Treatment Topical permethrin Oral ivermectin Pediculosis Pediculosis Infestation by the head lice Pediculus humanus capitis Lice are easily transferred by head- to-head contact https://www.skin-disorders.net/diseases/pediculosis-capitis.html © Gilles San Martin (2010)