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83 Cards in this Set
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Pityriasis versicolor
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Etiologic agent is the lipophilic yeast Pityrosporum furfur (unique in its requirement of oil or fatty acids in the medium for growth.
Chronic, mild, usually asymptomatic infection of the stratum corneum. The lesions are discrete and appear as discolored or depigmented areas of the skin. Fawn or dark brown patches may be observed, or the lesion may consist of one continuous scaling sheet. There is seldom any irritation or inflammatory response. Treatment is a topical or systemic azole or 2% selenium sulfide lotion (Selsun Blue) |
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Piedra
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White piedra is caused by Trichosporon cutaneum; Black piedra is caused by Piedraia hortae
Fungus infection of the hair shaft characterized by the presence of firm, irregular nodules. The nodules are composed of fungal elements cemented together anywhere along the hair shaft, and multiple infections of the same strand are common. Treatment with a topical azole is beneficial but relapse is common. |
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Tinea capitis
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Dermatophyte infection of the scalp, eyebrows, and eyelashes caused by species of the genera Microsporum and Trichophyton.
Characterized by the production of a scaly erythematous lesion and by alopecia that may become severely inflamed. In extensive lesions the infected hairs break off sharply at the follicular orifice, leaving a spore filled stub or "black dot". |
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Tinea corporis
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Microsporum are the predominant cause in children, who are more susceptible to these species.
Ringworm; infection of the stratum corneum of the epidermis in glaborous skin. Annular lesions have a center which are scaly and usually tend to heal; the periphery is an advancing circle of vesicles and papules. Vesicular lesion is characterized by an elevated inflamed margin with central scaling vesicles or crust. |
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Tinea cruris
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Trichophyton and Epidermophyton are the most frequently implicated fungi.
Involves the groin, perineum, and perianal region. The lesion is characteristically sharply demarcated, with a raised, erythematous margin and thin, dry epidermal scaring. It is usually severly pruritic (itchy). |
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Tinea pedis
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Trichophyton is most commonly involved.
Involves the feet, particularly the toe webs and soles (Athlete's foot). This is the most common dermatophytic fungal infection, with up to 65% of surveyed populations having evidence of infection. |
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Onychomycosis
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May be caused by Candida and other fungi.
Fungal infection of the nails, usually occurs as an extension of infections of adjacent toe or palmar skin. Nails become distorted, deformed, thickened, and discolored, with an accumulation of debris beneath them, and may have ragged or furrowed edges. |
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Onychomycosis treatment
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Onychomycosis is difficult to eradicate and require prolonged course (6 to 12 weeks) of systemic therapy with terbinafine or itraconazole. Relapses are common.
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Tinea treatment
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Can be accomplished topically with topical azole agents (e.g. miconazole, clotrimazole). Therapy of tinea corporis is more refractory and usually requires systemic therapy, such as itraconazole (azole). Terbinafine (topical, oral) is also used.
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Dermatophytes
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Molds that cause infections of keratinized tissues, epidermis, hair and nails. All of these fungi contain the enzyme keratinase with allows them to digest keratin for growth.
Genera of fungi that cause these infections are Microsporum, Trichophyton, and Epidermophyton. Infections include tinea and onychomycosis. |
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Sporotrichosis
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Caused by Sporothrix schenckii.
Associated with injuries by thorns or splinters (rose picker's disease). Cutaneous form - characterized by nodular lesions, which may ulcerate. Lymphocutaneous form - a chain of swollen, suppurating lymph nodes extends from the primary lesion and is highly suggestive of this organism. Azoles, particularly itraconazole, have shown excellent activity. Amphotericin B may be used as an alternative. |
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Sporothrix schenckii
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Typically, cigar shaped or rounded forms are seen surrounded by a stellate, periodic acid-Schiff (PAS)-positive, eosinophilic material known as an asteroid body.
Dimorphic fungus, growing as yeast at 37 C and a mold at 25 C. |
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Chromomycosis
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Primarily caused by species of dematiaceous or black-pigmented fungi belonging to the genera Phialophora, Cladiosporum, and Fonsecaea.
Chronic granulomatous infections of skin and subcutaneous tissue that occurs primarily in tropical and subtropical regions. Lesions start as small papules or nodules that may ulcerate, and if untreated, produced lobulated masses (cauliflower lesions). No bone involvement. May be treated with surgical resection. Prolonged systemic treatment with itraconazole is beneficial but relapses are common. |
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Mycetoma
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Any chronic, subcutaneous or tissue tumor caused by fungi. Originally described as "Madura foot". The disease is most frequently found in the tropics, but isolated cases occur virtually everywhere. Unlike chromomycosis, these lesions may involve the bone.
Surgical excision and systemic treatment with azoles or amphotericin B are required. |
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Histoplasmosis epidemiology
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The most common of the endemic mycoses; prevalent in the Ohio/Mississippi river valleys.
There appears to be a specific stimulating substance provided by bird manure that permits growth of Histoplasma. |
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Histoplasmosis pathogenesis
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Histoplasma capsulatum
May mimic TB; pulmonay disease with granulomas, calcification of lesions and lymph nodes, and chronic upper lobe lung disease. Acute pericarditis in 5% of cases. Complications include chronic cavitary disease and fibrosing mediastinitis (rare). |
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Progressive Disseminated Histoplasmosis
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Usually occurs in the very young, the elderly, persons infected with HIV-1, or patients with hematologic malignancies or steroid therapy.
Acute - fever, weight loss, diffuse lung infiltrates, pancytopenia, and hepatosplenomegaly. Less frequently maculopapular skin lesions and CNS disease. If untreated, is fatal within weeks. Subacute - chronic fevers, weight loss, hepatosplenomegaly, oropharyngeal lesions, skin nodules; adrenal involvement can lead to Addison's disease. |
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Histoplasmosis Treatment
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Most infections are self-limited and require no therapy.
Treat more severe pulmonary disease with oral itraconazole. Disseminated disease - IV amphotericin. |
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Histoplasmosis Diagnosis
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Tissue biopsy - caseating granulomas, yeast forms (silver methenamine, PAS stain), fungal culture takes up to 8 weeks
Histoplasma antibody - unreliable Histoplasma urinary antigen - 90% positive with disseminated disease, less sensitive with localized disease (25-75%) For disseminated Histoplasmosis Blood smear (insensitive) - may see yeasts within circulating macrophages with dissemination |
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Blastomycosis
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Blastomyces dermatitidis
Infrequent mycotic infection limited to areas rich in organic matter (pine forests, river basins). Primary pulmonary infection, commonly associated with skin lesions which are maculopapular, becoming pustular with seropurulent exudate and crusting. Patients may develop chronic pulmonary disease with cough, hemoptysis, and weight loss. Bone and joint involvement is present in approximately 10-15% of cases and typically presents with soft tissue abscesses or draining sinuses. |
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Blastomycosis Diagnosis
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Direct examination is the best way to diagnose the disease. KOH mount of sputum or aspiration of skin pustule shows thick walled, broad based budding yeast. Buds are attached to the parent with a thick isthmus.
Methenamine silver, H&E, and PAS stains are all useful. |
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Blastomycosis Treatment
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IV amphotericin B remains the mainstay of therapy. Intraconazole has excellent activity, especially in cutaneous or localized pulmonary disease.
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Coccidioidomycosis
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Coccidioides immitis
Dust born fungal disease geographically restricted to the desert southwest; associated with Saguaro cactus. Valley Fever - cough, pleuritic chest pain, fever, abnormal chest x-ray (50%; focal lung infiltrate, hilar adenopathy, pleural effusion, and thin "egg-shell" cavity in <10%), prolonged fatigue, and arthralgias common. Extrapulmonary complications - erythema nodosum, meningitis (<0.1%); musculoskeletal and skin disease are uncommon; <0.5% progresses to classical granulomatous disseminated form that has a high mortality. |
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Coccidioidomycosis Diagnosis
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Histopathology - spherules (large spores containing multiple endospores)
Coccidioides antibody - specific for recent infection, develops 1 to 3 weeks after onset of symptoms Fungal culture - warn lab is suspected, highly contagious |
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Coccidioidomycosis Treatment
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Healthy patients with limited acute disease need no treatment - should be observed up to 2 years for complications.
Treat patients with severe or prolonged disease with fluconazole or itraconazole. |
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Paracoccidioidomycosis
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Paracoccidioides brasiliensis
Indigenous to central and south america Primary lung disease, may later cause oral granulomas and lymphadenitis. Lesions are usually in the mouth, on the nose, or on the face but may involve viscera and adrenals. |
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Diagnosis of Paracoccidioidomycosis
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Histology - multiple budding, spherical, thick-walled yeasts with Ship's wheel appearance
Serology - specific for recent infection; excellent correlation of complement fixation and immunodiffusion tests with disease state. |
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Treatment of Paracoccidioidomycosis
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Oral azole antifungals, itraconazole in particular, are very effective.
Refractory cases may be treated with amphotericin B. |
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Candida
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The most common yeast infections of man; these organisms exist as part of our normal GI flora and the mucocutaneous regions.
Candida exist as true yeasts. They are found as round or oval yeast cells that reproduce by budding. A unique feature of Candida albicans is formation of germ tubes. Clinical manifestations include oropharyngeal, esophageal, chronic mucocutaneous, and hepatosplenic candidiasis, as well as candida vulvovaginitis, candidemia, and endophthalmitis. |
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Oropharyngeal candidiasis
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Thrush; the most common clinical manifestation of Candida infection.
It may occur spontaneously in infants or young children and is the most frequent finding in HIV positive persons with CD4 lymphocyte counts less that 200. Often lesions will resolve on their own with resolution of the underlying predisposing factor. Topical azoles (clotrimazole), nystatin, or systemic therapy with fluconazole are all effective treatment. |
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Chronic mucocutaneous candidiasis
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Debilitating disorder that occurs early in life and has been associated with various congenital immune defects. Systemic azole therapy has improved the prognosis for patients with this disorder.
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Candidemia
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Most commonly occurs as a result of infection of a central venous catheter, especially in patients receiving total parenteral nutrition.
Must treat and remove catheter. Check for endophthalmitis. |
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Hepatosplenic candidiasis
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Occurs after chemotherapy in patients with leukemia, paradoxically, as their neutropenia resolves. Characteristic "target" lesions are visualized on CAT scan of the liver and spleen.
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Treatment of Candida Infections
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Skin infections - topical azoles, nystatin (polyene)
Oral, vaginal yeast infections - topical azoles, nystatin, oral fluconazole |
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Treatment of Systemic Candidiasis
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Fluconazole is drug of choice (po, IV)
Amphotericin (IV) - polyene Caspofungin (IV) - echinocandin Voriconazole (po, IV) - azole active vs. Flu R species |
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Aspergillus
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Ubiquitous mold in nature which is inhaled into the lungs.
Produces a wide variety of clinical manifestations - allergic disease, colonization, and invasive disease. Aspergillus can be identified in tissue specimens by its dichotomous acute (45 degree) angle branching and septation of hyphae. |
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Allergic bronchopulmonary aspergillosis (ABPA)
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Respiratory disease in patients with underlying asthma or atopic illness. Aspergillus acts as an antigen and produces inflammatory pulmonary infiltrates, peripheral blood eosinophilia, and elevated levels of IgE.
Treatment can be accomplished by avoidance of potential provoking environments and steroid therapy. One study suggested a benefit from specific therapy with azoles (itraconazole). |
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Aspergilloma
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Colonization of preformed lung cavity caused by other diseases or may result de novo in the course of invasive disease in immunocompromised patients.
Characterized by the "fungus ball", a mass of fungal hyphae that grow within the cavity as a tangled mass of mycelia. X-ray has a radiolucent crest (Monod's sign) over the upper portion of an internal mass. Most of these infections are asymptomatic. Resection and systemic antifungal therapy are the preferred methods of treatment. |
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Invasive aspergillosis
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Associated with immunosuppression, especially prolonged neutropenia.
Lung disease is major manifestation, causing fever, cough, pleuritic chest pain, and hemoptysis. Invades vascular structures (angioinvasive), causing thrombosis and necrosis. Some patients have a slowly progressive course over a period of weeks to months to years, as the organism advances through their pulmonary tissue - chronic necrotizing pulmonary aspergillosis. Can also occur more quickly - fulminant necrotizing pulmonary aspergillosis. |
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Disseminated aspergillosis
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Occurs when the organism can no longer be contained in the lung. Lesions commonly found in the brain, kidney, and other vascularized structures. GI and bone disease is rare. My produce necrotic skin lesions.
Prognosis is dismal. |
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Aspergillus Diagnosis and Treatment
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Diagnosis is very difficult; blood cultures are rarely positive and the antigen tests are insensitive.
Tissue biopsy is the test of choice (septate hyphae, acute angle branching). For invasive aspergillus, surgical resection can be done if feasible. Voriconazole is the drug of choice. Amphotericin and caspofungin can also be used. |
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Cryptococcus neoformans
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Ubiquitous organism usually inhaled into lungs from contaminated soil. Pigeon droppings can contain a high concentration of cryptococcus.
Most common presentation is subacute meningitis. Usually presents as a non-specific illness characterized by headache. The organism may not be particularly inflammatory and so the usual findings of meningitis (stiff neck, photophobia) may be absent. Also causes pulmonary infection and skin lesions. An important reservoir of latent infection can be established in men in the prostate gland. |
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Cryptococcus neoformans Diagnosis
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India ink stain of CSF reveals the capsulated yeast in 20-30% of cases.
The cryptococcal capsule can be specifically stained with mucicarmine. PAS and silver stain are also useful. Organism is urea positive. The cryptococcal antigen is more sensitive than the India ink stain and should always be performed on CSF and serum. |
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Cryptococcal menengitis treatment
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Drug of choice - amphotericin with 5-fluorocytosine for induction therapy for >= 2 weeks (synergistic)
Fluconazole has excellent CNS penetration and can be used following a 2 week course of induction therapy with amphotericin and 5-FC. Echinocandins and caspofungin are NOT active. |
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Cryptococcal meningitis complications
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Elevated intracranial pressure - may cause acute worsening of headache and lethargy; blindness, dementia
Treatment - daily lumbar punctures, lumbar drain, and ventriculoperitoneal shunt if persists |
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Zygomycetes
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Causes invasive infections of the sinuses and CNS. The major species are Mucor, Rhizopus, Absidia, and Rhizomucor.
Angioinvasive, very difficult to treat Tissue biopsy shows large non-septate hyphae with 90 degree branching angles |
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Zygomycosis Treatment
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Surgical resection
Amphotericin is drug of choice Most azoles, caspofungin are NOT active; new azole posaconazole is active |
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Amphotericin B Mechanism
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Binds to ergosterol. Creates pores in the lipid bilayer. This increases permeability via A- associated pores in the fungal membrane. Electrolytes are lost.
The result is disruption of membrane function, a leaky cell, and cell death. Nearly insoluble. Not absorbed from GI. Colloid/liposomal preps try to make it soluble. Highly protein bound. Poor penetration into CSF, so give intrathecally if needed. Hepatic metabolism, but don't need to adjust. Not affected by renal or hepatic failure or dialysis. Half life is about 15 days. |
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Amphotericin B slower toxicity
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Nephrotoxicity - the use limiting toxicity with amphotericin; the severity is variable.
Reversible component - decreased renal perfusion Irreversible component - renal tubular injury. Cumulative doses > 4 gms. Renal tubular acidosis, severe wasting of K+ and Mg2+. Can “sodium load” prior to dose to try to protect kidneys. |
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Amphotericin immediate toxicity
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Infusion related
Due to release of interleukin 1 and TNF Fever, chills, tachypnea, muscle spasms, vomiting, headache, and hypotension. A 1 mg test dose can be given to gauge severity of reaction and to determine if pretreatment is necessary. Patients can be pretreated with antipyretics, antihistamines, corticosteroids to reduce infusion-related symptoms. Infusions typically given over at least one hour. Sometimes the daily dose is given over 24 hours. |
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What organisms are resistant to amphotericin B?
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Pseudallescheria boydii and Candida lusitaniae
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Flucytosine
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Inhibits the synthesis of ergosterol.
Human cells cannot efficiently convert 5-FC into any of the active/toxic metabolites (the limited extent which does occur accounts for most of 5-FC toxicity). Well absorbed from the GI tract (>90% bioavailability), minimal protein binding, penetrates well into CSF and other compartments, little metabolism, mostly excreted unchanged. Antineoplastic effects; synergistic with amphotericin or itraconazole. |
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Flycytosine activity
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Cryptococcus neoformans (maintanence), some Candida, some fungi. Useful in combination therapy for systemic candidiasis and cryptococcal meningitis (with Amphotericin B) or for chromoblastomycosis (with itraconazole).
Should not be used as monotherapy. When used as combination therapy, monitor serum levels of flucytosine. NOT FOR Aspergillus, Sporothrix, Blastomyces, Histoplasma, Coccidioides immitis. |
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Azole Structure and Mechanism
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5 member azole nucleus containing 2 N (imidazole) or 3 N (triazole)
Mechanism is reduction of ergosterol synthesis by inhibition of fungal cytochrome P450 system (they bind to the enzymes responsible for the demethylation of lanosterol to ergosterol). Specificity for fungal P450 > human P450, but still accounts for drug interactions and side effects with these drugs. |
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Name the Azoles
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Imidazoles: Ketoconazole, Clotrimazole (topical), and Miconazole (topical)
Triazoles: Fluconazole, Itraconazole (oral only), Posaconazole, Voriconazole |
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Ketoconazole Adverse Effects and Drug Interactions
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Requires acidic gastric pH for absorption; has the most effects on metabolic enzymes of any azole; hepatically eliminated; half live is <10 hrs
Adverse effects: blocks synthesis of adrenal and gonadal steroid hormones, gynecomastia, infertility, menstrual irregularities, anorexia, hepatic toxicity, dermatitis. Significant drug interactions: +cyclosporine = nephrotoxicity; +cisapride/astemizole = arrhythmias/long QT syndrome; antagonizes amphotericin B; rifamycins and isoniazid stimulate hepatic metabolism of Ketoconazole |
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Ketoconazole Activity and Uses
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Activity: nonmeningeal blastomycosis, cutaneous mycoses, oral and esophageal candidiasis, common dermatophytes and fungi
NOT aspergillus, cryptococcus, or mucormycosis Uses: limited by drug interactions, endocrine effects, and narrow therapeutic range; include mucocutaneous candidiasis, non-meningeal coccidioidomycosis |
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Fluconazole
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Good bioavailability; has best CSF penetration (thus used for meningitis in HIV patients); least effects on metabolic enzymes; 1 day+ half life
Adverse effects: GI, headache, rash, alopecia Drug interactions: warfarin, phenytoin, sulfonylureas, zidovudine, rifamycins, cyclosporine Activity: Candida, cryptococcus, blastomyces, histoplasma; NOT aspergillus, filamentous fungi Uses: Azole of choice for treatment and prophylaxis of cryptococcus, coccidioidal meningitis, candidemia, candida pharyngitis & esophagitis, vaginal candida yeast infections; has widest therapeutic index of azoles |
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Itraconazole
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Hepatic elimination; 1 day+ half life;
Adverse effects: Not for patients with CHF Drug interactions: Rifamycins, cisapride, erythromycin, calcium channel blockers, dofetilide Activity: Some activity against aspergillus Uses: Azole of choice for dermatophytosis and onychomycosis (fungal nail infections); also for aspergillus, histoplasma, blastomyces, lymphocutaneous sporotrichosis |
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Posaconazole
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Should be taken with a high fat meal; inhibits CYP3A4; 1+ day half life
Adverse effects: GI, headache, rash, alopecia, QT prolongation Drug interactions: Other drugs that are metabolized by CYP3A4 Activity: Some against aspergillus; also has activity against zygomycetes Uses: Prophylaxis of invasive aspergillus and candida in high-risk patients; salvage therapy for zygomycetes |
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Voriconazole
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Hepatic elimination; can half non-linear elimination
Adverse effects: Transient visual disturbances, skin, increased hepatic enzymes Drug interactions: Drugs that induce or inhibit CYP enzymes can affect metabolism and serum concentrations Activity: Aspergillus, approved for primary treatment of invasive aspergillus (DOC) Uses: Good activity against candida and invasive aspergillus, other rare fungi |
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Mechanisms for Azole Resistance
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Mutation in 14-alpha demethylase (decrease drug binding)
Mutation in Delta 5(6)-desaturase (accumulation of ergosterol precursor) Overexpression of drug efflux pumps Inceased copy numbers of target enzymes |
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Echinocandins
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Caspofungin, Micafungin, Anidulafungin
Structure: Large cyclic peptides linked to a long chain fatty acid Mechanism: Attack fungal cell wall by reducing synthesis of Beta (1,3)-D-glucan, an essential component of the fungal cell wall; non-competitive inhibition of a gene whose product is a cell membrane protein responsible for glucan synthesis |
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Caspofungin
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Not absorbed from GI; 95% bound to albumin; hepatic metabolism; long elimination half life; adjust for severe hepatic insufficiency
Adverse effects: Infusion may cause histamine release, anaphylaxis reported, avoid during pregnancy, rash, fever, mild hepatic toxicity Drug interactions: Cyclosporin, tacrolimus Activity: Fungicidal against candida; fungistatic against aspergillus Uses: FDA indications for invasive candidiasis and aspergillosis; used for salvage therapy with invasive aspergillosis who have failed amphotericin B |
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Micafungin
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Injection only
FDA pregnancy category C Candida prophylaxis in patients undergoing stem cell transplant and esophageal candidiasis |
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Anidulafungin
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No hepatic metabolism - degrades to inactive metabolites at body temperature and pH; no dosage adjustment required
Adverse effects: Hypokalemia, diarrhea, elevated ALT/GGT levels, HA Uses: Candidemia, candidal peritonitis, intrabdominal abcesses, esophageal candidiasis |
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Echinocandins Resistance
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Rare but has been reported
Amino acid substitutions in Fks-1, a major subunit of glucan synthesis; genetically dominant, cross resistance among all class members |
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Nikkomycin Z
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Targets chitin synthesis
Orphan drug status for coccidiomycoses (Valley Fever) |
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Sodarins
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Inhibits protein synthesis elongation cycle in yeasts
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Griseofulvin
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Fungistatic; disrupts mitotic spindle during fungal division; deposition in newly forming skin and nails and binds to keratin precursor cells, making them resistant
Dermatophyte infection can only be cured when infected skin is replaced by new keratin-containing Griseofulvin skin; therapy is long term and only static Absorption improved with fatty foods Can induce hepatic microsomal enzymes; eliminated through bile Adverse effects: Allergic reactions, hepatotoxicity, photosensitivity, CNS effects, teratogenic, carcinogenic; cross sensitivity with penicillin Drug interactions: warfarin, barbiturates, oral contraceptives, and others Uses: Dermatophytosis (infections of skin, hair, nails, feet caused by trichophyton, microsporum, epidermophyton) Fungistatic effects: scalp and hair - 1 month, fingernails - 6 months, toenails - 1 year No effects on filamentous fungi; main use should be when topical agents have failed |
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Terbinafine
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Fungicidal; prevents ergosterol synthesis by inhibiting squalene epoxidase; squalene accumulates inside the fungal cells and results in fungal cell death
Well absorbed; >99% bound to plasma proteins; long half life; decreased clearance with hepatic, renal impairment Adverse effects: Rare; GI upset, HA, rash and hypersensitivity reactions, hepatic failure; NOT for patients with chronic or active liver disease; pretreatment with AST/ALT Drug interactions: Decreased clearance of caffeine, cimetidine; increased clearance of cyclosporine; rifampin increases clearance In vitro inhibition of CYP2D6 mediated metabolism Activity: Epidermophyton (fungicidal), Candida albicans (fungistatic) Uses: Onychomycosis of nails due to dermatophytes (tinea unguium); once daily for 12 weeks |
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Lice
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Pediculus humanus capitis - hair
Pediculus humanus humanus - nit on clothing Phthirus pubis - large claw on back 2 legs (crab louse); genital areas, eyebrows, and axillae Nits measure 0.5 mm and are glistening white; eggs hatch in 4-14 days; adults seen 12-28 days after oviposition and live for approximately 30 days Transmission by person to person contact Local lesions where adult and nymphs feed leads to intense pruritus depending on the number of lice and sensitivity of the host; ONLY the body louse transmits epidemic typhus, trench fever, relapsing fever, and others Treatment - Medicated shampoo plus nit picking; repeat after one week to kill newly hatched lice; treatment of clothing and furniture includes heat, insecticides, or sealing off for 14 days |
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Cimex lectularius
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Bed bug
5 mm in length, no wings and covered with hairs; hinged proboscis for piercing skin to feed Can survive without feeding for 1 year No disease transmission |
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Triatomid
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Assassin bugs or Kissing bug
Hinged proboscis and have wings Male and female bite on face, lips and outer angle of eye; transmit Trypanosoma cruzi, which causes Chagas disease |
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Fly larvae
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Fly larvae (maggots) develop from eggs deposited on wound or on broken skin, nose, ears, lips or mouth
Myiasis is infection due to invasion by fly larvae which may be specific or accidental Treatment - petroleum jelly to cause the larvae to exit or surgical intervention |
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Fleas
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2.0 mm, wingless, long legs for jumping; 1 year lifespan
Not host specific Bite sensitization from salivary secretions; transmission of plague and typhus |
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Hard Ticks
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8 mm in length, dorsal scutum
Feeding lasts for long periods, beginning 24 hours after the mouthparts are inserted and requiring 7-9 days for engorgement Vector for Rocky Mountain Spotted Fever, Babesiosis, Lyme Disease, Ehrlichia, Tularemia Tick paralysis - Most serious when tick bites in the occipital region, back of neck, or along spinal column; rapidly developing ascending paralysis develops 24 hours after tick attaches; may be fatal if not removed |
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Soft Ticks
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No scutum on the dorsum of the leathery body
Bite is of short duration Transmit Endemic Relapsing Fever |
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Sarcoptes scabiei
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Mite causes Scabies or Mange
Most commonly seen in the interdigital webs and backs of hands, beneath the breasts and between the belly folds of babies Causes severe dermatitis due to secretions, excretions, egg shells, and dead adults causing short reddish linear lesions Norwegian scabies is seen in immunodeficient patients |
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Demodex folliculorum
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Mite
50-100% of adults are infected 0.1-0.4 mm in length with short stumpy legs Found in hair follicles and sebaceous glands of the face particularly in area of nose or forehead Usually unnoticed - rarely requires treatment |
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Scorpions
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Venom is a mixture of neurotoxic and hemotoxic substances
8 legs, claws at anterior end, stinger on tail Venom causes local pain leading to vascular failure, respiratory paralysis, and convulsions Death can occur within a few minutes or up to a day or two |
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Black Widow Spider
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Lactrodectus mactans
Venom is neurotoxic - starts with pain and swelling, leading to a severe burning and aching sensation; the venom disseminates within one hour leading dizziness, weakness, cramps with board-like rigidity of abdomen May lead to death in approximately 5% of cases Treat to eliminate muscle spasm and specific anti-venom |
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Brown Recluse Spider
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Venom is necrotoxic - severe pain first seen several hours after bite; leads to central necrosis as the skin becomes covered with vesicles and sloughs off
Spreads for months and healing is slow and disfiguring Treatment in most cases is not required; skin grafting, however, may be required for bites not healed after 6-8 weeks |
