infectious exam 3 – Flashcards
Unlock all answers in this set
Unlock answersquestion
| Host Defenses |
answer
| 1. intact epidermis 2. cidal properties of skin 3. phagocytosis by WBC 4. normal flora |
question
| Qualities of intact epidermis |
answer
| acid pH dryness salty sweat low surface temperature |
question
| cidal properties of skin |
answer
| excreted chemical compounds: sebum urea |
question
| normal flora of skin |
answer
| Propionibacterium acnes diphtheroids Coagulase-negative staphylococci |
question
| non-infectious causes of skin problems |
answer
| allergies cancer etc |
question
| Etiology of Skin infections: |
answer
| non-infectious causes (allergies, cancer) parasites or arthropods pathogenic patterns caused by microorganisms |
question
| Pathogenic Patterns of Skin Disease caused by microorganisms |
answer
| 1. systemic/blood-borne illness that causes skin manifestations 2. skin infections that have symptoms caused by exotoxins 3. primary skin infection - herpes simplex (most common virus), bacteria (p.acnes, s.aureus, s.pyogenes), fungi (t.rubrum) |
question
| Characteristics of primary skin infections |
answer
| type of lesion pattern recognition progression and distribution associated symptoms present? |
question
| type of lesion |
answer
| macule papule vesicle or bullae pustule ulcer petechiae or purpura blanching or hemorrhagic? |
question
| pattern recognition |
answer
| are all lesions the same or in same stage of development |
question
| progression and distribution |
answer
| method of spread and evolution of lesions |
question
| associated symptoms |
answer
| is there prodromefeverwhen in relation to rash? |
question
| Propionibacterium acnes -what does it cause? |
answer
| acne/acne vulgaris inflammatory acne/inflammatory acne vulgaris |
question
| Propionibacterium acnes -etiology |
answer
| gram positive non motile diphtheroid/pleomorphic rod anaerobic normal flora of skin |
question
| Propionibacterium acnes epidemiology |
answer
| acne is most common skin disease; involves hair canals in skin; happens in adolescents |
question
| Propionibacterium acnes --pathogenesis and clinical manifestations |
answer
| in absence of p. acnes microcomedones develop when: 1. increased sebum production after puberty 2. follicular canal of sebaceous follicles becomes plugged due to alterization in keratinization of cells lining the canal |
question
| Propionibacterium acnes --pathogenesis and clinical manifestations |
answer
| microcomedones will progress to non inflammatory comedones and possibly inflammatory comedones (papules, postules, nodules, cysts) 1. closed comedones - white heads; cant see; slightly raised; small papule 2. open comedones - black heads; follicular impaction of lipid, keratin, melanin causes brown or black appearance (not dirt!) |
question
| Propionibacterium acnes --pathogenesis and clinical manifestations |
answer
| if sebaceous gland / follicle becomes colonized by p.acnes, an inflammatory, self limiting diagnosis occurs -inflammatory acne -papules are most common and rarely result in scarring |
question
| Propionibacterium acnes -chronic --purpose of treatment |
answer
| Antikeratinizing Inhibit sebum production Anti-p.acnes Anti-inflammatory |
question
| Propionibacterium acnes --inhibition of physiological process |
answer
| Salicylic Acid Retinoic Acid (tretinoin), isotretitnoin, tazarotene, adapalene Azelaic Acid - naturally in wheat, rye, barley Benzoyl peroxide? |
question
| Propionibacterium acnes --inhibition of P. acnes |
answer
| salicylic acid Retinoic Acid Azelaic Acid - antibacterial (static and cidal) benzoyl peroxide Antibiotics in topics in combination with benzoyl peroxide (ie erythromycin) |
question
| Propionibacterium acnes --other treatments |
answer
| Gentle medicated cleansing OTC topical vitamin A or C (antioxidants; may work) OTC low dose retinol or OTC alphy hydroxy acids Severe acne - systemic antibiotics or corticosteroids Estrogens and antiandrogens |
question
| Propionibacterium acnes --ineffective / harmful therapy |
answer
| frequent, non medicated, vigorous scrubbing use of abrasive cleansing restricted diet squeezing pimples |
question
| Propionibacterium acnes --3 things pharmD should recognize |
answer
| 1. acne patients have levels of social and emotional problems as great as those with chronic asthma, diabetes, arthritis 2. Impact on quality of life does not correlate with severity of acne 3. Patients are usually misinformed (most think acne is curable and treatment is less than 6 months; neither is true) |
question
| Staphylococcus Aureus --etiology |
answer
| Coagulase Positive (produces coagulase) Gram positive cocci in pairs, short chains, or clusters |
question
| Staphylococcus Aureus --pyodermic infections that it causes |
answer
| these pyodermic infections are pyogenic (forms abscesses in any tissue) 1. folliculitis 2. furuncles 3. carbuncles 4. epidemic impetigo 5. bullous impetigo 6. staphylococcal scalded skin syndrome |
question
| Staphylococcus Aureus -folliculitis, furuncles, carbuncles, epidemic impetigo |
answer
| NONE are toxin mediated diseases ALL are contagious - that is, if you catch a strain you many not develop dx |
question
| Staphylococcus Aureus -folliculitis |
answer
| 1. superficial infection of individual hair follicle at apocrine regions 2. lesions: small erythematous, sometimes pruritic papule topped by central pustule occurring on any hair-bearing site on body |
question
| Staphylococcus Aureus --furuncles and carbuncles |
answer
| Developed from folliculitis Children 3-15 yrs Occur on neck, face, back, gluts, thighs infection of hair follicle and subcutaneous tissue |
question
| Staphylococcus Aureus --furuncles |
answer
| -boils/deep folliculitis -infection of individual hair follicle -painful, firm, discrete, tender, red nodule with purulent drainage -skin around furuncle is hot but no systemic signs |
question
| Staphylococcus Aureus --carbuncle |
answer
| -larger, deeper, indurated lesions than furuncles -involve several hair follicles -erythematous, edematous, painful lesions with central, necrotic crater -lesions coalesce - spreading, drain to surface along hair follicles -systemic signs of fever and malaise |
question
| Staphylococcus Aureus --epidemic impetigo (crusted skin) epidemiology |
answer
| Classic, nonbullous impetigo -caused primarily be s.aureus but also by strep pyogenes (GAS) or both -most common bacterial skin infection in children and third most common skin disease overall, after dermatitis and warts -children 2-5 yrs -often secondarily infects varicella lesions or lesions present in systemic diseases (AIDS or diabetes); causes scarring -autoinocculation causes spread |
question
| Staphylococcus Aureus --epidemic impetigo manifestations |
answer
| -in superficial epidermis, single macule or papule forms small vesicles that develop into pustules with little erythema, then ruptures -purulent discharge drying on top of lesion results in thickened amber colored adhesive crust that resolves in weeks without scarring -contagious; passed by fomites or person to person |
question
| Staphylococcus Aureus -community acquired infections CAI |
answer
| infections acquired in non health care settings -two strains USA300 or 400 -Resistant to beta lactams, macrolides, clindamycin, tetracyclin; need D test -associated with skin and soft tissue infections; less so a necrotizing (non-abscessogenic) pneumonia -strains appear to be more virulent and with greater pathogenicity, than HAI-MRSA strains |
question
| Staphylococcus Aureus -ET, ETA, ETB -exfoliatin exotoxins |
answer
| exotoxin mediated diseases caused by s.aureus: - bullous impetigo -SSSS (including ritter's disease of newborn) |
question
| Staphylococcus Aureus --pathogenesis of exotoxin mediated disease |
answer
| 1. caused by exfoliatin toxin 2. ET causes exfoliation of superficial intraepidermal layers of skin (cleavage in epidermis) by producing one or both: a-epidermal necrosis (sloughing of large layers of skin) b-bullae - flaccid, thin walled, white, serous fluid-filled sacks with hsarp margins and with no surrounding erythema which rupture - painful, moist lesion that dry in 1-2 days to think varnish-like light-brown crusted lesions that resolve without scarring in several weeks, unless secondary infection occurs |
question
| Staphylococcus Aureus --bullous impetigo |
answer
| 1. lesions: -occur in infants or young kids on diaper area, neck folds, legs -contain ET producing strain of s.aureus bUT NO OTHER microorganisms 2. toxin and agent do not disseminate in blood, lymph, etc |
question
| Staphylococcus Aureus -SSSS staphylococcal scalded skin syndrome |
answer
| 1. infants and kids less than 5 yrs or immunocompromised adults 2. focal infection by ET producing strains -dissemination of staphy is rare -hematogenous dissemination of ET that is elaborated in focal lesion -focal infection is contagious; exfoliated skin lesion/bullae are sterile |
question
| Staphylococcus Aureus -SSSS manifestations |
answer
| 2 syndromes SSSS and Ritters disease of newborn (most severe form) manifest with: fever wiespread, diffuse erythroderma (scarlatiniform rash) that progresses in 1-3 days to extensive in size, widely distributed, exfoliation of skin/bullae that progress as described above; within 5 days of onset, fine, flaky discolored total-body desquamation occurs |
question
| Staphylococcus Aureus -treatment of non-bullous and bullous impetigo, SSSS, and Ritters disease |
answer
| 1. supportive - pain management, fluid replacement 2. antibiotics - -penicillin resistant strains (MSSA) are common in community and hospital outbreaks of impetigo in nurseries -for impetigo involving limited body surface area, topical Ab like mupirocin and fusidic acid is preferred first line therapy -oral Ab that are effective = antistaphy penicillins, amoxicillin, cephalosporins, macrolids -erythromycin is less effective -for more extensive impetigo or systemic symptoms, use oral Ab -oral penicillin V, amoxicillin, topical bacitracin, and neomycin are not remcommended for impetigo -topical disfectants like hydrogen peroxide should NOT be used in impetigo! |
question
| Streptococcus pyogenes -etiology |
answer
| Group A beta-hemolytic strep Gram positive cocci in chains |
question
| Streptococcus pyogenes -classic impetigo |
answer
| epidemic in preschool children Unrelated to pharyngeal strep (different M types) complication: Acute Glomerulonephritis |
question
| Streptococcus pyogenes -cellulitis |
answer
| See other Erysipelas is a form of cellulitis associated with blocked lymphatics |
question
| Streptococcus pyogenes -scarlet fever |
answer
| Caused by strains producing streptococcal pyrogenic exotoxins (SPE) -AKA erythrogenic exotoxins - which are superantigens is a complication of streptococcal pharyngitis or classical impetigo signs and symptoms of either plus: 1. systemic signs that can lead to DS 2. enanthem - pronounced hyperemia of the entire pharynx with petechial lesions on palate, bleeding lips and gums, and white strawberry tongue that progresses to a red strawberry tongue and finally a raspberry tongue 3. exanthem: a. diffuse, generalized, blanching, macular erythroderma as base for scarlatiniform (fine, red, punctate, sandpaper like rash); worse in folds of skin b. rash first appears on trunk then spreads peripherally to cover whole body within hours or days c. rash resolves with desquamation of sheets of skin (esp palms and soles) which occurs 1-2 weeks after onset of illness 4. complications: RF or AGN |
question
| Streptococcus pyogenes -infections that it causes |
answer
| 1.classic impetigo 2. cellulitis / erysipelas 3. scarlet fever |
question
| Cellulitis -agents |
answer
| 1. gram positive cocci 2. gram negative rods 3. atypical mycobacteria 4. fungal agents |
question
| Cellulitis -gram positive cocci agents |
answer
| MUST ALWAYS INCLUDE THESE AGENTS IN COVERAGE FOR CELLULITIS (target therapy at GP and GN anaerobes) -s. pyogenes -s.aureus -s.pneumoniae |
question
| Cellulitis -Gram Negative Rods |
answer
| BOTH facultative and obligate anaerobes -MUST ALWAYS INCLUDE THESE AGENTS IN COVERAGE FOR CELLULITIS |
question
| Cellulitis - atypical mycobateria |
answer
| Cause Necrotizing skin lesions 1. mycobacterium ulcerans -buruli ulcer 2. mycobacterium marinum 3. M.fortuitum, M. abscessus, M. chelonae (fortuitum complex) |
question
| Cellulitis -fungal agents |
answer
| Agents of systemic mycoses 1. blastomycosis 2. histoplasmosis 3. coccidioidomycosis 4. mucormycosis (aka zygomycosis) - group of ubiquitous fungi |
question
| Cellulitis -epidemiology |
answer
| things that can cause cellulitis A. exposure to water (fresh or seawater) B. animal bite/scratch C. infections in areas around oral cavity or contaminated with oral secretions |
question
| Cellulitis -epidemiology -exposure to water |
answer
| predisposes to cellulitis with bacteremia as common complication Caused by: 1. facultative, anaerobic, GN rods 2. atypical mycobacteria a. mycobacterium marinum - fish tanks b. m. fortuitum, M. abscessus, M. chelonae - pedicures 3. vibrio vulnificus (saltwater) |
question
| Cellulitis -epidemiology -animal bites |
answer
| mostly cats and dogs bite/scratch predisposes to cellulitis caused by: 1. gram positive cocci 2. diphtheroids/corynebacteria 3. facultative anaerobic, GN rods a. pasteurella pestis and multicoida b. capnocytophaga canimorsus --TARGET THERAPY HERE 4. anaerobic GN rods |
question
| Cellulitis -epidemiology -infections by oral cavity |
answer
| infections in areas adjacent to oral cavity (head and neck soft tissues, sinuses, RT) or infections contaminated by oral secretions (bite and clenched hand; aka fist wounds) predisposes to cellulitis caused by: Eikenella Corrodens -facultative anaerobic, GN rod -Normal Flora of mucosal surfaces (oral, GI, UR tracts) |
question
| Cellulitis -initial portal of entry |
answer
| 1. lesions such as: interdigital tinea pedis skin fissures viral lesions psoriasis eczema 2. cuts surgical incision traumatic injury punctures/IV 3. animal/insect bites 4. diabetes --diabetes foot ulcer 5. abrasion 6. burns |
question
| Cellulitis -surgical wounds |
answer
| occur 0.1% suture line gets reddened, tender |
question
| Cellulitis -clinical manifestations; systemic signs |
answer
| infection of skin (deep dermis) and subcutaneous fat manifestations develop within few days after inciting event systemic signs: fever chills malaise leukocytosis --like carbuncles of s.aureus |
question
| Cellulitis --local infection signs |
answer
| 1. inflammation - pain, erythema, edema, warmth; never sharply demarcated (sharply demarcated is syphillis) 2. suppurative, local abscess can develop and small patches of overlaying skin may undergo necrosis 3. subcutaneous tissues can be palpated 4. lymphangitis or lymphadenitis can occur |
question
| Cellulitis -treatment |
answer
| IV ANTIBIOTICS MUST BE DONE symptoms resolve 1-2 days |
question
| Bacillus Anthracis -etiology |
answer
| Gram Positive Box car shaped rod aerobic ENCAPSULATED - polyglutamic acid facultative intracellular pathogen |
question
| Bacillus Antracis -epidemiology |
answer
| enzootic disease -herbivores (sheep, goats, cattle, horses) -excreted in feces, urine, saliva -spores survive for years in soil cutaneous anthrax requires DIRECT CONTACT with either: soil bearing spores, infected animals, or animal products bearing spores worldwide distribution, also in US |
question
| Bacillus Antracis -cutaneous anthrax |
answer
| -accounts for 95% of human cases -spores or cells enter skin through small abrasions and multiply locally -small, PAINLESS, papule develops, progresses to a vesicle filled with fluid, then ruptures, producing an eschar (painless ringed lesion with edematous ridge - malignant pustule) -death is due to both toxemia and bacteremia |
question
| Bacillus Antracis -differential diagnosis |
answer
| 1.ecthyma (pyoderma) gangrenosum -caused by p. aeruginosa 2. ulceroglandular tularemia -caused by rancisella tularensis 3. NOT ecthyma contagiosum (Orf pox) or ecthyma (GAS) |
question
| Bacillus Antracis -control |
answer
| -bury infected animals or bury -subunit purified vaccine for humans -live attenuated vaccine for livestock |
question
| Erysipelas - St. Anthony's Fire -etiology |
answer
| group a strep; strep pyogenes |
question
| Erysipelas -epidemiology |
answer
| -young and elderly -preceded by URT or skin infection caused by GAS -recurrent erysipelas due to lymphatic obstructions |
question
| Erysipelas -pathogenesis |
answer
| -distinctive form of rapidly progressing (hours) superficial cellulitis with involvement of cutaneous lymphatics -occurs on extremities and face |
question
| Erysipelas -symptoms |
answer
| same as cellulitis except lesions differ! -illness begins with systemic signs and burning or itching at site of infection than rapidly spreading (mins to hours) erythema forms that is bright RED and INDURATED - peau d'orange sharply demarcated! |
question
| Small pox |
answer
| vaccine is cow origin antiviral drug may work vaccine is open bottle w/cap; refrigerate --use "tyne?", not needle; dab and break skin to get into body - can be catastrophic with eczema so be careful in smallpox, lesions are same over time (unlike chicken pox) |
question
| Varicella Zoster Virus -synonyms |
answer
| chickenpox and zoster part of herpes virus group HHV3 |
question
| Varicella Virus- chickenpox -epidemiology |
answer
| -1-6 yr old -winter-spring -portal of entry: URT via direct contact with respiratory secretions or with lesions -highly contagious; all exposed manifest with disease -mild, self limiting childhood disease, but DOES CAUSE SIGNIFICANT morbidity and mortality in children, ESPECIALLY in adults -humans are sole host and reservoir |
question
| Varicella Virus - chickenpox -clinical manifestations |
answer
| -virus is in lesions of both varicella and zoster -lesions are contagious -incubation is long 2 weeks -no prodrome -actue onset of fever, flulike symptoms, pruritic exanthematous maculopapular lesions that become vesicles, then pustular, then crust, then scab -lesions develop first on head then spread to trunk and extremities -appear in successive crops for 3-6 days; every time with fever -different stages of lesions all at once -lesions can scar if they become secondarily infected by GAS s.aureus - most common cause for hospitalization in kids -in adults, morbidity and mortality is directly due to VZV's cytolytic activity - causes interstitial pneumonia, hepatitis, meningoencephalitis, and thrombocytopenia -virus becomes latent in nerves after primary infection; no way to remove it or cure it -zoster patient is infectious and a susceptible person infected with VZV from a zoster lesion manifests with varicless (chicken pox), NOT zoster (shingles |
question
| Herpes Zoster -synonyms |
answer
| Belt or Girdle aka Shingles Varicella Zoster Virus |
question
| Herpes Zoster (HHV3) -epidemiology |
answer
| incidence is rising -adults or immunocompromised children -cancer patients -no predisposing factor - stress or sunlight -no seasonality |
question
| Herpes Zoster -pathogenesis |
answer
| recrudescence of VZV - reactivated latent VZV infection due to waning cellular immunity |
question
| Herpes Zoster -manifestations |
answer
| -tingling - severe pain in innervated areas precedes -asymmetrical maculopapular or vesicular-crusting rash following a single thoracic dermatome (stops at midline) or cranial nerve distribution while tingling - severe pain continues - systemic signs of fever, malaise, headache |
question
| Herpes Zoster -complications |
answer
| 1. ophthalmic (ocular) zoster, herpes zoster oticus (ear) - refer to specialist 2. postherpetic neuralgia (severe burning, lancinating pain) can persist for months-years; can be debilitating, accompanied by allodynia (pain from non-noxious stimuli) 3. acute peripheral facial palsy, idiopathic peripheral facial palsy (bell's palsy) (either caused by VZV-no rash- or HSV reactivation) |
question
| VZV -treatment |
answer
| for symptoms in immunocompetent children with varicella: -lotion or antihistamines for pruritis -aspirin is contraindicated because of association with Reye's syndrome -post exposure prophylaxis VZIG; for adolescents, adults, leukemia patient, or pregnant women with no immunity |
question
| VZV -antiviral therapy |
answer
| 1. varicella: oral acyclovir administered within 9 days post infection or within 24 hours of onset of varicella symptoms can prevent/minimize signs and symptoms --only recommended for persons at high risk for severe disease 2. zoster: acyclovir, famciclovir, valacyclovir administer within 72 hrs of rash onset to reduce pain |
question
| VZV -prevention |
answer
| live attenuated vaccine for kids 13m-12yr same schedule as MMR vaccine HIGHLY EFFICACIOUS with 1 dose in children, 2 in adolescents and adults -children immunized with varivax will have a decline in immunity to both vaccine strain and wild-type VZV. THEY CAN MANIFEST WITH VARICELLA DUE TO VZV OR ZOSTER DUE TO VARIVAX STRAIN OR VZVA. HOWEVER, in all cases, symptoms are MILD and immunity to both are boosted recommendations for varivax administration: 3-5 days post exposure to prevent disease in immunocompetent persons or persons with HUMORAl deficiency contraindications: pregnant women immunocompromised children zostavax - prevent shingles in 60yr or older |
question
| Human Parvovirus B19 -epidemiology |
answer
| PVB-19 Erythema Infectiosum, fifth disease -winter, spring -enters URT via respiratory secretions -common in childhood, half of adults are immune - possess anti HPV B19 igG -erythema infectiosum primarily occurs in children 4-15 yrs; arthropathy is rare -arthropathy in adults, esp women |
question
| Human Parvovirus B19 -manifestations |
answer
| 3 presentations based on severity of symptoms: 1. erythema infectiosum (5th disease) 2. Arthropathy 3. Aplastic crisis 4. in pregnant women, mom not affected but unborn child can die and have CHF |
question
| Human Parvovirus B19 -erythema infectiosum (fifth disease) |
answer
| prodomal illness with mild symptoms that last 2-3 days -fever -headache -malaise -respiratory symptoms -sometimes GI symptoms; nausea, vomiting, abdominal pain fever quickly drops then: RASH. erythematous maculopapular lacy appearance rash; fever usually gone -initially on face (slapped cheek appearance) -may also involve limbs; maybe pruritic -rash resolves in 1-2 weeks -lesions are not contagioius |
question
| Human Parvovirus B19 -arthropathy |
answer
| also include other rheumatoid manifestations, vasculitis adults manifest with acute onset of flulike symptoms for 2-3 days then: polyarthralgia and symmetric polyarthropathy joints involved - hands, knees, wrists, ankles -usually self limiting 2 weeks up to a month -in adults, rash is less typical |
question
| Human Parvovirus B19 -aplastic crisis |
answer
| patient has aplastic crisis (severe anemia/reticulocytopenia) if they are infected with HPVB19 and suffer from: chronic hemolytic anemia sickle cell Dx acquired anemia chronic hemolysis -agent replicates in bone marrow where rbc are made; major loss of rbc --not age dependent like other two patient has severe anemia symptoms for 7-10 days: dyspnea fatigue malaise confusion maculopapular rash, polyarthropy may occur anemia may be protracted in immunocompromised patients who are unable to control the infection - chronic bone marrow failure in the immunocompromised patient |
question
| Human Parvovirus B19 -treatment |
answer
| supportive only -antipyretics, analgesics, nonsteroidal, anti inflammatory drugs -transfusions for patients in aplastic crisis or fetus with hydrops fetalis (detected in utero) |
question
| Human Herpes Virus 6 and 7 -infections it causes |
answer
| Exanthem subitum Roseola Infantum Sixth Disease |
question
| Human Herpes Virus 6 and 7 -etiology |
answer
| herpes DNA virus closely related to cytomegalovirus acyclovir/ganciclovir resistant |
question
| Human Herpes Virus 6 and 7 -drug resistance |
answer
| 1. acyclovir/famciclovir, and valacyclovir 2. ganciclovir sensitive, but less than CMV 3. foscarnet, valganciclovir sensitive |
question
| Human Herpes Virus 6 and 7 -epidemiology |
answer
| -in immunosuppressed persons, reactivation or re-infection of HH7 or HH6 can occur, causing severe disease -can be co-infection with CMV |
question
| Human Herpes Virus 6 -epidemiology |
answer
| -shed in saliva of adults; primary mode of transmission -primary infection is first 3 yrs of life; adults are seropositive for HH6 -most infants are asymptomatic -primary infections in infants 3m-3yr MAY lead to exanthem subitum -primary HHV6 in 6-12m is usually responsible for first febrile illness -primary HH6 infection in 6-12 m accounts for MANY visits to ER and MANY first time febrile seizures in kids under 2 yr -forms active, life long infections in salivary glands and latent persistent infections of PBMC (wbc) |
question
| Human Herpes Virus 7 -epidemiology |
answer
| -secreted in saliva -80% of kids 1-4 yr are seropositive -agent of pityriasis rosea? |
question
| Human Herpes Virus 8 -epidemiology |
answer
| -not in US so much, but high elsewhere -secreted in saliva, maybe chronically or just during infection -latent in B cells -associated with all forms of karposi sarcoma including: classical KS - mediterranean endemic KS - africa iatrogenic KS-organ transplant pt epidemic KS-AIDS pt |
question
| Human Herpes Virus 6 and 7 -manifestations |
answer
| -prodrome high fever 2-5 days -fever goes away and fine, macular, blanching rash appears that lasts 48 hr -virus NOT in lesions/rash -kids go to ER with high fever, no obvious cause; major cause for spinal taps (remember fever, lethargy, irritability = aseptic meningitis) -other signs:fever, no rash or rash, no fever, or both |
question
| Human Herpes Virus 6 and 7 -complications |
answer
| children: otitis media adults: mononucleosis-like syndrome aseptic meningitis seizures GI distress, hepatitis in utero infection for immunosuppressed, many organ systems can be involved |
question
| Measles -etiology |
answer
| Also called rubeoloa or hard measles ONE serotype enveloped ssRNA virus; cause syncytia formation |
question
| Measles -epidemiology |
answer
| -next to be eliminated -children less than 5 -winter, spring -enters URT; passed via respiratory secretions TWO DAYS BEFORE PRODROME or 5 days after onset of rash -highly contagious; nearly all infected get it; primary attack rate is high -infection without disease = lots and lots of spread complications - diarrhea or pneumonia are leading causes of death for kids 1-5yr in developing countries due to malnutrition, poor medical care |
question
| Measles -manifestations |
answer
| virus produces exanthem AND enanthem -prodrome occurs 10-12d post infection and 3-4d before rash -coryza (cold like symptoms) -cough -conjunctivitis----THREE C'S -fever -lymphadenopathy -koplik's spots on buccal mucosa; looks like grains of salt -pharyngitis -pathognomonic |
question
| Measles -manifestations part 2 |
answer
| prodromal manifestations continue and then exanthem appears: symmetrical, non pruritic, red maculopapular rash on face and scalp line; descends to lower extremities -rash is strong on head then thins and becomes discrete -rash appears 3 days after onset of prodrome -viral antigen IS IN lesion |
question
| Measles -manifestations 3 |
answer
| 24-48 hr later, as Ab titers rise, disseminated viremia halts and symptoms abort; rash clears in order it appears |
question
| Measles -complications |
answer
| severe otitis media is most common -pneumonia (leading cause of death bc of measles) -diarrhea -CNS-encephalitis -agent can cross placenta and infect unborn child |
question
| Measles -treament |
answer
| supportive administer vitamin A administer gamma globulin for immunocompromised or prevaccines within 6 days of exposure |
question
| Measles -vaccine |
answer
| trivalent measles, mumps, rubella live attenuated two doses-15-18m then 4-6yr or 11-13y three doses: 15-18m then 4-6 yr, then 11-13yr NOT RECOMMENDED FOR PREGNANT WOMEN |
question
| Rubella -synonyms |
answer
| German Measles Soft-mild-Measles 3 Day Measles Little Red -ssRNA virus |
question
| Rubella -epidemiology |
answer
| older children young adults -winter spring -enters URT; passed via respiratory secretions during prodrome or 2 weeks after onset of rash -asymptomatic infections occur, not as infectious as chicken pox or measles -due to vaccination, incidence of rubella and congenital disease is rare in US |
question
| Rubella -symptoms |
answer
| prodrome symptoms are minimal or absent (viral replicates in pharynx for up to 2 weeks) -conjunctivitis -coryza -lymph node enlargement -pharyngitis -malaise -low grade fever -discrete rash 3-5days; face then extremities -arthralgia occurs; more in women -all symptoms occur at same time; not prodrome like the other one |
question
| Rubella -complications |
answer
| Congenital Rubella Syndrome -no risk to mother -mom infects placenta -timing is crucial; first trimester is most critical -organogenesis is disrupted -chronic and persistent infection of child is likely -isolation of neonate because virus sheds for months in urine and respiratory secretions -CRS leads to cardiac, vision, hearing defects, and speech/learning deficits -lower the birth weight, more chance of severe complications |
question
| Rubella -diagnosis |
answer
| can be hard because many ECHO viruses mimic manifestations lab diagnosis for newborn - STORCH -measure specific igM Ab in cord blood -tests for immune status via LCAT at prenatal exam, not via TORCH |
question
| Rubella -treatment |
answer
| NOT RECOMMENDED to treat with IG!! -postexposure prophylaxis does not prevent rubella infection or viremia -if susceptible pregnant woman is exposed and will not terminate it, MAYBE IG will reduce risk --most physicians do therapeutic abortion if CRS is likely! |
question
| Rubella -prevention |
answer
| live attenuated trivalent vaccine for measles, mumps, rubella for CRS: vaccinate non-pregnant women; inform pregnant women to stay away from rashes |
question
| Fungal infections -superficial mycoses |
answer
| infections confined to outermost layers of skin - stratum corneum cause little tissue reaction and only mild symptoms |
question
| Fungal infections -cutaneous mycoses |
answer
| dermatomycoses infections involve entire cutis (epidermis, maybe dermis) prefer keratin containing tissue -ie candida albicans |
question
| Fungal infections -subcutaneous mycoses |
answer
| invade through superficial sources, cause chronic ulcerated lesions with regional lymph node involvement, numerous genera, sporotrichosis |
question
| Fungal infections -systemic mycoses |
answer
| most serious infections enter respiratory tract or break in skin |
question
| Fungal infections -opportunisitc infections |
answer
| normal flora and in environment; usually produce lesions on mucus membranes, skin, and RT of compromised host |
question
| Superficial Mycosis -agents that cause it |
answer
| infections confined to outermost layer of skin (stratum corneum) -malassezia furfur -piedra hortai -trichosporon beigelii -exophiala werneckii |
question
| Pityriasis Versicolor -agents that cause it |
answer
| -superficial AKA tinea versicolor caused by malassezia furfur aka pityrosporum orbiculare |
question
| Pityriasis Versicolor -malassezia furfur -epidemiology |
answer
| young adults predisposing factors: malnutrition, hyperridosis, antibiotics |
question
| Pityriasis Versicolor -malassezia furfur -pathogenesis |
answer
| chronic, mild, asymptomatic superficial infection when agent transitions from yeast form (NF) to hyphal form |
question
| Pityriasis Versicolor -malassezia furfur -manifestations |
answer
| brown colored or hypopigmented patches no itching non inflammatory lesions on chest, stomach, back; cosmetically unappealing causes pityrosporum folliculitis - papules pustules on trunk/upper arms that resemble acne causes dandruff - seborrheic dermatitis |
question
| Pityriasis Versicolor -malassezia furfur -therapy |
answer
| antifungal topicals -ketoconazole -ciclopirox for acute occurrence, use topical anti-inflammatory or steroid OTC: selenium sulfide - selson blue zinc pyritihon - head and shoulders salicylic acid use shampoo daily for 2wk, then maintain by using 2x per week chronic disease; relapses will happen |
question
| Black piedra - piedra hortai White piedra - trichosporon beigelii -epidemiology |
answer
| -superficial worldwide |
question
| Black piedra - piedra hortai White piedra - trichosporon beigelii -pathogenesis |
answer
| form ectothrix (sheath of arthrospores only on external hair shaft, most often on face; no involvement of epidermis or follicular hair portion |
question
| Black piedra - piedra hortai White piedra - trichosporon beigelii -manifestations |
answer
| no symptoms white piedra - resembles lice; results in unneeded toxic pesticide treatments black piedra - resembles ectothrix of microsporum NOTE: pediculosis captis is lice, lays eggs on outside of hair shaft near scalp |
question
| Black piedra - piedra hortai White piedra - trichosporon beigelii -treatment |
answer
| cut or shave off infected hair |
question
| Tinea nigrans (keratomycosis nigrans) hortaea (exophiala) werneckii -epidemiology |
answer
| -superficial tropical regions under 18 yr female direct contact or autoinoculation |
question
| Tinea nigrans (keratomycosis nigrans) hortaea (exophiala) werneckii -manifestations |
answer
| discrete brown macule on palm or fingers no inflammation, induration, or scaling differentiate between tinea nigrand and malignant melanoma and junctional nevus (birthmark) |
question
| Tinea nigrans (keratomycosis nigrans) hortaea (exophiala) werneckii -treatment |
answer
| topical keratinolytic agents |
question
| Cutaneous -Dermatophytoses -ringworm infections -etiology |
answer
| infections involve enture cutis caused by 3 fungal agents -know which fungi infect which tissues to have best therapy epidermophyton - skin and nails microsporum - hair and skin tricophyton - hair, skin, nails (t.rubrum is most common and most difficult to treat) |
question
| Cutaneous -Dermatophytoses -ringworm infections -epidemiology |
answer
| worldwide same risk factors as pityriasis versicolor acquired from: other humans, soil, or animals |
question
| Cutaneous -Dermatophytoses -ringworm infections -pathogenesis |
answer
| keratinolytic fungi have strong affinity for keratinized tissue of nails, hair, skin |
question
| Cutaneous -Dermatophytoses -ringworm infections -manifestations |
answer
| -cutaneous -ringworm tinea capitis: ringworm of scalp and hair t.pedis: athletes foot t.cruris: jock itch t.unguium: onychomycosis -nail infection t.manuum: hand t.barbae: barbers itch - beard t.corporis: smooth skin; ie trunk |
question
| Cutaneous -Dermatophytoses -ringworm infections -t. pedis, cruris, manuum, barbae |
answer
| etiology is big three: t.mentagrophytes t.rubrum e.floccosum manifests: scales, vesicles, or ulcers |
question
| Cutaneous -Dermatophytoses -ringworm infections -t.unguium |
answer
| onychomycosis etiology: big three predominate but ANY trichophyton species can be involved manifests: leukonychia mycotica; nails lose luster, opaque, brittle, have crumbling consistency |
question
| Cutaneous -Dermatophytoses -ringworm infections -t.capitis |
answer
| etiology: microsporum audouinii m. canis trichophyton mentagrophytes t.rubrum microsporum: ectothrix; spores produced OUTSIDE hair shaft; fluoresces; infected hair becomes dull, breaks off 3mm above scalp trichophyton: endothrix; spores produced inside hair shaft; breaks at scalp "blackdot" |
question
| Cutaneous -Dermatophytoses -ringworm infections -treatment |
answer
| depends on area, occupation, age, cost, severity -best way to treat is orally but requires blood work and monitoring; lot of agents available |
question
| Cutaneous -Dermatophytoses -ringworm infections -onychomycosis |
answer
| progressive, recurring superficial fungal infection that begins in nail bed and progresses to nail plate leukonychia: whitening of nail plate |
question
| Cutaneous -Dermatomycosis -cutaneous candidosis (candida albicans) -etiology |
answer
| any fungal infection of skin, nails or maybe hair, caused by fungi other than dermatophyte c.albicans has 3 INVASIVE forms: yeast pseudohyphae hyphae |
question
| Cutaneous -Dermatomycosis -cutaneous candidosis (candida albicans) -epidemiology |
answer
| risk factors: diabetes obesity pregnancy AIDS broad-spectrum ab |
question
| Cutaneous -Dermatomycosis -cutaneous candidosis (candida albicans) -manifestations |
answer
| intertriginous candidosis: "weeping" or "scaled skin" lesions paronychial/onychomycotic candidosis: chronic infection; painful reddened swelling up to paronychial edge; nail is hardened, thickend; grooved |
question
| Cutaneous -Dermatomycosis -cutaneous candidosis (candida albicans) -therapy |
answer
| for cutaneou candidosis: crystal violet topical antifuncal agents for candidal paronychia or onychomycosis with ointment and systemicallY: nystatin amphotericin B ketoconazole |
question
| Subcutaneous Mycoses -sporotrichosis (sprothrix schenckii) -etiology |
answer
| sporothrix schenckii -thermally dimorphic fungus |
question
| Cutaneous -Dermatomycosis -cutaneous candidosis (candida albicans) -epidemiology |
answer
| worldwide contact with plants (thorns, splinters) gardeners and lumber worker at risk |
question
| Cutaneous -Dermatomycosis -cutaneous candidosis (candida albicans) -manifestations |
answer
| painless chronic infection nodular lesions of subcutaneous or cutaneous tissues and adjacent lymphatics |
question
| Cutaneous -Dermatomycosis -cutaneous candidosis (candida albicans) -therapy |
answer
| apply heat to affected extremity 3-4 times a day give AIDS pt itraconazole or amphotericin B |
