micro_mod8_the_dregs

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soren101
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micro_mod8_the_dregs
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2011-05-05 15:03:26
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microbiology ms1 mod8
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filamentous bac spirochetes chlamydia rickettsia
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  1. ACTINOMYCES ISRALII
    Filamentous G+ rod

    strictly anaerobic

    Sulfur granules

    Endogenous flora of the mouth and GI tract

    Non-acid fast

    Trauma (abscessed tooth, appendicitis, wounds, dental extraction, broken jaw)

    bacteriaform filaments surrounded by areas of inflammation

    Actinomycosis – hard, non-tender swelling of the face/neck or abdomen, spreads through draining sinus tracts; NOT communicable

    Pelvic actinomycosis – in women with an IUD

    Hard yellow granules (sulfur granules)composed of filamentous mass form in pus

    Tx: penicillin G with drainage

    SNAP -- Sulfa for Nocardia; Actinomyses give Pen
  2. NOCARDIA ASTEROIDES
    Filamentous G+ rod

    facultative aerobe

    Found in exogenous environment (soil)

    Infection through inhalation

    Weak acid fast staining (esp. if weak HCl is used)

    Nocardiosis – immunocompromised person --> lung infection (pneumonia) --> abscesses, sinus tracts --> brain, skin, and kidneys; NOT communicable

    Ziehl-Neelsen stain

    Tx: trimethoprim-sulfamethoxazole

    SNAP -- Sulfa for Nocardia; Actinomyses give Pen
  3. TREPONEMA PALLIDUM: GENERAL
    spirochete, microaerophilic

    Not seen on Gram stain, use dark field microscopy or fluorescence

    Non-specific serology – positive in primary and secondary syphilis

    Venereal Disease Research Laboratory (VDRL) test: cardiolipin (antigen) combined with patient serum --> flocculation if reagin (non-specific antibody) is present; used for congenital syphilis because titer is higher in the baby vs. mother

    • Rapid Plasma Reagin (RPR) test: cardiolipin on charcoal + patient serum --> agglutination:
    • *False positive – if you have HBV, leprosy, or infectious mononucleosis
    • *False negative – prozone phenomenon

    Specific serology – stay positive for life, so you can’t use it to determine response to treatment

    Fluorescent treponemal antibody-absorption (FTA-ABS) test: serum is adsorbed with antigens from a nonpathogenic treponemal Reiter’s stain to remove antibodies that react with normal flora --> serum added to syphilis antigen on a slide --> fluorescent anti-human antibody detects syphilis antibodies

    Microhemagglutination test (MHA-TP) test: sheep or turkey RBCs are coated with syphilis antigens; agglutinates if added to serum with syphilis antibodies

    Transmission – sexual and transplacental

    Infects endothelium --> endarteritis (for all stages, but most important in tertiary stage)

    Congenital syphilis – Hutchinson’s or “mulberry” incisors, facial and tooth abnormalities seen by 2 years; in 3rd month of pregnancy, get skin and bone lesions with hepatosplenomegaly

    Immunity is incomplete

    Tx: benzathine penicillin for all stages – grows very slowly so you must treat for a long time. For neurosyphilis use aqueous penicillin (benzathine penicillin does not penetrate the CNS)

    Non-pathogenic treponemes are part of the normal flora and can be cultured
  4. TREPONEMA PALLIDUM: STAGES
    Primary syphilis – hard, painless chancre at site of contact (tissue damage with migration of neutrophils, lymphocytes, and macrophages to the entry site)

    heals spontaneously within 6 months and spreads systemically through the blood; contagious

    Secondary syphilis – in ½ of patients: spread from blood to lymph nodes, CNS, mucousmembranes, and skin --> lymphadenopathy and generalized rash on the palms and soles, patchy alopecia

    moist lesions on genitalia = condyloma lata; low fever, malaise, anorexia,headache, and maybe meningitis, hepatitis, or nephritis; contagious

    Latent stage – organisms persist in spleen and lymph nodes; 1/3 of cases, can last decades:

    Early: secondary symptoms can recur; contagious

    Late: no symptoms; not contagious

    Tertiary syphilis – ½ of people with latent syphilis; tissue destruction is caused by host response to treponemal antigens, get gummas (soft masses in bone and skin consisting of inflammatory cells and few treponemes) and hepatosplenomegaly; neurosyphilis (tabes dorsalis)
  5. BORRIELA BURGDORFERI
    motile spirochete

    microaerophilic

    LYME DISEASE

    can see it with dark field microscopy, Giemsa, and silver stain(but patient culture is usually negative)

    Most common tick-borne disease in US – transmitted from the white-footed mouse (reservoir) to humans via the bite of Ixodes scapularis (East coast) or Ixodes pacificus(West coast); Deer are needed for the life cycle; nymphal stage transmits more often

    Stage 1 – local; multiplication in the skin and dissemination to the blood; 1 – 5 weeks after bite get erythema migrans (target-like) lesion (but 25% do not get the rash) with flu-like symptoms

    Stage 2 – spread to nervous system, joints, heart, and eyes, with secondary annular skin lesions, meningitis, myocarditis, MSK pain, Bell’s palsy, and eye abnormalities; aseptic. Intermittent symptoms with latency

    Stage 3 – chronic infection of large joints, nervous system, or skin

    Lyme arthritis – autoimmune

    ELISA – IgM after 2 weeks, IgG after 30 days; confirm with Western or PCR(there are cross-reacting antibodies in the normal flora)

    Tx: for stage 1 give doxycycline or amoxicillin; for late stage give ceftriaxone; doxycycline for prophylaxis
  6. BORRIELA HERMSII
    aerobic spirochete

    may see in blood smear

    major antigenic proteins from linear plasmids that can undergo antigenic variation

    Transmitted from rodents (reservoir) to humans via the Ornithodoros tick bite

    In the US: endemic relapsing fever – blood --> multiplies in kidney, liver, eye,and/or brain --> headache, fever, chills, and organ dysfunction --> antibody responses kill pathogen --> antigenic variation --> fever again…

    Tx: tetracycline
  7. BORRIELA RECURRENTIS
    spirochete

    may see in blood smear

    Can produce major antigenic proteins from linear plasmids that can undergo antigenic variation

    Humans are the only known reservoir; transmitted by the human body louse

    In Africa: epidemic relapsing fever – blood --> multiplies in kidney, liver, eye, and/or brain --> headache, fever, chills, andorgan dysfunction --? antibody responses kill pathogen --> antigenic variation --> fever again…

    Tx: tetracycline
  8. Jarisch-Herxheimer reaction
    Treatment with penicillin causes flu-like symptoms due to endotoxin release uponbacteria lysis

    • occurs in:
    • Secondary syphilis
    • Lyme disease
    • Leptospirosis
    • Relapsing fever

    Mediated by TNF, so passive immunization with anti-TNF can prevent
  9. RAT BITE FEVER
    Spirillum minor and Streptobacillus moniliformis

    cause rat bite fever --> reddish brown rash with fever and local lymphadenopathy
  10. CHLAMYDIA: GENERAL
    stain G-negative

    non-motile

    lack peptidoglycan in cell wall

    Obligate intracellular with a complex life cycle – spore-LIKE elementary body enters the epithelial cell and changes into reticulate body that replicates by binary fission

    daughter reticulate bodies (these are seen as inclusions with Giemsa stain) eventually turn into elementary bodies and are released

    Cannot be cultivated because they can’t generate their own energy

    Infect epithelial cells and are rarely invasive

    All share group-specific LPS antigen that can be detected with complement fixation

    Exudates can be subjected to IF, ELISA, and DNA probes
  11. CHLAMYDIA TRACHOMATIS
    most common cause of preventable blindness

    most common cause of bacterial STD in US; 15 immunotypes that only infect humans

    Inclusions contain glycogen and will stain with iodine

    Reservoir – people with asymptomatic genitourinary tract infection

    Transmission is usually sexual or through the birth canal

    Trachoma (chronic conjunctivitis) – conjunctival scarring causes eyelashes to turn inward which scars the cornea and leads to vascularization (pannus) --> blindnessTypes A, B, and C

    Transmission – finger/fomite-to-eye

    Nongonococcal urethritis (TYPES D-K) --> disseminated disease involves epididymitis and salpingitis or pelvic inflammatory disease; infected cells are restricted to nonciliated epithelial cells on mucous membranes of the urethra, endocervix, endometrium, fallopian tubes, and rectum

    Extensive PID may cause infertility or ectopic pregnancy

    Tx: azithromycin

    Neonatal conjunctivitis (onset: 7 – 12 days) and pneumonia (onset: 2 – 12 weeks), Tx: erythromycin

    Lymphogranuloma venereum (LGV, TYPES L1-3) – highly invasive; primary genital lesion --> systemic spread and replication in mononuclear phagocytes in the lymphatics (swollen draining lymph nodes = buboes that can rupture and lead to abscesses). Most common in Africa, Asia, and South America. Tx: tetracycline, doxycycline

    Reiter’s syndrome – associated with genitourinary and gastrointestinal infections; urethritis, conjunctivitis, mucocutaneous lesions, and reactive polyarthritis (damages cartilage without infecting synovial fluid)

    Can’t see, can’t pee, can’t bend my knee

    Linked with the HLA-B27 haplotype (maybe autoimmune response/complexes formed?)

    10 – 30% are co-infected with N. gonorrheae, so always give azithromycin with thetetracycline

    Produces a cell-mediated response and antibodies but no immunity forms

    Serology is useless because infection rate is high
  12. OTHER THINGS THAT CAUSE REITER'S SYNDROME
    • Neisseria gonorrheae
    • Ureaplasma urealyticum
    • Salmonella spp.
    • Shigella spp.
    • Yersinia spp.
    • Campylobacter spp.
    • Chlamydia trachomatis
  13. CHLAMYDIA PSITTACHI
    Primary reservoir is birds (turkeys and parrots) – spread by inhalation of dried excretions

    INTRACELLULAR GROWTH

    Parrot fever (ornithosis) – infected alveolar macrophages spread infection to lungs (pneumonia with high fever) --> bloodstream --> spleen, heart, liver

    Rarely communicable

    Inclusions do not contain glycogen

    Can use serology – 1 immunotype

    Tx: tetracycline, doxycycline
  14. CHLAMYDIA PNEUMONIA
    Atypical pneumonia – URT, LRT

    sinusitis spread from person to person

    Inclusions do not contain glycogen

    Can use serology – 1 immunotype

    Associated with coronary artery disease

    Tx: tetracycline, doxycycline
  15. RICKETTSIA GENERAL
    Gram-negative (poor-staining) coccobacillus

    outer membrane and thin peptidoglycan layer

    Obligate intracellular parasite that multiplies intracellularly by binary fission

    Can synthesize some of the ATP needed for metabolism (not an energy parasite)

    Cause zoonotic disease transmitted by arthropod vectors and do not survive in the outside environment

    Infect vessel wall endothelium --> vasculitis --> hemorrhage and edema

    For R. rickettsii, R. prowazekii, and R. tsutsugamushi – antigen cross-reacts with the OX strain of Proteus vulgaris --> basis of agglutination in the Weil-Felix test using patient serumantibodies
  16. RICKETTSIA RICKETTSII
    ROCKY MOUNTAIN SPOTTED TICK FEVER

    Spread from dogs and rodents (reservoirs) to humans

    Dermacentor tick bite; US East coast

    Skin --> blood --> attach to endothelial cells of small blood vessels and enter by pathogen directed endocytosis

    Phagosome lysis via phospholipase A and growth in cytosol until the cell bursts --> hemorrhagic spots associated with a characteristic rash

    Rocky Mountain Spotted Fever – acute fever, headache, myalgia, prostration; macules appear first on hands and feet and progress to petechiae. Severe DIC and coma

    No person-to-person transmission

    Diagnosis by IFA, ELISA, and direct detection of antigens in skin biopsies

    Tx: need something that gets inside the host cell – doxycyline, tetracycline, or chloramphenicol

    Sulfa drugs exacerbate infection
  17. RICKETTSIA PROWAZEKII
    Epidemic typhus: 1–3 weeks after bite: sudden onset of chills, fever, headache with a maculopapular rash (that spares face, palms, and soles) coming a week later --> severe meningoencephalitis with rash --> delirium and coma (if nottreated)

    Spread by human body louse (Pediculus); only infects humans

    Associated with war and poverty

    Tx: tetracycline, chloramphenicol

    Recrudescent typhus – reactivation following latent infection with epidemic typhus; less severe than epidemic form. In the US, see it in people from WW2; called “Brill-Zinsser disease
  18. RICKETTSIA TSUTSUGAMUSHI
    Scrub typhus – transmitted by mites or chiggers from rodents
  19. RICKETTSIA AKARI
    Reservoir is mice, transmitted by mites

    Causes rickettsial pox
  20. RICKETTSIA TYPHI
    Reservoir is rodents, spread by fleas

    Causes endemic (murine) typhus

    May see it in California or Texas
  21. COXIELLA BURNETII
    Transmitted from cattle, sheep, or goats to humans by inhalation of dried excretions

    INTRACELLULAR GROWTH

    Spore-like structure makes it resistant to the environment and phagolysosome

    Q fever – fever, severe headache, chills, myalgia; may cause pneumonia with granuloma formation in the lungs, liver (--> hepatitis), bone marrow, and spleen; no rash!

    Phase I: isolated, virulent, has surface antigen

    Phase II: after repeated passage, nonvirulent, surface antigen is lost

    Chronic Q fever – associated with higher phase I titers, may involve heart valves as a subacute bacterial endocarditis that is blood culture-negative

    Very low ID50 – only need about 1 for infection

    INTRACELLULAR GROWTH
  22. EHRLICHIA CHAFFEENSIS
    Forms morulae in cytoplasm

    Endemic in dogs, transmitted by the Lone Star tick (Amblyomma and Dermacentor)

    Human monocytic ehrlichiosis (HME) – infection of monocytes and macrophages --> fever, headache, myalgia, thrombocytopenia, leukopenia, and increased liver enzymes

    Tx: doxycycline

    LONE STAR TICK

    The ehrlichioses are clinically indistinguishable
  23. EHRLICHIA EQUI
    Transmitted by Ixodes ticks

    Infection of granulocytes --> fever, headache, myalgia, thrombocytopenia, leukopenia, increased liver enzymes(ehrlichiosis)

    Tx: doxycycline

    The ehrlichioses are clinically indistinguishable

    renamed Anaplasma phagocytophilum
  24. TINEA VERSICOLOR
    CUTANEOUS MYCOSES

    DERMATOPHYTOSES

    hypopigmented skin patches inwarm humid areas of the skin (infects outer layer of dead cells)

    May get outbreaks in the NICU

    Transmitted through direct contact

    Tx: topical miconazole; selenium sulfide on skin
  25. MICROSPORUM CANIS
    CUTANEOUS MYCOSES

    DERMATOPHYTOSES

    infects skin, hair, and nails; characteristic targetlesion; get it from infected cats, dogs, and other people

    Causes tinea ______, or ringworm

    A zoonotic fungal pathogen

    Scrapings show macroconidia on short conidiophores and branched,septate hyphae; may also form microconidium – non-dimorphic mold

    Highly infectious/contagious

    Tx: topical miconazole, tolnaftate or undecylenic acid; oral griseofulvin

  26. TRICHIPHYTON AND EPIDERMOPHYTON
    CUTANEOUS MYCOSES

    DERMATOPHYTOSES

    Trichophyton tonsurans is the most common cause of outbreaks of tinea capitis in children; seasonal (September)

    Superficial fungal infection of skin = dermatophytosis

    Many major pathogens are dimorphic
  27. SPOROTHRIX SCHENCKII
    SUBCUTANEOUS MYCOSES

    Spirotrichosis, aka Roseberg’s disease – formation of local abscess orulcer with nodules in regional lymphatics (subcutaneous)

    Introduced into skin by thorns and other puncture wounds

    Mold – has a rosette/daisy pattern of oval conidia (chlamydiophore)

    Yeast – cigar-shaped with buds

    Dimorphic

    HIV & GARDENERS (THORNS)

    Tx: itraconazole,heat, iodine

    MOLD

    • YEAST (CIGAR)
  28. HISTOPLASMA CAPSULATUM
    SYSTEMIC MYCOSES

    endemic in Ohio and Mississippi River valleys

    Dimorphic – mold has tuberculate macroconidia and microconidia (looks like sea mines); yeast issmall and ellipsoid

    Extremely slow grower

    Can get in from bat caves (due to high levels of nitrogen in guano) and starling droppings, inhaled

    Phagocytosed, but can exist within or kill macrophages (produces bicarbonate and ammoniathat raise the pH of phagolysosome)

    After 2 weeks causes acute respiratory illness – fever, chills, night sweats, fatigue, headache, cough, myalgia, andweight loss

    Causes disseminated histoplasmosis in patients with compromised CMI – ulcerative lesions of tongue and gingiva,severe pulmonary infection

    RIA detects Histoplasma antigens or RNA (DNA probe); complement fixationand immunodiffusion

    Tx: amphotericin B, itraconazole is used for preventing disease in AIDS patients; fluconazole for meningitis

    • MOLD

    • YEAST (SMALL, ELLIPSOID)
  29. BLASTOMYCES DERMATITIDIS
    SYSTEMIC MYCOSES

    Dimorphic – mold has hyphae with pear-shaped microconidia; yeast is round with adoubly refractive wall and a single broad-based bud

    Causes blastomycosis – fever, productive cough, pleuritic chest pain, and weight loss,erythematous lesion and lung crackles; CXR shows nodular lesions

    Soil is natural reservoir – inhalation of aerosolized microconidia

    Endemic in eastern north America (Ohio, Mississippi, and St. Lawrence ribers)

    Affects AIDS patients but not as much as the others (disseminated disease – ulceratedgranulomas of skin, bone, or other sites)

    Tx: itraconazole, amphotericin B for severe disease

    • YEAST (BROAD-BASED BUD)

    • MOLD (w MICROCONIDIA @ 20^C)
  30. COCCIOIDES IMMITIS
    SYSTEMIC MYCOSES

    Endemic in Southwestern US and Latin America – lots in Phoenix and South Texas

    Hyphae w/alternating arthrospores (soil) and spherules filled withendospores (diagnostic because it isn’t a classic yeast, in tissues)

    Spherule – kind of a parasitic cycle

    Inhaled

    Causes coccidioidomycosis – influenza-like illness with fever, nightsweats, joint pain, dry cough, headache, and fatigue - patients maydevelop infiltrates or arthralgias;

    erythema nodosum (EN) - red, tendernodules, also called "desert bumps," may occur on extensor surfaces; it isa delayed hypersensitivity reaction to fungal agents and an indicator of good prognosis; NOT specific for Coccidioides (histoplasmosis, tuberculosis, and leprosy can do the same thing)

    Filipinos, African Americans, and pregnant women in 3rd trimester -higher incidence of disseminated disease

    Defect in CMI predisposes

    Complement-fixing antibodies are very increased in disseminated disease

    Tx: amphotericin B for disseminateddisease

    • SPHERULE

    • ARTHROSPORES (INHALED)
  31. PARACOCCOIDES BRASILIENSIS
    SYSTEMIC MYCOSES

    endemic in the soil of rural Latin America

    “captain’swheel” appearance of yeast in tissue (thick wall with multiple buds)

    Dimorphic

    Transmission through airborne conidia

    Causes paracoccidioidomycosis – ulcerations in the oral cavity and at bothangles of the lips; cough and purulent sputum; CXR shows bilateral micronodularinfiltration, some fibrosis, and a cavity in the upper right lung

    Tx: itraconazole

    • YEAST
  32. PNEUMOCYSTIS JIROVECII
    OPPORTUNISTIC MYCOSES

    Crushed ping-pong ball morphology

    CXR: diffuse interstitial pneumonia and bilateral infiltrates with a ground glass appearance

    Classified as a protozoan medically and a fungus genetically but has cholesterol (not ergosterol) in the cell membrane

    Major surface glycoprotein (encoded on multiple genes) exhibits antigenic variation

    Cysts are visualized with methenamine-silver, Giemsa, or fluorescent-abstaining

    Causes plasma cell pneumonia – sudden onset of fever, non-productivecough, progressive dyspnea, tachypnea, and fatigue

    Infection of alveoli leads to an inflammatory response with plasma cells and afrothy exudate that blocks oxygen exchange

    70% of the population has been infected (mostly asymptomatic)

    Found in domestic animals (horses and sheep) and rodents, but they are not areservoir

    Mortality is 100% if untreated

    Tx: trimethoprim and sulfamethoxazole

    Px: trimethoprim-sulfamethoxazole or aerosolized pentamidine should be usedas a chemoprophylaxis in patients whose CD4 counts are below 200

  33. MUCOR & RHIZOPUS
    OPPORTUNISTIC MYCOSES

    Mucormycosis (caused by Rhizopus, Mucor, and Absidia spp.) MOLD

    Fastest growing fungus – emergency surgery needed

    See it in people with diabetic ketoacidosis, burns, or leukemia

    Yeast: non-septate hyphae with right-angle branges and ribbon-likeappearance; mold: spores within a sporangium

    Saprophytic, non-dimorphic mold, transmission is through inhalation

    Invades and leaves the lungs to proliferate in the walls of blood vessels

    infarction and necrosis

    Chills, fever, pleuritic chest pain, bloody sputum, infiltrates on CXR; also likesthe paranasal sinuses: may get a necrotic lesion under the eye with periorbitalswelling and ptosis

    Tx: amphotericin B and removal of necrotic tissue

    • MOLD (CONTAINED)

    • YEAST (RIGHT-ANGLE BRANCHING)
  34. ASPERGILLUS
    OPPORTUNISTIC MYCOSES

    Aspergillus fumigatus

    Find it in any decomposing plant matter; very thermophilic

    Not dimorphic – only exists as a mold

    Outside the body: spores form radiating columns; inside the body: septate hyphae form V- shaped branches

    Risk factor – neutropenia, bone marrow transplant, cancer, and things that cause lungcavities (aerobic)

    AIDS patients – don’t expect it early on, but it may happen once their lungs are damaged

    Often associated with secondary colonization

    Causes a variety of different things: acute invasive pulmonary aspergillosis (dry cough,dyspnea, chest pain --> fever, bloody cough), aspergilloma, acute bronchopulmonaryaspergillosis (high eosinophils)

    Colonizes and invades lungs – hematogenous dissemination to organs may occur (abscessesin brain, kidney, heart, bone, and GI)

    More likely to get an aspergilloma if you had a TB granuloma or sarcoidosis

    Tx: amphotericin B

    • MOLD (RADIATING)

    • YEAST (V BRANCHES)
  35. CRYPTOCOCCUS NEOFORMANS
    OPPORTUNISTIC MYCOSES

    most common life-threatening fungal disease in AIDS patients

    Grows in soil that contains bird (esp. pigeon) droppings – gets to human throughinhalation

    Oval, budding yeast surrounded by a wide polysaccharide capsule (not dimorphic)

    India ink is used to see the capsule

    Forms a narrow-based bud

    Colonies will be very mucoid

    Cryptococcal antigen test (“crag”) – capsular antigen is detected through latexagglutination

    Highly elevated “opening pressure” when you do spinal tap

    It is neurotropic – brain has lots of dopamine compounds (melanin precursors), and Cryptococcus has the ability to make melanin (which functions as an electron sink)

    Causes cryptococcal meningitis – fever, headache, nausea, vomiting, nuchal rigidity, and disorientation

    Subcutaneous nodules may also appear in disseminated disease

    Tx: combined treatment with amphotericin B and flucytosine; use fluconazole for disease suppression long-term

    • YEAST (NARROW-BASED BUD)

    • INDIA INK
  36. CANDIDA ALBICANS
    OPPORTUNISTIC MYCOSES

    Oral thrush and diaper rash (red, weeping)

    Dimorphic – mold and yeast

    Germ tubes form in serum at 37 degrees celsius (serves to distinguish C. albicans frommost other Candida species)

    60% oral carriage, most infections are endogenous

    Infections with Candida are more frequent than those of all the other fungi combined

    Yeast is the form found in normal flora – hyphae = invasive phaseYeast cell = colonizersHyphae = invaders

    Budding yeasts are G+ and can be seen using calcofuor

    Forms chlamydospores at 37C but other spp. do not

    AIDS can predispose to systemic infection (defect in T cell immunity)

    Cadida glabrata may occur in organ transplants

    Skin tests with Candida antigens are uniformly positive in immunocompetent adults and are used as an indicator that theperson can mount a cellular response

    Tx: topical antifungals (clotrimazole or nystatin); fluconazole for oropharyngeal or esophageal thrush

    • YEAST/MOLD (SABOURAUD 25^C)

    • YEAST (PSEUDOHYPHAE, SEEM G+)

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