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347 Cards in this Set
- Front
- Back
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What are fungi
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- eukaryotic
- heterotrophic - unicellular to filamentous - rigid cell walled - spore bearing organisms that usually reproduce by both sexual and asexual means - eukarotes - have nuclei, mito, golgi, ER< and lysososomes = seperates fungi from bacteria heterotrophic - lack chlorophyll - seperates from plants and alage - saprobes - live on decaying batter - symbionts - live together in which the assoc is of mutual advantage - commensals - org living in close relationship in which one benefits and the other is neither benifited or harmed - parasites - organisms that live in or w/in a host from which they derive benefits w/o making any useful congribution in return - unicellular or fillamentous - fungi have 2 basic forms - single celled = yeast or filamentous -molds - like plants - righid walls - non-motile - seperates them from animals - spore bearing - formation of spores sexual (meiosis) or asexual (mitosis) |
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mycotic dx
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hypersensitivity - allergic rxn to molds and spores
mycotoxicosis - poisoning by food products contaminated by fungi - produce toxins from the grain substrate mycetismus (mushroom poisoning) pre-formed toxin infection |
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increased frequency of mycotic dx caused by
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1. more invasive procedures used on pt
2. increased use of immunosuppressive drugs 3. increase in immunosuppressive dx 4. increased awareness by physicians 5. better lab diagnostic tools 6. better trained lab personnel |
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morphology of yeast
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exist in 2 basic growth forms
- yeast - mold/hyphae (filamentous, mycelium) - dimorphic fungi exist in both forms - yeast/hyphae |
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yeast
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unicellular
non-filamentous oval or spherical 350 species ided 2 types based on how they multiply reproduce by simple budding to form blastoconidia - 2 types of asexual reproduction - 1. transverse 2. budding - colonies are usually moist or mucoid - yeasts-like fungi may be basidiomycetes or ascomycetes |
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hyphae
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aka filamentous, mycelium
- filamentous - 1 dimensional linear arrangement of cells - form as a consequence of cell division along single plain - grows at the tip - apical extension - rapid growth - reporduce by spores or conidaia - septate - lack separation of fully divided cells - septa that contain pores coenocytic - one continuous cytoplasm - aseptate tubular cells w/cell walls mass of hyphae = mycelia - tangle of hyphae - extensively permeate the substrate w/in which fungi grows structures like mushrooms - filaments tightly packed together vegetative - on or beneath the surface aerial - above the surface - produce structures known as conidia - blastic*budding) or thallic (fragment) |
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dimorphic fungi
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yeast form
- parasitic form - tissue form - cultured at 37 deg C Mycelial form - saprophytic form - cultured at 25 deg C |
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reproduction
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reproduce by the formation of spores
- sexual - fission of 2 nuclei - meosis - plasmogamy = cytoplasmic fusion of cells - , karyogamy = fusion of two nuclei - genetic recomb and meiosis - haploid spore = sexual spore (zygospore, ascospores, basidospore - sexual spore either formed by two different strains + and - = heterothallic - or from same stain - homothalic - asexual =mitosis - conidia - budding or differentiation of preformed hyphae - sporangia = forms asexual spores by successive cleavage of sporangium -major method for maintenance and dissemination of many fungi - some classes can produce both sexual and asexual spores - telemorph - sexual - anamorph - asexual |
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hyphae
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aka filamentous, mycelium
- filamentous - 1 dimensional linear arrangement of cells - form as a consequence of cell division along single plain - grows at the tip - apical extension - rapid growth - reporduce by spores or conidaia - septate - lack separation of fully divided cells - septa that contain pores coenocytic - one continuous cytoplasm - aseptate tubular cells w/cell walls mass of hyphae = mycelia - tangle of hyphae - extensively permeate the substrate w/in which fungi grows structures like mushrooms - filaments tightly packed together vegetative - on or beneath the surface aerial - above the surface - produce structures known as conidia - blastic*budding) or thallic (fragment) |
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dimorphic fungi
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yeast form
- parasitic form - tissue form - cultured at 37 deg C Mycelial form - saprophytic form - cultured at 25 deg C |
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reproduction
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reproduce by the formation of spores
- sexual - fission of 2 nuclei - meosis - plasmogamy = cytoplasmic fusion of cells - , karyogamy = fusion of two nuclei - genetic recomb and meiosis - haploid spore = sexual spore (zygospore, ascospores, basidospore - sexual spore either formed by two different strains + and - = heterothallic - or from same stain - homothalic - asexual =mitosis - conidia - budding or differentiation of preformed hyphae - sporangia = forms asexual spores by successive cleavage of sporangium -major method for maintenance and dissemination of many fungi - some classes can produce both sexual and asexual spores - telemorph - sexual - anamorph - asexual |
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Spores
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sexual
- less frequent than asexual - formed upon the mating of two fungi - genetically intermediate to the parental fungi asexual - formed by a single parental fungi - genetically identical to parent fungi - variety of types = conidiospores or sporangiospores |
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kingdom of fungi classifications
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zygomycetes
basidiomycetes archiascomytes hemiascomycetes euascomycetes |
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zygomycetes
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molds w/ broad, sparsely septate, coenocytic hyphae
root like structures = rhizoids produce sexual zygospores following fusion of 2 compatible mating types asexual spores are contained w/in sporangium - that is borne at the tips of the stalk-like sporangiospores - cause zygomycosis - Rhizopus, Mucor |
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Basidiomycetes
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mostly fillamentous but some typical yeasts
sex repro leads to formation of haploid basiodspores on the outside of the generative cell termed a basidium hyphae w/clamp connections asexual repro by budding = conidia most prominent human pathogens are the basidiomycetous yeast |
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Archiascomycetes
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new class
including pneumocystis carinii that was formally considered a protozoan sexualy reproduction by fusion of compatible mating types to form zygote = spherical cyst or spore case that contains 8 spores vegetative trophic form that reproduces asexually by binary fission |
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hemiascomycetes
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contains ascomycetous yeasts
proliferate by budding or fission anamorphs and telemorphs candida |
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euascomycetes
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repro sexually to form a thin walled sac or ascus that contains haploid ascospores
class has12 orders that include species pathogenic to humans budding yeasts, septate hyphae, conidia asexual repro by budding conidia septate molds aspergillus |
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pathogenic fungi
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normal host
- systemic pathogens - 25 species = deep infections of the internal organs - cutaneous pathogenous - 33 species - localized to the skin the hair and nails - subcutaneous pathogens - 10 species = infection confined do the dermis, subcutaneous tissue or adjacent structure Immunocompromised host - opportunistic fungi - 300 species = cause infection only in the immunocompromised not necessary step in fungi life cycle not communicable from person to person outbreak result of common environmental exposure |
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pathogenicity of fungi
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1. thermotolerance- most are mesophilic and cannot grow at 37 deg C
2. ability to survive in tissue environment - unique enzyme capacity 3. ability to withstand host defenses |
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establisment of fungal infection
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depends on
- size of inoculum - resistance of the host = cell mediated immunity - immune competent individuals usually can control infections - severity of dx seems to depend mostly on the immunologic statusof the host |
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PT history of mycotic dx
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medical
occupaitonal travel avocation |
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diagnosis of mycotic dx depends on 3 basic lab approaches
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1. microbiologic
2. immunologic 3. histopathologic |
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diagnosis of mycotic dx
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- stains and direct micro exam
- rapid and cos effective - less sensitive than culture - Approaches used: calcofluor white, gram, giemsa, GMS (silver stain), PAS, H&E, KOH - culture - most sensitive - nec to ID etiologic agents - grown on Sabouraud dextrose agar - add cycloheximide and Abx (penecillin, steptomycin etc) - 25 deg and 37 deg C inccubated seperately 2 plates= to reveal dimorphism - acid pH ~5.6 - not negative until after 4 weeks of incubation - serology - latex agglutination -IgM - immunodiffusion - IgG - EIA - IgG & IgM - Complement fixation - IgG antigen detection - cycptococcosis, histoplasmosis, aspergillosis - DNA probes - rapid 1-2 hrs - species specific - expensive - Ribosomal DNA hybridized to labeled DNA probe - skin testing - dermal hypersensitivity - use limited to: 1. determine cellular defense mechanisms 2. epidemiologic studies |
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treatment
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induce cell inj by causing cell membrane of fungus to become permeable
finding an agent that will selectively injure fungal cell walls w/o damaging the host cell Mammalian cells do not contain the enzymes that will degrade the cell wall polysaccharides of fungi. Therefore, these pathogens are difficult to eradicate by the animal host defense mechanisms. The cell membranes of all eukaryotic cells contain sterols; ergosterol in the fungal cell membrane and cholesterol in the mammalian cell membrane |
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primary anti-fungal
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1. polyenes
2. azoles 3. allylamines 4. echinocandins 5. antimetabolites 6. griseofulvin |
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Polyenes
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aka amphotericin B
used to tx of serious life threatening mycoses - fungicidal against most fungi - exerts iits anti-fungal effect by 2 mechanisms 1. binding to ergosterol causing leakage 2. direct membrane damage due to oxidative damage - also binds to cholesterol causing toxicity = nephrotoxicity, fever, chills, anemia last resort for severe infections adm intravenously - req hospitilization - often for months |
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azoles
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inhibit the fungal cytochrome P-450-dep enzyme lanosterol - alpha - demethylase
-inhibition of ergosterol synthesis which effects membrane synthesis results in inhibition of growth or cell death or cell death ketoconazole - orally abs - active against dimorphic fungi - can cause serious side effects Fluconazole - excellent oral bioavailability and low toxicity - not active against the opportunistic molds Itraconaxole - orally administered or by IV - broad spectrum of antifungal activity - often used in tx of dermatophytic infections - serious side effects are rare Voriconazole - orally administered or by IV - excellent penetration into CNS - generally well tolerated - can cause visual disturbances targtets 14alpha demethylase |
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allylamines
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used for dermatophyte infections
- decreases ergosterol syntehsis broad spectrum of activity tx of all dermatomycises targets squalene epoxidase |
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echinocandins
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inhibit 1,3 beta D glucan synthase forms glucan polymers in the cell wall
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flucytosine
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5FC only available antifungal agent that fns as an antimetabolite
interferes w/syn of DNA, RNA, and prot in the fungal cell excellent bioavailability major toxicities which serum levels exceed 100 microgram/mL inhibits RNA syn found main application in cryptococcosis administered orally |
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grisseofulvin
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very slow actingdrug used for severe skin and nail infections
inhibits fungal growth by interaction w/microtubules resulting in inhibition of mitosis administered orally tx of dermatophytes considered a second line agent assoc w/mild side effects |
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clinical classification
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superficial
cutaneous subcutaneous systemic opportunistic |
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superficial mycoses
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limited to very superficial surfaces of the skin and hair
nondestructive no living tissue invade no cellular response from host - no pathological changes elicited - innocuous pt unaware of condition ex = tinea nigra, pityriasis versicolor |
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cutaneous mycoses
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infections of keratinized layer of skin, hair and nails,
-may elicit a host response and becomes symptomatic - signs and sx = itching, scaling, broken hairs- ring like patches of skin and thickened discolored nals |
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subcutaneous mycoses
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involve the deeper layers of the skin
caused by broad spectrum fungi recognized by the host immune system tend to remain localized and rarely disseminate systematically chronic, localized infections following traumatic implantation of the agent causitive fngi are all soil saprophytes of regional epidemiology whose ability to adapt to the tissue enviro and elicit dx is extremely variable - form deep ulcerated skin lesions - most commonly involoving lower extremities |
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systemic mycoses
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caused by classic dimorphic fungal pathogens
exhibit thermal dimorphism often refered to as endemic mycoses cause primary infection in lung w/dissemination to other organs and tissues |
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opportunistic mycoses
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caused by ubiquitous saprophytes and occasional pathogens that invade tis of those pt who have
- predisposing dx - predisposing conditions have low or limited virulence |
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yeasts
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unicellular
single celled fungus reproduces by simple budding to form blastoconidia 2 types of asexual reproduction - transverse and buding colonies visible iin culture w/in 24-48 hrs soft moist colonies resemble bacterial cultures many species of yeast |
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yeast pathogens
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candida albicans
cryptococcosis neoformans |
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candida albicans info and morphology
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4th most common cause of nosocomal bloodstream infections
infection rates rising steadily in all age groups more than 100 species described but only a few have been implicanted in clinical infections canida albicans mostcommonly isolated from clinical material (90-100% of mucosal isolates and 50-70% of isolates from BSI) Morphology - exists as oval like forms that produce buds or blastoconidia - several species produce pseudohyphae and true hyphae - C. albicans forms germ tubes and terminal thick walled chlamyoconidia - stain poorly w/H&E and well w/the PMS and GMS stain - in culture - smooth, wite domed colonies - other specis and albicans undergo phenotypic switiching in which a single strain of candida may change reversibly among several different morphtypes - may explain the ability of C. albicans to survive in many different environmental types |
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canidida epidemiology
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known colonizers of humans and other warm-blooded animals
primary site of colonization is in the GI tract also found as commensals in the vagina and urethra on the skin and under nails - found in air, water, and soil - 25-50% of healthy individuals carry canidia as ppart of the normal flura of the mouth - C. albicans 70-80% of isolates - endogenous infection occurs when the host is compromised - transfer of organism from GI mucosa to bloodstream req overgrowth ofyeast and a breach in integrity of the GI mucosa -exogenous infection may also occur through contamination or transmission from healthcare workers usually occurs when pt has some alteration in alteration in cellular immunity, normal flora, or normal physiology - pdecreased cellular immunity, prolonged antibiotic or steroid = imbalance of normal flora - invasive procedures such as cardiac surgery and indwelling catheters produce alterations in the host can cause pneumonia, septicemia, endocarditis, esophagitis in the compromised pt |
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candida - clinical syndromes
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can cause infection in any organ system
- range from superficial mucosal and cutaneous candidiasis to widespread hematogenous dissemination involving target organs mucosal infections - seen in immunocompromised individuals - appearance - white cottage cheese like patches on mucosal surface - pseudomembranous type - erythematous type - candidal leukoplakia - angular cheilitis local skin infection skin lesions urinary tract involvement hematogenous involvement CNS involvement cardiac involvement eye infection bone and joint infection |
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lab diagnosis of candida
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histopathology
- clinical material to be sent to lab depends on the presentation of the dx - budding yeast-like forms and pseudohyphae are easily detected culture - culture on a standard mycologic medium will allow the isolation of the organism for subsequent identification to species blood cultures, vaginal discharge, urine, feces, nail clippings, or material from cutaneous or mucocutaneous lesions yeast form is gram positive and grows in 2-3 days on most bacterial and fungal media more virulent as it forms mycelia |
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treatment for candida
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drug of choice for vaginitis and cutaneous infections is nystatin (topical) and for those systemic infections are itraconazole and fluconazole, amphotericin B
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cryptococcosis
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sub-acute or chronic infection may affect the lungs or skin but most commonly manifests as a meningitis
worldwide distribution found in soil varieties include - Neoformans, Grubbi, Gatti |
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cryptococcosis morphology
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- systemic mycosis caused by encapsulated, yeast-like organism, 2-20 micrometers in diameter
- replication is by budding - single buds are usually formed - cells are surrounded by spherical zones (extracellular capsule) - cell wall contains melanin |
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cryptococcosis epidemiology
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- inhalation of aerosolized cells from the environment
- dissemination from lung to CNS produces clinical dx - most common cause of fungal meningitis most often encountered as an opportunistic pathogen pt w/defective cellular immunity occurs in pt w/AIDS initial exposure may be moths to years prior to manifestation of dx encountered as opportunistic pathogen - defective cellular immunity |
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cryptococcosis sx
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presents as pneumonic process or CNS infection, cutaneous infection occurs less common
pulmonary infection can be asymptomatic to pneumonia cerebromeningeal is most common form of dx skin lesions in 10-15% of pt fatal if untreated - death due to cerebral edema and increased intracranial pressure both meninges and underlying brain tissue are involved clinical presentation = fever, headache, visual disturbances, abn mental status and seizures and ultimately coma and death spinal tap for diagnosis |
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cryptococcosis diagnosis
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histopathology of blood, CSF or other clinical material = encapsulated budding yeast - visualized w/gram stain as well as with india ink
- mucicarmine stain is often used as it tints the capsule - usually no inflammatory rxn culture of blood, CSF, or other clinical material on mycologic media = colonies round, encapsulated, budding yeast cells w/in 3-5 days as culture ages it turns brown due to melain production by direct detection of the capsular polysaccaride Ag in serum or CSF using latex agglutination or EIA kits = rapid, sensitive, and specific. - decreasing titer has a good prognosis while increasing titer has a poor prognosis |
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cryptococcosis tx
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fatal if untreated
effective management of CNS pressure amphotericin B plus flucytosine (2 weeks) Fluconazole or itraconazole (8 weeks) |
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pityriasis vesicolor info and morphology
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caused by Malassezia furfur
- certain tropical environments it may affect up to 60% of the population appears as cluster of spherical or oval thick - walled yeast like cells 3-8 micrometers - may be mixed w/ short hyphae - budding - collar around bud initiation - show polar bud formation w/a lip or collor around the ppt of bud initiation on parent cell - cream-colored -> tan |
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pityriasis vesicolor epidemiology
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dx of helathy
occurs worldwide most prevalent in the tropics not found as saprophytte in nature infection from direct contact from infected keratinous material from one person to another |
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pityriasis (tinea) versicolor clinical syndromes
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lesions
upper trunk, arms, chest, shoulders, face and neck irregular shaped nterfere w/melanin production asymptomatic |
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pityriasis vesicolor lab diagnosis
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direct visualization of epidermal scales in
- 10% KOH w/ or w/o calcofluor white - H&E - PAS - culture may be performed in mycologic media at 30deg C for 5-7 days = not nec = colonies composed of budding yeast cells w/occasional hyphae |
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tx of pityriasis vesicolor
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dx is generally chronic and persistent
topical azoles or selenium sulfide shampoo - for more widespread infection use of ketoconazole or itraconazole |
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tinea nigra morphology
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caused by the black fungus Hortaea werneckii
dermatiaceous, frequently branched, septate hyphae (1.5-3 micrometers) elongate budding cells anelloconidia black mold in culture - standard mycologic media 25 deg C where it is black mold producing annelloconidia - conidia possessing annelids or rings superficial infection |
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tinea nigra epidemiology
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tropical or subtropical condition
traumatic inoculation most prevalent in africa. asai, central and south america children and young adults most often affected w/ higher incidence in females |
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tinea nigra clinical syndromes
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- solitary, irregular, pigmented macule
usually on palms or soles not contagious no discomfort or host reaction |
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tinea nigra lab diagnosis
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microscopic diagnosis of skin in 10-20% KOH
- h&E cultured on mycologic media w/abx = yeast colony appear in 3 weeks - micro examination = 2 celled cylindrical yeast-like cells |
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tinea nigra tx
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responds well to topical therapy including whitfield ointment, azole creams, and terbinafine
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white piedra morphology
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infection of hair caused by fungi of genus
Trichosporon hyphal elements arthroconidia - rectangular cells resulting from the gragmentation of hyphal cells blastoconidia |
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white piedra epidemiology
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occurs in tropical and subtropical regions
related to poor hygiene |
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white piedra cliical syndromes
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affects the hairs of the groin and the axillae
surrounds the hair shaft and forms a white to brown swelling along the hair strand soft and pasty doesn't damage hair shaft |
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white piedra lab diagnosis
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micro exam to reveal hyphal elements
arthoconidia or budding yeast infected hair placed on mycologic media = cream-colored dry colonies w/in 2-3 day |
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white piedra treatment
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topical azoles
improved hygine and shaving of infected area |
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black piedra morphology
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affects hair - primarily the scalp
causative agent = Piedraia hortae grows as a pigmented brown to redish black mold cutlure ages asci-containing, spindle shaped ascospores foremd w/in specialized structures these are also produced around the hair shaft |
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balck peidra epidemiology
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uncommon
reported in tropical areas (Latin america, and central africa) condition of poor hygiene |
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black piedra - clinical syndrome
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small dark nodules that surround the hair shafts
asymptomatic usually involves the scalp hyphal mass held together by cement like substance that contains asci and ascospores, the sexual phase of the fungus |
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black piedra lab diagnosis
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examination of nudule to reveal branched pigmented hyphae
culture on mycologic media (25 deg C) asci observed ranging from 4 to 30 micrometers containing up to 8 ascospores |
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black piedra treatment
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haircut
regular washings |
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dermatophytoses
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caused by dermatophytic fungi
refers to a complex of dx caused by any of several species of taxonomically related filamentous fungi - Trichophyton - epidermophyton - microsporum all possess the ability to cause dx in humans or animals have in common the ability to invade the skin, hair, or nails break down keratin surfaces skin infections - only invade the upper, outermost layer of the epidermis - stratum corneum various forms are referred to as TIneas or ring worm clinically classified according to the anatomic site or structure affected - tinea capitis of scalp, eyebrows and eyelashes - tinea barbae of the beard - tinea corporis of the smooth or glabrous skin - tinea cruris of the groin tinea pedis of the foot - tinea unguium of the nails |
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dermatophytoses morphology
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each genus is caracterized by a specific pattern of growth in culture and by the production of macroconidia and microconidia
further identification to species level requires consideration of colony morphology, spore porduction and nut req in vitro microsporum - ided by observation of its macroconidia - microsporum canis produces characteristic large multicellular thick and rough walled macroconidia Epidermophyton floccosum does not produce microconidia but is smooth -walled macroconidia borne in clusters of two or three are distinctive trichophyton rubrum - produces microconidia - teardrop or peg shapped and borne along the sides of h yphae trichophyton mentagrophytes produce both cigar shapped macroconidia and grapelike clusters of spherical microconidia trichophyton tonsurans produces variable sized and shaped microconidia when the hair is infected the pattern of fungal invasioin can be either ectothrix, endothrix or favic depending on the dermatophytic species |
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ectothrix
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arthroconidia are formed on the outside of the hair
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endothrix
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arthroconidia are formed inside the hair
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flavic pattern
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hyphae, arthroconidia and empty air spaces are formed inside the hair
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stains for seeing dermatophytes
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Hand E but best visualized w/GMS and PAS
appear as hyaline septate hyphae, chains of arthroconidia or dissociated chains for arthroconida that invade the stratum corneum, hair follicles or hair |
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dermatophytoses ecology and epidemiology
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classified into 3 different categories based on their natural habitat
1. geophilic - live in soil and are occasional pathogens of both animals and humans 2. zoophilic - normally parasitize the hair and skin of animals and can be transmitted to humans 3. anthropophilic - infect humans and may be transmitted directly or indirectly from person to person worldwide distribution - both sexes and all ages susceptible - individual dermatophyte species may vary in their geographic distribution and in their virulence anthropophilic fungi cause chronic relatively non-inflammatory infections that are difficult to cure zoofphilic and geophilic fungi tend to elicit a profound host reaction causing lesions that are highly inflammatory and respond well to therapy generally endemic but epidemic proportions in school children trichophyton rubrum and trichophyton mentagrophytes account for 80-90% of all infections |
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clinical syndromes of dermatophytes
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wide range of clinical presentations affected by species of dermatophyte, inoculum size, site of infection, immune status of the host,
classic pattern = ringworm pattern - ring of inflammatory scaling w/diminution of inflammation toward the center of the lesion tineas of hair bearing areas often presents as raised circular or ring-shaped patches of alopecia w/erythema and scaling or more diffusely scattered papules, pustules, vesicles, and kerions infections of smooth skin present as erythematous and scaling patches that expand in centripetal pattern w/central clearing dermatophytoses of the foot and hand may often become complicated where the nail plate is invaded and destroyed by the fungus - infection is usually chronic and nails become thickened, discolored, raised, friable and deformed |
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lab diagnosis of dermatophytes
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demonstration of fungal hyphae by direct microscopy of skin, hair, or nail samples and the isolation of organisms in culture
culture iin mycologic media such as sabouraud agar w/and w/o abx or dermatophyte test medium specimens mounted in a drop of 10-20% KOH on a glass slide and examined microscopically - filamamentous hyaline hyphal elements may be seen culture in mycologic media such as Sabouraud agar w/and w/o abx or dermatophyte test medium - colonies develp w/in 7-28 days |
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dermatophytes diagnosis
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localized and do not affect hair or nails treated topically
all others req oral therapy topical agents = azoles, terbinafine, and haloprogin oral antifungal agents w/systemic activity against dermatophytes include griseofulvin, itraconazole, fluconaole, and terbinafine |
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clinical syndromes of dermatophytes
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wide range of clinical presentations affected by species of dermatophyte, inoculum size, site of infection, immune status of the host,
classic pattern = ringworm pattern - ring of inflammatory scaling w/diminution of inflammation toward the center of the lesion tineas of hair bearing areas often presents as raised circular or ring-shaped patches of alopecia w/erythema and scaling or more diffusely scattered papules, pustules, vesicles, and kerions infections of smooth skin present as erythematous and scaling patches that expand in centripetal pattern w/central clearing dermatophytoses of the foot and hand may often become complicated where the nail plate is invaded and destroyed by the fungus - infection is usually chronic and nails become thickened, discolored, raised, friable and deformed |
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lab diagnosis of dermatophytes
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demonstration of fungal hyphae by direct microscopy of skin, hair, or nail samples and the isolation of organisms in culture
culture iin mycologic media such as sabouraud agar w/and w/o abx or dermatophyte test medium specimens mounted in a drop of 10-20% KOH on a glass slide and examined microscopically - filamamentous hyaline hyphal elements may be seen culture in mycologic media such as Sabouraud agar w/and w/o abx or dermatophyte test medium - colonies develp w/in 7-28 days |
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dermatophytes diagnosis
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localized and do not affect hair or nails treated topically
all others req oral therapy topical agents = azoles, terbinafine, and haloprogin oral antifungal agents w/systemic activity against dermatophytes include griseofulvin, itraconazole, fluconaole, and terbinafine |
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filamentous fungi
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one dimensional linear arrangement of cells
form as a consequence of cell divisioin along single plain grows at the tip (apical extensions) - rapid growth septate - lack separation of fully divided cells - septa thta contain pores coenocytic - one continuous cytoplasma, aseptate |
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filamentous fungal pathogens
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subcutaneous infections
1. chromoblastomycosis 2. mycetoma 3. subcutaneous zygomycosis aspergillious mucormycosis |
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subcutaneous mycoses
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involve the dermis, subcutaneous tis, muscle and fascia
commonly introduced traumatically through skin rarely spread to distant organs clincal course is chronic do not respond well to anti-fungal therapy low pathogenic potential - -isolated from soil, wood, or decaying vegetation exposure= occupational infected pts generally have no underlying immune defect |
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chromoblastomycosis
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chronic fungal infection affecting skin and subcutaneous tissues
slow growing nodules or plaques commonly seen in tropics organisms assoc w/chromoblastomycosis = pitmented fungi - FOnsecaea Cladosporium - exophiala - cladophialophora - rhinocladiella - phialophora warm moist environment and lack of protective footwear and clothing |
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chromoblastomycosis morphlogy
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dematiceous
morphologically diverse in culture in tissue form muriform cells - pigmented hyphae also prsent may be free w/in tissue or contained w/in macrophage chestnut b/c melanin in walls |
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chromoblastomycosis epidemiology
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affects individuals working in rural areas of tropics
agents grow on woody plants and in soil involve legs and arms most infections have been in men climatic factors influence distribution no person to person contact |
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chromoblastomycosis - clinical syndromes
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chronic , pruritic, progressive, indolent, and resistant to treatment
early leasions small, warty papules verrucous lesions to flat plaques ulceration and cyst formation may occur secondary bacterial infection possible established infections appear as multiple large warty cauliflower-like growths usually clustered w/in the same region limb is grossely distorted due to fibrosis and secondary lymphedema secondary bacterial infections may also occur |
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|
lab diagnosis of chromoblastomycosis
|
clinical presentation
histopathologic findings -KOH -H&E = chestnut brown muriform cells isolation in culture No serological tests available |
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|
tx of chromoblastomycosis
|
itraconazole
terbinafine posaconazole combined w/flucytosine heat or cryotherapy to shrink lesions squamous cell carcinoma may develop in longstanding lesions |
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|
mycetoma
|
localized, chronic, granulomatous, infections, process involving cutaneous and subcutaneous tissues
multiple granulomas and abscesses that contain grains or granules- grains made up ove large aggregates of fungal hyphae = contain cells that have marked modifications or internal and external structure abcesses drain to externally through the skin may cause destruction of mm and bone seen in tropics organisms assoc w/mycetoma - phaeoacremonium - curvularia - fusarium |
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mycetoma morphology
|
granules are composed of septate fungal hyphae (2-6micrometer) or greater in width = either dematiaceous or hyaline depending on the etiological agent
black grain or pale/white grain hyphae can be distorted in form and size large thick walled chlamydoconidia are often present hyphae embedded in sement like substance |
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|
mycetoma epidemiology
|
tropical areas w/low rainfall
most frequent in africa and the indian subcontinent infected via percutaneous implantation of the agent men more affected than women agents differ from region to region infection occurs through traumatic implantation - foot and hand are most common sites of infection not contagious |
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mycetoma clinical syndromes
|
most commonly present w/longstanding infection
small painless nodule or plaque that grows slowly infected area becomes disfigured as a result of chronic inflammation and fibrosis sinus tracts appear on the skin surface destroys mm and bone hematogenous or lymphatic spread is rare |
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mycetoma diagnosis
|
grains or granuolse - grossly visable while driaining sinus tracts or may be expressed onto a glass slide
material may also be obtained by deep surgical biopsy - visualized by mounting on 20%KOH - H&E, PAS or GMS - culture nec for definitive identification - grown on mycologic medium |
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|
mycetoma treatment
|
usually unsuccessful
terbinafine voriconazole posaconazole amputation determine whether eumycotic mycetoma or actinomycotic mycetoma - med therapy usually effective for the latter |
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|
subcutaneous zygomycosis
|
infection caused by zygomycetes - entomophthorales
occurs as a result of traumatic implantation of the fungus present in plant debris in tropical environments caused by: - conidiobolus coronatus causes loccalized infections to facial area in adults - basididbolus ranarum =causes subcutaneous infection of the proximal limbs in kids |
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subcutaneous zygomycosis morphology
|
hyphal elements are sparse and often appear as fragments surrounded by eosinophils
hyphal fragments are thin walled and stain poorly septa are infrequent not angioinvaasuve |
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subcutaneous zygomycosis epidemiology
|
seen most commonly in africa
saprophytes present in leaf and plant debris rare dx unknown predisposing factors infection due to B. ranarum occurs following traumatic implantation of the fungus C> coronatus infections occur following inhalation of the fungal spores which invade the tis of nasal cavity occurs in kids under 20 more often in males |
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subcutaneous zygomycosis clinical syndrome
|
B. ranarum
- pt have disk-shaped, rubbery, movable masses that can be quite large - the masses may eventually become ulcerated C. coronatus - infection is confined to the rhinofacial area - swellin causes facial deformity |
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subcutaneous zygomycosis diagnosis
|
req biopsy despite the characteristic clinically features
histopathology marked by focal clusters of inflammation w/eosinophils and fragmented hyphae can be cultured from clinical material on standard mycological medium |
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subcutaneous zygomycosis
|
both types of infection treated w/itraconazole
facial reconstructive surgery may be nec for c. coronatus |
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aspergillosis
|
wide variety of dx
range from allergic rxn to disseminated dx 19 species documented A. fumigatus A. flavus A. niger A. terreus |
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aspergillosis morphology
|
grow in culture as hyaline molds may be black, brown, green , yellow, white or other olories depending on the species and growh conditions
branched septate hyphae that produce conidial heads = infectious propagules hyphae uniform in width, regular septations and a progressive tree-like branching pattern branching is dichotomous may be seen w/in blood vessles (angioinvasion hyphae stain well w/PAS and GMS conidal heads not seen w/in tissue |
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|
aspergillosis epidemiology
|
common
conidia are present in air, soil and decaying matter infection depends mostly on host factors resp tract most common portal of entry abundant in hispital environment infection depends on viruelence or pathogenesis of species |
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aspergillosis clinical synddromes
|
1. allergic manifestations
- based on degree of hypersensitivity - bronchopulmonary form = astham, pulmonary infiltrats, peripheral eosinophilia, elevated serum IgE,and evidence or hypersensitivity = sinusitis form - shypersensitivity along w/ upper respiratory sx of nasal obstruction and discharge, headache, and facial pain 2. obstructive bronchial aspergillosis - usually occurs w/underlying pulmonary dx, occurs when the parasinuses and lower airways become colonized - bronchial casts or plugs form which are composed of hyphal elements and mucinous material - tx usually not nec unless pulm hemorrhage occurs - if it does occur then surgical excision of the cavity and the funguus ball may be necessary 3. invasive aspergillosis - range from superficially invasive dx to destructive invasive pulmonary dx or disseminated form - limited forms usually include necrotizing bronchial aspergillosis - cause wheezing, dyspnea, hemoptysis - ot assoc w/vascular invasion or dissemination - surgical resection of affected areas or antifungal therapy are efficacious in treating this condition 4. invasive pulmonary aspergillosis and disseminated aspergillosis - seen in neutropenic and immunodeficient pt - mortality 70% - pt w/ fever and pulmonary infiltrates - hematogenous dissemination is common due to the angioinvasive nature of the fungus |
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aspergillosis diagnosis
|
evaluation of tis using histopathology - surgically removed tis accompanied bypositive histopathology - moniliaceous, septate, dichotomously branching hyphae
- culture on mycologic media -lacking cyclohexamide - species det by id of conidia rarely documented by blood cultures -immunoassay in serum - detects the aspergillus galactomannan antigen in serum. best used as an early indication to begin antifungal therapy |
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|
aspergillosis treatment
|
prevention for high risk pt= filtered air
amphotericin B voriconazole for A. terreus decrease immunosuppression or improve host defenses surgical removal of infected areas |
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mucormycosis
|
aka zygomycosis
caused by the order mucorales - rhizopus - mucor infections are rare - acute and rapidly progressive w/mortality rates 70-100% |
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|
mucormycosis morphology
|
- fast growing producing grey to brown wooly colonies - 12-18hrs
microscopically they are wide, thin walled, sparsely septate, coencytic hyphae asexual spores are contained w/in a sporangium presence of root like structures in tissue they are seen as ribbon-like, aseptate or sparsely septate non-pigmented hyphae easily detected w/H&E |
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mucormycosis epidemiology
|
worldwide
food, soil, and organic debris infection may be acquired by inhalation, ingestion, or contamination of wounds w/sporangispores from the environment occurs in immunocompromised pt may cause infection in organ transplants, esp those w/diabetes mellitus risk factors include corticosteroid therapy, diabetic ketoacidosis, and renal failure |
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murcomyosis clinical syndromes
|
Rinocerebral infection - infection of sinuses and brain
- starts as sinus infection - progress to involve inflam of cranial n - may cause blood clots that block vessels to brain = thrombosis pulmonary mucormycosis - lung involvement -- pneumonia that gets worse quickly and may spread to the chest cavity, heart, and brain can also occur in the GI tract, skin and kidneys can also occur |
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mucormycosis diagnosis
|
collection of appropriate specimens can include scrapings of nasal mucosa, aspirates of sinus contents, bronchial alveolar lavage fluid, and biopsy of any necrotic infected tis
histopathology - direct examination of tis in KOH w/calcofluor white may reveal the broad, aseptate hyphae - stain w/H&E or PAS Culture - tissue can be cultured on standard mycologic media - negative cultures are common serology - there are no widely available serologic tests |
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mucormycosis treatment
|
amphotericin B = first line treatment
surgery |
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|
opportunistic mycoses
|
infection due to fungi of low virulence in pt who are immunologically compromised
1. saprophytic - from environment 2. endogenous - commensal orgainsm many species |
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|
host-pathogen equilibrium
|
number of organisms * virulence/ Host resistance
= disease opportunistic dx equation is tilted in favor of dx b/c host resistance is lowered for immunocompromised host no such thing hs non-pathogenic fungus = most commonly sprophytic or endogenous most common candida, aspergillus and mucor |
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|
pathogenic fungi
|
normal host
- systemic pathogens = 25 species - cutaneous pathogens - 33 species - subcutaneous pathogens - 10 species immunocompromised host - opportunistic fungi = 300 species |
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|
upward trend in opportunistic mycoses
|
1. increased clinical awareness
2. improved clinical diagnostic tools 3. improved lab diagnostic technics 4. increase in susceptible hosts 5. more invasive diagnostic and therapeutic procedures |
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|
predisposing factors
|
1. malignancies
2. drug therapies 3. abx 4. therapeutic procedures 5. AIDS 6. others - severe burns - diabetes - Tb - IV drug use |
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|
malignancies
|
predisposing factor for opportunistic fungal infection
leukemia lymphomas hodgkins dx fungal septicimias or pneumonias = 1/3 of all deaths hematological malignacies account for 60% of systemic fungal infections |
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drug therapies
|
anti-neoplastic
steroids immunosuppressive drugs predispose to fungal infections |
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abx
|
predispose to fungal infections
- overuse or inappropriate use of abx alter normal flora allowing fungal overgrowths |
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therapeutic procedures
|
that predispose to opportunistic fungal infections
1.. solid organ and bone marrow transplantation 2. open heart surgery 3. indwelling catheters - urinary, IV drugs, or parenternal hyperaliimentation - in cases of fungemia, the contaminated catheter must be removed before starting anti-fungal therapy 4. artificial heart valves 5. radiation therapy |
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|
AIDS pt and fungal
|
fungal infection sometime during the course of their illness
|
|
|
most serious opportunistic infections
|
candida species
aspergillus species mucor species (zygomyces) |
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|
candida species
|
C. albicans
C. glabrata C. krusei C. torulopsis C. parapsilosis C. lusitaniae C. Rugosa stined w/ GMS demonstrating budding yeasts and pseudohyphae |
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|
immuocompromised pt
|
can develop hepatic candidiasis
|
|
|
cryptococcus neoformans
|
may cause pulmonary and cutaneous infections as a meningitis
second most common fungal infection in AIDS pt 10-30% of AIDS pt have cryptococcal meningitis and they will require maintenance therapy w/fluconazole penetrates the CSF |
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|
other opportunistic yeast-like fungi
|
malassezia spp
trichosporon spp rhodotorula spp blastoschizomyces capitatus |
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|
cryptococcus neoformans ecological niche
|
pigeon droppings
chicken droppings |
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|
HIV and cryptococcus
|
CD4+ counts of less than 100/mm (usually <200/mm) are at high risk for CNS and disseminated cryptococcosis
amphotericin B 5FC - then fluconazole the remainder of their life - penetrates the CSF |
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|
cryptococccosis relapse rate
|
non AIDS pt 15-20%
AIDS pt 50% w/relapse there is a 60% mortality w/o treatment mortality = 100% w/treatment 20% |
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|
sporotrichosis
|
primarily a dx of the cutaneous tissues and LN
recently a pulmonary dx co-infection w/other fungi or TB is frequent portals of entry - inhalation, inoculation ecological associations - rose thorns - sphagnum moss - timbers - soil |
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|
aspergillus
|
lactophenol cotton blue preparation showing conidial heads
aspergillus in tissues showing acute angle branching, septate hyphae GMS amphotericin B = 72% mortality w/o Therapy = 90% |
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|
zygomycetes
|
rhizopus spp - in tissue showing broad, ribbon-like, aseptate hyphae
mucor spp rhizomucor spp absidia spp cunninhamella spp |
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|
zygomycetes/mucormycetes
|
Diabetes mellitus
Leukemias Corticosteroid therapy Intravenous therapy Severe burns |
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|
clinical presentation
|
1. Atypical signs and lesions.
As shown in the case report, the patient was irresponsive to antibiotic therapy. 2. Unusual Organ affinity. Candida may invade liver, heart valves; Oral thrush occurs in people who are relatively immunocompetent while esophageal candidiasis occurs in those patients who are immunologically compromised. 3. Infections with systemic dimorphic fungi occurring outside endemic areas. These factors complicate the diagnosis and management of these diseases. Histoplasmosis mainly in eastern states and southern states, occurrence in Northeastern states like Maine is rare. 4. Unusual Histopathology. Even the inflammatory reaction may be different in biopsy specimens. The normal host reaction to fungal invasion is usually pyogenic or granulomatous. In the immunodeficient host the reaction is necrotic. 5. Unusual Pathogens Pneumocystis jirovecii (formerly P. carinii) A common cause of pneumonia in AIDS patients and the most common opportunistic infection in these patients. Formerly thought to be a protozoan. Recently shown to be a fungus. Not able to grow in vitro. |
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|
improving treatment
|
1. New drugs – Lipid Amphotericin B, Third generation azoles (posaconazole, voriconazole). A new class of antifungal agents: echinocandins. An IV preparation of Nystatin is in clinical trials.
2. New therapeutic regimen – Combination therapy. 3. Aggressive therapy • Prophylactic – Before chemotherapy; Posaconazole now approved • Empirical – Patient at risk (fever and/or infiltrate without antibacterial response). • Pre-emptive – Some evidence of fungal infection 4. Conjunctive therapy • Monoclonal antibody plus antifungal agent • Immunotherapy plus antifungal agent. |
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biofilm
|
It has long been recognized that in patients with a microbial infection, any artificial device such as an indwelling catheter or prosthetic valve or joint, must be removed prior to initiating antibiotic therapy. The foreign body acts as a nidus, seeding the infection if it remains present. The exact mechanism was not clear. A biofilm is a microcolony of organisms with a polysaccharide slime, which adheres to a surface (catheter, implant, or dead tissue) and which resist removal by fluid movement and the organisms become resistant to antimicrobials. The slime may contain a single species of organism or be polymicrobic. This biofilm phenomenon, which occurs on the rocks in a stream, was first recognized as a public health problem in drinking water distribution pipes and was regarded as a source of coliform contamination of drinking water. Recent work in clinical microbiology has shown that biofilms occur in the human and animal body. These organisms develop a resistance to therapy because they are contained in a matrix, which acts like a tissue and becomes a barrier to antibodies, macrophages and antimicrobial agents. Candida species readily form biofilms and is the most prevalent organism isolated from catheters.
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dimorphic fungal pathogens
|
1. blastomyces dermatidis
2. coccidioides immitis 3. histoplasma capsulatum - H. capsulatum - H. dboisii 4. paracoccidioides brasiliensis 5. penicillium marneffei |
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|
blastomyces dermatitidis
|
blastomycosis is a systemic fungal infection caused by the dimorphic pathogen = blastomyces dermatididis
it isconfined to the geographic region of the mississippi river basin around the Great lakes and in the southeast region of US |
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|
blastomycosis morphology
|
mold form
- produces round to oval or pear shaped conidia (2-10micrometer) located on long or short terminal hyphal branches - white to tan filamentous mold colonies yeast form - spherical, hyaline, 8-15 micromemter in diameter, multinucleated and have thick double contoured walls - reproduce by formation of buds or blastoconidia attached to parent cell by broad bases |
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|
blastomycosis epidemiology
|
ecological niche is decaying organic matter
infection acquired following inhalation of aerosolized conidia outbreaks assoc w/occupational or recrreational contact w/soil can include individuals of all ages and both genders est that 1-2 cases of symptomatic blastomycosis req therapy occur per 100,000 pop annually |
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blastomycosis clinical syndromes
|
severity of sx depends on the extent of exposure that immune status of host
symptomatic dx occurs in less than half of infected individuals may present as pulmonary dx or an extrapulmonary disseminated dxx - pulmonary dx - asymptomatic - more severe infection resembles bacterial pneumonia (fever, lobar infiltrates, cough) - may resembles tb or lung cancer (pulmonary mass leesions or fibronodular infiltrates) inhalation ofconidia pt presents with loss of wt, fever, reproductive cough, hemoptysis, and night sweats obvious pulmonary dx cutaneous involvement - lesions - painless |
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blastomycosis lab diagnosis
|
produces granulomatous and suppurative tissue rxn - typical cutaneous lesion shows central healing w/in microabscesses at the periphery - yeasts demonstrated from KOH prep of pus from skin lesion
micro detection of fungus in tis - direct exam of stained material - fresh wet prep - typical broad-based budding yeast forms -culture of clinical material on mycologic media incubated at 25 and 37 deg C takes 2-3 weeks to grow at 25 deg - appears as white cottony mold on Sabouraud dextrose agar - fruiting bodies called miroconidia present but not distinctive - 37 deg C yeast grows in abt 7-10 days buttery like soft colony w/tan color - typical yeast serological tests -immunodiffusion - req 2-3 weeks after onset of illness to become positive - positive in abt 80% of pt w/blastomycosis close to 100% specificity - complement fixation = req 2-3 months after onset of dx to develop detectable ab - cross reacts w/other fungal infections - quantitative test and physician can follow pt response to the dx by monitoring the ab titer - enzyme immunoassay = test is easy to perform and Ab is dected early in the dx process |
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|
blastomycosis treatment
|
itraconozole drug of choice for mild cases
amphotericin B used for pt w/life threatening dx consider - cliical forma and severity of dx, immune status of pt, toxicity of antifungal agents who should be treated? pulmonary blastomycosis, hematogenous dissemination alternative tx = fluoconazole |
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|
coccidioidomycoisis
|
endemic mycosis
caused by - coccidioides immitis - coccidioides posadassii inhalation of infectious arthroconidia ranges from asymptomatic infection to progressive infection and death coccidioidal granuloma and san joaquin valley fever |
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|
coccidioidomycosis morphology
|
mold form
- exists in nature and when cultured in lab - initial growth is white to gray, moist and glabrous and occurs w/in 3-4 days - develops abundant aerial mycelia -mature colonies become tan to brown or lavendar - vegetative hyphae give rise to fertile hyphae that produce arthroconidia - barrel shaped w/frill at both ends - upon inhalation arthroconidia become rounded as they convert to spherules in the lung 0 at maturity spherules (20-60 micrometers) produce endospores b a process known as progressive cleavage - rupture of spherule walls release endospores NO yeast form the invasive form is the spherule |
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|
coccidioidomycosis epidemiology
|
endemic to the desert SW US
found in the soil, growth enhanced by bat and rodent droppings exposure greates in late summer and fall cycles of drought and rain enhance dispersion infection occurs by inhalation higher in elderly and HIV infected individuals ecologic niche = Sonoran desert airborn carried by woind = spread hundreds of miles in storms |
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coccidioides clinical syndromes
|
prob most virulent of all human mycotic pathogens
primarily a pulmonary dx 60% are endemic and asymptomatic 25% flu like illness pulmonary fungal dx = anorexia, wt loss, cough, hemoptysis and resembles tb arthralgia and erythema nodosum particularly on legs freq in female pt if symptomatic for 6 weeks or longer dx progresses to secondary cocidioidomycosis = extrapulmonary sites of infection = skin, soft tis, bones, joints, meninges much greater mortality rate in certain ethnic grous = filipino, african american, hispanic =25x more likely to develop progressive dx and death pregnant females also have greater incidence of dissemination dx as do elderly and AIDS pt males mortality in disseminated dx >90% if untreated |
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|
coccidioidomycosis dx
|
histopathologic exam of tissue
- direct micro exam - exudates w/10-20% KOH and calcofluor wihte - biopsy tissue w/H and E, GMS or PAS - Endospores incite a polymorphonculear response so large numbers of neutrophils can be seen. As the endospores mature, the acute reaction is replaced by lymphocytes, plasma cells and epithelioid cells. isolation of fungus in culture - culture on mycologic media - colonies develop w/in 3-5 days - sporulation seen in 5-10 days -serologic testing - combined used of ID and LP test - complement fixation - tube precipitin |
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|
coccidioidomycosis treatment
|
fluconazole and itraconazole
w/ amphotericin B reserved for more severe infections most individuals do not need therapy at risk = amphotericin immunocompromomised = amphotericin B and azole for maintenance for 1 year chronic cavitary pneumonia - oral azole for at least 1 year - surgical treatment - all other s oral azole |
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|
histoplasmosis
|
intracellular mycoses, attacking lungs, liver, spleen, BM and occasionally kidneys, adrenals and intestines = reticuloendothelial system
caaused by 2 varieties of histoplasma capsulatum - histoplasma capsulatum var. capsulatum = pulmonary and disseminated infections in eastern half of the US and most of latin america - hhistoplasma capsulatum var. dubosisii = predom skin and bone lesions - restricted to tropic areas of Africa systemic dx |
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|
histoplasmosis morphology
|
thermally dimorphic existing as a hyaline mold in nature and in culture at 25 deg C and as intracellular budding yeast int tis and in culture 37 deg C
mold colonies grow slowly and dev as white or brown hyphal colonies after several days to a week mold form produces 2 types of conidia 1. large thick-walled, spherical macroconidia w/spike-like projections that arise from short conidiosphores 2. small oval microconidia w/smooth or slightly rough walls that are sessile or on short stalks yeast are thin walled, oval and measure 2-4 micro meter capsulatum thicker walled and 8-15 micro meter - duboisii intracellular in vivo and are uninucleated |
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|
histoplasmosis epidemiology
|
natural habitat of mold form is soil w/high N content
outbreaks assoc w/exposures to bird roosts, caves, excavation aerosolization of microconidia most cases are asymptomatic immunocompromised individuas dev sx broad regions of Ohio and mississippi river valleys in the US and occurs throughout Mexico and central and south america duboisii - confined to tropical areas of africa one of the most common fungal infections, occuring in SC, particularly NW part of state |
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|
histoplasmosis clinical syndromes
|
- inhalation of microconidia
-microconidia phagocytosed H. capsulati - clinical presentation dependent on intensity of exposure and immunologic status of host - acute pulmonary histoplasmosis - flu -like illness - progressive pulmonary histoplasmosis - apical cavities and fibrosis -asymptmatic in 90% of individuals following low intensity exposure - disseminated histoplasmosis = chronic, subacute, acute - acute pulmonary histoplasmosis - flu-like illness w/fever, chills, headache, cough, and chest pain - progressive pulmonary histoplasmosis - assoc w/apical cavities and fibrosis and is more likely to occur in pt w/prior underlying pulmonary dx - disseminated histoplasmosis - much higher in kids and immunocompromised - include wt loss, fatigue, oral ulcers, splenomegaly duboisii - localized form is characterized by regional lymphadenopathy w/lesions of skin and bone - skin lesions progress to abcesses that ulcerate - dissemination to BM, liver, splee, and other organs occurs - marked by fever, anemia and wt loss |
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|
histoplasmosis diagnosis
|
direct microscopy
- yeast phase detected w/giemsa, GMS, or PAS - sputum or bronchial alveolar lavage - BM - peripheral blood source culture - conversion to mold phase - must confirm by converting from yeast to mycelium or vice versa - use DNA probe serology - AB and Ag detection - Ab detection include CF and ID - Ag by EIA - complement fixation - 2 ag one to yeast form and one to mold form - some pt react to one form or the other andsome to both - dev late in dx 2-3 months after onset - cross reacts w/other fungi - advantage is quantitive |
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histoplasmosis tx
|
severe acute pulmonary histoplasmosis = amphotericin B followed by oral itraconazole =12 weeks
chronic pulmonary histoplasmosis = amphotericin B followed by oral itraconazole (12-24 months) disseminated histoplasmosis - amphotericin B followed by oral itracomazole (6-18 months) histoplasmosis of CNS - amphhotericin B followed by oral fluconazole (9-12 months) |
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|
paracoccidioidomycosis
|
systemic fungal infection cuased by paracoccidioides brasiliensis or south american blastomycosis
major dimorphic endemic fungal infectio nin latin amercian countries primary infection as self-limited pulmonary process reactivation may result in chronic progressive pulmonary dx usually self limited pulmonary process chronic granulomatous dx of mucous membranes, skin, and pulmonary system |
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|
paracoccidioidomycosis morphology
|
mold phase
- grows slowly, colonies appear in 3-4 weeks - white w/velvet appearance - mycelial form is non-descript and non-diagnostic yeast phase - variable size 3-30 micrometers - oval - double refractile wals - single or multiple buds mold grows slowly at 25 deg C -apparent in 3-4 weeks - mycelia nondiagnostic - req conversion to yeast form yeast seen in tis and culture at 37 deg C |
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|
paracoccidioidomycosis epidemiology
|
most prevvalent in S. america
high humiditiy, rich vegetation, moderate temps and acid soil portal of entry - inhalation, inoculation dx most common in men 30-50 years endemic throughout latin america - more prevalent in S. america than in central america - highest incidence seen in brazil |
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|
paracoccidioidomycosis clinical syndrome
|
sub-clinical
progressive - acute or chronic pulmonary forms - acute, sub-acute, or chronic disseminated forms sub-acute disseminated form in younger pt and immunocompromised individuals adults usually preseent w/chronic pulmonary form result in dissemination in the absence of diagnosis or tx most are self limited common triad of sx - pulmonary lelsions, edentulous mouth, and cervical lymphadenopathy organism invade mucus membranes of mouth causing t eeth to fall out white plaques are also found in the buccal mucosa and along w/the triad is now used to differentiate from TB long latency period 10-20 years may pass btw infection and manifestation |
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|
paracoccidioidomycosis lab diagnosis
|
- microscopic examination
- demonstration of yeast forms on microscopic examination culture - -thermal dimorphism serology - serologic testing using ID or CF to demonstrate Ab |
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|
paracoccidioidomycosis lab diagnosis
|
- microscopic examination
- demonstration of yeast forms on microscopic examination culture - -thermal dimorphism serology - serologic testing using ID or CF to demonstrate Ab |
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|
paracoccidioidomycosis treatment
|
itraconazole for 6 months
severe infections may require amphotericin B followed by itraconazole |
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|
penicilliosis marneffei
|
disseminated mycosis caused by penicillium marneffei
involves the monoculear phagocytic system occurs primarily in HIV - infected individuals thailand and southern China |
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|
penicilliosis marneffei morphology
|
only species of penicillium that is a pathogenic dimorphic fungus
in its mold phase it exhibits sporulating structures identification is aidedby the formation of a soluble red pigment that diffuses into the agar the yeast form divides by fission and exhibits a transverse septum the yeast is intracellular in vivo |
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|
penicilliosis epidmeiology
|
primary mycotic pathogen among HIV infected individuals in SE asia
early indicator of HIV infection |
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|
penicilliosis marneffei clinical syndromes
|
inhalation of conidia from environment
may mimic tb, leishmaniasis and other AIDS related opportunistic infections pt present w/fever, cough, pulmonary infiltrates, lymphadenopathy, organomegaly, anemia, leukopenia, and thrombocytopenia skin lesions reflect hematogenous dissemination |
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|
penicilliosis marneffei lab diagnosis
|
in culture at 25-30 deg C isolation of mold that exhibits typical penicillium morphology and a diffusible red pigment
yeast phase 37 deg C exhibits elliptical fission inside phagocytes |
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|
penicilliosis marneffei treatment
|
amphotericin B (2 weeks) followed by itraconazole for 10 weeks
AIDS pt may req lifelong tx w/itraconazol |
|
|
penicilliosis marneffei lab diagnosis
|
in culture at 25-30 deg C isolation of mold that exhibits typical penicillium morphology and a diffusible red pigment
yeast phase 37 deg C exhibits elliptical fission inside phagocytes |
|
|
penicilliosis marneffei treatment
|
amphotericin B (2 weeks) followed by itraconazole for 10 weeks
AIDS pt may req lifelong tx w/itraconazol |
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parasite
|
organism that obtains food and shelter from another organism and derives all the benefits from this association
|
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|
obligate
|
when the parasite can live only in host
|
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|
facultative
|
when the parasite can live in the host as well as in free form
|
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|
endoparasites
|
when the parasite lives inside the body
|
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ectoparasites
|
when the parasite survives on the body
|
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pathogenic
|
when the parasite causes harm to the host
|
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commensals
|
those parasites which benefit from the host w/o causing harm
|
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|
host
|
the organism that harbors the parasite and suffers a loss caused by the parasite
|
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|
primary host or definitive host
|
in which the parasite reaches its maturity or reproduces sexually
|
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|
secondary host or intermediate host
|
where the parasite lives its asexual stage for a short period
|
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|
dead end host
|
an intermediate host that does not allow the transmssion to the definite host, thereby preventing the parasite from completing its development
|
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reservoir
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hosts other than humans that harbor the parasite, ensure the continuity of the life cycle and act as additionla sources of infection
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vector
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organism (usually an insect) that is responsible for transmitting the parasite infection
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characteristics of parasitic dx
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prevalance in underderdeveloped countries specially in the lower income group of population
low mortality and morbiditiy limited drug development no vaccines |
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intestinak and uro-genital protozoa of man
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1. entamoeba histolytica causes dysentery, liver and brain abscesses - 500 x 10^6 cases worldwide
2. giardia lamblia causes diarrhea - 200 x 10^6 cases world wide 3. balantidium coli causes dysentery - farm associated world wide 4. cryptosporidium causes diarrhea - sporadic epidemics - world wide 5. isospora belli causes diarrhea - rare, opportunistic 6. trichomonas vaginalis - sexual - frequent, common among prostiitutes world wide |
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amebiasis
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amebic dysentery, amebic hepatitis - liver, lung, branin and other abcesses
etioloty - entamoeba histolytica epidemiology - most common in ppl who live in developing countries w/poor sanitation - africa, latin america, inda, SE asia = endemic - US 4% pop prob carries parasite - mostly found in immigrants from developing countries -dogs cats rodants can be affected morphology = active trophozite stage exists only in the host and in the fresh loose stool - contains single nuc w/distinctive small central karyosome. endoplasm is fine and granular and may contain erythrocytes cysts often found in the stool survive outside of the host, in water, soil and on foods - refractile wall and contains dark staining chromatoidal bodies and 1-4 nuclei w/central karyosome and an evenly distributed peripheral chromatin life cycle = - ingestion of cyst in the contaminated water and food - excystation occurs in small intestine 8 trophozoites produced from one cyst - trophozoites migrate to large intestine where they multiply or may encyst for excretion - cysts exit host in the stool - larger bolus of infection some amoebae attach to and invade the mucosal tissue forming 'flask-shapped' lesions or craters. the orgnaisms encyst for mitosis and are passed thhrough w/feces |
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fecal oral life cycle of amebiasis
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cysts
1. passed in feces 2. nonmotile 3. resistant to hostile environment 4. does not multiply cysts => trophozoite via excystation trophozoite 1. metabolically actve 2. motile 3. multiplies by replication trophozoite => cyst via encystment |
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trematodes (flukes)
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schistosoma
- s.mansoni -s. hematobium -s. japonicum fasciolopsis buski fasciola hepatica opisthorchis - O. sinensis - O. felineus - O. viverini Paragonimus - P. westermani -P. kellicotti |
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schistosomiasis
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N. africa
Africa - middle - coast of brazil - have male and female - live in close assoc - life cycle - snail intermediate = male and females lay eggs causes hematuria |
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schistosomiasis sx
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skin - dermatitis - swimmers itch
GI - abd pain, ascities, diarrhea, bloody stool (mansoni and japonicum) - inflam response to eggs0 mucosal fibrosis urogenital - chronic cystitis and urethritis - granulomatous fibrosis due to egg depositis |
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schistosomiasis diagnosis
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history
sx histology eggs in urine / stool s. hematobium - terminal spine = africa S. manosoni - lateral spine africa and americ S. japonicum - smaller egg minute spine = fareast |
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treatment
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controling snail
praziquantel is effective avoid swimming in snail infested water sanitary disposal of sewage elimination of snails |
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schistosomiasis morphology
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Adult worms are 10-20 mm long; the male has an unusual lamelliform shape with marginal folds forming a canal in which the slender female worm resides. Unlike other trematodes, schistosomes have separate sexes
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fasciopolopsis buski
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giant intestinal fluke
central and SE asia elongate oval fluke 2-7 cm lives in sml intestines of men |
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fascioliosis buski life cycle
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man infected by ingesting water chestnuts contaminated w/metacercaria that find access to sml intestine
- attach themselves to mucosa - mature in 25-30 days - fluke eggs are passeed w/ feces and hatch in fresh water producing miracidia that must penetrait suitable snail w/in hrs - miracidium in the snail develops into cercaria and enter freshwater - attaches itself to water plants - water chestnut and encysts as metacercaria |
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fascola hepatica
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liver fluke more common with cows
water vegetation human consumption of improperly cooked watercress that harbors encysted larval metacercariae larval fluke penetrates duodenal wall and migrates to peritoneal cavity penetrates liver capsule and migrates into the bile duct where it matures adult fluke passes its eggs in stool that hatch in water to produce miracidia that must find appropriate snail to contiue the life cycle in the snail the miracidium divides and gives rise to cercariae exit snail and enzyst as metacercariae attached to watercress leaves |
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fascola hepatica sx
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passage of larva through liver produces tenderness and hepatomegaly
infection results in upper quadrant pain chills and fever accompanied by eosinophilia - presence of worm in bile duct - causes irritation resulting in hyperplasia of the epithelium and bile obstruction adult worms may invdade liver and cause necrotic foci |
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opisthorchis sinensis
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liver fluke
endemic in parts of western europe and japan spindloid flukes chineese liver fluke link to hepatic cancer |
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opisthorchis sinensis life cycle
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man is infected by eating raw or improp cooked fish
carries infective metacercaria in a cyst - cyst is digested and larval worm migrates up bile duct to liver matures to adult eggs deposited in biliary duct duct pass in feces and find way to fresh water ingestion by suitable fresh water operculate snail - egg hatches to produce miracidium in snail develops into cercaria and berak out in water to penetrate under scales of fish in fish cercaria encysts in mm and forms metacercaria that are infectious man cats and dogs can be reservoir hosts |
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paragonismus westermani
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mexico and some china
asia, africa, s america plump reddish brown oval worm |
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paragonismus westermani life cycle
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infects man (domestic carnifors) throu consumption of crab (shellfish) infected w/encysted metacercaria
metacercaria reach sml intestine wher they exit their shell and bore their way as young flukes through int wall and thoracic diaphragm and penetrate lung - there they become enclosed 1-2 cm cysts and reach maturity eggs found in sputum occasional if swallowed in feces 2-3 months after infection eggs when iintroduced in fresh water produce miracidia which penetrate the suitable snial dev in snail into cercaria break out in water and penetrate gills, muscle or viscera of fresh water crabs and become encycsted in flesh as metacercaria |
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paragonismus westermani symptoms
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fluke dev of fibrous tissue capsule in the lung - pulmonary granuloma
- w/ bloody purulent material containing eggs inflam infiltrate around capsule dry cough followed by prod of blood stained rusty brown sputum pulm pain and pleuisy may dev worms migrate to brain lay eggs -- rare =- granulomatous abscess formation resulting in sx sim to epilepsy |
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myiasis
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distributed world wide
burial of fly larvae in tissue - cochliomay new world screw warm - chysomya old world screw worm - dermatobia hominis, calliphora, oestrus sacrophaga, gastrophilus cordylobia antrhopophaga 0 african tumbu fly = brightly colored flys bumb - breating hole = healthy or necrotic tissue - mandibular hook aid by proteolytic enzyme - GI/urinary, cutaneous, arterial - cause mechanical damage and the affected area site of secondary infection -mostly in kids - require surgical removal of burrowed larvae - eggs and maggots may be washed from hair, skin, wounds w/soap and water - urinary usually self resolving - tx anthelmintic may be nec for GI myasis petrolum jelly/bacon come back a day later hygeine - avoid flies on open wounds - debridement wound abx for secondary bacterial infection |
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lice
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Pediculus humanus capitus - head lous
p. humanus humanus - body louse phthirus pubis - crab louse spend all life on very specific host both male and female feed on blood and leave the host only to transfer to another |
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head lice
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mostly kids - crowded enviro, adult secondarly, rarely AAA
2-10% kids light infections - itching - sensitization to louse saliva heavy infestations - fever, aches, secondary infections - finding live lice or empty eggshels (nits) attached to hair - often behind ears topical application of soothing lotions relieves irritation tx - washing hair w/shamoii cont permethrin or malathion or alt a mixture of pyrentins and pipronyl butoxide or ivermectin may be as effective and less toxic than benzene hexacholide |
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body lice
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in clothes - burn homeless
- carry dx - typhus ... - same tx as head lice cleanliness is essential |
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pubic lice aka crabs
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transmited sexually
infests coarse hair in pubic areas in adults found in eyelashes or head of kids - reportable - sexual abuse finding lice or nits in infested area treated in same manner as head lice severe intching in infected area - difficult to see tx - phasostigmine, yellow mercury oxide permethrin mouse containing ... |
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chiggers
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aka redbugs (trombiculidae)
- imp group of ectoparasites affecting humans - Eutrombiculae sp, leptotrombidium sp attach to skin in ankles waistline, armits perianal skin from long grassy enviro do not feed on blood but on lymph and partially digested cells from reactive of the saliva w/ host tissue host reacts to the mouthparts and saliva of the mite bite causes severe irritation and sometimes fever tx local anesthetic insect repellants may be effective in avoiding chigger bites |
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tapeworm structure
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scolex - attachment organ
zone of prolif - undiff area behind scolex - neck region strobilia - chain of segments - proglottidis - immature proglottidis - dev reproductive - mature - mature repro organs - favid proglottidis - contain eggs in uterus hermaphroditic |
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taeniasis geographic distribution
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world wide incidence dep on idetary habits as well as quality of battle ranching and pig farming
- t. saginata - beef tapeworm - more than 14 uterine branches - t. solium - pork tape worm - less than 14 uterine branches |
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acute amebiasis symptoms
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small and large intestines involved
- abd pain - freq bloody dysentery w/necrotic mucosa lasts a week to 10 days infectin may resolve or become dormant = chronic |
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chronic amebiasis symptoms
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small and large intestine - recurrent bloody and mucoid dysentery w/intervening constipation; appendicitis; pseudopolyps; perforation
liver - abcess, hepatitis lung - abcess; pneumonia brain - abcess; encephalitis mucosal erosion and crater formation |
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E. histolytica pathology and immunology
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- invassiveness and abscess formation are due to amoebic proteolytic enzymes
- abs are detectable in chronic infections but they are of questionable protective value intestinal ulcers due to enzymatic degradation of mucosal tissue |
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amebiasis differential diagnosis
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- diff from giardiasis and bacterial dysentery
- mucus and blood in stool - no high fever - no granulocytosis |
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E. Histolytica - diagnostic features
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when amebic dysentery is suspected, fresh fecal sample or swab should be examined under microscope
- examined quickly the colorless motile trophozoite can be seen the motile trophozoite has one nucleus staining lugol stain- general morphology iodine staining - glycogen iron/haematoxylin staining - chromatoidal bodies |
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E. histolytica prevention and treatment
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prevention - better hygiene
- efficient sewage tx and disposal tx - iodoquinol for acute amebiasis - metronidazole for chronic amebiasis |
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giardiasis
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etiologic agent - giardia lamblia
dx - giardia affects humans but most common parasites infecting cats, dogs and birds diarrhea, lipid and vit B12 and other nut mal-abs HIV most commonly infected ] most freq protozoan int dx in US - most common, ided waterborne dx assoc w/breakdown of water purification system, outdoorsmanship, day care centers , and travel to endemic areas (russia, india, rocky mtns) |
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giardia lamblia morphology
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active trophozoite attaches to the lining of sml int w/a sucker resp for causing signs and sx
NO mito trophozoite half-pear shapped w/8 flagella and 2 axostyles arranged in bilateral symmetry 2 ant located large suction discs cytoplasm cont 2 nuclei and 2 parabasal bodies cysts - smaller - ellipsoidal body and smooth well-defined wall. cytoplasm cont 4 nuclei and many structures seen in trophozoite |
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giardia lamblia life cycle
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infect occurs by ingestion of cysts in contaminated water
decystation occurs in duodenum and trophozoites (trophs) colonize the upper small intestine where they may swim freely or attach to the sub-mucosal epithelium via the ventral suction disc the free trophozoites encyst as they move downstream and mitosis takes place during the encystment cysts are passed in stool main primary host although beavers, pigs, and monkeys also infected and serve as reservoirs |
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giardiasis symptoms
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acute - small and large intestine - flatulence, foul smelling bulky light diarrhea - explosive, often watery; malabs, lactose intolerance; nausea - stool contains excess lipids but very rarely any blood or necrotic tis
chronic - small and large intestine - asymptomatic or sx described above = B12 malabs disaccharidase deficiency and lactose intolerance |
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giardiasis pathology and immunology
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path- covering epithelium by trophozoite and flattening of the mucosal surface results in malabs of nut
IgA and IgM ab play some role in resistance - increased incidence of giardiasis in immunodeficient individuals (AIDS) |
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giardiasis differential diagnosis
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different from amebiasis and bacterial dysentery
- NO mucus blood - No granulocytosis and no fever |
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giardiasis diagnosis, tx, prevention
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mainstay diagnosis of giardia is stool microscopy - distinctive oval cyst and motile trophozoite
based on sx, history, epidemiology duodenal content obtained using a string device - enterotest must be distinguished from nonpathogenic flagellate, trichomonas hominis, an asymmetrical flagellate w/ an undulating membrane prevention - better hygiene - efficient sewage treatment and disposal tx= metronidazole, iodoquinol |
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balantidium coli
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primarily a zoonotic intestinal parasite
- horses, cows, pigs farm workers at risk sx sim to amebiasis except - NO abscesses in peripheral organs morphology - largest protozoan and only ciliate known to parasitize humans - macro and micro nucleus - infected by ingestion of cysts in fecal material of farm animals - trophozoites reside in lumen of large int where they divide by transverse binary fission - encystation is triggered by dehydration of int content may also occur outside host diaggnosis - history, sx, finding typical trophozoites and cysts in stool prevention- avoid ingestion of mat cont w/ animal feces tx - tetracycline, iodoquinol, metronidazole man to man transmission is rare but possible metronidazole and iodoquinol are effective |
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balantidium coli
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primarily a zoonotic intestinal parasite
- horses, cows, pigs farm workers at risk sx sim to amebiasis except - NO abscesses in peripheral organs morphology - largest protozoan and only ciliate known to parasitize humans - macro and micro nucleus - infected by ingestion of cysts in fecal material of farm animals - trophozoites reside in lumen of large int where they divide by transverse binary fission - encystation is triggered by dehydration of int content may also occur outside host diaggnosis - history, sx, finding typical trophozoites and cysts in stool prevention- avoid ingestion of mat cont w/ animal feces tx - tetracycline, iodoquinol, metronidazole man to man transmission is rare but possible metronidazole and iodoquinol are effective |
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cryptosporidium parvum
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major csause of epidemic diarrhea
animal reservoir - domestic animals severe diarrhea and invasive infection in AIDS pt typically acute short term infection - parasite transmitted by oocytes that, once infected, excyst in the small intestine - oocysts release sporozoites in upper GI tract and attach to the gut mucosal cells where they divide to produce merozoites - which invade other mucosal cells and further multiply asexually some meroxoites differentiate into male and female gametocytes and form an oocyst in which they multiply and differentiate int sporozoite the mature oocyst is excreted w/fecal material and infects other individuals when a large number of humans in a community have diarrhea, is the most likely cause - small bolus of infection may cause diarrhea, larger intakke = copious watery diarrhea, cramping abd pain, flatulence and wt loss - severity and duration of sx are related to immunocompetence and bolus of infection - AIDS pt org prolonged severe diarrhea - org invade gallbladder, biliary tract and lung epithelium - diagnosis based on the presence of acid fast oocysts in the stool no approved effective tx for cryptosporidiosis - Paromycin used as an investigational drug - exact working mechanism is unknown self limiting - nitrazoxanide - proper sanitation and clean water supply |
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Isospora belli
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mostly found in tropical countries
infection occurs via oral fecal route - infective stage diagnostic stage of I. belli in fresh stiil oocyst w/1 sporoblast oocyts are thin walled transparent and ovoid shape causes giardiasis-like but milder symptoms self limiting in normal individuals severe and prolonged dx in AIDS pts tx - trimethoprim, sulphamethoxazole |
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trichomonas vaginalis morphology
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trichomoniasis one of the most widespread sexually transmitted dx world wide
human parasite only world-wide - 5% in norm population, 70% among prostitutes |
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trichomonas vaginalis symptoms and diagnosis
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man - rarely symptomatic, occasionally mild urethritis and/or prostatitis
women - often asymptomatic - mild to severe vaginitis in heavy infections -copious fowl-smelling yellow discharge - growth of organism favored by high pH >5.9 (N=3.5-4.5) diagnosed by giemsa stained - vag swab |
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life cycle of trichomonas vaginalis
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colonizes the vagina of women and the urethra sometimes prostate of men - infectoin occurs primarily via sexual contact - non-veneral possible
organism doesn't encyst and divides by binary fission - no non-human reservoir for organism causes contact depend metronidazole is effective in both males and females - vinegar douche useful personal hygiene or use of condom |
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trypanosomiasis
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african trypanosomiasis (sleeping sickness)
- T. brucei, rhodesiense - T. brucei gambiense American trypansosmiasis (Chagas' dx) T. cruzi |
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trypanosoma brucei morpphologic forms
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epimastigote (crithidial form) in the insect- crithidial - kinetoplast ant to nuc metacyclic trypomastigote (infectious form)
outer surface of trypomastigote form is densley coated w/layer of glycoprotein the variable surface glycoprotein trypomastigote (trypanosomal form) in the mammalian host spindle shaped body w/single central nucleus and a single flagellum originating at the kinetoplast and joined to the body by an undulating membrane human circulation the organism exists in a trypanosomal = posterior location of kinetoplast |
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african trypansoma life cycle
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infective metacyclic form - injected into the primary host durign bite by the vector - tsetse fly
or ganism transforms into a dividing trypanosomal blood form - trypomastigote enters the draining lymphatic and blood stream trypanosomal form enters the vector during the blood meal traavels through alimentary canal to the salivary gland where it prolifs as the crithidial form (epimastigote) matures into an infectious metacyclic trypomastigote trypomastigote traverse walls of blood and lymph to enter CT and at later stage cross the choroid plexus into the brain and cerebral spinal fluid - transmitted through blood transfusion |
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african trypanosomiasis symptoms
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bile reaction -= skin - non pustular bumps w/o pus, itchy, painful chancre, no scar 1-3 weeks after bite lasts 1-2 weeks
parasitemia- blood circulation and LN - malaise, lassitude, insomnia, fever which starts 2-3 weeks after bite , edema, lymphadenopathy = - painful sensitivity of palms and ulnar region to pressure ( Kerandel's sign) some caucasians, - enlargement of the glands of post cervical region - characteristic of Gambian dx = Winterbottoms sign - febrile episodes last a few months in Rhodesian or several years Gambian dx CNS stage - CNS T. gambiensee) heart (T. rhodesiense) = personality changes, shuffling gait, lack of interest, tremulous speech, mental retardation, sleepiness, cardiac fever - loss of interest and disinclination to work, avoidance of acquaintances, morose, melancholic attitude alternating w/exaltation, MR, and lethargy, low and tremulous speech, tremors of tongue and limbs, slow and shuffling gait, altered reflexes, males become impotent = slow progressive involvement of cardiac tissue later stages are characterized by drowsiness and uncontrollable urge to sleep - term stage wasting and emaciation - death from comma - intercurrent infection or cardiac fever rhodesian more acute = don't allow for typical progression to sleeping sickness - death due to cardiac failure w/in 6-9 months Rhodesian dx progresses more rapidly and sx are often more pronounced morepronounced in caucasians than in local african population divided into three stages- bite rxn parasitemia and CNS stage |
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african trypanosomiasis pathology and immunology
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inflammation
antigenic change CNS damage by organisms ab are not protective due to antigenic change polyclonal B cell expansion; hyper-IgM hypocomplementemia stimulates the reticuloendothelial system causes severe depression of cell mediated and humoral immunity to other Ag immunosuppression |
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diagnosis of T. brucei
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= history of travel and fly-bite
- sx = blood smear and/or CSF detection of parasites in bloodstream, lymph secretions and enlarged LN aspirate conc by centrifugation or b the use of anionic support media CSF must always be examined for organism and prot and cell counts immunoserology - ELISA, immunoflourescence) may be indicative but not definite diagnosis |
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treatment and control of african trypanosomiasis
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blood stage treated w/ reasonable success w/ pentamidine isethionate or Suramin = effective in prophylaxis although may mask early inf increase risk of CNS dx
- CNS involvement should be treated w/melarsoprol - organic arsenic cmpd - most effective preventive measure avoid contact w/tsetse flies -vector eradication impractical due to vast area immunization has not been effective due to Ag variation |
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american trypanosomias etiology
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chagas' dx
caused by protozoan hemoflagellate, trypanosoma cruzi scattered irregularly in central and S. America stretching from parts of mexico to argentina rare cases reported in Tx, Ca, Alabamma and maryland - est that 10 mil ppl infected and 50 mil at risk |
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american trypanosomias morphology
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occur indiff forms depending on the host environment
trypanosomal form in mammalian blood - long and sim to african crithidial -epimastigote form found in insect intestine leishmanial (amastigote) form found intracellularly or in psuedocysts in mamillian viscerai part myocardium and brain round or oval shape and laks a prominent flagellum |
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american trypanosomias life cycle
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transmitted to mammalian host by many species of the kissing bug (riduviid) most prominanetly by triatoma infestans, T. sordida, panstrongylus megistus and Rhodnius prolizus
transmission during the feeding of the bug which normally bites in facial area - hence - but defecates while it bites you metacyclic trypomastigote contained in fecal material gain access to mammalian tis and subsequently enter macrophages and multiply uninfected bugs acquire the organism when feed on infected animals trypomastigote divides longitudinally in the mid and hindgut of the insect where they develop into infective metacyclic trypomastigotes transmission may also occur from man to man by blood transfusion and by transplacentla route wild and domestic animals =reservoir - cattle, pigs, cats, dogs, rats, armadillo, raccoon, opossum naturally infected transmission assoc w/poor living conditions |
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symptoms of chagas
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primary lesion - skin - nonpurulent, edematous plaque - appears at site of infections w/in a few hours of bite surrounded by variable area of hard edema -
- enlargement of pre and post auricular and submaxillar y gland on side of the bite - infection of eyelid, resulting in unilateral conjunctivitis and orbital edema(Ramana's sign) commonest finding acute stage - 7-14 days - LN and heart - malaise, restlessness, lymphadenitis, hepatomegaly, splenomegaly, acute, myocarditis, generalized edema, sleeplessnes, increassing exhaustion, chills, fever ,bone and mm pains cervical, axillary and iliac adenitis -erythematous rash hepatomegaly and acute myocarditis - serious pericarditis and endocarditis kids = cause meningo-encephalitis and coma death in 5-10% - hematologic examination during the chills and fever episode = lymphocytosis and parasitemia chronic - hollow organs - mega colon, cardiomegaly, cardiac arrythmia - - can become carrier- asymptommatic - alternate btw asymptomatic remission and relapses characterized by sx as acute phase = particulary heart, colon, esophagus cardiac changes = myocardial insufficiency cardiomegally - AV conduction disturbances and adams stoke sndrome - disturbances of peristalsis lead to megaesophagus and megacolon |
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chagas pathology and immunology
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pathology
= directed damage to infected cells - acute - later stages destruction of autonomic nerve ganglion may be of significance immune mech - both mediated andh umoral - involving rxn to the org and to autologous tis - been implicated in pathogeneis Ab shown to lyse org but rarely causes eradication of organism due to intracellular localization activated macrophages kill org does not alter ag coat ab directed against heart and mm cells - detected autoimmune rxn - severe depression of both cell mediated and humoral immune responses chaga toxin |
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T. cruzi diagnosis
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thin blood smear
history of travel and sometimes cardiac problems romana's sign or chagoma organisms in the chagoma exudate, LN aspirate or blood easy in kids - cardiac dilation, mega colon, megaesophagus Ab detected by complement fixation or immunoflurescence |
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chagas tx
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no curative therapy available
most drugs innefective or highly toxic exp drugs Benzidazole and nifurtimox been used w/promising results in acute stage - side effects limit their prolonged use in chronic cases contorl measures reduce contact btw vectors and man attempts to create a vaccine not successful |
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Leishmaniasis
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L. donovani = visceral leishmaniasis
L. tropica - cutaneous leishmaniasis L. brazillensis = mucocutaneous leishmaniasis prevalent world wide - SEasia, Indo-pakastain, mediterranean, N and central Africa and S and central america |
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leishmaniasis morphology
|
amastigote (leishmania seen in mammal host
promastigote (leptomonad) seen in sand fly |
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Leishmaniasis life cycle
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organism transmitted by bite of several species of blood-feeding sand flies which carries the promastigote in the ant gut and pharynx gains access to mononuclear phagocytes wher transforms into amastigote and divide until the infected cell ruptures
released org infect other cells- sand fly acquires org during blood meal amastigotes transforms into flagellate promastigotes and multiply in the gut until the ant gut and pharynx are packed dogs and rodents common reservoirs congenital transmission of visceral leishmansis form symptomatic and non-symptomatic moms durign labor and in utero reported |
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leishmania sx
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visceral - liver, spleen, BM, LN, skin - no bite rxn, lymphadenopathy, splenomegaly, and hepatomegaly; parasitemia, chills, and fever, darkening of skin
cutaneous - skin - centrifugally growing papular lesion w/central crusting; heals spontaneously, permanent scar mucocutaneous - skin and mucoid tissue - initially same as cutaneous lesion but it does not heal, necrosis of mucoid tissue; metastasis to distant mucoid tissues; very disfiguring |
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visceral leishmania
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1-4 months - fever 102-104F , chills, diarrhea, dysentery
progressive hepato-spleomegaly skin hyperpigmentatoin (kala Azar) = black dx death if untreated org rapidly eliminated from site - rarely local lesion - minute papules described in kids localize and multiply in the mononuclear phagocytic cells of spleen, liver, LN< BM, intestinal mucosa, etc |
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cutaneous leishmanisis
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orientla sore, delhi ulcer, baghdad boil
org L. tropica multiplies locally, producing of a papule 1-2 weeksor as long as 1-2 months after bite papule grows gradually to form a relatively painless ulcer center of the ulcer encrusts while the satelite papules dev at periphery heals in 2-10 months even if untreated but leaves disfiguring scar dx may diseminate in case of depressed immune fn |
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mucocutaneous leishmaniasis
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espundia, Uta, chiclero
intial sx = same as those of cutaneous leishmaniasis except organisms can metastasize and the leisions spread to mucoid (oral, pharyngela and nasal) tissues and lead to their destruction and hence severe deformity organism responsible and L. braziliensis, L. mexicana, L peruviana |
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leishmania diagnosis
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history
lesions or sx organisms in the lesion montenegro test - type IV hypersensitivity detection of anti-leishmanial Ab by immunofluoresence indicative of exposure |
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leishmania pathology
|
due to immune rxn to org particularyly the cell mediated immunity
lab exam reveals marked leukopenia relative monocytosis and lymphocytosis, anemia, and thrombocytopenia IgM and IgG levels extremely elevated due to both specific ab and polyclonal activation leishmanial proteoglycan immunosuppression |
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treatment and control of leishmania
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no vaccine
control of sand fly and infected animals avoidance of sand fly pentosam - antimony cluconate = sodium stibogluconate pentamidine isethionate used as alternative |
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malaria etiology
|
plasmodium falciparum = malignant tertian malaria
plasmodium vivax = benign tertian malaria plasmodium ovale = ovale teritan malaria plasmodium malariae = quartan malaria |
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malaria epidemiology
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200 mil global cases w/ mortality of more than 1 mil
falciparum and malariae most common found in asia and africa vivax predom in latin america, indian, pakistan, ovale - almost exclusively found in africa most cases from california in US most vivax |
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malaria morphology
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malarial parasite trophozoites ring shaped - other forms = ameboid/band may exist
sexual forms - gametocytes much larger falciparum largest gametocyte - banana shaped while others are smaller and round vivax causes stippling of infected red cells |
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malaria life cycle
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- malarial parasite transmitted by infected female anopheline mosquito
- injects sporozoites present in the saliva of the insect sporozoites infect the liver parenchymal cells where they may remain dormant (hypnozoites) or undergo mitosis to produce schizonts and meronts (merozoites) when parenchymal cells rupture thousands of meronts are released into blood and infect the red cells P. ovale and vivax infect immature RBC P. malariae infect mature RBC Falciparum infect both parasites mature in RBC burst merozoites and released into circulation - some merozoites transform into male and female gametoctyes while others enter RBC to continue the erythrocyte cycle gametocytes ingested by female mosquito -> transforms into ookinete , fertilized forms an oocyst in the gut oocyte produces sporozoites (sporogony) migrate to salivary gland and are ready to infect another host liver (extraerythrocytic cycle) takes 5-15 days where as erythrocytic cycle takes 48-72 hrs Can be transmitted by transfusion and transplacentally |
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malaria etiology
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plasmodium falciparum = malignant tertian malaria
plasmodium vivax = benign tertian malaria plasmodium ovale = ovale teritan malaria plasmodium malariae = quartan malaria |
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malaria epidemiology
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200 mil global cases w/ mortality of more than 1 mil
falciparum and malariae most common found in asia and africa vivax predom in latin america, indian, pakistan, ovale - almost exclusively found in africa most cases from california in US most vivax |
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malaria morphology
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malarial parasite trophozoites ring shaped - other forms = ameboid/band may exist
sexual forms - gametocytes much larger falciparum largest gametocyte - banana shaped while others are smaller and round vivax causes stippling of infected red cells |
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malaria life cycle
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- malarial parasite transmitted by infected female anopheline mosquito
- injects sporozoites present in the saliva of the insect sporozoites infect the liver parenchymal cells where they may remain dormant (hypnozoites) or undergo mitosis to produce schizonts and meronts (merozoites) when parenchymal cells rupture thousands of meronts are released into blood and infect the red cells P. ovale and vivax infect immature RBC P. malariae infect mature RBC Falciparum infect both parasites mature in RBC burst merozoites and released into circulation - some merozoites transform into male and female gametoctyes while others enter RBC to continue the erythrocyte cycle gametocytes ingested by female mosquito -> transforms into ookinete , fertilized forms an oocyst in the gut oocyte produces sporozoites (sporogony) migrate to salivary gland and are ready to infect another host liver (extraerythrocytic cycle) takes 5-15 days where as erythrocytic cycle takes 48-72 hrs Can be transmitted by transfusion and transplacentally |
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malaria symptoms
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incubation period varies btw 10-30 days as parasite load becomes significant -
intervals 34-36 hrs in vivax and ovale 58-60 hours in malariae vivax and ovale - headache - lassitude - vague aching of bones and joints - chills and high fever 103-106 - n/v - convulsion - euphoria - profuse sweating - sx every other day and last 8-12 hrs - spontaneous recovery falciparum - same as above but no tertian pattern - may be daily spiking - no spontaneous recovery - ultimately fatal - renal and CNS involvement - sequestration of cap vasculature in brain, GI and renal tissues, leading to hemoglobinure( black water dx) chronic = hepatosplenomegaly and nephritc syndromes malariae - same as tertian but paroxysm occurs every 3 days - 2 day clear period chills --> teeth chattering overtly shaking chill, peripheral vasoconstriction resulting in cyanotic lips and nails (cold stage)- lasts for about an hour at the end of this stage body temp climbs and reaches 103=106 assoc w/ headache n/v and convulsions pt experiences euphoria and profuse perspiration and temp begins to drop w/in a few hours pt exhausted but symptomless and remains asymptomatic until next paroxysm = each paroxysm due to rupture of infected erythrocytes and release of parasites |
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malaria pathology and immunology
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sx of malaria due to release of massive number of merozoites into circulation
infection results in production of ab which are effective in containing the parasite load ab against merozoites and schizonts infection also results in the activation of the reticuloendothelial system (phagocytes) activated macrophages help in the destruction of infected (modified) erythrocytes and ab coated merozoites cell mediated immunity also may dev and help in the elimination of infected erythroblasts malarial infections is assoc w/immunosuppression |
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malarial diagnosis
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travel history
sx blood smear detection of parasite in giemsa stained blood smears |
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malarial treatment and control
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effective with quinine derivatives (quinine sulfate, chloroquinie,l mefloquine, and primaquin
drug resistance particularly in P. falciparum and to some extent in P. vivax major problem control measures are eradication of infected anopheline mosquitos vaccines developed and tried but non available for routine use control mosquito population - mosquito netting |
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babesiosis geograph and etiology and morphology
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etiologic agent = babesia microti
zoonotic infection deer are primary reservoir cases reported in NE part of US and europe sim to malarial parasite, but no schizonts or gametocytes up to 4 trophozoites per cell no sexual cycle |
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babesiosis life cycle
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organism (sporozoite) is transmitted by hard tick (ixodes) and enters the red cell where it undergoes mitosis and the progeny merozoites are released to infect other red cells
ticks acquie organism during feeding on infected individual - in tick the organism divides sexually in the gut and migrates into salivary gland |
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babesiosis symptoms
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assoc w/ hemolytic anemia, jaundice, fever, and hepatomegaly
usually 1-2 weeks after infection mild chills |
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babesiosis diagnosis
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sx
history of tick bite no malarial paroxysm characteristic organism in blood intraerythrocytic parasites |
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babesiosis treatement and control
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drug = clindamycin combined w/quinine
pt may recover spntaneously avoid tick exposure and if bitten remove tick from skin immediately |
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toxoplasmosis
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etiologic agent = T. gondii distributed worldwide
most of pop is seropositive w/o any symptomatic episode threat to immunosuppressed and unborn intracellular parasite (tachyzoite) - pear shaped org that are enclosed in a parasite membrane to form a cyst - cysts in cat feeces (oocysts) |
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toxoplasmosis life cycle
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natural life cycle is in cats and sml rodents but can grow in different organs (brain, eye, skeletal mm) of any mammal or bird
cat gets infected by ingestion of cysts in the flesh decystation occurs in the small int and org penetrate the submucosal epithelial cells where they undergo several generations of mitosis, finally resulting in dev of micro- (male) and macro- (female) gametocytes - fertilized macro-gametocytes dev into oocysts that are discharged into the gut lumen and excreted oocysts sporulate in the warm environment and are infectious to a variety of animals including rodents and man sporulated oocysts swallowed by mammals release sporozzoites in the small int these sporozoites penetrate the intestinal mucosa and find their way into macrophages where they divide very rapidly and form cysts which may occupy the whole cell infected cells ultimately burst and release the tachyzoites to enter other cells, including mm and n cells where they are protected from the host immune system and multiply slowly (hence the name bradyzoites) - these cysts are infectious to carnivores (including man) unless man is eaten by a cat - it is a dead end host |
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toxoplasmosis symptoms
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prenatal
- 1-5% aborted - 8-10% serious brain and eye damage - 10-13 less serious visual and mental prob - 70% late visual and mental prob norm adult = flu like immunocompromised - parasitemia, cysts in visceral organs, eye, and CNS often fatal |
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toxoplasma gondii pathology and immunology
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both humoral and cell mediated immune responses are stimulated in norm individuals
CMI is protective and humoral response is of diagnostic value |
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toxoplamosis diagnosis and treatemnt
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diagnosis
- history - CT scan - tonsil or LN biopsy - isolate organism tx - sulphonamide - pyrimethamine -SPiramycin = alternative preg women avoid cat litter, handle uncooked meet, carefully and not to consume undercooked meat |
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Facultative parasitic protozoa
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free living amoebae which occasionally cause a serious human dx
- particular significance in immunocompromised hosts 1. Negleria fowleri - flagellate may inhabit warm waterrs (spas, warm springs , heated swimming pools) and gain access via the nasal passage to the brain and cause encephalitis acanthamoeba - several species of free-libing acanthamoeba are pathogenic to man - norm reside in soil - infect kidds who swallow dirt while playing on ground - norm individuals infection causes mild pharyngitis or remain asymptomatic - immunodeficient - penetrate esophageal mucosa and reach the brain where it causes granulomatous encephalitis |
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pneumocystis carinii
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not a protozoan its a yeast
opportunistic major cause of pneumoia among AIDS pt tx - trimethoprim sulphamethoxazole |
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ascaris lumbricoides epidemiology
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large intestinal roundworm
epidemiology - annual global morbidity est at 1 bil w/mortality of 20,000 ascariasis can occur at all ages, but it is more prevalent in 5-9 years old incidence in poor, rural population |
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ascaris lumbricoides morphology
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average female worm 30 cm
male is relatively smaller |
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life cycle ascaris lumbricoides
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infection occurs by ingestion of food contaminated w/ infective effs that hatch in the upper small intestine
larvae penetrate intestinal wall and enter the venules or lymphatics larvae pass through liver, heart and lung to reach alveoli - 1-7 days during which period they grow to 1.5cm they migrate up the bronchi, ascend the trachea to the glottis and pass down the esophagus to small intestine where they mature in 2-3 months - female may live in the intestine for 12-18 months and has a capacity of producing 25 mil eggs at avg daily output of 200,000 eggs are excreted in feces and under suitable condition infective larvae are formed w/in eggs - eggs are resistant to chem disinfectant and survive months in sewage but are killed by heat 40 deg C for 15 hrs infection is man to man autoinfection can occur |
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ascaris lumbricoides symptoms
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symptoms relative to worm burden
light infestation 10-20 worms may go unnoticed except on routine stool exam most common complaint is vague abd pain severe cases - pt experience listlessness, wt loss, anorexia, distended abdomen, intermittent loose stool and occasional vomiting durign pulmonary stage there may be a brief period of cough, wheezing, dyspnea and sub sternal discomfort most sx are due to pysical presence of the worm small and large intestine - abd pain; distended abd, anorexia, wt loss, occasional vomiting and loose stool pulmonary - cough wheezing dyspnea substernal discomfort |
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ascaris lumbricoides diagnosis
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based on identification of eggs w/characteristic external mammillated layer in the stool
some cases the oter mammillated layer is absent (known as decorticated eggs) the eggs are often stained brown by bile |
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ascaris lumbricoides tx and prevention
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albendazole 400 mg once
mebendazole 100 mg BID for 3 days if effective good hygiene is the best preventive measure |
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trichinosis
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world wide distribution - not common in muslim countries
related to hog farming conditions - pork consumption trichinella spiralis |
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trichinosis moorphology
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larvae in the tissue are coiled in a lemon- shaped capsule
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trichinella spiralis life cycle
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infection occurs by ingestion of larvae, in poorly cooked meat, which immediately invade intesinal mucosa and sexually differentiate w/in 18-24hrs
female after fertilization, burrows deeply in the small intestinal mucosa, whereas the male is dislodged on abt the the 5th day eggs begin to hatch in the female worm and young larvae are deposied in mucosa from where they reach the lymphatics, LN and the blood stream (larval migration) larval dispersion occurs 4-16 weeks after infection larvae are deposited in mm fiber and in striated mm form the capsule which calcifies to form a cyst in the non striated tissue such as heart and brain - larvae do not calcify they die and disintegrate the cyst may persist for several years female worm produces 1500 larvae man is termina l host the reservoir include most carnivorous and omnivorous animals |
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trichinosis symptoms
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depend on severity of infection
mild infections may be asymptomatic larger bolus of infection produces sx according to severity and stage of infection and organs involved intestinal mucosa 24-72 hrs - n/v/d abd pain - headache circulation and mm - 10-21 days - edema - peri-orbital conjunctivits - photophobia - fever - chill - sweating - mm pain - spasm - eosinophilia myocardium -10-21 days - chest pain - tachycardia - ECG changes - edema of extremities - vascular thrombosis Brain and meninges - 14-28 days - headache (supraorbital - vertigo - tinnitus - deafness - mental apathy -delirium - coma - loss of reflexes |
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trichinosis diagnosis
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- sx
- recent history of eating under- cooked pork, seal or bear - eosinophilia - increased serum creatinine phosphate and lactate dehydrogenase - positive serology |
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trichinosis - treatment and prevention
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tx - corticosteroids for symptomatic relief
- albendazole or mebendazole for killing parasite prevention - elimination of parasite from hogs - cooking meat well - freeze pork immediately after packaging - steroids used for tx of inflammatory sx and albendazole or mebendazaole used to elimnate worms |
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trichuriasis epidemiology
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tripical disease primarily of kids
65% of 1 billion cases seen in asia and africa seen in rural (low country) SC caused by trichuris trichiura (whipworm) |
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trichinosis pathology and immunology
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presence of large number of larvae in vital mm and host rxn to larval metab
mm fibers become enlarged edematous and deformed the paralyzed mm are infiltrated by neutrophils, eosinophils and lymphocytes splenomegaly is dependent on the degree of infection worm induces a strong IgE response which in assoc w/eosinopphils contributes to the parasite death |
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trichuris trichiuri morphology
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female organism long and slender ant and thicker post end
male is smaller and has coiled post end trichuris eggs are lemon or football shaped and have terminal plugs at both ends |
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life cycle of trichuris trichiura
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infection occurs by ingestion of embryonated eggs in fecally contaminated soil
the larva escapse the shell in the upper small intestine and penetrates the villus where it remains for 3-10 days upon reaching adolescence the larvae pass to the cecum and embed in the mucosa reach the ovipositing age in 30-90 days from infection = produce 3000, 10,000 eggs per day and live as long as 5-6 years eggs passed in feces embryonic in moist soil w/in 2-3 weeks eggs are less resistant to desiccation, heat and cold than ascaris eggs embryo killed under desiccation at 37deg w/in 15 minutes temp 52 deg C and -9 deg C are lethal |
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trichuris trichiura sx
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abd pain
chronic profuse diarrhea w/mucus and blood wt loss and anemia prolapsed rectum heavy infection less than 10 worms are usually asymptomatic heavier infections infection may result in malnutrition, wt loss and anemia and sometimes death |
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tricuris trichuria diagnosis, prevention and treatment
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symptoms
examine stool for eggs prevention - sanitary eating habits, improved hygiene tx - mebendazole is effective 100 mg BID for 3 dyas |
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pinworm epidemiology
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enterobius vermicularis
enterobiasis most common helminthic infection in US urban dx of kids in crowded environment adults get from kids |
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pinworm morphology
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female 8mm eggs small ovoid but asymmetrically flat on one side
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life cycle of pinworm
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infection occurs when embryonated eggs are ingested from the environment, with food or by hand to mouth contact
embryonic larvae hatch in the duodenum and reach adolescence in jejunum and upper ileum adult worms descend into lower ileum, cecum and colon and live there for 7-8 weeks gravid females containing more than 10,000 eggs migrate at night to the perianal region and deposit their eggs there eggs mature in oxygenated, moist environment and are infectious 3-4 hours later man-to-man and autoinfection are common man is the only host |
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pinworm symptoms
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enterobiasis relatively innocuous and rarely produces serious lesions
most common sx is perianal, perineal, and vaginal irritation caused by femal migration the itching results in insomnia and restlessness in some cases GI sx (pain, n/v) may develop mental distress termed pinworm neuropathy, consisting of mental distress , a guilt complex and desire to conceal the infection from their friends, is perhaps the most imp trauma of this persistent, pruritic parasite |
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diagnosis pinworm
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diagnosis is made by finding, the adult worm or eggs in the perianal area, particularly at night Scothc tape is used to obtain eggs
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pinworm treatment and control
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2 doses of pyrantel pamoate 2 weeks apart achieves a very high cure rate
mebendazole is an alternative whole family should be treated to avoid reinfection bedding and underclothing must be sanitized between the 2 treatment doses personal cleanliness is the most effective means of prevention |
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strongyloides stercoralis epidemiology
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prevalent in the tropics
southern US and PR threadworm akak cochin-china diarrhea poor saniation |
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threadworm morphology
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varies depending on whether it is parasitic or free living
parasitic female is larger than the free living worm |
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life cycle of threadworm
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infective larvae of S. stercoralis penetrate the skin of man enter the venus circulation and pass through the right heart to lungs where they penetrate into the alveoli
from there the adolescent parasites ascend to the glottis, are swallowed, and reach the upper part of the small intestine where they develop into adults ovipositing females develop in 28 days from infection the eggs in the intestinal mucosa hatch and dev into rhabditiform larvae in man the maturation into filariform larvae can allow penetration through the mucosa and cycle back into blood circulation, lung, glottis, and duodenum and jejunum, thus producing an autoinfection cycle alt they are passed in the feces, develop into infective filariform larvae and enter another host to complete the direct cycle if no suitable host is found the larvvae mature into free-living worm and lay eggs in the soil eggs hatch in the soil and produce rhabditiform larvae which dev into infective filariform larvae and enter another host to complete the direct life cycle if no suitable host is found the larvae mature into free-living worm and lay eggs in the soil the eggs hatch in the soil and produce rhabditif orm, larval , which develop into infective filariform larvae and enter a new host indirect cycle or mature into adult worms to repeat the free-living cycle |
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strongyloides stercoralis symptoms
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skin - ithching and red blotches during migrationthrough lung - bronchial verminous pneumonia
pulmonary - verminous, pneumonitis GI tract - mid-epigastric pain - n/v/d/c bloody dysentery general - wt loss and anemia |
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strongyloides stercoralis diagnosis
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larvae in stool w/in 24 hrs
histology |
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treatment and control of `strongyloides sterocoralis
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ivermectin or albendazole can be used effectively
direct and indirect infections are controlled by improved hygeine and autoinfection controlled by chemo |
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hookworms epidemiology
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hookworms parasitize 900 mil ppl and cause daily blood loss of a cumulative 7 mil litters
ancylostomiasis is most prevalent and second only to ansacariasis N. americanus (new world hookworm) is most common in the americas, central and southern america, southern asia, indonesia, australia, and pacific islands a. duodenale (old world hokworm dominate species in mediterranean region and Northern asia |
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hookworm morphology
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adult female hookworms 1mm
males smaller ant end of N. americanus is armed w/ a pair of curved cutting plates whereas A. duodenale is eqquipped w/one or more pairs of teeth hookworm eggs have a segmented embryo often enter through the feet common in areas where sewage disposal is inadequate |
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life cycle of the hookworm
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identical to that of threadworms except that hookworms are not capable of a free-living or auto infectious cycle
A. duodenale can infect by oral route |
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sx of hookworm
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depend on the site the worm is present and the burden of worms
light infection may not be noticed dermal - local erythema, macules, papules - ground itch - cutaneous invasion and subcutaneous migration of larrva pulmonary - bronchitis, pneumonitis and sometimes eosinophilia - migration of larvae through lung, bronchi adnd trachea gastrointestinal - anorexia, epigastric pain and gastrointestinal hemorrhage - attachment of adult worms and inj to upper int mucosa hematologic - iron deficiency, anemia, hypoproteinemia, edema, cardiac failure - intestinal blood loss |
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hookworm diagnosis
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identification of typicalsegmented eggs in fresh or preserved feces
species of hookworms cannot be distinguished by egg morphology |
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hookworm prevention and treatment
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sanitation- good hygiene and sanitary disposal of sewage are primary contorl measuures - walking parefoot in infested areas avoided
anthelmintic - - mebendazole - albendazole - pyrantel pamoate |
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dracunculus medinensis epidemiology and morphology
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aka Guinea worm
aka fiery serpent of the israleites - small amt of pppl infected - originated in sudan - WHO eradication effort <5000 infected adult female worm 50-120 cm by 1mm male half the size of the female |
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dracunculus medinensis life cycle
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infection caused by ingestion of water contaminated w/ water fleas (Cyclops) infected w/larvae
rhabtidiform larvaee penetrate the human digestive tract wall, lodge in loose CT mature to adult form in 10-12 weeks - in about a year thegravid female mibrates to the subcutaneous tissue of organs that norm come in contact w/water and discharges its larvae in water larvae picked up by cyclops in which they develop into infective form in 2-3 weeks |
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dracunculus medinesis sx
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if worm does not reach skin it dies and causes little reaction
superficial tissue it liberates a toxic substance that produces a local inflammatory rxn in the form of a sterile blister w/ serous exudation worm lies in a subcutaneous tunnel w/post end beneath the blister which contains clear yellow fluid the course of the tunnel is marked w/induration and edema the contamination of the blister produces abcesses, cellulitis, extensive ulceration, and necrosis |
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draculus medinensis diagnosis,, treatment, and control
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diagnosis - local blister, worm or larvae
outline of worm under skin may be revealed by reflected light tx extraction of adult worm by rolling it a few cm per day or perferably by multiple surgical incisions under local anesthesia no drug is efficacious protection of drinking water from being contaminated w/ cyclops and larvae or filtration are effective preventive measures |
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toxocara canis/ toxocara catti
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roundworms of dogs and cats
infection occurs when egg from animal feces is swallowed larvae migrate to visceral organs and produce inflammatory rxns can cause blindness |
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toxocara canis or T. catti life cycle
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eggs from feces of infected animals are swallowed by man and hatch in the intestine
larvae penetrate the mucosa enter circulationcarried to liver, lungs, eyes and other organs where they cause infllammatory necrosis |
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toxocara canis/T. catti sx, tx
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due to inflam rxn at site of infection
most serious consequence loss of sight - if worm localizes in the eye tx= albendazole/mebendazole avoidance of infected dogs/cats |
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ancylostoma braziliensis, ancylostoma caninum
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hookworms of dogs and cats
rarely infection has been assoc w/ eosinophilic enteritis larvae penetrate the skin and migrate in the epidermis producing pruritis along inflammatory tracts prevalent in many tropical and subtropical countries and in the us esp along Gulf and southern atlantic states larval persistaence = 2-10 weeks light infection tx by freezing the involved area heavier infections treated w/albendazole or ivermectin infection avoided by keeping away from water and soil contaminated w/infected feces |
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wuchereria bancrofti and W. (brugia) Malayi (elephantiasis)
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W. bancroftistrictly a human pathogen
distributedd in tropical areas worldwide whereas B. malayi infects a number of wild and domestic animals and restricted to SE asia mosquitos are vectors |
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toxocara canis/ toxocara catti
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roundworms of dogs and cats
infection occurs when egg from animal feces is swallowed larvae migrate to visceral organs and produce inflammatory rxns can cause blindness |
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toxocara canis or T. catti life cycle
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eggs from feces of infected animals are swallowed by man and hatch in the intestine
larvae penetrate the mucosa enter circulationcarried to liver, lungs, eyes and other organs where they cause infllammatory necrosis |
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toxocara canis/T. catti sx, tx
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due to inflam rxn at site of infection
most serious consequence loss of sight - if worm localizes in the eye tx= albendazole/mebendazole avoidance of infected dogs/cats |
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ancylostoma braziliensis, ancylostoma caninum
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hookworms of dogs and cats
rarely infection has been assoc w/ eosinophilic enteritis larvae penetrate the skin and migrate in the epidermis producing pruritis along inflammatory tracts prevalent in many tropical and subtropical countries and in the us esp along Gulf and southern atlantic states larval persistaence = 2-10 weeks light infection tx by freezing the involved area heavier infections treated w/albendazole or ivermectin infection avoided by keeping away from water and soil contaminated w/infected feces |
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wuchereria bancrofti and W. (brugia) Malayi (elephantiasis)
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W. bancroftistrictly a human pathogen
distributedd in tropical areas worldwide whereas B. malayi infects a number of wild and domestic animals and restricted to SE asia mosquitos are vectors |
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morphology of W> bancrofiti and B. malayi
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very similiar in morphology
w. bancrofi - found in LN and lymphatic channels 10 cm - males 1/2 the size B. malayi - half the size and its microfilaria are slightly smaller than W. bancrofti |
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W. bancrofiti and B. malayi life cycle
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filariform larvae enter the human body during the mosquito bite and migrate to tissues
there they may take up to a year to mature and produce microfilaria which migrate to lymphatics and at night enter the blood circulation mosquitos infected during blood meal microfilaria grow 4-5 fold in mosquito in 10-14 days and become infective for man |
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W, bancrofiti and B. malayi sx
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include lymphadenitis and recurrent high fever every 8-10 weeks which lasts 3-7 days
progressive lymphadenitis due to inflam response to parasite lodged in the lymphatic channels and tissues as worm dies the rxn continues and produces a fibroprolifefrative granuloma which obstructs lymph channels and causes lymphedema and elephantiits the stretched skin susceptible to traumatic injury and infections microfilaria cause eosinophilia and some splenomegally not all infections lead to elephatiitasis prognosiss in absence of elephantiasis = good |
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W> bancrofiti and B. malayi diagnosis, treatment, and control
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diagnosis based on history of mosquito bite in endemic areas, clinical findings, and presence of microfilaria in blood samples collected at night
tx - diethylcarbamzine quickly kills adult worms or sterilizes female steroids helpful alleviating inflam sx surgery avoid endemic areas cooler climate reduce inflam rxn |
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onchocerca volvulus epidemiology
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aka blinding filariasis
aka river blindness africa - prevalent through out eastern, central and western - major cause of blindness americas = guatemala, mexico, colombia, and venezuela confined to areas of low elevation w/rapidly flowing small streams where black flies breed man is the only host |
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onchocerca volvulus morphology
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male worms are much smaller
females = 50 cm |
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onchocerca volvulus life cycle
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infective larvae are injected into human skin by female black fly (simulium damnosum
dev into adult worms in 8-10 months adutlst inhabit as group of worms 2-3 females and 1-2 males tightly coiled gavid female releases microvilariae larvae which are distributed through the skin - picked up by black fly inthe skin - during a blood meal larvae migrate from the gut of the black fly to the thoracic mm where they develop into infective larvae in 6-8 days larvae migrate to the head of the fly then transmitted to a second host |
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onchocerca volvus sx
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nodular and erythematous lesion in the skin and subcutaneous tissue due to the chronic inflammatory response to persistnat worm inflammation
during incubation period 10-12 months = eosinophilia and urticaria occular involvement results from the entrapment of microfilaria in the in the cornea, choroid, iris, and anterior chambers leading to photophobia, lacrimation, and blindness |
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ochocerca volvus diagnosis
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based on sx
history of exposure to black flies and presence of microfliarial in nodules |
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onchocerca volvus tx and control
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ivermectin effective in killing larvae but does not affect adult worm
phase III clinical trial moxidectin in progress - kills adulats and microfilaria vector control - tx of infected individuals and avoidance of black fly |
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loa loa morphology/epidemiology
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loasis sim to onchocercaisis
can cause blindness central africa- equatorial rain forrest larger female org 66mm male 35 mm aka eye worm life cycle identical to that of onchocerca except the vector = deer fly |
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loa loa sx
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results in subcutaneous (calabar) swelling meassuring 5-10 cm in diameter marked by erythema and angioedema usually in the extremities
organism migratess under the skin at a rate of up to an inch every 2 minutes swelling appears spontaneously, persists 4-7 days and disappears known as fugitive or Calabar swelling worm causes no serious prob except when passing through orbital conjunctiva or bridge of nose |
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loa loa dx
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based on sx, history of deer fly bite and presence of eosinophilia
recovery of worm from conjunctiva confirmatory tx and control achieved w/diethylcarbamazine |
