Term
| alpha proteins of hsv replication encode? |
|
Definition
|
|
Term
| beta proteins of hsv replication encode? |
|
Definition
| proteins for viral replication |
|
|
Term
| gamma proteins of hsv replication encode? |
|
Definition
|
|
Term
| what is LMP-1 (latent infection membrane protein)? |
|
Definition
| in EBV, interacts with TNF and may inhibit apoptosis (leading to B-cell immortality) |
|
|
Term
|
Definition
| helps maintain latent EBV infection by binding to the EBV viral promoter oriP |
|
|
Term
| EBV infection occurs first in which area of the body? which cell surface protein is involved in infection? |
|
Definition
| nasopharynx then lymphocytes via CD21 |
|
|
Term
| which genes of high-risk hpv are associated with immortalization and transformation functions? |
|
Definition
|
|
Term
| which proteins are used in hpv vaccine? |
|
Definition
| structural capsid proteins L1 |
|
|
Term
| HPV E6 protein. what is the significance? |
|
Definition
| its an oncogene protein that binds p53 and promotes its degradation (inhibits apoptosis) |
|
|
Term
| HPV E7 protein. what is its significance? |
|
Definition
| hpv oncogene protein, binds to p105RB |
|
|
Term
| fungi dont have peptidoglycan but instead have? |
|
Definition
| glucans, mannoproteins, chitin |
|
|
Term
| what is the name of the special media used to culture fungi? and what's in it? |
|
Definition
| sabouraud's dextrose agar - acid-balanced, glucose, room temp incubation, use of bacterial inhibitors (bc lots of fungi take a while to grow and can easily be outgrown by bac colonies) |
|
|
Term
| give 2 examples of vegetative conidiation |
|
Definition
| arthroconidia and chlamydoconidia (develop directly from hyphal cells) |
|
|
Term
| give 2 examples of aerial conidiation |
|
Definition
| condidiophores (i.e. ascomycetes) and sporangioconidia (i.e. zygomycetes) also micro and macro conidia |
|
|
Term
| describe some characteristics of ascomycetes |
|
Definition
| "sac" fungi; yeast and mold (septate hyphae branching at acute angles); dimorphic species, includes most of the major pathogens |
|
|
Term
| describe some characteristics of basidiomycetes. |
|
Definition
| "club" fungi; mushrooms, rusts, smuts, some yeast; a few are infectious, others cause toxinoses (fungal intoxication!) |
|
|
Term
| describe some characteristics of zygomycetes. |
|
Definition
| very fast growing, primitive molds with broad, aseptate hyphae branching at right angles - agents of the most acute fungal infection, rhinocerebral zygomycosis |
|
|
Term
| what is a special stain that will allow us to get the best visualization of specific structures in tissue sections (fungi)? |
|
Definition
|
|
Term
| what is calcofluor white and how does it work? |
|
Definition
| it is a stain that we use to visualize fungal cell walls (namely, chitin) --> under black light this stain fluoresces bright blue |
|
|
Term
| what is india ink prep used for? |
|
Definition
| it is a negative stain used to show polysaccharide capsule of fungi. used esp to identify CRYPTOCOCCUS NEOFORMANS which is an impt OI in aids patients. |
|
|
Term
| in what situations would a delayed-type hypersensitivity skin test for fungi be useful? |
|
Definition
| epidemiology, to r/o particular dx, indicator for possible immunodeficiency |
|
|
Term
| visualization of germ tubes identifies which fungal organism? |
|
Definition
|
|
Term
| describe the dermatophyte test medium |
|
Definition
| selective against other species. tests dermatophyte ability to grow and produce an acid rxn on keratin-based agar medium. medium yellow @ acid-pH --> dermatophytes present? --> digest keratin (alkaline rxn) --> color change to red |
|
|
Term
| fungal 'farmer's lung' is associated with what type of rxn? |
|
Definition
| type III hypersensitivity (inhale conidia or mycelial elements occurring over long periods --> chronic lung disease) |
|
|
Term
| what is the most serious mushroom-poisoning toxin and what is the general development of sx? |
|
Definition
| death angel mushroom (amanita phalloides, amatoxins/amanitin). severe GI sx --> full recovery --> liver failure --> death (death within several days d/t multiorgan failure) |
|
|
Term
| why is ergotism (st. anthony's fire) dangerous and where do we get it? |
|
Definition
| fungal plant pathogen growing on food crops during growth or storage --> release toxins that cause disease upon ingestion. we get it from ingestion of RYE containing claviceps purpurea. --> choreic movements as sx |
|
|
Term
| what is the danger of aspergillus and where are they found? |
|
Definition
| found in contaminated stored crops (esp peanuts) --> release aflatoxins (hepatotoxins in large doses, carcinogens in chronic low dose) |
|
|
Term
| what 2 pathogens are responsible for superficial or cutaneous mycosis? |
|
Definition
| c. albicans and dermatophyte molds |
|
|
Term
| how are subcutaneous mycoses acquired? |
|
Definition
| usually through skin breaks (usually in feet) followed by lymphatic spread |
|
|
Term
| tinea is caused by which genera of dermatophytes? |
|
Definition
| microsporum, trichophyton and epidermophyton |
|
|
Term
| hair shaft infections can be subdivided... |
|
Definition
| ectothrix (fungus on surface of shaft) and endothrix (fungus invading the shaft) |
|
|
Term
| chronic mucocutaneous candidiasis (CMC) is a frequent manifestation of? |
|
Definition
| autoimmune polyendocrinopathy syndrome type 1 (APECED) - central tolerance defect |
|
|
Term
|
Definition
| allergic contact dermatitis, photoallergic dermatitis, eczematous drug eruptions, atopic eczematous dermatitis (unknown etiology) |
|
|
Term
| clinical features of eczematous dermatitis |
|
Definition
| polymorphous, ill-defined pruritic lesions characterized by thickening and scaling of the skin with gray scales and moist crusts. erythema, edema, oozing and crusting (vesicles in severe cases) this is an ACUTE inflammatory disorder |
|
|
Term
| what is the histopathologic hallmark of eczematous dermatitis? |
|
Definition
| spongiosis (intercellular edema of epidermis) --> abnormal keratinization with parakeratosis and serum in the cornified layer |
|
|
Term
| clinical features of psoriasis |
|
Definition
| chronic relapsing disorder, red round plaques (elevated lesion) and patches (flat lesions) with white scale with elbows knees and scalp most commonly affected. |
|
|
Term
| what are the histopathologic characteristics of psoriasis? |
|
Definition
| microabsesses (munro's) in the epidermis, parakeratosis, psoriasiform epidermal hyperplasia, dilated blood vessels in dermis |
|
|
Term
| clinical features of lichen planus |
|
Definition
| pruritic purple papules commonly affecting flexor surfaces of wrist and ankles, also mucous membranes, genitals and nails. |
|
|
Term
| histopathologic characteristics of lichen planus? |
|
Definition
| lichenoid infiltrate (dense band-like infiltrate filling the papillary dermis, obscuring dermoepidermal junction) NO parakeratosis, thickened cornified and granular layers, degeneration of basal layer |
|
|
Term
| clinical features of dermatophyte infections |
|
Definition
| ring shaped lesions, peripheral scale erythema |
|
|
Term
| histopathologic characteristic of dermatophyte infections? |
|
Definition
| fungal hyphae in cornified layer (periodic acid-schiff reaction stains organisms blue) |
|
|
Term
| histopathologic characteristic of c. albicans? |
|
Definition
| spores and pseudoseptate hyphae in cornified layer (PAS stain helpful) |
|
|
Term
| histopathologic characteristics of HSV |
|
Definition
| intraepidermal vesicles with epidermal necrosis and ballooning degeneration of the squamous cells. multinucleated keratinocytes |
|
|
Term
| demographic of people affected with pemphigus? level of morbid/mort? |
|
Definition
| (autoimmune) high level of morbidity/mortality, pt 35-65 |
|
|
Term
| demographic for pemphigoid? morbid/mort rate? |
|
Definition
| (autoimmune) low morbiditiy and mortality, adults over age of 60 |
|
|
Term
| clinical features of pemphigus? |
|
Definition
| flaccid blisters, easily rupture, arise on NORMAL skin, affects head/trunk/mouth |
|
|
Term
| clinical features of pemphigoid? |
|
Definition
| tense pruritic blisters that arise on erythematous edamatous plaques, commonly on groin/axilla/flexural surfaces of extremities |
|
|
Term
| histopathologic characteristic of pemphigus? and pathophys |
|
Definition
| intraepidermal vesicles above basal cell layer, discohesion of keratinocytes (acantholysis) auto-abs attack desmosomes |
|
|
Term
| histopathologic characteristics of pemphigoid? |
|
Definition
| subepidermal vesicles with eosinophils, split occurs in lamina lucida of the basement membrane zone comple. epidermis basically lifted off of the skin. hemidesmosome = target |
|
|
Term
|
Definition
| auto-abs attack bullous pemphigoid ag1 and 2 (lamina lucida) --> unhinges epidermis from basal cell layer |
|
|
Term
| where do basal cell carcinomas typically appear? |
|
Definition
| almost exclusively on hair-bearing areas esp sun-damaged skin of the face |
|
|
Term
| what are the most important predisposing factors for basal cell carcinoma? |
|
Definition
| light skin color and prolonged exposure to light |
|
|
Term
| clinical presentation of basal cell carcinoma? |
|
Definition
| elevated tumor nodule with elevated, pearly, shiny, ulcerated edges. outgrows blood supply. |
|
|
Term
| are basal cell carcinomas dangerous? |
|
Definition
| LOCALLY destructive, do NOT metastasize. can be dangerous IF they gain entry into the orbit or to any nerves that innervate the face (can damage brain and cause death, rare) |
|
|
Term
| histopathologic characteristics of basal cell carcinoma |
|
Definition
| proliferation of atypical basaloid cells forming nests/lobules in DERMIS. basal cells show peripheral palisading of nuclei; nests exhibit artifactual retraction from surrounding stroma. |
|
|
Term
| who is most at risk for actinic keratoses? |
|
Definition
| severely sun-damaged skin in older ppl (excessive exposure to sunlight for many years w/o protection) |
|
|
Term
| clinical presentation of actinic keratoses? |
|
Definition
| commonly seen on face, dorsum of hands and bald portions of scalp in men. multiple, elevated scaly red patches |
|
|
Term
| are actinic keratoses dangerous? |
|
Definition
| should be viewed as earliest stage in evolution of squamous cell carcinoma aka pre-cancerous. it is slow-developing so if it's caught early enough it can be treated before it turns cancerous. |
|
|
Term
| histopathologic characteristics of actinic keratoses? |
|
Definition
| thickened cornified layer, stains way more pink (usually more blue) d/t keratin overproduction, nuclei much larger and darker than normal (in lower 1/3 of epidermis) |
|
|
Term
| where would we most expect to find squamous cell carcinomas? |
|
Definition
| anywhere on the skin and mucous membranes. often on sun-damaged skin (assoc. with pre-existing actinic keratoses), on longstanding scars (esp burn scars) |
|
|
Term
| when are squamous cell carcinomas more likely to metastasize? |
|
Definition
| LOW propensity to metastasize when they're on sun-damaged skin; HIGH propensity on lip, scars, chronic sinus tracts, eyes, mouth, genitals (up to 30%) i.e. in areas involving mucocutaneous junctions bc can gain entry into lymphatics/blood |
|
|
Term
| clinical presentation of squamous cell carcinomas? |
|
Definition
| elevated, irregular, hyperkeratotic neoplasms, often ulcerated |
|
|
Term
| histopathologic characteristics of squamous cell carcinoma? |
|
Definition
| collections of very pink staining cells forming irregular nests, lobules, and strands within inflamed stroma (bc abn cells are proliferating, trying to produce keratin), pleiomorphic nuclei (nuclei stain with diff colors and sizes bc chr all messed up, all cells have diff # of chr), dyskeratosis |
|
|
Term
| where would we expect to find malignant melanomas? |
|
Definition
| trunk of fair-skinned men and lower legs of fair skinned women. rarely, on eyes and mouth. |
|
|
Term
| what are the risk factors for malignant melanomas? |
|
Definition
| family hx of malignant melanomas, dysplastic or large congenital nevi (nevus= mole, benign, melanocyte grows abn, benign collection of melanocytes in nests within epidermis dermis or both), fair skin, freckling, light hair, excessive exposure to UV light, hx of blistering sunburns and immune suppression |
|
|
Term
| histopathologic characteristics of malignant melanomas? |
|
Definition
| poorly circumscribed proliferation of atypical melanocytes wtihin epidermis arranged as irregular nests along dermoepidermal junction and extending to higher levels of epidermis. |
|
|
Term
| what are some malignant signs of a melanoma just by observation? |
|
Definition
| brown, black and white. >6mm diameter, irregular border |
|
|
Term
|
Definition
| when you see a primary melanoma with satellite spots. indicates that the primarily lesion has disseminated through the lymphatics and is going back and causing re-growth. bad prognosis. |
|
|
Term
| what's an example of natural passive immunization? |
|
Definition
| transplacental transfer of maternal IgG |
|
|
Term
| what's an example of artificial passive immunization? |
|
Definition
| antitoxins and antivenoms, also pooled human IgG (IVIg) for prophylaxis against infections in immunodeficiency disease |
|
|
Term
| what's an example of natural active immunization? |
|
Definition
| person's own immune response to antigens of an infectious agent |
|
|
Term
| what's an example of artificial active immunization? |
|
Definition
| innoculation of the pathogen itself, its antigens, or other cross-reacting pathogens or antigens or nucleic acids encoding antigens |
|
|
Term
| how is prevention of infection different from prevention if disease? |
|
Definition
| prevention of infetion involves removing the protected individual from the chain of transmission in the population |
|
|
Term
| when would we use immunization as a means of treating an ongoing disease? |
|
Definition
| when the natural immune response to the pathogen is poorly protective and where there is a lack of good tx alternatives |
|
|
Term
| what are some examples of vaccines we use today that are live-attenuated? |
|
Definition
| measles, mumps, chickenpox, and polio (until recently) |
|
|
Term
| describe the IPV (inactivated poliovirus vaccine) |
|
Definition
| killed mixture of the 3 serotypes (SALK vaccine). parenterally given, results in circulating abs (IgG). this did not provide mucosal immunity against the virus and did not prevent infection of intestinal cells when the immunized person later encountered wild poliovirus, but it did stop the viremic phase of infection and prevented symptomatic CNS infection (fatal) |
|
|
Term
| describe OPV (oral poliovirus vaccine) |
|
Definition
| SABIN vaccine. mixture of one attenuated variant of each of the wild strains. provides stimulation of the normal course of inf --> induces mucosal immunity in the GI tract, rendereing immunized resistant to inf by wild virus as well as to symptomatic disease. reduces the spread of virus in the population. opv itself spreads in the population after immunization, extending benefits of vaccine to non-immunized people. |
|
|
Term
| what is the major downside of OPV? |
|
Definition
| two of the viral strains is stable but the third is not --> exhibits reversion to virulence at a measurable but low rate --> few cases of paralytic disease every year |
|
|
Term
| what is the major live-attenuated bacterial vaccine? |
|
Definition
| bacille-calmette-guerin (BCG) vaccine against TB (attenuated variant of mycobacterium bovis). |
|
|
Term
| what are 3 examples of a killed-pathogen vaccine? |
|
Definition
| influenza virus vaccine, rabies virus vaccine, pertussis vaccine |
|
|
Term
| why is protection only partial in killed-pathogen vaccines for diseases like influenza and pertussis? |
|
Definition
| killed-pathogen vaccines work fine for diseases that depend on extensive spread through body before sx produced. influenza and pertussis produce sx much earlier, so the protection will cause a lesser version of the disease but will not prevent sx altgoether |
|
|
Term
| what are the most prominent examples of subunit vaccines? |
|
Definition
| toxoids and capsular polysaccharides |
|
|
Term
| what kind of diseases do we use subunit vaccines for? |
|
Definition
| for the kind of bacterial infections whose ill effects are totally or mostly attributable to protein toxins produced by the bacteria (diptheria, tetanus) |
|
|
Term
| how do adjuvants work to stimulate immunity? |
|
Definition
| induce inflammation (stimulation of lys proliferation and activation by early cytokines such as IL-1); by facilitating uptake and presentation of ags via complex formation; and by prolonging the presence of ag in tissues by formation of insoluble depots such as ag in mineral oil |
|
|
Term
| what are 3 ways we're trying to mimic the effects of an intracellular infection to improve induction of CMI in vaccines? |
|
Definition
| use of micelle-forming immune-stimulatory complexes to deliver ags directly into the cytosol; use of recombinant live viruses to express ags from other pathogens during an intracellular inf; immunization with genes encoding such ags in the form of naked molecules of dna or rna |
|
|
Term
| what happens after anthrax spores are inhaled? |
|
Definition
| travel to alveoli, ingested by macrophages, carried to mediastinal lymph nodes --> hemorrhagic necrotizing mediastinitis w/systemic toxemia and bacteremia --> death |
|
|
Term
| what 4 bacterial virulence factors are involved in the pathogenesis of anthrax? |
|
Definition
| antiphagocytic capsule, lethal factor (cytolytic toxin, induces release of pro-inflammatory factors like TNF-a), edema factor (alters IC signaling --> changes in water homeostasis and immune func), protective antigen (binds to cellular receptor, facilitates uptake of LF and EF by cells) |
|
|
Term
| what do you treat anthrax with? |
|
Definition
| fluoroquinolones (cipro), tetracyclines (doxy), amoxicillin |
|
|
Term
| how do we treat a botulism attack? |
|
Definition
| there is no infection so antibiotics play no role in tx. toxoid vaccine exists, but would have to be given in advance of attack (antitoxin), and risk of attack is not high enough to justify immunization. |
|
|
Term
| what are the 3 forms of plague? |
|
Definition
| bubonic (massive lymphadenopathy), pneumonic (from vector-acquired bubonic or septicemic plague by hematogenous spread or by inhalation), septicemic. unlike other bioterrorist threats, pneumonic plague spreads efficiently person-to-person --> 2ndary spread after an attack expected |
|
|
Term
| what are the bacterial virulence factors for plague? |
|
Definition
| yersinia outer membrane proteins (yops - invasive cytotoxic outer membrane proteins), proteinaceous capsule, thrombolytic protease (activates plasminogen), endotoxin |
|
|
Term
| what do you treat plague with? |
|
Definition
| streptomycin, gentamycin, doxy, cipro, chloramphenicol |
|
|
Term
| what are the 2 class A bioterrorist agents that can be spread person to person? |
|
Definition
|
|
Term
| what's the tx for smallpox in bioterrorist attack? |
|
Definition
| vaccine can be used for post-exposure prophylaxis |
|
|
Term
| what are the 7 presentations of tuleremia? |
|
Definition
| ulceroglandular (skin), glandular (vector), oculoglandular (eye), oropharyngeal (ingestion or inhalation), typhoidal (systemic febrile illness with enteric involvement), septic |
|
|
Term
|
Definition
| streptomycin, gentimicin, doxy, chloramphenicol, cipro |
|
|
Term
| what are 4 classes of viruses that can lead to hemorrhagic fevers? |
|
Definition
| flavivirus (yellow fever), filoviruses (ebola and marburg viruses), arenaviruses (lassa), bunyaviruses (rift valley fever) |
|
|
Term
| tx for hemorrhagic fever? |
|
Definition
| ribavirin for arenaviruses and bunyaviruses |
|
|
Term
| how do we test for toxoplasmosis |
|
Definition
| serologic testing - sabin-feldman test: methylene blue + accessory factor + serum --> clear if infected (d/t antisera) and blue if non-infected (no antisera); or indirect fluorescent antibody test |
|
|
Term
| how do we dx leishmaniasis? |
|
Definition
| smear and stain (giemsa), culture scrapings from lesion margin, positive leishmanin skin test (montenegro test) demonstrates DTH |
|
|
Term
| how does toxoplasma gondii survive intracellularly |
|
Definition
| prevents fusion of lysosome and endosome |
|
|
Term
| how does leishmaniasis survive intracellularly? |
|
Definition
| can survive in phagolysosome |
|
|
Term
| how does trypanosoma cruzii survive intracellularly? |
|
Definition
| escape from phagolysosome/phagosome |
|
|
Term
| which form of trypannosomiasis protozoa are infectious for humans? |
|
Definition
| metatrypomastigotes (in tsetse fly, epimastigotes transform into metatrypanomastigotes) |
|
|
Term
| what is winterbottom's sign and what is it diagnostic for? |
|
Definition
| characteristic of Gambian trypanosomiasis |
|
|
Term
| pathogenesis of african trypanosomiasis |
|
Definition
| fly bite --> metatrypanomastigote introduced to skin --> lodge in local tissue and multiply extracellularly --> inflammatory rxn subsides in 1-2 weeks (primary lesion seen in caucasions usually) --> trypomastigotes reach blood in 2 weeks of inf --> hyperplasia of vascular endothelium + perivascular infiltration by leukocytes and inflam of lymph nodes and hepatosplenomegaly |
|
|
Term
| clinical presentation of african trypanosomiasis |
|
Definition
| headache, frequent febrile paroxysms, extreme weakness, rapid weight loss, rapidly progressive, fatal. CNS involvement --> disturbed vision, mental confusion, delayed response to pain, emaciation, continuous sleep, death |
|
|
Term
| describe antigenic variation in association with african trypanosomiasis |
|
Definition
| parasite changes variant surface glycoprotein by random switching of VSG genes --> changed antigenic profile --> antibody response to VSG results in waves of parasitemia |
|
|
Term
| diagnosis of african tryapnosomiasis |
|
Definition
| sx, hx of exposure, parasites in blood, csf or lymph node aspirates, serology |
|
|
Term
| how do we get infected with chagas disease? |
|
Definition
| reduviidae insects - metatrypomastigotes in insect feces rubbed into bite wound, skin abrasions, or intact mucosa (esp conjunctiva; also via blood transfusion, congenital and oral transmission |
|
|
Term
| 2 things/signs that may happen at primary infection site of chagas disease |
|
Definition
| romana's sign (in children, unilateral painless, erythematous edema around eye, with periauricular and/or submaxillary lymphadenitis); chagoma (erythematous, itching, desquamated and rarely ulcerated skin lesion) |
|
|
Term
| what happens in chagas disease after we're introduced to the metatrypomastigotes? |
|
Definition
| metatrypomastigotes enter macrophages --> transform into amastigotes and multiply --> transform into trypomastigotes and leave infected cell to infect other cells or to be picked up by insect (in insect --> transform to epimastigotes --> multiply in midgut --> go to hindgut and transform into metatrypomastigotes --> infect humans) |
|
|
Term
| diagnosis of chaga's disease |
|
Definition
| parasites in blood lymph or infected tissues; culture; animal inoculation; xenodiagnosis (feed uninfected bugs on pt --> examine insect gut for parasites); serologic tests |
|
|
Term
| what efficiently kills all intracellular parasites? |
|
Definition
| INF-y-treated (activated) macrophages |
|
|
Term
| describe the pathogenesis of pneumocystis jirovecci (PCP) |
|
Definition
| alveolar pathogen without tissue invasion --> extracellular trophozoites and cysts in pulmonary alveoli (along with cellular debris and macrophages) --> pulmonary injury from inflammatory response |
|
|
Term
| describe the clinical presentation of PCP |
|
Definition
| can be a chronic asymptomatic infection in immunocompetent; fulminant pulmonary and extrapulmonary disease in immunocompromised. pt experiences progressive dyspnea, nonproductive cough, low-grade fever and hypoxia) |
|
|
Term
|
Definition
| cysts and trophozoites in induced sputum or bronchoalveolar lavage fluid |
|
|
Term
| toxoplasma gondii, leishmania spp., and trypanosoma cruzi are all intracellular parasites. what cells do they infect? |
|
Definition
| toxoplasma and trypanosoma cruzii infect all nucleated cells (macrophages, smooth skeletal and cardiac muscle, neurons of CNS and PNS); leishmania spp only infect macrophages |
|
|
Term
| chronic infection with trypanosoma cruzii leads to what sx? |
|
Definition
| cardiomyopathy, megaesophagus and megacolon |
|
|
Term
| pediculites aka lice - how many legs? |
|
Definition
|
|
Term
| what do scabies insects look like? how are they spread? |
|
Definition
| microscopic, 4 pairs of legs, 2 anterior and 2 posterior, indistinct head. spread person to person or via fomites |
|
|
Term
| how long do lice live? how many eggs produced each day? how long til maturation? |
|
Definition
| live 30 days, 5-10 eggs/day, eggs hatch in 4-14 days, takes 12-28 days to mature |
|
|
Term
| how long do scabies bugs live? where do they reide? how many eggs/day? how long til eggs hatch? larva become adults in a week? |
|
Definition
| live for 8 weeks in cutaneous burrows/tunnels; 1-2 eggs at a time; eggs hatch in 3-5 days; larvae become adults in a week |
|
|
Term
| what causes the itching in pediculosis? |
|
Definition
| louse saliva produce pruritic papules |
|
|
Term
| what causes the itching in scabies? |
|
Definition
| fecal pellets, eggs and remains of dead mites provoke hypersensitivity rxns --> inflammation --> itching |
|
|
Term
|
Definition
| infestation of the body with larvae of dipterous flies (flies deposit eggs or larvae in wounds, ulcers, sores, and orifices) |
|
|
Term
| how do larvae cause damage in myiasis? |
|
Definition
| debride necrotic tissue (in the wounds, ulcers, sores that they are deposited in) --> sometimes cause extensive damage to surrounding healthy tissue --> painful lesions |
|
|
Term
| what is the toxin in scorpion venom? |
|
Definition
| its a neurotoxin called chlorotoxin. crosses BBB --> targets glioma or primary brain tumor cells. we use it in imaging to localize tumors |
|
|
Term
| what does scorpion venom stimulate? |
|
Definition
| sustained release of acetylcholine and catecholamines (epi) --> initial cholinergic and later adrenergic sx |
|
|
Term
| what happens at the site of the scorpion sting immediately after puncture? |
|
Definition
| intense local pain, local edema, regional lymph node swelling and tenderness, blistering and necrosis |
|
|
Term
| what are the early sx of a poisonous scorpion sting? |
|
Definition
| salivation, vomiting, profuse sweating, alternating brady and tachycardia, abdnominal colic, diarrhea, loss of sphincter control, priapism, widely dilated pupils |
|
|
Term
| what are the late sx of a poisonous scorpion sting? |
|
Definition
| hypertension, pulmonary edema, respiratory paralysis, convulsions, hematemesis, hyperglycemia, acute pancreatitis, shock, coma, death |
|
|
Term
| what is the danger in a black widow spider bite? |
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Definition
| (first, is a systemic arachnidism, does not produce local tissue necrosis) toxin = alpha-latrotoxin --> binds irreversibly to neurons --> sustained release and eventual depeletion of NT (acetylcholine and norepi) --> painful muscle cramps in extremities and trunk (other sx: salivation, vomiting, tachycardia, HA, resp or cardiac failure, possibly fatal) |
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Term
| whats the pathogenesis behind a brown recluse spider bite? |
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Definition
| (first, its NOT systemic, its local) it has a catalytic toxin that has enzyme activity --> cleaves extracellular matrix proteins --> pain, erythematous and pruritic bite site --> lesions resolve or become hemorrhagic/necrotic with blackeneed eschar --> necrotic ulcer |
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Term
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Definition
| if attached for several days --> tick paralysis (tick salivary toxin --> inhibits acetylcholine release --> acute, ascending flaccid paralysis (gone as soon as tick removed, but if tick not removed, 10% mortality from resp paralysis) |
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Term
| what is the pathogenesis of malaria (from bite to sx) |
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Definition
| infected female bites human --> inject saliva and sporozoites --> sporozoites enter hepatocytes and multiply --> become merozoites infective of RBC --> successive progenies of merozoites in rbc --> major manifestations of malaria |
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Term
| how does sexual reproduction of malaria take place in mosquito? |
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Definition
| some merozoites in human RBC differentiate into gametocytes --> gametocytes ingested by mosquitos --> give rise to gametes in mosquito stomach where fertilization takes place --> zygote --> oocyst --> sporozoites develop in oocyst --> oocyst ruptures upon maturation --> sporozoites released migrate to salivary gland |
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