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109 Cards in this Set
- Front
- Back
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Mycobacterium: shape, nutrition, classification?
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Non-spore forming aerobic rods
Grow very slowly Acid fast |
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Transmission of M. leprae?
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direct skin contact with respiratory secretions and wound exudates; possibly inhalation of infectious aerosols.
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Tuberculoid leprosy: symptoms? histology? infectivity?
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associated with strong CELLULAR IMMUNE RESPONSE
Symptoms: erythematous or hypopigmented plagues on skin. Peripheral nerve damage and complete sensory loss. Histology: many lymphocytes and granulomas; few or no bacteria visible Infectivity: low confirmed by skin test (reactivity to lepromin) |
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Immunological aspect of tuberculoid leprosy
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cell mediated immune response
granuloma formation most intracellular bacteria killed in macrophages activated by INF-gamma - IFN - gamma functions to: 1. drive differentiation of CD4+ cells to th1 2. activate macrophages 3. induces antibody isotypes that promotes phagocytosis through attachment to Fc receptors and activation of complement 4. stimulate the expression of class 2 MHC molecules on APCs Disease progresses slowly Characteristic of Th1 activity Cytokine profile reflects Th1 |
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What is WHO recommended treatment for tuberculoid leprosy?
If they cant tolerate rifampin or is infection with a resistant strain? |
Rifampin + dapson OR
rifampin + clofazimine Resistant: Clofazimine + oflaxacin + minocyclin |
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Lepromatous leprosy: symptoms? histology? infectivity?
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Associated with strong ANTIBODY RESPONSE, combined with specific defect in cellular immune response
Symptoms: erythematous macules, papules, nodules on skin - extensive tissue destruction - diffuse nerve involvement with patchy sensory loss Histology: foamy macrophages; few lymphos, lack of Langerhans cells, lots of bacteria Infectivity: high Confirmed by acid fast staining |
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Immunological aspect of lepromatous leprosy
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you can assume you dont have good cell mediated immunity
Strong Ab response Growth of bacteria in macros widely disseminated by macros to tissues such as bone and cartilage Cytokine production characterisitc of Th2 - naive t-cells differentiate to Th2 cells under influence of IL4 - Th2 cell make IL4 activate more T cells - Th2 cells produce IL4 which stimulates the production of IgG AB and neutralizing isotypes of IgG but do not promote phagocytosis - th2 cells produce il5 IL-10 suppresses macro activation |
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Rickettsia shape? nutrition?
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Aerobic poorly staining
gram negative rods Obligate intracellular |
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Rickettsia rickettsii: reservoir? Vector?
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Mammalian: wild rodents
Vector: arthropod |
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Rickettsia rickettsii: disease?
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Rocky Mtn Spotted Fever
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Rickettsia rickettsii: pathogenesis
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Outer memrane protein A facilitates attachment to endothelial cells
bacteria penetrate and replicate in endothelial cells and move from cell to adjacent cell Damage to endo cells --> leakage of fluid from blood vessels --> hypovolemia Inflammatory and cell mediated immune responses cause most damage and symptoms |
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RMSF: incubation, symptoms?
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Incubation: 2-14 days
Sudden high fever and headache often associated with myalgias, nausea, vomiting, diarrhea, abdominal pian Macular rash in 90% of pts after 3 days - starts on wrists, arms, ankles, then spread to trunk (different pattern than most rashes that go trunk-->extremities) - may evolve to spotted petechial form (indicator of serious disease) |
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RMSF: complications?
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Possible complications in untreated cases:
-neurological -pulmonary and renal failure -cardiac abnormalities |
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Resevoir for rickettsia akari? Vector
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wild rodents
urban mite |
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Rickettsialpox: incubation, symptoms? Caused by?
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Rickettsia akari
1 week First phase: papule at site of bite; quickly ulcerates and progresses to eschar formations Second phase: (after 7-24 additional days) - sudden high fever with chills, severe headaches, sweats, myalgias, photophbia - general papulovesicular rash Usually mild and uncomplicated, even if not treated |
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Erysipelothrix rhusiopathiae: shape, nutrition, reservoirs?
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gram positive
non-spore forming rod faculatively anaerobic Zoonotic disease: people who work with animals at most risk |
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Erysipeloid: caused by? symptoms?
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Erysipelothrix rhusiopathiae
Inflammatory skin lesion (violaceous, raised edge) that spreads peripherally Painful and pruritic (produces burning, throbbing sensation) - usually non-suppurative |
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Staph aureus skin diseases
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SSSS
Bullous impetigo Non-bullous impetigo Folliculitis Furuncles (boils) and carbuncles Cellulitis |
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Strep pyogenes skin diseases
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impetigo (pyoderma)
erispelas cellulitis |
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P. aeruginosa skin diseases
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folliculitis
cellulitis burn infections swimmer's ear (outer ear) |
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Capnocytophaga skin diseases
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filamentous gram negative rods
infections related to cat and dog bites |
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Pasteurella multocida skin diseases
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gram negative coccobacillus
infections related to animal bites |
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Batonella henselae skin diseases
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cat scratch disease
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bacillus anthracis skin diseases
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gram positive spore forming rod
cutaneous anthrax |
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Herpes simplex viruses skin diseases
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oral herpes
herpes whitlow herpes gladiatorum eczema herpaticum genital herpes |
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Varicella-Zoster virus: pathogenesis
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initial replication/amplifcation in respiratory mucosa (primary site of infection)
viremia transports virus to lymphatic system, cells of reticuloendothelial system (secondary amplification) Secondary viremia (after 3-11 days) transports virus to skin Replication at skin --> chicken pox lesions Latent infection established in DRG or cranial nerve ganlia after primary infection if reactivated, virus travels along neural pathway to skin and produces shingles lesions Shingles typically involve single dermatome |
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Varicella-Zoster virus: transmission:
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droplet infection or contact with skin vesicles
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Chicken pox: incubation? symptoms? caused by?
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varicella zoster virus
14 days Fever and maculopapular rash (thin-walled vesicles on erythematous base) Vesicles --> pustular, crust over, and become scabbed Successive crops of lesions develop over 3-5 days Generalized rash, but more severe on trunk than on extremities Lesions itch and cause scratching (can lead to secondary bacterial infections and scarring) Primary infections --> viral pneumonia in 20-30% of adult cases |
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Shingles: incubation? symptoms? caused by?
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Recurrence of active infeciton in neuron --> severe pain in area innervated by nerve and skin lesions
Rash usually limited to single dermatome chronic pain (postherpetic neuralgia) may persist for month to years Progressive disease in IC hosts |
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Roseola infantum: incubation? symptoms? caused by?
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HHV6 and HHV7
5-15 days Sudden fever, sometimes with slight anorexia, vomiting, rhinorrhea, and/or cough Rash develops suddenly as fever subsides: - numerous pale, pink, almond shaped macules - appear on neck and trunk and become confluent - fade in few hours to 2 days |
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Poxviruses: shape? genome? enveloped?
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Enveloped virus with brick shaped nucleocapsids
linear double stranded DNA Only DNA virus that replicate in cytoplasm of host Humans are only hosts for molluscum contagiosum and variola (smallpox) viruses All others are zoonotic |
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What is the only DNA virus that replicates in cytoplasm of host?
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poxvirus
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What are the poxviruses that are only human hosted?
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molluscum contagiosum
variola (smallpox) |
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Molluscum contagiosum: incubation? symptoms? caused by?
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poxvirus
2-8 weeks Papules develop and lead to pearl like or wart like nodules with easily expressed central plug - lesions most common on trunk, genetalia and proximal extremities (often in clusters of 5-20 nodules) - disappear in 2-12 months more common in children than adults |
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What are the poxvirus zoonotic diseases most likely to be seen in US?
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orf
pseudocowpox These come from direct contact with lesions on animals Can be occupational hazard for vets and farmers |
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Papillomaviridae: shape? genome? enveloped?
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non-enveloped
double stranded DNA genomes HPV |
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HPV pathogenesis
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infect and replicate and stimulate proliferation of epi cells in:
- sqamous epi of skin (warts) - mucous membranes (genital, oral, and conjunctival papillomas) |
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Papillomaviridae: human infections acquired by?
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- direct contact with wart or fomite
- via sexual intercourse - chewing on warts Virus enters through a break in skin or mucous membrane Warts most frequent in children and young adults Some HPV tpyes sexually transmitted |
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Skin warts: caused by? symptoms
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HPV
Benign, self-limited proliferations of skin, usually on hands and/or feet Invading virus stimulates cell growth, thickening in basal and prickle layers (stratum spinosum and stratum granulosum) Average wart takes 3-4 months to develop Infection remains local; usually regresses on its own (recurrences possible) |
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Rubella: enveloped? genome? host?
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togaviridae family: enveloped virions with icosahedral capsids
+ sense ss-RNA genomes Humans are only host |
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Rubella transmission?
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respiratory droplets
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Rubella virus: pathogenesis
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infects upper respiratory tract epithelium
migrates to local lymph nodes (lymphadenopathy) Viremia distributes virus to other tissues, especially skin (characteristic skin rash) Prodromal period (before rash) lasts up to 2 weeks (patient highly contagious at this time) Can cross placenta in pregnant women, infect fetus, and replicate in many tissues |
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Rubella virus: disease? incubation period? symptoms?
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rubella (german measles) -- different from regular measles
14-21 days Maculopapular rash (lasts 3 days) and swollen glands Generally benign in children; in adults, may lead to bone and joint pain, thrombocytopenia, or postinfectious encephalophathy |
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What is rubella congenital syndrome?
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fetus at major risk of infection until 20th week; maternal immunity prevent infection
most frequent symptoms: cataracts, deafness, mental retardation mortality high in utero and until the first year after birth most states screen mothers for ABs |
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What are superficial mycoses?
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mostly cosmetic in nature
- skin infections limited to outermost layers of stratum corneum - hair infection limited to cuticle Do not cause physical discomfort (infections limited to dead tissues - no immune response) Relatively easy to Dx and treat |
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What is pityiasis versicolor?
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Superficial mycoses
caused by: malassezia furfur - member of normal skin flora - lives in areas rich in sebaceous glands Lesions on upper torso, abdomen, and arms - may be hyperpigmented or hypopigmented - scale easily - affected areas have dry, chalky, appearance |
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Disease caused by malassezia furfur?
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pityiasis versicolor
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What is tinea nigra?
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superficial mycoses
caused by hortaea werneckii - dimorphic fungi with brown-black pigmentation Brown or black macular lesions - often on palms or soles, but can occur elsewhere - enlarge by peripheral extension |
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What disease is caused by hortaea werneckii?
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Tinea nigra
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What is a subcutaneous mycoses?
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usually associated with injury that implants fungus in underlying tissues
infections initially involve deeper layers of dermis, subQ tissues or bone (depending on depth of injury) Later extend into epidermis and lead to skin lesions Most often occur in portions of body most prone to trauma (feet, legs, hands, arms, butt) Rare in US except lymphocutaneous sporotrichosis |
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What is lymphocutaneous sporotrichosis?
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SubQ mycoses
Caused by sporothrix schenckii (which also causes systemic fungal disease when inhaled) Chronic infection --> nodular ulcerative lesions along lymphatic glands draining primary site of infection Painless subQ nodules that may ulcerate and discharge pus |
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What disease is caused by sporothrix schenckii?
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lymphocutaneous sporotrichosis
(and other systemic fungal infections) |
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Propionibacterium: shape? nutrition?
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Gram positive bacilli
ferment carbs to propionic acid colonize skin, conjunctiva, oropharynx, ears |
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Propionibacterium: important species?
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P. acnes
P. propionicum |
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Acne vulgaris
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caused by Propionibacterium acnes
bacteria grow in sebaceous follicles, secrete peptide that attracts leukocytes Phagocytosis of bacteria --> release of bacterial proteases, lipases, neuraminidase, hyaluronidase Released products --> local inflammatory response --> swelling and eventual rupture of follicle |
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What disease is associated with early development of rash limited to cheeks that looks like a "slapped cheek"?
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Erythema infectiosum (Fifth Disease)
Parvovirus B-19 |
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What causes fifth disease?
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Parvovirus B-19 (only human pathogen in parvoviridae family)
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What is pathologic process of Parvovirus B19?
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B-19 replicates in upper resp tract, migrates to bone marrow
Lytic infection and death of RBC precursor cells and halt in production of RBCs for about 1 week Many viruses appear in bloodstream by 8 days after infection (coincides with early symptoms) Many viruses in oral, respiratory secretions as well (facilitates transmission via droplets) AB responses eventually clear virus from bloodstream but also contribute to symptoms: - second stage of disease mediated by immune response Primarily in ages 5-18 |
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Skin warts: caused by? symptoms
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HPV
Benign, self-limited proliferations of skin, usually on hands and/or feet Invading virus stimulates cell growth, thickening in basal and prickle layers (stratum spinosum( and stratum granulosum Average war takes 3-4 months to develop Infection remains local; usually regresses on its own (recurrences possible) |
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Rubella: enveloped? genome? host?
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togaviridae family: enveloped virions with icosahedral capsids
+ sense ss-RNA genomes Humans are only host |
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Rubella transmission?
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respiratory droplets
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Rubella virus: pathogenesis
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infects upper respiratory tract epithelium
migrates to local lymph nodes (lymphadenopathy) Viremia distributes virus to other tissues, especially skin (characteristic skin rash) Prodromal period (before rash) lasts up to 2 weeks (patient highly contagious at this time) Can cross placenta in pregnant women, infect fetus, and replicate in many tissues |
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Rubella virus: disease? incubation period? symptoms?
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rubella (german measles) -- different from regular measles
14-21 days Maculopapular rash (lasts 3 days) and swollen glands Generally benign in children; in adults, may lead to bone and joint pain, thrombocytopenia, or postinfectious encephalophathy |
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What is B-19 presentation in adults?
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arthryalgias and joint issues (arthritis)
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What is rubella congenital syndrome?
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fetus at major risk of infection until 20th week; maternal immunity prevent infection
most frequent symptoms: cataracts, deafness, mental retardation mortality high in utero and until the first year after birth most states screen mothers for ABs |
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What does the parvovirus B19 cause in persons with a chronic hemolytic disease?
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sudden transient aplastic crisis
pts with sickle cell anemia, paroxysmal nocturnal hemoglobinuria, erythrocyte enzyme deficiency Death of RBC precursor cells, halt in production of new RBCs --> transient reticulocytopenia for 7-10 days May have fever, chills, etc. |
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What are superficial mycoses?
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mostly cosmetic in nature
- skin infections limited to outermost layers of stratum corneum - hair infection limited to cuticle Do not cause physical discomfort (infections limited to dead tissues - no immune response) Relatively easy to Dx and treat |
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Parvovirus B19 in IC pts
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cannot eliminate B19
chronic transfusion dependent anemia |
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What is pityiasis versicolor?
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Superficial mycoses
caused by: malassezia furfur - member of normal skin flora - livers in areas rich in sebaceous glands Lesions on upper torso, abdomen, and arms - may be hyperpigmented or hypopigmented - scale easily - affected areas hace dry, chalky, appearance |
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Disease caused by malassezia furfur?
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pityiasis versicolor
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Parvovirus B19 in pregnant women?
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Can infect fetus
increased risk of death in seronegative mothers - does same thing in fetus as it does in kids and adults -- goes after RBC precursor cells Infection in seropositive mothers usually has no adverse effects on fetus |
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what is an exanthems?
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disease that produce skin eruptions
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What is tinea nigra?
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superficial mycoses
caused by hortaea werneckii - dimorphic fungi with brown-black pigmentation Brown or black macular lesions - often on palms or soles, but can occur elsewhere - enlarge by peripheral extension |
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What viral diseases can looks like classic measles?
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German measles
Fifth disease after dissemination Roseloa |
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What time period is associated with classic measles?
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1960s-ish
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What are some bacterial diseases that look like classic measles?
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Rocky Mtn Spotted Fever
Scarlet Fever Typhus |
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What is the one truly unique symptoms of classic measles?
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Koplik's Spots on buccal mucosa
1-2 mm blue-white spots on bright red background Easily overlooked and disappear soon after onset of rash |
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What is the causative agent of classic measles?
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rubeola virus
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how is measles transmitted?
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air via droplet infection
one of the most contagious diseases known early symptoms like influenza or heavy cold (no reason to suspect measles) |
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How does classic measles progress? What are the skin lesions from?
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virus migrates from upper resp to lymph system to bloodstream
Viremia may lead to infection of conjuctiva, remaining part of resp tract, urinary tract Maculopapular skin rash caused by immune T cells target against virus infected endothelial cells in small blood vessels under surface of skin |
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Classic measles prognosis?
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usually self limiting
dangerous complications are rare - viral pneumonia - others |
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What two organisms cause >90% of cellulitis?
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Staph aureus
Strep pyogenes |
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How do staph and strep forms of cellulitis differ?
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Staph: spreads out directly from central localized infection AT POINT OF ENTRY (signified by an absess or something like that)
Strep: more rapidly spreading and diffuse; symptoms often do not surround or extend directly from original point of entry |
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What other agents cause cellulitis?
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>90% of infections are endogenous (caused by normal skin flora - strep and staph)
haemophilus influenzae type b --> cellulitis in children wide variety of exogenous bacteria |
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What is oncycomucosis?
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Tinea uinguim - ringworm of the toes
fungi cause this Most caused by dermatophyte funi |
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80% of fungal nail infections caused by?
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trichophyton rubrum
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Who is most likely to get trichophyton?
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40-60 yrs old
rarely occurs prior to puberty men affected more than women more frequent in those with diabetes, peripheral vascular disease, or any condition that supresses immune system |
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What are some predisposing factors to nail infection by trichophyton?
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wearing occlusive footwear
physical exercise follwoed by communal showering incomplete drying of feet after bathing Onchyomycosis frequently associated with athlete's foot |
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What do you use to treat a fungal nail infection?
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Systemic anti-fungal
terbinafine itraconazole alternative first line |
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what are the only skin lesions likely to be confused with impetigo
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herpetic lesions (HSV1 and VZV)
BUT: - oral herpes lesions usually appear as more discrete - chicken pox wide spread over body |
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Which two microbes are associated with non-bullous impetigo?
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Staph aureus
Strep pyogenes |
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what is tinea corpis?
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ringworm of the body
nothing to do with worms actually Lesion characterisitics: Expanding annular appeaance, inflamed, raised and well demarcated margins |
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What causes tinea corpis?
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dermatophyte fungi
Trichophyton is most likely |
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How can you get infected with tinea corpis?
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direct contact with others who are infected
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What is suggested by the combo of nausea, vomiting, and persistent RUQ pain, especially with a positive Murphy's sign?
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Acute cholecystitis
Fever is consistent with this dx Also could be hep |
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Murphy's Sign
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Sign they use to dx cholecystitis
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What is acalculous cholecystitis?
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cases of cholecystitis that cannot be attributed to gallstones
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What factors most frequently predispose a person to acalculous cholecystitis?
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Serious trauma or burns
Postpartum period after prolonged labor Post operative period following orthopedic or other non-biliary major surgery Vasculitis, carcinmona, diabetes |
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What infectious agents can cause acalculous cholecystitis
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Usually in AIDS pts:
Cytomegalovirus (CMV) Cryptosporidium |
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CMV - family, characterisitcs
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Herpesviridae
Enveloped DS DNA |
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Pathogenesis - CMV
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Replicated in various human cells
establishes latent infections in mononuclear lymphocytes, stromal cells of bone marrow, etc. Cell mediated immunity essential for resolving active infections and controlling latent infections Virus can be reactivated |
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How is CMV transmitted
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Congenital
Oral Sexual Tissue/organ transplantation Leading cause of congential disease in US |
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What is suggested by the combo of nausea, vomiting, and persistent RUQ pain, especially with a positive Murphy's sign?
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Acute cholecystitis
Fever is consistent with this dx Also could be hep |
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What is the leading cause of congenital disease in US?
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CMV
Small size at birth, thrombocytopenia, jaundice, rash, heptasplenomegaly, retardation |
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Murphy's Sign
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Sign they use to dx cholecystitis
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What happens in immunocompetent adults who get CMV?
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it remains latent and the person remains asymptommatic.
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What is acalculous cholecystitis?
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cases of cholecystitis that cannot be attributed to gallstones
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What factors most frequently predispose a person to acalculous cholecystitis?
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Serious trauma or burns
Postpartum period after prolonged labor Post operative period following orthopedic or other non-biliary major surgery Vasculitis, carcinmona, diabetes |
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What infectious agents can cause acalculous cholecystitis
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Usually in AIDS pts:
Cytomegalovirus (CMV) Cryptosporidium |
