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75 Cards in this Set
- Front
- Back
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of the A/B toxin:
1. what is the function of the A subunit? 2. what is the function of the B subunit? |
1. A subunit has toxin activity
2. B subunit is required for binding and translocation |
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give two examples of toxins that have the A/B toxin subunits.
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1. cholera toxin
2. pertussis toxin |
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which two bacteria are the "most important" in regards to their superantigen production?
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1. Staph aureus
2. Strep pyogenes |
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superantigens cause?
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polyclonal activation of T cells leading to the release of proinflammatory cytokines
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describe toxin production by Bacillus anthracis
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- has a protective antigen
- this antigen is cleaved by the host protease - pore is formed - Lethal factor + PA = lethal toxin - Edema factor + PA = edema toxin upon cellular entry PA binds to either lethal factor or edema factor |
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the cholera toxin targets which protein?
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G proteins
(alters ion transport) |
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the pertussis toxin targets which protein?
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G protein
results in an increase of cAMP |
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some toxins result in cell cycle arrest of the host cell. In what phase are these cells arrested in?
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G2
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what is the most potent toxin known?
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Botulinum toxin
(from Clostridium botulinum) |
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both the botulinum and the tetanus toxin alter what?
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vesicular trafficking in the nervous system
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via what mechanism do many bacteria induce apoptosis?
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via activation of the caspases
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give two examples of bacteria that induce apoptosis
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1. shigella
2. salmonella *many bacteria induce apoptosis* |
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give an example of a bacteria that BLOCKS apoptosis
Why would it want to do that? |
Rickettsia rickettsii (RMSF)
*it is an obligate intracellular parasite |
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type III secretion is characterized by?
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secretion of proteins across 3 membranes
(bacterial cytosol to eukaryotic cytosol) |
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which type of secretion do conjugal DNA transfer systems use?
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Type IV secretion
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besides DNA, what else is transported via type IV secretion? (2)
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1. nucleoprotein complexes
2. multisubunit toxins |
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acute lymphadenitis is most often caused by?
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local trapping of microbes
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diffuse lymphadenitis is most often caused by? (3)
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viral infection
bacteremia diseases caused by exotoxins |
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which type of infections would cause acute suppurative lymphadenitis?
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pyogenic (pus-forming) infections
(these are characterized by acute inflammatory neutrophilic rxn and are caused by drainage of bacteria from the infected site) |
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which two bacteria are known to cause acute suppurative lymphadenitis?
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staph aureus
group A strep (above are referred to as the pyogenic cocci) |
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which organism, responsible for cat-scratch disease, causes a regional self limiting lymphadenitis?
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Bartonella henslae
(gram negative rod) |
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what happens in a Bartonella henslae infection?
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- starts as a small papule 3-10 days after infection
- organism spreads to regional lymph nodes *host usually limits the infection here |
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which organism causes "uncontrolled cat scratch disease"
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Bacillary angiomatosis
bacteria multiply freely and are disseminated into the bloodstream *sepsis occurs * get skin erruptions resembling Kaposi's sarcoma |
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which one of 3 antibiotics would we use to treat cat scratch disease?
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erythromycin
doxyxycline azithromycin |
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what is a scrofula?
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TB that has caused cervical lymphadenitis
*caused by spread from the lung *firm red painless mass on SCM or in supraclavicular area |
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inguinal lymphadenopathy is caused by what three things?
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1. STDs
2. Plague 3. Tularemia |
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lymphadenitis caused by Haemophilus decreyi (an STD) is known as?
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a chancroid
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organism causing the plague?
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Yersinia pestis
(small gram - rod) |
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are most Yersinia infections intra or extra cellular?
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extracellular
(although it is a facultatively intracellular pathogen) |
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in current times, where in the US are most Yersinia infections seen?
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southwest
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Yersinia pestis has a bipolar staining. what does it look like in the blood?
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safety pin appearance
extracellular |
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how is the Bubonic plague transmitted?
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flea bites
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in Bubonic plague:
describe what happens from the flea bite up until death |
- infection spreads from flea bites to regional lymph nodes
- inflammed lymph nodes form buboes (painful) - bacteria spreads from lymph nodes to lung, liver, spleen - death from septic shock |
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how does septicemic plague differ from bubonic plague?
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disease progression occurs without the formation of buboes
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what is the difference between pneumonic plague and the other two types of plague?
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direct inoculation into the lung via aerosols
- almost always fatal - human to human transmission |
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what aspect of Yersinia pestis is used as a diagnostic tool?
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F1 capsule
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function of F1 capsule?
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prevents phagocytosis
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function of Pla (plasminogen activator) protease in Yersinia pestis?
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helps in dissemination from peripheral tissue
also cleaves C3 |
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treatment for Yersinia pestis?
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1. supportive care
2. antibiotics (streptomycin, doxycycline, quinolones) |
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what is a major "attribute" of anthrax that contributes to its virulence?
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it can form endospores
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what are the three forms of an anthrax infection?
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In order of severity:
1. Cutaneous 2. Gastrointestinal 3. Inhalational |
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treatment for anthrax?
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penicillin G (sometimes with an aminoglycoside)
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prophylactic treatment for anthrax?
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cipro
must take for over 2 months because of endospores |
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describe the pathogenesis of inhalational anthrax up until death
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- inhaled endospores germinate in alveolar macrophages
- bacteria replicate in regional lymph nodes - progresses to mediastinal hemorrhage |
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which organism causes Tularemia?
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Francisella tularensis
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what is notable about F. tularensis?
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probably the most infectious bacteria known
(infectious dose as low as 10-50 organisms) |
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is F. tularensis intra or extra cellular?
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F. tularensis is a facultative intracellular parasite
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treatment for Tularemia?
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streptomycin or other aminoglycoside
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prophylaxis for Tularemia?
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doxycycline
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what is notable about the clinical course of Leptospirosis?
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Biphasic course (typical of spirochetes)
1. sepsis 2. menigneal inflammation, rash, uveitis |
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relapsing fever is most often caused by which microorganism?
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Borrelia recurrentis
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B. recurrentis is transmitted by?
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lice
(when lice are crushed they enter through mucous membranes or broken skin) |
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describe the relapsing fever seen with Borrelia recurrentis infection
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first fever lasts 3-6 days
fever recurs in 7-10 day intervals (fever is present when spirochetes are in blood, when there is no fever they are in organs) |
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what is the leading cause of bacteremia and meningitis in neonates?
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group B Strep
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most common symptom of Group B Strep infection in the neonate?
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meningitis
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what are the two major types of Rickettsial infections?
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1. Typhus group
2. Spotted Fever group |
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Is rickettsia an intra or extra cellular parasite?
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obligate intracellular parasites
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where do Rickettsia multiply?
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in vascular endothelium - this causes pathology in skin, CNS, liver
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describe the pathogenesis of Rocky Mountain Spotted Fever
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Rickettsia rickettsii replicate at the site of the tick bite
-spread to blood and vascular endothelium of lungs, spleen, skin, brain - 1 wk incubation period - fever, headache, myalgia, respiratory symptoms - maculopapular rash - splenomegaly and sepsis occur |
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what is the mortality rate of Typhus in epidemic areas?
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40%
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what is the animal reservoir of endemic Typhus?
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rodent
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Bartonella quintana causes?
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trench fever
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what is characteristic of trench fever?
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intense tibial pain
fever recurs every 5 days with decreasing severity |
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Q fever is caused by?
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Coxiella burnetti
(coccobacillus) |
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is coxiella an intra or extra cellular parasite?
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obligate intracellular parasite
(infects primarily monocytes and macrophages) |
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how is Q fever diagnosed?
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serology
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Erlichia is transmitted by?
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tick bites
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HHV-6 causes? and has a possible association with ?
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causes exanthum subitum (rash)
possible association with MS |
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HTLV-1 is associated with what diseases? (2)
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1. Adult T-cell leukemia/lymphoma
2. HTLV associated myelopathy/tropical spastic paraparesis |
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HTLV-2 is associated with? (1)
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HTLV-associated myelopathy/tropical spastic paraparesis
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What is the causative agent of infectious mononucleosis?
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EBV
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EBV is also assiciated with what 2 neoplasms?
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1. Burkitt's lymphoma
2. nasopharyngeal carcinoma |
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where does the latent EBV infection "hang out"
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B lymphocytes
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describe the virion and capsid seen in EBV
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enveloped virion
icosahedral capsid |
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structurally, what makes EBV different from other herpes viruses?
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one predominant glycoprotien on cell surface
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