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333 Cards in this Set
- Front
- Back
Describe Mycobacteria
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strict aerobes, rod-shaped bacteria, Gram +, acid-fast, very resistant to dessication
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What are the two forms of Mycobacteria causing the majority illness in humans?
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M. tuberculosis
M. leprae |
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What is immediately attached to the peptidoglycan matrix of the Mycobacterial cell wall and what is its function?
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An arabanogalactan (polysaccharide) layer that anchors the long chain mycolic acids
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60% of the mycobacterial cell wall is compased largely of what molecules?
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Mycolic acids (complex lipid-containing molecules)
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What is the hallmark of mycobacteria?
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Acid-fastness (once stained, they resist de-staining in acidified alcohol
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What morphological feature will virulent strains of M. tuberculosis show on culture?
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cord factor/cording morphology
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Which comorbidities are closely associated with TB?
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diabetes, HIV/AIDS, silicosis, malnurished, elderly, poor, smokers, chronic alcoholics
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What is the route of transmission for TB infection?
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inhalation of airborne droplet nuclei; human to human spread (no animal reservoirs)
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Which immunological mechanism controls TB infections?
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cell-mediated immunity
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Describe the mechanism by which cell mediated immunity controls/kills TB infection
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Antigen-specific CD4+ T-helper cells activate macrophages; activated macrophages are able to kill intracellular bacteria (or slow their growth)
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Which two factors produced by macrophages is necessary for the control of TB?
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IFN-g and TNF-a
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What is contained in the "tubercle" of tuberculosis?
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granulomas consisting of epithelioid cells, giant cells, and lymphocytes
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What is the charcteristic necrosis of the granulomas in TB?
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Caseous
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What constitutes a Ghon complex?
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a TB lesion in the lung and the draining bronchial lymph node
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What is the evidence on chest X-ray of a primary infection?
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fibrotic or calcified healed lesions
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T/F: TB is able to live in granulomas for long periods of time
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True; this is the cause reactivation of latent TB
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Wher eis the most common site of TB reactivation?
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Apex of the lung (most highly oxygenated)
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Where in the lung do TB bacteria multiply?
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in resident alveolar macrophages
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Virulence of the TB organism is directly related to what feature?
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its ability to grow in macrophages and survive for long periods even in activated macrophages
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What is the general mechanism by which TB bacteria are able to live in activated macrophages?
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TB interferes with membrane controlled trafficking and arrests the phagosome at a stage when no harm can be done to the pathogen and nutrients come in unimpeded
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What are the three players in TB that arrest the maturation of the host phagosome?
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PIM, ManLAM, SapM
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What is the function of PIM?
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Stimulates the fusion between phagosomes and early endosomes -> constant nutrient supply to the phagosomal compartment
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What is the function of ManLAM?
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inibits the maturation of phagosome
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What is the function of SapM?
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cleaves the late endosomal vesicular marker (PI3P) in the phagosome membrane -> prevents fusion of phagosome to lysosome
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Cathelicidin requires what substance in order to be expressed in macrophages?
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Vitamin D
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What is the function of cathelicidin?
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found in macrophages and is responsible for killing intracellular M. tuberculosis in human macrophages
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What is the primary goal of TB control?
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to identify active infectious cases and treat them in order to save the individual and stop transmission
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What are the symptoms of pulmonary TB?
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cough, chest pain, hemoptysis
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What are the symptoms of systemic TB?
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fever, chills, night sweats, appetite loss, weight loss, fatigue
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T/F: Mantoux TB skin test is the primary method for diagnosing TB.
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False; it is used to test for infection but not dx because 20% of TB cases will have a negative skin test
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What test has been approved for the diagnosis of LATENT tuberculosis infection?
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Interferon gamma release assays (IGRAs)
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What are the first line agents in the tx of TB?
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Isoniazid
Rifampin Pyrazinamide Ethambutol |
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Which two TB drugs are continued through the entire course of TB treatment?
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Rifampin and Isoniazid
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How long is the typical treatment regimen for TB?
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6 months
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What is the mechanism by which M. tuberculosis acquires drug resistance?
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genetic mutation (NOT by acquiring foreign DNA that encodes resistance)
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What is the immunological basis for the mechanism of the Mantoux skin test?
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cell-mediated delayed hypersensitivity reaction to a preparation of tubercular protein
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What does PPD stand for?
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purified protein derivative
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What are the criteria for positive results in Low, Intermediate and High risk pts?
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Low: >15 mm
Intermediate: > 10 High: > 5 |
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What are the three main advantages to an interferon gamma release assay over the TB skin test?
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1. less cross-reactivity from vaccination with BCG and non-TB mycobacteria
2. less susceptible to reader variability 3. requires only one pt visit |
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Where is TB most likely to be located in HIV patients?
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extrapulmonary: lymph node, bone marrow, GI and CNS
often fatal |
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How is Nontuberculosis bacteria acquired
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Environmental sources (soil and water)
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What is the most common NTM causing lung disease?
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M. avium-intracellulare
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How long are NTM infections treated?
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At least 18 months - resistant to usual anti TB drugs
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In children, what is the most common syndrome associated with Mycobacterium avium complex (MAC)?
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cervical lymphadenitis
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What is one of the only ways to distinguish the pulmonary syndrome from M. kansasii from that of TB?
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Lung cavities in M. kansasii are thin walled
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What is the third most common mycobacterial disease after TB and leprosy?
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M. ulcerans (Buruli ulcer)
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What produces the typical ulcer of M. ulcerans?
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a toxin. mycolactone, inducing tissue necrosis
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Why do M. leprae tend to affect skin and appendages?
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grows best at low temperatures
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What is the route of transmission for M. leprae?
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person to person but very low transmission
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What are the two forms of leprosy?
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Lepromatous and tuberculoid
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What is the MOA of the Lepromatous leprocy?
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it actively suppresses the hosts cell mediated response to lepromin; malignant
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What are the symptoms lepromatous leprosy?
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loss of eyebrows, thickened/enlarges nares, ears, cheeks, loss of local sensation
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What is the prognosis for tuberculoid leprosy?
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better than lepromatous, most cases are self-limiting
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What are the signs of tuberculoid leprosy?
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blotchy red lesions on the face, trunk, and extremities with loss of local sensation (more sensory nerve damage than lepromatous)
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99% of the bacteria that inhabit the GI tract are aerobes or anaerobes?
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Anaerobes
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The most common aerobic bacteria of the GI tract in adults are of what family of bacteria?
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Enterobacteriaceae (Salmonella, Shigella, Yersinia), non-dextrose fermenting Gram-negative rods, and non-hemolytic and alpha-hemolytic strep
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Who ar ethe primary actors in upper respiratory infections?
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viral agents and GAS
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What are two of the most common normal flora organisms?
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N. subflava
Staph epidermidis |
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What test is used to determin species designation for Staph?
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Coagulase test: aureus is coag positive and epidermidis is negative
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Which genus of Strep is sensitive to Taxo-A discs?
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S. pyogenes
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Which test is used to differentiate S. pneumoniae from viridans?
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Optochin
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Alpha-hemolytic organisms appear as what color on a Blood Agar Plate?
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Green
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Beta-hemolytic organisms appear as what color on a Blood Agar Plate?
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clear
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Satelite colonies of what organism appear on a Blood Agar Plate in the vicinity of Staph?
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H. influenzae
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Why do satelite colonies of H. influenza appear in the vicinity of Staph?
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Staph (and some other organisms) produce the necessary NAD and hematin fromt he lysed RBCs
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Why is Chlamydia an obligate intracellular pathogen?
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Because it cannot synthesize ATP or NADP
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Describe Chlamydia:
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small, round/oval, gram negative obligate intracellular pathogen with a biphasic life cycle
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Describe the binary life cycle of Chlamydia:
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Elementary body infects, reticulate bodies multiply and re-organize into EBs the cell, cell lysis = EB release
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What is the main cause of preventable blindness worldwide?
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Trachoma
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What percentage of women with Chlamydia are asymptomatic? Men?
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75% of women and 50% of men
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Your patient with symptoms of a urogenital tract infection has a gram stain showing diplococci inside PMNs. What is the diagnosis?
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Gonorrhea
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What are the symptoms of chlamydial infection in men? Women?
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Men: dysuria, discharge; Women: mucopurulent urethritis, cervicitis or salpingitis
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What population in the U.S. has recently seen an increase in lymphogranulosum venereum?
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homosexual men
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What clinical course does lymphogranulosum venereum follow?
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ulcer on genitals and inguinal lymph node swelling, node becomes a draining sinus after 2-6 weeks
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What clinical syndromes are associated with chlamydia pneumoniae?
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atypical pneumonia and sinusitis
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Describe n. gonorrhoeae:
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gram negative diplococcus, kidney shaped individual coccus
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What clinical syndromes are associated with a disseminated gonococcal infection?
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septic arthritis, dermatitis-arthritis-tenosynovitis, RARELY endocarditis and meningitis
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Why are newborns given silver nitrate drops at birth?
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to prevent gonococcal or chlamydial conjuctivitis
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What laboratory techniques are used to determine the presence of pathogenic N. gonorrhoeae?
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Grows on Thayer-Martin and Chocolate (but NOT blood) Agar plate in CO2, positive oxidase test, NAAT
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Why is it important to do more than one test for gonorrhea lab diagnosis in children?
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Legal requirement to present evidence of sexual abuse
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What subspecies of Treponema are associated with syphilis?
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pallidum
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Describe treponema:
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spiral, motile bacilli with endoflagella corkscrew appearance, gram -ve, hard to see on light microscopy (need darkfield)
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What syphilis test may not be accurate in the first two weeks?
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Direct fluorescence antibody, because it may take the body 2 weeks to make Ab
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What virulence factors does N. gonorrhoeae have?
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pili, Opa, LOS, IgA protease
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What is meant by antigenic vs. phase variation in N. gonorrheae?
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there are hundreds of different types of pili (antigenic variation) and the bacteria can turn expression on or off (phase variation)
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What is the recommended treatment for a gonorrheal infection?
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3rd generation cephalosporin or a quinolone
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What is the recommended treatment for a Chlamydial infection?
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azithromycin (macrolide) or tetracycline (doxy)
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After exposure to syphilis, how long might it be before a patient notices a lesion? What will the lesion likely be?
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3 week incubation period, local ulceration on genetalia (chancre)
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What percentage of patients spontaneously heal after primary syphilis?
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25
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What are some of the common symptoms of secondary syphilis?
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maculopapular rash, lymphadenopathy, chancre may still be present
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How long might a patient experience latent, aysmptomatic syphilis before tertiary symptoms appear?
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3 to 30 yrs
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What is a gumma? Where on the body can they present? What stage of syphilis are they associated with?
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soft, granulomatous growth ass'd with tertiary syphilis, found on the liver, brain, heart, skin, bone, testis
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What might happen to a fetus if the mother is infected but untreated for syphilis?
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stillbirth, teeth/facial deformities or developmental abnormalities if born
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Why might it be difficult to defeinitely diagnose the cause of tertiary syphilis?
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organisms are rarely visualized in late lesions, many symtptoms are related to immune response
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What are nontreponemal antigen tests? What are some examples?
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Ab to syphilis cross-react, but test is not specific for anti-TP Ab. VDRL or RPR
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What is the recommended treatment for syphilis? How do you treat neurosyphilis in a pt with an allergy?
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PCN (very little resistance if any has developed); desensitize to PCN in neuro (i.e. do NOT use another medication)
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What happens in tabes dorsalis?
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Nerve fibers are slowly demyelinated and degenerated
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Besides gummas and neurosyphilis, what other lesions can appear in tertiary syphilis?
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Cardiovascular - aortic lesion and heart failure
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What behaviors are associated with syphilis outbreaks?
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illicit drug use, exchange of money/drugs for sex
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How long will a patient remain contagious during early syphilis?
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3-5 yrs
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How is leptospirosis spread?
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contaminated water or food
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How does water become a reservoir for leptospirosis?
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infected animals have kidney infection, shed the organism in the urine
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What might be the clinical presentation of a patient infected with leptospirosis?
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fever, jaundice, hemmorhage and N retention (due to infection/necrosis of kidney or liver), aseptic meningitis after IgM titer rises
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What differences exist between n. meningitidis and n. gonorrhoeae?
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Meningitidis has a polysaccharide capsule and utilizes maltose; n. gonorrhoeae does not do either
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A 22yof presents with dysuria, white vaginal discharge and suprapubic pain x2d. What is your dDx?
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cervicitis, vaginitis, urethritis, cystitis
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What symptoms might help you distinguish between a genital tract vs. a urinary tract infection?
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genital tract: more prominent discharge and pain with intercouse, but sxs do overlap
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How can you distinguish between an upper and lower urinary tract infection?
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Lower: dysuria, increased frequency and urgency; upper: fever, casts, CVA/back pain
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What findings diagnose a UTI?
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urine culture (might not be done on uncomplicated pt), microscopic analysis (pos leukocyte esterase and nitrates on urine) and clinical syndrome
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What defenses does the body have to prevent UTIs?
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urine chemistry (low pH, high osmolarity), Ab, nl flora and voiding
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What organisms cause UTIs in an uncomplicated pt? In a hospitalized or more complicated pt?
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e. coli (#1), Proteus, Klebsiella; complicated pt: s. aureus,pseudomonas, fungi
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What things might increase the risk of contracting a UTI?
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anatomic variation (decreased clearance of pathogens) neurogenic bladder, obstruction of urinary flow (BPH, stones, strictures) and sexual activity (honeymoon cystitis)
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What organisms commonly cause genital ulcers? How might you distinguish between them?
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HSV1 or 2: painful and multiple lesions, tender lymphadenopathy; syphilis: non-painful single lesion, non-tender lymphadenopathy; haemophilus ducreyi (chancroid):draining lymph, ragged edged lesion + exudate
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What is the Jarisch-Herxheimer reaction?
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following treatment of syphilis, many bacterial cells die and release toxin --> fever, pain, headaches and palpitations 1-2 d after antibiotics started
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What is meant by antigentic drift and antignenic shift in influenza?
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drift: multiple small mutations; shift: reassortment of genome segments --> majoy simultaneous change in epitope of the hemagglutinin protein
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What is the role of hemagglutinin in orthomyxovirus infection? How is it activated?
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It binds the N-acetyl neuraminic acid receptor on glycoproteins; activated by proteolytic cleavage of HA0 to HA1 and HA2 by viral furin or host trypsin
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Who is at high risk for contracting influenza?
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elderly pts, chronic heart and lung dz pts, pregnant women, nursing home patrons, diabetes.metabolic disorder pts
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What are some of the complications of influenza?
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primary or secondary pneumonia, encephalitis, pericarditis, rhabdo, Reye's, Guillian-Barre
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What is the role of neuraminidase in orthomyxovirus infection? What drugs block this EZ's activity?
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destroys the receptor on host cell, plays a role in viral penetration and release from infected cell; zanamivir and oseltamivir inhibits
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What is the difference in antibody production mediated by influenza vaccine vs. infection?
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Vaccine --> secretory IgA in respiratory epithelium; infection --> IgM and IgG (no prevention of infection)
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Where do virions preferentially bud with influenza infection?
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from the apical side of respiratory epithelium
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What virulence factor was enhanced in the H5N1 strain of orthomyxovirus?
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highly cleavable HA0 (longer sequence of basic amino acids at cleavage site = higher virulence)
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What differences exist between H5N1 spread in humans vs. birds?
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systemic spread in birds, poor human-to-human transmission
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About how effective is the flu vaccine each year?
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70%
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What does Matriz protein 2 do to protect HA2 during influenza?
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M2 is an ion pump that raises pH, prevents conformational change in HA2 which would otherwise inactivate it with endosomal induced acidity; also works on the ay out with the pH of secretory vessicles
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What flu drug targets the M2 protein?
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amantadine and rimantadine
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What happened in the 1918 epidemic when the HA and NA proteins mutated and grew better in human hosts?
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healthy young adults were killed
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Why can't rhinoviruses cause enteric infection?
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inactiavated by low pH and cannot replicate at 37C
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How do rhinoviruses enter host cells?
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ICAM-1 and LDL receptor
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How does most transmission of rhinovirus occur?
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contaminated hands (rather than droplets)
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What important viruses are members of the family paramyxoviridae?
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parainfluenza, morbillivirius(measles), mumps, and pneumovirus(RSV)
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What virus of the paramyxo family causes cytoplasmic and late nuclear inclusions? What are these inclusions?
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measles(morbillivirus); helical nucleocapsids, viral RNA and protein
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What is the significance of the HN and F proteins in paramyxoviral infection?
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HN binds the host cell receptor (neuraminic acid) and F glycoprotein (following proteolytic cleavage) allows fusion of the viral envelope with cell membrane
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What clinical syndromes are associated with parainfluenza infection?
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upper respiratory tract infection (+otitis media in 15-30% of cases), bronchiolitis and pneumonia in infants, croup
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What is the most important cause of lower respiratory tract infection in infants and young children?
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RSV (Who knows what important means)
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What percentage of children have recurrent wheezing following RSV infection?
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40-50%
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How is RSV spread?
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contaminated hands and large respiratory droplets
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What accounts for the increased severity of symptoms in an infant with RSV?
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inflammation and edema in narrow airways, differences in Cell Mediated Immunity
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What drug can be used to treat RSV infection? What can be used to prevent infection for infants at high risk of RSV death?
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Ribavirn; IV anti-RSV monoclonal Ab
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What clinical syndrome is associated with metapneumovirus?
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Community acquired interstitial pneumonia in adults
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What percentage of common colds are caused by coronavirus? What complications may occur?
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15-30%; otitis media and sinusitis
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What was the source of SARS-CoV? How many amino mutations are needed to allow efficient human-to-human spread?
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Bats in southeast asia; only 2 amino acids confer specificity for receptor (which is ACE2)
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What is the significance of polyomavirus infection? What strains have been detected in the respiratory tract?
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they have oncogenic potential; WU and KI (role unknown)
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What is primary atypical pneumonia?
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acute infectious pulmonary disease caused by m. pneumoniae, Rickettsia, Chlamydia and viruses (adeno and parainfluenza)
|
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What makes primary atypical pneumonia atypical?
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patchy lymphocytic infiltrate, peribronchial (not alveolar) pathology, insidious onset, constitutional sxs predominate over respiratory complaints
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Describe mycoplasma pneumoniae.
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small, pleomorphic, no cell wall, small, slow-growing colonies
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What are the mechanisms by which mycoplasma pneumoniae causes cell injury?
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ciliostasis, superantigen --> cytokine mediated damage, CARDS toxin
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How is mycoplasma pneumoniae transmitted? How does it maintain a tight association with host cells?
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respiratory secretions, attachment to ciliated epithelium mediated by attachment protein P1 on host neuraminic acid
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Describe legionella pneumophila.
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motile, pleomorphic gram neg. rod, has beta-lactamase, oxidase and catalase
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What two clinical syndromes are associated with legionella pneumophila?
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pontiac fever (self-limited febrile illnes) and legionnaire's disease
|
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What are the symptoms of legionnaire's disease?
|
fever, malaise, chills, and cough due to an acute pneumonia with interstitial inflammation
|
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How does legionella pneumophila evade endosome-lysosome fusion?
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endosomes become associated with endoplasmic reticulum - forms ribosome-studded phagosomes
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How is legionella pneumophila spread?
|
contaminated water via aerosol inhalation
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What tests are available to diagnose legionella pneumophila?
|
silver stain on intracellular culture, inmmunofluorescence, !Urine Antigen!
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What role does the E6 protein play in HPV infection?
|
binds p53 and marks it for degradation, inhibiting cell apoptosis
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What role does the E7 protein play in HPV infection?
|
binds RB, releasing EF2 and promoting cell growth
|
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What layer of epithelium does HPV initially infect? From what layer is it released?
|
Basal; surface
|
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What happens when active HPV infection persists for a long period (1 yr)?
|
viral DNA is integrated into host chromosome; E2 protein (which suppresses E6 and E7) is disrupted with integration
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What strains of HPV are associated with the majority of cervical cancers in the U.S.? Which are associated with venereal warts?
|
High risk = 16, 18; low risk = 6, 11 (8)
|
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How does Gardasil protect against HPV infection?
|
L1 capsid proteins are recominantly grown in eukaryotic cell, (VPLs) and elicit Ig Ab
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What virus is associated with renal graft failure in kindney transplant patients and hemorrhagic cystitis in bone marrow transplant patients?
|
BKV
|
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What virus is associated with PML in AIDS patients and in MS patients treated with Natalizumab?
|
JCV
|
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What percentage of people are infected with BKV and JCV?
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80%
|
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What is the second leading worldwide cause of cancer death in women?
|
HPV related cervial cancer
|
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What are the role of L1 and L2 proteins in HPV infection?
|
capsid proteins
|
|
Describe rabies virus
|
Rhabdovirus: bullet-shaped enveloped viron, non-segmented, negative single strand RNA
|
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How many serotypes of rabies virus exist?
|
One
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How long is the incubation of rabies virus?
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weeks to months
|
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Where does the rabies virus replicate?
|
in peripheral nerves at the site of the wound
|
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Once rabies virus is in the brain where does it spread to next?
|
Parotid/salivary glands
|
|
What test is used to dx rabies in a human and what are you looking for?
|
HnE stain looking for Negri bodies - eosinophilic inclusion bodies of virus in cytoplasm of infective cells
|
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What are th first two things you should do in a pt in whom you suspect rabies?
|
1. Wash the wound with soap and water (breaks down envelope
2. Give both PASSIVE and ACTIVE immunization |
|
In what vector is the rabies vaccine produced?
|
Human diploid cells (HDRV)
|
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What are the leading cause of rabies in US? What about other parts of the world?
|
US: bats
Worldwide: dogs |
|
How do humans get infeted with Hantaan virus?
|
inhalation of rodent urine or feces
|
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How does human infection of Hantaan virus manifest itself?
|
hemorrhagic fever, fever with renal syndrome (HFRS) or pulmonary syndrome
|
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When the patient presents with Hantaan virus, how long doe s the pt have before death?
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About 3 days - quick dx and treatment is key
cytokine explosion |
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What tx is used to get pt through hantaan virus crisis period?
|
Intubation
Heart-lung bypass (24 hrs) |
|
What family of virus is Monkeypox?
|
Orthopoxvirus
|
|
What animals serve as the reservoir for monkeypox?
|
rodents
|
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Is there a vaccine to protect against monkeypox?
|
Yes, the smallpox vaccine will protect against smallpox, but no one is vaccinated for small pox anymore = reemergence
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What are the signs of monkeypox?
|
looks like a milder version of smallpox ; also monkepox will cause lymph nodes to swell
|
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What is the treatment for monkeypox?
|
there is no specific tx for monkeypox; CDC guidelines for who should get vaccinated with smallpox
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Where do anaerobes like to colonize?
|
sebaceous glands of the skin, gingival crevices of the gums, lymphoid tissue of the throat, lumen of GI
|
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Where in the body do we have the most anaerobe flora?
|
Colon
|
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What special technique must be used to cultivate anaerobes?
|
GasPak jars and anaerobe glove boxes
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What factos of the aerobic environment are particularly toxic to anaerobes?
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the production of hydrogen peroxide and superoxide
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What enzymes do strict anaerobes lack that make oxygen toxic?
|
catalase and superoxide dismutase
|
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Anaerobic organisms that are part of the normal flora cause disease through what mechanism?
|
Autoinfection
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Which anaerobic normal flora are the frequent cause of infection?
|
Bacteroides fragilis
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T/F: anaerobes typically associated with dz are somewhat aerotolerant.
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True: some may even produce catalase and SOD (vir factors)
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anaerobic infections tend to be polymicrobial or mixed infections. In the early acute stage of the infection, which organisms predominate?
|
aerobes and facultative organisms
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How are the later stages of mixed infections (where anaerobes predominate) characterized?
|
chronic abscess formation
|
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What is the function of abscess formation in an anaerobic infection?
|
maintains low oxygen tension, providing protection from host defenses and antimicrobial agents
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What are the sx of the acute stage in an mixed infection?
|
febrile, hypotensive
|
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Which organism is associated with > 80% of intra-abdominal infections?
|
Bacteriodes fragilis
|
|
Describe B. fragilis
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aerotolerant, anaerobic, gram (-) rod, pleomorphic and irregular stain
Catalase + |
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B. fragilis is resistant to which antimicrobials?
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kanamycin, vancomycin, colistin
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What are the virulence factors of B. fragilis?
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1.Fimbrae (pili) to adhere to epithelial cells
2. Phospholipase A/C, collagenase - tissue damage 3. SOD and catalse 4. Polysaccharide capsule (MOST IMPORTANT) - helps contribute to formation of abcess (also taget for humoral/cellular immunity) |
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Which part of the host immune system is required for the protection against abscess formation?
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T-cell immunity
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Clostridium, gram + anaerobes, are unique in that they form what feature?
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spores
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What is the advantage of spore formation in Clostridium?
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They can stay alive for long periods of time even in aerobic conditions. Spore not affected by oxygen
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Where is C. tetani found?
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In the environment; enters through wounds
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How doe sthe C. tetani toxin reach the CNS?
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retrograde axonal transport along peripheral motor neurons
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What is the pathophys of C. tetani?
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blocks the release of inhibitory neurotransmitters (GABA, glycine) causing constant muscle contraciton
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What are the signs/sx of tetanus?
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trismus (lockjaw), neck stiffness, difficulty swallowing, rigidity of ab and back muscles, fever
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What is the tx for tetanus?
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1. supportive therapy
2. Debridement of wound 3. antimicrobials |
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T/F: antimicrobials and passive immunization can eliminate tetanus from a pt
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False: they can neutralize free toxin, but once toxin is bound to nerve endings, it cannot be neutralized with antibody
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Why don't you become immune to tetanus after infection?
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Because the amount it takes to kill you is so small, you cannot launch an effective immune response in enough time
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Where is C. botulinum found?
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Contaminated food; home canning
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What is the pathophys of C. botulinum?
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toxin blocks the release of the neurotransmitter ACh at the neuromuscular junctions in periphery = flacid paralysis
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What are the three types of botulism?
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1. Classic/food bourne
2. Infant botulism 3. Wound botulism |
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Which unique form of botulinum toxicity is being developed for bioterrorism?
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Inhalation botulism
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Which Clostridium species is a frequent cause of wound infection?
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C. perfringens
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What won't be seen on microscopy in C. perfringens?
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PMNs: alpha toxin (PLP-C) effectively destroys PMNs as they arrive to the site
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What is an oportunisitic infection?
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an infection that occurs in a compromised host by an organism that would not normally infect a healthy host
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What is a nosocomial infection?
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infections that occur in an institutional setting
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What is an iatrogenic infection?
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infection resulting fromt he activity of a physician or other health care giver; does not imply fault
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What clinical diseases are commonly associated with C. perfringens?
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soft tissue infections like: cellulitis, fasciitis, myonecrosis (gas gangrene)
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What is the treatment for C. perfringens injuries?
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surgical debridement to remove dead tissue and antibiotic therapy; hyperbaric oxygen may be useful to inhibit growth and toxin production
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Which is the only clostridial disease in which there is significant risk of person-to-person spread?
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C. diff
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What two toxins are produced by C. diff?
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cytotoxin and enterotoxin
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What is the single most important typical bacterial agent for community acquired pneumonia?
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Strep pneumoniae followed by H. influenzae
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What other test should be done in young adults with community acquired pneumonia?
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HIV test since risk of pneumococcal pneumnia is 10x greater in HIV-infected individuals
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T/F: all patients who present with signs and symptoms of pneumonia should have their sputum tested?
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False: reccomendations are to not routinely test sputum for patients that will be treated as outpatients
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What does it mean when a lab reports of a sputum stain: < 10 epithelial cells and > 25 WBC per low power field?
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that an adequate sputum specimen have been obtained
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Which patients are at increased risk for penicillin-resistant pneumococci?
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over 65
day care exposure beta-lactam treatment in the last 3 months misc complicated med problems |
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What is the tx regimen for typical pneumonia?
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beta-lactam + macrolide/doxycycline OR fluoroquinolone
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What is aspiration pneumonitis?
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often difficult to distinguish from aspiration pneumonia: due to a chemical cause from the effects of sterile gastric contents with low pH; inflammation but no infection
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What other agents should be considered in a pt who does not respond within 3 days to therapy?
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Legionella, Coxiella, endemic fungi, mycobacterium TB
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What are some common co-factors in patients with CAP?
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smoking, preceding viral illness, excess ETOH
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T/F:antibiotic prophylaxis for patients with the flu or who have aspirated is not an effective treatment against CAP?
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True: only leads to an increased cost in treating resistant bugs
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What factors can predispose a patient to an opportunistic infection?
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granulocytopenia, immune dysfunction (cellular or humoral), obstruction, CNS dysfunction, iatrogenic procedures
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What ultimately leads to septic shock?
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Endotoxin (LOS or LPS of gram negative organism) -> TNFα and IL-I -> endothelial cell damage by macrophage
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What is meant by the term nutritional immunity? How does the body accomplish this?
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ability of a host to withhold nutrients from a pathogen; increase iron storage and decrease absorption, fever, load substances with iron-binding proteins
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What microbial mechanisms are aimed at overcoming nutritional immunity?
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sideophores (compete with host proteins for iron binding)
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What is the opportunistic pathogen with the highest mortality rate?
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pseudomonas
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What is the morphology of p.aeruginosa?
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gram neg rod
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What leads to the antibiotic resistance seen in p. aeruginosa?
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chromosomal mediated (Not plasmid) efflux pumps
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What virulence factors does p. aeruginosa have?
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exotoxin a, phospholipases, proteases
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What does exotoxin A in p. aeruginosa do? How is it regulated?
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ADP-ribosylater of EF-2 (stops protein synthesis), regulated by iron
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What are the functions of the multiple phospholipases in p. aeruginosa?
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substrates are precursors to highly potent inflammatory mediators and cell signalling molecules (one is highly endothelially toxic -> vascular thrombosis)
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You see a patient in your preceptor's office who has Ecthyma Gangrenosum. What has caused their infection?
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p. aeruginosa - pathognomonic, cuased by the phospholipase that is endothelially toxic
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What is quorum sensing?
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complex cell-to-cell signaling in p. aeruginosa, mediated by homoserine lactones, which regulates the release of extracellular virulence factors and the assembly/maturation of the biofilm
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What diseases are commonly associated with p. aeruginosa?
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burn wound infections, septicemia, urinary tract infections, opthalmic infections, skin infections (hot tub, water slides, loofAH sponges), pulmonary infections
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What do most cystic fibrosis pateints die of?
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p. aeruginosa infection
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What special set of circumstances leads to virtually unclearable p. aeruginosa infection in CF pts?
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highly viscous mucus so p. aeruginosa can't be cleared, high osmolarity and Ca++ induces alginate slime, also ab complexes may form
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Describe the pattern of Arbovirus transmission.
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virus replicates to high titer in vector, vector infects dead-end host
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What viruses are blood-borne but not arboviruses?
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HCV, HIV, HBV - not infective to mosquito
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What alphavirus is not an arbovirus? What Flavivirus is not an arbovirus?
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Rubella is alpha, HCV is flavi
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What percentage of arbovirus infections are subclinical?
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90%
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What are the symptoms of Colorado Tick Fever?
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fever, chills, myalgia, general malaise (3-7% will develop encephalitis)
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Where in the U.S. is California Encephalitis Virus most common?
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midwestern states
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What diseases are associated with arbovirus infection other than encephalitis?
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arthralgia, hemorrhagic fever
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What arboviruses are associated with hemorrhagic fever syndromes?
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yellow fever, dengue
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Why does the dengue cuase hemorrhagic fever only on the second infection?
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First infection causes production of a NON-neutralizing Ab, upon 2nd infection these antibodies allow phagocytic cell uptake, the virus replicates inside phagocytic cells
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What are the symptoms of Yellow Fever?
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Range from fever, chills, headache and vomioting to jaundice, internal bleeding and kidney failure
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Where in the world do Yellow Fever cases occur?
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South America (mostly forestry workers) and Africa
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Who should be vaccinated for Japanese Encephalitis?
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travelers who intend to be in rural areas for four weeks or more
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Who is at increased risk for acquiring a zoonotic bacterial infection?
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farmers, hunters, hikers, slaughterhouse workers, veterinarians, and pet owners
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Describe the morphology of Yersinia pestis.
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bipolar staining GNR, member of enterobacteria
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What are the virulence factors of y. pestis?
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YOPs: anti-phagocytic capsule, subversion of normal phagocyte activation, iron uptake system, coagulase system that allows transmission to fleas
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What reservoirs exist for y. pestis? How is infection transmitted from reservoir to humans?
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rodents to fleas or through cat infection (pneumonia)
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What three clinical syndromes are associated with y. pestis?
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bubonic (fever & painful lymphadenopathy), septicemia, and pneumonia
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What is the treatment for y. pestis?
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streptomycin 1st line, alternate: tetracycline, chloramphenical, fluoroquinolones
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Describe the morphology of f. tularensis.
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small, aerobic, pleomorphic, gram neg coccobacillus,
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How is f. tularensis transmitted?
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arthropod vectors, contact with infected rabbits
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What important difference exists between y. pestis and f. tularensis pulmonary infection?
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pneumonic plague with y, pestis can rapidly spread from person to person
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What clinical syndromes are associated with tularemia?
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abrupt onset of flu-like syndrome, glandular, pulmonary, occular and pharyngeal involvement possible
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Describe the morphology and important virulence factor of brucella.
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small, aerobic, gram neg coccobacillus, replicate within phagocytic cells, LPS acts are virulence factor
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How is brucella transmitted?
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consumption of unpasteurized dairy products (esp goat cheese)
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What can happen to a vet who accidentally inoculates themselves with brucella vaccine intended for animals?
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chronic infection with Brucella
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What are the clinical features of Brucella illness?
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prolonged flu-like syndrome or localized disease of the bones, joints, or CNS
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What organism causes Lyme disease?
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Borrelia Burgdorferi
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Describe morphology of Borrelia.
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Spirochete
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Describe the pathophys of Borrelia.
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Evades immune effector cells, readily crosses intracellular junctions, requires humoral immunity
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In what regions of the U.S. is Lyme disease prominent? What are the animal reservoirs?
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Northeast, upper Midwest, Far West; white footed mice and deer.
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What are the clinical features of Borrelia infection?
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Bullseye rash, septic arthritis, CNS infection, or cardiac conduction block
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How is Borrelia infection diagnosed?
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ELISA CONFIRMED BY WESTERN BLOT, RULE OUT BABESIA AND EHRLICHIA
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Describe coxiella burneti.
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obligate intracellular bacteria
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What human factor can induce the growth of B. abortus?
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erythritol
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What accounts for Coxiella burneti infection in humans?
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domesticated herds shed highly infections fecal parts, inhalation of a single organism can produce infection
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What are the virulence factors of C. burneti?
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Superoxide dismutase, catalyase, acid phosphotase, and LPS
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What are the complications of flu-like illness seen with C. burneti infection?
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Hepatitis, pneumonia, myocarditis, perocarditis, and meningoencephalitis
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Describe Bartonella species.
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Gram negative, pleomorphic rods, slow-growing and capable of extracellular growth
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What is Oroya Fever? What is verruga peruana?
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fever is serious infections anemia, followed by eruptive stage two to eight weeks later, caused by B. bacilliformis, transmitted by sandflys
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What accounts for the clinical manifestations of B. bacilliformis?
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pathogen invades erithrocytes and produces a membrane-deforming protein, invades endothellial cells leading to swelling, occlusion, and thrombosis
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How is B. Bacilliformis diagnosed?
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Inclusion bodies in erithrocytes, serology
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What disease is caused by B. quintana, and how is it transmitted?
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trench fever; louse bite or feces
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What causes the self-limited illness catscratch disease?
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Ted Nugent; B. henselae infects endothellial cells of capilaries
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Who is at risk for the angioproliferative and peliosis hepatic diseases caused by Bartonella?
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immuno-compromised patients, especially AIDS patients
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What is the morphology of Rickettsia?
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Gram neg, paired rods or single coccobacilli
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How can you effectively stain and see Rickettsia?
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Giemsa (stains poorly otherwise)
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What are the clinical signs and symptoms of Rickettsia?
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fever, headache, rash (petechiae due to vascular focal infections, leading to increase permeability and edema). Late sxs: thrombosis and extravasation
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What two Rickettsia species cause typhus and which are milder?
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R. prowazekii causes epidemic typhus and milder Brill's dz, r. typhi causes mider endemic typhus (both have worldwide distribution)
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What are the symptoms of typhus?
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rash starts on trunk and spreads to extremeties. in severe dz: bacteremia, high fever, renal failure, prostration and stupor
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How can you prevent/treat Rickettsia typhus?
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Live attenuated vaccine given to armed forces, tx = doxyxcycline
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What distinguishes scrub typhus from typhus?
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rash is absent, eschar at site of chigger bite, caused by orienta tsutsugamushi, short-lived immunity after infection
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How is scrub typhus treated?
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doxy or chloramphenicol
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What causes spotted fever diseases?
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rickettsia rickettsii
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How are spotted fever diseases transmitted to humans?
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ticks and mites - takes tick 4 hours before transmission can occur
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How is the rash in spotted fever different from that seen in typhus?
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starts on the extremities (wrists and ankles) and moves to trunk
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Where and when is Rocky Mountain Spotted fever most prevalent?
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mid-atlantic states (VA, SC, NC) - summer when ticks are active
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How is spotted fever treated?
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doxy
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How do ehrlichia and anaplasma differ from Rickettsia?
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Target phagocytic cells instead of endothelial, live in phagosome instead of cytosol, cause similar dz but without rash and with hematologic abnormalities (leucopenia and thrombocytopenia)
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What is Human monocytothrophic Ehrlichiosis?
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caused by ehrlichieae transmitted from deer to tick to human
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Where in the U.s. is Ehrlichia most prominent? Anaplasma?
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E: south central and southeast US, A: northeast and upper midwest
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What is Human granulocytic Ehrlichiosis?
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caused by anaplasma and transmitted from deer to tick to human, emerging dz in U.S., less severe than HME
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What THREE tests should be performed when TB is suspected in a pt?
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Sputum AFB smear, PPD Skin test, Chest x-ray
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TRUE or FALSE: A positive Sputum AFB smear indicates active TB infection.
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NO: 50% of postive smears in US are due to non-B mycobaceria (i.e. M.avium or M.kansasii)
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Can empirical TB treatment be prescribed for pts with negative AFB smear and ppd tests?
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Yes, in cases where TB likelihood is high and when elays in tx may result in trnasmission (i.e. daycare employee)
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What are the overall rates of TB infection and active TB in worldwide?
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33% infected, 10% active
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What is the standard drug therapy for TB?
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Rifampin, Isoniazid, Pyrazinamide, Ethambutol for 2 months, then just Rif. And INH for the next 4 months
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What percentage of known contacts of an active TB pt develop active TB? What is the PPD threshold?
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1-2%, 5mm
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What percentage of dog and cat bites become infected?
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3-20% dog, 50% cats
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What are the risk factors for post-bite infection?
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Age (very young or old), location (hand>arm>leg>face), wound type (puncture) time till tx
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What drugs should be used for bite -infection treatment?
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Augmentin (amoxicillin-clavulanate) with clindamycin for anaerobes
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What is the most common organism isolated from animal bite infections?
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Pasteruella multocida (50% of dogs, 75% cats)
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What two vaccines should be considered with respect to animal bites?
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Tetanus and Rabies
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What features of joint pain suggest an infectious etiology?
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single joint involved, acute onset, IV drug use, fever, knee (>50%)
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What signs differentiate synovitis from extra-articular inflammations?
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passive AND active ROM decreased (only active affected by tendonitis, bursitis, muscle injury, etc)
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What THREE main catergories of disease should be considered with acute monoaricular Sx?
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Tramua, infection, crysalline disease (Gout, Pseudogout)
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What is the treatment for bacterial arthitis?
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I&D, antibiotics (vanco for g+, ceftazadime for g-)
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What bug is the most likely cause of septic arthitis?
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s, aureus (others: n.gon. In young adults, coag- staph in prosthetic joints/IVDU, polymicrobial RARE)
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What is the most common etiology of septic arthitis?
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hematogenous spread (75% cases) from transient/self-limiting bacteremia)
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How is osteomyelitis diagnosis confirmed?
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Direct bone culture and radiographic finding (CT/MRI); superficial culture swabs are USELESS!
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What bugs are the most common cause of Osteomyeletis?
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Staph (aureus and coag-)
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What drugs should be used for Osteomyelitis?
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Pperacillin/tazobactam (Zosyn) or ticarcillin/clavulanate (Timentin)
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Why are obligate anaerobes incapable of growing in oxygen?
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They lack cytochrome systems for respiration. Aerotolerants will have SOD/catalase to defend against oxiditive damage.
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Why are anaerobes so common in wound infections?
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Normal body flora and common in soil/water that commonly enter wound during trauma
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Why are abcesses frequently polymicrobial?
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Symbiotic relationships: aerobes use up oxygen early on, allow anaerobes to take over and wall off abcess.
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Where are anaerobes found as normal body flora?
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GI tract. Mouth, vagina, skin
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What factors influence anaerobic spore formation?
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Starvation, high cell density
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What treatment is used for sever histotoxic anaerobic wound infections?
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hyperbaric oxygen
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