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54 Cards in this Set
- Front
- Back
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describe the general characteristics, side from the crazy cell wall structure, of the mycobacterium.
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rods with a gram + lineage but do not stain, DAP not lysine in PG, non motile, acid fast, slow growth (up to 2 mo's), aerobic, facultative intracellular parasite of alveolar macs
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what causes mycobacterium to be difficult to treat and to have very slow growth when cultured?
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the unusual cell wall
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describe the cell wall structure of mycobacterium and point out the differences between it and gram positives.
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gram pos orgs have a plasma membrane and then a peptidoglycan layer which mycobac also has except the peptidoglycan contains N-GM instead of NAM. In addition mycobac also have an arabinogalactin sugar layer outside of the peptidoglycan and a mycolic acid layer outside of the arabinogalactin (note mycolic layer is responsible for waxy appearance on colonization, hydrophobicity, and overall resilience of the bac). Mycobac also contains LAM (lipid, arabinose, and mannose) that extends from the membrane through all the layers.
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describe how the structure of mycolic acid gives the mycobac special properties and what are these special properties?
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it contains many long fatty acid chains that make the org very hydrophobic and resistant to detergents, drying, antibiotics, and staining.
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describe the staining methods for mycobacs as well as results interpretation.
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acid fast stain is done by adding carbol fuchsin dye to specimen while BOILING, use ethyl alcohol to decolorize then add methylene blue. Acid fast orgs like mycobac will be red and others will be blue. Auramine-rhodamine fluorescence is also used; the bacs will be yellow in a sea of green.
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describe the attachment of mycobacs to the target host cells and name the host cells type.
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they attach to complement receptors on alveolar macs. CR4 is attachment site in unstimulated macs (CR4 usually binds C3b which will stimulate the mac to phagocytoze existing bacs). Activated macs can still be infected by mycobac binding to the CR3 complement receptor which has the same function as CR4 in unactivated macs. LAM on the bac is what binds the complement receptors
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what critical property of mycobac allows them to be phagocytized by macs and not be destroyed?
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they prevent lysosome-phagosome fusion and thus prevent lysosome hydrolysis and acidification.
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of the ppl infected with mycobac, how many of them develop disease?
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about 10%
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what 2 factors are critical in determining if an infected individual will develop disease?
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number of mycobacs in the inoculum and multiplication as well as the immune status of the host (especailly T cell status which is reduced in transplant pts or T cell immunosuppression). NOTE that the strain of TB, prior exposure, and vaccination also have roles in disease development.
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T/F: all ppl that are infected will progress through the five stages of disease.
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False
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describe stage 1 of TB progression.
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aerosolized droplets are inhaled from another, large droplets get stuck in the throat while smaller ones travel down to the alveolar sacs where they are eaten by macs and start to replicate; note if I-dose is small and immune system healthy, the macs will activate and claer infection
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describe stage 2 of TB progression.
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1 - 3 wks post infection. the bac is multiplying unrestrictedly in th mac, mac bursts and release the bacs, additional macs extravasate to the scene (some activated that can kill the bacs, while others are not and are hosts)
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describe stage 3 of TB progression.
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histiological evidence for clinical TB. lymphocytes infiltrate (T cells activated by TB antigen and make IFN gamma which activates the macs to destroy TB bacs). pt. is no TB skin test pos from CMI response. Immune pathology begins via stuff like TNF alpha, IL1, IFN gamma, lyososomal enzymes. Tubercle formation begins via macs fusing to form langhans giant cells, and these cells with other macs and T cells form around focus of damaged tissue containing bacs walling off the area forming a granuloma/tubercle. center of tubercle has caseation necrosis and the bacs persist but do not replicate (lack of oxygen and low pH in tubercles); example of host/pathogen truce.
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what is a ghon complex?
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enlarged hilar lymph node plus primary tubercle lesion in lung
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describe stage 4 of TB disease?
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bacs replicate in poorly activated macs at periphery of tubercles, growing tubercle may invade the bronchus, spread to rest of lung and into blood stream, secondary lesions formed
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describe stage 5 of TB disease.
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caseous centers of the tubercle liquefy, bacilli escape the tubercle, tubercle cavitates. Pt's can be highly infectious, bacs grow and multiply extracellularly, bronchi become necrotic and rupture, bacs disseminate throughout the lung: called miliary TB == lotsa small millet seed sized granulomas. Bacs disseminate throughout the body; kidneys, bones, GU, joints, nodes, and peritoneum get infected (mainly kidney and bones)
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how can TB become chronic.
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If in stage three, the bacs are in a stage of latency, and may later become reactivated: granuloma must persist
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why aren't the virulence factors of TB studied that much? what is one that is and what are its properties?
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it is believed that most of the disease severity is due to the hosts T cell response (or lack there of). The cord factor is a virulence factor that is known; it is a trehalose mycolic acid compound that makes the bacs form serpentine like structures in the culture and is responsible for granuloma formation during stage three as well as inducing TNF-a (fever). It is also a component of Freund's adjuvant (vaccine related)
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describe the transmission of pathogenic species of mycobacterium.
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person to person via inhalation of droplets is seen in M. TB and M. leprae. M. avium (also causes TB) is obtained by ingesting contaminated food
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describe the important facts about M. TB epidemiology.
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1/3 world infected, mainly in 3rd world countries, recent resurgence probly due to increased pop, age, MDR-TB, HIV, decrease in surveillance/intervention. 2-3 million deaths/year. #1 bacterial infectious disease worldwide. #2 pathogen worldwide behind HIV. # cases/ yr in US ranges, note 2006 was an all time low. one of 1st opportunistic infections seen in HIV+.
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what is the disease caused by M. avium?
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TB - M. avium intracellular complex AKA MAC
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define MDR TB.
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resistant to at least isoniazid and rifampin which are two of the key drugs used to treat
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what are two important stats about MDR-TB in the US?
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1-2% of all TB isolates and most of them are found in immigrants
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what makes a strain of TB XDR-TB?
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extensively drug resistant... resistant to the first lines of isoniazid and rifampin, but then resistant to fluoroquinolones (next in line) and to at least one other secondline injectable (amikacin, capreomycin, kanamycin) PLUS resistance to least two other anti TB drugs
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interpret results of the skin PPD test in various populations.
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immunosuppressed - only 5mm of induration will be considered positive. Prisoners, foreign born, and healthcare workers are positive at 10mm and above. Everyone else is positive at 15 mm plus
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what does a positive PPD test mean?
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it is suggestive, some ppl have received the BCG vaccine and thus they will always be positive and not necessarily infected; thus a positive result indicates more testing to be performed
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what are important history items that indicate TB?
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very recent and rapid weight loss, HIV status, and hemoptysis (coughing up bloody sputum)
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T/F the antibiotics for TB and M. avium complex are the same
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false
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what does the presence of an acid fast bacilli in the sputum indicate?
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mycobacterium or rhodococcus
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why is culturing mycobacterium so important ?
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it is definitive diagnosis and also allows for antimicrobial susceptibility testing. NOTE recent improvements in culturing have made the culture time only 10 to 14 days...
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what is the purpose of PCR in mycobacterium?
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can use it to look for some antibiotic resistance like isoniazid
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what does treatment of TB depend upon?
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TB strain, patient's immune status, age of pt, how serious disease is
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what are the 1st line of drug treatments for TB and what do each of the drugs do?
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isoniazid (mycolic acid inhibitor), rifampin (RNA pol inhibitor), ethambutol (arabinogalactin biosynt inhibitor), pyrazinamide (fatty acid synthesis inhibitor/blocks membrane transport and NOTE it is only used for 2 mos bc of hepatotoxicity with rifampin), and streptomycin. Use the 1st 4 until susceptability known and if it is INH/RIF sensitive stop ethambutol and PZA. MUST take for 6-9 months
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what is the treatment for TB is it if isoniazid resistant?
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use rif, ethambutol (or streptomycin) and PZA (only 2 months) and fluoroquinolones for 6-9 mos
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how do you treat MDR-TB?
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use 4 of following: fluoroquinolones and streptomycin (or new aminoglycoside) must be used in combo with ethambutol, PZA, cycloseine or ethionamide for 18-24 months
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if pt is TB+ and HIV+, how do you treat?
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same as normal but add to 9-12 months.
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why is drug compliance important with TB?
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lack of it can lead to MDR TB strains and clinical failure
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what patient populations are prophylactively treated?
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HIV+ and patient contacts of those who are TB+
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what is the bCG vaccine made of? How effective is it? why don't we use it in the US?
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avirulent M. bovis. Effectiveness can be from 0 to 80% depending upon how the country making it packages the vaccine. We do not use it here because we have very few cases and a cheap diagnostic PPD test.
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what are the major differences between M. TB and MAC?
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MAC has no person to person transmission, is obtained from iingestion of food or water, can cause more severe disseminated disease in HIV + including nearly every organ, is more prevalent in AIDS patients, is seen in male smokers, is seen in middle aged female nonsmokers with bronchiectasis and history of suppressing cough reflex, is more antibiotic resistant and uses a macrolide + ethambutol + rifabutin drug regimine for over 9 months
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where is the only place that mycobacterium leprae can be cultured?
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on armadillos feet
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T/F:
1. M. leprae prefers cooler temperatures than 37 degrees. 2. half of its genes are psuedogenes and are in genetic meltdown. |
1. T
2. T |
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what is the treatment for M. leprae?
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dapsone+rifampin+clfazimine for lepromatous. Dapsone with or without rifampin for tuberculoid form. lifelong treatment is recommended
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how deos the bCG vaccine affect M. leprae?
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may have limited prophylactic value
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in terms of diagnosis, infectiousness, immune response, histopathology, skin lesions, and disease severity, distinguish between M. leprae lepromatous form and tuberculoid form.
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Lepromatous form is diagnosed by acid fast stain, is highly infectious, uses CD4 T cells and thus more Ab's and is not that affective, see lotsa AFB in skin lesions and organs with foamy macs, and has erythematous macules, papules and nodules with extensive tissue destruction of bones and cartilage and no nerve enlargement. The tuberculoid form is diagnosed by the lepromin skin test, is not highly infectious, uses CD8+ T cells mainlly with normal Ig levels and is thus more effective, see large infiltrates of lymphocytes, langerhans cells, and few AFB. Skin lesions have few macules with hypopigmentation, nerve damage and nerve enlargement.
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about how many ppl in the US get leprosy per year and how do they get it?
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~100 and they get it from other countries
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how is M. leprae transmitted?
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person to person by close contact or inhalation of aerosols
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what is the second most common mycobacterium disease and what organism causes it?
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Buruli ulcers which is caused by M. ulcerans
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How is M. ulcerans transmitted?
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possible zoonosis, not person to person
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is M. ulcerans extracellular or intracellular?
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extracellular
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where are buruli ulcers endemic?
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mainly in west Africa and Australia.
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what orgs have low virulence and cause disease mainly in severely immunocompromised patients?
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M. kansasii and bovis cause TB like disease while M. marinum causes more of a cutaneouus infection
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what orgs have low virulence and cause disease mainly following trauma or iatrogenic (med/surgery treatments) infections and are rapid growing mycobacs that are easier to treat?
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M. fortuitum, chelonae, and abscessus
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which mycobacterium has been linked to Crohn's disease?
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M. avium subspecies paratuberculosis
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