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100 Cards in this Set
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tell me about...
1. Ehrilichia chaffeensis: 2. Anaplasmosis 3. Q fever: |
1. Ehrilichia chaffeensis: worldwide, SE/MW US. reservoir in horse, deer, dog, rick, vector is lone star tick. infected macro. low mortality. there is cholesterol in membrane. NO LPS
2. Anaplasmosis: seen worldwode, MW/NE US. reservoir in lots of small mammlas, vector is black legged ticks. infects PMN. super low mortality. cholesterol in membrane, NO LPS 3. Q fever: worldwide, uncommon in US. seen in birds, ricks etc. NO VECTOR, ITS INHALED. lung macro, can cause pneumonia, hepatitis, endocarditis. chronic disease has high mortality. weak LPS activity, does AG variation ALL are gram - and DOC is doxy |
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what are like the 2 most unique things about Q fever
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1. NO VECTOR, its inhaled
2. weak LPS, does phase variation to escape us |
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this vectors causes... and infects these cells
1. lone star tick: 2. BLack legged tick: |
lone star: erlichoisis, macro
black legged: anaplasmosis, PMN NO person to person spread |
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erlichia and anaplasmosis are transmitted how
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arthropod
erlichia: amblyomma americanum: lone star tick (likes macro) Anaplasmosis: ixodes, black legged (likes PMN) recall thse 2 are intracellular and replicate in cytoplasmic vesicles called morulea |
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ehrilichoisis and anaplasmosis micro
gram intra/extra transmission |
gram - (no LPS)
cholesterol in membrane intracellular! can make own ATP though non motile. replicate in morulae adn LOVE WBC |
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whats a morulae
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intracytoplasmic vesicle that has ehrilicholisis and anaplasmosis replicating. thse 2 love WBC
inhibits lysosome fusion and NADPH oxidase |
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tell me where E chaggeensis is found and what the vector, reservoir is
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seen in OK, area
infected by lone star tick reservoir: horse, deer, dog, tick |
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what all is transmitted by the lonestar tick
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ehrlisheria
borellia ricketssia parkeri |
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E chaffeensis causes what disease
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HME- human monocytic ehrlichiosis
**organism enters from lone star tick bite and gets into macrophages and replicates in morula, then it is released by exocytosis clinical: HA, fever, rash Labs: leukopenia, thrombocytopenia, elevated CRP, ESR minimal elevation, mild increase in serum transaminase |
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HME is what
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the disease caused by E chaggeenis, it infects macrophages and causes Faver, AH, rash. can progress and cause problems in liver, lung, encephalitis. mortality is low but treat ASAP
passed by lone star tick. reservoir in horse, deer, tick |
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whats E ewingii
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its like E chaffeensis that causes HME but e ewingii affects dogs
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tell me about anaplasmosis phagocytophilim, where is it seen, what vector, what reservoir
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seen in upper MW, mighigan area
Vector: blacklegged tick (ixodes, same as lyme disease) Revervoir: lots of small mammlas RARE to have rash |
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if the black legged tick bites you and your PMN are infected what was the cause
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anaplasmosis, A phagocytophilum
rash is RARE |
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what disease is it RARE to have a rash
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anaplasmosis
infectes PMN from black legged (ixodes) tick bite |
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how is anaplasmosis dx
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PCR
IFA x4 increase in AB titer |
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whats the tx for anaplasmosis
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doxy, same as all the ricketesia and HME
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A 63 y/o female camping in Tennessee removed an engorged tick attached to her back. She believes the tick became attached 48 hours earlier during a hike. Two days later she had onset of backache followed by fever, HA, myalgia, fatigue, abdominal pain, and a nonproductive cough. She was admitted to the hospital two days later due to progression of her symptoms.
Labs: Pancytopenia (WBC 2600/uL, RBC 3500/uL, platelets 88,000/uL), increased ALT, AST, and LDH. Atypical pneumonia and hepatitis were suspected, and IV erythromycin was initiated. A consulting physician suspected ehrlichiosis or RMSF, so IV doxycycline was added to the treatment regimen. Because of persistent abdominal pain and tenderness with mildly elevated bilirubin, ALT, and AST, an ultrasonogram of the gall bladder was performed. The wall appeared thickened, so on day 2 of admission, she had it removed. Analysis of a blood sample obtained on admission was negative for E. chaffeensis and R. rickettsii. Do you change your treatment at this point? Eight days later, an IFA titer to E. chaffeensis was 1024. Continue with doxycycline. This patient recovered and was released after nearly 4 wks |
this is actually a case of ehchilerosis and this tx is NOT effevtive, need doxy
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A 47 y/o male residing in upstate NY was admitted to the hospital with a 3 day history of fever, HA, sweats, and cough. He frequently walked in the forest, but does not recall being bitten by ticks. At admission, he presented with flu-like symptoms.
Lab results: WBC 2600/uL; platelets 119,000/uL LDH: 633 IU/L, CRP: 149 mg/L, fibrinogen: 6.2 g/L, ALT: 90 IU/L, AST: 69 IU/L CXR: bilateral interstitial infiltrates Blood cultures were negative What is on your differential diagnosis at this point? The pt was thought to have atypical pneumonitis and treatment was initiated accordingly. What organisms do you suspect and what antibiotic(s) would cover them? A serum sample obtained two days after admission was negative for antibodies to C. pneumoniae, M. pneumoniae, L. pneumophila, and C. burnetii. Since he lives in an area endemic for many ticks, the acute phase serum was also tested for antibodies to various tick-borne pathogens (Rickettsia, Ehrlichia, Anaplasma, and Borrelia). All tests were negative. 24 Now what? After 5 days of treatment, his fever resolved. A convalescent-phase serum sample was collected 4 weeks later and showed an IgG titer of 256 to A. phagocytophilum. Why didn’t these antibodies show up on the first test? |
anaplasmosis: seen in upper states, ehricherlosis is lower midwest
fiirst didnt show bc you need to wait for the AB titer rise. it was too early for AB production to be apparent on serology |
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coxiella burnetii causes what? what are the 2 forms of the organism
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Q fever, NO vetor, its inhaled. gram -
1. SCV- long lived, infectious 2. LCV- survived in the phagolysosome. its intracellular |
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what disease has SCV and LCV
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coxiella, Q fever
SCV- lives in environemnt, infectious LCV- lives in us, intracellular |
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what bug does phase variation
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coxciella, q fever
Phase I: resistant to phago, more virulent Phase II: killed easier **AB to both AG can be found in serum |
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where is Q fever seen
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world side, in western midwest in US. NM, UT, CO, MT, NB
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what is the reservoir and vector for coxciella
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reservoir: lots of animals, birds, ticks
vector: ticks, ZOONOTIC disease, doesnt require a vector transmission: inhale contaminated milk bite |
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what can be passed through inhalation, milk, or tick bite
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Q fever
high risk: farmers, vets, lab workers |
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tell me about the sx of Q fever
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1. Acute: you inhaled it and it infects alv mecrophages. fever, HA,
-mimics atypical pneumonia -liver granuloma!!! 2. CHRONIC (focus ehre) -subacute endocarditis |
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what can lead to subacute endocarditis w/chronic infection
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coxciella, Q fever
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how is Q fever dx
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1. CXR- mimica atypical pneumonia, liver granuloma,
Serology to phase I AND II AG. Acute: IgM to I/II, IgG to phase II Chronic: IgG and IgA to phase I, w/decrease in phase II AB |
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what is the serology for acute and chronic Q fever
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Acute: IgM to phase I II AG, IgG to phase II
CHRONIC: IgG, IgA to phase I decline in phase II |
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how is q fever tx and prevented
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doc is doxy and add another for chronic infection
inactive vaccine!!!!! dont touch infected animals, dont eat unpasturized milk |
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whats the most common cause of gastroenteritis/enterocolitis
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s typhimutium
reportable disease, so is yersinia |
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what is typhoid
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reportable disease that causes delirum in 3 week of untreated illness
** |
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who is the carrier for typhoid fever
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human ONLY, not super common in US, reportable
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what is paratyphoid fever
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its less severe than typhoid, caused by S paratyphoid
humans are only host, common in places with little sanitation |
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what host system protects us from sal pyphoid
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1. gastric acid
2. normal flora 3. IgA prevents it from attahing to intestinal epithelium *CFTR Hz also have acquired resistance, can be effective or not IgM, IgG, CTL cells |
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what is HZ CFTR good for
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prevent salmonella typhoid
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whts the micro of sal typhi
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gram -
motile anerobe grow on regular medium: make black H2S no lactulose fermentation, clear colonies on MacConkey |
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what grows black on agar
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sal typhi (gram - bacilli) anerobe, lactulose non fermenter- clear on macconkey
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who gets sal typhi
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school kids, young adults
in US most cases are from international travel, some rare outbreaks from contaminated food or infected food handler - typhoid mary. REPORTABLE |
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where is sal typhi common
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places with little sanitation
asia africa latin america caribbean oceania not common in US, gram - bacilli. anerobic, makes H2S black colonies. lactose non fermenter |
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whats teh transmission of sal typhi
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1. oral: person sheds bacteria in stool or urine and can contamiate food/beverage. or sewage contaminated water/food
2. Hand to mouth: after using contaminated toilet and not washing hands |
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what disease can you get from the toilet seat
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sal typhi, unsanitary conditions, not washing hands
also spread through infected food/water or infected food handler REPORTABLE disease, gram - bacilli |
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what are the virulence factors assocaited with sal typhi
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it lives in macrophages
invasive: type III secretory system to do bacteria mediated endocytosis, cell ruffling. gets in through M cells and enterocytes. LPS, O AG, H AG, pathogenicity islands |
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what are the salmonella pathogenicity islands
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SPI1 SPI2
other sal typhi virulence includes. LPS, O/H AG, they live in macrophages |
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what is the Vi AG
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specific to S typhi
also has K AG, which is seen in E coli as well as others |
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whats PAMP
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pathogen associated moleular patterns- thse usually let bugs get eaten up but in the case of sal typhi these are covered. part of its virulence to prevent phago
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what allows salmonella to attach to M cells in GI
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fimbriae, pilli
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whats the pathogensisi of sal typhi
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1. microbes get in through food/drink
2. they live in the stomach acid 3. use fimbria/pili to attach to M cells in distal ileum 4. type III secretory to induce its own endocytosis 5. taken up by macro and start replicating 6. taken to RES- liver, spleen, BM, 7. start to kill the host macro 8. released into bloodstream FEVER BEGINS 9. repete circut, shed in stool/urine |
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when does the fever start w/sal typhi
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when the bug is released from macrophages and enters the blood
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are pts w/achlorhydria more or less susceptible to sal typhi
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MORE!! the bug can tolerate stomach acid but when there is less acid a person is MORE susceptible
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once in the GI whree does sal typhi like to go, what does it do once it gets there
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peyers patches in distal ileum
fimbrea attach to CFTR or M cells and induce bacterial mediated endocytosis once in the phagolysosome they activate their pathogenicity islands |
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M cells and peyers patches are associated with what disease
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sal typhus
attachment to MV in the M cells, they change through Bacterial Mediated endo- cell ruffle adn are taken into the cell. Effectors secreted by type III secretory system can break junction and let bacteria just slide in. Once inside it redirects MT and gets to BM |
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where does sal typhi replicate
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in teh macros in peyers patches, then they are released to RES and eventually kill the macro, spill into blood and cause FEVER
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the secondary bacteremia (kills macro and then bursts into blood) in sal typhi causes what
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GB infction: colecystitis,
**when bile gets infective you poop out the bug for a LONG time Peritonitis from perforation |
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what factors are associated with long term sal typhi excretion in the poo
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gallstones!! the bug gets stuck in the stones and so is ever present
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what does sal typhi manifastation look like in the first week
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get stepwise fever pattern, rises in that day and drops by AM. increases then to about 104. then you get bacteremia and then decrease HR,
pulse temp disassocaiteion |
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what happens in week 2 of sal typhi
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abd pain
rose spots on trunk constipation/diarrhea |
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what happens in week 3 of sal typhi infection
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1. hepatosplenomegaly
2. intestinal bleeding 3. perforation: bc of payers hyperplasis 4. septic shock, death |
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what happens in week 4 of sal typhi
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gradual resolve (if you didnt die from sepsis in week 3 of course)
some survivors will be asx carriers. common in women or pts w.gallstones |
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whats the clinical for sal typhi
week 1 week 2 week 3 week 4 |
1: fever pattern, increase drop, increase. bacteremia. pulse temp disassocaiteion
2. abd pain, rose spots, constipation/diarreha 3. sepsis, die, perforation, bleed, large liver/spleen 4. resolve so asx carrier (women, biliary abnormality) |
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we spent a lot of time knowing the fever pattern, rose spots, peritonitis/sepeis, recovery/asx carrier
is this ALWAYS the case |
geographical variation
but 88% DO have that steady insidious onset fever |
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sal typhi clinical lab dx
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criterion std = culture isolation
susceptibility tests are essential |
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how is sal typhi revocered for dx
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bone marrow aspirate, its super sensitive but PAINFUL
can also do blood, stool a week after incubation. |
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whats the typhidot
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serology for sal typhi dx
*ELISA that detects igM and IgG AB to s typhi outer membrane protein used to confirm carrier status |
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do you do sensitivity testing for s typhi
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YES!
resistance to nalidoxic acid, fluoroquinolo |
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sal typhi tx
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start ASAP! give emperic if there is a person w.unexplained dx w/recent travel, consuption of food by unknown carrier
start definitive treatment when you get sensitivity back |
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what do we do for long time sal typhi carriers
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AB tx for a LONG time, or can take out GB, the bug can hang out here
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how can you prevent sal typhi
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vaccinate ppl who are going to endemic or outbreak areas (haiti)
several vaccines are available 1. Live attenuated: 1 cap po, q2days for 4 doses. >6yo 2. Purified Vi capsule: injected 1 time. need to be .2 yo |
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can you vaccinate animals to erradicate sal typhi
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nOPE! only infects humans
give vaccine, clean water, education, sweage disposal, |
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what causes the plague
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yersinia pestis. **reportable
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whats teh micro of yersinia pestis
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no spore
pleomorphic gram - pai stained bipolar safety pin appearance |
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what is the bipolar, safety pin, appearance w.wayson stain
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persinia pestis
causes the plague |
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what has a wide range of temperature tolerance
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plague, yersinia pestis
also is NON motile, has AG protein F1 |
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where is yersinia found
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humans AND fleas
intracelluar in human macrophages multiplies in fleas |
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in what parts of the world is yersinia found
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africa, asia,
**HUGE increase in risk in native americans if in US its localized to western states. |
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who is at risk of yersinia
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native americans
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do flea bites increase risk of yersinia or sal typhi
what about cats |
yersinia, also increase plague risks with rats, field mice, prarie dogs e
cats: pneumonic plague |
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what are risk factors for the plague
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1. flea bite:
2 endemic areas (SW US, africa, asia, vietnam) 3. if you eat rats, or have rats near the home 4. occupation: researccher, vets 5. outdoor recreation 6. handling/inhaling contaminated tissue: hunters, medical/lab techs |
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risk factors for pneumonic plague
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crowded areas
cats |
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is yersinia zoonotic
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yep
humans are accidental hosts, reservoir: rodents, feral mammals, domestic cats 1 bacterium is infectious dose *contact w/infected carcas (anthrax) |
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whats the infectious dose for yersinia transmissin. what is the transmission like for this disease
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1 bacterium!!!!
WOW reservoir are rodents, feral (wild) mammals, domestic cats cantact w/infected animal carcas --> anthrax |
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is there human to human transmission of the plague
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NO!
well sometimes during pneumonic plague epidemics only |
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what are the virulence factros associated with yersinia
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1. temperature has wide regulation
2. fibrinolysin/phospholipase facilitate multiplication 3. coagulase:, polysaccharide biofilm. block proventriculus 4. YOPS: yersinia outer membrane protein- destroy host cell, block cell signaling 5. F1 envelope AG: anti phago 6. plasminogen activator- helps mets 7 endotoxin- not temp regulated |
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whats YOPS
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yersinia outer mmebrane protein, its the virulence factor
**kill host cell, disrupt signaling path of host, inhibit cytokine production |
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does yersinia have the virulence factors F1 envelope AG and plasminogen activator
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yep
F1- resist phago plasminogen activator- METS |
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tell me about the endotoxin assocated with yersinia
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1. not temp regulated
hemorrhage, vascular collapse, DIC, focal necrosis |
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what s the pathology of bubonic plague
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1. yersinia pestis
flea eats blood from infected rat or what ever -coagulase causes a blood clot in flea GUT, the bacilli then MULTIPLY - the flea then infectes the next things it feeds on 2. so the yersinia bacilli are now in you and are taken up by PMN and go to LN 3. they then lyse and yersini is everywhere it continues to grow in blood and then invades other organs |
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we has a flea eat an infected animal and now the flea has yersinia. the yersinia has coagulase which makes a big old GI clot so it can replicate. now the flea bites you.. what happens
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bubonic plague!!!!
bacilli enter us and get in macrophages/PMN, multiply in the cell and travel to LN macro/PMN then lyse and we get bacteremia and the microbe grows like craxy in the blood and invades other organs |
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what are hte sx of bubonic plague
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(from yersinia pesits)
bubonic is most common form! 2-6 days after flea bite (recall they went to macro/PMN replicated went to LN, lysed spilled bacilli everwhere and now are in other organs) you get sudden FEVER, chills, HA. then BUBOES- the painful swollen lymph glands |
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what are buboes
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its seen in bubonic plague
when yersinia are int eh LN and make them HUGE, its painful swollen lymph glands will have sidden onset fever, HA, chills 2-6 days after flea bite |
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if you dont tx bubonic plage what 2 thigns happen
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1. disseminate--> septicemia
2. spread to lungs --> pneumonic plague |
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whats teh pneumonic plague
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from yersinia, not as common as bubonic
can be primary from inhalation (cats, crowds) or secondary to bubonic septicemia HIGHLY CONTAGIOUS- transmitted by aerosol drops or handing infected animals fever chills CHEST PAIN |
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is bubonic or pneumonic plague associated w/chest pain
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penumonic
super contageous, may or may not have bubeosis 100% mortaliy in 24 hrs if not treated |
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whats the septicemic plague
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resulf of bubonic, or pneumonic plague
HIGH mortality: DIC, septic shock< MODS necrosis of small vessels. full body ecchymosis NO bubeos |
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if you have buneos what plage
if you have zero |
have: bubonic
penumonic are +/- buboes septicemis is NO buboes both septicemic and pneumonic are fatal in 24 hrs of not tx |
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how do you dx plague
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cal CDC
aspirate fluid from LN, sputum. Wayson stain shows those bipolar safety pin thigns F1 AG serology and IFA blood culture CXR |
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what does he think looks like starry night
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plague! yersinia
its an IFA, the F1 AG stains |
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how do you treat yersinia
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call rodent control, call public health call WHO, CDC
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whats teh tx for yersinia pestis
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IV gentamicin
**pt needs to be in respiratory isolation for 72 hrs after you start AB |
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do you prophylax ofr yersinia
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ya if you have been exposed start on doxy. recall gentimicin is the tx
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is there a vaccine for yersinia
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whole cell w/inactivated formaldehyde-not anymore,
UK plague- F1, V AG DoD- F1, V AG, tobacco plants, at ASU proposed nasal to prevent bioterrorism none effective for pneumonic 2 for sal typhi |
