Official Step 1 HY Microbio Concepts & Discussion Thread

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Mr. Mojo Risin

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Here is a Question from Kaplan Qbank.

A 42 yo woman comes to the physician because of a headache and nausea. She underwent a heart transplant 14 months ago. Vital signs are normal. Physical examination does not show any focal neurologic deficits. A CT scan of the head is shown. Examination of tissue obtained on biopsy of the brains shows multiple cystlike structures. Cultures of the lesions are negative. Which of the following is the best explanation for the syndrome in this patient?


Screen Shot 2015-01-10 at 6.07.58 PM.png


A. infected whole-blood transfusion
B. ingestion of cysts in poorly cooked beef
C. ingestion of oocysts from cat feces
D. reactivation of latent infection
E. transplant of an infected organ

Correct Answer: D

f
Highlight for correct answer. Explain how you came up with your answer. Thanks.
 
Here is a Question from Kaplan Qbank.

A 42 yo woman comes to the physician because of a headache and nausea. She underwent a heart transplant 14 months ago. Vital signs are normal. Physical examination does not show any focal neurologic deficits. A CT scan of the head is shown. Examination of tissue obtained on biopsy of the brains shows multiple cystlike structures. Cultures of the lesions are negative. Which of the following is the best explanation for the syndrome in this patient?


View attachment 188395

A. infected whole-blood transfusion
B. ingestion of cysts in poorly cooked beef
C. ingestion of oocysts from cat feces
D. reactivation of latent infection
E. transplant of an infected organ

Correct Answer: hh

f
Highlight for correct answer. Explain how you came up with your answer. Thanks.

I Think the correct answer is D. As she probably is on immunosuppressive drugs and there is a reactivation of toxoplasmosis. It seems like cystic lesions.

Kindly let us know the answer.

Thanks
 
I Think the correct answer is D. As she probably is on immunosuppressive drugs and there is a reactivation of toxoplasmosis. It seems like cystic lesions.

Kindly let us know the answer.

Thanks

Toxo would be my choice as well. Look at that ring-enhancing lesion.
 
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Choice C also describes Toxo

This is true. I meant reactivation of latent infection with Toxo. Many people are already infected, and since this woman is likely immunosuppressed from the heart transplant, D is a better answer than C.
 
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The correct answer is D but I originally assumed C as a correct answer. You all should be able to highlight for the correct answer on my original post if I did it correctly. It's a Kaplan qbank question.
 
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A groom-to-be develops pneumonia after an unorthodox bachelor party involving spelunking, quad biking, and hand gliding a few hours drive outside the Strip in Las Vegas. What do you expect to find under the microscope?

A: Acute branching, septate hyphae
B: Perpendicular branching, non-septate hyphae
C: Yeast forms engulfed within macrophages
D: Spherules with endospores
E: Dimorphic cigar-shaped yeasts
 
The correct answer is D but I originally assumed C as a correct answer. You all should be able to highlight for the correct answer on my original post if I did it correctly. It's a Kaplan qbank question.
B, C, and D could all be toxo. Worth knowing that for most people it will be a reactivation of latent infection vs new infection (D).

A groom-to-be develops pneumonia after an unorthodox bachelor party involving spelunking, quad biking, and hand gliding a few hours drive outside the Strip in Las Vegas. What do you expect to find under the microscope?

A: Acute branching, septate hyphae
B: Perpendicular branching, non-septate hyphae
C: Yeast forms engulfed within macrophages
D: Spherules with endospores
E: Dimorphic cigar-shaped yeasts

I think spelunking is a red herring to get you to choose histoplasma (C), which I wouldn't expect to see in Vegas. Probably inhaled spores of coccidiodomycosis while quad biking, and so you'd see spherules with endospores (D).
 
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I think spelunking is a red herring to get you to choose histoplasma (C), which I wouldn't expect to see in Vegas. Probably inhaled spores of coccidiodomycosis while quad biking, and so you'd see spherules with endospores (D).

Yup. Also according to Goljan cocci is in caves as well (the quad biking was just a random desert activity that popped into my head).
 
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Yup. Also according to Goljan cocci is in caves as well (the quad biking was just a random desert activity that popped into my head).
Haha, would've been trickier without the quad biking for me, but I guess you can still go mostly by geography.
 
A groom-to-be develops pneumonia after an unorthodox bachelor party involving spelunking, quad biking, and hand gliding a few hours drive outside the Strip in Las Vegas. What do you expect to find under the microscope?

A: Acute branching, septate hyphae
B: Perpendicular branching, non-septate hyphae
C: Yeast forms engulfed within macrophages
D: Spherules with endospores
E: Dimorphic cigar-shaped yeasts

I would go with D based on the region.... so coccidio
 
23 year old is intubated and over the next few days develops pneumonia. Sputum gram stain shows encapsulated oxidase-positive GNB. Susceptibility testing reveals resistance to aminoglycosides. Which of the following mechanisms causes this organism to be resistant to this antibiotic?

A. Acetyltransferase production
B. PBP mutation
C. Topoisomerase mutation
D. Enzymatic inactivation
E. Beta-lactamase production

Hint: FA won't tell you the answer.
 
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23 year old is intubated and over the next few days develops pneumonia. Sputum gram stain shows encapsulated oxidase-positive GNB. Susceptibility testing reveals resistance to aminoglycosides. Which of the following mechanisms causes this organism to be resistant to this antibiotic?

A. Acetyltransferase production
B. PBP mutation
C. Topoisomerase mutation
D. Enzymatic inactivation
E. Beta-lactamase production

Hint: FA won't tell you the answer.
It's A right?
 
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It's A right?

Nope. According to Kaplan klebsiella and enterobacter do A, but pseudomonas uses a different mechanism. I've been tested on abx resistance mechanisms before, but never organism-specific mechanisms...
 
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Nope. According to Kaplan klebsiella and enterobacter do A, but pseudomonas uses a different mechanism. I've been tested on abx resistance mechanisms before, but never organism-specific mechanisms...
Did you get that q from Kaplan qbank?
 
Nope. According to Kaplan klebsiella and enterobacter do A, but pseudomonas uses a different mechanism. I've been tested on abx resistance mechanisms before, but never organism-specific mechanisms...
From what I've seen pseudomonas uses acetylation, phosphorylation and adenylation to inactivate aminoglycosides. Was there a explanation why D was correct over A?

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0017224
http://www.uphs.upenn.edu/bugdrug/antibiotic_manual/aminoglycosideresistance.htm
http://aac.asm.org/content/49/2/479
 
From what I've seen pseudomonas uses acetylation, phosphorylation and adenylation to inactivate aminoglycosides. Was there a explanation why D was correct over A?

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0017224
http://www.uphs.upenn.edu/bugdrug/antibiotic_manual/aminoglycosideresistance.htm
http://aac.asm.org/content/49/2/479

Nope. Explanation was basically "pseudomonas does enzymatic inactivation and/or efflux pumps for aminoglycosides. kleb and enterobacter use plasmid-mediated acetyltransferase for gentamicin"

Pretty dumb if you ask me since both acetyltransferase and enzymatic inactivation are well known mechanisms of aminoglycoside resistance. I wasn't (still am not) entirely sure if acetyltransferase isn't "enzymatic inactivation" via acetylation...
 
Nope. Explanation was basically "pseudomonas does enzymatic inactivation and/or efflux pumps for aminoglycosides. kleb and enterobacter use plasmid-mediated acetyltransferase for gentamicin"

Pretty dumb if you ask me since both acetyltransferase and enzymatic inactivation are well known mechanisms of aminoglycoside resistance. I wasn't (still am not) entirely sure if acetyltransferase isn't "enzymatic inactivation" via acetylation...
Especially since acetylation via acetyltransferase is a form of enzymatic inactivation.
 
It's D because you can use a variety of mechanisms to inactivate. Choice A is too narrow. Gotta love Kaplan qbank. Plus I have my shelf exam tomorrow, so I have been looking over this.
 
It's D because you can use a variety of mechanisms to inactivate. Choice A is too narrow. Gotta love Kaplan qbank. Plus I have my shelf exam tomorrow, so I have been looking over this.

Choice D is the answer for kleb and enterobacter. I don't think this is a test taking skills question. I think Kaplan was testing organism specific info.
 
Choice D is the answer for kleb and enterobacter. I don't think this is a test taking skills question. I think Kaplan was testing organism specific info.

I was being a little sarcastic about kaplan's testing of detailed minutiae.
 
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Could anyone explain why sulfonamides lead to hemolytic anemia in G6PD def patients? Would it be because the RBCs are unable to be synthesized well? Or is it because the sulfonamides cause some sort of oxidative damage to RBCs -> their destruction?
 
Could anyone explain why sulfonamides lead to hemolytic anemia in G6PD def patients? Would it be because the RBCs are unable to be synthesized well? Or is it because the sulfonamides cause some sort of oxidative damage to RBCs -> their destruction?
Oxidative damage --> oxidized glutathione --> no NADPH for reducing --> heinz bodies --> hemolytic anemia
 
Thanks. Was just curious about the actual oxidative damage, since sulfonamides are folate synth inhibitors and not something that causes ROS.
 
Thanks. Was just curious about the actual oxidative damage, since sulfonamides are folate synth inhibitors and not something that causes ROS.
TMP-SMX could cause a megaloblastic anemia due to folate deficiency but that would be separate from G6PD deficiency with hemolytic anemia
 
What if a patient who has chronic hepatitis B gets vaccinated? What serum markers would be present in this patient?
 
I got two:

A 25 year old woman has a 4 year old son who is now recovering from Group A strep pharyngitis. Out of curiosity, the pediatrician does a throat culture on the mother which is positive for Group A strep even though she doesn't have a sore throat. The pediatrician also does an ASO titer and anti DNAse B assay on her both of which are negative. At this point we would say that she:
A. Has asymptomatic infection
B. Has opportunistic infection
C. Is a carrier
D. Is immunosuppressed
E. Is immunocompromised

A 7 year old boy with a history of recurrent granulomatous skin infections and a prior episode of Aspergillus pneumonia undergoes a partial hepatectomyto treat a poorly draining liver abscess. Genetic analysis reveals an inactivating mutation affecting a structural component of a neutrophil oxidase enzyme. This patient most likely has and increased vulnerability to infections caused by which of the following pathogens?
A. Enterococcus Faecalis
B. Giardia Lamblia
C. Strepococcus Pyogenes
D. Streptococcus Pneumoniae
E. Burkholderia Cepacia
F. Herpes Simplex Virus Type 1
 
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I got two:

A 25 year old woman has a 4 year old son who is now recovering from Group A strep pharyngitis. Out of curiosity, the pediatrician does a throat culture on the mother which is positive for Group A strep even though she doesn't have a sore throat. The pediatrician also does an ASO titer and anti DNAse B assay on her both of which are negative. At this point we would say that she:
A. Has asymptomatic infection
B. Has opportunistic infection
C. Is a carrier
D. Is immunosuppressed
E. Is immunocompromised

A 7 year old boy with a history of recurrent granulomatous skin infections and a prior episode of Aspergillus pneumonia undergoes a partial hepatectomyto treat a poorly draining liver abscess. Genetic analysis reveals an inactivating mutation affecting a structural component of a neutrophil oxidase enzyme. This patient most likely has and increased vulnerability to infections caused by which of the following pathogens?
A. Enterococcus Faecalis
B. Giardia Lamblia
C. Strepococcus Pyogenes
D. Streptococcus Pneumoniae
E. Burkholderia Cepacia
F. Herpes Simplex Virus Type 1

Is the first one C?

E for the second question.
 
It's actually listed in FA 2015 on p.216, but there's no other info about it aside from the fact that it's a possible pathogen in patients with decreased granulocytes.
Thanks.
that's cute, thanks FA. hidden away with a small note :wtf:
 
With anaerobic infections, are the infections always going to be foul smelling and mixed? I heard that in one of my micro lectures, but i couldnt find it anywhere and didnt understand the association
 
Does Staph Aureus have a capsule or not? I've been finding conflicting info about it on the internet + I know that the first aid list is not complete
 
What microorganism comes to your mind if I give you a case of a guy falling off of his bike and develop a wound on his knee and that wound having a "foul smell"?
 
I thought about perfringens too and that's a better response given the extent of immunization for tetanus
Wait, you're (accepted)? What on earth are you doing in this thread. Go enjoy your summer.

They also gave no physical exam findings associated with tetanus, which they love to do, and I've never heard of a tetanus infection being particularly associated with a foul smell. Immunizations can wane or be ignored, not a good rule out reason.
 
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