Slide Deck 3 Flashcards

1
Q

What type of bacteria is this, and what is its characteristic makeup?

A

Spirochete: spiral, with axial filament (endoflagellum)

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2
Q

Syphilis genus species name?

How is it grown on agar?

A

cannot be grown on agar! only rabbit testicles (humans are the only reservoir)

Treponema Pallidum Pallidum

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3
Q

Describe the progression of syphilis, post sexual contact.

A

Incubation: Median of 21 days

Primary lesion: lasts three to six weeks

A few months later….

Secondary syphilis: may have a variety of symptoms, including a maculopapular rash (lasts several months) condylomata lata

Becomes latent for myabe five years

Tertiary syphilis: gummas (soft swelling) in CNS (eg meningitis) and cardiovascular system

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4
Q

bilateral small pupils that constrict when the patient focuses on a near object, but do not constrict when exposed to bright light. What is this called, and what is it a sign for?

A

Argyll Robertson pupils (“AR pupils”) are bilateral small pupils that constrict when the patient focuses on a near object (they “accommodate”), but do not constrict when exposed to bright light (they do not “react” to light).

also are slitted and irregular

Sign of neurosyphilis (tertiary)

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5
Q

When does transplacental transmission of syphilis occur? If you find mother with syphilis, how can you prevent it? What are the consequences of congenital syphilis

A

after 18 weks of gestation – SO TEST DURING FIRST TRIMESTER, and administer penicillin before or during 16 weeks of pregnancy

Stillbirth, notched “Hutchinsons” teeth, snuffles (with infectious snot)

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6
Q

How do you diagnose syphilis?

A

Visualize organisms in primary lesion by immunofluorescence or dark field microscopy

You can screen, (with false positive being a risk) with non-treponemal antibody screening test (VDRL)

But a sepcific test for treponemal antibody (more expensive) would be FTA-ABS: fluorescent treponemal antibody-absorption)

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7
Q

What type of bacteria are clostridia?

A

Gram positive, obligate anaerobic, spore forming rods

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8
Q

in what conditions does clostridia form spores? If it’s not in the sporulation cycle, what is it doing?

A

forms spores in tissues, ie in presence of oxygen (then it divides not symmetrically, as it does in vegetative cycle).

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9
Q

Differentiate between the nature of paralysis induced by Clostridium tetani and Clostridium botulinum.

A

Clostridium tetani blocks release of inhibitory mediators, causing spastic paralysis.

Clostridium botulism causes a descending flaccid paralysis by blocking Ach motor neuron release.

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10
Q

What is the most common neurotoxin for botulinum, and how is it used nonmedically? What does it target?

A

A, used in botox, targets SNAP-25, a snare protein involved in Ach release

B targets synaptobrevin, another snare protein

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11
Q

How does Clostridium botulinum exert its effects?

A

It causes flaccid paralysis by blocking the release of acetylcholine at the myoneuronal junction.
Cleaves SNARES to make this happen

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12
Q

How si botulinum transmitted? Specifically, what kind f foods might induce it in adults v. infants?

A

Foodborne/traumatic implantaation

Adults are suscpetible to preformed toxin ingested (in poorly canned alkaline vegetables) – you should heat all canned foods

Infants are vulnerable to ingesting the spore, like in honey

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13
Q

What is this symptom, and what is it associated with?

A

Risus sardonicus: associated with clostridium tetani

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14
Q

What is this symptom, and what is it associated with?

A

ophisthotonus: arched back, associated with tetanus

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15
Q

How do you treat tetanus and botulism?

A

antitoxin

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16
Q

Gas gangrene has its characteristic, gassy vesicles, due to production of what ? what bacterium is responsible?

A

H2

Clostridium perfringens

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17
Q

Toxoinotype A of Clostridium perfringens is responsible for what human disease? What about C?

A

A: causes gas gangrene, gastrointestinal disease

C: necrotic enteritis (pig bel, rare in US)

18
Q

What is the main toxin responsible for Clostridium perfringens to spread? How can it be detected on agar?

A

Phospholipase C: disrupts membranes

It can be detected by the Nagler reaction: egg yolk agar plate. You compare the side that has Phospholipase C with the side that does not.

19
Q

Clostridium perfringens can cause diarrhea because of what toxin?

A

Enterotoxin: produced in intestines in food poisioning disrupting ion transport and resulting in watery diarrhea

20
Q

Diarrhea in hospital patient…likely cause? How can you diagnose?

A

Clostridium dificile, often seen after antibiotic therapy

This is commensal, so you have to differentiate with asymptomatic strain (only the toxigenic strains, tcdA and tcdB, cause infection).

So, you do a stool exam for toxin production

21
Q

How do clostridium dificile toxins A and toxins B work?

A

Toxin A: enteotoxin damaging mucosa leading to fluid increase, attraction of granulocytes

Toxin B: cytotoxin ADP ribosylation and depolymerizaiton of actin, increased bacterial adherence

22
Q

How do you treat clostridium dificole?

A

It’s hard because those spores are out there. Here you have to give oral vancomycin, but that has really high recurrence (you’ve killed vegetative, but spores grow after the antibiotics end). It has a 78% success rate

oral metronidazole is the inferior treatment also suggested

23
Q

C dif is often secondary to antibiotic use, especially ____ or ____. It is also associated with ____ use.

A

clindamycin or ampicillin, associated with proton pump inhibitor use

24
Q
A

Pseudomembranous colitis, C dificile!

25
Q

We talked about clinical trials that had antibody treatment targeting C dificile toxin A and B. The rate of recurrent CDI was significantly lower with which one?

A

Bazlotoxumab which targeted B

as opposed to actoxumab, which targeted A

26
Q

What does EPEC stand for, and how does it exert its effect? Who does it most effect?

A

EPEC forms no toxin. It adheres to the apical surface, flattening villi and preventing absorprtion. Organisms form small microcolony aggregates on epithelium. It causes diarrhea, usually in children (Pediatrics)

27
Q

Which E . coli organism goes past the intestinal lining and basement membrane, causing necrosis and inflammation? What are the symptoms, and what other bacterium does this resemble?

A

EIEC: Enteroinvasive E coli– bloody diarrhea (dysentery)

Similar to Shigella

28
Q

What is the major cause of traveler’s diarrhea, as well as malnourished infant diarrhea? How do you treat?

A

Enterotoxigenic E. coli, which is acquired from feces contaminated food or water

Oral rehydration, no antibiotics necessary

29
Q

What is Hemolytic uremic syndrome? It ocurs in just 1% of cases of this E. coli, what form of E. coli is associated?

A

Renal failure, anemia, thrombocytopenia

symptoms: watery diarrhea, sometimes bloody

EHEC: enterohemorrhagic, also called Shiga-like

H for hamburgers, often transmitted by undercooked meat, raw leafy vegetables

30
Q

What is the Shiga toxin? How does it function, and in which diseases?

A

carried in Shigella and in STEC or EHEC, B5 subunit binds to Gb3 glycolipid on host cells,

A is cleaved by furin to generate A1 and A2, A1 functions as RNA N-glycosidase to cleave rRNA, blocking ribosomal protein synthesis.

(its the 60s minute glass in the shiga video, and the little baby she gorilla in the e coli video)

31
Q

What is the common name for shigellosis?

A

Bacillary dysentery: bloody/watery/mucoid diarrhea

32
Q

What types of cells does Shigella invade?

A

M cells

icrofold cells (or M cells) are found in the gut-associated lymphoid tissue (GALT) of the Peyer’s patches and in the mucosa-associated lymphoid tissue (MALT) of other parts of the gastrointestinal tract. These cells are known to initiate mucosal immunity responses on the apical membrane of the M cells and allow for transport of microbes and particles across the epithelial cell layer from the gut lumen to the lamina propria where interactions with immune cells can take place

33
Q

What is the predominant strain that causes UTI in women, and what is the thing responsible?

A

E. coli, P-pili is what it uses to get the bladder, forms intracellular biofilms and lives inside the cells until it pops out with recurrent infections

34
Q

Associated with abdominal pain, fever,

A

Here you see typhoid fever: rose spots on abdomen, constipation, abdominal pain, fever

It is caused by salmonella typhi, and you treat with ceftriaxone or fluoroquinolone.

35
Q

Salmonella gastroenteritis usually stems from what cause?

A

raw poultry, eggs, pets, and turtles

36
Q

How effective are the rapid serologic tests for tpyhoid fever (Tubex TF, TyphiDot?)

A

Neither diagnositic nor specific

37
Q

How do salmonella enteridis and typhi get into host, and where do they replicate?

A

INavde in the small intestine

  1. comes in M cell of Peyer patches

or

  1. Type III secretion to come into colonic epitheilium

survive inside lymphoid cells, in SCV: “Salmonella containing vacuole,” which eventually kills the cell for release

38
Q

How do you prevent typhoid fever?

A

ViPS: Vi polysaccharide antigen for >= 2 yoa

or

live attenuated oral vaccine

new: conjugate vaccine, but short-term only

39
Q

rice-water diarrheal illness caused by this gram - disease? in developing countries–requires IMMENSE amounts of bacteria in food/water to be human relevant. How do you treat? Can you prevent?

A

Vibrio cholera: comma shaped disease

Treat with prompt oral rehydration, quarantine

Prevent by short-term vaccines

40
Q

How does cholera exert its efect?

A

enterotoxin permanently activates Gs, increases cAMP

41
Q

Carbapenem-resistant enterobacteriacea occur in what settings? How is the prognosis?

A

They are hospital associated pathogens, especially endoscopes

CRE infections in hospital-patients are associated with high mortality

42
Q
A