A sterile agar plate, I, is streaked with a pure culture of bacteria by means of aseptic techniques. Paper discs treated with the antibiotics Aureomycin (A) and penicillin (P) are placed at opposite sides of the plate, as shown in the diagram above. The plate is examined after a 24-hour incubation period, and a clear ring is discovered around disc A, but not around disc P. Within the clear ring around disc A, a single bacterial colony with physical characteristics like those of the pure culture is observed. A second sterile agar plate, II, is then streaked with this single colony and also incubated with antibiotics.

Which of the following would most likely be observed in plate II after 24 hours?

Question

A sterile agar plate, I, is streaked with a pure culture of bacteria by means of aseptic techniques. Paper discs treated with the antibiotics Aureomycin (A) and penicillin (P) are placed at opposite sides of the plate, as shown in the diagram above. The plate is examined after a 24-hour incubation period, and a clear ring is discovered around disc A, but not around disc P. Within the clear ring around disc A, a single bacterial colony with physical characteristics like those of the pure culture is observed. A second sterile agar plate, II, is then streaked with this single colony and also incubated with antibiotics.

Which of the following would most likely be observed in plate II after 24 hours?

BlackTom AI · Accepted Answer

To tackle this question, let’s break down what the observations on plate I imply and how they translate to plate II.
Option 1: There would be a clear ring around both disc A and disc P.
- A clear ring (zone of inhibition) around a disc indicates the bacteria are sensitive to that antibiotic. In plate I, a clear ring is seen only around disc A, not around disc P. This means the bacteria are susceptible to Aureomycin but not to penicillin. Therefore, predicting a clear ring around both discs on plate II would contradict the observed susceptibility pattern and the lineage of the colony used in plate II. This option is inconsistent with plate I data.
Option 2: There would not be a clear ring around either disc A or disc P.
- The colony used to inoculate plate II originates from a spot inside the Aureomycin inhibition zone on plate I, suggesting a possible Aureomycin-resistant variant (it survived within the A zone). If this colony is then tested again on plate II, it could be resistant to Aureomycin. Additionally, the initial plate showed no inhibition by penicillin, suggesting the isolate is also resistant to penicillin. Thus, no zones of inhibition around either disc on plate II would be consistent with a double-drug resistant phenotype and matches the inference from plate I to plate II. This option aligns with the described sequence of events.
Option 3: A clear ring larger than that around disc A in plate I would appear around disc P only.
- A larger inhibition zone around P than A would imply that the colony is more susceptible to penicillin than to Aureomycin, contradicting its origin from the Aureomycin-inhibition zone and the lack of a P zone on plate I. It also conflicts with the reasoning that the plate II colony could be Aureomycin resistant. This option is inconsistent with the observed data and the probable resistance profile.
Option 4: A clear ring smaller than that around disc A in plate I would appear around disc P only.
- A smaller P zone than A would suggest partial susceptibility to penicillin, yet plate I showed no ring around P at all, indicating strong resistance to penicillin in the original culture. Expecting a smaller but present P zone on plate II would not fit the initial lack of inhibition by P. This option misreads the plate I result and the lineage of the colony used for plate II.
Option 5: A clear ring larger than that around disc A in plate I would appear around disc A only.
- If plate II showed a larger A-zone but not a P-zone, that would imply increased Aureomycin sensitivity after passaging, which contradicts the premise that the colony came from within the Aureomycin inhibition zone and is likely resistant to Aureomycin. Moreover, the question’s setup expects the plate II result to reflect the resistance characteristics of the colony, not an increased susceptibility. This option is inconsistent with the expected behavior of a colony originating from within an inhibition zone of A.
In summary, considering that the plate I observation places the isolated colony inside Aureomycin’s inhibition zone (suggesting a resistant subpopulation) and absent P inhibition (penicillin resistance), the most coherent outcome on plate II is the absence of a clear zone around both discs A and P. This aligns with a resistant phenotype to both antibiotics and follows logically from the described experimental sequence.

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