Step 1: Recall what an opsonin actually does. An opsonin is a molecular tag that sticks to a microbe and makes it tastier to phagocytes, increasing the efficiency of engulfment. So we need the complement fragment that physically deposits on the bacterial cell wall.
Step 2: Within the complement cascade, $C3$ is split by C3 convertase into $C3a$ and $C3b$. The smaller piece $C3a$ floats away as an anaphylatoxin; the larger piece $C3b$ covalently bonds to the pathogen surface.
Step 3: Phagocytes carry complement receptors that grab surface-bound $C3b$, so $C3b$ is the classic complement opsonin. This is true in both the classical and the alternative pathways, which is why $C3b$ is central to innate defence.
Step 4: Eliminate the rest: $C3a$ and $C5a$ trigger inflammation and chemotaxis (anaphylatoxins), and $C6$ joins $C5b$, $C7$, $C8$ and $C9$ to build the lytic membrane attack complex. None of these coat bacteria for phagocytosis.
Therefore the opsonin among the options is C3b.\[\boxed{\text{C3b}}\]