The shapes and arrangements of bacteria

Shape and arrangement narrow a diagnosis, but they cannot close it, and understanding why is the difference between using a laboratory report well and misusing it. Several organisms that are unrelated in their biochemistry, their virulence and their treatment share an identical microscopic outline. A coccobacillus such as Haemophilus influenzae can be read as a coccus; rods of very different genera differ only in the shape of their ends. The same species can also change its appearance with age, with the medium and with the smear: young, actively dividing cultures tend to look longer and more uniform, while old cultures may be pleomorphic, showing swollen, branched or granular forms that do not resemble the textbook picture at all. This is why identification is a cascade rather than a single observation. The Gram reaction is the next layer, separating organisms whose shape is the same but whose cell wall is radically different. After that comes biochemistry: catalase and oxidase tests, coagulase for suspected Staphylococcus aureus, urease for Proteus, sugar fermentation patterns, and the Lancefield grouping of the streptococci. Further layers follow when those are not decisive — serology, molecular methods, mass spectrometry and gene sequencing — and finally susceptibility testing answers the separate question of what will actually treat the patient. For a nurse, the practical consequence is simple: a preliminary description is a working hypothesis that justifies precautions and an empirical drug, not a species name to be announced to the family. Treating it as final leads to wrong counselling, and occasionally to the wrong antibiotic, precisely because the shape was the only thing that had been established at the time the decision was made.

The arrangement is not merely a microscopic curiosity; it tracks with how the organism spreads and therefore with what the nurse must do. Streptococci divide in one plane and travel as chains. Streptococcus pyogenes, the group A beta-haemolytic streptococcus, causes pharyngitis, impetigo and scarlet fever, and in its invasive form it can produce necrotising fasciitis, in which the infection races along tissue planes and destroys muscle and fat within hours. Because the organism moves as a chain through lymph and tissue, prompt recognition of a sore throat matters more than it seems: untreated streptococcal pharyngitis can be followed weeks later by acute rheumatic fever, which damages heart valves. Prompt antibiotic treatment of the sore throat prevents that sequela, but it does not prevent post-streptococcal glomerulonephritis, the kidney inflammation produced by the same immune response, which in fact more often follows a streptococcal skin infection such as impetigo. These are not complications of the antibiotic but consequences of the immune response to an infection that was allowed to run its course, which is why completing treatment and recognising the illness early are nursing responsibilities. Staphylococci behave differently. Staphylococcus aureus divides in changing planes and clings in clusters, which makes it a master of the skin and of pus-filled, walled-off collections. It causes boils, wound abscesses, food poisoning and, in the wrong circumstances, toxic shock syndrome and bloodstream infection. Its clusters help it persist on hands, on clothing and on equipment, and its ability to acquire resistance gave us methicillin-resistant Staphylococcus aureus, a major cause of hospital-acquired infection. The nursing translation is precise. For a cluster-former, hand hygiene and environmental cleaning are the dominant defences, because the organism survives on surfaces and transfers by contact; drainage of a collection matters as much as the drug, because the walled-off pus does not receive it. For a chain-former, early recognition and full treatment of the primary infection are the dominant defences, because the later damage comes from the immune response rather than from the organism itself.

Why a coccus becomes a chain and another becomes a cluster comes down to a small set of proteins that assemble at mid-cell and to the chemistry of the wall they build there. Division begins when a ring of the protein FtsZ, a relative of the tubulin of human cells, polymerises around the inside of the cytoplasmic membrane and marks the future septum. FtsZ then recruits the other components of the divisome, including the enzymes that synthesise peptidoglycan, the mesh of sugar chains cross-linked by short peptides that gives the bacterium its shape and its strength. The cross-links are made by transpeptidases, the proteins that penicillin binds and inactivates, which is why penicillin kills only cells that are actively dividing: a cell that is not building a septum has no transpeptidase at work for the drug to attack. The position of the FtsZ ring is not random. In rod-shaped cells the Min system, a set of proteins that oscillates from pole to pole, blocks FtsZ from assembling near the ends so that the septum forms at the middle, and nucleoid occlusion prevents a ring from forming over the chromosome before it has been copied. Between the two systems the cell divides at the right place at the right time. What happens after the septum is built varies with the organism. Some cells release enzymes called autolysins that digest the connecting wall and let the daughters fall apart; others keep the wall intact, and the daughters remain joined. When the ring always forms in the same orientation, the result is a chain, as in the streptococci. When successive divisions take place in different orientations, the cells pile up in three dimensions and form a cluster, as in the staphylococci. The point for practice is that the shape and arrangement written on a laboratory report are the visible end of a precise molecular process, and that process is also the target of some of the most widely used antibiotics in the world.