Bacterial infections

“Tissue destruction and toxins” become clearer once you follow the sequence a bacterium actually uses. First it must adhere: surface structures let it stick to a mucosal cell or a wound rather than being washed away. Then it multiplies, and some species invade — they secrete enzymes such as hyaluronidase and collagenase that break down the connective tissue holding cells together, which is how an infection spreads sideways through a limb. Others stay at the surface and cause damage from a distance. The toxins they make fall into two families with different behaviour. Exotoxins are proteins actively secreted by living bacteria; they are often specific, acting on one target such as nerve endings (the paralysis of tetanus or botulism) or on the gut lining (the watery diarrhoea of cholera). Because exotoxins are proteins, they can be neutralised by antibodies and are the basis of toxoid vaccines such as tetanus. Endotoxins are different: they are part of the outer membrane of Gram-negative bacteria and are released mainly when the bacterium dies and breaks apart. They are not specific and trigger a general inflammatory cascade. In large amounts, endotoxin release produces fever, low blood pressure and widespread clotting — the picture of septic shock. This distinction has practical consequences. A Gram-negative infection treated with a rapidly bactericidal antibiotic can briefly worsen as many bacteria die at once and dump endotoxin into the blood, which is one reason severely ill patients are monitored closely during the first hours of treatment. Gram staining, the first step in identifying a bacterium, separates organisms that retain the stain (Gram-positive, often exotoxin producers) from those that do not (Gram-negative, endotoxin carriers).

Antibiotic resistance does not appear because a patient’s body becomes used to a medicine. It appears because bacteria are selected. Bacterial populations are not identical: random mutations mean that a few cells in a large population are slightly less affected by a given antibiotic. When a patient takes the full course, the drug concentration stays high long enough to kill even those less sensitive cells. When the patient stops early, the concentration falls while the tougher cells are still alive, and those survivors now multiply without competition — this is natural selection happening inside one patient in a matter of days. A single surviving bacterium can rebuild a whole population: many species divide roughly every twenty minutes, so one cell can become more than a million in about seven hours. The second road is genetic sharing. Bacteria can pass resistance genes directly to one another, even between different species, through small circular pieces of DNA called plasmids. In a process called conjugation, one bacterium builds a bridge to another and transfers a plasmid carrying, for example, the gene for an enzyme that destroys penicillin. This is horizontal gene transfer — resistance is not only inherited from parent to daughter cell, it is also acquired from neighbours, which is why resistance can appear in a patient who has never taken the antibiotic involved. Several hospital organisms, including resistant staphylococci and enterobacteria, spread their resistance genes this way. The nursing consequences follow directly: give the right dose at the right interval so the concentration never drops into the “training zone”, never stop a course without a prescriber’s instruction, use narrow-spectrum drugs when the laboratory identifies the organism, and apply hand hygiene and isolation between patients so that resistant organisms do not get the chance to meet and swap plasmids.

Knowing the mechanisms changes what a nurse does at the bedside, in a fixed order. First, obtain the specimen before the first dose whenever possible: blood cultures or a wound swab taken after the antibiotic has started often grow nothing, and the chance to identify the organism and its sensitivity is lost. Then check the practical details that decide whether the drug works — the prescribed dose, the interval, the route, the patient’s allergies, and the patient’s weight, kidney and liver function, because the same dose clears more slowly in a patient with reduced kidney function and can become toxic. Oral and IV routes are not simply interchangeable: oral treatment suits a stable patient who can absorb the drug, while an IV is chosen for severe infection or when the gut cannot be relied on, and the patient is usually switched from IV to oral once they improve — a deliberate step called IV-to-oral switch, not a random change. Observe and document the response at both levels described in the short notes: the local wound and the systemic fever curve. A fever that falls and a wound that shrinks indicate the antibiotic fits the organism; a fever that persists after two or three days is a signal to reassess rather than to add a second drug blindly. Finally, teach adherence in concrete terms. Ask the patient to repeat back when and how they will take each dose, check whether they can afford to finish the course, and explain what to do about a missed dose. This is antibiotic stewardship seen from the bedside: the goal is not to give more antibiotics but to give the right one, for the right duration, so that today’s bacteria stay treatable tomorrow. Nurses also protect patients from the opposite harm, because broad-spectrum antibiotics disturb the normal flora and can allow other organisms, including fungi, to overgrow.