Spirochaetes, rickettsiae and chlamydiae

Ordinary diagnostic bacteriology rests on one assumption: place the specimen on a nutrient agar plate, incubate it overnight at 37 °C, and the organism will appear as colonies. Spirochaetes, rickettsiae and chlamydiae each break that assumption, and each breaks it for a different reason. Rickettsiae and chlamydiae are obligate intracellular organisms: they cannot generate enough ATP of their own and must be inside a eukaryotic cell, so a plate of agar — however rich — supplies nutrients but no host cell, and nothing grows. Spirochaetes are not intracellular in the same way, but they are fastidious and slow: Treponema pallidum has never been cultured routinely on artificial media, and Leptospira needs a specialised medium containing serum or albumin, grows slowly, and is easily overgrown or lost. The laboratory therefore reaches for other tools. Spirochaetes are demonstrated directly: dark-ground or phase-contrast microscopy shows living, motile, tightly coiled cells in a fresh specimen, while silver impregnation stains and direct fluorescent antibody tests reveal them in tissue. Rickettsiae and chlamydiae are demonstrated indirectly: cell culture using living monolayers (McCoy cells are the classic line for Chlamydia trachomatis), embryonated hen’s eggs or laboratory animals for rickettsiae, and above all nucleic acid amplification and serology. Serology is the workhorse, and it carries a rule the nurse must know: because antibodies take one to two weeks to rise, a single early serum sample is often negative, and a second, convalescent sample taken about two weeks later must be paired with it. A missing convalescent sample is not a laboratory delay; it is a follow-up failure by the clinical team. Specimen choice changes too: whole blood in an anticoagulant tube for molecular testing of leptospirosis, a midstream urine or endocervical swab in the correct transport medium for chlamydial nucleic acid testing, and a biopsy or skin lesion for rickettsial polymerase chain reaction. Because none of these results is available at the bedside within the hour, treatment for a seriously ill patient begins empirically, on the clinical pattern and the exposure history.

Two diseases in this group show how the lifestyle of the organism produces the symptoms. Relapsing fever is caused by Borrelia species. The supplied notes print “Bornelia recurrentis”; the correct name is Borrelia recurrentis, and the genus is Borrelia. Borrelia recurrentis is louse-borne: the body louse takes the organism up when it feeds on an infected person, and infection passes to the next person when the crushed louse is rubbed into a bite or a scratch. Tick-borne relapsing fever, caused by other Borrelia species transmitted by soft ticks of the genus Ornithodoros, behaves in much the same way clinically. Fever comes in attacks separated by afebrile intervals of several days because the organism performs antigenic variation: as the patient’s antibodies clear the dominant surface protein, called the variable major protein, a small sub-population that has switched to a different version survives and multiplies, producing the next attack. This is why a patient can look well and be discharged, then return with fever, and why a single blood film taken during an afebrile interval may be negative. Nurses should expect rigors and a rising temperature after the first effective dose — the Jarisch–Herxheimer reaction — and monitor the blood pressure rather than dismiss it as a drug allergy. Weil’s disease is the severe form of leptospirosis, most often caused by Leptospira interrogans. The notes print “Leptora interrogans”; the correct genus is Leptospira. After entering through broken skin or a mucous membrane, the organism spreads through the blood and then settles in the kidney, the liver, the meninges and the eye. Capillary walls are damaged, so plasma leaks into the tissues and small haemorrhages appear, which is why the patient has muscle pain and red eyes, then jaundice with a high bilirubin, and later acute kidney injury from tubular damage. The illness can progress to haemorrhage into the lungs or gut, myocarditis and death. Treatment is a penicillin or doxycycline plus supportive care, and dialysis in severe cases. The nursing priorities follow from the mechanism: strict fluid balance and daily weight, accurate urine output, watching for bleeding gums, epistaxis, haemoptysis and black stool, and monitoring for confusion that may signal meningitis. Jaundice with a falling urine output in a patient who has waded in flood water is a medical emergency, not a reason to wait for a serology result that will arrive in two weeks.

The choice of drug for these infections follows from one rule of pharmacology: an antimicrobial reaches only the compartments it can enter. A bacterium free in the blood or in interstitial fluid is exposed to the drug concentration in plasma. A bacterium inside a macrophage, an endothelial cell or an epithelial cell is exposed only to the concentration inside that cell, so the decisive property is not how potent the drug looks in a test tube but how well it crosses the human cell membrane and accumulates where the organism sits. Doxycycline is strongly lipophilic, enters human cells readily and inhibits the bacterial ribosome at the 30S subunit. Macrolides — azithromycin, erythromycin and clarithromycin — are also concentrated inside cells, where they bind the 50S subunit. Both classes are therefore active against rickettsiae and chlamydiae. Beta-lactams act on the peptidoglycan wall of a multiplying bacterium in the extracellular space; for organisms living inside cells that target may be absent or unreachable, and in chlamydial infection the metabolically active form has a different surface chemistry, so penicillins are not the drugs of choice. Azithromycin has a further advantage: it reaches high concentrations inside cells, remains there for days, and can be given as a single 1 g dose for uncomplicated genital chlamydial infection, which matters enormously for adherence and for treating the partner. The nursing detail is equally pharmacological. Doxycycline should be swallowed with a full glass of water while sitting or standing and not at bedtime, because it can ulcerate the oesophagus if it lodges there. It chelates calcium, iron and magnesium, so milk, antacids and iron tablets must be separated from the dose by at least two hours, otherwise the drug is swallowed but never absorbed. It causes photosensitivity, so the patient needs sun protection and advice, and it is avoided in pregnancy and in young children except when a serious rickettsial infection makes the benefit greater than the risk. Finally, adherence is a microbiological act: an interrupted course lets surviving organisms return, and for chlamydial infection it also leaves the partner untreated and the patient reinfected. The nurse who explains why the tablets must be taken with water and away from milk, and who arranges treatment for the partner, is applying cell biology at the bedside.