Borrelia and Relapsing Fever
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Direct answer
Fever that spikes, clears for days, then returns — each crisis milder than the last — is the pattern the name promises. Relapsing fever borreliae are long, loosely coiled spirochaetes that, unlike Treponema, stain readily with Giemsa, Leishman and Wright stains and circulate in peripheral blood during febrile episodes, so the diagnostic move is a simple thick and thin smear taken during the fever. Two epidemiological forms: louse-borne relapsing fever from Borrelia recurrentis, transmitted when the human body louse is crushed and its haemolymph contaminates abraded skin; and tick-borne relapsing fever from species such as B. duttoni and B. hermsii, delivered by painless, fast-feeding Ornithodoros soft ticks. The relapses are pure antigenic variation: a repertoire of silent variable membrane protein genes converts into an expressed locus, so each new serotype escapes the antibody response that cleared the previous wave.
What you must remember
- Morphology and staining: coarse, irregular spirals, 10-30 by 0.3 micrometres, with hooked ends; readily visible in peripheral blood stained with Giemsa or Wright — the decisive contrast with Treponema pallidum, which is too thin to see by light microscopy.
- Vector distinction: louse-borne B. recurrentis — Pediculus humanus corporis, crushed-louse transmission, humans the sole reservoir, epidemic; tick-borne species — painless night-feeding Ornithodoros soft ticks, minutes-long feeds, transovarial maintenance, endemic and sporadic.
- The relapse mechanism: silent vmp cassettes in the genome recombine into the expression site by gene conversion, switching the major outer membrane protein; each febrile episode equals a new dominant serotype; the antibody response clears each wave but cannot anticipate the next.
- Clinical pattern: sudden fever, headache, myalgia, hepatosplenomegaly; crisis ends with defervescence and risk of shock; louse-borne disease has fewer relapses (often one to three) but higher untreated mortality; tick-borne disease relapses more often but kills less.
- Complications to quote: myocarditis, splenic rupture, hepatic dysfunction, abortion, iridocyclitis and Jarisch-Herxheimer reaction during therapy — rigors, fever and hypotension within two hours of the first dose, driven by tumour necrosis factor and interleukin-6 release.
- Diagnosis: Giemsa-stained thick and thin films during fever (highest yield at peak fever), darkfield microscopy of blood, PCR in reference laboratories; serology is unhelpful — no routine specific test, and Weil-Felix is negative.
- Treatment: doxycycline seven days for tick-borne disease; louse-borne responds to a single dose of tetracycline (erythromycin in pregnancy); monitor for Jarisch-Herxheimer — fatal reactions are described.
- Delousing logic: epidemic control is delousing of contacts, not quarantine — the louse, not the patient, is the target.
One patient, three serotypes
Follow the immunology through a natural history. Day one: fever, spirochaetes flooding the blood, Giemsa-positive. Day five: antibodies against the dominant variable membrane protein rise, opsonise the circulating borreliae, and clearance produces the crisis — fever, rigors, sometimes hypotension as the spleen filters the debris. A week of health follows, but in the bone marrow and spleen a few borreliae have silently switched their expression site to a different vmp gene; these escapees multiply below the antibody radar, and day ten brings fever number two, a different serotype on the smear. Wave three is smaller, and untreated, the cycle exhausts itself into carrier state or cure. This is antigenic variation compressed from influenza's years into weeks — one reason no vaccine exists.
Overlay treatment: a single tetracycline dose kills the population within hours — releasing a lipoprotein bolus that triggers the Jarisch-Herxheimer reaction, why the first dose is given where fluids and monitoring exist.
Where students slip
The Treponema comparison trips the maximum: students expect all spirochaetes to be invisible on light microscopy, but Borrelia is the fat, stainable exception — and the answer to "which spirochaete do you diagnose from a peripheral smear". Second, the Weil-Felix reflex: relapsing fever shares nothing antigenically with Proteus, and the test is negative. Third, vector details get flattened — soft Ornithodoros ticks feed in minutes at night and are rarely noticed when the fever begins, so "no tick bite history" excludes nothing; the louse-borne form transmits by crushing, not biting. Finally, do not confuse Jarisch-Herxheimer with drug allergy or with cerebral malaria in the febrile post-dose patient — the timing within two hours of therapy and the cytokine explanation should be written explicitly.
Frequently asked questions
Why does relapsing fever relapse?
Sequential antigenic variation: borreliae switch their expressed variable membrane protein from a silent gene library, so each relapse is a new serotype escaping the antibodies that cleared the previous wave.
How is relapsing fever diagnosed in a district laboratory?
By Giemsa or Wright-stained thick and thin peripheral blood films taken during the febrile peak, where the loosely coiled spirochaetes circulate; PCR is available in reference laboratories.
How do louse-borne and tick-borne relapsing fever differ?
Louse-borne Borrelia recurrentis is epidemic, transmitted by crushing the body louse, relapses fewer times and kills more; tick-borne species are endemic, transmitted by painless night-feeding Ornithodoros, relapse more and kill less.
What is the Jarisch-Herxheimer reaction in this setting?
A cytokine storm — tumour necrosis factor and interleukin-6 driven — of rigors, fever and hypotension within two hours of the first antibiotic dose, managed supportively with fluids and monitoring.
Is the Weil-Felix test useful in relapsing fever?
No; relapsing fever borreliae share no antigens with Proteus strains, so the test is negative — microscopy during fever, not serology, makes this diagnosis.