Relapsing Fever and Lyme Disease

Borrelia Genus

Large, loosely coiled spirochete, Gram-negative-staining but distinct. Motile (periplasmic flagella). VISIBLE on Giemsa/Wright blood smear during fever (larger than most blood bacteria).

Relapsing Fever

Two Forms

LBRF (louse-borne): B. recurrentis ONLY. Vector: body louse (Pediculus humanus). Transmission: CRUSHING infected louse on broken skin (not bite) → hemolymph release. Epidemic — war/famine/refugee crises.

TBRF (tick-borne): multiple species (B. duttonii, B. hermsii, etc, geography-dependent). Vector: soft ticks (Ornithodoros) — brief painless NIGHT feeding, often unnoticed. Reservoir: rodents. Sporadic/endemic (caves, cabins, burrows).

Pathogenesis — Antigenic Variation

Mechanism of relapses: periodic change in major surface protein → new antigenic variant → old antibody doesn’t recognize → unchecked multiplication (fever episode) → new Ab response clears variant (afebrile interval) → next variant emerges → repeat.

LBRF: 1-2 relapses untreated. TBRF: MANY more (10+) — larger genomic variation repertoire.

Clinical Manifestations

Each episode: abrupt high fever, rigors, headache, myalgia, arthralgia. Lasts 3-7 days (resolves spontaneously as Ab clears variant). Afebrile interval ~1 week before next relapse. Splenomegaly, hepatomegaly common. Petechial/macular rash possible. Severe complications (myocarditis, hepatic failure, pregnancy loss/preterm labor) — MORE common in LBRF.

Laboratory Diagnosis

Peripheral blood smear (thick+thin, Giemsa/Wright) DURING febrile episode = standard/practical method (high spirochete count). Dark-field wet blood = motile organism demonstration. Serology complicated by SAME antigenic variation (Ab vs one variant ≠ react to another). PCR = reference labs.

Treatment

Tetracycline (doxycycline) or macrolide (erythromycin). LBRF: single dose can suffice. TBRF: longer course (relapsing tendency).

Jarisch-Herxheimer reaction: systemic reaction (fever, rigors, hypotension) within hours of FIRST antibiotic dose — sudden antigen release from mass organism killing. MORE severe/common in LBRF. Monitor closely after first dose.

Lyme Disease

Cause: Borrelia burgdorferi sensu lato complex. Vector: Ixodes hard ticks. Reservoir: deer, rodents. Unlike relapsing fever Borrelia — NO dramatic antigenic-variation relapsing pattern. Instead: STAGED progression if untreated.

Early localized: Erythema migrans — expanding “bull’s-eye” rash at bite site, days-weeks post-bite. + fever, malaise, headache, myalgia. MOST recognizable/useful diagnostic feature.

Early disseminated (wk-mo later): multiple 2° EM lesions, neuro (facial palsy, lymphocytic meningitis, radiculopathy = “neuroborreliosis”), cardiac (AV block typically).

Late (mo-yr later): Lyme arthritis — recurrent LARGE joint (knee classic) oligoarthritis = DOMINANT late manifestation. Chronic neuro involvement — less common.

Laboratory Diagnosis

Classic EM = CLINICAL diagnosis (endemic area + exposure) — lab confirmation often unnecessary/misleading (Ab not yet developed early).

Serology needed for disseminated/late/atypical: TWO-TIER TESTING — screening ELISA (sensitive) → IF positive/equivocal → confirmatory Western blot (ELISA alone has false+ from cross-reacting Ab).

PCR: role in SYNOVIAL FLUID for Lyme arthritis (higher organism burden there). Blood PCR = insensitive (unlike relapsing fever Borrelia, not high blood numbers).

Treatment

Early localized: oral doxycycline (or amoxicillin/cefuroxime if doxy contraindicated — young children, pregnancy) ×10-14 days, usually curative. Disseminated neuro/cardiac: IV ceftriaxone. Lyme arthritis: longer oral course, escalate to IV if oral fails.

Prevention

Tick-bite avoidance (protective clothing, repellents), prompt tick removal (risk rises sharply with attachment time, generally needs ≥24-48hr attachment for transmission), environmental tick control. Human vaccine exists in some regions, not universal.

The Genus Borrelia

Borrelia is a genus of large, loosely coiled spirochetes, Gram-negative-staining but distinctive enough to be classified separately, motile via periplasmic flagella, and — unlike most bacteria of medical importance — genuinely visible on a standard Giemsa- or Wright-stained peripheral blood smear during febrile episodes, since it is larger than most other blood-borne bacteria. Different species cause two clinically distinct diseases: relapsing fever and Lyme disease.

Relapsing Fever

Two Epidemiological Forms

Louse-borne relapsing fever (LBRF) is caused by a single species, Borrelia recurrentis, transmitted by the human body louse (Pediculus humanus) — humans are infected not by the louse’s bite but by crushing an infected louse against broken skin, releasing infected haemolymph. Because lice thrive in crowded, unhygienic conditions, LBRF is classically an epidemic disease of war, famine, and refugee crises.

Tick-borne relapsing fever (TBRF) is caused by multiple Borrelia species (B. duttonii, B. hermsii, and others, varying by geography), transmitted by soft ticks of the genus Ornithodoros, which feed briefly and painlessly at night, often going unnoticed. Rodents serve as the animal reservoir, and the disease is typically sporadic/endemic rather than epidemic, tracking wherever the tick vector lives (caves, rustic cabins, rodent burrows).

Pathogenesis — the Mechanism Behind “Relapsing”

The defining feature of relapsing fever — the relapses themselves — comes from antigenic variation: Borrelia periodically alters the structure of its major surface protein, generating a new antigenic variant that the host’s existing antibody response no longer recognizes. Each febrile episode corresponds to one antigenic variant multiplying unchecked until the immune system catches up and mounts a new antibody response, clearing that variant and producing a symptom-free interval — until the next variant emerges and the cycle repeats. Untreated LBRF typically has 1–2 relapses; TBRF can relapse many more times (up to 10+), since it has a larger genomic repertoire for variation.

Clinical Manifestations

An abrupt high fever, rigors, headache, myalgia, and arthralgia mark each febrile episode, lasting roughly 3–7 days before resolving spontaneously (as antibody clears that variant), followed by an afebrile interval of about a week before the next relapse. Splenomegaly and hepatomegaly are common; a petechial or macular rash can occur. Severe complications — myocarditis, hepatic failure, and, in pregnancy, miscarriage or preterm labour — are more frequent in LBRF.

Laboratory Diagnosis

Direct microscopy of a peripheral blood smear (thick and thin, Giemsa/Wright stain), taken during a febrile episode when spirochetes are circulating in high numbers, is the standard and most practical diagnostic method — dark-field examination of wet blood can also demonstrate motile organisms directly. Serology exists but is complicated by the same antigenic variation that drives relapses, since antibody raised against one variant may not react well against another; PCR is available in reference settings.

Treatment

Tetracyclines (doxycycline) or macrolides (erythromycin) are effective; a single dose can suffice for LBRF, while TBRF typically needs a longer course given its relapsing tendency. A genuinely important treatment complication is the Jarisch-Herxheimer reaction — a systemic reaction (fever, rigors, hypotension) occurring within hours of the first antibiotic dose, from the sudden release of spirochetal antigens as large numbers of organisms are killed at once; it is more severe and more common in LBRF, and patients should be monitored closely after the first dose.

Lyme Disease

Lyme disease (Lyme borreliosis) is caused by the Borrelia burgdorferi sensu lato complex, transmitted by hard ticks of the genus Ixodes, with deer and rodents as reservoir hosts. Unlike relapsing fever’s Borrelia, B. burgdorferi does not show the same dramatic antigenic-variation-driven relapsing pattern; instead, Lyme disease progresses through recognizable clinical stages if untreated.

Early localized disease: erythema migrans — an expanding, often target-like (“bull’s-eye”) red rash at the tick-bite site, appearing days to weeks after the bite, frequently accompanied by fever, malaise, headache, and myalgia. This is the single most recognizable and diagnostically useful feature of the disease.

Early disseminated disease (weeks to months later): multiple secondary erythema migrans lesions, neurological involvement (facial nerve palsy, lymphocytic meningitis, radiculopathy — collectively “neuroborreliosis”), and cardiac involvement (most typically atrioventricular conduction block).

Late disease (months to years later): Lyme arthritis (recurrent, large-joint — classically the knee — oligoarthritis) is the dominant late manifestation in most regions; chronic neurological involvement is less common but described.

Laboratory Diagnosis

Diagnosis for classic erythema migrans is primarily clinical in an endemic area with a compatible exposure history — laboratory confirmation is often unnecessary and can be misleading early in infection, since antibody hasn’t yet developed. Where serology is needed (disseminated or late disease, or atypical presentation), a two-tier testing approach is standard: an initial sensitive screening ELISA, and — only if that is positive or equivocal — a confirmatory Western blot, since ELISA alone has a meaningful false-positive rate from cross-reacting antibodies. PCR has a role in synovial fluid analysis for Lyme arthritis specifically, where organism burden is higher; blood PCR is generally insensitive, since B. burgdorferi is not typically present in high numbers in circulating blood the way relapsing-fever Borrelia is.

Treatment

Early localized disease: oral doxycycline (or amoxicillin/cefuroxime where doxycycline is contraindicated, e.g. young children, pregnancy) for 10–14 days, usually curative. Disseminated neurological or cardiac disease may need IV ceftriaxone. Lyme arthritis is treated with a longer oral course, escalating to IV therapy if oral treatment fails.

Prevention

Tick-bite avoidance (protective clothing, repellents), prompt tick removal (transmission risk rises sharply the longer an infected tick remains attached, generally requiring at least 24–48 hours of attachment), and environmental tick control in endemic areas. A human vaccine exists in some regions but is not in universal use.