Yes — this is a well-documented pattern in lymphatic filariasis

Why it "hides" and then flares

• The adult worms live for years inside the lymphatics/lymph nodes (often 5-8 years, sometimes longer), quietly causing low-grade lymphatic damage (dilation, valve destruction, scarring) without any visible symptoms in between attacks - "the affected body part appears clinically normal in between these episodes" (Dermatology, 2-Vol Set 5e, p. filariasis ch.).
• Superimposed on this chronic damage, people get recurrent acute attacks - classically called acute adenolymphangitis (ADL) or acute dermatolymphangioadenitis (ADLA). These episodes:
  • Last about a week
  • Recur roughly 1 to 10 times per year in a given affected limb
  • Present with sudden limb swelling, redness/warm skin, ascending lymphangitis (streaking up the limb), tender regional lymph nodes (groin/axilla), fever, chills, and malaise
  • Are usually one-sided (matches the "single leg" pattern you describe) - Dermatology, 2-Volume Set 5e
• These flares are typically triggered by a secondary bacterial or fungal superinfection, often entering through a tiny skin break (commonly between the toes, e.g. from fungal interdigital infection). Because the lymphatics are already damaged from the underlying worm infection, even a minor skin breach in the same limb repeatedly sets off inflammation there - hence why it's the same leg each time rather than random sites.
• Seasonal clustering makes sense too: heat, humidity, minor foot fungal infections, and mosquito-transmission cycles all tend to peak in certain seasons in endemic regions, which can make these ADL/ADLA flares appear "yearly" or tied to a particular time of year.

The bigger picture

• Each recurrent attack causes a bit more lymphatic scarring. Over 10-15 years, repeated episodes progress to chronic disease - persistent lymphedema and eventually elephantiasis (Dermatology, 2-Volume Set 5e).
• So it is not truly "dormant" worms reactivating on a schedule - it's chronic, ongoing lymphatic damage from worms/dead worm debris, punctuated by acute inflammatory flares (often infection-triggered) that happen to recur periodically.

Important caveat

• Filarial ADL/ADLA (if you're in or have lived in an endemic area - South Asia, Sub-Saharan Africa, parts of South America/Pacific)
• Recurrent bacterial cellulitis/erysipelas (very common cause of one-sided leg swelling + fever, and it doesn't require filariasis at all - lymphedema of any cause predisposes to recurrent cellulitis, which becomes a self-perpetuating cycle)
• Or another cause of secondary lymphedema entirely

Treatment & Prevention Plan for Recurrent Filarial Leg Swelling

1. Antifilarial drug treatment (targets the worms/microfilariae)

• Diethylcarbamazine (DEC) - the traditional first-line agent, 6 mg/kg/day in divided doses for 12 days in individual treatment, or as a single annual dose in mass programs
• Albendazole - added for broader antiparasitic coverage, weaker alone against filariae but boosts the combination
• Ivermectin - added in some regimens, especially where onchocerciasis co-exists
• Current WHO/program strategy is a single-dose triple-drug regimen (ivermectin + DEC + albendazole, "IDA"), shown in trials (including a large Papua New Guinea study) to be markedly more effective at clearing microfilariae than two-drug regimens - Katzung's Basic and Clinical Pharmacology, 16th Ed; Goodman & Gilman's Pharmacological Basis of Therapeutics.
• In endemic countries this is given as annual mass drug administration (MDA) to the whole at-risk community for several years (WHO recommends 4-6+ rounds), because the disease keeps being re-transmitted by mosquitoes if only individuals are treated - Dermatology, 2-Volume Set 5e (Treatment).
• Note: DEC and ivermectin kill microfilariae rapidly and can occasionally trigger short-term inflammatory reactions (Mazzotti-like reactions) - this is usually managed with antipyretics/antihistamines and is not a reason to stop treatment.

2. Preventing the recurrent attacks (this is what actually stops your "seasonal" pattern)

• Daily hygiene - wash the affected limb (and the other leg too, even if unaffected) with pH-neutral soap and water, at least once daily, ideally before bed
• Meticulous foot/skin care - dry thoroughly between toes, treat any fungal infection (interdigital tinea is the classic entry point for the bacteria that trigger ADLA) promptly with antifungal cream, keep nails trimmed, treat any cuts/wounds immediately with antiseptic
• Limb elevation at rest and at night to encourage lymphatic drainage
• Regular exercise/movement of the limb to promote lymph flow (avoid prolonged standing)
• Wearing shoes to prevent skin injuries and fungal entry
• Some programs also use prophylactic antibiotics (e.g., penicillin) for patients with frequent ADLA recurrences, similar to how recurrent cellulitis with lymphedema is managed elsewhere

3. Mosquito bite prevention (stops new infection/re-infection)

• Sleep under a mosquito net, use repellent on exposed skin, wear long sleeves/pants especially at dusk/night when the relevant mosquito vectors bite
• This matters even after treatment, since re-infection is possible if you remain in or travel to an endemic area

4. For advanced swelling (hydrocele/elephantiasis)

• Hydrocele can be corrected surgically (excision and eversion of the sac)
• Surgery for reducing chronically swollen limbs is rarely done/rarely successful and is not first-line - Bailey & Love's Short Practice of Surgery, 28th Ed

Bottom line

1. Get tested to confirm filarial infection.
2. If confirmed, take the antifilarial drug course (DEC/albendazole/ivermectin combination) under medical supervision.
3. Regardless of drug treatment, start daily limb hygiene, foot/skin care, elevation, and exercise now - this is the single most effective way to reduce how often that leg flares up with swelling and fever going forward.
4. Use mosquito prevention measures if you're in or visiting an endemic region, to avoid reinfection.

Two distinct entities get lumped together as "filarial attacks"

• This is the genuine filaria-driven event: fever, lymphadenitis, retrograde lymphangitis (spreading peripherally, which is what distinguishes it from ordinary bacterial lymphangitis), and edema lasting days to a week
• It's triggered either by the living adult worm irritating the lymphatic vessel/node, or more classically by the death of an adult worm, which releases a burst of parasite antigen and provokes an intense immune/inflammatory reaction - Campbell-Walsh-Wein Urology
• So true ADL does need worm activity (live or dying) as the trigger - it's not purely a consequence of old damage

• This is what you're describing when attacks keep recurring year after year, often long after any worms are dead or treated
• It presents with fever, chills, myalgia, and painful edematous/inflamed skin plaques, often starting at a visible skin injury or fungal entry point (classically between the toes)
• Mechanism: no active worm is required. Once the lymphatics are structurally damaged (dilated, valve-incompetent, obstructed) from earlier filarial injury, that limb becomes a vulnerable, poorly-draining pocket. Any minor bacterial or fungal breach of the skin in that limb then spreads unchecked through the damaged lymphatics, causing the inflammatory flare - Dermatology, 2-Volume Set 5e; Campbell-Walsh-Wein Urology
• This is exactly why these episodes continue to recur even after successful antifilarial drug treatment has cleared the worms - the anatomical damage (not the parasite) is now the driver
• It's also why WHO's prevention strategy for recurrent attacks is hygiene and skin/entry-lesion care, not repeated antiparasitic dosing - once the lymphatics are damaged, killing more worms won't stop these episodes, but keeping the skin intact and infection-free will

Bottom line for your case

What a low-titer/mild positive on echinococcus serology usually means

• Echinococcus antibody tests (ELISA, IHA) are screening tests, not confirmatory ones. Even textbooks note ELISA positivity rates of only ~85% in confirmed hepatic hydatid disease and roughly 50% sensitivity in pulmonary disease - so serology alone, especially a weak/borderline result, is unreliable on its own (Schwartz's Principles of Surgery, 11th Ed; Murray & Nadel's Textbook of Respiratory Medicine).
• Serology is meant to be used alongside imaging (ultrasound or CT looking for a cystic lesion in liver/lung, the two most common sites), not as a standalone diagnosis - Bailey and Love's Short Practice of Surgery, 28th Ed; Maingot's Abdominal Operations.

Important: cross-reactivity, particularly relevant to you

• Other cestodes, especially Taenia solium (cysticercosis) - a "strong cross-reaction" is well described
• Other helminths, including filarial nematodes - Public Health Ontario's echinococcosis serology reference specifically lists filarial nematodes, along with Taenia, Schistosoma, and Strongyloides, as causes of cross-reactive false positives on echinococcus antibody testing
• Also: cysticercosis, schistosomiasis, collagen vascular disease, liver cirrhosis, and some cancers - CDC DPDx; Tietz Textbook of Laboratory Medicine

What I would NOT do

• Don't start antihelminthic treatment (albendazole) or pursue surgery/PAIR based on serology alone, especially a mild/borderline result.
• Don't assume it's unrelated or dismiss it either - it needs to be worked up properly rather than ignored.

What should happen next

1. Imaging - abdominal ultrasound (liver is the most common site, ~65-70% of hydatid cysts) and a chest X-ray or CT if there's any respiratory symptom, to look for an actual cyst. If no cyst is seen anywhere, a mild positive serology on its own is very unlikely to represent active disease.
2. Repeat/confirmatory serology - if there's real concern, request a more specific confirmatory test rather than relying on the screening ELISA: immunoblot, or antigen-specific tests (Antigen B, Antigen 5, or Em2/recEm18 for alveolar echinococcosis) which have far less cross-reactivity - Current Surgical Therapy, 14th Ed.
3. Correlate with eosinophil count and exposure history - hydatid disease classically causes eosinophilia and is linked to exposure to dogs/livestock in endemic sheep/cattle-raising regions (echinococcus needs a dog-livestock cycle, unlike filariasis which is mosquito-borne) - so travel/animal contact history matters here.
4. Tell your treating physician about the filariasis - they should factor in the known cross-reactivity risk before acting on this result.

Why you can't get a precise percentage from serology alone

• Echinococcus ELISA specificity in different studies has ranged from roughly 77% to 100%, and sensitivity from ~79-90% (Mahajan et al. 2019; Erganis et al. 2024)
• Critically, when specificity isn't perfect and the disease is not highly prevalent in the tested population, the positive predictive value (PPV) can be quite low - one comparative immunoassay study found PPV as low as 52-60%, even though the negative predictive value stayed high (94-100%) (Fecková et al. 2020, PMC7425236). That means in some settings, closer to half of all positive results were false positives.
• This is exactly why textbooks (CDC DPDx, Public Health Ontario, Schwartz's Principles of Surgery) all say echinococcus serology should never stand alone - it needs imaging correlation.

Applying this to your specific situation

1. "Mild" (low titer) result - weak positives are disproportionately more likely to represent cross-reactivity or nonspecific reaction than strong positives. Antibody titer roughly correlates with the strength of true antigen-driven response; a borderline reading sits right in the zone where cross-reactive false positives cluster.
2. A known, documented cross-reactor is present - you have confirmed/suspected filarial infection, and filarial nematodes are explicitly listed as a cause of false-positive echinococcus serology (Public Health Ontario reference). This isn't speculative on my part - it's a recognized interference.
3. No imaging finding mentioned - if you haven't had an ultrasound/CT showing an actual cyst in the liver or lung, that absence matters a lot. Serology without a corresponding lesion carries much less weight.
4. No mention of eosinophilia, travel/exposure to livestock-dog cycle (echinococcus needs dog-sheep/cattle transmission, unlike mosquito-borne filariasis), or relevant symptoms (RUQ pain, hepatomegaly, biliary symptoms, or a lung mass) - these would raise suspicion if present.

My honest assessment

• Ultrasound/CT showing a cystic lesion in liver or lung → raises probability substantially (this is the deciding factor)
• Peripheral eosinophilia → raises probability somewhat
• A repeat, more specific confirmatory test (immunoblot, Antigen B/Antigen 5-specific assay) staying positive → raises probability
• Normal imaging plus a repeat test that reverts to negative or stays only weakly positive → strongly favors false positive/cross-reactivity