Symptoms of the initial and peak stages of the disease
The disease starts acutely, accompanied by a powerful intoxication syndrome (Anamnesis morbi). In the initial stage, patients complain of severe chills and high fever. Headache, photophobia, anorexia, insomnia, and thirst are characteristic. Intense myalgia, localized predominantly in the calf muscles, is considered a pathognomonic clinical sign. In the peak stage, the initial symptoms persist and progress. Signs of internal organ involvement join in:
- Abdominal pain and dyspeptic disorders occur.
- Lower back pain appears, and the color and volume of excreted urine change.
- The skin acquires a yellowish hue.
- Hemorrhagic syndrome manifests: nosebleeds, rash, and hemorrhages on the mucous membranes and skin.
In some cases, the development of meningeal symptoms is possible.
Laboratory and instrumental findings
Nonspecific tests reflect the systemic inflammatory process and target organ damage:
- Complete blood count: reveals pronounced leukocytosis (12–20 × 10⁹/L), neutrophilia with a left shift of the leukocyte differential, and moderate anemia. The erythrocyte sedimentation rate (ESR) is significantly accelerated — up to 40–60 mm/h.
- Urinalysis: demonstrates proteinuria, leukocyturia, cylindruria, and frequently hematuria.
- Cerebrospinal fluid (CSF) analysis (if meningitis is suspected): CSF pressure is elevated, with a moderate increase in protein level, normal glucose, and lymphocytic (less commonly neutrophilic) pleocytosis.
- X-ray: may show small focal infiltrates in the lungs, signs of pulmonary edema, or enlargement of cardiac borders.
Specific infection diagnostics
Confirmation of the diagnosis requires identifying the pathogen itself, its DNA, or specific antibodies.
- Bacterioscopy: dark-field microscopy of a crushed blood drop (in early stages) or examination of urine and CSF (at the peak of the disease).
- Serology: hemagglutination inhibition, microscopic agglutination test (MAT), agglutination test, complement fixation test. The diagnosis is confirmed with a titer of 1:100 or higher against the background of typical clinical findings, or with a fourfold increase in low titers (1:20–1:40) over time.
- Immunology and molecular genetics: detection of Leptospira DNA using PCR, detection of antigens by ELISA and RIA (at a concentration of more than 100 bacteria per 1 mL), and detection of specific IgM antibodies by ELISA.
- Bacteriological method: culture of blood, CSF, or urine. Due to slow growth of the culture (from 2 weeks to 3 months), it has only retrospective value. A biological test on guinea pigs is also used.
Treatment and management tactics
Patients are subject to hospitalization with strict bed rest (especially with signs of renal or hepatorenal failure) and diet.
- Etiotropic therapy: for mild to moderate cases, doxycycline is prescribed orally (per os) at 100 mg twice daily for a 7-day course. Alternatives include oral ampicillin, amoxicillin, or azithromycin. For severe cases, the drug of choice is benzylpenicillin intramuscularly (6–12 million IU/day, up to 24 million for meningitis) or intravenous penicillin G.
- Specific immunotherapy: heterologous antileptospiral immunoglobulin is used. It is administered strictly fractionally using Besredka's method.
- Pathogenetic therapy: includes detoxification, correction of hemostasis and electrolyte balance. If acute renal failure progresses, hemodialysis is indicated.
Differential diagnosis
At the initial stage, leptospirosis is differentiated from other acute fevers:
- Influenza: differs by autumn-winter seasonality, short course (up to 5 days), tracheobronchitis, and leukopenia. Jaundice, hepatosplenomegaly, and kidney damage are atypical for it.
- Epidemic typhus: characterized by pronounced meningeal syndrome, facial hyperemia, Govorov-Godelier sign, and roseolous-petechial rash starting from days 4–6.
- Typhoid fever: differs by gradual onset, facial pallor at the peak of fever, roseola on the abdomen, relative bradycardia, and leukopenia.
When organ damage develops, it is important to exclude:
- Viral hepatitis: cyclicity, improvement in well-being upon the appearance of jaundice, high aminotransferase levels.
- HFRS (Hemorrhagic Fever with Renal Syndrome): jaundice and hepatolienal syndrome are absent, and antibacterial therapy is ineffective.
- Malaria: characterized by a clear sequence of febrile paroxysm phases (chills — fever — sweating) and the detection of plasmodia in a blood smear.
To remember the classic clinical picture of the peak stage of leptospirosis, use the triad: Myalgia (especially calf muscles) + Kidneys (oliguria, hematuria) + Jaundice (liver damage).
Class and exam questions
Which clinical symptom is considered pathognomonic for leptospirosis?
Pronounced calf muscle pain (myalgia) that appears from the first days of high fever.
How to distinguish leptospirosis from hemorrhagic fever with renal syndrome (HFRS)?
In HFRS, hepatolienal syndrome and jaundice are absent, and antibacterial therapy does not provide a therapeutic effect.
What criteria confirm the diagnosis serologically?
The minimum diagnostic antibody titer in serological reactions is 1:100. The diagnosis is also confirmed by a 4-fold increase in initially low titers over time.
How is the specific antileptospiral immunoglobulin administered?
The drug is administered strictly fractionally according to Besredka's method: on the 1st day, a diluted preparation (1:10) is first administered subcutaneously, followed by the undiluted preparation intramuscularly.
What else to study on this topic
- Collection of epidemiological history (water, occupational factors, contact with animals)
- Algorithm for differential diagnosis with yersiniosis and sepsis
- Dispensary Observation of Convalescents
- Sanitary and veterinary prevention measures and vaccination
- Emergency drug prophylaxis
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