Etiology and Epidemiology
The TBSF group is caused by pathogenic rickettsiae. In the Russian Federation, natural foci are represented by two nosologies: Mediterranean spotted fever (causative agent: Rickettsia conorii) and North Asian tick-borne rickettsiosis (Rickettsia sibirica). These pathogens belong to the subgenus Dermacentroxenus, due to their unique ability to parasitize and form colonies not only in the cytoplasm, but also intranuclearly. Intracellular vegetative forms are motile thanks to flagella-like structures, and invasion into target cells is mediated by the enzyme phospholipase A2.
The diseases are natural focal zoonoses. Ixodid ticks serve as the reservoir and specific vector. Rickettsiae can persist asymptomatically in the tick organism for over 18 months and be transmitted transovarially to the progeny.
Routes of human transmission:
- Vector-borne (primary) — the pathogen enters the wound with the tick's saliva during blood-sucking.
- Contact or aerogenic (alternative) — when infected hemolymph or dry feces of a crushed tick get onto damaged skin and mucous membranes.
The infection is not transmitted from person to person, and robust post-infection immunity is established after recovery.
Pathogenesis and vascular lesions
The basis of the pathogenesis of all TBSFs is the development of acute specific panvasculitis. The pathogen invades endothelial cells of venous and lymphatic vessels of the microvasculature.
The development of the disease goes through several stages:
- At the site of rickettsial inoculation (tick bite), a local immune-mediated reaction occurs with the participation of CD8+ T killers. This leads to local skin necrosis, forming the primary affect. Interestingly, when infection occurs through mucous membranes, a typical primary affect does not form.
- In the initial period, a primary "minor" rickettsiemia develops with the formation of secondary foci. Vascular lesions have the character of proliferative-desquamative vasculitis: the endothelium swells and proliferates, and inflammatory cells accumulate around the vessels.
- As the infection disseminates, the process transitions to the stage of acute destructive thrombovasculitis, the external manifestation of which is exanthema (rash).
Despite systemic vascular involvement, the disease most often runs a benign course. This is facilitated by the low replication rate of rickettsiae (doubling every 12 hours), long-term preservation of the integrity of affected cells (the pathogen exits via filopodia without rapid cell destruction), and early death of some bacteria in the primary affect zone.
Clinical presentation
The disease is characterized by cyclicity: incubation period (3 to 12 days), initial period (2–5 days), peak period (3–7 days), and convalescence.
Typical clinical presentation includes:
- Presence of a primary affect (epidermal defect over the wedge-shaped necrosis zone).
- Regional lymphadenopathy.
- Abundant polymorphic maculopapular rash.
- Pronounced intoxication syndrome with fever, caused by the action of inflammatory mediators and endothelial cell breakdown products (eicosanoids).
Most tick-borne rickettsioses are characterized by a mild or moderate course. The exception is Rocky Mountain spotted fever, which runs a severe course with high mortality, pronounced intoxication and hemorrhagic syndromes, while the primary affect and regional lymphadenopathy are not typical for it.
Diagnostics and treatment
A provisional diagnosis is made based on the clinical triad and a carefully taken epidemiological history (stay in a natural focus from April to October, tick bites). Laboratory confirmation is provided by serological reactions (CF_T, HIAT, IFA). It is important to remember that antibodies are produced against the entire group of tick-borne rickettsioses, so cross-reactivity is observed.
Mild forms are treated out-patiently, severe ones in a hospital.
Etiotropic therapy:
- Drugs of choice: tetracycline antibiotics (primarily oral doxycycline). Administration is continued up to and including the second day of normal body temperature.
- Alternative drugs: fluoroquinolones (ciprofloxacin, ofloxacin) or rifampicin for a short 4–5 day course.
- Special groups: erythromycin is prescribed for children and pregnant women.
- Important: penicillins and cephalosporins are ineffective in rickettsioses.
In case of severe intoxication, detoxification therapy is performed as indicated via intravenous drip infusions of crystalloid and colloid solutions.
Briefly: answers to topical questions
What complications can occur in Rocky Mountain spotted fever?
In severe Rocky Mountain spotted fever, disseminated intravascular coagulation (DIC) can develop. Adverse outcomes are associated with progressive functional failure of vital organs—the heart, kidneys, and central nervous system—as well as the activation of secondary microflora. The disease is characterized by a severe course, pronounced intoxication and hemorrhagic syndromes, and high mortality.
The symptom triad of TBSF is easily remembered by the acronym ALS: Affect (primary at the bite site) + Lymphadenopathy (regional) + Rash (polymorphic).
Class and exam questions
Why do tick-borne rickettsioses most often have a benign course?
This is due to the slow division rate of rickettsiae, prolonged preservation of the integrity of infected endothelial cells, and local death of some pathogens in the area of primary affect necrosis.
Where do tick-borne spotted fever pathogens multiply inside the cell?
Unlike some other rickettsiae, TBSF pathogens (subgenus Dermacentroxenus) are capable of parasitizing and forming colonies not only in the cytoplasm, but also inside the nucleus of the infected cell.
Which disease from the TBSF group runs an extremely severe course?
The exception to the group is Rocky Mountain spotted fever. It is distinguished by high mortality, massive hemorrhagic syndrome, and a primary affect is not formed.
Which antibiotics are strictly unsuitable for treating TBSF?
Penicillins and cephalosporins are ineffective in the treatment of tick-borne spotted fevers. The drugs of choice are tetracyclines.
What else to study on this topic
- Morphological differences of Rickettsia conorii and Rickettsia sibirica from the epidemic typhus agent
- Mechanism of the local immune-mediated reaction involving CD8+ T killers in the formation of the affect
- Differential diagnosis of tick-borne spotted fevers with pseudotuberculosis and measles
- Features of the pathomorphological picture of destructive thrombovasculitis during the peak period
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