Rickettsias are numerous infectious diseases associated with a common etiology (pathogens are rickettsias) and epidemiology (they have a predominantly transmissible transmission mechanism). Disease occurs with the occurrence of primary affect (with tick-borne rickettsias), febrile and intoxication syndromes, generalized vasculitis and skin rashes. Serological diagnostics (RIGA, RSC, RNIF, ELISA) allows to confirm the diagnosis and verify its clinical form. Etiotropic therapy is carried out with antibacterial drugs from the tetracycline group and chloramphenicol.
Rickettsias is a term used in relation to vector–borne febrile diseases caused by intracellular pathogens — rickettsias. The group of human rickettsias includes typhus (endemic and epidemic), tick-borne fevers (Rocky Mountain spotted fever, Volyn fever, Marseille fever, vesicular rickettsias, North Asian tick-borne rickettsias), paroxysmal rickettsias (trench fever, tick-borne paroxysmal rickettsias), tsutsugamushi fever and Q fever. Despite the etiological differences, all these diseases are characterized by some common epidemiological, pathogenetic, pathomorphological, immunological and clinical signs that allow them to be united by a common name – rickettsias. The prevalence is ubiquitous; the greatest incidence is observed in developing countries, where they account for 15-25% in the structure of fevers of unclear etiology.
According to their cultural qualities, rickettsias are an intermediate link between bacteria and viruses. They are brought closer to microbial pathogens by morphological signs (gram–negative rod-shaped or coccoid forms), and with viral agents – the ability to intracellular parasitism. The following types of rickettsia are pathogenic to humans:
- R. Prowazekii – causes epidemic (lice) typhus and its distant relapse – Brill’s disease
- R. Typhi – causes endemic (rat, flea) typhus
- R. Sibirica – causes North Asian tick-borne rickettsias
- R. Conorii – causes Marseilles fever
- R. Rickettsii – causes Rocky Mountain spotted fever
- R. Australis – causes Australian tick–borne rickettsias
- R. Quintana (Rochalimea quintana) – causes Volyn fever
- R. Akari — causes vesicular rickettsias
- R. Japonica – causes Japanese spotted fever
- R. Orientalis – causes tsutsugamushi
- R. Burneti (Coxiella burnetii) – causes Ku-fever
Rickettsioses are divided into anthroponotic, in which a person acts as a source of infection, and lice are carriers, and zoonotic, characterized by transmission from animals through tick bites. Typhus and trench fever belong to anthroponoses; all other rickettsioses belong to natural focal zoonoses.
Rickettsias are not stable in the external environment: heating and exposure to disinfectants are detrimental to them. However, at low temperatures and drying, rickettsias can persist for a long time. There may be several ways of infecting a person with rickettsias – transmissible, hemotransfusion and transplacental; in some cases (for example, with fever, Cu – contact, aspiration, alimentary). The entrance gate for rickettsias is most often the skin, where a local inflammatory reaction – primary affect – can develop at the site of the pathogen introduction. Subsequent hematogenic dissemination of the pathogen causes the development of feverish intoxication syndrome and generalized vasculitis.
Rickettsias of the typhus group
Epidemic (lice) typhus occurs with fever, intoxication, roseolus-petechial rash on the skin, damage to the vascular and nervous system. The incubation period takes from 5 to 21 days. Rickettsias manifests with an increase in body temperature and general intoxication symptoms, which reach maximum severity by the 3rd-6th day of the disease. During this period, there is pronounced hyperemia and puffiness of the face, injection of sclera, enanthema on the soft palate. Approximately on the 5th day, a bright characteristic roseolus-petechial rash appears on the skin of the lateral surface of the chest, abdomen, flexor surfaces of the arms. After a week, the rash pales, and at 2-3 weeks from the onset of the disease disappears. At the same time, the temperature decreases and intoxication disappears, but post-infectious asthenia persists for several more weeks. In severe rickettsias, there is a central nervous system lesion in the form of meningitis or encephalitis. Complications of epidemic typhus can include otitis media, mumps, pneumonia, myocarditis. Brill’s disease, or recurrent typhus, manifests itself with the same symptoms, but less pronounced.
Endemic (rat or flea) typhus begins acutely and in the initial period is characterized by general infectious symptoms (fever, fever, arthralgia, headache). At the height of the febrile period, a rash appears on the chest, abdomen and extremities, which has a predominantly roseolous-papular character. Arterial hypotension, bradycardia, general weakness, dizziness are characteristic. In general, the disease proceeds more easily than epidemic typhus.
Rickettsioses of the spotted tick fever group
North Asian tick-borne rickettsias, or tick-borne typhus of North Asia is transmitted through the bites of ixodic ticks. A typical sign of tick–borne rickettsias is primary affect – the primary inflammatory reaction of the skin at the site of penetration of the pathogen. It is a painful seal surrounded by a zone of hyperemia and covered with a brown scab in the center. Simultaneously with the appearance of primary affect, body temperature rises, regional lymphadenitis and intoxication syndrome develop. Skin rashes appear on the 2nd-3rd day and are represented by polymorphic roseolous-papular elements located on the trunk and around the joints. There is hyperemia of the face and pharyngeal mucosa, bradycardia, hypotension, moderate hepatosplenomegaly. The course of North Asian tick-borne rickettsias is benign; recovery usually occurs by the 14th day of the disease.
Marseille fever is also characterized by the presence of a primary affect at the site of the introduction of the tick, fever, lymphadenitis, spot-papular rash. The initial signs of rickettsias are similar to tick-borne typhus in Northern Asia. The primary affect looks like a dense infiltrate with central necrosis, which later ulcerates and epithelizes only in the period of convalescence (after 3-4 weeks). Against the background of feverish intoxication manifestations, hyperemia of the oropharyngeal mucosa, sore throat, conjunctivitis are expressed. A distinctive feature of Marseille fever is a rash that affects not only the body, but also the face, palms and soles. Usually the rash has a spotty-papular character, but it can transform into pimples (“pimple fever”) with hemorrhagic contents. The fading of the rash is gradual, pigmentation persists in its place for a long time.
Rocky Mountain spotted fever refers to rickettsias with a severe course. In the acute period, the disease is accompanied by chills, alternating fever; severe headache and muscle pain, nosebleeds. Neurological changes include insomnia, impaired consciousness (deafness, prostration), seizures, para- and hemiplegia, visual and hearing impairments. There is no primary affect. The rash with this type of rickettsias is abundant, petechial, tends to merge with the formation of large spots. The mortality rate from this rickettsias reaches 7%.
Paroxysmal rickettsias occurs with recurrent febrile attacks, recurring every 5 days (with Volyn fever) or 2-3 days (with paroxysmal tick-borne rickettsias). During an attack, the temperature rises to 39.0–40.5 ° C, chills, ossalgia, myalgia, arthralgia, headaches appear. Primary affect, skin rashes and regional lymphadenitis are not constant companions of paroxysmal rickettsias and are often absent. The course of fevers is usually prolonged, but benign.
Identification and differential diagnosis of rickettsioses is carried out in several directions: collection of epidemiological anamnesis, analysis of clinical data and laboratory verification of the pathogen. In the epidemiological status, the emphasis is on the natural focal nature of the infection, the connection of the disease with tick bites, pediculosis, etc. When analyzing the clinical symptoms of rickettsias, the main attention is paid to the presence of primary affect, the nature and localization of the rash.
Laboratory diagnostics of rickettsioses is carried out using serological methods (IFT, IRF, ELISA), which allow identifying the pathogen by determining its antigens and specific antibodies. In some cases, it is possible to isolate rickettsias from blood, urine, cerebrospinal fluid, biopsies, tick biomass, and skin allergy tests. Differential diagnosis of rickettsioses is carried out with influenza, measles, hemorrhagic fevers, meningococcal infection, typhoid fever, enterovirus infection, allergies, etc.
Tetracycline antibiotics (tetracycline, doxycycline), chloramphenicol, fluoroquinolones are used as means of etiotropic therapy of rickettsias. Usually, the course of treatment lasts the entire febrile period and 2-3 days after the normalization of body temperature. At the same time, detoxification, desensitizing, anti-inflammatory therapy is carried out. In severe rickettsias, corticosteroid hormones are used.
Prognosis and prevention
According to the course, outcomes and mortality rates, the most severe rickettsioses include epidemic typhus, Rocky Mountain spotted fever and tsutsugamushi. The remaining rickettsioses are more benign and rarely accompanied by complications. Prevention of rickettsias infection involves the fight against pediculosis, ticks and rodents, compliance with personal protection measures against the attack of blood-sucking insects. In case of tick bites, emergency chemoprophylaxis with doxycycline or azithromycin is recommended. In order to prevent typhus and Ku fever, vaccination is carried out. Patients with typhus are subject to strict isolation; persons in contact with the patient are monitored; sanitary treatment is carried out in the focus of infection.