Vesicular rickettsiosis is an acute transmissible natural focal infection. Characteristic signs are primary affect with central necrosis and abundant rash on the body. Fever, symptoms of general intoxication and a relatively benign course are noted. The main method of diagnosis is the isolation of the rickettsia gene material (PCR), the detection of antibodies to the pathogen using serological techniques. Therapeutic measures include etiotropic antibacterial therapy, the use of detoxification, antipyretic, angioprotective and other means.
ICD 10
A79.1
General information
Vesicular rickettsiosis (smallpox, gamase rickettsiosis, Kew Garden spotted fever) is a zoonotic rickettsiosis disease. The first mention of the infection dates back to 1946, when cases of vesicular fever were recorded in New York. Subsequently, similar symptoms were described in other cities of the USA, Croatia, Ukraine, Belarus, Moldova, and Central Africa. Isolated cases of the disease are registered annually with a seasonal rise in May-September. Among the patients, men predominate mainly over the age of 60, women become infected less often, usually at the age of 45.
Causes
The causative agent of the disease is rickettsia Rickettsia akari. Reservoirs and sources of infection are domestic mice, dogs, cats. The transmission of rickettsia in the vast majority of cases is carried out by mouse ticks, in conditions of a large animal population, human vectors do not attack. Among ticks, transovarial transmission of the pathogen often occurs. Cases of aerogenic human infection have been reported when working with rickettsias in laboratories.
The importance of vesicular rickettsiosis for modern infectology is due to the high incidence among injecting drug users, homeless and antisocial persons. This rickettsiosis pathology is in second place after bartonellosis; currently, the number of cases of the once-casuistic possibility of hemocontact transmission is increasing. The prevalence of HIV infection in the human population contributes to the emergence of complicated forms of the disease.
The main risk factors are intravenous drug use, low social adaptation, work in agriculture, granaries associated with the extermination of rodents. Tourists, military personnel, recipients of donated organs and blood products, as well as the population of endemic areas are at high risk. A number of studies have found that the expression of TLR-2 and TLR-4 receptors on human cell membranes increases the risk of not only Crohn’s disease, tuberculosis and a number of other pathologies, but also vesicular rickettsiosis.
Pathogenesis
The pathogenesis of vesicular rickettsiosis has not been studied sufficiently due to the benign course and the small number of deaths. After penetration into the human body, when the rickettsia vector is bitten, a specific granuloma is formed. The main cells affected by pathogens are macrophages with the CD-68 receptor. Rickettsias are capable of exiting the phagosome and entering the cytoplasm of macrophages. Restriction of replication of pathogens in cells occurs through complex, not fully understood reactions involving interleukins.
TLR-2/4 receptor proteins on the cell surface of the human body are activators of chemokines and proinflammatory cytokines that affect the indirect induction of interleukin-8 and TNF-alpha expression during R. akari recognition. In parallel, there is moderate toxinemia, multi-organ spread through the lymphatic system. Endotheliocytes can be involved in the pathological process as a breeding ground for rickettsias, but most often characteristic panvasculitis is caused by toxic reactivation of the immune system.
Symptoms
The incubation period is 7-12 days, more often – 10 days. The disease begins with the appearance of a small painless compacted spot at the site of the tick suction, the diameter of which does not exceed 5 cm. The skin around the primary affect is hyperemic. Then a tubercle is formed in the center, followed by a bubble with transparent contents, then an ulcer with a dark crust; a scar may form. Approximately during this period, the patient notes the onset of fever with pronounced weakness, headaches and dizziness.
The temperature reaction of the body reaches 39-40 ° C, chills, muscle and joint pain occur. Fever usually lasts 5-7 days, can last up to 12 days. Sometimes there is a painful enlargement of the lymph nodes, stool disorders, abdominal pain, dry cough. About 2-4 days of the disease, an abundant polymorphic rash appears with localization on the scalp, trunk, limbs. The elements of the rash are extremely diverse (bumps, spots, bubbles), cause moderate itching, persist for up to 10 days of the disease, disappear without a trace. Organ lesions are uncharacteristic.
Complications
Vesicular rickettsiosis rarely occurs with complications, usually their appearance is preceded by a late request for medical help or an immunosuppressive condition. Skin infections caused by other bacteria, lymph node lesions with the formation of purulent lymphadenitis are more often detected. Cardiovascular insufficiency, transient pathological dysfunction of the central nervous system occur with severe toxinemia. Hemorrhagic strokes and cerebral infarctions are considered rare complications of vesicular rickettsiosis.
Diagnostics
The diagnosis of vesicular rickettsiosis is verified by an infectious disease specialist. A thorough collection of epidemiological anamnesis is carried out for tick sucking, staying in endemic areas. Other specialists (most often dermatovenerologists and therapists) are involved for consultations if there are indications. The main diagnostic laboratory and instrumental signs of the disease are:
- Physical data. Objective examination reveals primary ulcerative affect, covered with a dark crust; spotty papular, vesicular exanthema on the body, limbs and scalp; moderate enlargement, painlessness of lymph nodes, less often – lymphadenitis. Percussive, auscultative and palpatory signs of visceral pathology are usually absent.
- Laboratory tests. A general clinical blood test has no specific markers, leukopenia, neutropenia, thrombocytopenia, and an increase in ESR are detected. Leukocytosis occurs with a complicated course of rickettsiosis. In the biochemical analysis, there is a transient increase in the activity of ALT, AST. In the general analysis of urine against the background of fever, traces of protein, erythrocyturia can be determined.
- Identification of infectious agents. Isolation of rickettsias in cell culture is a laborious, long and expensive process. The most informative method of detecting pathogens is multiplex PCR, carried out with smears-prints of primary affect, skin biopsies. Serological reactions (ELISA) should be repeated at intervals of at least 10-14 days to fix the growth of the antibody titer.
- Instrumental techniques. For the purpose of differential diagnosis, patients are chest X-ray. According to the indications, ultrasound examination of the abdominal cavity, kidneys, soft tissues, lymph nodes is recommended. To exclude toxic myocardial damage, an ECG is prescribed, with neurological disorders, MRI, CT with contrast is advisable.
Differential diagnosis is carried out with typhus, characterized by severe course, the presence of roseolus-petechial rash and neurological lesions; chickenpox with true polymorphism of rashes, enanthema and the phenomenon of sprinkling; infectious mononucleosis, for which pronounced lymphadenopathy, tonsillitis and hepatosplenomegaly are typical. The differences of meningococcal infection are considered to be a true hemorrhagic rash starting from the lower extremities, severe intoxication, symptoms of CNS involvement.
Signs of measles are rashes starting from the face and upper half of the body, conjunctivitis, mucosal lesions; ixodic tick-borne borreliosis occurs with migrating erythema, liver damage, musculoskeletal system. Systemic lupus erythematosus is characterized by erythematous photodermatitis, telangiectasia, Sjogren’s syndrome, symmetrical lesions of large joints. Thrombocytopenic purpura occurs without an increase in body temperature, typical manifestations are spontaneous polymorphic hemorrhages in the skin and mucous membranes, bleeding.
Treatment
Patients with suspected of this pathology are subject to hospitalization only in case of severe course or if differential diagnosis is necessary. Bed rest is prescribed until the normalization of body temperature and for 2-3 days of a persistent non-sporadic period. A special diet has not been developed, it is recommended to refuse to take potential food allergens, nicotine and alcohol, due to the possible side effects of antibiotics used – from hard-to-digest food. The water load increases in the absence of contraindications.
Conservative therapy
The drugs of choice for the treatment of vesicular rickettsiosis are antibiotics. The greatest sensitivity of the pathogen was noted to doxycycline, chloramphenicol, tetracycline, macrolides. The use of penicillins, vancomycin, aminoglycosides requires high-dose injections. Be sure to prescribe angioprotectors and anti-inflammatory drugs, perform oral and intravenous detoxification. Aspirin and analogues should be used with caution. Symptomatic treatment is selected taking into account the clinical need for a particular patient.
Prognosis and prevention
The prognosis is favorable, characterized by self-limitation of the disease with spontaneous recovery. In the case of a complicated course, severe premorbid conditions, the mortality rate reaches 2.8%. The duration of vesicular rickettsiosis usually does not exceed 7-10 days. Specific prevention (vaccine) has not been developed. Non-specific protection measures include planned deratization, the use of acaricidal treatment, anti-tick sprays, clothing with long sleeves and trousers, gloves when in the natural focal areas of the habitat of gamas mites.
