Tsutsugamushi is an acute rickettsiosis that occurs with fever, focal vasculitis and perivasculitis of various organs – the central nervous system, heart, lungs, kidneys. Clinical manifestations are characterized by the presence of high body temperature, primary affect, spotty-nodular rash on the skin, generalized lymphadenopathy. Frequent complications are meningoencephalitis, myocarditis, pericarditis, pleurisy, glomerulonephritis, peritonitis. The diagnosis is established using immunological methods (IFT, RPH, IFA, ELISA). Tsutsugamushi fever is treated with antibiotics (tetracyclines, macrolides, chloramphenicol, etc.).
A75.3 Typhus caused by Rickettsia tsutsugamushi
Tsutsugamushi (Japanese river fever, jungle typhus, red-cell rickettsiosis) is a tick-borne fever with a natural focal prevalence caused by rickettsias. Like other rickettsioses, tsutsugamushi proceeds with intoxication, typical primary affect, lymphadenopathy, macular-papular rash.
The main natural foci of tsutsugamushi fever are located in the countries of Central, East and Southeast Asia, Indonesia, Australia, Oceania. The susceptibility to the disease is quite high: in some regions, fever develops in 3% of the population every month. The greatest incidence of tsutsugamushi is affected by rural residents and visitors (mainly tourists).
The causative agent fever is a small gram-negative stick Rickettsia tsutsugamushi, or Rickettsia orientalis. The bacterium has a coccoid or rod-shaped shape, a length of 0.8-2 microns and a width of 0.3-0.5 microns. Rickettsia tsutsugamushi are obligate parasites that multiply in the cytoplasm of affected cells. Different strains of the pathogen differ in antigenic properties and virulence, so tsutsugamushi fever can occur in both mild and clinically pronounced forms. Rickettsias are sensitive to environmental conditions; heating, exposure to disinfectants, drying are detrimental to them.
The guardians and carriers of infection in natural foci are the larvae of red-bodied mites that transmit the pathogen tsutsugamushi transphase and transovarially. Also, small rodents, insectivores, and marsupials are involved in the process of rickettsia circulation in natural foci. The causative agent of the disease obtained by blood sucking is transmitted by the larva to nymphs, and then to adult ticks, which carry out transovarial transmission of rickettsias to the next generation of larvae. Thus, only a new generation of larvae of red-bodied mites in the next season can be a carrier of tsutsugamushi.
Larvae attack animals and humans in grassy shrubby thickets. Infection occurs transmissively during blood sucking. The seasonality of tsutsugamushi fever varies in different epidemic foci; usually the peak incidence occurs in May and September. Immunity after infection is strictly specific and short-lived; repeated cases of tsutsugamushi disease are possible after 3 years.
At the site of the tick bite and the introduction of the pathogen, a focal skin change occurs – the primary affect. The further spread of rickettsias along the lymphatic pathways is accompanied by an inflammatory reaction in the form of regional lymphadenitis and lymphangitis. When they enter the bloodstream, rickettsias begin to multiply in the vascular endothelium, causing desquamation of endothelial cells, granulomatous inflammation, the development of focal vasculitis and perivasculitis in internal organs: kidneys, heart, lungs, central nervous system. The development of massive rickettsiemia is accompanied by intoxication.
The incubation period can last from 5 to 21 days (on average 7-11 days). The severity of tsutsugamushi fever varies from erased and mild to extremely severe forms that end fatally.
The typical onset of tsutsugamushi is sudden – with a sharp increase in temperature to 38-39 ° C, which lasts from 1 to 3 weeks without treatment. Fever is accompanied by chills, increasing symptoms of intoxication, regional lymphadenitis. A thorough examination of the skin of a tsutsugamushi patient reveals a primary affect at the site of the infection gate in the form of an inflammatory infiltrate that tends to increase in size.
Initially, at the site of the bite of the tick larva, there is a seal and hyperemia of the skin with a diameter of 0.2 cm, at the top of which a vesicle forms. In place of the opened vesicle, an ulcer is formed, covered with a scab, with a corolla of hyperemia along the periphery. As a result of transformations, the area of the altered skin increases to 2-3 cm. The primary affect persists for 2-3 weeks.
From the first days of tsutsugamushi fever, patients develop hyperemia and swelling of the face, symptoms of conjunctivitis and scleritis. By the end of the first week, abundant macular-papular rashes appear on the skin of the abdomen, chest and extremities. In the severe course of tsutsugamushi fever, the rash is hemorrhagic in nature; “sprinkling” is characteristic – the periodic appearance of new elements. Usually after 3-6 days, the rash disappears, leaving behind peeling, sometimes skin pigmentation. A typical manifestation of tsutsugamushi fever, which distinguishes it from other rickettsioses, is the development of generalized lymphadenopathy (secondary rickettsiosis polyadenitis). Half of the patients have moderate enlargement of the liver and spleen.
The defeat of the cardiovascular system in tsutsugamushi fever is accompanied by bradycardia, which, with the development of myocarditis, is replaced by tachycardia, a moderate decrease in blood pressure, ECG changes. On the part of the respiratory system, signs of pharyngitis, tracheitis and tracheobronchitis are detected. In severe forms of tsutsugamushi, interstitial pneumonia occurs due to the formation of granulomas in small vessels.
With the layering of secondary bacterial infection, focal and even lobular pneumonia are possible. Severe headaches, disturbances of consciousness, delirium, visual hallucinations, meningeal symptoms, tremors, convulsions, etc. indicate the defeat of the central nervous system in tsutsugamushi fever. During the convalescence period, complications may develop in the form of pericarditis, pleurisy, lung abscess, meningoencephalitis, glomerulonephritis, peritonitis, thrombophlebitis.
The starting points for making a preliminary diagnosis are epidemiological anamnesis data (stay in natural foci of tsutsugamushi), the presence of fever, primary affect, skin rash, generalized lymphadenopathy, signs of damage to the nervous, cardiovascular, respiratory, excretory systems. Laboratory confirmation of tsutsugamushi is carried out using serological reactions (IFT, RPH, IFA, ELISA). Isolation of R.tsutsugamushi culture is used in experiments on white mice.
Tsutsugamushi fever should be differentiated from diseases with similar clinical manifestations:
Tetracycline antibiotics (tetracycline, doxycycline), chloramphenicol, macrolides, fluoroquinolones, rifampicin are the drugs of choice for etiotropic therapy of tsutsugamushi fever. Antibacterial therapy can significantly reduce the duration of the febrile period and prevent death. Pathogenetic treatment of tsutsugamushi fever includes infusion detoxification therapy, according to indications – the use of cardiac glycosides, glucocorticosteroids.
Prognosis and prevention
Before the use of antimicrobial drugs, the mortality rate from tsutsugamushi fever reached 20% or more. Currently, thanks to modern antibiotic therapy, deaths are practically not recorded. Prevention of epidemic outbreaks of tsutsugamushi in endemic areas is achieved through anti-tick measures: deforestation of thickets of shrubs, processing of breeding sites of red-bodied mites. Individual protection is provided by the use of special clothing and repellents. A live attenuated vaccine and an antibiotic vaccine have been developed for the active prevention of tsutsugamushi.