OVERVIEW
Human ehrlichiosis is caused by tick-borne transmission of ehrlichia. The pathogen invades monocytes or neutrophils and forms mulberry-shaped inclusions in the cytoplasm. Patients have a sudden onset of symptoms resembling Rocky Mountain spotted fever, with a rare rash. Leukopenia and thrombocytopenia are associated with hepatocellular damage and abnormal liver function. It can cause death if there are severe complications. Because its epidemiology and clinical manifestations are similar to those of rickettsial diseases, some people categorize it as spotted fever.
Etiology
There are more than 10 species of Ehrlichia, the main human pathogenic E. canis, E. phagocytophilia, E. sennetsu and E. risticii, in particular, E. canis can cause canine severe thrombocytopenia. 1986, a case of Ehrlichia was found in the United States, the mononuclear cytoplasm of which was found to be mulberry-shaped inclusion bodies, and the patient’s serum and the patient’s serum were different from that of Ehrlichia. In 1986, a case of ehrlichiosis was found in the United States, in which mulberry-shaped inclusion bodies were found in the plasma of mononuclear cells; the patient’s serum had an agglutination reaction with canine ehrlichiosis with a gradual increase in potency, and smear staining of peripheral blood mononuclear cells identified this pathogen, which had been isolated from a mutant tick, which is a vector for the spread of spotted fever in Los Angeles.In 1949, a type of ehrlichiosis was also found in the United States in which the inclusion bodies were found in granulocytes (whereas the inclusion bodies of E. canis were found in mononuclear cells). The inclusion bodies are located in monocytes), so it was named human granulocytic ehrlichiosis (HGE), so there are at least two types of ehrlichiosis that cause disease in humans.
Tick-borne ehrlichiosis is through the bite of the tick into the human body, through the microvascular or lymphatic channels into the relevant organs, the pathogen in the monocyte macrophage growth and reproduction, directly causing damage to host cells, or induced by the body’s immune system response, so that the immune cells to release a variety of cytokines and other inflammatory mediators, resulting in tissue damage, focal necrosis and granuloma formation, etc., in the bone marrow, the visible formation of myeloma, the formation of myeloma. In the bone marrow, bone marrow granuloma formation, myelodysplasia and megakaryocyte hyperplasia are seen; in the liver, annular granulomas and focal hepatic necrosis are formed; in the lungs, extensive alveolar damage, interstitial pneumonitis and pulmonary hemorrhage can be seen; not only that, lymphocytic infiltration can be seen around the blood vessels in the kidneys, spleen, heart, liver, brain, meninges, lungs and other organs, and the decrease of lymphocytes in the peripheral blood.
Symptoms
Incubation period of 12 to 14 days, patients with clinical manifestations and Rocky Mountain spotted fever is almost difficult to distinguish, both sudden onset, chills, high fever, often accompanied by bradypnea (<90 beats / min), headache, muscle pain, nausea, vomiting, fatigue, malaise, physical examination without obvious signs, about 20% of Chaffee ehrlichiosis infection of patients with a rash, but human granulocytic ehrlichiosis (HGE) infection of the patients do not have a rash, the rash The rash is multiform, with a maculopapular or papular rash, or a maculopapular, hemorrhagic, or erythematous rash, commonly on the chest, legs, and arms.The rash appears about 5 days after onset of the disease, and the natural course of the disease averages 7 days (3 to 19 days).
The natural course of the disease is 7 days (3-19 days). Elderly patients are prone to severe disease, which may include renal failure, meningitis, coma, disseminated intravascular coagulation (DIC), and even thrombocytopenia and regenerative disorders of the bone marrow hematopoietic cells, and disruption of the separation of blood constituents (i.e., phagocytosis syndrome), which may lead to death if not treated promptly.
Examination
Decreased white blood cell count (<4×109/L), decreased absolute lymphocyte count (<1.5×109/L, with a median count of 0.41×109/L), decreased platelets, (49-75) ×109/L, abnormal liver function, and a rise to peaks in alanine aminotransferase (ALT) and alanine oxal transaminase (AST) at the end of the 1st week of the course of the disease, 90-583 U/L, and a rise in the lymphocyte and mulberry-shaped inclusion bodies are seen in lymphocytes and monocytes or neutrophils.
Diagnosis
The diagnosis is made on the basis of epidemiological data that the patient has traveled to an area where the disease is endemic, has a history of tick bites, or has entered a tick-prone area, accompanied by the above clinical manifestations and laboratory abnormalities, and the diagnosis can be made by leukocyte smear staining with mulberry-like inclusions, and the diagnosis can be confirmed by immunofluorescence and polymerase chain reaction (PCR) to measure antibodies to ehrlichia or deoxyribonucleic acid (DNA).
Treatment
Early application of tetracycline antibiotics reduces fever after 1 to 2 days and has a favorable prognosis. Doxycycline is used continuously until at least 3 days after the fever subsides, and tetracycline or chloramphenicol may also be used. Heparin is not necessary, as symptoms such as pancytopenia may resolve quickly after antibiotic therapy has controlled the symptoms.