Human Ehrlichiosis
المؤلف:
Mary Louise Turgeon
المصدر:
Immunology & Serology in Laboratory Medicine
الجزء والصفحة:
5th E, P254-255
2025-08-23
384
Human ehrlichiosis was first described in the United States in 1986; since then, reports of tickborne illnesses have increased. Unlike Lyme disease, which tends to be indolent, Rocky Mountain spotted fever and ehrlichiosis can be fatal and must be recognized and treated promptly.
Etiology
Tickborne rickettsiae of the genus Ehrlichia have been recognized as a cause of human illness in the United States. Ehrlichia spp. belong to the same family as the organism that causes Rocky Mountain spotted fever. Ehrlichia chaffeensis, the etiologic agent of human monocytic ehrlichiosis in the United States, was demonstrated to cause disease in a patient from Arkansas with tick bites in 1987. Since then, two more Ehrlichia spp., Ehrlichia ewingii and an Ehrlichia phagocytophila–like agent that differs antigenically and genetically from E. chaffeensis, have been identified as the cause of anaplasmosis (human granulocytic ehrlichiosis).
Epidemiology
Although the prevalence rates are low, human ehrlichiosis is endemic in the United States. Some fatalities have been reported. Incidence rates increase with age and are higher in men than women. Human ehrlichiosis occurs most frequently in the southern Mid-Atlantic and south central states during spring and summer.
The major vector for E. chaffeensis is the lone star tick, Amblyomma americanum. The principal reservoir for E. chaffeensis is the white-tailed deer, which hosts all stages of A. americanum. The primary tick vector for the agent of human granulocytic ehrlichiosis is I. scapularis in the eastern United States and I. pacificus in California. Dermacentor variabilis represents a second tick vector in the United States. The major reservoir for infection may be the white-footed mouse in the eastern United States. The onset of illness in spring and early summer for most cases parallels the time when A. americanum and D. variabilis ticks are most active.
Signs and Symptoms
Ehrlichiosis is a general term for human granulocytic ehrlichiosis, now called anaplasmosis, and human monocytic ehrlichiosis (HME). The syndrome of human ehrlichiosis is not typically recognized by physicians, but should be considered in patients with a history of tick exposure and an acute febrile, flulike illness. Most patients are not suspected of having a rickettsial infection. Because ehrlichiosis can cause fatal infections in humans, early detection and treatment with tetracycline or chloramphenicol appear to offer the best chance for complete recovery.
Symptoms are nonspecific and include fever, chills, and headache. Fever and skin rashes are the most common physical findings. In children, fever and headache are universal. Myalgias, nausea, vomiting, and anorexia are also common.
Diagnostic Evaluation
Laboratory studies have indicated that the hematologic, hepatic, and central nervous systems are usually involved in human ehrlichiosis. Definitive diagnosis is based on inclusion in leukocytes (Fig. 1). Ehrlichia spp. undergo three developmental stages, as follows:
1. Elementary bodies enter a leukocyte by phagocytosis and multiply rapidly.
2. After 3 to 5 days, small numbers of tightly packed elementary bodies (initial bodies) are visible.
3. During the next 7 to 12 days, the initial bodies develop into morular, or mulberry, forms.
Fig1. Schematic representation of the growth cycle of ehrlichiae in an infected cell. Elementary bodies (EBs; individual ehrlichiae) enter the leukocyte by phagocytosis and multiply. After 3 to 5 days, small numbers of tightly packed EBs are observable and are called initial bodies. During the next 7 to 12 days, additional growth and replication occur, and the initial bodies develop into mature inclusions, which appear by light microscopy as mulberry (morular) forms. This morula is a hallmark of ehrlichial infection. (From McDade J: Ehrlichiosis—a disease of animals and human beings. J Infect Dis 161:609 617, 1990.)
For anaplasmosis, direct observation of intraleukocytic morulae in Wright-Giemsa–stained peripheral blood or buffy coat smears is a rapid and inexpensive laboratory test. If clinical symptoms and the epidemiologic history are compatible with rickettsial infections, the following diagnostic tests should be used during the acute stage of illness and when antibiotic treatment is initiated:
• PCR test on skin biopsy of rash or eschar, or an ethylenediaminetetraacetic acid (EDTA) whole blood specimen
• Specific immunohistologic detection of rickettsiae in skin biopsy of rash or eschar
In anaplasmosis, the diagnosis is confirmed by seroconversion or by a single serologic titer higher than 1:80 in patients with a supporting history and clinical symptoms. Seroconversion is defined as a fourfold rise in the titer of paired acute and convalescent sera. Detection of IgM class antibody alone should not be interpreted as recent exposure to the rickettsial agents and should be confirmed by detection of IgG or, preferably, IgG seroconversion by parallel evaluation with a convalescent phase serum collected 4 to 6 weeks after onset of the illness.
In HME the diagnosis is confirmed by seroconversion or by a serologic titer higher than 1:128 in patients with a supporting history and clinical symptoms. Serum or CSF can be analyzed for IgM and IgG antibodies to Ehrlichia spp.
PCR-based detection of the E. phagocytophila–like agent of anaplasmosis represents the most sensitive and direct approach to diagnosis. PCR detection of E. chaffeensis includes the amplification of sequences with 16SrDNA.
Treatment and Prevention
HME patients and those with anaplasmosis are treated with doxycycline. No established guidelines have been established for long-term therapy. Prevention consists of reducing the risk of exposure to ticks (see earlier discussion of Lyme disease prevention).
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