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Microbiology · Anaplasmas, Ehrlichiae

Anaplasmosis and ehrlichiosis

Anaplasmosis and ehrlichiosis are acute vector-borne infections transmitted to humans through the bites of infected arthropods. The diseases are characterized by a febrile syndrome, lymphatic system involvement, rash development, and formation of a primary affect at the pathogen's site of entry.

Infectious doseExtremely low; the penetration of single cells is sufficient for infection development
EndemicityCoastal regions of the western Pacific, including Japan and Oceania
Incubation periodRanges from 5 to 21 days, averaging 7–10 days
TherapyHigh efficacy of tetracyclines: resolution of the process in 4–5 days
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Epidemiology and Ecology

The infectious process is closely linked to the existence of natural foci. The geographical distribution of the pathogen mainly covers the coastal territories of the western Pacific (Japan, Oceania countries). In the Russian Federation, the historical natural focus in the south of Primorsky Krai has currently self-extinguished, so the disease does not pose a serious epidemiological threat to the country.

The reservoir and mechanism for maintaining the focus in the wild are small rodents and arthropods. A crucial biological feature is the pathogen's ability to persist in vector populations through two transmission pathways:

  • Transovarial transmission — from an infected female to offspring via eggs.
  • Transstadial transmission — persistence of the pathogen during transition from one tick developmental stage to another.

The incidence has a distinct seasonal pattern directly dependent on the activity of tick larvae of various species. There are two main infection peaks: the spring-summer period (April–June) and the autumn period (September–November).

Pathogenesis and clinical presentation

The portal of entry for the infection is the skin. Humans are infected when attacked by tick larvae, while the bite itself remains completely painless. A specific marker, the primary affect, forms at the attachment site.

The incubation period lasts an average of 7–10 days (ranging from 5 to 21 days). The infection is characterized by a high frequency of asymptomatic (inapparent) forms—up to 2/3 of all cases, depending on the virulence of the specific strain.

When a manifest form develops, the disease debuts acutely:

  1. Chills, fever, intense headache, and myalgia occur.
  2. Hypotension is registered on the part of the cardiovascular system.
  3. The lymphatic system responds with the development of regional lymphadenitis, which subsequently progresses to generalized lymphadenopathy.

On days 4–7 from the onset of the disease, exanthem (rash) appears. By its character, it is predominantly maculopapular, less often hemorrhagic. The rashes are located mainly on the skin of the torso, whereas involvement of the palms and soles is extremely rare.

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Immunity and Antigenic Structure

The pathogen is distinguished by pronounced antigenic variability—there are many different antigenic variants (orientations) of the pathogen in nature.

The immunity formed after the disease is strictly type-specific. This means that protective antibodies do not exhibit persistence against heterologous strains of the microorganism. Consequently, a past infection caused by one antigenic type does not protect a person from infection by another type, due to which recurrent cases of the disease are possible.

Diagnostics, treatment, and prevention

Laboratory verification of the diagnosis is based on serological and molecular genetic methods:

  • Molecular genetic methods: detection of pathogen DNA by PCR.
  • Nonspecific serology: detection of antibodies to Proteus OX19.
  • Specific serology: CFT, IFA, ELISA to detect antibodies against tick group antigens. These methods are also suitable for retrospective diagnostics, as antibodies can persist in the blood for up to 20 years.

The basis of etiotropic therapy is antibacterial drugs of the tetracycline series. They demonstrate exceptionally high efficacy: clinical recovery occurs in just 4–5 days.

Specific prophylaxis (vaccination) has not been developed. The main emphasis is placed on nonspecific measures—anti-tick control. For individuals at risk (tourists, military personnel) in endemic areas, emergency chemoprophylaxis is provided: administration of the antibiotic doxycycline once a week.

Briefly: answers to topical questions

Which target cells does the agent of human granulocytic anaplasmosis affect?

The agent of human granulocytic anaplasmosis predominantly affects neutrophils, as well as macrophages in various internal organs.

  • Neutrophils — inside their cytoplasm, the pathogen forms specific clusters called morulae.
  • Macrophages — cells of the spleen, liver, lymph nodes, and bone marrow are affected, with the development of focal necrosis.

Which target cells does the agent of human monocytic ehrlichiosis affect?

The agent of human monocytic ehrlichiosis affects blood monocytes and macrophages of internal organs.

  • Monocytes — inside their cytoplasm, bacteria multiply within vacuoles and form characteristic clusters (morulae).
  • Macrophages — cells of the bone marrow, liver, spleen, and lymph nodes are affected, where lymphohistiocytic infiltrates form.

What changes in the complete blood count are characteristic of the acute period of anaplasmosis and ehrlichiosis?

The acute period of anaplasmosis and ehrlichiosis is characterized by leukopenia, thrombocytopenia, lymphopenia, monocytopenia, band neutrophilemia, and an elevated ESR.

  • Leukopenia — detected in 60% of patients.
  • Thrombocytopenia — observed in 68% of cases.
  • Band neutrophilemia.
  • Lymphopenia and monocytopenia.
  • Elevated ESR.

Which tick species are the main vectors of anaplasmosis in Eurasia?

The main vectors of the granulocytic anaplasmosis agent in Eurasia are ixodid ticks.

  • Castor bean tick (Ixodes ricinus) — the sheep tick involved in the transmission of the infection.
  • Taiga tick (Ixodes persulcatus) — a specific vector and reservoir of the pathogen.

Both species act as reservoirs of infection in the wild, along with wild ungulates and small rodents.

How to memorize

To memorize the seasonality of the infection: SS-AS — Spring-Summer (April-June) and Autumn Seasons (September-November) correspond to the two peaks of tick activity.

Class and exam questions

How does the pathogen persist in the vector population?

The pathogen persists due to transovarian (transmission to offspring via eggs) and transtadial (persistence between developmental stages) transmission.

Does lasting immunity form after recovery?

Immunity is type-specific and does not protect against other antigenic variants (orientations), therefore reinfections are possible.

What skin manifestations are typical for this infection?

At the site of the painless tick bite, a primary affect arises, and on days 4–7, a maculopapular rash appears on the torso.

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What else to study on this topic

  • Mechanisms of transovarial and transstadial transmission of infections
  • Antigenic variants of the pathogen and their effect on immunity
  • Features of the nonspecific reaction with Proteus OX19
  • Protocols for emergency chemoprophylaxis with doxycycline

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