Two related bacteria, two different ticks, two overlapping but distinct US regions, one antibiotic that works for both. Ehrlichiosis and anaplasmosis are the dominant rickettsial tick-borne illnesses in the United States after Rocky Mountain spotted fever, and CDC case reports have grown roughly sevenfold since 2000. The disease they produce can be mild or quickly lethal, especially in elderly and immunocompromised patients. The diagnosis is often missed because the early symptoms are flu-like and most clinicians do not see many cases.
CDC counted 2,093 ehrlichiosis cases and 5,655 anaplasmosis cases in 2019, both up sharply from baseline. True incidence is much higher because passive case reporting catches only confirmed laboratory diagnoses. Co-infection with Lyme is common in deer tick regions, and patients who fail to improve on doxycycline for Lyme often have one of these instead, or in addition. The Lyme disease tick prevention guide covers vector-shared exposures, and the babesiosis post walks through the parallel parasitic infection. Parent pillar: outbreak-aware travel guide.
Key Takeaways
- Ehrlichia chaffeensis causes human monocytic ehrlichiosis (HME), transmitted by Amblyomma americanum (Lone Star tick) in southeastern and south-central US.
- Anaplasma phagocytophilum causes human granulocytic anaplasmosis (HGA), transmitted by Ixodes scapularis (deer tick) in northeastern and upper midwestern US.
- Both produce fever, headache, muscle aches, low white blood cell count, and low platelets within 1 to 2 weeks of tick bite.
- Severe disease and death concentrate in elderly, immunocompromised, and patients with delayed treatment; HME mortality runs 2 to 3 percent.
- Doxycycline is first-line for both, even in children, even before lab confirmation.
- Cases have climbed steadily since 2000, driven by tick range expansion and better diagnostic recognition.
What are ehrlichiosis and anaplasmosis?
Both are bacterial infections caused by obligate intracellular pathogens of the family Anaplasmataceae. The bacteria live and multiply inside white blood cells, forming clusters called morulae that are visible on stained blood smears in some cases.
Ehrlichia chaffeensis infects monocytes (a type of white cell), producing human monocytic ehrlichiosis. Anaplasma phagocytophilum infects granulocytes (a different white cell type), producing human granulocytic anaplasmosis. The two diseases are related, look clinically similar, and have overlapping but distinct geographic distributions.
A third agent, Ehrlichia ewingii, causes human ewingii ehrlichiosis primarily in immunocompromised patients in the same southeastern US range as E. chaffeensis. A newer species, Ehrlichia muris eauclairensis, has been recognized in Minnesota and Wisconsin since 2009 and is transmitted by deer ticks alongside anaplasmosis and babesiosis.
How do they spread?
Tick vectors differ between the two main pathogens:
| Disease | Pathogen | Vector tick | Main US region |
|---|---|---|---|
| Ehrlichiosis (HME) | Ehrlichia chaffeensis | Amblyomma americanum (Lone Star) | Southeast, south-central |
| Ehrlichiosis (E. ewingii) | Ehrlichia ewingii | Amblyomma americanum | Southeast |
| Anaplasmosis | Anaplasma phagocytophilum | Ixodes scapularis (deer tick) | Northeast, upper midwest |
| Anaplasmosis (west) | A. phagocytophilum | Ixodes pacificus | West coast |
| Ehrlichiosis (EME) | E. muris eauclairensis | Ixodes scapularis | Upper midwest |
Reservoir hosts differ as well. White-tailed deer maintain E. chaffeensis cycles in the southeast. White-footed mice (Peromyscus leucopus) maintain A. phagocytophilum cycles in the northeast. Both ticks bite humans aggressively when given the chance.
Transmission requires roughly 12 to 24 hours of tick attachment for efficient bacterial transfer. Prompt removal reduces but does not eliminate risk.
Where are they active?
Ehrlichiosis cases concentrate in Missouri, Arkansas, Oklahoma, Tennessee, Virginia, Kentucky, Maryland, and North Carolina. The Lone Star tick range has expanded northward, and ehrlichiosis cases now appear in southern New England and lower midwestern states as well.
Anaplasmosis is heaviest in Minnesota, Wisconsin, New York, Massachusetts, Connecticut, Rhode Island, Vermont, New Hampshire, and northern Pennsylvania. The geographic profile matches Lyme disease closely because the vector is identical.
Cases peak May through August, with smaller spring and fall shoulders. Late-season cases continue into October in warmer years and in southern states.
What are the symptoms?
Symptoms appear 1 to 2 weeks after tick bite. The early presentation is nonspecific and resembles influenza, COVID-19, or many other febrile illnesses.
- Common: fever (often 39 to 40C), headache, muscle aches, fatigue, chills, nausea, anorexia
- Less common: rash (more common in ehrlichiosis than anaplasmosis, opposite of Rocky Mountain spotted fever), cough, joint pain, abdominal pain
- Lab abnormalities: leukopenia, thrombocytopenia, elevated liver enzymes (almost universal); useful red flags when present in a patient with tick exposure
- Severe disease: acute respiratory distress, renal failure, disseminated intravascular coagulation, septic shock, meningoencephalitis, death
Severe disease and mortality concentrate in patients over 60, immunocompromised hosts, and those with delayed treatment. HME has higher mortality (2 to 3 percent overall) than HGA (under 1 percent overall). Both can be rapidly fatal in elderly patients within days of symptom onset if not treated promptly.
The rash difference matters clinically. About 30 percent of HME cases develop a rash, often maculopapular or petechial, but classic Rocky Mountain spotted fever rash (palmar and plantar petechiae) is uncommon. HGA only causes rash in about 10 percent of cases.
How are they diagnosed?
Treatment should not wait for confirmation. Empiric doxycycline starts when clinical suspicion is reasonable, because mortality rises sharply when treatment is delayed past day 5 of illness.
Available tests:
- PCR on whole blood: most sensitive for acute disease, available at reference labs and many large hospitals; turnaround 1 to 3 days
- Peripheral blood smear: can show morulae inside white blood cells; positive in 20 to 80 percent of HGA cases, lower in HME
- Serology: IgG and IgM by indirect fluorescent antibody; useful for retrospective confirmation, not for acute decisions because antibodies appear 7 to 14 days into illness
- Acute and convalescent paired serology: fourfold rise in titer confirms infection
CDC case definitions require either PCR positive, morulae visualization, fourfold serology rise, or compatible clinical illness with single elevated titer plus tick exposure. The PCR vs antigen vs serology post explains the underlying tests.
How are they treated?
Doxycycline is first-line for both, regardless of age. CDC explicitly endorses doxycycline for children including those under 8, because the dental staining risk traditionally cited was overstated and the alternative for these life-threatening rickettsial diseases is inadequate.
- Doxycycline: 100 mg twice daily orally or IV in adults; 2.2 mg/kg twice daily in children
- Duration: at least 3 days after fever resolves, typically 7 to 14 days total
- Severity: IV doxycycline for hospitalized patients with severe disease
Defervescence within 24 to 48 hours of starting doxycycline is the expected response and helps confirm the empiric diagnosis. Patients who do not improve on doxycycline within 48 hours need re-evaluation, often for an alternative or co-infecting pathogen.
Rifampin has been used in pregnancy where doxycycline is relatively contraindicated, though doxycycline can still be used in pregnant women when life-threatening rickettsial disease is suspected. Chloramphenicol is not effective and should not be substituted.
How do you prevent them?
Same as all tick-borne disease prevention:
- Permethrin-treated clothing in endemic regions during peak season
- DEET 25 to 35 percent or picaridin 20 percent on exposed skin
- Thorough skin inspection within hours of outdoor exposure
- Prompt removal of attached ticks with fine-tipped tweezers, grasped at the skin level
- Tumble dry clothing on high heat for 10 minutes after returning indoors
- Shower within 2 hours of indoor return
The Lyme disease tick prevention guide covers the full prevention strategy that applies equally here.
FAQ
How do I tell ehrlichiosis from anaplasmosis without testing?
You generally can't on clinical grounds alone, but geography and tick exposure point the way. A patient with Lone Star tick exposure in Arkansas is more likely to have ehrlichiosis; one with deer tick exposure in Minnesota is more likely to have anaplasmosis. The treatment is the same either way, which is why doxycycline starts empirically before confirmation.
Can you have both at the same time?
Co-infection with Lyme disease, babesiosis, or both is common in deer-tick regions, because the same tick transmits all of them. Patients on doxycycline for Lyme are already being treated for anaplasmosis, but a patient who is not improving may have babesiosis added, requiring atovaquone plus azithromycin separately. See the babesiosis post for the co-infection picture.
Should children receive doxycycline?
Yes, when ehrlichiosis or anaplasmosis is suspected. CDC, AAP, and IDSA all support doxycycline for children of any age in suspected rickettsial disease. The historical concern about tooth staining was based on tetracycline, not doxycycline, and short courses of doxycycline have not been shown to cause dental staining in modern studies.
Why does treatment have to start before confirmation?
Mortality rises substantially when doxycycline is delayed past day 5 of symptoms. Most lab confirmation takes 1 to 3 days or more, by which time severe disease can develop. Empiric doxycycline for compatible illness in tick-exposed patients is the standard of care, and the test results inform downstream decisions rather than initial treatment.
Are there vaccines?
No human vaccine exists for ehrlichiosis or anaplasmosis. Veterinary vaccines exist for canine Ehrlichia canis in some markets. Human vaccine development has been hindered by the relatively small case counts compared to other tick-borne diseases, the obligate intracellular nature of the bacteria, and antigenic variability.