Literature

Clinical Pearls & Morning Reports

Posted by Carla Rothaus

Published May 23, 2018

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What are the most sensitive diagnostic tests for anaplasmosis during the first week of illness?

A: Anaplasmosis is a tickborne illness, with a peak incidence during the spring. There are two areas of the United States in which anaplasmosis is hyperendemic: the upper Midwest (Minnesota and Wisconsin) and New England. Among persons who do not have the traditional epidemiologic risk factors for tickborne disease, Anaplasma phagocytophilum may be transmitted perinatally and by blood transfusion. Read the latest Case Records of the Massachusetts General Hospital here.

Clinical Pearls

Q: What are some of the clinical manifestations of anaplasmosis?

A: Anaplasmosis has a wide range of clinical manifestations, and symptoms may be absent or subclinical. Most patients who present for care are older, and the classic prominent symptoms are fever, diffuse myalgias, and lethargy. There is usually involvement of at least one organ system, and common symptoms are anorexia, cough, nausea, diarrhea, and headache. Rash occurs in a minority of patients; it is typically limited to erythema on the head, chest, and upper back, and it very infrequently has a palpable papular component. The presence of rash in a patient with anaplasmosis should raise suspicion about coinfection with Lyme disease.

Q: What tickborne disease may be confused with anaplasmosis due to substantial clinical overlap?

There is substantial overlap between the clinical syndrome of anaplasmosis and that of human monocytic ehrlichiosis due to Ehrlichia chaffeensis. The hallmark laboratory findings of human granulocytic anaplasmosis are leukopenia, thrombocytopenia, and abnormal liver function. Similar findings are also seen in human monocytic ehrlichiosis. Intracellular morulae in leukocytes could be diagnostic of human monocytic ehrlichiosis or human granulocytic anaplasmosis.

Morning Report Questions

Q: What are the most sensitive diagnostic tests for anaplasmosis during the first week of illness?

A: During the acute phase of anaplasmosis, when symptoms have been present for a week or less and antimicrobial therapy has not yet been initiated, direct detection methods — such as nucleic acid testing and examination of a peripheral-blood or buffy-coat smear for intracytoplasmic morulae in granulocytes — are more sensitive than indirect (serologic) detection methods for the diagnosis of A. phagocytophilum infection. Studies of the specificity of blood-smear examination are lacking, but the technique most likely leads to false positive results with some regularity, since there are several causes of true or apparent intracytoplasmic inclusions in granulocytes besides A. phagocytophilum morulae. However, many hospital laboratories do not offer on-site nucleic acid testing for A. phagocytophilum, and there may be a substantial delay in obtaining the results. In the meantime, a blood-smear examination can be a useful exercise, although morphologic findings should be correlated with clinical features and epidemiologic risk factors, especially when classic morulae are not found.

Q: What is the recommended treatment for anaplasmosis, and what is the expected course with appropriate therapy?

A: Data from controlled trials of treatments for anaplasmosis are limited. A 10-to-14-day course of doxycycline is the treatment of choice, and A. phagocytophilum is not known to have resistance to this agent. In patients with uncomplicated anaplasmosis, the fever diminishes rapidly, resolving within 48 to 72 hours after treatment is initiated. If the fever and other symptoms persist, alternative diagnoses and the possibility of coinfection should be further explored. Organ failure — such as acute renal failure, the acute respiratory distress syndrome, or rhabdomyolysis — can develop. Development of critical illness is unusual and is typically due to exacerbation of an underlying coexisting condition. In rare cases, the neutropenia leads to complication with an opportunistic infection, such as invasive aspergillosis or candidal esophagitis.

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