Disease Course

In the vast majority of cases, the course of the disease is mild and favorable, with reported clinical improvement within 24 to 48 hours after doxycycline therapy and complete recovery

TABLE 2 Meta-analysis of Clinical Manifestations and Laboratory Abnormalities in Patients with HGA (36,64,102)

All North America Europe

All North America Europe

TABLE 2 Meta-analysis of Clinical Manifestations and Laboratory Abnormalities in Patients with HGA (36,64,102)

Symptom or sign

Mean %

n

Mean %

n

Mean %

n

Fever

93

521

92

448

99

73

Myalgia

77

516

79

448

66

68

Headache

76

385

71

316

95

69

Malaise

94

288

96

271

53

17

Nausea

38

258

36

207

47

51

Vomiting

26

90

34

41

19

49

Diarrhea

16

95

22

41

11

54

Cough

19

260

22

207

10

53

Arthralgias

46

504

47

448

41

56

Rash

6

357

6

289

5

68

Stiff neck

21

24

22

18

17

6

Confusion

17

211

17

207

0

4

Laboratory abnormality

Leucopenia

49

336

50

282

46

54

Thrombocytopenia

71

336

72

282

63

54

Anemia

37

59

37

59

n.d.

n.d.

Elevated serum AST or ALT

71

177

79

123

53

54

Elevated serum creatinine

43

72

49

59

15

13

Abbreviations. ALT, alanine transaminase; AST, asperate transaminase; HGA, human granulocytic anaplasmosls; n.d., not determined.

Abbreviations. ALT, alanine transaminase; AST, asperate transaminase; HGA, human granulocytic anaplasmosls; n.d., not determined.

within two months, even without appropriate antibiotic treatment (67,69,111). Elderly patients are more prone to severe infections and death as are individuals with underlying medical conditions (e.g., immunosuppressive treatment, malignancies) or with delayed specific antibiotic treatment (60,92,106,112). A severe course of HGA can present as a septic or toxic-shock-like syndrome, myositis, rhabdomyolysis, myocarditis, or neurological involvement, such as brachial plexopathy or demyelinating polyneuropathy (38,41,109,113-116). Life-threatening complications were described in 7% (30 of 457) of patients in 2001-2002 (59), including acute respiratory distress syndrome (three patients), disseminated intravascular coagulation (one patient), renal failure (three patients), and others. The long-term outcome for HGA is usually favorable, showing no differences in physical functioning, general health, and vitality in one case-controlled study; however, HGA patients showed lower scores for "pain and health" relative to one year earlier (117).

No convincing clinical data support increased severity of Lyme disease with HGA (37,44,97,117), and there is no evidence for chronic or persistent HGA in humans (41,111). In contrast, experimental coinfection with A. phagocytophilum and B. burgdorferi in mice results in increased B. burgdorferi burden and severity of Lyme arthritis (118-120), and antibody response to A. phagocytophilum but not to B. burgdorferi is decreased in coinfected C3H/HeN mice (119). Moreover, coinfection in vitro facilitates migration of B. burgdorferi through endothelial cell barriers, including models of the blood-brain barrier (121). Much more study of how these interactions mechanistically explain the biological alterations is required.

The case-fatality rate is estimated at 0.7% based on U.S. surveillance data (59). So far, only one fatal case has been reported in Europe (122). In most unfavorable outcomes, opportunistic infections superimposed on HGA are observed. These included disseminated candidiasis, invasive pulmonary aspergillosis, necrotizing herpes esophagitis, and cryptococcosis, among others (41,114,123-125).

Not all A. phagocytophilum infections result in disease. Asymptomatic A. phagocytophilum seroconversion (68,74,111,126) and high seroprevalence rates in North America, Europe, and Asia suggest that most infections are subclinical or asymptomatic (69-71,74,127,128). Whether the serologic reactions represent true A. phagocytophilum infection that is cleared, infections by "nonpathogenic" strains, or simply false-positive serologic tests is not known (70,129,130).

FIGURE 2 A. phagocytophilum appears as a cluster of small, dark-stained stipples in the cytoplasm of peripheral blood neutrophils and immature granulocytes, as shown here [Romanowsky (Hema-3) stain; original magnification: X1060],

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