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Most patients acquire babesiosis, human monocytic ehrlichiosis, and HGA between May and September with reported spikes in June and July. ticks infected with B microti is higher when they feed on mice that are coinfected with B burgdorferi and B microti, rather than with B microti alone.8 In studies of I scapularis from different locales, 2.2% to 26% were coinfected with B burgdorferi and A phagocytophilum; in fact, 3% to15% of patients in Connecticut and Wisconsin were found to be coinfected.4 Disease concomitance is important to recognize as patients who are coinfected tend to have increased duration and severity of infection, and treatment of B microti is different from the other disorders.9 Pathophysiology, Clinical Manifestations, and Associated Laboratory Features

In babesiosis, sporozoites are delivered to the dermis within 36 to 72 hours of tick attachment.Therefore, removal of the tick during the first 24 to 36 hours of attachment greatly minimizes risk of transmission, similar to Lyme disease. In a process similar to the actions of protozoa that cause malaria, the Babesia sporozoites migrate to the bloodstream where they invade erythrocytes, mature into merozoites, and lyse the host cell to be released back into the bloodstream to invade new erythrocytes. The host’s splenic macrophages play a critical role in clearing Babesia-infected erythrocytes. Clinical manifestations of babesiosis range from asymptomatic to flu-like symptoms, but patients with asplenia, those aged >50 years, or those with immune system compromise (ie, from HIV/AIDS, malignancy, chemotherapy, radiation, or immunosuppressant therapy) are at risk for severe, life-threatening babesiosis.3,10 The release of merozoites into the circulation stimulates the host’s inflammatory response involving pyrogenic cytokines (ie, tumor necrosis factor-alpha, interleukin-6), which induce symptoms characteristic of a viral-like illness such as fever, chills, diaphoresis, headache, anorexia, myalgia, fatigue, nausea, and vomiting. The lysis of erythrocytes results in hemolytic anemia with associated jaundice, and hemoglobinuria may cause resultant renal injury. This anemia is compounded by Babesia-induced generation of reactive oxygen species, loss of erythrocyte membrane integrity, and opsonization, all of which promote clearance of erythrocytes by splenic macrophages. Hepatosplenomegaly may be noted on physical examination. The same cytokines may contribute to complications associated with severe babesiosis such as acute respiratory distress syndrome and disseminated intravascular coagulation (DIC).10 The pathology of babesiosis is reflected in laboratory findings that may include hemolytic anemia with reticulocytosis and unconjugated hyperbilirubinemia, thrombocytopenia, lymphopenia, and elevated aminotransferases.

Ehrlichia species preferentially infect peripheral leukocytes, with E chaffeensis associated with human monocytic cells (ie, monocytes and macrophages); infection of neutrophils with E ewingii has been reported. Multiorgan involvement is known to occur, with organisms detected in the spleen, lymph nodes, bone marrow, and peripheral blood. A phagocytophilum preferentially infects granulocytes, particularly neutrophils. HME and HGA typically present as similar acute illnesses; however, a wide spectrum of disease exists from subclinical and self-limited to subacute or chronic infection. It is likely that symptoms are due to the host inflammatory response rather than to direct damage caused by the bacteria.5 Ehrlichia has an incubation period of 1 to 2 weeks, but a shorter period may be seen. In a study of 18 adults with HGA, symptoms appeared an average of 5.5 days after tick bite.4 Constitutional symptoms such as fever, chills, headache, malaise, and myalgia occur in the majority of patients, while nausea, vomiting, arthralgia, and cough occur in 25% to 50%.4,11 In HME, cough and respiratory symptoms are more common in adults than in children.5 A minority of patients (up to 36%) with HME may present approximately 5 days into illness with a nonpruritic, erythematous rash that may be macular, maculopapular, or petechial and is more frequent in children.4,5 Rash is not typical in anaplasmosis. In both HME and HGA, laboratory evaluation demonstrates thrombocytopenia, leukopenia, and increased aminotransferase levels. Although HME and HGA have similar clinical manifestations, HME is often more serious, with hospitalization occurring in 50% of patients and increased risk of sepsis or shock-like presentations, particularly in immunosuppressed hosts and the elderly.4 Central nervous system involvement occurs in 20% of patients, and symptoms may progress to acute respiratory distress syndrome or coagulopathy.5 The CDC reports mortality rates of 1% to 3% in patients who present for medical care of ehrlichiosis.5 In HGA, 5% to 7% of patients require intensive care, and at least 7 deaths associated with delayed diagnosis and treatment and development of opportunistic infections have been identified. In HGA, infection diminishes CD4 and CD8 counts and impairs phagocytosis, antibody responses, neutrophil emigration, and intracellular killing.11 An intact immune system is important for recovery from HGA, and HGA further antagonizes immune dysfunction.11 Other complications of HME and HGA include acute abdominal syndrome, rhabdomyolysis, myocarditis, acute renal failure, and demyelinating polyneuropathies and/or cranial nerve palsies.


Profile for The Clinical Advisor

June 2019 Clinical Advisor  

June 2019 Clinical Advisor