Ehrlichiosis and anaplasmosis

Bacterial species	Ehrlichia chaffeensis	Ehrlichia ewingii	Ehrlichia muris-like agent	Anaplasma phagocytophilum	Candidatus Neoehrlichia mikurensis
Tick vector	Amblyomma americanum	A. americanum	Ixodes scapularis	Ixodes scapularis (USA) Ixodes pacificus (USA) Ixodes ricinus (Europe) Ixodes persulcatus (Asia) Haemaphysalis concinna (Asia)	Ixodes ricinus (Europe) ?Ixodes ovatus (Japan)
Clinical illness	HME	HEE	EMLA infection	HGA	No name
Year first reported	1987	1999	2009	1994	2009
Known geographic distribution	Atlantic USA Southeast USA South Central USA	South Central USA	Upper Midwest (USA)	Upper Atlantic (USA) Upper Midwest (USA) Pacific coast (USA) North and central Europe Asia (China, Korea, Japan, Eastern Russia)	Central Europe Northeast China
Target leukocyte	Monocyte Macrophage	Neutrophilic granulocyte	Monocyte	Neutrophilic granulocyte	?Neutrophilic granulocyte
Incidence rate (cases/100 000)	14	Unknown	Unknown	20	Unknown
Reported cases (n)^a	9411	≤50	44	12 764	15

^a As of 09/13/2013 per MMWR Weekly Reports, CDC.

When the tick takes a blood meal, bacteria become injected with the tick saliva into the host. Once injected, the bacteria infect specific circulating leukocytes and cause a nonspecific febrile illness. Ehrlichia chaffeensis and EMLA typically infect monocytes and macrophages, whereas E. ewingii and A. phagocytophilum infect neutrophilic granulocytes; Candidatus N. mikurensis has been observed only once in human neutrophils but its definitive target is not yet established. The bacteria adhere to leukocyte membrane receptors to enter cells by endocytosis. There are key differences in the vacuoles with E. chaffeensis and A. phagocytophilum, underscoring that the agents induce distinct pathogenetic pathways. Regardless, the bacteria reside within cytoplasmic vacuoles, where they interact with the host cell to access nutrients, delivering effector proteins to the host cytosol and nucleus that subvert host cell functions, including intracellular signaling, cell cycle regulation, innate immune responses such as respiratory burst or induction of immune activation, delayed induction of apoptosis, and subversion of autophagy, among others. During this interval, the bacteria multiply in the vacuole to form aggregates called morulae. Eventually, each morula fuses with the cell membrane through exocytosis or the cell is mechanically lysed, liberating bacteria to infect other cells. Most recent investigations of disease pathogenesis focus on the induction of innate, inflammatory, and immune-mediated injury as the major consequence of infection. This suggests that an important target for control of disease could include control of inflammatory and immune responses.

Even though they differ with respect to biology, epidemiology, and ecology, HME, HEE, HGA, and infection with EMLA present as clinically similar illnesses with characteristic, albeit nonspecific alterations in hematology and chemistry laboratory tests. The incubation period for HME, HEE, HGA, and EMLA varies between 1 and 2 weeks following tick exposure or tick bite. The symptoms and signs range from asymptomatic to fatal, and clinical severity increases with patient age and comorbid illnesses. Ehrlichiosis presents as a clinical syndrome most commonly manifest by abrupt onset of fever, shaking chills, severe headache, and myalgia (Table 171.2); a specific diagnosis can be difficult because of the undifferentiated nature of the signs and symptoms. Between one-third and one-half of symptomatic patients require hospitalization for 1 week or longer. Infection with Candidatus N. mikurensis can result in either a severe febrile illness that lasts for weeks in the absence of therapy, as observed in Europe where most patients had pre-existing immune compromise, or as a mild to moderate and self-limited illness, as observed in Asia where most patients were not immune compromised.

Table 171.2

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