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Update on Human Granulocytic Ehrlichiosis

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Update on Human Granulocytic Ehrlichiosis UC Agriculture & Natural Resources Proceedings of the Vertebrate Pest Conference Title Update on Human Granulocytic Anaplasmosis Permalink https://escholarship.org/uc/item/7313k3h6 Journal Proceedings of the Vertebrate Pest Conference, 22(22) ISSN 0507-6773 Author Foley, Janet Publication Date 2006 DOI 10.5070/V422110093 eScholarship.org Powered by the California Digital Library University of California Update on Human Granulocytic Anaplasmosis JanetFoley SchoolofVeterinaryMedicine,UniversityofCalifornia,Davis,California ABSTRACT : Granulocytic anaplasmosis (GA) is a disease of humans, domestic animals, and wildlife caused by Anaplasma phagocytophilum, formerly Ehrlichia phagocytophila, E. equi, and the unnamed agents of “human granulocytic ehrlichiosis” (HGE). This pathogen is inoculated into host skin by the bite of Ixodes spp. ticks, including I. pacificus in California and I. scapularis in the eastern U.S. After inoculation, A. phagocytophilum disseminates to the blood and is phagocytosed into host neutrophils.TheclinicalcharacteristicsofGAinpeoplevaryfromnosymptomstofever,headache,neurologicalsymptoms,and occasionallydeath.Horses withGAmayexperiencehighfever,depression,reducedabilitytoeat,limbedema,jaundice,andataxia. GAisanemergingdiseaseintheeasternU.S.butonlyahandfulofhumancaseshavebeenreportedinthewesternU.S.,despite relativelycommonreportsofdiseaseinhorsesanddogs.Wildlifeanddog-sentinelstudieshaveclarifiedthatinfectioniscommon in the coast range mountains and Sierra Nevada foothills, with ongoing research focusing on ecological determinants that can modifytheprevalenceofinfectioninanyparticulararea.Oneknownreservoiristhedusky-footedwoodrat.However,important, poorlyunderstoodecologicaldeterminantsservetomodifytheprobabilityofrodentaswellashumaninfections,includingclimate, vegetation, and possibly the presence of other reservoir-competent rodents and nidicolous woodrat-specialist ticks such as I. spinipalpis. KEYWORDS :Anaplasmaphagocytophilum ,disease, dusky-footedwoodrat, Ixodespacificus ,Ixodesspinipalpis ,Neotoma fuscipes ,tick-bornedisease Proc.22 nd Vertebr.PestConf. (R.M.TimmandJ.M.O’Brien,Eds.) PublishedatUniv.ofCalif.,Davis. 2006. Pp.318-323. THEORGANISMANDDISEASE phagosome. A. phagocytophilum-infected neutrophils PhylogenyandBiologicalCharacteristics secretechemokinesthatrecruitmacrophages,whichthen Granulocytic anaplasmosis (GA) is a disease of secreteIFN-γandIL-10andamplifylocalandsystemic humans, domestic animals, and wildlife caused by the inflammation (Dumler et al . 2000, Klein et al . 2000). newly renamed pathogen, Anaplasma phagocytophilum Within the phagosome, A. phagocytophilum can inhibit (Dumler et al . 2001) . This new species combines fusionofthisprotectedenvironmentwiththelysosome, Ehrlichia phagocytophila , E. equi , and the unnamed overcoming initial host immune attacks against the agents of “human granulocytic ehrlichiosis” (HGE), bacteria. Ultimately, however, when host cells are which cross-react serologically (Walker and Dumler primedwithIFN-γ,theyareabletokilltheintracellular 1995)andareindistinguishablemorphologically(Popov A. phagocytophilum (Webster et al . 1998, Mott et al . etal .1998).Thereismicrovariabilityinthe16SrRNA 1999). geneofstrainsfromtheuppermidwestern,eastern,and western U.S. among different host species (Chen et al. ClinicalOutcomesofInfection 1994,Reubel etal .1998),butanalysisofthe16S,444ep- The clinical characteristics of GA in people are Ank,andgroESLheatshockproteingeneticregionsfrom variable including pyrexia, headache, myalgia, nausea, equine and human-origin isolates from northern and ataxia (Goodman et al . 1996). More severe cases CaliforniasuggestedthattheHGEagentand E.equi in mayresultinorganfailure,susceptibilitytoopportunistic theU.S.aresynonymous,withmultiplestrainsthatmay infections, neuritis, or respiratory complications, with a vary geographically but do not appear to be host- case fatality rate up to 5% (Walker and Dumler 1995, differentiated(Chae etal .2000). Foley2000).GAinhorses ischaracterizedbyhighfever, A. phagocytophilum shares common biological depression, reduced ability to eat, limb edema, characteristics and immunopathological mechanisms in petechiation,icterus,andataxia(Madigan1993).Counts hostswithotherehrlichialandrickettsialbacteria.This ofbloodcellsmaydocumentanemia,lowplateletcounts, organism is inoculated into host skin by tick bite, in andlowwhitebloodcellcounts.Becausemuchofthe contextwithticksaliva,whichcontainsanarrayofanti- pathogenesis of GA is immune-mediated, there may be inflammatory and immunomodulatory chemicals during downstream immune-mediated sequelae, including feeding to prevent host blood clotting, platelet possiblepolyarthritisandvasculitis. aggregation,NKcellactivity,andT H1cytokineresponses (Wikel 1999). After tick inoculation and local host LaboratoryFindingsinGAandDiagnosis immune responses, A. phagocytophilum disseminates to AlthoughmostcasesofGAoccurinareaswheretick the blood, where this obligate intra-cellular pathogen bitingiscommon,notallhumanpatientsreportatickbite must persist within host neutrophils. The bacterium and not all dog or horse owners recognize that their enterstheneutrophilafterattachingviaanoutersurface animalhasbeeninfected.Thesymptomsandlaboratory protein to a host cell receptor and being phagocytosed diagnosticresultsofGAarenon-specificandmayinclude into a small host membrane-bound site called a elevated liver enzymes, thrombocytopenia, and neutro- 318 penia.Insomecases,thesymptoms(e.g.,headacheand and I.spinipalpis inthewesternU.S. fever) are severe, and yet there are only mild or no Thespatialdistributionofhumanandequinecasesof laboratoryabnormalities. GA in the western U.S. corresponds with the range of ProbablythemostrapidmethodfordiagnosisofGA Ixodes pacificus , the western black-legged tick, a is to find the characteristic membrane-bound inclusions common tick throughout much of low mountain (morulae) in neutrophils on blood smears, but the California (Furman and Loomis 1984, Madigan and proportionofneutrophilswithvisiblemorulaemaybeas Gribble1987,Richter etal .1996).I.pacificus hasbeen low as 1-2%. The Centers for Disease Control (CDC) recordedfrom55of58countiesinCalifornia,andadult I. criteria for a confirmed diagnosis require that pacificus containing A.phagocytophilum DNAhavebeen visualization of morulae be accompanied by positive detected in Alameda, El Dorado, Humboldt, Napa, titers ( ≥64), probably because some cellular inclusions Orange, Sacramento, Santa Cruz, Sonoma, and Yolo may appearsimilarto morulae. Althoughasingletiter Counties (Barlough et al . 1997, Kramer et al . 1999; ≥64maybepartofapresumptivediagnosis,thisdoesnot Nicholson etal .1999;Lane etal .2001),althoughtick document active infection. However, a 4-fold rise in surveillancehasbeenlimited.Thevectorcompetenceof specifictiterover4weeksisconsideredconfirmatoryfor I. pacificus for A. phagocytophilum has been evaluated. GA.Titersbecomepositiveapproximately2weeksafter Infected I. pacificus individuals can be found in nature onsetofclinicalsignsandremainelevatedafterexposure (Richter etal. 1996;Barlough etal .1997,Kramer etal . formonthstoyears,sothereisabriefwindowearlyin 1999, Lane et al . 2001); horses can be experimentally theinfectionwhenthepatientmaybeillbutseronegative. infected using field-caught, naturally-infected ticks Culture of A. phagocytophilum is time-consuming, (Reubel et al . 1998); and the agent can be transmitted specialized,andsomewhatexpensive.Polymerasechain from experimentally-infected horses to naïve horses by reaction (PCR) for specific DNA is extremely valuable feedingof I.pacificus (Richter etal .1996) . for confirming a suspected diagnoses but generally not Theprevalenceof A.phagocytophilum inticksranges available rapidly enough in practice for use in primary from0-51%intheeasternU.S.(Magnarelli etal .1995, diagnosis and to guide treatment. There are multiple Pancholi et al . 1995, Daniels et al . 1997, Varde et al . published protocols for PCR of A. phagocytophilum . 1998), but typically is much lower in the western U.S., PCRmaybemostusefulearlyinacuteinfectionbefore from0.8-11%(Barlough etal .1997,Kramer etal .1999, the patient seroconverts, late in infection to rule-out Nicholson etal .1999,Lane etal .2001).Theprevalence chronic infection, or when serological titers to several in I. pacificus nymphs is also low, with 0/465 nymphs agentsaresimilar. positiveevenwheretheadultprevalencewas11%(Lane et al . 2001) and only 1/47 pools positive from Sonoma ECOLOGY County(Barlough etal .1997).Yet,nymphsmaycause Emergence mosthuman,deer,andmountainlioncases,becausethese Human granulocytic anaplasmosis (HGA) has peak typically in June and July, corresponding to emergeddramaticallyintheeasternandmidwesternU.S. nymphaltickabundance(Lane1990;Foley etal .1998, overthepast25years.SincefirstreportedinWisconsin 1999 b, 2001; CDC 2000). In contrast, cases in horses in1994,over400casesofHGAhavebeendiagnosedin and dogs seem to peak in the winter, corresponding to the upper midwestern and northeastern United States peakactivityof I.pacificus adults(MadiganandGribble (CDC2000).Incontrast,only8humancaseshavebeen 1987,Vredevoe etal .1999,Foleyetal .2001),although documentedinCaliforniaasofApril2002,despitebeing dog cases also occur in late spring, at the time of the reportable to the California Department of Health emergence of nymphs (Foley et al . 2001). A. Services (CDHS), availability of diagnostic laboratory phagocytophilum isnottransovariallytransmittedamong support,
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