First clinical case of canine granulocytic anaplasmosis in Korea and genotypic analyses of Anaplasma phagocytophilum

Granulocytic anaplasmosis is an emerging infectious disease affecting dogs and humans in the United States and other regions of the world. Relatively few cases have been described in pregnant women, and perinatal transmission appears to occur infrequently in humans. Infection in pregnant dogs has not been reported. Diagnosis of infection during pregnancy poses therapeutic challenges, because doxycycline, the treatment of choice, is teratogenic. Also, infection during pregnancy may result in more severe disease. When infection is diagnosed after parturition, knowledge of the risk of perinatal transmission to offspring is important, because prophylactic therapy in neonates is also not without risk. In this report, we describe relatively severe clinical manifestations of Anaplasma phagocytophilum infection in a postpartum bitch and a lack of perinatal transmission to her puppies.

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Exposure to Anaplasma phagocytophilum in two dogs in Belgium

Vlaams Diergeneeskundig Tijdschrift ◽

10.21825/vdt.v84i1.16621 ◽

2015 ◽

Vol 84 (1) ◽

pp. 39-46 ◽

Cited By ~ 2

Author(s):

S. Elhamiani-Khatat ◽

P. Defauw ◽

S. Marynissen ◽

I. Van de Maele ◽

A. Van Dongen ◽

...

Keyword(s):

Antibody Titer ◽

Anaplasma Phagocytophilum ◽

Kidney Injury ◽

Granulocytic Anaplasmosis ◽

First Case ◽

Immune Mediated ◽

Positive Antibody ◽

Vector Borne ◽

The Relationship ◽

Canine Granulocytic Anaplasmosis

In this report, two dogs are described, which were exposed to Anaplasma phagocytophilum in Belgium. The first case was presented for acute weakness and collapse, and was diagnosed with immune mediated hemolytic anemia. Vector-borne serology panel revealed a positive antibody titer for A. phagocytophilum, and the dog recovered during doxycycline therapy. The second patient suffered from an immune mediated glomerulopathy, and concurrently had a highly increased antibody titer for A. phagocytophilum. The relationship between canine granulocytic anaplasmosis and both IMHA and protein-losing nephropathy is unclear in these cases. However, it is suspected that A. phagocytophilum could be associated with kidney injury, as it is described in the second case.

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Expression of perilipin in human promyelocytic cells in response to Anaplasma phagocytophilum infection results in modified lipid metabolism

Journal of Medical Microbiology ◽

10.1099/jmm.0.47504-0 ◽

2008 ◽

Vol 57 (2) ◽

pp. 159-163 ◽

Cited By ~ 16

Author(s):

Raúl Manzano-Roman ◽

Consuelo Almazán ◽

Victoria Naranjo ◽

Edmour F. Bloui ◽

Katherine M. Kocan ◽

...

Keyword(s):

Lipid Metabolism ◽

Anaplasma Phagocytophilum ◽

Intracellular Pathogen ◽

Mrna Levels ◽

Rt Pcr ◽

Obligate Intracellular ◽

Granulocytic Anaplasmosis ◽

Obligate Intracellular Pathogen ◽

Canine Granulocytic Anaplasmosis

The obligate intracellular pathogen Anaplasma phagocytophilum is transmitted by ticks and causes human granulocytic anaplasmosis, tick-borne fever of ruminants, and equine and canine granulocytic anaplasmosis. In a previous study, the perilipin (PLIN) gene was identified as one of the genes differentially expressed in human promyelocytic HL-60 cells in response to infection with A. phagocytophilum. PLIN is a major adipocyte lipid droplet-associated phosphoprotein that plays a central role in lipolysis and cholesterol synthesis. Host cholesterol and other lipids are required by A. phagocytophilum for infection and multiplication in human cells. In this study, it was hypothesized that PLIN may be involved in infection of human HL-60 cells by A. phagocytophilum. To test this hypothesis, a combination of real-time RT-PCR, immunofluorescence and RNA interference was used to study the expression of PLIN. The results of these studies demonstrated that A. phagocytophilum modulates lipid metabolism by increasing PLIN mRNA levels and facilitates infection of HL-60 cells. The results of these studies expand our knowledge of the role of lipid metabolism in A. phagocytophilum infection and multiplication in HL-60 cells and suggest a mechanism by which A. phagocytophilum modulates lipid metabolism.

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Granulocytic anaplasmosis in captive ring-tailed lemur (Lemur catta) in Poland

BMC Veterinary Research ◽

10.1186/s12917-021-02827-8 ◽

2021 ◽

Vol 17 (1) ◽

Author(s):

Łukasz Adaszek ◽

Anna Wilczyńska ◽

Jerzy Ziętek ◽

Marcin Kalinowski ◽

Oliwier Teodorowski ◽

...

Keyword(s):

Anaplasma Phagocytophilum ◽

Polymerase Chain Reaction Test ◽

Anaplasma Ovis ◽

Case Presentation ◽

Granulocytic Anaplasmosis ◽

Pcr Product ◽

Polymerase Chain ◽

Obligate Intracellular Bacteria ◽

Chain Reaction Test ◽

Anaplasma Bovis

Abstract Background Anaplasma are obligate intracellular bacteria and aetiological agents of tick-borne diseases of both veterinary and medical interest. The genus Anaplasma comprises six species: Anaplasma marginale, Anaplasma centrale, Anaplasma ovis, Anaplasma phagocytophilum, Anaplasma bovis and Anaplasma platys. They can infect humans, carnivores, ruminants, rodents, insectivores, birds and reptiles. The aim of this study was to present the first clinical case of granulocytic anaplasmosis in a captive ring-tailed lemur in Poland. Case presentation A 4-year-old female lemur presented anorexia, epistaxis and tick infestation. The microscopic examination of a blood smear revealed morulae in neutrophils. Polymerase chain reaction test and sequencing of obtained PCR product confirmed infection by the GU183908 Anaplasma phagocytophilum strain. Therapeutic protocol included doxycycline (2.5 mg/kg p.o., b.i.d.) for 3 weeks and the lemur recovered within 24 h. Conclusions This is the first report on granulocytic anaplasmosis in a ring-tailed lemur in Europe, indicating that A. phagocytophilum infection must also be considered in differential diagnosis in this animal species, especially in individuals with thrombocytopenia associated with Ixodes ricinus parasitism.

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CXCR2 Blockade Influences Anaplasma phagocytophilum Propagation but Not Histopathology in the Mouse Model of Human Granulocytic Anaplasmosis

Clinical and Diagnostic Laboratory Immunology ◽

10.1128/cdli.11.5.963-968.2004 ◽

2004 ◽

Vol 11 (5) ◽

pp. 963-968 ◽

Cited By ~ 34

Author(s):

Diana G. Scorpio ◽

Mustafa Akkoyunlu ◽

Erol Fikrig ◽

J. Stephen Dumler

Keyword(s):

Anaplasma Phagocytophilum ◽

Tissue Injury ◽

Treated Group ◽

Obligate Intracellular Bacterium ◽

Human Granulocytic Anaplasmosis ◽

Obligate Intracellular ◽

Liver Histopathology ◽

Granulocytic Anaplasmosis ◽

Infected Cells ◽

And Control

ABSTRACT Anaplasma phagocytophilum is an obligate intracellular bacterium that infects neutrophils and causes human granulocytic anaplasmosis. Infection induces neutrophil secretion of interleukin-8 or murine homologs and perpetuates infection by recruiting susceptible neutrophils. We hypothesized that antibody blockade of CXCR2 would decrease A. phagocytophilum tissue load by interrupting neutrophil recruitment but would not influence murine hepatic pathology. C3H-scid mice were treated with CXCR2 antiserum or control prior to or on day 14 after infection. Quantitative PCR and immunohistochemistry for A. phagocytophilum were performed and severity of liver histopathology was ranked. Control mice had more infected cells in tissues than the anti-CXCR2-treated group. The histopathological rank was not different between treated and control animals. Infected cells of control mice clustered in tissue more than in treated mice. The results support the hypothesis of bacterial propagation through chemokine induction and confirm that tissue injury is unrelated to A. phagocytophilum tissue load.

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Draft Anaplasma phagocytophilum Genome Sequences from Five Cows, Two Horses, and One Roe Deer Collected in Europe: TABLE 1

Genome Announcements ◽

10.1128/genomea.00950-16 ◽

2016 ◽

Vol 4 (6) ◽

Cited By ~ 1

Author(s):

Thibaud Dugat ◽

Marie-Noëlle Rossignol ◽

Olivier Rué ◽

Valentin Loux ◽

Sylvain Marthey ◽

...

Keyword(s):

Anaplasma Phagocytophilum ◽

Roe Deer ◽

Intracellular Bacterium ◽

Genome Sequences ◽

Sequence Capture ◽

Granulocytic Anaplasmosis ◽

Alternative Approaches

Anaplasma phagocytophilum is a zoonotic tick-borne intracellular bacterium responsible for granulocytic anaplasmosis. As it is difficult to isolate and cultivate, only 20 A. phagocytophilum genomes have been sequenced to date. Here, we present eight A. phagocytophilum genome sequences obtained using alternative approaches based on sequence capture technology.

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Anaplasma phagocytophilum Has a Functional msp2 Gene That Is Distinct from p44

Infection and Immunity ◽

10.1128/iai.72.7.3883-3889.2004 ◽

2004 ◽

Vol 72 (7) ◽

pp. 3883-3889 ◽

Cited By ~ 31

Author(s):

Quan Lin ◽

Yasuko Rikihisa ◽

Suleyman Felek ◽

Xueqi Wang ◽

Robert F. Massung ◽

...

Keyword(s):

Outer Membrane ◽

Anaplasma Phagocytophilum ◽

Ixodes Scapularis ◽

Outer Membrane Proteins ◽

Gene Families ◽

Single Copy ◽

The United States ◽

Granulocytic Anaplasmosis ◽

The United Kingdom ◽

Membrane Protein Gene

ABSTRACT The msp2 and p44 genes encode polymorphic major outer membrane proteins that are considered unique to the intraerythrocytic agent of Anaplasma marginale and the intragranulocytic agent of Anaplasma phagocytophilum, respectively. In the present study, however, we found an msp2 gene in A. phagocytophilum that was remarkably conserved among A. phagocytophilum strains from human granulocytic anaplasmosis (HGA) patients, ticks, and a horse from various regions in the United States, but the gene was different in a sheep isolate from the United Kingdom. The msp2 gene in the A. phagocytophilum strain HZ genome was a single-copy gene and was located downstream of two Ehrlichia chaffeensis omp-1 homologs and a decarboxylase gene (ubiD). The msp2 gene was expressed by A. phagocytophilum in the blood from HGA patients NY36 and NY37 and by A. phagocytophilum isolates from these patients cultured in HL-60 cells at 37°C. The msp2 gene was also expressed in a DBA/2 mouse infected by attaching ticks infected with strain NTN-1 and in a horse experimentally infected by attaching strain HZ-infected ticks. However, the transcript of the msp2 gene was undetectable in A. phagocytophilum strain HZ in SCID mice and Ixodes scapularis ticks infected with strain NTN-1. These results indicate that msp2 is functional in various strains of A. phagocytophilum, and relative expression ratios of msp2 to p44 vary in different infected hosts. These findings may be important in understanding roles that Msp2 proteins play in granulocytic ehrlichia infection and evolution of the polymorphic major outer membrane protein gene families in Anaplasma species.

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Sequential Analysis of Anaplasma phagocytophilum msp2 Transcription in Murine and Equine Models of Human Granulocytic Anaplasmosis

Clinical and Vaccine Immunology ◽

10.1128/cvi.00417-07 ◽

2007 ◽

Vol 15 (3) ◽

pp. 418-424 ◽

Cited By ~ 16

Author(s):

Diana G. Scorpio ◽

Christian Leutenegger ◽

Jeannine Berger ◽

Nicole Barat ◽

John E. Madigan ◽

...

Keyword(s):

Anaplasma Phagocytophilum ◽

Complete Blood Count ◽

Clinical Manifestations ◽

Clinical Severity ◽

Human Granulocytic Anaplasmosis ◽

High Passage ◽

Granulocytic Anaplasmosis ◽

Low Passage

ABSTRACT Anaplasma phagocytophilum causes human granulocytic anaplasmosis by inducing immunopathologic responses. Its immunodominant Msp2 protein is encoded by a family of >100 paralogs. Msp2 (msp2) expression modulates in the absence of immune pressure, and prolonged in vitro passage modulates in vivo virulence. Because programmed MSP2 expression occurs in Anaplasma marginale, we hypothesized a similar event in A. phagocytophilum in vivo, with specific Msp2 expression triggering immunopathologic injury or clinical manifestations of disease. We examined msp2 transcripts in 11 B6 mice and 6 horses inoculated with low- or high-passage A. phagocytophilum Webster strain. Blood was sequentially obtained through 3 weeks postinfection for msp2 reverse transcription-PCR. Horses were additionally assessed for clinical manifestations, seroconversion, complete blood count, blood chemistry, and cytokine gene transcription. In both species, there was no consistent emergence of msp2 transcripts, and all 22 msp2 variants were detected in both passage groups. Clinical severity was much higher for high-passage-infected than for low-passage-infected horses, preceded by higher levels of blood gamma interferon transcription on day 7. Antibody was first detected on day 7, and all horses seroconverted by day 22, with a trend toward lower antibody titers in low-passage-infected animals. Leukocyte and platelet counts were similar between experimental groups except on day 13, when low-passage-infected animals had more profound thrombocytopenia. These findings corroborate studies with mice, where msp2 diversity did not explain differences in hepatic histopathology, but differ from the paradigm of low-passage A. phagocytophilum causing more significant clinical illness. Alteration in transcription of msp2 has no bearing on clinical disease in horses, suggesting the existence of a separate proinflammatory component differentially expressed with changing in vitro passage.

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