Severe Thrombocytopenic Purpura in a Child with Brucellosis: Case Presentation and Review of the Literature

Makis, Alexandros; Perogiannaki, Aikaterini; Chaliasos, Nikolaos

doi:10.1155/2017/3416857

Cited by 11 publications

(4 citation statements)

References 18 publications

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“…In humans, the BM shows histopathological alterations such as granulomas and an augmented number of inflammatory cells. Later, neutropenia, thrombocytopenia, anemia, and, in severe cases, pancytopenia, myelodysplasia, and hemophagocytosis are common BM alterations (198,200,201). Brucella organisms can persist in the BM of infected mice for protracted periods and induce significant changes in this tissue.…”

Section: Pmn Recruitment In the Course Of Brucellosismentioning

confidence: 99%

The Role of Neutrophils in Brucellosis

Moreno

Barquero-Calvo

2020

Microbiol Mol Biol Rev

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SUMMARY Brucellosis is a bacterial disease of domestic animals and humans. The pathogenic ability of Brucella organisms relies on their stealthy strategy and their capacity to replicate within host cells and to induce long-lasting infections. Brucella organisms barely induce neutrophil activation and survive within these leukocytes by resisting microbicidal mechanisms. Very few Brucella-infected neutrophils are found in the target organs, except for the bone marrow, early in infection. Still, Brucella induces a mild reactive oxygen species formation and, through its lipopolysaccharide, promotes the premature death of neutrophils, which release chemokines and express “eat me” signals. This effect drives the phagocytosis of infected neutrophils by mononuclear cells that become thoroughly susceptible to Brucella replication and vehicles for bacterial dispersion. The premature death of the infected neutrophils proceeds without NETosis, necrosis/oncosis, or classical apoptosis morphology. In the absence of neutrophils, the Th1 response exacerbates and promotes bacterial removal, indicating that Brucella-infected neutrophils dampen adaptive immunity. This modulatory effect opens a window for bacterial dispersion in host tissues before adaptive immunity becomes fully activated. However, the hyperactivation of immunity is not without a price, since neutropenic Brucella-infected animals develop cachexia in the early phases of the disease. The delay in the immunological response seems a sine qua non requirement for the development of long-lasting brucellosis. This property may be shared with other pathogenic alphaproteobacteria closely related to Brucella. We propose a model in which Brucella-infected polymorphonuclear neutrophils (PMNs) function as “Trojan horse” vehicles for bacterial dispersal and as modulators of the Th1 adaptive immunity in infection.

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Section: Pmn Recruitment In the Course Of Brucellosismentioning

confidence: 99%

The Role of Neutrophils in Brucellosis

Moreno

Barquero-Calvo

2020

Microbiol Mol Biol Rev

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“…However, in all brucellosis cases, the BM displays histopathological alterations, whether or not the bacterium is isolated from this tissue. Common hematological signs are neutropenia, thrombocytopenia, and anemia, and in severe cases, pancytopenia has also been reported [4, 5, 11]. In most patients, the BM cellular alterations ameliorate or disappear after antibiotic treatment [4].…”

Section: Introductionmentioning

confidence: 99%

Persistence of Brucella abortus in the Bone Marrow of Infected Mice

Gutiérrez-Jiménez

Hysenaj

Alfaro-Alarcón

et al. 2018

Journal of Immunology Research

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Brucellosis is a zoonotic bacterial infection that may persist for long periods causing relapses in antibiotic-treated patients. The ability of Brucella to develop chronic infections is linked to their capacity to invade and replicate within the mononuclear phagocyte system, including the bone marrow (BM). Persistence of Brucella in the BM has been associated with hematological complications such as neutropenia, thrombocytopenia, anemia, and pancytopenia in human patients. In the mouse model, we observed that the number of Brucella abortus in the BM remained constant for up to 168 days of postinfection. This persistence was associated with histopathological changes, accompanied by augmented numbers of BM myeloid GMP progenitors, PMNs, and CD4+ lymphocytes during the acute phase (eight days) of the infection in the BM. Monocytes, PMNs, and GMP cells were identified as the cells harboring Brucella in the BM. We propose that the BM is an essential niche for the bacterium to establish long-lasting infections and that infected PMNs may serve as vehicles for dispersion of Brucella organisms, following the Trojan horse hypothesis. Monocytes are solid candidates for Brucella reservoirs in the BM.

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“…In another paper by Makis et al, a case of a 5-year-old girl with Brucella melitensis infection presenting with severe thrombocytopenic purpura was described. Treatment included intravenous immunoglobulin and a combination of antibiotics [12] . In Saudi Arabia, a series of 115 children with brucellosis was reported, four of whom had severe thrombocytopenia.…”

Section: Discussionmentioning

confidence: 99%