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Background: Thrombocytopenia is commonly observed in patients with sepsis and is an independent risk factor for poor prognosis. However, the changes of platelet count caused by different pathogens can vary significantly. Our study aims to evaluate the quantitative changes in platelet count in response to various pathogens., Material and Methods: We retrospectively analysed data of 3044 patients with sepsis from Medical Information Mart for Intensive Care (MIMIC, 2008-2019) database and prospectively collected data of 364 patients with sepsis from our local cohort of the Shandong Bloodstream Infection and Sepsis Collaboration Study (SBISC, 2020-2022). Propensity score matching (PSM) was employed to control for baseline differences in variables, except for the causative pathogen., Results: Multivariate logistic analyses of both original and PSM populations identified Candida , Escherichia , Klebsiella , and Serratia species posing a higher risk for thrombocytopenia compared to others. Restricted cubic spline (RCS) curves showed L- or U-shaped associations between platelet count and 28-mortality with various cut-off values among different pathogens: ranging from 96 × 10 9 /L in Candida species - 190 × 10 9 /L in Klebsiella species., Conclusion: Our present findings indicate a pathogen-specific effect on platelet count, highlighting the importance of monitoring thrombocytopenia in patients infected with above microorganisms. Clinicians need to consider pathogen-specific thresholds when intervene on platelet count.

Previous studies suggest that sepsis remains a common critical illness with a global incidence of 31.5 million. The aim of this study was to evaluate the comparative therapeutic value of recombinant human thrombopoietin (rhTPO) in treating sepsis patients with thrombocytopenia. We conducted a comprehensive electronic search of PubMed, EMBASE, the Cochrane Library, and CNKI from its inception through December 31, 2021. Thirteen randomized controlled trials (RCTs) involving 963 patients were included. Network meta-analyses showed that rhTPO 300 U/kg/day and rhTPO 15000 U/day significantly increased the platelet (PLT) levels on the 7 th day and decreased the requirement of transfusion of red blood cells (RBCs), plasma, and PLT compared with IVIG and NAT. SUCRA showed that rhTPO 300 U/kg/day ranked first in terms of 28-day mortality (85.5%) and transfusion, including RBC (88.7%), plasma (89.6%), and PLT (95.2%), while rhTPO 15000 U/day ranked first for the length of the intensive care unit (ICU) stay (95.9%) and PLT level at day 7 (91.6%). rhTPO 300 U/kg/day may be the optimal dose to reduce 28-day mortality and transfusion requirements. However, rhTPO 15000 U/day may be the optimal dose for shortening the ICU stay and increasing the PLT level on the 7th day. However, additional studies to further validate our findings are needed., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2022 Dandan Chen et al.)

Background: Our aim was to characterize etiologic diagnoses obtained from bronchoalveolar lavage fluid (BALF) and blood specimens, and to identify risk factors for mortality in systemic lupus erythematosus (SLE) patients with pneumonia and respiratory failure., Methods: We conducted a retrospective analysis of SLE patients with pneumonia and respiratory failure. Clinical characteristics, laboratory profiles, and microbiology in BALF and blood samples were evaluated. We performed univariable analyses to identify mortality risk factors., Results: All 24 patients (F:M = 21:3, median age 46.5 years; disease duration 11 years) received mechanical ventilation (median duration: 11 days). Pathogens identified in BALF included Pneumocystis jiroveci (12 patients [50%]), cytomegalovirus (CMV, 7 patients [29.2%]), and bacteria (11 patients [45.8%]). Thirteen patients (54.2%) yielded pathogens in blood (CMV in 8 patients [33.3%] and Escherichia coli in 5 patients [20.8%]). Eight developed septic shock, and 9 died within 30 days. Univariable analysis identified thrombocytopenia (odds ratio [OR]: 8.0, 95% confidence interval [CI]: 1.23-52.25), bacteremia within 30 days before or after endotracheal intubation (OR: 8.0, 95% CI: 1.23-52.5), and P. jiroveci pneumonia (PJP, OR: 7.0, 95% CI: 1.04-46.95) as risk factors for 30-day mortality. Kaplan-Meier analysis confirmed an increased risk of 30-day mortality with thrombocytopenia and bacteremia., Conclusion: There are high prevalence rates of PJP and CMV infections as evidenced by BALF analyses in SLE patients with pneumonia and respiratory failure. BALF analysis can facilitate rescue therapy per pathogen. Thrombocytopenia, bacteremia, and PJP in SLE patients can increase their 30-day mortality, so warrant early and aggressive treatments., Competing Interests: Declaration of Competing Interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (Copyright © 2020. Published by Elsevier B.V.)

Background: Well known for their hemostatic function, platelets are increasingly becoming recognized as important immunomodulators. The purpose of the present study was to assess the impact of platelet depletion on antimicrobial host defense in a mouse model of periprosthetic joint infection (PJI)., Methods: Thrombocytopenia (TCP) was induced in C57BL/6 mice with use of a selective antibody against platelet CD41 (anti-CD41). Whole blood from pre-treated mice was incubated with Staphylococcus aureus to assess antimicrobial efficacy with use of bioluminescent imaging, quantitative histological staining, and colony forming unit (CFU) quantification. In parallel, untreated heterologous platelets were added to TCP blood to assess potential rescue of antimicrobial efficacy. In vivo, TCP and control mice underwent placement of a titanium implant in the femur inoculated with bioluminescent Xen36 S. aureus. Longitudinal bioluminescent imaging was performed postoperatively to quantify the evolution of bacterial burden, which was confirmed via assessment of S. aureus CFUs on the implant and in peri-implant tissue on postoperative day (POD) 28., Results: Anti-CD41 treatment resulted in significant dose-dependent reductions in platelet count. Ex vivo, platelet-depleted whole blood demonstrated significantly less bacterial reduction than control blood. These outcomes were reversed with the addition of untreated rescue platelets. In vivo, infection burden was significantly higher in TCP mice and was inversely correlated with preoperative platelet count (r2 = 0.63, p = 0.037). Likewise, CFU quantification on POD28 was associated with increased bacterial proliferation and severity of periprosthetic infection in TCP mice compared with controls., Conclusions: Thrombocytopenia resulted in an increased bacterial burden both ex vivo and in vivo in a mouse model of PJI., Clinical Relevance: In orthopaedic patients, deficiencies in platelet quantity or function represent an easily modifiable risk factor for PJI., Competing Interests: Disclosure: This study was supported by the H&H Lee Research Program and the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health. On the Disclosure of Potential Conflicts of Interest forms, which are provided with the online version of the article, one or more of the authors checked “yes” to indicate that the author had a relevant financial relationship in the biomedical arena outside the submitted work (http://links.lww.com/JBJS/G396)., (Copyright © 2021 by The Journal of Bone and Joint Surgery, Incorporated.)

Anaplasma phagocytophilum (AP) is the causative agent of human granulocytic anaplasmosis (HGA), a tick-borne illness with highest incidence in north-eastern regions of the United States. This condition presents with vague constitutional symptoms and has been associated with laboratory derangements such as leukopenia, thrombocytopenia and transaminitis1. Rhabdomyolysis, however, is not one of these associations. We report a case of confirmed HGA associated with severe rhabdomyolysis, where no other cause was identified. The etiology of rhabdomyolysis secondary to AP infection is still unknown. A presumptive diagnosis of HGA can be made in the presence of fever, non-specific symptoms such as myalgias, laboratory derangements such as leukopenia and thrombocytopenia in an individual residing in an endemic area3. Serological confirmation should not delay treatment, given the rapid progression of this dangerous infection. Rhabdomyolysis should also be considered as part of supporting data in the diagnostic consideration for HGA., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Castleman-Kojima disease, also known as idiopathic multicentric Castleman disease with TAFRO syndrome (iMCD-TAFRO), is a recently recognized systemic inflammatory disorder with a characteristic series of clinical symptoms, including thrombocytopenia (T), anasarca (A), fever (F), reticulin fibrosis (R), and organomegaly (O). Patients with iMCD-TAFRO often develop severe abdominal pain, elevated alkaline phosphatase levels, and systemic inflammation, but the etiological factors are unknown. To investigate the potential role of bacterial infection in the pathogenesis of iMCD-TAFRO, we performed polymerase chain reaction (PCR) for the bacterial 16S rRNA gene with DNA extracted from liver specimens of three patients with iMCD-TAFRO, four patients with amyotrophic lateral sclerosis, and seven patients with inflammatory conditions. Sequencing of the PCR product showed 99% DNA sequence identity with Campylobacter jejuni in all three patients with iMCD-TAFRO and in two patients with inflammatory conditions. Immunohistochemical and electron microscopy analyses could not identify C. jejuni in patients with iMCD-TAFRO. The findings indicated that C. jejuni infection is not the pathological cause of iMCD-TAFRO; however, this ubiquitous bacterium may play a role in uncontrolled systemic hypercytokinemia, possibly through the development of cross-reactive autoantibodies., (© 2019 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.)

TAFRO syndrome is a novel disease concept characterized by Thrombocytopenia, Anasarca, myeloFibrosis, Renal dysfunction, Organomegaly, multiple lymphadenopathy and a histopathological pattern of atypical Castleman's disease. A 58-year-old man was diagnosed as TAFRO syndrome by clinical and histopathological findings. After receiving intensive immunosuppressive therapy, his thrombocytopenia and anasarca had not improved. He developed complications such as methicillin-resistant Staphylococcus aureus sepsis , gastrointestinal bleeding, peritonitis caused by Stenotrophomonas maltophilia , gastrointestinal perforation, and disseminated candidiasis resulting in death. Autopsy revealed disseminated candidiasis and hemophagocytic lymphohistiocytosis, with no evidence of TAFRO syndrome. During treatment, we regarded his lasting thrombocytopenia and anasarca as insufficient control of TAFRO syndrome. However, the autopsy revealed that thrombocytopenia was caused by secondary hemophagocytic lymphohistiocytosis caused by over-immunosuppression. We reviewed the published literature to identify indicators of adequate treatment, which suggested improvement of platelet count and anasarca several weeks after initial therapy. This indicated that we could not depend on the platelet count and anasarca in acute medical care after initial treatment. We should treat TAFRO syndrome based on patients' clinical status and obviate the risk of treatment-related complications caused by over-immunosuppression., Competing Interests: The authors declared no conflict of interests for this article.

Thromobocytopenia predicts mortality in patients with melioidosis in Thailand. We analyzed platelet counts in two large cohorts of melioidosis patients in tropical northern Australia to assess utility in a different clinical setting. Admission platelet counts were compared between subgroups of patients with different clinical outcomes. Patients with more severe disease (indicated by bacteremia, septic shock, and death) had significantly lower platelet counts than those with less severe disease. Logistic regression analysis was carried out for potential predictors of mortality among various clinical parameters, and platelet count was shown to be an independent predictor of mortality. Furthermore, in patients critically ill with melioidosis, an increasing platelet count after admission was associated with a significantly greater chance of survival. However, given that most patients with severe disease still had platelet counts within the normal range, platelet count is not a useful biomarker for predicting the severity of melioidosis in a clinical context.

BACKGROUND Murine typhus is a rare bacterial infection caused by Rickettsia typhi, which is transmitted from rodents to humans through the infected Xenopsylla cheopis flea. The disease presentation is often non-specific, leading to unnecessary tests, and a delay in diagnosis and treatment. CASE REPORT A report is presented of a 22-year-old, previously healthy man, who presented with several symptoms and signs that increased in severity, requiring admission to the medical intensive care unit (MICU). After an extensive bacterial and viral laboratory workup, IgM and IgG titers confirmed the diagnosis of murine typhus due to infection by Rickettsia typhi. The patient was treated with doxycycline, which resulted in significant clinical improvement. CONCLUSIONS Murine typhus can present with a characteristic triad of fever, headache, and rash but also with other symptoms and signs and can vary in severity. Given its increasing prevalence in coastal cities, awareness of this infection and early diagnosis and treatment with doxycycline can reduce patient morbidity.

Scrub typhus is becoming a clinically important cause of acute undifferentiated febrile illness in Taiwan. The incubation period is between 6 and 21 days after exposure. It is transmitted by chiggers (larva of trombiculid mite) in long grasses and in dirt-floor homes, with infection characterized by a flu-like illness of fever, headache, and myalgia lasting approximately 1 week. It has various systemic manifestations, including GI symptoms. In some, the illness progresses to multiorgan dysfunction syndrome and death. We report on a 13-year-old boy who lived in Taipei City and who had initially tentative diagnosis of acute pyrexia of unknown origin with high fever up to 40.3°C for 1 week, but later had thrombocytopenia and diffuse abdominal pain with peritoneal sign suspected acute appendicitis. During the clinical course, septic shock and disseminated intravascular coagulopathy (DIC) were noted. There were skin rash in his trunk and extremities and an eschar with black crust surrounded by a scaling erythematous rim on his right buttock. In addition, we got the information of his travel history in Green Island and Orchid Island for 10 days.With the correct antibiotics, vancomycin, meropenem, and doxycycline, the patient was getting better and corresponding with high level of granulysin and tumor necrosis factor-alpha. The diagnosis of scrub typhus was confirmed by the biopsy of eschar and high quantitative real-time polymerase chain reaction values of Orientia tsutsugamushi (16sRNA and 56 kDa) tested by Centers for Disease Control and Prevention, Taiwan. Histopathological findings of the eschar revealed the leukocytoclastic vasculitis, crust and thrombus formation with many gram-negative microorganisms, O. tsutsugamushi demonstrated by 47 kDa monoclonal antibody immunohistochemical stain and electromicroscopy., Outcomes: After the careful selection of appropriate antibiotics including meropenem, vancomycin, and doxycycline, he recovered and was subsequently discharged 7 days after admission., Lesson Subsections: This case highlights that scrub typhus infection can mimic acute abdomen and septic shock with DIC. This rare presentation of acute abdomen and septic shock with thrombocytopenia and DIC caused by scrub typhus should remind physicians to be alert to the possibility of acute abdomen and febrile illness resulting from scrub typhus.

Arthropod-borne pathogens are medically important because of their ability to cause diseases in their hosts. The purpose of this study was to detect the occurrence of Ehrlichia spp., piroplasmids and Hepatozoon spp. in dogs with anemia and thrombocytopenia in southern Brazil. EDTA-whole blood was collected from 75 domestic dogs presenting anemia or/and thrombocytopenia from Guarapuava, state of Paraná, Brazil. DNA samples were subjected to conventional PCR assays for Ehrlichia spp. (dsb), piroplasmids (18S rRNA) and Hepatozoon spp. (18S rRNA), followed by sequencing and phylogenetic analyses. Among the 75 dogs, one (1.33%) was positive for Hepatozoon sp. and six (8%) were positive for piroplasmids in 18S rRNA cPCR assays. None of the dogs showed positive results in Ehrlichia spp.-cPCR targeting dsb gene. The phylogenetic analyses revealed that three piroplasm sequences were clustered with Rangellia vitalii, while one sequence was grouped with B. vogeli. The only sequence obtained from Hepatozoon spp.-PCR protocol was pooled with H. canis. Therefore, there is urgent need for differential molecular diagnosis of the two piroplasm species cited as etiological agents in clinical cases of canine hemoparasitic diseases, given the higher pathogenic potential of R. vitalii than of B. vogeli.

Sepsis is associated with thrombocytopenia and microvascular thrombosis. Studies have described platelets implication in this pathology but their kinetics of activation and behavior remain poorly known. We show in a mouse model of peritonitis, the appearance of platelet-rich thrombi in organ microvessels and organ damage. Complementary methods are necessary to characterize platelet activation during sepsis as circulating soluble markers and platelet-monocyte aggregates revealed early platelet activation, while surface activation markers were detected at later stage. A microfluidic based ex-vivo thrombosis assay demonstrated that platelets from septic mice have a prothrombotic behavior at shear rate encountered in microvessels. Interestingly, we found that even though phosphoinositide-3-kinase β-deficient platelet mice formed less thrombi in liver microcirculation, peritoneal sepsis activates a platelet alternative pathway to compensate the otherwise mandatory role of this lipid-kinase to form stable thrombi at high shear rate. Platelets are rapidly activated during sepsis. Thrombocytopenia can be attributed in part to platelet-rich thrombi formation in capillaries and platelet-leukocytes interactions. Platelets from septic mice have a prothrombotic phenotype at a shear rate encountered in arterioles. Further studies are necessary to unravel molecular mechanisms leading to this prothrombotic state of platelets in order to guide the development of future treatments of polymicrobial sepsis.

We discuss a child with severe thrombocytopenia and mild anemia admitted to the Hematology service who quickly deteriorated to a life-threatening state. However, once rickettsial disease was considered in the differential diagnosis and empiric doxycycline begun, she quickly and fully recovered. A diagnostic panel, including Rickettsia typhi serology, confirmed the diagnosis of murine typhus but this occurred weeks after she had recovered. Given the potential severity of rickettsial diseases and the ease of modern travel across geographic borders, hematology-oncology providers everywhere must consider rickettsial diseases in their differential diagnosis of critically ill children and begin empiric therapy with doxycycline promptly.

Neonatal adenovirus infection is infrequent, but in most cases the outcome of the infection is fatal. In this case report we describe the hospital course of a 3 day old newborn patient presenting with bloody stools and thrombocytopenia that remained clinically stable and had a benign course following Adenovirus 40/41 infection detected in stool. Neonatal adenovirus infection should be considered in the differential diagnosis of neonatal sepsis and pneumonia but also in patients that present with hematochezia, thrombocytopenia and/or other less specific signs and symptoms of viral illness.

Purpose: Fungaemia is associated with substantial morbidity and mortality in neonates admitted to neonatal intensive care units (NICUs). We report an outbreak of fungaemia in a NICU due to rare yeast, Pichia kudriavzevii (a teleomorph of Candida krusei). To the best of our knowledge, this is the first report of neonatal sepsis due to P. kudriavzevii., Methodology: Between August and September 2014, blood cultures from nine neonates diagnosed with late-onset sepsis in the NICU yielded yeast-like organisms. The molecular identification and typing of these isolates was performed by sequencing the D1/D2 region of 26S rDNA and fluorescent amplified fragment length polymorphism (FAFLP) respectively. Antifungal susceptibility was tested by broth microdilution as per the Clinical Laboratory Standards Institute (CLSI) guidelines. Sampling from environmental sources and the hands of healthcare workers (HCWs) in the NICU was performed., Results: Of the nine neonates, eight were preterm and six had very low birth weight (VLBW). Thrombocytopenia was present in two neonates. Sequencing identified all the isolates as P. kudriavzevii and FAFLP showed their clonal origin. Antifungal susceptibility testing revealed the susceptibility of all isolates to the antifungals tested. Treatment with voriconazole was advised. However, only seven neonates were treated successfully and discharged after improvement, whereas two were lost for follow-up. Cultures from the environment and the hands of HCWs were negative. The outbreak was controlled by the strict implementation of infection control practices., Conclusion: This study emphasizes the importance of accurate identification of the aetiological agent of sepsis and vigilant monitoring for the possibility of an outbreak in NICUs.

Group B Streptococcus (GBS) causes life-threatening bacterial sepsis, especially in newborns and pregnant women. Patients suffering from sepsis often display low platelet counts, characterized by thrombocytopenia, because of platelet activation. In the present study, the roles of six GBS strains from septic patients in platelet aggregation, as well as the underlying mechanisms, were investigated. Incubation of platelets with three of the strains induced platelet aggregation, increased the secretion of cellular adhesin molecule CD62P and activation of GPIIb/IIIa. Furthermore, the GBS strains that induced platelet activation also caused an increase in the expression of Toll-like receptor (TLR) 2 in platelets. Pre-incubation of platelets with anti-TLR2 monoclonal antibody, but not anti-TLR4 monoclonal antibody, inhibited these functional responses induced by GBS. TLR2 stimulation also activated the phosphoinositide 3-kinase (PI3-K)/Akt signalling pathway in platelets, and inhibition of PI3-K significantly reduced GBS-induced platelet responses. Our results indicate that three of the GBS strains from the septic patients can trigger platelet activation by interacting with platelets, which involves the elevation of platelet TLR2 expression., (© 2016 John Wiley & Sons Australia, Ltd.)

Hantaviruses cause potentially fatal two different systemic infectious diseases in humans named as hemorrhagic fever with renal syndrome (HFRS) and Hantavirus pulmonary syndrome. The clinical features of HFRS are hemorrhage, fever, thrombocytopenia and acute renal insufficiency frequently observed. HFRS shows distinctive clinical manifestations throughout from acute influenza-like febrile illness to shock. Although a large portion of HRFS patients present with a complaint of abdominal pain, acute pancreatitis is a rare complication of HFRS. No specific treatment protocol has been described for HRFS and supportive treatment is the basic approach. The rate of success enhanced with early diagnosis and intensive care support. Clinicians should be alert to the HFRS in patients with acute pancreatitis associated with systemic viral infection. We describe a case with HFRS who has presented with acute kidney injury, thrombocytopenia and acute pancreatitis. The patient was treated by supportive management successfully., (© Acta Gastro-Enterologica Belgica.)

Clostridium difficile infection (CDI) is a common cause of nosocomial diarrhea and colitis. The incidence and prognostic significance of thrombocytopenia as related to mode of acquisition (hospital vs. community), NAP1/027 strain, and disease severity has not been examined. We performed a single-institution retrospective analysis of all adult inpatients from 2013 to 2014 diagnosed with CDI during their hospitalization to document the incidence/prevalence of thrombocytopenia and associated outcomes. Severe disease was defined by a composite endpoint of inpatient death, death within 30 days of discharge, presence of septic shock, or need for colectomy during hospitalization. Of the 533 patients diagnosed with CDI, moderate thrombocytopenia (platelet count <100 × 10 9 /L at time of CDI diagnosis) was present in 15 % of the total cohort and incident thrombocytopenia developed in 3 % of patients after admission. Thrombocytopenia was more common in hospital-acquired disease and associated with increased length of stay, but was not associated with treatment failure. Those with moderate thrombocytopenia were more likely to have severe disease, after controlling for white blood cell count, albumin, and creatinine. Moderate thrombocytopenia is associated with poor prognosis and is a potential risk stratification tool for severe CDI.

Prevalence of Anaplasma, Ehrlichia, Neorickettsia, and Wolbachia DNA in blood of 479 cats collected in different veterinary clinics in Southern Germany was determined using a previously published conventional PCR using 16S-23S intergenic spacer primers (5' CTG GGG ACT ACG GTC GCA AGA C 3' - forward; 5' CTC CAG TTT ATC ACT GGA AGT T 3' - reverse). Purified amplicons were sequenced to confirm genus and species. Associations between rickettsial infections, and feline immunodeficiency virus (FIV), as well as feline leukemia virus (FeLV) status were evaluated. Rickettsial prevalence was 0.4% (2/479; CI: 0.01-1.62%). In the two infected cats, Anaplasma phagocytophilum DNA was amplified. These cats came from different environment and had outdoor access. Both were ill with many of their problems likely related to other diseases. However, one cat had neutrophilia with left shift and the other thrombocytopenia potentially caused by their A. phagocytophilum infection. There was no significant difference in the FIV and FeLV status between A. phagocytophilum-negative and -positive cats. A. phagocytophilum can cause infection in cats in Southern Germany, and appropriate tick control is recommended., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: Human granulocytic anaplasmosis (HGA) is an acute tick-borne infectious disease with increasing morbidity and mortality, but is rarely considered in clinical practice. Because human-to-human transfusion or nosocomial transmission can occur, diagnosis is difficult when the history of tick bites is not clear., Methods: We present clinical features and laboratory data of HGA patients who had no clear tick bite history., Results: All patients in the study presented with a high fever, petechiae, purpura, nose bleeding and leukopenia, and patients had abnormally high levels of serum ferritin and C-reactive protein. Morulae in leukocytes were observed in three patients. Foamy histiocytes and slight erythrophagocytic activity were only found in severely ill patients., Conclusion: In patients with fever and thrombocytopenia in whom no other diagnosis is evident on clinical assessment, HGA should be considered in the differential diagnosis, and tested for serologically if possible. For patients in whom the diagnosis of HGA is possible, and to whom tetracyclines can safely be given, it is apparent that these drugs hasten recovery and improve the prognosis., (© The Author(s) 2015.)

We report a fatal case of suspected Clostridium (Cl.) perfringens septicemia in a previously healthy woman in her eighties. At first, she presented at the hospital complaining of upper abdominal discomfort and vomiting, and was discharged the next day after ruling out any fatal conditions. However, her condition deteriorated approximately 10h after discharge and she died shortly after. The postmortem computed tomography (PMCT) performed 29h postmortem revealed an excessive systemic gas accumulation compared with the postmortem external appearance and time elapsed since her death, which suggested the presence of a gas-forming infection. Histopathological examination showed diffuse proliferation of Gram-positive bacilli in almost all the organ tissues, especially in blood vessels. Along with these findings, hyperthermia 3h postmortem, and severe anemia and thrombocytopenia without an obvious site of hemorrhage suggested hemolysis due to Cl. perfringens septicemia. These findings suggested the diagnosis before performing the conventional autopsy. To the best of our knowledge, this is the first case report to describe PMCT findings of gas-forming infection and septicemia in contrast with the external appearance and histopathological findings in a medico-legal autopsy setting., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Introduction: Leptospirosis is a worldwide zoonosis caused by the spirochete Leptospira interrogans. The spectrum of symptoms reported in leptospirosis is extremely broad. Thrombocytopenia is common during the acute phase of leptospirosis but its pathophysiological mechanism remains not well defined., Case Report: We report a 56-year-old man hospitalized for severe sepsis with acute kidney injury and liver failure. Because of the recent flood of his house, we suspected leptospirosis. The diagnosis was rapidly confirmed. Blood tests revealed thrombocytopenia at 9 G/L associated with hyperferritinemia and hypertriglyceridemia. Cytological examination of bone marrow showed abundance of megakaryocytes and hemophagocytosis which confirmed the diagnosis of hemophagocytic syndrome. Clinical symptoms resolved and blood tests returned to normal values in the same time., Conclusion: We suggest that hemophogocytosis is a possible mechanism of thrombocytopenia in leptospirosis and that examination of bone marrow should be performed to confirm the diagnosis., (Copyright © 2014. Published by Elsevier SAS.)

A 67-year-old man was referred to our hospital because of acute kidney injury, thrombocytopenia and hyperbilirubinemia. Despite severe kidney failure, hypokalemia was present. One infectious cause explained the whole clinical picture., (2015 BMJ Publishing Group Ltd.)

Although liver involvement is frequently seen in brucellosis, acute hepatitis is a rare clinical entity. In its progress, haematological findings are non-specific and vary in respect to severity. In this paper, we present a case of brucellosis with acute hepatitis and bicytopenia without anaemia. A 19-year-old man presented with a 2-week history of fever, sweating, low back and leg pain, lassitude, loss appetite, nausea and vomiting. He gave a history of raw milk ingestion and animal contact. Physical examination showed signs of icteric skin and sclera, tenderness in the right hypochondriac region and hepatosplenomegaly. On admission to hospital, laboratory tests showed WBC 3500/mmc (polymorphs 63% and lymphocytes 33%), haemoglobin 13.8 g/dL, platelet 89000/mmc, erythrocyte sedimentation rate 19 mm/h, and C-reactive protein 21.7 mg/dL (N<0.8 mg/dL). Biochemical tests were as follows: AST 771 U/L, ALT 471 U/L, ALP 355 U/L, GGT 432 U/L, total bilirubin 2.61 mg/dL, direct bilirubin 1.45 mg/dL and albumin 3.7 g/dL. Viral hepatitis markers were found to be negative (HBsAg, anti-HBc total, anti-HBc IgM, anti-HAV IgM, and anti-HCV). Blood culture grew Brucella melitensis. Leukopenia and thrombocytopenia returned to normal levels at the 7th and 14th day of his admission, respectively. Liver function tests improved at the 28th day. Treatment of the brucellosis was performed with antibiotics (tetracycline 500 mg orally four times daily for 6 weeks and streptomycin 1 g IM once daily for 21 days). Finally, a case of brucellosis with acute hepatitis and bicytopenia was treated with a successful outcome. In conclusion, we suggest that due consideration be taken of bicytopenia/pancytopenia and acute hepatitis in brucellosis cases in Turkey, an endemic region.

Anaplasma platys is the causative agent of infectious cyclic thrombocytopenia in dogs. This infection is worldwide and reported with a higher incidence in tropical and subtropical areas such as South America. Until now, there has been no report of this bacterium in French Guiana. The aim of this study was molecular investigation of A. platys occurrence in the blood of autochthonous dogs in this region. A total 65 blood samples were taken from the shelter dogs in the cities of Cayenne and Kourou, and from dogs of private owners in the city of Cayenne. The results show that at least 15.38% (10/65) were positive to this pathogen. The strain identified in this study has been reported worldwide. These findings should be considered in the way that local veterinarians handle suspected cases of canine anaplasmosis and ehrlichiosis.

Sepsis is one of the oldest and most elusive syndromes in medicine. With the confirmation of germ theory by Semmelweis, Pasteur, and others, sepsis was considered as a systemic infection by a pathogenic organism. Although the germ is probably the beginning of the syndrome and one of the major enemies to be identified and fought, sepsis is something wider and more elusive. In this chapter clinically relevant themes of sepsis will be approached to provide an insight of everyday clinical practice for healthcare workers often not directly involved in the patient's management.

A 54-year-old woman was seen by her primary care internist for a general health maintenance visit. Her major chronic illness was immune thrombocytopenic purpura (ITP) for which she had been treated with prednisone therapy for the past 15 years. Recent review of possible aetiologies of her chronic thrombocytopenia revealed infection with Helicobacter pylori. Successful eradication resulted in complete resolution of her thrombocytopenia within 2 months. She was weaned from steroid therapy and at 1-year follow-up, her platelet counts remained in the normal range. This case report summarises what is known about the association of H. pylori infection and ITP., (2014 BMJ Publishing Group Ltd.)

Objective: To determine frequency of thrombocytopenia and thrombocytosis, the MPV (mean platelet volume) and PDW (platelet distribution width) in patients with probable and culture proven neonatal sepsis and determine any association between platelet counts and mortality rate., Study Design: Descriptive analytical study., Place and Duration of Study: NICU, Fazle Omar Hospital, from January 2011 to December 2012., Methodology: Cases of culture proven and probable neonatal sepsis, admitted in Fazle Omar Hospital, Rabwah, were included in the study. Platelet counts, MPV and PDW of the cases were recorded. Mortality was documented. Frequencies of thrombocytopenia (< 150000/mm3) and thrombocytosis (> 450000/mm3) were ascertained. Mortality rates in different groups according to platelet counts were calculated and compared by chi-square test to check association., Results: Four hundred and sixty nine patients were included; 68 (14.5%) of them died. One hundred and thirty six (29%) had culture proven sepsis, and 333 (71%) were categorized as probable sepsis. Thrombocytopenia was present in 116 (24.7%), and thrombocytosis was present in 36 (7.7%) cases. Median platelet count was 213.0/mm3. Twenty eight (27.7%) patients with thrombocytopenia, and 40 (12.1%) cases with normal or raised platelet counts died (p < 0.001). Median MPV was 9.30, and median PDW was 12.30. MPV and PDW of the patients who died and who were discharged were not significantly different from each other., Conclusion: Thrombocytopenia is a common complication of neonatal sepsis. Those with thrombocytopenia have higher mortality rate. No significant difference was present between PDW and MPV of the cases who survived and died.

Introduction: This case report details the second described case of Whipple's disease-related thrombocytopenia in the medical literature. Whipple's disease is a rare multisystem infection caused by the actinomycete Tropheryma whipplei, first described by George Whipple in 1907. The key clinical manifestations are weight loss, diarrhoea and malabsorption, but arthralgia and endocarditis are also well described., Case Presentation: A 62-year-old Caucasian female presented with weight loss, anaemia and behavioural changes but denied any abdominal symptoms. Thrombocytopenia subsequently developed rapidly. Bone marrow examination showed abundant megakaryocytes in keeping with peripheral platelet sequestration. In addition, there was significant polyclonal plasmacytosis. She was also found to have a 1.6 cm tricuspid vegetation. The diagnosis was confirmed by presence of foamy macrophages on duodenal biopsy, positive periodic acid-Schiff staining and visualisation of T whipplei actinomycetes on electron microscopy. Tissue PCR performed mid-treatment showed traces of T whipplei DNA. The infection was treated with a 2-week intravenous course of ceftriaxone followed by 12 months of oral co-trimoxazole. The thrombocytopenia and anaemia resolved rapidly with antibiotic therapy, her behaviour returned to normal and she remains clinically well., Conclusions: This report confirms the association of thrombocytopenia with Whipple's disease, likely due to peripheral platelet sequestration, which resolves rapidly with treatment. In patients with a long history of unintended weight loss, Whipple's disease is a rare but important differential diagnosis as it is ultimately fatal if left untreated.

In a small percentage of patients with immune thrombocytopenia (ITP), H. pylori eradication has a positive effect on platelet counts. Whether H. pylori infection is associated with a lower thrombocyte count in persons without clinical ITP is unknown. We performed a cross-sectional study to compare thrombocyte count between H. pylori infected (n=108) and H. pylori non-infected patients (n=600) who underwent a diagnostic gastroscopy. The mean thrombocyte count in H. pylori negative patients was 257 × 10(9)/l, in H. pylori positive patients 252 × 10(9)/l (mean difference 5 × 10(9)/l, 95% CI: -23 to 14). Subgroup analysis did not show significant differences either. In the patient group without apparent comorbidity, there were no subjects with thrombocyte counts <120. In 36 H. pylori positive patients in whom data post-eradication was available, platelet counts pre- and post-eradication were similar. In conclusion, this study could not demonstrate a lower thrombocyte count in H. pylori infected patients or in subgroups of H. pylori infected patients compared to non-infected subjects.

Iliopsoas abscesses (IPAs) from methicillin-resistant Staphylococcus aureus (MRSA) are rare; however, IPAs from community-associated MRSA (CA-MRSA) may be increasing. In Japan, we previously described an adolescent athlete case of Panton-Valentine leukocidin (PVL)-positive ST30 CA-MRSA (strain NN12). In this study, we describe an IPA and discitis case from a variant of the successful PVL-negative CA-MRSA clone (ST8 CA-MRSA/J) in Japan. The patient was a 62-year-old man with intractable eczema, who had been diagnosed with IPAs and discitis (L1-L2). CA-MRSA (strain NN55) was isolated from blood, pus, and joint fluid. The invasive infections seemed to have originated in his intractable eczema, and the characteristics of this case, systemic myalgia and marked thrombocytopenia, seemed to have been caused by an exotoxin. Molecular genetic analysis revealed that NN55 possessed genotype ST8/spa606(t1767)/agr1/CoaIII and SCCmecIV of a novel subtype (encoding new cell-wall-anchored surface protein/J [CWASP/J]), exhibited enhanced expression of the cytolytic peptide genes, psmα and hld, and was resistant to gentamicin (caused by aacA-aphD), similar to ST8 CA-MRSA/J; however, NN55 lacked pathogenicity island SaPIj50 [carrying tst, encoding toxic shock syndrome toxin-1 (TSST-1)] of ST8 CA-MRSA/J, suggesting a variant (ST8 CA-MRSA/Jv). Strains NN12 and NN55 both caused bacteremia, IPAs, and adjacent musculoskeletal infections, preceded by intractable skin infections, and possessed high potential for adherence and enhanced expression of psmα and hld. The data suggest the role of a combination of CA-MRSA adhesin/cytolytic peptides (not PVL or TSST-1) in the pathogenesis of IPAs (and perhaps of systemic myalgia and marked thrombocytopenia).

Hemolytic uremic syndrome (HUS) is a disease of microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. About 90% of cases are secondary to infections by Escherichia coli strains producing Shiga-like toxins (STEC-HUS), while 10% are associated with mutations in genes encoding proteins of complement system (aHUS). We describe two patients with a clinical history of STEC-HUS, who developed end-stage renal disease (ESRD) soon after disease onset. They received a kidney transplant but lost the graft for HUS recurrence, a complication more commonly observed in aHUS. Before planning a second renal transplantation, the two patients underwent genetic screening for aHUS-associated mutations that revealed the presence of a heterozygous CFI mutation in patient #1 and a heterozygous MCP mutation in patient #2, and also in her mother who donated the kidney. This finding argues that the two cases originally diagnosed as STEC-HUS had indeed aHUS triggered by STEC infection on a genetic background of impaired complement regulation. Complement gene sequencing should be performed before kidney transplantation in patients who developed ESRD following STEC-HUS since they may be undiagnosed cases of aHUS, at risk of posttransplant recurrence. Furthermore, genetic analysis of donors is mandatory before living-related transplantation to exclude carriers of HUS-predisposing mutations., (© Copyright 2013 The American Society of Transplantation and the American Society of Transplant Surgeons.)

Background and Aim: Helicobacter pylori infection is reported to be associated with some extragastrointestinal manifestations, such as hematological diseases (thrombocytopenia, anemia), obesity, and fatty liver disease. The length or the volume ratio of liver to spleen was suggested to be changed in some hematological and hepatobiliary disorders. We hypothesized that the liver-to-spleen ratio may be affected in H. pylori-positive patients. In this respect, we aimed to evaluate the effect of H. pylori infection on the liver-to-spleen ratio and platelet indices., Method: A total of 174 patients with functional dyspepsia were included in the study. Patients were divided into group 1 (H. pylori-positive gastritis) (n=95) and group 2 (H. pylori negative, control group) (n=79). Liver, spleen length measurement, and liver steatosis scores were performed by ultrasonography by the same physicians who were blinded to the H. pylori results. Blood count values including the platelet count and the mean platelet volume (MPV) were compared between the two groups. BMI was also evaluated as a potential confounding factor for fatty liver., Results: The liver-to-spleen ratio, platelet-to-spleen ratio, MPV-to-spleen ratio, and the MPV-to-liver ratio were significantly lower in the H. pylori-positive group compared with the H. pylori-negative group (P<0.001, <0.001, <0.001, and 0.038, respectively). Fatty liver was significantly more frequent in H. pylori-positive patients., Conclusion: Liver-to-spleen ratio and the MPV-to-spleen ratio are important indices in the pathogenesis of H. pylori-linked liver and spleen manifestations, and thrombocytopenia.

Objective: To describe clinical findings and the use of a tick-associated pathogen panel in a series of patients with human granulocytic anaplasmosis (HGA) at a suburban Boston hospital., Patients and Methods: Medical records were reviewed for inpatients and outpatients at Newton-Wellesley Hospital with a positive polymerase chain reaction (PCR) result for Anaplasma phagocytophilum during the study period March 1 through November 30, 2009. A PCR panel was used to test for tick-borne pathogens. Postal ZIP code data from the patients' areas of residence were used to estimate the area of disease transmission., Results: Thirty-three cases were confirmed during the 2009 transmission season, and 14 of these patients (42%) required hospitalization. Thrombocytopenia and/or leukopenia were observed at the time of presentation in 25 of 30 patients (86%) in whom both white blood cell and platelet counts were determined, and 28 of 33 patients (85%) reported fever. Rash occurred in only 2 of the 33 patients (6%), and 25 (76%) reported one or more respiratory or gastrointestinal symptom. Cases were geographically distributed diffusely throughout the hospital catchment area, with one possible focus of infection identified in Weston, MA. Due to a lack of clinical data reporting to the Massachusetts Department of Public Health, only 20 of 32 HGA cases (63%) fulfilled the case confirmation criteria., Conclusion: Diagnosis of HGA requires a high suspicion for infection even in endemic areas. Use of a tick-associated pathogen panel that includes PCR assays for several organisms could improve detection of underrecognized tick-borne diseases in endemic areas. Lack of epidemiological follow-up to confirm corroborating clinical findings prevents accurate case reporting and assessment of the true HGA burden., (Copyright © 2012 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.)

Background: Immediate removal of central venous catheters (CVCs) is not possible in patients with candidemia requiring total parenteral nutrition (TPN). This study analyzed the possible prognostic factors for survival time after onset of candidemia among nonneutropenic adults requiring TPN., Methods: We conducted a retrospective analysis from September 2003 to August 2005., Results: A total of 59 nonneutropenic adults with candidemia and requiring TPN were identified retrospectively. All Candida isolates were susceptible to flucytosine and amphotericin B. With the exception of one C glabrata isolate, all other isolates were susceptible to fluconazole and itraconazole. The only predictor of 30-day survival rate after onset of candidemia identified in our analysis was an Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 23 points or less. Adults with higher APACHE II scores, who did not have their CVCs changed, did not receive antifungal treatment, or who had thrombocytopenia had shorter survival times after the onset of candidemia., Conclusions: APACHE II scores, thrombocytopenia, antifungal agents, and CVCs changes are associated with survival time in nonneutropenic adults requiring TPN after the onset of candidemia., (Copyright © 2011. Published by Elsevier B.V.)

Hematologic abnormalities of mild anemia and leucopenia have been frequently associated with acute brucellosis, but thrombocytopenia are less frequently seen. In the present study, we documented 5 (2.6%) isolated thrombocytopenic patients with the manifestations of brucellosis observed during the course of active infection. Five (2.6%) patients, 4 boys and 1 girl, with ages ranging from 2 to 14 years, had isolated thrombocytopenic at diagnosis. In 5 (2.6%) patients, platelet counts ranged from 39,000 to 120,000/mm(3). Tube agglutination tests for brucellosis were positive for all patients (1/160-1/1280). All patients recovered completely, and their thrombocytopenia returned to normal by 2 to 4 weeks after antibiotic treatment of brucellosis. In our study, we present 5 patients with Brucella-induced thrombocytopenia mimicking idiopathic thrombocytopenic purpura to emphasize the isolated thrombocytopenia and the resolution of thrombocyte counts following treatment of brucellosis.

Aeromonas hydrophila leads to both intestinal and extraintestinal infections in animals and humans, and the underlying mechanisms leading to mortality are largely unknown. By using a septicemic mouse model of infection, we showed that animals challenged with A. hydrophila die because of kidney and liver damage, hypoglycemia, and thrombocytopenia. Pretreatment of animals with quorum-sensing-associated signaling molecules N-acyl homoserine lactones (AHLs), such as butanoyl and hexanoyl homoserine lactones (C(4)- and C(6)-HSLs), as well as N-3-oxododecanoyl (3-oxo-C(12))-HSL, prevented clinical sequelae, resulting in increased survivability of mice. Since little is known as to how different AHLs modulate the immune response during infection, we treated mice with the above AHLs prior to lethal A. hydrophila infection. When we compared results in such animals to those in controls, the treated animals exhibited a significantly reduced bacterial load in the blood and other mouse organs, as well as various levels of cytokines/chemokines. Importantly, neutrophil numbers were significantly elevated in the blood of C(6)-HSL-treated mice compared to those in animals given phosphate-buffered saline and then infected with the bacteria. These findings coincided with the fact that neutropenic animals were more susceptible to A. hydrophila infection than normal mice. Our data suggested that neutrophils quickly cleared bacteria by either phagocytosis or possibly another mechanism(s) during infection. In a parallel study, we indeed showed that other predominant immune cells inflicted during A. hydrophila infections, such as murine macrophages, when they were pretreated with AHLs, rapidly phagocytosed bacteria, whereas untreated cells phagocytosed fewer bacteria. This study is the first to report that AHL pretreatment modulates the innate immune response in mice and enhances their survivability during A. hydrophila infection.

Two dogs in France were diagnosed with Anaplasma phagocytophilum infection by real-time PCR. The most remarkable hematologic and biochemical findings were severe thrombocytopenia, mild neutrophilia, morulae in neutrophils, and increased serum concentration of the α2-globulin fraction detected by agarose gel electrophoresis of serum proteins. Using sequencing of the partial 16S rRNA and ankA genes, molecular characterization of the A. phagocytophilum strains showed that the organisms from both dogs were identical to the European strains isolated from horses and people. Based on phylogenetic analysis, the ankA gene was more discriminating than the 16S rRNA gene in distinguishing the majority of European and American strains of A. phagocytophilum infecting people and animals. Three isolates of A. phagocytophilum, 1 from Spain (cow) and 2 from Norway (sheep and deer), were external to the European and American clades., (©2011 American Society for Veterinary Clinical Pathology.)

Linezolid is an effective antibiotic for treatment of infections caused by resistant Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA). However, thrombocytopenia has been reported in a certain proportion of patients receiving linezolid treatment. We investigated the risk factors for linezolid-related thrombocytopenia in MRSA-infected patients after digestive surgery. Forty-three patients who were treated with linezolid for postoperative MRSA infection were enrolled. We compared the characteristics of the patients who developed thrombocytopenia during linezolid therapy with those of the patients who did not. Thrombocytopenia was defined as a platelet ratio (post/pre-treatment with linezolid) of < 0.7. Twenty-one (48.8%) patients developed thrombocytopenia. In univariate analysis, long treatment duration, high pre-treatment levels of total-bilirubin and transaminases, and the coexistence of chronic liver disease (CLD) were found to be significant risk factors for development of thrombocytopenia. Other factors, for example pre-treatment platelet count, serum creatinine and albumin levels, and previous hepatic resection were not associated with thrombocytopenia. In the multivariate regression analysis, only CLD remained as an independent factor associated with thrombocytopenia. In addition, thrombocytopenia was more common among patients with indocyanine green retention at 15 min (ICG-R15) of more than 10% than in those with an ICG-R15 of 10% or less. Our results suggest that patients with CLD are at high risk of developing linezolid-related thrombocytopenia. Therefore, they should be targeted for more intense platelet count monitoring during linezolid therapy.