Splenic abscess is a rare entity, with a reported incidence of 0.1-0.7%, often necessitating source control of infection with percutaneous drainage or even partial or complete splenectomy in refractory cases. It carries a high morbidity and mortality risk despite treatment, with immunocompromised states such as malignancy, immunosuppressive medications, acquired immunodeficiency syndrome (AIDS), end-stage kidney disease, cirrhosis, and contiguous sites of infection acting as predisposing factors. We report the case of a 19-year-old lady with lupus nephritis who presented with persistent high-grade fever and sepsis-associated acute kidney injury. After extensive evaluation for potential sources of infection, imaging revealed an abscess in the spleen measuring 6 × 4 × 3 cm. Percutaneous pigtail catheter drainage of the collection under ultrasonography guidance was done. Cultures from pus revealed nontyphoidal Salmonella. She also developed progressively worsening thrombocytosis, which was attributed to functional asplenia and was managed with prophylactic antiplatelet to alleviate thrombotic risk, in addition to hydroxyurea therapy. This is the first reported case of nontyphoidal Salmonella-associated splenic abscess and further complications in a case of lupus nephritis.

Overwhelming post-splenectomy infection (OPSI) is a rare but life-threatening complication that can occur at any time after splenectomy, most often involving encapsulated organisms such as Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. We report the case of a 36-year-old Caucasian female, 26 years post-splenectomy for immune thrombocytopenic purpura, who presented with flu-like symptoms and altered mentation. On arrival, she was hypotensive, tachycardic, febrile, and hypoglycemic with purpura fulminans and conjunctival injection. She rapidly progressed to septic shock requiring vasopressors, disseminated intravascular coagulation, and acute respiratory failure necessitating mechanical ventilation. Blood cultures revealed Streptococcus pneumoniae bacteremia, and the pneumonia panel identified non-COVID-19 coronavirus, adenovirus, Haemophilus influenzae, and Staphylococcus aureus. Her course was complicated by acute kidney injury requiring continuous renal replacement therapy and bilateral lower limb ischemia. Despite aggressive management, she deteriorated rapidly and died within 48 hours of admission. This case underscores the critical nature of OPSI and purpura fulminans in asplenic patients and emphasizes the importance of prompt recognition and treatment. While vaccination against encapsulated organisms reduces risk, vaccination failures remain possible. Thorough patient education regarding prodromal symptoms and the integration of prophylactic measures, including early antibiotic initiation, are essential. The high mortality associated with OPSI, even decades after splenectomy, highlights the necessity of ongoing preventive strategies, vigilant monitoring, and rapid intervention to mitigate fatal outcomes.

We report the case of a 45-year-old man with a history of HIV infection (on antiretroviral therapy with a preserved CD4 count) and prior splenectomy, who presented with vomiting, diarrhea, confusion, and worsening headache. He was found to have Streptococcus pneumoniae meningitis complicated by intracranial hypertension requiring external ventricular drain placement and extensive cerebral venous sinus thrombosis. This case highlights the risk of severe pneumococcal infection in asplenic and immunocompromised patients and underscores the importance of prompt recognition and management.

Autosplenectomy, defined as the spontaneous loss of splenic tissue in the absence of trauma or surgery, is most commonly associated with sickle cell disease and is rarely described in patients with autoimmune conditions. We present a case of a 54-year-old woman with systemic lupus erythematosus (SLE) and Sjögren's overlap syndrome who was incidentally found to have a complete absence of the spleen on computed tomography (CT), despite prior imaging demonstrating a normal splenic anatomy. The patient presented with polyarthralgia, fatigue, and systemic inflammation. Laboratory investigations revealed elevated anti-dsDNA titers, hypocomplementemia, and a positive extractable nuclear antigen (ENA) profile. Imaging confirmed splenic absence, and extensive evaluation excluded infectious, malignant, infiltrative, and hematological causes of splenic agenesis. Serial imaging findings, combined with the presence of an active autoimmune disease, supported the diagnosis of a probable autoimmune-mediated autosplenectomy. This case highlights a rare but clinically significant manifestation of systemic autoimmune diseases. Recognition of asplenia is critical because of the associated risk of overwhelming infection, necessitating vaccination and the implementation of prophylactic strategies. Clinicians should consider splenic dysfunction in patients with autoimmune diseases, particularly when unexplained infections or atypical imaging findings are present.

Platelets are a component of blood produced in the bone marrow that plays a vital role in the blood clotting process. The normal platelet count in adults and children is 150,000/microL to 450,000/microL (150 to 450 x 10/L), but the normal range may vary in different clinical laboratories. Thrombocytosis is a condition where the platelet count exceeds 450,000/μl.[1] It is also referred to as thrombocythemia. Thrombocytosis can be divided into two groups:  primary thrombocytosis and secondary (or reactive) thrombocytosis.[2]  This distinction between primary and secondary thrombocytosis is important as it carries implications for evaluation, prognosis, and treatment. Primary thrombocytosis is due to the unregulated abnormality of platelet production of bone marrow progenitor cells.[3] They are usually associated with the myeloproliferative neoplasms group. Primary thrombocytosis, especially essential thrombocythemia and polycythemia vera, have an increased risk of thrombosis and bleeding compared to secondary thrombocytosis.[4] Secondary thrombocytosis, also known as reactive thrombocytosis defined as an abnormally high platelet count due to underlying events, disease, or the use of certain medications. Secondary thrombocytosis is the more common type and is usually identified in routine laboratory results. Among individuals with thrombocytosis, 80% to 90% are known to have secondary thrombocytosis.[5] Reactive causes of thrombocytosis include transient processes such as acute blood loss, acute infection, or sustained forms of reactive thrombocytosis include iron deficiency, asplenia, cancer, chronic inflammatory, or infectious diseases. Secondary thrombocytosis (reactive thrombocytosis) is a laboratory anomaly that resolves when the underlying causative condition is addressed. In most cases, the symptoms are due to an underlying disorder and not the thrombocytosis itself. Extreme thrombocytosis may rarely result in thrombotic events such as acute myocardial infarction, mesenteric vein thrombosis, and pulmonary embolism.[6] Even though secondary thrombocytosis is benign, the underlying etiology of thrombocytosis (e.g., malignancy, connective tissue disorders, chronic infections) can be associated with an increased risk of adverse outcomes.

Capnocytophaga canimorsus is a gram-negative, anaerobic bacillus commonly found in the oral flora of dogs and cats. While often transmitted through animal bites or scratches, severe infections can occur even without documented exposure, particularly in immunocompromised individuals such as asplenic patients. Although rare, mycotic aneurysms caused by C. canimorsus are associated with high mortality. We report the case of a 53-year-old male with a history of splenectomy due to diffuse large B-cell lymphoma, currently in remission, who presented with malaise, fever, dyspnea, and abdominal pain. He rapidly progressed to septic shock and multiorgan failure, including coagulopathy consistent with disseminated intravascular coagulation (DIC). Despite broad-spectrum antibiotics and intensive support, the patient died within hours of admission. Blood cultures later confirmed C. canimorsus bacteremia. Postmortem examination revealed a ruptured aortic aneurysm. This case highlights the fulminant progression of C. canimorsus infection in an asplenic patient, culminating in a fatal aortic aneurysm rupture. Notably, there was no history of animal exposure, reinforcing the need for high clinical suspicion, especially in high-risk populations. Although empiric therapy with beta-lactam/beta-lactamase inhibitors is recommended, early recognition and possible surgical intervention remain crucial for survival. Infections caused by C. canimorsus should be considered in septic patients with risk factors such as splenectomy, even in the absence of animal contact. Rapid deterioration and rare complications, like aortic aneurysm rupture, underscore the importance of early diagnosis and aggressive multidisciplinary management.

BACKGROUND Capnocytophaga canimorsus is a gram-negative bacillus found in the oral cavity of dogs and cats. Human infection is uncommon but can cause severe sepsis. Although classically associated with asplenia, alcohol use disorder, or immunosuppression, a substantial proportion of cases occur in patients without identifiable risk factors. Diagnosis may be delayed due to the fastidious nature of the organism and the impact of prior antibiotic exposure on culture yield. CASE REPORT A 75-year-old woman presented with fever and right upper-quadrant abdominal pain 6 weeks after right total hip arthroplasty. She had no history of animal bite but reported close contact with dogs. Initial investigations did not identify a source of infection, and empirical ceftriaxone was initiated. Blood cultures became positive after extended incubation (Day 10), with identification of C. canimorsus by MALDI-TOF mass spectrometry. Imaging studies were inconclusive for prosthetic joint infection. The patient was treated with high-dose amoxicillin for 14 days, with favorable clinical and biological outcomes. CONCLUSIONS C. canimorsus infection should be considered in patients presenting with sepsis or persistent fever and a history of dog or cat exposure, even in the absence of a bite. Close collaboration with microbiology laboratories may be required to ensure appropriate culture conditions. Clinicians should also be aware of the potential for diagnostic uncertainty in patients with recent prosthetic implants.

Infective endocarditis involving the aortic valve carries a high risk of rapid valvular destruction and hemodynamic compromise, particularly when complicated by sepsis. Patients with sickle cell disease are uniquely susceptible to severe infection due to functional asplenia, chronic hemolysis, endothelial dysfunction, and frequent exposure to intravascular devices, yet native valve endocarditis in this population remains rarely described. We report the case of a 51-year-old man with sickle cell disease who presented with sepsis and was found to have native aortic valve endocarditis caused by Staphylococcus capitis. Initial transthoracic echocardiography on hospital day three demonstrated a small aortic valve vegetation with mild-to-moderate aortic regurgitation. Despite initiation of appropriate antimicrobial therapy, transesophageal echocardiography performed thereafter on hospital day six revealed rapid progression to moderate-to-severe aortic regurgitation with associated atrial dilation, indicating accelerated valvular deterioration. The patient subsequently developed worsening volume overload and hemodynamic instability, prompting cardiothoracic surgical intervention. He underwent successful aortic valve replacement with perioperative transfusion support tailored to the hematologic and hypoxic risks associated with sickle cell disease and demonstrated clinical improvement postoperatively. This case highlights how sepsis-related inflammatory activation, superimposed on baseline vascular and hematologic abnormalities in sickle cell disease, may accelerate valvular destruction, even in infections caused by organisms traditionally considered low-virulence, underscoring the importance of serial echocardiographic assessment and timely multidisciplinary management.

Melioidosis, caused by Burkholderia pseudomallei, is an emerging infection in the tropics. Most of the melioidosis patients have underlying co-morbidities or occupational exposures. Hemoglobinopathies, such as thalassemia, are established risk factors for melioidosis; however, the association of SCD with melioidosis is infrequently reported. We report two culture-confirmed melioidosis cases from eastern India: a 58-year-old male with SCD on hydroxyurea and another 44-year-old with sickle cell trait, both presenting with cavitary lung lesions mimicking tuberculosis. SCD-related functional asplenia may heighten susceptibility. These cases emphasise the need for clinical vigilance in endemic areas and further research into SCD/SCT-associated immune vulnerabilities.

Meningococcal disease is a serious bacterial infection caused by Neisseria meningitidis. Serogroups B, C, W, and Y cause the majority of cases of this disease in the United States. These serogroups are targeted by different meningococcal vaccines available in the United States. Two quadrivalent (serogroups A, C, W, and Y) meningococcal conjugate vaccines (MenACWY) (MenACWY-CRM [Menveo, GSK] and MenACWY-TT [MenQuadfi, Sanofi Pasteur]) and two serogroup B meningococcal vaccines (MenB) (MenB-4C [Bexsero, GSK] and MenB-FHbp [Trumenba, Pfizer]) are licensed for use in the United States and recommended by CDC's Advisory Committee on Immunization Practices (ACIP). Indications for MenACWY and MenB vaccination have not changed since indications for their use were published in 2020. A pentavalent (serogroups A, B, C, W, and Y) meningococcal vaccine (MenABCWY) (MenACWY-TT/MenB-FHbp [Penbraya, Pfizer]) has been licensed and recommended for use since October 2023. On February 14, 2025, the Food and Drug Administration licensed a second pentavalent MenABCWY vaccine (MenACWY-CRM/MenB-4C [Penmenvy, GSK]) for prevention of invasive disease caused by N. meningitidis serogroups A, B, C, W, and Y in persons aged 10-25 years, the same indication for which MenACWY-TT/MenB-FHbp is licensed. On April 16, 2025, ACIP recommended that MenACWY-CRM/MenB-4C may be used when both MenACWY and MenB are indicated at the same visit for 1) healthy persons aged 16-23 years (routine schedule) when shared clinical decision-making favors administration of MenB vaccine and 2) persons aged ≥10 years who are at increased risk for meningococcal disease (e.g., because of persistent complement deficiencies, complement inhibitor use, or functional or anatomic asplenia). Different manufacturers' serogroup B-targeting vaccines are not interchangeable; therefore, when MenACWY-CRM/MenB-4C is used, MenB-4C should be used for the other MenB doses. This report summarizes evidence considered for these recommendations and provides clinical guidance for the use of MenACWY-CRM/MenB-4C.

Asplenia means the absence of a spleen. Asplenia can occur in a variety of clinical settings, and it can refer to an anatomic absence of the spleen or functional asplenia secondary to a variety of disease states. The spleen is one of the primary extramedullary lymphoid organs. It is located in the left upper quadrant of the abdomen. Normally, the spleen is not palpable on physical exam and measures on average 10.65 by 5.16 cm. Normal spleen size can vary by gender and race. For example, men on average have larger spleens than females, and whites, on average, tend to have larger spleens compared to African American individuals.[1] When palpable or notably enlarged on imaging, the clinician must consider a variety of underlying disease states (whether acquired or inherited) contributing to the enlargement. Functionally, the spleen’s primary physiologic role is the filtration and processing of senescent blood cells (predominantly red blood cells or RBCs) and immunologically helps protect against encapsulated microorganisms and respond to infectious pathogens. It contains both hematopoietic and lymphopoietic elements, providing a basis for extramedullary hematopoiesis when necessary.[2] The spleen has two functionally and histologically distinct tissues where these processes take place: the white pulp and the red pulp. The white pulp has a large mass of lymphoid tissue that produces antibodies against recognized antigens, whereas the red pulp has a tight network of sinusoids called the cord of Billroth which helps in blood filtration.[3] As the body's largest filter of blood, it helps to remove old RBCs from the circulation aiding in the removal of blood-borne microorganisms.[4] Beyond the spleen, the lymphatic system of the body consists of a complex myriad of lymphatic vessels, lymph nodes, and other specific extramedullary lymphoid organs including the thymus, tonsils, and appendix, which collectively play a very important role in immune defenses. Asplenia can be caused by damage to the white pulp, the red pulp, or both. The spleen is a direct and indirect site of potential toxicity that can secondarily arise from underlying disease processes or infection.[2] One must understand and appreciate the various etiologies and potential complications of asplenia, such as being a great risk factor for encapsulated microorganisms. Bacterial infections with Neisseria meningitides or Streptococcal pneumoniae, among many others, can become life-threatening if untreated in patients with anatomic or functional asplenia.[5] Patients without a spleen have a 200-fold greater risk of death from septicemia compared to those with an adequate functioning spleen. There are many case reports in the medical literature reporting of asplenic patients, unfortunately, succumbing to infectious disease leading to death. One notable example reported by Heubner ML et al. (2015) described the rare case of a patient who had required splenectomy due to refractory immune thrombocytopenia (ITP).[6] He subsequently developed a pneumococcal meningitis infection and died despite best supportive efforts.  The rate of invasive bacterial infection and mortality in asplenic patients is significantly higher compared to normal controls – 69% in meningitis, 64% in septicemia, and 7% in Purpura fulminans.[5]

Acute chest syndrome (ACS) is a life-threatening complication of sickle cell disease (SCD) with complex infectious and non-infectious etiologies. Bacterial pathogens, including Streptococcus pneumoniae, Haemophilus influenzae, and atypical organisms such as Mycoplasma pneumoniae, play crucial roles in ACS pathogenesis, particularly in immunocompromised SCD patients with functional asplenia. Despite the importance of infectious triggers, regional data on pathogen identification rates and antimicrobial management strategies in ACS remain limited, especially from high-prevalence SCD regions. This study aimed to investigate the infectious etiologies, pathogen identification patterns, and antimicrobial management outcomes of ACS in adult SCD patients in Eastern Saudi Arabia. A five-year retrospective analysis was conducted on patients aged ≥14 years with SCD who were admitted with ACS to Dammam Medical Complex between 2018 and 2022. Comprehensive microbiological evaluation included blood cultures, sputum cultures, and atypical pathogen testing (Mycoplasma pneumoniae, Chlamydia pneumoniae). Data on antimicrobial regimens, pathogen identification rates, vaccination status against encapsulated bacteria, and clinical outcomes were systematically analyzed. Empirical antibiotic strategies and their effectiveness in this immunocompromised population were evaluated. A total of 60 adult SCD patients experiencing 80 episodes of ACS were included. Despite comprehensive microbiological workup, specific infectious pathogens were identified in only 8 (10.0%) episodes, highlighting the complex multifactorial etiology of ACS. Blood cultures yielded pathogens in 5 (6.3%) cases, sputum cultures in 4 (5.0%) cases, and Mycoplasma pneumoniae was identified in 3 (3.8%) episodes. All patients received empirical broad-spectrum antimicrobial therapy, with ceftriaxone and azithromycin combination being the most frequent regimen (76 cases, 95.0%), providing coverage for both typical and atypical bacterial pathogens. Antibiotic escalation was required in 16 (20.0%) episodes. Vaccination rates against Streptococcus pneumoniae were suboptimal at 30 (50.0%), representing a significant risk factor for invasive bacterial infections in this functionally asplenic population. The intensive care unit (ICU) admission rate was 15 (18.8%), and in-hospital mortality was 3 (3.8%), with infectious complications contributing to severe outcomes. In this cohort of SCD patients, ACS demonstrated low rates of specific pathogen identification despite systematic microbiological investigation, supporting the multifactorial infectious and non-infectious etiology of this syndrome. The predominant use of broad-spectrum antimicrobial therapy targeting both typical and atypical bacterial pathogens proved effective in this immunocompromised population. However, suboptimal vaccination rates against encapsulated bacteria represent a critical gap in infection prevention strategies. These findings emphasize the importance of empirical antimicrobial coverage for suspected bacterial pathogens in ACS management and highlight the urgent need for enhanced vaccination programs to prevent infectious complications in functionally asplenic SCD patients.

Babesiosis is a tick-borne protozoal infection that can cause life-threatening disease in asplenic or immunocompromised patients. We report a 71-year-old woman with prior distal pancreatectomy and splenectomy who developed severe babesiosis complicated by pulmonary involvement and complement-mediated hemolysis. Initial therapy with clindamycin-atovaquone and partial exchange transfusion was required due to a reported azithromycin allergy; following successful rechallenge, she tolerated guideline-based azithromycin-atovaquone. Despite parasite clearance, she developed complement-mediated hemolysis confirmed by a complement C3-positive, IgG-negative direct antiglobulin test. A 71-year-old woman with a history of distal pancreatectomy and splenectomy for pancreatic carcinoma (without recurrence) presented from upstate New York with one week of fever, chills, headache, fatigue, and myalgias. She denied a known tick bite but reported a small pink skin lesion. Initial laboratory evaluation revealed thrombocytopenia, transaminitis, and hyperbilirubinemia; hepatitis, Epstein-Barr virus, and cytomegalovirus testing were negative, while Babesia microti polymerase chain reaction (PCR) was positive. Because of a reported azithromycin allergy manifesting as hives, she was started on clindamycin-atovaquone. On admission to Memorial Sloan Kettering Cancer Center, her hemoglobin was 7.6 g/dL, lactate dehydrogenase (LDH) 392 U/L, and parasitemia 9.7%. Partial exchange transfusion (four of nine units) lowered parasitemia to 5.2%. The clinical course was complicated by recurrent fevers, hypotension, and hypoxia requiring a high-flow nasal cannula; chest CT demonstrated bilateral ground-glass opacities and pleural effusions. On hospital day 10, an azithromycin challenge was tolerated, and therapy was transitioned to azithromycin-atovaquone, with parasitemia clearing by day 16. Despite clearance of parasitemia, the patient developed worsening hemolysis characterized by a complement C3-positive, immunoglobulin (IgG)-negative direct antiglobulin test, consistent with complement-mediated hemolysis; cold agglutinin titer was negative. She experienced a hemoglobin nadir of 6.5 g/dL, lactated dehydrogenase peaking at 1,573 U/L, haptoglobin <8 mg/dL, and mild transient elevations in liver enzymes. She required multiple transfusions, though immunosuppressive therapy was avoided, and hematologic parameters improved as the infection resolved. Echocardiography revealed preserved systolic and diastolic function with a left ventricular ejection fraction of 68%. This case highlights several important aspects of severe babesiosis. First, asplenic patients represent a high-risk population, prone to higher parasitemia and serious complications. Second, therapeutic challenges may arise in the setting of drug allergies, but careful reevaluation can allow the use of guideline-based azithromycin-atovaquone therapy. Third, this case underscores the emerging recognition of complement-mediated autoimmune hemolysis in babesiosis, demonstrated by worsening hemolysis despite parasite clearance and a complement C3-positive, immunoglobulin G (IgG)-negative direct antiglobulin test. Finally, optimal outcomes required a multidisciplinary approach involving infectious disease, hematology, and transfusion medicine specialists, reflecting the complexity of management in severe and atypical babesiosis.

Sparing or removing the accessory spleen (AS) in patients undergoing diagnostic splenectomy for lymphoproliferative disorders (LPD) is an unsolved issue rarely considered. Usually, a healthy AS can be preserved. Reporting a case of our own, this paper aims to review existing literature and propose a tailored approach. A 59-year-old woman presented with unexplained anemia. A FDG-PET-CT scan revealed splenomegaly and two hypermetabolic splenic nodules, pathological upper and lower diaphragmatic lymph nodes, and a non-FDG-avid AS around splenic hilum. The patient underwent diagnostic splenectomy and AS removal. The histopathological examination of the spleen disclosed a diffuse large B-cell lymphoma (DLBCL), whereas the AS was uninvolved, consistent with the preoperative FDG-PET-CT findings. The post-operative course was uneventful. The patient was discharged on the 5th post-operative day. Asplenia following splenectomy increases the risk of severe infections. It is hypothesized that sparing a healthy AS could help maintain immune competence. However, there is currently insufficient evidence to guide the decision on whether to remove or spare an AS during splenectomy for diagnostic purposes in suspected LPD cases, and to understand the potential prognostic impact (both oncological and infectious) of this strategy. The preoperative finding of a non-FDG-avid AS may recommend surgical sparing.