Acute Systemic Infection Research Articles

Tissue-resident memory CD8 T cell diversity is spatiotemporally imprinted.

Tissue-resident memory CD8 T (TRM) cells provide protection from infection at barrier sites. In the small intestine, TRM cells are found in at least two distinct subpopulations: one with higher expression of effector molecules and another with greater memory potential1. However, the origins of this diversity remain unknown. Here we proposed that distinct tissue niches drive thephenotypic heterogeneityof TRM cells. To test this, we leveraged spatial transcriptomics of human samples, a mouse model of acute systemic viral infection and a newly established strategy for pooled optically encoded gene perturbations to profile the locations, interactions and transcriptomes of pathogen-specific TRM cell differentiation at single-transcript resolution. We developed computational approaches to capture cellular locations along three anatomical axes of the small intestine and to visualize the spatiotemporal distribution of cell types and gene expression. Our study reveals that the regionalized signalling of the intestinal architecture supports two distinct TRM cell states: differentiated TRM cells and progenitor-like TRM cells, located in the upper villus and lower villus, respectively. This diversity is mediated by distinct ligand-receptor activities, cytokine gradients and specialized cellular contacts. Blocking TGFβ or CXCL9 and CXCL10 sensing by antigen-specific CD8 T cells revealed a model consistent with anatomicallydelineated, early fate specification. Ultimately, our framework for the study of tissue immune networks reveals that T cell location and functional state are fundamentally intertwined.

First Description of the Role of the Relationship Between Serum Amyloid P Components and Nuclear Factors/Pro-Cytokines During Critical Periods of Toxoplasmic Encephalitis.

Background/Objectives:Toxoplasma gondii (T. gondii), an obligate food-borne intracellular parasite, causes severe neuropathology by establishing a persistent infection in the host brain. We have previously shown that T. gondii infection induces severe neuropathology in the brain manifested by increased nitric oxide production, oxidative stress, glial activation/BBB damage, increased pro-inflammatory cytokine glia maturation factor-beta and induced apoptosis. Methods: The aim of this experimental study was to investigate the serum amyloid P (SAP) components, nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), caspase 1 (Casp 1), tumor necrosis factor-alpha (TNF-α) and complement 3 (C3) gene expressions on the 10th, 20th and 30th days after infection with T. gondii in the neuroimmunopathogenesis of toxoplasmic encephalitis (TE) in mouse brains by real-time quantitative polymerase chain reaction. The study also aimed to determine whether there was a correlation between the markers included in the study on these critical days, which had not previously been investigated. The mRNA expression levels of SAP components, NF-κB, IL-1β, Casp 1, TNF-α and C3 were examined. Results: The most notable outcome of this investigation was the observation that SAP components exhibited a 13.9-fold increase on day 10 post-infection, followed by a rapid decline in the subsequent periods. In addition, IL-1β expression increased 20-fold, while SAP components decreased 13-fold on day 20 after infection. Additionally, the TNF-α, Casp 1 and NF-κB expression levels were consistently elevated to above normal levels at each time point. Conclusions: This study identified SAP components, NF-κB, IL-1β, Casp 1 and TNF-α expressions as playing critical roles in TE neuroimmunopathogenesis. Furthermore, to the best of our knowledge, this is the first study to investigate SAP components during the transition from acute systemic infection to early/medium chronic and chronic infection and to explore the relationship between SAP components and other nuclear factors/pro-cytokines.

Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid

Aging changes the responsiveness of our immune defense, and this decline in immune reactivity plays an important role in the increased susceptibility to infections that marks progressing age. Aging is also the most pronounced risk factor for development of age-related macular degeneration (AMD), a disease that is characterized by dysfunctional retinal pigment epithelial (RPE) cells and loss of central vision. We have previously shown that acute systemic viral infection has a large impact on the retina in young mice, leading to upregulation of chemokines in the RPE/choroid (RPE/c) and influx of CD8 T cells in the neuroretina. In this study, we sought to investigate the impact of systemic infection on the RPE/c in aged mice to evaluate whether infection in old age could play a role in the pathogenesis of AMD. We found that systemic infection in mice led to upregulation of genes from the crystallin family in the RPE/c from aged mice, but not in the RPE/c from young mice. Crystallin alpha A (CRYAA) was the most upregulated gene, and increased amounts of CRYAA protein were also detected in the aged RPE/c. Increased CRYAA gene and protein expression has previously been found in drusen and choroid from AMD patients, and this protein has also been linked to neovascularization. Since both drusen and neovascularization are important hallmarks of advanced AMD, it is interesting to speculate if upregulation of crystallins in response to infection in old age could be relevant for the pathogenesis of AMD.

Effect of IL-6R blockade on plasma lipids and clinical outcomes among hospitalized patients with COVID-19 infection

Plasma lipid levels are modulated by systemic infection and inflammation; it is unknown whether these changes reflect inflammatory responses or caused directly by pathogen presence. We explored the hypothesis that anti-inflammatory intervention via interleukin 6 receptor (IL-6R) blockade would influence plasma lipid levels during severe infection and evaluated the association of plasma lipid changes with clinical outcomes. Sarilumab (monoclonal antibody blocking IL-6R) efficacy was previously assessed in patients with coronavirus disease 2019 (COVID-19) (NCT04315298). This analysis determined whether strong inflammatory reduction by sarilumab in patients with COVID-19 pneumonia of increasing severity (severe, critical, multisystem organ dysfunction) affected plasma lipid changes between day 1 and day 7 of study therapy. Baseline lipid levels reflected the presence of acute systemic infection, characterized by very low HDL-C, low LDL-C, and moderately elevated triglycerides (TGs). Disease severity was associated with progressively more abnormal lipid levels. At day 7, median lipid levels increased more in the sarilumab versus placebo group (HDL-C +10.3%, LDL-C +54.7%, TG +32% vs. HDL-C +1.7%, LDL-C +15.4%, TG +8.8%, respectively). No significant association between lipid changes and clinical outcomes was observed. In conclusion, severe-to-critical COVID-19 pneumonia causes profound HDL-C depression that is only modestly responsive to strong anti-IL-6R inflammatory intervention. Conversely, LDL-C depression is strongly responsive to IL-6R blockade, with LDL-C levels likely returning to the predisease set point. These results advance our understanding of the complex relationship between serum lipids and infection/inflammation and suggest that HDL-C depression during acute contagious disease is driven by infection and not IL-6–mediated inflammation.

A Comprehensive Review of Toxoplasmosis: Serious Threat to Human Health

Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii. Despite infecting a major fraction of the global population, T. gondii rarely results in clinically significant disease. Cats are the only known definitive host for this parasite, which sheds millions of oocysts in its feces every day, which then sporulate and become infective in the environment. This comprehensive review article aims to explain the etiology, pathogenesis, epidemiology, transmission, clinical symptoms, diagnosis, risk factors, public health importance, economic effect, treatment, and prevention of toxoplasmosis. A search for various publications in English with the criteria of reviewing articles explaining toxoplasmosis was carried out. T. gondii reproduces through two life cycles, namely the sexual cycle and the asexual cycle. In general, consuming parasite cysts in tainted food or water is how humans and other warm-blooded animals become infected with T. gondii. Nearly every region of the world has reported incidences of toxoplasmosis in humans, and around one-third of people are susceptible to latent infection. According to the reports, the main ways through which diseases spread are by water, tainted food, eating tissue cysts or oocysts, and congenital transmission. Infected individuals may experience asymptomatic cervical lymphadenopathy during an acute systemic infection. Diagnostic evaluation is very important for early detection, prevention of transmission, and as a reference for treatment options for infected pregnant women. Consuming undercooked meat is traditionally seen as a significant risk factor for developing toxoplasmosis. The impact of toxoplasmosis is very significant in humans because it causes abortion and disease in newborns, resulting in serious economic losses. To treat toxoplasmosis, dihydropteroate synthetase and dihydrofolate reductase inhibitors are advised. Toxoplasma transmission to humans can be avoided by thoroughly washing your hands with soap after handling meat, poultry, or shellfish.

Systemic virus infection results in CD8 T cell recruitment to the retina in the absence of local virus infection.

During recent years, evidence has emerged that immune privileged sites such as the CNS and the retina may be more integrated in the systemic response to infection than was previously believed. In line with this, it was recently shown that a systemic acute virus infection leads to infiltration of CD8 T cells in the brains of immunocompetent mice. In this study, we extend these findings to the neurological tissue of the eye, namely the retina. We show that an acute systemic virus infection in mice leads to a transient CD8 T cell infiltration in the retina that is not directed by virus infection inside the retina. CD8 T cells were found throughout the retinal tissue, and had a high expression of CXCR6 and CXCR3, as also reported for tissue residing CD8 T cells in the lung and liver. We also show that the pigment epithelium lining the retina expresses CXCL16 (the ligand for CXCR6) similar to epithelial cells of the lung. Thus, our results suggest that the retina undergoes immune surveillance during a systemic infection, and that this surveillance appears to be directed by mechanisms similar to those described for non-privileged tissues.

Passive Transfer of Animal-Derived Polyclonal Hyperimmune Antibodies Provides Protection of Mice from Lethal Lassa Virus Infection.

Lassa virus (LASV) can cause severe acute systemic infection in humans. No approved antiviral drugs or vaccines are currently available. Antibody-based therapeutics are considered a promising treatment strategy in the management of LASV disease. We used chimeric Ifnar-/- C57BL/6 (Ifnar-/- Bl6) mice, a lethal LASV mouse model, to evaluate the protective efficacy of polyclonal antibodies purified from sera of rabbits hyperimmunized with virus-like particles displaying native-like LASV glycoprotein GP spikes. Polyclonal anti-LASV GP antibodies provided 100% protection against lethal LASV infection in a pre- and post-exposure treatment setting and prevented LASV disease. Treatment also significantly lowered viremia level and virus load in organs. When treatment was initiated at the onset of symptoms, the hyperimmune antibodies provided partial protection and increased the survival rate by 80%. Our findings support the consideration of animal-derived hyperimmune antibodies targeting GP as an effective treatment option for highly pathogenic LASV.

Sclerotherapy of lower limb veins: Indications, contraindications and treatment strategies to prevent complications - A consensus document of the International Union of Phlebology-2023.

Sclerotherapy is a non-invasive procedure commonly used to treat superficial venous disease, vascular malformations and other ectatic vascular lesions. While extremely rare, sclerotherapy may be complicated by serious adverse events. To categorise contraindications to sclerotherapy based on the available scientific evidence. An international, multi-disciplinary panel of phlebologists reviewed the available scientific evidence and developed consensus where evidence was lacking or limited. Absolute Contraindications to sclerotherapy where the risk of harm would outweigh any benefits include known hypersensitivity to sclerosing agents; acute venous thromboembolism (VTE); severe neurological or cardiac adverse events complicating a previous sclerotherapy treatment; severe acute systemic illness or infection; and critical limb ischaemia. Relative Contraindications to sclerotherapy where the potential benefits of the proposed treatment would outweigh the risk of harm or the risks may be mitigated by other measures include pregnancy, postpartum and breastfeeding; hypercoagulable states with risk of VTE; risk of neurological adverse events; risk of cardiac adverse events and poorly controlled chronic systemic illness. Conditions and circumstances where Warnings and Precautions should be considered before proceeding with sclerotherapy include risk of cutaneous necrosis or cosmetic complications such as pigmentation and telangiectatic matting; intake of medications such as the oral contraceptive and other exogenous oestrogens, disulfiram and minocycline; and psychosocial factors and psychiatric comorbidities that may increase the risk of adverse events or compromise optimal treatment outcomes. Sclerotherapy can achieve safe clinical outcomes provided that (1) patient-related risk factors and in particular all material risks are (1a) adequately identified and the risk benefit ratio is clearly and openly discussed with treatment candidates within a reasonable timeframe prior to the actual procedure; (1b) when an individual is not a suitable candidate for the proposed intervention, conservative treatment options including the option of 'no intervention as a treatment option' are discussed; (1c) complex cases are referred for treatment in controlled and standardised settings and by practitioners with more expertise in the field; (1d) only suitable individuals with no absolute contraindications or those with relative contraindications where the benefits outweigh the risks are offered intervention; (1e) if proceeding with intervention, appropriate prophylactic measures and other risk-mitigating strategies are adopted and appropriate follow-up is organised; and (2) procedure-related risk factors are minimised by ensuring the treating physicians (2a) have adequate training in general phlebology with additional training in duplex ultrasound, procedural phlebology and in particular sclerotherapy; (2b) maintain their knowledge and competency over time and (2c) review and optimise their treatment strategies and techniques on a regular basis to keep up with the ongoing progress in medical technology and contemporary scientific evidence.

Using T cell lymphokines of hyperimmunized chickens with Salmonella pullorum to protect layer hens against Salmonella pullorum infection

Salmonella pullorum (SP) is well adapted to cause an acute systemic infection in hens with a high mortality rate. This study aimed to assess the efficacy and safety of a salmonella-immune lymphokine (SILK) produced by hyperimmunized pullets with Salmonella pullorum during the layer hens' production stage to boost their immune response against Salmonella pullorum infection. In this study, two groups of 25 pullets were used to produce lymphokines; the first group received three doses of the Salmonella pullorum vaccine at 12, 14, and 16 weeks, while the second group only received phosphate buffer saline (PBS), which served as the control. At 18 weeks, non-immune lymphokines (NILK) were isolated from the T cells of the second group, and salmonella-immune lymphokines (SILK) were isolated from the T cells of the first group. Then, 100-layer hens (ISSA Brown), at 30 weeks old, which entered the production stage, were separated into four groups, each with 25 chickens. G1: infected with SP and treated with SILK. G2: infected with SP and treated with NILK. G3: untreated and SP-challenged G4: no treatment or challenge. The current study aimed to describe the host humoral immune responses to infection in serum samples and bacterial shedding in hens challenged with SP during 31-33 weeks by qPCR techniques. Internal organ bacterial loads were estimated to evaluate the persistence of bacteria. The results show that the spleen, liver, and caecal tonsils tested were positive for bacteria in both groups (G2, G3), proving that Salmonella was not eliminated from the birds and suggesting that internal organ colonization bacteria may act as a reservoir for ongoing bacterial shedding with low IgG titer in compared to G1 with extremely low persistence and high IgG titer in weeks 31, 32, and 33. The current investigation shows that using SILK provides layer hens with better homogenous protection against SP and less internal organ persistence.

CONSTRUCTION AND CHARACTERIZATION OF STEE DELETION MUTANT OF SALMONELLA PULLORUM

Salmonella Pullorum (S. Pullorum) is one of the host-restricted serotypes causing systemic infection in poultry. After S. Pullorum infection, chicks and turkeys usually have acute systemic infection. The main clinical symptoms are white dysentery and dyspnea, and the mortality can be as high as 100%. In adult chickens, local and chronic infections are the most common without obvious clinical symptoms, and can be transmitted vertically to offspring through ovary. Although the use of antibiotics reduces the death of sick chickens, it can not completely eliminate the pathogenic microorganisms in hosts, and is prone to public health problems such as drug resistance and drug residues. No study has ever reported the role of steE in HD-11 cells infected by S. Pullorum. The growth and biochemical characteristics of S. Pullorum ΔsteE were similar to that of S. Pullorum. Furthermore, we also observed the effects of steE on cell proliferation and apoptosis in S. Pulloruminfected HD-11 cells.In order to define the pathogenicity of steE gene of S. Pullorum, the steE deletion strain of S. Pullorum and its complemented strain were successfully constructed, and then its characterization were analyzed. S. Pullorum was preserved by the microbiology laboratory of the college of animal science and veterinary medicine, Henan Institute of Science and Technology. The pKD4, pKD46 and pCP20 or pBR322 plasmids were used for the λ-Red recombination system or complementary strain. The biological characteristics of S. Pullorum ΔsteE were consistent with those of its parent strain S. Pullorum and complementary strain S. Pullorum ΔsteE (pBR322-steE). Construction and confirmation of the ΔsteE strain. To identify the roles of steE in S. Pullorum, the steE deletion mutant of S. Pullorum was correctly constructed.The virulence test showed S. Pullorum ΔsteE decreased the proliferation and apoptosis of HD-11 cells compared to that of S. Pullorum and S. Pullorum ΔsteE (pBR322-steE). Taken together, our data demonstrate that the deletion of steE in S. Pullorum had no effect the growth and biochemical characteristics, but its proliferation ability decreased significantly in HD-11 cells, which decreased cell apoptosis, indicating that steE was closely related to virulence of S. Pullorum. Altogether, our research suggest that the steE gene was required for S. Pullorum virulence, which laid a foundation for further related research in S. Pullorum vaccine strains.

Acute posterior multifocal placoid pigment epitheliopathy associated with infectious mononucleosis

This case report describes the association between acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and Epstein-Barr virus (EBV) infection. A 26-year-old female presented with acute bilateral blurred vision and paracentral scotoma. The patient also had prodromal flu-like symptoms. Funduscopic examination showed bilateral yellow-white placoid lesions at the level of retinal pigment epithelium (RPE). Fluorescein Angiography showed characteristic early hypofluorescence and late hyperfluorescence of the lesions. The diagnosis of APMPPE was made based on these findings. Laboratory investigation showed a positive result for EBV serology test. Severe dry eye symptoms were presented at the end of 6-month follow-up. APMPPE may be associated with acute systemic EBV infection.

Current practices in pediatric hospital‐acquired thromboembolism: Survey of the Children's Hospital Acquired Thrombosis (CHAT) Consortium

BackgroundA rise in hospital‐acquired venous thromboembolism (HA‐VTE) in children has led to increased awareness regarding VTE prophylaxis and risk assessment. Despite no consensus exists regarding these practices in pediatrics. ObjectiveTo describe common practices in VTE prophylaxis, VTE risk assessment models, and anticoagulation dosing strategies in pediatric hospitals that are members of the Children's Hospital Acquired Thrombosis (CHAT) Consortium. MethodsAn electronic survey of 44 questions evaluating practices surrounding pediatric HA‐VTE risk assessment and prevention was distributed between August 9, 2021, and August 30, 2021, to the primary investigators from the 32 institutions within the CHAT Consortium. ResultsThe survey response rate was 100% (n = 32). In total, 85% (n = 27) of the institutions assess HA‐VTE, but only 63% (n = 20) have formal hospital guidelines. Within the institutions with formal guidelines, 100% (n = 20) include acute systemic inflammation or infection and presence of a central venous catheter (CVC) as risk factors for VTE. Pharmacologic prophylaxis is prescribed at 87% (28) of institutions, with enoxaparin being the most frequent (96%, n = 27). Variability in responses persisted regarding risk factors, risk assessment, thromboprophylaxis, dosing of prophylactic anticoagulation or anticoagulant drug monitoring. A majority of providers were comfortable providing thromboprophylaxis across all age groups. In addition, the global coronavirus disease 2019 increased the providers' use of prophylactic anticoagulation 78% (n = 25). ConclusionPractices among institutions are variable in regard to use of HA‐VTE prophylaxis, risk assessment, or guideline implementation, highlighting the need for further research and a validated risk assessment model through groups like the CHAT Consortium.

In vivo molecular imaging of the neuroinflammatory response to peripheral acute bacterial infection in older patients with cognitive dysfunction: A cross-sectional controlled study

IntroductionChronic neuroinflammatory events have been implicated in the pathophysiology of neurodegenerative conditions but no studies have directly examined the neuroinflammatory response to acute systemic infection in older people with dementia. The objective of this study was to determine the magnitude of the neuroinflammatory response triggered by acute systemic infection in older subjects with dementia and/or delirium compared to cognitively healthy controls.MethodsWe recruited 19 participants (4 with delirium, 4 with dementia, 4 with delirium superimposed on dementia, 7 cognitively healthy) hospitalized with acute systemic bacterial infection not involving the Central Nervous System. Participants underwent [11C]-PK11195 PET and a neuropsychological assessment during hospital stay. The distribution volume ratio was estimated in the regions-of-interest using the Hammers’ brain atlas.ResultsIn the subcortical analysis, we found that the cognitively healthy group presented regions with significantly higher DVR intensity than the other groups in the choroid plexus. Mean choroid plexus DVR positively correlated with MoCA (r = 0.66, p = 0.036).ConclusionThis study suggests that dementia and/or delirium is associated with a reduced neuroinflammatory response to acute systemic bacterial infection which can be the result of an immunosuppressive brain environment.

An Audit of Clinical Cases of Dengue Fever and the Usage of Platelets in Such Cases in a Tertiary Care Hospital in Hyderabad

Background and Objectives: Dengue is an acute self-limited systemic viral infection caused by the dengue virus of the family Flaviviridae. The incidence of dengue fever has been increasing for the past few years and dengue has become a global problem. The current data required for further improving the treatment policies are scanty. Our study aims to capture the demographic and clinical characteristics of the patients enrolled in the study, to see any correlation between thrombocytopenia and bleeding tendencies and other transfusion-related parameters. Methods: The study is a prospective cohort study. All seropositive dengue cases were included in the study. A format was prepared for documenting the demographic data, history, clinical characteristics, spectrum of the disease, the laboratory details of the patient (platelet count, prothrombin time, activated partial thromboplastin time, Hematocrit, and indication). All the transfusion requirement data were collected from the blood center registers. Overall mortality in the study group, number of hospital readmissions, and episodes of exacerbation of symptoms was recorded separately. Results: A total of 270 cases were included in the audit who fulfilled the inclusion and exclusion criteria. The median age of the patient pool was 27 (4–66 years range). Twenty-six percent of the cases developed hemorrhages. Eighty-four single-donor platelets (SDPs) and 340 random-donor platelets (RDPs) were used. A mean of 270 ml of products was transfused per patient. The mortality rate was 0.8%. The mean duration of hospitalization was 1 week. In 72% of cases, platelet count was restored in single-unit transfusion. Ninety-nine percent of the product utilization were within the guidelines recommended. Conclusion: A good monthly audit of blood product utilization is a good guide for treatment. Quality control and rational use of SDPs and RDPs are important in sick and thrombocytopenic patients resulting in better clinical outcomes.

Association between infection with Chlamydia pneumonia and cerebral noncardioembolic ischemic stroke

Introduction: Stroke is the third most common cause of mortality and the most common disability disorder among adults. We aimed to study the relationship between Chlamydia pneumonia infection and non-cardio Ambulatory ischemic stroke.Methods: This case-control study was performed on 162 patients with non-cardio ambulatory ischemic stroke admitted to Shahid Beheshti Hospital of Kashan in 2019 as the case group and patients with neurological headache and degenerative diseases as the control group. After filling out the questionnaire for all subjects, we took blood samples. We analyzed all three anti-chlamydia pneumonia antibodies (IgM, IgG, IgA) by ELISA method after data were analyzed by Chi-square and Fisher tests.Results: The findings of this study showed that positive IgA in the stroke group was significantly higher than in the control group (p=0.001); it was also found that the risk factors of HTN (p=0.001), HLP (p=0.001), DM (p=0.001), and age (p = 0.049) were significantly higher in the stroke patients’ group than the control group. On the other hand, there was not a significant difference in serum IgG level (p = 0.349), IgM (p = 0.745), smoking (p = 0.211) and gender (p = 0.157) in understudied groups.Conclusion: Chlamydia IgA antibodies can be a complementary tool for predicting prognosis and monitoring new therapies for ischemic stroke. This study provides a way for further studies, especially with other markers of acute and chronic systemic Chlamydia pneumonia infection. Antibiotic treatment significantly helps to reduce mortality and stroke complications.

Helminth Infections in Children.

Helminth Infections in Children.

Histopathological and Haematological Manifestations of Typhoid Fever in Pediatric Age Group

Background: Typhoid fever is an acute systemic infection caused by Salmonella Enterica Serovar Typhi. Organism is transmitted by fecal-oral route. Aim: To determine frequency of various histopathological & hematological manifestations of typhoid fever in pediatric age group. Study design: Cross-sectional survey. Methodology: Complete blood count, pro-thrombin time and activated partial thromboplastin time were performed on the patients (n=140) to find out various hematological manifestations. Histopathological findings of patients undergoing colonoscopy and biopsy due to gastrointestinal presentations were also noted. Results: Present study had 65% males with 35% females. Almost 65.7% cases presented with anemia. Around 50.7% patients had leucopenia while eosinopenia was 67.1%. Cases (39.3%) presented with prolonged activated partial thromboplastin time while 32.1% cases had prolonged pro-thrombin time. Among histopathological manifestation, 3(2.14%) presented with Typhoid colitis/enteritis, 2(1.43%) with gastrointestinal bleeding due to ulcers and only 1(0.71%) with peritonitis. Conclusion: It was concluded that most common haematological manifestation in typhoid fever was eosinopenia which was most frequently found in coexistence with thrombocytopenia. However, histopathological abdominal complications were quite rare but could be dreadful and should be kept in mind. Keywords: Typhoid Fever, Hematological, Histopathological Manifestations, Abdominal complications and Children.

Measles-Associated CNS Complications: A Review

AbstractMeasles virus infection is a common infectious disease of childhood, incidence of which is still high in developing countries. Other than the morbidity associated with the acute systemic infection, the measles virus can cause serious fatal neural complications. It can either enter the brain leading to acute encephalitis like primary measles encephalitis and acute post infectious measles encephalomyelitis or it may persist in brain cells (as mutated virus) leading to long-term neurodegenerative diseases like measles inclusion body encephalitis and subacute sclerosing pan encephalitis. The patho-clinical features, treatment, and the outcomes of these complications are different and should be identified in time for early diagnosis and management.

Middle Ear Effusion in Intensive Care Unit Patients at Al-Sadder Teaching Hospital in Al-Najaf City-Iraq (A Prospective Randomized Comparative Clinical Study)

Background: Middle ear effusion (MEE) is one of the commonest chronic otological conditions in childhood but has a lower incidence in normal adult. By definition it is an accumulation of non-purulent fluid in the middle ear. It is an inflammatory effusion behind an intact tympanic membrane that is not associated with acute otological symptoms or systemic signs. Aim: To explore factors related to the occurrence of MEE in the intensive care unit (ICU) patients with prolonged oral endotracheal intubation in Al-Najaf city/Iraq. Methods: Forty patients (80 ears) with a prolonged endotracheal intubation (> 5 days) in the ICU were studied. Information of the age, gender, level of consciousness, duration of endotracheal intubation and placement of nasogastric tube were retrospectively collected from history and patient`s data. All patients were subjected to otoscopic examination, tympanometry studies and acoustic reflectometry for evidences of MEE. Results: Out of the 80 ears examined, 46 ears had MEE (57.5%), 22 ears were normal (27.5%), and 12 ears (15%) had negative pressure in the middle ear by tympanometry. Patients who were intubated for more than 11 days and those with conscious disturbance had a significantly high incidence of MEE. No episodes of acute otitis media or systemic infection were encountered. Conclusion: Prolonged endotracheal intubation (more than 11 days), age advancing and conscious disturbance contribute significantly to the occurrence of MEE in adult ICU patients. Recommendation: Middle ear pathology like MEE in the ICU patients with prolonged intubation should not be underestimated.

Pathogenesis and Treatment of Cytokine Storm Induced by Infectious Diseases.

Cytokine storm is a phenomenon characterized by strong elevated circulating cytokines that most often occur after an overreactive immune system is activated by an acute systemic infection. A variety of cells participate in cytokine storm induction and progression, with profiles of cytokines released during cytokine storm varying from disease to disease. This review focuses on pathophysiological mechanisms underlying cytokine storm induction and progression induced by pathogenic invasive infectious diseases. Strategies for targeted treatment of various types of infection-induced cytokine storms are described from both host and pathogen perspectives. In summary, current studies indicate that cytokine storm-targeted therapies can effectively alleviate tissue damage while promoting the clearance of invading pathogens. Based on this premise, “multi-omics” immune system profiling should facilitate the development of more effective therapeutic strategies to alleviate cytokine storms caused by various diseases.