Inflammation Of Internal Organs Research Articles

Hearing Loss in Systemic Onset Juvenile Idiopathic Arthritis (Sojia) -A Single Case Study

Juvenile Rheumatoid Arthritis is a common type of arthritis in children under the age of sixteen. Females are more affected than males with ratio of 2:1. Systemic onset Juvenile Idiopathic Arthritis (SoJIA) is an immune driven inflammatory condition that develops in children. Although SoJIA can occur any time during childhood it usually starts before age five. Inflammation of internal organs and MAS (macrophage activation syndrome) is closely associated with SoJIA. Children with SoJIA have high levels of two powerful inflammatory protein (cytokines) called Interleukin -1 and Interleukin-6. The management of SoJIA follows up with NSAIDs, Corticosteroids, DMARDs and inflammatory cytokine blockade. The incudomalleolar and incudostapedial joint are synovial in nature and hence could be involved in inflammatory process. Immune complex mediated vasculitis and ototoxic side effects may cause a pathological inner ear. Thus individuals with SoJIA are at higher risk of hearing impairment.

SAT440 DRESS/DHIS-associated Thyroiditis And Hypophysitis

Abstract Disclosure: I.R. Ranasinghe: None. M.S. Elston: None. V. Boyle: None. Introduction: Drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms (DRESS/DIHS) is a severe life-threatening adverse reaction to specific drugs, including cephalosporin antibiotics (1). It is characterised by rash, fever, eosinophilia, lymphadenopathy, and inflammation of internal organs. Endocrine complications in the form of thyroid disease and Type 1 Diabetes have been reported following DRESS/DIHS (2). We report a case of thyroiditis and hypophysitis following cephalosporin-associated DRESS/DIHS. Case: A 21-year-old male farmer suffered a tractor crash accident resulting in hospitalization for bilateral compound distal femur fractures. He had no past medical history of note. One month later, he developed a maculopapular rash involving his limbs, mouth ulcers, fever, liver function derangement and eosinophilia. Punch biopsy was consistent with DRESS/DHIS. A 2- week tapering course of prednisone was initiated at 40mg daily in conjunction with a topical corticosteroid for 9 days with resolution of rash. Review of medication charts identified the most likely causative agent as cefazolin. An Endocrine consult was requested a month later due to new hypercalcemia. Investigations revealed new onset thyrotoxicosis and a decreasing morning cortisol over the following week despite having stopped all steroids one month earlier, normal ACTH, mildly elevated prolactin and secondary hypogonadism. Short Synacthen test showed suboptimal response. TRAb were negative and technetium thyroid scanning demonstrated a thyroiditis. MRI pituitary was unremarkable. He was commenced on hydrocortisone replacement for symptomatic cortisol deficiency. Biochemical abnormalities gradually normalized and his hydrocortisone ceased with symptomatic resolution. Endocrine involvement, particularly pancreas and thyroid has previously been reported in cases of DHIS/DRESS (3) (4). In this case, DHIS/DRESS-associated hypophysitis with thyroiditis may explain the clinical findings of pituitary dysfunction affecting multiple pituitary axes and the gradual recovery to normal pituitary function.

Вплив нематоди Contracaecum (Ascaris) на риб водойми-охолоджувача Запорізької атомної електростанції

Purpose: To determine species composition and localization of anisakidosis pathogens, infestation of fish species in the Zaporizhzhia NPP cooling reservoir, and identify trends in their infestation compared to monitoring epizootic studies of the last year. Methodology. In the course of the work, we used the generalized results of the studies conducted in the summer and autumn of 2021. The fish species composition in the ZNPP cooling reservoir as well as the species composition of parasites of Anisakidae family and their localization were determined. The studies were carried out using the method of incomplete parasitological dissection of fish at the laboratory. Nematode larvae were detected by visual inspection. The parasites were identified using identification keys. The detected parasites were washed with a saline and stored in 70% ethanol. For the quantitative analysis of the parasitofauna, we used such parameters as prevalence (%) and intensity (ind./ fish). Findings. The parasitological analysis showed that Contracaecum (Ascaris) larvae were found in European, channel and redtail catfishes, which were localized as cysts or free-living in the abdominal cavity. The infestation intensify reached 86 ind./fish, and prevalence reached 100%. The parasites caused hyperemia (redness) and inflammation of internal organs. At the same time, no Contracaecum larvae were found in common and silver carps. Compared to 2020, the infestation of fish was less pronounced, namely: no monogenean Dactylogirus were found on the gills of carps as well as ciliates including Trichodina and Apiosoma, which were found in small amounts on the body surface and gills of common and silver carps. The Contracaecum larvae invasion intensity in catfish decreased by 17 %. Originality. For the first time, a large tendency to the spread of Contracaecum larvae among fish of the ZNPP cooling reservoir was detected, namely in European, channel and redtail catfishes. The importance of the threat of this invasion for fish was established. Practical value. The obtained results can be used to identify timely trends in the infestation of fish by Anisakidae and to develop sanitary and preventive measures in the reservoir. Key words: nematodes, parasites Contracaecum (Ascaris), fish, ZNPP, anisakidosis, prevalence, invasion intensity, anisakids (Anisakidae).

A Case of Mycobacteriosis in Cultured Japanese Seabass (Lateolabrax japonicus) in Southern China

Japanese seabass (Lateolabrax japonicus) is an important species of cultured marine fish with high economic value in China. Nevertheless, from May to November 2019, mass mortality among cultured Japanese seabass occurred in Zhuhai City, Guangdong Province of China. Approximately 0.2–0.5% mortality was recorded daily, and the cumulative mortality was up to 30% during this disease outbreak. In this study, the clinical signs and pathological characteristics of diseased fish were investigated. Furthermore, the pathogenicity and antibiotic sensitivity of identified pathogenic bacteria from diseased fish were analyzed. The infected fish showed clinical signs of uncoordinated swimming; anorexia; pigment changes; and a number of 1–5 mm grayish-white nodules in the liver, spleen, and kidney tissues was also found. A bacterial strain, which was designated as ZHLJ2019, was isolated from the diseased fish. To ensure that ZHLJ2019 isolate was the causative agent, a Koch postulate trial was performed. Healthy Japanese seabass were infected by the intraperitoneal injection of 5 × 104, 5 × 105 and 5 × 106 CFU/fish, and cumulative mortalities within 42 days were 75%, 90%, and 100%, respectively. The bacteria colony had traditional morphological and biochemical characteristics similar to that of Mycobacterium marinum. Phylogenetic molecular analyses of 16S rRNA, rpoB, hsp65, erp, and ITS genes confirmed that the isolated strain ZHLJ2019 was M. marinum. The granulomatous inflammation in internal organs of Japanese seabass naturally and experimentally infected with ZHLJ2019 isolate was consistent with the classic pathological features of mycobacteriosis. Drug susceptibility of ZHLJ2019 isolate to 11 antibiotics was determined by broth dilution method in vitro. The minimum inhibitory concentrations (MICs) of minocycline, rifampicin, ethambutol, isoniazid, streptomycin, doxycycline hydrochloride, kanamycin sulfate, levofloxacin, roxithromycin, and prothionamide against the strain ZHLJ2019 were 4, 2, 8, 4, 16, 8, 8, 8, 4, and 8 μg/mL, respectively. The results of this study suggest that M. marinum is the causal agent responsible for the morbidity and mortality of Japanese seabass cultured in intensive brackish water dirt ponds in southern China.

Novel Loci Controlling Parasite Load in Organs of Mice Infected With Leishmania major, Their Interactions and Sex Influence.

Leishmaniasis is a serious health problem in many countries, and continues expanding to new geographic areas including Europe and USA. This disease, caused by parasites of Leishmania spp. and transmitted by phlebotomine sand flies, causes up to 1.3 million new cases each year and despite efforts toward its functional dissection and treatment it causes 20–50 thousands deaths annually. Dependence of susceptibility to leishmaniasis on sex and host's genes was observed in humans and in mouse models. Several laboratories defined in mice a number of Lmr (Leishmania major response) genetic loci that control functional and pathological components of the response to and outcome of L. major infection. However, the development of its most aggressive form, visceral leishmaniasis, which is lethal if untreated, is not yet understood. Visceral leishmaniasis is caused by infection and inflammation of internal organs. Therefore, we analyzed the genetics of parasite load, spread to internal organs, and ensuing visceral pathology. Using a new PCR-based method of quantification of parasites in tissues we describe a network-like set of interacting genetic loci that control parasite load in different organs. Quantification of Leishmania parasites in lymph nodes, spleen and liver from infected F2 hybrids between BALB/c and recombinant congenic strains CcS-9 and CcS-16 allowed us to map two novel parasite load controlling Leishmania major response loci, Lmr24 and Lmr27. We also detected parasite-controlling role of the previously described loci Lmr4, Lmr11, Lmr13, Lmr14, Lmr15, and Lmr25, and describe 8 genetic interactions between them. Lmr14, Lmr15, Lmr25, and Lmr27 controlled parasite load in liver and lymph nodes. In addition, Leishmania burden in lymph nodes but not liver was influenced by Lmr4 and Lmr24. In spleen, parasite load was controlled by Lmr11 and Lmr13. We detected a strong effect of sex on some of these genes. We also mapped additional genes controlling splenomegaly and hepatomegaly. This resulted in a systematized insight into genetic control of spread and load of Leishmania parasites and visceral pathology in the mammalian organism.

Characterization of Histopathological and Ultrastructural Changes in Channel Catfish Experimentally Infected with Virulent Aeromonas hydrophila.

A highly virulent clonal population of Aeromonas hydrophila (vAh) has been the cause of recent motile Aeromonas septicemia epizootic in channel catfish (Ictalurus punctatus) farms in the Southeastern United States. The pathology of the disease caused by vAh has not been studied well yet. Thus, our aim was to determine histopathological and ultrastructural changes in channel catfish following vAh challenge. To accomplish this, catfish fingerlings were challenged with vAh (strain ML09-119) by bath. Six fish per each time point were collected at 1, 3, 5, 6, 24, and 48 h for light microscopy, and six fish were collected at 48 h for transmission electron microscopy (TEM). The first pathological lesions were detected in the spleen and stomach at 1 h post-challenge (HPC) while intestine, gills, kidney, and liver lesions were observed at 24 and 48 HPC. Histopathological examination revealed degenerative changes, necrosis, extensive edema, and inflammation in internal organs. The TEM showed severe tissue destruction with multiple bacterial cells secreting outer membrane vesicles, especially in spleen and gills and far number in the stomach. Degenerated bacterial cells were observed in the intestinal lumen and the phagosomes of phagocytic kidney cells. We identified, for the first time, degranulate eosinophilic granular cells, and dendritic cells like (DC-like) cells in the necrotic intestinal epithelium. These findings suggest that vAh rapidly proliferated and spread through the catfish organs following bath challenge.

Stenotrophomonas maltophilia as an opportunistic pathogen in cultured African catfish Clarias gariepinus (Burchell, 1822)

Indian catfish production is increasing over the years so as the frequency of diseases. In this report, the isolation of Stenotrophomonas maltophilia from the kidney of Clarias gariepinus juvenile with distended abdomen along with its phenotypic, molecular and phylogenetic characteristics was described. The diseased catfish juveniles in an earthen pond (1500m3) with high stocking density (≈60nos/m3) had body discoloration, fin/tail rot, focal cutaneous hemorrhage, distended abdomen, inflammation of internal organs and visceral hemorrhage. The abdominal cavity was filled with transparent jelly-like mass. The bacterial strain isolated from the kidney of catfish formed a monophyletic group with other strains of S. maltophilia based on genotypic characters and phylogenetic analyses. The strain S. maltophilia SK1 (NCBI accession number KP898215) was alpha-hemolytic, protease and lipase positive and weakly pathogenic to C. gariepinus juveniles. It caused only 35±5% mortality at a level of 1.40×107 cells/fish via intraperitonial injection. While the intramuscular injection caused only 10% mortality. The dead fish up on challenge had distended abdomen with jelly-like mass. Understanding the pathology and pathogenesis of this emerging pathogen in cultured catfish would help manage the disease. Statement of relevance1Stenotrophomonas maltophilia is considered as an opportunistic pathogen of human and fish.2This species is emerging as a pathogen in cultured catfish Clarias gariepinus (Burchell, 1822).3Understanding the pathology and pathogenesis of this species would help manage the disease.

On the skin of a soldier: The story of flogging

After Farrier-Major Critton struck the 150th lash on the back of Private Frederick John White, at the end of a common disciplinary session at Hounslow Barracks, West London, in 1846, the soldier, whistling, walked himself to the infirmary to have his wounds dressed. His skin healed promptly, but 4 weeks later, he was found dead in his dormitory. The army medical officers, after performing an autopsy, reached the conclusion that the soldier had died from inflammation of internal organs but excluded any connection with flogging. This version of facts did not convince the coroner for Middlesex, who decided to open an inquest. After 3 more weeks of inquiry and 2 more postmortem examinations, the famous dermatologist Erasmus Wilson contradicted the army officers by affirming that the soldier had indeed died from the effects of flogging as the analysis of the cutaneous lesions and underneath would demonstrate. This contribution will detail how the inquest into the death of Private John White sparked a medical debate on the effects of military flogging to the skin. The discussion raised by the publication of the details of the autopsies demonstrated that different and opposing points of view coexisted in the Victorian period concerning the relation between external lacerations and internal organs in cases of flogging.

DRESS syndrome due to Anti-Tuberculous Drug

DRESS (Drug Rash with Eosinophilia and Systemic Symptoms) is a potentially life threatening syndrome caused by exposureto certain medications. That may cause skin rash, fever, inflammation of internal organs, lymphadenopathy, and characteristichematologic abdnormalities such ad eosinophilia, thrombocytopenia, and typical atypical lymphocytosis. The interval between thestarting of drug therapy and the onset of cutaneous reactions may be at least one month. Aromatic anticonvulsants(phenytoin, phenobarbital, carbamazepine) and sulfonamides are the most common causes of DRESS. There has been only afew case reports of DRESS syndrome induced by anti-tuberculous medication, Ethambutol, Rifampin, Isoniazid, Pyrazinamide. Wereport a case of Ethambutol induced DRESS syndrome and multiple drug hypersensitivity to other antituberculosis drugs thatwere used at after DRESS syndrome developed.

Gemcitabine-induced radiation recall phenomenon in a post-operative and post-radiotherapy case of peri-ampullary carcinoma during adjuvant chemotherapy

Radiation recall phenomenon is an inflammatory process occurring at sites of previous radiation subsequent to administration of pharmacologic agents. The most common chemotherapeutic agents implicated with radiation recall phenomenon are anthracyclines and taxanes. Skin is the most common site for radiation recall. About 63% of the radiation recall events are reported to manifest as dermatitis. This finding differs from radiation recall due to Gemcitabine, in which approximately 70% cases manifested as inflammation of internal organs or tissues and 30% manifested as dermatitis. Here, we report a case of post-operative peri-ampullary carcinoma who developed radiation recall dermatitis during adjuvant chemotherapy with inj. Gemcitabine and inj. Carboplatin after concurrent chemoradiation with capecitabine.

Exophiala angulospora causes systemic ­inflammation in Atlantic cod Gadus morhua

Species of Exophiala are opportunistic fungal pathogens that may infect a broad range of warm- and cold-blooded animals, including salmonids and Atlantic cod. In the present study, we observed abnormal swimming behaviour and skin pigmentation and increased mortality in cod kept in an indoor tank. Necropsy revealed foci of different sizes with a greyish to brownish colour in internal organs of diseased fish. The foci consisted of ramifying darkly pigmented fungal hyphae surrounded by distinct layers of inflammatory cells, including macrophage-like cells. In the inner layer with many hyphae, the macrophage-like cells were dead. We observed no apparent restriction of fungal growth by the inflammatory response. A darkly pigmented fungus was repeatedly isolated in pure culture from foci of diseased fish and identified as Exophiala angulospora using morphological and molecular characters. This species has not been previously reported to cause disease in cod, but has been reported as an opportunistic pathogen of both marine and freshwater fish. Based on the morphology and sequence analysis presented here, we conclude that E. angulospora caused the observed chronic multifocal inflammation in internal organs of cod, leading to severe disease and mortality.

Effects of D-4F on vasodilation, oxidative stress, angiostatin, myocardial inflammation, and angiogenic potential in tight-skin mice

Systemic sclerosis (scleroderma, SSc) is an autoimmune, connective tissue disorder that is characterized by impaired vascular function, increased oxidative stress, inflammation of internal organs, and impaired angiogenesis. Tight skin mice (Tsk(-/+)) have a defect in fibrillin-1, resulting in replication of many of the myocardial and vascular features seen in humans with SSc. D-4F is an apolipoprotein A-I (apoA-I) mimetic that improves vascular function in diverse diseases such as hypercholesterolemia, influenza, and sickle cell disease. Tsk(-/+) mice were treated with either phosphate-buffered saline (PBS) or D-4F (1 mg.kg(-1).day(-1) for 6-8 wk). Acetylcholine and flow-induced vasodilation were examined in facialis arteries. Proinflammatory HDL (p-HDL) in murine and human plasma samples was determined by the cell-free assay. Angiostatin levels in murine and human plasma samples were determined by Western blot analysis. Hearts were examined for changes in angiostatin and autoantibodies against oxidized phosphotidylcholine (ox-PC). Angiogenic potential in thin sections of murine hearts was assessed by an in vitro vascular endothelial growth factor (VEGF)-induced endothelial cell (EC) tube formation assay. D-4F improved endothelium-, endothelial nitric oxide synthase-dependent, and flow-mediated vasodilation in Tsk(-/+) mice. Tsk(-/+) mice had higher plasma p-HDL and angiostatin levels than C57BL/6 mice, as did SSc patients compared with healthy control subjects. Tsk(-/+) mice also had higher triglycerides than C57BL/6 mice. D-4F reduced p-HDL, angiostatin, and triglycerides in the plasma of Tsk(-/+) mice. Tsk(-/+) hearts contained notably higher levels of angiostatin and autoantibodies against ox-PC than those of control hearts. D-4F ablated angiostatin in Tsk(-/+) hearts and reduced autoantibodies against ox-PC by >50% when compared with hearts from untreated Tsk(-/+) mice. Angiogenic potential in Tsk(-/+) hearts was increased only when the Tsk(-/+) mice were treated with D-4F (1 mg.kg(-1).day(-1), 6-8 wk), and cultured sections of hearts from the D-4F-treated Tsk(-/+) mice were incubated with D-4F (10 microg/ml, 5-7 days). Failure to treat the thin sections of hearts and Tsk(-/+) mice with D-4F resulted in loss of VEGF-induced EC tube formation. D-4F improves vascular function, decreases myocardial inflammation, and restores angiogenic potential in the hearts of Tsk(-/+) mice. As SSc patients have increased plasma p-HDL and angiostatin levels similar to the Tsk(-/+) mice, D-4F may be effective at treating vascular complications in patients with SSc.

Rickettsia-like organism infection in a freshwater cultured fish Ophiocephalus argus C. in China*

From 2001 to 2002, a new and emergent infectious disease of Ophiocephalus argus occurred in a fishery in Hubei Province, China, with an incidence of 60% similar to 70% and a mortality as high as 100 %. The diseased fish showed an enlarged abdomen, the millet-like nodules in internal organs, and the swollen kidney which was composed of 5 similar to 10 sarcoma-like bodies in cream or gray-white colour or ulcerated into beandregs-like substance. Light microscopic observation revealed the basophilic or acidphilic inclusions in cytoplasm of the cells and the granulomas, a diffusive chronic inflammation in internal organs. Further analysis under an electron microscope indicated that the intracytoplasmic inclusions were rickettsia-like organisms (RLOs) that are either spherical or coccoid, with variable size, ranging from 0.5 similar to 1.5 mum in diameter, and enclosed within membrane-bound cytoplasmic vacuoles. RLO had a central nucleoid region with some fine filamentous structures and an electron-dense granule. Its cytoplasm contained abundant ribosomal bodies. Occasionally, RLO appeared to be divided by binary fission. RLOs were also observed in the homogenized tissue of infected fish. The results suggested that the death of cultured O. argus was caused by RLO infection.