Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the winter of 2002, an outbreak of mycoplasma infection in Vaal rhebok (Pelea capreolus) originating from South Africa occurred 15 weeks after their arrival in San Diego, Calif. Three rhebok developed inappetence, weight loss, lethargy, signs related to pulmonary or arthral dysfunction, and sepsis. All three rhebok died or were euthanized. Primary postmortem findings were erosive tracheitis, pleuropneumonia, regional cellulitis, and necrotizing lymphadenitis. Mycoplasmas were detected in numerous tissues by electron microscopy, immunohistochemistry, and PCR. The three deceased rhebok were coinfected with ovine herpesvirus-2, and two animals additionally had a novel gammaherpesvirus. However, no lesions indicative of herpesvirus were seen microscopically in any animal. The rheboks' mycoplasmas were characterized at the level of the 16S rRNA gene, the 16S-23S intergenic spacer region, and the fructose biphosphate aldolase gene. Denaturing gradient gel electrophoresis was carried out to address the possibility of infection with multiple strains. Two of the deceased rhebok were infected with a single strain of Mycoplasma capricolum subsp. capricolum, and the third animal had a single, unique strain most closely related to Mycoplasma mycoides subsp. mycoides large-colony. A PCR survey of DNA samples from 46 other ruminant species demonstrated the presence of several species of mycoplasmas in the mycoides cluster, including a strain of M. capricolum subsp. capricolum identical to that found in two of the rhebok. These findings demonstrate the pervasiveness of mycoplasmas in the mycoides cluster in small ruminants and the potential for interspecies transmission and disease when different animal taxa come in contact.
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PMID:Systemic disease in Vaal rhebok (Pelea capreolus) caused by mycoplasmas in the mycoides cluster. 1575 Jan 4

CASE DESCRIPTION-A 12-week-old female English Springer Spaniel was evaluated for lethargy, vomiting, and pyrexia 1 week after treatment of patent ductus arteriosus (PDA) via coil occlusion. CLINICAL FINDINGS-Test results were consistent with septicemia, and the assumption was made that the PDA occlusion coils were infected. Radiography revealed partial migration of the coil mass into the pulmonary artery and signs of congestive heart failure. TREATMENT AND OUTCOME-After successful treatment of the septicemia and heart failure, surgical removal of the coils and resection of the PDA were undertaken. Although the coil that embolized to the pulmonary vasculature was left in place, the dog's clinical signs resolved. CLINICAL RELEVANCE-This case highlights the fact that as PDA coil occlusion devices become more widely used in dogs, practitioners must be prepared to treat implant infections aggressively, with both medical and surgical interventions if necessary.
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PMID:Septicemia in a young dog following treatment of patent ductus arteriosus via coil occlusion. 1678 81

Neonatal septicemia acquired by vertical transmission of Pasteurella multocida is very rare. The authors report a case of Pasteurella multocida septicemia in a 2-day-old male infant. His mother had a history of prolonged premature rupture of membranes and subsequently developed fever. The patient had fever and lethargy at 36 hours of age, then developed severe pneumonia, sepsis, persistent pulmonary hypertension, renal failure and liver failure. Although the appropriate antibiotics were given, he continued to deteriorate and eventually died.
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PMID:Neonatal septicemia due to Pasteurella multocida: the first case report in Thailand. 1704 43

Sickness behaviour (SB) consists of the set of adaptive responses of the host to severe infections and inflammation. It includes, among others, the thermoregulatory responses such as regulated increase (fever) and/or decrease (anapyrexia) of body temperature (T(b)), decrease of motor activity (lethargy), and loss of appetite (hypophagia) resulting in a transient loss of body weight. It is thought that SB is partially induced by the immune-derived mediators such as cytokines and prostaglandins acting on the central nervous system. It has repeatedly been shown, on the other hand, that severe infections (pneumonia, tissue septicemia) can impair processes of the gases exchange both in the lungs and in distal tissues including brain, which may lead to hypoxia of the affected organs. Therefore, we have tested the hypothesis that hypoxia may also provoke SB. The study was conducted on freely moving biotelemetered mice kept at 28 degrees C ambient and 12/12 h light/dark cycle. We demonstrate that mice exposed for 7 days to hypoxia (11%O(2)) displayed all symptoms of SB. Interleukin-6 deficient mice (IL-6 KO) revealed reduced SB symptoms under hypoxic conditions. Recovery of the hypoxia-exposed mice to a normal rhythm in T(b), motor activity and feeding was unaffected by mepacrine, a phospholipase A(2) blocker. The recovery, however, was significantly impaired by indomethacin, a cyclooxygenase inhibitor. Exposure to hypoxemia resulted in significant elevation of plasma IL-6 in both untreated and treated with lipopolysaccharide (LPS) mice. It inhibited, however, a generation of blood prostaglandins (PGE(2)) in mice. Based on these data we conclude that IL-6 and accumulation of free arachidonic acid in biomembranes contribute to hypoxemia- induced SB.
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PMID:Hypoxia-induced sickness behaviour. 1724 71

Cryptosporidium oocysts were identified by phase contrast microscopy on smears from flotations of greenish-yellow pasty feces obtained from two foals. One foal, a one week old Percheron was recumbent, anorectic and lethargic, believed to be the result of a septicemia of undetermined etiology. Despite therapy and nursing care the animal died. Using light and electron microscopy, numerous stages of Cryptosporidium sp. were seen protruding from the surface of epithelial cells of intestinal villi. The other foal, a six week old Arabian had a mild diarrhea. The diarrhea and passage of oocysts eventually ceased. Immunological tests on sera of both these foals provided no evidence of abnormal immune function. This report is the first to describe cryptosporidiosis in apparently immunocompetent horses.
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PMID:Cryptosporidiosis in two foals. 1742 22

The dermatology staff was called to evaluate abnormal hair on a 22-month-old Hispanic girl whose parents were first cousins. Her medical history was significant for leptomeningitis with subsequent neurologic devastation, gastroesophageal reflux disease, and recurrent respiratory infections. Her hospital course was complicated by sepsis, liver dysfunction, pan-cytopenia, and disseminated intravascular coagulation. She had developed normally for the first year of life. At 13 months she became progressively lethargic and developed floppy muscle tone; a delay in mental and motor milestones was recognized. Results of a metabolic workup were negative. On examination she was noted to have generalized excessively fair skin when compared with her parents. She had silver-gray hair (Figure 1) and white eyebrows and body hair. Her maternal grandfather and granduncles had silver hair since childhood, but were without health problems. A maternal family member was said to have light skin. The presumed diagnosis before pathologic examination was Chediak-Higashi syndrome. Hematoxylin and eosin stain tests revealed prominent melanocytes in the basal layer of the epidermis. The melanocytes were large and distended with a large volume of melanin (Figure 2). The adjacent keratinocytes were completely devoid of melanin. Application of Masson-Fontana ammoniac silver stain highlighted prominent melanocytic melanin and a relative paucity of melanin in the adjacent keratinocytes (Figure 3). Microscopic examination of her hair revealed clumps of melanin of various sizes and shapes irregularly distributed throughout the hair shaft. Ultrastructural examination of the epidermis showed the melanocytes were distended by an accumulation of large stage IV mature melanosomes. Peripheral blood smear failed to show abnormal granules, even after repeated examination. Based on the clinical features and the pathologic findings, a diagnosis of Griscelli syndrome type 2 was made.
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PMID:Griscelli syndrome. 1748 61

Infant botulism is a rare cause of hypotonia in young infants. It may present with vague symptoms such as poor feeding and lethargy. We present 4 cases of infant botulism presenting to 2 community hospitals in central Maryland. In each case, poor feeding and lethargy were the chief complaints. One patient was referred to the emergency department with suspected sepsis and one with suspected intussusception. Three patients required endotracheal intubation. All were treated with botulism immune globulin, and all eventually made full recoveries. We discuss the differential diagnosis and provide an overview of infant botulism.
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PMID:Infant botulism presenting with poor feeding and lethargy: a review of 4 cases. 1766 36

There is paucity of data about the predictive values and likelihood ratios of clinical signs of late onset nosocomial sepsis in neonates. A clinical score comprising of seven items had been derived from analysis of individual signs and had been published by this group in the Journal of Tropical Pediatrics in 2003. The current study was done to validate the score in a fresh validation cohort, to evaluate the score at 0 and 24 h after onset of clinical signs of sepsis and to evaluate the sepsis screen in combination with the clinical score. The seven clinical signs in the clinical score included grunting, abdominal distension, increased prefeed aspirates, tachycardia, hyperthermia, chest retractions and lethargy. A total of 220 episodes of sepsis among 208 babies were evaluated. The clinical score was calculated at 0 h and 24 h. A sepsis screen (micro erythrocyte sedimentation rate, C reactive protein, absolute neutrophil count and immature/total neutrophil ratio) and blood culture were performed in all subjects at enrollment. Sepsis screen was considered 'positive' if any two parameters were positive. The outcome of interest was 'definite sepsis', defined as blood culture positive. The 0-h clinical score had sensitivity, specificity, PPV, NPV, LR(+) and LR(-) of 90, 22.5, 30.3, 85.7, 1.16 and 0.44%, respectively. The 24-h score had higher specificity (60.6%) but lower sensitivity than the 0-h score. Sepsis screen per se had a sensitivity and NPV of 48.3 and 78.3% but when combined with the 0-h clinical score, the sensitivity and NPV rose to 95 and 90.6%, respectively. The 'clinical score' in combination with sepsis screen result can be used by clinicians to rule out sepsis.
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PMID:Validation of a clinical score for the diagnosis of late onset neonatal septicemia in babies weighing 1000-2500 g. 1769 86

Application of liver transplantation to methylmalonic acidemia (MMAemia) is controversial because MMAemia is caused by a systemic defect of methylmalonyl-CoA mutase. The clinical courses of seven pediatric patients with MMAemia undergoing living donor liver transplantation (LDLT) were reviewed. Serum and urinary methylmalonic acid (MMA) levels were found to be significantly decreased after LDLT, whereas serum and urinary MMA levels did not return to normal in any patient. One patient died of sepsis 44 days after LDLT. The other six patients are currently doing well. All patients had preoperative history of acute metabolic decompensation and/or metabolic stroke. However, no episode of acute metabolic decompensation or metabolic stroke was observed postoperatively in any surviving patients. In the preoperative period, all patients showed lethargy and cognitive deficit, both of which were eradicated after LDLT in all surviving patients. Preoperatively, all patients were subjected to dietary protein intake restriction and tube feeding, and were administered several metabolism-correcting medications. The metabolism-correcting medications being administered remained mostly unchanged after LDLT, whereas protein restriction was liberalized and tube feeding became unnecessary in all surviving patients. In addition, physical and neurodevelopmental growth delay remained in all surviving patients during the observation period, which ranged from 4 to 21 months with a median of 10.5 months.
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PMID:Efficacy of living donor liver transplantation for patients with methylmalonic acidemia. 1790 73

A 3-year-old Irish Wolfhound was evaluated because of acute onset of lethargy and fever. Severe neutropenia (0/microL; reference interval 2500-11,200/microL) was associated with granulocyte aplasia in the bone marrow (myeloid:erythroid ratio, 0.009:1). Antineutrophil antibodies were assessed by an indirect immunofluorescence assay using flow cytometry. When normal canine leukocytes were incubated with the patient's serum and anti-IgG, a marked shift was observed in the forward-angle light scatter of the neutrophil population, and the monocyte cluster disappeared, possibly the result of fragmentation or lysis. Both neutrophil fluorescence intensity (309 +/- 11 median channel units [MCU], control values 107-152 MCU) and the percentage of neutrophils with increased fluorescence intensity (61 +/- 5%, control values 3.8-13.7%) were increased in the patient's serum, consistent with the presence of antineutrophil antibodies. Repeated episodes of neutropenia occurred while treatment with steroidal and nonsteroidal immunosuppressive therapy was initiated and modified. The neutrophil count eventually stabilized in the low-normal range, and the dog was maintained for the next 15 months on prednisone (0.4 mg/kg PO q 48 h) and azathioprine (2 mg/kg daily). During this period, the dog developed immune-mediated hemolytic anemia and thrombocytopenia, decubital ulcers, nasal aspergillosis, and eventually, multi-organ septicemia, which led to euthanasia on day 784. A diagnosis of pure white cell aplasia was made in this dog, based on the many similarities to human patients with pure white cell aplasia, including severe neutropenia with selective granulocyte aplasia, serum antineutrophil antibodies, remission dependent on treatment with immunosuppressive therapy, and recurrent bacterial infections.
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PMID:Pure white cell aplasia in a dog. 1804 6


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