Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brucellosis has always been an unusual disease in children and, concomitant with the control of the disease in domestic animals, reports have become sparse. The pediatrician, therefore, may not be aware of the protean clinical manifestations of childhood brucellosis. In 1973, nine cases occurred during a three-month period in El Paso, Texas. All cases were marked by spiking fevers and lethargy of four days to four weeks in duration. Tender hepatomegaly or splenomegaly was striking in seven patients. Other characteristics included epistaxis, arthralgia, myalgia, and weight loss. Leukopenia and leukemoid reaction were found in five patients. All of the patients tested had elevated liver enzymes. Febrile agglutinins were invaluable in screening for an early clue to diagnosis. When Brucella abortus antigen agglutinated serum from patients with a positive screen in dilutions greater than 1:320, a presumptive diagnosis of brucellosis was made. Brucella was isolated from the blood or bone marrow in seven patients and the time of incubation proved crucial for successful recovery. Bacterial blood cultures are usually discarded at ten days of age, as were cultures from the only two patients from whom the organism was not recovered. All of the cultures incubated for 12 to 15 days grew B. melitensis, an unusual causative species in the United States. However, several patients admitted eating cheese from the State of Chihuahua, Mexico, made from unpasteurized goat's milk, the presumed source of the infection. Within one to three days, all patients responded dramatically to antibiotics; tetracycline was given orally for 21 days and streptomycin intramuscularly for 14 days. Pediatricians caring for patients in areas where consumption of unpasteurized milk products is likely would do well to consider brucellosis in a child with obscure fever or toxic hepatosplenomegaly.
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PMID:Brucellosis in childhood. 80 83

Knowledge of the natural history of symptomatic congenital cytomegalovirus (CMV) infection in the newborn is essential in order to anticipate complications and assess the potential benefit from antiviral therapy. To define the disease course we reviewed data on 106 neonates with symptomatic congenital CMV infection diagnosed and managed by the investigators. Petechiae, jaundice and hepatosplenomegaly were each noted in 70% or more patients. Microcephaly was noted in 54 of 102 (53%) at birth. Elevated alanine aminotransferase, conjugated hyperbilirubinemia and thrombocytopenia were seen in 83, 81 and 77%, respectively. Eighty-six percent had at least two of the manifestations highly suggestive of congenital infection. Platelet count fell to its nadir during the second week of life whereas elevated alanine aminotransferase and direct bilirubin persisted past the first month. In spite of the difficulty in assessing central nervous system function in the newborn, evidence of damage was present in the majority. Seventy-two had microcephaly, poor suck, lethargy/hypotonia or seizures. Abnormal computerized tomographic scan was present in 16 of 20 (80%) and decreased hearing in 20 of 39 (56%). Cerebrospinal fluid protein was greater than 120 mg/dl in 24 of 52 (46%) and this elevation was associated with neurologic abnormalities as well as hearing loss. The mean length of hospital stay was 13 and 22.4 days for term and preterm infants, relatively. Thirteen infants (12%) died during the first 6 weeks of life. Disseminated CMV infection with multiorgan involvement was evident in 7 of 9 at postmortem examination. We conclude that neonates with symptomatic congenital CMV infection have a multi-system disease with significant morbidity and mortality.
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PMID:Symptomatic congenital cytomegalovirus infection: neonatal morbidity and mortality. 131 Oct 66

Seven English Springer Spaniels (6 adult males and 1 female) with chronic hemolysis and sporadic intravascular hemolytic crises were determined to have a deficiency in erythrocyte phosphofructokinase (PFK) activity, a key regulatory enzyme of anaerobic glycolysis. Intermittent severe pigmenturia concomitant with weakness, lethargy, and anorexia were the major clinical signs and commonly were related to exercise or other stressful situations that caused panting or barking (hyperventilation). Pale or icteric mucous membranes, fever, mild hepatosplenomegaly, and muscle wasting sometimes were evident. Results of routine laboratory testing indicated a persistent marked bilirubinuria and reticulocytosis with normal PCV, to severe anemia and intermittent hemoglobinuria and hyperkalemia. Erythrocyte PFK activities were severely reduced to 8% to 22% of values for control dogs. The block of glycolysis at the PFK step caused a markedly diminished erythrocyte 2,3-diphosphoglycerate content, resulting in an increased hemoglobin-oxygen affinity and compensatory accelerated erythrocyte production. Phosphofructokinase-deficient erythrocytes had increased alkaline fragility in vitro and in vivo. Hemolytic crises were induced in vivo by hyperventilation that caused transient, mild alkalemia. Studies of family members of a PFK-deficient dog suggested an autosomal recessive mode of inheritance. Carrier dogs with half-normal erythrocyte PFK activities appeared clinically normal.
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PMID:Hemolysis caused by phosphofructokinase deficiency in English springer spaniels: seven cases (1983-1986). 295 37

Peripheral lymph node enlargement was found in 14 of a series of 132 feline lymph node biopsy specimens. Six of nine cats tested had antibodies for feline leukemia virus (FeLV). Half of the cats were clinically normal while the remainder had fever, lethargy, anorexia, and hepatosplenomegaly. There was severe distortion of lymph nodal architecture with variable loss of discernible follicles and sinuses. Histiocytes, lymphocytes, immunoblasts, and plasma cells were present in expanded paracortical regions which encroached on, and occasionally effaced, lymphoid follicles. Postcapillary venules were numerous and prominent throughout the paracortex. The lymphadenopathy was most commonly transient (86% of cases) with subsequent development of lymphoma in one cat. Lymph nodes from seven kittens with experimental FeLV infection were compared with spontaneously enlarged lymph nodes; four of seven had B and T lymphocyte hyperplasia with normal nodal architecture. Three had partial loss of nodal architecture as a result of expanded paracortical regions populated largely by histiocytes and lymphocytes. Proliferation of postcapillary venules was not prominent in nodes from FeLV-infected cats. The cause of spontaneous lymph node hyperplasia of young cats was not determined. However, the similarity of lesions to those of kittens with experimental FeLV infection and the association with FeLV by serologic tests in six of nine cats suggest that this retrovirus may be involved in the pathogenesis of the lesion.
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PMID:Distinctive peripheral lymph node hyperplasia of young cats. 375 Jul 32

The clinical and pathologic features of 4 dogs with malignant histiocytosis were evaluated. The most common clinical signs were weight loss, lethargy, lymphadenopathy, hepatosplenomegaly, and anemia. Neoplastic histiocytic infiltrates most commonly were found in the spleen, bone marrow, liver, or lymph nodes. Malignant histiocytosis was considered as a differential diagnosis for anemic dogs with lymphadenopathy and/or hepatosplenomegaly.
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PMID:Malignant histiocytosis in four dogs. 405 15

A toxin associated with Toxoplasma gondii infection was obtained from the trophozoites and culture medium used to propagate the parasite in cell cultures. The toxin, named Toxofactor (TF), administered parenterally or nonparenterally in adult mice, produces transient symptoms of lethargy, ruffled fur, and body weight loss. Organ changes which accompanied the outward symptoms included hepatosplenomegaly and involuted thymus. TF activity was detected in extracts of the blood, peritoneal fluid, liver, and spleen of infected mice. Severe damage to embryonal and fetal development was induced when TF was administered during pregnancy. Resorption, abortion, and congenital abnormalities were produced, dependent upon the stage of development at the time of exposure. Adult mice which had reacted to and recovered from an initial intraperitoneal injection to TF were protected against a secondary challenge from TF. Fetal development was also protected from damage when TF was used to challenge adults previously exposed to TF. Mouse and rabbit anti-TF sera neutralized TF activity in the adult. In no instance did control mice show any deleterious effect when exposed to soluble cell lysate from the uninfected cell line (BHK-21) used to propagate the organism plus the used medium from these same uninfected cells. TF activity was not attributed to bacterial, myocoplasmal, or viral contamination. TF toxic activity is labile to elevated temperature and high or low pH, which also destroy its protective properties. TF activity was sensitive to trypsin and was obtained in the elution fraction (alpha-methyl-D-mannoside) from affinity chromatography (concanavalin A-Sepharose 4B). Ultrafiltration indicated the molecular weight to be between 50,000 and 100,000. TF, apparently a glycoprotein, was quantitated for activity by a weight loss assay. A unit of activity was defined as the minimum quantity of TF (highest dilution) which produced at least a 10% average body weight loss in adult Nya:NYLAR female mice between days 7 and 12 post-intraperitoneal injection.
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PMID:Toxofactor associated with Toxoplasma gondii infection is toxic and teratogenic to mice. 668

Acute clinical malaria caused by Plasmodium inui was diagnosed in an adult female cynomolgus monkey (Macaca fascicularis) 4 years after importation into the United States. Stress and immunosuppression associated with experimentation completed 2 weeks earlier may have contributed to the development of severe clinical disease. Clinical findings included severe regenerative anemia, hepatosplenomegaly, weakness, lethargy, weight loss, and anorexia. The infection was treated and successfully eliminated with chloroquine hydrochloride administered intramuscularly at a dose of 5 mg/kg base given at 0, 6, 24, 48, and 72 hours. Treatment also included a blood transfusion and intensive supportive care.
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PMID:Acute clinical malaria (Plasmodium inui) in a cynomolgus monkey (Macaca fascicularis). 683 80

A 54-year-old male was hospitalized because of lethargy, weight loss, an upper abdominal mass, hepatosplenomegaly and peripheral blood plasmacytosis of 66%. The diagnosis of acute plasma cell leukaemia was established, and after chemotherapy was initiated, the patient entered complete remission. 6 months later, he developed extramedullary plasmacytoma with involvement of the gastrointestinal tract, right inguinal lymph nodes and right orbit. Response to chemotherapy was poor and he died without evidence of plasma cell leukaemia. The possibility of the existence of extramedullary plasmacytoma at the onset of the disease, expressed by the appearance of plasma cell leukaemia only at the beginning and by extramedullary spreading at the terminal stage is discussed.
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PMID:Acute plasma cell leukaemia followed by extramedullary plasmacytoma. 737 11

A 3.5-year-old male Golden Retriever with lethargy, generalized lymphadenopathy, and hepatosplenomegaly was determined to have malignant histiocytosis, based on the morphologic appearance of neoplastic cells by light and electron microscopic examination, evidence of erythrophagocytosis, the presence of diffuse nonspecific esterase activity, and immunohistochemical demonstration of vimentin intermediate filaments. Because of the appearance of abundant iron stores in the bone marrow, serum was obtained for determination of iron, total iron binding capacity, and ferritin values. Serum ferritin concentrations were markedly increased. Measurement of serum ferritin concentrations may be useful in supporting a diagnosis of malignant histiocytosis, and the monitoring of serum ferritin concentrations may be useful for assessing treatment and regression of the disease.
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PMID:Hyperferritinemia associated with malignant histiocytosis in a dog. 782 79

Simian T-cell leukemia virus type 1 (STLV-1), a type C retrovirus associated with leukemia/lymphoma in Old World monkeys, is closely related to human T-cell leukemia virus type 1, the etiologic agent of adult T-cell leukemia/lymphoma in humans. In a colony of 3200 baboons, the prevalence of antibodies to STLV-1 is more than 40%. Seropositivity is more frequent in female baboons than in males and increases with age. Of 27 STLV-1 antibody-positive baboons with non-Hodgkin's lymphoma, 20 were females and 7 were males, ranging in age from 3 to 21 years (mean, 13 years). Non-Hodgkin's lymphoma was not found in STLV-1 antibody-negative baboons. Clinical signs and laboratory findings were variable but generally included lethargy, low body weights, anemia, dyspnea, lymphadenopathy, hepatosplenomegaly, pneumonia, nodular skin lesions, and leukemia with or without multilobulated lymphocytes in peripheral blood. Radiography revealed pulmonary infiltrates consistent with pneumonia in 17 of the baboons. Serum chemical values were normal except for hypercalcemia in one baboon. Lymphocytosis was found in 18 of the baboons, with leukemia diagnosed in 11. At necropsy, variable enlargement of lymph nodes and other lymphopoietic tissue was usually found. Pale tan to white space-occupying foci typical of proliferative lymphoid tissue were often found in various organs, including lungs, spleens, livers, skin, and hearts. The lungs in 14 baboons had thickened pleuras, congestion,edema, and large tan to brown areas of consolidation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneously generated non-Hodgkin's lymphoma in twenty-seven simian T-cell leukemia virus type 1 antibody-positive baboons (Papio species). 790 50


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