UMLS:C0023380 - FACTA Search

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Query: UMLS:C0023380 (lethargy)
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Sixteen pregnant queens were inoculated orally with tissue cysts of Toxoplasma gondii, and fetal membranes and offspring were examined for T gondii infection by bioassay in mice. Queens appeared clinically normal, although all shed T gondii oocysts. Toxoplasma gondii was isolated from tissues of 7 of 33 fetuses or kittens from 5 litters (at 13, 23, 26, 27, and 29 postinoculation days) from 8 queens euthanatized between 10 and 31 postinoculation days. Infection with T gondii was found in kittens from all 8 litters from the 8 queens that were allowed to undergo parturition and nurse their kittens. A total of 43 kittens were born to these 8 queens. Toxoplasma gondii was isolated from tissues of 26 of 40 kittens bioassayed; in 3 kittens, tissues were not available for bioassay. Toxoplasmosis was severe in full-term kittens born to 5 queens; all 25 kittens from these litters died or were ill by 24 days of age. Anorexia, lethargy, hypothermia, and sudden death were the most common manifestations. Cytologic examination of peritoneal fluid aspirate samples and determination of hepatic-associated enzyme concentrations in affected kittens, as well as measurement of anti-T gondii antibodies in serum of kittens and queens, were helpful in the diagnosis of neonatal toxoplasmosis. Transplacental transfer of anti-T gondii antibodies was not observed in cats. Toxoplasma gondii oocysts were found in fecal samples of 3 kittens from different litters at 16, 24, and 63 days of age.
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PMID:Diagnosis of induced toxoplasmosis in neonatal cats. 760 11

Infection of 60 to 90% of neutrophils with the protozoa, Hepatozoon canis, was detected in 2 dogs. Clinical signs included lethargy, anorexia, and weight loss. Both dogs had severe anemia, leukocytosis, and thrombocytopenia as well as hypoalbuminemia, hyperglobulinemia, and high activities of serum alkaline phosphatase and creatine kinase. Both dogs were treated with imidocarb dipropionate and doxycycline. One dog recovered clinically, with disappearance of parasites from WBC. The other dog died, despite treatment. Necropsy revealed widespread dispersion of schizonts in the parenchymal tissues, but no involvement of skeletal muscle tissues. The disease syndrome that has been identified in the Texas Gulf region is characterized by gait abnormalities associated with multifocal pyogranulomatous myositis, thus, it is distinct clinicopathologically from the syndrome observed in these 2 dogs.
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PMID:Hepatozoon canis infection in two dogs. 779 Mar 3

Infection causes major morbidity and mortality in patients with cerebrospinal fluid (CSF) shunts. The prognosis of CSF shunt infections caused by Gram-negative bacteria (GNB) has been thought to be particularly poor. The authors reviewed all GNB shunt infections treated at Children's Memorial Hospital from January 1986 to January 1990 (n = 23). Of these infections 20 (87%) occurred within 4 weeks after shunt revision (median, 10 days). The most frequent symptoms were fever, lethargy, and irritability; the illness was not severe in the majority of these patients. Escherichia coli was isolated from 12 of 23 patients (52%), Klebsiella pneumoniae from 5 (22%), and mixed GNB from 3 (13%) patients. Initial treatment always included immediate shunt removal, externalized ventricular drainage, and intravenous antibiotics. Extraventricular drainage revision and/or intraventricular antibiotics were required in four patients whose CSF cultures were persistently positive for GNB. At admission, these patients had CSF glucose levels of < 10 mg/dl and CSF positive for GNB by Gram's stain. The overall cure rate was 100%, and no recurrence was observed; however, a subsequent infection with a different organism developed in four patients. Only 2 of 19 patients (11%) who were followed up suffered apparent CNS damage. One patient died of unrelated causes shortly after treatment. Our findings indicate that 1) patients with GNB CSF shunt infections often appear relatively well at presentation; 2) CSF positive for GNB by Gram's stain and very low CSF glucose levels predict continued positive CSF cultures, despite appropriate antibiotic therapy; and 3) GNB CSF shunt infections can be successfully treated by prompt shunt removal, extraventricular drainage, and intravenous antibiotics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventriculoperitoneal shunt infections with gram-negative bacteria. 826 83

Sleeping sickness (SS; African trypanosomiasis) is an anthropozoonosis transmitted by the tsetse fly. Infection with Trypanosoma brucei in humans is associated with adynamia, lethargy, anorexia, and more specifically amenorrhea/infertility in women and loss of libido/impotence in men. Recent evidence suggests that experimental infection in animals with Trypanosoma brucei species causes polyglandular endocrine failure by local inflammation of the pituitary, thyroid, adrenal, and gonadal glands. In a cross-sectional study we investigated the prevalence and significance of neuroendocrine abnormalities in 137 Ugandan patients with SS. In the untreated stage of the disease, there was a high prevalence of adrenal insufficiency (27%), hypothyroidism (50%) and hypogonadism (85%). Pituitary function tests suggested an unusual combined central (hypothalamic/pituitary) and peripheral defect in hormone secretion. Specific therapy resulted in a rapid recovery of adrenal/thyroid function, whereas hypogonadism persisted for years in a substantial portion of patients. We did not detect pituitary, thyroid, adrenal, and gonadal autoantibodies in patients with endocrine dysfunction, ruling out an autoimmune origin of the endocrine abnormalities. However, the presence of hypopituitarism correlated with high cytokine concentrations (TNF-alpha, IL-6) which--together with direct parasitic infiltration of the endocrine glands--are involved in the pathogenesis of SS-associated endocrine dysfunction.
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PMID:Neuroendocrine dysfunction in African trypanosomiasis. The role of cytokines. 962 7

The feasibility of water channel gene delivery to kidney tubules and microvessels was evaluated by delivery of an adenovirus encoding aquaporin 1 (AQP1-Ad5) to transgenic AQP1 null mice. In wild-type mice, AQP1 is expressed in kidney proximal tubule, thin descending limb of Henle, and descending vasa recta, where urine osmolality (Uosm) increases from 1000-1500 mOsm (before) to 2500-3500 mOsm after 36 hr of water deprivation. Uosm in AQP1 null mice remains nearly fixed at 650-750 mOsm. AQP1-Ad5 (with a CMV promoter) was generated and purified. Infection of CHO cells gave strong uniform AQP1 expression with plasma membrane localization and eightfold increased water permeability over noninfected cells. AQP1-Ad5 was delivered to 20 to 25-g AQP1 null mice by tail vein infusion (0-10(10) PFU). At 3-7 days, AQP1 protein expression was strongest in liver (approximately 20 microg of AQP1 protein per liver) and next strongest in kidney, with expression in proximal tubule apical and basolateral membranes, and renal microvessels. Functional analysis showed increased water permeability in apical membrane vesicles from proximal tubule. AQP1 expression was not detected in glomerulus, limb of Henle, or collecting duct. In water-deprived null mice receiving 5 x 10(9) PFU of AQP1-Ad5, Uosm increased by up to 510 mOsm (mean increase, 225 +/- 24 mOsm; n = 33 mice). Whereas the control null mice became lethargic and lost 34.2 +/- 0.6% body weight, the virus-treated mice remained relatively active and lost 32.3 +/- 0.7% body weight. Viral DNA and AQP1 transcript were detected in kidney and liver of null mice up to 17 weeks after virus infusion; partial correction of the urinary concentrating defect persisted for 3-5 weeks. These results demonstrate partial functional correction of a urinary concentrating defect by adenoviral delivery of the AQP1 gene.
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PMID:Partial correction of the urinary concentrating defect in aquaporin-1 null mice by adenovirus-mediated gene delivery. 1072 35

Schistosomiasis japonica is a serious communicable disease and a major disease risk for more than 30 million people living in the tropical and subtropical zones of China. Infection remains a major public health concern despite 45 years of intensive control efforts. It is estimated that 865,000 people and 100,250 bovines are today infected in the provinces where the disease is endemic, and its transmission continues. Unlike the other schistosome species known to infect humans, the oriental schistosome, Schistosoma japonicum, is a true zoonotic organism, with a range of mammalian reservoirs, making control efforts extremely difficult. Clinical features of schistosomiasis range from fever, headache, and lethargy to severe fibro-obstructive pathology leading to portal hypertension, ascites, and hepatosplenomegaly, which can cause premature death. Infected children are stunted and have cognitive defects impairing memory and learning ability. Current control programs are heavily based on community chemotherapy with a single dose of the drug praziquantel, but vaccines (for use in bovines and humans) in combination with other control strategies are needed to make elimination of the disease possible. In this article, we provide an overview of the biology, epidemiology, clinical features, and prospects for control of oriental schistosomiasis in the People's Republic of China.
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PMID:Schistosomiasis in the People's Republic of China: prospects and challenges for the 21st century. 1129 39

The aim of this study was to present neurological complications of influenza infections. Infections caused by influenza viruses can be very serious and may lead even to death resulted from the post-infectious complications. The most often occurring complications are pneumonia, bronchitis, bronchiolitis, myocarditis and otitis media. The other group is neurological post-influenza complications, including dementia, epileptic disorders, cerebrovascular disease, febrile convulsions, toxic encephalopathy, encephalitis, meningitis, subarachnoid hemorrhages, lethargic encephalitis, psychosis or increase in the number of cases of Parkinson's disease. The first way of prevention of influenza is vaccination that results in healthy, social and economic benefits.
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PMID:[Neurological complication of influenza infections]. 1219 26

Mortalities among juvenile paua Haliotis iris Martyn 1784 in a commercial culture facility were reported in April 2000. Histology of moribund paua showed heavy systemic infections of a uni- to multi-nucleate stage of a novel organism later confirmed by transmission electron microscopy (TEM) and molecular studies to be a haplosporidian. Multinucleate plasmodia up to 25 microm diameter with up to 17 nuclei were detectable in wet preparations of hemolymph from heavily infected paua. The presence of the haplosporidian in the affected facility was associated with mortalities of slow growing 'runt' paua during the summer months. Total mortalities in affected raceways 6 mo after mortalities began were between 82.5 and 90%. Heavily infected paua exhibited behavioural abnormalities including lethargy, loss of righting reflex, and were easily detached from surfaces. Some heavily infected paua exhibited oedema and pale lesions in the foot and mantle, but no reliable gross signs of disease were noted. Light infections of the haplosporidian were also found in apparently healthy paua from the facility. Histology indicated that the early stages of infection were characterised by small numbers of plasmodia in the connective tissue surrounding the gut, amongst glial cells adjacent to nerves in the mantle and foot and within gill lamellae. In heavy infections, large numbers of small plasmodia (mean size 5.5 x 7 microm in histological sections) were present in the hemolymph, gills, heart, kidneys, mantle, foot, epipodium and connective tissue of the digestive gland. Infections were not transferred horizontally at 14 and 19 degrees C after cohabiting heavily infected paua with uninfected paua for 3 mo in aquaria, or 3 mo after injecting healthy paua with hemolymph containing haplosporidian plasmodia. This may indicate that the prepatent period for disease is longer than 3 mo, that disease is not expressed below 20 degrees C, or that an intermediate host is required for transmission. Spore formation was not observed in juvenile paua but sporocyst-like bodies containing putative spores were observed amongst haplosporidian plasmodia in the right kidney of poorly performing adult paua collected from the wild.
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PMID:Pathology of cultured paua Haliotis iris infected with a novel haplosporidian parasite, with some observations on the course of disease. 1221 78

The guidance in this report is for evaluation and treatment of patients with complications from smallpox vaccination in the preoutbreak setting. Information is also included related to reporting adverse events and seeking specialized consultation and therapies for these events. The frequencies of smallpox vaccine-associated adverse events were identified in studies of the 1960s. Because of the unknown prevalence of risk factors among today's population, precise predictions of adverse reaction rates after smallpox vaccination are unavailable. The majority of adverse events are minor, but the less-frequent serious adverse reactions require immediate evaluation for diagnosis and treatment. Agents for treatment of certain vaccine-associated severe adverse reactions are vaccinia immune globulin (VIG), the first-line therapy, and cidofovir, the second-line therapy. These agents will be available under Investigational New Drug (IND) protocols from CDC and the U.S. Department of Defense (DoD). Smallpox vaccination in the preoutbreak setting is contraindicated for persons who have the following conditions or have a close contact with the following conditions: 1) a history of atopic dermatitis (commonly referred to as eczema), irrespective of disease severity or activity; 2) active acute, chronic, or exfoliative skin conditions that disrupt the epidermis; 3) pregnant women or women who desire to become pregnant in the 28 days after vaccination; and 4) persons who are immunocompromised as a result of human immunodeficiency virus or acquired immunodeficiency syndrome, autoimmune conditions, cancer, radiation treatment, immunosuppressive medications, or other immunodeficiencies. Additional contraindications that apply only to vaccination candidates but do not include their close contacts are persons with smallpox vaccine-component allergies, women who are breastfeeding, those taking topical ocular steroid medications, those with moderate-to-severe intercurrent illness, and persons aged < 18 years. In addition, history of Darier disease is a contraindication in a potential vaccinee and a contraindication if a household contact has active disease. In the event of a smallpox outbreak, outbreak-specific guidance will be disseminated by CDC regarding populations to be vaccinated and specific contraindications to vaccination. Vaccinia can be transmitted from a vaccinee's unhealed vaccination site to other persons by close contact and can lead to the same adverse events as in the vaccinee. To avoid transmission of vaccinia virus (found in the smallpox vaccine) from vaccinees to their close contacts, vaccinees should wash their hands with warm soapy water or hand rubs containing > or = 60% alcohol immediately after they touch their vaccination site or change their vaccination site bandages. Used bandages should be placed in sealed plastic bags and can be disposed of in household trash. Smallpox vaccine adverse reactions are diagnosed on the basis of clinical examination and history, and certain reactions can be managed by observation and supportive care. Adverse reactions that are usually self-limited include fever, headache, fatigue, myalgia, chills, local skin reactions, nonspecific rashes, erythema multiforme, lymphadenopathy, and pain at the vaccination site. Other reactions are most often diagnosed through a complete history and physical and might require additional therapies (e.g., VIG, a first-line therapy and cidofovir, a second-line therapy). Adverse reactions that might require further evaluation or therapy include inadvertent inoculation, generalized vaccinia (GV), eczema vaccinatum (EV), progressive vaccinia (PV), postvaccinial central nervous system disease, and fetal vaccinia. Inadvertent inoculation occurs when vaccinia virus is transferred from a vaccination site to a second location on the vaccinee or to a close contact. Usually, this condition is self-limited and no additional care is needed. Inoculations of the eye and eyelid require evaluation by an ophthalmologist and might require therapy with topical antiviral or antibacterial medications, VIG, or topical steroids. GV is characterized by a disseminated maculopapular or vesicular rash, frequently on an erythematous base, which usually occurs 6-9 days after first-time vaccination. This condition is usually self-limited and benign, although treatment with VIG might be required when the patient is systemically ill or found to have an underlying immunocompromising condition. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. EV occurs among persons with a history of atopic dermatitis (eczema), irrespective of disease severity or activity, and is a localized or generalized papular, vesicular, or pustular rash, which can occur anywhere on the body, with a predilection for areas of previous atopic dermatitis lesions. Patients with EV are often systemically ill and usually require VIG. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. PV is a rare, severe, and often fatal complication among persons with immunodeficiencies, characterized by painless progressive necrosis at the vaccination site with or without metastases to distant sites (e.g., skin, bones, and other viscera). This disease carries a high mortality rate, and management of PV should include aggressive therapy with VIG, intensive monitoring, and tertiary-level supportive care. Anecdotal experience suggests that, despite treatment with VIG, persons with cell-mediated immune deficits have a poorer prognosis than those with humoral deficits. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. Central nervous system disease, which includes postvaccinial encephalopathy (PVE) and postvaccinial encephalomyelitis (or encephalitis) (PVEM), occur after smallpox vaccination. PVE is most common among infants aged < 12 months. Clinical symptoms of central nervous system disease indicate cerebral or cerebellar dysfunction with headache, fever, vomiting, altered mental status, lethargy, seizures, and coma. PVE and PVEM are not believed to be a result of replicating vaccinia virus and are diagnoses of exclusion. Although no specific therapy exists for PVE or PVEM, supportive care, anticonvulsants, and intensive care might be required. Fetal vaccinia, resulting from vaccinial transmission from mother to fetus, is a rare, but serious, complication of smallpox vaccination during pregnancy or shortly before conception. It is manifested by skin lesions and organ involvement, and often results in fetal or neonatal death. No known reliable intrauterine diagnostic test is available to confirm fetal infection. Given the rarity of congenital vaccinia among live-born infants, vaccination during pregnancy should not ordinarily be a reason to consider termination of pregnancy. No known indication exists for routine, prophylactic use of VIG in an unintentionally vaccinated pregnant woman; however, VIG should not be withheld if a pregnant woman develops a condition where VIG is needed. Other less-common adverse events after smallpox vaccination have been reported to occur in temporal association with smallpox vaccination, but causality has not been established. Prophylactic treatment with VIG is not recommended for persons or close contacts with contraindications to smallpox vaccination who are inadvertently inoculated or exposed. These persons should be followed closely for early recognition of adverse reactions that might develop, and clinicians are encouraged to enroll these persons in the CDC registry by calling the Clinician Information Line at 877-554-4625. To request clinical consultation and IND therapies for vaccinia-related adverse reactions for civilians, contact your state health department or CDC's Clinician Information Line (877-554-4625). Clinical evaluation tools are available at http.//www.bt.cdc.gov/agent/smallpox/vaccination/clineval. Clinical specimen-collection guidance is available at http://www.bt.cdc.gov/agent/smallpox/vaccination/vaccinia-specimen-collection.asp. Physicians at military medical facilities can request VIG or cidofovir by calling the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) at 301-619-2257 or 888-USA-RIID.
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PMID:Smallpox vaccination and adverse reactions. Guidance for clinicians. 1261 10

A 2-year-old female Quarter Horse was evaluated for hind limb lameness, fever (40 degrees C [104 degrees F]), and lethargy of 2 weeks' duration. Hypoproteinemia characterized by hypoalbuminemia and hyperfibrinogenemia was detected. Abdominal ultrasonography revealed thickening of the right dorsal colon wall. Treatment was instituted for putative right dorsal coliis. Lameness evaluation localized signs of pain to the lumbar vertebrae or pelvis. Radiography performed with the horse standing and nuclear scintigraphy revealed no abnormalities. Ventrodorsal pelvic radiography revealed a focal area of bony lysis and proliferation involving the cranial portion of the pubic symphysis. Aspiration yielded purulent exudate containing Rhodococcus equi, which was susceptible to erythromycin. Treatment included surgical debridement of the abscess and oral administration of erythromycin and rifampin. The horse's hind limb lameness completely resolved within 20 days. Infections of the pubic symphysis should be considered when lameness localized to the pelvis is associated with fever and an inflammatory leukogram.
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PMID:Osteomyelitis of the pelvis caused by Rhodococcus equi in a two-year-old horse. 1268 88

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