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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

Prions are a novel class of infectious agents that cause subacute encephalopathy in man and animals as human Creutzfeldt-Jakob disease (CJD), sheep scrapie and bovine spongiform encephalopathy (BSE). Previously, prions were shown to be transmitted by neuro- and ophthalmosurgical measures and by application of brain-derived therapeutic hormones. Recently, prions have been detected in blood specimens of experimentally infected monkeys indicating a principal threat to transfusion medicine, furthermore in human or bovine materials used in reconstructive surgery. In this article the risk of prion transmission from the surgeon to the patient or vice versa during (orthopedic) surgery is reevaluated including the issues of blood transfusion. This is accomplished based on recent epidemiologic findings and biometric calculations on the spread of prions in animals and humans as well as in terms of experimental data on artificially contaminated medical materials and devices. The overall risk of prion transmission in orthopedic surgery is considered very low if adequately prepared and sterilized materials and devices are used.
Infection 2003 Jun
PMID:Prions and orthopedic surgery. 1278 74

Infection with influenza viruses produces a spectrum of clinical responses, ranging from upper respiratory illness to central nervous system (CNS) involvement. Recently, the number of reports of influenza-associated encephalopathy in Japan has increased. During the winters of 1997-1998 and 1998-1999, when epidemics of type A influenza (H3N2) occurred, many pediatricians reported cases of influenza-associated encephalitis or encephalopathy in children. The prominent indicators of influenza-associated encephalopathy are the abrupt onset of seizures and coma within a few days of developing a high-grade fever. These patients often develop multi-organ failure and have high morbidity and mortality. The pathogenesis of influenza-associated encephalopathy remains unclear. Because not all patients with influenza develop encephalopathy, infection with the influenza vieus is necessary, but not sufficient, for the development of influenza-associated encephalopathy. Viral RNA is rarely detected in the cerebrospinal fluid (CSF), and the presence of viral antigen in the brain has not been proven. Pathological findings, including the lack of detectable viral antigen and inflammatory cells in brain tissues, suggest that direct viral invasion and inflammation are unlikely to be causes of this disease. In influenza-associated encephalopathy, serum and CSF concentrations of several proinflammatory cytokines and cytokine receptors--such as interleukin (IL)-6, IL-1beta, and soluble tumor necrosis factor (TNF) receptor-1 (sTNF-R1)--are elevated and are related to the clinical severity of the disease. Moreover, the damage of vascular endothelial cells has been shown. Using SNPs, molecular analysis of whole genome of the patients are now on going.
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PMID:[Influenza-associated encephalopathy]. 1565 45

Infection with HIV-1 has spread exponentially in recent years to reach alarming proportions. It is estimated than more than 33 million adults and 1.3 million children are infected worldwide. Approximately 16,000 new cases are diagnosed every day and almost 3 million people die every year from AIDS, making it the fourth leading cause of death in the world. Since the introduction of highly active anti-retroviral therapy (HAART) in the mid 1990s, the morbidity and mortality associated with HIV-1 infection has significantly decreased and AIDS has become a chronic disorder. However, neuropathological conditions associated with AIDS are still present in approximately 70 to 90% of patients and can be the result of HIV itself or of opportunistic infections. Here we briefly review the pathology and pathophysiology of AIDS-Encephalopathy, of some of the significant opportunistic infections affecting the brain in the context of AIDS, including Progressive Multifocal Leukoencephalopathy (PML) a demyelinating disease caused by the human neurotropic JC virus, Toxoplasmosis, Cryptococcosis and of primary CNS lymphoma, a brain malignancy frequently associated with HIV-1 infection, all of them considered AIDS defining conditions.
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PMID:HIV disorders of the brain: pathology and pathogenesis. 1614 64

Certain arthropod-borne infections are common in tropical regions because of favorable climatic conditions. Water-borne infections like leptospirosis are common due to contamination of water especially during the monsoon floods. Infections like malaria, leptospirosis, dengue fever and typhus sometimes cause life threatening organ dysfunction and have several overlapping features. Most patients present with classicial clinical syndromes: fever and thrombocytopenia are common in dengue, malaria and leptospirosis; coagulopathy is frequent in leptospirosis and viral hepatitis. Hepatorenal syndrome is seen in leptospirosis, falciparum malaria and scrub typhus. The pulmonary renal syndrome is caused by falciparium malaria, leptospirosis, Hantavirus infection and scrub typhus. Fever with altered mental status is produced by bacterial meningitis, Japanese B encephalitis, cerebral malarial, typhoid encephalopathy and fulminant hepatic failure due to viral hepatitis. Subtle differences in features of the organ failure exist among these infections. The diagnosis in some of these diseases is made by demonstration of antibodies in serum, and these may be negative in the first week of the illness. Hence empiric therapy for more than one disorder may be justified in a small proportion of cases. In addition to specific anti-infective therapy, management of organ dysfunction includes use of mechanical ventilation, vasopressor drugs, continuous renal replacement therapy and blood products. Timely transfer of these patients to well-equipped ICUs with experience in managing these cases can considerably decrease mortality and morbidity.
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PMID:Tropical infections in the ICU. 1694 13

In a retrospective review, 3 (3.8%) of 78 patients developed recurrent posterior reversible encephalopathy syndrome. Underlying clinical conditions included sickle cell disease, antibody-positive autoimmune disease, and allogeneic bone marrow transplantation. Infection (bacterial/viral) was suspected or documented in both episodes in all 3 patients. Evidence of endothelial injury (schistocyte formation and increased lactate dehydrogenase) was documented in all patients, and multiple organ dysfunction syndrome developed during the hospital course of all admissions.
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PMID:"Recurrent" posterior reversible encephalopathy syndrome: report of 3 cases--PRES can strike twice! 1725 48

Dengue fever, one of the common endemic viral fevers, often presents with fever, rash, and mild liver dysfunction. However, plasma leakage induced by dengue virus infection can lead to dengue hemorrhagic fever and dengue shock syndrome, and it can cause severe complications including liver failure and encephalopathy. Infection of dengue virus with other pathogens is an unusual but serious complication. We report a case of dengue shock syndrome with liver failure and impaired consciousness. The patient developed a disseminated Candida tropicalis infection, which may have been due to translocation of the fungus from the intestine damaged by the dengue virus.
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PMID:Dengue hemorrhagic shock and disseminated candidiasis. 1760 49

Infection is a risk factor for adult stroke and neonatal encephalopathy. We investigated whether exposure to bacterial endotoxin increases hypoxia-induced brain cell death and impairs cerebral metabolic compensatory responses to hypoxia. Prehatching chicken embryos (incubation day 19) were exposed to bacterial lipopolysaccharide (LPS) (3 mg Salmonella typhimurium LPS per egg) or hypoxia (4% ambient O(2) for 1 h), alone or in combination with LPS, followed 4 h later by hypoxia. Cerebral cell death and glial activation were assessed histologically. Further, chicken embryo brains were studied by magnetic resonance imaging (MRI) and spectroscopy (MRS) to assess haemodynamic and metabolic responses. In most brain areas, combined LPS/hypoxia resulted in a 30- to 100-fold increase in terminal deoxynucleotidyl transferase dUTP nick end labelling -positive cells, compared to control and single-insult groups. Glial activation correlated with the severity of cell death and was significantly greater in the combined-insult group (P<0.05). Hypoxia was associated with a 10-fold increase in lactate/N-acetyl-aspartate (NAA), an approximately 20% increase in total creatine/NAA, rapid decreases in T2 and T2(*), and a reduction in direction-averaged brain-water diffusion (D(av)) by approximately 15%. Liposaccharide pretreatment did not alter the magnitude or timing of these responses, but engendered baseline shifts (increased Cho/NAA, Cr/NAA, and Dav, and reduced T2(*)). In conclusion, LPS greatly increased hypoxia-induced brain damage in this model and induced changes in baseline haemodynamics and metabolism but did not affect the magnitude of the glycolytic response to hypoxia. The damage-enhancing effects of LPS are not because of additional energy depletion but because of a synergistic toxic component.
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PMID:Greater hypoxia-induced cell death in prenatal brain after bacterial-endotoxin pretreatment is not because of enhanced cerebral energy depletion: a chicken embryo model of the intrapartum response to hypoxia and infection. 1803 Mar 3

A case of Susac syndrome in a child is reported with a review of the literature. A 14-year-old girl presented with headache, left hemiparesis, sphincter deficit, and cognitive deficits. The assessment consisted of neurological and ocular examination, imagery by cerebral magnetic resonance, lumbar puncture, and a biological and immunological assessment. Magnetic resonance imaging revealed numerous high signal intensities on T2-weighted images in the white and grey matter. The ophthalmologic examination found bilateral branch retinal artery occlusions. Twelve months later, she developed hearing loss. Infection assessment was negative and immunologic tests were normal. Susac syndrome is a rare disorder with a clinical triad of encephalopathy, branch retinal artery occlusions, and hearing loss. It is caused by a microangiopathy affecting the precapillary arterioles of the brain, retina, and inner ear. Susac syndrome usually affects young women in young adulthood and is extremely rare during childhood. The pathogenesis of this syndrome is unknown. The clinical course of Susac syndrome is characterized by recurrent attacks. Resolution usually occurs spontaneously. However, sensory and neurologic sequelae may be present. Treatment is not well codified and may include steroids, immunosuppressant drugs, and immunoglobulin. Susac syndrome should be considered in children when evaluating patients with branch retinal artery occlusion and encephalopathy.
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PMID:[Susac syndrome and ocular manifestation in a 14-year-old girl]. 1826 43

Prematurity remains a public health problem with a considerable psychosocial impact. Premature infants are discharged home more fragile and more precociously than infants born at term. Post-discharge nutrition and growth of the preterm infants should be carefully followed because of specific needs of these infants. Infections and cardiorespiratory abnormalities are more frequent in ex-premature infants. Some cerebral lesions may be shown by brain imaging suggesting future sequelae. However, estimation of their real consequences remains imperfect and long term prognosis contains many uncertainties. Cerebral palsy seems to be less severe nowadays, but all current gravity is due to disabilities which express later: hearing disorders, visual impairments, alterations of eye-hand coordination skills, attention deficit disorders, psychological troubles and school difficulties. Multidisciplinary consultations are designed for these children because early screening and adapted care can improve long term prognosis. All this underlines the importance of prolonged follow-up program after discharge for premature infants and others who presented worse suffer from hypoxic/ischemic encephalopathy.
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PMID:[Care and follow-up of premature infants after discharge]. 1857 75


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