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Dive into the research topics where Sally Slavinski is active.

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Featured researches published by Sally Slavinski.


Journal of Clinical Microbiology | 2004

Epidemiologic and Molecular Characterization of an Outbreak of Candida parapsilosis Bloodstream Infections in a Community Hospital

Thomas A. Clark; Sally Slavinski; Juliette Morgan; Timothy J. Lott; Beth A. Arthington-Skaggs; Mary E. Brandt; Risa M. Webb; Mary Currier; Richard H. Flowers; Scott K. Fridkin; Rana Hajjeh

ABSTRACT Candida parapsilosis is an important cause of bloodstream infections in the health care setting. We investigated a large C. parapsilosis outbreak occurring in a community hospital and conducted a case-control study to determine the risk factors for infection. We identified 22 cases of bloodstream infection with C. parapsilosis: 15 confirmed and 7 possible. The factors associated with an increased risk of infection included hospitalization in the intensive care unit (adjusted odds ratio, 16.4; 95% confidence interval, 1.8 to 148.1) and receipt of total parenteral nutrition (adjusted odds ratio, 9.2; 95% confidence interval, 0.9 to 98.1). Samples for surveillance cultures were obtained from health care worker hands, central venous catheter insertion sites, and medical devices. Twenty-six percent of the health care workers surveyed demonstrated hand colonization with C. parapsilosis, and one hand isolate was highly related to all case-patient isolates by tests with the DNA probe Cp3-13. Outbreak strain isolates also demonstrated reduced susceptibilities to fluconazole and voriconazole. This largest known reported outbreak of C. parapsilosis bloodstream infections in adults resulted from an interplay of host, environment, and pathogen factors. Recommendations for control measures focused on improving hand hygiene compliance.


JAMA | 2017

Birth Defects Among Fetuses and Infants of US Women With Evidence of Possible Zika Virus Infection During Pregnancy

Margaret A. Honein; April L. Dawson; Emily E. Petersen; Abbey M. Jones; Ellen H. Lee; Mahsa M. Yazdy; Nina Ahmad; Jennifer Macdonald; Nicole Evert; Andrea Bingham; Sascha R. Ellington; Carrie K. Shapiro-Mendoza; Titilope Oduyebo; Anne D. Fine; Catherine M. Brown; Jamie N. Sommer; Jyoti Gupta; Philip Cavicchia; Sally Slavinski; Jennifer L. White; S. Michele Owen; Lyle R. Petersen; Coleen A. Boyle; Dana Meaney-Delman; Denise J. Jamieson

Importance Understanding the risk of birth defects associated with Zika virus infection during pregnancy may help guide communication, prevention, and planning efforts. In the absence of Zika virus, microcephaly occurs in approximately 7 per 10 000 live births. Objective To estimate the preliminary proportion of fetuses or infants with birth defects after maternal Zika virus infection by trimester of infection and maternal symptoms. Design, Setting, and Participants Completed pregnancies with maternal, fetal, or infant laboratory evidence of possible recent Zika virus infection and outcomes reported in the continental United States and Hawaii from January 15 to September 22, 2016, in the US Zika Pregnancy Registry, a collaboration between the CDC and state and local health departments. Exposures Laboratory evidence of possible recent Zika virus infection in a maternal, placental, fetal, or infant sample. Main Outcomes and Measures Birth defects potentially Zika associated: brain abnormalities with or without microcephaly, neural tube defects and other early brain malformations, eye abnormalities, and other central nervous system consequences. Results Among 442 completed pregnancies in women (median age, 28 years; range, 15-50 years) with laboratory evidence of possible recent Zika virus infection, birth defects potentially related to Zika virus were identified in 26 (6%; 95% CI, 4%-8%) fetuses or infants. There were 21 infants with birth defects among 395 live births and 5 fetuses with birth defects among 47 pregnancy losses. Birth defects were reported for 16 of 271 (6%; 95% CI, 4%-9%) pregnant asymptomatic women and 10 of 167 (6%; 95% CI, 3%-11%) symptomatic pregnant women. Of the 26 affected fetuses or infants, 4 had microcephaly and no reported neuroimaging, 14 had microcephaly and brain abnormalities, and 4 had brain abnormalities without microcephaly; reported brain abnormalities included intracranial calcifications, corpus callosum abnormalities, abnormal cortical formation, cerebral atrophy, ventriculomegaly, hydrocephaly, and cerebellar abnormalities. Infants with microcephaly (18/442) represent 4% of completed pregnancies. Birth defects were reported in 9 of 85 (11%; 95% CI, 6%-19%) completed pregnancies with maternal symptoms or exposure exclusively in the first trimester (or first trimester and periconceptional period), with no reports of birth defects among fetuses or infants with prenatal exposure to Zika virus infection only in the second or third trimesters. Conclusions and Relevance Among pregnant women in the United States with completed pregnancies and laboratory evidence of possible recent Zika infection, 6% of fetuses or infants had evidence of Zika-associated birth defects, primarily brain abnormalities and microcephaly, whereas among women with first-trimester Zika infection, 11% of fetuses or infants had evidence of Zika-associated birth defects. These findings support the importance of screening pregnant women for Zika virus exposure.


Emerging Infectious Diseases | 2003

Acute Flaccid Paralysis and West Nile Virus Infection

James J. Sejvar; A. Arturo Leis; Dobrivoje S. Stokic; Jay A. Van Gerpen; Anthony A. Marfin; Risa M. Webb; Maryam B. Haddad; Bruce C. Tierney; Sally Slavinski; Jo Lynn Polk; Victor Dostrow; Michael Winkelmann; Lyle R. Petersen

Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a peripheral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic features of this paralysis syndrome, we evaluated acute flaccid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hospitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnormalities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropriate treatment and diagnostic testing.


Muscle & Nerve | 2003

Clinical spectrum of muscle weakness in human west nile virus infection

A. Arturo Leis; Dobrivoje S. Stokic; Risa M. Webb; Sally Slavinski; Jonathan D. Fratkin

Poliomyelitis has recently been identified as a cause of muscle weakness in patients with West Nile virus (WNV) infection. However, the clinical spectrum of WNV‐associated weakness has not been described. We reviewed data on 13 patients with WNV infection. Patients with muscle weakness were classified into one of three distinct groups based on clinical features. Group 1 comprised five patients who developed acute flaccid paralysis, four with meningoencephalitis and one without fever or other signs of infection. Paralysis was asymmetric, and involved from one to four limbs in individual patients. Electrodiagnostic studies confirmed involvement of anterior horn cells or motor axons. Group 2 involved two patients without meningoencephalitis who developed severe but reversible muscle weakness that recovered completely within weeks. Muscle weakness involved both lower limbs in one patient and one upper limb in the other. Group 3 consisted of two patients who experienced subjective weakness and disabling fatigue, but had no objective muscle weakness on examination. In addition to the three distinct groups, two other patients developed exaggerated weakness in the distribution of preexisting lower motor neuron dysfunction. We conclude that the clinical spectrum of WNV‐associated muscle weakness ranges from acute flaccid paralysis, with or without fever or meningoencephalitis, to disabling fatigue. Also, preexisting dysfunction may predispose anterior horn cells to additional injury from WNV. Awareness of this spectrum will help to avoid erroneous diagnoses and inappropriate treatment. Muscle Nerve 28: 302–308, 2003


Obstetrics & Gynecology | 2016

Prolonged Detection of Zika Virus RNA in Pregnant Women.

Dana Meaney-Delman; Titilope Oduyebo; Kara N. D. Polen; Jennifer L. White; Andrea Bingham; Sally Slavinski; Lea Heberlein-larson; Kirsten St. George; Jennifer L. Rakeman; Susan L. Hills; Christine K. Olson; Alys Adamski; Lauren Culver Barlow; Ellen H. Lee; Anna Likos; Jorge L. Muñoz; Emily E. Petersen; Elizabeth Dufort; Amy B. Dean; Margaret M. Cortese; Gilberto A. Santiago; Julu Bhatnagar; Ann M. Powers; Sherif R. Zaki; Lyle R. Petersen; Denise J. Jamieson; Margaret A. Honein

OBJECTIVE: Zika virus infection during pregnancy is a cause of microcephaly and other fetal brain abnormalities. Reports indicate that the duration of detectable viral RNA in serum after symptom onset is brief. In a recent case report involving a severely affected fetus, Zika virus RNA was detected in maternal serum 10 weeks after symptom onset, longer than the duration of RNA detection in serum previously reported. This report summarizes the clinical and laboratory characteristics of pregnant women with prolonged detection of Zika virus RNA in serum that were reported to the U.S. Zika Pregnancy Registry. METHODS: Data were obtained from the U.S. Zika Pregnancy Registry, an enhanced surveillance system of pregnant women with laboratory evidence of confirmed or possible Zika virus infection. For this case series, we defined prolonged detection of Zika virus RNA as Zika virus RNA detection in serum by real-time reverse transcription-polymerase chain reaction (RT-PCR) 14 or more days after symptom onset or, for women not reporting signs or symptoms consistent with Zika virus disease (asymptomatic), 21 or more days after last possible exposure to Zika virus. RESULTS: Prolonged Zika virus RNA detection in serum was identified in four symptomatic pregnant women up to 46 days after symptom onset and in one asymptomatic pregnant woman 53 days postexposure. Among the five pregnancies, one pregnancy had evidence of fetal Zika virus infection confirmed by histopathologic examination of fetal tissue, three pregnancies resulted in live births of apparently healthy neonates with no reported abnormalities, and one pregnancy is ongoing. CONCLUSION: Zika virus RNA was detected in the serum of five pregnant women beyond the previously estimated timeframe. Additional real-time RT-PCR testing of pregnant women might provide more data about prolonged detection of Zika virus RNA and the possible diagnostic, epidemiologic, and clinical implications for pregnant women.


Lancet Infectious Diseases | 2003

West Nile poliomyelitis.

A. Arturo Leis; Jonathan D. Fratkin; Dobrivoje S. Stokic; Theresa Harrington; Risa M. Webb; Sally Slavinski

gen, and alpha fetoprotein, were negative. The x-ray films of the chest and computed tomography scan of the thorax and abdomen were normal. The patient was treated with subcutaneous heparin and diclophenac, and fever and migratory thrombophlebitis subsided. Because the patient had been working with manure several days before his initial symptoms, Q fever serologic testing was requested. The antibody levels measured by complement fixation (CF) against phase II Coxiella burnetii antigen was 1:512. By indirect immunofluorescence, the titers of IgM and IgG against phase I and II were 1:64 and 1:512 and 1:256 and >2,048, respectively. Antibody titers against Mycoplasma, Chlamydia, Legionella, enterovirus, and influenza were negative. Recovery was uneventful and the patient was asymptomatic during a follow-up visit 3 weeks later. Antiphospholipid antibodies were negative. Three months after the acute phase of the infection, new titers of antibodies (CF) against C. burnetii were 1:128. Two years after the episode the patient was asymptomatic. This patient is unique in that he had acute Q fever with migratory thrombophlebitis. A diagnosis of Trousseau’s syndrome associated with an occult malignancy was considered on admission, but it was excluded soon. The recent history of exposure to manure was the key for the clinical diagnosis. Although specific anti-coxiella treatment was not given, the patient followed a self-limited course, and both clinical and laboratory abnormalities promptly subsided. Microscopic vasculitis and thrombosis are commonly found in patients with other rickettsial infections (5), but vascular phenomena must be considered an exceptional event in patients with Q fever. However, thrombophlebitis and pulmonary embolisms have been occasionally reported (6–8). These unusual manifestations have been associated with aPL during the course of acute Q fever (7,8). Antibodies to phospholipids have been found in 80% of patients in a large series of acute Q fever (9). None of the patients in the study showed thrombotic events or cardiac valve involvement in contrast to patients with lupus or primary aPL syndrome in whom clinical manifestations attributed to aPL developed (9). This observation could be explained by the fact that aPL found in patients with lupus and primary aPL syndrome are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation, which has been characterized as a β2-glycoprotein I (apolipoprotein H). This glycoprotein seems to inhibit the activation of the contact phase system of the intrinsic pathway of blood coagulation (10). On the other hand, apolipoprotein H is not necessary for the aPL activity observed in patients with Q fever and other infectious diseases (10). According to these studies, the observation of low titers of aPL in the serum of our patient during the acute phase of Q fever must be seen as a finding of uncertain importance not necessarily associated with migratory thrombophlebitis. In short, migratory thrombophlebitis (Trousseau’s syndrome) should be added to the evergrowing list of unusual manifestations of Q fever.


Javma-journal of The American Veterinary Medical Association | 2008

Compendium of Animal Rabies Prevention and Control, 2016.

Catherine M. Brown; Sally Slavinski; Paul Ettestad; Tom J. Sidwa; Faye E. Sorhage

505 Rabies is a fatal viral zoonosis and serious public health problem.1 All mammals are believed to be susceptible to the disease, and for the purposes of this document, use of the term animal refers to mammals. The disease is an acute, progressive encephalitis caused by viruses in the genus Lyssavirus.2 Rabies virus is the most important lyssavirus globally. In the United States, multiple rabies virus variants are maintained in wild mammalian reservoir populations such as raccoons, skunks, foxes, and bats. Although the United States has been declared free from transmission of canine rabies virus variants, there is always a risk of reintroduction of these variants.3–7 The rabies virus is usually transmitted from animal to animal through bites. The incubation period is highly variable. In domestic animals, it is generally 3 to 12 weeks, but can range from several days to months, rarely exceeding 6 months.8 Rabies is communicable during the period of salivary shedding of rabies virus. Experimental and historic evidence documents that dogs, cats, and ferrets shed the virus for a few days prior to the onset of clinical signs and during illness. Clinical signs of rabies are variable and include inapCompendium of Animal Rabies Prevention and Control, 2016


Emerging Infectious Diseases | 2010

Lymphocytic choriomeningitis virus meningitis, New York, NY, USA, 2009.

Deborah Asnis; Owen Muana; Do Gyun Kim; Minerva Garcia; Pierre E. Rollin; Sally Slavinski

We describe a case of lymphocytic choriomeningitis virus (LCMV) meningitis in a New York, NY, resident who had no apparent risk factors. Clues leading to the diagnosis included aseptic meningitis during winter and the finding of hypoglycorrachia and lymphocytosis in the cerebrospinal fluid. LCMV continues to be an underdiagnosed zoonotic disease.


Emerging Infectious Diseases | 2012

Trap-Vaccinate-Release Program to Control Raccoon Rabies, New York, USA

Sally Slavinski; Lee Humberg; Martin Lowney; Richard Simon; Neil Calvanese; Brooke Bregman; Daniel Kass; William Oleszko

In 2009, an outbreak of raccoon rabies in Central Park in New York City, New York, USA, infected 133 raccoons. Five persons and 2 dogs were exposed but did not become infected. A trap-vaccinate-release program vaccinated ≈500 raccoons and contributed to the end of the epizootic.


Journal of Wildlife Diseases | 2017

HEALTH SURVEY OF FREE-RANGING RACCOONS (PROCYON LOTOR) IN CENTRAL PARK, NEW YORK, NEW YORK, USA: IMPLICATIONS FOR HUMAN AND DOMESTIC ANIMAL HEALTH

Kimberly L. Rainwater; Krysten Marchese; Sally Slavinski; Lee Humberg; Edward J. Dubovi; Jodie A. Jarvis; Denise McAloose; Paul P. Calle

Abstract We conducted health assessments on 113 free-ranging raccoons (Procyon lotor) in Central Park, New York City, US, in February 2010, September 2010, and November 2011 in conjunction with a trap-vaccinate-release program to control a raccoon rabies epizootic. Five individuals were sampled at two time points for 118 raccoon examinations in total. We tested 13 of 13 and 8 of 13 euthanized raccoons for rabies and canine distemper virus (CDV), respectively, by antigen testing on brain tissue; all were negative for both viruses. Endoparasitism was the most common necropsy finding, with definitive identification of Baylisascaris procyonis in six of eight (75%) necropsied raccoons. Multiple intestinal parasites were detected in feces of living raccoons, including ascarid-type ova in 25 of 80 (31%) raccoons, with B. procyonis confirmed in one sample. Median blood lead level was 7.3 μg/dL (n=104). Rabies virus neutralizing antibody titer was ≥0.5 IU/mL in 9 of 88 (10%) raccoons naive to rabies vaccination and in 13 of 20 (65%) previously vaccinated raccoons. The majority of raccoons we tested were seropositive for canine parvovirus-2 (54/59, 92%) and Toxoplasma gondii (39/60, 65%). Fewer were seropositive for Rickettsia rickettsii (3/30, 10%). None were seropositive for CDV (n=108), canine adenovirus-1 (n=60), or Borrelia burgdorferi (n=30). Ectoparasites found during 16 of 118 (13.6%) physical examinations included Ixodes texanus ticks (15/118, 12.7%) and Trichodectes octomaculatus lice (1/118, 0.8%). We detected Campylobacter jejuni in 5 of 79 (6%) fecal samples. We detected 11 Salmonella enterica serotypes in 70 of 111 (63.1%) enteric cultures, the most common of which were Salmonella Newport (20/70, 29%) and Salmonella Oranienburg (20/70, 29%). These results indicate that raccoons in Central Park likely are involved in the environmental occurrence and potential disease transmission of a variety of infectious and noninfectious diseases of concern for human, wildlife, and domestic animal health.

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A. Arturo Leis

University of Mississippi Medical Center

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Lyle R. Petersen

Centers for Disease Control and Prevention

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Risa M. Webb

University of Mississippi Medical Center

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Anne D. Fine

New York City Department of Health and Mental Hygiene

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Ellen H. Lee

New York City Department of Health and Mental Hygiene

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Jennifer L. Rakeman

New York City Department of Health and Mental Hygiene

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Jonathan D. Fratkin

University of Mississippi Medical Center

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Andrea Bingham

Florida Department of Health

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Anthony A. Marfin

Centers for Disease Control and Prevention

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