Catherine M. Brown

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

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.

Compendium of Animal Rabies Prevention and Control, 2011

the disease, and for purposes of this document, use of the term animal refers to mammals. The disease is an acute, progressive encephalitis caused by a lyssavirus. 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. 2–6 The 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. 7 Rabies is communicable during the period of salivary shedding of rabies virus. Experimental and historic evidence document that dogs, cats, and ferrets shed virus a few days prior to clinical onset and during illness. Clinical signs of rabies are variable and include inappetence, dysphagia, cranial nerve deficits, abnormal behavior, ataxia, paralysis, altered vocalization, and seizures. Progression to death is rapid. There are currently no known effective rabies antiviral drugs.

Evidence for a 4-dose vaccine schedule for human rabies post-exposure prophylaxis in previously non-vaccinated individuals

After exposure, human rabies is preventable by prompt application of post-exposure prophylaxis. Historically, the total number of rabies vaccine doses administered during human prophylaxis has decreased, as modern biologics have improved and scientific knowledge has grown. A review of the literature on rabies virus pathogenesis, experimental animal studies, clinical trials, epidemiological surveillance, and economic analyses was conducted to determine the potential utility of reducing the current 5-dose intramuscular series of human rabies vaccine administered in the United States. Based upon the available evidence, a reduced schedule of cell-culture rabies vaccine, administered on days 0, 3, 7, and 14, given in conjunction with rabies immune globulin, was supported and recommended by the United States Advisory Committee on Immunization Practices.

Compendium of Animal Rabies Prevention and Control, 2016.

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

Phylogenetic and epidemiologic evidence of multiyear incubation in human rabies

Eight years after emigrating from Brazil, an otherwise healthy man developed rabies. An exposure prior to immigration was reported. Genetic analysis revealed a canine rabies virus variant found only in the patients home country, and the patient had not traveled internationally since immigrating to the United States. We describe how epidemiological, phylogenetic, and viral sequencing data provided confirmation that rabies encephalomyelitis may present after a long, multiyear incubation period, a consideration that previously has been hypothesized without the ability to exclude a more recent exposure. Accordingly, rabies should be considered in the diagnosis of any acute encephalitis, myelitis, or encephalomyelitis. ANN NEUROL 2014;75:155–160

Brill-Zinsser Disease in a Patient Following Infection with Sylvatic Epidemic Typhus Associated with Flying Squirrels

Recrudescent Rickettsia prowazekii infection, also known as Brill-Zinsser disease, can manifest decades after untreated primary infection but is rare in contemporary settings. We report the first known case of Brill-Zinsser disease in a patient originally infected with a zoonotic strain of R. prowazekii acquired from flying squirrels.