Search

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.

Human Brucella canis infection incidence is unknown. Most identified cases are associated with pet dogs. Laboratory-acquired infections can occur following contact with Brucella spp. We identified a paediatric B. canis case, the source and other exposed persons. A 3-year-old New York City child with fever and dyspnoea was hospitalized for 48 h for bronchiolitis. After her admission, blood culture grew B. canis, she was prescribed anti-microbials and recovered. B. canis was also isolated from blood of the child's pet dog; these isolates were genetically similar. The dog originated from an Iowa breeding facility which was quarantined after identification of the dog's infection. Additionally, 31 laboratory workers were exposed and subsequently monitored for symptoms; 15 completed post-exposure prophylaxis. To our knowledge, this is the first report strongly suggesting B. canis zoonotic transmission to a child in the United States, and highlights the need for coordinated control policies to minimize human illness., (© 2014 Blackwell Verlag GmbH.)

Animal bites continue to pose major public health challenges, and the clinical sequelae of bite injuries can extend far beyond simple wound management. Identification of people bitten by animals remains incomplete, and inconsistencies in data collection preclude meaningful conclusions about bite circumstances and predisposition of specific breeds of dogs to bite or inflict severe bites.

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.

Context: During the 1999 New York City West Nile virus (WNV) outbreak, 4 patients with profound muscle weakness, attributed to Guillain-Barré syndrome, were autopsied. These cases were the first deaths caused by WNV, a flavivirus, to be reported in the United States. The patients' brains had signs of mild viral encephalitis; spinal cords were not examined. During the 2002 national epidemic, several patients in Mississippi had acute flaccid paralysis. Electrophysiologic studies localized the lesions to the anterior horn cells in the spinal gray matter. Four of 193 infected patients in Mississippi died and were autopsied. All 4 experienced muscular weakness and respiratory failure that required intubation. Postmortem examinations focused on the spinal cord., Objective: To emphasize apparent tropism of WNV for the ventral gray matter of the spinal cord., Design: Cerebral hemispheres, basal ganglia, diencephalon, brainstem, cerebellum, and spinal cord sections were stained with hematoxylin-eosin and incubated with antibodies to T cells, B cells, and macrophages/microglial cells., Results: We identified neuronophagia, neuronal disappearance, perivascular chronic inflammation, and microglial proliferation in the ventral horns of the spinal cord, especially in the cervical and lumbar segments. Loss of ganglionic neurons, nodules of Nageotte, and perivascular lymphocyte aggregates were found in dorsal root and sympathetic ganglia. Severity of cellular reaction was proportional to the interval length between patient presentation and death., Conclusion: West Nile virus caused poliomyelitis. Injury to spinal and sympathetic ganglia mirrored the damage to the spinal gray matter. The disappearance of sympathetic neurons could lead to the autonomic instability observed in some WNV patients, including labile vital signs, hypotension, and potentially lethal cardiac arrhythmias.

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.

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.