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New York City reports first cases of West Nile virus

New York City reports first cases of West Nile virus


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The first cases of an encephalitis outbreak are reported in New York City on August 23, 1999. Seven people die from what turns out to be the first cases of West Nile virus in the United States.

A cluster of eight cases of St. Louis encephalitis was diagnosed among patients in the borough of Queens in New York City in August 1999. The sudden cases of critical brain swelling were found exclusively among the elderly. At about the same time, people noticed an inordinate number of dead crows throughout the city. Other birds, including exotic varieties housed at the Bronx Zoo, were also found dead.

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The Center for Disease Control (CDC) was called in to investigate. They found that the West Nile virus, previously found only in Uganda and the Middle East, had been contracted by birds throughout the area, including robins, ducks and eagles. In addition to birds and humans, horses have also been known to be susceptible to the virus, which is spread by mosquitoes.

Upon further investigation, the victims thought to have had St. Louis encephalitis had actually had been infected with West Nile. It causes flu-like symptoms and can be deadly in both the elderly and small children. By the end of the summer, there were 56 confirmed cases of West Nile in New York, though the CDC estimates that 80 percent of people infected with West Nile show no symptoms and therefore would not seek medical help.

In subsequent years, the West Nile virus moved steadily westward across the United States.

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West Nile virus in the United States

The West Nile virus quickly spread across the United States after the first reported cases in Queens, New York in 1999. The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence. The disease spread quickly through infected birds. Mosquitoes spread the disease to mammals. It was mainly noted in horses but also appeared in a number of other species. The first human cases usually followed within three months of the first appearance of infected birds in the area except where cold weather interrupted the mosquito vectors. Since the virus has become widely established in the U.S., an average of 130 deaths a year occurred.

Differences in surveillance and reporting between health departments and generally increased surveillance as the disease spread cause some problems in direct comparison of the number of cases and the mortality rate. The reported number of infected in 2009 was 720, but the estimated total number of infected the same year was 54,000. [2] The true mortality rate is thought to be much lower because most cases are so mild they go undiagnosed. Some estimates put severe cases at only 1% of all cases. It is believed that the elderly or people with weak immune systems are most vulnerable to serious illness or death if bitten by a mosquito infected by West Nile. [3] [ unreliable medical source? ] Most but not all mild cases go undiagnosed. In addition, some more severe but non-neuroinvasive cases are not reported to the CDC. Some mild cases are discovered during blood donation screening. 1,039 West Nile-tainted blood donations were discovered between 2003 and mid-2005. 30 cases of West Nile from blood transfusion were known, the majority from 2002 before blood screening was instituted.

In the first ten years since the virus arrived in the U.S., over 1,100 deaths occurred with human cases reported from every U.S. state except Maine, Alaska and Hawaii. (Animal cases have been occasionally found in Maine and in Puerto Rico.) [4] In 2012, there was a widespread outbreak with the highest death toll and second-highest total case numbers. Maine and Puerto Rico reported one case each, the first time the disease was reported in those places. [5]


The First Case Report of West Nile Virus-Induced Acute Flaccid Quadriplegia in Canada

The 1999 New York City outbreak of West Nile virus (WNV) was associated with a high incidence of West Nile virus neuroinvasive disease (WNVND) where the outcomes for these patients were very poor. We describe a case of West Nile virus neuroinvasive disease (WNVND) characterized by acute flaccid quadriplegia with a favorable outcome in Winnipeg, Manitoba, Canada.

1. Introduction

WNV, a member of the Japanese encephalitis serocomplex belonging to the genus Flavivirus and family Flaviviridae, is transmitted by Culex spp. mosquitoes [1–3]. Up to 20% of WNV-infected persons are symptomatic ranging from mild to severe neuroinvasive diseases. West Nile virus neuroinvasive disease (WNVND) may manifest as meningitis, encephalitis, or acute flaccid paralysis and comprises less than 1% of the total number of cases [4, 5]. Our patient experienced a prolonged hospitalization with acute flaccid quadriplegia before his recovery.

2. The Case

A previously healthy 69-year-old white male from rural Manitoba, Canada, was admitted to hospital through the emergency department on August 1, 2012, with a 3-day history of an upper respiratory illness characterized by nasal discharge, sore throat, chills, and fever. On day 5 of his illness, he began experiencing weakness and paresthesia in both hands and feet and an unsteadiness of gait. He had a past medical history of spinal stenosis associated with chronic back pain, for which he had been prescribed nonsteroidal anti-inflammatory drugs. He denied sustaining any recent mosquito bites or contact with horses or dead birds.

An initial evaluation showed that his vital signs were within normal limits, and he was oriented to time, place, and person. A neurological examination identified no meningismus or cranial nerve deficits. However, he was noted to have symmetrical antigravity (3/5) strength in the upper extremities and reduced resistance (4/5) strength in the lower extremities. Furthermore, he manifested a symmetrical stocking-glove distribution of hypoesthesia in the lower and upper extremities and was symmetrically areflexive in the upper and lower extremities. The rest of the physical examination was normal.

Initial investigations including the complete blood count, erythrocyte sedimentation rate, liver enzymes, bilirubin, and lactate dehydrogenase were normal. The cerebrospinal fluid (CSF) was clear, with a total nucleated cell count of <1 × 10 6 /L (normal 0–5 × 10 6 /L), of which neutrophils constituted 2%, lymphocytes 80%, and monocytes 18%. The CSF protein was elevated (0.79 g/L normal < 0.45 g/L), and the CSF-to-serum glucose ratio was 0.7 (3.5 and 5.0 mmol/L, resp., (normal > 0.6)). The CSF Gram stain demonstrated no bacteria, and bacterial culture of the CSF was sterile. The magnetic resonance imaging of the brain and spinal cord revealed no acute process or abnormality. Retrospectively, repeating magnetic resonance neuroimaging (MRNI) may disclose some changes later in the course of WNVND, however, due to the neurological improvement repeating the MRI neuroimaging was felt to be unnecessary throughout the hospital course neither for diagnostic nor for management purposes.

Based on the clinical findings of ascending flaccid paralysis, a working diagnosis of Guillain–Barré syndrome (GBS) was considered, and the patient was prescribed a five-day course of intravenous immunoglobulin (IVIG) 500 mg/kg/day (40 g/day). The paralysis progressed, requiring intubation and ventilation due to respiratory muscle failure seven days after initial symptoms. A second course of IVIG 500 mg/kg/day (40 g/day) for 5 days was given seven days after the first course was completed.

Diagnostic serology testing for herpes simplex virus, varicella-zoster virus, enteroviruses, neuroborreliosis, and syphilis was negative in the CSF. West Nile virus neuroinvasive disease (WNVND) was suspected by the detection of WNV IgM by the enzyme-linked immunosorbent assay (ELISA) in both CSF and serum specimens and by a plaque reduction neutralization test (PRNT90) serum titre of 40 for the WNV-specific antibody in the acute serum sample. Four weeks later, the WNV PRNT90 of the convalescent serum specimen showed a fourfold rise in the WNV neutralizing titre of 160, confirming West Nile virus neuroinvasive disease (WNVND) [1].

Delayed clinical improvement prompted a biopsy and histopathological examination of the medial antebrachial nerve of the left forearm during the 7th week of illness which demonstrated an inflammatory neuropathy characterized by inflammatory changes in the endoneurium, perineurium, and epineurium. No evidence of vasculitis was observed. Myelin damage and axonal degeneration were also noted. Electron microscopy examination of the neural tissue revealed macrophage-mediated myelin stripping, similar to the process of demyelination observed in the acute inflammatory demyelinating neuropathy (AIDN) and chronic inflammatory demyelinating polyradiculopathy (CIDP) variants of GBS reported in association with a related flavivirus, Zika virus [2]. These findings suggested a probable AIDP triggered by WNV.

On week 8 of hospitalization, the patient began to manifest twitching movements in his deltoid muscles bilaterally. He was extubated on week 10, and by week 13, he was sufficiently stable to be referred to a rehabilitation programme. A neurological examination disclosed symmetrical reduced muscle power (3/5 proximally but 0/5 distally in the upper extremities and 3/5 in the lower extremities), persistent stocking-glove distribution of hypoesthesia in both lower and upper extremities, trace biceps reflexes, and absence of reflexes in the lower extremities. Bilateral lower motor facial nerve (VII) palsy was also noted. His blood pressure was consistently low (80/40 mmHg), without evidence for tissue hypoperfusion, consistent with an autonomic neuropathy further suggesting AIDP. After 4 months of rehabilitation and prior to hospital discharge, his strength testing improved to 5/5 proximally and 4/5 distally in both upper extremities and 4/5 proximally and 3/5 distally in both lower extremities. The patient was able to walk 450 feet (137 m) with a cane and assistance.

3. Discussion

Of the 66 Culex mosquito species known to support the growth of the WNV, only Cx. pipiens, Cx. quinquefasciatus, and Cx. tarsalis are able to act as vectors to transmit the virus to humans. Transmission to humans has also been reported through blood transfusions and organ transplantation and may be transmitted by pregnant women to the fetus or to an infant through breast milk [3, 4].

Acute flaccid quadriplegic paralysis is rare and may occur in 3–19% of those with West Nile virus neuroinvasive disease (WNVND). The syndrome has been more commonly observed in the elderly, patients with chronic renal failure, and patients with diabetes [4]. However, WNVD syndrome’s clinical features may overlap reflecting focal, segmental, or disseminated WNV-driven lesions that have prognostic importance [5].

The CSF profile in neuroinvasive disease may be characterized by a lymphocytic pleocytosis in up to half of the cases, a neutrophil pleocytosis in up to 45% of cases, or a noninflammatory profile in up to 5% of cases of neuroinvasive diseases [6], as was the case in our patient. Moreover, our case had normal MRI neuroimaging. Although the majority (up to 80%) of cases with normal MRI findings may require only short periods of hospitalization (up to 13 days) and have complete recovery [7], our patient required a lengthy seven-month period of hospitalization and was left with residual deficits. Clinical response after IVIG therapy for West Nile virus neuroinvasive disease (WNVND) may require four to eight weeks. The prolonged time-to-improvement in our patient’s case may have been a function of the degree of virus-mediated inflammatory neurological damage sustained prior to the administration of IVIG. Alternatively, a patient manifesting GBS due to West Nile virus neuroinvasive disease (WNVND) may require increased or multiple doses of IVIG to increase the level of IgG effectively to dampen the autoimmune and autoinflammatory response [8].

Between 2002 and 2017, the total number of reported Canadian WNVD cases was 5603. Non-neuroinvasive, neuroinvasive, and unclassified WNVD cases comprised 22.6%, 72.4%, and 5.1%, respectively (Table 1). The case fatality rate was 1.2% (Table 1) [8]. In 2003, the highest seroprevalence proportion of WNVD cases in North America (17%) was reported in the Canadian province of Saskatchewan where 937 cases of WNV were reported with an attack rate of 93/100,000 compared to 1.2/100,000 in Manitoba [9, 10]. Similarly, in the United States, the highest incidence was seen in North Dakota (neighboring Manitoba) (8.9/100,000), South Dakota (6.8/100,000), Nebraska (2.9/100,000), and Wyoming (2.8/100,000) [11]. The Culex spp. mosquito vector of WNV is endemic in the midwest United States and in the Canadian Prairie provinces, which correlates with the higher attack rates in these regions (Table 1) [10].

By the end of 2017, Ontario, Quebec, Manitoba, and Saskatchewan accounted for a total of 81.3% of West Nile virus neuroinvasive disease (WNVND) and 81.9% of West Nile virus non-neuroinvasive disease (WNVNND) cases in Canada, respectively (Table 1) [8].

The first case of WNV was documented in Uganda in 1937, and the first case report of West Nile virus neuroinvasive disease (WNVND) was traced to an outbreak in Israel in 1951 [4]. Five decades later, the appearance of a first outbreak of WNV infection in the western hemisphere occurred in New York City during the summer of 1999 when sixty-two cases were reported, including 7 deaths and 59 cases of West Nile virus neuroinvasive disease (WNVND) due to the WNV genotype New York 99 (NY99) [4]. In 2002, an invasive WNV genotype, WNO2, replaced NY99 and may have contributed to the spread of West Nile virus disease (WNVD) cases across North America and to subsequent outbreaks in 2002-2003 and other years, where our patient was diagnosed, with West Nile virus inducing an acute flaccid quadriplegia, as a first case in Manitoba, Canada however, the genotyping was not done [12].

West Nile virus is the most common arboviral disease that causes 95% of West Nile virus neuroinvasive diseases (WNVNDs) the incidence is 0.41 in 100,000 and the case fatality rate is up to 9% between 1999 and 2017 in the United States of America [5, 13, 14].

West Nile virus disease (WNVD) is known to be symptomatic in minority of cases up to 20%, where these cases present in a form of febrile illness called West Nile fever (WNF) that may mimic flu-like symptoms. About 1% of these cases developed West Nile virus neuroinvasive disease (WNVND), which carry various ranges of outcomes including complete recovery and various minor or major residual neurological defects or mortality. The long-term outcomes are not always directly correlated with the severity of WNVND at the presentation [5, 13, 15].

In the absence of vaccine or proven therapy for West Nile virus diseases (WNVDs) to date, WNVND treatment remains supportive. The polyclonal intravenous immunoglobulin (IVIG), interferons, ribavirin, and steroids have been tried without proven benefit [13, 16, 17]. WNVND clinical syndromes are associated with various degrees of natural variability in recoveries where treatments’ response and outcomes need to be evaluated and interpreted cautiously. Intravenous immunoglobulin (IVIG) demonstrates association with good outcome in immunocompromised and old individuals with WNVND in case reports [16, 17]. Similarly, the recovery of our patient was our experience where IVIG was introduced at the early stage of the disease as described.

4. Conclusion

This case represents, to our knowledge, the first description of life-threatening acute flaccid quadriplegia due to WNV in this region of Canada. The patient’s incomplete recovery from the WNV-mediated Guillain–Barré Syndrome (GBS) required a lengthy period of hospitalization and rehabilitation. He was treated with two doses of IVIG consistent with recommendations [15]. This case illustrates that a compatible clinical syndrome and seasonal context for West Nile virus neuroinvasive diseases (WNVNDs) should prompt testing for the presence of WNV IgM in serum and CSF.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

Acknowledgments

The authors wish to acknowledge Dr. Hui Zheng, Public Health Agency of Canada, for his valuable assistance in providing additional Canadian West Nile virus cases and epidemiological data described in this report.

References

  1. Centers for Disease Control and Prevention, National Notifiable Disease Surveillance System (NNDSS). Arboviral Diseases, Neuroinvasive and Non-Neuroinvasive 2015 Case Definition, 2015, https://wwwn.cdc.gov/nndss/conditions/arboviral-diseases-neuroinvasive-and-non-neuroinvasive/case-definition/2015.
  2. V. M. Cao-Lormeau, A. Blake, S. Mons et al., “Guillain-Barré syndrome outbreak caused by Zika virus infection in French Polynesia,” The Lancet, vol. 387, no. 10027, pp. 1531–1539, 2016. View at: Publisher Site | Google Scholar
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  7. M. Ali, Y. Safriel, J. Sohi et al., “West Nile virus infection: MR imaging findings in the nervous system,” American Journal of Neuroradiology, vol. 26, no. 2, pp. 289–297, 2005. View at: Google Scholar .
  8. H. Zheng, M. A. Drebot, and M. B. Coulthart, “West Nile virus in Canada: ever-changing, but here to stay,” Canada Communicable Disease Report, vol. 40, no. 10, pp. 173–177, 2014. View at: Google Scholar
  9. T. L. Schellenberg, M. F. Anderson, M. A. Drebot et al., “Seroprevalence of West Nile virus in Saskatchewan’s Five Hills Health Region, 2003,” Canadian Journal of Public Health, vol. 97, pp. 369–373, 2006. View at: Google Scholar
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Copyright

Copyright © 2018 Yahya Salim Yahya Al-Fifi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Results

For the 2 Long Island counties with human cases of WNV disease in 2001, weekly DCD Ϡ.1 were seen more than 1 month before onset of human cases ( Figure 2 ). DCD increased before the first WNV-positive bird was reported (1𠄳 weeks after it was found). However, the highest peaks in weekly DCD occurred after viral activity was confirmed and may have been influenced by increased interest in reporting dead crows after the media had reported WNV in the area. For other New York counties, weekly DCD remained lower (π.1), and no human cases were detected.

Dead crow densities (DCD, dead crows per square mile) and number of cases of human West Nile virus (WNV) disease, by week, 2001. Horizontal dashed line indicates DCD = 0.1. F, date that the first bird with confirmed WNV infection was found R, date that the laboratory result of the first bird with WNV infection was reported.

In 2002, Long Island (Nassau and Suffolk counties) had the most human cases ( Figure 3 ). However, almost as many human cases were reported for Erie and Broome counties further north. Eight other counties reported 1𠄴 cases. In general, DCD Ϡ.1 occurred several weeks before the onset week of the first human case in most counties, with the peak density around the period of the human case onset, except in sparsely populated rural counties (Clinton, Orleans, Wayne, and Yates), which reported 1 human case each. Suffolk County is notable for its relatively lower weekly DCD. Two counties had DCD Ϡ.1 without human cases. The first WNV-positive bird of the season was typically reported 1𠄴 weeks after the bird was found. Sharp increases in DCD immediately after the report of the first WNV-positive bird were not generally noted in 2002.

Dead crow densities (DCD, dead crows per square mile) and number of cases of human West Nile virus (WNV) disease, by week, 2002. Horizontal dashed line indicates DCD = 0.1. F, date that the first bird with confirmed WNV infection was found R, date that the laboratory result of the first bird with WNV infection was reported.

A similar pattern was seen in 2003, with Long Island (Nassau and Suffolk counties) again leading the number of human cases ( Figure 4 ). All 3 counties with ϡ human case had DCD Ϡ.1 in the week of, or the weeks before, the first human case onset. A similar pattern was seen for Monroe County with 1 human case. Onondaga County, with 1 human case, had a weekly DCD Ϡ.1 after the human case onset. The DCD approached 0.1 in Dutchess County 2 weeks before the week of the human case onset. The DCD remained low in the sparsely populated counties (Cattaraugus, Schuyler, Warren, and Yates) with 1 human case. Two counties had DCD Ϡ.1 without human cases. In 2003, laboratory confirmation of viral activity in a dead bird was available 1𠄲 weeks after the bird was found. DCD increases after those reports were observed for some, but not all, counties.

Dead crow densities (DCD, dead crows per square mile) and number of cases of human West Nile virus (WNV) disease, by week, 2003. Horizontal dashed line indicates DCD = 0.1. F, date that the first bird with confirmed WNV infection was found R, date that the laboratory result of the first bird with WNV infection was reported.

For each year and for the 3 years combined, the CMH pooled estimate of risk for WNV disease among residents of counties with DCD Ϡ.1 was Ϣ times the risk among residents of counties with DCD π.1 ( Table 2 ). Relative risks were highest in 2001 residents of counties with elevated DCD had 7.6𠄸.6 times the risk of contracting WNV disease than residents of counties with lower DCD. Relative risks were lower in 2002 (2.0𠄲.3) but increased in 2003 (5.3𠄶.5). During the 3-year period, residents of counties with elevated DCD had 3.4𠄳.8 times the risk of contracting WNV disease within the next 2 weeks than residents of counties reporting fewer dead crows per square mile.

Table 2

Counties with elevated DCD†2001 RR (95% CI)2002 RR (95% CI)2003 RR (95% CI)2001� RR (95% CI)
2 weeks before onset8.6 (1.8�.8)2.2 (1.1𠄴.6)5.4 (2.1�)3.5 (2.0𠄶.0)
1 or 2 weeks before onset7.9 (2.9�.1)2.3 (1.1𠄴.8)6.5 (2.6�.3)3.8 (2.2𠄶.6)
0, 1, or 2 weeks before onset7.6 (1.6�.8)2.0 (0.95𠄴.4)5.3 (2.2�.8)3.4 (1.9𠄵.9)

*Versus residents of counties without elevated DCD in the previous 2 weeks risk is calculated for exposure to elevated DCD only 2 weeks before, 1 or 2 weeks before, and during the same week or 1 or 2 weeks before week of onset. SAS provides risk estimates by 2 methods because zero values occur in 2൲ tables for some weeks, we report results by the adjusted logit method, which uses a 0.5 correction for zero-value cells. RR, relative risk CI, confidence interval.
†Weekly DCD Ϡ.1.


Most Read

The city has done nine rounds of pesticide spraying and seven aerial larvicide treatments to go after mosquitos this season. While the focus has been on preventing the Zika virus, the anti-mosquito tactics also reduce the risk of West Nile.

Zika has not been found in any mosquitos in New York.

Some 318 New Yorkers have been diagnosed with West Nile virus since it was first found in the United States in 1999.

People over 60 are particularly at risk for the virus, which causes flu-like symptoms or no symptoms at all in most people but can lead to a serious and sometimes fatal infection of the brain and spinal cord.

"Wearing mosquito repellent when you are outdoors, getting rid of standing water, and installing window screens will reduce your risk of getting bitten. New Yorkers age 60 and older or people with weakened immune systems should be especially careful as they are more likely to become seriously ill, and in rare cases die, if infected," Bassett said.


WN virus is maintained in nature in a mosquito-bird-mosquito transmission cycle. Mosquitoes of the genus Culex are generally considered the principal vectors of WNV, in particular Cx. Pipiens. WNV is maintained in mosquito populations through vertical transmission (adults to eggs).

Birds are the reservoir hosts of WNV. In Europe, Africa, Middle East and Asia, mortality in birds associated with WNV infection is rare. In striking contrast, the virus is highly pathogenic for birds in the Americas. Members of the crow family (Corvidae) are particularly susceptible, but virus has been detected in dead and dying birds of more than 250 species. Birds can be infected by a variety of routes other than mosquito bites, and different species may have different potential for maintaining the transmission cycle.

Horses, just like humans, are &ldquodead-end&rdquo hosts, meaning that while they become infected, they do not spread the infection. Symptomatic infections in horses are also rare and generally mild, but can cause neurologic disease, including fatal encephalomyelitis.


West Nile virus: Uganda, 1937, to New York City, 1999

West Nile virus, first isolated in 1937, is among the earliest arthropod-borne viruses discovered by humans. Its broad geographical distribution, not uncommon infection of humans, transmission by mosquitoes, and association with wild birds as enzootic hosts were well documented by the mid-1960s. However, West Nile virus was not considered to be a significant human pathogen because most infections appeared to result in asymptomatic or only mild febrile disease. Several epidemics had been documented prior to 1996, some involving hundreds to thousands of cases in mostly rural populations, but only a few cases of severe neurological disease had been reported. The occurrence between 1996 and 1999 of three major epidemics, in southern Romania, the Volga delta in southern Russia, and the northeastern United States, involving hundreds of cases of severe neurological disease and fatal infections was totally unexpected. These were the first epidemics reported in large urban populations. A significant factor that appeared in common to all three outbreaks was the apparent involvement of the common house mosquito, Culex pipiens, as a vector. This species had not previously been implicated as important in the transmission of West Nile virus. In addition the epidemic in the northeastern United States was unusual in the association of West Nile virus infection with fatal disease of birds, suggesting a change in the virulence of the virus toward this host. Understanding the risk factors that contributed to these three urban epidemics is important for minimizing the potential for future occurrences. This review will attempt to compare observations on the biology of West Nile virus made over about 60 years prior to the recent epidemics to observations made in association with these urban epidemics.


Epidemic West Nile encephalitis, New York, 1999: results of a household-based seroepidemiological survey

Background: In the summer of 1999, West Nile virus was recognised in the western hemisphere for the first time when it caused an epidemic of encephalitis and meningitis in the metropolitan area of New York City, NY, USA. Intensive hospital-based surveillance identified 59 cases, including seven deaths in the region. We did a household-based seroepidemiological survey to assess more clearly the public-health impact of the epidemic, its range of illness, and risk factors associated with infection.

Methods: We used cluster sampling to select a representative sample of households in an area of about 7.3 km(2) at the outbreak epicentre. All individuals aged 5 years or older were eligible for interviews and phlebotomy. Serum samples were tested for IgM and IgG antibodies specific for West Nile virus.

Findings: 677 individuals from 459 households participated. 19 were seropositive (weighted seroprevalence 2.6% [95% CI 1.2-4.1). Six (32%) of the seropositive individuals reported a recent febrile illness compared with 70 of 648 (11%) seronegative participants (difference 21% [0-47]). A febrile syndrome with fatigue, headache, myalgia, and arthralgia was highly associated with seropositivity (prevalence ratio 7.4 [1.5-36.6]). By extrapolation from the 59 diagnosed meningoencephalitis cases, we conservatively estimated that the New York outbreak consisted of 8200 (range 3500-13000) West Nile viral infections, including about 1700 febrile infections.

Interpretation: During the 1999 West Nile virus outbreak, thousands of symptomless and symptomatic West Nile viral infections probably occurred, with fewer than 1% resulting in severe neurological disease.


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Case Reports

Patient 1. On 12 August 1999, a 60-year-old man was admitted to the hospital with complaints of fever, weakness, and nausea for 3 days. Physical examination revealed a well-tanned man with a maximum temperature of 39.7°C but with no other remarkable symptoms. A chest radiograph suggested bibasilar infiltrates and the patient was placed on iv erythromycin and ceftriaxone. On day 4, he was found to be confused, with proximal muscle weakness, decreased deep tendon reflexes, and respiratory difficulty. There also was urinary retention. He was placed on bilevel positive airway pressure ventilatory assistance. A lumbar puncture (LP) and CT scan of the head were done ( table 1). The medications were changed to iv ceftriaxone and acyclovir. Electromyogram/nerve conduction velocities studies (EMG/NCV) showed axonal type polyneuropathy. Guillain-Barre syndrome (GBS) was thought to be a possible diagnosis, so plasmapheresis was initiated. Over the next several weeks, his muscle weakness and mentation improved. Bladder catheterization, however, was still required. He was subsequently transferred to another institution for rehabilitation for 1 month. Five months after his primary infection, he walks with a quad cane, has left side weakness, and has episodes of recent memory loss.

CSF and CT head scan findings for 8 patients in New York City with West Nile virus.

CSF and CT head scan findings for 8 patients in New York City with West Nile virus.

Patient 2. On 15 August, an 80-year-old man with a history of mild congestive heart failure was admitted with complaints of fever, headache, weakness, and diarrhea for 1 week. On the day of admission, his wife found him unresponsive, and paramedics were called. After tracheal intubation, he developed ventricular tachycardia and asystole. He was successfully resuscitated. At the hospital, his temperature was 40°C, and his exam revealed a sun-tanned, well-built man without any abnormalities except that he was obtunded and on a ventilator. He was given iv ceftriaxone and clindamycin for possible aspiration pneumonia. A head CT and LP were performed ( table 1). Medical complications that developed included an anterior wall myocardial infarction requiring dobutamine, hypotension requiring vasopressor agents (dopamine and norepinephrine), ischemic hepatopathy, renal insufficiency, and disseminated intravascular coagulation. On day 3, the amylase was 672 IU/L. Over the next few days he became flaccid an EMG/NCV showed motor axonopathy without sensory involvement. After 3 weeks, life support was removed, and the patient died. Autopsy revealed encephalitis. Microscopic exam showed microglial nodules scattered in the gray and white matter of the cerebrum. Scanty mononuclear inflammatory infiltrate was present in the leptomeninges. The general autopsy was limited at the family's request and revealed only hemorrhagic pancreatitis.

Patient 3. On 18 August, a 75-year-old man with a history of prostate cancer presented with a sudden change in mental status, fever, and urinary incontinence. On admission, his temperature was 39.5°C. Neurologically he was oriented to person and place, with neck rigidity and diffuse tremors in both upper and lower extremities. Deep tendon reflexes were brisk. A CT scan of the head and LP were performed ( table 1). He was placed on iv ampicillin, ceftriaxone, and acyclovir. On day 2, he required mechanical ventilation. Subsequently he developed diffuse muscle weakness and decreased deep tendon reflexes. EMG/NCV showed diffuse polyneuropathy with axonal involvement. After 3 weeks, he died. Autopsy revealed encephalitis. On microscopic sections, microglial nodules were present in the medulla, cere-bellum, and thalamus. Rare lesions were also present in the cerebrum, particularly the hippocampus. Perivascular inflammation was seen in the medulla. There was no leptomeningeal inflammation. In some cranial nerve roots of the medulla, there was focal mononuclear inflammation. The remainder of the autopsy showed no histologic evidence of pancreatitis, myocarditis, or hepatitis.

Patient 4. On 20 August, an 87-year-old woman with a history of breast and colon cancer was admitted with complaints of 1 week of headache, loose stools, fever, and weakness. In the hospital, she appeared dehydrated but alert, with a normal physical exam except for some mild dysarthria. On day 6 the patient became obtunded, with diffuse muscle weakness, and was intubated. Her temperature rose to 38.7°C. Her presumed diagnosis was GBS, and she underwent plasmapheresis. An LP was done ( table 1), and she was started on iv ceftriaxone and acyclovir. An EMG/NCV showed diffuse motor axonal polyneuropathy without sensory involvement. On day 10, she died. Autopsy revealed encephalitis with microglial nodules in the gray and white matter ( figure 1A, 1B). Mononuclear perivascular inflammation was also evident. The medulla and the thalamus were most severely involved. The remainder of the autopsy showed no histologic evidence of pancreatitis, myocarditis, or hepatitis.

A, Hematoxylin and eosin-stained section of the medulla from patient 4. In the white matter adjacent to the olivary nucleus, note the microglial nodule (arrowhead) composed of histiocytes and occasional lymphocytes (original magnification, ×100). B, Microglial nodule (original magnification, ×200).

A, Hematoxylin and eosin-stained section of the medulla from patient 4. In the white matter adjacent to the olivary nucleus, note the microglial nodule (arrowhead) composed of histiocytes and occasional lymphocytes (original magnification, ×100). B, Microglial nodule (original magnification, ×200).

Patient 5. On 27 August, a 57-year-old man with a history of alcohol abuse was admitted with complaints of fever, vomiting, and confusion for 3 days. In the hospital, his temperature was 39°C, and examination revealed a combative man who was confused. A CT scan of the head and LP were performed ( table 1). He was given iv ampicillin, ceftriaxone, and acyclovir. He improved and was discharged after 2 weeks without any sequelae.

Patient 6. On 23 August, a 79-year-old man presented with complaints of generalized weakness, anorexia, and confusion for 3 days. On admission, his temperature was 39.2°C, and the examination was normal except for mild muscle weakness and confusion. An LP and CT scan of the head were performed ( table 1). He was started on iv ampicillin and ceftriaxone until the CSF culture was negative. He improved and was discharged to home within 11 days.

Patient 7. On 31 August, a 29-year-old woman presented with fever, headache, rash, nausea, vomiting, diarrhea, and weakness that started 8 days earlier. In the hospital, her temperature was 39°C, and the rest of her exam was normal except for a stiff neck and a few macular lesions on her back. The rash started on her limbs 6 days before and then spread to her trunk and back. An LP was done ( table 1). She was given iv ceftiaxone until CSF culture was negative. She was discharged to home after 5 days with mild weakness and memory loss that resolved after 3 months.

Patient 8. On 2 September, a 49-year-old man presented with a 4-day history of fever, headache, anorexia, arthralgias, weakness, and a questionable rash on his legs and arms. On admission, his temperature was 39°C, and his physical exam was normal. An LP was done ( table 1). He was started on iv ceftriaxone. He was discharged after a week and resumed work but still felt weak for ∼2 weeks.


New York State Department of Health Reminds New Yorkers to Protect Against Mosquitoes and Ticks During Outdoor Activities

ALBANY, N.Y. (June 9, 2021) &ndash The New York State Department of Health today reminded New Yorkers to take precautions to protect against diseases that are transmitted by mosquitoes and ticks, now that warm weather has arrived and people are spending more time outdoors.

"As we continue our efforts to defeat COVID-19 and return to normal, including returning to the activities we love, we encourage all New Yorkers to enjoy the outdoors while also taking the proper steps to protect themselves from mosquitos and ticks to avoid potential illness," New York State Health Commissioner Dr. Howard Zucker said."As infected mosquitoes and ticks can be found in outdoor areas across the state, prevention remains the most effective method to protect yourself and others from exposure to mosquitoes and ticks that can transmit diseases like West Nile virus, eastern equine encephalitis virus or Lyme disease."

WEST NILE VIRUS

West Nile virus (WNV), an infection that can cause serious illness and, in some cases, death, is transmitted to humans and some animals through the bite of an infected mosquito. Not all mosquitoes carry WNV, which was first identified in New York State in 1999. Since 2000, approximately 900 human cases of WNV and 100 deaths have been reported statewide.

Most people infected with WNV do not develop any signs or symptoms. If illness develops, symptoms usually occur 3-15 days after the bite from an infected mosquito. People with mild cases of mosquito-borne disease may develop fever, headache, body aches and occasionally a skin rash or swollen glands. People with severe cases of WNV usually have a sudden onset of headache, high fever, neck stiffness, muscle weakness, altered mental status, tremors, convulsions, paralysis, inflammation of the brain or the membranes of the brain and spinal cord or coma.

The following precautions are highly recommended to reduce risk of infection from mosquito-borne diseases including West Nile virus:

  • Cover your skin as completely as possible when outside when mosquitoes are present and active. Wear long sleeves, pants and socks.
  • Use insect repellent on exposed skin and follow label directions. Repellents that include DEET, picaridin, or oil of lemon eucalyptus are recommended.
  • Make sure there are screens in your home's windows and doors. Make sure the screens are free of rips, tears and holes.
  • Eliminate all standing water in yards and around your home and property where mosquitoes can breed, including: plastic containers, pool covers, wading pools, ceramic pots, clogged drainpipes, and wheelbarrows. Also change water in bird baths twice a week.

LYME AND OTHER TICK-BORNE DISEASES

Tick bites can transmit several diseases including Lyme disease, which is the most-commonly reported tick-borne disease in New York State. Over the last 10 years, NYS has averaged more than 7,500 new cases each year. Lyme disease is a bacterial infection that spreads when an infected black-legged tick &ndash commonly called a deer tick, which is the most common tick in New York &ndash bites a person and remains attached for 36 hours or more. In most cases, an expanding rash resembling a bull's eye or solid patch will appear near the site of the bite. If an expanding rash with a diameter of more than two inches appears or flu-like symptoms occur over a 30-day period following a tick bite, individuals should contact their health care provider immediately.

Some of the less common tick-borne diseases include babesiosis and anaplasmosis, averaging 483 and 613 cases annually since 2010, respectively. Other diseases are rare, such as Rocky Mountain Spotted Fever, averaging 33 cases annually since 2010 and Powassan encephalitis, totaling 31 cases since 2010. While these diseases vary in their severity, all can cause serious illness and even death, if untreated.

In 2018, the Asian longhorned tick was identified in New York State for the first time and has now been found in several locations in New York City, Long Island and the Lower Hudson Valley. While this tick has transmitted disease to humans in other parts of the world, more research is needed to determine whether this can occur in the United States. To date, the Department has tested more than 1,500 of these ticks and has not found disease-causing agents. Regardless, New Yorkers should continue to take measures to protect themselves, their children and their pets against all ticks and tick-borne diseases that are present in New York State. In addition, the longhorned tick is also a concern for New York's agricultural industry and may pose a threat to livestock.

The Department of Health and its partners routinely collect and analyze ticks from across the state to better understand the tick population, tick behavior and regional trends in diseases carried by ticks. Current and retrospective tick collection and testing results are publicly available on the Department's Health Data NY website.

While hiking, working, or spending time in wooded areas, follow these simple steps to help prevent tick bites:



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