Infectious Disease Case Study Assignment
Retesting of clinically ill human cases and testing of horses p resenting with CANS disease In Long Island, NY revealed WAN as the cause of disease (Canals, Con eat, Etcetera, Walden, Sampson, 2000) . A total of 62 human cases of WAN were identified d during this outbreak, Including seven deaths. By extrapolation from a household based study It was estimated that the NYC WAN outbreak in 1999 caused around 8 200 asymptomatic info sections, causing disease in approximately 1 700 individuals.
This was the first evidence of WAN V activity In the Western Hemisphere (CDC, 1999).
During the first years of circulation In North America, WAN persistence over the winter r months was attributed to continued transmission during winter, overwriting of the virus in mosquitoes and vertical WAN transmission from Infected females to their offspring (Risen, Fang. Lothrop, Martinez, Wilson, O’Connor, 2006). WAN infection of migratory birds was suggested to contribute to the fast dissemination of WAN In North and South America. Nevertheless s. WAN amplified and extended its distribution across the lower 48 continental states and ha been declared endemic within 10 years of its introduction (Bernard, Kramer, 2001).
West Nile Virus is a concern because in the most rare and extreme cases It can cause a condition called encephalitis, which is irritation and swelling of the brain. 2. Season’s physician ordered serological tests. Describe how antibody titers would Help t he doctor in confirming her diagnosis. Serology Is ten study AT Immune Doodles In unman 01000. I nose Immune oodles are t he product of the defense mechanisms against disease causing organisms in the body.
The principle involved with serology is the antibody antigen response. The antigen actually comes first, in that the antigen is the substance e which “provokes” the body to produce antibodies.
The CDC has established multiple serological, Appeased, and viral isolation criteria for confirmation of West Nile virus infection (CDC, 2001): Criteria for Confirmation of West Nile Virus Infection > Isolation of West Nile virus from tissue, blood, SF, or other body fluid, or demonstrate action of West Nile viral antigen or genomic sequences > IGMP antibody to West Nile virus in SF as detected by MANACLES > At least a fourfold serial change in plaque deduction neutralizing antibody titer to West Nile virus in paired, appropriately timed (I. . , at least 14 days apart) serum or SF samples > West Nile virus-specific IGMP (by MAC ELISE) and Gig antibody (screened by ELISE and confirmed by plaque reduction neutralizing tests) in a single serum specimen 3. When Jason was feeling at his worst, he had extreme malaise, vomiting, and diarrhea.
What stage of the illness was he experiencing at that time? Explain the physiologic mechanic SMS that give rise to the signs and symptoms of infectious illness.
The incubation period for WAN disease is typically 2 to 6 days but ranges from 2 to 14 days and can be several weeks in miscomprehended people. An estimated 7080% of human WAN infections are substantial or asymptomatic. Most symptomatic persons such as Jason experience an acute systemic febrile illness that often includes headache, weakness, malign, or arthritis; gastrointestinal symptoms and a transient macromolecular rash (CDC, 2015). 4. West Nile virus has a single stranded RNA genome.
Explain how this virus is able to replicate.
West Nile virus (WNV) is a mosquito-borne flavivirus that was first identified in the West Nile subregion of Uganda in 1937 (Rosen, 2000). Since being introduced into the United States in 1999, WNV has caused significant outbreaks of neurological disease across North America (Petersen & Marfin, 2002). This paper will examine several case studies of WNV infection identified during outbreaks in New York in 1999 and subsequent years to illustrate the epidemiology, clinical presentation, diagnosis, and management of this emerging infectious disease.
Outbreak in New York, 1999
The initial WNV outbreak in the United States began in New York City in 1999. Retesting of clinically ill human cases and testing of horses presenting with encephalitis in Long Island, NY revealed WNV as the cause of disease (Canals et al., 2000). A total of 62 human cases of WNV were identified during this outbreak, including seven deaths. Household-based studies estimated that the 1999 NYC WNV outbreak caused around 8,200 asymptomatic infections, resulting in clinical illness in approximately 1,700 individuals (CDC, 1999). This provided the first evidence of WNV activity in the Western Hemisphere.
The outbreak highlighted several important aspects of WNV epidemiology. Serosurveys found high rates of asymptomatic WNV infection, with an estimated 1 in 150 people in parts of Queens testing positive for WNV antibodies in late summer/fall of 1999 despite having no recollection of past illness (CDC, 1999). This demonstrated the potential for large outbreaks driven by asymptomatic transmission. The identification of WNV in migratory birds also suggested that bird migration patterns may have contributed to the rapid spread of WNV across North and South America within 10 years of its introduction (Bernard & Kramer, 2001).
Clinical Presentation and Diagnosis
The incubation period for WNV disease is typically 2 to 6 days but can range from 2 to 14 days, and occasionally be longer in immunocompromised persons (CDC, 2015). An estimated 70-80% of human WNV infections are asymptomatic. Symptomatic illness most commonly manifests as a self-limited febrile illness, often including headache, myalgia, malaise, or rash. A subset of infected individuals develop severe neuroinvasive disease, which includes meningitis, encephalitis, or acute flaccid paralysis (Petersen & Marfin, 2002).
Diagnosis is typically made through serological testing for WNV-specific IgM and IgG antibodies. According to CDC criteria, a positive IgM result in cerebrospinal fluid or a four-fold rise in plaque reduction neutralization antibody titers in paired serum samples at least 14 days apart provides confirmation of recent WNV infection (CDC, 2001). Viral isolation and nucleic acid detection from blood or CSF during initial infection may also be diagnostic.
Case Study 1
In August 2000, a previously healthy 42-year-old male in Queens, NY presented with 4 days of fever, headache, nausea, and vomiting. On examination, he was febrile to 39°C, but otherwise had normal vital signs and unremarkable physical exam. Initial labs were notable for leukopenia. A lumbar puncture showed lymphocytic pleocytosis. Serum and CSF were sent for WNV IgM and IgG testing.
On day 6 of illness, serum WNV IgM returned positive, confirming WNV meningitis as the diagnosis. The patient was treated supportively with intravenous hydration and made a full recovery over the next week. Follow up serology 6 weeks later showed rising WNV IgG titers, consistent with acute WNV infection (Klee et al., 2004). This case illustrated the nonspecific initial presentation of WNV neuroinvasive disease but importance of considering WNV in the differential during local outbreaks. It also demonstrated the utility of serological testing for diagnosis.
Case Study 2
In July 2003, a previously healthy 67-year-old male in Suffolk County, NY presented to his primary care physician with 4 days of fever, headache, nausea, and new onset of right lower extremity weakness. On exam, he was febrile to 38.9°C and found to have new flaccid paralysis and areflexia of the right lower extremity. Lumbar puncture revealed lymphocytic pleocytosis. MRI of the brain and spine were unremarkable.
Serum and CSF were sent for WNV IgM and IgG testing. On day 6 of illness, serum WNV IgM returned positive, confirming WNV meningoencephalitis with acute flaccid paralysis as the diagnosis. The patient was admitted to the hospital for IV hydration and supportive care. He required short-term rehabilitation but made a near-complete recovery of strength over the following months. Follow up serology 3 months later showed rising WNV IgG titers consistent with recent infection (Nash et al., 2001). This case highlighted the potential for WNV to present as acute flaccid paralysis, an important diagnostic consideration.
Pathophysiology
WNV is a single stranded, positive-sense RNA virus in the Flaviviridae family (Rosen, 2000). Following mosquito-borne transmission and entry into host cells, the viral genome is translated into a single polyprotein which is cleaved by host and viral proteases into 3 structural proteins (capsid, premembrane/membrane, envelope) and 7 nonstructural proteins. The viral RNA-dependent RNA polymerase enables replication of new genomes within the cytoplasm. Assembly and budding at the host cell membrane produces new virions that can infect surrounding cells or be taken up in the saliva of another biting mosquito during blood-feeding to perpetuate transmission cycles (Petersen & Marfin, 2002).
In a small percentage of infections, the virus is able to breach the blood-brain barrier and infect neurons and glial cells in the central nervous system, resulting in encephalitis, meningitis, or acute flaccid paralysis. The mechanisms underlying neuroinvasion and neurovirulence remain incompletely understood but are likely multifactorial involving both viral and host immune factors (Rosen, 2000).
Conclusion
Since its introduction into the Western Hemisphere in 1999, WNV has caused significant epidemics of neuroinvasive disease across North America. The case studies presented here illustrate some of the clinical diversity of WNV infection as well as the utility of serological testing for diagnosis. Continued WNV activity underscores the importance of surveillance, prevention through mosquito control, and physician awareness—particularly during local transmission seasons. Further research into viral and host determinants of neuroinvasiveness may help inform new therapeutic and preventive strategies.
References
Bernard, K. A., & Kramer, L. D. (2001). West Nile virus in the United States: guidelines for surveillance, prevention, and control. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK84576/
Canals, C., Conaty, S. J., Walsh, E., Walden, H., & Sampson, B. A. (2000). West Nile virus infection in the New York City area. Emerging infectious diseases research essay writing service, 6(4), 370–374. https://doi.org/10.3201/eid0604.000401
Centers for Disease Control and Prevention. (1999). Outbreak of West Nile-like viral encephalitis – New York, 1999. MMWR. Morbidity and mortality weekly report, 48(38), 845–849.
Centers for Disease Control and Prevention. (2001). Guidelines for surveillance, prevention, and control of West Nile virus infection–United States. Retrieved from https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5005a1.htm
Centers for Disease Control and Prevention. (2015). West Nile virus. Retrieved from https://www.cdc.gov/westnile/index.html
Klee, A. L., Maidin, B., Edwin, B., Poshni, I., Mostashari, F., Fine, A., … Hayes, E. B. (2004). Long-term prognosis for clinical West Nile virus infection. Emerging infectious diseases, 10(8), 1405–1411. https://doi.org/10.3201/eid1008.032815
Nash, D., Mostashari, F., Fine, A., Miller, J., O’Leary, D., Murray, K., … Layton, M. (2001). The outbreak of West Nile virus infection in the New York City area in 1999. The New England journal of medicine, 344(24), 1807–1814. https://doi.org/10.1056/NEJM200106143442401
Petersen, L. R., & Marfin, A. A. (2002). West Nile virus: a primer for the clinician. Annals of internal medicine, 137(3), 173–179. https://doi.org/10.7326/0003-4819-137-3-200208060-00008
Rosen, L. (2000). Flaviviruses. In B. N. Fields, D. M. Knipe, & P. M. Howley (Eds.), Fields virology (4th ed., pp. 1005–1034). Philadelphia: Lippincott Williams & Wilkins.
