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Hantavirus infection in British Columbia: An atypical case history ...
Hantavirus infection in British Columbia: An atypical case history …

Although the diagnosis is rare, hantavirus infections do occur in British Columbia. Hantavirus pulmonary syndrome has a crude mortality rate of approximately 40% to 50% and is usually characterized by fever, chills, and myalgia followed by the sudden onset of respiratory distress and hypotension, often require ventilation. In 2002, cases of hantavirus pulmonary syndrome at presentation as is usually diagnosed in a 46-year-old man from the Okanagan region. It highlighted the case of a doctor needs to be aware of such an atypical case history, epidemiology and laboratory investigations are required, and the epidemiology of hantavirus infections in British Columbia, including transmission and common risk factor for disease. Physicians should also be aware of national definitions and the BC case, the specimen collection procedures, differential diagnosis, clinical management, and the importance of reporting cases.

A patient with such symptoms usually eventually found to have hantavirus pulmonary syndrome.

history Case

at the beginning of July 2002, 46-year man presented to the department complained emergency epigastric discomfort followed by vomiting significantly and right upper quadrant pain intense. He was hospitalized and within 2 days developed drenching night sweats and mild shortness of breath, headache, but no diarrhea. initial X-ray showed interstitial pneumonitis with bilateral effusions; Oxygen saturation was 84% ​​on room air but is enhanced with the provision of oxygen (94% in 4 L of O2). Patient developed cough by the fourth day in the hospital and crackles just fine present throughout both lung fields. Several bilateral chest pain is present but this is not typical pleuritic pain. The highest recorded temperature was 38.1 ° C patients on day 2, with fluctuations between 36 ° C and 38 ° C. BUN and creatinine levels it was initially normal, but he went to the temporary kidney failure (creatinine maximum 260). Study of liver function is normal except for GGT of 160 (normal 12-50 U / L). normal WBC count at 6:18, with 3.40 and 0.19 polymorphonuclear leukocytes band, but smear showed rare nucleated red blood cells and mature granulocytes, which are considered abnormal. Similarly, many of lymphocytes that are abnormal in appearance. the number of initial hemoglobin is 166 but on rehydration fell to 115. Her platelet count was 90 000 in the presentation, fell to 65 000 two days later, and then slowly recover. His chest X-ray finally revealed interstitial edema with a small pleural effusion.

Diagnostic investigation

initial examination concentrated on the causes of severe stomach pain patients. Ultrasound showed gallstones and cholecystitis; upper endoscopy and colonoscopy failed to show a significant lesions. Within 2 days in the hospital, laboratory tests are required to respiratory pathogens, including Chlamydia species, Legionella species, Mycobacterium tuberculosis, Mycobacterium pneumoniae, and Sin Nombre virus, hantavirus species. A four-fold was observed in immunoglobulin M antibodies to the virus Sin Nombre from acute to recover sera (1: 1600 to 1: 400) with a concurrent rise in immunoglobulin G antibody (1: 600-1:> 6400). Sera reactive with antibodies to other respiratory pathogens.

The case was eventually proved to be an example of an atypical presentation of hantavirus pulmonary syndrome (HPS). Despite the increase, not fever reached 38.3 ° C, the threshold is recognized in patients with HPS. Chills and myalgia, common to most patients with HPS, which recorded only on one day. respiratory disorders are mild with minimal cardiopulmonary involvement; The dominant symptom is a severe abdominal pain. In this case, as in about 80% of cases of HPS, a platelet count below 150 000 units. The combination of atypical lymphocytes, especially the increase in cell bands (and even mielosit, metamyelocytes, and promyelocytes), and thrombocytopenia in the setting of pulmonary edema is highly suggestive of hantavirus infection. While less typical, abdominal pain, nausea, and vomiting are considered manifestations often HPS (see), show that hantavirus infection should be considered in the differential diagnosis of individuals who experience gastrointestinal complaints, especially when a complaint is accompanied by evidence of radiological bilateral spread infiltrates.

The classic presentation of HPS include early symptoms are relatively nonspecific prodrome of fever lasts 3 to 5 days. Fever is usually accompanied by chills and myalgia. Less often, the patient presents with headaches, dizziness, productive cough, nausea, vomiting, abdominal pain, and diarrhea. Indication of the upper respiratory tract disease, including sore throat, colds, sinusitis, and ear pain, usually no. Cough and tachypnea usually do not develop until day 7 and signal the onset of pulmonary edema and hypoxia, usually requiring mechanical ventilation. It is accompanied, in some patients, severe myocardial depression, which can progress to the next sinus bradycardia with electromechanical dissociation, ventricular tachycardia or fibrillation. After the fever and cardiopulmonary phase of the disease, spontaneous diuresis occurs, so that clearance of pulmonary edema fluid and resolution of fever and shock.

epidemiological investigation

According to the national US registry HPS cases, Sin Nombre virus incubation period is estimated to range from 9-33 days, with an average of 14 to 17 days. Other estimates put outside the range of the incubation period of 6 weeks. In the case under discussion, face to face interviews conducted using standard national questionnaires to assess the potential exposure and disease risk factors.

Exposure assessment. In times of illness, the patient lived in a mobile home on a large rural property in southern BC. Two years earlier, the mobile home has been infested with rats. To overcome these problems, the mobile home has been set on concrete blocks, particles have been used to cover the space of the ground floor of the house, and the poison had been placed in this crawl space. No rat has been seen anywhere since the early infestation.

In mid-May, about six weeks before the start of symptoms, the patient was employed to clean the top floor of a barn on the property. The warehouse floor has been unused for nearly 10 years after the closure of the chicken farm operation. Chicken feeder is still intact and the required removal. Some of them still are leftover chicken feed and rodent droppings. Warehouse floor covered with a layer of sawdust and chicken manure so thick that door over-swinging into the warehouse could not be opened to ventilate the area before cleaning. Patients are working to remove debris for more than 2 hours a day for 3 days. The environment is not wetted and become very dusty. For protection during cleanup, patients wearing yellow work gloves nylon (cloth-type, not rubber) and a dust mask. Barn door was eventually released and the area is well ventilated. The property owner also install the fan in the upstairs barn in an attempt to dislodge the dust.

In early May, two months before the onset of symptoms, the patients also have turned on the water pipe, which involved crawling under the car home to reach the taps. Additional activities during the incubation period of 6 weeks, including hiking in a wooded area of ​​agricultural property and four one-day fishing where it is not exposed to a fishing lodge or cabin. In addition to cleaning the barn, the patient had been working nearby branch pruning in the garden for 3 days in early May. Cleaning warehouse, unventilated area shows clear evidence of rodent infestation, is the most likely source of exposure, given the level of exposure and the length of the incubation period. While patients do wear some protective equipment, a dust mask offers adequate protection against aerosol droplets known to transmit hantavirus.

mousetrap. Rodent traps carried out over a period of 2-night, from 18 September to 20 September 2002 with the use of 82 Sherman traps. Traps are set in and around the patient’s home as well as inside and outside the warehouse where cleanup is done. Trap is emptied every morning and speciated rats caught and dissected. A total of 29 rodents (23 deer mice, squirrels 3, 3 rats, and one rat) stuck. Blood samples were taken from each rodent and tested for the presence of immunoglobulin G antibodies against Sin Nombre virus

The serum of mice had titers of 1 :. 400, suggests exposure Sin Nombre virus. The remaining 28 specimens have a titer of <1: 100, indicating that theynot infected with Sin Nombre virus. Positive mouse stuck on the barnyard on 19 September 2002. There are no rats caught from a trap placed in a motor home patients.

The environmental assessment. Environmental assessment examined rodent-proofing around the barn and house cars and activities identified to reduce the possibility of future exposure to rodents. As the cleaning has not been completed, the advice given on a safe method to clean the barn floor above. Owners are advised to wear protective equipment during cleanup including disposable clothes, rubber boots or shoe covers, rubber gloves, goggles and masks suitable (negative-pressure respirator with a HEPA filter or air purifier with a HEPA filter respirator powered). It was suggested that a well-ventilated barn for a few days before the cleanup is to start and that the heavy layer of moistened sawdust covering the floor. This is to be achieved by fogging or misting machines in a way that will not interfere if any infectious particles. potentially infective material is removed from the top floor of the warehouse along with personal protective equipment used in the cleanup must be burned or deep-buried on the site. Basic serology requested on all individuals involved in the clean-up procedures in the case of an infection developed after cleaning.

The patient filed a claim for Workers’ Compensation Board of British Columbia based on information obtained during an epidemiological investigation and the claim was finally approved.

Epidemiology hantavirus

HPS was first recognized in 1993 during an outbreak in the Four Corners region of the United States, an area bordering New Mexico, Arizona, Colorado, and Utah. Although hantavirus then regarded as the emerging diseases, retrospective analysis showed serological evidence of infection in the United States dating back to 1959. In Canada, the HPS was first recognized in BC in 1994 as a result of active surveillance; subsequent investigation identified the previous case, which occurred in Alberta beginning in 1989. Between 1989 and 1999, 32 laboratory-confirmed cases identified in Canada. Until now, the case has been restricted to western provinces of BC, Alberta, Saskatchewan, and Manitoba. Alberta has identified more than 60% of the reported cases (20/32). This parallels the observed distribution of cases in the western United States; cases tend to occur in less densely populated areas of both countries. Since 1994, BC has reported seven cases of HPS () from the largely rural province, from the Okanagan Valley in the south to Williams Lake in the north. Between 1996 and 2002 no cases of HPS were reported in BC. While it is known that climate change and the dynamics of the rodent population can contribute peak or trough year, a complete absence of reported cases is probably due to the recognition of the disease were inadequate and supervision. This is especially possible given that during this period of time Alberta continues to report cases. Compare BC and Canadian fatality rate and the age and gender distribution of HPS cases reported between 1989 and 1999. High levels of deaths in BC may reflect the approximate unstable due to small sample size or most of the cases occurred in 1994 BC and 1995, immediately after the discovery of the virus in North America with the recognition of HPS is often delayed.

Some seasonal seems to exist with HPS infection. Most patients SM started to ache during the spring, especially during the month of April (3/7). Canadian data show seasonal bimodal distribution with peaks in the spring and late autumn.

Although it is present in North America, HPS reported nearly three times more frequent in the countries of Central and South America, especially Brazil, Argentina, and Chile. HPS is not known outside the United States. Other viruses of the genus Hantavirus causes a spectrum of disease are collectively referred to as hemorrhagic fever with renal syndrome, present in Europe, Asia, and the Middle East. This disease differs clinically from HPS.

cause HPS virus mainly transmitted to humans through inhalation aerosol mouse urine and feces. infectious airborne particles can be produced for human activities that disturb contaminated soil, litter, or nesting material. Another route transmission rare but potentially involve direct inoculation through bite infected mice, as the virus is known to be present in the saliva of mice. Another theoretical -rute of infections including ingesting food contaminated with rodent feces, and exposure of the membrane of the nose or mouth into the hands contaminated. Although person-to-person transmission has not been reported in North America, molecular evidence of transmission of person-to-person documented in HPS outbreak in Argentina in 1996. The species of hantavirus involved in this person-to-person outbreak, Andes virus, yet associated with human disease in Canada. Animals, ticks, mosquitoes and other biting arthropods are not known to carry disease.

Each type of hantavirus usually associated with species of rodent hosts. BC cases of HPS associated with Sin Nombre virus, the main reservoir environment is deer (Peromyscus maniculatus), commonly found throughout British Columbia. deer tendency to enter human settlements and surrounding buildings is an important factor in transmission. serological and genetic studies conducted on deer mice populations in Canada have identified the infected mice in all provinces except Prince Edward Island and Nova Scotia. The absence of human cases in the eastern province may be the result of the intensity of supervision combined with geographic differences in rodent and human behavior.

While most infections have been associated with exposure to rodent known, not all infected patients have reported contact with rodents, droppings, or nesting material. However, the density of the higher rodents has been demonstrated in and around the home of cases compared with control homes. In Canada, 34% of cases of HPS were probably infected during domestic activity and 25% have exposure associated with agriculture. Domestic high-risk activities including cleaning the mice-infested areas, especially the closed or restricted without adequate ventilation. This may include activities such as open cabins or other buildings after a period of use or cleaning barns, garages, or storage areas containing machinery or farm equipment. While some infections HPS clearly a direct result of occupational exposure, 8 serologic studies of high-risk occupation groups in areas known to harbor infected mice have not shown seropositive. Despite the reports of person-to-person transmission of nosocomial Argentina, hantavirus transmission in hospital settings has not been confirmed. No immunoglobulin G antibodies were detected in 67 health personnel in Chile affected patients with HPS. Another study found no increased risk of hantavirus exposure, measured by the presence of immunoglobulin G and immunoglobulin M antibody, in hospital workers exposed to HPS patients than those without contact with the patient.

case definitions and sample collection

To meet the definition of national and BC cases, confirmed cases of hantavirus require laboratory confirmation coupled with clinical signs of the disease (see). If you suspect a case of HPS, collect 7 mL of blood (clotted in the red-top tube) when the patient is febrile, and before starting antiviral therapy. Specimens must be submitted for testing hantavirus antibodies with clinical and epidemiological information that is relevant and all specimens should be transported to the BC Center for Disease Control laboratory according to Transport Dangerous Goods regulations. A cured specimen takes 2 to 4 weeks after the first specimen collection.

Differential diagnosis

There are many diseases with symptoms similar to hantavirus pulmonary syndrome. The most important part of the diagnosis is to consider the possibility of hantavirus infection. Some of exposure, clinical, and laboratory features that are highly suggestive of hantavirus. Although it failed to explain the exposure might be described well, most of the cases, including all those diagnosed in BC, has had a strong history of exposure to rodents or rodent droppings. Each patient with pneumonia, especially among those who live in or have visited the BC Interior, should be asked about the exposure. Some exposure is as clear as the patient described here, while others may be more subtle, including just being in places where rodents or their droppings may be present.

Usually, the clinical course of HPS is different from most cases of respiratory diseases. Patients usually have minor symptoms several days with little or no respiratory symptoms, and then into a fever and more than 1 to 3 days of developing symptoms and findings suggestive of acute pulmonary edema and respiratory insufficiency noncardiogenic. Unlike many cases of severe pneumonia, most cases do not involve the underlying disease. In an effort to further distinguish between HPS and similar diseases, a US study that followed 135 patients with an adequate specimen with suspected hantavirus infections; Ultimately, 30 patients received a laboratory confirmed diagnosis of hantavirus while 105 did not. Those with hantavirus are significantly more likely to complain myalgia (85% versus 61%, OR 3.6) throughout their initial illness, nausea before hospitalization, and both nausea and diarrhea at the time of hospitalization. They were significantly less likely to complain of respiratory symptoms at the beginning of their illness. Cough at 23% compared to 72%, dyspnea in 8% compared to 60%, and chest pain in 4% compared to 30%

features typical laboratory including hemokonsentrasi, a left shift is marked on the blood smear (usually with the total number of cells normal white blood), a decrease in platelet count, and hypocapnia. Imaging studies typically show diffuse bilateral infiltrates more suggestive of acute respiratory distress syndrome of pneumonia.

In the US study mentioned above, alternative diagnoses were made in 55 of 105 patients without hantavirus, and a large number of causes of infectious and noninfective identified. 1999 document “Hantavirus in the Americas: Guidelines for Diagnosis, Treatment, Prevention and Control” () provide additional information about hantavirus diagnosis and management

Clinical management

Because none. curative treatment for HPS, management support. A high index of suspicion is required at the beginning so that a correct diagnosis can be made. Because respiratory symptoms secondary to an increase in immune-mediated diffuse capillary permeability of the lung microvasculature, efforts to optimize the balance of fluids to avoid fluid overload are important, such as the provision of adequate oxygenation and hemodynamic monitoring. Since HPS was rare among those who have respiratory complaints, even in areas where hantavirus general, most patients will require antimicrobial for possible sepsis. Doxycycline would be necessary if the history of epidemiology indicates insect or rodent exposure and the possibility of tularemia, plague, erhlichiosis, or rickettsiosis.

The case report

Although it is unlikely to affect the treatment, laboratory confirmation and reporting of cases of HPS is important from a public health perspective. routine diagnosis allows surveillance for changes in the epidemiology of the disease (for example, an increase in the number of cases and the increase in atypical clinical presentation as the case described here). reporting cases also allow monitoring of the geographical expansion of the disease into areas that were previously unknown provinces infected mice harbor. In the end, the collection of surveillance information enabling an accurate picture of the risk of disease in the province and identify changes over time. In addition, the characteristics of the disease risk factors (obtained through the investigation of cases of laboratory-confirmed cases) prevention messages can be targeted to those most at risk.

Competing interests
None stated.

Acknowledgments
diagnostic laboratories given by Dr. Robbin Lindsay at the National Microbiology Laboratory in Winnipeg. Rodent traps done with the help of Keerthi Fernando of the BC Center for Disease Control. Assistance from environmental health officers from the Interior Health Authority appreciated the follow-up cases.

Table 1. Symptoms of hantavirus pulmonary syndrome, with symptoms of the case being discussed is highlighted.

Source: Center for Disease Control and Prevention. (Accessed August 19, 2003).

Table 2. Descriptive epidemiology of hantavirus pulmonary syndrome.

, Table 3. National and BC the case definition for hantavirus pulmonary syndrome case

An authenticated confirmation requires both laboratory and clinical signs of disease

Laboratory confirmation of infection .:
• Detection of hantavirus-specific IgM antibodies or a four-fold or greater increase in specific antibody titers of IgG hantavirus
Or
• Detection of hantavirus-specific ribonucleic acid sequences by polymerase chain reaction in the appropriate clinical specimens
Or
• Detection of hantavirus antigens by immunohistochemistry

PLUS

clinical signs of disease:
• fever (temperature> 38.3 ° C oral) requiring supplemental oxygen
And
• bilateral diffuse infiltrates (may resemble acute respiratory distress syndrome)
And
• The disease that develops within 72 hours of hospital in previously healthy people
Or
• Unexplained illness that results in death, followed by autopsy examination showed pulmonary edema noncardiogenic no specific cause can be identified death

1. Centers for Disease Control and Prevention. All about hantavirus: clinical manifestations of disease. (Accessed August 19, 2003).
2. Young JC, Hansen GR, Graves TK, et al. The incubation period of hantavirus pulmonary syndrome. Am J Trop Med Hyg 2000; 62: 714-717.
3. Control of Communicable Diseases Manual, 17th ed. James Chin (ed). Washington, DC: American Public Health Association; 2000.
4. Drebot MA, Artsob H, Werker D. Hantavirus Pulmonary Syndrome in Canada, 1989 – 1999. Canada Communicable Disease Report. 26. 15 April 2000 Vol.
5. Hantavirus Pulmonary Syndrome (HPS) Case: The Americas through 2000. Washington, DC: PAHO; 1999.
6. Padula P, Edelstein A, Miguel SD, et al. Hantavirus pulmonary syndrome (HPS) outbreak in Argentina: Molecular evidence of person-to-person transmission of Andes virus. Virology 1998; 241: 323-330.
7. Childs JE, Krebs, JW, Ksiazek TG, et al. A household-based, case-control study of environmental factors associated with hantavirus pulmonary syndrome in the southwestern United States. Am J Trop Med Hyg 1995; 52: 393-397.
8. Jay M, Hjelle B, Davis R, et al. Exposure leading to a hantavirus pulmonary syndrome in the employees of the utility company. Clin Infect Dis 1996; 22: 841-844.
9. Zeitz PS, Graber JM, Voorhees RA, et al. The risk assessment work hantavirus infection in Arizona and New Mexico. J occup Environ Med 1997; 39: 463-467.
10. C Castillo, Mardones J, Villagra E. Prevalence of anti-hantavirus antibodies in health workers in direct contact with patients with hantavirus pulmonary syndrome in Temuco, Chile 1997 – 1999. Rev Med Chil 2000; 128: 735-739.
11. Chaparro J, Vega J, Terry W, et al. Rate person-to-person transmission of hantavirus pulmonary syndrome in hospital Chile. J Hosp Infect 1988; 40: 281-285.
12. LE Chapman, Ellis BA, Koster FT, et al. Discriminator between an infected person and -uninfected hantavirus enrolled in the trial of intravenous ribavirin for alleged hantavirus pulmonary syndrome. Clin Infect Dis 2002; 34: 293-304.

L. MacDougall, MSc, M. Fyfe, MD, MSc, William R. Bowie, MD, FRCPC, K. Cooper, CPhI (C), GD McCauley, MD, FRCPC, M. Morshed, PhD

Ms MacDougall is a field with a Canadian epidemiological field Epidemiology Program, Health Canada, and the Infectious Disease Epidemiology Services, British Columbia Center for Disease Control (BCCDC), Vancouver, BC. Dr. Fyfe is a communicable disease epidemiology Epidemiology physician Services, BCCDC. Dr Bowie is a professor in the Division of Infectious Diseases, Faculty of Medicine, University of British Columbia. Mr. Cooper is an environmental health officer with the Interior Health Authority of British Columbia. Dr. McCauley is respirologist / intensivist at Kelowna General Hospital, Kelowna, British Columbia. Dr Morshed is the head of zoonoses and Emerging Pathogens, Laboratory Services, BCCDC.

The above is the information needed to cite this article in the paper or presentation. The International Committee
of Medical Journal Editors (ICMJE) recommends the following citation style, which is now almost universally
citation style accepted for scientific work:
Halpern SD, Ubel PA, Caplan AL, Marion DW, Palmer AM, Schiding JK, et al. Solid-organ transplantation in HIV-infected
patient. N Engl J Med. 2002; 347: 284-7.

ICMJE is a small group of general medical journal editors who first met informally in Vancouver, British Columbia,
in 1978 to establish guidelines for the format of manuscripts submitted to their journals. The group became known as
Vancouver Group. requirements for manuscripts, including formats for bibliographic references developed by the US
National Library of Medicine (NLM), first published in 1979. The Vancouver Group Expanded and develop into
International Committee of Medical Journal Editors (ICMJE), which meets annually. The ICMJE created the
to help writers and editors create and distribute accurate, clear, easily accessible reports of biomedical studies.

An alternative version of the style ICMJE is for an additional month list the number of problems, but because most journals using continuous
pagination, short form providing enough information to find references. NLM now lists all authors.

BCMJ standard citation style is a slight modification of the style ICMJE / NLM, as follows:

For more information about the ICMJE Recommendations for Conduct, Reporting, Editing, and scientific publications Work
The Medical Journal, visit www.icmje.org

The above is the information needed to cite this article in the paper or presentation. The International Committee
of Medical Journal Editors (ICMJE) recommends the following citation style, which is now almost universally
citation style accepted for scientific work:
Halpern SD, Ubel PA, Caplan AL, Marion DW, Palmer AM, Schiding JK, et al. Solid-organ transplantation in HIV-infected
patient. N Engl J Med. 2002; 347: 284-7.

ICMJE is a small group of general medical journal editors who first met informally in Vancouver, British Columbia,
in 1978 to establish guidelines for the format of manuscripts submitted to their journals. The group became known as
Vancouver Group. requirements for manuscripts, including formats for bibliographic references developed by the US
National Library of Medicine (NLM), first published in 1979. The Vancouver Group expanded and evolved into
International Committee of Medical Journal Editors (ICMJE), which meets annually. The ICMJE created the
to help writers and editors create and distribute accurate, clear, easily accessible reports of biomedical studies.

An alternative version of the style ICMJE is for an additional month list the number of problems, but because most journals using continuous
pagination, short form providing enough information to find references. NLM now lists all authors.

BCMJ standard citation style is a slight modification of the style ICMJE / NLM, as follows:

For more information about the ICMJE Recommendations for Conduct, Reporting, Editing, and scientific publications Work
The Medical Journal, visit www.icmje.org

BC Medical Journal is a general medical journal published by the Physicians of BC. It provides continuing medical education with a focus on evidence-based medicine.

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