¡ Whoa...Hantavirus!

Tania Cruz <tania-ivonne@msn.com>

Nicole Montes <nm.montes@gmail.com>
Shirley Mori <shirleym@ucla.edu>
Yoshua Kenneth <yosh237@gmail.com>
Laura-Jo Ortega <laura.jo.ortega@gmail.com>
Henry Chien <asok_d_intern@yahoo.com>
Gracie Charles <gracie16@hotmail.com>
Rosa Sanchez <rsanchez10@mail.csuchico.edu>
Lori Bautista <lorrainebautista@gmail.com>
Ramin Pouriran <Ramin_pouriran@hotmail.com>
Jen Gulas <jennifergulas@gmail.com>
Mona G <monaggg@gmail.com>

UAG 2010
Third Semester
Microbiology Presentation
 Taxonomy:
Hantaviruses belong to the Bunyaviridae family of viruses. The Bunyaviridae family is divided into 5 genera:
Orthobunyavirus, Nairovirus, Phlebovirus, Tospovirus, and Hantavirus.

Genomic Description:
The hantavirus genome consists of an enveloped, linear, negative sense, single-stranded RNA made up of 3616
base pairs.
 Diagnosis:
Following an incubation period of 5-33 days, patients usually report:
Myalgia
Fatigue
High Fever
Headache
Nausea
Vomiting and Diarrhea

Next phase is 4-6 days later:

Abrupt onset of dyspnea and hypoxia, rapidly progressing to noncardiogenic pulmonary edema and respiratory
failure (Hantavirus Pulmonary syndrome)
Hypotension or shock with myocardial depression
DIC and renal failure commonly observed

Also:
Additionally, HPS is clinically defined as a febrile illness (temperature >38.3°C) with bilateral diffuse infiltrates that
cause respiratory compromise requiring supplemental oxygen within 72 hours of hospitalization. Moreover, a case
may also be defined postmortem as an unexplained, fatal respiratory illness, with noncardiogenic pulmonary
edema of unknown cause.

Labs:
Elevated hematocrit
Leukocytosis with left shift
Immaure myeloctyes and immunoblasts in peripheral smear
Thrombocytopenia

DX:
Clinical presentation
Serology: Hantavirus SNV immunoglobulin IgM and IgG
Western Blot
RT-PCR
 Pathophysiology
•
Following inhalation exposure to
hantavirus in rodent excrement
there is an incubation period of 9
to 33 days.

•
Viremia is then produced that
infects target endothelial cells
mainly the lungs and stimulates T
cells.

•
Immune-stimulated T cells
distribute to areas of hantavirus
concentration.

•
Disease results from infected
endothelial cell function being
disturbed and local T-cell
cytokine production.

•
Which in turn increases vascular
permeability causing the
capillaries to leak fluid into the
surrounding tissue and organs.

•
Later causing pulmonary edema,
 Complications

The most important complication of this virus is Hantavirus Cardiopulmonary Syndrome. At first the symptoms are
general and flu like fever around 101 to 104, headache, stomach pain, pain in the joints and lower r back,
coughing, and nauseas. The main symptom is difficulty breathing as the lungs fill with fluid. The virus infects
the walls of the capillaries in the lungs and making them leak and flooding the lungs with fluid. Hantavirus
pulmonary syndrome is transmitted mainly by rodents through urine, droppings, and saliva. The symptoms
include tachycardia and tacchypnea which lead to cardiovascular shock. Pulmonary syndrome is often deadly
primary to lung infection. HPS is fatal to more than half of those who become infected. Most cases of
Hantavirus pulmonary syndrome progress rapidly to the second stage, the cardiopulmonary phase. The
features of this stage include a rapid clinical decomposition with hypotension and respiratory insufficiency
followed by dead. If the patient survives the cardiopulmonary stage, he or she enters the convalescent phase,
which is characterized by rapidly improving oxygenation, hemodynamic stabilization, and diuresis.
Extracorporeal membrane oxygenation has been shown to benefit a limited number of patients. Thus, early
recognition of Hantavirus pulmonary syndrome is important so that the appropriate supportive measures can
be undertaken. In the below radiograph the sever Hantavirus Pulmonary Syndrome is present. This is a case
of a 58 year old man who presented with shortness of breath and flulike symptoms. Within 24 hr. patient died.
Progression to extensive perihilar and upper lung zone consolidation with associated air Bronchgrams can be
seen.
 New Research

•
Currently scientists are trying to create a vaccine
for this virus, But until the now the best way of
control is through the control of the rodent
population.
 Treatment for Hantavirus Pulmonary Syndrome:


There is no cure and specific
treatment options are limited;
therefore early recognition,
immediate hospitalization and
adequate respiratory support are
required.
Ribavarin has been used with
LIMITED success, but its
effectiveness remains controversial.
Supportive treatments such as
maintaining fluids, blood pressure,
and electrolytes are necessary.

Mechanical ventilation with oxygen
may be necessary for Sin Nombre
virus infections.
 Epidemiology
 SNV occurs wherever its reservoir rodent carrier,the deer mouse Peromyscus maniculatus is
found.

SNV and HCPS (Hantavirus cardiopulmonary syndrome) are especially common in western
states & Canada

Peak incidences for HCPS has been reported in regions in which there is a lot of contact
between humans and mice (New Mexico, Arizona) and in states with exceptionally large rural
populations such as California.

SNV can be contracted through the inhalation of virus-contaminated deer mouse excreta.

The case fatality ratio of SNV-induced HCPS in the USA was reported to be about 66.7%

Since that time the case fatality ratio has steadily declined as more mild cases came to be
recognized.

By 2007 the CFR had declined to about 35%
 Control
 Sin Nombre virus (SNV) was first
isolated from rodents collected on
the initial HPS patients in the Four
Corners region. Isolation was
achieved through blind passage in
Peromyscus maniculatus and
subsequent adaptation to growth in
Vero E6 cells.
 Control of this disease includes
rodent control as well as no contact
with infected rodents and their
droppings. Care must me taken to
avoid inhaling aerosolized dried
droppings when cleaning rodent-
infested areas.
 Reference Material
Taxonomy & Genome:
http://en.wikipedia.org/wiki/Hantavirus
http://www.ncbi.nlm.nih.gov/nuccore/NC_005219.1

Diagnosis:
Venes, M.D., D. (2009). Taber's cyclopedic medical dictionary, 21st edition (thumb index version). Philadelphia, Pa: F A Davis Co.
McPhee, SJ, & Papadakis, MA. (2008). Viral & rickettsial infections. In H Koo (Ed.), Lange 2008 current medical diagnosis & treatment (pp. 1178-1226). USA:
McGraw-Hill Companies, Inc.
Centers for Disease Control and Prevention. Outbreak of acute illness-southwestern United States, 1993. MMWR Morb Mortal Wkly Rep 1993;42:421-4.
Khan AS, Khabbaz RF, Armstrong LR, Holman RC, Bauer SP, Graber J, et al. Hantavirus pulmonary syndrome: the first 100 U.S. cases. J Infect Dis
1996;173:1297-303.
Duchin JS, Koster FT, Peters CJ, Simpson GL, Tempest B, Zaki SR, et al. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly
recognized disease. N Engl J Med 1994;330:949-55.

Pathogenesis:
http://bestpractice.bmj.com/best-practice/monograph/928/basics/pathophysiology.html
http://www.cdc.gov/ncidod/diseases/hanta/hps/noframes/FAQ.htm

Complications:
Of mice, men, and microbes. Author Davide R. Happer, Andrea S. Meyer.

Treatment:
Http://www.cdc.gov/ncidod/eid/vol5no5/kitsutani.htm
Kitsutani, Paul T., Robert W. Denton, CurtisL. Fitz, Robert A. Murray, Randall L. Todd W. John Pape, J. Wyatt Frampton, Joni C. Young, Ali S. Khan, Clarence J.Peters, and
Thomas G. Ksiazek. "Acute Sin Nombre Hantavirus Infection without Pulmonary Syndrome, United States." Centers for Disease Control and Prevention. 5.5 (2000):
Print.

Epidemiology:
Erin M. Lehmer, Christine A. Clay, et.al, Differential regulation of pathogens: the role of habitat disturbance in predicting prevalence of Sin Nombre virus. 2008. OECOLOGIA
Volume 155, Number 3, 429-439

Control:
Special pathology lab. http://www.cdc.gov. 14 June 2004. 29 September 2010
Brooks, Geo. Butel, Janet. Carrol, Karen, and Morse, Stephen. Medical Microbiology. 24th edition. 2004