Transcript Biological Weapons: A Module for Nursing Professionals

Biological Weapons: Essential
Information on Category C Agents
Felissa R. Lashley, RN, PhD, FAAN, FACMG
Professor, College of Nursing, and
Interim Director, Nursing Center for Bioterrorism
and Infectious Disease Preparedness, College of
Nursing
Rutgers, The State University of New Jersey
This module on the use of biological agents
as bioweapons covers general material, the
classification of biological agents as to their
use in bioterrorism and gives the most
important information regarding the
Category C agents according to the Centers
for Disease Control and Prevention (CDC)
classification. Separate modules address
Category A and Category B agents. This
module was supported in part by USDHHS,
HRSA Grant No. T01HP01407.
OBJECTIVES
At the completion of this module, participants will
be able to:
1. Identify at least 10 factors that make a
biological agent or biological toxin suitable for
use as a bioterror agent.
2. List the 3 CDC categories for critical biological
agents and why they are so categorized.
3. Identify and list CDC Category C biological
agents with potential for use in a bioterrorism
attack.
4. Describe signs and symptoms of infection with
Category C agents.
5. Discuss isolation precautions for each Category
C agent.
Using Biological Agents as
Bioweapons
Biological Agents and Bioterrorism



Includes microorganisms, especially certain
bacteria and viruses, and biological toxins as
botulinum toxin, which act like chemical agents.
May be directed at humans, plants, animals, and
be a threat to crops, livestock, food products
(agroterrorism) during processing, distribution,
storage and transportation which could cause
illness and also have severe economic
consequences such as bovine spongiform
encephalopathy, and foot and mouth disease.
Biological agents can be used as weapons in:



Biocrimes
Bioterrorism
Biowarfare
Biological Agents and Bioterrorism-2
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Definition: The North Atlantic Treaty Organization
(NATO) defines a biological weapons as "the
provision of any infectious agent or toxin by any
means of delivery in order to cause harm to
humans, animals, or plants."
Various definitions for bioterrorism have been
given. The following may be used: "the
intentional use or threat of use of biological
agents on a population to achieve political, social,
religious, ethnic, or ideological ends by causing
illness, death and wide scale panic and
disruption." The aim may not be maximum
damage but rather a political statement.
Biological Agents and Bioterrorism-3



The technology exists to modify existing
biological agents, or weaponize them, to,
for example, make it easier to disseminate
and/or cause greater harm in their
dissemination.
The use of biological agents for
bioterrorism has been referred to as the
"poor man's nuclear bomb."
All involve the use of biological agents in
order to obtain an outcome: political,
social, economic, theological, personal.
Agents with Potential for USE in
BIOTERRORISM

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Varies according to source
NATO handbook lists 39 agents
World Health Organization (WHO) has another list
Centers for Disease Control and Prevention (CDC)
lists biological agents in various categories, A, B
&C
National Institute for Allergy and Infectious
Diseases (NIAID), National Institutes of Health
(NIH) also lists categories A, B & C, but they
differ somewhat from how CDC categorizes
agents and lists a greater number of agents
Others
The Following are Desirable Characteristics
for Biological Agents to be Used for Harmful
Intent


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Generate high levels of panic among
population
Easy to obtain
Inexpensive
Easy to produce in mass quantities
Can be relatively easily “weaponized” or
altered for maximum effect (even with
genetic manipulation)
High infectivity
High person-to-person contagion
High mortality
The Following are Desirable Characteristics
for Biological Agents to be Used for Harmful
Intent-2
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Lack of effective treatment
Need for intensive care, straining resources
High potential for casualities/morbidity
Result in lengthy illness with prolonged care
needed
Non-specific symptoms, especially early, delaying
recognition
Long incubation periods
Hard to diagnose
Great degree of helplessness from effect
Examples of Historical Uses of the
Deliberate Release of Biological Agents



Known as early as the 6th century BC
Soldiers dropped corpses of those who
died of plague over city walls during siege
of Kaffa to start a plague epidemic and
force surrender.
British soldiers used variola contaminated
blankets to spread smallpox to American
Indians during the French and Indian Wars
(1754-1767).
Examples of Historical Uses of the
Deliberate Release of Biological
Agents-2


Followers of Bhagwan Shree Rajneesh
intentionally contaminated salad bars in
The Dalles, Oregon with Salmonella. The
purpose was to keep people from voting in
a local election in November, 1984. More
than 750 people were affected.
The Aum Shinrikyo group in Japan
attempted to carry out attacks using
aerosolized anthrax spores and botulinum
toxin before releasing sarin in the Tokyo
subway in 1995.
Examples of Historical Uses of the
Deliberate Release of Biological
Agents-3

Intentional distribution of anthrax spores
mainly through the US mail to various
people occurred in the fall of 2001. In all,
there were 22 known cases of anthrax; 11
were inhalational.
Pictures from CDC
Categories of Critical Biological
Agents as Specified by CDC

Three Categories of Agents:
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Category A Agents: Pose the greatest
threat to national security
Category B Agents: Second highest
priority to national security
Category C Agents: Third highest
priority agents include emerging
pathogens that could be engineered for
mass dissemination in the future
Category A Agents

Pose a threat to national security
because they:

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
Can be easily disseminated or
transmitted person-to-person
Cause high mortality with potential for
major public health impact
Might cause public panic and social
disruption
Require special action for public health
preparedness
Category B Agents

Second highest priority to national
security:
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Are moderately easy to disseminate
Cause moderate morbidity and low
mortality
Require specific enhancements of CDC's
diagnostic capacity and enhanced
disease surveillance
Category C Agents

Third highest priority agents include
emerging pathogens that could be
engineered for mass dissemination in
the future because of:
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Availability
Ease of production and dissemination
Potential for high morbidity and
mortality and major health impact
Category C Agents

These agents include the following organisms
with the disease in parentheses. Each is
individually discussed in the following material:

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Hantaviruses (Hantavirus pulmonary syndrome and
hemorrhagic fever with renal syndrome
Mycobacterium tuberculosis (multidrug-resistant) [MDRTB]
Nipah virus (encephalitis)
Tickborne encephalitis virus
Tickborne hemorrhagic fever viruses
Yellow fever virus (yellow fever)
Other emerging pathogens such as melioidosis
and SARS (not covered here)
Source: CDC (2000). Biological and chemical terrorism: Strategic
plan for preparedness response. MMWR, 49(RR-04), 1-14.
Hantaviruses

Description:

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
The genus hantavirus contains many
worldwide viruses.
Hantaviruses belong to the Bunyavirus
family.
They are RNA viruses.
In humans, infection may result in


Hantavirus pulmonary syndrome (HPS) or
Hemorrhagic fever with renal syndrome
(HFRS) depending on the type of virus.
Hantaviruses-2

Epidemiology:
The virus types that are known as Old World
include such viruses as Puumala, Hantaan,
Seoul, Dobrava, and Saaremaa and are found
mostly in Europe and Asia. The clinical
presentation is that of HFRS.
 Those known as New World hantaviruses,
naturally found in the U.S., and the Americas
include the Sin Nombre virus first identified in
May 1993 in the U.S. Four Corners area.
 Infection with Sin Nombre, Andes, bayou, New
York and similar hantaviruses can result in
HPS.

Hantaviruses-3

Transmission:

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
Hantaviruses are transmitted to humans from
small mammal carriers that are chronically
infected, especially rodents.
Most hantaviruses are associated with a
particular species of small mammal.
The infected rodent sheds virus in feces, saliva
and urine. They are transmitted via
aerosolization of rodent feces, salive or urine,
through the bite of an infected rodent or
contamination of broken skin by rodent saliva
or excreta, or possibly through ingestion of
food or water that are contaminated.
Hantaviruses-4

Incubation
period:
For HFRS, typically
2 to 4 weeks.
 For HPS, 5 days to
4 weeks, typically
14 to 17 days.

Photo from CDC
Hantaviruses-5
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Clinical manifestations:

HFRS –
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Depends somewhat on which virus causes infection.
Infection varies from subclinical to fatal.
Typically there is a febrile phase followed by
headache and then nausea, vomiting and abdominal
pain.
Visual disturbances have been noted, particularly a
thickening of the lens.
Flushing may be seen.
Hypotension and shock may develop rapidly.
Renal symptoms including back pain and tenderness,
may begin at approximately the 3rd or 4th day, and
oliguria, anuria and acute renal failure may occur.
Hemorrhagic manifestations such as petechiae,
hematuria or melena may be seen.
A diuretic phase with polyuria may occur with
recovery, and full recovery may take weeks. Dobrava
infection may be more severe than Puumula
infection.
Hantaviruses-6

Clinical manifestations cont.:

HPS 
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Typically there is a prodromal stage that is
characterized by a flu-like illness including fever,
chills, malaise and myalgia especially of large muscle
groups in legs, shoulders, thighs and lower back.
Other symptoms include nausea, vomiting, diarrhea,
headache and then cough.
May have thrombocytopenia.
After this, a cardiopulmonary phase with increasing
respiratory and cardiovascular compromise occurs
with shortness of breath, tachypnea and tachycardia
as well as decline in oxygen saturation and
hemoconcentration.
Symptoms may resemble adult respiratory distress
syndrome. Patients may need mechanical ventilation.
In some, milder cases occur.
Hantaviruses - Diagnosis


HFRS: Diagnosis based on serological and
clinical findings.
HPS: From characteristic clinical findings,
exposure to rodent contaminated areas in
history (not useful in bioterrorism),
radiological appearance of bilateral diffuse
interstitial pulmonary infiltrates but
confirmed with serological diagnosis such
as Western blot assay or by viral
identification in tissues.
Hantaviruses & Treatment

HFRS:



IV ribavirin useful in some cases.
Supportive care (see below).
HPS:
Requires aggressive cardiopulmonary support
preferably in intensive care.
 Patients may need mechanical ventilation,
hemodynamic monitoring with a pulmonary
artery catheter, supplemental oxygen,
appropriate fluid management to maintain
cardiac output, and pressors.
 In the initial care of patients in New Mexico in
the early 1990s, extracorporeal membrane
oxygenation was useful.
 Antiviral therapy with ribavirin has been tried
with varying reports of success.

Hantaviruses cont.

Nursing care:
Intensive supportive care as discussed above under treatment.
 Standard isolation precautions.
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Vaccination:
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Inactivated vaccines used for old world hantaviruses and in
development for others.
Other:
Although classified as a category C agent, several characteristics
make it unlikely for use by terrorists, including difficulty in
production and because it is not usually transmitted between
humans.
 Many preventive techniques are available for naturally occurring
hantavirus infection not covered here.

Sources:
Clement, J.P. (2003). Hantavirus. Antiviral Research, 57, 121-127.
Lashley, F.R., & Durham, J.D. (Eds.). (2007). Emerging infectious diseases:
Trends and Issues,2nd edition . New York: Springer Publishing Co.
Lednicky, J.A. (2003). Hantaviruses. Archives of Pathology and Laboratory
Medicine, 127, 30-35.
Snell, N.J. (2004). Novel and re-emerging respiratory infections. Expert Review in
Anti-Infective Therapy, 2, 405-412.
Vapalahti, O., Mustonen, J., Lundkvist, A., et al. (2003). Hantavirus infections in
Europe. Lancet Infectious Diseases, 3, 653-661.
Multidrug-Resistant Tuberculosis
(MDR-TB)
MDR-TB is
considered as a
Category-C biological
agent by the CDC in
regard to its
potential for use in
bioterrorism.
MDR-TB

Definition:
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
MDR-TB is defined as a case of TB
caused by a strain of M. tuberculosis
that is resistant to two or more
antituberculosis drugs.
Some define MDR-TB as a case of TB
caused by a strain of M. tuberculosis
that is resistant to isoniazid and
rifampin.

XDR-TB (extensively resistant
tuberculosis) refers to cases of TB
that are resistant to isoniazid,
rifampin, the second line drugs, the
fluoroquinolones, and at least one of
three injectable drugs, such as
amikacin, kanamycin or capreomycin
MDR-TB-2
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Etiology:
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Both tuberculosis infection and tuberculosis
(TB) are due to the tubercle bacilli.
The most common in the US is Mycobacterium
tuberculosis.
M. tuberculosis is a nonmotile, non-spore
forming rod shaped bacillus with no capsule.
It does not produce toxin.
It is known as acid fast because of staining
characteristics.
It can survive for long periods under adverse
conditions.
MDR-TB-3
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Description:
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Infection with M. tuberculosis can be
pulmonary or extrapulmonary.
Pulmonary TB is the most common form in
developed countries.
In extrapulmonary TB, signs and symptoms
depend on the affected organ system as well
as systemic symptoms.
Major concerns about MDR-TB arose in the
early 1990s when nosocomial outbreaks
occurred.
MDR-TB-4
Epidemiology

MDR-TB is particularly common in:
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Resource poor areas
Global "hot spots" such as some areas
in the former Soviet Union, India, the
Dominican Republic, Ivory Coast, and
others
Congregate settings such as prisons or
long-term care facilities
MDR-TB
Epidemiology cont.-2

In practice, MDR-TB develops either
because the person is infected
initially with a:
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Drug-resistant strain (primary), or
Susceptible strain that becomes
resistant (secondary)
Primary resistance would be most likely
in regard to bioterrorism use
MDR-TB
Epidemiology cont.-3

Reasons for secondary resistance are
numerous and complex:
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Wrong drugs used in an improper way
Failure to assess drug susceptibility
patterns of the organism
A large bacterial load, especially in the
case of cavitation
Poor adherence to the treatment
regimen
MDR-TB
Epidemiology cont.-4
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TB (including MDR-TB) and HIV co-infections are
relatively common globally and each condition
adversely affects the other.
In the US in 2007, the overall number of TB
cases reported in the U.S. was 13,293
In the U.S. between 1993 and 2006, 49 cases of
XDR-TB were reported, and in 2006, 116 cases of
MDR-TB were reported. The overall case rate was
4.4 cases per 100,000 population. U.S. born
blacks and foreign born persons account for a
disproportionate number of cases.
MDR-TB
Epidemiology cont.-5

TB remains a major global problem.
Each year about 2 million people die
of TB each year worldwide, and
overall one-third of the world’s
population is infected.
MDR-TB

Transmission:

Person-to-person through inhalation of
droplet nucleii
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Infected person usually coughs or sneezes
and projected infected droplet nucleii into
the air
Ingestion of contaminated food or water
(rare in US)
Direct inoculation (rare) although
infection through transplant has
occurred.
MDR-TB
Outcomes of Contact with M. tuberculosis
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Many factors determine outcome
such as:
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Host susceptibility, such as genetic
factors and immune status
Organism characteristics, such as
virulence
Environment, such as length of time
and proximity of contact between the
susceptible person and the person with
TB
MDR-TB
Sequence of Events in Brief:
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After M. tuberculosis enters the
body, possible events include:
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No infection
Tuberculous infection
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Remains dormant in latent form (90%)
Progression to clinical disease (10%)
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Within a year or two (5%)
Years later (5%)
MDR-TB
Thus, persons may have:
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Latent TB infection in which they are infected
with tubercle bacilli but are not infectious to
others nor show clinical symptoms but do usually
have a positive reaction to the tuberculin skin
test but usually negative chest radiograph. They
may be candidates for preventive drug therapy,
OR
Active TB in which they are infected with tubercle
bacilli, usually have positive sputum smears and
cultures, usually have a positive reaction to the
tuberculin skin test, usually have clinical
symptoms, and may be infectious to others
before treatment is effective.
MDR-TB
Clinical Manifestations
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MDR-TB or XDR-TB are not clinically
distinguishable from drug-susceptible
TB at the outset.
Signs, symptoms and radiological
findings are similar initially to drugsusceptible TB.
MDR-TB
In the non-bioterrorist setting, reasons to suspect
drug resistance are:
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A history of previously treated TB in a person
presenting with active TB
High community rates of drug resistant TB
Positive HIV status
High likelihood of exposure to nosocomial, prison
or community sources of MDR-TB
The infected person is from a country with a high
MDR-TB rates
Contacts with persons with MDR-TB
Infected person has received inadequate
treatment regimens for >2 weeks
Smears or cultures remain positive despite 2
months of treatment for TB
MDR-TB
Symptoms of Pulmonary TB include:
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Cough (usually
productive and maybe
bloody)
Low-grade fever
Sweating
Chills at night
Fatigue
Malaise
Anorexia
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Weight loss
Dull, aching chest pain
or tightness
Symptoms of
extrapulmonary TB
depend on the organ
system involved but
may include systemic
symptoms such as
malaise
MDR-TB
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Diagnosis generally consists of:
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Medical history,
Clinical signs and symptoms,
Chest x-ray for pulmonary TB,
Sputum smear and/or culture for acidfast bacilli, and possibly
A tuberculin skin test.
MDR-TB
Diagnosis Notes
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Tuberculin skin test with purified protein
derivative as screen; anergy may be seen in
elderly and the immunosuppressed.
Chest x-ray or radiograph of extrapulmonary site
shows characteristic findings of abnormalities in
apical or posterior segments of upper lobe or
superior segments of lower lobe but is not used
to confirm diagnosis of pulmonary TB.
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Appearance may be unusual in HIV-positive persons
Sputum smears and cultures for tubercle bacilli.
MDR-TB
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Treatment
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Initial non-MDR-TB therapy especially in
drug-susceptible disease calls for 8
weeks of therapy with isoniazid,
rifampin, pyrazinamide, and ethambutol
followed by a continuation regimen of
isoniazid and rifampin for 18 more
weeks as the most frequent option.
Aggressive treatment is suggested.
MDR-TB
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Treatment cont.
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Usually the regimen for MDR-TB will
consist of at least 3 TB drugs the
patient has not used before (a single
drug should never be added) and as
many as 6 drugs.
There are detailed dosages and possible
options available depending on many
factors. Newest guidelines should
always be consulted
MDR-TB
Treatment cont.
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MDR-TB treatment depends on the
drug resistance pattern present:
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It may include directly observed therapy
Occasionally, surgical resection may be
used in treatment
Detailed information about management
options are given in the references (see
CDC reference in particular)
MDR-TB
Prevention

MDR-TB may be prevented by
clinicians:
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
Choosing the appropriate therapeutic
regimen based on clinical,
microbiological, pathological,
radiological and epidemiological
information, and
Assuring a regimen with the highest
likelihood of adherence to therapy.
MDR-TB
Management, including Infection Control
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Teaching the patient and family about
preventing transmission, especially
etiquette and hygiene, use of masks
where indicated, and handwashing.
Isolation precautions are usually needed
until there have been 3 negative sputum
cultures.
Ascertaining likelihood of adherence and
using measures to enhance adherence.
Promptly isolate persons suspected or
known to have TB.
Use appropriate infection control.
MDR-TB
For sputum positive pulmonary MDR-TB,
appropriate infection control includes:
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Special airborne infection isolation control
precautions, including isolation in a negative
pressure isolation room.
Staff should wear appropriate personal protective
devices, and close door behind them.
Staff should remove personal protective devices
before exiting anteroom and sanitize hands after
leaving room. See infection control module
details, and CDC, (2005). Guidelines for
preventing the transmission of Mycobacterium
tuberculosis in health care settings.
MDR-TB References
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CDC. (2003). Treatment of TB. American Thoracic Society,
Centers for Disease Control and Prevention, and Infectious
Disease Society of America. MMWR, 52 (RR-11), 1-88.
CDC (2008). Trends in tuberculosis- United States, 2007. MMWR
57, 281-85.
CDC (2005) Guidelines for preventing the transmission of
Mycobacterium in healthcare settings, 2005. MMWR, 54, 1-141.
Lashley, F. R., & Durham, J. D. (Eds.). (2007). Emerging
infectious diseases: Trends and issues. 2nd edition New York:
Springer Publishing Co.
Mukherjee, J. S., Rich, M. L., Socci, A. R. et al. (2004).
Programmes and principles in treatment of multidrug-resistant
tuberculosis. Lancet, 363, 474-481.
Murphy, R.A. (2008) The emerging crisis of drug-resistant
tuberculosis in South Africa: Lessons from New York City. Clinical
Infectious Diseases 46, 1729-1732.
Yew, W.W. and Leung, C.C. (2008) Management of multidrugresistant tuberculosis: Update 2007. Respirology, 13, 21-46.
Nipah Virus Infection
CDC
Nipah Virus Infection-2
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
Etiologic agent: Nipah virus, a
paramyxovirus
Epidemiology:




First identified in 1998 after an outbreak of
encephalitis in farm and laboratory workers in
Malaysia at the same time as illness in pigs.
Later spread to Singapore.
Bats appear to be the natural host of the virus.
Believed that environmental events such as
drought and tree cleaning led to bats being
closer to pigs, transmitted virus to pigs, then
to humans.
Nipah Virus Infection-3

Incubation period:

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
Transmission:



4 days to 2 months
In most, 2 weeks or less
Transmitted between bats, humans, and pigs
Humans infected secondarily by droplet
transmission
Clinical course:
Can be similar to subacute sclerosing
panencephalitis, caused by the measles virus
 Infected people can be initially asymptomatic
and develop encephalitis months after
exposure. May also cause pneumonitis.

NIPAH Virus Infection-4

Clinical manifestations may include:
Encephalitis with myoclonus
 Pneumonitis-in some fever, headache
 Fever
 Dizziness
 Headache
 Vomiting
 Reduced levels of consciousness
 Confusion
 Brain-stem dysfunction
 Aneflexia
 Hypotonia
 Hypertension
 Tachycardia

NIPAH Virus Infection-5

Complications may include:





Septicemia
GI bleeding
Renal impairment
Of those recovering, about 1/4 had
residual neurological defects
Mortality: May approach 40% of
those with severe illness
NIPAH Virus Infection-6

Treatment:



Supportive
Ribavirin appears useful
Nursing Considerations:



Standard isolation precautions
Human to human spread not known
Supportive and symptomatic nursing management
Sources:
CDC. Hendra virus disease and Nipah virus encephalitis, October 19, 2007.
Solomon, T. (2003). Exotic and emerging viral encephalitis. Current Opinion
in Neurology, 16, 411-418.
Wong, K.T., Shieh, W.J., Zaki, S.R., et al. (2002). Nipah virus infection, an
emerging paramyxoviral zoonosis. Springer Seminars in
Immunopathology, 24, 215-228.
Tick-Borne Encephalitis

Etiology:


Tick-borne
encephalitis virus
(TBEV), a flavivirus
Has 3 subtypes: Far
Eastern, Siberian,
and European
TBEV-2

Epidemiology:



Endemic to central and eastern Europe, and
the far east.
Natural habitat is forest undergrowth in Europe
and Asia where TBEV is maintained in a cycle
involving ticks and animal hosts especially
rodents but also larger animals such as goats,
cows, and sheep.
These ticks need certain climactic conditions
that determine their distribution. Global
satellite data have contributed to this
knowledge.
TBEV-3

Transmission:

Under natural conditions, most commonly through






Bite of infected tick
Ingestion of unpasteurized milk
Laboratory cases have been acquired through needlestick and through aerosol infection when glass bottles
with high TBEV concentrations were accidentally broken.
There could be a potential for freeze-dried TBEV to be
stored in glass and then broken to allow release of TBEV
into the air.
A small number of cases from blood transfusion, breast
feeding and slaughter of goats have been described.
May be excreted in urine and feces.
Could cause “significant problems on small scale” if used
in bioterrorism.
TBEV-4

Incubation period:


7-14 days typically but can be 2 to 28 days.
Clinical manifestations:


70-95% of naturally-acquired human infections
in endemic areas are subclinical or
asymptomatic.
Onset is usually abrupt, and early symptoms
include fever, fatigue, nausea, vomiting,
muscular pain especially in neck, shoulder,
lower spine and limbs.
TBEV-5

Clinical manifestations cont.:




After the initial symptoms, there are various
forms of TBE that may develop (discussed in
following frames), and a short afebrile period
may occur.
The Eastern subtype is said to follow a
monophasic course.
The Western subtype tends to be biphasic.
In the febrile form (occurring in about 1/3), no
neurological symptoms are seen and recovery
is usually complete.
TBEV-6

Clinical manifestations cont.:
1.
Meningeal form severe headaches, photophobia and pain in the
eyes.
b. Fever may last 1 to 2 weeks. Recovery is gradual.
a.
2.
Meningoencephalitis form hallucinations, may become unconscious.
b. Can develop bradycardia, gastric hemorrhage,
hyperkinesia, hemiparesis, and hemiplegia as well
as epileptic seizures.
c. Mortality is up to 30%; recovery is slow, and
hemiplegia may last.
a.
TBEV-7

Clinical manifestations cont.:
3. Poliomyelitic form a. Weakness, numbness or paralysis in a
limb.
b. May have paresis of neck, shoulder and
upper limbs, wrist drop and drooping head
on standing, muscle atrophy.
c. Patients show progressive deterioration,
and about half show partial recovery from
the neurological manifestations.
TBEV-8

Clinical manifestations cont.:
4. Polyradiuculoneuritic form –
a. After onset in first phase, temperature returns to
normal for 1 to 2 weeks after which symptoms of
CNS damage and meningeal and focal neurological
symptoms occur.
b. There is peripheral nerve pain.
c. Recovery is usually complete.
5. Chronic form –
a. After the acute disease symptoms, neurological
symptoms may develop over a long period even
years and can include lateral sclerosis, progressive
muscle atrophy and a Parkinson like disease.
b. Mental deterioration and dementia may also occur.
TBEV-9

Treatment:



Supportive, depends on manifestations.
Close observation is needed because neuromuscular
paralysis leading to rapid respiratory failure may
develop quickly, and ventilatory support with intubation
may be needed.
Nursing Considerations:



Use standard precautions for infection control.
Supportive depending on manifestations.
Close observation is needed because neuromuscular
paralysis leading to rapid respiratory failure may
develop quickly, and intubation and ventilatory support
may be needed.
TBEV-10

TBEV Vaccine:


Active vaccines are available
Other:

Postexposure passive immunization with
specific immunoglobulin is no longer
recommended.
Sources:
Dumpis, U., Crook, D., & Oksi, J. (1999). Tick-borne encephalitis.
Clinical Infectious Diseases, 28, 882-890.
Gritsun, T.S., Lashkevich, V.A., & Gould, E.A. (2003). Tick-borne
encephalitis. Antiviral Research, 57, 129-146.
Lindquist, L, and Vapalahti,O. (2008). Tick-borne encephalitis. Lancet
371, 1861-1871.
Tickborne Hemorrhagic Fever
Viruses

Includes:




Omsk hemorrhagic fever virus
Kyasanur forest disease virus
Both are small, single stranded RNA
flaviviruses
Diseases caused:


Omsk hemorrhagic fever
Kyasanur forest disease
Tick borne Hemorrhagic Fever
Viruses-2

Epidemiology:




Both are transmitted through infected ticks.
For Kyasanur forest disease virus, the natural
host are monkeys, and the region where it is
typically found is Northern India. Forest
workers are at particular risk.
For Omsk hemorrhagic fever virus, the hosts
are typically rodents especially muskrats and
voles, and the region where it is typically
found is Siberia.
Incubation period:

2 to 9 days for both
Tickborne Hemorrhagic Fever
Viruses-3

Clinical manifestations:

Omsk hemorrhagic fever 



Begins with fever, cough, conjunctivitis,
maybe hyperemia of face and trunk but no
rash
There may be papulovesicular eruption in
throat, lymphadenopathy, splenomegaly.
May see nosebleeds, conjunctival
hemorrhaging, gastrointestinal bleeding.
May develop pneumonia and/or central
nervous system dysfunction.
Tickborne Hemorrhagic Fever
Viruses-4

Clinical manifestations cont.:

Kyasanur Forest disease 





Similar to Omsk but biphasic appearance of
symptoms is common.
Begins with sudden onset of fever and headache,
backpain, pain in extremities and prostration.
Conjunctivitis may be seen and bradycardia may be
present.
After initial symptoms may see an afebrile period of 9
to 21 days.
Up to about half develop meningoencephalitis.
On autopsy, see liver and spleen degeneration as
well as hemorrhagic pneumonia in some.
Tickborne Hemorrhagic Fever
Viruses-5

Mortality:


Treatment:


Up to 10%
Supportive
Nursing Considerations:



Supportive, depending on symptoms.
Standard isolation precautions in clinical
setting.
In laboratory, precautions are taken to protect
against airborne droplets, and this may be
necessary if widely aerosolized in attack.
Tickborne Hemorrhagic Fever
Viruses-6

Vaccine:


Inactive virus vaccine is available for
Kyasanur Forest disease.
Other:

Handled as biosafety level 4.
Sources:
Borio, L., Inglesby, T., Peters, C.J., et al. (2002). Hemorrhagic
fever viruses as biological weapons. JAMA, 287, 23972405.
Kyasanur Forest disease. Traveler's health prevention against
diseases abroad. Retrieved July 26, 2008 from:
http://www.traveldoctoronline.net/vk_home/index.htm.
Gowld, E.A., and Solomon, T. (2008). Pathogenic
flaviriviruses. Lancet 371, 500-509.
Yellow Fever



Etiology: Yellow fever virus, a flavivirus
causing viral hemorrhagic fever
Epidemiology: Occurs mainly in tropical
Africa and South America
Has two cycles:



Urban pattern of interhuman transmission,
with the mosquitos of Aedes aegypti as vectors
Sylvatic cycle, involving monkeys and
Haemogogus and Sabethes mosquitos
Considered a zoonotic infection
Yellow Fever-2


Incubation period: 3-6 days usual
Clinical manifestations:




Clinical disease can range from non-specific to
hemorrhagic fever.
Person appears acutely ill.
Symptoms include: fever, chills, malaise,
headache, dizziness, nausea, myalgia, lower
back pain, bradycardia, and may have
congested conjuctivae.
May progress to: prostration, hemorrhage,
shock.
Yellow Fever-3

Clinical course:



Acute illness gives way to apparent remission
for about 24 hours; and in some, disease
"aborts."
In 15-25%, illness reappears and is more
severe (period of intoxication).
In this phase, may see:







Fever
Vomiting, may be black
Epigastric pain
Jaundice and hepatic injury
Renal failure
Myocardial injury
May be major hemorrhagic manifestations, such as
epitaxis, melena, hematemesis, ecchymoses
Yellow Fever-4

Diagnosis:


Detection of virus or viral antigen in blood, serologic
diagnosis by measurement of IgM antibodies by ELISA.
Complications:

Before death, may see:








Hypotension
Delirium
Stupor
Coma
Metabolic acidosis
In those surviving, there is a long convalescent period
with weakness and fatigue.
There may be tubular necrosis requiring dialysis, as well
as pneumonia and hepatic injury.
Mortality:

20-50% of patients with hepatorenal disease die.
Yellow Fever-5

Treatment:


Vaccination:


Largely supportive, depending on manifestations. Higerdose ribaviris with interferons may hold promise.
Live, attenuated 17D vaccine available
Nursing Considerations:

Supportive care with standard isolation precautions
Sources:
Bryant, J., Wang, H., Cabezas, C., et al. (2003). Enzootic transmission of
yellow fever virus in Peru. Emerging Infectious Diseases, 9(8), 926-934.
Marfin, A.A., Eidex, R.S., Kozarsky, P.E., & Cetron, M.S. (2005). Yellow fever
and Japanese encephalitis vaccines: Indications and complications.
Infectious Disease Clinics of North America, 19, 151-168.
Monath, T.P. (2008). Treatment of Yellow fever: Antiviral Research 78, 116124.