Transcript Preparedness Against Biological Weapons: A Module for

Biological Weapons: Essential
Information on Category A 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 A Agents
according to the Centers for Disease
Control and Prevention (CDC)
classification. Separate modules address
Category B and Category C agents. This
module was supported in part by
USDHHS, HRSA Grant No. T01HP01407.
The format and information in this module
focuses on the use of the agent or outbreak of
disease particularly in regard to bioterrorism
including emphasis on management with
nursing applications and infection control
material. Detailed material on general
transmission of disease, infection control and
isolation precautions is in a separate module
and this should be consulted. Aspects of
preparedness are also in a separate module.
Note that for the care of persons exposed to
any biological agent, the nurse should be sure
he/she is adequately protected first.
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 A biological agents
with potential for use in a bioterrorism attack.
4. Describe the signs and symptoms of infection
with Category A agents.
5. Discuss isolation precautions for each Category A
agent.
Using Biological Agents as
Bioweapons
Biological Agents and Bioterrorism


Includes microorganisms, especially
certain bacteria and viruses, and biological
toxins such 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 and Bioterrorism-2

Biological agents can be used as weapons
in:
• Biocrimes
• Bioterrorism
• Biowarfare

Definition: North Atlantic Treaty
Organization (NATO) defines a biological
weapon as “the provision of any infectious
agent or toxin by any means of delivery in
order to cause harm to humans, animals,
or plants.”
Biological Agents and Bioterrorism-3

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-4



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






Varies according to source
NATO handbook lists 39 agents
World Health Organization (WHO) has another list
CDC lists biological agents in various categories, A,
B, and C
National Institute for Allergy and Infectious Diseases
(NIAID), National Institutes of Health (NIH) also lists
categories A, B, and 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








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








Lack of effective treatment
Need for intensive care, straining
resources
High potential for casualties/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 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.
Picture from CDC. Inhalational
anthrax.
Categories of Critical Biological
Agents as Specified by CDC

Three Categories of Agents:
• 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:
• 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:
• 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:
• Availability
• Ease of production and dissemination
• Potential for high morbidity and
mortality and major health impact
Category A Agents

These agents include the following
diseases, with the organism in
parentheses. Discussion of each individual
organism listed below follows:
•
•
•
•
•
•
•
•
Anthrax (Bacillus anthracis)
Botulism (Clostridium botulinum)
Ebola hemorrhagic fever (Ebola virus)
Lassa Fever (Lassa virus)
Marburg hemorrhagic fever (Marburg virus)
Plague (Yersinia pestis)
Smallpox (Variola virus)
Tularemia (Francisella tularensis)
Category A Agents-2

Other hemorrhagic fever viruses, such
as:
• Junin virus (Argentine hemorrhagic fever)
• Guanarito virus (Venezuelan hemorrhagic
fever)
• Machupo virus (Bolivian hemorrhagic
fever)
• Sabia virus (Brazilian hemorrhagic fever)
Anthrax (Bacillus anthracis)

Etiology:
• A gram-positive rod-like bacteria, B.
anthracis
• Capable of aerobic spore formation
• Spores can last 40 years or more
• Non-motile
• Forms capsule
Anthrax-2

Description – has several clinical types:
• Cutaneous (skin) anthrax most common.
• Gastrointestinal (GI) anthrax



Rare in developed countries
Results from infected meat that is undercooked or
raw
Can affect oropharynx or esophagus, causing ulcers
• Inhalational (respiratory) anthrax



Abrupt respiratory distress
No person-to-person transmission
Other names –
• Was known as woolsorters or ragpickers
disease.
Anthrax-3

Epidemiology:
• A zoonotic disease, primarily of animals such
as cattle, sheep, goats, deer and horses.
• Worldwide there can be up to 100,000 cases
per year. Most natural cases occur in the
Middle East, India, Asia, Africa and Latin
America. Usually rare in the US and western
Europe.
• Until the deliberate release of anthrax spores
in the US in 2001, inhalational anthrax had not
been reported in the US for more than 20
years. In 2001, 22 cases of human anthrax
were reported in the US, 2 in 2002, none in
2003, 2004, and 2005, 1 in 2006, and none in
2007.
Anthrax-4

Transmission:
• Animals become infected through ingestion of spores in
soil which germinate and produce toxins.
• Humans usually contract anthrax from contact with
anthrax infected animals or contaminated animal hair,
hides, flax, wool, excretions, blood and products such as
bone meal.
• Direct contact from infected person’s skin lesions.
• Inhalational anthrax is acquired by inhaling aerosolized
spores.
• Gastrointestinal anthrax results from eating
undercooked or raw meat or dairy products from
infected animals.
• Inhalational and gastrointestinal anthrax are not known
to be transmitted person-to-person.
• Humans may also become infected through intentional
exposure.
Anthrax-5

Transmission cont.:
• Occupational exposure in humans has been the
most usual way in which anthrax was acquired.
• Examples include farm workers, laboratory
workers or industrial exposure (see below).
• Cutaneous and inhalational anthrax cases
formerly occurred during the manufacturing
process of infected wool, hair and hides. In
2006, one case occurred in a man who
acquired the disease from an infected animal
hide he brought back from Africa to make
drums.
Anthrax-6
Incubation period:
• Cutaneous anthrax: a few hours to 12
days
• Gastrointestinal anthrax: 1 to 7 days
• Inhalational anthrax: Less than 7 days
(usually 4-6 days) but up to 2 months.
Anthrax-7

Clinical manifestations:
• Cutaneous anthrax






Local response is itching followed by small
red macule progressing to papule formation
(3-5 days usual), resembling an insect bite.
This becomes a vesicle with a painless ulcer
formation that may enlarge to 1 to 3 cm.
Black eschar develops within 7-10 days with
surrounding edema.
Typically seen on arms, hands, head or
neck.
May also have lymphadenitis and fever,
malaise and headache.
Septicemia can occur.
Cutaneous Anthrax
(Notice the edema and typical lesions)
Photos from CDC.
Notice the edema and typical lesions
Further examples of Cutaneous
Anthrax lesions Photos from CDC.
Black eschar,
redness remains
Ulcer and vesicle ring
Anthrax-8

Clinical manifestations cont.:
• Gastrointestinal anthrax




Symptoms initially are nausea, vomiting,
anorexia, fever, followed by abdominal pain,
hematemesis and bloody diarrhea.
Symptoms depend on site of lesions.
If there are lesions in oral pharynx, may
swell to affect the airway, and there may be
dysphagia and throat pain.
In gastrointestinal anthrax, ascites may
develop as may septicemia within 5 days
after onset.
Anthrax-9

Clinical manifestations cont.:
• Inhalational anthrax





There are usually two phases.
Initial symptoms are nonspecific and consist of
malaise, low grade fever, nonproductive cough and
gastrointestinal complaints such as nausea and/or
vomiting.
Sometimes there is improvement for a few days
followed by a second phase with dry cough, dyspnea,
high fever, chills, diaphoresis, tachypnea and
respiratory distress.
Bacteria enter the blood causing bacteremia, and
seeding of the meninges and gastrointestinal tract.
Abdominal pain, hematemesis, melena, cyanosis,
confusion and hemorrhagic, purulent meningitis
develop.
Anthrax-10

Clinical manifestations cont.:
• Inhalational anthrax cont. –



Meningitis occurs in about 50%.
Cardiovascular collapse and death follow if
untreated.
Because early symptoms are non-specific,
the presence of nausea and vomiting and
neurological symptoms help to differentiate
it from other disorders and a widened
mediastinum on x-ray is suggestive of
inhalational anthrax.
Inhalational Anthrax
Mediastinal widening and pleural effusion on Chest X-Ray in inhalational
anthrax
Anthrax-11

Diagnosis:
• For all, blood cultures may be done if
organism has spread.
• Lab may do rapid screening followed by
confirmatory testing.
• Combine lab testing with clinical
findings.
Anthrax-12

Diagnosis cont.:
• Cutaneous –


Gram stain, PCR, culture of exudate or eschar
Should be done before antibiotic therapy
• Gastrointestinal –


Blood cultures
Oropharyngeal swabs
• Inhalational –



Chest x-ray findings especially widened mediastinum,
pleural effusions, and pulmonary congestion
Tissue biopsy
Fluid for gram stain, PCR or culture if from sterile site
Anthrax-13

Mortality:
• Cutaneous - if untreated can be 10%20%, less than 1% with treatment
• Gastrointestinal - depends on site,
25%-60%
• Inhalation - mortality can be 45%-97%
with antibiotic therapy. The case fatality
rate may be as high as 75%.
Anthrax-14

Treatment:
• Cutaneous anthrax –


Initial therapy in adults is usually ciprofloxacin or
doxycycline; in children both are also used, although
care must be taken in children as doxycycline may
discolor teeth.
Therapy may be oral.
• Inhalational anthrax –




For adults and children, ciprofloxacin or doxycycline
are used with one or two additional antimicrobials.
Initial therapy is IV, switching to oral therapy when
appropriate.
Therapy may be as long as 60 days.
Therapy may be combined with a 3 dose regimen of
anthrax vaccine for prophylaxis.
Anthrax-15

Treatment cont.:
• Gastrointestinal anthrax –

May be treated with the same antibiotic regimens as
inhalation because of potential to spread to
respiratory tract.
• Note: Post-exposure prophylaxis may be given
to those exposed to an initial release of
anthrax as soon as possible after exposure.
This is usually administered orally for 60 days
with ciprofloxacin and doxycycline being the
most desired followed by amoxicillin which is
preferred for pregnant women. If organism is
susceptible, children may also be switched to
amoxicillin.
Anthrax-16

Nursing considerations:
•
•
•
•
Be sure decontamination has taken place.
Appropriate isolation precautions.
Supportive care as needed for symptoms.
If associated with intentional release, psychosocial
support/therapy is needed.
• In analysis of survivors of fall 2001 anthrax release, a
year later survivors had reported lower health-related
quality of life and greater overall psychological distress.
Those who had inhalation anthrax reported loss of
functional capacity, and some still had respiratory
abnormalities.
• Adherence may be an issue for persons on long-term
antimicrobial therapy and nurses should plan to address
this.
Anthrax-17

Isolation Precautions:
• Cutaneous anthrax – Standard and the
transmission based contact precautions. Avoid
any contact with skin lesions or drainage.
• Inhalational anthrax – Both standard and
contact precautions have been recommended
in addition to respurology N95 mask or PAPR &
protective clothing for environmental aerolized
powder on person.
• Gastrointestinal anthrax – Standard
precautions.
Anthrax-18

Vaccine:
• Multidose vaccine available but currently used for special
populations such as the military.
• Both live cellular and live acellular vaccines are available.
Recombinant vaccines are in development.

Other:
• Persons known to be exposed to anthrax spores should
remove clothing and shoes and leave at worksite and wash
exposed skin including any jewelry and glasses.
• Removed clothing should be bagged.
• At home, systematic showering with systematic cleaning
from hair down should be done if at risk for higher
contamination.
• Care needs to be taken when removing outer clothing to
keep inner clothing from being contaminated.
• Biosafety level 2 handling.
Anthrax – Special Considerations
Re: Bioterrorism

Anthrax is considered one of the most
important biological agents with potential
for use as a bioterror agent.
• It can be weaponized in an aerosolized stable
spore form.
• One deep breath at the site of intentional
release can result in inhalational anthrax with
high mortality.
• Environmental surveillance and assessment is
needed.
• Decontamination procedures are needed.
Anthrax – Special Considerations
Re: Bioterrorism-2

Anthrax potential for use as bioterror
agent cont.:
• Pre-exposure immunization available for
defined population segments.
• If anthrax is suspected, one part of the patient
assessment is to assess whether there is an
epidemiological linkage to a plausible
environmental exposure such as through the
person’s occupation.
• Antimicrobial prophylaxis will be used for
persons potentially exposed to anthrax. In
those who are demonstrated not to be
exposed, prophylaxis can be discontinued. For
others, this will be continued for about 60
days.
Botulism
(Clostridium botulinum toxin)

Etiology:
• Toxin from Clostridium botulism, a sporeforming bacillus.
• Seven known types cause disease.
• These toxins are potent neurotoxins.
• Toxin prevents acetylcholine release and
blocks neuromuscular transmission,
presynaptic inhibition affecting autonomic and
motor receptors.
• Minute quantities of botulinum toxins can
cause death, as they are extremely poisonous.
• Infective dose: 0.001 micrograms.
Botulism-2

Types:
•
•
•
•


Foodborne – most common
Wound
Infant
Inhalational - rare, may be intentional
Incubation period: For foodborne botulism:
18-36 hours usual but can be 6 hours to 10
days.
Incubation period for inhalation botulism is
24-72 hours after exposure.
Botulism-3

Epidemiology:
• Most cases of foodborne botulism occur
through improperly canned or prepared foods
especially those that are of low acidity such as
corn, beans, tomato sauce.
• Improperly heated and stored sauteed onions
were the cause of one outbreak in Peoria,
Illinois.
• Botulinum toxins have been weaponized to be
delivered by aerosol means.
• Wound and infant botulism are not discussed
here.
Botulism-4

Transmission:
• Ingestion,
inhalation (in
deliberate release
situation) or
absorption.
• Not transmissable
from person-toperson.
Botulism-5

Clinical manifestations:
•
•
•
•
•
•
•
Blurred vision
Dilated pupils
Diplopia
Ptosis
Dry mouth, and
Photophobia
These may be followed by:





Dysarthria
Dysphagia
Dysphonia
Generalized weakness, and
A symmetrical descending progressive paralysis
leading to respiratory failure.
Botulism-6

Clinical manifestations cont.:
• Cranial nerve palsies are responsible for
symptoms, such as difficulty in speaking
or swallowing.
• Symptoms such as constipation and
urinary retention may be seen and
nausea and vomiting may be present.
• Patients are usually alert and afebrile.
Botulism-7

Diagnosis:
• By detection of
toxin in serum,
stools or gastric
secretions.
Botulism-8

Treatment:
• Important to recognize botulism early and
administer botulism antitoxin as soon as
possible to neutralize the circulating toxin or
progression will continue to occur.
• Antitoxin does not reverse paralysis but limits
it.
• In cases of aerosol exposure, the antitoxin is
effective before clinical symptoms are present
but if given later will not prevent respiratory
failure.
Botulism-9

Treatment cont.:
• Full recovery can take a long time—months-as presynaptic axons regenerate and new
synapses are formed.
• In the botulism outbreak in Peoria in the
1980s, symptoms such as fatigue, headache,
and weakness lasted for years.
• Therapy includes rapid administration of
botulism antitoxin, monitoring of vital capacity
to institute rapid ventilatory support when vital
capacity falls below 12 ml/kg.
Botulism-10

Nursing considerations:
• Use of standard precautions
• Isolation room not required
• Observe for possible respiratory distress which
can occur rapidly
• Assist patient with communication if on a
mechanical ventilator
• Prevent nosocomial infections through use of
good hygiene
• Prevent deep vein thromboses (DVT)
• Give appropriate bowel and bladder care
Botulism-11

Nursing considerations cont.:
• May need extensive rehabilitation for
swallowing, speech, muscle strength and so
on.
• Address psychosocial issues and fears
associated with the progressive paralysis and
loss of voluntary movement and speech.
• CDC recommends decontamination of patients
and their clothing with soap and water if
exposed to aerosolized botulism toxins and
decontamination of exposed surfaces by
cleaning with a bleach solution.
Botulism-12

Other:
• In case of use in bioterrorism, resources such
as ventilatory support (which may be needed
in the long term) and supportive intensive care
services would be overwhelmed, as would the
availability of antitoxin.
Prevention:
• Pre-exposure vaccination with toxoid is
available for military personnel and laboratory
workers at high risk of exposure.
• Development of recombinant toxoid vaccines
for wider use is underway.
Ebola Hemorrhagic Fever
(Ebola virus)

Etiology:
• Ebola virus, a rod-shaped RNA
virus in the filovirus family.
• Changes shape rapidly.
• The filamentous form is
associated with high infectivity.
• Has 4 (possibly 5 )
subtypes to date:





Zaire
Sudan
Reston
Cote d’Ivoire (Ivory Coast)
A possible new subtype
responsible for the outbreak in
Uganda in 2007-8
Picture from CDC
Ebola-2

Description:
• Is a viral hemorrhagic fever caused by the
Ebola virus.
Epidemiology:
• Ebola virus occurs naturally in Africa.
• While subclinical infections have been noted,
typically Ebola hemorrhagic fever emerges in
sporadic outbreaks.
• Outbreaks have been reported in the
Democratic Republic of the Congo, Gabon,
Sudan, the Ivory Coast, Uganda and Republic
of the Congo.
Ebola-3

Epidemiology cont.:
• First outbreaks
recognized in 1976 in
Sudan and in Zaire,
now part of the
Democratic Republic of
the Congo.
• It is believed to be a
zoonotic virus normally
maintained by a natural
host native to Africa.
Photo from CDC.
Ebola-4

Epidemiology cont.:
• The natural reservoir for Ebola virus is not known, but it
is believed that human outbreaks occur when a person
is exposed to an infected animal. Fruit bats have been
suggested as having a role.
• Outbreaks also occur among gorillas and chimpanzees.
• Ebola-Reston occurred in infected monkeys in the
Phillipines, but is not known if Ebola is also native to
Asia since there have not been other recognized
outbreaks there.
• The most recent reported outbreaks are in The
Democratic Republic of the Congo (2007) and Uganda
(2007-2008)
• The outbreak in Uganda is believed due to a previously
unknown subtype with a lower mortality rate.
Ebola-5

Transmission:
• Person-to-person spread may occur when a person
comes into contact with infected blood, tissues,
secretions, or excretions of another person.
• Infection may also occur through contact with
contaminated objects.
• Infection may further occur in hospitals or health care
settings through:



The use of contaminated medical equipment, such as
reused needles and syringes,
Contaminated multivials of medicine, and/or
Lack of appropriate infection control.
• Traditional burial ceremonies involving contact with the
infected corpse may spread Ebola virus.
• Handling of infected wild animal carcasses, such as
chimpanzees, gorillas and duikers, including food
preparation activities.
Ebola-6


Incubation period: 2 to 21 days.
Clinical manifestations:
• Asymptomatic infection may occur.
• In most cases, the onset of illness is abrupt
with fever, headache, myalgia, weakness,
malaise and pharyngitis.
• These may be followed by nausea, diarrhea
and vomiting as well as stomach pain.
• A maculopapular rash may appear around the
5th day and desquamation can occur.
• Conjunctival injection, hiccups, and
hemorrhage from orifices as well as petechiae
and ecchymoses may be seen.
• Blindness can occur.
• Obtunding may occur.
Ebola-7

Diagnosis:
• By antigen-capture enzyme-linked
immunosorbent assay (ELISA), IgM
ELISA, polymerase chain reaction
(PCR), and virus isolation.

Mortality:
• The mortality rate is high, usually 25%
to 90%.
Ebola-8

Treatment:
• Supportive



This may include maintenance of appropriate fluid
and electrolytes, oxygenation and blood pressure,
and treating complications promptly.
Immune plasma from convalescent patients has been
used in some instances.
Nursing considerations:
• Limit number of staff approaching patient, use
mask, gown, gloves, goggles, leg coverings,
and shoe coverings.
• Be sure health care staff understands the
infection control procedures in use.
• Prevent other cases by preventing nosocomial
transmission, including to health care staff.
Ebola-9

Nursing considerations cont.:
• Appropriate infection control critical.
• Should use immediate isolation of suspected case with
airborne and contact precautions, as well as standard
precautions and barrier nursing.
• Because of the severity of the disease, many
practitioners in the field use double masks, gowns,
gloves and so on in implementing precautions.
• Individual room with negative air pressure.
• In places where no negative pressure isolation rooms
exist, the patient should be put in a private room with a
HEPA filtration unit.
• Limit unnecessary blood draws and other procedures.
• Use N95 or higher respirators for aerosol generating
procedures in settings where AIIRs are unavailable.
Ebola-10

Nursing considerations cont.:
• The patient should remain in their room with
doors and windows closed.
• In full service hospitals, an anteroom may be
used between the private room and the corridor.
• If there are a large number of patients needing
care, a designated nursing unit may be created
with a barrier plan to seal off the existing
ventilation system from other hospital areas and
limiting access to the unit.
• In cases of mass numbers, a whole facility or
large gym may be dedicated.
• Prevent cases through education of family and
community about methods of spread and how to
avoid them and why these precautions are
necessary.
Ebola-11

Nursing considerations cont.:
• Be sure staff fully understand isolation
precautions.
• During some Ebola outbreaks, governments
outlawed traditional ways of preparation of
bodies and other burial practices.
• Specific guidelines are available online for
infection control for viral hemorrhagic fever in
the African health care setting at:
http://www.cdc.gov/ncidod/dvrd/spb/mnpages
/vhfmanual.htm
• Supportive care depending on manifestations
including maintaining appropriate fluid and
electrolytes.
Ebola-12

Vaccine:
• Experimental
vaccine in animals
Ebola-13

Prevention:
• Prevent other cases by preventing
nosocomial transmission including to
health care staff.
• Prevent cases through education of the
family and community about methods of
spread and how to avoid them.
• The latter should include information
that Ebola virus may be transmitted in
semen up to 12 weeks after infection.
Ebola-14

Social, behavioral and cultural issues:
• Affected families may be stigmatized and not be
allowed in other dwellings or schools.
• Families tend not to seek medical care because
of:




Cost,
Mistrust of hospitals (nosocomial spread supports these
fears),
Belief in traditional remedies and healers, and
Problems of transportation to health care facilities
especially in rainy season.
• Traditional burial practices contribute to personto-person spread.
• Civil unrest and wars can exacerbate outbreaks
through overcrowding, poor sanitation, and
economic dispair.
Ebola-15

Other notes:
• Ebola outbreaks tend to burn out
relatively quickly because of the high
mortality rates.
• Ebola virus is studied in a level 4
biosafety facility.
• There are great fears that the Ebola
virus could mutate into a form that is
more easily transmitted from human-tohuman or becomes airborne.
Lassa Fever (Lassa virus)

Etiology:
• Lassa virus, a single
stranded RNA virus in
the arenavirus family.

Description:
• Is a viral hemorrhagic
fever caused by the
Lassa virus.
Lassa virus electron
micrograph. Image
courtesy, C.S.
Goldsmith and M.
Bowen (CDC).
Lassa Fever-2

Epidemiology:
• Endemic in West Africa, where it kills thousands per year,
especially in Sierra Leone.
• Fewer cases are seen in Nigeria, Guinea and Liberia.
• Subclinical infection commonly occurs in areas of rural West
Africa where Lassa virus is endemic. This is known through
the high prevalence of antibodies to Lassa virus in the
serum in seropositivity studies in West Africa.
• Occasional outbreaks occur, often with high mortality rates.
• In 2004, a case was identified in a New Jersey man who had
recently returned to the Trenton area from Africa, and in
2006 a case was diagnosed in a man who returned to
Germany from Sierra Leone.
Lassa Fever-3

Epidemiology
cont:
• The natural hosts
are rodents of the
Mastomys genus.
• These rodents
prefer to live in or
around human
dwellings. These
rodents are
persistently infected
and shed virus in
excreta.
Lassa Fever-4

Transmission:
• Infection results through:





Direct contact with infected rodent urine or
droppings,
Through touching objects or eating food
contaminated by infected excreta,
Through breaks in the skin,
Through inhalation of infected rodent excreta in
aerosol form, such as when cleaning a heavily
contaminated area, and
Through food preparation or consumption of infected
rodents. These rodents are considered a delicacy in
this part of Africa.
Lassa Fever-5

Transmission cont.:
• Richmond & Baglole (2003) note that Lassa viral
antibodies occur after a febrile illness in twice as
many people who eat these rodents than in those
who do not, and deafness (one of the sequelae of
Lassa fever) occurs four times more frequently.
• Person-to-person spread may occur when a
person comes into contact with:




Infected blood,
Tissues,
Secretions, or
Excretions.
Lassa Fever-6

Transmission cont.:
• Lassa virus is found in semen up to 3 months
after infection and in urine a month after
disease onset.
• Infection may also occur in hospitals or health
care settings through use of contaminated
medical equipment such as needles and
syringes that may be reused or through
overcrowding and poor hygiene.
• Traditional burial ceremonies involving contact
with the infected corpse may spread Lassa
virus (see cultural considerations under Ebola).
Lassa Fever-7

Transmission cont.:
• Lassa virus may be excreted in urine up to 9
weeks after infection, and excreted in semen
up to 3 months after infection.


Incubation period: 5 to 21 days.
Clinical manifestations:
• In about 80%, affected persons are
asymptomatic or mildly affected.
• In 20%, symptoms may be severe and may
mimic other hemorrhagic fevers.
Lassa Fever-8

Clinical manifestations cont.:
• Richmond & Baglole (2003) divide clinical
stages and symptoms as follows:

Stage 1 (days 1-3)
• Symptoms include general weakness and malaise, high
fever, about 39o C with higher peaks.

Stage 2 (days 4-7)
• Symptoms include sore throat (with white exudative
patches); headache; back, chest, side, or abdominal
pain; conjunctivitis; nausea and vomiting; diarrhea;
productive cough; proteinuria; low blood pressure
(systolic <100 mm/Hg); and anemia.

Stage 3 (after 7 days)
• Symptoms include facial edema; convulsions; mucosal
bleeding (mouth, nose, eyes); internal bleeding; and
confusion or disorientation.

Stage 4 (after 14 days)
• Symptoms include coma and death.

Not all progress through all stages.
Lassa Fever-9

Diagnosis:
• Reverse transcription polymerase chain
reaction (PCR) can diagnose close to 100% but
takes time.
• Enzyme linked immunosorbent assays (ELISA)
for Lassa virus antigen and for virus IgM are
more than 85% sensitive and specific together.
• If laboratory tests are not available, clinical
diagnosis should be suspected in patient with
fever at or above 38o C or 100.4o F who do not
respond adequately to antibiotics or
antimalarial drugs.
Lassa Fever-10

Complications:
• Includes mucosal bleeding, sensorineural
deafness, hair loss, loss of coordination,
spontaneous abortion in women, and both
pleural and pericardial effusion

Treatment:
• Supportive such as fluid replacement.
• Intravenous ribavirin is effective especially
when given early.
• Thus, early diagnosis and clinical suspicion is
needed.
Lassa Fever-11

Management:
• Strict standard, contact and droplet isolation of
suspected cases and maintaining procedures
for handling body fluids and excreta as well as
appropriate infection control procedures.
• Stringent barrier nursing procedures.
• Limit number of staff approaching patient.
• Use N95 or higher respirators when performing
aerosol – generating procedures.
Lassa Fever-12

Management cont.:
• Use mask, face shield, gown, gloves, leg
coverings, and shoe coverings.
• Be sure health care staff understands
the infection control procedures in use.
• Consult
http://www.cdc.gov.mcidod.dhgp/pdf/isolation2007.pdf
Lassa Fever-13

Management cont.:
• Nurses should provide education to patients
and families regarding why these precautions
and procedures are necessary and how to
prevent the spread of the virus.
• Specific guidelines are available online for
infection control for viral hemorrhagic fevers in
the African health care setting at:
http://www.cdc.gov/ncidod/dvrd/spb/mnpages
/vhfmanual.htm
Lassa Fever-14

Prevention:
• Prevent other cases by preventing nosocomial
transmission including to health care staff.
• Prevent cases through education of the family and
community about methods of spread and how to avoid
them.


Vaccination: Experimental
Mortality:
• Varies.
• In general population may be 1 to 2%, but in those who
are hospitalized, is generally estimated at up to 25%.
• In Sierra Leone, one study indicated that 25% of all
maternal deaths were due to Lassa fever (Price, FisherHoch, Craven & McCormick, 1988).
Lassa Fever-15

Social, behavioral and cultural
issues:
• Because Lassa virus is spread through
rodents, families may wish to continue
to eat the “sweet meat” of this rodent
and not associate that practice with
developing Lassa fever since in many
cases, infection will be asymptomatic or
mild.
• Affected families may be stigmatized
and not be allowed in other dwellings or
schools.
Lassa Fever-16

Social, behavioral and cultural issues
cont.:
• Families tend not to seek medical care because
of:






Cost,
Mistrust of hospitals (nosocomial spread supports
these fears),
Belief in traditional remedies and healers,
Non-availability of a quick early diagnostic test in the
field,
Problems of transportation to health care facilities
especially in rainy season, and
Attribution of some complications, such as
miscarriage, to “witchcraft” or fault of the woman.
Lassa Fever-17

Social, behavioral and cultural
issues cont.:
• Traditional burial practices contribute to
person-to-person spread.
• The resulting deafness in some may
lead to social isolation.
• Civil unrest and wars can exacerbate
outbreaks through overcrowding, poor
sanitation, and economic dispair.
Lassa Fever-18

Other notes:
• Lassa fever has been diagnosed in
travelers including relief workers and UN
peacekeepers returning from West
Africa to Europe and North America.
• A case was imported to New Jersey in
August 2004. The patient was
hospitalized and subsequently died. No
further transmission was identified.
• Lassa fever is studied in a level 3
biosafety facility.
Marburg Hemorrhagic Fever
(Marburg virus)

Etiology:
• Marburg virus, a RNA
virus in the filovirus
family, the only other
member of which is
Ebola virus.

Description:
• Is a viral hemorrhagic
fever caused by the
Marburg virus.
• Also called Marburg
disease.
Image courtesy of Russell Regnery,
Ph.D., DVRD, NCID, CDC.
Marburg hemorrhagic fever-2

Epidemiology:
• Marburg hemorrhagic fever was first
recognized in 1967 among workers in
laboratories in Germany and was then
Yugoslavia.
• The source of this infection was infected green
monkeys imported from Africa, specifically
Uganda.
• The next reported index case was in 1975 in a
tourist who apparently acquired the infection in
Zimbabwe, and who was hospitalized in South
Africa. He transmitted Marburg virus to his
travel companion and to a nurse who cared for
him.
Marburg hemorrhagic fever-3

Epidemiology cont.:
• In 1998, an outbreak occurred in the
Democratic Republic of the Congo, and the
index case was believed to have acquired
infection from a source in a gold mine there.
• In late 2004 and 2005, an outbreak occurred
in Angola. Of the 175 identified cases as of
4/4/05, 155 had been fatal. Other outbreaks
were relatively small. Another small outbreak
occurred in a mining community in Uganda in
2007. In July 2008 a Dutch tourist returned to
the Netherlands with Marburg fever.
• The natural host for Marburg virus is unknown.
Marburg hemorrhagic fever-4

Transmission:
• Person-to-person spread may occur when
a person comes into contact with infected
blood, tissues, secretions, or excretions, or
has close contact with an infected person.
• Infection may also occur through contact
with contaminated objects or through
droplets of body fluids.
• The virus is still found in seminal fluid
months after infection, and sexual
transmission from a male to a female has
been documented.
Marburg hemorrhagic fever-5

Incubation period:
• Typically 3-10 days

Clinical manifestations:
• In most cases, the onset of illness is abrupt
with fever, chills, headache, and myalgia.
• Nausea, vomiting, chest pain, pharyngitis,
abdominal pain and severe diarrhea may be
seen.
• A maculopapular rash may appear around the
5th day.
Marburg hemorrhagic fever-6

Clinical manifestations cont.:
• Other severe symptoms such as jaundice;
pancreatitis; severe weight loss; delirium;
shock; liver failure; massive hemorrhage
through vomitus, eyes, skin, and vagina; and
multiorgan dysfunction may be seen.
• Recovery is prolonged and may include
hepatitis, transverse myelitis, uvietis, and/or
orchitis in men as well as prolonged hepatitis.
Marburg hemorrhagic fever-7

Diagnosis:
• By antigen-capture enzyme-linked
immunosorbent assay (ELISA), IgM capture
ELISA, polymerase chain reaction (PCR), and
virus isolation.
• Diagnosis can be difficult because signs and
symptoms can be similar to diseases such as
malaria or typhoid fever or be nonspecific,
especially initially.
• Diagnosis is particularly difficult when only one
or a few cases appear.
Marburg hemorrhagic fever-8

Treatment:
• Supportive, and may include:






Maintenance of appropriate fluid and
electrolytes,
Oxygenation,
Frequent blood pressure checks,
Replacement of lost blood and clotting
factors, and
Treating complications promptly.
Immune plasma from convalescent patients
has been used in some instances.
Marburg hemorrhagic fever-9

Management:
• Strict isolation of suspected cases and
maintaining procedures for handling
body fluids and excreta as well as
appropriate infection control procedures
using standard, contact, and airborne or
droplet precautions.
• Stringent barrier nursing procedures.
• Do not wear jewelry.
• Limit number of staff approaching
patient.
Marburg hemorrhagic fever-10

Management cont.:
• Use mask, fluid-proof long-sleeved gown,
gloves, goggles, leg coverings and shoe
coverings that are at least ankle high and fluid
proof (may need to be higher if floor is visibly
soiled).
• Use double disposable gloves if handling any
sharp device, and be sure gloves cover cuff of
gown.
• Use hair covering and disposable face shields if
needed.
Marburg hemorrhagic fever-11

Management cont.:
• Disposable N-95 respirators should be
worn when entering room.
• Remove shoe covers and gloves as well
as gowns before exiting.
• Wash hands immediately on leaving
room with antimicrobial agent.
• Use disposable equipment when
possible or dedicated equipment such as
stethoscopes to be kept in patient’s
room.
Marburg hemorrhagic fever-12

Management cont.:
• Be sure health care staff understands the
infection control procedures in use.
• Prevent other cases by preventing nosocomial
transmission including to health care staff.
• Specific guidelines are available online for
infection control in the African health care
setting at
http://www.cdc.gov/ncidod/dvrd/spb/mnpages
/vhfmanual.htm
• Also see information in module discussing
infection control, and at
http://www.cdc.gov/ncidod/dhgp/pdf/isolation
2007.pdf
Marburg hemorrhagic fever-13

Prevention:
• Prevent other cases by preventing
nosocomial transmission including to
health care staff.
• Prevent cases through education of the
family and community about methods of
spread and how to avoid them.
• Should include information that Marburg
virus may be transmitted in semen as
long as 3 months after infection.
Marburg hemorrhagic fever-14

Mortality:
• The mortality rate is high, usually 23 to 25%
or more.

Vaccine:
• Experimental vaccine is being looked at in
animals.

Other notes:
• Marburg virus is studied in a level 4 biosafety
facility.
• Knowledge of Marburg hemorrhagic fever and
Marburg virus is somewhat limited due to the
few number of cases known.
Plague (Yersinia pestis)

Plague is considered a Category A agent
for bioterrorism because:
• Plague bacteria are not difficult to obtain,
• Aerosolized plague bacteria are easily
transmitted,
• There is a high attack rate,
• Clinical disease is severe, and
• The word “plague” has a high psychological
impact.

A sudden outbreak of disease due to an
intentional release might present as
severe pneumonia and sepsis.
Plague-2
Picture from CDC
Plague-3

Etiology:
• Yersinia pestis, a small gram-negative
rod-like bacilli.

Description:
• Was known as the Black death in the
bubonic form in the middle ages when it
killed 20-30 million in Europe.
• In the mid 1800s, it killed 12 million in
China.
Plague-4

Epidemiology:
• Plague is
considered a
zoonosis.
• Y. pestis is
transmitted from
infected rodents
such as rats, mice,
gerbils, chipmunks,
and prairie dogs to
humans via infected
fleas.
Picture from CDC
Plague-5

Epidemiology cont.:
• Cats and dogs, also may become infected by
eating infected rodents.
• Plague occurs worldwide.
• In the US there are generally 10 to 15
reported cases of plague each year, most
commonly in rural areas of New Mexico,
Colorado, Arizona, California, Oregon and
Nevada.
• Worldwide there are 1,000-3,000 cases
reported each year.
Plague-6

Epidemiology cont.:
• In the fall of 2002, a hospital in New
York City admitted a couple who were
found to have plague acquired in their
home state of New Mexico before
traveling to New York.
• Most cases occur in summer.
• About 30% of cases occur in
southwestern US.
• Suspicion should be raised if it occurs in
other geographic areas.
Plague-7

Clinical types:
• Bubonic – infected lymph nodes leading
to development of buboes. Most
common.
• Septicemic – organisms are bloodborne, primary through dried inoculation
or secondary from bubonic or
pneumonic plague.
• Pneumonic – is transmissible by aerosol.
Rarest, high mortality.
Plague-8

Transmission:
• Via bite of infected fleas,
• Through contact with infected animals or their
fluids, and
• In pneumonic plague, animal-to-person, or
person-to-person via droplets.
• In bioterrorism, organisms would most likely
be transmitted through aerosol dispersion.

Incubation period:
• Bubonic – 2 to 8 days after exposure
• Pneumonic – 1 to 4 days after exposure
Plague-9

Clinical manifestations:
• Y. pestis produces an endotoxin that
can lead to shock, sepsis, disseminated
intravascular coagulation (DIC), and
multiorgan failure.
• Bubonic –

May experience abrupt onset of flu-like
symptoms such as fever, chills, headache,
and malaise shortly before or at the same
time as the bubo which is a swollen, warm,
reddened (often around the edges), very
tender lymph node(s) usually in the
inguinal, axillary or cervical region.
Plague-10

Clinical
manifestations
cont.:
• Bubonic cont. –


Patients may
become prostrated
with episodes of
agitation and
restlessness.
Secondary
septicemia may
result and this can
lead to secondary
pneumonic plague.
Picture from CDC
Plague-11

Clinical manifestations cont.:
• Pneumonic (primary) –



Presentation is severe, fulminant, rapidly
progressing pneumonia.
Signs and symptoms include fever, dyspnea,
and cough with hemoptysis, and chest pain.
May also have nausea, vomiting, diarrhea,
purpura, and abdominal pain.
Plague-12

Clinical manifestations cont.:
• Septicemic (primary) –



Presentation resembles other gram-negative
septicemias including high fever, chills,
malaise, hypotension, nausea, vomiting and
diarrhea.
May also have purpura and disseminated
intravascular coagulation (DIC).
May spread rapidly to central nervous
system resulting in meningitis, lungs and
other sites.
Plague-13

Diagnosis:
• There are three levels of laboratory test
criteria for diagnosis according to CDC:



Suspected
Presumptive
Confirmed
Plague-14

Diagnosis cont.:
• Diagnosis is by compatibility of clinical symptoms:



Along with stain or smear positive specifically for Y.
pestis, or if a single serum specimen is tested and the
anti-F-1 titer by agglutination is greater than 1:10
(presumptive),
Or a small gram-negative coccobacilli from affected
tissue (suspected), or if an isolated culture is lysed by
specific bacteriophage,
If two serum specimens demonstrate a four-fold anti-F-1
antigen titer difference by agglutination testing, or if a
single serum specimen tested by agglutination has a titer
of more than 1:128, and the patient has no previous
history of plague exposure or vaccination history
(confirmed).
Plague-15

Mortality:
• Bubonic – Untreated bubonic plague has a
mortality of 40 to 60% but with treatment is
less than 10%.
• Pneumonic – Untreated pneumonic plague has
a mortality rate of 95% to 100%. With
treatment the mortality rate may still approach
60%. It is essential that antimicrobial
treatment begin within 24 hours.
• Septicemic – Untreated septicemic plague has
a mortality rate of essentially 100%. With
treatment the mortality rate may still approach
60%. It is essential that antimicrobial therapy
begin within 24 hours.
Plague-16

Treatment:
• Streptomycin, IM every 12 hours has been the
therapy of choice followed by gentamicin (5
mg/kg per day) which is more readily available
in the US.
• Doxycycline and the fluoroquinolones are
considered alternate therapies.
• Supportive care, including hemodynamic
monitoring, especially for septic shock is
necessary.
• Buboes are generally not incised and drained,
but regress with antibiotic treatment.
• Chloramphenicol may be used for treatment of
plague meningitis if it occurs.
Plague-17
Prophylaxis and Vaccination
• Post-exposure prophylaxis with doxycycline or
ciprofloxacin may be used for those with
known exposure or close contact with an
infected person.
• Pre-exposure prophylaxis is not available in
the US.
• A killed cell vaccine is said to be available in
the UK.
• Usually will become non-infective after several
days of antimicrobial therapy.
Plague-18

Nursing considerations:
• Standard and droplet isolation
precautions should be used for the
pneumonic type and the ??? continued
until sputum is negative.
• Standard and contact precautions used
for bubonic if open wounds unless
progression to lungs occurs.
• Avoid contact with drainage.
• See module on infection control or CDC
site for details.
Plague-19

Nursing considerations cont.:
• Supportive nursing care varies
according to type and symptoms and
includes appropriate information to
patients, family and staff about:



Information on infection control (included in
another module as is instruction on largescale outbreak management).
Consider emotional impact of word,
“plague.”
On first patient contact with possible plague
case, assess travel history, animal contacts
and any infected insect bites especially from
fleas.
Smallpox (Variola virus)

Description and Etiology:
• Caused by the variola virus, a DNA virus
member of the orthopox virus family.
• Other orthopoxes include monkeypox,
camelpox and chickenpox.

Epidemiology:
• The last natural human case of smallpox
occurred in 1977 in Somalia.
• No animal reservoir has been identified.
• Identification of even one case of smallpox
constitutes an international public health
emergency.
Smallpox-2

Transmission:
• Droplet
• Aerosol
• Direct person-to-person contact including skin lesions
and secretions or
• Through contact with contaminated linens, clothing,
surfaces, and other fomites
• Smallpox is highly contagious

Incubation:
• Typically 12 to 14 days after infection but can be 7 to 17
days.
• The person may be contagious during prodrome phase
and is most contagious as rash forms.
• Is contagious until all scabs are gone.
• Typically virus is transmitted from an infected person by
coughing or sneezing to the oral mucosa of a susceptible
person.
Smallpox-3

Clinical manifestations:
• Usually begins with the flu-like symptoms of
fever (typically 101o to 103o F), malaise,
headache, and body aches (prodrome).
• In most people, about 90% develop a rash
first as red spots on tongue and in mouth
which develop into sores in mouth.
• A rash starts on face, then to arms and legs
and hands and feet within 24 hours.
• Over days, the rash becomes raised bumps
which fill with opaque fluid and have a
depression in center (said to look like a belly
button).
Smallpox-4
Picture from CDC
Smallpox-5

Clinical manifestations cont.:
• Bumps become pustules (often said to
feel like BB pellets embedded).
• The pustules crust over to form scabs.
• The scabs generally fall off after about a
total of 3 weeks after the rash first
appeared.
• Pitted scars are left at site of scabs.
• Lesions are generally round and 6-10
mm. in diameter with concentration on
face and extremities.
Smallpox-6

Clinical manifestations cont.:
• May be distributed in a centrifugal
pattern.
• In some 5-10% of patients, a
hemorrhagic form occurs during which
the erythematous lesions are confluent,
and the skin is said to look like crepe
rubber.
• There may be bleeding into the skin
with petechiae and ecchymoses.
• This form is usually fatal within a week.
Smallpox-7

Clinical manifestations cont.:
• There is also a flat type with an atypical rash
that never becomes pustules and has a high
mortality.
• Less severe forms may occur in those with
partial immunity from vaccination.
• Note: In contrast to chickenpox, smallpox skin
lesions in the same area develop at same pace
and appear similar while in chickenpox, the
lesions develop in crops and lesions that are
scales, vesicles and pustules may be seen
simultaneously. Chickenpox lesions are rarely
seen on palms of hands or soles of feet.
Smallpox-8

Diagnosis:
• Sample from lesion should be taken by a
recently vaccinated health care worker under
appropriate precautions.

Mortality:
• About 30%.

Treatment:
• Supportive including hydration, sedation and
pain management.
• Cidofovir may be promising.
• Post-exposure vaccination if given within 2 to
3 or possibly up to 5 days post-exposure may
prevent or ameliorate disease.
Smallpox-9

Management and nursing
considerations:
• Supportive.
• Appropriate infection control critical.
• The smallpox virus is small in size and can be
carried by air currents or on dust particles over
long distances and thus be transmitted to
susceptible persons in a small amount of time.
• An actual or suspected case of smallpox should
be treated as a public health emergency and
reported as appropriate in the staff member’s
institution per their disaster plan.
Smallpox-10

Management and nursing
considerations cont.:
• Should use immediate isolation of suspected
case with airborne, contact, and standard
precautions and barrier nursing.
• Individual room with negative air pressure is
desirable.
• In places where no negative pressure isolation
rooms exist, the patient should be put in a
private room with a HEPA filtration unit.
Smallpox-11

Management and nursing
considerations cont.:
• The patient should remain in their room with
doors and windows closed.
• If there are a large number of patients needing
care, a designated nursing unit may be created
with a barrier plan to seal off the existing
ventilation system from other hospital areas
and limiting access to the unit.
• In cases of mass numbers, a whole facility or
large gym may be dedicated to smallpox
cases.
Smallpox-12

Management and nursing
considerations cont.:
• Unvaccinated visitors should remain at home
until vaccinated.
• Health care workers should use the personal
protective equipment (PPE) appropriate to the
degree of exposure and tasks.
• Disposable N95 respirators that filter particles
to 0.02 microns or powered air-purifying
respirators should be worn when entering the
room, and removed after leaving.
• Unless absolutely necessary, the smallpox
patient should not leave their room.
Smallpox-13

Management and nursing
considerations cont.:
• If the patient must leave their room, they
should wear a N-100 mask, have their body
completely covered, including the head and
face (nose and mouth should not be covered)
except with mask.
• Hallways should be cleared and anyone with
the patient should wear PPE including N95
respirators.
• Use disposable patient care equipment and
dedicated non-disposable equipment.
Smallpox-14

Management and nursing considerations
cont.:
• Linens should be placed in one bag, sealed and then
placed in a second leak-proof bag with clear
identification as contaminated and chutes should not be
used.
• If patient dies, they should be placed in leak-proof
container.
• Specific infection control information is in another
module or can be found on the CDC website.
• Provide psychological support to patient and family.
• Unvaccinated personnel should not care for smallpox
patients if an immune healthcare worker is available.
Smallpox-15

Vaccination:
• Available.
• Uses vaccinia virus for vaccination.
• Complications of vaccination occur particularly
in immunocompromised persons.
• Post-exposure vaccination may be useful. See
above.
• Passive immunization with vaccine
immunoglobulin may be given especially if
more than 3 days have elapsed since
exposure.
Smallpox-16

Vaccination cont.:
• Vaccination often performed for
contacts as ring vaccination. In this
model, contacts of the patients are
identified and vaccinated with further
case identification, surveillance contact
identification and vaccination in
concentric “rings.” This has been
proposed rather than universal
vaccination in which many more
reactions to the vaccine would be seen.
Smallpox-17

Other notes:
• Requires biosafety level 4.
• Staff caring for patients with smallpox may be
asked to monitor their temperatures daily, not
use main hospital entrance, shower and
change before leaving and not enter main
hospital area during work.
• Some recommend not admitting smallpox
patients to hospitals but maintaining them in
the home because smallpox is so contagious
that hospitalization could increase the number
of people at potential risk of transmission.
Tularemia (Francisella tularensis)

Description:
• Is a category A agent because of
infectivity, ease of dissemination, and
ability to cause serious illness.

Other names:
• Deer-fly fever, Glandular tick fever, Market
man’s disease, Rabbit fever, and O’Hara’s
disease
Tularemia-2

Etiology:
• Francisella tularensis, a tiny, gram-negative,
non-spore forming, hardy, aerobic
coccobacillus.
• Two subspecies:




Type A is more common in North America and is
more virulent than
Type B, found in Asia, Europe and North America.
Type A typically associated with rabbits.
Type B typically associated with rodents or wet
environment.
Tularemia-3

Epidemiology:
• A zoonotic infection.
• Occurs in the US, Europe, and Asia. Has
diverse small mammal animal hosts, including
rabbits, squirrels, muskrats, mice, water rats,
and others that are natural reservoirs of
infection.
• F. tularensis may be recovered from soil,
water, and vegetation.
• In the US, fewer than 200 recognized cases
occur each year.
• Disease is endemic in Martha’s Vineyard.
• Is occupational risk for hunters, trappers, and
others who handle infected animal carcasses.
Tularemia-4

Transmission:
• Direct contact with infected animal fluids or
tissues,
• Ingestion of contaminated water,
• Ingestion of contaminated undercooked meat,
water or soil,
• Bites of infected arthropods, such as ticks,
• Inhalation of infectious aerosols, such as
contaminated dust, or deliberate release in
laboratory, or
• Direct contact with contaminated food, water, or
soil.
• Person-to-person spread is unusual.
Tularemia-5

Incubation period:
• 1 to 21 days, typically 3 to 5 days

Clinical manifestations:
• Extremely variable depending on type, route of
inoculation and dose.
• Occurs in six recognized clinical forms:
ulceroglandular, glandular, oculoglandular,
oropharyngeal, pneumonic, and typhoidal.
• Tularemia sepsis may follow dissemination and
be severe leading to disseminated
intravascular coagulation (DIC), acute
respiratory distress syndrome (ARDS), and
organ failure if not treated immediately and
appropriately.
Tularemia-6

Clinical manifestations cont.:
• Ulceroglandular – is the most common
type.




Occurs following the bite of an infected
arthropod or handling an infected animal.
Begins as chills, fever, headache, generalized
aches, and can disseminate to lymph nodes,
and their enlargement or lymphadenopathy
may resemble buboes in bubonic plague.
A skin papule develops that becomes pustular
and eventually ulcerates.
The skin lesion can last for months.
Tularemia-7
Tularemia-8

Clinical manifestations cont.:
• Glandular – similar to above but without the
ulcer.
• Oculoglandular – occurs after eye contamination
causing conjunctival ulceration, inflamed eyelids
and nodules, vasculitis and possibly regional
lymphadenopathy
• Oropharyngeal – occurs after ingestion of
contaminated food or water.


Results in pharyngitis with yellow-white
pseudomembrane, and tonsillitis with cervical or
retropharyngeal lymphadenopathy.
In some cases, diarrhea and bowel ulceration may occur.
Tularemia-9

Clinical manifestations cont.:
• Pneumonic (primary) – from inhaling
infected aerosols.



Can present as atypical pneumonia or
present as acute illness with fever, fatigue,
chills, headache and malaise.
Cough, usually nonproductive,
manifestations of bronchitis, pneumonitis,
chest pain and dyspnea may occur.
Erythema multiforme may occur, and a rash
or erythema nodosum may be seen in about
one-third.
Tularemia-10

Clinical manifestations cont.:
• Typhoidal – acute septicemic illness with
fever and prostration leading to delirium
without skin lesion or lympohadenopathy.



Pneumonia is common.
May exhibit abdominal pain, vomiting and
diarrhea.
Mortality rate is about 35% to 60%.
Tularemia-11

Diagnosis:
• Clinical suspicion.
• Serological testing, culture sputum for
gram stain culture and other testing.
• Identification of organism in other
tissues as appropriate.

Mortality:
• If untreated, ranges from 5% to 35%,
overall.
• With prompt treatment may be only
1%.
Tularemia-12

Treatment:
• Preferred treatment is parenteral streptomycin
or intravenous gentamicin or aminoglycosides
for 10 days.
• Fluoroquinolones show promise in treatment.
• In a mass casualty situation, doxycycline and
ciprofloxacin given orally is recommended.
• Postexposure prophylaxis with ciprofloxacin or
doxycycline for 14 days is recommended to
prevent clinical disease if begun during the
incubation period.
Tularemia-13
Nursing considerations:
• Standard isolation precautions are recommended.
• Supportive care.

Vaccine:
• One form was available and recommended for
certain occupations but some difficulties were
found.
• The live attenuated vaccine is still being
investigated.

Other:
• Studied in biosafety lab 3.
• For laboratory workers, negative pressure
microbiological cabinets as well as face masks
are recommended.
Tularemia-14

Prevention:
• In natural cases:





Avoid tick-infested areas
Avoid tick and mosquito bites through
protective clothing, repellents, tick checks.
Use gloves, masks, protective eye-cover
when handling wild animals.
Cook wild game thoroughly.
Avoid drinking untreated water.
Other Hemorrhagic Fever Arenaviruses

The category includes 5 arenaviruses that
cause viral hemorrhagic fevers.
• Lassa virus (Lassa fever), which is one of
these, is discussed separately in this module.

Other arenaviruses and the viral
hemorrhagic fevers they can cause
include:
•
•
•
•
Virus
Junin virus
Sabia virus
Machupo virus
Guanarito virus
Disease
Argentine hemorrhagic fever
Brazilian hemorrhagic fever
Bolivian hemorrhagic fever
Venezuelan hemorrhagic
fever
SAHF-2




These four viruses are sometimes known
collectively as South American hemorrhagic fever
(SAHF) viruses and are discussed collectively
first. Then Junin virus causing Argentine
hemorrhagic fever is discussed specifically next
along with information about the other SAHF
viruses.
The SAHF viruses each cause diseases of similar
symptomatology.
Specific species of rodents are natural hosts for
the viruses.
The typical incubation period is 7 to 14 days but
may extend from 5 to 21 days. Case fatality rates
are estimated as 15 to 30%.
SAHF-3

Rodents are implicated in
transmission through contaminated
food, water or direct contact with
infected secretions or through
inhalation of infectious secretions or
excretions such as infected rodent
urine. Person-to-person transmission
may occur especially for Machupo
virus.
SAHF-4

Clinical features tend to be similar with:
• Gradual onset of fever
• Malaise followed by myalgia, back pain,
headache and dizziness with hyperesthesia of
the skin
• Hemorrhagic manifestations include
hemorrhaging from gums, vagina and
gastrointestinal tract leading to hypovolemic
shock
• Neurological manifestations include tremors,
inability to swallow, grand mal convulsions and
coma.
SAHF-5

Clinical features cont.:
• Some symptoms are more specifically
associated with individual viruses.


For example, in Guanarito virus,
pharyngitis, vomiting, and diarrhea are
more commonly seen.
In Junin and Machupo viral infections,
petechiae, erythema, facial edema,
hyperesthesia of the skin and shock may be
more frequent. Both of these have a high
fetal mortality if occurring in pregnant
women.
SAHF-6


Clinical features noted during an outbreak of
Venezuelan hemorrhagic fever included fever,
conjunctivitis, pharyngitis, thrombocytopenia,
myalgia, and hemorrhagic manifestations. Facial
edema was also observed. In this outbreak, 9 of
15 cases died. A few hundred cases have been
reported.
Clinical features noted in an outbreak of Bolivian
hemorrhagic fever included: fever, chills,
malaise, arthralgias, severe lower back pain,
headache and hemorrhagic manifestations. The
incubation period was 1 to 2 weeks. The case
fatality rate is estimated at 20%. Nosocomial
transmission has been noted.
SAHF-7




If used for bioterrorism, viremia may be
high with a higher transmission rate and
higher mortality as well as a greater
frequency of secondary cases because of
the large number of patients flowing into
emergency facilities due to nosocomial
transmission.
Standard, contact and airborne isolation
precautions.
Barrier nursing precautions as outlined for
Lassa fever should be followed.
Biosafety containment level 4 is used for
these viruses.
Junin Virus & SAHF Viruses

Etiology:
• Junin virus is a RNA virus in the
arenavirus family.
• It belongs to what is commonly known
as the New World arenavirusesMachupo virus, Guanarito virus and
Sabia virus.
• Each of these can cause a viral
hemorrhagic fever similar to the
Argentine hemorrhagic fever caused by
Junin virus.
Junin Virus & SAHF Viruses -2

Epidemiology:
• Junin and other new world viruses have mostly
been identified from the 1950s to date.
• The natural hosts are rodents.
• The at-risk region is mainly Argentina.
• It tends to be seasonal with a peak during the
corn harvest from March to June.
• Most of those infected are agricultural workers
who inhale infected aerosols from rodent excreta
or when rodents are caught in mechanical
harvesters.
• Aerosol infections have been noted in laboratory
workers.
• Sabia virus infection has only been documented
rarely. In one case, it was laboratory acquired in
the US and the researcher was treated with
ribavirin and survived.
Junin Virus & SAHF Viruses -3

Transmission:
• Contact with infected rodents, inhalation of
infectious rodent secretions or excretions.
• Person-to-person airborne spread has been
described for Machupo virus as well as Lassa
virus (discussed earlier).
• Machupo virus has been transmitted to
spouses 1-3 weeks after onset of illness.
• Nosocomial transmission mediated by infected
blood and excretion contact is described as
possible as is contact with medical equipment
that has been contaminated by virus.
Junin Virus & SAHF Viruses -4

Incubation period:
• Typically 7 to 14 days, but can be 2 to 21
days.

Clinical manifestations:
• Are similar but not identical for the South
American hemorrhagic fevers.
• Typical onset is gradual with fever, malaise
followed by headache, myalgia, back pain,
dizziness, and hyperesthesia of the skin.
• Guanarito virus infections tend to include
pharyngitis, vomiting and diarrhea more
frequently than others.
Junin Virus & SAHF Viruses -5

Clinical manifestations cont.:
• Junin and Machupo infections tend to include
petechiae, erythema and flushing of face and
trunk, facial edema and lymphadenopathy.
• Hemorrhagic and neurological manifestations
may occur alone or together.
• Hemorrhagic manifestations include
hemorrhaging from the gums and orifices,
especially the gastrointestinal tract and vagina
in females leading to shock, and capillary leak
syndrome with thrombocytopenia.
Junin Virus & SAHF Viruses -6

Clinical manifestations cont.:
• Neurological manifestations include tremors,
inability to swallow, dysarthria, convulsions,
coma and death which may occur 7 to 12 days
after onset.
• Recovery is usually complete but there may be
a temporary loss of scalp hair.
• Pregnant women are more likely to have a
fatal outcome if infected with Junin virus and
both Junin and Machupo viruses are associated
with high fetal mortality.
Junin Virus & SAHF Viruses -7

Mortality:
• Mortality rate is 15-30%.

Treatment:
• Ribavirin as been used successfully intravenously
for about 10 days, and is recommended for atrisk contacts orally for a week. Limited number of
studies are available though.
• Other treatment is generally non-specific and
supportive, including fluid and electrolyte balance,
monitoring, and clotting factor or platelet
replacement may be done in cases of serious
hemorrhage.
• Convalescent or immune serum therapy has been
used for Junin and Machupo viral infections.
Junin Virus & SAHF Viruses -8

Nursing considerations:
• Strict barrier nursing precautions should be
used, including standard and contact isolation
precautions, and in the interests of absolute
safety, airborne precautions.
• Educate patient about isolation precautions
being used.
• Indicate what is expected of them in regard to
cooperation if they are able to cooperate and
understand.
• See infection control module for details and
CDC site as well as material previously
discussed under Lassa, Ebola and Marburg
viruses.
• Supportive care.
Junin Virus & SAHF Viruses -9

Other notes:
• Biosafety level 4
conditions are used
for study.
Picture from CDC.