biologic agent of conasdcern
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categories A,B and C were created in
order to classifyBiological agent thesebiological agent of concerns.
Agents were ranked based on severalfactors including public health, disease
and mortality rates, dissemination
potential, public perception and the needfor special public health preparations.
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CATEGORY A
The most deadly microbes known to man
Easily disseminated or transmitted from
person to person
Have high mortality rates as well as thepotential for severe public health
consequences including public panic and
social disruption.
Their high infectivity poses a danger not only
to those infected with disease but also to
those with who treating the infected patients.
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CATEGORY A AGENTS
Anthrax (Bacillus anthracis)
Botulinu toxin (Clostridium botulinum) Plague (Yersinia Pestis)
Smallpox (Variola major)
Tularemia (Francisella tularensis) Hemorrhagic fever viruses
- Ebola
- Marburg- Lassa machupo
- Junin
- Guanarito
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CATEGORY B
Second highest priority
Share certain characteristic such as the
potential for moderate morbidity and lower
mortality rate
Moderately easy to disseminate and
require specific diagnostic capabilities
Agents are extremely toxic but are difficult
to disseminate or has lower infectivity
compared to category A
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CATEGORY B AGENTS
Brucellosis
Epsilon toxin of clostridium perfringens Food safety threats (salmonella, shigella, E.
coli, etc.)
Melioidosis
Psittacosis
Q fever
Ricin toxin from castor beans
Staphylococcal enterotoxin B Viral encephalitis
Water safety threats
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CATEGORY C
Emerging agents that is potential futureinfective threats such as Nipah fever
and Hantavirus.
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ANTHRAX
A zoonotic disease found in herbiboresuch as sheep, goats and cattle thatingest spores fro infected soil.
wool sorters disease
Bacillus Anthracis
Occurs in 3 distinct forms
- Cutaneous
- Inhalational
- gastrointestinal
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1.Cutaneous anthrax
- Contact with abraded skin derivedfrom infected herbivores.
2. Inhalational anthrax
- Contacted by inhalation of sporesfrom infected animals
3. Gastrointestinal anthrax
- Rare and is contracted viaconsumption of meat from infected
animals.
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INHALATIONAL ANTHRAXSUBJECTIVE Sx
Cough, chest pain, dyspnea, viral URI(sorethroat, myalgias, mild fever) during
prodrome
Meningeal signs -Hemorrhagic meningitisOBJECTIVE FINDINGS
Lympadenopathy, widened mediastinum on
chestNOTES
S/S are progress to respiratory failure,
sepsis, and hemodynamic collapse in pre
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CUTANEOUS ANTHRAX
SUBJECTIVE SxRaised bump on face, hands or arms,
typically with black painless ulceration.
OBJECTIVE FINDINGSUlcer with black eschar, moderate to
severe localized edema and
lympadenopathyNOTES:
Time course is 1-7 days until appearnce
oof typical ulcer.
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GASTROINTESTINAL ANTHRAX
SUBJECTIVE SxVomiting, diarrhea and abdominal pain
OBJECTIVE FINDINGS
Diarrhoea may be bloody. Acuteabdomen may be present with or
without ascites
NOTES:Fluid volume loss may be severe.
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BIO SAFETYISSUES,
PROTECTION ANDISOLATION
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Biosafety Level II
Precautions are recommended forlaboratory personnel who come incontact with anthrax specimen.
Handling of specimen in a laminarflow hood with protective eyewear,
using gloves pulled over lab coatsand avoiding activities that mayproduce aerosol or droplet dispersal
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BIOSAFETY LEVEL III
Precautions are recommended forpersonnel who worked extensively
with anthrax specimen (research
purposes)
Precautions similar to BSL II,
- respiratory protective equipment
- Controlled access to lab- Decontamination of all waste
- Negative air pressure in the laboratory
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Health care workers who come in
contact with patients in whom anthrax
is suspected should use universal
precautions at all times, including the
use of rubber gloves, disposal of
sharps AND FREQUENTHANDWASHING
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VACCINATION AND POST EXPOSUREPROPHYLAXIS
An anthrax vaccine is available butreserved for laboratory and military
personnel who may come in contact
with disease. AVA Anthrax Vaccine Adsorbed
No currently licensed for use to
civilian populations
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TREATMENT
CUTANEOUS ANTHRAX 60 day oral
course of either ciprofloxacin or
doxycycline.
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TREATMENT
Ciprofloxacin or doxycycline plus
additional antimicrobials and adjunctive
therapies for inhalational anthrax.
INHALATIONAL ANTHRAX 60 days of
IV course of cipro or doxy plus one or
two additional microbials to which
anthrax has historically been sensitive
such as AMINOGLYCOSIDES OR
CLINDAMYCIN
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Anthrax has been traditionally
resistant to CEPHALOSPORIN such
as CEFTRIAXONE.
Accumulation of haemorrhagic pleural
effusion - CHEST TUBE DRAINAGE
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It is a food borne illness caused by
Clostridium botulinum .
Most poisonous substance known to
mankind less than 1 mcg is a fatal dose
for an adult.
4 types of botulism
1. Foodborne botulism
2. Infantile botulism
3. Wound botulism
4. Intestinal botulism
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CLASSIFICATION AND ETIOLOGY
TYPE A AND B
Associated with the consumption ofhome canned vegetables, fruits , and
meat productsTYPE E
Seen with marine products
INFANTILE BOTULISM involves theingestion of botulism spores which iscommonly found in honey.
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CLINICAL MANIFESTATIONS ANDDIAGNOSIS
Nausea, vomiting and diarrhea
(initial neurologic symptoms)
Constipation becomes prominent in later
stage. INFANTILE BOTULISM
- Constipation is often the main symptom
- Flaccidity characteristic (floppy baby)- Poor suck reflex
- Poor feeding
- Poor head control
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Pitfalls in the diagnosis of botulism
include failure to recognize the
symptoms and to institute adequate
ventilatory support.
Underdiagnosed and Mistaken for a
number of neuromuscular andneurologic disorders.
- Diptheria
- Encephalitis- Poliomyelitis
- Guillain -Barre syndrome
- congenital neuropathies and myopathies
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Ushroom (muscarinic) poisoning are
diagnoses potentially similar in
presentation to botulism
Laboratory test includes:
- F/A- gastric samples of aspirate or food
samples
- C.Botulinum cultures can also beobtained
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LABORATORY ISSUES , PROTECTIONAND ISOLATION
Extremely poisonous to humans, Coats ,face, gloves, face shield and
protective cabinets are recommendedfor handling botulism specimen.
Ideally lab personnel should bevaccinated with C.botulinum antitoxin
Universal precaution should be used
when caring for patients suspected ofbotulism.
Isolation is not necessary but droplet
precaution should be instituted.
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PUBLIC HEALTH IMPLICATION
every case of foodborne botulismshould be treated as public health
emergency.
Every effort should be made toeliminate toxin containing food items
still available for public consumption
to avoid mortality and morbidity.
Cases that happened in geographical
areas should be rapidly investigated.
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VACCINATION AND POST EXPOSURE
PROPHYLAXIS
Botulinum toxoid an investigational
agent intended for lab worker who
work regularly with botulinum toxin.
Post exposure prophylaxis is not
recommended at this time for
asymptomatic patient
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TREATMENT
Ventilatory support
Administration of botulinum antitoxin
trivalent equine antitoxin provides
antibodies to botulinum toxin TypesA,B and E
Cathartics and enemas
Antibiotics are not recommendedexcept for tx of secondary infectious
complication such as pneumonia.
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HISTORY
Most feared infectious disease in thehistory of humankind.
Yersinia Pestis the bacterium
responsible for plague Black death of the middle ages plague
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EPIDEMIOLOGY
Plague is still present worldwide.
The introduction of the disease to
human populations occurs when
plague infected fleas , which
typically infest rodent host, cause
the death of these rodents in large
numbers.
Fleas then move fro their naturalhosts to human, causing outbreaks
of plague.
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CLASSIFICATION AND ETIOLOGY
Transmission to human is typically
through the bite of an infected flea.
Droplet spread from patients withpneumonic plague is another route of
infection.
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3 FORMS
1. BUBONIC
Most common form of plague,
responsible for the European
pandemics
Presents with painful, swollen lymph
nodes the bubo of bubonic plague
Axilla, groin, neck
Following by generalized bacteremia
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3 FORMS
2. SEPTICEMIC
The infected fleabite vector is the
same but rather than develop
buboes, patient develop sepsis
followed by multiple organ failure.
Usually develop gangrene and
necrosis of fingers and toes
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3 FORMS
3. PNEUMONIC PLAGUE
Spread by droplet dispersal from
infected patients and severe
pulmonary involvement is the
cardinal sign.
The most deadly form of plague,
when Y. pestis infects the lungs
causing :
severe hemorrhagic , necrotizing
bronchopneumonia
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This process can either occur by
hematogenous spread of thebacterium (secondary pneumonic
plague)
Droplet spread from infected person
directly to the patient via inhalation
(primary pneumonic plague)
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CLINICAL MANIFESTATIONS
Nausea and vomiting and cough
productive of bloody sputum are
also seen
Chest pain, dyspnea and hemoptysis
are later symptoms are later
symptoms typical of pneumonic
plague
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A history of contact with infected
rodents or fleas is important to elicit.
Ground squirrels, pairie dogs and
rats are reported plague vectors.
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BIOSAFETY ISSUES, PROTECTION AND
ISOLATION
Strict isolation should be
maintained for all patients
suspected of Y. pestis infection.
Gowns, gloves, masks and eye
protection should be worn for at
least the 1st 48 hours of treatment.
VACCINATION AND POST EXPOSURE
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VACCINATION AND POST EXPOSURE
PROPHYLAXIS
Vaccines available protected only an
individual from bubonic plague but notwith pneumonic plague.
Administered only for military and
laboratory personnel working inplague endemic areas researchersworking with plague infected animalsor fleas.
Antibiotic prophylaxis isrecommended for contacts of patientwith plague as well as close
surveillance of contacts refusing
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Doxycycline and Ciprofloxacin are
recommended post exposure
prophylaxis to adult, children and
pregnant women.
Tetracyclines, sulfonamides and
chlorampenicol are also effective as
post exposure prophylaxis against thedisease.
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TREATMENT
Streptomycin antibiotic of choice for
the treatment of plague.
Gentamicin another preferred
antibiotic
Patients with pneumonic plague may
also require advance medical
supportive therapy in addition to
antibiotics.
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HISTORY
Tularemia is a highly infectious
zoonotic disease caused by the
bacterium Francisella tularensis.
First described in Tulare, Country,
California
Tularemia can cause fever, skin or
mucous membrane ulceration,
lympadenopathy and occasionallylife threatening pneumonia
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Its major threat comes from its
extreme infectivity, inhalation orinoculation of as few as 10 organisms
is enough to cause disease.
If untreated can produce severe
disease and death .
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EPIDEMIOLOGY
Primarily a rural disease
Males tend to be more often infected
than females
It may be related to the specificoutdoor activities that may
predispose individuals to contracting
tularemia such as farming, hunting,
trapping and butchering
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CLASSIFICATION AND ETIOLOGY
Tularemia is caused by gram (-)
aerobic bacterium. It can present clinically in several
forms:
- Ulceroglandular- Glandular
- Oculoglandular
- Oropharyngeal- Pneumonic
- Typhoidal
- Septic forms
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It is typically found in animals such asrabbits and rodents
Can be transmitted to humans inseveral ways.
- Contact with infected animal carcasses
- Ingestion of contaminated meat, soil orwater
- Inhalation of the bacterium(laboratoryworkers)
- Inoculation of the bacterium via cuts orabrasion
- Via bites of infected arthropods such as
ticks
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CLINICAL MANIFESTATIONS AND DIAGNOSIS
Ulceroglandular and typhoidal forms
make up the majority of tularemia
patients
Initially presents with abrupt onset of
- high fever
- Headache
- Rigors- Coryza
- Sorethroat
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CLINICAL MANIFESTATIONS AND DIAGNOSIS
Dry cough, sweats, fever and chills
occur as the disease continues.
Ulceroglandularform presents with
skin and mucous membrane ulcers ,
lympadenopathy or both.
A cutaneous chancre like ulcer is the
most common finding.
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CLINICAL MANIFESTATIONS AND DIAGNOSIS
Typhoidal form has less significant
lymph node involvement and skinlesion are absent.
Pulmonary involvement is prominent
The differential diagnosis of tularemiaalso includes otherdiseases with
prominent skin manifestations orpulmonary findings such as plague,diphtheria, psittacosis, Q fever andother tick-borne diseases.
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Definitive diagnosis of tularemia is by
culture typically from sputum.
ELISA, bacterial agglutination and
immunofluorescent are also available.
BIOSAFETY ISSUES PROTECTION
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BIOSAFETY ISSUES, PROTECTION
AND ISOLATION
Extremely infectious in aerosol form Biosafety precaution II should be
used for initial evaluation then
specimen should be forwarded to aBSL 3 laboratory for further testing.
Human to human transmission of
tularemia is not at risk , isolation isnot needed.
Universal precautions are
recommended.
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TREATMENT
As the for the treatment of plague ,
streptomycin and gentamicin are theDOC.
Doxycycline and chloramphenicol havealso been used but more treatmentfailures have been reported with theseregimens.
Ciprofloxacin is another alternative
therapy. For the first line regimens aswell as ciprofloxacin, a 10 day course ofIV antibiotics is recommended.
For second line therapies , 14 days are
recommended.
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EPIDEMIOLOGY
Smallpox occurs in two forms:
- Variola major(the most dangerous
and formerly widespread form of
disease)
- Variola minor
Person to person transmission of
the disease occurs by droplet
spread from infected persons or by
contact with contaminated clothing
or bedding
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Viral hemorrhagic fevers are group
of febrile illnesses caused by RNA
viruses from several viral families.
Fiviruses (Ebola and marburg)
Arenaviruses (Lassa and NewWorld arenaviruses)
Bunyaviruses (rift valley river)
Flaviviruses (yellow fever, amongothers)
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These leads to potentially lethal
syndrome characterized by:
- Malaise
- fever
- vomiting
- mucosal and GI bleeding
- edema
- hypotension.
Th t t i b f thi
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The most notorious member of this
group is EBOLA outbreaks which
have been associated with casefatality rates.
These disease are generally
contracted via an infected animal or
arthropod vector.
Bats are considered to be the natural
reservoir for Ebola .
Mastomys rodent - natural reservoir
for Lassa virus.
American arenaviruses are also
spread by rodent contact typically
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Infected mosquito rift valley fever
and yellow fever
Tick bite of flavivirus carrying
anthropods- omsk hemorrhagic
fever and kyasanur forest disease.
PATHOGENESIS
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PATHOGENESIS
The primary defect in patients with
VHF is that of increased vascular
permeability.
H. fever viruses have an affinity for
the vascular system , leading tomucous membrane hemorrhage
with accompanying hypotension
and shock. All of the viruses can also lead to
thrombocytopenia and depletion of
clotting factors
CLINICAL MANIFESTATIONS AND DIAGNOSIS
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CLINICAL MANIFESTATIONS AND DIAGNOSIS
Incubation period --- 2-21 days
Non specific early symptoms
include :
- High fever , head ache, myalgias,
arhralgias, fatigue, flushing and
abdominal pain.
Patients with Ebola infection oftendemonstrate a petechial rash by
Day 5.
Jaundice is common in patients
BIOSAFETY ISSUES, PROTECTION AND
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,
ISOLATION
BSL 4 precautions are necessary
when handling specimens from
patient suspected of VHF infection.
All medical personnel who have
had close contact with patient
suspected of VHF infection before
the safeguards were institutedshould be placed under medical
surveillance.
SPECIFIC RECOMMENDATION FOR PATIENT
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SUSPECTED OF HAVING VHF INFXN:
Strict hand washing
Double gloving Impermeable gowns
N-95 masks or powered air purifying respiratorsand negative pressure isolation rooms
Leg and shoe coverings
Face shields and goggles
restricted access to patient rooms
Environmental disinfection If multiple patient are present, they should be
cared for in one area of the hospital to minimizeexposure to other patients and health care
personnel.
VACCINATION AND POST EXPOSURE
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PROPHYLAXIS
No approved vaccines exists forany f the VHF infections other than
yellow fever.
Ribavirin a nucleoside analog isrecommended for post exposure
prophylaxis forLassa and other
arenaviruses.
But has no efficacy against
filovirus or flavivirus.
TREATMENT
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TREATMENT
Supportive, IVF and electrolyte
replacement
Hemodialysis, invasive monitoring,
and vasopressor therapy may also
be needed.
IM injection, use of aspirin and
other NSAID and anticoagulants
should be put into consideration.
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