BIOTERRORISM
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Transcript of BIOTERRORISM
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BIOTERRORISM
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HISTORY
• Microbial pathogens were used as potential weapons of war or terrorism from ancient times:– the poisoning of water supplies in the sixth century
B.C. with the fungus Calviceps purpurea (rye ergot) by the Assyrians
– the hurling of the dead bodies of plague victims over the walls of the city of Kaffa by the Tartar army in 1346
– the spreading of smallpox via contaminated blankets by the British to the native American population loyal to the French in 1767.
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Key Features of Biologic Agents Used as Bioweapons
• High morbidity and mortality • Potential for person-to-person spread • Low infective dose and highly infectious by aerosol • Lack of rapid diagnostic capability • Lack of universally available effective vaccine • Potential to cause anxiety • Availability of pathogen and feasibility of production • Environmental stability • Database of prior research and development • Potential to be “weaponized”
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CLASSIFICATION• Centers for Disease Control and Prevention (CDC) classifies potential
biologic threats into three categories: A, B, and C• Category A agents are the highest-priority pathogens:
– can be easily disseminated or transmitted from person to person– result in high mortality rates– have the potential for major public health impact– might cause public panic and social disruption– require special action for public health preparedness.
• Category B agents include those that are moderately easy to disseminate, result in moderate morbidity rates and low mortality rates, and require specifically enhanced diagnostic capacity.
• Category C agents include emerging pathogens– the general population lacks immunity– could be engineered for mass dissemination in the future because of
availability, ease of production, ease of dissemination– The recent emergence of novel viruses leading to outbreaks of severe
acute respiratory syndrome (SARS), Nipah, hantavirus are examples
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Category A agents
• Anthrax (Bacillus anthracis)• Botulism (Clostridium botulinum toxin)• Plague (Yersinia pestis)• Smallpox (Variola major)• Tularemia (Francisella tularensis)Viral hemorrhagic fevers: • Arenaviruses: Lassa, New World (Machupo, Junin,
Guanarito, and Sabia)• Bunyaviridae: Crimean Congo, Rift Valley • Filoviridae: Ebola, Marburg • Flaviviridae: Yellow fever; Omsk fever; Kyasanur Forest
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Category B agents• Brucellosis (Brucella spp.)• Epsilon toxin of Clostridium perfringens• Food safety threats:
– Salmonella sp.– Escherichia coli 0157:H7– Shigella sp.
• Water safety threats– Vibrio cholerae– Cryptosporidium parvum)
• Glanders (Burkholderia mallei)• Melioidosis (B. pseudomallei)• Psittacosis (Chlamydia psittaci)• Q fever (Coxiella burnetii)• Ricin toxin from Ricinus communis (castor beans)• Staphylococcal enterotoxin B• Typhus fever (Rickettsia prowazekii)• Viral encephalitis
– alphaviruses (e.g., Venezuelan, eastern, and western equine encephalitis)
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Anthrax as a Bioweapon• Anthrax may be the prototypic disease of bioterrorism
although rarely spread from person to person• U.S. and British government scientists studied anthrax
as a biologic weapon beginning approximately at the time of World War II (WWII).
• Soviet Union in the late 1980s stored hundreds of tons of anthrax spores for potential use as a bioweapon
• At present there is suspicion that research on anthrax is ongoing by several nations and extremist groups
• One example of this is the release of anthrax spores by the Aum Shrinrikyo cult in Tokyo in 1993. Fortunately, there were no casualties associated with this episode.
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Anthrax as a Bioweapon II• 1979: the accidental release of spores into the atmosphere from a Soviet
Union bioweapons facility in Sverdlosk:– at least 77 cases of anthrax were diagnosed with certainty, of which 66 were fatal– victims have been exposed in an area within 4 km downwind of the facility– deaths due to anthrax were also noted in livestock up to 50 km away from the
facility– interval between probable exposure and development of clinical illness ranged from
2 to 43 days (the majority of cases were within the first 2 weeks)– death typically occurred within 1 to 4 days following the onset of symptoms– the anthrax spores can lie dormant in the respiratory tract for at least 4 to 6 weeks
• September 2001: anthrax spores delivered through the U.S. Postal System. – CDC identified 22 confirmed or suspected cases of anthrax (11 patients with
inhalational anthrax, of whom 5 died, and 11 patients with cutaneous anthrax - 7 confirmed - all of whom survived)
– cases occurred in individuals who opened contaminated letters as well as in postal workers involved in the processing of mail
– one letter contained 2 g of material, equivalent to 100 billion to 1 trillion spores (inoculum with a theoretical potential of infecting up to 50 million individuals)
– The strain used in this attack was the Ames strain - was susceptible to all antibiotics
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Bacillus anthracis
• Aerobic, sporing Gram-positive rod: infection usually transmitted by spores
• Generally more sensitive to antibiotics than other Bacillus species, but multi drug resistant strains have been found in nature
• BUT not sensitive to 3rd generation cephalosporins
• Easily dismissed as a contaminant when identified in general hospital laboratories
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B.anthracis, forming spores
Typical, wavy chains of bacilli, appearance like railway trucks
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B. anthracis toxins
• Lethal toxin (LeTx): intracellular endopeptidase, probably directly damages endothelial cells; also immunosuppressive.
• Oedema toxin (ETx): potent adenyl cyclase; contributes to shock and potentiates LeTx.
• Protective antigen: the portion of the binary LeTx and ETx complexes which mediates attachment to target cells
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Bacillus anthracis: epidemiology
• Spores of B. anthracis are widely dispersed in nature: in soil, animal carcases and skins, and items made from skin, wool or hair (eg drums made with animal skins, bags, fur robes, plaster reinforced with horse-hair etc)
• It is relatively difficult to infect humans: usually skin inoculation or a large inhalational exposure is required
• The organism is therefore classified at biosafety level 3 (CL 3)
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Anthrax presentations
• Inhalational: ‘flu’ followed by mediastinitis and pneumonitis
• Cutaneous• Gastrointestinal• Meningitic
CUTANEOUS ANTHRAXMost common presentation:Look for black eschar; halo ofvesicles; extensive oedema
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Cutaneous Anthrax: Early lesions
(CDC Public Health Image Library)
(courtesy AB Christie, Liverpool)
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Cutaneous Anthrax
( CDC. www.bt.cdc.gov/agent/cutaneous.asp)
• 95% of naturally occurring cases• Subcutaneous inoculation of
spores• Hands, forearm, head• Incubation: <1 to 7 days• Small painless papule ulcer
with marginal vesicles (24-48h)• Painless oedema surrounds
lesion• Develops into eschar (2-6 d)• Untreated mortality 20%
(treated v. rare)
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Cutaneous Anthrax
Note extensive oedema in relation to lesion size
( CDC www.bt.cdc.gov/agent/cutaneous.asp)
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Cutaneous Anthrax: Differential Diagnosis
• Necrotic ulcers
• Rickettsial eschar
• (e.g. tick typhus)
• Pox virus infection
• (e.g. cowpox, orf)
• Spider bites
Cowpox (courtesy Dr D. Baxby, Liverpool)
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Cutaneous anthrax: oedema
• Rarely, bacteraemia can accompany cutaneous anthrax
• Always investigate, and treat sepsis with high-dose IV antibiotic
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Intestinal Anthrax
(Armed Forces Institute of Pathology, USA)
• Ingestion of contaminated meat
• Incubation: <1 - 7 days
• Fever, acute abdomen, vomiting, bloody diarrhoea
• Intestinal eschar (similar to cutaneous lesion)
• Progression to sepsis syndrome
• Mortality 50 - 100% despite treatment
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Inhalational anthrax
• Flu’-like onset, respiratory failure develops abruptly after 3-4 days-fatal in 1 or 2 days
• CXR suggestive, but features can be subtle
• Blood cultures pos.(CL3)• PCR possible (ref.lab)• responds to early
vigorous treatment
Jernigan et al. EID 2001; 7: 933
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Confirmed anthrax cases associated with bioterrorism: U.S., 2001. A. Geographic location and clinical manifestation of the 11 cases of confirmed inhalational and 7 cases of confirmed cutaneous anthrax. B. Epidemic curve for the 18 confirmed cases of inhalational and cutaneous anthrax and 4 cases of suspected cutaneous anthrax.
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Progression of chest x-ray findings in a patient with inhalational anthrax. Findings evolved from subtle hilar prominence and right perihilar infiltrate to a progressively widened mediastinum, marked perihilar infiltrates, peribronchial cuffing, and air bronchograms.
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Recognising inhalational anthrax• 10 cases of inhalational anthrax: USA
• WCC 7.5-13.3 x109/l (6 < 10.0)
• 6/6 had >70,000 RBCs in pleural fluid, with high protein and low WBCs
• 6/6 had PaO2 80mmHg or less on air
• 5/7 treated within 5 days of onset survived
• 1/3 treated after 5 days survived
JA Jernigan et al. EID 2001; 7: 933
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Treating inhalational anthrax
• Severe chest infection of unknown cause.
• DON’T use 3rd gen. Cephalosporin alone.
• Use a penicillin eg.co-amoxyclav plus a macrolide/ciproflox.
• Or add gentamicin.
• Antibiotics effective for anthrax.
• Ciprofloxacin.• Benzyl penicillin.• Macrolides.• Gentamicin (plus
pen.).• Doxycycline.• Chloramphenicol.
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Vaccination and Prevention• The first successful vaccine for anthrax was developed
for animals by Louis Pasteur in 1881. • At present, the single vaccine licensed for human use is
a product from the cell-free culture supernatant of an attenuated, nonencapsulated strain of B. anthracis (Stern strain) - anthrax vaccine adsorbed (AVA).
• Clinical trials for safety in humans and efficacy in animals are currently under way to evaluate the role of recombinant protective antigen (one of the major components, along with lethal factor and edema factor, of B. anthracis toxins) as an alternative to AVA.
• The efficacy of AVA in a postexposure setting in humans has not been established.
• The current recommendation for postexposure prophylaxis is 60 days of antibiotics (ciprofloxacin or doxycycline).
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Chemo-prophylaxis ofanthraxProphylaxis Adult doses Child doses
Ciprofloxacin 500mg orally bd for 6 weeks
20-30mg/kg bd
Doxycycline (if cipro x tolerated /indicated)
100mg orally bd 5mg/kg orally in two divided doses
Although normally used with caution or contraindicated, these drugs may be given in pregnancy, lactation and childhood to protect against anthrax
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PLAGUE
MICROBIOLOGICAL FEATURES:gram-negative, rod-shaped, facultative anaerobic
bipolar staining, non-motile, non-sporulating
BIOLOGICAL SURVIVAL:15 minutes in 55° C/ few hours in sunlight
weeks in water, grains, moist soil, dry sputum, flea feces
lives months/years at just above 0°C
HOST RANGE:zoonotic disease of rodents: rats, mice, ground squirrels
intracellular organism: monocytes/macrophages
=> long-term survival requires host
=> Circumstances for natural human outbreaks:disasters/ disruption of rat habitats/ rat dis- or relocation
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SYNDROMIC PRESENTATION – SESSION 1PLAGUE EPIDEMIOLOGY INATURALLY OCCURING PLAGUE
Since 1965: approximately 1500 cases/year
25 countries reported cases
50% Eastern and South Africa, esp. Madagascar
1980-1994: 18,739 cases reported from 20 countries to WHO
2000 – 2005: Zambia, Algeria, Malawi, DR Congo
December 2007: n=1, marmoth hunter, China
Endemic in U.S. 1947-96: 390 cases/y1970-2003: 5-15 cases/y
83% Bubonic15% Septicemic2% Primary Pneumonic
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SYNDROMIC PRESENTATION – SESSION 1PLAGUE TRANSMISSION
4 ROUTES FOR HUMAN INFECTION
1. Flea-bite (most common)
=> Rat-borne urban epidemics in history
=> Human overcrowding, indoor contacts
2. Handling infected animals (skin contact, scratch, bite)
=> Endemic sylvatic plague with sporadic outbreaks
=> Occupational risks
3. Inhalation of contaminated aerosol (human/animal)
=> Only pneumonia capable of person to person spread
4. Ingestion of infected meat
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3 TYPES OF DISEASE
Bubonic
Septicaemic
Pneumonic
SYNDROMIC PRESENTATION – SESSION 1PLAGUE CLINICAL COURSE I
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Plague: Clinical FormsBubonic
(CDC image library)
• Common form of naturally occurring plague, following bite of infected flea • Inguinal, axillary, or cervical lymph nodes are the most commonly affected• 80% can become bacteraemic• 60% mortality if untreated
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SYNDROMIC PRESENTATION – SESSION 1PLAGUE CLINICAL COURSE II1. “CLASSIC” Bubonic Plague
ENTRY: Bite of infectious flea
Contact/ ingestion of infected animals
Contact/ ingestion of infectious material
BUBOES: Enlarged tender lymphnodes (unilateral)
Usually inguinal/ femoral in adults
Cervical/ submaxillary common < 10y
CFR: 40-60% untreated, <5% treatedOverall 14% in U.S. (delayed diagnosis/ therapy)
COMPLICATION: BACTERAEMIA
secondary septicaemic plague
secondary pneumonic plaguesecondary plague meningitis
www.cdc.gov
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3. Pneumonic Plague
US cases: 2% PRIMARY PNEUMONIC12% SECONDARY PNEUMONIC
PRIMARY: Result of droplet inhalation Only few cases in endemic areas
ENTRY: Aerosol => other patients/ infected animals/ BW
SECONDARY: Hematogenously spread to lungsInitially: interstitial pattern/ later: abscess
CFR: ~ 100% if untreated/ therapy delayed > 18-24h after onsetRemains high despite treatment: Overall 57%
(U.S.)
DEATH WITHIN 2-4 DAYS (max 6d): cyanosis, stridor, resp. failure
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Plague: Differential Diagnosis
Pneumonic• Bioterrorism threats• Anthrax- Tularaemia- Melioidosis
• Other pneumonias,esp. “atypicals”
• Leptospirosis (haemorrhagic)
Bubonic• Staph/strep adenitis
• Glandular tularaemia
• Cat scratch disease
• LGV & chancroid
Septicaemic• Other Gram-negative sepsis
• Meningococcaemia
• Rickettsia
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SYNDROMIC PRESENTATION – SESSION 1PLAGUE TREATMENTFIRST LINE:
STREPTOMYCIN =>bacteriocidalCHILDREN: 30 mg/kg IM divided q8-12h (max 2g/day)ADULTS: 1g IM bid
GENTAMYCIN => as effective, qd dosageCHILDREN: 2.5mg/kg im/iv q8hADULTS: 5mg/kg iv qd (check levels) OR
load 2mg/kg, then 1.7mg/kg q8h
SECOND LINE:
DOXYCYCLIN => good in vitro + good human data1. Single 200mg iv loading dose2. 100mg iv bid or 200 mg iv qd
adults/ kids >45kg=> 1st choice po therapy for mass
casualties/ PEP
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Smallpox
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The variola virus
• A member of the family of Orthopoxviridae
• The largest viral genome: double-stranded DNA
• An enveloped virus, but the envelope is not essential for infectiousness
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The Yugoslavia outbreak 1972
• Single index case spent time in Iraq– 11 contacts developed smallpox
• 100 secondary cases in contacts and other hospital patients
• 14 tertiary cases
• Spread to other cities
• Total 175 cases, 35 deaths
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Variola: first and second day of rash (4th-5th day of fever)
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Variola: 4th day of rash
•For the first time-on the fourth day of the rash and the fifth day of infectiousness, a typical vesicular appearance is seen
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Variola major: drying rash (7-9 days)
•The rash is becoming less infectious
•Conjunctival lesions are usually benign and heal completely
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Variola major: confluent on day 7 of rash
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Variola major: scabbing of rash: day 11
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Smallpox Clinical Course
• Prodrome (day 1-3)• Erythematous rash (days 2-3)• Maculopapular rash (days 4-6) • Vesicular pustular rash (days 8-14+)
(Fenner F et al. Smallpox and its eradication. WHO 1998.http://whqlibdoc.who.int/smallpox/9241561106.pdf )
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Boys aged 13 years, infected from the same source-admitted same day: right-unvaccinated; left-vaccinated in infancy
Variola major: variation in severity
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Diagnosis of smallpox: (must be in CL4 facility)
• Classical testsEM of vesicle fluid for
poxvirusVirus culture(CFT and ELISA for plasma
antibodies-not reliable)
PCR: rapid, specific, can distinguish between poxviruses-performed on blood or vesicle fluid
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Smallpox vs. Chickenpox
• Smallpox• Incubation 7-17d• Severe illness • Prodrome• Headache and back pain • Centrifugal• Synchronous• Rash not initially itchy• Lesions round• Scabs form 10-14d• Scabs separate 14-28d
• Chicken pox• Incubation 14-21 d• Usually mild• Prodrome • Mild malaise• Centripetal• Asynchronous• Rash initially itchy• Lesions oval• Scabs form 4-7d• Scabs separate <14d
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Management of smallpox• General supportive measures
• Analgesia (the rash is very painful)
• Good hygiene (secondary infection is a danger-the skin is a common portal of entry)
• Antibiotics to treat secondary infection and limit scarring
• ?antiviral drugs
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Smallpox vaccine• Live vaccinia vaccines
Lister-Elstree NYCBH 2nd generation live (Modified vaccinia and others)
• Given by scarification
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Burkholderia pseudomallei– Aerobic, gram-negative, motile bacillus– Found in water and moist soil– Opportunistic pathogen– Produces exotoxins– Can survive in phagocytic cells
• Latent infections common
MELIOIDOSIS
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disease of rice farmers endemic in tropics and subtropics:
Southeast Asia, Australia, the Middle East, India, China, Caribbean
U.S. and EU cases linked with travel abroad
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS V Epidemiology II
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Clinical disease uncommon
in endemic areas– antibodies in 5-20% of
agricultural workers– no history of disease
Seasonal increase (wet season)– heavy rainfall– high humidity or temperature
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS VI Epidemiology III
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WOUND INFECTION– Contact with contaminated soil
or water
INGESTION– Contaminated water
INHALATION– Dust/ contaminated soil
RARELY– Person-to-person– Animal-to-person
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS VIII Transmission
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INCUBATION PERIOD: 1-21 days (~ 9 days) up to 30 years
Always Fever, chills, malaise
Soft tissue: AbscessPulmonary: Productive cough, dyspnoeaSepticaemic/disseminated: Multiple abscesses, Septic shock
MOST INFECTIONS ASYMPTOMATIC/ LATENT
MODE OF TRANSMISSION INDUCES DIFFERENT CLINICAL FORMS:
INOCULATION => Focal (wound) infectionINHALATION => Acute pulmonary infection
Both can result in secondary SEPTICEMIACNS involvement is rare
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS IX Clinical Course I
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Abscess/ granuloma formation
– Skin– Bone and/or muscle– Joints– Internal organs– Genitourinary– Nervous system (infrequent)
FOCAL INFECTIONS
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS X Clinical Course II
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Most common form:
High fever, headache
Dull aching chest pain
Cough, tachypnea, rales
Chest X-rays– Upper lobe consolidation– Nodular lesions– Pleural effusion
ACUTE PULMONARY INFECTION
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS XI Clinical Course III
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PULMONARY INFECTION - RADIOLOGY FINDINGS
USE CTIF AVAILIABLE !
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS XII Clinical Course IV
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DIAGNOSIS:Clinical suspicion => travel to endemic areas
low budget, outdoor travel
=> occupational exposure
medical, military
Microbiology => Isolation of organism
=> Various serological tests
PREVENTIONAvoid contact with soil/water => Chlorination if needed
Handling infected animals with care
Thorough cleaning of wounds
SYNDROMIC PRESENTATION – SESSION 1MELIOIDOSIS XIVDiagnosis and prevention