Download Biological Warfare Agents

Biological Warfare Agents
Categories
A: high risk; readily disseminated, high mortality, require public health preparedness
Smallpox – 30% mortality, no antiviral therapy, stable virus in aerosol form, small dose needed,
aerosol/direct contact, infectious during incubation period, no current vaccination herd immunity
Anthrax, botulism, plague, tularemia, viral haemorrhagic fevers, adenaviruses
B: moderate risk; moderate disseminated, moderate morbidity, low mortality, require diagnostic
surveillance; foodbourne/waterbourne normally
Brucellosis, C. perfringens, Salmonella, E coli, shigella, glanders, meliodiosis, psittacosis, Q fever, staph
enterotoxin B, typhus fever, viral encephalitis, cholera
C: potential pathogens (eg. Nipah virus)
Recognition of
Attack
 number of patients (exponentially); unusual disease presentation; unresponsive to standard treatment
Anthrax
Bacillus anthracis: Spore-forming; rod-shaped; G+ive; extracellular; aerobic; Contact with farm and wild
animals usually; spores ground into powder for biological warfare; lethal toxin and oedema toxin cause
symptoms and death; no person-person transmission
Cutaneous anthrax: 95% of naturally occuring infections; painless pruritic
papule  ulcer  vesicle within 2 days  enlarges, with surrounding
erythema and lympadenopathy  vesicle ruptures  ulcer covered with
painless depressed black eschar 1-3cm diameter which dries and falls off in
1-2/52; lymphangitis; bacteraemia rare; mortality rate 20% without
antibiotics
Inhalational anthrax (wool sorter’s disease): inhaled  alveolar spaces  macrophages mediastinal
lymphadenopathy  spores germinate and release toxins
Stage 1: 1-6/7 prodromal illness  fever, cough, flu-like illness but no runny nose
Stage 2:  abrupt onset worsened fever, hypoxia, sweating; SOB (80%); chest pain (65%) 
haemorrhagic mediastinitis, oedema, necrosis, focal haemorrhagic necrotising lesions, pleural
effusions, stridor, resp failure, cyanosis, bacteriaemia  haemorrhagic meningitis in 50%; shock and
death in hrs-days
GI anthrax: eating undercooked meat; nausea, abdominal pain, vomiting  severe, bloody diarrhoea;
acute abdomen; mortality >50%
Investigation: widened mediasinum (70%), pleural effusions (80%), lesions in midzone; CT scan; pleural
aspirate; blood culture; ELISA; blood gases, U+E (hypocalcaemia, hyperkalaemia), BSL, FBC; culture skin
lesions, stool culture
Management: immediate notification of public health; standard barrier isolation, no need for air filter
masks; no direct contact with skin lesions; surface decontamination with bleach and water; urgent
antibiotics; assume resistance to penicillin and tetracycline if terrorist attack; use ciprofloxacin 400mg IV
BD + rifampicin / vancomycin / penicillin / imipenem / clindamycin; treat for 60/7
Plague
Yersinia pestis: Facultative intracellular; Fleabites (blocks gut of flea, flea vomits before feeding); aerosol;
Toxins; Proliferate in lymphoid tissue  kill host phagocytes
Bubonic plague: infected fleabite on legs, with small pustule/ulceration 
large tender lymph nodes (buboes) in few days, soft and plum coloured 
infarct / rupture through skin; rapid onset fever, shock, MOF, death
Septicaemic plague: all LN's big; GI symptoms, DIC and widespread
haemorrhage and thrombi, MOF, rapid death
Pneumonic plague: most likely manifestation of bioterrorism; most rapidly
progressive and fatal; incubation 1-6/7; watery, mucoid, frothy, bloody
sputum, symptoms of pneumonia +/- GI symptoms
Investigation: microscopy of blood / sputum / CSF / buboe  G-ive bacilli; pneumonia on CXR
Management: respiratory isolation; antibiotics ASAP = streptomycin / gent best; also doxycycline /
ciprofloxacin
Smallpox
DNA virus: only infectious disease to have
been eradicated; spread would be fast by
droplet/aerosol
Symptoms: 90% have classical presentation;
incubation 7-17/7; infective once
maculopapular rash develops (mucous
membranes, face, forearms, trunk, legs;
spares palms and soles)  vesicular and
pustular in 1-2/7 (all at same stage of
development, unlike varicella)  high
fever and toxaemia, malaise, headache,
backache, abdominal pain, delirium on
D3-8  infectivity wanes as scabs develop
(D8-9)  scarring; 30% mortality from variola major, 1% from minor; multiplies in spleen, bone marrow,
lymph nodes; death in 30%, in week 2 10% atypical: haemorrhagic (more severe; fatal; dusky erythema,
petechiae, frank haemorrhage in skin and MM); malignant (similar to haemorrhagic, but slower), minor
(milder)
Investigation: swab lesions for microscopy
Management: international health emergency; isolate all face-to-face contacts; standard disinfectants
work; cremate if die; supportive treatment only; can vaccinate within 4/7 exposure (post vaccine
encephalitits in 1:300,000, 25% fatal/severe morbidity; post-vaccine gangrene (often fatal); smallpox
disease)
Tularemia
Francisella tularensis: aerobic, G-ive coccobacillus; highly infective +++; animal hosts  human infected
by bites, faeces, soil, water; no human-human transmission; causes granulomatous necrotic lesions;
results in ulceroglandular disease (papulepustuleulcer, eschar), oculoglandular, oropharyngeal
(exudative tonsillitis), pneumonia (mortality 30-60%), sepsis (potentially severe and fatal), meningitis;
typhoidal tularemia lacks these cutaneous / MM lesions (and may have prominent GI symptoms, pulse /
T differentiation); mortality 5-15% for type A; overall mortality 2%
Management: streptomycin, gentamicin; if mass involvement, doxycycline / ciprofloxacin
Botulism
Clostridium botulinum: from soil into food (home canned food, foiled wrapped potatoes, garlic in oil,
yoghurt, cream cheese, infant formula, cream cheese) / wound  toxin absorbed; major potential in
bioterrorism, inhaled; most poisonous substance known to man; no human-human spread; toxin in
blood  peripheral cholinergic synapses and neuromuscular junction  blocks acetylcholine action
 acute, afebrile, symmetrical, descending flaccid paralysis always beginning in bulbar muscles, multiple
cranial nerve palsies, vision/speech/swallowing problems, constipation, ptosis, large, sluggish pupils;
normal LOC, no sensory changes, arreflexia; usually 12-72hrs after ingestion, ?72hrs INH
Investigation: clinical diagnosis; EMG
Differential Diagnosis: Guillian Barre syndrome, MFS, myasthenia gravis, CNS disease
Treatment: supportive care; antitoxin will  subsequent nerve damage, but doesn’t reverse existing
paralysis