Download Biological Warfare Agents

Biological Warfare Agents
Categories
Cat 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
Cat B: mod risk; mod disseminated, mod 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
Cat C: potential pathogens (eg. Nipah virus)
Incr no pt (exponentially); unusual disease presentation; unresponsive to standard trt
Recognition
of attack
Anthrax
Plague
Smallpox
Tularemia
Botulism
Viral
haemorrhagic
fevers
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 ABx
Inhalational anthrax (wool sorter’s disease): inhaled  alveolar spaces  macrophages mediastinal LN --> 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%); CP (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, abdo pain, vomiting --> severe, bloody diarrhoea; acute abdo; mortality >50%
Investigation: widened mediasinum (70%), pleural effusions (80%), lesions in MZ; CT scan; pleural aspirate; blood culture; ELISA; blood gases, U+E
(hypoCa, hyperK), BSL, FBC; culture skin lesions, stool culture
Mng: 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 Abx; assume resistance to penicillin and tetracycline if terrorist attack; use cipro 400mg IV BD +
rifampicin / vanc / penicillin / imipenem / clindamycin; trt for 60/7
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 LN's (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, Sx of pneumonia +/- GI symptoms
Investigation: microscopy of blood / sputum / CSF / buboe  G-ive bacilli; pneumonia on CXR
Mng: resp isolation; Abx ASAP = streptomycin / gent best; also doxy / cipro
DNA virus: only infectious disease to have been eradicated; spread would be fast by droplet/aerosol
Sx: 90% have classical presentation; incubation 7-17/7; infective once maculopapular rash develops (MM, 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, AP, delirium on D3-8  infectivity wanes as scabs develop (D8-9)  scarring; 30% mortality from variola major, 1% from minor;
multiplies in spleen, BM, LN; death in 30%, in wk 2
10% atypical: haemorrhagic (more severe; fatal; dusky erythema, petechiae, frank haemorrhage in skin and MM); malginant (similar to
haemorrhagic, but slower), minor (milder)
Investigation: swab lesions for microscopy
Mng: international health emergency; isolate all face-to-face contacts; standard disinfectants work; cremate if die; supportive trt 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)
Francisella tularensis: aerobic, G-ive coccobacillus; highly infective +++; animal hosts  human infected by bites, faeces, soil, water; no humanhuman 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 Sx, pulse / T differentiation); mortality 5-15% for type A; overall mortality 2%
Mng: streptomycin, gentamicin; if mass involvement, doxycycline / cipro
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  peri cholinergic synapses and NMJ  blocks Ach action
 acute, afebrile, symmetrical, descending flaccid paralysis always beginning in bulbar muscles, multiple CN palsies, vision/speech/swallowing,
probs, constipation, ptosis, large, sluggish pupils; normal LOC, no sensory changes, arreflexia; usually 12-72hrs after ingestion, ?72hrs INH
Investigation: clinical diagnosis; EMG
DD: GBS, MFS, MG, CNS disease
Trt: supportive care; antitoxin will decr subsequent nerve damage, but doesn’t reverse existing paralysis
See febrile traveller fact sheet
Notes from: Dunn