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Dr. Marwan Jabr Alwazzeh Assoc. Prof. of Medicine Consultant Internist/Infectious Diseases University of Dammam.

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Presentation on theme: "Dr. Marwan Jabr Alwazzeh Assoc. Prof. of Medicine Consultant Internist/Infectious Diseases University of Dammam."— Presentation transcript:

1 Dr. Marwan Jabr Alwazzeh Assoc. Prof. of Medicine Consultant Internist/Infectious Diseases University of Dammam

2 What is Biological Warfare? The use, for hostile purposes, of living organisms, whatever their nature, or infective material derived from them, which are intended to cause disease or death in man, animal, or plants

3 Bioweapens recent history Bioweapons have a long history. Recent uses include: U.S, Canada, Great Britain, Japan, and the Soviet Union with anthrax during World War II Post World War II, NATO and the Warsaw Pact nations had bioweapons programs Other countries Bioterrorism

4 The threat of biological warfare Biologic agents are likely to be used as weapons because: Relatively easy to procure Potentially inexpensive to produce Unless the terrorists announced the release of agent, detection of the attack would be challenging (odorless, colorless and tasteless) Can be used to attack people, economies and food supplies Cause fear, panic and social disruption

5 Biological warfare arsenal of the Cold Ware Superpowers (U.S) Anticrop weaponsIncapacitating agentsLethal agents Wheat-stem rust Rye-stem rust Rice-blast spore Venezuelan equine encephalitis Staphylococcal Enterotoxin B Brucella suis Coxiella burnetii Bacillus anthracis Botulinum toxin Francisella tularensis

6 Biological warfare arsenal of the Cold Ware Superpowers (Soviet Union) Smallpox Yersinia pestis Bacillus anthracis Botulinum toxin Venezuelan equine encephalitis virus Francisella tularensis Coxiella burnetii Marburg virus Influenza virus Burkholderia mallei Rickettsia typhi

7 The Ideal Bioweapon Contagious Virulent Robust Difficult to detect Drug-resistant User-controllable

8 Characteristics of biological attacks Incubation periods A delay is likely between the release of the agent and the knowledge that the occurrence is a sinister act A short window of opportunity exists between the first wave and the second wave

9 Characteristics of Biological attacks Victims widely dispersed and likely to present for days to weeks Potential for many casualties “First responders” may be health care providers

10 Hypothetical dissemination of some infectious agents Total casualtiesDeathsDownwind carriageAgent >>20 kmAnthrax kmPlague >20 kmTularemia kmPlague kmTick-borne encephalitis kmEpidemic typhus kmBrucellosis >20 kmQ-fever kmVenezuelan equine encephalitis Casualty figures assume 50 kg of dried agent, disseminated along a 2-km line upwind of a population center of

11 Critical agents for public health preparedness Category CCategory BCategory A Emerging threat agents (e.g., nipah virus, hantaviruses, pandemic influenza viruses) Coxiella burnetii Brucellae Burkholderia mallei Burkholderia pseudomallei alphaviruses Rickettsia prowazekii Certain toxins (e.g., ricin, SEB) Chlamydia psittaci Food safety threat agents (e.g., salmonellae, E. coli O 157:H7) Water safety threat agents (e.g., vibrio cholera) Variola virus Bacillus anthracis Yersinia pestis Botulinum toxin Francisella tularensis Filoviruses and arenaviruses

12 CDC CATEGORY A AGENTS Agents that would have maximum impact on population: Ease of dissemination Person-to-person transmission High mortality Need for public health preparedness

13 ANTHRAX Infectious agent: Bacillus anthracis – rod-shaped, Gram- positive, spore forming bacteria Primarily endemic and epidemic zoonotic disease

14 ANTHRAX Bacillus anthracis has characteristics that make it attractive as biological weapon: Easy to obtain Grows readily in easily prepared media Can be easily induced to form spores Spore size and durability


16 CLINICAL FORMS OF ANTHRAX Cutaneous form: 7 days after exposure to infected hides or meat, a painless or mildly pruritic papule forms The lesion rapidly enlarges and ulcerates, often accompanied by significant surrounding edema and regional lymphadenopathy The case fatality rate of cutaneous anthrax is 20% without antibiotic treatment, and <1% with antibiotics.

17 Gastrointestinal form Rare natural occurrence Results from consumption of insufficiently cooked meat of infected animals Typically develop massive gastrointestinal bleeding and sepsis Fatal outcome in 50% of cases Oropharyngeal anthrax CLINICAL FORMS OF ANTHRAX

18 Inhalational form Present within 1-6 days of exposure (but perhaps up to several month later) Person-to-Person spread extremely rare Nonspecific febrile prodrome Pneumonia is rare, but there is usually mediastinitis and plural fusion Fatal outcome in 45-85% of cases Anthrax Meningitis manifests in 50% of Inhalational Anthrax patients CLINICAL FORMS OF ANTHRAX

19 CXR classically shows mediastinal widening with clear lung fields Non-contrast chest CT was useful in leading to a presumptive diagnosis in some patients

20 Blood culture (on blood agar) is the gold standard and is very specific (100% before antibiotic initiation) Culture from the cutaneous lesion (from vesicle) Stool culture Immunohistochemical stains PCR Diagnosis

21 Cutaneous form Systemic and route unknown: Initial empirical should be include ciprofloxacin or doxycycline plus one or tow additional effective antibiotics Human anthrax immune globulin (in clinical trials) Treatment

22 Oral ciprofloxacin, levofloxacin or doxycycline for at least 60 days Anthrax Vaccine Adsorbed (AVA) (under investigation) Contact precautions Postexposure prophylaxis

23 SMALLPOX Variola virus - Orthopox virus Two forms: Variola Major and Variola Minor Global eradication was in 1980, but remaining viral stocks exist

24 Droplet-borne infection Person-to-person spread very rapid and would likely infect 35-50% of unvaccinated case contacts Incubation period: 7-17 days Nonspecific influenza-like symptoms of prodromal phase The rash appears in centrifugal pattern Mortality: less than 1% in the minor form and 20 to 50 % in the major form SMALLPOX






30 The Diagnosis primarily clinical Viral culture (vesicle fluid) PCR Electron microscopy Diagnosis

31 There is no specific treatment Supportive care Antiviral drugs (Cidofovir) Vaccina immune globulin Treatment

32 Strict contact and respiratory isolation until all scabs have separated Smallpox vaccine (within 4 days of exposure) Near complete protection lasting at least 5-10 yrs Vaccinia immune globulin is also effective the antiviral drug cidofovir Postexposure prophylaxis

33 Plague Infectious agent: Yersinia pestis – a non-motile, Gram-neg., coccobacillus

34 Plague is primarily a zoonotic disease In nature, fleas living on rodents spread infection to humans As a bioterrorist weapon – inhalation of aerosol leads to pneumonia and sepsis Plague

35 Three forms: Bubonic plague (rare person-to-person spread) Pneumonic plague (person-to-person spread) Septicemic (rare person-to-person spread) Plague

36 Bubonic Plague Incubation period: 2-6 days Bite of infected flea Characteristic “bubos” grossly enlarged, extremely tender lymph nodes Suppurative lymphadenopathy and fever

37 Bubonic Plague If untreated, can lead to pneumonic or septicemic forms of plague

38 Pneumonic Plague Aerosolized bacilli Short incubation: 2 to 3 days Short, febrile prodrome Rapid progression to severe pneumonia Fatality: 100% if untreated within 24 hours of symptom onset

39 Septcemic Plague Rare, usually seen secondary to pneumonic or bubonic forms of plague Progression: Purpura Disseminated intravascular coagulation (DIC) Acral necrosis Often fatal even when treated “Black Death”

40 Wayson, Wright’s, Giemsa stains Blood, sputum and CSF culture Serologic tests provide a diagnosis retrospectively Diagnosis

41 Rapid antibiotic therapy Streptomaycin or Gentamycin Alternative ciprofloxacin or doxycycline Beta-lactams,rifampin, and macrolides are ineffective Treatment

42 Strict respiratory isolation until 48 hrs of effective antibiotic therapy Ciprofloxacin or doxycycline for 7 days after exposure Postexposure prophylaxis

43 Tularemia A zoonotic, bacterial infection caused by Francisella tularensis, a tiny, pleomorphic, poorly staining Gram-negative coccobacillus

44 Tularemia Commonly found in ticks living on rabbits and transmitted by handling the animal or by tick bite

45 Inhalation of aerosol leads to pneumonia and sepsis Incubation period: 3 to 5 days (range 1 to 14) Person-to-person transmission is unusual Sudden onset with influenza-like symptoms such as fever, chills, malaise, profuse sweating, headache and nausea Pulse-temperature dissociation Tularemia

46 CLINICAL FORMS Ulceroglandular (Most common form in naturally occurring cases) Glandular Occuloglandular Oropharyngeal Tularemia

47 CLINICAL FORMS Pneumonic (Primary pleuro-pulmonary disease) Typhoidal Abrupt onset of febrile illness in 3-5 days Rapid progression to life-threatening pneumonitis in 80% of typhoidal cases Case fatality rate for typhoidal tularemia is 35% in untreated patients Tularemia


49 Sputum Gram’s stain is invariably negative Culture of Blood, sputum or plural fluid is slow and insensitive Serologic tests more sensitive PCR available Diagnosis

50 Rapid antibiotic therapy (Mortality rate > 60% in untreated cases) Streptomaycin or Gentamycin Alternative ciprofloxacin or doxycycline Cefteriaxone is ineffective Treatment

51 Strict contact precautions Ciprofloxacin or doxycycline for 14 days after exposure A live attenuated vaccine available, but not recommended for postexposure prophylaxis Postexposure prophylaxis

52 Botulism Clostridium botulinum – a spore forming, anaerobic Gram-positive bacillus No person-to- person transmission Incubation period: 12 to 72 hours

53 Botulism There are 7 neurotoxins (A-G) LD 50 =0.001 µg/kg (the most potent chemical warfare agent) Affect the motor nerve terminus with irreversibly blocks the release of acetylcholine Muscle paralysis lasts until axonal branches regenerate

54 Botulism Food-born botulism (ingested toxin) Gastrointestinal and Infant botulism (Clostridium botulinum) Wound botulism(Clostridium botulinum) Iatrogenic botulism (Botox) Pulmonary botulism(inhaled aerosolized toxin)

55 Classic triad: Lack of fever Clear sensorium Symmetric descending flaccid paralysis Symptoms include ptosis, diplopia, dysarthria, dysphagia, d ry mouth, and Muscle weakness Botulism

56 Cases presenting with the classic syndrome can be diagnosed clinically Mouse bioassay (confirmatory test) Diagnosis

57 Supportive care particularly ventilatory support Botulinum antitoxins (IV) Treatment

58 Asymptomatic persons: Botulinum antitoxin is not recommended for prophylaxis (10% hypersensitivity reactions) Symptomatic persons: Botulinum antitoxin and carefully monitoring Postexposure prophylaxis

59 Viral Hemorrhagic Fevers (VHFs) Virus FamilyDisease (Virus)Natural Distribution Usual Source of Human Infection Respiratory transmission Incubation (Days) Arenaviridae ArenavirusLassa feverAfricaRodentyes5-16 Argentine HF (Junin)South AmericaRodent7-14 Bolivian HF (Machupo)South AmericaRodent9-15 Brazilian HF (Sabia)South AmericaRodent7-14 Venezuelan HF (Guanarito)South AmericaRodent7-14 Bunyaviridae PhlebovirusRift Valley feverAfricaMosquito2-5 NairovirusCrimean-Congo HFEurope, Asia, AfricaTickyes3-12 Hantavirus Hemorrhagic fever with renal syndrome, hantavirus pulmonary syndrome Asia, Europe, worldwideRodent9-35 Filoviridae FilovirusMarburg and EbolaAfricaUnknownyes3-16 Flaviviridae FlavivirusYellow fever Tropical Africa, South America Mosquito3-6 Dengue HFAsia, Americas, AfricaMosquitoUnknown for dengue HF, 3-5 for dengue

60 Viral Hemorrhagic Fevers (VHFs) All share the potential for severe disruption of vascular permeability (vascular endothelial damage) and bleeding diathesis (DIC) Think at VHF in every case with unexplained leukopenia, thrombocytopenia and hepatitis

61 Sudden onset of fever, muscle aches, headache, followed by vomiting, diarrhea, rash and bleeding Viral Hemorrhagic Fevers (VHFs)

62 Progresses rapidly to hypotension, shock, mucosal and GI bleeding, edema and end-organ failure Viral Hemorrhagic Fevers (VHFs)

63 Confirmed diagnosis can be made for most VHFs serologically Some viruses can be cultured Supportive therapy is crucial for all patients Antiviral therapy (Ribavirin IV) has been used experimentally for Crimean-Congo HF, Lassa, Rift Valley fever and HF caused by hantaviruses

64 Postexposure prophylaxis All patients should be placed in respiratory and contact isolation Oral Ribavirin can be used after high-risk exposure to Crimean-Congo HF, Lassa, Rift Valley fever and HF caused by hantavirus

65 Horses or Zebras? Outbreak of rare disease Seasonal disease at wrong time Unusual age distribution Unusual clinical symptoms Unusual epidemiologic features Outbreak in region normally not seen

66 Horses or Zebras? Rapidly increasing disease incidence in a healthy population Multiple diseases in one patient Dead animals (especially multiple species) History of visible cloud Claims by aggressors Fulminant disease presentations Travel history

67 The Ideal Bioweapon Contagious Virulent Robust Difficult to detect Drug-resistant User-controllable

68 “Please, don’t forget these zebras”

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