Week 15: Impaired Immunity Flashcards Preview

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Flashcards in Week 15: Impaired Immunity Deck (77):

Systemic inflammatory response syndrome (SIRS), triggers, criteria needed, what does it advance to?

*Generalized inflammation in organs remote from  initial insult

*Consider fairly reversible.  Problem is that it advances to MONS

Criteria (2 or more needed):

  • Fever greater than 38.0 or less than 36
  • hr greater than 90
  • RR greater than 20
  • WBC above 12,000, less than 4,000
  • Bands greater than 10%


  • Mechanical tissue trauma: burns, crush injuries, surgical procedures
  • Abscess formation: intra-abdominal, extremities
  • Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
  • Microbial invasion: Bacteria, viruses, fungi
  • Endotoxin release: Gram-negative bacteria
  • Global perfusion deficits: Post–cardiac resuscitation, shock states
  • Regional perfusion deficits: Distal perfusion deficits




Multiple organ dysfunction syndrome (MODS)

  • failure of two or more organ systems
  • Homeostasis cannot be maintained without intervention-Results from SIRS
  • SIRS and MODS represent ends of a continuum
  • Transition from SIRS to MODS DOES NOT occur in a clear-cut manner




Consequences of inflammatory response

  • Low BF
  • Release of mediators
  • Direct damage to endothelium
  • Hypermetabolism
  • Vasodilation leading to dec SVR
  • Inc in vascular permeability
  • Activation of coagulation cascade 
  • Inflammation can travel to other organs and cause the same response in other organs


SIRS and MODS patho and stages

  • Organ and metabolic dysfunction
  • Hypotension
  • Decreased perfusion
  • Formation of microemboli
  • Redistribution or shunting of blood 

Stage 1:

local cytokine relase

Stage 2:

release of cytokines into systemic system

stage 3:

Humoral cascade (clotting cascade being released systemically in multiple organs)



SIRS/MODS in respiratory system

  • Alveolar edema
  • Decrease in surfactant
  • Increase in shunt
  • V/Q mismatch
  • End result: ARDS 
  • 70% will go into MODS, so the VAP protocols are essential


Cardiovascular system SIRS/MODS patho

  • Myocardial depression and massive vasodilation
  • decreased CO, decreased preload, increased afterload leading to ischemia to the heart
  • Depressed cardiac muscle function



Renal system SIRS/MODS  patho

Acute renal failure

  • Hypoperfusion leading to ischemia
  • Release of mediators
  • Activation of renin–angiotensin– aldosterone system to compensate (which causes vasoconstriction, furthering ischemia)
  • Nephrotoxic drugs, especially antibiotics further the insult.  Quinolines, Sulfas, Vancomycins




GI system SIRS/MODS patho

  • Motility decreased: Abdominal distention and paralytic ileus
  • Decreased perfusion: Risk for ulceration and GI bleeding
  • Potential for bacterial translocation

Hypermetabolic state

  • Hyperglycemia–hypoglycemia
  • Insulin resistance
  • Catabolic state
  • Liver dysfunction
  • Lactic acidosis


Hematologic system SIRS/MODS patho

  • DIC
  • Electrolyte imbalances
  • Metabolic acidosis


SIRS/MODS collaborative care prevention

  • Prognosis for MODS poor
  • Goal: Prevent progression of SIRS to MODS
  • Vigilant assessment-ongoing monitoring to detect early signs of deterioration or organ dysfunction-critical
  • Prevention and treatment of infection
    • Aggressive infection control strategies to dec risk for nosocomial infections
    • Once an infection suspected, institute interventions to control source !~


SIRS/MODS collaborative care oxygenation

Maintain tissue oxygenation

  • Dec O2 demand
    • Sedation

    • Mechanical ventilation (on volume control)

    • Paralysis

    • Analgesia

  • Optimize O2 delivery
    • Maintain normal hemoglobin level
    • Maintain normal PaO2
      • Individualize tidal volumes with PEEP ( don't want too much volume, can cause barotrauma)




Maintenance of tissue oxygenation with SIRS/MODS

Maintenance of tissue oxygenation
Enhance CO

  • Increase preload or myocardial contractility: dopamine and dobutamine
  • Reduce afterload: Nipride or nitro drip, 
  • Give levofed to cause vasoconstriction: cuts circulation into the periphery increasing SVR and preload


SIRS/MODS collaborative care with nutrition

  • Nutritional and metabolic needs
  • Goal of nutritional support: Preserve organ function-total energy expenditure-often inc 1.5 to 2.0 times: need HIGH PROTEIN feed.
  • Nutritional and metabolic needs
  • Use of enteral route preferred to parenteral nutrition
  • Monitor plasma transferrin  & prealbumin levels to assess hepatic protein synthesis


SIRS/MODS failiing organs

Support of failing organs

  • ARDS: Aggressive O2 therapy and mechanical ventilation
  • DIC: Appropriate blood products
  • Renal failure: Continuous renal replacement therapy or dialysis


Shock, classifications

  • Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
    • Imbalance in supply/demand for O2 and nutrients
  • Classification of shock


cardiogenic shock


  • Systolic or diastolic dysfunction
  • Compromised cardiac output (CO)

Precipitating causes

  • Myocardial infarction
  • Cardiomyopathy
  • Blunt cardiac injury
  • Severe systemic or pulmonary hypertension
  • Cardiac tamponade
  • Myocardial depression from metabolic problems



patho of cardiiogenic shock


decrease in filling that leads to a decrease in stroke volume.  Up to 85% die

CO lesss than 4 or cardiac input of less than 2.5


Manifestations of Cardiogenic shock

Early manifestations

  • Tachycardia; Hypotension
  • Narrowed pulse pressure
  • ↑ myocardial O2 consumption

Physical examination

  • Tachypnea, pulmonary congestion
  • Pallor; cool, clammy skin
  • Dec capillary refill time
  • Anxiety, confusion, agitation

-↑ in pulmonary artery wedge pressure
-Dec renal perfusion and UO


Absolute hypovolemia

loss of intravascular fluid volume

  • Hemorrhage; GI loss (e.g., vomiting, diarrhea)
  • Fistula drainage; Diabetes insipidus
  • Hyperglycemia; Diuresis


relative hypovolemia

  • Results when fluid volume moves out of vascular space into extravascular space (e.g., interstitial or intracavitary space)
  • Termed third spacing


patho of hypocolemic shcok

  • greater than 40% volume loss is irreversible and there will be permanent damage.  Body tries to autoregulate, but can't past this 40%, causing ischemia and damage to all organs
  • Look at H&H, (see an increase with diabetes insipidous or third spacing, otherwise it will go down), look at electrolytes (increase in K+), ABGS, CV o2 sat, watching UO hourly (have to be cathed)


clinical manifestations of hypovolemic shock

  • Anxiety
  • Tachypnea
  • Inc in CO, heart rate
  • Dec in stroke volume, PAWP, urinary output
  • If loss is >30%, blood volume is replaced.


Distributive shock/neurogenic shock and clinical manifestations

  • Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and  last up to 6 weeks
  • Can occur in response to spinal anesthesia
  • Results in massive vasodilation > lead to pooling of blood in vessels

Clinical manifestations

  • Hypotension
  • Bradycardia
  • Temperature dysregulation (resulting in heat loss) (warm skin from vasodilation, then it cools and get hypothermia)
  • Dry skin
  • Poikilothermia (taking on the temperature of the environment)




distributive shock/anaphylactic shock, manifestations, treatment

Acute, life-threatening hypersensitivity reaction

  • Massive vasodilation; Release of mediators
  • ↑ capillary permeability

Clinical manifestations

  • Anxiety, confusion, dizziness
  • Sense of impending doom; Chest pain
  • Incontinence
  • Swelling of the lips and tongue, angioedema
  • Wheezing, stridor; Flushing, pruritus, urticaria
  • Respiratory distress and circulatory failure


  • A (establish this quick) BCDE
  • If you don't have an epi pen, have them in a position to help with vasodilation, so you want their feet elevated
  • Epi (adrenaline) lasts only 20 minutes, then it needs to be repeated (give every 3-5 minutes in hospital until you get a response)
  • High flow oxygen is appropriate for these patients (veni mask, face mask)
  • IV fluids: Adults 500-1,000, children crisiloid 20ml/kg
  • Give steroids and medications to help with allergic reactions (hydrocortisone, chloriphenamine




Distributive/Septic shock, clinical manifestations

-Sepsis: systemic inflammatory response to documented or suspected infection
-Severe sepsis = Sepsis + Organ dysfunction

  • Presence of sepsis with hypotension despite fluid resuscitation
  • Presence of tissue perfusion abnormalities

Clinical manifestations

  • ↑ coagulation and inflammation
  • ↓ fibrinolysis
  • Formation of microthrombi
  • Obstruction of microvasculature
  • Hyperdynamic state: increased CO and decreased SVR
  • Tachypnea/hyperventilation
  • Temperature dysregulation
  • ↓ urine output
  • Altered neurologic status
  • GI dysfunction
  • Respiratory failure common.



obstructive shock

(pulmonary embolis) Develops when physical obstruction to blood flow occurs with decreased CO

  • From restriction to diastolic filling of right ventricle due to compression
  • Abdominal compartment syndrome

Patient  experience

  • Dec CO
  • Increased afterload
  • Variable left ventricular filling pressures

Rapid assessment and immediate treatment important


initial stage of shock

  • Usually not clinically apparent
  • Usually considered reversible
  • Metabolism changes from aerobic to anaerobic.
    • Lactic acid accumulates -must be removed by blood and broken down by liver.
    • Process requires unavailable O2.
  • Clinically apparent –Neural, Hormonal &Biochemical compensatory mechanisms
  • Attempts  aimed to overcome consequences of anaerobic metabolism and maintaining homeostasis.




compensatory (or initial?) stage of shock

  • Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP.
    • Vasoconstriction while blood to vital organs maintained-
  • ↓ blood to kidneys  > activates renin– angiotensin system ↑ venous return to heart, CO, BP
  • Impaired GI motility- Risk for paralytic ileus
  • Cool, clammy skin from blood
    • Except septic patient who is warm and flushed


complensatory stage

  • Shunting blood from lungs increases physiologic dead space.
    • ↓ arterial O2 levels
    • Increase in rate/depth of respirations
    • V/Q mismatch
  • SNS stimulation increases myocardial O2 demands.
  • If perfusion deficit corrected, patient recovers with no residual sequelae
  • If deficit not corrected, patient enters progressive stage




progressive stage of shock

  • Begins when compensatory mechanisms fail
  • Aggressive interventions to prevent multiple organ dysfunction syndrome (MODS)
  • Hallmarks -↓ cellular perfusion & altered capillary permeability
    • Leakage of protein into interstitial space
    • ↑ systemic interstitial edema


  • Fluid leakage affects solid organs and peripheral tissues.
  • ↓ blood flow to pulmonary capillaries

Movement of fluid from pulmonary vasculature to interstitium

  • Pulmonary edema
  • Bronchoconstriction
  • ↓ residual capacity

Fluid moves into alveoli

  • Edema-Dec surfactant
  • Worsening V/Q mismatch
  • Tachypnea, Crackles
  • Inc work of breathing

CO begins to fall

  • Dec peripheral perfusion
  • Hypotension
  • Weak peripheral pulses
  • Ischemia of distal extremities

Myocardial dysfunction results in

  • Dysrhythmias
  • Ischemia; Myocardial infarction
  • End result: complete deterioration of cardiovascular system

Liver fails to metabolize drugs and waste.

  • Jaundice;  Elevated enzymes
  • Loss of immune function
  • Risk for DIC and significant bleeding

Mucosal barrier of GI system becomes ischemic

  • Ulcers
  • Bleeding
  • Risk of translocation of bacteria
  • Dec ability to absorb nutrients



irreversible stage of shock

  • Exacerbation of anaerobic metabolism
  • Accumulation of lactic acid
  • ↑ capillary permeability
  • Profound hypotension and hypoxemia
  • Tachycardia worsens.
  • Failure of one organ system affects others.
  • Recovery unlikely




diagnostic studies for shock

  • Thorough history and physical examination
  • No single study to determine shock
    • Blood studies
      • Elevation of lactate
      • Base deficit
    • 12-lead ECG
    • Chest x-ray
    • Hemodynamic monitoring 


successful management of shock includes

  • Identification of patients at risk for shock
  • Integration of patient’s history, physical examination, and clinical findings to establish diagnosis
  • Interventions to control or eliminate cause of dec perfusion
  • Protection of target and distal organs from dysfunction
  • Provision of multisystem supportive care




Management strategies of shock general

  • General management strategies
    • Ensure patent airway.
    • Maximize oxygen delivery (sat above 90%)
  • Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = Volume expansion
    • Isotonic crystalloids (e.g., normal saline) for initial resuscitation of shock
    • 2-3 liters fluid, then give a blood produc
  • Volume expansion
    • If patient does not respond to 2 to 3 L of crystalloids, blood administration & central venous monitoring may be instituted.
      • Complications of fluid resuscitation: Hypothermia & Coagulopathy


primary goal of drug therapy in shock

Primary goal of drug therapy = Correction of decreased tissue perfusion

  • Vasopressor drugs (e.g., norepinephrine)
    • Achieve/maintain MAP >60 to 65 mm Hg.
    • Reserved for patients unresponsive to fluid resuscitation
  • Vasodilator therapy (e.g., nitroglycerin, nitroprusside)
    • Achieve/maintain MAP >65 mm Hg.




nutrition in shock care

Nutrition is vital to decreasing morbidity from shock.

  • Initiate enteral nutrition within the first 24 hours.
  • Initiate parenteral nutrition if enteral feedings contraindicated or fail to meet at least 80% of caloric requirements
  • Monitor protein, nitrogen balance, BUN, glucose, electrolytes
  • Need high calories/protein


collaborative care cardiogenic shock

  • Restore blood flow to myocardium by restoring  balance between O2 supply and demand.
  • Thrombolytic therapy
  • Angioplasty with stenting
  • Emergency revascularization
  • Valve replacement
  • Hemodynamic monitoring
  • Drug therapy (e.g., diuretics to reduce preload)
  • Circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device)
  • to decrease contractility: beta blockers




hypovolemic shock collaborative care

  • Management focuses on stopping loss of fluid and restoring circulating volume.
  • Fluid replacement is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss). 
  • may need a vasopressor if this isn't working


collaborative care septic shock

  • Fluid replacement to restore perfusion
    • Hemodynamic monitoring
  • Vasopressor drug therapy
  • Vasopressin for patients refractory to vasopressor therapy
  • IV corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP
  • Antibiotics after cultures obtained (e.g., blood, wound exudate, urine, stool, sputum)
  • Drotrecogin alfa (Xigris)-Major side effect: bleeding
  • Glucose levels <150 mg/dL (combination of tpn and nutrition)
  • Stress ulcer prophylaxis with histamine (H2)-receptor blockers
  • Deep vein thrombosis prophylaxis with low-dose unfractionated heparin or low-molecular-weight heparin




pt. with neurogenic shockIn spinal cord injury: spinal stability


In spinal cord injury: spinal stability

  • Treatment of hypotension and bradycardia with vasopressors and atropine
  • *Fluids used cautiously as hypotension generally is not related to fluid loss
  • Monitor for hypothermia (warming blankets)


general treatment for anaphylactic

  • Epinephrine, diphenhydramine
  • Maintaining patent airway
    • Nebulized bronchodilators
    • Endotracheal intubation or cricothyroidotomy may be necessary.
  • Aggressive fluid replacement
  • Intravenous corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive 


obstructive shock general care

  • Early recognition and treatment is primary strategy.
  • Mechanical decompression
  • Radiation or removal of mass
  • Decompressive laparotomy


nursing assessment in shock

  • ABCs: airway, breathing, and circulation
  • Focused assessment of tissue perfusion
    • Vital signs
    • Peripheral pulses
    • Level of consciousness
    • Capillary refill
    • Skin (e.g., temperature, color, moisture)
    • Urine output
  • Brief history
    • Events leading to shock
    • Onset and duration of symptoms
  • Details of care received before hospitalization
  • Allergies
  • Vaccinations 


nursing diagnosis

  • Ineffective tissue perfusion: renal, cerebral, cardiopulmonary, GI, hepatic, and peripheral
  • Fear
  • Potential complication: organ ischemia/dysfunction



Goals for patient

  • Assurance of adequate tissue perfusion
  • Restoration of normal or baseline BP
  • Return/recovery of organ function
  • Avoidance of complications from prolonged states of hypo-perfusion


nursing implementation

Health promotion

  • Identify patients at risk.
    • Elderly patients
    • Those with debilitating illness
    • Those who are immunocompromised
    • Surgical or accidental trauma patients
  • Planning to prevent shock
    • Monitoring fluid balance to prevent hypovolemic shock
    • Maintenance of hand washing to prevent spread of infection 

Acute interventions

  • Monitor the patient’s ongoing physical and emotional status to detect subtle changes in the patient’s condition.
  • Plan and implement nursing interventions and therapy.
  • Evaluate the patient’s response to therapy.
  • Provide emotional support to patient and family.
  • Collaborate with other members of health team when warranted. 

Neurologic status: orientation and level of consciousness

Cardiac status

  • Continuous ECG
  • VS, capillary refill
  • Hemodynamic parameters: central venous pressure, PA pressures, CO, PAWP
  • Heart sounds: murmurs, S3, S4
  • Respiratory status

Respiratory rate and rhythm

  • Breath sounds
  • Continuous pulse oximetry
  • Arterial blood gases
  • Most patients will be intubated and mechanically ventilated.

-Urine output
-Tympanic or pulmonary arterial temperature
-Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection
-Bowel sounds
-Nasogastric drainage/stools for occult blood
-I&O, fluid and electrolyte balance
-Oral care/hygiene based on O2 requirements
-Passive/active range of motion

Assess level of anxiety and fear.

  • Medication PRN
  • Talk to patient
  • Visit from clergy
  • Family involvement
  • Comfort measures
  • Privacy
  • Call light within reach




nursing evaluation

  • Normal or baseline, ECG, BP, CVP, and PAWP
  • Normal temperature
  • Warm, dry skin
  • Urinary output >0.5 mL/kg/hr
  • Normal RR and SaO2 ≥90%
  • Verbalization of fears, anxiety


When assessing a patient in shock, the nurse recognizes that the hemodynamics of shock include:

1. Normal cardiac output in cardiogenic shock.
2. Increase in central venous pressure in hypovolemic shock.
3. Increase in systemic vascular resistance in all types of shock.
4. Variations in cardiac output and decreased systemic vascular resistance in septic shock. 

4. Variations in cardiac output and decreased systemic vascular resistance in septic shock. 


The nurse determines that the patient in shock has progressed beyond the compensated stage when laboratory tests reveal:

1. Increased blood glucose levels.
2. Increased serum sodium levels.
3. Increased serum potassium levels.
4. Increased serum calcium levels.

3. Increased serum potassium levels.


  • 26-year-old man arrives via paramedics to ED with multiple gun shot wounds to abdomen.
  • Unresponsive, BP 58/30, HR 146
  • Three units type O packed RBC given for profuse blood loss before surgery
  • Surgery successful in removing bullets and repairing blood vessels
  • Surgeon estimated he lost at least
    3 L of blood before surgery and 1 L more during surgery.He is admitted to ICU.

1. What complications will you anticipate with this amount of blood loss?

2. What fluids can you expect to administer?

3. What medications will likely be ordered?

4. What should you monitor hourly or every 2 hr?



1. hypovolemic shock

2. Administer LR, PRBCS, NS

3. Give levofed

4.  Monitor LOC, Cardiac Monitor/tele


Ideal Qualities for a Biologic Terrorist Agent

  • High rate of illness among those exposed
    • High attack rate
  • High rate of death among those who get ill
    • High case fatality rate
  • Short time between onset of illness and death
    • Small window to start treatment
  • Low level of immunity in the population
  • No effective or available treatment
  • Can be transmitted person to person
  • Easy to produce and disseminate
  • Difficult to diagnosis either clinically or diagnostically (i.e. laboratory identification)




Priority Biological Agents 


  • Anthrax
  • Plague
  • Tularemia
  • Brucellosis
  • Q fever
  • Other
    • food borne pathogens
    • waterborne pathogens


  • Smallpox
  • Viral Hemorrhagic Fevers
  • Viral Encephalitis


  • Botulism
  • Staph Enterotoxin B
  • Ricin toxin
  • Tricothecene mycotoxins



  • Gram positive spore forming bacterium Bacillus anthracis
  • Primarily disease of herbivores which are infected by ingesting spores in soil
  • Natural transmission to humans by contact with infected animals or contaminated animal products
    • “Woolsorter’s disease”
  • Three forms of disease
    • Cutaneous
    • Inhalational
    • Gastrointestinal (GI)


Epidemiology and transmission of anthrax

direct contact, ingestion (lesion), and inhalation


cutaneous anthrax

  • Accounts for 80% of naturally occurring Anthrax cases
  • Enters through openings in skin from abrasions, lacerations
  • 20% progress to systemic form if untreated
  • Most cases recover

A image thumb

anthrax inhalation

  • Inhalation of spores
  • Incubation, 2-3 days (range up to 60 days)
  • Spores engulfed by macrophages and transported to mediastinal and peribronchial lymph nodes
  • Insidious onset:  malaise, low grade fever, nonproductive cough
  • Abrupt development of respiratory distress
  • Hemorrhagic mediastinitis
  • Hematogenous spread
  • Meningitis in 50%, usually fatal

A image thumb

pt. care of inhalation anthrax


  • 400 mg intravenous every 12 hours for adults
  • 10 -15 mg/kg intravenous every 12 hours for children


  • 100 mg intravenous every 12 hours for adults and children > 8 yr and > 45 kg
  • 2.2mg/kg every 12 hours for children
  • < 8 yr (up to 200 mg/day)



  • One or two additional anti-microbial agents effective against anthrax (e.g. imipenem, clindamycin, rifampin, macrolides)

Additional issues

  • Penicillin should never be used as a monotherapy
  • If meningitis is suspected, an antibiotic with good CSF penetration should also be administered (e.g. rifampin or chloramphenicol)
  • Supportive therapy for shock, fluid volume deficit and airway management may be needed.
  • Drainage of pleural effusions may improve clinical outcome

Anthrax Immune Globulin (AIG) can be used to neutralize anthrax toxin.


Anthrax: Post-Exposure Prophylaxis 

Start 60 days of oral antibiotics ASAP after exposure

  • Ciprofloxacin or Levofloxacin


  • Doxycycline


  • Amoxicillin or Penicillin (if known PCN sensitive)

Vaccine: Can be given post-exposure in conjunction with antibiotics



  • Variola virus, two forms of the disease:  minor and major
  • Spread via respiratory droplets or aerosols expelled from the oropharynx
  • May also spread via direct contact
  • Patients are most contagious during the time at which the skin rash is present
  • Approx. 30% of patients exposed go on to develop the disease
  • Approx. 30% mortality with ordinary smallpox


smallpox characteristics

  • Febrile Syndrome – occurring 1-4 days prior to rash.
  • Classic Smallpox lesion – deep-seated, firm/hard, round, well-circumscribed; lesion may become umbilicated or confluent.
    • Can be mistaken chicken-pox
  • Febrile Syndrome – occurring 1-4 days prior to rash.
  • Lesion in Same Stage of Development – Evolve from macules → papules → pustules at the same time.
  • Centrifugal distribution – First lesion on oral mucosa, face, or forearms.
  • lesions on palms and soles 

A image thumb

smallpox vs. Chickenpox distribution


Spares the trunk: Smallpox

Primarily the trunk: chickenpox

A image thumb

clinical timeline for smallopox

  • exposure
  • incubation period: 12 days (range 7-19 days)NOT Infectious
  • Prodrome phase (2 - 4 days): Abrupt onset of fever >38.3°C, Malaise/myalgia, Headache, Nausea/vomiting, Backache,
    Usually NOT Infectious
  • Early Rash Phase: Mucous membrane lesions.  Small red spots on the tongue and throat.  Lesions enlarge, ulcerate, then shed virus.  Infectious 24 hours before visible skin rash
  • Rash Phase: (21 days) macules, papules, vesicles, pustules, scabs, Infectious until all scabs fall off


Smallpox:  Medical Management

  • Strict respiratory/contact isolation of patient
    • Patient infectious until all scabs have separated
  • Treatment is supportive care only
  • Antivirals are under evaluation
    • Cidofovir
    • ST246


Smallpox: Prevention and Control

  • Immediate vaccination of ALL close contacts (< 6 ft) and ALL contacts of patients contacts (Ring vaccination)
  • Vaccination within 4 days of exposure may prevent or lessen disease
  • Mass vaccination may be necessary and/or everyone may want to be vaccinated


Smallpox current vaccine

  • Live vaccinia virus
  • Because it is a live virus, there can be adverse events from vaccination
    • Occurs mostly in immunologically suppressed persons
  • Immunity is not life-long, but having been vaccinated in the past may reduce morbidity and mortality


Plague and types

  • Plague is a severe bacterial disease of humans and animals produced by the gram negative nonsporulating bacillus Yersinia pestis
  • Bite of a rodent flea that is carrying the plague bacterium, or by handling an infected animal
  • Hundreds of millions of people died
  • when human dwellings were inhabited
  • by flea-infested rats
  • Modern antibiotics are effective, but without prompt treatment the disease can likely cause illness or death


  • Bubonic
  • Septicemic
  • Pneumonic






plague epidemiology and natural transmission

Routes of Plague Transmission

Animal Resovior

A = Bite of Flea
B = Contact with animal or carcass
C = Inhalation of respiratory droplets
D = Contact with sputum or fluid



Clinical Presentation of Pneumonic Plague


*IncubationPeriod: 1-6 days

*Early Presentation: Abrupt onset of fever, malaise, headache, myalgia, Chest pain and dyspnea, Tachypnea (particularly in young children), Productive cough (sputum may be purulent or watery, frothy, blood-tinged), Hemoptysis

*Antibiotic therapy in the first 24 hours can prevent septicemia, cardio-respiratory failure, shock, and death

*Late Presentation

  • Rapid progression to pulmonary disease/ARDS
  • Pulmonary edema, dyspnea, cyanosis
  • Meningitis may be a complication
  • Hypotension, DIC, septicemia, and death
  • Lab findings -- bacterial infection and sepsis
  • Organism usually seen on sputum gram stain
  • Mortality approaches 100% if untreated in 24 hours


Plague:  Patient Care 

Early antibiotic treatment* is paramount to patient survival


  • Streptomycin 1 gm IM b.i.d. for 10 days (DRUG OF CHOICE);
  •   Chloramphenicol 25 mg/kg IM or IV 4 times daily for 10 days
  •   Gentamicin 5 mg/kg IM or IV once daily for 10 days;   
  • Doxycycline 100 mg IV b.i.d. or 200 mg IV once daily for 10 days; 
  •   Ciprofloxacin 400 mg IV b.i.d. for 10 days;


  • Streptomycin 15 mg/kg IM twice daily for 10 days (max 2  gm/day);
  • Chloramphenicol 25 mg/kg IV 4 times daily for 10 days (max 4 gm/day)
  • Gentamicin 2.5 mg/kg IM or IV 3 times daily for 10 days;
  • Doxycycline 2.2 mg/kg IV twice daily for 10 days (max dose 200mg/day);
  • Ciprofloxacin 15 mg/kg IV twice daily for 10 days (max 1 gm/day)

*CDC recommends initiating treatment with two drugs believed effective against Y. pestis until antimicrobial susceptibility data is available on isolates. 


Plague:  Prophylaxis

  • Pneumonic plague contacts (transmitted via droplets)
    • Oral Doxycycline or Ciprofloxacin
    • For 7 days after last exposure
  • Vaccine no longer manufactured





Caused by toxin from Clostridium botulinum

  • Colorless, odorless and tasteless
  • Lethal dose for 70kg human is 1ng/kg
    • Botulinum toxin is the most lethal neurotoxin known to man
    • Dispersal of aerosolized toxin, 1 gm of aerosolized toxin could kill up to 1.5 million people


botulism epidemiology and natural transmission

  • C. botulinum in the soil, flora and fauna (in honey and botox)
  • Toxin production in foods prepared or stored at ambient temperature
  • Colonization and toxin production in an open wound
  • Intestinal colonization and toxin production in susceptible infants and adults
  • Botulism:Acute, symmetric, descending flaccid paralysis with bulbar palsies


clinical presentation of botulism


Incubation Period

  • Inhalational: 24-72 hours
  • Foodborne: 18-36 hours (range 2 hours to 8 days)  Dependent on toxin dose

Cranial Nerve Palsies: Cranial Nerves III, IV, VI, VII, IX

  • Blurry vision
  • Diplopia
  • Ptosis
  • Expressionless Facies
  • Regurgitation
  • Dysarthria/Dysphagia

Descending Flaccid Paralysis: Symmetric Paralysis
Voluntary Muscles

1. Neck
2. Shoulders
3. Upper extremities
4. Lower extremities

*BP often normal; Mental status normal


Botulism: Medical Management

  • Early administration of antitoxin: within 24 hours, 1 vial per person, acts by binding to free toxins in the system
  • Supportive care
    • Monitoring respiratory function
    • Providing mechanical ventilation
    • May be needed for weeks or months





Viral Hemorrhagic Fevers (VHF)

Hemorrhagic fever viruses (RNA) belong to four taxonomic families:

  • Filoviridae (Ebola/Marburg)
  • Arenaviridae (Bolivian HF))
  • Bunyaviridae (Congo-Crimean HF)
  • Flaviviridae (Dengue)

Natural vectors – virus dependent

  • Rodents, mosquitoes, ticks

No natural occurrences in U.S.


VHF as a Biological Weapon

These viruses are considered suitable weapons because:

  • they have a low infectious dose
  • they cause high morbidity and mortality
  • they cause fear and panic in the general public
  • effective vaccines are either not available, or supplies are limited


Clinical timeline for VHF


incubation period:

  • 2-21 days (depending on the virus)

Early Manifestations 

  • High fever
  • Headache
  • Myalgia
  • Arthralgia
  • Anorexia
  • Varying degrees of  nausea, vomiting and   diarrhea

Later Manifestations

  • External and internal hemmorage
    • Ecchymosis
    • Petechiae
    • Bleeding from puncture site
    • Bleeding from nose and gums
    • Hemorrhagic conjunctivitis
    • Gastrointestinal bleeding
    • Severe vaginal bleeding
    • Pleural effusion
    • Renal Failure
    • Shock 
  • Laboratory Findings
    • Leukopenia or leukocytosis
    • Thrombocytopenia
    • Elevated Liver Function Tests
    • Anemia or Hemoconcentration
    • Prolonged PT, PTT 


VHF Clinical Management

  • Aggressive supportive care with intravenous fluids, colloids, blood products as needed
  • Specific therapy (ribavirin) may be helpful in bunyaviruses and arenaviruses
  • Avoid IM injections or invasive procedures (due to bleeding)
  • Strict aerosol precautions (i.e. respiratory isolation)