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Typhoid Mary: History for Today

Chances are that if you lived in the United States in early 1930’s you were concerned about numerous diseases that don’t have today’s media headlines. Typhoid Fever is one of those diseases which garnered much attention during that time in United Sates history, but today receives little or no attention. Although it lacks the marquee value of other diseases such as MRSA, smallpox, and anthrax, there are many lessons to be applied from the impact of Typhoid. One such lesson is that taught by Mary Mallon…better known as Typhoid Mary.

Mary Mallon (September 23, 1869 – November 11, 1938) has the dubious honor of being the first person in history to be a carrier of typhoid fever. Between 1901 and 1907 Mary Mallon held several positions with institutions and in private homes as cook. Many of the jobs were held here in New York State. During here working time she is alleged to have infected 22 people with typhoid fever and accused of the resulting single death. Typhoid illness and deaths spiked in her presence as she moved from city to city. The incidence of disease and deaths seemed to follow her from Mamaronek, NY to Manhattan to Long Island. It seems that within two weeks of Mary Mallon’s arrival, outbreaks of typhoid occurred.

Defending her innocence to the accusations of being a carrier of typhoid, Mallon refused to submit stool and urine samples in 1904, and in 1906 the possibility of a human carrier of typhoid was published in the June issue of the Journal of the American Medical Association. Later Mallon, now know by the popular Typhoid Mary name was taken into custody and held for three years. Her involuntary isolation came at her protests that the law was against her and claims of harassment because she was an Iris immigrant. She was eventually released on condition that not work with food, but took job as a hospital cook under an assumed name and infected twenty-five other people with typhoid. Two of those infected died. After this latest outbreak of typhoid, Mary “Brown” was discovered to actually be “Typhoid” Mary Mallon. She was arrested and re-admitted (involuntarily) for life-long isolation.

At the age of 69, on November 11, 1938, “Typhoid” Mary Mallon died of pneumonia. On postmortem exam, live typhoid bacteria was found in her gallbladder. Despite her overwhelming denial of her role in the typhoid cases and deaths, she in fact, produced the situations resulting in numerous cases and deaths from typhoid.

What relevance can we bring to today’s bio-security awareness society from Typhoid Mary? There are several historical points that should be considered. First, Mary’s situation was almost certainly unintentional. That is, Mary Mallon did not intend to harm anyone or spread disease. Would a change in the intent change the outcome or the circumstances of the situation? I think so. We have become accustomed to the “suicide bomber” scenarios played on the evening news. Consider the possibility of a “Biological Bomber”…a person who intentionally infects himself/herself with a disease in order to spread the disease and effect a bioterrorist event. Can you imagine the impact of one person infected with some disease walking into a hospital and contacting immunological suppressed patients, visitors, and health care workers?

And what if Mary was alive today and incarcerated on the suspicion of being a health carrier of a deadly disease; what would be said about her civil rights? Would public health authorities have the ability today to impose isolation? Think back to the media circus surrounding Mr. Speaker, the international traveler with extremely drug resistant tuberculosis. Can you imagine what would have happened had a fellow traveler contracted TB? Further, what will the effects be on society during an actual public health emergency? During a public health crisis I’m not convinced that the imposition of isolation or quarantine measures will be effective. During the Sever Acute Respiratory Syndrome (SARS) outbreak of 2003, the city of Toronto found that a majority of citizens voluntarily complied with social distancing. These high levels of compliance may be contributed to community education efforts and use of the modern media. With the SARS situation in mind, I am still skeptical that a similar outcome would be possible in the United States despite the Constitutional and legal ability to do so.

The Public Health Services Act (1944) provides for quarantine authority of the Federal government and authorizes “…apprehension, detention, and conditional release of individuals to prevent spread of communicable disease” This statute applies to persons infected with a communicable disease in a qualifying stage Title 42 U.S.C. Section 264 (Section 361 of the Public Health Service Act) gives the Secretary of Health and Human Services responsibility for preventing the introduction, transmission, and spread of communicable diseases from foreign countries into the U.S. and within the U.S. and its territories/possessions, and CDC has the authority to “detain, medically examine, or conditionally release individuals suspected of carrying a communicable disease” under regulations found at 42 C.F.R. Parts 70 and 71. Violation of a quarantine and isolation order is a federal criminal misdemeanor.

On April 4, 2003, at the request of the CDC, President Bush signed Executive Order 13295, adding SARS to the list of communicable diseases for which federal isolation and quarantine is authorized. And earlier in 2007, President Bush signed Homeland Security Presidential Directive 51 authorizing the Office of the President to declare and define “threats to continuity of government”.

The fact remains that during a public health crisis resources would be few and one has to wonder if quarantine would be possible at all.

Preparing for Biological Terrorism: An Emergency Service Planning Guide. George Buck, Ph.D ISBN 1-4018-1094-2
Critical Care Study Guide. Criner/D’Alonzo ISBN 0-387-95164-4
Emergency Management: Principles and Practice for Local Government. ICMA ISBN 0-87326-082-1. Century History. “Typhoid Mary” accessed Nov. 30, 2007
Typhoid Mary: Villain or Victim? Judith Walzer Leavitt accessed Dec. 2, 2007
The Most Dangerous Woman in America. NOVA accessed Dec. 01, 2007
Women’s Health, Prevention works for women. Centers for Disease Control and Prevention accessed Dec. 1, 2007


Emerging Diseases and the Hygiene Hypothesis

The media has been full of stories warning the public of a new “super bug” that is threatening the health of our communities. Despite the advances in cleaning products, antimicrobial agent soaps, and an emphasis public health, these infectious diseases continue to thrive and seek out new targets for disease. In the late 1990’s West Nile Virus gained concern as the never before pathogen, spread by mosquito bite and carried by wild birds, began showing up in wild birds across the United States. Our awareness to biological agents was thrust to the forefront of our culture as a result of the anthrax attacks following 9/11. Avian flu, or H5N1, has had our attention on and off for the last few years as the hotly debated question of mutation and the possibility of pandemic is discussed. Several incidents of illness and death have been cited due to pathologic Escherichia coli (E. coli) O157:H7, and most recently, the so-called super bug Methicillin Resistant Staphylococcus aureus or MRSA.

Methicillin Resistant Staphylococcus aureus or MRSA, along with its counterpart ORSA (Oxacillin Resistant Staphylococcus aureus) have been nosocomial, or hospital acquired infections of concern for quite some time infecting the patient who has undergone an invasive procedure or the long term care patient with a compromised immune system. Hospital and other health care workers can become infected with ORSA/MRSA as a result of the performance of their duties. Health care providers may become infected with ORSA/MRSA by 1) contact with colonized or infected patients, 2) colonized or infected sites of the personnel (clothing or unprotected areas) and, 3) exposure to contaminated surfaces or items such as medical devices, or environmental surfaces. The good news is that practicing standard body substance isolation and good personal hygiene (hand washing) can prevent many of these exposures.

The question remains, however, as to why these diseases continue to flourish in a society rich with countermeasures such as anti-microbial soaps and cleaners. Why do they continue to evolve to resist traditional treatment and migrate to infect otherwise healthy people in the community?

Certain theories propose that cleaner is not always better. One such theory is the Hygiene Hypothesis which began circulation as a theory on the relationship between exposure to viruses and bacteria and the development of a healthy immune system around 1989. The Hygiene Hypothesis proposes that exposure to environments that are less than germ-free as an infant or toddler builds a stronger immune system and reduces the risk of developing disease later in life.
How can this be possible? It seems counterintuitive to claim that a more microbe-free environment is not automatically equated to better health. We can, in fact, look to a simple analogy of the immune system for a better perspective. Let’s compare the immune system to voluntary muscle for a moment. When voluntary muscle is stressed, as in the case of exercise, the muscle becomes stronger; the hygiene hypothesis is merely suggesting the same principle applies to the immune system. The exposure a young, developing immune system to repeated small doses of various virus and bacteria endemic to a given environment can be considered as exercise for the immune system. “That which does not kill us makes us stronger” may be a better name for the hypothesis.

Although debated, several findings suggest that early infection with certain bacteria have reduced the severity of later immune response to allergens in mice.
The Hygiene Hypothesis has been implicated as a factor in the rise of asthma and some community acquired immunologic diseases. Research suggests that our society’s overuse of anti-microbial/anti-biotic materials, such as cleaners and soaps, has caused people to be exposed to fewer diseases during immune system development. Scientists point out that asthma and other diseases linked to the immune system have been on the rise for the last 30-40 years despite exposure to fewer infectious organisms. The thought is that these organisms are a key component in training and creating a healthy immune system. Without early exposure, the developing immune system fails to respond at an appropriate level and may actually overreact to irritants that would otherwise be inconsequential. The result is an increased overreaction of the immune system equating to conditions such as asthma. Other research has indicated that children who are exposed to high levels of the bacterial compound, endotoxin, found in house dust may actually be less likely to develop eczema during their first year of life3. Finding such as this support the hygiene hypothesis by indicating that early exposure to infectious or inflammatory agents cause changes in the immune systems and reducing the risk of developing allergy-related conditions later in life.

The hygiene hypothesis remains unproven but continues to be tested by a variety of researchers. I think my analogy comparing the immune system to the voluntary muscular system make a lot of sense. For an immune system to work property it must be trained and experienced, but if training and experience is lacking, the immune system defaults to “going to war” when all that may be needed is to fire a single shot. Our approach to develop items such as anti-bacterial soaps is not entirely bad…I think the marketing and media hold much of the responsibility for this situation.

1.Bacterial Infections Alter Allergic Response; Findings Support Hygiene Hypothesis. Science Daily/national Jewish Medical and Research Center accessed 10 October 2007 accessed 10 October 07
2.Bacterial toxin may protect infants from asthma. National Institutes of Health; Medical News Today accessed 10 October 07
3.Infants who have fevers become children with fewer allergies. National Institute of Allergy and Infectious Diseases; Medical News Today accessed 12 October 07
4.S.B. Levy: Antibacterial Household Products: Cause for Concern. Emerging Infectious Diseases vol. 7, No. 3 Supplement, June 2001 accessed via PDF 12 October 07
5.Erwin W. Gelfand, MD. The Hygiene Hypothesis Revisited: Pros and Cons from Selected Coverage of the 60th Anniversary Meeting of the American Academy of Allergy, Asthma and Immunology accessed 13 October 07 via Medscape
6.Study dishes the dirt on hygiene’s role in disease. CBC News 2006/16/rats-hygiene.html accessed 12 October 07
7.The hygiene hypothesis: Are cleaner lifestyles causing more allergies for kids? Science Daily accessed 12 October 07
8.Edward Willett: The hygiene hypothesis. Online weblog accessed 12 October 07
9.MRSA in Healthcare Settings, Centers for Disease Control and Prevention accessed 15 October 07
10.Information About MRSA for Healthcare Personnel, Centers for Disease Control and Prevention accessed 15 October 07


E. coli:A Cause of Renal Failure and Disseminated Intravascular Coagulation

Rick Russotti, CI/C, EMTP September 2007

Another outbreak of pathologic Escherichia coli (E. coli) O157:H7 has emerged in the United States as a result of contaminated hamburger meat. Contaminated meat and meat products are the major cause of food-borne E. coli infection. Other routes of infection include contaminated water, non-pasteurized milk and juice, and some raw lettuce/vegetables. Although food- and water-borne vectors may account for many E. coli infections, transmission of the bacteria can occur by person-to-person contact.

E. coli O157:H7 was discovered in the human colon in 1885 by German bacteriologist Dr. Theodor Escherich and identified as a disease causing agent, or pathogen, as a result of an outbreak of gastrointestinal illness in 1982. E. coli is a bacterium that lives in the intestine of healthy cattle and has been found in the intestines of healthy chickens, deer, sheep, and pigs. Because these animals lack the specific protein receptors for the disease, they do not get sick but are reservoirs for the bacteria. The O157:H7 indicates the subspecies of the E. coli bacteria; the O157 designates the specific carbohydrate and the H7 identifies the flagella protein. Although hundreds of variations of E. coli exist, the O157:H7 strain is different and belongs to a class of pathologic E. coli known as enterohemorrhagic Escherichia coli or EHEC. This strain of E. coli has the ability to produce a toxin; Verocytoxin E. coli (VTEC) or Shiga-like toxin (STEC). These toxins are known to cause severe complications from E. coli infection.

As previously noted, infection with E. coli can occur from eating undercooked contaminated meat, ingesting contaminated water or un-pasteurized beverages, contact with contaminated surfaces, or person to person contact. Contaminated meat looks and smells perfectly normal and the number of microbes needed to cause infection is very small. Transmission of the disease can occur from eating produce exposed to contaminated run-off or irrigation. Contamination of irrigation and soil can occur from infected manure being spread as fertilizer. As the bacteria can penetrate plant material; crops, even those not normally considered as a reservoir for E. coli, can harbor the bacteria and cause infection. Person-to-person contact among family members, close contact work environment, and child care centers can be difficult to manage. Bacteria found in the loose stool of a person infected with E. coli can be passed via the fecal/oral route if hygiene is lacking. Hand washing is of particular importance in the prevention of contamination and infection from the fecal/oral route.

Signs and symptoms of E. coli range from mild to severe and most often include brutal bloody diarrhea and abdominal cramps, with or without fever. Symptoms often resolve within ten-days and require little medical treatment. Oral and intravenous fluid replacement can be helpful, but antidiarrheal agents and antibiotics should be avoided. According to the Centers for Disease Control, antibiotics may actually precipitate renal complications. Deaths from E. coli occur annually in the United States and are caused by complications of the toxins (VTEC/STEC). These toxins are responsible for a condition known as Hemolytic Uremic Syndrome or HUS with approximately 2% to 7% of E. coli infections progressing with this complication. Hemolytic Uremic Syndrome (HUS) causes several life-threatening conditions including Acute Renal Failure (ARF) and Disseminated Intravascular Coagulation (DIC). Acute Renal Failure and Disseminated Intravascular Coagulation impact long-term health and recovery of E. coli patients. HUS causes 61 deaths annually (about 2-7% of E. coli patients) and another 8% go on to suffer complications of ARF such as high blood pressure, seizure, blindness and paralysis. ARF is diagnosed on the basis of increased blood urea nitrogen (BUN) and can be further classified as oliguric (urine output<400ml/24h)>
The development of DIC is more ominous. DIC is a condition of blood coagulation throughout the entire body. E. coli, sepsis, and viral hemorrhagic fevers are infectious causes of DIC. Other medical causes include amniotic emboli, eclampsia and Abrutio Plancentae; with burn trauma and profound decompensated shock states as traumatic causes. DIC can also be caused by some species of venomous snakes. Complications of renal failure and DIC are most often associated with patients in extremes of age; particularly children under five-years of age and the elderly. Increased potential of renal failure and DIC in the patient with a compromised immune system is not clear. Treatment for these conditions in the pre-hospital setting is to support the ABC’s and initiate intravenous fluid replacement per local protocol and medical direction.
There are a number of steps that can be taken to prevent E. coli infection. Since cattle intestine is the major source of the bacteria, strict adherence to regulations for the slaughter and processing of meat may decrease the contamination of meat products. Manure is another source of E. coli O157:H7 and can contaminate the environment, including ground and irrigation water. Containment and prevention of infection at the source, during processing and packaging, is key to abatement of outbreaks. There are numerous actions that can be taken to prevent infection and spread of E. coli; cooking all meat products thoroughly, proper storage of meat products, washing fruits and vegetables, consuming pasteurized milk, ciders, and juices, and by avoiding swallowing of pool water or lake water while swimming. For those engaged in patient care in the pre-hospital setting the most important preventative strategy is the easiest to employ: simple hand washing with soap and water and good hygiene practice coupled with body substance isolation and infection control practices. Each agency is required to have and implement an infection control plan. These plans are required to address agency-specific policy regarding body substance isolation and exposure incidents, reporting requirements, post exposure prophylaxis and treatment. The foundation of any infection control program and plan is based on training, management/employee buy-in, and prevention.
Situational awareness and education are the best defense against the spread of diseases like E. coli. Pre hospital care providers at all levels must arm themselves with the information needed to make good clinical decisions for their patients and good protective choices for themselves.

Recommended Reading:
Escherichia coli O157:H7; Wikipedia accessed 27 September 2007

E. coli O157:H7 - Escherichia coli O157:H7; accessed 16 September 2007

Escherichia coli O157:H7, General Information; CDC Bacterial, Mycotic Diseases accessed 16 September 2007

E. coli Questions and Answers; CDC

E. coli Outbreak from Fresh Spinach, October 12, 2006; CDC accessed 21 September 2007

For a copy of this and other articles, and the weekly All-Hazards podcast, visit Mitigation Journal website at


Influenza: The H’s and N’s

A tremendous amount of media attention has been placed on avian flu and pandemic situations. Hyped media attention and public confusion on the topic underscores the need for emergency responders to have the basic information and understanding of key concepts regarding types of influenza, terminology, and other details. Responders not armed with a basic understanding may lack the ability to gain situational awareness placing themselves, the public, and potentially their families at risk.

The term influenza is not synonymous with Avian Flu or pandemic. Influenza can be categorized in a variety of ways, but in general, influenza or flu is caused by a family of viruses known as Orthomyxoviridae and can be broken out into three types; type A, B, and C. There are numerous illnesses that can be responsible for the classic flu symptoms like body aches, chills and fever. Symptoms can range from mild to severe and include serious complications such as bacterial infections and pneumonia. Type A influenza crosses species and is the most hearty, or virulent, of the three strains. Highly Pathogenic Avian Influenza, or HPAI, is a type A flu virus. Type B flu virus targets only humans, is common and less severe than type A while type C, which impacts humans and swine, is rare and my have only mild symptoms or none at all.

Type A flu viruses receive much of our attention and is home to H5N1 or avian flu. The H’s and N’s represent designation of proteins of the virus and are important to the classification of Type A flu. Understanding the role of the H’s and N’s will also aid in understanding why vaccine development can be difficult. Designations such as H5N1 are used to further classify one type A virus from another. The “H” stands for hemagglutinin antigen (sometimes HA is used rather than just H). There are fifteen different hemagglutinin antigen (H/HA) proteins. The H proteins give the virus the ability to attach to the host cell. The “N” represents neuraminidase antigen (again, sometimes documented as NA rather than N). The neuraminidase protein allows the virus to be released from the cell and spread infection. There are nine neuraminidase antigen (N/NA) proteins. The numerous combinations of H’s and N’s allow the type A virus to infect such a large number of species. Remember, there are 15 different H proteins and 9 N proteins...that means there are 135 combinations of protein variations for type A influenza virus. Here’s the catch; a vaccine designed to work for one combination of proteins will not work for another and since type A (and B) influenza changes slightly from one flu season to another, creation of a vaccine for that particular season is tricky business. Keep in mind that the virus wants to survive and to do so will have to change; either slightly or drastically. A slight change in the virus is known as antigenic drift while drastic changes are called antigenic shifts. It is the antigenic shift that can cause a virus to change enough to cause severe disease or pandemic.

References: Pandemic Planning and Preparedness


CYANIDE: The Deadly Partner of Carbon Monoxide

Warnings have emerged on the presence and dangers of cyanide in smoke produced by the burning of ordinary combustible materials. At least two large-scale studies (Paris, France/Dallas, Tx.) have evaluated cyanide as a major contributor of inhalational injury (smoke inhalation) and death from exposure to the products of combustion. Hydrogen cyanide is found in smoke generated by products such as wool, silk, cotton and paper as well as combustion of synthetic materials (plastics/polymers). Generally speaking, any materials containing carbon and nitrogen can create cyanide as a by-product of incomplete combustion. Cyanide is a histo-toxin, a substance that destroys the ability of the cells to use oxygen, while carbon monoxide binds efficiently to the hemoglobin preventing oxygen uptake.

Study data from Paris, France and Dallas, Texas suggest that cyanide poisoning is a significant contributor to fire-related deaths. Cyanide may have a larger role than carbon monoxide (CO) in causing death and coexposure to carbon monoxide and cyanide was frequent. Monkeys exposed to low levels of cyanide were quickly incapacitated and unable to self-evacuate, suggesting that greater toxic exposure would follow. The Paris Fire Study on Cyanide concluded the cyanide and carbon monoxide were both important determinants of smoke inhalation morbidity and mortality. The Paris study also found that cyanide concentrations were directly related to the probability of death and may have predominated over carbon monoxide as cause of death in some fire victims. The Paris study suggests that cyanide and carbon monoxide may potentate the toxic effects of one another. The Dallas, Texas Fire study noted similar findings as well as noting elevated cyanide concentrations among smoke inhalation victims may be directly related to deaths.

Cyanide (CN) has a notorious history and can be found in numerous forms including hydrogen cyanide (HCN), thiocyanate (SCN-), sodium cyanide (NaCN) and potassium cyanide (KCN). Cyanide, a blood agent, has been used in chemical warfare, cult mass-suicide as well as domestic and international terrorist events. Cyanide abruptly stops the ability of the red blood cell to carry and distribute oxygen to the tissues by binding with the hemoglobin. Cyanide-toxic hemoglobin is not able to function either by distributing oxygen or removing the waste products of metabolism thereby creating a hypoxic state. Organs and body systems that are sensitive to decreased oxygen and hypoxic states are also most vulnerable to cyanide. The cardiovascular, pulmonary and central nervous systems have a low-threshold of tolerance for decreased oxygen levels and cyanide exposure may manifest signs and symptoms in these systems first. Signs and symptoms associated with cyanide poisoning include tachycardia, dypsnea, altered mental status and confusion. Continuous exposure to cyanide results in nausea, hypotension, seizure-like activity, cardiac collapse, non-cardiogenic pulmonary edema and coma. Differential diagnosis of carbon monoxide should be considered but is difficult due to the similarities in symptoms with cyanide exposure.

Treatment of cyanide exposure and poisoning begins with a high index of suspicion and situational awareness. Firefighters or civilian victims with significant exposure to smoke from a fire who exhibit symptoms should be evaluated and suspected of having been exposed to cyanide and carbon monoxide until proven otherwise. When signs or symptoms of exposure are present, exposure takes place without respiratory protection or in an enclosed space; differential diagnosis for cyanide and carbon monoxide poisoning must be undertaken. The basic treatment of cyanide exposure should support the ABC’s, ventilation/oxygen delivery, and cardiac function. Cyanide antidote kits should be considered if available and providers are trained in their use. Cyanide kits, also know as Lilly Kits, Taylor Kits or Pasadena Kits, contain Sodium Nitrite for injection, Sodium Thiosulfate and Amyl Nitrate inhalants. Sodium Nitrite reacts with the hemoglobin to form methemoglobin, in turn removing cyanide ions from tissues producing cyanmethemoglobin; with a low level of toxicity. Thiosulfate converts cyanide into thiocyanate (rhodanese reaction) and is excreted in the urine. The FDA recently approved a new medication for the treatment of cyanide poisoning. Hydroxocobalamin is the main medication in the Cyanokit. In the presence of cyanide, hydroxocobalamin takes up the cyanide and transforms into cyanocobalamin, a form of vitamin B12, to be excreted in the urine.

Cyanide and carbon monoxide work in a similar fashion; they both take up the space on the red blood cell normally occupied by oxygen resulting in a lack of oxygen to the tissues. The result is not much different from that of a patient with shortness of breath from a medical cause. If you can remember that simple principle you can remember the signs, symptoms and basic treatment. A patient with low levels of oxygen (from any cause) is hypoxic and should receive oxygen via mask. If the hypoxia becomes severe to the point of respiratory failure; ventilate the patient with high flow oxygen. The same simple advice will help you remember how the cyanide kits work. Forget about memorizing the big words and chemical cascades. Remember that each medication in the kits reacts with cyanide to change it into something else. That something else, thiosyanate in the case of Sodium Thiosulfate administration or vitamin B12 in the case of hydroxocobalamin administration, is a material that can be excreted by the body in some way. We want to stop the cyanide from doing damage and then get rid of it…usually in the urine. Think of it like a house fire; you stop the fire from doing damage (extinguishment), change the heat into steam and then you get rid of the steam and left over smoke (ventilation).

The firefighter and EMS professional must recognize that cyanide exists in smoke and fire victims (civilian or others) must be evaluated for cyanide toxicity along with carbon monoxide exposure especially if the exposure has taken place in a confined environment. Since there is no process for measuring cyanide levels in the body without blood samples, EMS professionals must remain aware of the signs and symptoms of both cyanide and CO exposure. Fire service and EMS managers should consider purchasing new technology capable of non-invasive measuring of CO and methemoglobin. Firefighters and EMS professionals must be aware that exposure to potentially lethal cyanide at “routine” fires is more frequent than we have previously recognized. Exposure to cyanide may be difficult (if not impossible) to differentiate from carbon monoxide poisoning and, although cyanide may actually play a larger role in death, the combination of carbon monoxide and cyanide has severe consequences.

Key terms and abbreviations:
AC: Hydrogen Cyanide (HCN) or Zyclon B
CK: Cyanogen Chloride (CHCL)
CN: Cyanide
Thiosulfate (S2O3-2)
Thiosyanate (SCN-)
Cyanogenic = Cyanide forming

Details of Care: Follow Local Protocol for the treatment of cyanide patients!

1. Oxygenation and ventilatory support are at the cornerstone of treatment. Including delivery of 100% oxygen and control of the airway as needed.
2.Supplemental oxygen can make a difference even in the cyanide patient
3. Establish an IV line…be alert for pulmonary edema
4. Place patient on cardiac Monitor with pacer/defibrillator available.
5. Cyanide Kit/Cyanokit administration
6. Be ready for seizures and difficult airway

Notorious Cyanide Events:
WWI: French use Cyanide during open-field campaign
WWII: Nazis use Zyclon B in death camps
Chicago, 1982: Seven people died after taking cyanide-tainted Tylenol.
Washington State, 1991: Three people developed acute cyanide poisoning after having taken over-the-counter Sudafed capsules tainted with cyanide. Two died.
NYC 1993: Cyanide suspected in first WTC attack (incinerated by explosion)
Tokyo 1995: Cyanide used as secondary agent in subway attack