Infectious Diseases: Annual, Recurrent and Emerging

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Objectives

  • Describe the difference between an infectious disease and a communicable disease.
  • Describe the pathophysiology of influenza, pertussis and cholera.
  • Explain the body substance isolation procedures that should be employed when treating the patient with influenza, pertussis and cholera.
  • List the signs and symptoms of influenza, pertussis and cholera.
  • Discuss the management of the patient with suspected influenza, pertussis and cholera.

   An infectious disease is an illness resulting from the presence of a pathogenic biological organism in a host organism. Examples of pathogenic organisms include bacteria, viruses, fungi, protozoa, parasites and prions, all of which are able to cause illness and death in their host. A prion is an infectious agent composed of proteins normally found in the brain. Unlike the other pathogenic organisms, prions do not contain any genetic material. Prions are the cause of a number of diseases in mammals, including bovine spongiform encephalopathy (also known as "mad cow disease") in cattle and Creutzfeldt-Jakob disease (CJD) in humans.

   While they are often used synonymously, the terms infectious disease and communicable disease do not have the same meaning. A communicable disease is an infectious disease that is easily spread from one human to another. As such, all communicable diseases are infectious diseases, but not all infectious diseases are communicable.

   As EMTs and paramedics, we learn about many infectious and communicable diseases, some of which we see on a regular basis, like influenza, the common cold, croup or sexually transmitted diseases. Other infectious diseases, like epiglottitis, are more obscure. This article discusses influenza, an infectious disease that occurs yearly and affects many persons in the community; pertussis, a disease that until fairly recently has been encountered infrequently, but is presently enjoying a bit of a resurgence in the United States; and discuss cholera, an infectious disease that is not a problem in the United States, but current conditions in other parts of the world and ease of travel make it increasingly likely that emergency care personnel may encounter it in the field here at home.

Influenza

   Influenza, commonly referred to as "the flu," is an acute, contagious respiratory illness caused by infection with one of the many influenza viruses. Symptoms can range from mild illness with fatigue to respiratory failure and death. Three types of influenza are recognized:

  • Type A is associated with most epidemics and pandemics and most of the deaths from influenza.
  • Type B evolves slower than Type A, and results in regional or widespread epidemics every 2 to 3 years.
  • Type C is rare and associated with sporadic cases.

   Identifying the type is the first step in naming the influenza virus, followed by the subtype, which is named after the class of surface protein located on the viral surface. The two broad classes of surface proteins are hemagglutinin (HA) and neuraminidase (NA). There are 16 HA subtypes (designated H1-H16) and 9 NA subtypes (designated N1-N9). All of the possible combinations of influenza A subtypes infect birds, but only those containing the H1, H2, H3 and N1 and N2 do so to any great extent. The H5 subtype is considered a candidate for a new sub-type for broad human infectivity, and, as a result, we may be hearing about it in upcoming influenza seasons.

   Persons of all age groups are at risk of contracting the influenza virus, although rates of infection are highest among children. Risks for complications, hospitalization and death from influenza are higher among persons aged 65 years and older, young children, and persons of any age with medical conditions that place them at increased risk for complications.1

   There are a number of reasons why flu seasons are unpredictable. Influenza viruses are constantly evolving and vary from season to season, making it common for new flu strains to appear each year. In the U.S., flu activity typically peaks in January or February, although activity can continue as late as May. Although the flu season occurs every year, the timing, severity and length of the outbreak depend on many factors, including what influenza viruses are spreading and whether they match the viruses in the flu vaccine for that year. If the spreading viruses and flu vaccine are closely matched, it can be anticipated that vaccine effectiveness will be higher; if they are not closely matched, vaccine effectiveness may be lower. The CDC reports that the vaccine for the 2010-2011 flu season will protect against three different flu viruses: H3N2, influenza B and the H1N1 virus that caused so much illness last season.2

   The last flu season is most likely still on the minds of healthcare providers, when the 2009 H1N1 influenza virus ("swine flu") created the first influenza pandemic (global outbreak of disease) in more than 40 years. This is a variant of the flu strain that was responsible for the Spanish flu pandemic that killed some 50-100 million people worldwide in 1918 and 1919. While not certain, it is likely that the 2009 H1N1 virus will continue to spread along with seasonal viruses in the United States during the 2010-2011 flu season.2

Pathophysiology of Influenza

   Once inoculation of the upper respiratory tract occurs, an incubation period of 1-4 days ensues. The virus invades upper airway epithelial cells, and, once sequestered within the host cell, takes over the cell's DNA-replicating machinery, replicates viral RNA, and produces a new virus that bursts from the cell, destroying it. The virus then goes on to infect other cells and reproduce in the same manner. Local and systemic effects result from the release of inflammatory mediators and include swelling, cough and fever. If the infection spreads further down the respiratory tree, abnormal lung sounds such as rhonchi or wheezing may be auscultated. The most common cause of death from influenza is not the influenza virus itself, but additional "superinfection" by bacterial pneumonia.

History and Clinical Exam Findings

   A patient with the flu will typically describe a rather acute onset of symptoms, including sore throat (a common reason why patients seek medical attention), mild to severe myalgia (muscle pain), fever that can range from low-grade to high, and frontal/retro-orbital headache that can range from mild to severe. Weakness and fatigue are common, and rhinorrhea may be described.

   The physical examination can reveal patients who clinically range in appearance from mildly to severely ill. Tachycardia may be present secondary to fever or hypoxia, and tachypnea may be present. If present, fever may range from low to high, and skin signs can range from normal to warm to hot, depending on temperature. If the infection has spread to the lower airways, lung sounds such as rhonchi or wheezing may be auscultated.

Prehospital Management of the Patient with Suspected Influenza

   As with all infectious diseases, the first line of management is preventing the spread of infection to the healthcare provider. The CDC recommends that all high-risk groups, which include healthcare personnel, receive the influenza vaccination. PPE used by the healthcare provider should include gloves and a surgical mask. Place a surgical or some other mask over the patient's mouth and nose to prevent the release of aerosolized droplets when they cough, sneeze or talk. The best way for healthcare providers to prevent the spread of infection is by washing hands thoroughly after contact with a patient suspected of having influenza. Additionally, clean all stretcher linen and ambulance surfaces after completion of the call with appropriate cleaning solutions like EPA-registered disinfectants or a bleach solution of 1 tablespoon of bleach in 1 quart (4 cups) of water. For a larger supply of disinfectant, add ¼ cup of bleach to 1 gallon (16 cups) of water.

   Treatment of the patient with influenza is mostly supportive. There is no treatment for the influenza virus itself, which must be allowed to run its course. Treatment includes ensuring proper ventilation and oxygenation and correcting any fluid volume deficits. If SpO2 is below 95%, oxygen should be administered via the appropriate delivery device. If breathing is inadequate, bag-mask ventilations should be provided. If the patient shows signs of dehydration, a distinct possibility in the setting of fever and limited fluid intake common to patients with influenza, initiate IV access and administer an isotonic crystalloid bolus of 20 cc/kg, or as local protocol requires.

Pertussis

   Pertussis, also known as whooping cough, is a respiratory tract illness caused by the bacterium Bordetella pertussis. First identified in the 16th century, when an epidemic swept through Paris, it was a significant cause of infant and child morbidity and mortality until introduction of the pertussis vaccine, which was combined with the diphtheria and tetanus toxoids (known as the Tdap vaccine) and made widely available in the United States in the 1940s. Pertussis literally means "violent cough," which is the hallmark of the disease.

   Since the 1980s, there has been an increase in the number of cases of pertussis, especially among teens (10-19 years of age) and babies younger than 6 months. In 2009, there were nearly 17,000 reported cases in the U.S., including 14 deaths.3 Pertussis incidence increases cyclically, with peaks every 2-5 years.4

   More recently, the news media have reported on outbreaks of pertussis across the United States. On June 23, 2010, California declared a pertussis epidemic. As of December 15, 2010, California had documented 7,824 cases of confirmed (62%), probable (19%) or suspected (19%) cases of pertussis since the previous January 1. Of those, there were 10 deaths, with nine of the fatalities in infants younger than 2 months who had not received a dose of pertussis vaccine.5 Vaccination is the best defense against whooping cough; however, immunity from vaccines wears off over time, and pertussis booster vaccine rates in adolescents and adults are low. As a result, pertussis continues to circulate widely in California, and especially affects infants who are too young for the shots.6

   This potential for disease is not unique to California, and outbreaks have occurred in other areas of the country as well. On August 5, 2010, the Pennsylvania Department of Public Health issued an alert to physicians noting unusually high rates of pertussis among 8- to 12-year-olds in the Philadelphia suburbs. Outbreaks have also been reported in Upstate New York, South Carolina and Michigan.

Pathophysiology of Pertussis

   Humans are nature's sole reservoir for B. pertussis, which is spread via airborne transmission of aerosolized droplets. Infants are typically infected by parents, other caregivers or siblings who are not aware that they have the disease. After inoculation, the organism adheres to ciliated respiratory epithelial cells, releasing toxins that act both locally and systemically. Local effects include inflammation of the respiratory mucosal lining and resultant congestion.

   The incubation period for pertussis is typically about 3-12 days, and the disease progresses in three phases: catarrhal, paroxysmal and convalescent.

   Phase 1, the initial phase, occurs after the incubation period and is characterized by common upper respiratory infection (URI) symptoms, including rhinorrhea, congestion, sneezing, tearing and low-grade (100.4°F-102.2°F) fever. This phase may last up to two weeks, and its end is usually heralded by the onset of a dry cough.

   Phase 2, the paroxysmal phase, begins as the dry cough increases in frequency and the low-grade fever subsides. Paroxysms (short, sudden bursts) of staccato-like coughing can occur up to 50 times per day and can be followed by a characteristic "whoop" resulting from the vigorous inhalation following the coughing fit. A great online resource that provides audio files with examples of the sounds associated with whooping cough can be found at http://health.utah.gov/epi/diseases/pertussis/pertussis_sounds.htm.

   Phase 3, the convalescent phase, is characterized by a residual persistent cough that can last for several months. This coughing does not indicate ongoing or recurrent infection with pertussis.

   Major complications associated with pertussis include development of severe pneumonia, central nervous system effects like seizures (secondary to hypoxia) and otitis media. In addition, complications resulting from frequent, forceful coughing, such as pneumothorax, pneumomediastinum and diaphragmatic rupture can occur.7

History and Clinical Exam Findings

   Patients with pertussis, or more likely their caregivers, will often describe a 1- to 2-week history of URI-like symptoms that progress to a dry cough, which will increase in frequency and evolve into the characteristic coughing paroxysms and resulting "whooping" sound. In addition, the caregiver may describe, or the clinician may observe, episodes of diaphoresis; cyanosis; excessive, thick respiratory secretions and salivation; lacrimation; and protrusion of the tongue during the coughing paroxysms. In addition, post-tussive emesis (forceful coughing followed by vomiting or apnea) may occur.7

   Inquire about the patient's immunization status, as children who are not immunized are at significantly higher risk for developing the disease.

Prehospital Management of the Patient with Suspected Pertussis

   All patients with suspected pertussis should be transported to an emergency department for evaluation, regardless of the perceived severity of the disease, as significant complications can develop quickly, especially in the very young. Patients with suspected pertussis and severe paroxysms will most likely be hospitalized, as will children under age 1 who are not immunized. Neonates with suspected pertussis will most likely be admitted to an intensive care unit, as apnea and significant cardiac complications can occur without warning.

   It is recommended that all prehospital care providers receive a Tdap booster vaccine and wear appropriate PPE to prevent transmission of the disease via aerosolized droplets. At a minimum, gloves, a surgical mask and eye protection should be used. Keep the patient as comfortable as possible and not agitated. If signs of hypoxia are present, administer oxygen via the most appropriate delivery method that results in as little patient agitation as possible, with a goal SpO2 greater than 95%. If the patient's breathing is inadequate, assist ventilation with a bag-valve mask to ensure adequate minute volume. Provide suctioning as necessary; it may be required after paroxysms. Intravenous fluid replacement can be provided to patients who present with dehydration. Administer 10-20 ml/kg boluses of isotonic crystalloid solution for patients with signs of hypovolemia.

Cholera

   Cholera is an acute intestinal illness that occurs secondary to infection with the bacterium Vibrio cholerae and is usually the result of ingesting food or water contaminated with the organism. The resulting diarrhea and subsequent profound water losses can kill within hours; up to 50% of infected individuals can die if left untreated. An estimated 3-5 million cholera cases occur worldwide every year, resulting in about 100,000-120,000 deaths.8

   With advances in hygiene, sanitation and water delivery, cholera has been almost nonexistent in industrialized nations since the turn of the 19th century and is not a threat in the United States; however, it is still common in other parts of the world, including sub-Saharan Africa and the Indian subcontinent. Natural disasters can create conditions favorable for an outbreak of cholera.

   For a cholera outbreak to occur, two conditions must be present: 1) There must be significantly insufficient hygiene, sanitation and water infrastructure used by a large population of persons, permitting large-scale contamination of and exposure to water containing Vibrio cholerae organisms, and 2) cholera (the disease) must be present in the population. The earthquake that struck Haiti on January 12, 2010, created the required damage to its water, sanitation and hygiene infrastructure. What is not as easily identifiable is how the Vibrio cholerae organism was reintroduced to Haiti.

   According to the Centers for Disease Control and Prevention (CDC), an outbreak of cholera was confirmed in Haiti on October 21, 2010.9 On November 26, the Haitian Ministère de la Sante Publique et de la Population (MSSP) and the Pan American Health Organization (PAHO) together reported cumulative figures to November 24, 2010. A total of 72,017 cases of cholera had been seen in Haiti, with a total of 1,648 deaths. The case fatality rate at that time was 2.3%.10

   On November 17, a woman living in Florida was diagnosed with cholera after traveling to Haiti to visit her family. New cases were expected to emerge in Florida, because the state has around 241,000 Haitian-born residents, many of whom travel to and from Haiti and have done so with increased frequency since last January's earthquake.11 In addition to persons returning to Haiti to visit family members, large numbers of non-Haitians are traveling to Haiti to lend assistance to the earthquake recovery efforts and risk bringing the disease back to their home locations when they return. As of December 18, 2010, the Florida Department of Health had confirmed five cases of cholera in the state. Four of the five patients were hospitalized, including two who had been evaluated in an emergency department, discharged the same day, and readmitted 2-3 days later.12 It is beneficial for responders to be familiar with the disease so it can be readily identified if encountered in the field.

Pathophysiology of Cholera

   The dose of V. cholerae necessary to result in clinical disease varies by the mode of transmission. If inoculation occurs with contaminated water, the infectious dose is 103-106 organisms. If inoculation occurs with contaminated food, fewer organisms (102-104) are required to produce disease. The naturally acidic environment of the stomach is the body's first line of defense against becoming infected with cholera. Use of proton pump inhibitors, antacids and histamine receptor blockers reduces gastric acidity, increases the risk of cholera infection and predisposes the patient to a more serious course of disease.

   Once colonized in the small intestine, V. cholerae produces an enterotoxin (protein toxin released by microorganisms) that promotes a shift of fluid and electrolytes out of the bloodstream into the small intestine. The large intestine, or colon, is not as sensitive to the enterotoxin and can absorb fluid in a normal fashion. However, the large intestine cannot reabsorb the large volumes of fluid produced upstream in the small intestine, resulting in severe diarrhea and electrolyte losses.

History and Clinical Exam Findings

   Patients infected with V. cholerae will typically exhibit symptoms 24 to 48 hours after inoculation. More often than not, infection results in a subclinical course, with patients presenting as relatively asymptomatic with mild diarrhea that is clinically indistinguishable from other causes of gastroenteritis. However, an estimated 5% of infected patients will progress to cholera gravis, the most severe form of cholera that is characterized by profuse, painless, watery diarrhea; vomiting; muscle cramping; and signs and symptoms of dehydration.

   The diarrhea of cholera is unique in that it is profuse, has what is described as a fishy odor, and has a "rice water" appearance. An untreated adult with cholera can produce 10-20 liters of diarrhea per day, leading to rapid and profound dehydration, electrolyte imbalance and death.13 Vomiting can also contribute to water and gastric acid losses, leading to acid/base disturbances. Signs of dehydration include excessive thirst, hypotension, tachycardia, dry mucous membranes, and weakness or fatigue. Profound, life-threatening dehydration is characterized by sunken fontanels in children, sunken eyes, poor skin turgor, oliguria, somnolence and coma.

   It is important to identify those persons at risk for cholera infection, and a good history can help lead you in the right direction. Inquire about recent travel, especially international travel and travel to areas with a high risk of or active problems with cholera. Also ask if the patient has been in contact with persons who have traveled to those areas or anyone who has been ill with gastrointestinal complaints.

   Cholera can often be diagnosed or placed high on the list of differential diagnoses based on the combination of a good medical/travel history and physical examination. Once clinically suspected, treatment can be started immediately while waiting for confirmatory testing. Confirmation of the diagnosis is made through laboratory culture of a stool or rectal specimen—a process that may take hours or days to complete.

Prehospital Management of the Patient with Suspected Cholera

   Consider proper personal protective equipment necessary when assessing and treating a patient with suspected cholera in order to protect yourself from contaminated vomitus and diarrhea. A clean, non-sterile, full-sleeved gown is recommended, in addition to clean, non-sterile gloves that cover the cuffs of the gown. In addition, all healthcare providers should wash their hands with soap and water or an alcohol-based hand rub after contact with a patient suspected of having cholera.14

   After ensuring that the airway is open and breathing is adequate, the prehospital treatment of cholera, or any infection that produces profound diarrhea, water loss and dehydration, revolves around fluid replacement therapy. The World Health Organization has created an oral rehydration formula that has been used successfully to treat dehydration secondary to cholera worldwide, but oral administration of fluids is not typical protocol for prehospital care providers.15 As such, initiate IV access and administer an isotonic crystalloid (normal saline or lactated Ringer's) per protocol for hypovolemia.

   After providing patient care or coming into contact with a patient's clothes, bed linen or any equipment that may be contaminated, it is important to wash your hands thoroughly with soap and clean water.

References

   1. Prevention & Control of Influenza-Recommendations of the Advisory Committee on Immunization Practices (ACIP) 2008. MMWR 57(RR07):1-60, Aug 8, 2008.
2. Centers for Disease Control. Questions & answers: 2010-2011 flu season. www.cdc.gov/flu/about/qa/1011season.htm.
3. CDC. Pertussis: What you need to know. www.cdc.gov/features/pertussis/.
4. Cherry JD, Heininger U. Pertussis and other Bordetella infections. In: Feigin RD, Demmler GJ, Cherry JD, Kaplan SL, eds. Textbook of Pediatric Infectious Diseases, Vol. 1, 5th ed. Philadelphia, PA: WB Saunders Co., pp. 1588-1608, 2004.
5. Pertussis report 2010-12-15. California Department of Public Health. www.cdph.ca.gov/programs/immunize/Pages/PertussisSummaryReports.aspx.
6. California Department of Public Health. Pertussis (Whooping Cough). www.cdph.ca.gov/healthinfo/discond/pages/pertussis.aspx.
7. Fernandez-Frackelton M. Infectious diseases: Bacteria. In: Marx: Rosen's Emergency Medicine, 7th ed. Mosby, 2009.
8. World Health Organization. Media center: Cholera. Fact sheet N107, June 2010. www.who.int/mediacentre/factsheets/fs107/en/index.html.
9. CDC. 2010 cholera outbreak. www.cdc.gov/haiticholera/situation/.
10. Pan American Health Organization. PAHO responds to cholera outbreak in Haiti. http://new.paho.org/disasters/index.php?option=com_content&task=view&id=1423&Itemid=1 .
11. Tasker F. Miami Herald Online. Fla. woman diagnosed with cholera after trip to Haiti. www.miamiherald.com/2010/11/17/1930271/florida-woman-diagnosed-with-cholera.html.
12. Centers for Disease Control and Prevention. MMWR 59(50);1637-1641, 2010.
13. Sack DA, Sack RB, Nair GB, Siddique AK. Cholera. Lancet 363 (9404): 223-233, 2004.
14. Pan American Health Organization. Infection control in cholera outbreaks. http://tinyurl.com/29fykuq.
15. WHO. Position paper on oral rehydration salts to reduce mortality from cholera. www.who.int/cholera/technical/en/.

Scott R. Snyder, BS, NREMT-P, is the EMS education manager for the San Francisco Paramedic Association in San Francisco, CA, where he is responsible for the original and continuing education of EMTs and paramedics. Contact him at scottrsnyder@me.com.

David A. Vitberg, MD, EMT-P, is an intensivist in critical care medicine at St. Agnes Hospital in Baltimore, MD, and an attending physician in the Department of Emergency Medicine at the Baltimore Washington Medical Center in Glen Burnie, MD. He stays close to his EMS roots in his role as an EMS physician with the Baltimore County Fire Department. Contact him at dvmd01@verizon.net.

Kevin T. Collopy, BA, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also a flight paramedic for Spirit Ministry Medical Transportation in central Wisconsin and a lead instructor for Wilderness Medical Associates. Contact him at kcollopy@colgatealumni.org.

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