CHAPTER 38. Communicable Diseases

Sherri-Lynne Almeida

An infection is the detrimental colonization of a host organism by a foreign species. Three factors form the chain of infection: agent, host, and mode of transmission. ⁹ In an infection, the infecting organism seeks to use the host’s resources to multiply (usually at the expense of the host). The infecting organism, or pathogen, interferes with the normal functioning of the host and can lead to chronic wounds, gangrene, loss of an infected limb, and even death. The host’s response to infection is inflammation. A pathogen is usually considered a microscopic organism, though the definition is broader and includes bacteria, parasites, fungi, and viruses. The property of an infectious agent that determines the extent to which overt disease is produced or the power of an organism to produce disease is called pathogenicity. Some agents are highly pathogenic and routinely cause disease, whereas other agents cause disease only when normal host defenses are impaired.

A susceptible host is one who lacks effective anatomic and physiologic resistance to a pathogenic agent. Characteristics that influence susceptibility include nutritional and immunization status, hormonal influences, age, medical and medication history, underlying pathologic condition, and specific insult to the body such as trauma. The severity with which a pathogen causes disease in a specific host, the severity of the resulting diseases, the efficiency with which the organism is transmitted to or from the host, or a combination of these factors is known as the virulence of the pathogen.

Transmission of pathogens is essential to their ultimate survival. Major modes of transmission are contact (direct and indirect), airborne, and droplet. Direct transmission occurs when person-to-person contact occurs between an infected source and susceptible host with a receptive portal through which human or animal infection can enter. Examples of direct contact include biting, sexual intercourse, direct inoculation with contaminated blood (needlestick injury), or direct projection of droplet spray onto conjunctiva of the eye, nose, or mouth during sneezing, coughing, spitting, or vomiting. Indirect transmission occurs when susceptible hosts come in contact with an inanimate object contaminated with an infectious agent and the agent is transported and introduced into the host through a suitable portal of entry.

Vehicle-borne agents are contaminated, inanimate materials such as patient care equipment, soiled linen, surgical instruments, dressings, food, water, milk, and biologic products such as blood, serum, plasma, tissues, or organs. Vector-borne transmission occurs with injection of saliva during biting, regurgitation, or dermal exposure to feces or other material capable of penetrating nonintact skin. And finally, airborne transmission is defined as dissemination of microbial aerosols through a portal, usually the respiratory tract. Close contact with an infected source that is coughing or sneezing can transmit large infectious particles through the air. Factors that influence airborne transmission include ambient airflow, proximity, and spatial orientation to the infected person.

INFECTION PREVENTION IN THE ACUTE CARE SETTING

In the hospital environment, transmission of an infectious agent to a susceptible host occurs by contact and inhalation exposure. Nosocomial infections, also known as hospital-acquired infections, are infections acquired during hospital care that were not present or incubating at admission. Infections occurring more than 48 hours after admission are usually considered nosocomial.

Many factors contribute to the frequency of nosocomial infections: hospitalized patients are often immunocompromised, they undergo invasive examinations and treatments, and patient care practices and the hospital environment may facilitate the transmission of microorganisms among patients. The selective pressure of intense antibiotic use promotes antibiotic resistance. Although progress in the prevention of nosocomial infections has been made, changes in medical practice continually present new opportunities for development of infection.

Inappropriate or lack of hand washing is the most significant factor for development of nosocomial infections, and universal compliance with hand hygiene recommendations is poor. This is due to a variety of reasons, including lack of appropriate accessible equipment, high staff-to-patient ratios, allergies to hand-washing products, insufficient knowledge of staff about risks and procedures, and the duration of time recommended for washing.

When hands or other skin surfaces are contaminated with blood or other body substances, the area should be cleaned as soon as possible. Hands should be washed before and after every patient contact regardless of whether gloves are worn.

In addition to the protection of patients from infectious agents, clinical and nonclinical health care personnel need to protect themselves as well. Health care personnel are at risk for occupational exposure to bloodborne pathogens, including hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus (HIV). Exposures occur through needlesticks or cuts from other sharp instruments contaminated with an infected patient’s blood or through contact of the eyes, nose, mouth, or skin with a patient’s blood. Important factors that influence the overall risk for occupational exposure to bloodborne pathogens include the number of infected individuals in the patient population and the type and number of blood contacts. ¹ Many needlesticks and other penetrating exposures can be prevented by using safer techniques (for example, not recapping needles by hand), disposing of used needles in appropriate sharps disposal containers, and using medical devices with safety features designed to prevent injuries. Using appropriate barriers such as gloves, eye and face protection, or gowns when contact with blood is expected can prevent many exposures to the eyes, nose, mouth, or skin.

Exposure to bloodborne pathogens is of concern in health care settings. The emergency nurse will encounter a number of communicable diseases, depending on where he or she works and how mobile the patient population is. Most of the focus has been on HBV, HCV, and HIV, but any infectious agent presents a potential risk under the right circumstances. To control the spread of hepatitis A and E, enteric precautions should be implemented. Needlestick prevention and blood precautions will assist in the control of hepatitis B, C, and D.

DISEASES OF CONCERN

Hepatitis

Hepatitis is an acute or chronic viral infection of the liver that may be mild or life threatening. Acute viral hepatitis is caused by five agents, the hepatitis A, B, C, D, and E virus. Of the hepatitis viruses, only HBV, HCV, and hepatitis D (HDV) can cause chronic hepatitis.

Hepatitis A

Hepatitis A, one of the oldest diseases known to humankind, is a self-limited disease that results in fulminant hepatitis and death in only a small proportion of patients. However, it is a significant cause of morbidity and socioeconomic losses in many parts of the world.

Transmission of HAV is typically by the fecal-oral route. ^7.^10.^{and 12.} Because HAV is abundantly excreted in feces and can survive in the environment for prolonged periods of time, it is typically acquired by ingestion of feces-contaminated food or water. Direct person-to-person spread is common under poor hygienic conditions. ⁷ Occasionally HAV is also acquired through sexual contact (anal-oral) and blood transfusions. ⁷ People who have never contracted HAV and who are not vaccinated against hepatitis A are at risk for infection. The risk factors for HAV infection are related to resistance of HAV to the environment, poor sanitation in large areas of the world, and abundant HAV shedding in feces. ⁷ In areas where HAV is highly endemic, most HAV infections occur during early childhood.

Nosocomial HAV transmission is rare. Outbreaks have occasionally been observed in neonatal intensive care units when an infant acquires the infection from transfused blood and subsequently transmits hepatitis A to other infants and staff. ¹⁰ Outbreaks of hepatitis A caused by transmission from adult patients to health care workers are typically associated with fecal incontinence, although the majority of hospitalized patients who have hepatitis A are admitted after onset of jaundice, when they are beyond the point of peak infectivity. ¹⁰ Data from serologic surveys of health care workers have not indicated an increased prevalence of HAV infection in these groups compared with that in control populations.

The course of hepatitis A may be extremely variable. ⁷ Patients with inapparent or subclinical hepatitis have neither symptoms nor jaundice. Children generally belong to this group. Asymptomatic cases can be recognized only by detecting biochemical or serologic alterations in the blood. ⁷ Patients may develop anicteric or icteric hepatitis and have symptoms ranging from mild and transient to severe and prolonged, from which they either recover completely or develop fulminant hepatitis and die. The severity of the disease increases with age at time of infection. ⁷ The course of acute hepatitis A can be divided into four clinical phases identified in Table 38-1.

**Table 38-1** C linical P hases of H epatitis A
HAV, Hepatitis A virus.
Incubation or preclinical period	Ranging from 10 to 50 days, during which the patient remains asymptomatic despite active replication of the virus. In this phase, transmissibility is of greatest concern.
Prodromal or preicteric phase	Ranging from several days to more than a week, characterized by the appearance of symptoms such as loss of appetite, fatigue, abdominal pain, nausea and vomiting, fever, diarrhea, dark urine, and pale stools.
Icteric phase	Jaundice develops at total bilirubin levels exceeding 20-40 mg/L. Patients often seek medical help at this stage of their illness. The icteric phase generally begins within 10 days of the initial symptoms. Fever usually improves after the first few days of jaundice. Viremia terminates shortly after hepatitis develops, although feces remain infectious for another 1-2 weeks. Extrahepatic manifestations of hepatitis A are unusual. Physical examination of the patient by percussion can help to determine the size of the liver and possibly reveal massive necrosis. The mortality rate is low (0.2% of icteric cases), and the disease ultimately resolves. Occasionally, extensive necrosis of the liver occurs during the first 6-8 weeks of illness. In this case, high fever, marked abdominal pain, vomiting, jaundice, and the development of hepatic encephalopathy associated with coma and seizures are the signs of fulminant hepatitis, leading to death in 70%-90% of the patients. In these cases mortality is highly correlated with increasing age, and survival is uncommon over 50 years of age. Among patients with chronic hepatitis B or C or underlying liver disease who are superinfected with HAV, the mortality rate increases considerably.
Convalescent period	When resolution of the disease is slow, but patient recovery uneventful and complete. Relapsing hepatitis occurs in 3%-20% of patients 4-15 weeks after the initial symptoms have resolved. Cholestatic hepatitis with high bilirubin levels persisting for months is also occasionally observed. Chronic sequelae with persistence of HAV infection for more than 12 months are not observed.

Hepatitis A cannot be differentiated from other types of viral hepatitis on the basis of clinical or epidemiologic features alone. Serologic testing to detect immunoglobulin M (IgM) antibody to the capsid proteins of HAV (IgM anti-HAV) is required to confirm a diagnosis of acute HAV infection. In the majority of persons, serum IgM anti-HAV becomes detectable 5 to 10 days before onset of symptoms. ^8.^{and 11.} IgG anti-HAV, which appears early in the course of infection, remains detectable for the person’s lifetime and provides lifelong protection against the disease. In the majority of patients, IgM anti-HAV declines to undetectable levels less than 6 months after infection. ^8.^{and 11.}

Better hygienic and sanitary conditions and development of the hepatitis A vaccine have led to a decline in the overall incidence of hepatitis A in the United States over the past several decades. The vaccines containing HAV antigen that are currently licensed in the United States are the single-antigen vaccines HAVRIX (manufactured by GlaxoSmithKline) and VAQTA (manufactured by Merck & Co., Inc.) and the combination vaccine TWINRIX (containing both HAV and HBV antigens; manufactured by GlaxoSmithKline). All are inactivated vaccines. An inactive hepatitis A vaccine has been shown to be safe, immunogenic, and efficacious. Protection against clinical HAV may begin in some people 14 to 21 days after a single dose of vaccine; nearly all have protective antibodies by 30 days. Hepatitis A immunization is recommended for anyone who plans to travel repeatedly or reside for long periods in areas where people are at risk for infection and for children living in communities with the highest rates of infection and disease. Individuals employed in hospitals or day care centers should also be immunized.

For proven cases of hepatitis A, enteric precautions are necessary during the first 2 weeks of illness but for no more than 1 week after onset of jaundice. Persons who have been recently exposed to HAV and who have not previously received hepatitis A vaccine should be administered a single dose of immune globulin (IG) (0.02 mL/kg) as soon as possible after exposure. Efficacy when administered more than 2 weeks after exposure has not been established. Persons who have been administered one dose of hepatitis A vaccine at greater than or equal to 1 month before exposure to HAV do not need IG. Hepatitis A vaccine and IG are not indicated for contacts if they do not fall into the following categories: close personal contacts, including household, sexual, or drug using; day care center attendees/workers if one or more cases of hepatitis A are identified; and common-source outbreak related to food handling.

The World Health Organization (WHO) has recommendations for the use of hepatitis A vaccine. In industrialized nations with low endemicity and high rates of disease in specific high-risk populations (men who have sex with men, injecting drug users, all susceptible persons traveling to or working in countries where HAV is endemic, persons who work with HAV-infected primates or in research laboratories), vaccination of these populations may be recommended.

Hepatitis B

HBV is a widely distributed pathogen that produces acute and chronic infection. Chronically infected people represent the major source of infection. Individuals have an increased risk for mortality and morbidity associated with chronic liver disease and primary hepatocellular carcinoma. HBV is a worldwide problem existing even in the most remote and isolated populations of the world. Prevalence of HBV infection varies widely. The disease is highly endemic in most of the developing world but is minimally endemic in developed countries. Of the 2 billion people who have been infected with HBV, more than 350 million have chronic (lifelong) infections. These chronically infected persons are at high risk for death from cirrhosis of the liver and liver cancer, diseases that kill about 1 million persons each year. Although the vaccine will not cure chronic hepatitis, it is 95% effective in preventing chronic infections from developing and is the first vaccine effective against a major human cancer. Despite vaccine availability, it is estimated that over 4 million new acute clinical cases occur each year.

Hepatitis B virus is transmitted by contact with blood or body fluids (saliva; cerebrospinal fluid; peritoneal, pleural, pericardial and synovial fluid; amniotic fluid; semen and vaginal secretions and any other body fluid containing blood; and unfixed tissues and organs) of an infected person. Transmission occurs by exposure to infected body fluids via the percutaneous or per mucosal route.

Worldwide, the major modes of HBV transmission include sexual or close household contact with an infected person, mother-to-infant transmission, the reuse of unsterilized needles and syringes, and nosocomial. Sexual transmission from infected men to women is about three times more efficient than that from women to men, and anal intercourse is associated with an increased risk for infection. The transmission of HBV in household occurs primarily from child to child. Perinatal transmission is common when the mother is hepatitis Be antigen (HBeAg)-positive. Intravenous (IV) drug users are at risk if they share syringes and needles contaminated with blood. In addition, hepatitis B virus is the major infectious occupational hazard of health care workers, despite the fact that most health care workers have received the hepatitis B vaccine.

The incubation period for HBV averages 60 to 80 days, with the norm 45 to180 days; however, the incubation period can range from 2 weeks to 6 to 9 months when hepatitis B surface antigen (HBsAg) appears. Extreme variation in the incubation period is related in part to the amount of virus in the inoculum, mode of transmission, alteration of viral pathogenicity by chemical or physical means, administration of a specific antibody, and unusual virus-host interactions. ⁷

All people who are HBsAg-positive and HBeAg-positive are potentially infectious. Both antigens are detectable 1 to 3 weeks after exposure and 4 to 5 weeks before onset of jaundice. Infectivity of chronically infected individuals varies from highly infectious (HBeAg-positive) to sparingly infectious (anti–HBe-positive). ⁷

Diagnosis of HBV is based on clinical, serologic, and epidemiologic findings. Detection of HBV infection serologic markers—HBsAg—confirms hepatitis B infection. Infection may present with a variety of symptomatology: acute illness with jaundice followed by recovery, subclinical infection followed by recovery, acute illness that progresses to chronic active hepatitis, subclinical infection followed by chronic active hepatitis, and fulminant disease. ⁷ Viral hepatitis is the most common infectious cause of jaundice. A short prodromal phase, varying from several days to more than a week, may precede onset of jaundice. Typical symptoms include anorexia, weakness, and fatigue. Nausea, vomiting, and diarrhea may also occur. Many patients complain of right upper quadrant abdominal pain. The preicteric phase may be characterized by fever (usually 103° F [39° C] or more), malaise, myalgia, and headache. Other symptoms are similar to serum sickness: arthritis, arthralgia, and urticaria or maculopapular rash. ⁷ The icteric phase begins with the appearance of dark urine resulting from bilirubinuria, followed by light or gray stools, and yellowish discoloration of mucous membranes, sclera, conjunctivae, and skin. Jaundice becomes apparent when total bilirubin levels exceed 2.0 to 3.0 mg/dL. Hepatic tenderness and hepatomegaly are also present. ⁷ Recovery begins with the disappearance of jaundice and other symptoms. HBsAg and HBeAg also disappear. The appearance of antibodies (anti-HBs and anti-HB) indicates the infection is subsiding. Liver failure may occur in 1% to 3% of patients with acute hepatitis B. ⁷ This potentially fatal disease is characterized by mental confusion, emotional instability, bleeding manifestations, and coma. The case fatality rate is about 1% higher in those over 40 years of age.

The most effective method of infection control against hepatitis B is the hepatitis B vaccine. Hepatitis B vaccine prevents hepatitis B disease and its serious consequences such as hepatocellular carcinoma (liver cancer). Hepatitis B vaccine has been available since 1982. The current vaccine used in the United State is a recombinant product derived from HBAg grown in yeast. Vaccines licensed in different parts of the world may have varying dosages and immunization schedules. In the United States the vaccine is primarily administered in three intramuscular (IM) doses. For infants, the first dose is administered at birth with subsequent doses at 1 to 2 and 6 to 18 months of age. In adults, the immunization schedule consists of three IM doses. After the first dose, subsequent doses are administered at 1 to 2 and 4 to 6 months. Current data show that vaccine-induced hepatitis B surface antibody (anti-HBs) levels may decline over time; however, immune memory (amnestic anti-HBs response) remains intact indefinitely following immunization. Therefore persons with declining antibody levels are still protected against clinical illness and chronic disease. Postvaccination testing for adequate antibody response is not necessary after routine vaccination of infants, children, adolescents, or adults. A combination of active and passive immunization is used for nonimmunized persons who have sustained a percutaneous or mucous membrane exposure to blood that might contain HBsAg. If the decision is made to provide postexposure prophylaxis, then a single dose of hepatitis B immune globulin (HBIG) (0.06 mL/kg) should be given as soon as possible, or at least within 24 hours of a high-risk needlestick, and the hepatitis B vaccine series should be started. If the vaccine cannot be given, a second dose of HBIG should be provided 1 month after the first.

WHO’s hepatitis B prevention strategy is based on routine universal newborn or infant immunization. The current strategy in the United States includes screening of all pregnant women, providing HBIG and hepatitis B vaccine to infants of HBsAg- positive mothers, providing hepatitis B vaccine to susceptible household contacts, providing routine hepatitis B vaccine for all infants, and providing catch-up immunizations to unimmunized children and adolescents. In addition, there is also an effort to immunize adolescents and adults in defined risk groups.