CDEWorld > Courses > Infection Control In The Dental Office: A Review For A National Infection Control Exam – Part 2

CE Information & Quiz

Infection Control In The Dental Office: A Review For A National Infection Control Exam – Part 2

Eve Cuny, MS, and Charles J. Palenik, PHD, MS, MBA

Course - Expires Sunday, December 31st, 2023

American Dental Assistants Association


Human health and safety including infection control is essential to every dental practice. The well-being of dental practitioners, patients and the surrounding community is very important. These areas are in constant flux. New products, equipment and processes seemingly appear on a daily basis. In addition, governmental agencies and professional associations regularly release new rules, regulations and recommendations. 

Dental practices must comply with certain requirements, but the methods involved often seem complex, time consuming and relatively expensive. However, there really is no alternative to an effective workplace health and safety program. Each dental practice must make the commitment to establish and maintain a safe work and treatment environment. 

In December of 2003, the Center for Disease Control and Prevention (CDC) released an extensive review and set of recommendations regarding infection control in dental environments. This document as well as others will serve as “guiding lights” for this course. The guidelines update previous CDC recommendations, incorporating relevant infection control measures, and discuss a number of concerns not previously addressed in dentistry. 

Every dental practice should have a copy of the 2003 CDC infection control guidelines for dentistry. Every person having a dental license received a copy. Electronic copies also are available at 

One effective way dental practices can improve and maintain compliant health and safety programs is through the appointment of a safety coordinator (compliance officer). The CDC indicates that a knowledgeable infection control coordinator (a member of the practice team) or a person willing to be trained should be given the responsibility for coordinating the program. The educated dental assistant should be readily capable of performing the tasks required.

You must be signed in to read the rest of this article.

Login Sign Up

Registration on CDEWorld is free. Sign up today!
Forgot your password? Click Here!


Chapter 4: Human Oral Flora

The human oral cavity is home to normal oral microbiota (normal oral flora). These microorganisms colonize and are continually present on the teeth and soft tissues, as well as in saliva. These microorganisms do not cause harm except when they accumulate in the form of dental plaque or move from the mouth to deeper tissues, such as the tooth pulp, gingival tissues or to other body sites, such as the bloodstream.

Normal Oral Microbiota/Normal Flora

The human mouth is usually first exposed to microorganisms at birth during passage through the birth canal. Most of the mother's vaginal bacteria that enter the child's mouth are transient(short-lived) and usually do not establish themselves as regular members of the oral microbiota. Over time, the child is exposed to microorganisms from the environment and other humans. It appears that the main source of microorganisms that colonize the child's mouth come from oral tissues and saliva of other people, particularly the mother and other close family members.

For microorganisms to become established members of the oral microbiota, they must be able to attach well to oral surfaces and must be able to multiply in the oral environment. Eruption of the primary teeth results in a major change, providing tooth surfaces and gingival crevices. New bacteria, such as Streptococcus mutans, appear that can survive only on teeth. Anaerobes increase because of additional anaerobic sites around the teeth.

Different sites in the mouth (tongue, buccal epithelium, supragingival tooth surfaces, subgingival tooth surfaces, and crevicular epithelial surfaces) support different combinations of microorganisms. They serve as specific ecological niches. With age, more microorganisms colonize the mouth. Usually, the composition (mix of microorganisms) stabilizes by the early teen years.

Bacteria comprise the majority of the normal oral microbiota. However, about 40% of the population also has yeast, such as Candida albicans, as part of their normal flora. The oral microbiota is quite diverse, with approximately 30 genera of bacteria represented, although not every person has all of these varied microorganisms present all of the time. Each genus may be represented by several species, resulting in a very complex group of gram-positive and gram-negative bacteria. A gram of dental plaque (about one fourth of a teaspoonful) contains approximately 200 billion bacteria, and saliva contains approximately 10 million to 100 million bacteria per milliliter.

Prevention of Plaque-Associated Diseases

The two most common plaque-associated diseases are dental caries and periodontal disease. Regular brushing and flossing as well as professional dental care are useful for preventing plaque-associated diseases. Also, fluoride and pit and fissure sealants are effective against caries. Caries and periodontal diseases still occur; however. Other preventive methods and materials continue to emerge.

One current approach involving microbiology is the use of antimicrobial mouth rinses. Other approaches still under investigation include more effective means of delivering antimicrobial agents to sites of infection, slow release of active agents, developing new antimicrobial agents, replacement of oral pathogens with nonpathogenic strains, and use of vaccines or other chemical agents that may prevent bacterial attachment or disrupt preformed plaque.

Acute Oral Infections

As carious lesions progress and approach the tooth pulp, microbial byproducts may enter the pulp and cause inflammation called pulpitis. As the disease continues, the bacteria enter the pulp chamber, enhancing the inflammation and destroying the pulp tissue. Further progression may extend the infection through the tooth apex, causing a periapical infection.

Depending on the host response and probably the types of bacteria involved, the surrounding facial tissues may become infected, producing a cellulitis.

Other Infections

The slightest trauma in the mouth that results in bleeding (e.g., tooth brushing, biting the cheek, dental procedures) may permit members of the normal oral microbiota to enter the bloodstream, causing a transient bacteremia. Normally, the phagocytes in the blood rapidly destroy these bacteria before they have a chance to cause problems. If a person has had previous damage to their heart valves, however, such as in rheumatic heart disease, certain oral bacteria in the blood may induce further damage to these valves or cause subacute bacterial endocarditis (inflammation of the inside of the heart). This is why some dental patients with previous heart damage must be given prophylactic antibiotics when they receive dental care. When bacteria do enter the bloodstream and cause damage to tissues, it is referred to as septicemia rather than bacteremia.

Other harmful infections caused by oral microorganisms are those resulting from a bite, or a puncture or cut from a contaminated dental instrument. Several microorganisms are implanted through the skin in these instances, which can lead to a harmful infection that may require antibiotic treatment. Thus many members of the normal oral microbiota have pathogenic potential, if they are allowed to gain entrance to deeper tissues or if they gain entrance to the bodies of others.

Chapter 5: Bloodborne Pathogens

As described in Chapter 4, the patient's mouth is the most important source of potentially pathogenic microorganisms in the dental office. Pathogenic agents may occur in the mouth as a result of four basic conditions: bloodborne diseases, oral diseases, systemic diseases with oral lesions, and respiratory diseases. The bloodborne diseases will be presented here, while oral and respiratory diseases will be presented in Chapter 6.

Bloodborne Pathogens

Bloodborne pathogens may infect different blood cells or other tissue of the body. Pathogens exist or are released into the blood or other body fluids, which may include semen, vaginal secretion, intestinal secretions, tears, mothers' milk, synovial (joint) fluid, pericardial (around the heart) fluid, amniotic fluids (surround the developing fetus), and saliva. Because blood or other body fluids may contain the pathogens, the disease may be spread from one person to another by contact with the fluids. Thus the diseases are called bloodborne diseases. A patient's blood may enter their mouth during dental procedures since many procedures induce bleeding. Some of the blood of these patients will contain bloodborne pathogens. Thus contact with saliva during such procedures may result in exposure to these pathogens if present. Because it is very difficult to determine if blood is actually present in saliva, saliva from all dental patients should be considered potentially infectious.

Viral Hepatitis

There are at least six hepatitis viruses that cause clinically similar diseases: hepatitis A, B, C, D, E, and G (Table 5). Hepatitis A and E transmit through the consumption of contaminated food and water (fecal-oral route of spread); hepatitis B, C, D, and G are bloodborne diseases usually transmitted by direct contact with infected body fluids. Hepatitis also may be caused by excessive alcohol consumption, exposure to some hazardous chemicals, and as a complication of other viral infections such as cytomegalovirus.

Hepatitis B

Hepatitis B, an inflammation of the liver, is a major health problem in the United States and is endemic (occurs regularly) in other parts of the world. In the United States, the Centers for Disease Control and Prevention estimate that 100,000 people are infected with the hepatitis B virus (HBV) each year. Between 800,000 and nearly 1.2 million people in the U.S. are believed to be chronic carriers of HBV, meaning that they continue to be able to transmit the disease to others through the bloodborne disease route. About 3,000 people die each year of hepatitis B-related chronic liver disease, including cirrhosis, liver cancer, fulminate liver disease, and about one health care worker dies each day.

HBV is an enveloped DNA virus that infects and multiplies in human liver cells. During the course of an infection, the virus and cells containing the virus are released in high numbers into the bloodstream and other body fluids, explaining its description as a bloodborne disease agent. A milliliter of blood from an infected person may contain as many as 100 million virus particles, meaning that only small amounts of blood or other body fluids are necessary to transmit the disease to others. The virus has three components that are important antigens; one is on its surface (HBsAg) and two are inside the virus (HBcAg and HBeAg). The hepatitis B vaccines consist of the HBsAg that is synthesized in the laboratory by genetic engineering techniques. Hepatitis B virus has been shown to be killed or inactivated by commonly used methods of sterilization and disinfection, including the steam autoclave, and 10-minute exposure to 1:100 diluted bleach, 1:16 diluted phenolic glutaraldehyde, 75 parts per million iodophor, and 70% isopropyl alcohol. Thus HBV is relatively easy to kill when outside the body, provided the killing agent comes into direct contact with the virus. Hepatitis B virus is more easily killed than Mycobacterium tuberculosisand bacterial spores.

Approximately 90% of those infected with HBV have a complete recovery without developing a carrier state. Approximately 5% to 10% become carriers of the virus, with approximately one half of these eliminating the virus from their bodies within 2.5 years. The other one half (2.5%-5% of all those originally infected) become chronic carriers. The carrier state is defined as being HBsAg-positive on at least two occasions when tested at least 2 months apart or being HBsAg positive and IgM anti-HBc negative at a single test. Anyone who is positive for HBsAg has a potential to spread the disease to others. Those who are also HBeAg positive have very high concentrations of the virus in their blood and, therefore, are considered highly infectious. Persons who have chronic hepatitis have approximately a 200 to 300 times greater chance of later developing liver cancer.

Hepatitis B virus is spread percutaneously (through the skin) or permucosally (through mucous membranes) by contact with infected body fluids, for example, at birth, during sexual activities, or with contaminated needles or other sharp objects. Also, the virus may be spread in environments involving frequent close contact with an infected person, as in households or institutions for developmentally disabled children. This latter route of spread likely involves unnoticed contact of infected body fluids with skin lesions or mucosal surfaces.

Populations considered to be at an increased risk for infection with HBV include:

• Infants born to infected mothers

• Sex partners of infected persons

• Sexually active persons who are not in a long-term, mutually monogamous relationship (e.g., >1 sex partner during the previous 6 months)

• Men who have sex with men

• Injection drug users

• Household contacts of persons with chronic HBV infection

• Healthcare and public safety workers at risk for occupational exposure to blood or blood-contaminated body fluids

• Hemodialysis patients

• Residents and staff of facilities for developmentally disabled persons

• Travelers to countries with intermediate or high prevalence of HBV infection

Spread of HBV through transfused blood or blood products is now rare because of routine testing of blood for HBsAg and donor screening. Hepatitis B is not commonly transmitted by the fecal-oral route. In approximately 30% of the hepatitis B cases, however, the exact mode of transmission is not identifiable.

If symptoms develop after infection, they begin to appear approximately 90 days after exposure. Roughly one-third of those infected (Table 6) exhibit the more easily recognizable symptoms of yellowing of the skin (jaundice) and whites of the eyes, light-colored stools, dark urine, joint pain, fever, a rash, and itching. Approximately another one third develop less descript mild symptoms that may include malaise ("not feeling good"), loss of appetite, nausea, and abdominal pain. The other one-third will develop no symptoms at all. Thus two-thirds of all those infected develop no symptoms or have mild nondescript symptoms that often are unrecognized as being related to hepatitis. Yet both symptomatic and asymptomatic cases can spread the virus to others. This unrecognizable infection with HBV and with other viruses (such as human immunodeficiency virus [HIV], described later) serves as the basis for standard precautions-applying infection control procedures during care for all patients, not just for those who are known to be infected.

Development of a hepatitis B chronic carrier state may occur more commonly in those who are asymptomatic and is more likely to occur in the young. As many as 90% of newborns infected by their mothers become chronic carriers and from 25% to 50% of children infected before age 5 become carriers. Women who are pregnant should seek the advice of their personal physician about being tested for hepatitis B, so that, if infected, proper procedures can be instituted to protect the newborn. Approximately 5% to 10% of infected adults become carriers. Chronic carriers are at high risk of developing chronic hepatitis that may lead to cirrhosis of the liver or primary liver cancer. Thus one could be unknowingly infected with HBV, not develop any recognizable symptoms, become a chronic carrier, unknowingly spread the virus to others, and die years later of HBV liver damage. Hepatitis B is an insidious disease.

There is a risk for the dental team. In the early to mid 1980s, approximately 10,000 to 12,000 cases of hepatitis B a year (approximately 4% of all cases) occurred in people who had an occupational risk for exposure to body fluids. In 1994, this number dropped to about 1,000 cases, showing approximately a 90% decrease in hepatitis B among health care workers.

The greatest dental occupational risks for exposure are:

• Injuries from contaminated sharps (needlesticks, instrument punctures, cuts, bur lacerations).

• Blood and saliva contamination of cuts and cracks on the skin on ungloved hands or hands with torn gloves.

• Spraying of blood and saliva onto open lesions on the skin or onto mucous membranes.

Several blood testing surveys of dental workers conducted between 1975 and 1982 attempted to determine how many of the different types of dental workers had been infected with HBV. Although some of the studies involved only small groups of workers, the results suggested that approximately 13% of dental assistants, 17% of dental hygienists, 14% of dental laboratory technicians, and 9% to 25% of dentists had been infected. It is estimated that approximately 5% of the general population has been infected. Thus unvaccinated members of the dental team are at least two to five times more likely to become infected with HBV than the general population. Use of the HBV vaccine and implementation of infection control barriers such as masks, gloves, and protective eyeglasses that prevent exposure to blood and saliva help prevent hepatitis in health-care workers, but some are still being infected through injuries with contaminated sharp instruments and needles.

There is little risk of dental patients contracting HBV during treatment. The chances of a patient acquiring any disease in a dental office are extremely low. In the past, HBV has been spread from dentists to patients, as documented in ten separate instances. In each instance, the dentist was highly infectious (HBeAg-positive) and apparently did not routinely wear gloves. There has been one documented case of a patient to patient transmission of HBV that was published in 2007. In this instance the exact mode of transmission was not established, but the examination of the viral DNA confirmed that the transmission was from one patient to another in an oral maxillofacial office.

It is extremely fortunate that safe and effective vaccines for hepatitis B are available. Because there is no successful medical treatment to cure this disease, prevention is of paramount importance. Details on the vaccination for health care workers are presented in Chapter 11. The vaccines are strongly recommended for all members of the dental team. The Occupational Safety and Health Administration (OSHA) of the U.S. Department of Labor actually requires dentist-employers to offer the hepatitis B vaccine series free of charge to office staff who may have any potential for exposure to blood or saliva. OSHA requires this of employers in all health-care and other professions related to body fluid exposures.

Hepatitis C

Hepatitis C was previously called parenterally transmitted non-A, non-B hepatitis. The hepatitis C virus (HCV) is thought to cause approximately 30% of acute viral hepatitis cases in the United States. Hepatitis C is a bloodborne disease. It is estimated that about 170,000 people in the U.S. become infected with HCV every year, but only about 25% of those infected have any recognizable symptoms.

Hepatitis C has been transmitted to health-care workers through needlestick injuries and two reports of HCV transmission through blood splashes to the eyes have been reported. The following populations are considered to be at increased risk for HCV infection:

• Current or former injection drug users, including those who injected only once many years ago

• Recipients of clotting factor concentrates made before 1987, when more advanced methods for manufacturing those products were developed

• Recipients of blood transfusions or solid organ transplants before July 1992, when better testing of blood donors became available

• Chronic hemodialysis patients

• Persons with known exposures to HCV, such as

• healthcare workers after needlesticks involving HCV-positive blood

• recipients of blood or organs from a donor who tested HCV-positive

• Persons with HIV infection

• Children born to HCV-positive mothers

An alarming fact about hepatitis C is that 75%-85% of those infected become chronic carriers, which may involve 1% to 3% of the entire U.S. population. This disease is thought to cause from 8,000 to 10,000 deaths per year. Until recently, hepatitis C was diagnosed by indirect means, showing that the patient did not have type A or type B hepatitis. The causative virus was first isolated in 1989, and a blood test for antibodies to HCV was designed in 1991. This test aids in diagnosing the disease, identifying those who are or have been infected, and in screening potential blood donors and tissues intended for transplant. As yet there is no vaccine for hepatitis C but development of the badly needed test for HCV is leading to more firm information on modes of spread of this virus. Neither the hepatitis A nor the hepatitis B vaccines provide any protection against hepatitis C.

Hepatitis D

Infection with hepatitis D virus (HDV), also known as the Delta agent, appears to be a complication of hepatitis B. This virus may cause infection only in the presence of an active HBV infection. Hepatitis D virus is a defective virus that needs a part of the HBV to complete its life cycle. Infection with HDV may occur as a coinfection with HBV (both HDV and HBV infect simultaneously) or as a superinfection of HDV in an HBV carrier. Both instances usually result in clinical acute hepatitis and coinfection usually resolves, whereas superinfection frequently causes chronic HDV infection and chronic active hepatitis. Hepatitis D virus is transmitted by routes similar to those of HBV, and outbreaks of hepatitis D have been reported in the United States. Thus those who are susceptible to HBV infection, occupationally or otherwise, are also susceptible to HDV infection. Successful vaccination against hepatitis B also should prevent hepatitis D.

HIV Disease

The human immunodeficiency virus (HIV) causes HIV disease, which involves HIV infection that progresses to a final phase called acquired immunodeficiency syndrome (AIDS). AIDS was reported as a new clinical disease in the summer of 1981, and the Centers for Disease Control and Prevention now estimate that approximately 1,140,400 adults and adolescents were living with HIV in the United States. In 2006, the CDC estimates that more than 56,000 new infections with HIV occurred in the U.S. Approximately 24%-27% of people infected with HIV are unaware of their infection, underscoring the need for standard precautions in infection control. Worldwide, it is estimated that more than 37 million people are living with HIV and that 2.1 million die each year as a result of HIV disease.

HIV disease involves destruction of the body's immune system, making the individual susceptible to life-threatening opportunistic infections or cancers. Progression from the initial phase of the disease (HIV infection) to the terminal phase of the disease (AIDS) may take from approximately 2 to 12 or more years, with an average of approximately 10 years.


Human immunodeficiency virus is a member of a group of RNA viruses called retroviruses. Human immunodeficiency virus type 1 is the most common worldwide cause of HIV disease. Human immuno-deficiency virus type 2 causes another less aggressive immunodeficiency syndrome in Western Africa. Infection with HIV-2 in the United States is uncommon, with most cases occurring in immigrants from Africa and in injection drug abusers.

Human immunodeficiency virus type 1 primarily infects T4 lymphocytes but also can infect macrophages and a few other cell types. These special lymphocytes are the cells that regulate the immune response. Human immunodeficiency virus type 1 selectively attaches to and enters T4 lymphocytes (also called CD4 lymphocytes), where the virus RNA is quickly converted into viral DNA, which is incorporated as viral genes into the lymphocyte chromosomes. Thus the lymphocyte and its succeeding generations of cells are permanently infected with the HIV-1 genes. These genes may remain latent (delayed) for prolonged periods but they induce the production of new virus particles within the lymphocytes. This virus production occurs throughout HIV disease but at widely different rates in different patients. Virus production destroys the lymphocytes and yields more viruses that can infect and destroy more lymphocytes. This eventually depletes the body of T4 cells.

Thus HIV-1 produces a latent infection in which the infected person is usually asymptomatic until the level of T4 lymphocytes becomes critically low. Human immunodeficiency virus type 1 may undergo mutations that produce several different genetic forms as the virus replicates inside lymphocytes and other cells. This genetic variation may explain the difference in the course of HIV disease in different individuals, with some strains of HIV-1 being more virulent than others. This genetic variation also is one reason why a vaccine for prevention has not yet been developed. A vaccine made against one HIV type 1 strain may not protect against other strains. Although there is no known approach to kill HIV type 1 after it is in the body, it can be easily killed when outside the body. It is readily killed by all forms of heat and gas sterilization and by the commonly used liquid sterilants and surface disinfectants, provided the killing agent comes into direct contact with the virus. Human immunodeficiency virus type 1 is much more easily killed on instruments and surfaces than Mycobacterium tuberculosisand bacterial spores.

Disease States and Symptoms

HIV infection. At approximately four weeks after initial infection with HIV type 1, a person may experience sore throat, fever, swollen glands, diarrhea, joint pain, and fatigue. This is called a retroviral syndrome, or acute HIV syndrome, signifying acute HIV-infection but is not unlike that which occurs with many viral infections. These symptoms may be slight or even unnoticed. Antibodies to HIV type 1 usually develop within 6 to 12 weeks after initial infection, and by 6 months 95% of those infected have developed antibodies (seroconverted). Unfortunately, these antibodies do not protect against the disease; although they do provide a means to diagnose HIV disease. A person with antibodies to HIV is referred to as being "HIV-positive," indicating that the person is infected with the virus.

After acute HIV infection has occurred, most people infected have no further clinical symptoms until months or years later, when the killing of T4 lymphocytes or other cells becomes prominent. Nevertheless, people with asymptomatic HIV infection still can transmit the virus to others. Some HIV-positive persons experience persistent swollen glands under the arms and in the groin but are otherwise asymptomatic. The condition is referred to as generalized lymphadenopathy.

AIDS. Replication of HIV type 1 in T4 lymphocytes kills the lymphocytes, and as more and more cells are killed the immune system becomes progressively weaker. This immunodeficiency results in increased susceptibility to opportunistic disease agents that normally do not cause infections or cause less severe infections in those with healthy immune systems. When an HIV-positive patient experiences one or more of these indicator opportunistic infections or a cancer, the patient is diagnosed as having AIDS. The symptoms experienced depend on the type of infection or cancer that occurs, examples of which are listed in Table 7. Eventually, one of these diseases causes death. The infectious diseases may be caused by bacterial, viral, fungal, or protozoan agents; the leading cause of death in an AIDS patient is Pneumocystis cariniipneumonia.

Oral Manifestations of AIDS

In many instances, early manifestations of AIDS occur as oral lesions. Oral manifestations include fungal diseases, such as candidiasis (thrush), histoplasmosis, geotrichosis, or cryptococcosis; viral diseases such as warts, hairy leukoplakia, or human herpesvirus type 1 (herpes simplex) infection; bacterial diseases such as rapidly progressing periodontitis or gingivitis; cancerous diseases such as Kaposi's sarcoma (recently associated with human herpes virus type 8) and non-Hodgkin's lymphoma.


Human immunodeficiency virus type 1 is transmitted from an infected person through:

• Intimate sexual contact (vaginal, anal, oral) involving contact or exchange of semen or vaginal secretions.

• Exposure to blood, blood-contaminated body fluids, or blood products.

• Perinatal contact (from infected mother to child).

Other exposures resulting in HIV-infection are variations of these three basic modes of transmission. Human immunodeficiency virus infection is not spread by casual contact.

Sexual contact. Nationwide, unprotected sex has resulted in the greatest number of AIDS cases. The risk of exposure to HIV type 1 is present when unprotected genital or anal intercourse is performed with individuals whose HIV status is not known, be it homosexual, bisexual, or heterosexual contact. Having multiple sex partners of unknown HIV status even further increases this risk. Clearly, HIV disease is a sexually transmitted disease, as are genital herpes, gonorrhea, syphilis, nongonococcal urethritis, genital warts, and several other conditions. The presence of a sexually transmitted disease, particularly herpes, syphilis, or chancroid, increases 100 to 200 times the chance of acquiring HIV infection if exposed.

Although AIDS was first recognized in the male homosexual population in the U.S., spread through heterosexual activity occurs. In fact, between 1990 and 1991, the largest increase in the number of reported AIDS cases (21.0%) occurred among heterosexuals, with the second highest increase (15%) among women. Approximately 31% of all AIDS cases in the U.S. are now due to high-risk heterosexual activity. Injection drug abuse results in 12% of all cases and male to male sexual contact accounts for 53% of the cases of HIV infection in the U.S. today.

Exposure to blood. Intravenous drug abuse is a high-risk behavior when injection needles are shared, allowing the transfer of blood remaining in the used needles from one person to another. Injection of infected blood directly into the bloodstream is a very efficient route of transmission. Percutaneous (through the skin) injuries with contaminated needles or other sharp objects and contamination of skin or mucous membranes containing small cuts or abrasions or dermatitis are variations of this "shared needles" mode of transmission.

Administration of infected blood products (e.g., to those with bleeding disorders such as hemophilia) or transfusions with infected blood have caused approximately 3% of the total reported cases of AIDS. In 1985, however, tests were developed that detect HIV infected blood, and since then these modes of transmission essentially have been eliminated.

Human immunodeficiency virus type 1 has been isolated from numerous body fluids, including blood, semen, vaginal and cervical secretions, cerebrospinal fluid, synovial fluid, amniotic fluid, pericardial fluid, saliva, tears, breast milk, and urine. Although HIV type 1 has been isolated from saliva, so far no cases of transmission have been documented by this route in casual or household contact. Also, transmission was shown not to occur in a 2.5-year follow-up study of 198 health-care workers, 30 of whom were bitten or scratched by an HIV-infected patient. The extremely low risk for transmission through saliva may be attributable to the low concentration of the virus in the saliva of infected persons. A proteinaceous factor in human saliva also has been shown to interfere with the HIV type 1 infection process. Nevertheless, "saliva in dentistry" is still considered potentially infectious because of the intimate contact with the patient's mouth during dental care and because most dental procedures result in varying degrees of bleeding into the mouth. Also, some natural bleeding may occur in the mouths of dental patients who have gingivitis or other oral soft tissue lesions. Thus, "saliva in dentistry" commonly contains blood.

Mother to child. Approximately one half of infants who have HIV-positive mothers are infected before birth by passage of the virus across the placenta, at the time of birth by contact with mother's blood during delivery, or, less commonly, through breast milk. Approximately 1.7% of all reported AIDS cases in the United States have occurred in children younger than age 13 (pediatric AIDS cases), and 85% of these occurred by spread from infected mothers, with the remainder involving hemophilia or transfusion cases. Advances in HIV research, prevention, and treatment have continued and these advances have made it possible for many women with HIV to give birth to babies who are free of HIV. According to the CDC, the annual number of HIV infections through perinatal transmission has declined by more than 95% since the early 1990s.

Risk for the Dental Team

The risk of HIV disease transmission from dental patients to members of the dental team is extremely low. Nevertheless, there is some small potential for this to occur. Through June 1997 (the last year the CDC provided figures for occupational transmission), the Centers for Disease Control and Prevention received reports of 57 health-care workers in the U.S. with documented, occupationally acquired HIV infections and an additional 138 with possible occupationally acquired HIV-infection (Table 7). In 1992, these numbers were 32 and 69. A "documented" case involves seroconversion (HIV-negative at the time of exposure, later becoming HIV-positive) following a percutaneous or mucocutaneous (mucous membrane and skin) occupational exposure to blood, body fluids, or tissues. A "possible" case involves persons with no determined behavioral or transfusion risks who report past percutaneous or mucocutaneous occupational exposure to blood, other body fluids, or tissues but did not have a documented seroconversion. Although there are no documented cases of occupational spread to dental workers, there are six cases in which this may have occurred (see Table 7).

Of the 57 "documented" cases described in Table 7, 86% had percutaneous exposure (e.g., sharps injuries), 10% had mucocutaneous exposure, and 2% had both; 90% were exposed to HIV-infected blood, 3% to a concentrated HIV-1 culture in the laboratory, and 3% were exposed to an unknown body fluid. Most of the 138 "possible" cases involved exposure to body fluids of unknown infectivity.

Risk for Dental Patients

The risk for a dental patient of acquiring HIV disease in the office from a member of the dental team must be extremely low. Although the bloodborne HBV has been spread in rare instances from dentist to patient (described early in this chapter), spread of HIV type 1 is suggested in only one instance. Apparently, a dentist with HIV infected six of his patients being treated in his Florida dental office during the years 1987 to 1990. The investigation of this case involved a comparison of the HIV type 1 from the dentist with the viruses isolated from the infected patients, and this demonstrated significant similarity in the viruses. Unfortunately, the investigation did not discover the mode of virus spread from the dentist to the six patients but the final conclusion by the investigators from the Centers for Disease Control and Prevention and the Florida Department of Health suggested that direct spread from the dentist to the patients was most likely rather than spread from contaminated instruments, equipment, or surfaces.

Until recently, this Florida dentist case was the only known instance in all of dentistry and medicine of possible spread of HIV disease from a health-care worker to patients. It still remains the only known instance in dentistry, but in February of 1997, the French government reported that a woman patient contacted HIV disease from a physician in France in 1992. All of the details are not available but evidence released so far supporting this transmission (comparing the viruses from the patient and the physician) is compelling. The available information suggests that the physician (an orthopedic surgeon) may have contracted the disease from a patient in 1983 but was not tested for HIV status until 1994. The physician performed an orthopedic procedure of some 10 hours in length on the woman patient in 1993; it is assumed that this is when the transmission occurred. To date, 968 of this physician's surgery patients have been tested and only the one woman has been found to be HIV-positive. Further attempts have been made to identify and define the low risk of spread from health-care workers to patients by performing HIV testing on patients who have been cared for by other HIV-positive health-care workers. Of approximately 28,000 medical and dental patients tested so far, none have been shown to have acquired HIV diseases from any of the 63 infected dentists or physicians involved. Nevertheless, it is important to maintain proper infection control during care for all patients.


Sexual contact. Recommendations for preventing the spread of HIV type 1 through sexual contact include abstinence or limiting sexual activities to one partner who is not infected and who does not have any other sex partners. A lesser level of protection is offered by safer sex practices such as the use of condoms to eliminate or minimize contact of each partner with body fluids that may contain HIV type 1.

Blood contact. Injection drug abusers must not use blood-contaminated needles. Continued screening for HIV-infectivity of blood for transfusion and of blood products began in June of 1985 and continues today. All members of the dental team and other health-care workers must protect themselves from exposure to blood, and all other potentially infectious body fluids including saliva. Contaminated sharps must be handled with care and disposed of properly. Gloves, mask, and protective eyewear and clothing must be used during the care of all patients and in other instances to prevent direct or indirect contact with body fluids. Also, all health-care workers must prevent their blood or body fluids from coming into contact with the patients being treated and instruments and equipment used on more than one patient must be properly decontaminated before reuse.

HIV Post-Exposure Prophylaxis (PEP). Numerous medications are used in the treatment of HIV infection. There is some evidence that the use of these medications in post exposure management may provide a reduced risk for infection after exposure. Thus the management of occupational exposures to body fluids should be provided by a health care practitioner knowledgeable in post exposure management, including the use of the multitude of medications available. If such prophylaxis is to be taken, it should begin within hours after the exposure, so a rapid post-exposure response is important.

Chapter 6: Oral and Respiratory Tract Infections

Oral and respiratory diseases can spread in dental offices. Often, the infectious agents associated with these infections are present in asymptomatic carriers. Transmission in some cases is by directly touching lesions or contacting infectious saliva. In other cases, disease spread requires exposure to spatter or inhalation of contaminated aerosols.

Table 8 lists important oral diseases and systemic diseases with oral manifestations. Proper aseptic technique, such as the application of standard precautions, holds the chances of occupation acquisition to an absolute minimum. Thus, universal use of protective barriers, such as gloves, is extremely important.

Upper Respiratory Infections

Inhalation of contaminated aerosolized particles can cause respiratory infections. Such infections may involve bacteria, viruses, protozoans and fungi. Spread may involve either respiratory or salivary fluids. Thus, exposure of both patients and practitioners may occur with the generation of spatter and aerosols. These infections can be divided into upper and lower respiratory infections (Table 9).


Influenza ("the flu") is a contagious respiratory illness caused by two types of influenza viruses. Symptoms range from mild to severe with life threatening complications. On average, hospitalization of 200,000 people for flu-related complications occurs each year. Over 36,000 people in the United States die annually because of influenza. Hospitalizations and deaths are most common among those older than 65 years, young children and all ages with underlying health conditions, such as congestive heart failure, asthma or diabetes.

In the United States, winter is the time for flu. The flu season can range from November through March and even past March in some years. For more than two decades, the heaviest flu activity (peak month) occurred in February.

Symptoms of flu include fever (usually high), headache, extreme tiredness, dry cough, sore throat, runny or stuffy nose and muscle aches and pains. Gastro-intestinal symptoms, such as nausea, vomiting and diarrhea, are much more common among children than adults. Sometimes the term "stomach flu" is associated with gastrointestinal symptoms ("sick to your stomach"). These illnesses do not involve influenza viruses, but rather other viruses, bacteria or even parasites. Flu is a respiratory disease and not a stomach or intestinal affliction.

The flu and the common cold are both respiratory illnesses caused by different viruses that often develop at the same time of the year. Because these two types of illnesses have similar symptoms, it can be difficult to tell the difference between them (Table 10).

Because colds and flu share many symptoms, it can be difficult (or even impossible) to tell the difference between them based on symptoms alone. Special tests that usually must be done within the first few days of illness can be carried out, when needed, to tell if a person has the flu.

In addition to the flu and the common cold, other respiratory viruses circulate during the flu season and cause symptoms and illness similar to those seen with a flu infection. One of the most important is the respiratory syncytial virus, which is the most common cause of severe respiratory illness in young children as well as the leading cause of death from respiratory illness in these aged 65 years and older.

There are three types of influenza viruses - Type A, Type B and Type C. Types A and B cause human illness throughout the world. Type A is more common and is usually associated with the more serious epidemics and pandemics. Type B causes more regional outbreaks. Type C infections result only in mild respiratory illness and are not involved with epidemics.

Flu is a contagious disease. The main way influenza spreads is from person-to-person in respiratory droplets associated with coughs and sneezes. This is droplet spread. This can happen when droplets from a cough or sneeze of an infected person are propelled through the air (usually up to one meter). The droplets deposit on the nose and mouths of persons nearby. Less frequently, flu viruses are spread when a person touches respiratory droplets on another person or an object and then touches their own mouth or nose or some one else's mouth or nose before washing their hands.

By far, the single best way to prevent the flu is for individuals, especially people at high-risk for serious complications from the flu, to get vaccinated each fall. The flu shot is an inactivated vaccine (killed virus) that is injected usually in the arm. Three of the antiviral drugs used to treat influenza can prevent to some extent influenza. These drugs are not substitutes for vaccination. All three are prescription drugs. All persons that have contact with dental patients should receive a flu vaccination every year.

Lower Respiratory Infections

A wide variety of microorganisms causes lower respiratory infections. These infections involve the bronchial tree, the lungs or both. Some diseases, such as tuberculosis, involve a single species, while other infections involve a range of different organisms (Table 11).


Although Mycobacterium tuberculosis(TB) is not commonly transmitted in dental settings, infected patients occasionally seek dental care. The CDC has published guidelines for TB in dental settings.

Carriage of TB is through airborne infective droplet nuclei that can be generated when persons with pulmonary or laryngeal TB sneeze, cough, speak and sing. The infectious particles are small enough (one to five mm) to stay suspended in air for hours.

Infection occurs when a susceptible person inhales droplet nuclei containing M. tuberculosis, which then migrate to the alveoli of the lungs. Usually within two-twelve weeks after initial infection with TB, an immune response prevents further spread, although the bacteria can remain viable in the lungs for years. This condition is a latent infection. Persons with latent TB infection commonly develop a reactive tuberculin skin test, do not demonstrate symptoms of active disease and are not infectious. However, they can develop active disease (recrudescence) later in life.

About 5% of recently infected untreated persons will develop active disease within one to two years. Another 5% will develop active disease later in life. Thus, 90% of persons with latent TB never progress to active TB. Only persons with active TB are contagious and present a risk of disease transmission.

Criteria for diagnosis of active TB vary according to setting. Persons with persistent cough (e.g., lasting two weeks or more) are possible candidates. Common symptoms include fever, night sweats, weight loss, shortness of breath, hemoptysis (coughing blood) and chest pain.

Tests for the diagnosis of TB vary in sensitivity, specificity, speed and cost. The TB skin test is widely used as a screening tool to identify persons that have been recently infected with the TB bacillus. A positive skin test is not an indicator of active infection and a person should not be denied dental treatment based on skin test alone. Additional diagnostic tests such as chest x-rays and sputum smears should be performed and the person evaluated for possible TB infection by a physician. Even with additional tests, culturing of the sputum of the person suspected of being infected is required for definite diagnosis and is essential for drug-susceptibility testing. The sputum smear is inexpensive and quickly performed. However, only 50% - 80% of persons with culture-confirmed pulmonary TB have positive smears. So, smear negative people are involved with 15% - 20% of TB transmissions.

TB is the world's second most common cause of death from infectious disease, after HIV/AIDS. There are an estimated eight million to nine million cases of TB each year. The majority are unreported. One-third of the world's population is infected with TB. Among those infected, approximately 9 million will develop active disease each year. About three-four million are sputum-smear positive, the most infectious form of the disease. In the U.S. in 2007 there were 13,299 cases of TB reported. This is a 3.3% decline in the number of new cases from the previous year.

The global TB caseload appears to be growing slowly overall. Declines have been steady in western and central Europe, North and South America and the Middle East. In contrast, marked increases have occurred in the former Soviet Union and in sub-Saharan Africa. In the former Soviet Union, since 1991 there has been economic decline and general failure at TB control and other health services. Some studies indicate that as much as 10% of new cases involve multiple-drug resistant TB. Resistance is a byproduct of TB emergence in these countries, not the primary cause of it.


General Recommendations

Bolyard EA, Tablan OC, Williams WW, Pearson ML, Shapiro CN, Deitchman SD, Hospital Infection Control Practices Advisory Committee. Guideline for infection control in health care personnel, 1998. Am J Infect Control 1998;26:289--354.

CDC. Guidelines for prevention of transmission of human immunodeficiency virus and hepatitis B virus to health-care and public-safety workers: a response to P.L. 100-607 The Health Omnibus Programs Extension Act of 1988. MMWR 1989;38(suppl No. 6S).

US Department of Labor, Occupational Safety and Health Administration. 29 CFR Part 1910.1030. Occupational exposure to bloodborne pathogens; needlesticks and other sharps injuries; final rule. Federal Register 2001;66:5317--25. As amended from and includes 29 CFR Part 1910.1030. Occupational exposure to bloodborne pathogens; final rule. Federal Register 1991;56:64174--82. Available at

US Department of Labor, Occupational Safety and Health Administration. OSHA instruction: enforcement procedures for the occupational exposure to bloodborne pathogens. Washington, DC: US Department of Labor, Occupational Safety and Health Administration, 2001; directive no. CPL 2-2.69.

US Department of Labor, Occupational Safety and Health Administration. 29 CFR 1910.1200. Hazard communication. Federal Register 1994;59:17479.

CDC. Immunization of health-care workers: recommendations of the Advisory Committee on Immunization Practices (ACIP) and the Hospital Infection Control Practices Advisory Committee (HICPAC). MMWR 1997;46(No. RR-18).

CDC. Updated U.S. Public Health Service guidelines for the management of occupational exposures to HBV, HCV, and HIV and recommendations for postexposure prophylaxis. MMWR 2001;50(No. RR-11).

CDC. Guidelines for preventing the transmission ofMycobacterium tuberculosisin health-care facilities, 1994. MMWR 1994;43(No. RR-13).

Smart ER, Macleod RI, Lawrence CM. Allergic reactions to rubber gloves in dental patients: report of three cases. Br Dent J 1992;172:445--7.

Cleveland JL, Robison VA, Panlilio AL. Tuberculosis epidemiology, diagnosis and infection control recommendations for dental settings: an update on the Centers for Disease Control and Prevention guidelines. J Am Dent Assoc. 2009 Sep;140(9):1092-9.

Kanjirath PP, Coplen AE, Chapman JC, Peters MC, Inglehart MR. Effectiveness of gloves and infection control in dentistry: student and provider perspectives. J Dent Educ. 2009 May;73(5):571-80.

Policy on infection control. American Academy on Pediatric Dentistry Clinical Affairs Committee-Infectious Disease Control Subcommittee; American Academy on Pediatric Dentistry Council on Clinical Affairs. Pediatr Dent. 2008-2009;30(7 Suppl):85.

OSAP. Creating a successful infection control program. Dent Assist. 2008 Nov-Dec;77(6):19-22, 24-6, 30-1.

Smith A, Creanor S, Hurrell D, Bagg J, McCowan M. Management of infection control in dental practice. J Hosp Infect. 2009 Apr;71(4):353-8.

Boyce R, Mull J. Complying with the Occupational Safety and Health Administration: guidelines for the dental office. Dent Clin North Am. 2008 Jul;52(3):653-68.

Herd S, Chin J, Palenik CJ, Ofner S. The in vivo contamination of air-driven low-speed handpieces with prophylaxis angles. J Am Dent Assoc. 2007 Oct;138(10):1360-5.

OSAP.OSAP'S safety and infection control report card. Dent Assist. 2006 Nov-Dec;75(6):6-10.

Basquill LC, Govoni M, Bednarsh H.OSHA--what is its role in dentistry and how do we provide training? Compend Contin Educ Dent. 2005 Mar;26(3 Suppl):10-3.

Palenik CJ. An overview of OSHA training for dentistry. Compend Contin Educ Dent. 2005 Mar;26(3 Suppl):6-8.

Weissenbock, H. (2010). Zoonotic mosquito-borne flaviviruses; Worldwide presence of agents with proven pathogenicity and potential candidates of future emerging diseases. Veterinary Microbiology 140 (3-4), pages 271-280.

Globally Harmonized System of Classification and Labelling of Chemicals(Second revised ed.), New York and Geneva: United Nations, 2007, ISBN 978-92-1-116957-7, ST/SG/AC.10/30/Rev.2 ("GHS Rev.2")

Werner BG, Grady GF. Accidental hepatitis-B-surface-antigen-positive inoculations: use of e antigen to estimate infectivity. Ann Intern Med 1982;97:367--9.

Shapiro CN. Occupational risk of infection with hepatitis B and hepatitis C virus. Surg Clin North Am 1995;75:1047--56.

Cleveland JL, Siew C, Lockwood SA, Gruninger SE, Gooch BF, Shapiro CN. Hepatitis B vaccination and infection among U.S. dentists, 1983--1992. J Am Dent Assoc 1996;127:1385--90.

CDC. Recommendations for preventing transmission of human immunodeficiency virus and hepatitis B virus to patients during exposure-prone invasive procedures. MMWR 1991;40(No. RR-8).

US Department of Labor, Occupational Safety and Health Administration. 29 CFR Part 1910.1030. Occupational exposure to bloodborne pathogens; final rule. Federal Register 1991;56:64004--182.

Cleveland JL, Gooch BF, Shearer BG, Lyerla RL. Risk and prevention of hepatitis C virus infection: implications for dentistry. J Am Dent Assoc 1999;130:641--7.

Gruninger SE, Siew C, Azzolin KL, Meyer DM. Update of hepatitis C infection among dental professionals [Abstract 1825]. J Dent Res 2001;80:264.

Ciesielski C, Marianos D, Ou CY, et al. Transmission of human immunodeficiency virus in a dental practice. Ann Intern Med 1992; 116:798--805.

Ashkenazi M, Fisher N, Levin L, Littner MM. Seroepidemiology of hepatitis C antibodies among dentists and their self-reported use of infection control measures. Community Dent Health. 2009 Jun;26(2):99-103.

Azarpazhooh A, Fillery ED. Prion disease: the implications for dentistry. J Endod. 2008 Oct;34(10):1158-66

Cristina ML, Spagnolo AM, Sartini M, Dallera M, Ottria G, Lombardi R, Perdelli F. Evaluation of the risk of infection through exposure to aerosols and spatters in dentistry. Am J Infect Control. 2008 May;36(4):304-7

Redd JT, Baumbach J, Kohn W, Nainan O, Khristova M, Williams I.Patient-to-patient transmission of hepatitis B virus associated with oral surgery. J Infect Dis. 2007 May 1;195(9):1311-4. Epub 2007 Mar 21. Erratum in: J Infect Dis. 2007 Jun 15;195(12):1874

COST: $0
PROVIDER: American Dental Assistant Association
SOURCE: American Dental Assistants Association |

Learning Objectives:

Upon completion of this course, the dental professional should be able to:

• List and describe microorganisms present in the oral cavity and body fluids.
• Describe how disease can be transmitted within dental environments.
• Describe the importance of microbiology in relation to infection control.
• Describe the natural defenses of the human body against infection.


The author reports no conflicts of interest associated with this work.

Queries for the author may be directed to