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46 Cards in this Set
- Front
- Back
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Dental Caries
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Dental Caries "• Most common infectious disease of human beings
– Main reason for tooth loss – As many as 47% of US population over 65 have lost all of their teeth" |
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Dental Caries
Symptoms |
"– Usually advanced before symptoms arise
– Once symptoms develop they include • Throbbing pain • Noticeable discoloration, roughness or defect in tooth – Tooth can break while chewing" |
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Dental Caries
Causative Agent |
"– Streptococcus mutans most common cause
• Colonize teeth – Cannot colonize mouth • Thrive in acidic conditions – Produce lactic acid from sugar metabolism • Produce glucans from sucrose – Glucans essential for production of dental caries" |
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Dental Caries
Pathogenesis |
"– Begins with adherence of bacteria to specific receptors on teeth
– Production of glucans from dietary sucrose • Glucans bind organisms together and to tooth – Formation of cariogenic plaque • Dietary sugar produces drop in pH – Acidic environment causes calcium phosphate in teeth to dissolve, which creates pits and fissures for colonization" |
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Dental Caries
Epidemiology |
"– Worldwide distribution
• Incidence varies – Mainly on availability of dietary sucrose and dental care – Heredity significant factor – Young people more susceptible than old • Pits and fissures wear down with age" |
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Dental Caries
Prevention |
"– Restriction of dietary sucrose
• Most important preventative – Fluoride required for teeth to resist acid • Makes tooth enamel harder – More resistant to dissolving in acid" |
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Dental Caries
Treatment |
"– Mechanical removal of plaque via tooth brushing and dental floss
• Reduces incidence by approximately 50% – Pits and fissures prevented by application of sealant – Treatment of caries requires drilling out cavity and filling (with amalgam, composite)" |
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Periodontal Disease
Symptoms |
– Majority of cases asymptomatic
– Common symptoms • Bleeding gums • Gum sensitivity • Bad breath • Teeth become loose and discolored • Receding gums |
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Periodontal Disease
Causative Agent |
– Caused by dental plaque
• Plaque forms at area where gum joins the teeth – Numerous bacteria reside in plaque |
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Periodontal Disease
Pathogenesis |
– Plaque forms on teeth at gum line often referred to as tartar
• Extends into gingival crevice • Inflammation occurs known as gingivitis – Progression results from enzymes released from organisms that weaken gingival tissue • Causes gingival crevice to widen and deepen – Gram-negative organisms increase and release exotoxins • Exotoxins attack host tissue – Membranes and bone softens » Tooth may be lost |
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Periodontal Disease
Epidemiology |
– Mainly disease of individuals over 35 • 90% of those over 65 have some periodontal disease
• People with underlying immunodeficiency often have severe disease |
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Periodontal Disease
Prevention and treatment |
– Careful flossing and brushing
• Combined with semi-annual polishing and cleaning – Treated by cleaning out inflamed gingival crevice and removing plaque – In advanced cases surgery is usually required • To expose root of teeth for cleaning |
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Trench Mouth
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• Also known as Vincent’s disease or acute necrotizing ulcerative gingivitis
– ANUG • Condition distinct from other forms of periodontitis • Disease rampant during World War I – Soldiers in trenches unable to attend to proper mouth care |
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Trench Mouth
Symptoms |
– Abrupt onset
– Fever – Bleeding and painful gums – Foul odor |
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Trench Mouth
Causative Agent |
– Oral spirochete from Treponema genus
– Bacteria most likely work synergistically with other anaerobic bacteria of mouth |
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Trench Mouth
Pathogenesis |
– Precise mechanism unknown • Presumed to act with other bacteria to destroy tissue
– Plaque is always present – Bacterial invasion causes necrosis and ulceration • Mainly of gums between teeth |
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Trench Mouth
Prevention and Treatment |
– Control directed at daily brushing and flossing • With semi-annual cleaning
– Antibacterial treatment directed at spirochetes and anaerobic bacilli • Relives acute symptoms • Must be followed up with extensive plaque removal |
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Trench Mouth
Epidemiology |
– Can occur at any age
• Arises in association with poor dental hygiene – Stress, malnutrition or immunodeficiency may contribute – Disease not contagious |
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Herpes Simplex
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– Many manifestations • Most common form begins
in mouth and throat – Infection persists for life – Virus transmissible with saliva – Disease usually insignificant • BUT: Disease can be fatal in immunodeficiency |
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Herpes Simplex
Symptoms |
– Typically begin during
childhood – Common symptoms include • Fever and blisters – First lesions which lead to ulcers • Ulcers in mouth and throat – Generally painful – Heal without treatment – After healing disease becomes latent – Symptom recurrence usually begins on the lips • Marked by tingling, itching, burning or painful sensation |
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Herpes Simplex
Causative Agent |
– Herpes simplex virus (HSV)
• Medium-sized • Enveloped • Double-stranded DNA genome • Two types – HSV 1 » Occurs mainly on the lips and mouth – HSV 2 » Responsible for most genital infections |
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Herpes Simplex
Pathogenesis |
– HSV 1
• Virus multiplies in epithelial cells of mouth or throat • Blisters form – Blisters contain large numbers of mature virions • Some virions carried to lymph vessels and nodes – Immune response produced limits infection • Some virions enter sensory nerves as latent virus – Latent virus can become infectious • Viruses are carried by nerves to skin or mucous membranes – Viruses produce recurrent disease – Stress can precipitate recurrences |
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Herpes Simplex
Epidemiology |
– Extremely widespread
• Infects 90% of some US inner-city populations • Estimated 20% to 40% of Americans suffer from recurrent disease – Transmitted by close physical contact • Virus can survive for several hours on plastic and cloth • Greatest risk of transmission is contact with lesion or infected saliva |
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Herpes Simplex
Prevention and Treatment |
– Antivirals such as acyclovir have proved effective in treatment
• Prevents DNA replication • Medications do not affect latent viruses |
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Hepatatis A
Pathogenesis |
– Transmission from ingestion of contaminated food or water
– Ingested virus reaches liver by unknown route • Liver main site of viral replication • Only tissue know to be damaged – Virus is released into bile • Virus-laden bile eliminated in feces |
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Hepatatis A
Epidemiology |
– Spreads via fecal-oral route
– Many outbreaks originated from restaurants • Due to infected food handler – Raw shellfish frequent source of infection – Low socioeconomic groups make up high percentage of infected – High risk groups include people in day care and nursing homes and homosexual men |
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Hepatatis A
Causative Agent |
– Hepatitis A virus (HAV)
– Small – Single-stranded RNA genome – Belongs to picornavirus family – Given name hepatovirus – Only one serotype • Makes good target for vaccine |
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Hepatatis A
Prevention and Treatment |
– Vaccine available since 1995
• Indicated for travelers to deprived regions, homosexual men, sewer workers and healthcare workers – Gamma globulin contains HAV antibody, can be given to individuals that have been exposed • Afford short term protection if given within 2 weeks of exposure |
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Hepatatis B
Symptoms |
– Similar to hepatitis A
• Symptoms for hepatitis B more severe – Causes death in 1% to 10% of hospitalized cases – Formerly known as serum hepatitis |
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Hepatatis B
Causative Agent |
– Hepatitis B virus (HBV)
• Double-stranded DNA genome • Enveloped • Part of the hepadnavirus family • Virus contains 3 important HBV antigens – HBsAg » Surface antigen – HBcAg » Core antigen – HBeAg » e antigen |
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Hepatatis B
Pathogenesis |
– HBV carried in liver
– Mechanism of liver damage unknown • Damage most likely results from immune response – Virus replicates via reverse transcriptase • Viral DNA transported to host nucleus • Host mRNA makes RNA copy • RNA copy transcribed by viral reverse transcriptase – New DNA copy is genome for new virus – New viruses bud from host cell HBV |
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Hepatatis B
Epidemiology |
– Progressive rise in reported cases between 1965 and 1985
• Incidence appears to have plateaued – HBV spread mainly by blood, blood products and semen – Carriers are of major importance • Often unaware of infection – Risk factors for infection include • Sharing needles • Tattooing and piercing with contaminated instruments • Shared toothbrushes, razors and towels – Sexual intercourse responsible for nearly 50% of cases in United States |
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Hepatatis B
Prevention and Treatment |
– Vaccine approved in 1980s
• New more effective vaccine available since 1986 • Vaccination against HBV can help prevent liver cancer caused by the virus – Passive immunization with HBIG (hepatitis B immune globulin) offers immediate protection – No curative treatment |
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Hepatitis C
Symptoms |
– Same as hepatitis A and hepatitis B
• Generally milder • 65% are asymptomatic • 25% have jaundice |
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Hepatitis C
Causative Agent |
– Hepatitis C virus • Enveloped
• Single-stranded RNA genome • Member of flavivirus family • Considerable genetic variability – Virus divided into type and subtype |
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Hepatitis C
Pathogenesis |
– Few details known
– Infection transmitted via contact with infected blood – Incubation period average 6 weeks – Over 80% develop chronic infections – Virus infects the liver • Incites inflammatory and immune responses – Disease comes and goes • Individuals have times of near normalcy – 10% to 20% will develop cirrhosis or liver cancer |
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Hepatitis C
Epidemiology |
– Mechanism of exposure not
always obvious – Risk factors include • Sharing toothbrush, razors, towels • Tattooing and piercing with unclean instrument • Sharing syringes – 60% of US cases due to sharing needles – Transmission via intercourse most likely rare • Can occur if multiple partners |
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Hepatitis C
Prevention and Treatment |
– No vaccine for HCV
• Vaccination against A and B seem to give some protection – Avoidance of alcohol to limit effect on liver – No satisfactory treatment • Some are helped by interferon therapy – Often has undesirable side effects – Interferon usually combined with ribavirin |
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Mumps
Pathogenesis |
– Transmitted by inhalation of infected droplets
– Long incubation period • 15 to 20 days – Virus reproduces in the upper respiratory tract • Virus spreads throughout body via bloodstream • Produces symptoms after infecting tissues – In salivary glands • Virus multiplies in epithelium of salivary ducts – Destroys epithelium and releases virus into saliva • Inflammation produced – Inflammation responsible for symptoms and pain |
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Mumps
Epidemiology |
– Humans only natural host
– Natural infection confers lifelong immunity – Virus is spread by asymptomatic individuals in high numbers – Virus can be present in saliva of symptomatic persons • Virus may be present for up to a week before symptoms appear to 2 weeks after |
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Mumps
Prevention and Treatment |
– Prevention directed at immunization
• Usually given in same injection as measles and rubella – MMR • Immunization prevents latent recurrent infections – Due to only one viral serotype – No effective antiviral treatment |
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Helicobacter pylori Gastritis
Symptoms |
– Range from belching
to vomiting – Most are asymptomatic – Symptoms occur when infection is complicated with ulcers or cancer – Symptoms include • Abdominal pain • Tenderness • Bleeding |
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Helicobacter pylori Gastritis
Causative Agent |
– Helicobacter pylori • Short
• Spiral • Gram-negative • Microaerophile • Multiple polar flagella |
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Helicobacter pylori Gastritis
Pathogenesis |
• Pathogenesis
– Bacteria survive extreme acidity of the stomach • Able to neutralize environment – Organism uses flagella to corkscrew through mucosal lining – Inflammatory response begins – Mucus production decreases • Without mucus stomach lining not protected from acidic environment – Infection persists for years • Possibly for a lifetime |
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Helicobacter pylori Gastritis
Epidemiology |
– Infections tend to cluster in
families – Transmission most likely fecal-oral route • Flies also capable of transmission – 20% of US population infected • Incidence increases with age – Almost 80% of those over 75 infected • Rates highest in lower socioeconomic groups |
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Helicobacter pylori Gastritis
Prevention and Treatment |
– No proven prevention
measures – Infection can usually be eradicated with combined antibiotic treatment • Medication is also used to inhibit production of stomach acid |
