1. Infectious Diseases
&
Infection Control
In Dentistry

2. Types of Microorganisms
Pathogenic (causing disease)
Potentially Pathogenic
Non-Pathogenic
Some infections only occur in individuals who are immunocompromised because their immune system is unable to fight the potential pathogen. These are called opportunistic infections.

3. How do Infections Occur?
Pathogens
Virus
Bacteria
Fungi
Protozoa
Rickettsia
Helminthes
Since a number of diseases can be transmitted during routine dental care, it is important to understand the principles behind the infection control
Body has normal resistance to most pathogens

4. How are diseases transmitted in the dental setting?
From the patient to the dental worker
From the dental worker to the patient
From one patient to another
From the dental office to the community
Transmission can be…
Direct- from an infected person to another person who is not immune
Indirect- from contact with objects that are contaminated, like surfaces or instruments
Droplet-from spray or splatter contact with mucous membranes, or contact with aerosols (stay suspended in the air for longer periods of time)

5. For Infection to Occur…
Pathogen
Quantity
Vulnerability
Entry Site/Mode

6. The Process of Infection
7. Termination
The Process of Infection
6. Recovery or
Relapse
5. Clinical Stage
4. Prodormal
Period
3. Incubation
Period
2. Infection
1. Exposure

7. Recommendations for Adult Immunizations
Diphtheria , Polyomyelitis , Tetanus ( DPT )
Hepatitis B
Hepatitis A ? ? ?
Measles, Mumps and Rubella ( MMR )
Varicella (Chickenpox) ?
Meningococcal Disease ?
Influenza ?
Pneumococcal Disease ?

8. Infectious Diseases for Dentist
Common Cold
Influenza
Herpes simplex
Mononucleosis
Meningitis
Group A and Group B Strep Infection
Staphylococcus aureus Diseases
Tetanus
Anthrax
New Infectious Treats

9. Common Cold Facts Spring & Summer Colds Treatments for the Common Cold
There are 200 distinct cold viruses.
Spring & Summer Colds
Rhinoviruses causing symptoms above the neck
Stuffy nose, headache and runny nose.
Treatments for the Common Cold
Ibuprofen
Antihistamines
Watch for drowsiness
Individuals with hypertension , diabetes, heart disease, or thyroid disorders should limit products containing pseudoephedrine.

10. Influenza ( Flu ) Facts
The flu causes more severe, longer lasting symptoms than a cold.
Influenza A and influenza B.
Transmission
The flu is very contagious and is spread by coughs, sneezes, laughs, and even normal conversation.
Vaccinations : Annually
Antiviral Drugs Relenza and Tamiflu

11. Student Snapshot – Colds and Flu on Campus
Student Snapshot, p. 402 11

12. Individuals Who Should Get FluVaccine
Individuals aged 65 years and older.
Individuals aged 2 to 64 years with chronic health conditions.
Children aged 6 to 23 months.
Pregnant women.
Health-care personnel
Household contacts and caregivers.

13. Herpesviruses Large family; 8 infect humans
HSV-1 –Herpes simplex 1 – Herpes Labialis , Whitelows
HSV-2 –Herpes simplex 2 – Genetal Herpes , Encephalitis
VZV – Varicella zoster virus - Chicken pox ,Shingles
EBV – Epstein-Barr virus –I.M , Burkitt Lymphoma
HHV-6 –Herpevirus 6 –Roseola Infantum
HHV-7 –Herpevirus 7 - ? No disease assocciation
HHV-8 –Herpevirus 8 – Kaposi Sarcoma 13 13

14. 14 14

15. Oral-Facial Herpes Acute Gingivo stomatitis
Acute gingivostomatitis is the commonest manifestation of primary herpetic infection.
The patient experiences pain and bleeding of the gums mm ulcers with necrotic bases are present.
Neck glands are commonly enlarged accompanied by fever.
Usually a self limiting disease which lasts around 13 days.
Herpes labialis (cold sore)
Following primary infection, 45% of orally infected individuals will experience reactivation. The actual frequency of recurrences varies widely between individuals.
Herpes labialis (cold sore) is a recurrence of oral HSV.
A prodrome of tingling, warmth or itching at the site usually heralds the recurrence. About 12 hours later, red­ness appears followed by papules and then vesicles.

16. H. Labialis ( Cold Sore )

17. Herpetic whitlows 17 17

18. HHV – 6 : Roseala Infantum

19. HHV – 8 : Kaposi Sarcoma
Originally isolated from cells of Kaposi’s sarcoma (KS)
Now appears to be firmly associated with Kaposi’s sarcoma
Most patients with KS have antibodies against HHV-8

20. Diagnosis, Treatment, and Control of Herpes Simplex
Vesicles and exudate are typical diagnostic symptoms
Scrapings from base of lesions showing giant cells
Culture and specific tests for diagnosing severe or disseminated HSV
Direct fluorescent antibody tests
Treatment: Acyclovir, Famciclovir, Valacyclovir; Topical medications 20 20

21. Parvoviruses . B . 19
B19 cause of erythema infectiosum (fifth disease); rash of childhood (“slapped face” )
Children may have fever and rash on cheeks
Severe fatal anemia can result if pregnant woman transmits virus to fetus 21 21

22. Varicella Zooster Virus
Primary infection results in varicella (chickenpox)
Incubation period of days
Presents fever, lymphadadenopathy. a widespread vesicular rash.
The features are so characteristic that a diagnosis can usually be made on clinical grounds alone.
Complications are rare but occurs more frequently and with greater severity in adults and immunocompromised patients.
Most common complication is secondary bacterial infection of the vesicles.
Severe complications which may be life threatening include viral pneumonia, encephalititis, and haemorrhagic chickenpox.

23. Varicella Zooster Virus
Varicella (chickenpox) and herpes zoster (shingles) are distinct clinical entities cause by the varicella-zoster virus (VZV).
In young children, prodromal symptoms of chickenpox are uncommon, but in older children and adults, the manifestation of the rash may be preceded by two or three days of fever and chills, malaise, headache, backache, sore throat, and dry cough.
The rash begins on the face and scalp and spreads rapidly to the trunk, with relative sparing of the extremities.
New lesions arise in crops, usually appearing centrally. Each crop proceeds through the developmental phase described below, so that at any given time, a patient can have macules, papules, vesicles, pustules, and crusts. (Scarring is rare )
In smallpox, by contrast, at any given time, all lesions on the patient's body are in the same phase of development.

24. Chicken Pox - Rash

25. Chicken Pox - Rash

26. Differential Dx - Chickenpox
Begins on the face and scalp, spreads to the trunk
Lesions in various stages of development can simultaneously be present on the patient's skin
Variola (Smallpox)
Begins centrally, then spreads outward to face and extremities
All lesions are always in a single stage of development

27. Treatment & Preventive Care
More severe form in adults
May cause pneumonia, disseminated infection in adults
Handwashing
Isolation of children from public places until lesions are crusted and dry
Antivirals to lessen symptoms mostly in adults
HCW with out past exposure to chickenpox may consider chickenpox vaccine
Varicella zoster immune globulin recommended if pregnant and with a substantial exposure

28. Herpes Zoster (Shingles)
Herpes Zoster mainly affect a single dermatome of the skin.
It may occur at any age but the vast majority of patients are more than 50 years of age.
The latent virus reactivates in a sensory ganglion and tracks down the sensory nerve to the appropriate segment.
It is characterized by unilateral radicular pain and a vesicular eruption that is typically limited to one or two dermatomes innervated by a spinal or cranial nerve.
The most distinctive characteristics of herpes zoster are its localization and it distribution, which is almost always unilateral.
There is a characteristic eruption of vesicles in the dermatome which is often accompanied by intensive pain which may last for months (postherpetic neuralgia)
Herpes zoster affecting the eye and face may pose great problems.
As with varicella, herpes zoster in a far greater problem in immunocompromised patients in whom the reactivation occurs earlier in life and multiple attacks occur as well as complications.
Complications are rare and include encephalitis and disseminated herpes zoster.

29. Relationship between varicella and zoster29 29

30. Herpes Zoster (Shingles)

31. Epstein-Barr Virus (EBV)
Transmission – direct, oral contact and contamination with saliva
In industrialized countries, college-age population is vulnerable to infectious mononucleosis (mono or kissing disease)
By mid-life, 90-95% of all people are infected
Infectious mononucleosis – sore throat, high fever, cervical lymphadenopathy; develop after day incubation
Dormancy in B cells; reactivated; may be asymptomatic 31 31

32. Disease Association 1. Infectious Mononucleosis 2. Burkitt's lymphoma
3. Nasopharyngeal carcinoma
4. Lymphoproliferative disease and lymphoma in the immunosuppressed.
5. Oral leukoplakia in AIDS patients

33. Infectious Mononuclosis
Primary EBV infection is usually subclinical in childhood. However in adolescents and adults, there is a 50% chance that the syndrome of infectious mononucleosis (IM) will develop.
IM is usually a self-limited disease which consists of fever, lymphadenopathy and splenomegaly. In some patients jaundice may be seen which is due to hepatitis.
Atypical lymphocytes are present in the blood.
Complications occur rarely but may be serious e.g. splenic rupture, meningoencephalitis, and pharyngeal obstruction.
In some patients, chronic IM may occur where eventually the patient dies of lymphoproliferative disease or lymphoma.
Diagnosis of IM is usually made by the heterophil antibody test and/or detection of EBV IgM.
There is no specific treatment.

34. Tumors Associated with EBV
Burkitt lymphoma – B cell malignancy; usually develops in jaw and grossly swells the cheek; central African children 4-8 years old; may be associated with chronic coinfections with malaria, etc.
Nasopharyngeal carcinoma – malignancy of epithelial cells; occurs in older Chinese and African men
Anyone with an immune deficiency is highly susceptible to EBV 34 34

35. Epstein-Barr Virus 35 35

36. Diagnosis, Treatment, and Prevention
Differential blood count shows lymphocytosis, neutropenia, and large atypical lymphocytes; serological assays to detect antibodies and antigen
Treatment directed at relief of symptoms of fever and sore throat
Disseminated disease may be treated with IV gamma globulin, interferon, acyclovir, and monoclonal antibodies 36 36

37. Skin Structure Infections by Site
Compartment
Epidermis
Dermis
Hair follicle
Subcutan.
fat
Fascia
Muscle
(Pseudomonas aeruginosa)
myositis
Clostridia, Strep. pyogenes

38. Staphylococcus aureus : Diseases
Pyoderma : pyogenesis in the (skin)
Impetigo - multiple pustules with erythematous base on face and extremities
Furuncles - large, painful, nodules filled with pus and necrotic tissue = boil
Carbuncles - multiple boils which coalesce in deep subcutaneous tissue
Wound infections - erythrema, edema, pain in/around wounds
Bacteremia - bacteria in the blood from other infections sites
Osteomyelitis - infection of highly vascularized area of bone
Endocarditis - infection of the endocardium
Toxic shock syndrome
Scalded skin syndrome
Food poisoning
intoxication
Pneumonia - response to the presence of bacteria in the lungs

39. Folliculitis, Furuncle, Carbuncle, and Cutaneous Abscess
Folliculitis is characterized by the formation of a circumscribed, conical pustule around a hair follicle.
A furuncle is a deep, necrotizing form of folliculitis, with pus accumulation. Several furuncles may coalesce to form a carbuncle.
A carbuncle is larger than a furuncle, typically occurring at the nape of the neck or on the back or thighs. The lesion is red, indurated, painful, and multiple pustules soon appear on its surface, draining around multiple hair follicles. The lesion develops a yellow-gray crater at the center and heals slowly by granulation.
An abscess (boil) is a localized accumulation of purulent material deep in the dermis or subcutaneous tissue. Pus may not be visible on the surface of the skin. An abscess is warm, red, and tender; it frequently begins as folliculitis.
Most furuncles and carbuncles are caused by Staphylococcus aureus. Fever and malaise sometimes accompany carbuncles and abscesses.
A furuncle starts as a hard, tender, red nodule in hair-bearing skin that enlarges and becomes painful and fluctuant. Rupture may occur with drainage of pus. The pain then subsides, and the redness and swelling subside over several days or weeks.

40. Impetigo

41. Furuncle

42. Carbuncle

43. Streptococcus pyogenes
Group A Streptococcal Diseases
Pharyngitis- suppurative erythematous inflammation of the pharynx
sore throat with exudate and cervical lymphadenopathy
accompanied by fever, malaise and headache
also known as “strep throat”
Scarlet fever - pharyngitis with diffuse erythematous rash on head/extrem
rash blanches when pressed, raw red tongue= strawberry tongue
no rash around mouth or palms/soles
Pyoderma - purulent(pus forming) lesions on face, arms, and legs
vesicles fill with pus, rupture, and crust over
Erysipelas - acute infection of the skin with fever, chills, leukocytosis
inflamed areas is distinctly raised from uninfected skin
Cellulitis - localized inflammation of subcutaneous tissues
accompanied by fever, chills, leukocytosis

44. Streptococcus pyogenes
Group A Streptococcal Diseases
Necrotizing fasciitis - infection of deep subcutaneous tissues
extensive destruction muscle(gangrene) and fat
spreads along facial planes
often results in systemic toxicity, organ failure, and death
Streptococcal toxic shock syndrome – multi system toxicity
begins with localized soft tissue inflammation and pain
accompanied by fever, chills, malaise, vomitting, diarrhea
toxicity causes liver, heart, and lungs to fail
patient is bacteremic and often has necrotizing faciitis
Bacteremia - beta hemolytic streptococci in the blood
accompanies necrotizing faciitis and toxic shock syndrome
does not occur with pharyngitis, pyoderma, or erysipelas
Rheumatic fever - nonsuppurative sequalae to group A Strep infection
inflammatory changes in heart, joints, blood vessels, and subcutaneous
chronic progressive damage to the heart valves often occurs
Glomerulonephritis - nonsuppurative sequalae to group A Strep infection
acute inflammation of glomeruli
accompanied by edema, hypertension, hematuria, and proteinuria

45. Impetigo Group A streptococcus, Staphylococcus arueus
Superficial blistershoney colored crusts on erythematous base
No systemic signs
Mainly in children
May be associated with glomerulonephritis
Treat with penicillin/antistaphylococcal penicillin

46. Cellulitis
Deeper infection usually involving skin and subcutaneous tissue
Erythema, pain and swelling often with distinct border (erysipelas)
Fever and lymphangitis or adenitis common
Gp A streptococcus, Staphylococcus aureus most common
Treat with antistaphylococcal penicillin unless culture positive

50. Necrotizing Fasciitis
Streptococcal gangrene (Gp A strept)
Deeper infection involving fascia and often muscle
Extreme toxicity and rapid spread (“flesh-eating virus”)
May have associated toxic shock
Treatment – surgical removal of necrotic tissue and antibiotics
Penicillin and clinidamycin

51. Streptococcus pyogenes
Diagnosis of Streptococcal Diseases
Symptoms
Pharyngitis - with or without tonsillar exudate
Fever, rash, inflammation or swelling
Laboratory Tests
Gram stain from specimen or culture
Culture
Antigen detection (microantigen)
Detect group specific C-carbohydrate in throat cultures
React antigen with antibody bound to membrane or latex particles
Antibody detection
Anti-streptolysin O (ASO test) indicates recent( 3-4 wks) streptococcal infection and helps confirm rheumatic fever or acute glomerulonephritis
Anti-DNase B - helps confirm pyoderma or pharyngitis associated with glomerulonephritis

52. Characteristics of Pharyngitis
Agent
Exudate
Lymph nodes
Treatment
Gp A strept +
Submandibular
Penicillin
Viral -
None
C. Diphtheriae
Membrane
“Bull neck”
Antitixon
Erythromycin, Penicillin
Infectious mononucleosis
Diffuse

53. Food Poisoning Agent Mechanism Incubation Clinical S. Aureus
Enterotoxin
1-8 h
Nausea, vomiting, diarrhea
B. Cereus
Toxin
4 h
Diarrhea
Clostridium perfirngens
Sporulation toxin
8-16 h
Salmonella
12-48 h
Fever, pain and diarrhea

54. Infectious Diarrhea Fever Enterotoxin E. Coli - V. cholerae Invasive
Salmonella +
Shigella
C. jejuni
E. coli O157:H7
Y. Enterocolitica

55. Meningitis - An Emergency
Etiology
Viral
Pneumococcus
Haemophilus influenzae
Meningococcus
Listeria
Coccidioides immitis
Diagnosis LP
Blood cultures (BEFORE antibiotics) - very important
CT scan in selected patients

56. MENINGOCOCCAL MENINGITIS

57. Meningococcal Diseases
Prevention
Eradicate the pool of healthy carriers
those identified can be treated prophylactically with antibiotics
also exposed susceptible(s) can be treated chemoprophylactically
polysaccharide vaccines exist for some serogroups
Treatment
Antibiotic treatment if started earlier can alter the course of the disease
mortality approaches 100% in untreated cases
Penicillin(s) are currently agents of choice
antibiotic resistant strains have begun to occur

58. Viral infections of the (CNS)
Clinical syndrome
Part of CNS affected
Encephalitis
Brain Parenchyma
Aseptic meningitis
Meninges
Myelitis
Spinal Cord
Neuritis
Peripheral Nerves

59. Common symptoms of Encephalitis
Lethargy
Sudden fever
Headache
Change in consciousness
Irritability or restlessness
Tremors or convulsions
Vomiting and diarrhea

60. Encephalitis vs.V. Meningitis
Viral Meningitis
Constitutional symptoms
Fever
Yes
Headache, nausea, vomiting, lethargy
Photophobia, neck stiffness No
Neurologic dysfunction
Seizures
Minimal
Cranial nerve palsies, paralysis
Altered mental status (i.e. confusion, coma)

61. Differentiating Viral from Bacterial
Viral Meningitis
CSF clear to cloudy
↑ initial pressure
↑ protein
normal glucose
↑ cells (not over 1000/mcL, polys on day 1, then more lymphs)
a specific virus is incriminated by rising titer after patient is better
Bacterial Meningitis
CSF clear to purulent
↑ initial pressure
↑ protein
↓ glucose
↑ polys (often more than 1000/mcL)
↑ lymphs (some, typically after treatment)
positive gram stain, culture, and/or meningitis antigens

62. New Infectious Threats
Severe Acute Respiratory Syndrome (SARS)
Avian Flu
Swine Flu
Bioterror Threats
Anthrax
Smallpox
Botulism
Tularemia

63. Anthrax – Bacillus anthracis
Gram positive, spore-forming rod with capsule ,Spores in soil, or animal products
Enter through skin, alimentary, respiratory tracts
Toxin: (cyclase), lethal factor
Painless ulcer with marked local edema
Pneumonia (mediastinitis) meningitis
Necrotizing enteritismeningitis
Diagnosis-culture
Treatment: ciprofloxacin+clindamycin+rifampin, penicillin if susceptible

64. Cutaneous Anthrax

65. TETANUS Diseases caused by Clostridium tetani
Incubation period is usually 3-21 days.
tetanus maximum sustained contraction of skeletal muscles
Generalized most common form involving masseter muscles, back contractions, cardiac arrhythmias, profuse sweating
Cephalic : primary site of infection is the head
Localized : symptoms confined to musculature at site of infection
Death is most often due to paralysis of the respiratory muscles.
Basis of Virulence
Tetanospasmin
Neurotoxin blocks release of inhibitory neurotransmitters causing unregulated excitatory synaptic activity in motor nerves
plasmid-encoded, heat labile
A-B toxin, released upon cell lysis, binds irreversibly
Tetanolysin
oxygen-labile hemolysin

66. TETANUS DIAGNOSIS MODE OF TRANSMISSION
Tetanus spores are introduced into the body, usually through a puncture wound contaminated with soil or feces.
Incubation period of usually 3-21 days.
DIAGNOSIS
The diagnosis of tetanus is made by observation of uncontrolled contraction of skeletal muscle, following puncture wounds, burns, or trauma to body parts.
The organism is rarely recovered from the site of infection, and usually there is not detectable antibody response.

67. TETANUS Prevention of Tetanus Treatment of Tetanus
Proper treatment of deep puncture wounds
clean and disinfect the wound
stop the bleeding
keep aerobic
Immunization
basis in artificial active immunity
vaccine contains tetanus toxoid inactive/antigenic tetanospasmin
given in the polyvalent vaccine, DPT or DT
Treatment of Tetanus
Antitoxin (TIG). Artificial passive immunity
Antibioitic

68. IMMUNIZATIONS
Vaccination series for 1 to 3 month old babies consists of 3 injections given 2 months apart as part of DPT.
A booster dose about 1 and 4 years later.
Children immunized have protection for 10 years.
Additional booster dose every 10 years.

69. Botulinum Food Poisoning
Diseases caused by Clostridium botulinum
Botulism: bilateral descending weakness of peripheral muscles terminating with respiratory paralysis
other symptoms = Blurred vision, dry mouth, constipation, abdominal pain
Food borne intoxication
Wound botulism same symptoms
due to infection in soil contaminated wounds
Basis of Virulence
botulinum toxin(s)
binds specifically to cholinergic nerves
blocks the release of acetylcholine at peripheral synapses
A-B toxin with seven antigenic variants- A, B, E, F, are most common
binds irreversibly

70. Clostridium botulinum
Epidemiology of botulism
common source food borne poisoning of the intoxication type
commonly associated with water-based canned foods
home canned foods account for 85% of botulism cases
commercially canned foods for 15% of botulism cases
some cases involve other types of foods
Prevention of botulism
sterilization of water-based canned foods
freezing
avoid giving honey to infants
Treatment of botulism
Botulism antitoxins, A, B, E, artificial passive immunity
Gastric lavage

71. Clostridium perfringens : Gas Gangrene
Diseases/Infections involving Clostridium perfringens
Gas gangrene (myconecrosis) : Extensive muscle necrosis
Soft tissue infections(cellulitis) : Organism grows in the fascial planes
Food poisoning :Abdominal cramps and diarrhea
Necrotizing enteritis : Acute necrosis of the jejunum
Septicemia : Generally not significant
Basis of Virulence
alpha toxin : Lecithinase, hemolytic, >vascular permeability
a lecithinase, zinc metallophospholipase, hydrolyzes the phosphatylcholine and sphingomyelin in eucarytoic cell membrane = cell death
Clostridium group A toxin responsible for myonecrosis
beta toxin : Necrosis, causes release of catecholamine
iota toxin : Necrosis and increased vascular permeability
Enterotoxin : Cytotoxic, alters membrane permeability

72. Clostridium perfringens
Epidemiology
Portal of Entry integument via wounds, gastrointestinal tract via ingestion of endospores
Example meat, fish, or poultry containing endospores is cooked; spores are not killed; food is incubated at warm(room) temperature and spores germinate; if food is not adequately reheated, vegetative cells are ingested and sporulate in the intestine; This sporulation process releases the enterotoxin
Prevention
rapid and adequate treatment of wounds
debridement
keep aerobic
refrigerate high risk foods to prevent spores from germinating

73. Clostridium difficile
Diseases caused by Clostridium difficile
antibiotic associated colitis
antibiotic associated pseudomembranous colitis
Basis of Virulence
enterotoxin - stimulates neutrophil chemotaxis, cytokine release with accompanying inflammation, hypersecretion of fluid, and hemorrhagic necrosis
cytotoxin - depolymerizes actin, thus destroying the cellular cytoskeleton
adhesin factor mediates binding to colonic cells, esp ileum
hyaluronidase hydrolyzes intestinal hyaluronic acid
spore formation past for long term survival
Epidemiology of Antibiotic-associated enterocolitis
This is an example of opportunism
Clostridium difficile is part of the normal microflora in many healthy and hospitalized people
In most people it is sufficiently antagonized and its endospores are latent
Many antibiotics, especially those taken orally, kill the antagonistic microflora, thus allowing this organism to germinate and grow
Prevention
This condition is difficult to prevent
The organism is common in hospitals
Antibiotics are necessary to control other infections

74. Mucormycosis
DM (DKA), leukemia/neutropenia, transplant, deferoxamine therapy
Rhinocerebral Mucormycosis
Fever, sinus/facial pain/edema, H/A, CN palsies, retinal vein thrombosis, cavernous sinus thrombosis
Surgical debridement & Amphotericin B: Posaconazole (60% response rate)