Emerging/Reemerging Diseases: Update 2003: Emerging/Reemerging Diseases: Update 2003 Louis G. DePaola, DDS, MS Professor
Department of Diagnostic Sciences and Pathology
Dental School
University of Maryland Baltimore
Emerging Infectious Diseases/Agents in the USA, 2003: Emerging Infectious Diseases/Agents in the USA, 2003 Chlamydia
Diphtheria
Encephalitis
West Nile
St. Louis
E. coli
N gonorrhea
H. Influenzae
Hantavirus Hepatitis A-G
Human herpes viruses
HHV 1-8
HIV/AIDS
Human papilloma viruses
Influenza
Emerging strains
Legionella pneumophila
Lyme Disease
Emerging Infectious Diseases/Agents in the USA, 2003: Emerging Infectious Diseases/Agents in the USA, 2003 Measles
Meningococcus
MRSA/VRSA
Pertussis
Poliomyelitis
Rabies
Rocky Mt. Spotted Fever
Rubella
SARS
Severe Acute Respiratory Syn
Salmonellosis
Shigellosis
S. pneumoniae
Syphilis
Tetanus
Toxic-Shock Syndrome
Tuberculosis
Vaccinations Prevent Disease: Vaccinations Prevent Disease
Immunization Programs : Immunization Programs National guidelines for immunization of, and PEP for, HCP, which includes DHCP, are provided by the US Public Health Service’s Advisory Committee on Immunization Practices
ACIP, CDC/ACIP 1997 and 2001
Based on studies of health-care infections, susceptible HCP are considered to be at occupational risk for acquiring:
HBV or HCV infection,
And at risk for acquiring or transmitting influenza, measles, mumps, rubella, and chicken pox (varicella).
The ACIP recommends that all HCP be vaccinated or have documented immunity to all vaccine-preventable diseases
HBV
Influenza
MMR
Varicella
Immunization Programs : Immunization Programs Immunizations are an essential part of prevention and infection control programs for DHCP and dental health-care facilities are encouraged to formulate a comprehensive immunization policy.
These policies should include a checklist of required and recommended vaccinations for specific job categories, including:
Immunization Programs : Immunization Programs Appropriate vaccination and booster schedules;
Determination of the immune status of newly hired employees;
And considerations for DHCP unable or unwilling to be vaccinated as required or recommended.
Policies also should reflect the regulations and recommendations on the vaccination of HCP established by individual states and professional organizations
Vaccine Preventable Diseases Adults: Vaccine Preventable Diseases Adults Diphtheria**
Hepatitis A
Hepatitis B
Influenza**
Lyme Disease
Measles*
Haemophilis influenza type B (Hib)
Mumps*
Pneumococcus**
Polio
Rubella*
Tetanus**
Varicella* * May not be needed if certain conditions are met ** Very important in adults over 65 www.cdc.gov, 2/4/2002
Vaccination of Pregnant Women: Vaccination of Pregnant Women Risks are largely theoretical
Generally live-virus vaccines contraindicated
Benefit of vaccination outweighs risk if:
Risk for exposure to disease is high
Infection poses a risk to fetus
Vaccine is unlikely to cause harm
Acceptable
Hepatitis B
Influenza
Tetanus/Diphteria
Meningococcus
Rabies
Contraindicated
Measles
Mumps
Rubella
Varicella
BCG
Vaccinia National Immunization Program; www.cdc.gov/nip
Vaccine Preventable Diseases Children: Vaccine Preventable Diseases Children Diphtheria
Hepatitis A
Hepatitis B
Pertussis
Measles*
Haemophilis influenza type B (Hib)
Mumps*
Polio
Rubella*
Tetanus
Varicella www.cdc.gov, 02/02 * Single vaccine - MMR
Rubella: Rubella Respiratory transmission of the virus
Highly contagious; Incubation 12-23 days
Replication in nasopharynx/lymph nodes
Viremia 5-7 days post-exposure
Placenta and fetus infected during viremia
Rash, low grade fever, malaise, adenopathy
Fainter rash than measles and non-coalescent
Disastrous disease in early gestation
Infection at < 12 weeks - Most dangerous
Causes: Congenital Rubella Syndrome
Multiple organ damage; death
Prevention paramount!!!
Vaccination: MMR National Immunization Program
www.cdc.gov/nip
MMR Vaccine Not Associated With Increased Incidence of Autism: MMR Vaccine Not Associated With Increased Incidence of Autism Dales, L, et al: JAMA; 2001; 285:1183-1185
Compared the number of autism cases reported in CA between 1980-94 with rates of MMR vaccination during the same period.
The incidence of autism exploded by 373%, but the % of children who received MMR vaccination by age 2 increased only moderately, from 72% to 82% over the 14-year period.
"There is no correlation to show that [MMR vaccination] is a major factor, or even a factor at all, in autism."
Kaye J, et al: Brit Med Jour; 2001;322
Although the incidence of autism rose between 1988-99, the prevalence of MMR vaccination remained constant at 97% during that period
Exposure to MMR cannot explain rapid increase in autism
Other factors are responsible for increase
Recognition of lesser forms of disease
Environmental factors; Other?
MMR Vaccination Not Associated With Autism Danish Study:2002 : MMR Vaccination Not Associated With Autism Danish Study:2002 537,303 children born in Denmark between 1/1/91 and 12/31/98 were studied.
440,655/537,303 (82%) had received the MMR vaccine.
316 children diagnosed with autism and
422 diagnosed with other autistic-spectrum disorders.
The risk of autism remained similar in vaccinated and unvaccinated children after taking into account factors such as birth weight, gestational age, socioeconomic status, mother's education and gender
The results of the large population-based study provide "strong evidence" that the measles, mumps and rubella (MMR) vaccine is not a cause of autism.
There was a lack of association between MMR vaccination and autism no matter how how the data was analyzed.
Madsen et al. N Engl J Med 2002;347:1477-1482.
Vaccines Bioterrorist Agents: Vaccines Bioterrorist Agents Anthrax
Cell-free culture of an avirulent, non-encapsulated, derivative of a bovine isolate-V770
2-dose efficacy in monkeys
Estimated > 90% effective against cutaneous anthrax
Botulism
Pentavalent toxoid (A-E)
3 doses 100% effacicious in primates
Tulermia
Live attenuated vaccine
80% protection
Plaque
Suspension of killed Y. pestis
Questionable immunity
Smallpox
Vaccinia vaccine; Effective in one dose; Side effects
VHF
No vaccine available
Emerging/Re-emerging Diseases: Emerging/Re-emerging Diseases Newly recognized
Changes in known organisms
Emerging / Re-emerging Diseases: HIV/AIDS/Opportunistic infections
Hepatitis A-G, Other ?
Herpes, Flu, Other viral diseases
Candiaiasis, Other fungal diseases
Bacterial/Drug resistant bacterial:
E. coli 015.7:H7
Other food/H2O-borne
S. Pneumonia, MRSA, VRSA
Vancomycin resistant Enterococcus
Multiple-drug resistant TB (MDRTB)
Bio-engineered agents
Emerging / Re-emerging Diseases
Emerging Viral Diseases: Emerging Viral Diseases
Slide20: First reported 6/5/81 by CDC
Epidemiologic Notes and Reports
Pneumocystis Pneumonia --- Los Angeles
In the period October 1980-May 1981, 5 young men, all active homosexuals, were treated for biopsy-confirmed Pneumocystis carinii pneumonia at 3 different hospitals in Los Angeles, California. Two of the patients died. All 5 patients had laboratory-confirmed previous or current cytomegalovirus (CMV) infection and candidal mucosal infection. Case reports of these patients follow.
June 5, 1981 / Vol. 30/ No. 21
HIV: HIV Very dynamic virus
109 viral particles/day
Loss of 108-109 CD4 cells/day
Replicate every two days
680,000 viral particles produced and cleared daily
95% of virus produced from newly infected cells
HIV: Twenty Years in Review: HIV: Twenty Years in Review 1981: The first cases of AIDS reported
June 5, 1981 (MMWR 1981;30:250)
1982: Term AIDS replaces GRID
1983: Universal precautions introduced
MMWR 1983;32:101
The virus that causes AIDS identified
Gallo- HTLV III; Montagnier-LAV
Name changed to human immunodeficiency virus (HIV)
1985: First serologic test for HIV licensed by FDA
Rock Hudson died of AIDS on 10/2/85
1986: AZT approved by FDA
Record approval time of 6 months
Bartlett JG; Hopkins HIV Report, July 2001
HIV: Twenty Years in Review: HIV: Twenty Years in Review 1989: U.S. AIDS cases reported at 100,000
1991: Estimated HIV infected in USA 1.5 million
Magic Johnson announces he is HIV positive
1993: Multiple drugs fail in clinical trials
Period of extreme pessimism for HIV infected
1995: First protease inhibitor approved:
Inverase,saquinivir
HIV kinetics reported at 10 billion virions/day Bartlett JG; Hopkins HIV Report, July 2001
HIV: Twenty Years in Review: HIV: Twenty Years in Review 1996:
HIV viral load testing
Becomes major method to assess ART
Mellors J; Ann Intern Med 1997;126:946
ACTG 076 shows benefit of AZT in reducing perinatal transmission
NEJM 1996;335:1621
Initial reports of benefit of HAART
Ritonavir and indinavir approved
Fisrt NNRTI, nevirapine approved
First triple combination HAART study
Eradication of HIV might be possible with HAART
Dr. David Ho Time “Man of the Year” Bartlett JG; Hopkins HIV Report, July 2001
HIV: Twenty Years in Review: HIV: Twenty Years in Review 1997: 13% decrease in AIDS deaths
60-80% reduction in new AIDS-defining conditions, hospitalizations and deaths
Palella et al, NEJM 1998;338:853,
Mocroft at al, Lancet 1998;352:1725
1999: HIV spread to humans from chimpanzees
Occurred in Africa decades before recognition
2000: AIDS pandemic raging in “Third World”
36.1 million people infected with HIV
21.8 million deaths
14,000-16,000 new infections/day
2001: Two distinct epidemics
Bartlett JG; Hopkins HIV Report, July 2001
HIV Natural History: HIV Natural History Viral Transmision:
Primary HIV INfection:
Seroconversion syndrome: Symptomatic: Fever (96%), Adenopathy (74%),Pharyngitis (70%), Rash (70%), Other Symptoms;Onset 2-4 weeks, but > 10 months documented; Frequently diagnosis overlooked
Seroconversion: 3-12 weeks, median 63 days; > 95% seroconversion in 5.8 months Bartlett J: Medical Mgmt. of HIV Disease, 2001
Slide27: Symptoms appear 2-4 weeks after transmission
Fever
Sore throat
Lymphadenopathy
Rash
Maculopapular
Resolves spontaneously
Seroconversion Syndrome
HIV Natural History: Clinical Latent Period: Asymptomatic - May have PGL; Viral set point at 6 month: Equilibrium between immune system and HIV; Persists for years; Gradual, relentless degradation of immune function
Early Symptomatic HIV Infection: CD4 < 500; Opportunistic Infection(s)
AIDS: CD4 < 200; AIDS Defining Illness(s)
Advanced HIV Infection: CD4 < 50; Serious Opportunistic Infection(s); Death HIV Natural History Bartlett J: Medical Mgmt. of HIV Disease, 2001
How Is HIV Spread?: How Is HIV Spread? Routes of Transmission:
Sexual
IDU
Inhalation drug abuse
Exposure to blood/blood products
Occupational exposure
Mother to child
Breast feeding
Cocaine Abuse: Cocaine Abuse Yagiela J. JAMA Vol. 130 May 1999, 701-709. Cocaine abuse is a growing problem and interaction with drugs commonly use in dentistry can be lethal
Patient’s often do not report cocaine usage
Potential adverse interaction between cocaine and adrenergic vasoconstrictors and other drugs
Suspect cocaine use when:
Confronted by patient showing agitation, tremor, sympathetic arousal and dysrhythmias
Damage to nasal septum or skin lesions on the forearms
Vasoconstrictors should not be used for 24 hours after cocaine
Mother-to-Child Transmission Global Situation: Mother-to-Child Transmission Global Situation Wiktor SZ, et al. XIIIth IAC, Durban, 2000. Abstract 354 Estimated 2.4 million HIV-positive women give birth annually to 600,000 HIV-positive babies
1800 new infections each day
90% in sub-Saharan Africa
<1% (1000) in USA and Europe
Transmission rates
USA/Europe: 13–30% without ART, approaching 1–3% with ART
Developing countries: 20–43% without ART, lower rates with ART, even with short-course therapy
Breast feeding for 6 months
Additional 5–10% infections, with the highest rates of transmission occurring in the first and second months post-partum
Mother-to-Child Transmission Prevention: Mother-to-Child Transmission Prevention Regimen recommended for pregnant HIV + women
Standard: Reduces HIV transmission by two thirds
Zidoduvine (ZDV) 100mg 5 x daily beginning week 14-34 of gestation and continued until delivery
During labor 2mg/kg infusion for 1 hr; then a continuous infusion of 1mg/kg per hr until delivery
8-12 hrs after birth, infants given oral ZDV syrup; 2mg/kg q6h for the 1st 6 weeks of life
Short Course
Nevirapine (NVP) 200 mg tablet
Administered to mother once at the onset of labor
NVP 200 mg to infant within 72 hours of birth
50% decrease in HIV transmission compared to ZDV www.hivatis.org August 30, 2002
Adults and Children With HIV/AIDS, 12/31/02 : Adults and Children With HIV/AIDS, 12/31/02 North America
980,000
Western Europe
570,000 Eastern Europe & Central \Asia
1,200,000 Caribbean
440,000 Latin America
1,500,000 Sub Saharan Africa
29,400,000 North Africa & Middle East
550,000 East Asia & Pacific
1,200,000 South & South-East Asia
6,000,000 Australia & New Zealand
15,000 People living with HIV/AIDS .......................... 42 million
New HIV infections in 2002 ........................... 5 million
Deaths due to HIV/AIDS in 2002 .................... 3.1 million
Treatment of HIV Disease : Treatment of HIV Disease HAART
Management of opportunistic infection(s)
Current HAART Medications & Abbreviations: Current HAART Medications & Abbreviations NRTI
Abacavir ABC
Didanosine ddI
Lamivudine 3TC
Stavudine d4T
Zidovudine ZDV
Zalcitabine ddC
Trizivir TRZ
NNRTI
Delavirdine DLV
Efavirenz EFV
Nevirapine NVP
PI
Amprenavir AMP
Indinavir IND
Lopinavir LOP
Nelfinavir NLF
Ritonavir RIT
Saquinavir SAQ
soft gel SGC
hard gel HGC
Drugs Commonly Used in Dentistry That Should Not Be Used With Protease Inhibitors or NNRTIs* : Drugs Commonly Used in Dentistry That Should Not Be Used With Protease Inhibitors or NNRTIs*
Nevirapine: No drugs contraindicated;
*Non-nucleoside reverse transcriptase inhibitors
** Alternatives:
Analgesics-ASA, oxycodone, acetaminophen;
Antihistamine-loratadine, fexofenadine, cetirizine;
Psycotrophic-temazepam, forazepam
Modified from Bartlett JG & Gallant J: Medical Management of HIV Infection, 2001-2002 Edition
Adverse Effects: Adverse Effects NRTIs
Zidovudine
HA, GI
Bone marrow suppression
Didanosine
GI intolerance
Pancreatitis
Stavudine
Peripheral neuropathy
Zalcitabine
Peripheral neuropathy
Abacavir
HA, GI
Hypersensitivity reaction
NNRTIs
Nevirapine
Rash, liver
Delavirdine
Rash
Efavirenz
Teratogenic in primates,
CNS, rash
PIs
Indinavir
Nephrolithiasis
Ritonavir
GI intolerance
Nelfinavir
Diarrhea
Amprenavir
GI intolerance
Lopinavir
diarrhea
Metabolic and Morphologic Abnormalities: Metabolic and Morphologic Abnormalities Morphologic:
Lipo-atrophy
Central fat accumulation
Fat deposition
Buffalo hump
Lipomas
Ectodermal dysplasia (?)
Metabolic:
Elevated blood lipids
Cholesterol
Triglycerides
Elevated C-peptide
Insulin resistance,
Elevated blood glucose
Diabetes mellitus
Osteopenia (?)
Avascular necrosis (?) Carr A. (State of the Art Lecture) 8th CROI, Chicago, 2001. Issues in Metabolic Complications
Hepatitis and Liver Disease: Hepatitis and Liver Disease
Liver Disease: Liver Disease 500-1000 therapeutic agents implicated in hepatitis
15-20 million Americans are alcoholics
Chronic Liver Disease: Tenth leading cause of death in USA
25,000 deaths/year
1% of all deaths
40 % of chronic liver disease HCV-related
8-10,000 deaths/year.
HCV associated end stage liver disease is the most frequent indication for liver transplant
As HCV population ages incidence of chronic liver disease could increase substantially
Chronic Liver Disease MMWR 1998 Vol. 47/ No. RR-19
Hepatitis: Inflammation of the Liver: Hepatitis: Inflammation of the Liver Hepatitis
Asymptomatic - anicteric
Mild symptomatic - anicteric
Classic icteric infection
Fulminant hepatitis
Chronic hepatitis
Slide43:
Viral Hepatitis - Overview A B C D E Source of virus feces blood/ blood-derived/body fluids
feces Route of transmission fecal-oral Percutaneous/permucosal
fecal-oral Chronic infection no yes yes yes no Prevention pre/post- exposure immunization pre/post- exposure immunization blood donor screening; risk behavior modification pre/post- exposure immunization; risk behavior modification ensure safe drinking water Type of Hepatitis
Viral Hepatitis Sherker, AH: Hepatitis, 1998: Viral Hepatitis Sherker, AH: Hepatitis, 1998
Hepatitis A: Hepatitis A Family: Picornavirus Incubation: 15-40 days Onset: Usually acute Prodrome: None Transmission: Oral/fecal Carrier state: None Mortality: 0.1-0.2%
Hepatitis B: Hepatitis B Family:
Incubation:
Onset:
Prodrome:
Transmission:
Carrier state:
Mortality: Hepadnavirus
50-180 days
Slow, insidious
Sometimes
Blood, sex, perinatal
Yes (5-10%)
1-2%
Serologic Tests for HBV Infection : Serologic Tests for HBV Infection CDC, MMWR April 27, 2001/ Vol. 50 /No. RR-5
Hepatitis C: Hepatitis C Family:
Incubation:
Onset:
Prodrome:
Transmission:
Carrier state:
Chronic disease:
Mortality: 1-2%
Prevalence: 1.8% USA Flavivirus
1-5 months
Insidious
Sometime
Parenteral, sex
> 85 %
70%;
Hepatitis C Virus: Hepatitis C Virus Acute Infection:
HCV-RNA detectable in 1-3 weeks post-exposure
All patients develop liver cell injury
Documented by increased ALT; occurring within average of 50 days (range: 15-150)
Majority are asymptomatic and anicteric
25-35 % develop malaise, anorexia, weakness; some become icteric; fulminent liver failure-rare
HCV-antibody almost always detectable
Only 15 % of cases self-limiting: disappearance of HCV-antibody Management of Hepatitis C; NIH Consensus Statement 1997; 15(3):1-41
Hepatitis C Virus: Hepatitis C Virus Chronic Infection
At least 85 % of patients fail to clear the virus within 6 months
All have anti-HCVor HCV-RNA
One in three have normal ALT
Clinical course insidious usually w/o symptoms in the 1st two decades
Progression may lead to inflammation, liver cell death and fibrosis
Necroinflammatory changes & severe fibrosis can progress to cirrhosis which develops in 20% of patients and marks transition to uncompensated liver disease Management of Hepatitis C; NIH Consensus Statement 1997; 15(3):1-41
Slide51: Hepatitis C Virus Hepatitis C rate of chronic disease > 80%
35,000 new infection/yr
HCV has high propensity to mutate
Escapes immune surveillance
Lack of vigorous T-cell response promotes chronicity NIH Consensus Development Conference, 2002
Hepatitis C Virus: Hepatitis C Virus Infects 1.8 % of general population
About 4 million Americans
Highest prevalence:
Adults aged 40-59 yrs
6.1% of African Americans
8-10,000 deaths/yr from chronic infection
Latency period for up to 20 years
Occupational transmission documented
2-5% risk
70- 90% of IDU’s chronically infected
Rapidly acquired in IDU’s:
50-80 % acquisition in 6-12 months
Homeless, inmates and hemophiliacs 15-50%
NIH Consensus Development Conference, 2002
HCV Testing: HCV Testing Two primary tests available for detection of HCV antibodies:
Anti-hepatitis C antibody (anti-HCV Ab)
EIA:
Enzyme immunoassays
RIBA:
Recombinant immunoblot assays
NIH Consensus Development Conference, 2002
HCV Testing- EIA: HCV Testing- EIA First HCV EIA developed in 1989
Three generations of EIA since
EIA is main screening test for HCV
Advantages:
Assays are easy to perform
Inexpensive
Highly sensitive, specificity not established
Disadvantages:
Require confirmatory assay for HCV diagnosis
False positives in low risk and in pts with autoimmune disease Bernstein D, Medscape, Gastroenterology Clinical Management Volume1 //I.d.medscape.com/Medscape/gastro/ClinicalMgmt
NIH Consensus Development Conference. 1997 March 24-26; 15(3):1-41.
Hepatitis D: Hepatitis D Family: Incubation: 21-90 days Onset: Usually acute Prodrome: Unknown Transmission: Usually parenteral
Chronicity: Yes Mortality: 2-20% Satellite
Hepatitis E: Hepatitis E Family: Calcivirus Incubation: 2-9 weeks Onset: Usually acute Prodrome: Not present Transmission: Oral/fecal,food/H2O 3rd World Carrier state : None Mortality: 1-2% in gen. pop.; 20% in pregnancy
Hepatitis G: Hepatitis G Family:
Incubation:
Transmission:
Carrier state:
Chronic disease:
Mortality:
Prevalence: Flavivirus
Unknown
Parenteral, sex?
Probable
Unknown
Unknown
1.7% blood donors
Hepatitis: SIGNS AND SYMPTOMS
Fatigue, nausea, vomiting, diarrhea,
Joint and muscle pain,
Jaundice, hepatomegaly,
Abdominal and gastric distention,
Clay colored stools, dark urine,
Fever, bruising, rash, chills,
Anorexia ,distaste for cigarettes and food Hepatitis
Liver Dysfunction: Liver Dysfunction Inflammation
Monitored by evaluating serum liver enzyme levels:
AST - Aspartate aminotransferase
ALT - Alanine aminotransferase
Transaminase levels also useful in determining the course of the disease
As values decrease, the patient may be resolving the infection.
AST - SGOT ALT - SGPT: AST - SGOT ALT - SGPT Jaundice:
2.5 mg/100 ml Bilirubin
Medical Management of Hepatitis: Non specific - palliative/bed rest
Nutrition and high caloric diet
Corticosteroids
Interferon therapy
Antiviral therapy
Combination therapy
Medical Management of Hepatitis
Hepatitis Treatment: Hepatitis Treatment 1. Interferon Therapy
Regimen: 3 MU 3X/Week X 12 Months
Infergen: Interferon alfa-1
Intron A : Interferon alfa-2a
Referon-A: Interferon alfa-2a
Rebetron: Rebetol (ribavirin) & Interferon alfa 2b
2. Antivirals/antiretrovirals
3TC (Epivir-HBV) FDA Approved
Adefovir & other antiretroviral drugs
Famciclovir & other antivirals
Dental Management of the Hepatitis Patient: Dental Management of the Hepatitis Patient
Laboratory Tests: Laboratory Tests Latest CD4 count, viral load
CBC with differential: WBC > 1,000 CELLS/mm3
Platelet count : > 100,000 CELLS/mm3
PT, PTT, INR, bleeding time
PPD
LFT’S (ALT, AST)
Common Laboratory Tests In Liver Disease: Common Laboratory Tests In Liver Disease ALT - Alanine Aminotransferase:
Enzyme produced in hepatocytes
Increases when hepatocytes damaged/killed
Level may correlate with degree of inflammation
Correlation variable; Biopsy needed for accuracy
AST - Aspartate Aminotransferase:
Similar to ALT but less specific for liver
Alakaline Phosphatase:
Enzyme(s) produced in bile ducts
Also in intestine, kidney, placenta and bone
Elevation suggests disease of bile ducts
Coagulation Tests: Coagulation Tests Indicate patient’s clotting ability
Increase indicates abnormal clotting mechanism(s)
Coagulation tests: - Prothrombin time (PT) - International normalized ratio (INR) - Partial thromboplastin time (PTT) - Bleeding time
PROTHROMBIN TIME (PT): PROTHROMBIN TIME (PT) NORMAL VALUE:
11-16 SECONDS *Note: prior to any surgical procedure patient should be checked to ensure it is less than twice normal.
Management of the Medically Compromised Dental Patient: Management of the Medically Compromised Dental Patient Assess patient: Pre-op, during & post-op for susceptibility to:
Bleeding/hemostasis
Infection
Drug interaction(s)/ contraindications
Ability to withstand dental treatment
International Normalized Ratio (INR): International Normalized Ratio (INR) INR for patients not on anticoagulants:
0.9-1.1
INR for patients on anticoagulants (controlled):
2.0-3.0
INR for patients with prosthetic valves or MI:
2.5-3.5
Evaluates level of anticoagulation
Slide70: Treatment of the
Hepatitis Patient The major complication encountered with treatment of the hepatitis patient is hemorrhage.
Coagulation tests should include:
Platelet Count,
Bleeding Time,
International Normalized Ratio (INR) or Prothrobin Time (PT)
Partial Thromboplastin Time (PTT)
Slide71: If coagulation tests are not within normal limits, consider for all surgical procedures:
Avoidance of aspirin containing products
A 10 mg dose of Vitamin K administered IM or IV prior to dental procedures.
Re-evaluation PRN Treatment of the
Hepatitis Patient
Treatment of the Hepatitis Patient: Treatment of the Hepatitis Patient To avoid stress to the patient’s coagulation mechanisms all surgical dental procedures should be:
Scheduled in small increments.
Gelfoam or topical thrombin should be used in extraction sites; And
Suturing of all overlying tissues/gingiva should be considered to control hemorrhage after surgery
Slide73: Pressure dressings on operative sites as necessary
Soft diet for 48 to 72 hours after surgical procedure
Avoid substances that may cause hepatic inflammation. Treatment of the Hepatitis Patient
Use with Caution : Use with Caution DRUGS METABOLIZED BY THE LIVER
Slide75: Drugs Metabolized By The Liver Local Anesthetics
Lidocaine (Xylocaine)
Mepivacine (Carbocaine)
Prilocaine (Citinest)
Bupivacaine (Marcaine)
Slide76: Analgesics
Aspirin
Acetaminophen
NSAIDS
Codeine
Meperidine (Demerol) Drugs Metabolized By The Liver
Slide77: Antibiotics
Amoxicillin
Ampicillin
Tetracycline
Erythromycin
Clindamycin Drugs Metabolized By The Liver
Slide78: Drugs Metabolized By The Liver Sedatives
Diazepam (Valium)
Barbiturates
Chlordiazepoxide (Librium)
Human Herpes Viruses: Human Herpes Viruses
Human Herpesviruses: Human Herpesviruses Alpha Herpesviruses:
Herpes Simplex Virus Type 1 (HSV-1)
Herpes Simplex Virus Type 2 (HSV-2)
Varicella Zoster Virus (HZV)
Beta Herpesviruses:
Cytomegalovirus (CMV)
Human Herpesvirus Type 6 (HHV-6)
Human Herpesvirus Type 7 (HHV-7)
Gamma Herpesviruses:
Epstein-barr Virus (EBV)
Human Herpesvirus Type 8 (HHV-8)
Kaposi’s Sarcoma Asso. Herpesvirus
Sandstrom and Whitley: International Herpes Management Forum Strategies Workshop and 3rd Annual Mtg, 1999
Viruses Herpes; HSV-1 & 2: HSV-1:
Oral/genital/mucocutaneous lesions;
Acute gingivostomatitis;
Pharyngitis;
Herpes labialis;
Keratoconjunctivitis;
Encephalitis;
Herpetic Whitlow;
HSV-2:
Oral/genital/mucocutaneous lesions;
At least 1:4 persons > 12 y.o. infected;
70-90% asymptomatic shedding;
Only about 20% of HSV-2 Ab+ know they are infected Viruses Herpes; HSV-1 & 2
Varicella-Zoster (VZV): Chickenpox: Ubiquitous infection of childhood
Primary infection results in the characteristic disseminated cutaneous lesions.
The virus then establishes lifelong latency in dorsal root ganglia from whence it may reactivate to cause localized cutaneous eruptions known as herpes zoster or shingles.
Herpes zoster usually occurs later in life as a consequence of immunosuppressive illness or immunosuppressive medical therapy.
Declining VZV-specific immunity later in life is associated with an increased risk of herpes zoster.
Varicella-Zoster (VZV)
Herpes Viruses : EBV:
Infects > 85% of population;
Agent of infectious mononucleosis
Cause of oral hairy leukoplakia;
Oncogenic: Burkitt’s Lymphoma;
Linked to Hodgkin’s Disease/ other malignancies
CMV:
Problematic in immumocomp. pts; Retinitis, enteritis;
Linked to vasculopathies, CAD?
Role in organ transplant rejection;
Other graft/host involvement Herpes Viruses
Herpes Simplex Virus Initial Treatment: Mild HSV:
acyclovir, (Zovirex) 400 mg, po, tid or
famciclovir, (Famvir) 250 mg, po, tid or
valacyclovir, (Valtrex) 1.0 gm bid
All given 7-10 days
Severe or refractory HSV:
acyclovir up to 800 mg, po, X 5 days or
acyclovir 15-30 mg/kg IV/day X at least 7 days
valacyclovir 1 gm, po, bid-tid X 7-10 days
Herpes Simplex Virus Initial Treatment Barlett J, Medical Management of HIV Infection: 2000-2001
Herpes Simplex Virus Topical Treatment: Recurrent Herpes Labialis:
Penciclovir 1% cream; Rx
Denavir 1.5 gram tube; 10mg penciclovir/gram
Apply every 2 hrs when awake X 4 Days
As soon as prodromal symptoms appear
Docosanol 10% cream; OTC
Apply 5x daily when awake X 4 days
As soon as prodromal symptoms appear
Herpes Simplex Virus Topical Treatment Siegle M, J Amer Dent Asso. 2002; 133:1245-49.
Human Papillomavirus HPV : Human Papillomavirus HPV
Human Papillomavirus: Most common viral STD
Infects about 1/3 of sexually active population in USA
>60 strains have been identified
25 strains associated with genital tract infections/cancer
Strongly associated with:
Cervical cancer
Causative agent
Oral cancer
Peri-anal/testicular cancer
Especially severe in HIV infected Human Papillomavirus
Papilloma; Focal Epithelial Hyperplasia (FEH): Papilloma; Focal Epithelial Hyperplasia (FEH) Etiological agent:
Human papilloma virus (HPV)
“Wart”
Clinical appearance:
Flat (FEH)
Siky
Cauliflower-like
Slide89: WNV
In USA WNV
is spreading
rapidly
throughout
the country 12/11/02
WNV in USA: 12/31/2002: WNV in USA: 12/31/2002 www.cdc.gov/od/oc/media/wncount.htm In 2002, 5 States Il, MI, OH, LA and IN accounted for
62.2 % of WNV cases
70.5% of deaths
West Nile Virus Clinical Presentation: Incubation period 3 - 14 days
20% develop “West Nile fever”
1 in 150 develop meningoencephalitis
Advanced age primary risk factor for severe neurological disease and death
Mild dengue-like illness of sudden onset
Duration 3 - 6 days
Fever, lymphadenopathy, headache, abdominal pain, vomiting, rash, conjunctivitis, eye pain, anorexia
Symptoms of West Nile fever in contemporary outbreaks not fully studied
West Nile Virus Clinical Presentation
West Nile Virus Clues and Clinical Presentation: West Nile Virus Clues and Clinical Presentation Suspect WNV when:
Symptoms consistent with WNV
Unexplained bird or horse deaths
Mosquito season
Age > 50 years
Symptoms:
Most cases asymptomatic or mild dengue-like illness
Incubation period usually 5 (3) to 15 days
Fever, lymphadenopathy, headache
Abdominal pain, vomiting, rash, conjunctivitis
Muscle weakness and /or flaccid paralysis, hyporeflexia
EMG/NCV showing axonal neuropathy
Lymphocytopenia
MRI:
Shows enhancement of leptomeninges and/or periventricular area
CNS involvement and death in minority of cases
Severe Acute Respiratory Syndrome (SARS): Severe Acute Respiratory Syndrome (SARS)
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) The Initial Epidemic
Outbreak of atypical pneumonia in Hong Kong in March 2003
Between 03/11/03 and 03/25/03 156 patients were hospitalized with SARS
138 were identified as secondary or tertiary cases as a result of exposure to index case(s)
112 secondary cases
26 tertiary cases
Includes 69 HCWs
20 MDs
34 Nurses
15 Allied HCWs
54 patients on ward or visitors
16 medical students
32 of the 138 patients (23.2%) had severe respiratory failure
5 patients died (3.6%)
All had been hospitalized with a major medical condition
Lee N et al. NEJM April 7, 2003. www.nejm.org
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) The Clinical Presentation- Initial 138 Cases
Incubation period was 2-10 days from initial exposure to onset of fever
Median incubation period was 6 days
The most common clinical symptoms were:
Fever (100%) > 100.50
Chills, rigors or both (73.2%)
Myalgia (60.9%)
Cough (57.3%)
Headache (55.8%)
Dizziness (42.8%)
Less common symptoms included:
Sore throat, sputum production, coryza, nausea, vomiting, and diarrhea Lee N et al. NEJM April 7, 2003. www.nejm.org
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Routes of Transmission:
The principal way SARS appears to be spread is through droplet transmission1,2
Namely, when a SARS patient coughs or sneezes droplets into the air and someone else breathes them in.
It is possible that SARS can be transmitted through the air or from objects that have become contaminated.1,2
People at risk: 1,2
Direct close contact with an infected person
Sharing a household with a SARS patient
HCWs who did not use infection control procedures while caring for a SARS patient.
In the United States, there is no indication of community transmission at this time.1,2 CDC. April 4, 2003. http://www.cdc.gov/ncidod/sars/faq.htm.
http://www.ada.org/prof/prac/issues/topics/sars.html
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Respiratory illness of viral etiology with onset since February 1, 2003, and the following criteria:
Measured temperature > 100.5°F (>38° C) AND
One or more clinical findings of respiratory illness
Cough
Shortness of breath
Difficulty breathing
Hypoxia
Radiographic findings of either pneumonia or acute respiratory distress syndrome
AND
http://www.cdc.gov/ncidod/sars/casedefinition.htm
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Travel within 10 days of onset of symptoms to an area with documented or suspected community transmission of SARS:
Peoples' Republic of China
Mainland China
Hong Kong Special Administrative Region
Hanoi, Vietnam
Singapore
Toronto, Canada (04/21/03)
OR
http://www.cdc.gov/ncidod/sars/casedefinition.htm
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Close contact within 10 days of onset of symptoms with either a person with a respiratory illness who traveled to a SARS area or a person known to be a suspect SARS case.
Close contact is defined as having:
Cared for
Lived with
Direct contact with respiratory secretions and/or body fluids of a patient known to be suspect SARS case. http://www.cdc.gov/ncidod/sars/casedefinition.htm
Severe Acute Respiratory Syndrome (SARS) Case Definition 04/20/03 : Severe Acute Respiratory Syndrome (SARS) Case Definition 04/20/03 Suspected Case:
Travel within 10 days of onset of symptoms to an area with documented or suspected community transmission of SARS
Excludes areas with secondary cases limited to healthcare workers or direct household contacts)
Travel includes transit in an airport in an area with documented or suspected community transmission of SARS. Areas with documented or suspected community transmission of SARS:
People's Republic of China
Mainland China
Hong Kong Special Administrative Region
Hanoi, Vietnam;
Singapore
Toronto, Canada. http://www.cdc.gov/ncidod/sars/casedefinition.htm
Severe Acute Respiratory Syndrome (SARS) Case Definition 04/20/03 : Severe Acute Respiratory Syndrome (SARS) Case Definition 04/20/03 Suspected Case:
Close contact within 10 days of onset of symptoms with a person known to be a suspect SARS case.
Close contact is defined as having cared for, having lived with, or having direct contact with respiratory secretions and/or body fluids of a patient known to be suspect SARS case.
Probable Case:
A suspected case with one of the following:
Radiographic evidence of pneumonia or respiratory distress syndrome
Autopsy findings consistent with respiratory distress syndrome without an identifiable cause http://www.cdc.gov/ncidod/sars/casedefinition.htm
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Cause of SARS
Scientists at CDC and other laboratories have detected a previously unrecognized coronavirus in patients with SARS.1-4
Confirmed as causative agent by WHO on 04/16/03
Virus a member of the coronavirus family, never before seen in humans 1. http://www.cdc.gov/ncidod/sars/casedefinition.htm
2. Peiris J et al, Lancet 2003 http://image.thelancet.com/extras/03art3477web.pdf
3. Drosten C et al. NEJM 2003 www.nejm.org
4. Ksiazek T et al. NEJM 2003 www.nejm.org
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Cause of SARS
Coronaviruses are a group of viruses that have a halo or crown-like (corona) appearance when viewed under a microscope.
These viruses are a common cause of mild to moderate upper-respiratory illness in humans and are associated with respiratory, gastrointestinal, liver and neurologic disease in animals.
Coronaviruses can survive in the environment for as long as three to four hours. 1. http://www.cdc.gov/ncidod/sars/casedefinition.htm
2. Peiris J et al, Lancet 2003 http://image.thelancet.com/extras/03art3477web.pdf
3. Drosten C et al. NEJM 2003 www.nejm.org
4. Ksiazek T et al. NEJM 2003 www.nejm.org
Severe Acute Respiratory Syndrome (SARS) Dental School, University of Maryland : Severe Acute Respiratory Syndrome (SARS) Dental School, University of Maryland Precautions for Dental Patients Who May Have Been Exposed to SARS:
While taking initial medical histories and at periodic updates, all dental patients at the Dental School will routinely be asked about:
Recent travel of patient or immediate family members to areas where SARS is endemic
Peoples' Republic of China
Mainland China
Hong Kong Special Administrative Region
Hanoi, Vietnam;
Singapore
Toronto, Canada DePaola L, 2003, University of Maryland Baltimore
Severe Acute Respiratory Syndrome (SARS) Dental School, University of Maryland : Severe Acute Respiratory Syndrome (SARS) Dental School, University of Maryland Precautions for Dental Patients Who May Have Been Exposed to SARS:
Recent respiratory illness:
Cough
Shortness of breath
Difficulty breathing
Hypoxia
Radiographic findings of either pneumonia or acute respiratory distress syndrome
Close contact with anyone suspected of being infected with SARS
While taking initial medical histories and at periodic updates, all dental patients at the Dental School will routinely be asked whether they have a history of and/or S & S suggestive of SARS DePaola L, 2003, University of Maryland Baltimore
Severe Acute Respiratory Syndrome (SARS) Dental School, University of Maryland : Severe Acute Respiratory Syndrome (SARS) Dental School, University of Maryland Precautions for Dental Patients Who May Have Been Exposed to SARS:
Patients with a medical history or signs and symptoms of SARS will be immediately referred to the University of Maryland Medical System, or their private physician for medical evaluation for possible infectiousness.
Such patients should not remain in the Dental School any longer than required to arrange the referral.
Elective dental treatment will be deferred until a physician confirms that the patient does not have SARS. DePaola L, 2003, University of Maryland Baltimore
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Infection Control Procedures Suspected Cases:1-3
Isolate patients in a separate waiting area
Give patients a surgical mask to wear
Instruct patients to cover mouth when coughing or sneezing
HCW’S utilize surgical mask
Healthcare personnel should apply:
Standard precautions
Hand hygiene
Soap and water or alcohol-based hand rub
Contact precautions when aerosol-generating procedures are being performed on patients who may have SARS.
Gloves, gown, and eyewear
Airborne precautions
Respiratory protective devices with a filter efficiency of greater than or equal to 95%
Recommended with confirmed SARS patients
http://www.cdc.gov/ncidod/sars/infectioncontrol.htm.
http://www.ada.org/prof/prac/issues/topics/sars.html
DePaola L, 2003, University of Maryland Baltimore
Severe Acute Respiratory Syndrome (SARS) : Severe Acute Respiratory Syndrome (SARS) Infection Control Procedures:
For known SARS patients
Due to rapid development of symptoms it is unlikely that SARS will be seen in the dental office
HCW’S utilize NIOSH respirators appropriate for TB
Defer all elective treatment until patient has been evaluated
Refer patients for urgent/emergency care to locations equipped with TB Isolation Areas, i.e. local hospitals
Follow the Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities http://www.cdc.gov/mmwr/preview/mmwrhtml/00035909.htm
In summary, healthcare personnel should apply:
Standard precautions
Contact precautions
Airborne precautions
http://www.cdc.gov/ncidod/sars/infectioncontrol.htm.
http://www.ada.org/prof/prac/issues/topics/sars.html
DePaola L, 2003, University of Maryland Baltimore
Slide109: An outbreak of unexplained illness occurred in May 1993 an area of the Southwest shared by NM, AZ, CO, and UT (Four Corners).
A number of previously healthy young adults suddenly developed acute respiratory symptoms; about half soon died.
A hantavirus, which is transmitted by rodents, was suspected.
The virus named Sin Nombre virus (SNV) and its principal carrier, the deer mouse were positively identified.
A "bumper crop" of rodents there, due to heavy rains during the spring of 1993.
Determined that person to person transmission of SNV was unlikely.
SNV had actually been present, but unrecognized, at least as early as 1959.
Since the discovery in 1993, hantavirus pulmonary syndrome (HPS) has been identified in over half of the states of the U.S. Hantavirus Pulmonary Syndrome (HPS)
Slide110: Influenza
Influenza: Acute, febrile illness, usually self limited
Headache, malaise, myalgias
Fever - 104oF-106oF (days 1-3)
URI symptoms
Nasal discharge, sore throat, cough (days 2-7)
Cervical adenopathy (children > adults) and rhonchi
Attack rate: 10 - 40%
Viral shedding:
One day before - until 10 days after symptom onset
Peak day 3-4
Shedding is prolonged in young children
Transmission:
Person to person via small particle aerosols
Virus is relatively stable and favors low humidity and cool temperatures
Influenza www.cdc.gov/ncidod/diseases/flu/fluvirus.htm
Slide112: http://www.cdc.gov/nip/Flu/Public.htm#Facts
Flu Facts: Flu Facts Influenza (flu) is a serious disease
Flu is not a cold!
It is far more dangerous than a bad cold
The virus infects the lungs.
It can lead to pneumonia/other sequellae.
Every year in the USA approximately:
114,000 people are hospitalized
20,000 people die because of the flu.
Most who die are over 65 years old. But small children less than 2 years old are as likely as those over 65 to have to go to the hospital because of the flu. http://www.cdc.gov/nip/Flu/Public.htm#Facts
Influenza Vaccine: Influenza Vaccine www.cdc.gov/ncidod/diseases/flu/fluvirus.htm Type: Inactivated split or whole virus
Route/schedule: 0.5 IM annually
Efficacy: 70-90%
Indications:
Age > 65
Health care or day care workers
Nursing home/chronic care residents
Adults and children with pulmonary and cardiovascular disorders, chronic metabolic disease (diabetes mellitus), renal dysfunction, immunosuppression
Teenagers and children on ASA
Women in the 2nd and 3rd trimester of pregnancy
Contraindications: Anaphylaxis to eggs
Side effects:
Local pain, occasional myalgias and rare allergic reactions
Prevention and Control of Influenza Recommendations of the Advisory Committee on Immunization Practices (ACIP) : Prevention and Control of Influenza Recommendations of the Advisory Committee on Immunization Practices (ACIP)
The 2002 recommendations include five principal changes or updates:
The optimal time to receive influenza vaccine is during Oct. and Nov.
However, because of vaccine distribution delays during the past 2 years, ACIP recommends that vaccination efforts in Oct. focus on persons at greatest risk for influenza-related complications and health-care workers and that vaccination of other groups begin in November.
Vaccination efforts for all groups should continue into Dec. and later, for as long as vaccine is available.
Because young, otherwise healthy children are at increased risk for flu-related hospitalization, influenza vaccination of healthy children aged 6--23 months is encouraged when feasible.
Vaccination of children aged >6 months who have certain medical conditions continues to be strongly recommended.
The 2002--2003 trivalent vaccine virus strains are A/Moscow/10/99 (H3N2)-like, A/New Caledonia/20/99 (H1N1)-like, and B/Hong Kong/330/2001-like strains.
A limited amount of influenza vaccine with reduced thimerosal content will be available for the 2002--2003 influenza season. MMWR. April 12, 2002 / 51(RR03);1-31
Slide116: http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5103a1.htm The 2002--2003 trivalent vaccine virus strains are:
A/Moscow/10/99 (H3N2)-like
A/New Caledonia/20/99 (H1N1)-like
B/Hong Kong/330/2001-like strains
Tuberculosis: Tuberculosis
Tuberculosis (TB): Tuberculosis (TB) TB is not on the decline.
One third of the world's population is infected with TB
In 1999 TB caused 8,000 deaths/day
The most deaths from TB in history
7- 8 million people become infected with TB/year
5-10 % of these people will develop active TB
Between 1993 and 1996, TB increased 13 %
TB accounts for more than 1/4 of all preventable adult deaths the developing world.
nfid.org/factsheets The number one single infectious disease killer
Tuberculosis (TB): Tuberculosis (TB) Someone is newly infected with TB every second !
TB is the leading killer of women
TB outranks all causes of maternal mortality
TB creates more orphans than any other infectious disease
TB is the leading cause of death among HIV-positive individuals nfid.org/factsheets The number one single infectious disease killer
Tuberculosis Transmission: Tuberculosis Transmission Caused by Mycobacterium tuberculosis
Spread by: - Airborne route - Droplet nuclei
Affected by: - Infectiousness of patient - Environmental conditions - Duration of exposure
Most persons exposed do not become infected
Pathogenesis Latent M.tuberculosis Infection: Pathogenesis Latent M.tuberculosis Infection Inhaled droplet nuclei with M. tuberculosis :
- Reach alveoli
- Are taken up by alveolar macrophages
- Reach regional lymph nodes
- Enter bloodstream and disseminate
Chest radiograph may have transient abnormalities
Specific cell-mediated immune response controls further spread
Pathogenesis Active M. tuberculosis Infection: Pathogenesis Active M. tuberculosis Infection Active disease state
Symptoms present:
Cough
Fever
Chills
Night sweats
May be infectious
Disease both treatable & preventable
Diagnosis of Active TB: Diagnosis of Active TB History and epidemiologic clues
Think TB!!!
Chest X-ray
Tuberculin skin test
AFB smear
AFB culture
Nucleic acid amplification
Fast but sensitivity poor in smear neg.
Empiric treatment trial
Slide124: Administering the Tuberculin Skin Test Inject intra-dermally:
0.1 ml of 5 TU PPD tuberculin
Produce wheal:
6 mm to 10 mm in diameter
Do not recap, bend, or break needles, or remove needles from syringes
Follow universal precautions for infection control
Slide125: Reading the Tuberculin Skin Test Read reaction:
48-72 hours after injection
Measure only induration!
Record reaction in millimeters
Dental Offices: Dental Offices “….No specific dental procedure has been classified as cough inducing. In light of these observations the following additional considerations appear prudent in dental settings: Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132
Risk of Occupational TB Transmission: Risk of Occupational TB Transmission Considered minimal
Follow CDC/ADA guidelines
No OSHA regulations (to date) Private Dental Offices Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132
TB Guidelines: TB Guidelines During initial medical history and periodic updates DHCW should:
Routinely ask all patients about a history of TB;
And signs and symptoms suggestive of TB Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132
TB Guidelines: TB Guidelines All elective dental care should be deferred until a physician determines:
That the patient doesn’t have TB ; or
Anti-TB therapy has been rendered and the patient is no longer infectious! Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132
TB Guidelines: TB Guidelines Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132 If urgent care must be provided for a patient with active TB or signs & symptoms suggestive of TB,
TB isolation practices should be implemented
DHCW should use appropriate respiratory protection while performing procedures on these patients
Emergency Dental Treatment for TB Patients: Emergency Dental Treatment for TB Patients Perform treatment in facilities with TB isolation capability
Use recommended respiratory protection
Fit tested HEPA filter mask
Select least invasive treatment options
Accomplish definitive care after patient is no longer infectious
Sputum Negative for Acid Fast Bacillus (AFB) Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132
Tuberculosis: Tuberculosis Dental-care in “high risk” facilities
Use engineering controls similar to those in general use areas of medical facilities with similar risk profile.
Evaluation of Dental HCW TB symptoms
Evaluate promptly
Do not return to clinic until:
TB Diagnosis is ruled out or;
DHCW is on therapy and non-infectious Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132
CDC/ADA Dental Office TB Recommendations: CDC/ADA Dental Office TB Recommendations Protocol for referring TB patients to dental isolation facility
Protocol for identifying and referring patients for medical evaluation for TB
DHCW education, training, counseling and screening
Periodic risk assessment and updates Written Plan Should Include: Guidelines for Preventing the Transmission of Mycobacterium tuberculosis in Health-Care Facilities, MMWR; October 28, 1994 / 43(RR13);1-132
Slide134: Louis G. DePaola, DDS, MS (410) 706-7628
lgd001@dental.umaryland.edu
I Questions?