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PATH II > infectious diseases > Flashcards

infectious diseases Flashcards

1
Q

pathogens

A

• Organism that is capable of causing disease

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2
Q

levels of virulence

A

–High - causes disease in a healthy population
–Low - causes disease only in susceptible populations

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3
Q

Opportunistic Infections
example?

A

• Non-pathogenic organism with Low virulence
• Immunocompromised host
C. albicans

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4
Q

Mutualism

A

• Interaction between two organisms
• Both organism benefits

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5
Q

Commensalism, example

A

Commensalism
• Interaction between two organisms
• One organism benefits
• Other is neither harmed nor helped
• C. albicans

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6
Q

How do pathogens injure cells and cause tissue damage?

A

• Bind to or enter host cells
• Release endotoxins or exotoxins
• Release enzymes that degrade tissue components
• Damage blood vessels and cause ischemic injury
• Induce host inflammatory and immune responses

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7
Q

general types of pathogens

A

• Prions
• Viruses
• Bacteria
• Chlamydia
• Rickettsia
• Mycoplasma
• Fungi
• Protozoa
• Helminths
• Ectoparasites

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8
Q

General Principles of Viral Infections
intracell?
tropism?
latent?

A

• Intracellular parasites, cannot replicate on their own
• Cell type specific
• Viral latency
A virus is a nucleic acid looking for a home

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9
Q

Viral Infection and Replication process

A

• Attach
• Penetrate
• Reproduce
• Assemble virions
• Release, usually kills

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10
Q

types of Viral Infections

A

• Transient infections
• Chronic latent infections
• Chronic productive infections
• Transforming infections/oncogenic

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11
Q

transient infection example

A

HepA

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12
Q

Chronic latent infection example

A

HSV

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13
Q

chronic productive infection example

A

HepB

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14
Q

oncogenic viruses examples

A

EBV, HPV

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15
Q

HHV
reservoir?
states?

A

• Humans are the natural reservoir
• Latency
• Reactivation

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16
Q

Human Herpes Virus types and names

A

• HHV-1= Herpes Simplex Virus Type 1
• HHV-2= Herpes Simplex Virus Type 2
• HHV-3= Varicella Zoster Virus
• HHV-4= Epstein Barr Virus
• HHV-5= Cytomegalovirus
• HHV-8= Kaposi Sarcoma associated virus

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17
Q

Transmission HSV
symptomatic?
Asymptomatic

A

• Contact with affected individual shedding virus can be done with:
–Symptomatic active lesions
–Asymptomatic viral shredding

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18
Q

HSV1 mostly causes infections where?
presents as?

A

oral infections, vesicles form and rupture with ulcerative transudate

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19
Q

Herpes Simplex Virus Type 2 mostly effects?

A

• Mostly genital infections, still ulcerations and ruptured vesicles

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20
Q

Primary Infection With. Herpes Simplex Virus
when does this usually occur?
symptoms?

A

• Initial exposure to virus in an individual without immunity
• Generally occurs at young age after physical contact with infected individual
• Mostly subclinical disease–80% of US population has antibodies to HSV, asymptomatic

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21
Q

Primary Herpetic Gingivostomatitis
S/S?

A

systemic and symptomatic
• Flu-like illness with fever, malaise, arthralgia, headache
• Cervical lymphadenopathy
erythematous marginal gingiva

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22
Q
A

primary herpetic gingivostomatitis

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23
Q

what oral tissues can be affected in primary gingivostomatits?

A

both bound and unboud tissues (keratinized and non-kertinized)

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24
Q

is primary gingivostomatitis acute or chronic? duration?

A

acute process with rapid onset and duration of 2-3 weeks

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25
Q

Recurrent Herpes Labialis
only affects?

A

only affects the lips
clustered vesicles that will rupture

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26
Q
A

recurrent herpes labialis

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27
Q

Recurrent Intra-Oral Herpes
usually on?
what can lesions do?

A

usually on the hard palate/ keratinzed and bound tissue
lesions can coalesce to form larger ulcers

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28
Q
A

recurrent intraoral herpes

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29
Q

Where is HSV dormant in affected indidivuals

A

trigeminal ganglion, can reactivate to cause S/S

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30
Q

HSV histology

A

form blisters with thin epithelium filled with transudate/ Tzanck cells= dying cells

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31
Q

HSV cytopathic effect

A

creates multinucleated cells

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32
Q

herpes whitlow

A

dentists without gloves, infection by HSV

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33
Q

herpes gladiatorium

A

usually close contact sports, can affect extra-oral tissues

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34
Q

HSV autoinoculation

A

usually affects the eye, infected indivivduals touch lesions then the eye
can result in herpes simplex keratitis

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35
Q
A

herpes simplex keratitis

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36
Q

What Is Recurrent Aphthous Stomatitis?
presentation?
cells involved?
viral?

A

• Focal mucosal destruction, “kanker sore”, exudate surrounded red halo forming an ulcer
• T lymphocyte mediated cytotoxic reaction, NOT VIRAL

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37
Q

Evolution Of An Aphthous Ulcer

A
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38
Q

Precipitating Factors for Recurrent Aphthous Stomatitis

A

• Sodium lauryl sulfate (SLS), toothpaste component
• Stress
• Trauma
• Allergies
• Acidic foods / juices
• Gluten
• Endocrine alterations

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39
Q

duration of Recurrent Aphthous Stomatitis

A

2-3 weeks

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40
Q

what tissues are affected by Recurrent Aphthous Stomatitis

A

non-keratinzed tissue, moveable and non-bound

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41
Q

Clinical Forms of Recurrent Aphthous Stomatitis

A

minor, major, and herpetic Aphthae

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42
Q

Minor Aphthae
occurance?
presentation?
healing time?

A

• Recurrent disease
• Shallow, painful ulcerations on non-keratinized mucosa
• Solitary or multiple lesions
• Heal in two weeks

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43
Q
A

minor aphthae

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44
Q

Major Aphthae
size?
depth?
healing?

A

• Larger (> 0.5cm)
• Deeper - may heal with scarring
• Heal slowly - weeks to months

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45
Q
A

major aphthae

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46
Q
A

scarring of major aphthae

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47
Q

Herpetiform Aphthae presentation?
healing time?
remission?

A

• Crops of small, shallow, painful ulcers (mimics herpes clusters)
• Heal in two weeks
• Short remissions

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48
Q

Herpetiform aphthae Resembles Recurrent Intra-oral Herpes Simplex
BUT

A

Located on non-keratinized mucosa and Does not begin as vesicles

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49
Q

Clinical Differential Diagnosis of recurrent herpes and recurrent aphthae
vesicular stage?
number of lesions?
location?

A
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50
Q

Aphthous-like Lesions May Be Associated With _________? examples?

A

systemic dx
• Behcet’s Syndrome
• Reiter’s Syndrome

• Inflammatory Bowel Disease
– Ulcerative colitis
– Crohn’s Disease

• Malabsorption Syndromes
– Gluten Sensitive Enteropathy

• Cyclic Neutropenia

• HIV / AIDS

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51
Q

Primary And Recurrent Infections With Varicella Zoster Virus

A

• Primary Infection -Varicella (Chicken Pox)
• Recurrent Infection -Zoster (Shingles)

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52
Q

Varicella (Chicken Pox)
transmission?
clinical or nonclinical?
symptoms?
lesions where?
waves?
scarring?

A

Varicella (Chicken Pox)
• Transmission by inspirationof infected droplets
• Clinical disease in mostindividuals
• Constitutional symptoms
• Skin lesions begin on face/trunk
• Vesicles in repeated waves
• Heal without scarring

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53
Q

can varicella have oral lesions

A

yes

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54
Q

how does varicella resolve

A

immunity created, virus becomes dormant in doral root ganglia

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55
Q

how does zoster occur

A

reactivation of the virus in doral root ganglia, leads to unilateral signs in associated dermatome

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56
Q

prodrome of zoster

A

pain and parathesia

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57
Q

can zoster present facially and orally?

A

yes, vesicles can form in mouth and on face and rupture.

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58
Q

does zoster have scarring

A

yes, lesion on skin may scar with healing

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59
Q

zoster and bone, dental correlation?

A

can lead to bone necrosis, seen on hard palate

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60
Q

zoster on the palate difference from herpes?

A

will have similar appearance but have a longer duration and intense pain

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61
Q

chronic pain of zoster

A

post-herpetic neuralgia (lasting pain in affected area) can occur after the prodromal and acute pain of zoster

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62
Q

Epstein Barr Virus
HHV?
most adults?
latent?
tropism?
infects epithelial cells where?

A

• Herpesvirus (HHV-4)
• Most adults EBV+
• Latency
• Tropism for B lymphocytes
• Infects epithelial cells of oral mucosa, oropharynx and nasopharynx

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63
Q

Dx’s associated with EBV

A
  1. Infectious Mononucleosis
  2. Lymphomas –NHL and HL (Burkitt lymphoma (NHL))
  3. Nasopharyngeal Carcinoma
  4. Oral Hairy Leukoplakia
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64
Q

Clinical Features of Infectious Mononucleosis
limiting?
usually occurs in what demographic? why?
signs and symptoms?

A

• Debilitating EBV infection
• Self-limiting
• Young adults- Salivary transmission
• Fatigue
• Malaise
• Lymphadenopathy
• Fever
• Sore throat

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65
Q

infectious mononucleosis infects what cells?
results in?

A

• Peripheral blood lymphocytosis
• Lymphocytes, not monocytes
• Atypical lymphocytes (Downey Cells)

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66
Q

infectious mononucleosis effects on the palate

A

petechia hemmorhages common

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67
Q

Infectious Mononucleosis effect on gingiva

A

Necrotizing Ulcerative Gingivitis

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68
Q

tests for mono
ab? binds to? specific to EBV?
spot test?
specific tests?

A

• Heterophile antibody
– IgM antibody - induced by EBV infection
– Binds to Paul-Bunnell antigen of sheep and bovine RBCs
– Non-specific antibody - not specific for EBV

• Monospot Test - detects heterophile antibody

• EBV-specific testing

69
Q

Infectious MononucleosisTreatment

A

• Symptomatic
• Bed rest, prevent splenic rupture

70
Q

Oral Hairy Leukoplakia
associated with?
location?
may also occur in association with?

A

• Epithelial hyperplasia associated with EBV infection
• Lateral border of tongue –common location
• May occur in any immunodeficiency state

71
Q
A

oral hairy luekoplakia

72
Q
A

hairy tongue on dorsal

73
Q

how to diagnose oral hairy leukoplakia

A

biopsy

74
Q

Cytomegalovirus
HHV#?
most are affected by what age?
most are symptomatic or asym?

A

• CMV (HHV –5 )
• Most of population affect by age 60
• Most CMV infections are asymptomatic

75
Q

stages of CMV infection

A

inital infection > latent > reactivation

76
Q

Acute Infection by Cytomegalovirus presentation.
heterophile ab test?
rare cases may have what oral effects?

A

• Similar to infectious mononucleosis (EBV)
• Heterophile antibody negative
• Rarely acute sialadenitis (salivary gland infection)with painful swelling and xerostomia

77
Q

Cytomegalovirus Infections in Immunocompromised Individuals could lead to?

A

• Retinitis –blindness
• Colitis

78
Q

Coxsackie Virus
occurs in what age?
transmission?

A

• Coxsackievirus Group A
• Self-limited disease that occurs in epidemics of flu-like symptoms in young children
• Transmitted by fecal-oral and airborne routes

79
Q

Herpangina
caused by?
presentation? location?

A

caused by coxsackie virus
• Constitutional symptoms
• Begins as small vesicles that rupture and ulcerate
• Posterior oral cavity and oropharynx

80
Q

hand, foot and mouth dx

A

caused by coxsackie
Vesicular eruption of hands, feet and anterior mouth

81
Q

Measles (Rubeola)
age?
communicable?
symptom?
vax?

A

• Childhood infection
• Communicable disease
• Skin rash
• Measles, Mumps, Rubella vaccine (MMR) Immunization

82
Q

oral sign of mealses

A

Koplik Spots
• “Grains of salt” on an erythematous base
• Foci of epithelial necrosis

83
Q

what is this? what is it indicative of?

A

koplik spots, indicative of measles

84
Q

Acute Viral Parotitis (Mumps) –Endemic Parotitis
age?
communicable?
vax?

A

• Childhood infection
• Communicable disease
• Measles, Mumps, Rubella vaccine (MMR) Immunization

85
Q

what virus causes measles and mumps

A

paroxyvirus

86
Q

what virus causes rubella

A

togovirus

87
Q

mumps
%subclinical?
prodromal symptoms?
salivary glands?

A

• 30% subclinical infection
• Prodromal constitutional symptoms
• Salivary gland swelling and discomfort

88
Q

Laboratory Findings in Mumps
what is elevated in the serum?
types of tests?

A

• Elevated serum amylase
–Released from granules during lysis of acinar cells
• Specific serologic tests

89
Q

Complications of Mumps
age group differences?

A

• Complications rare in the young and more common in older individuals
• Orchitis (testicle inflamm), oophoritis (ovary inflamm), mastitis (breast tissue inflamm), meningitis, thyroiditis, pancreatitis
• Sterility, hearing loss

90
Q

bacterial infection can be?

A

• Transient bacterial infections
• Localized infections
• Systemic infections

91
Q

bacteria intra or extracellular

A

either

92
Q

bacteria produce?

A

toxins

93
Q

bacteria grow on?

A

media

94
Q

Tuberculosis
caused by?
most common place of infection?
extra/intracellular?
type of dx?

A

• Mycobacterium tuberculosis
• Pulmonary infection most common
• Intracellular pathogen
• Granulomatous disease

95
Q

how much of the pop in infected with TB, leading cause of death?

A

1/3
• Leading infectious cause of death after AIDS

96
Q

Disadvantaged populations for TB?
Active tuberculosis cases increasing?

A

Disadvantaged populations– Homeless– Malnourished– Overcrowded
Active tuberculosis cases increasing– HIV infection– Immigration

97
Q

Infection vs Active Disease in Tuberculosis

A

• Infection - growth of the organism in a patient
• Active disease - destructive, symptomatic disease

98
Q

Transmission of Tuberculosis

A

• Droplet nuclei (1 - 5 microns)
• Stay airborne for long periods of time
• Reach the pulmonary alveoli

99
Q

Primary Pulmonary Tuberculosis
• what persons?
• lesions?
• what controls infection?
• what events may occur in the tissue?
• what can be in the lesions?
• reactivation?

A

• Previously unexposed (unsensitized) person
• Gohn complex (parenchymal lung lesion and hilar nodal lesion)
• Cell-mediated immunity controls infection
• Fibrosis and calcification
• Viable organisms dormant in lesions (latent disease)
• May reactivate if immune defenses lowered

100
Q
A

gohn focus of primary pulmonary TB

101
Q

Secondary Pulmonary Tuberculosis
how does this happen?
what can be the result?

A

• Reactivation of dormant primary lesions in a previously sensitized host
• Cavitation leads to erosion into airway and production of contaminated sputum

102
Q

Pulmonary systemic Miliary Tuberculosis

A

can enter lymphatics and dessimate to other organs

103
Q

what kind of inflammation occurs with tuberculosis
necrosis?

A

necrotizing granulomatous inflammation
caseating necrosis

104
Q

Tuberculosis histo

A

would have granulomas with giant cells/ epithelioid histocytes surrounded with lymphocytes and plasma cells

105
Q

stain for TB

A

acid fast

106
Q

how does mycobacterium TB behave as an intracellular pathogen

A

TB cord factor- prevents the formation of the phagolysosome

107
Q

chronic TB ulcers oral manifestations
where?
similar to?

A

can occur on lateral tongue, could be similar to SCC

108
Q

Tuberculosis Diagnosis

A

• Chest radiograph
• Sputum culture
• Molecular biologic tools

109
Q

TB tx

A

Multi-drug regimens
– Isoniazid
– Rifampin
– Ethambutol
– Streptomycin
– Pyrazinimide
– Rifabutin

110
Q

TB symptoms

A

• Chronic cough
• Hemoptysis
• Weight loss
• Night sweats
• Fever

111
Q

TB dx of spine

A

potts dx= curvature with osseous breakdown

112
Q

PPD Test
type of hypersensitivity?
what is injected?
what is recruited to the area?
result is positive?

A

• Type IV delayed hypersensitivity reaction to protein from M. tuberculosis
• Intracutaneous tuberculin injection
• T-cells sensitized by prior infection recruited to area
• Produces an area of induration

113
Q

Positive Tuberculin Skin Test:
indicates?
what exists?
is the dx active?

A

usually with induration >4cm
• Individual has been infected
• Cell-mediated hypersensitivity exists
• Does not indicate active disease

114
Q

Bacillus Calmette-Guerin (BCG)
Vaccination

A

• Live, attenuated strain of Mycobacterium bovis
• Causes positive PPD reaction
• Effectiveness uncertain
• Not used in United States

115
Q

Scrofula

A

• Tuberculous lymphadenitis of neck
• Mycobacterium bovis infection from infected milk
• Pasteurization of milk counters this
• Tuberculosis control for cattle

116
Q

SYPHILLIS
organism?
transmission?
stages?
latent?

A

Treponema pallidum
• Sexually-transmitted systemic disease
• Sequential clinical stages
• Years of latency

117
Q

2 FORMS OF SYPHILLIS

A

• Acquired syphilis -sexual transmission
• Congenital syphilis - in utero transmission

118
Q

Clinical Stages of Untreated Acquired Syphilis
time frame of each?

A

• Primary - 1 week to 3 months
• Secondary - 1 to 12 months
• Tertiary (Late) - 1 to 30 years

119
Q

lesion of primary syphilis

A

chancre, can be genital or oral
hard/indurated

120
Q

Lesions of Secondary Syphilis

A

• Skin rash= mucopaplar rash, all over skin
• Mucous patch, can be tx
• Condyloma lata (skin lesion= most infective)

121
Q

Tertiary Syphilis
lesions present
NS?
CVS?

A

• Most destructive stage
• Gumma lesions
• Syphilitic glossitis (papilla affected)
• Nervous system –neurosyphilis– Tabes dorsalis: slow degeneration of the nerve cells and nerve fibers that carry sensory information to the brain.
• Cardiovascular system– Aneurysm of ascending aorta

122
Q

gumma of tertiary syphillis
type of inflammation? cells present?
infectious?

A

granulomatous inflamm, typical cells
can cause perforation of the palate and nasal collapse
non-infectious (no viral shedding)

123
Q

infectivity of syphillis lesions

A
124
Q

Lesions of Congenital Syphilis

A

• Snuffles
• Saddle nose- depressed nasal bridge
• Rhagades- cracks or fissures of skin
• Hutchinson’s incisors
• Mulberry molars

125
Q

Dental Stigmata of Congenital Syphilis

A

• Hutchinson’s incisors
• Mulberry molars

126
Q

Hutchinson’s Triad of Congenital Syphilis

A
  1. Blind - intersitital keratitis
  2. Deaf
  3. Dental anomalies
127
Q

Laboratory Tests for Syphilis
can it be cultured?
microscopy?
serologic tests?

A

• Culture –cannot culture
• Microscopy –dark field or fluorescence microscopy
Serologic tests for Syphilis possible

128
Q

Serologic tests for Syphilis:

A

• Non -Treponemal Tests - reagin - antibody to cardiolipin
– RPR –Rapid Plasma Reagin

• Treponemal Tests –specific for T. pallidum
– FTA-ABS –Fluorescent Treponemal Antigen Absorption
– MHA-TP –Microhemagglutinin –Treponema pallidum

129
Q

dx caused by fungi
genera examples?

A

• Superficial - skin, hair, nails– Dermatophytes
• Subcutaneous - dermis and subcutaneous tissue– Sporotricosis
• Systemic - deep infections of internal organs– Histoplasmosis
• Opportunistic –immunocompromised host– Candidiasis

130
Q

Mucormycosis
pts?
presentation? progression?

A

immunocompromised pts
black necrotic area of palate that can lead to perforation

131
Q
A

mucomycosis

132
Q

Histoplasmosis
endemic to?
transmission? source?
level of infection?
symptoms/additional name?

A

• Endemic to Mississippi River Valley
• Transmission by inhalation of spores
– Bird droppings, dust particles
• Sub-clinical infection usual
• Flu-like syndrome
Mississippi Valley Fever

133
Q

Histoplasmosis results in

A

Deep Fungal Infection of the Lung

134
Q

how is histoplasmosis contracted?
main mech of defense?
creates?

A

• Inhalation of spores
• Phagocytosis
• Specific immunity/ Killing of organism

135
Q

histoplasmosis calcification?

A

dystrophic calcification
calcified hilar and medistinal nodes
calcified lung nodules

136
Q

Histoplasma Capsulatum morphology

A

• Dimorphic fungus - yeast at body temperature, mold in nature
• 80% - 90% population infected

137
Q

most common systemic fungal infection in usa

A

histoplasma capsulatum

138
Q

disseminated histoplasmosis
populations?
spreads to?
common lesions?

A

• Elderly, debilitated, immunosuppressed, AIDS
• Spreads to extra-pulmonary sites
• Adrenal lesions (Addison’sdisease) and Oral lesions are common

139
Q

desimminated histoplasmosis gingiva presents as?

A

nodular ulcerative masses

140
Q

Coccidioidomycosis
tissues involved?
symptoms?
dissemination possible?
virulence?

A

• Deep fungal infection of the lungs
• 40% develop respiratory symptoms
• Disseminated disease may occur
MOST VIRULENT OF THE FUNGI

141
Q

Disseminated Coccidioidomycosis presents where?

A

oral
skin granulomas

142
Q

Sarcoidosis
fungal?
cause?
demograpics?

A

NOT FUNGAL
• Multi-system granulomatous disorder
• Unknown cause
• Young adults
• African-Americans - 10:1

143
Q

sarcoidosis common findings
lymphadenpathy?
common location of lesions?

A

– Hilar lymphadenopathy
– Skin and eye lesions

144
Q

Hilar Lymphadenopathy in Sarcoidosis presents as?

A

non-caseating granulomas

145
Q

diagnosing sarcoidosis
ways to diagnose?
what can be elevated in the serum?
what biopsy could be done?
how can we use histopathology?

A

Sarcoidosis is a Diagnosis of Exclusion

• Clinical
• Radiographic

• Laboratory –elevated Angiotensin Converting Enzyme (sACE), serum Calcium

• Biopsy
– Bronchoscopic biopsy
– Salivary gland biopsy

• Histopathologic –non-caseating granulomas
– Special stains negative
– Cultures negative

146
Q

contents of sarcoidosis non caseating granulomas, are these specific to sarcoidosis?

A

schaumann bodies and asteroid bodies, not specific to sarcoidosis
An eosinophilic star-burst inclusion within a giant cell is an asteroid body.
Schaumann bodies are cytoplasmic, laminated calcifications.

147
Q

oral lesions of sarcoidosis

A

uncommon
non-specific submucosal papule affecting any site

148
Q

salivary gland involvemtn in sarcoidosis

A

partoid enlargement
xerostomia
facial nn weakness

149
Q

Treatment of Sarcoidosis
mild and severe

A

Mild disease –observation, no treatment, may resolve spontaneously
Severe disease - systemic corticosteroids

150
Q

Clinical Forms of Oral Candidiasis

A
151
Q

Acute Pseudomembranous Candidiasis

A

thrush
cottage cheese appearence
wiped away with an red base remaining

152
Q
A

thrush

153
Q

b

A

thrush, c. albicans

154
Q

tx pseudomembraneous candidasis

A
155
Q

atrophic candidasis
appearence?
associated with?
symptom?

A

erythmatous area on the tongue
associated with long term broad spectrum Ax use
burning sensation

156
Q

atrophic candidasis agar?

A

sabaurand agar- low pH and gentamyacin inhibit bacterial growth

157
Q

Erythematous Candidiasis

A

redness of the tongue

158
Q

Erythematous Candidiasis tx

A
159
Q

steroid inhaler and candidasis

A

will create an environment for c albicans growth

160
Q

angular chelitis

A

corners of the mouth
due to change in OVD

161
Q
A

angular chelitis

162
Q

angular Cheilitis tx

A
163
Q

hyperplastic candidasis
how to diagnose

A

leukoplakia on buccal mucosa
req a biopsy to diagnose

164
Q

candidasis histo

A

hypahe mixed in with the superficial epithelium

165
Q

Central Papillary Atrophy indicates?
associated with?

A

Median Rhomboid Glossitis, associated with chronic candidia infections

166
Q
A

median rhomboid glossitis

167
Q

Chronic Mucocutaneous Candidiasis due to?
affects what tissues?

A

T cell defects
affects both mucosa and skin

168
Q

candidasis in HIV infection affects what oral tissues?

A

affects palate and tongue

PATH II (32 decks)

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