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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
Recurrent Herpes Labialis only affects?
only affects the lips clustered vesicles that will rupture
26
recurrent herpes labialis
27
Recurrent Intra-Oral Herpes usually on? what can lesions do?
usually on the hard palate/ keratinzed and bound tissue lesions can coalesce to form larger ulcers
28
recurrent intraoral herpes
29
Where is HSV dormant in affected indidivuals
trigeminal ganglion, can reactivate to cause S/S
30
HSV histology
form blisters with thin epithelium filled with transudate/ Tzanck cells= dying cells
31
HSV cytopathic effect
creates multinucleated cells
32
herpes whitlow
dentists without gloves, infection by HSV
33
herpes gladiatorium
usually close contact sports, can affect extra-oral tissues
34
HSV autoinoculation
usually affects the eye, infected indivivduals touch lesions then the eye can result in herpes simplex keratitis
35
herpes simplex keratitis
36
What Is Recurrent Aphthous Stomatitis? presentation? cells involved? viral?
• Focal mucosal destruction, "kanker sore", exudate surrounded red halo forming an ulcer • T lymphocyte mediated cytotoxic reaction, NOT VIRAL
37
Evolution Of An Aphthous Ulcer
38
Precipitating Factors for Recurrent Aphthous Stomatitis
• Sodium lauryl sulfate (SLS), toothpaste component • Stress • Trauma • Allergies • Acidic foods / juices • Gluten • Endocrine alterations
39
duration of Recurrent Aphthous Stomatitis
2-3 weeks
40
what tissues are affected by Recurrent Aphthous Stomatitis
non-keratinzed tissue, moveable and non-bound
41
Clinical Forms of Recurrent Aphthous Stomatitis
minor, major, and herpetic Aphthae
42
Minor Aphthae occurance? presentation? healing time?
• Recurrent disease • Shallow, painful ulcerations on non-keratinized mucosa • Solitary or multiple lesions • Heal in two weeks
43
minor aphthae
44
Major Aphthae size? depth? healing?
• Larger (> 0.5cm) • Deeper - may heal with scarring • Heal slowly - weeks to months
45
major aphthae
46
scarring of major aphthae
47
Herpetiform Aphthae presentation? healing time? remission?
• Crops of small, shallow, painful ulcers (mimics herpes clusters) • Heal in two weeks • Short remissions
48
Herpetiform aphthae Resembles Recurrent Intra-oral Herpes Simplex BUT
Located on non-keratinized mucosa and Does not begin as vesicles
49
Clinical Differential Diagnosis of recurrent herpes and recurrent aphthae vesicular stage? number of lesions? location?
50
Aphthous-like Lesions May Be Associated With _________? examples?
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
51
Primary And Recurrent Infections With Varicella Zoster Virus
• Primary Infection -Varicella (Chicken Pox) • Recurrent Infection -Zoster (Shingles)
52
Varicella (Chicken Pox) transmission? clinical or nonclinical? symptoms? lesions where? waves? scarring?
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
53
can varicella have oral lesions
yes
54
how does varicella resolve
immunity created, virus becomes dormant in doral root ganglia
55
how does zoster occur
reactivation of the virus in doral root ganglia, leads to unilateral signs in associated dermatome
56
prodrome of zoster
pain and parathesia
57
can zoster present facially and orally?
yes, vesicles can form in mouth and on face and rupture.
58
does zoster have scarring
yes, lesion on skin may scar with healing
59
zoster and bone, dental correlation?
can lead to bone necrosis, seen on hard palate
60
zoster on the palate difference from herpes?
will have similar appearance but have a longer duration and intense pain
61
chronic pain of zoster
post-herpetic neuralgia (lasting pain in affected area) can occur after the prodromal and acute pain of zoster
62
Epstein Barr Virus HHV? most adults? latent? tropism? infects epithelial cells where?
• Herpesvirus (HHV-4) • Most adults EBV+ • Latency • Tropism for B lymphocytes • Infects epithelial cells of oral mucosa, oropharynx and nasopharynx
63
Dx's associated with EBV
1. Infectious Mononucleosis 2. Lymphomas –NHL and HL (Burkitt lymphoma (NHL)) 3. Nasopharyngeal Carcinoma 4. Oral Hairy Leukoplakia
64
Clinical Features of Infectious Mononucleosis limiting? usually occurs in what demographic? why? signs and symptoms?
• Debilitating EBV infection • Self-limiting • Young adults- Salivary transmission • Fatigue • Malaise • Lymphadenopathy • Fever • Sore throat
65
infectious mononucleosis infects what cells? results in?
• Peripheral blood lymphocytosis • Lymphocytes, not monocytes • Atypical lymphocytes (Downey Cells)
66
infectious mononucleosis effects on the palate
petechia hemmorhages common
67
Infectious Mononucleosis effect on gingiva
Necrotizing Ulcerative Gingivitis
68
tests for mono ab? binds to? specific to EBV? spot test? specific tests?
• 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
Infectious MononucleosisTreatment
• Symptomatic • Bed rest, prevent splenic rupture
70
Oral Hairy Leukoplakia associated with? location? may also occur in association with?
• Epithelial hyperplasia associated with EBV infection • Lateral border of tongue –common location • May occur in any immunodeficiency state
71
oral hairy luekoplakia
72
hairy tongue on dorsal
73
how to diagnose oral hairy leukoplakia
biopsy
74
Cytomegalovirus HHV#? most are affected by what age? most are symptomatic or asym?
• CMV (HHV –5 ) • Most of population affect by age 60 • Most CMV infections are asymptomatic
75
stages of CMV infection
inital infection > latent > reactivation
76
Acute Infection by Cytomegalovirus presentation. heterophile ab test? rare cases may have what oral effects?
• Similar to infectious mononucleosis (EBV) • Heterophile antibody negative • Rarely acute sialadenitis (salivary gland infection)with painful swelling and xerostomia
77
Cytomegalovirus Infections in Immunocompromised Individuals could lead to?
• Retinitis –blindness • Colitis
78
Coxsackie Virus occurs in what age? transmission?
• 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
Herpangina caused by? presentation? location?
caused by coxsackie virus • Constitutional symptoms • Begins as small vesicles that rupture and ulcerate • Posterior oral cavity and oropharynx
80
hand, foot and mouth dx
caused by coxsackie Vesicular eruption of hands, feet and anterior mouth
81
Measles (Rubeola) age? communicable? symptom? vax?
• Childhood infection • Communicable disease • Skin rash • Measles, Mumps, Rubella vaccine (MMR) Immunization
82
oral sign of mealses
Koplik Spots • “Grains of salt” on an erythematous base • Foci of epithelial necrosis
83
what is this? what is it indicative of?
koplik spots, indicative of measles
84
Acute Viral Parotitis (Mumps) –Endemic Parotitis age? communicable? vax?
• Childhood infection • Communicable disease • Measles, Mumps, Rubella vaccine (MMR) Immunization
85
what virus causes measles and mumps
paroxyvirus
86
what virus causes rubella
togovirus
87
mumps %subclinical? prodromal symptoms? salivary glands?
• 30% subclinical infection • Prodromal constitutional symptoms • Salivary gland swelling and discomfort
88
Laboratory Findings in Mumps what is elevated in the serum? types of tests?
• Elevated serum amylase –Released from granules during lysis of acinar cells • Specific serologic tests
89
Complications of Mumps age group differences?
• 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
bacterial infection can be?
• Transient bacterial infections • Localized infections • Systemic infections
91
bacteria intra or extracellular
either
92
bacteria produce?
toxins
93
bacteria grow on?
media
94
Tuberculosis caused by? most common place of infection? extra/intracellular? type of dx?
• Mycobacterium tuberculosis • Pulmonary infection most common • Intracellular pathogen • Granulomatous disease
95
how much of the pop in infected with TB, leading cause of death?
1/3 • Leading infectious cause of death after AIDS
96
Disadvantaged populations for TB? Active tuberculosis cases increasing?
Disadvantaged populations– Homeless– Malnourished– Overcrowded Active tuberculosis cases increasing– HIV infection– Immigration
97
Infection vs Active Disease in Tuberculosis
• Infection - growth of the organism in a patient • Active disease - destructive, symptomatic disease
98
Transmission of Tuberculosis
• Droplet nuclei (1 - 5 microns) • Stay airborne for long periods of time • Reach the pulmonary alveoli
99
Primary Pulmonary Tuberculosis • what persons? • lesions? • what controls infection? • what events may occur in the tissue? • what can be in the lesions? • reactivation?
• 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
gohn focus of primary pulmonary TB
101
Secondary Pulmonary Tuberculosis how does this happen? what can be the result?
• Reactivation of dormant primary lesions in a previously sensitized host • Cavitation leads to erosion into airway and production of contaminated sputum
102
Pulmonary systemic Miliary Tuberculosis
can enter lymphatics and dessimate to other organs
103
what kind of inflammation occurs with tuberculosis necrosis?
necrotizing granulomatous inflammation caseating necrosis
104
Tuberculosis histo
would have granulomas with giant cells/ epithelioid histocytes surrounded with lymphocytes and plasma cells
105
stain for TB
acid fast
106
how does mycobacterium TB behave as an intracellular pathogen
TB cord factor- prevents the formation of the phagolysosome
107
chronic TB ulcers oral manifestations where? similar to?
can occur on lateral tongue, could be similar to SCC
108
Tuberculosis Diagnosis
• Chest radiograph • Sputum culture • Molecular biologic tools
109
TB tx
Multi-drug regimens – Isoniazid – Rifampin – Ethambutol – Streptomycin – Pyrazinimide – Rifabutin
110
TB symptoms
• Chronic cough • Hemoptysis • Weight loss • Night sweats • Fever
111
TB dx of spine
potts dx= curvature with osseous breakdown
112
PPD Test type of hypersensitivity? what is injected? what is recruited to the area? result is positive?
• 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
Positive Tuberculin Skin Test: indicates? what exists? is the dx active?
usually with induration >4cm • Individual has been infected • Cell-mediated hypersensitivity exists • Does not indicate active disease
114
Bacillus Calmette-Guerin (BCG) Vaccination
• Live, attenuated strain of Mycobacterium bovis • Causes positive PPD reaction • Effectiveness uncertain • Not used in United States
115
Scrofula
• Tuberculous lymphadenitis of neck • Mycobacterium bovis infection from infected milk • Pasteurization of milk counters this • Tuberculosis control for cattle
116
SYPHILLIS organism? transmission? stages? latent?
Treponema pallidum • Sexually-transmitted systemic disease • Sequential clinical stages • Years of latency
117
2 FORMS OF SYPHILLIS
• Acquired syphilis -sexual transmission • Congenital syphilis - in utero transmission
118
Clinical Stages of Untreated Acquired Syphilis time frame of each?
• Primary - 1 week to 3 months • Secondary - 1 to 12 months • Tertiary (Late) - 1 to 30 years
119
lesion of primary syphilis
chancre, can be genital or oral hard/indurated
120
Lesions of Secondary Syphilis
• Skin rash= mucopaplar rash, all over skin • Mucous patch, can be tx • Condyloma lata (skin lesion= most infective)
121
Tertiary Syphilis lesions present NS? CVS?
• 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
gumma of tertiary syphillis type of inflammation? cells present? infectious?
granulomatous inflamm, typical cells can cause perforation of the palate and nasal collapse non-infectious (no viral shedding)
123
infectivity of syphillis lesions
124
Lesions of Congenital Syphilis
• Snuffles • Saddle nose- depressed nasal bridge • Rhagades- cracks or fissures of skin • Hutchinson’s incisors • Mulberry molars
125
Dental Stigmata of Congenital Syphilis
• Hutchinson’s incisors • Mulberry molars
126
Hutchinson’s Triad of Congenital Syphilis
1. Blind - intersitital keratitis 2. Deaf 3. Dental anomalies
127
Laboratory Tests for Syphilis can it be cultured? microscopy? serologic tests?
• Culture –cannot culture • Microscopy –dark field or fluorescence microscopy Serologic tests for Syphilis possible
128
Serologic tests for Syphilis:
• 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
dx caused by fungi genera examples?
• Superficial - skin, hair, nails– Dermatophytes • Subcutaneous - dermis and subcutaneous tissue– Sporotricosis • Systemic - deep infections of internal organs– Histoplasmosis • Opportunistic –immunocompromised host– Candidiasis
130
Mucormycosis pts? presentation? progression?
immunocompromised pts black necrotic area of palate that can lead to perforation
131
mucomycosis
132
Histoplasmosis endemic to? transmission? source? level of infection? symptoms/additional name?
• 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
Histoplasmosis results in
Deep Fungal Infection of the Lung
134
how is histoplasmosis contracted? main mech of defense? creates?
• Inhalation of spores • Phagocytosis • Specific immunity/ Killing of organism
135
histoplasmosis calcification?
dystrophic calcification calcified hilar and medistinal nodes calcified lung nodules
136
Histoplasma Capsulatum morphology
• Dimorphic fungus - yeast at body temperature, mold in nature • 80% - 90% population infected
137
most common systemic fungal infection in usa
histoplasma capsulatum
138
disseminated histoplasmosis populations? spreads to? common lesions?
• Elderly, debilitated, immunosuppressed, AIDS • Spreads to extra-pulmonary sites • Adrenal lesions (Addison’sdisease) and Oral lesions are common
139
desimminated histoplasmosis gingiva presents as?
nodular ulcerative masses
140
Coccidioidomycosis tissues involved? symptoms? dissemination possible? virulence?
• Deep fungal infection of the lungs • 40% develop respiratory symptoms • Disseminated disease may occur MOST VIRULENT OF THE FUNGI
141
Disseminated Coccidioidomycosis presents where?
oral skin granulomas
142
Sarcoidosis fungal? cause? demograpics?
NOT FUNGAL • Multi-system granulomatous disorder • Unknown cause • Young adults • African-Americans - 10:1
143
sarcoidosis common findings lymphadenpathy? common location of lesions?
– Hilar lymphadenopathy – Skin and eye lesions
144
Hilar Lymphadenopathy in Sarcoidosis presents as?
non-caseating granulomas
145
diagnosing sarcoidosis ways to diagnose? what can be elevated in the serum? what biopsy could be done? how can we use histopathology?
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
contents of sarcoidosis non caseating granulomas, are these specific to sarcoidosis?
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
oral lesions of sarcoidosis
uncommon non-specific submucosal papule affecting any site
148
salivary gland involvemtn in sarcoidosis
partoid enlargement xerostomia facial nn weakness
149
Treatment of Sarcoidosis mild and severe
Mild disease –observation, no treatment, may resolve spontaneously Severe disease - systemic corticosteroids
150
Clinical Forms of Oral Candidiasis
151
Acute Pseudomembranous Candidiasis
thrush cottage cheese appearence wiped away with an red base remaining
152
thrush
153
b
thrush, c. albicans
154
tx pseudomembraneous candidasis
155
atrophic candidasis appearence? associated with? symptom?
erythmatous area on the tongue associated with long term broad spectrum Ax use burning sensation
156
atrophic candidasis agar?
sabaurand agar- low pH and gentamyacin inhibit bacterial growth
157
Erythematous Candidiasis
redness of the tongue
158
Erythematous Candidiasis tx
159
steroid inhaler and candidasis
will create an environment for c albicans growth
160
angular chelitis
corners of the mouth due to change in OVD
161
angular chelitis
162
angular Cheilitis tx
163
hyperplastic candidasis how to diagnose
leukoplakia on buccal mucosa req a biopsy to diagnose
164
candidasis histo
hypahe mixed in with the superficial epithelium
165
Central Papillary Atrophy indicates? associated with?
Median Rhomboid Glossitis, associated with chronic candidia infections
166
median rhomboid glossitis
167
Chronic Mucocutaneous Candidiasis due to? affects what tissues?
T cell defects affects both mucosa and skin
168
candidasis in HIV infection affects what oral tissues?
affects palate and tongue

PATH II (32 decks)

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