3. Bacterial Infections Flashcards
(104 cards)
1
Q
What is impetigo?
A
Superficial infection of skin caused by Staphylococus aureus and/or Streptococus pyogenes
2
Q
What allows bacteria to cause impetigo?
A
Breaks of skin:
cut
scratch
abrasion
dermatitis
3
Q
What populations tend to get impetigo?
A
Children
adults with systemic conditions
4
Q
What determines if a patient will develop impetigo when bacteria enters?
A
Immune status
bacterial load
5
Q
How does impetigo clinically progress?
A
Vesicles with clear fluid at site of injury → large bullae or ulcerated/crusted
6
Q
Dx of impetigo?
A
clinilcal presentation & history
pattern corresponds to scratches/breaks of skin
7
Q
Tx of impetigo
A
prevention and topical antibiotics
will heal by itself in most cases
8
Q
Which pathogen that causes impetigo is most worrysome? why?
A
MRSA
Resistant to typical antibiotics and if left untreated will spread systemically
9
Q
Steptococcus pyogenes is aka what?
A
Group A ß-hemolytic streptococcus (GAS)
10
Q
What is pharyngitis/tonsilitis?
A
Infection in the throat. the two conditoins usually occur together
11
Q
How is pharyngitis spread?
A
Respiratory droplet
Oral secretion
12
Q
What kind of pathogen causes the majority of pharyngitis? Tx?
A
Virus
No Tx needed or suppurative
13
Q
What bacteria causes the majority of bacterial pharyngitis?
A
GAS
14
Q
What population is most commonly affected by bacterial pharyngitis?
A
School aged children who then spread it to their family
15
Q
S/S of bacterial phayrngitis
A
Sore throat
redness of oropharynx and tonsil
cervical lymphadenopathy
NO VESICLES unlike viral pharyngitis
16
Q
Dx of bacterial pharyngitis?
A
Rapid direct antigen test (5-10 mins)
culture (gold standard, 1-2 days)
17
Q
Bacterial pharyngitis Tx
A
Antibiotics
Necessary to prevent complications
18
Q
How does scarlet fever begin?
A
Untreated strep throat that has spread throughout body but has not developed antitoxin Ab
19
Q
What causes the red skin in scarlet fever?
A
GAS produces erythrogenic toxin.
The toxin attacks small blood vessels cusing the skin rash all over hte body and mucosa
20
Q
What is exanthem?
A
skin rash
21
Q
What is enanthem?
A
Mucosa rash
22
Q
What population is most often affected by scarlet fever?
A
Children
23
Q
How does the skin rash in scarlet fever resolve?
A
Fades in a week followed by desquamation
24
Q
Where is oral cavity petechiae most obvious in scarlet fever?
A
Soft palate
25
How is the tongue affected in scarlet fever?
Hyperplastic
erythematous fungiform papillae against white background
Initially white strawberry; later red strawberry (5-7 days). White coat (keratin) sheds off like the skin rash leaving the red coloration
26
What complications from pharyngitis are most concerning?
Rheumatoid fever
Glomerulonephritis
27
Why do bacterial pharyngitis systemic complications occur?
GAS produces M protein which the body forms ABs against
Due to M proteins similarity to host tissue, the M protein ABs will cross react with antigens from host tissue causing tissue damage
28
Why are recurrent infections of bacterial pharyngitis concerning?
Recurrent infections will increase M protein Ab production which will cause significant organ destruction from constant cross reaction
29
If a patient with GAS infection has a family history of RF, how does this affect treatment?
Pt with family history of Rf requires a post therapeutic lab test to ensure that all of the bacteria has been cleared
30
What pathogen causes tuberculosis?
Mycobacterium tubercolosis
31
What characteristic of M. tuberculosis confers it so much strength? What adidtional strengths are gained?
* High lipid content of its cell wall
* Resistance to killing by phagocytosis
* Inhibits penetration of antimicrobial agents
* Resistance to drying and remain viable in dried sputum
32
Tx for M tuberculosis?
Combination of antibiotics
33
What is tuberculosis?
Communicable chronic granulomatous dz
34
What populations are most affected by TB?
Elderly
Poor
AIDS
Immunocompromised
35
What is the #1 risk factor for TB?
AIDS
36
What is the leading cause of death in HIV infected pts?
TB
37
What causes damage in TB?
NOT toxin mediated
Host immune response causes damage (type IV hypersensitivity)
Bacterial antigens are presented to t cells. T cells become sensitized and release cytokines that attract macrophages and T cells to get rid of Mycobacterium.
Macrophages are ineffective in killing mycobacterium. Inability to kill mycobacterium causes T cells to continue releasing cytokines which recruits more T cels and macrophages.
Macrophages then fuse to form giant cells. This walls off bacteria for containment
this forms granules called tubercles with central necrosis called caseous
38
What are the two classifications of TB?
Primary - non-sensitized individuals contacting TB for first time
Secondary - reactivation or re-infection of the bacilli in a previously sensitized host
39
When does sensitivity occur in primary TB?
Second week of infection patient will develop immune response. No initial imune response because pt is not sensitized
40
How does primary TB manifest in pts?
Arrested/self-limited
Tubercle is walled off by calcified connective tissue
Walling off of organism prevents active disease and spread of TB from patient
41
How is TB reactived to cause secondary TB?
Imunosuppression
42
how does damage occur in secondary TB?
An immune response will occur within 2-3 dys after reactivation or reexposure causing greater inflammation which leads to significant destruction of lung tissue
43
How can TB become systemic?
Granulomatous lesions can break into blood causing systemic infection. Only occurs in small percentage of secondary patients
44
What is primary progressive TB?
Pts that are immunosuppressed and quickly develop systemic TB from primary TB because they cannot effectively wall off bacteria.
45
What patients tend to develop primary progressive TB?
HIV patients with high degree of immunosuppression
46
how does oral TB occur?
cut in the oral mucosa contaminated by sputum with M. tuberculosis.
Very rarely, occurs in patients with systemic TB (PPT or secondary)
47
S/S of oral TB?
Chronic non-healing ulcer or swellings (granulation tissue like)
Osteomyelitis in pts with systemic TB (very rare)
48
Dx of oral TB
Biopsy is a must.
Cannot tell from clinical presentation
49
Dx of TB?
* Mantoux test (PPD skin test)
* inject purified protein isolated from bacteria
* if body has antigen against bacteria (sensitized), will illicit a reaction within 2-3 days against protein
* great for screening but not very accurate
* Culture
* Takes a long time (3-6 weeks)
* Gold standard
* Good for determining use of treating antibiotic
* Stain
* acid fast bacilli
* non-specific
* PCR
* quick and specific
* $$$
50
What is leprosy?
Chornic granulomatous dz from Mycobacterium leprae
51
Transmission of leprosy
Unclear but possibly ihalation of contaminated respiratory droplets
52
Site of leprosy involvement?
Skin and nerves (main)
mucous membrane and resp tract (minor)
53
What are the two classifications of leprosy?
Tuberculoid (Paucibacillary)
Lepromatous (Multibacillary)
54
What population of pts develop paucibacillary leprosy?
Pts with high immune response
55
Test for paucibacillary leprosy?
Positive lepromin test (a skin test to heat killed bacteria)
56
Is paucibacillary leprosy localized or diffuse?
Localized
57
S/S of paucibacillary leprosy
Manifests as small number of well circumscribed, hypopigmented skin lesions
Nerve involvement leads to loss of sensation in affected skin
58
Paucibacillary leprosy histology
granulomatous inflammation with well formed granulomas (multinucleated giant cells surrounded by lymphocytes)
Acid fast stain will show some but few bacteria demonstrating proper immune system function
59
what kind of patients develop multibacillary leprosy?
Pts with reduced immune response
60
Test for multibacillary leprosy?
Negative lepromin test due to poor immune fxn
61
Is multibacillary leprosy diffuse or localized?
Diffuse
62
S/S of multibacillary leprosy
numerous ill defined hypopigmented lesions
With time, lesions become thickened
loss of skin appendages (replaced with granulomatous inflammation)
skin enlargement leads to facial distortion
All areas of involvement have no sensation
Nerve involement spread to most of body
63
Histology of multibacillary leprosy?
Granulation tissue with ill formed granuloma (multinucleated giant cells mixed with T lymphocytes)
Numerous bacteria in acid-fast stain demonstrating poor immune response
64
What oral lesions manifest in multibacillary leprosy?
Soft tissue -- ulceration, necrosis and loss of tissue
Bone - resorption and perforation of palate
Facies leprosa - resorption of anterior nasal spine and anterior maxillary alveolar edge (pts end up with collapsed nose and lose front teeth)
65
Dx of leprosy?
Characteristic skin lesions with diminished sensation
Prove presence of M. leprae
66
Tx for leprosy
Eradicate infection with MDR
Treat complication of nerve drug
Reconstruction of damage
67
What bacteria causes Syphilis?
Treponema pallidum
68
Transmission of syphilis?
Sexual contact
Mother to fetus
bacteria is vulnerable to drying
69
What accounts for the recent hike in syphilis cases?
Unprotected oral sex and AIDs
70
What condition complicates syphilis?
AIDS
71
What stages of syphilis are treatable by antibiotics?
All (primary, secondary, tertiary)
72
Wha is the trend of a patients infectiousness after contracting syphilis?
High -\> Low
Primary \> secondary \> tertiary
73
S/S of primary syphilis?
Chancre (Most often at genitalia but oral cavity, lip is most common extragenital site)
Ulcer
Regional lymphadenopathy
highly infectious
74
Dx of primary syphlis
* Serology
* Microscopy (IHC or dark-field)
* only good for chancre on genitals not oral cavity bc oral cavity naturally has spirochete bacteria
75
how does secondary syphilis develop?
If primary syphilis is untreated, will develop secondary syphilis 4-10 weeks after initial infectoin.
May overlap with primary syphilis
76
how does secondary syphilis resolve?
spontaneously heal in 3-12 weeks
May relapse
77
Dx of secondary syphilis
Serology
Microscopy
PCR
78
S/S of secondary syphilis?
**Maculopapular rash**
* often on face, trunk and **palmar and plantar areas **
* rarely in oral cavity
**Mucous patch**
* elevated white patch in oral cavity
* split papules when on commissure of mouth
**Lues maligna**
* appear on skin and mucosa
* most severe form of secondary syphlis (aka malignany syphilis)
* multiple nodules that become encrusted very quickly then heal with scars that may lead ot disfigurement
* mostly seen in HIV pts
Condyloma lata
* skin and mucosa
* wart-like lesions
79
What is the typical patient that develops tertiary syphilis now?
HIV+ patients
80
What kind of systemic damages arise from tertiary syphilis?
CV and CNS damage
81
S/S of tertiary syphilis?
Gummas
82
What is congenital syphilis?
Transplacental infection of T. pallidum during fetal development
83
What is the most common clinical manifestation of congenital syphilis?
Hutchison's triad
84
What is hutchnson's triad?
1. Dental anomalies (hutchinson's incisors and mulberry molars)
2. Deafness (8th nerve damage)
3. Blindness (interstitial keratosis)
85
What is the pathology of Bartonella in healthy patients?
Pt mounts an immune response and forms granulomatous inflammation
This reaction is normally sufficient in eradicating bacteria without Tx
example = cat scratch dz
86
What is the pathology of bartonella in immunocompromised patients?
Pt cannot mount immune response and bacteria promotes vessel formation (angiogenesis)
Leads to bacillary angiomatosis which is a bartonella infection that looks like a tumor
Requires antibiotic
87
What is cat scratch dz?
Benign self limiting infection of bartonella hensellae transmitted from cat to human via scratch
88
S/S of cat scratch dz?
1-2 weeks: primary skin lesion along scratch line
3-7 weeks: regional lymphadenopathy, may have fever. Primary lesion may be resolved
Scratch on face usually develop submandibular lymphadenopathy
89
Dx of cat scratch dz
Base on clinical history and demonstrate the bacteria in the specimen or a positive titer of Ab to B. henselae
Culture not effective
90
Tx of cat scratch dz
None needed
follow up with patient to ensure resolution (usually clear by 4 weeks)
91
What is Actinomyces?
Gram + filamentous anaerobic bacteria mostly present in head and neck region
92
What is the most common Actinomyces in oral flora?
A. isrealii
93
S/S of actinomycosis
Acute deep suppurative abscess with an associated draining sinus tract
Colonies of actinomycotic organisms surrounded by neutrophils
Sulfur granules (yellowish flecks seen clinically representing colonies of actinomyces)
94
Dx of actinomycosis
Histology + culture
95
Tx of actinomycosis
Surgical drainage/debridement and antibiotics
96
What is tonsillar concretions?
When a large mass forms into the invaginations of the crypts of the palatine tonsils
97
What is tonsillolithiasis?
When the tonsillar concretions become calcified
98
S/S of tonsillar conretions and tonsillolithiasis
Usually asymptomatic
Radiograph will show tonsilloliths in ramus area of mandible
If pts feel mass, gargle salt water to prevent further accumulation and growth
99
Tx of tonsillar concretions and tonsillolithiasis?
Usually unneeded
surgery if symptomatic
100
What is a noma?
opportunistic infection caused by components of the normal flora in patients that are severely immunocompromised (HIV & malnourished children)
101
S/S of noma
Begins as necrotizing ulcerative gingivitis, extends to involve adjacent soft tissue and beyond
normal flora becomes flesh eating
most patients will die without treatment
Extensive necrosis and marked tissue destruction
facial disfigurement
102
Noma Tx
correct underlying dz
antibiotics
debridement
103
What are gummas?
granulomatous inflammation causing ulceration and necrosis
extensive tissue destruction
can involve many tissues including perforating the palate
104
How long does it take for primary syphilis to develop and resolve?
Develops in 3-90 days and heals spontaneously in 3-8 weeks
