Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Micro last plus one anatomy 5 > bacterial infections of the skin and soft tissue III > Flashcards

bacterial infections of the skin and soft tissue III Flashcards

1
Q

clostridium- what are most infections of ?

A
  • skin, soft tissue and food poisoning as well as antibiotic associated diarrhea/colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

clostridium
type
features
where do they live

A

gram positive rod, SPORE-FORMING

  • anaerobic
  • spores are resilient and last years
  • ubiquitous to soil, water, sewage and GI commensal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are some virulence factors of clostridium

A
  • hemolysin, neurotoxin, enterotoxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q 
Clostridium perfringens
type
what does it produce
spores?
toxins?
what does it cause?
A
  • gram pos, non-motile rod, anaerobic, beta hemolytic
  • growth is associated with LARGE PRODUCTION OF HYDROGEN AND CARBON DIOXIDE
  • rarely see spores
  • makes lots of toxins A-E- mostly A
  • causes GAS GANGRENE (CLOSTRIDIAL MYONECROSIS) AND GASTROENTERITIS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what toxins does c. perfringens produce and what do they do?

A
  • alpha toxin- MOST IMPORTANT- phospholipase that hydrolyzes lecithin and sphingomyelin to disrupt cell membranes
  • beta toxin- leads to loss of mucosa and formation of necrotic lesions that lead to necrotizing enteritis
  • enterotoxin- binds small intestine altering its permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what type of soft tissue diseases does C perfringens cause?

A
  • cellulitis
  • fasciitis
  • suppurative myositis
  • myonecrosis (gas gangrene)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is gas gangrene?

A
  • it is a c. perfringens disease that are obtained by a surgical wound or a traumatic (war) wound via environment or GI
  • surgery is usually during a colon surgery
  • begins as wound infection and IS ACCOMPANIED BY GAS PRODUCTION (CREPITATIONS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the progression of disease for gas gangrene

A
  • starts of as cellulitis that turns in to myositis with PUS IN THE MUSCLE LAYER
  • this progresses to muscle necrosis and systemic spread with high mortality
  • CHARACTERISITIC RED/BROWN, FOUL SMELLING DISCHARGE
  • ALPHA TOXINS THAT LEAD TO EDMA AND NECROSIS
  • INCREASED VASCULAR PERMEABILITY OF TOXINS CAN LEAD TO DEATH WITHOUT BACTEREMIA-TOXIN INDUCED SHOCK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can come up on an xray that would indicate that the infection was clostridium perfringens?

A
  • there are clear spaces in the infected area that can be seen in an xray. it is a result of the gas production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how can c. perfringens be diagnosed? treatment?

A
  • gas bubbles in xray
  • gram pos rods in specimen WITHOUT LEUKOCYTES
  • treat: surgical debridement with PCN or clindamycin and metronidazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is clostridium tetani?

A
  • motile, spore forming, Gram pos rod
  • STRICT ANAEROBE
  • DRUMSTICK APPEARANCE =spores
  • found in soil and GI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does c. tetani enter the body?

A
  • wound thru nail or splinter
  • nonsterile technique
  • ** key point- results from a wound that goes necrotic and provides great medium by which infection can occur locally and TETANOSPASMIN CAN ACT AND CAN MAKE ITS WAY TO THE CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the two toxins of c. tetani

A

A) tetanolysin- oxygen-liable hemolysin

B) TETANOSPASMIN- heat-liable neurotoxin**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

tetanospasmin

A
  • in c. tetani
  • INACTIVATES PROTEINS THAT CONTROL RELEASE OF INHIBITORY NEUROTRANSMITTERS (GLYCINE AND GAMMA AMINOBUTARIC ACID) which causes unregulated excitation and SPASTIC PARALYSIS
  • binding is irreversible but rapidly degraded in GI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the three generalized presentations of c. tetani

A

1) generalized- involve masseter muscles-lock jaw- sweat, back spasms, autonomic involvement
2) localized- disease just at infected musculature, head
3) neonatal- umbilical stump infected, 90% mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is risus sardonicus

A

-caused by c. tetani
- sustained contraction of facial muscles
“sardonic smile”-abnormal, cynical like sustained grin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

opsithotonic posturing

A
  • spinal musculature curving and weirdness due to c. tetani infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

diagnosis and treatment of C. tetani

A
  • diagnosis- cant really culture, so clinical pres is important, masseter, spasms
  • treat- debride wound, metronidazole, HTIG-HUMAN TETANUS IMMUNOGLOBULIN VACCINATION (antibody that recognizes the toxin and kills it)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

prevention for c. tetani

A
  • childhood vaccination

- booster 10 yr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

mycobacterium
type?
cell wall?
what are some important characteristics about mycobacterium

A
  • gram pos rod
  • acid fast
  • aerobic
  • cell wall is LIPID RICH
  • NONSPORE FORMING
  • STAIN BRIGHT PINK- FROM MYCOLIC ACID IN THE CELL WALL (FATTY ACID)
  • CONTAINS LAM-LIPOARABINOMANNAN (LIKE LPS)- proinflammatory cell wall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is important to note about mycobacterium and its resistance? what about it’s growth rate?

A
  • it is resistant to many cleaning detergents, antibiotics, immune responses, and disinfectants
  • slow growing therefore slow disease process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is important to note about the disease process when it comes to mycobacteria

A
  • it is slow and follows a chronic course that leads to granuloma formation
  • there are no endo or exotoxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what type of immunity helps to kill mycobacteria?

A

CELL MEDIATED

24
Q

what is Mycobacteria tuberculosis

A
  • caused by mycobacteria
  • slow growing
  • NONPIGMENTED OR TAN COLONIES
  • usually obtained via inhalation of droplets
25
Q

what can result from a long-term mycobacteria tuberculosis infection?

A
  • you can get upper lumbar and lower thoracic vertebrae problems via hematogenous spread from the respiratory tract - potts disease, tuberculus vertebral osteomyelitis and skeletal TB
26
Q

how is m tuberculosis osteo probs diagnosed

A
  • travel hx
  • back pain and GIBBUS DEFORMITY
  • radiographic evidence
  • positive PPD
  • aspirate or biopsies of spinal lesions
27
Q

pathogenesis of m. tuberculosis

A
  • infect and live in macrophages so the macrophages cant kill them
  • macrophage secretes IL-12 and TNF-alpha in response
  • T cells differentiate intoTH1 AND PRODUCE IFN-GAMMA
  • MACROPHAGE INCREASES KILLING POTENTIAL IN RESPONSE TO IFN-GAMMA
  • mycobacteria resti the effects so the immune system , like T cells, compensates by surrounding macrophages to form a granuloma over time
28
Q

treatment and prevention of m tuberculosis

A
  • treat- resistance due to lipid rich cell wall =challenge!
    I-REP: isoniazid, rifampin, ethambutol, pyrazinamide
    -combo of four given over SIX TO 9 MONTHS

Prevention: vaccine for kids, prophylaxis with isoniazid

29
Q

what is mycobacterium leprae

A
  • obligate intracellular parasite
  • no growth on lab media
  • human and armadillo reservoirs
  • causes leprosy
  • slow disease course with granulomas
  • no endo or exo toxins
30
Q

what does m. leprae target? what’s its cell wall like

A
  • schwann cells and macrophages

- cell wall- proinflammatory, PHENOLIC GLYCOLIPID

31
Q

Transmission of m. leprae

A

-nasal secretions

32
Q

what are the stages of m. leprae

A
  • 2 stages
    a) tuberculoid (th1)- paucibacillary- containing few bacilli
  • cell mediated so gets rid of it

b) lepromatous (th2)- HENSEN’S DISEASE- multibacillary, chronic disease of the skin and dermal macrophages as well as peripheral nerves (schwann cells)
- humoral or antibody mediated so does not get rid of it

33
Q 
presentation of tuberculoid leprosy vs lepromatous leprosy
skin lesions-
histopathology-
infectivity-
immune response- 
immunoglobulin levels-
erythema noduosum-
A

skin lesions- few hypopigment plaques with flat centers and raised boarders, peripheral nerve involvement ////many erythmatous macules, extensive tissue destruction, diffuse nerve involvement

histopathology-few or no acid fast rods/// numerous

infectivity- low/// high

immune response- th1///th2

immunoglobulin levels-normal///hi

erythema noduosum: absent/// usually present (inflammation of fat cells)

34
Q

diagnosis of m. leprae

A
  • diagnosis- mostly clinical observation
    LEPROMIN TEST- inject inactivated m. leprae and see if there is a delayed response (lepromatous leprosy) and no reaction with tuberculoid leprosy

-CULTURE IS IMPOSSIBLE

  • you can confirm lepromatous with nose or ear smear
  • tuberculoid you do a skin biopsy
35
Q

treatment of m leprae

A
  • tuberculoid- sulones (dapsone) and rifampin for SIX MONTHS
    -lepromatous- dapsone, rifampin, clofazimine for 12 months
    -
36
Q

what are nocardiosis and actinomycosis

A
  • actinobacteria
  • cause cutaneous skin infections and bronchopulmonary disease that bring cough, dyspnea and fever
  • thought to be fungi because HAVE FILAMENTS THAT LOOK LIKE HYPHAE
37
Q

Nocardia
type
stain
special feature

A
  • gram pos rod but most appear gram neg with intracellular gram pos beads
  • WEAKLY ACID FAST- CELL WALL STRUCTURE IS SIMILAR TO MYCOBACTERIA WITH BRANCHED CHAIN FATTY ACIDS IN CELL WALL
  • have BRACHED FILAMENTS THAT RESEMBLE HYPAHE
  • slow growing
  • HAVE AERIAL HYPHAE THAT GROW UPWARD- look hairy
38
Q

what is mycetoma?

A
  • mycetoma is caused by nocardia infection
  • chronic infection of the skin, underlying tissues and sometimes bones/viscera
  • tropics
  • slowly progressive and PAINLESS
  • usually starts with minor injury- FOOT IS THE MOST COMMON SITE
  • CAUSES SINUS TRACT FORMATION
39
Q

what forms of disease can nocardia present with?

A
  • 1) cellulits and subcutaneous abscesses like mycetoma
    2) lymphocutaneous diease- starts as cutaneous and spreads to lymph nodes forming chronic granulomas and ulcers
    3) 1/3 get meningitis
40
Q

diagnosis of nocardia

A
  • hx- indicates direct exposure from environment via gardening, farming***
    -directly examine branched. filamentous gram pos weakly acid fast organism
    culture
    biospy
41
Q

treatment of nocardia

A

-tetramethoprim and sulfamethoxazole

42
Q

actinomyces israellii
What do they look like
where do they colonize
when do they infect

A
  • FILAMENTOUS bacteria that look like fungi
  • anaerobe
  • colonizes mucosa of upper respiratory tract and GI and female genital tract
  • opportunistic pathogen- breach in barrier LIKE IN DENTAL WORK
43
Q

what is the infection of actinomyctes israelli like

A
  • pyogenic abscesses connected with sinus tracts

- abscesses have sulfur granules that look like grains of sand- yellow/orange

44
Q

treatment of a. israellii

A
  • PCN
45
Q

what is cervicofacial actinomycosis

A
  • nodules on face around jaw
  • usually dental- poor hygiene or surgery
  • abdominal, pelvic and chest wall involvement sometimes seen
  • result of a. israelli
46
Q

diagnosis and treatment of actinomycosis

A
  • direct examination of draining material and culture with biopsy - has a gram stain and filaments
  • colonies appear5-7 days but two weeks may be needed

treat: PCN

47
Q

how do you distinguish actinomycetes israelli from nocardia

A

nocardia is acid fast and actinomycets are not

48
Q

actinommyocis vs nocardiosis

A

clinical pattern- lump with draining sinuses (mouth)//// sporotrichoid cellulitis and myocetoma

site- cervicofacial, thorax,ab, pelvis/// extremities

source- endogenous/// environment

most common causative agent - actinomyces israelli////nocardia brasilensis

49
Q

acne vulgaris -what are the four key elements?

A

1) follicular epidermal hyperproliferation
2) excess sebum
3) inflammation
4) presence and activity of PROPRIONIBACTERIUM ACNES

50
Q

What kind of bacteria are acne vulgaris? what does it do?

A
  • small, anaerobic , gram positive rod

- causes an inflammatory response

51
Q

treatment of acne vulgaris?

A
  • topical with benoyle peroxide and antibiotics like erythromysin and clindamycin
  • followed by oral- doxycycline and isotretenoin
52
Q

gingivitis and periodontitis -what clinical pres are they

A
  • gingivitis - inflammation of gingiva
  • periodontitis- chronic inflammatory disease that includes gingivitis along with loss of connective tissue and bone support for the teeth
53
Q

what can periodontitis cause

A

CAD, preterm birth, and chronic kidney disease

54
Q

what is gingivitis and periodontitis caused by

A
  • dental plaque that is a biofilm on enamel of teeth that many microbes bind on that causes inflammatory response in gingival tissues or the bone supporting teeth
  • POLYMICROBIAL AND ANAEORBIC
  • common bacteria: poryphyomonas gingivalis and treponema denticola
55
Q

what are dental caries and what is the main causative agent

A
  • cavities

- streptococcus mutans

56
Q

what is the cause of the underlying disease in caries?

A
  • acid products made during the interaction of strepto mutans with multiple species of biofilm are the cause

Micro last plus one anatomy 5 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions