Brainscape's Knowledge GenomeTM

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


See full index

Pulmonary Physiology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is the mechanism of the Diptheria Toxin?

A

Blocks host cell protein synthesis
AB domain binds, A domain is endocytosed, B domain assists in acidification and translocation of A domain to cytosol, A domain ADP ribosylates EF2 blocking hydrolysis of GTP which is required for movement of ribosomes.

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

How to Superantigens work?

A

They complex MHC molecules with TCRs to stimulate antigen independent activation of lymphocytes and creation of IgM.

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

What are the most common agents responsible for diseases of the nasopharynx?

A

Rhinovirus, coronavirus, other respiratory viruses, Staph Aureus.

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

What at the most common agents responsible for disease in the oropharynx?

A 
Group A Strep
Corynebacterium Diptheria
EBV
Adenovirus
Enterovirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the most common agents responsible for disease in the middle ear and paranasal sinuses?

A

Strep Pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Strep Pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the most common agents of infection of the epiglottis?

A

Haemophilus influenzae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the microbiological characteristics of Group A strep?

A 
Gram positive cocci in chains
Catalase Negative
Beta hemolytic (have clear space)
Bacitracin sensitive
Confirmed with anti-lancefield A test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is Group A strep identified and differentiated from Staph Aureus?

A

Staph Aureus is catalase positive and that is the easiest way to tell the two apart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the characteristics of viral pharyngitis?

A

More nasal discharge
Fever less common in adults
Paucity of clinical findings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the characteristics of bacterial pharyngitis?

A

More erythema and swelling
High fever
Tender cervical lymph nodes
Absence of conjunctivities, cough, and rhinorrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the major virulence determinants of group A strep?

A 
M protein (IgG response to this responsible for scarlet fever)
Helical antiphagocytic protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the growth media requirements for Haemophilus Influenzae

A

Chocolate agar consisting of Hemin and NAD or NADP (will not grow without both)
Grows best in 5-10% CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What clinical features distinguish H. Influenzae

A

Requires Chocolate Agar
Oxidase positive
Requires Hemin and NAD

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

What are the Characteristics of the H. Influenzae B capsule?

A

Antiphagocytic

Protective against antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What types of diseases are associated with encapsulated H. Influenzae B?

A

Meningitis
Epiglottitis
Pneumonia (seen often with COPD in adults)

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

What diseases are typically caused by non-encapsulated H. Influenzae?

A

Acute otitis media, sinusitis
Exacerbation of COPD
Conjunctivitis
Invasive infection in immunocompromised

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

How is the H. I-B virus destroyed in the body?

A

Anti-capsular antibodies are extremely important in the elimination.
Antibodies mediate complement dependent phagocytosis. Complement can also cause lysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do you treat H I B?

A

Start with 3rd generation cephalosporin, if organism is susceptible to ampicillin switch to that. (Meningitis often treated empirically with both)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is in the conjugate vaccine?

A

HIB coupled with Diptheria toxoid.

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

What is the recommended vaccination schedule for HIB?

A

2 months, 4 months, 6 months, and 12 months (Recommended that mother gets revaccinated to confer IgG immunity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you identify C diptheriae in the lab?

A

Turns black on tellurite agar, catalase positive, typically appears as “chinese letters” on H&E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the clinical features of diptheria?

A

Incubation period 2-5 days
May involve any mucous membrane
Classified based on site of infection
Creates a pseudomembrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do you treat diptheria?

A

Antitoxin (horse origin may cause serum sickness)
Antibiotics to eradicate organisms
Both must be given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the cellular receptor for binding of the major group of rhinoviruses?

A

ICAM-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the general structure of the rhinovirus?

A

+ssRNA is infectious
Small, Icosahedral
>100 serotypes
Temperature sensitive (likes nasopharynx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does replication of rhinovirus occur?

A

VP4 binds cellular receptor, virus mRNA directly binds to ribosomes, viral proteases cleave into VP0-VP1 and VP3, Viral RNA dependent RNA poly generates -ssRNA and makes +ssRNA from it. VPo is cleaved into VP2 and VP4, genome and proteins self assemble and the virus is released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Where does the RNA polymerase for Rhinovirus come from?

A

The virus encodes it’s own RNA polymerase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is Rhinovirus transmitted?

A

Aerosol droplets and directs contact, primarily in the fall and winter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does the virus cause disease?

A

Immunopathologic
Causes nasal discharge, congestion, and sneezing, sorethroat, muscle aches, fatigue…etc
May get into lower respiratory system of immune compromised people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is immunity conferred?

A

Mucosal IgA is protective against already encountered serotypes, interferons fight virus but cause pathogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the general structure of RSV?

A

Enveloped
-ssRNA genome
Two major envelope proteins (G for grab, F for fusion)
Encodes it’s own Rna dependent Rna Poly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the characteristics of RSV?

A

Transmitted by aerosol droplets and direct contact
Nosocomial spread common
Disease can be severe in immunocompromised people, babies born prematurely, or in children less than 8 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When is RSV the worst?

A

Primarily during the winter months because droplets stay in the air longer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the pathogenesis of RSV?

A 
Runny nose
Fever
Tachypnea
Wheezing and breathlessness with edema of the bronchioles (LRT)
Continuous coughing (LRT)
Cyanosis (LRT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where is immunity conferred against RSV?

A

Immunity is typically conferred against both serotypes only in the LRT, URT reinfection is common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is RSV treated?

A

There is no licensed vaccine to date
Ribavirin has been used but is of limited efficacy
If severe, supportive care is given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Why is there currently no vaccine against RSV?

A

Infants who were put on a trial with the vaccine developed a severe course of the disease upon re-exposure leading to hospitalization and death is two cases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is Respigam?

A

Polyclonal antibody used for passive therapy in patients with sever lower respiratory tract infection by RSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is Synagis?

A

Monoclonal antibody indicated in use for patients with high risk of severe LRT infection by RSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the structure of Adenovirus?

A

Unenveloped
ds linear DNA genome
51 serotypes are known
Replicates in the nucleas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does adenovirus replicate?

A 
Temporal replication in the nucleas. 
Binds via CAR to ICAM-1
Encodes it's own DNA polymerase
E1-E1B-E2A-E2B-E3-E4
L1-L5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How is Adenovirus transmitted?

A

Direct contact via FO, contaminated water, or aerosol droplets
Immunity against virus is serotype specific
Lytic in mucoepithelial cells, latent in adenoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What serotypes of adenovirus cause which pathogenic process?

A

Ad3, 7 cause pharyngoconjunctival fever in crowded places

Ad4, 7 cause acute respiratory disease in military recruits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What respiratory diseases are caused by adenovirus?

A 
Febrile, undifferentiated URI
Pharyngoconjunctival fever
Acutre respiratory distress
Pertussis-like symptoms
Pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What other adenovirus serotypes commonly cause disease?

A

8, 19 37 cause Keratoconjunctivitis
11 causes hemorrhagic conjunctivitis
11,4,7,1,21 cause acute hemorrhagic cystitis
40-42, 31, 25, 28 cause gastroenteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is immunity conferred against adenovirus?

A

Cell mediated immunity is crucial for clearing infection, long term immunity is conferred against one serotype by antibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is adenovirus treated?

A

Symptomatic treatment
Should resolve in 7-10 days
New live vaccine tablet was approved in 2011 for use during basic training

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is EBV?

A 
y-herpesvirus
Enveloped
Linear dsDNA
Encodes it's own DNA-dependent DNA poly
Replicates in the nucleas
Encodes numerous host proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the epidemiology of EBV?

A

95% of adults thought to have latent infection
Adolescents are major risk group
Transmission primarily though saliva
Incubation of 6-8 weeks and symptoms persist 2-3 weeks.
Infects and replicates in epithelial and Bcells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How does EBV infection present?

A

Sore throat, inflammed tonsils, swollen cervical lymph nodes, splenomegaly, nausea, chills, photophobia, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the most common symptoms of infectious Mono?

A

Pharyngitis, cervical lymphadenopathy, Sore throat, >10% atypical lympocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What genes allow for latency of EBV?

A

EBER and EBNA1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How is EBV diagnosed?

A

Atypical lymphocytes, agglutination test for heterophile antibodies, EBV antibody ELISA, PCR for EBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is characteristic of typical pneumonia?

A

High fever, chills, chest pain, lobar consolidation

55
Q

What is the most common cause of Typical CAP?

A

Strep Pneumoniae
Staph Aureus
H. Influenzae

56
Q

What is atypical CAP?

A

less severe illness, dry cough, headache, diffuse pattern on xray

57
Q

What are the most common causes of atypical CAP?

A 
Mycoplasm pneumoniae
Chlamydia pneumonia
Legionella pneumophila
Viruses
Coxiella
58
Q

What are the bacterial characteristics of Strep Pneumoniae?

A

Alpha hemolytic (green color due to breakdown of heme by pneumolysin)
Mucoid colonies
Gram positive, catlase negative, susceptible to optochin and bile

59
Q

What is the major virulence factor of Strep Pneumo?

A

Thick polysaccharide capsule which interferes with deposition of C3b on bacterial surface, no phagocytosis
90+ serotypes prevent immunity against all types
Loss of capsule = loss of virulence

60
Q

What are predisposing factors to pneumococcal pneumonia?

A 
Viral URT infection
Compromised pulmonary fx
Age
Black, Indians, Inuits
Impaired immunity
Type 3 serotype of S. pnuemoniae in URT
61
Q

What are the signs and symptoms of pneumococcal pneumonia?

A

Sudden onset, rusty sputum, pleuritic chest pain, lobar consolidation

62
Q

What are possible sequelae of Pneumococcal pneumonia?

A

Death
Neurological deficits from meningitis
Hearing impairment secondary to otitis media

63
Q

Who is most susceptible to drug resistant pneumococcal pneumonia?

A

Most is resistant to penicillin

The very young and very old are more susceptible

64
Q

Why is the conjucate PCV13 vaccine more effective?

A

Conjugation allows for recognition (not superantigen) this allows for IgG creation, somatic hypermutation, and a secondary response.

65
Q

What makes mycoplasma unique?

A

Smallest bacteria
Can pass through .45 um filters
Lack cell wall (no peptidoglycan)
Surrounded by lipid bilayer containing sterols

66
Q

What forms of mycoplasma are normally human pathogens?

A

M. Pneumoniae
M. Hominis (ureteritis)
M. Genitalium (ureteritis)
Ureaplasma species (ureteritis)

67
Q

How do mycoplasm colonies look in culture?

A

Require serum for growth and have a fried egg appearance under a microscope

68
Q

What is the epidemiology of M. pneumoniae?

A 
No seasonality
Higher in young and old
Spreads in dorms and barracks
Transmission through close contact via droplets
2-3 week incubation period.
69
Q

What are the pathogenic mechanisms of M. Pneumoniae infections?

A

Respiratory entry, attaches to epithelium of LRT via P1 adhesin to NA containing glycoprotein
Produces CARDS toxin which has ADP-ribosyltransferase activity causing deterioration of the cilia
Phagocytosis by Ms leads to inflammation
Vigorous CMI leads to sever clinical form

70
Q

How is M. Pneumoniae diagnosed?

A

Serology, cold agglutinins

71
Q

What antibiotics are recommended for M. Pneumonia?

A

Tetracycline
Macrolides (emerging resistance)
B-lactams not effective

72
Q

What Chlamydia forms cause pneumonia?

A

C. Pneumoniae

C. Psittaci (birds)

73
Q

What are characteristics of Chlamydiceae?

A 
Have DNA, RNA, and 70s ribosomes
Divide by binary fission
Small genome
Carry plasmids
Cell Envelope
74
Q

What is the infectious process of chlamydia?

A

Elementary bodies are phagocytosed, reticulate bodies form and begin to multiply by binary fission, chlamydia antigens are expressed and released from cell surface, reticulate bodies reorganized to elementary bodies and are released to cause further infection

75
Q

What are the pathogenic mechanisms of chlamydia?

A

Cytopathic effect on host cells
Immunopathogenesis causing inflammation and scarring in effort to clear disease
Establishes persisten infection

76
Q

How is C. Pneumoniae diagnosed?

A

Serology Igm titer greater that a 1:64 or a four fold rise of IgG titer is acuted serum and 4 week later serum

77
Q

How does psittaci infection occur?

A

Zoonotic infection causes wasting disease in birds, transmissible to humans via dried feces or direct contact
Patients usually are poultry industry workers, vets, or exotic bird owners
Presents with pneumonia and confusion

78
Q

How is chlamydia treated?

A

Doxycycline
Macrolides
(empiric therapy for all atypical pneumonias)

79
Q

What does pertussis look like on H and E?

A

Blue Safety pin shaped rod

80
Q

What is the environmental niche of Legionella?

A 
Gram negative
Lives in iron rich soil
Lives in water
Endures extreme temp
Resists chlorination
Survives inside amoebas
81
Q

What are the risk factors for Legionella?

A

Immunosuppression, smoking, renal failure, age over 50, cancer, male sex, alcohol abuse

82
Q

How does legionella live intracellularly?

A

Taken up by coiling phagocytosis, ribosomes surround phagosome, bacteria multiplies, host cell lyses and bacteria escapes.

83
Q

How do you identify legionella?

A

Gram negative slender bacilli
Need to do bronchoalveolar lavage to get MACs in which they live
Growth media is Buffered Charcoal Yeast Agar which has amino acids, iron, and trace metals

84
Q

What is pontiac fever?

A

Disease associated with legionella causing flu like symptoms.

85
Q

How do you diagnose Leginella?

A

UA done with ELISA for LPS antigen
BAL with Flourescent staining or Dieterles silver stain
4 fold antibody rise in serum

86
Q

What antibiotics treat Legionella?

A

Macrolides (-romycin)
Flouroquinolones (-oxacin)
B-lactams ineffective

87
Q

What is the environs for Psedomonas Aureginosa?

A

Gram negative rods
Flagellated
Strict aerobes
(Nonfermenters)

88
Q

Where is psudomonas found?

A

Everywhere
Fresh Fruits and Veggies
Hot Tubs
Respiratory Therapy Equipment

89
Q

What are the most important virulence factors of pseudomonas?

A 
LPS (cytokine agonist)
Alginate Capsule (resists opsonization)
Pili (adherence)
Flagella (motility)
Exotoxin A
90
Q

What does pseudomonas Auereginosa cause?

A 
Folliculitis
Swimmers ear
Pneumonia in CF patients
Burn infections
Nosocomial infections
Cellulitis
UTIs
91
Q

What is the alginate capsule?

A

1-4 linked B-D-mannuronate and its C-5 epimer a-L-guluronate

92
Q

Why is Pseudomonas less susceptible to antibiotics in CF patients

A

Biofilm formation

93
Q

How is P. Auruginosa characterized in the lab?

A 
Lactase - growth on McConkey Agar
Oxidase positive
Pyocyanin production (green)
Glucose oxidation only
Smells like grape soda
94
Q

What antibiotics are useful against Pseudomonas?

A 
Aminoglycosides
Carbapanems
Carboxypenicillins
Ureidopenicillins
Cephalosporins
Flouroquinolones
Monobactam
95
Q

What are the characteristics of Klebsiella Pneumonia?

A

Aspiration pneumonia
Gram -, Lac +
Mucoid Capsule
Targets alcoholics

96
Q

What are important concepts of endemic mycoses?

A

All acquired by inhalation of spores
Specific geographic locations
Acute or reactivated
Range in severity

97
Q

What are the typical characteristics of Histoplasmosis?

A 
Similar appearance to TB
White or Brown hyphal colonies
Yeast form appears as "dot disease"
Transmitted in soil in areas contaminated by bird or bat droppings
Mostly in mississippi river valley
98
Q

What is the pathogenesis of Histo?

A

Spores get into the lungs where they are taken up by dust cells in their yeast form, travel to lymph nodes and spread everywhere (lungs, lymph, liver, spleen, bone marrow)
Small amounts remain in granules and can become reactivated years later

99
Q

What is the most common clinical finding in Histo?

A

None

100
Q

What predisposes somboy to progressive disseminated Histo?

A

TNF-a inhibition

101
Q

How is Histo diagnosed?

A

Culture (takes a while)
Fungal stain (low sensitivity)
Serology (can have false negs or pos)
Antigen

102
Q

How are dimorphic fungi treated?

A 
Moderate disease (Itraconazole)
Severe disease (Amphoteracin B)
103
Q

What does Blastomyces look like?

A

White tan filamentous mold colonies with round to over conidia
Spherical yeast with thick double contoured walls
Reproduces by broad base budding
Dogs are 10x more susceptible than humans

104
Q

Where is blastomyces found?

A

Southern Mississippi river valley

105
Q

What is the pathogenesis of blastomyces?

A

Inhalation of conidia into alveoli causes yeast form to multiply by budding leading to hematoginous dissemination (it is the great pretender)
Most common in lungs, skin, bone and genitals
Typically presents like anything else but doesn’t respond to antibiotics

106
Q

What is coccidioidomycosis?

A

Mold form grows quickly and forms anthroconidia
Yeast form forms spherules which produce endospores
Found in San Juaquin Valley of CA
Can cause eosinophilia

107
Q

How does coccy typically present?

A

Like pneumonia, usually disseminated to skin, bone, and meninges (uncommon in immunocompetent hosts)
Filipinos and Blacks get it worse
Late pregnancy and post-partum is bad

108
Q

How do you diagnose coccy?

A

Microscopic evaluation of tissue
Serology
Calcaflour white stain
Methanamine silver stain

109
Q

What is the epidemiology of TB?

A

70% of new contacts not infected
30% are infected
95% of new infected develop latent infection
5% develop disease within two years
5% with latent infection develop active tuberculosis

110
Q

Typical presentation of TB?

A 
Cough
Weight loss
Hemoptysis
Constitutional
Chest pain
Fatigue
111
Q

Who is at risk for TB?

A 
Close contact with TB
Foreign born from TB Area
Prisoners
Health Care Workers
Underserved
Ethnic minorities
Children exposed to adults with TB
IV druggies
112
Q

Where is Latent Vs. REactivated TB found?

A

Latent found near the hilum and in the nearest lymph node in the form of a ghon complex
Reactivated in the upper lobe of the lung
Can proceed to miliary TB and proceed to other locations in the body causing potts disease, meningitis, or lymphadenitis or any other disease

113
Q

How do you screen for TB?

A

Positive PPD, Interferon Y test. BCG vaccine can give false positive on PPD
Acid Fast bacilli are found on sputum
Cavitary lesion in upper lobe on Xray (can be histo)

114
Q

What are the major components of the cellular envelope of TB?

A 
Waxes
Mycolic acids
Polysaccharides
Peptidoglycan
PGL-I (so it can get phagocytosed)
Lipoarabinomannan
115
Q

What stain causes TB to flouresce?

A

Auramine-Rhodamine stain

116
Q

On what agar is TB grown?

A

Lowenstein-Jensen agar (buff colonies after 3 weeks)

117
Q

How is TB treated?

A

Latent (9 months Isoniazid)

Active (Rifampin, Isoniazid, Pyrazinamide, Ethambutol) R.I.P.E

118
Q

What are the innate defenses in the urinary tract?

A 
Low pH
Urea
Organic Acids
Tamm-horsfall protein
lactoferrin
Lipocalcin
Antimicrobial peptides
119
Q

What are the signs and symptoms of cystitis?

A

Dysuria
Frequent urination
Suprapubic pain

120
Q

What are the signs and symptoms of pyelonephritis?

A 
Flank pain
Fever
Nausea
Increased CRP
Bacteremia
121
Q

What are the major players in Uncomplicated UTI?

A

Members of the Enterobacteriaceae family (normal intestinal flora)
E. Coli, K. Pneumoniae, Proteus Mirabalis…
Gram negative, oxidase negative

122
Q

What are the virulence factors of uropathogenic E. Coli?

A

Type 1 fimbriae (colonization of bladder)
P pili (adhere to digalactoside receptors, colonization of kidneys)
Hemolysin (damages cell membranes)
CNF toxin (inhibits Rho GTPases of cytoskeleton)

123
Q

What is a gram positive cause of UTI?

A

S. Saprophyticus

124
Q

How is S. Saprophyticus identified in a lab?

A

Gram positive cocci in clusters
Non-hemolytic, white
Catalase positive
Coagulase Negative

125
Q

What are complicated UTI?

A

Associated with metabolic disorders that are secondary to anatomic or functional abnormalities (UTI + kidney stones)

126
Q

What are catheter associated UTIs?

A

80% of nosocomial UTIs related to catheterization

Fever, leukocytosis, pyuria

127
Q

What are the players in Complicated and Caterter UTI?

A 
Enterobactericeae (Straight rods, glucose fermenters, oxidase negative)
Proteus mirabilis
E. Coli
Klebsiella
Pseudomonas
S aureus
128
Q

What common organisms form biofilms on indwelling catheters

A

Extracellular crosslinking polymers that facilitate adhesion are found in
S epidermidis, S aureus, E. faecalis, Candida albicans, pseudomons, klebsiella, E. coli, P. Mirabilis

129
Q

What is the most common cause of catheter associate UTIs?

A

Proteus Mirabilis
Produces swarming motility on solid agar
Produces urease
Prediliction of UUT

130
Q

What is the relationship between bacterial urease and renal calculi?

A

Bacterial urease causes stones to precipitate

This is found in Proteus Mirabellis

131
Q

What are the characteristics of Pseudomonas?

A 
Gram negative rods
Non-fermenters
Non-lactose fermenters
Oxidase positive
Pyoverdin (green)
132
Q

What is the criteria for uncomplicated UTI plating?

A

> 10^5 bacteria/ml of a single species

133
Q

What is the criteria for a complicated UTI

A

10^2-10^4 bacteria/ml

134
Q

What is a positive suprapubic tap?

A

Isolation of any organism

Pulmonary Physiology (5 decks)

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