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supplemental micro > Bacteria > Flashcards

Bacteria Flashcards

0
Q

What does the plane of replication influence?

A

Whether or not the cocci grow in chains

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1
Q

What are common test results shared by streptococci?

A

Gram positive, catalase negative and grow in chains

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2
Q

What are the virulence factors for group A strep?

A

Pilli, M protein and toxins

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3
Q

What two test results indicate group A strep?

A

Beta hemolytic and bacitracin sensitive

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4
Q

What are the test differences between group A and group B strep?

A

bacitracin test and CAMP test

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5
Q

What is the reservoir and transmission for group a strep?

A

Many people are carriers. Transmitted through direct contact

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6
Q

What do you use to treat group A strep?

A

Penicillin (no resistance) or erythromycin

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7
Q

Where does group B strep reside and who does it transmit to?

A

In 1/4 of women’s vaginas. Transmits to children when they are born

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8
Q

When do you give a woman prophylactic penicillin before childbirth?

A

If she has a fever, if she has a positive strep B culture, if she had a child who contracted group B strep or if her membrane has been broken >3 hrs

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9
Q

What tests indicate group B strep?

A

Beta hemolytic, resistant to bacitracin and CAMP positive

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10
Q

What is a distinct morphological feature of s pneumoniae?

A

It is diplococcus

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11
Q

What test results ID s pneumoniae?

A

Alpha hemolysis and sensitive to optochin (bile)

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12
Q

What two streptococci have capsules as their major virulence factors?

A

Group B strep and s pneumoniae

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13
Q

What circumstances make you more susceptible to a pneumoniae

A

Inhibited mucous clearance in lungs: virus, smoking, depressed cough reflex ect

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14
Q

How is a pneumoniae treated?

A

Treat underlying cause and give penicillin after antibiotic sensitivity test

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15
Q

What test results in ID of s viridans?

A

Alpha hemolysis and resistance to optochin

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16
Q

What is caused by s viridans?

A

Dental carries and endocarditis if it gets into the blood

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17
Q

What is the virulence factor for s viridans?

A

Sugar metabolizing enzyme that produces acid

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18
Q

Which streptococci are gamma hemolytic?

A

S fecalis

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19
Q

What test result verifies that a staph infection is a aureus?

A

Coagulate positive

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20
Q

What test results would indicate staphlococci?

A

Gram positive, catalase positive and growth in clumps

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21
Q

What are the virulence factors for a aureus

A

Protein A, capsule, coagulase and toxins

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22
Q

How do you treat s aureus?

A

Check for antibiotic resistance before choosing

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23
Q

How do you ID s epidermidis?

A

Staph with negative coagulase

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24
Q

What kind of culture do you grow nisseria on?

A

Chocolate agar

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25
Q

What test determines the two types of nisseria?

A

Ferments maltose: n meningitides

Does not: n gonorrhoea

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26
Q

What are the two virulence factors of n meningitides?

A

Capsule and LPS

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27
Q

What are the two virulence factors for n gonorrhoea?

A

Pilli an LOS

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28
Q

What is the reservoir and transmission of n meningitides?

A

Respiratory tract and droplets

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29
Q

How does one prevent n meningitides?

A

Vaccine, treat with penicillin

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30
Q

How is transmission of n gonorrhoea to a neonate prevented?

A

Neonatal eye droplets

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31
Q

Do you treat n gonorroae with penicillin?

A

No because there is plasmid resistance. Do resistance panel first

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32
Q

By what process do anaerobic bacteria derive all ATP from?

A

fermentation

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33
Q

A bacterium is an obligate anaerobe if it lacks what?

A

enzymes to remove ROS (catalase and superoxide dismutase)

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34
Q

what are the two types of anaerobic infectious agents?

A

normal flora that become opportunistic pathogens and soil organisms that enter the body as spores (in wounds or vacuum packaged foods)

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35
Q

what are some ways to ensure that anaerobic bacteria grow in a liquid culture?

A

treat with reducing agents and tightly stopper in a full container

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36
Q

what components of anaerobic culture jars permit anaerobic growth?

A

air tight lid, chemical system to remove oxygen and an anaerobic indicator

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37
Q

what are the gram staining results for anaerobes?

A

all of them stain positively except for the GNAB

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38
Q

What are the major pathogenic anaerobes?

A

Clostridium, GNAB and actinomyces

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39
Q

Which normal flora anaerobic bacterial cause infection?

A

GNAB, actinomyces and C difficile

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40
Q

Where does one acquire Clostridia infections?

A

soil infected wounds or vacuum packaged foods

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41
Q

what is the major virulence factor of anaerobic bacteria?

A

exotoxins
tetanus and botulism: neurotoxin
gas gangrene and abscess: tissue degrading enzymes

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42
Q

what is the appropriate treatment for an anaerobic infection?

A

drain abscess if applicable, provide antitoxin if applicable and conclude with antibiotics

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44
Q

What are the seven defining characteristics of enterobacteriaceae?

A

Gram -, nonsporulating, straight rods, facultative aerobes, catalase positive, oxidase negative and ferment glucose

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45
Q

are all enterobacteriaceae caught by ingestion?

A

no-ICU infections like Klebsiella

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46
Q

what is a major struggle when treating enterobacteriaceae infections?

A

extreme antibiotic resistance. promiscuous to new DNA (introduces new resistances and virulence factors)

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47
Q

what are the steps of antimicrobial sensitivity testing?

A

spread liquid culture on nutrient agar plate, place disks of antibiotics on plate before overnight incubation, compare zones of clearing to table to determine most effective antibiotics

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48
Q

what are the important virulence factors of enterobacteriaceae in the gut?

A

pilli (allow attachment in GU and GI tract) and type 3 secretion systems (adhesion, enterotoxins, and macrophage takeover)

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49
Q

How do enterobacteriaceae often infect a host?

A

sampled by M cells in Peyer’s patches then alter the local macrophages to avoid destruction. Macrophages are apoptosed and enterocytes are infected on exterior surface with T3SS

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50
Q

how do enterobacteriaceae spread systemically?

A

take over macrophages to bring them around the body. these macrophages are apoptosed at a specific time (quorum sensing) in lymph nodes

51
Q

What is the foodborne infection route for Enterobacteriaceae and how can they be prevented?

A

fecal- oral rout. prevented by water treatment, handwashing, food pasteurization and cooking

52
Q

Which enterobacteriaceae can cause hemolytic uremic syndrome and what population does this affect?

A

shigell and enterohemorrhagic E coli infection. it is primarily a pediatric complication

53
Q

what is the mechanism of hemolytic uremic syndrome?

A

bacteria escape the gut and release shiga toxin into the bloodstream

54
Q

what human antigen predisposes a patient to develop reactive arthritis?

A

HLA- B27

55
Q

What are the major symptoms of reactive arthritis and what kind of disease is it?

A

conjunctivitis, urethritis and arthritis. it is autoimmune

56
Q

which bacterial infections may lead to reactive arthritis?

A

Shigella, salmonella, yersinia, campylobacter and chlamydia

57
Q

What are ICU bugs?

A

major opportunistic nosocomial infections (seldom cause symptoms in previously healthy people) caused by Klebsiella, Enterobacter, Serratia, Proteus, Providencia and Morganella

58
Q

How do you prevent ant treat ICU bugs?

A

prevention: switch catheters, scrub down patients and the ICU, and minimize hospital stays. Difficult to treat, use antibiotic sensitivity testing

59
Q

what prevented the eradication of TB?

A

AIDS

60
Q

what are the present concerns when considering TB?

A

multi drug resistance

61
Q

what are some culture characteristics of TB?

A

gram stain poorly, acid-fast stain (mycolic acid) and grow very slowly

62
Q

describe the acid fast procedure

A

boil with carbolfuschin stain, use acid/alcohol to decolorize and conterstain with methylene blue

63
Q

how is TB transmitted and disseminated in the body?

A

transmitted by inhalation, infects GI by swallowing infected speutum and travels with macrophages to lymph nodes, kidney, bones and CNS

64
Q

how do TB outcomes differ depending on the immune status of the host?

A

Immunocompetent hosts force latency with an appropriate cell mediated response (most likely will never be active). Immunosuppressed will more likely have active infection

65
Q

how does the body attempt to destroy TB?

A

CD4 cells activate infected macrophages and CD8 cells kill infected macrophages, establishing caseating granulomas. TNF alpha also helps with containment.

66
Q

what are the symptoms of classic pulmonary TB?

A

cough, weight loss, fever, night sweats, hemoptysis and chest pain.

67
Q

how is active TB diagnosis confirmed and the appropriate antibiotic treatment determined?

A

determine expsure with PPD of TST and/or IGRA speutum culture and microscopy and chest X ray. perform antibiotic resistance tests when cultures grow

68
Q

what are the extrapulmonary manifestations of TB?

A

scrofula, GU, CNS, skeletal (arthritis of one joint or pott disease), GI and miliary

69
Q

Which disease is directly obserbed therapy now a standard for?

A

Tuberculosis

70
Q

Is there an effective vaccine for TB in the US? What complication does the vaccine impose in testing?

A

yes, a live attenuated virus (not for immune compromised). it is not cost effective in the US and creates false positive in TST PPD

71
Q

what is the most effective way to reduce the incidence of TB in a population?

A

good diet and housing-latent cases are not contagious

72
Q

how are TB patients treated?

A

they are isolated in negative pressure rooms with high efficiency masks for first 2 weeks. Then they are treated with directly observed therapy with a 4 drug regimen for 3 mo-1 year. monitor hepatic toxicity monthly.

73
Q

which of the following mycobacterial infection that resembles TB is treated by the same drugs:
M. scrofulaceum, M avium, M kansasii or M marinum?

A

M. kansasii

74
Q

what is the main difference between TB and atypical mycobacteria?

A

TB is caught from other people, atypical mycobacteria from the environment

75
Q

what is the presentation of an atypical mycobacteria in an immunocompetant adult usually?

A

cutaneous infection

76
Q

which infections are immunosupressed hosts most likely to have systemic infections of?

A

M. kansasii and MAI

77
Q

what is a similarity between atypical mycobacteria and TB treatment?

A

both are hard to treat. use multiple antibiotics and worry about resistance

78
Q

how do you culture M leprae?

A

you cannot. it will not grow

79
Q

What is the optimum temperature for M leprae?

A

30-37 C

80
Q

what is the difference in immune response and symptoms of tuberculoid and lepromatous TB?

A

tuberculoid has a correct Th1 response that activates macrophages to kill the microbe. symptoms are immunogenic
lepromatous has an unhelpful Th2 response with more severe cutaneous symptoms and nerve damage

81
Q

what does the lepromin PPD test demonstrate?

A

whether or not the host is having a correct immune response to the pathogen

82
Q

how do you treat Hansen’s Disease?

A

dapsone and rifampin for two years

83
Q

how are spirochetes transmitted?

A

wide variety of methods: sexual, insect vector and environmental included

84
Q

how do spirochetes cause multiorgan infection so quickly?

A

they travel easily into the bloodstream and some cross the blood brain barrier

85
Q

what is the primary virulence factor for spirochetes and how is it accomplished?

A

immune evasion. they are not very immunogenic and they down regulate the host respoonse

86
Q

are there any vaccines to spirochetes?

A

there is not since they are not very immunogenic

87
Q

why is diagnosis for syphilis challenging?

A

disease phases are very far apart and they cannot be seen under light microscope

88
Q

what is a unique exam that can diagnose syphilis?

A

the Argyll-Robertson pupil test. one or both pupils do not constrict to light stimulus but do to focus

89
Q

what is the treatment for syphilis and what is a possible complication?

A

treat with penicillin (little resistance). Jarisch Herxheimer reaction is possible-resembles sepsis

90
Q

what are the three stages of syphilis?

A
  1. painless chancre 2. variable rash with flu like symptoms 3. cardiac or CNS involvement after latent period
91
Q

how is lyme disease acquired and where and when is it most common?

A

by tick bite, in the Northeast in the summer

92
Q

how can lyme be prevented once a tick has bitten you?

A

prompt removal (takes 24 hrs to transmit) and prophylaxix with doxycycline possible

93
Q

what are the three phases of lyme?

A
  1. skin infection 2. immune and neurological issues 3. chronic lyme with severe immunopathology, neuropathology and fibromyalgia
94
Q

how long is treatment for lyme?

A

a month and no longer.

95
Q

what are recurring themes demonstrated by spirochete infection?

A

variety of transmission methods, cross easily into bloodstream, virulence factors for immune evasion, challenging diagnosis, little antibiotic resistance and Jarisch-Herxheimer reaction to treatment

96
Q

What is the morphology of vibrios and where do they reside?

A

curved, gram - rods that are ocean dwelling

97
Q

what major pathogenesis do vibrios cause?

A

gastroenteritis but can also infect wounds

98
Q

the most pathogenic V cholerae strands contain what genetic marker?

A

O1 marker of colonization by lysogenic bacterophage

99
Q

what is the infectious dose of V cholerae and why?

A

very high because it is killed by stomach acid

100
Q

how does V cholerae colonize?

A

it secretes mucinase to attach to intestine

101
Q

how does the enterotoxin of V cholerae cause disease?

A

it interferes with signal transduction by chronically activating adenylate cyclase. This causes leakage of chloride and water into the colon

102
Q

how is V cholerae treated?

A

give IV fluids and correct electrolytes primarily. antibiotics are unnecessary because the infection is self limiting

103
Q

what pathogen causes most stomach ulcers

A

H. pylori

104
Q

how does H pylori colonize and survive in the stomach?

A

colonizes with flagella that anchor it. urease turns urea into ammonia, neutralizing the stomach

105
Q

what are the ulcers in H pylori infection caused by?

A

irritation from the ammonia and induction of apoptosis of neighboring cells

106
Q

how is H. pylori diagnosed?

A

cannot grow in culture. use urea breath test to see if patients who swallow radioactive urea exhale radiolabeled CO2 (positive)

107
Q

how is H. pylori treated?

A

10-14 day treatment of three antibiotics, pepto bismol and a proton pump inhibitor

108
Q

what is the difference between facultative and obligate intracellular parasites?

A

facultative can divide independently while obligate require host resources to muliply

109
Q

how do intracellular pathogens evade humoral and surface innate immunity?

A

by infecting macrophages to transport them around the body and by taking over actin polymerization to spread to a next door cell

110
Q

what is the main virulence factor that establishes an intracellular infection?

A

type 3 secretion system

111
Q

what are the two most common functions of a T3SS that establishes an intracellular infection?

A

enhances phagocytosis by target cell and prevents endosomal fusion with lysosome

112
Q

what is the biggest barrier to treating intracellular infections?

A

antibiotics must be able to cross the human cell membrane and either be active or activatible after doing so

113
Q

what is the first choice of antibiotic for an intracellular infection?

A

tetracycline

114
Q

what is the most common mechanism of L. monocytogenes infection and what illness does it cause?

A

by eating cold stored prepared foods. it causes gastroenteritis

115
Q

are L monocytogenes, R rickettsiae and Chlamydia facultative or obligate intracellular bacteria?

A

L monocytogenes is facultative, R rickettsiae and Chlamydia are obligate

116
Q

what are possible complications of L monocytogenes with immunosupression?

A

dangerous disseminated diseases in other organ systems, particularly meningitis. can also complicate pregnancy

117
Q

what is the vector for R rickettsiae?

A

ticks

118
Q

what virulence factors does R rickettsiae employ?

A

adhesion, cell entry, endosomal escape and actin based cell to cell spread

119
Q

what tissue is infected by rickettsia rickettsiae and what disease is caused by it?

A

vascular endothelium and Rocky Mountain Spotted Fever

120
Q

what are some of the possible complications of Rocky Mountain Spotted Fever

A

coma, DIC and circulatory collapse

121
Q

what is the replication strategy of Chlamydia?

A

elementary bodies are infectious particles that unpack into reticulate bodies in the cell (noninfectious). A T3SS allows endosome escape and reploication occurs. reticulate bodies repack into elementary bodies and either endocytose or lyse the cell

122
Q

what is a possible delayed complication of Chlamydia infection?

A

reactive arthritis

123
Q

If a person comes back in after treatment with a new infection with Chlymidia, do you assume there was antibiotic resistance?

A

no, they probably were reinfected by their still infected partner

124
Q

Which enteric bacteria use Trojan horse macrophages and where do they travel to?

A

Yersina travels locally. S. typhi goes systemically

supplemental micro (8 decks)

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