Bacteria Flashcards
0
Q
What does the plane of replication influence?
A
Whether or not the cocci grow in chains
1
Q
What are common test results shared by streptococci?
A
Gram positive, catalase negative and grow in chains
2
Q
What are the virulence factors for group A strep?
A
Pilli, M protein and toxins
3
Q
What two test results indicate group A strep?
A
Beta hemolytic and bacitracin sensitive
4
Q
What are the test differences between group A and group B strep?
A
bacitracin test and CAMP test
5
Q
What is the reservoir and transmission for group a strep?
A
Many people are carriers. Transmitted through direct contact
6
Q
What do you use to treat group A strep?
A
Penicillin (no resistance) or erythromycin
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
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
9
Q
What tests indicate group B strep?
A
Beta hemolytic, resistant to bacitracin and CAMP positive
10
Q
What is a distinct morphological feature of s pneumoniae?
A
It is diplococcus
11
Q
What test results ID s pneumoniae?
A
Alpha hemolysis and sensitive to optochin (bile)
12
Q
What two streptococci have capsules as their major virulence factors?
A
Group B strep and s pneumoniae
13
Q
What circumstances make you more susceptible to a pneumoniae
A
Inhibited mucous clearance in lungs: virus, smoking, depressed cough reflex ect
14
Q
How is a pneumoniae treated?
A
Treat underlying cause and give penicillin after antibiotic sensitivity test
15
Q
What test results in ID of s viridans?
A
Alpha hemolysis and resistance to optochin
16
Q
What is caused by s viridans?
A
Dental carries and endocarditis if it gets into the blood
17
Q
What is the virulence factor for s viridans?
A
Sugar metabolizing enzyme that produces acid
18
Q
Which streptococci are gamma hemolytic?
A
S fecalis
19
Q
What test result verifies that a staph infection is a aureus?
A
Coagulate positive
20
Q
What test results would indicate staphlococci?
A
Gram positive, catalase positive and growth in clumps
21
Q
What are the virulence factors for a aureus
A
Protein A, capsule, coagulase and toxins
22
Q
How do you treat s aureus?
A
Check for antibiotic resistance before choosing
23
Q
How do you ID s epidermidis?
A
Staph with negative coagulase
24
What kind of culture do you grow nisseria on?
Chocolate agar
25
What test determines the two types of nisseria?
Ferments maltose: n meningitides
| Does not: n gonorrhoea
26
What are the two virulence factors of n meningitides?
Capsule and LPS
27
What are the two virulence factors for n gonorrhoea?
Pilli an LOS
28
What is the reservoir and transmission of n meningitides?
Respiratory tract and droplets
29
How does one prevent n meningitides?
Vaccine, treat with penicillin
30
How is transmission of n gonorrhoea to a neonate prevented?
Neonatal eye droplets
31
Do you treat n gonorroae with penicillin?
No because there is plasmid resistance. Do resistance panel first
32
By what process do anaerobic bacteria derive all ATP from?
fermentation
33
A bacterium is an obligate anaerobe if it lacks what?
enzymes to remove ROS (catalase and superoxide dismutase)
34
what are the two types of anaerobic infectious agents?
normal flora that become opportunistic pathogens and soil organisms that enter the body as spores (in wounds or vacuum packaged foods)
35
what are some ways to ensure that anaerobic bacteria grow in a liquid culture?
treat with reducing agents and tightly stopper in a full container
36
what components of anaerobic culture jars permit anaerobic growth?
air tight lid, chemical system to remove oxygen and an anaerobic indicator
37
what are the gram staining results for anaerobes?
all of them stain positively except for the GNAB
38
What are the major pathogenic anaerobes?
Clostridium, GNAB and actinomyces
39
Which normal flora anaerobic bacterial cause infection?
GNAB, actinomyces and C difficile
40
Where does one acquire Clostridia infections?
soil infected wounds or vacuum packaged foods
41
what is the major virulence factor of anaerobic bacteria?
exotoxins
tetanus and botulism: neurotoxin
gas gangrene and abscess: tissue degrading enzymes
42
what is the appropriate treatment for an anaerobic infection?
drain abscess if applicable, provide antitoxin if applicable and conclude with antibiotics
44
What are the seven defining characteristics of enterobacteriaceae?
Gram -, nonsporulating, straight rods, facultative aerobes, catalase positive, oxidase negative and ferment glucose
45
are all enterobacteriaceae caught by ingestion?
no-ICU infections like Klebsiella
46
what is a major struggle when treating enterobacteriaceae infections?
extreme antibiotic resistance. promiscuous to new DNA (introduces new resistances and virulence factors)
47
what are the steps of antimicrobial sensitivity testing?
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
48
what are the important virulence factors of enterobacteriaceae in the gut?
pilli (allow attachment in GU and GI tract) and type 3 secretion systems (adhesion, enterotoxins, and macrophage takeover)
49
How do enterobacteriaceae often infect a host?
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
50
how do enterobacteriaceae spread systemically?
take over macrophages to bring them around the body. these macrophages are apoptosed at a specific time (quorum sensing) in lymph nodes
51
What is the foodborne infection route for Enterobacteriaceae and how can they be prevented?
fecal- oral rout. prevented by water treatment, handwashing, food pasteurization and cooking
52
Which enterobacteriaceae can cause hemolytic uremic syndrome and what population does this affect?
shigell and enterohemorrhagic E coli infection. it is primarily a pediatric complication
53
what is the mechanism of hemolytic uremic syndrome?
bacteria escape the gut and release shiga toxin into the bloodstream
54
what human antigen predisposes a patient to develop reactive arthritis?
HLA- B27
55
What are the major symptoms of reactive arthritis and what kind of disease is it?
conjunctivitis, urethritis and arthritis. it is autoimmune
56
which bacterial infections may lead to reactive arthritis?
Shigella, salmonella, yersinia, campylobacter and chlamydia
57
What are ICU bugs?
major opportunistic nosocomial infections (seldom cause symptoms in previously healthy people) caused by Klebsiella, Enterobacter, Serratia, Proteus, Providencia and Morganella
58
How do you prevent ant treat ICU bugs?
prevention: switch catheters, scrub down patients and the ICU, and minimize hospital stays. Difficult to treat, use antibiotic sensitivity testing
59
what prevented the eradication of TB?
AIDS
60
what are the present concerns when considering TB?
multi drug resistance
61
what are some culture characteristics of TB?
gram stain poorly, acid-fast stain (mycolic acid) and grow very slowly
62
describe the acid fast procedure
boil with carbolfuschin stain, use acid/alcohol to decolorize and conterstain with methylene blue
63
how is TB transmitted and disseminated in the body?
transmitted by inhalation, infects GI by swallowing infected speutum and travels with macrophages to lymph nodes, kidney, bones and CNS
64
how do TB outcomes differ depending on the immune status of the host?
Immunocompetent hosts force latency with an appropriate cell mediated response (most likely will never be active). Immunosuppressed will more likely have active infection
65
how does the body attempt to destroy TB?
CD4 cells activate infected macrophages and CD8 cells kill infected macrophages, establishing caseating granulomas. TNF alpha also helps with containment.
66
what are the symptoms of classic pulmonary TB?
cough, weight loss, fever, night sweats, hemoptysis and chest pain.
67
how is active TB diagnosis confirmed and the appropriate antibiotic treatment determined?
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
what are the extrapulmonary manifestations of TB?
scrofula, GU, CNS, skeletal (arthritis of one joint or pott disease), GI and miliary
69
Which disease is directly obserbed therapy now a standard for?
Tuberculosis
70
Is there an effective vaccine for TB in the US? What complication does the vaccine impose in testing?
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
what is the most effective way to reduce the incidence of TB in a population?
good diet and housing-latent cases are not contagious
72
how are TB patients treated?
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
which of the following mycobacterial infection that resembles TB is treated by the same drugs:
M. scrofulaceum, M avium, M kansasii or M marinum?
M. kansasii
74
what is the main difference between TB and atypical mycobacteria?
TB is caught from other people, atypical mycobacteria from the environment
75
what is the presentation of an atypical mycobacteria in an immunocompetant adult usually?
cutaneous infection
76
which infections are immunosupressed hosts most likely to have systemic infections of?
M. kansasii and MAI
77
what is a similarity between atypical mycobacteria and TB treatment?
both are hard to treat. use multiple antibiotics and worry about resistance
78
how do you culture M leprae?
you cannot. it will not grow
79
What is the optimum temperature for M leprae?
30-37 C
80
what is the difference in immune response and symptoms of tuberculoid and lepromatous TB?
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
what does the lepromin PPD test demonstrate?
whether or not the host is having a correct immune response to the pathogen
82
how do you treat Hansen's Disease?
dapsone and rifampin for two years
83
how are spirochetes transmitted?
wide variety of methods: sexual, insect vector and environmental included
84
how do spirochetes cause multiorgan infection so quickly?
they travel easily into the bloodstream and some cross the blood brain barrier
85
what is the primary virulence factor for spirochetes and how is it accomplished?
immune evasion. they are not very immunogenic and they down regulate the host respoonse
86
are there any vaccines to spirochetes?
there is not since they are not very immunogenic
87
why is diagnosis for syphilis challenging?
disease phases are very far apart and they cannot be seen under light microscope
88
what is a unique exam that can diagnose syphilis?
the Argyll-Robertson pupil test. one or both pupils do not constrict to light stimulus but do to focus
89
what is the treatment for syphilis and what is a possible complication?
treat with penicillin (little resistance). Jarisch Herxheimer reaction is possible-resembles sepsis
90
what are the three stages of syphilis?
1. painless chancre 2. variable rash with flu like symptoms 3. cardiac or CNS involvement after latent period
91
how is lyme disease acquired and where and when is it most common?
by tick bite, in the Northeast in the summer
92
how can lyme be prevented once a tick has bitten you?
prompt removal (takes 24 hrs to transmit) and prophylaxix with doxycycline possible
93
what are the three phases of lyme?
1. skin infection 2. immune and neurological issues 3. chronic lyme with severe immunopathology, neuropathology and fibromyalgia
94
how long is treatment for lyme?
a month and no longer.
95
what are recurring themes demonstrated by spirochete infection?
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
What is the morphology of vibrios and where do they reside?
curved, gram - rods that are ocean dwelling
97
what major pathogenesis do vibrios cause?
gastroenteritis but can also infect wounds
98
the most pathogenic V cholerae strands contain what genetic marker?
O1 marker of colonization by lysogenic bacterophage
99
what is the infectious dose of V cholerae and why?
very high because it is killed by stomach acid
100
how does V cholerae colonize?
it secretes mucinase to attach to intestine
101
how does the enterotoxin of V cholerae cause disease?
it interferes with signal transduction by chronically activating adenylate cyclase. This causes leakage of chloride and water into the colon
102
how is V cholerae treated?
give IV fluids and correct electrolytes primarily. antibiotics are unnecessary because the infection is self limiting
103
what pathogen causes most stomach ulcers
H. pylori
104
how does H pylori colonize and survive in the stomach?
colonizes with flagella that anchor it. urease turns urea into ammonia, neutralizing the stomach
105
what are the ulcers in H pylori infection caused by?
irritation from the ammonia and induction of apoptosis of neighboring cells
106
how is H. pylori diagnosed?
cannot grow in culture. use urea breath test to see if patients who swallow radioactive urea exhale radiolabeled CO2 (positive)
107
how is H. pylori treated?
10-14 day treatment of three antibiotics, pepto bismol and a proton pump inhibitor
108
what is the difference between facultative and obligate intracellular parasites?
facultative can divide independently while obligate require host resources to muliply
109
how do intracellular pathogens evade humoral and surface innate immunity?
by infecting macrophages to transport them around the body and by taking over actin polymerization to spread to a next door cell
110
what is the main virulence factor that establishes an intracellular infection?
type 3 secretion system
111
what are the two most common functions of a T3SS that establishes an intracellular infection?
enhances phagocytosis by target cell and prevents endosomal fusion with lysosome
112
what is the biggest barrier to treating intracellular infections?
antibiotics must be able to cross the human cell membrane and either be active or activatible after doing so
113
what is the first choice of antibiotic for an intracellular infection?
tetracycline
114
what is the most common mechanism of L. monocytogenes infection and what illness does it cause?
by eating cold stored prepared foods. it causes gastroenteritis
115
are L monocytogenes, R rickettsiae and Chlamydia facultative or obligate intracellular bacteria?
L monocytogenes is facultative, R rickettsiae and Chlamydia are obligate
116
what are possible complications of L monocytogenes with immunosupression?
dangerous disseminated diseases in other organ systems, particularly meningitis. can also complicate pregnancy
117
what is the vector for R rickettsiae?
ticks
118
what virulence factors does R rickettsiae employ?
adhesion, cell entry, endosomal escape and actin based cell to cell spread
119
what tissue is infected by rickettsia rickettsiae and what disease is caused by it?
vascular endothelium and Rocky Mountain Spotted Fever
120
what are some of the possible complications of Rocky Mountain Spotted Fever
coma, DIC and circulatory collapse
121
what is the replication strategy of Chlamydia?
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
what is a possible delayed complication of Chlamydia infection?
reactive arthritis
123
If a person comes back in after treatment with a new infection with Chlymidia, do you assume there was antibiotic resistance?
no, they probably were reinfected by their still infected partner
124
Which enteric bacteria use Trojan horse macrophages and where do they travel to?
Yersina travels locally. S. typhi goes systemically
