Bacterial Flashcards
1
Q
symptoms of vibrio cholerae infection
A
stomach cramps, watery diarrhea (cloudy white stool), rapid dehydration, acidosis (bicarbonate base is lost in stool)
2
Q
what body region does vibrio cholerae infect
A
small intestine - causes onset of violent GI symptoms
3
Q
T/F: vibrio cholerae can cause rapid dehydration and death in a matter of 12 hours if left untreated
A
true
4
Q
T/F: vibrio cholerae that have recently been shed by another human are hyper-infectious and better able to survive passage of stomach
A
true
5
Q
how does vibrio cholerae infect the small intestine
A
Bacterium uses flagellum as propeller (guided by chemotaxis) to surface of intestine. Produces enzyme (mucinase) to digest mucous lining and penetrate surface. Uses fimbriae (thread-like appendages) to attach to epithelial cells. Secretes cholera toxin which disrupts Cl- channels. Large amount of Cl-, followed by Na+, enter the lumen, and water can no longer be absorbed. Bacteria replicates and exits host via watery stools.
6
Q
what does cholera toxin do
A
disrupts function of Cl- channels in epithelial cells. This causes Cl- to flow out of cells, followed by Na+. This causes disruption of water absorption in lumen of small intestine –> watery diarrhea
7
Q
what route of infection vibrio cholerae
A
fecal-oral route - common in parts of world where running water and sanitation aren’t available
8
Q
what is the first line of treatment for vibrio cholerae infection?
A
ORS - oral rehydration solution (water, sugar, salt)
the sodium and glucose use a different transporter which is not affected by cholera toxin
9
Q
vibrio cholerae is gram +/-? what shape is it?
A
gram negative, rod-shaped with single flagellum
10
Q
T/F: TB affects 1 in 3 people around the world
A
true
11
Q
what body region does mycobacterium tuberculosis affect
A
most frequently lungs (pulmonary TB), but can infect many parts of the body
12
Q
T/F: mycobacterium tuberculosis can stay dormant for years
A
true
13
Q
symptoms of mycobacterium tuberculosis infection
A
hemoptysis (coughing up blood), fever, fatigue, loss of appetite (anorexia), weight loss, night sweats
14
Q
how does mycobacterium tuberculosis survive in alveolar macrophages?
A
usually phagosome fuses with lysosome to kill microbe. TB modify the phagosome so it can’t fuse with lysosome. When macrophage eventually dies it releases TB, as well as content of lysosomes which causes local inflammation
15
Q
tuberculous granuloma
A
chronic inflammatory lesion - local collection of mycobacterium tuberculosis walled off by immune cells (because of the local inflammation they evoked)
infection is contained so it does not cause symptoms or organ damage/ can lay dormant –> latent/primary TB infection (LTBI)
16
Q
caseating granuloma
A
lesion formed by accumulation of caseous (cheese-like) material made of necrosis in the center of the tuberculosis granuloma
often causes collapse of granuloma and spread of infection to surrounding areas
17
Q
miliary TB
A
occurs when a large number of mycobacterium tuberculosis spread through the blood
seen as a millet-like seeding of TB bacilli on chest x-ray
18
Q
how is TB diagnosed
A
Tuberculin skin test - to detect latent TB
Acid Fast Bacilli (AFB) test - microscopically identifies mycobacterium tuberculosis (retain color after acid wash). Can be done as smear test (rapid) or culture test (confirmatory)
chest x-ray - to look for cavitary lesion (gas-filled space representative of area of dead cells)
lumbar puncture - for TB meningitis, collects CSF
19
Q
what does a miliary pattern on a chest x-ray suggest about a TB infection?
A
mycobacterium has spread out of lungs to other organs
20
Q
what are the symptoms of a Shiga-toxigenic E. coli (StEC) infection?
A
stomach pain, bloody diarrhea, inflammatory colitis, entero-hemorrhage
21
Q
what types of tests can be used to diagnose E. coli infection?
A
blood test, stool culture
22
Q
what route of infection is E. coli?
A
fecal-oral - E. coli is a commensal bovine bacteria (cow)
23
Q
why is StEC bacterium a particularly pathogenic strain of E. coli in humans?
A
DNA has been altered by bacteriophage - causes production of Shiga toxin, giving it enhanced adhesion capabilities
24
Q
how does Shiga-toxigenic E. Coli colonize the gut?
A
uses fimbriae to attach to epithelial cells in gut lumen, then uses Type III secretion system to inject virulent factors. Once colonized, it produces two-part Shiga toxin. B subunit forms donut-shaped entry portal through which A subunit enters enterocytes –> cell death and cytokine release –> local inflammation. Shiga-toxin enters inflamed blood vessels causing endothelial damage there –> bloody diarrhea
25
what do the A and B subunits of Shiga toxin do?
B creates portal into enterocytes through which toxic A subunit enters and kills cell
26
how can StEC infection cause hemolytic uremic syndrome (HUS)?
Shiga toxin causes local inflammation of blood vessels through which it enters systemic circulation. Inside vessels, Shiga toxin causes detachment of endothelial cells and thrombosis. Blood clots cause damage to small vessels of kidneys --> renal failure
27
signs of renal failure/ hemolytic uremic syndrome
shistocytes (blood cell fragments) in blood smear, high blood creatinine levels, protein and RBC in urinalysis
28
why is treatment for StEC mainly supportive during early stages of infection?
genes for Shiga toxin production are upregulated when E.coli detects it is in danger of being destroyed - so aggressive treatment could cause more damage
29
subacute bacterial endocarditis (SBE)
Type of infective endocarditis. Associated with history of rheumatic fever. Has a long incubation period and typically involves bacteria with low virulence (like streptococcal viridans). Typically requires prior structural abnormalities of the heart valves in order for infection to occur (because of low virulence of bacteria)
30
acute bacterial endocarditis (ABE)
Type of infective endocarditis. Associated with history of rheumatic fever. Has short incubation period and typically involves more virulent bacteria (like staph aureus). Often no prior structural damage to heart required for this form of bacterial endocarditis to develop
31
Janeway lesions are a classic physical finding of what type of infection?
non-painful erythematosus lesions on palms and soles. Indicate infective endocarditis
32
symptoms of streptococcal pharyngitis
sudden and severe sore throat, pain in swallowing, fever, enlarged lymph nodes and tonsils, white or yellow spots at the back of a red throat
33
cause of infective endocarditis
bacteria (like streptococci) enter blood stream and settle in heart lining, heart valve, or blood vessel, causing infection of inner lining of heart
34
Roth's spots
hemorrhage in the retina with a small, clear, white center. Often associated with bacterial endocarditis
35
T/F: streptococcus viridans is a commensal bacteria associated with acute bacterial endocarditis
true. Commonly found in mouth and intestine
36
what are the symptoms of streptococcus pneumoniae (pneumococcus) infection?
SOB, fever, tachycardia, tachypnea, low blood oxygen saturation (hypoxemia), chest pain
37
what might you find on a chest examination of a patient infected with pneumococcus?
dullness to percussion, decreased breath sounds, crackles and rhonchi (low-pitched rattling caused by obstruction)
38
pneumococcus is gram +/-? and what shape is it?
gram + diplococci (found in pairs)
39
T/F: Type I pneumocytes can act as phagocytes to engulf invading pneumococcus
FALSE: Type II pneumocytes can act as phagocytes
Type II pneumocytes secrete surfactant
40
why is emphysema from smoking a risk factor for pneumococcus infection?
emphysema causes scarring of lung tissue and enlargement of alveolar spaces --> altered gas exchange, impaired mucociliary clearance, diminished local inflammatory response
41
how is pneumococcus spread?
airborne
42
what is the most common cause of acute bacterial pharyngitis?
streptococcus pyogenes, aka group A streptococcus
43
symptoms of streptococcus pyogenes infection, when complicated with scarlet fever?
pain swallowing, sandpaper rash, fever, headache, epigastric pain, tachycardia, red strawberry tongue (red and bumpy), circumoral pallor (flushed cheeks but pallor around the mouth), erythema, cervical lymphadenopathy (swollen lymph nodes)
44
scarlet fever
delayed type of skin reaction to one of the streptococcal exotoxins
characteristic red rash covering most of body, strawberry tongue, sore throat, fever, pain on swallowing, cervical lymphadenopathy
45
streptococcus pyogenes (group A) is grame +/- and what shape?
gram + cocci that grow in chains
46
T/F: streptococcus pyogenes are normal inhabitants of the nasopharynx
true
47
what do M proteins of streptococcus pyogenes (group A) do?
project outside of hyaluronic acid capsule, block complement-mediated phagocytosis by neutrophils and macrophages
48
what are the most common suppurative (pus-forming) complications of group A streptococcus pharyngitis (pyogenes)?
peritonsillar abscess (pus-filled sore) and cervical lymphadenitis (infection of lymph nodes)
non-suppurative complications are immune mediated
49
T/F: streptococcus pyogenes is one of the leading causes of acquired heart disease in developing countires
true: acute rheumatic fever can occur as a complication (damages heart tissue) months-years after untreated streptococcal infection (stemming from immune mediated complications)
50
what tests can be used to diagnose Helicobacter pylori infection?
blood test (for antibodies), stool antigen test, endoscopy (to visual gastric/ duodenal ulcers and obtain biospy)
51
symptoms of Helicobacter pylori infection?
bloating, nausea, weight loss, loss of appetite (anorexia), postprandial eructation (belching after meals)
52
T/F: helicobacter pylori infection is the strongest risk factor for both peptic ulcers and gastric cancer
true
53
T/F: helicobacter pylori transmission requires close contact
true
54
what route of infection is helicobacter pylori?
oral-oral or gastric-oral (when microbes are regurgitated from stomach to mouth)
transmitted through contaminated food and water
55
helicobacter pylori produce this enzyme to protect itself from the acidity of the stomach
urease - catalyzes breakdown of urea into ammonia and carbon dioxide --> alkaline ammonia neutralizes acidic environments
56
what does the VacA toxin of helicobacter pylori do?
pore-forming toxin
57
more virulent strains of helicobacter pylori have a CagA protein which does what?
secreted through specialized type 4 secretion system, affects functioning of epithelium
increases risk of cancer
58
what are the symptoms of Neisseria meningitides?
lethargy, profuse sweating (diaphoresis), fever, headache, neck stiffness, vomiting, sensitivity to light and sound (photo/phonophobia), hypotension, tachycardia, tissue ischemia, non-blanching petechiae
59
meningitis vs encephalitis (including symptoms)
meningitis - inflammation of meninges. Presents with fever, severe headache, neck stiffness, vomiting, lethargy
encephalitis - infection of brain itself. Presents with diffuse or focal neurological deficits (behavior changes, disorientation, partial loss of voluntary movement)
60
Neisseria meningitides (meningococcemia) is gram +/- and what shape?
gram negative, diplococci
61
how does Neisseria meningitides (meningococcemia) enter human host? What 2 things does it use to evade immune system?
crosses nasopharyngeal mucosa. A capsule protects it from complement-mediated bacteriolysis. IgA proteases prevent it from being tagged for phagocytosis.
Displays neurotropism and replicates in CSF.
62
what toxin of Neisseria meningitides triggers inflammation and clotting inside small blood vessels (possibly leading to tissue ischemia)?
endotoxin, aka LPS (lipopolysaccharide)
endotoxins are less potent than exotoxins
63
systemic inflammatory response syndrome (SIRS) requires two of what four conditions
abnormal body temperature, tachycardia, tachypnea, abnormal white blood count
when caused by an infection SIRS is called sepsis
64
Gram staining of abscess fluid shows numerous neutrophils and gram + cocci in clusters. Bacterial culture shows yellowish colonies with beta hemolysis on Sheep Blood Agar. Antibiotic susceptibility shows that the bacterial colonies grow normally in the presence of several beta-lactam antibiotics. However, growth is inhibited by clindamycin and trimethoprim-sulfamethoxazole. What bacteria could it be?
these tests confirm diagnosis of MRSA - methicillin resistant staph aureus
65
what does MRSA stand for? what shape is it? is it gram + or -?
MRSA = methicillin resistant staph aureus
| gram + cocci
66
what gene allows MRSA to be resistant to penicillin and how does it work?
mecA gene - encodes particular form of penicillin-binding protein (PBP2A) that inhibits penicillin binding --> most beta-lactam antibiotics won't work
mecA is located on cassette (staphylococcal chromosome cassette - SCCmec), mobile genetic element, that can be passed via horizontal gene transfer
67
where is the mecA gene of MRSA located?
not on bacterial chromosome, located on cassette (staphylococcal chromosome cassette)
transferred to other bacteria via horizontal transfer
68
where is the gene for the pore-forming cytotoxin of MRSA found?
carried on a bacteriophage virus infecting staph aureus
causes widespread necrosis
69
pustule vs cellulitis vs abscess
pustule - small collection of puss, appears as white bump with red around it, often in sweat glands and hair follicles
cellulitis - diffuse bacterial soft tissue infection with no localized area of pus for drainage (cannot be drained), often occurs in skin and lower legs, area is warm/red/swollen
abscess - localized collection of pus, area is warm/red/swollen, has a drainage point
70
granulation tissue
new connective tissue and microscopic blood vessels that form on surface of healing wound. typically grows from the base of the wound and then fills wound
71
pyogenic membrane
limiting layer of an abscess or area of suppuration. Layer of pus cells lining the abscess that have not yet been autolyzed
72
exudate
fluid rich in protein and high content of cellular debris, oozes out of blood vessels due to inflammation and gets deposited in nearby tissues
73
what do beta lactam antibiotics contain (organic chemistry structure) and what do they bind? For what bacterial infection are they ineffective?
possess nitrogen-containing beta lactam ring that binds to penicillin-binding proteins (PBP) on surface of bacteria
ineffective against MRSA which has modified PBP (PBP2A)
74
what does MRSA (methicillin resistant staphylococcus aureus) usually cause?
skin lesions or pneumonia
75
what antibiotic-resistant bacterial infection are clindamycin and TMP-SMX (trimethoprim/sulfamethoxazole) used to treat?
MRSA (methicillin resistant staph aureus)
76
what bacteria causes syphilis?
treponema pallidum
77
what shape is treponema pallidum?
spiral, from spirochete family. So small it can only be seen with specialized dark-field microscopy
(causes syphilis)
78
how is treponema pallidum transmitted?
direct contact: sexually or congenital (mother-to-child)
| cannot survive outside the human body
79
T/F: treponema pallidum, the bacterium causing syphilis, can survive outside the human body
FALSE - must be transmitted directly (sexually or congenital)
80
T/F: some babies born with congenital syphilis appear healthy at birth
TRUE - infection can remain undetected for first few years of life. If untreated child can develop permanent complications
81
what are the permanent complications that can occur from congenital syphilis infection (by treponema pallidum)
Saber shin - anteriorly bow-shaped tibia (shaped like saber sword)
Hutchinson teeth - smaller and widely spaced teeth
Interstitial keratitis - inflammation of the cornea, blood vessels grow into cornea, causes cornea to become hazy
82
what common antibiotic can be used to effectively eliminate treponema pallidum infection? (syphillis)
penicillin
83
congenital syphilis
infection of treponema pallidum from mother to child through the placenta
84
Saber shin can be caused by what bacterial infection?
anterior bowing of the shin, deformity caused by congenital syphilis
85
Hutchinson teeth can be caused by what bacterial infection?
smaller and widely shaped teeth in babies, deformity caused by congenital syphilis
86
what is the most common cause of interstitial keratitis?
syphillis (treponema pallidum infection)
inflammation of the cornea in which blood vessels grow into the corneal tissue, causes cornea to become hazy and eventually lead to vision loss
87
what are the symptoms of primary syphilis infection?
chancres - painless, firm, round ulcer occurring on genitalia or on lips/in mouth. Can last 1-5 weeks
enlarged lymph nodes in the area surrounding the ulcer
88
what are the symptoms of secondary syphilis infection?
rashes on palms and soles
desquamation (shedding of skin's outer layer, often after a rash fades)
rhinorrhea (runny nose)
lymphadenopathy
fever, sore throat, patchy hair loss, muscle ache, fatigue
89
what are the symptoms of tertiary syphilis infection?
damage to internal organs like heart, brain, nerves, bones, joints, liver:
hepatomegaly (enlarged liver)
aortic aneurysm
tabes dorsalis - slow progressive degeneration of nerves of spinal cord, causing intense pain, unsteady gait, joint degeneration, dementia, blindness, deafness
90
tabes dorsalis can be caused by the tertiary stage of what bacterial infection
tertiary syphilis caused by treponema pallidus infection
slow progressive degeneration of nerves in spinal cord
91
what serious and potentially life-threatening condition can Group A streptococcus cause?
necrotizing fasciitis ("flesh eating disease"
92
what are the symptoms of necrotizing fasciitis (caused by Group A streptococcus)?
fever, hypotension, tachycardia, red and swollen (erythematous) infected area with seemingly disproportionate severity of pain around lesion - feels like "cooking under the skin"
93
what kinds of tests can be used to diagnose necrotizing fasciitis (caused by Group A streptococcus)?
CBC with differential, arterial blood gas measurements, blood cultures, urinalysis, CT scan (to delineate extent of infection)
94
a CT scan of an area under an infected lesion shows extensive soft tissue inflammation and thickening of the fascial planes. what kind of diagnosis does this support?
necrotizing fasciitis caused by Group A streptococcus
fascial plane - sheath of fibrous tissue that creates potential space or compartment around muscles, vessels, nerves
95
what is the treatment for necrotizing fasciitis (caused by Group A streptococcus)?
surgical debridement (removal of necrotized tissue), because the infection spreads rapidly and cuts off blood supply to tissues that would be required for antibiotic dissemination
96
Group A streptococcus is also known as
streptococcus (or just strep) pyogenes
97
strep pyogenes is gram +/-?
aka Group A streptococcus, gram +
98
how does strep pyogenes cause necrotizing fasciitis?
aka Group A streptococcus
enters through break in skin, releases exotoxin that leads to production of inflammatory cytokines, which damage endothelial lining of blood vessels and promotes coagulation, which occludes blood vessels and causes ischemic damage. Resulting necrosis facilitates growth of other microbes in area, such as anaerobic microbes which produce H and N gas which accumulate in subcutaneous tissues
can cause disseminated intravascular coagulopathy (DIC) - overactivity of clotting proteins
99
in necrotizing fasciitis caused by strep pyogenes infection, accumulation of H and N gases in subcutaneous tissues due to anaerobic bacteria can be felt during physical examination. What is this physical finding called?
crepitus - characterized by crackling or crinkly sound
| can also be seen in imaging (CT)
100
patients presenting with necrotizing fasciitis are LEAST likely to present with:
fever, high pulse rate, pain disproportionate to lesion, high blood pressure
HBP - patients with necrotizing fasciitis will present with LOW blood pressure
101
asymptomatic bacteriuria can be caused by what medical/treatment error?
in patients with indwelling bladder catheters (such as Foley catheter) for extended period of time, bacterial overgrowth in the catheter bag can be mistaken for a UTI, when the colonization is in fact only within the catheter tube and bag
patient has no symptoms of UTI but is treated with unnecessary antibiotics which can lead to negative consequences, such as destruction of normal gut flora which compete and protect against harmful microbes
102
how does clostridium (C) difficile cause infection?
produces toxin A and toxin B cytotoxins, leading to release of inflammatory mediators/increase in vascular permeability
C diff then causes degradation of colonic epithelial cells, then release hydrolytic enzymes to breakdown local connective tissue
plaque forms from necrotized tissue, fibrin, and WBC, causing GI symptoms - toxic megacolon, bowel perforation (--> disseminated infection)
103
how is C diff (clostridium difficile) often transmitted between patients in hospitals
through ingestion of spores carried by staff
| spores can survive a long time on surfaces and are resistant to alcohol-based cleansers (but can be killed with bleach)
104
adults with C diff (clostridium difficile) infection are treated with ___
children with mild to moderate symptoms are treated with ___
adults - oral vancomycin
| children - oral metronidazole
105
anaerobic, gram + bacteria that grow in chains. They are part of normal gut flora and normally found in human feces but can cause UTI and wound infections. They are known to be antibiotic resistant. What are...?
enterococcus
106
clostridium difficile is gram +/-?
gram +
spore-forming. tolerated in the gut of some individuals, but can cause infection following overuse of antibiotics that kill normal/protective gut flora
can cause pseudomembranous colitis - swelling/inflammation of large intestine/colon
107
pathognomonic
sign or symptom so characteristic of a disease that it can be used to make diagnosis
108
pediatric pt presents with fever, tachycardia, soft tissue swelling and redness around L eye, which protrudes anteriorly from the orbit (proptosis). Visual acuity is normal but pt is reluctant to move eye due to pain. Pupils show normal pupillary relfex and red reflex is intact. Your differential diagnosis will distinguish this condition between which two diagnoses?
common and more benign preseptal cellulitis and rare ophthalmic emergency orbital cellulitis
the difference is where the infection is - anterior or posterior to orbital septum (connective tissue extension of periosteum that projects in front of orbit all the way into upper and lower lids)
109
preseptal cellulitis
infections in skin and soft tissues anterior to the orbital septum
110
how can a sinus infection lead to orbital cellulitis?
orbit is separated from nasal sinuses only by thin, bony structures of skull (lamina papyracea). Viral/bacterial infection of sinuses can lead to inflammation of drainage pathway, decreased mucociliary clearance. Microbe is then able to invade orbit through bony structure. This could lead to cavernous sinus thrombosis and sixth nerve palsy (dysfunction of abducens nerve)
111
sixth nerve palsy can be caused by what kind of condition
dysfunction of abducens nerve (contracts lateral rectus), can be caused by orbital cellulitis
112
how can differential diagnosis be made between preseptal cellulitis and orbital cellulitis?
both cause eye pain, swelling, and erythema
but orbital cellulitis also causes inflammation of extraocular muscles within the orbit, leading to proptosis (anterior protruding of eye out of orbit)
113
most common cause of orbital cellulitis
sinus infection
114
tachycardia and tachypnea with blood work finding dangerously low white blood count (leukopenia, especially neutropenia) indicates what diagnosis
systemic inflammatory response syndrome (SIRS) - collection of physical findings like abnormal body temp, tachycardia/pnea, abnormal white blood count that together suggest widespread dysregulation of inflammatory response
115
when is SIRS considred sepsis
system inflammatory response syndrome is considered sepsis when it occurs as result of a confirmed infection
116
what is the initial inflammatory response to gram negative bacteria?
toll-like receptors (TLRs) on macrophages recognize lipopolysaccharides (LPS) endotoxin on surface --> leading to activation of nuclear factor kappa beta (NFkB) transcription factor --> inflammatory cytokines, chemokines, and NO
117
TLRs recognize LPS on gram [+/-] bacteria?
gram negative. Causes activation of pro-inflammatory NFkB transcription factor
118
what pro-inflammatory transcription factor is activated in macrophages in response to TLRs recognizing LPS on gram - bacteria?
NFkB (nuclear factor kappa beta)
119
why does sepsis tachycardia and tachypnea?
circulating cytokines (activated by NFkB of macrophages) cause increased vascular permeability. Some plasma leaks from blood vessels into tissues --> lowered blood pressure
120
what is given to patients with sepsis to treat their low blood pressure when fluids cannot be given because increased vascular permeability is causing fluid to enter the lungs?
norepinephrine (noradrenaline)
121
Escherichia coli, Salmonella, Shigella, Vibrio cholerae, Klebsiella, and Pseudomonas are examples of gram [+/-] bacteria?
gram negative (have LPS endotoxin on surface, lose crystal violet stain in Gram's method)
122
LPS is an [endo/exo]toxin on gram - bacteria?
endotoxin
