1050 Unit 5 Flashcards
1
Q
-describe symbiotic relationship
A
–hosts and microbes live together long term
–indigenous microbiota (must be careful not to stimulate immune response)
–3 types: communalistic, mutualistic, and parasitic
2
Q
how does indigenous microbiota exist?
A
–through co-evolution, co-adaption and co-dependency between bacteria and host
3
Q
Describe communalistic relationship
A
–no benefit or harm to either organism
–communalistic bacteria = describing bacteria recovered from culture that do not have pathogen present
4
Q
Describe mutualistic relationship
A
–both host and microbes benefit
5
Q
Describe parasitic relationship
A
–microbes cause harm to the host
6
Q
describe infectivity
A
–organisms ability to establish an infection
–horizontal transmission (person to person spread)
–“contagious”
7
Q
describe pathogenicity
A
–ability of an organism to cause disease
–qualitative trait of an organism determined by genetic makeup
8
Q
describe virulence
A
–extent of pathology caused by an organism when it infects a host
–quantitative trait refers to extent of damage
9
Q
what is avirulent?
A
–bacteria strain not capable of causing disease
10
Q
what are 3 functions of virulence factor?
A
1) may increase an organisms ability to establish itself on/in the host
2) invade or damage host cells
3) evade the host immune response
11
Q
what are the structural features of bacteria that contribute to increased virulence
A
–endotoxin
–pili
–flagella
–capsule
–exotoxins
12
Q
how do endotoxins contribute to increased virulence
A
–lipid A portion of LPS in gram-negative cell walls
–powerful stimulator of cytokine release
13
Q
how do pili contribute to increased virulence?
A
–adherence to host cells
–resistance to phagocytosis
14
Q
how do flagella contribute to increased virulence?
A
–adherence to host cells
–motility
15
Q
how do capsules contribute to increased virulence?
A
–blocks phagocytosis
–antibody attachment
–usually polysaccharides
16
Q
how do exotoxins contribute to increase virulence>?
A
–potent, toxic proteins released from living bacteria
–neutrophils, cytotoxins, and enterotoxins
17
Q
what type of cell is a bacteria cell?
A
–prokaryote cell
18
Q
what is peptidoglycan?
A
–primary component of cell shape and rigidity of bacteria
19
Q
what are two variations of a bacterial cell wall?
A
–gram-negative
–gram-positive
20
Q
describe gram-negative cell wall
A
–contains LPS (polysaccharide layers)
–LPS has 3 layers
—->outer core polysaccharides
—->inner core polysaccharides
—->lipid A1
21
Q
what is fimbrae?
A
–composed of proteins
–involved in specific attachment to prokaryotic surface ligands. “common pili”
22
Q
what is afimbrial?
A
–caused by attachment by presence of surface molecules
–non-pili-dependent
23
Q
describe bacteria defenses in innate immunity
A
–intact skin and mucosal surfaces (barriers to entry)
–antimicrobial defense peptides
–complement proteins, cytokines, acute-phase reactants
–recognition of PAMPs by PRRs such as TLRs
–defensins
–contributes heavily to bodies ability to overcome bacterial infection
24
Q
what are defensins?
A
–soluble peptides
–have 3 classes: Alpha, beta and theta
–theta not found in humans
25
describe alpha denfensins
--produced by neutrophil, certain macrophages and paneth cells of the small intestine
--disrupt microbial membrane
26
describe beta defensins
--produced by neutrophils, epithelial cells lining various organs
--increase resistance of epithelial cells to colonization
27
describe bacterial defenses in adaptive immunity
--antibody production --> bind of C, opsonization, neutralization of bacterial toxins
--cell-mediated immunity--> CD4 T cells produce cytokines that induce inflammation, cytotoxic T lymphocytes attack host cells that contain intracellular bacteria
28
what are bacterial evasion mechanisms?
1) inhibiting chemotaxis
2) blocking adherence of phagocytes to bacterial cells
3) blocking digestion
4) inhibiting complement C3b binding
5) cleavage IgA
29
what is primary effect that occurs when phagocyte adherence is blocked?
--release of lysosome contents into cytoplasm of phagocytic cell, killing WBC.
30
Describe endotoxins
--lipid A
-- found in LPS of cell walls of gram negative bacteria
--activates complement cascade --> leads to formation of anaphylaxis C3a and C5a
--immunogenic but does not result in production of protective antibodies
31
describe exotoxins
--protein molecules that are released from living bacteria (mostly gram positive)
--most potent molecule to harm living life
--may be classified as neurotoxins, cytotoxins, or enterotoxins
--have subunits that bind to receptors
--extremely immunogenic
--induce production of protective antibodies`
32
what are the 5 laboratory means of detecting causative agent or bacterial infection?
1)culture of the causative agents
2)microscopic examination
3)detection of bacterial agents
4)molecular detection of bacterial DNA or RNA
5)serological testing
33
describe "culture of causative agent" of bacterial defenses
--grows on broth or solid media
--major means of diagnosis, but may take time or may not be possible
--enriched media usage
--limitations
---->several bacterial pathogens have not been made for clinical use
---->recovery may take to long for some bacteria
---->some may present as dangerous to technologist
34
describe "microscopic examination" of bacterial defenses
--gram stains or special stains (fluorescent)
---->purple means gram positive is present
---->pink means gram negative is present
--direct fluorescent antibody assay (DFA)-->not used much anymore because not sensitive and not readily available
35
describe "detection of bacterial antigens" of bacterial defenses
--rapid testing by ELISA, LFA or LA
--LFA and LA are advantageous because relative ease, low cost, and raid turnaround time
36
describe "molecular detection of bacterial DNA or RNA" of bacterial defenses
--can obtain results in few hours with real-time PCR ( most widely known)
--compact hybridization and gene amplification assays (easy to use)
--Nucleic acid-based assays are more sensitive but have limitations:
---->very few FDA approved assays on market for several infectious agent
---->laboratories usually do not approve costs on these
37
describe "serological testing" of bacterial defenses
--detect antibodies to bacterial agents
38
what are some uses of serological testing?
--to detect and confirm infections with no other test available
--to diagnose infection when symptoms are not well known
--current infection indicated by presence of IgM, high IgG titer, or fourfold rise in antibody between acute and convalescent samples
--to determine past exposure to organism with IgM/IgG
--to access reactivation or exposure
39
what are disadvantages of serological testing
--delay between start of infection and production of antibodies
--low antibody production by immunosuppressed patients
40
describe lateral flow immunochromatographic assays
--LFA
--involves movement of a liquid sample containing analyte of interest
--strip passed through various zones containing labeled antibodies specific to analyte
--used to detect bacterial, viral, fungal, or parasitic antigens
--if antigen-antibody complex is present, it is captured by another antibody at the end of the strip, resulting in visible line
41
what is LFA commonly used for?
--to diagnose streptococcal pharyngitis
42
what are common exotoxins produced by GAS and the role they play in contributing to virulence of streptococcus pyogenes?
--streptolyins O (hemolysis)
--deoxyribonucleases B (produced when GAS positive)
--streptokinase (dissolve blood clots)
--NADase (catalyst of hydrolysis)
--pyrogenic exotoxins (activate T cells and stimulate production of inflammatory cytokines
43
Describe rheumatoid fever
--develops 1 to 3 weeks after pharyngitis/tonsillitis in 2-3% of infected individuals
--most likely caused by immune responses to streptococcal antigens that cross-react with human heart tissue
--does not occur because of skin infection
--follows upper respiratory infections
44
what are symptoms of rheumatoid fever?
--fever
--joint pain
--inflammation of heart
45
Describe poststreptococcal glomerulonephritis
--may follow strep infection of skin/pharynx
--deposits of immune responses to streptococcal antigens in glomeruli (stimulate immune inflammatory that damages and impairs kidney)
--renal function usually impaired
46
what are symptoms of poststreptococcal glomerulonephritis?
--hematuria
--proteinuria
--edema
--hypertension
--malaise
--back ache
--abdominal discomfort
--renal function is usually impaired
47
Describe streptococcus pyogenes
--Group A streptococcal or GAS
--primary cause of bacterial pharyngitis and skin infection called impetigo
--untreated can lead to sequelae known as acute glomerulonephritis or rheumatic heart disease
48
what do production of exotoxins contribute to?
--the infections caused by GAS
49
describe Scarlett fever
--occurs in small % of individuals with GAS
--caused by production of erythrogenic exotoxins that may also result in toxic shock syndrome
49
describe Scarlett fever
--occurs in small % of individuals with GAS
--caused by production of erythrogenic exotoxins that may also result in toxic shock syndrome
50
what are laboratory diagnosis's of GAS infection?
--culture and detection of acute infections
--anti-streptolysin O antibody detection of for Sequelae GAS
--anti-DNAsa B antibody detection of sequelae
51
describe streptozyme test
--measures 5 extracellular streptococcal antigens
--positive in majority of patients with acute poststreptococcal glomerulonephritis caused by GAS pharyngitis
52
what are the five extracellular streptococcal antigens detected in a streptozyme test?
--anti-streptolysin (ASO)
--anti-hyaluronidase (AHase)
--anti-streptokinase (ASKase)
--anti-nicotinamide-adenine dinucleotide (anti-NAD)
--anti-DNAse B antibodies
53
describe Helicobacter Pylori`
--leading cause of gastric carcinoma
--produces a large amount of urease that protects the organism from the acidic environment is stomach
54
what is the primary screening method for detecting H. pylori?
---serological testing
--urase can also be used for detection and diagnosis
55
describe mycoplasma pneumoniae
--leading cause of community-acquired pneumonia
--referred to as walking pneumonia
56
M. pneumoniae may result in what clinical manifestations?
--dermatological --causing Stevens-Johnson syndrome and Raynaud syndrome
57
Describe Raynaud syndrome
--manifestation that is observed with M. pneumoniae
--reversible variable vasospasms of the digits in which the fingers turn white when exposed to cold
58
give characteristics of cold agglutinins
--production of cold agglutinins is observed in 50%$ of individuals with M. pneumoniae
--demonstration of cold agglutinins is neither specific nor sensitive when detecting infection by the organism
59
what is the most useful diagnosis assay that most likely indicates recent infection of M. Pneumoniae
--detection of M. pnuemoniae-specific IgM immunoglobulin
60
what are 4 testing methods of M. pneumoniae ?
--culture
--antibodies to M. pneumonia
--cold agglutinins
--molecular methods
61
what is the leading cause of respiratory infections worldwide?
--M. pneumoniae
62
what is the incubation period of M. pneumoniae
1-3 weeks
63
Steven-Johnson not clearly known but may be caused by what?>
--immune response of the host or by augmented sensitivity to antibiotics while being treated for M. pneumoniae
64
what induces production of autoantibodies
M. pneumoniae
65
what is the most widely used assay for M. pneumoniae?
enzyme-linked immunoassays --> can detect IgM and IgG direct against M. pneumoniae
66
what is the primary immunoglobulin in response to infection of M. pneumoniae
IgM, but testing for IgG is required because adults may only elicit IgG response
67
describe methods of molecular diagnosis of M. pneumoniae
--nested multiplex PCR and able to detect 20 respiratory viruses and bacteria.
--illuminagene myoplasmdirect by Merdian Bioscience
---->detect M. pneumoniae in throat swab
----> uses loop-mediated isothermal amplification (LAMP)
68
Describe Rocky Mountain spotted fever
--caused by R rickettsii
--prevalent from may to september
--once introduced, spreads through circulatory and lymphatic system
--invades vascular endothelium by means of OmpA and OmpB ligands
--doxycycline reduces severity of infection
69
what are the 3 species of ticks that transmit RMSF?
--american dog tick
--brown dog tick
--rocky mountain wood tick
70
what are the symptoms of RMSF?
--headache
--nausea
--fever (3 to 5 days after tick bite)
--vomiting
--diarrhea
--skin-rash (3 to 5 days after fever) (on hands and soles of feet)
--death
--symptoms observed occurs 2-14 days (7 day median)after tick bite
71
how to diagnose RMSF?
--clinical presentation
-- serology by IFA (indirectimmunofluorescence assays)
72
what would need to be ruled out to diagnose RMSF?
--typhoid fever
--measles
--rubella
--enteroviral infection
--respiratory tract infection
73
what main event caused by RMSF?
--endothelial cell damage
74
what are symptoms endothelial cell damage?
--hypertension
--hypoalbinismia
--edema (increased vascular permeability)
--hypovolemia
75
how long does a tick need to feed to transmit RMSF?
6-10 hours, the organism is injected into the host from salivary gland
76
describe indigenous microbiota
--varies at different sites of the body
77
how is symbiotic relationship beneficial?
--protecting against infection
--stimulating the immune system
--aiding in digestion of food
--producing various vitamins
78
What do endotoxins induce production of?
—IL-6, IL-8, TNF and PAF
—these cytokines production lead to production of prostaglandins and leukotrienes
79
What do exotoxins induce production of?
Protective antibodiesuse
80
describe treponema pallidum
--causative agent of syphilis
--no reservoir, must multiple within living host
--3 subspecies
--6 to 14 coils
--TROMPS
81
what are the 3 subspecies of T. pallidum
--pertenue- agent of yaws (found in tropics)
--endemicura - cause of nonvenereal endemic syphilis (found in desert regions)
--treponema carateum - agent of pinta (found in central and south america)
82
what is TROMPS
--treponemal rare outer membrane protein
--scarcity of this protein will delay host immune response
82
what is TROMPS
--treponemal rare outer membrane protein
--scarcity of this protein will delay host immune response
83
describe borrelia burgdorferi
--causative agent of Lyme disease
--loosely coiled spirochetes
--outer membrane (consists of glycolipids and proteins) is extremely fluid and loosely associated to organism
--organism divides by binary fission (~12 hours)
84
what is spirochetemia?
spirochetes in blood
85
describe Leptospira
--thin, flexible, tight coiled spirochetes
--pointed ends with bent into a hook shape
--primarily 28-30C
86
what are the two main species in Leptospira?
--Leptospira interrogans (pathogenic saprophytes)
--Leptospira biflexa (enviromental saprophytes)
87
how do you distiguinsh between the 2 subspecies?
serotyping
88
what artificial cultures are used in leptospira
--fletcher semisolid
--ellinghausen-McCollogh-johnson- harris semisolid medium
--stuart liquid medium
